Download Common congenital malformations: Name 7

Common congenital malformations: Name 7 common congenital
malformations
(1) Heart Defects (congenital rubella) (2) Hypospadias (3) Cleft lip with or
without cleft palate (4) congenital hip dislocation (5) spina bifida (6)
anencephaly (7) pyloric stenosis (associated with polyhydramnios &
projectile vomiting)
Common congenital malformations: Name 2 neural tube defects (NTDs)
Spina bifida and anencephaly
Common congenital malformations: Name 2 diagnostic associations with
NTDs during gestation
increased serum and amniotic fluid levels of a-fetoprotein
Common congenital malformations: How can the incidence of NTDs be
reduced?
Folate ingestion during pregnancy
Congenital Heart Disease: What kind of shunts cause early cyanosis?
R-to-L "blue babies"
Congenital Heart Disease: What kind of shunts cause late cyanosis?
L-to-R "blue kids"
Congenital Heart Disease: Name 3 common R-to-L shunts.
The 3 T's: Tetralogy of Fallot (most common cause of early cyanosis),
Transposition of the great vessels, truncus arteriosus
Congenital Heart Disease: What might you see children with a R-to-L shunt
do to relieve discomfort?
Squat to increase venous return
Congenital Heart Disease: Name 3 common L-to-R shunts.
VSD, ASD, PDA
Congenital Heart Disease: Rank them in order of frequency
VSD > ASD > PDA
Congenital Heart Disease: What are the auscultatory signs of an Atrial Septal
Defect?
Loud S1; wide, fixed split S2
Congenital Heart Disease: How do you treat PDA?
Indomethacin
Congenital Heart Disease: Name 3 sequelae of L-to-R shunts.
1) Increased pulmonary resistance due to arteriolar thickening. 2) Progressive
pulmonary HTN 3) R-to-L shunt (Eisenmenger's)
Eisenmenger's Syndrome: What are signs/symptoms of Eisenmenger's?
Late cyanosis, clubbing, polycythemia
Tetrology of Fallot: What is the Tetrology?
(1) Pulmonary Stenosis (2) RVH (3) Overriding aorta (4) VSD (mnemonic:
PROVe)
Tetrology of Fallot: What is the direction of the shunt in the tetralogy?
right-to-left across the VSD
Tetrology of Fallot: What is the x-ray finding on the tetralogy?
Boot-shaped heart due to RVH
Tetrology of Fallot: What is the embryological cause of the tetralogy?
Anterosuperior displacement of the infundibular septum.
Transposition of great vessels: The transposition occurs because of a failure
of the --------------- --------- to -------
failure of the aorticopulmonary septum to spiral
Transposition of great vessels: In transposition of the great vessels, the aorta
leaves ------------ and the pulmonary trunk leaves the ------------
aorta leaves the RV (anterior) and the pulmonary trunk leaves the LV
(posterior)
Transposition of great vessels: How might transposition of the great vessels,
be compatible with life?
If a shunt (e.g. VSD, PDA or patent foramen ovale) exists, blood from the
systemic and pulmonary circulations can mix. Clinicians use PGE to keep
PDA open.
Transposition of great vessels: Transposition of the great vessels is a common
congenital heart disease in offspring of mothers with what disease?
Diabetes
Coarctation of aorta: Where is the aortic stenosis in the infantile type of
coarctation?
Preductal (proximal to insertion of ductus arteriosus) - INfantile (in close to
heart)
Coarctation of aorta: Where is the aortic stenosis in the adult type of
coarctation?
Postductal (distal to ductus arteriosus). - ADult (Distal to Ductus)
Coarctation of aorta: Name 3 symptoms in adult type coarctation?
(1) Notching of the ribs (2) HTN in uper extremities (3) Weak pulses in uper
extremities
Coarctation of aorta: What is the Male-to-Female ratio in coarctation?
3-to-1
Coarctation of aorta: What pulses should you check on physical exam?
Femoral
Patent ductus arteriosus: Which direction is the shunt in a neonate with PDA?
Left-to-right
Patent ductus arteriosus: What change occurs to the heart in PDA?
RVH and failure
Patent ductus arteriosus: What is the auscultatory finding in PDA?
Continuous, "machine-like" murmur.
Patent ductus arteriosus: How is patency maintained in PDA?
prostaglandin (PGE) synthesis and low Oxygen tension.
Patent ductus arteriosus: What drug is used to close a PDA?
Indomethacin
Patent ductus arteriosus: How is a PDA kept open?
porstaglandin--PGE
Patent ductus arteriosus: Why would you want to keep a PDA open?
To sustain life in conditions such as transposition of the great vessels.
Autosomal trisomies: What is the most common chromosomal disorder and
cause of congenital mental retardation?
Down Syndrome (trisomy 21), 1:700
Autosomal trisomies: In Down syndrome, 4% of cases are due to ------translocation, and 1% are due to -------- mosaicism
Robertsonian; Down
Autosomal trisomies: 95% of Down syndrome cases occur because of ----------------- of homologous chromosomes
meiotic nondisjunction
Autosomal trisomies: What is the type and cause of the most common
congenital heart malformation in Down syndrome?
Septum-primum-type ASD due to endocardial cushion defects
Autosomal trisomies: Name 8 findings in trisomy 21
(1) mental retardation (2) flat facial profile (3) prominent epicanthal folds (4)
simian crease (5) duodenal atresia (6) congenital heart disease (7)
Alzheimer's in affected >35 yrs old (8) Increased risk of ALL
Autosomal trisomies: Name a risk factor for Down Syndrome
Advanced maternal age (1:500 < 20 yo; 1:25 > 45 yo)
Autosomal trisomies: What is the name of the syndrome associated with
trisomy 18?
Edwards' syndrome (Election age = 18)
Autosomal trisomies: Name 7 findings in trisomy 18
(1) severe mental retardation (2) rocker bottom feet (3) low-set ears (4)
microngathia (5) congenital heart dz (6) clenched hands (flexion of fingers)
(7) prominent occiput
Autosomal trisomies: What is the life expectancy in trisomy 18?
Death usually w/in 1 year of birth
Autosomal trisomies: What chromosomal anomaly is found in Patau's
syndrome?
trisomy 13 (1:6000)
Autosomal trisomies: Name 7 findings in Patau's
(1) severe mental retardation (2) microphthamlia (3) microcephaly (4) cleft
lip/palate (5) abnormal forebrain structures (6) polydactyly (7) congenital
heart dz
Autosomal trisomies: What is the life expectancy in Patau's?
Death usually w/in 1 year of birth
Genetic gender disorders: What is the chromosomal anomaly in Klinefelter's
syndrome?
XXY (1:850) - male
Genetic gender disorders: Name 5 characteristics of Klinefelter's syndrome
(1) Testicular atrophy (2) Enuchoid body shape (3) Tall, long extremities (4)
Gynecomastia (5) Female hair distribution
Genetic gender disorders: What is a Barr body and is it found kin
Klinefelter's syndrome?
It is the inactivated X chromosome. Yes.
Genetic gender disorders: What is the chromosomal anomaly in Turner's
syndrome?
Female XO; (1:3000)
Genetic gender disorders: Name 4 characteristics of Turner's syndrome
(1) Short stature (2) Ovarian dysgenesis (streak ovary) (3) Webbing of next
(4) Coarctation of the aorta
Genetic gender disorders: Turner's syndrome is the most common cause of
primary ------------
amenorrhea
Genetic gender disorders: Is there a Barr body in Turner's syndrome?
No
Genetic gender disorders: Double Y males have what genotype?
XYY (1:1000) - male
Genetic gender disorders: What is the double Y phenotype?
Normal phenotype, very tall, severe acne, antisocial behavior (seein in 1-2%
of XYY males; seen increasingly among prison inmates)
Muscular dystrophies: How are muscular dystrophies diagnosed?
Elevated CPK and muscle biopsy
Muscular dystrophies: What is the gene involved in muscular dystrophy?
Dystrophin
Muscular dystrophies: What is the mutation in Duchenne's MD?
Frame-shift mutation - deletion of dystrophin gene - accelerated muscle
breakdown.
Muscular dystrophies: What is the age of onset in Duchenne's MD?
Before 5 years
Muscular dystrophies: In what muscles does weakness begin with Duchenne's
MD?
Pelvic girdle muscles and progresses superiorly
Muscular dystrophies: Name 3 diagnostic characteristics of Duchenne MD.
(1) Pseduohypertrophy of calf muscles due to fibrofatty replacement of
muscle (2) Cardiac myopathy (3) Use of Gowers' maneuver, requiring
assistance of uper extremities to stand up - indicates proximal lower limb
weakness
Muscular dystrophies: What distinguishes Becker's from Duchenne's MD?
Less severe mutation in Becker's. Less debilitating.
Pseudohermaphroditism: What is pseudohermaphroditism?
Disagreement between the phenotypic (external genitalia) and gonadal (testes
vs. ovaries) sex.
Pseudohermaphroditism: A female pseudohermaphrodite has ------- present,
but external genitalia are -------- or -----------.
ovaries; virilized or ambiguous
Pseudohermaphroditism: What causes female pseudohermaphroditism?
Excessive and inapropraite exposure to androgenic steroids during early
gestation (i.e.,congenital adrenal hyperplasia or exogenous administration of
androgens suring pregnancy).
Pseudohermaphroditism: What are the phenotypes in female and male
pseudohermaphroditism?
female - XX; male - XY
Pseudohermaphroditism: A male pseudohermaphrodite has ------- present, but
external genitalia are --------- or ---------.
testes; female or ambiguous
Pseudohermaphroditism: What is the most common form of male
pseudohermaphroditism?
Testicular feminization (androgen insensitivity), which results from a
mutation in the androgen receptor gene (x-linked); blind-end vagina
Pseudohermaphroditism: What determines gender identity?
External genitalia and sex of upbringing.
True Hermaphrodite (46,XX or 47, XXY): What is a true hermaphrodite?
Both ovary and testicular tissue present; ambiguous genitalia.
True Hermaphrodite (46,XX or 47, XXY): What are the genotypic
possibilities for a true hermaphrodite?
46,XX or 47,XXY
Testicular Feminization syndrome (46, XY): What is the molecular defect in
testicular feminization syndrome?
Defect in DHT receptor resulting in normal-apearing female
Testicular Feminization syndrome (46, XY): What genitalia are present in
testicular feminization syndrome?
female genitalia with rudimentary vagina; uterus and uterine tubes generally
absent; develop testes (often found in labia majora; surgically removed to
prevent malignancy)
Testicular Feminization syndrome (46, XY): What are the genotype and
horomone levels in testicular feminization syndrome?
46, XY; levels of testosterone, estrogen and LH are all high
5a-reductase deficiency: What is the biochemical consequence of
5a-reductase deficiency
Unable to convert testosterone to DHT.
5a-reductase deficiency: Describe genital development in 5a-reductase
deficiency.
Ambiguous genitalia until puberty, when increased testosterone causes
masculinization of genitalia.
5a-reductase deficiency: What are the hormone levels in 5a-reductase
deficiency.
Testosterone/estrogen levels are normal; LH is normal or elevated.
Cri-du-chat syndrome: What is the mutation in Cri-du-chat syndrome?
Congenital deletion of short arm of chromosome 5 (46,XX or XY, 5p-)
Cri-du-chat syndrome: What are the findings in Cri-du-chat
Microcephaly, severe mental retardation, high-pitched crying/mewing,
epicanthal folds, cardiac abnormalities.
Cri-du-chat syndrome: What does Cri-du-chat mean in english, which might
help remember the symptoms?
Cry of the cat.
Fragile X syndrome: What is the 2nd most common cause of genetic mental
retardation?
Fragile X syndrome
Fragile X syndrome: What genetic change is involved in Fragile X
syndrome?
x-linked defect affecting the methylation and expression of the FMR1 gene.
Fragile X syndrome: Name 4 physical features associated with Fragile X
syndrome?
(1) macro-orchidism (enlarged testes) (2) Long face with a large jaw (3) large
everted ears (4) autism
Cystic Fibrosis (CF): What is the genetic defect in cystic fibrosis?
Autosomal-recessive defect in CFTR gene on chromosome 7
Cystic Fibrosis (CF): What is the molecular defect in CF?
Defective Cl- channel
Cystic Fibrosis (CF): What are the consequences of the defect in CF?
The defective chloride channel causes secretion of abnormally thick mucus
that plugs lungs, pancreas and liver, which leads to recurrent pulmonary
infections (pseudomonas species and S. aureus), chronic bronchitis,
bronchiectasis, pancreatic insufficiency (malabsorption and steatorrhea),
meconium ileus in newborns.
Cystic Fibrosis (CF): Name a diagnostic test for CF.
Increased concentration of Cl- ions in sweat test.
Cystic Fibrosis (CF): Why does CF cause infertility in males?
Absent vas deferens.
Cystic Fibrosis (CF): What vitamins are often deficient in CF?
Fat-soluble - A,D,E,K
Most common lethal genetic disease of Caucasians.
Cystic Fibrosis
Cystic Fibrosis (CF): What is the treatment for CF?
N-acetylcysteine to loosen mucous plugs.
Autosomal-dominant diseases: A patient presents with flank pain, hematuria,
hypertension, progressive renal failure and has a mutation in one of his copies
of APKD1 (chromosome 16); what is the diagnosis?
Adult polycystic kidney disease. N.B. the juvenile form is recessive.
Autosomal-dominant diseases: Name 2 other characteristics of adult
polycystic kidney disease.
(1) always bilateral, (2) massive enlargement of the kidneys due to multiple
large cysts.
Autosomal-dominant diseases: What sequelae are associated with adult
polycystic kidney disease?
(1) polycystic liver disease (2) berry aneurysms (3) mitral valve prolapse
Autosomal-dominant diseases: What disease involves elevated LDL owing to
defective or absent LDL receptor?
Familial hypercholesterolemia (type IIA)
Autosomal-dominant diseases: What are the average cholesterol levels in
heterozygotes and homozygotes with familial hypercholesterolemia (tyype
IIA)?
heterozygotes (1:500) - 300 mg/dL homozygotes - 700+ mg/dL
Autosomal-dominant diseases: What are 3 sequelae of familial
hypercholesterolemia (type IIA)?
(1) severe atherosclerotic disease early in life (2) tendon xanthomas
(classically in the Achilles tendon) (3) MI may develop before age 20
Autosomal-dominant diseases: What is the genetic defect in Marfan's
syndrome?
Fibrillin gene mutation leads to connective tissue disorders.
Autosomal-dominant diseases: What are the skeletal abnormalities in
Marfan's?
tall with long exteremities, hyperextensive joints, and long, tapering fingers
and toes.
Autosomal-dominant diseases: What are the cardiovascular risks in Marfan's?
cystic medial necrosis of aorta leads to aortic incompetence and dissecting
aortic aneurysms; flopy mitral valve.
Autosomal-dominant diseases: What are the ocular risks in Marfan's?
Subluxation of lenses.
Autosomal-dominant diseases: What is another name for Neurofibromatosis
type 1?
von Recklinghausen's disease
Autosomal-dominant diseases: What chromosome is affected in NF type 1?
Long arm of chromosome 17 (17 letters in von Recklinghasen's)
Autosomal-dominant diseases: What are 5 classic characteristics of people
with NF type 1?
(1) café-au-lait spots (2) neural tumors (3) Lisch nodules (pigmented iris
hamartomas) (4) skeletal disorders (e.g., scoliosis) (5) Increased tumor
susceptibility
Autosomal-dominant diseases: What disease is associated with bilateral
acoustic neuroma?
Neurofibromatosis type 2
Autosomal-dominant diseases: What gene is affected in neurofibromatosis
type 2?
NF2 gene on chromosome 22; (type 2 = 22)
Autosomal-dominant diseases: What is the genetic mutation in
Von-Hippel-Lindau disease?
Deletion of VHL gene (tumor supressor) on chromosome 3p. (Von
Hipel-Lindau = 3 words for chromosome 3)
Autosomal-dominant diseases: What are the clinical findings in
Von-Hippel-Lindau disease?
hemiangioblastomas of retina/cerebellum/medulla; about half of affected
individuals develop multiple bilateral renal cell carcinomas and other tumors.
Autosomal-dominant diseases: What is the diagnosis in a 20-50 year old
person who presents with depression, progressive dementia, choreiform
movements, caudate atrophy, and decreased levels of GABA and Ach in the
brain?
Huntington's disease
Autosomal-dominant diseases: What chromosome holds the gene involved in
Huntington's?
Chromosome 4; triplet repeat disorder ("Hunting 4 food")
Autosomal-dominant diseases: What disease is responsible for a colon that
ecomes covered with adenomatous polyps after puberty?
Familial adenomatous polyposis (FAP)
Autosomal-dominant diseases: What is the progression in Familial
adenomatous polyposis if colon not resected?
Colon cancer
Autosomal-dominant diseases: What is the genetic defect in Familial
adenomatous polyposise?
deletion on chromosome 5 - 5 letters in polyp
Autosomal-dominant diseases: What are 3 characteristics of hereditary
spherocytosis?
(1) spheroid erythrocytes (2) hemolytic anemia (3) increased MCHC
Autosomal-dominant diseases: What is the cure for hereditary spherocytosis?
splenectomy
Autosomal-dominant diseases: What is the genetic defect in achondroplasia?
Autosomal dominant cell-signaling defect of fibroblast growth factor (FGF)
receptor 3.
Autosomal-dominant diseases: What are the physical characteristics of
achondroplasia?
Dwarfism, short limbs, but head and trunk are normal size.
X-linked or AR:: Cystic fibrosis
AR
X-linked or AR:: albinism
AR
X-linked or AR:: Fragile X
X-linked
X-linked or AR:: Duchenne's muscular dystrophy
X-linked
X-linked or AR:: hemophilia A and B
X-linked
X-linked or AR:: a1-antitrypsin deficiency
AR
X-linked or AR:: Fabry's
X-linked
X-linked or AR:: G6PD deficiency
X-linked
X-linked or AR:: Hunter's syndrome
X-linked
X-linked or AR:: Phenylketonuria (PKU)
AR
X-linked or AR:: thalassemias
AR
X-linked or AR:: sickle cell anemias
AR
X-linked or AR:: ocular albinism
X-linked
X-linked or AR:: glycogen storage diseases
AR
X-linked or AR:: mucopolysaccharidoses (except Hunter's)
AR
X-linked or AR:: sphingolipidoses (except Fabry's)
AR
X-linked or AR:: infant polycystic kidney
AR
X-linked or AR:: Lesch-Nyhan syndrome
X-linked
X-linked or AR:: Bruton's agammaglobulinemia
X-linked
X-linked or AR:: hemochromatosis
AR
X-linked or AR:: Wiskott-Aldrich syndrome
X-linked
X-linked or AR:: What are femal carriers of x-linked recessive disorders
rarely affected?
Inactivation of X chromosomes in each cell
Neural Tube Defects (NTD): Name two associations with neural tube defects
during pregnancy.
(1) Low folic acid intake (2) Elevated a-fetoprotein in amniotic fluid
Neural Tube Defects (NTD): What NTD is associated with failure of bony
spinal canal to close, but no structural herniation?
Spina bifida occulta
Neural Tube Defects (NTD): Which NTD is involved with herniation of
meninges through spinal canal defect?
Meningocele
Neural Tube Defects (NTD): What is the NTD that involves herniation of
meninges AND spinal cord through spinal canal defect?
Meningomyelocele
Neural Tube Defects (NTD): Which NTD is usually seen at lower vertebral
levels?
Spina bifida occulta
Neural Tube Defects (NTD): Take a look at the figures in the book for good
visualization of the NTDs.
0
Fetal Alcohol Syndrome: Who is at greatest risk of FAS?
Newborns of mothers who consumed significant amounts of alcohol
(teratogen) during pregnancy (highest risk at 3-8 weeks).
Fetal Alcohol Syndrome: Name 5 congenital abnormalities in FAS?
(1) pre and postnatal developmental retardation (2) microcephaly (3) facial
abnormalities (4) limb dislocation (5) heart and lung fistulas
Fetal Alcohol Syndrome: How does FAS rank among congenital
malformations in the U.S.?
It's number 1
Fetal Alcohol Syndrome: What is the presumed mechanism of FAS?
Inhibition of cell migration?
Fetal Alcohol Syndrome: AUTHOR
Neha Pathak
NEOPLASTIC PROGRESSION: when cells increase in number it is called?
hyperplasia
NEOPLASTIC PROGRESSION: what are two enzymes that allow neoplastic
cells to invade th ebasement membrane?
collagenase and hydrolase
NEOPLASTIC PROGRESSION: when cells have an increased nulear to
cytoplasmic ratio but have not invaded the basement membrane, it is called?
carcinoma in situ
_ -PLASIA DEFINITIONS: squamous _________ occurs in the trachea and
bronchi of smokers
metaplasia
_ -PLASIA DEFINITIONS: what is it called when a cell has reversible
preneoplastic changes with abnormal shape and size?
dysplasia
_ -PLASIA DEFINITIONS: abnormal cells that lack differentiation are
called?
anaplastic cells
TUMOR STAGE VS. GRADE: staging of a tumor takes into account what
factors?
TMN size of tumor, node involvment, metastases
TUMOR STAGE VS. GRADE: histolgy of a tumor is used to determine?
grade
TUMOR STAGE VS. GRADE: what has more prognostic value? Grade or
stage?
stage
TUMOR NOMENCLATURE: the term _________ implies epithelial origin,
whereas _________ implies mesenchymal origin
carcinoma, sarcoma
TUMOR NOMENCLATURE: a tumor of blood vessels is called what when
it is benign? When it is malignant?
hemangioma, angiosarcoma
TUMOR NOMENCLATURE: what is a benign tumor of skeletal muscle
called?
rhabdomyoma
DISEASES ASSOCIATED WITH NEOPLASMS: Kaposi's sarcoma and
aggressive malignant lymphomas are associated with what disease
AIDS
DISEASES ASSOCIATED WITH NEOPLASMS: Actinic Keratosis
predispose to what disease?
squamous cell carcinoma of skin
DISEASES ASSOCIATED WITH NEOPLASMS: down syndrome is
associated with what neoplasm?
ALL
ONCOGENES: c-myc oncogenes are associated with what neoplasm?
burkitt's lymphoma
ONCOGENES: breast, ovarian, and gastic carcinomas all have this oncogene
mutation in common?
erb B2
ONCOGENES: MEN II and III are associated with what oncogenic
mutation?
ret
TUMOR SUPRESSOR GENES: Name the associated tumor witht the
following tumor supressor gene mutations: Rb, APC, WT1
retinoma blastoma, colorectal cancer, wilms tumor
TUMOR SUPRESSOR GENES: p53 is on what chromosome
17p
TUMOR SUPRESSOR GENES: osteosarcoma is associated with what tumor
supressor gene mutation
Rb
TUMOR MARKERS: TRAP is a tumor marker for what neoplasm
hairy cell leukemia
TUMOR MARKERS: what tumor marker is elevated in hyatidiform moles
beta-HCG
TUMOR MARKERS: ovarian tumors are associated with what tumor marker
CA-125
ONCOGENIC VIRUSES: the virus associated with burkitts and
nasopharyngeal cancer is?
ebv
ONCOGENIC VIRUSES: hpv is responsible for what cancers?
cervical, penile, and anal carcinoma
ONCOGENIC VIRUSES: what virus is responsible for kaposis sarcoma?
hhv8
CHEMICAL CARCINOGENS: aflatoxin, vinyl chloride and ccl4 damage
what organ?
liver
CHEMICAL CARCINOGENS: nitrosamines cause cancer in what organs?
esophagus or stomach
CHEMICAL CARCINOGENS: asbestos causes what types of cancer?
bronchogenic and mesothelioma
LOCAL EFFECTS OF TUMORS: When the following are obstructed, what
can occur: bronchus? Biliary tree? Left colon?
pneumonia, jaundice, constipation
LOCAL EFFECTS OF TUMORS: tumor mass in the brain can cause the
following
seizure, increased intracranial pressure, mass effect and herniation
LOCAL EFFECTS OF TUMORS: compression of the recurrent laryngeal
nerve can cause what?
hoarseness
PROSTATIC ADENOCARCINOMA: what lobe/zone is most often involved
in prostatic cancer?
posterior lobe, peripheral zone
PROSTATIC ADENOCARCINOMA: what is a common site of metastases
for prostate cancer?
bone
PROSTATIC ADENOCARCINOMA: what are useful tumor markers for
prostate CA
psa, and prostatic acid phosphatase
SKIN CANCER: this type of skin cancer has palisading nuclei
basal cell carcinoma
SKIN CANCER: dyplastic nevi are a precursor fot this type of cancer
melanoma
SKIN CANCER: this type of skin cancer is associated with keratin pearls
squamous cell carcinoma of skin
PRIMARY BONE TUMORS: the translocation 11;22 is associated with this
cancer of the bone that occurs most commonly in young boys
ewing's sarcoma
PRIMARY BONE TUMORS: this tumor is characterized by a "double
bubble" or "soap bubble" appearance
benign giant cell tumor
PRIMARY BONE TUMORS: this is the most common benign bone tumor,
usually in men younger than 25, with a rare transformation to malignancy
osteochondroma
PRIMARY BONE TUMORS: AUTHOR
Gabe Pitta
Primary Brain Tumors-Adult peak incidence: Most common adult brain
tumor?
Glioblastoma multiforme (grade IV astrocytoma) See pseudopalisading tumor
cells, central necrosis and hemorrhage.
Primary Brain Tumors-Adult peak incidence: Second most common adult
tumor?
Meningioma, occurring in convexities of hemispheres and parasagittal region.
See psammoma bodies.
Primary Brain Tumors-Adult peak incidence: Benign, slow-growing tumor in
frontal lobes?
Oligodendroglioma, look for fried egg apearance, often calcified.
Primary Brain Tumors-Adult peak incidence: Third most common tumor,
often localized to CN8?
Schwannoma, see it in acoustic Schwannoma. Antoni A (compact) and
Antoni B (loose) patterns.
Primary Brain Tumors-Adult peak incidence: Most common forms are
prolactin-secreting?
Pituitary Adenoma, which derives from Rathke's Pouch and can produce
secondary bitemporal hemianopsia and hypopituitarism
Primary Brain Tumors-Child Peak Incidence: Highly malignant cerebellar
tumor?
Medulloblastoma, can compress 4th ventricle and cause hydrocephalus. See
rosettes or pseudorosettes.
Primary Brain Tumors-Child Peak Incidence: Cerebellar tumor associated
with von Hippel-Landau syndrome?
Hemangioblastoma, see foamy cells and high vascularity, can produce excess
EPO-->polycythemia.
Primary Brain Tumors-Child Peak Incidence: Commonly found in fourth
ventricle, causing hydrocephalus?
Ependyomomas, which have perivascular rosettes and rod-shaped
blepharoblasts near nucleus on exam.
Primary Brain Tumors-Child Peak Incidence: Diffusely infiltrating glioma,
usually found in posterior fossa?
Low-grade Astrocytoma
Primary Brain Tumors-Child Peak Incidence: Benign tumor often confused
with pituitary adenoma?
Craniopharyngioma, which also is derived from Rathke's pouch, also presents
with bitemporal hemianopsia, also calcified.
Common sites that receive metastatic tissue: To Brain?
Lung, Breast, Skin (melanoma), Kidney (renal cell carcinoma), GI. Lots of
Bad Stuff Kills Glia. 50% of brain tumors are due to metastases.
Common sites that receive metastatic tissue: To liver?
Colon>Stomach>Pancreas>Breast>Lung. Cancer Sometimes Penetrates
Benign Liver. Metastases much more common than primary liver tumors.
Common sites that receive metastatic tissue: To bone?
Breast, lung, thyroid, testes, kidney, prostate.=> "BLT with a Kosher Pickle."
Common sites that receive metastatic tissue: Most common organ receiving
metastases?
Adrenal medulla, then cortex.
Common sites that receive metastatic tissue: Most common organ sending
metastases?
Lung>Breast/Stomach
Paraneoplastic effects of tumors: Cushing's Syndrome
ACTH/ACTH-like peptide from small-cell lung CA
Paraneoplastic effects of tumors: SIADH
ADH/ANP from small cell lung CA and intracranial neoplasms.
Paraneoplastic effects of tumors: Hypercalcemia
PTH-related peptide/TGF-alpha/TNF-Alpha/IL-2 from squamous cell lung
CA, renal cell CA, Breast CA, multiple myeloma, bone metastasis.
Paraneoplastic effects of tumors: Polycythemia
EPO from renal cell CA.
Paraneoplastic effects of tumors: Lambert-Eaton Syndrome
Antibodies against presynaptic Ca2+ channels at NMJ, generated by
Thymomas and bronchogenic CA.
Paraneoplastic effects of tumors: Gout
Hyperuricemia due to excess nucleic acid turnover, found in various
neoplasms.
Cancer Epidemiology: Male incidence?
Prostate(32%)>Lung(16%)>Colon and Rectum (12%)
Cancer Epidemiology: Male Mortality?
Lung(33%)>Prostate(13%)
Cancer Epidemiology: Female incidence?
Breast (32%)>Lung(13%)>Colorectal(13%)
Cancer Epidemiology: Female Mortality?
Lung(23%)>Breast(18%)
HEMATOLOGIC PATHOLOGY: Anemia
0
HEMATOLOGIC PATHOLOGY: Anemia presenting with increased TIBC,
decreased ferritin, decreased serum iron.
Mycrocytic, Hypochromic, usually secondary to iron deficiency. Also seen
with Thalassemia, lead poisoning
HEMATOLOGIC PATHOLOGY: Anemia in patients with B12/Folate
deficiency
HEMATOLOGIC PATHOLOGY: Anemia in patients with normocytic,
normochromic smears?
Macrocytic (MCV>100), presents with PMN hypersegmentation on blood
smear. B12 deficiency presents with neuro effects, folate deficiency much
easily reached through bad diet. Also seen in patients taking drugs blocking
DNA synthesis (sulfa drugs, AZT)
Hemorrhagic, autoimmune hemolytic, enzyme defects (G6PD), bone marrow
dz, anemia of chronic dz. Decreased serum haptoglobin and increased LDH
indicate RBC hemolysis. Direct Coomb's test can show an immune-mediated
process.
HEMATOLOGIC PATHOLOGY: Anemia in patients with a decreased
TIBC, decreased serum iron, and decreased iron saturation?
Anemia of chronic disease
HEMATOLOGIC PATHOLOGY: Anemia in patients with an increased
TIBC, decreased serum iron, and normal iron saturation?
Iron-deficiency anemia.
HEMATOLOGIC PATHOLOGY: Patient with normal TIBC, increased
serum iron, and 100% iron saturation (normal is 20-50%)
Iron overload (hemosiderosis)
Aplastic Anemia: Patient presentation of Aplastic Anemia?
Patients with pancytopenia characterized by severe anemia, neutropenia, and
thrombocytopenia caused by failure or destruction of multipotent myeloid
stem cells.
Aplastic Anemia: What causes aplastic anemia?
Radiation, benzene, chloramphenicol, alkylating agents, antimetabolites, viral
agents, Fanconi's anemia, idiopathic causes.
Aplastic Anemia: Common Sx?
Fatigue, malaise, pallor, purpura, mucosal bleeding, petechiae, infection.
Aplastic Anemia: How do the blood smear and bone marrow aspirate appear?
Blood smear: pancytopenia with normal cell morphology.
Aspirate:hypocellular marrow with fatty infiltration.
Aplastic Anemia: What's the treatment of aplastic anemia?
Withdraw offending agent, BMT, RBC/platelet transfusion, G-CSF or
GM-CSF.
Hereditary Spherocytosis: How do patients with hereditary psherocytosis
present (smear and labs)?
Smear shows microcytic RBCs that are small and round with no central
pallor. The patients will have normal Hgb and MCV.
Hereditary Spherocytosis: What's the cause of hereditary spherocytosis?
Intravascular hemolysis due to spectrin defect.
Hereditary Spherocytosis: How is it confirmed and tested?
Will be Coombs' negative (unlike warm antibody hemolysis), can perform
osmotic fragility test.
Hereditary Spherocytosis: What are some associated diseases?
Gallstones, splenomegaly, anemia, and jaundice.
Blood Dyscrasias-Sickle Cell Anemia: What is the HbS mutation?
Glutamate-->Valine in a Beta chain. Heterozygotes are usually
malaria-resistant. *% of Af-Ams carry the HbS trait, 0.2% have the disease.
Blood Dyscrasias-Sickle Cell Anemia: What can precipitate sickling?
Low O2, dehydration.
Blood Dyscrasias-Sickle Cell Anemia: What are the common complications
of HbS homozygotes?
aplastic crises from parvovirus infection, autosplenectomy, risk of
encapsulated organism infection, salmonella osteomyelitis, vaso-occlusive
pain crises, and splenic sequestration crises.
Blood Dyscrasias-Sickle Cell Anemia: What is the HbC defect?
Different Beta-chain mutation, the patients with HbC or HbSC have milder
dz than HbSS patients.
Blood Dyscrasias-Sickle Cell Anemia: What are the treatment options?
Hydroxyurea (increased HbF) and bone marrow transplantation.
Blood Dyscrasias-Alpha-Thalassemia: What populations have the most
prevalence?
Mediterranean populations. (thalaSEAmia)
Blood Dyscrasias-Alpha-Thalassemia: What is the etiology?
Underproduction of the alpha-globin chain, with no compensatory increase of
any other chains. HbH has Beta-4 tetramers and lacks 3 alpha-globin genes.
Blood Dyscrasias-Alpha-Thalassemia: What is the presentation of a patient
lacking all four alpha-globin genes?
hydrops fetalis and intrauterine fetal death.
Blood Dyscrasias-Beta-Thalassemia: Patient Presentation of
Beta-Thalassemia major?
severe anemia requiring blood transfusion. Cardiac failure is often due to
secondary hemochromatosis.
Blood Dyscrasias-Beta-Thalassemia: Etiology of Beta-Thalassemia major?
Beta chain is absent, fetal Hgb production is compensatorily increased but is
inadequate.
Blood Dyscrasias-Beta-Thalassemia: Etiology of Beta-thalassemia minor?
The Beta chain is underproduced, again see fetal HgB compensatory increase.
HbS/Beta-thalassemia heterozygote has mild to moderate disease.
DIC: What is the definition of DIC?
Activation of the coagulation cascade leading to microthrombi and global
consumption of platelets, fibrin, and coagulation factors.
DIC: What causes DIC?
Obstetric complications (most common cause), gram-negative sepsis,
transfusion, trauma, malignancy, acute pancreatitis, nephrotic syndrome.
DIC: What are the lab findings in DIC?
Increased PT, increased PTT, incrased fibrin split products (D-dimers),
decreased platelet count.
Bleeding Disorders: What disorder type presents with mucous membrane
bleeding, petechiae, purpura, and prolonged bleeding time?
Platelet abnormalities (microhemorrhages), which can be caused by ITP
(antiplatelet antibodies and increased megakaryocytes), TTP (schistocytes),
drugs, and DIC (increased fibrin split products).
Bleeding Disorders: What disorder type presents with hemarthroses (bleeding
into joints), easy brusing, prolonged PT and/or PTT?
Coagulopathies (macrohemorrhages), which can be caused by Hemophilia
A/B and von Willebrand's disease (most common)
Bleeding Disorders: What is the deficiency in Hemophilia A?
Factor VIII
Bleeding Disorders: What is the deficiency in Hemophilia B?
Factor IX
Bleeding Disorders: What is the deficiency in vW dz?
Deficiency of von Willebrand's antigen.
Bleeding Disorders: Which factors does the PT measure?
Extrinsic: Factors II, V, VII, and X.
Bleeding Disorders: Which factors does the PTT measure?
Intrinsic: All factors except VII and XIII.
Hemorrhagic disorders: What presents with increased bleeding time, normal
platelet count, and normal PT/PTT and platelet count?
Qualitative platelet defects, can be Bernard Soulier disease (defect in
adhesion) or Glanzmann's thrombasthenia (defect in aggregation). Can also
see these labs in vascular bleeding.
Hemorrhagic disorders: What presents with decreased platelet count,
increased bleeding time, and normal PT/PTT?
Thrombocytopenia
Hemorrhagic disorders: Which diseases present with increased PTT and
normal PT, platelet count, and bleeding time?
Hemophilia A and B
Hemorrhagic disorders: What presents with a high PTT, normal PT, normal
platelets, and increased bleeding time?
vW disease
Hemorrhagic disorders: What presents with increased Bleeding time/Pt/PTT
and decreased platelet count?
DIC
Lymphomas: Hodgkin's Versus NHL: Which one presents with
Reed-Sternberg cells?
Hodgkin's
Lymphomas: Hodgkin's Versus NHL: Which one is associated with HIV and
immunosuppression?
NHL
Lymphomas: Hodgkin's Versus NHL: Which one involves multiple,
peripheral nodes, with common extranodal involvement?
NHL
Lymphomas: Hodgkin's Versus NHL: Which one is localized to a single
group of nodes, with contiguous spread and rare extranodal involvement?
HL
Lymphomas: Hodgkin's Versus NHL: Which one presents with constitutional
signs/symptoms: low-grade fever, night sweats, weight loss?
HL (NHL has few signs/symptoms)
Lymphomas: Hodgkin's Versus NHL: Which one presents with mediastinal
lymphadenopathy?
HL
Lymphomas: Hodgkin's Versus NHL: Which one involves mostly the B cells
(except lymphoblastic origin)?
NHL
Lymphomas: Hodgkin's Versus NHL: Which one has
hypergammaglobulinemia?
neither. Multiple Myeloma has hypergammaglobulinemia, where the excess
B cells are in the resting state.
Lymphomas: Hodgkin's Versus NHL: Which one has a 50% association with
EBV?
HL
Lymphomas: Hodgkin's Versus NHL: Which one has bimodal age
distribution?
HL (NHL has peak incidence at 20-40 years old)
Lymphomas: Hodgkin's Versus NHL: Which one has more common male
presentation?
HL
Hodgkin's: What factors denote a good prognosis?
Increased lymphocytes, decreased RS cells.
Hodgkin's: Which HL type has the best prognosis?
Nodular sclerosing (65-75%), which has least RS cells and lots of
lymphocytes. Lymphocyte-predominant LH also has excellent prognosis.
Hodgkin's: Which HL type is the most common?
Nodular sclerosing, affecting women more than men and primarily young
adults.
Hodgkin's: What is the prognosis of mixed cellular HL?
Intermediate. There are lots of lymphocytes but also lots of RS cells.
Hodgkin's: Which HL type has the worst prognosis?
Lymphocyte-depleted, which affects older males with disseminated disease.
Hodgkin's: Which HL type has the most RS cells?
Mixed cellular.
NHL: Which NHL type has only B cells?
Small Lymphocytic lymphoma, follicular lymphoma, Burkitt's
NHL: Which NHL type has a mix of B cells and T cells?
Diffuse large cell , occurring mostly in elderly but sometimes in children.
NHL: Which NHL type has only T cells?
Lymphoblastic Lymphoma, which has immature T cells. It is a very
aggressive T-cell lymphoma.
NHL: Which type is associated with a t(8;14) c-myc gene mutation?
Burkitt's Lymphoma, occurring mostly in children. Has a high-grade "starry
sky" apearance.
NHL: Which type is associated with a t(14;18) mutation and overexpression
of bcl-2?
Follicular lymphoma, which is difficult to cure but has an indolent course.
NHL: Which type is associated with EBV infection and is endemic in africa?
Burkitt's
NHL: Which is the most common childhood NHL?
Lymphoblastic Lymphoma, which also presents with ALL and a mediastinal
mass.
NHL: Which is the most common adult version of NHL?
Follicular lymphoma.
NHL: Which types occur in adults?
Small lymphocytic lymphoma, follicular lymphoma.
NHL: Which types occur in children?
Lymphoblastic lymphoma, Burkitt's lymphoma.
NHL: Which one has a distribution of 80% adults and 20% children?
Diffuse large cell lymphoma, which ALSO has an 80% B cells 20% T cell
distribution.
NHL: Which low-grade NHL type presents like CLL?
Small Lymphocytic lymphoma.
NHL: AUTHOR
John Peoples
Leukemias: Peripheral and bone marrow characteristics
Increased circulating leukocytes, bone marrow infiltrates of leukemic cells
Leukemias: Consequences of marrrow failure
Anemia (dec. RBC's), infections (dec. WBC's), hemorrhage (dec. platelets)
Leukemias: Common organs of infiltration
Liver, spleen, lymph nodes
Leukemias: Characteristics of acute leukemias
Blasts predominate, children or elderly, short or drastic course
Leukemias: ALL characteristics (4)
Lympholasts (pre-B or pre-T), children, most responsive to therapy,
associated with Down's Syndrome
Leukemias: AML characteristics
Myeloblasts, adults, auer rods
Leukemias: Characteristics of chronic leukemias
More mature cells, midlife age range, longer, less devastating course
Leukemias: CLL characteristics - cells
Lymphocytes, non-Ab producing B cells, increased smudge cells on
peripheral blood smear
Leukemias: CLL - population
older adults
Leukemias: CLL - presentation and course
lymphadenopathy, hepatosplenomegaly, few sx., indolent course
Leukemias: CLL is similar to?
very similar to SLL (small lymphocytic lymphoma)
Leukemias: CLL is associated with what type of anemia?
warm antibody autoimmune hemolytic anemia
Leukemias: CML cell characteristics
Myeloid stem cells, increased neutrophils and metamyelocytes
Leukemias: CML translocation?
Ph Chromosome, t(9;22), bcr-abl
Leukemias: CML acute complications?
blast crisis (AML)
Chromosomal translocations - the following disorder is associated with what
translocation?: CML
Ph chromosome, t(9;22), bcr-abl
Chromosomal translocations - the following disorder is associated with what
translocation?: Burkitt's lymphoma
t(8;14), c-myc activation
Chromosomal translocations - the following disorder is associated with what
translocation?: Follicular lymphomas
t(14;18), bcl-2 activation
Chromosomal translocations - the following disorder is associated with what
translocation?: AML- M3 type
t(15;17), responsive to all-trans retinoic acid (ATRA)
Chromosomal translocations - the following disorder is associated with what
translocation?: Ewing's sarcoma
t(11;22)
Chromosomal translocations - the following disorder is associated with what
translocation?: Mantle cell lymphoma
t(11;14)
Lymphomas and Leukemias: What are the chronic leukemias associated with
T-lymphoblasts?
Sezary Syndrome, CLL-T (both L2)
Lymphomas and Leukemias: What are the acute leukemias associated with
T-lymphoblasts?
ALL-T (L2), ALL-null (L1), ALL-common(L1)
Lymphomas and Leukemias: What are the chronic leukemias associated with
B-lymphoblasts?
CLL-B (L3)
Lymphomas and Leukemias: What are the acute leukemias associated with
B-lymphoblasts?
ALL-B (L3)
Lymphomas and Leukemias: What are the chronic leukemias associated with
monoblasts?
Chonic monocytic (M5), chronic myelomonocytic (M4)
Lymphomas and Leukemias: What are the acute leukemias associated with
monoblasts?
Acute monocytic (M5), acute myelomonocytic (M5)
Lymphomas and Leukemias: What are the chronic leukemias associated with
myeloblasts?
CML (M1, 2 and 3), Polycythemia rubra vera (M1), myelofibrosis (M1)
Lymphomas and Leukemias: What are the acute leukemias associated with
myeloblasts?
AML (M2 and M1), Promyelocytic (M1)
Lymphomas and Leukemias: What are the chronic leukemias associated with
eos-myeloblasts?
Eosinophilic (rare)
Lymphomas and Leukemias: What are the chronic leukemias associated with
normoblasts?
Chronic erythroid (M6, rare)
Lymphomas and Leukemias: What are the acute leukemias associated with
normoblasts?
acute erythroleukemia (M6)
Lymphomas and Leukemias: What are the chronic leukemias associated with
megakaryoblasts?
Idiopathic thrombocytopenia (M7)
Lymphomas and Leukemias: What are the acute leukemias associated wwith
megakaryoblasts?
acute megakaryocytic leukemias (M7)
Multiple Myeloma: What type of cell proliferates in MM, and what is its
histologic appearance
Monoclonal plasma cell, fried egg apearance
Multiple Myeloma: Where does MM arise?
bone marrow
Multiple Myeloma: The 2 most common ab's, in order, are:
IgG (55%), IgA (25%)
Multiple Myeloma: Common symptoms are:
lytic bone lesions and hypercalcemia, renal insifficiency, increased
suscpetibility to infection, anemia
Multiple Myeloma: This disease is associated with:
primary amyloidosis
Multiple Myeloma: Ig light chains are also called:
Bence Jones proteins
Multiple Myeloma: 3 key diagnostic features:
lytic bone lesions on x-ray, M-spike on serum protein electrophoresis,
Bence-Jones proteins in urine
Multiple Myeloma: Red blood cell appearance on peripheral smear:
Rouleaux formation (poker chips)
Multiple Myeloma: What 2 differences are seen in Waldenstrom's
macroglobulinemia?
M-spike is IgM, no lytic lesions
Achalasia: Achalasia results from:
failure of relaxation of lower esophogeal sphincter due to loss of the
myenteric plexus (Aeurbach's). [A-chalasia = absence of relaxation]
Achalasia: Achalasia causes:
progressive dysphagia
Achalasia: Diagnosis is made by:
barium swallow showing "bird beak" dilated esophagus with distal stenosis.
Achalasia: Secondary achalasia may result from this protozoan disease:
Chagas disease (treponema cruzi)
Achalasia: Associated with increased risk of:
esophageal carcinoma
Barrett's esophagus: The distal esophageal colummnar epithelium is replaced
with….
Gastric columnar epithelium
Barrett's esophagus: Barrett's results from:
Reflux
Barrett's esophagus: Barrett's can progress to:
adenocarcinoma
Esophageal Cancer: Risk factors are (ABCDEF):
achalasia, barrett's esophagus, corrosive esophagitis/cigarettes, diverticuli
(e.g. zenker's), esophogeal web/EtOH, familial
Esophageal Cancer: The most common esophageal cancer in the world is:
squamous cell carcinoma
Esophageal Cancer: The most common esophageal cancer in the US is:
equal between squamous cell and adenocarcinoma (decreased cigarette use).
Esophageal Cancer: Esophageal Adenocarcinoma is found where?
lower third
Esophageal Cancer: Esophageal squamous cell carcinoma is found where?
uper 2/3
Congenital Pyloric Stenosis: What does this cause in infant?
Projectile vomiting at aproximately 2 weeks of age
Congenital Pyloric Stenosis: Treatment entails:
surgery
Malabsorption syndromes: Autoantibodies are seen to what in Celiac Sprue?
Gluten (gliaden) in wheat and other grains
Malabsorption syndromes: The histologic appearance of celiac sprue:
villous flattening, lymphocytic infiltrate
Malabsorption syndromes: Tropical sprue is due to what type of agent?
Infectious, treated with Antibiotics
Malabsorption syndromes: What are you infected with if you have Whipple's
Disease?
Tropheryma whipelli
Malabsorption syndromes: Histologic cell type seen in Whipple's disease:
PAS+ macrophages
Malabsorption syndromes: What is the most common disaccharide deficiency
leading to malabsorption?
lactase => milk intolerance
Chronic Gastritis: Fundal gastritis (type A) is characterized by 4 A's, what are
they?
Autoimmune disorder with Autoantibodies to parietal cells, pernicious
Anemia, Achlorydia
Chronic Gastritis: Antral gastritis (Type B) is caused by:
a Bug, H. Pylori infection
Chronic Gastritis: Both forms of gastritis carry an increased risk of what?
Gastric carinoma
Peptic Ulcer Disease: 2 etiologic agents underlying gastric ulcers are:
H. pylori (70%) and NSAID's
Peptic Ulcer Disease: Degeneration of what leads to gastric ulcers?
Gastric mucosal protection v. gastric acid
Peptic Ulcer Disease: Does the pain of a gastric ulcer increase or decrease
with meals?
Increases => weight loss
Peptic Ulcer Disease: One etiologic agent underlies duodenal ulcers - what is
it?
H. pylori (100%)
Peptic Ulcer Disease: 2 pathogenic mechanisms are thought to lead to
development of duodenal ulcer - what are they?
Increased gastric acid secretion and decreased mucosal protection
Peptic Ulcer Disease: What tends to hypertrophy with duodenal ulcers?
Bruenner's glands
Peptic Ulcer Disease: The margins of a doudenal ulcer are:
clean and punched out
Peptic Ulcer Disease: The 4 common complications of of duodenal ulcers are:
bleeding, penetration, perforation, and obstruction (not necessarily
pre-cancerous)
Peptic Ulcer Disease: Does the pain of a duodenal ulcer increase or decrease
with meals?
Decreases => weight gain
Peptic Ulcer Disease: How is H.pylori infection treated?
triple therapy (metronidazole, bismuth salicylate, amoxocillin or tetracycline)
with or without proton pump inhibitor
Peptic Ulcer Disease: Does smoking effect peptic ulcer development?
Yes, it is 2x as common in smokers
IBD: The possible etiology of Crohn's disease is:
Infectious
IBD: The location and lesion type of Crohn's disease is:
Skip lesions in any portion of GI tract, usually terminal ileum, SI, and colon.
Rectal sparing.
IBD: Gross Morphological features (6) of Crohn's disease are:
Transmural inflammation, cobblestone mucosa, creeping fat, bowel wall
tickening (string sign on x-ray), linear ulcers, and fissure. (FAT OLD
CRONE SKIpING DOWN A COBBLESTONE ROAD)
IBD: The microscopic morphological features of Crohn's disease are:
non-caseating granulomas
IBD: The four major complications of Crohn's disease are:
Strictures, fistulas, perianal diease, malabsorption leading to nutritional
depletion.
IBD: Two major extraintestinal manifestations associated with Chron's
disease are:
migratory polyarthritis and erythema nodosum
IBD: The possible etiology of UC is:
autoimmune
IBD: Location and lesion type of UC is:
continuous lesions of colon with rectal involvement
IBD: The two gross morphological features of UC are:
mucosal inflammation, friable mucosal pseudopolyps with freely hanging
mesentery.
IBD: The microscopic morphological features of UC are:
crypt abcesses, ulcers
IBD: 3 severe complications of UC are:
severe stenosis, toxic megacolon, and colorectal carcinoma
IBD: Two major extraintestinal manifestations associated with UC are:
pyoderma gangrenosum, sclerosing cholangitis
Diverticular Disease: Diverticuli are blind pouches found in the:
alimentary tract
Diverticular Disease: Diverticuli are lined by (3 layers):
Mucosa, muscularis, and serosa
Diverticular Disease: The 4 GI tract locations of diverticuli are:
esophagus, stomach, duodenum and colon
Diverticular Disease: Why are most diverticuli termed false?
They lack or have an attenuated muscularis mucosa.
Diverticular Disease: Percent of older patients likely to get diverticulosis
(many diverticula):
50% of patients >60
Diverticular Disease: The reasons for increasing number of diverticula with
age are:
Increased intraluminal pressure and focal weaknes in the colonic wall.
Diverticular Disease: What type of diet is diverticulosis associated with?
low-fiber
Diverticular Disease: Sx of diverticulosis?
usually asymptomatic, sometimes vague discomfort.
Diverticular Disease: Diverticulitis commonly presents with pain where?
LLQ
Diverticular Disease: Complications of diverticulitis include:
perforation, peritonitis, abcess formation, bowel stenosis
Intussusception and Volvulus: What is intussuception?
telecoping of 1 bowel segment into distal segment.
Intussusception and Volvulus: Complication of intussusception is:
compromised blood suply.
Intussusception and Volvulus: What is volvulus?
Twisting of portion of the bowel around its mesentery.
Intussusception and Volvulus: What volvulus lead to?
obstruction.
Stomach Cancer: What is the most common type of stomach cancer?
adenocarcinoma
Stomach Cancer: Is this cancer aggresive?
Yes, it has early aggressive local spread and node/liver mets
Stomach Cancer: Stomach Cancer is associated with what 3 etiologic factors?
dietary nitrosamines, achlorhydria, chronic gastritis
Stomach Cancer: What is stomach cancer termed when it is diffusely
infiltrative with thickened and rigid appearance?
Linitis plastica
Stomach Cancer: What does Virchow's node signify?
involvement of supraclavicular node by stomach mets
Stomach Cancer: What is Krukenberg's tumor?
bilateral stomach cancer mets to the ovary
Stomach Cancer: What are characteristics of Krukenberg's tumor?
Abundant mucus, "signet ring" cells
Hirschprung's Disease: What is Hirschprung's diease?
congential megacolon
Hirschprung's Disease: What is missing?
enteric nerve plexus (both Auerbach's and Meissner's). Seen on biopsy
Hirschprung's Disease: What is the cause of this disease?
failure of neural crest migration.
Hirschprung's Disease: How does this disease present?
Chronic constipation early in life.
Hirschprung's Disease: Which part of the colon is dilated?
That part proximal to the aganglionic segment - aganglionic portion is
constricted.
Colorectal cancer risk factors: The risk factors are:
colorectal villous adenoma, IBD, low-fiber diet, age, FAP, HNPCC, personal
and family hx. of colon cancer.
Colorectal cancer risk factors: What is Peutz-Jeghers, and does it lead to
colorectal cancer?
It is a benign polyposis syndrome which is not a risk factor.
Colorectal cancer risk factors: Who schould be screened for colorectal cancer
and how?
People over age 50, screen with stool occult blood test.
Cirrhosis/Portal HT: Cirrho in Greek means:
tawny yellow
Cirrhosis/Portal HT: Cirrhosis is:
diffuse fibrosis of the liver with destruction of norml architecture, nodular
regeneration.
Cirrhosis/Portal HT: Cause of micronodular cirrhosis (nodules <3mm,
uniform in size) is:
metabolic insult
Cirrhosis/Portal HT: Causes of macronodular cirrhosis (nodules >3mm,
varied in size) are?
Significant liver injury leading to hepatic necrosis (post-infectious,
drug-induced hepatitis)
Cirrhosis/Portal HT: Cirrhosis is assocated with what type of cancer?
hepatocellular carcinoma
Cirrhosis/Portal HT: The effects of portal hypertension are:
esophageal varices (hemetemesis, melena), peptic ulceration (melena),
splenomegaly, caput medusae, ascites, hemmorhoids, and testicular atrophy
Cirrhosis/Portal HT: Portal hypertension may be relieved by what method?
Portacaval shunt between splenic vein ad left renal vein.
Cirrhosis/Portal HT: What are the effects of liver cell failure?
Coma, scleral icterus, fetor hepaticus (breath smells like a freshly opened
corpse), spider nevi, gynecomastia, jaundice, loss of sexual hair, asterixis,
bleeding tendency, anemia, ankle edema
Alcoholic Hepatitis: Hepatocytes in alcoholic hepatitis are:
swollen and necrotic
Alcoholic Hepatitis: Other histologic changes seen in aloholic hepatitis are:
neutrophil infiltration, mallory bodies (hyaline), fatty change, and sclerosis
areound central vein
Alcoholic Hepatitis: SGOT (AST):SGPT (ALT) ratio is:
usually more than 1.5 (A Scotch and Tonic: AST elevated)
Budd Chiari Syndrome: What is Budd-Chiari Syndrome?
Occlusion of the IVC or hepatic veins with centrilobular congestion and
necrosis, leading to congestive liver disease
Budd Chiari Syndrome: The features of congestive liver disease are:
hepatomegaly, ascites, abdominal pain, and eventual liver failure
Budd Chiari Syndrome: Budd-Chiari Syndrome is associated with what 3
conditions:
polycythemia vera, pregnancy, hepatocellular carcinoma
Wilson's Disease: Wilson's disease is?
Coper accumulation, especially in liver, brain and cornea
Wilson's Disease: It is due to what?
failure of coper to enter circulation in the form of ceruloplasmin
Wilson's Disease: What is another name for Wilson's Disease?
Hepatolenticular degeneration
Wilson's Disease: What are the symptoms of Wilson's Disease? (A,B,C-6,D)
Asterixis, basal ganglia degeneration (parkinsonian symptoms),
Ceruloplasmin decrease, cirrhosis, corneal deposits (kayser-fleischer rings),
coper accumulation, carcinoma (hepatocellular), choreiform movements,
Dementia
Hemochromatosis: What is hemosiderosis?
Deposit of iron (hemosiderin) - this causes hemochromatosis
Hemochromatosis: The traid of sx. are?
micronodular cirrhosis, pancreatic fibrosis, and skin pigmentation ("bronze"
diabetes)
Hemochromatosis: Possible complications include?
CHF, increased risk of hepatocellular carcinoma
Hemochromatosis: What is primary form?
inherited, Autosomal recessive
Hemochromatosis: What is secondary form due to?
chronic transfusion therapy
Hemochromatosis: What are ferritin, iron, TIBC and transferrin saturation
levels?
Ferritin increased, iron increased, TIBC decreased => transferrin saturation is
increased
Hemochromatosis: How much iron may the body contain?
As much as 50g, enough to set off airport metal detectors
Hemochromatosis: How is this condition treated?
Phlebotomy, deferoxamine
Hemochromatosis: AUTHOR
Tzevan Poon
Jaundice: bacteria convert conjugated bilirubin into what? what happens to
some of this?
urobilinogen --> some which is reabsorbed, some which is excreted.
(urobilinogen that's reabsorbed is converted to urobilin= yellow pigment in
urine)
Jaundice: which is soluble in water/urine: conjugated or unconjugated
bilirubin?
conjugted of course!
Jaundice: check out the 3 jaundice types: what are they? ***cover up the
various parts of the chart in the text and test yourself.
heptocellular vs. obstructive vs. hemolytic jaundice
Heriditary hyper-bilirubinemias: What is the biochemical disorder in
GILBERTS SYNDROME?
mild ↓ in UDP-glucuronyl transferase (this is key enzyme in conjugation of
bilirubin)
Heriditary hyper-bilirubinemias: what are the symptoms?
asymptomatic
Heriditary hyper-bilirubinemias: what type of bilirubin is seen upon the lab
findings? Do you have do you have major hemolysis?
unconjugated bilirubin is elevated w/o overt hemolysis
Heriditary hyper-bilirubinemias: What is the syndrome called when you have
an ABSENCE of UDP-glc-ur-transferase?
Crigler-Najjar (CN) syndrome type 1 (type 2 is LESS severe)
Heriditary hyper-bilirubinemias: when does it present in life? What is the
prognosis?
presents early in life: pts die in a few years.
Heriditary hyper-bilirubinemias: name 3 findings of C-N syndrome?
jaundice, kernicterus, ↑ unconjugated bilirubin
Heriditary hyper-bilirubinemias: type 2 is more sever or less severe? What do
you treat it with?
less severe than type 1; treat type 2 with phenobarbital.
Heriditary hyper-bilirubinemias: what do you treat type 1 with (name 2)?
plasmapheresis + phototherapy (breaks down unconj. Bilirubin)
Heriditary hyper-bilirubinemias: What is Dubin Johnson syndrome?
↑↑ hyperbilirubin (conjugated) due to defective liver EXCRETION
Heriditary hyper-bilirubinemias: what does the liver look on gross exam?
black liver grossly
Heriditary hyper-bilirubinemias: what is the name of the less severe
syndrome akin to Dubin Johnson?
Rotor's syndrome: also no black liver.
Heriditary hyper-bilirubinemias: see drawing: it's nice.
0
Primary sclerosing cholangitis: what is the pathophysiology
segmental inflammation and fibrosis of bile ducts: unaffected parts are
dilated.
Primary sclerosing cholangitis: what test do you do to see this
stricture/dilating/beading pattern?
ERCP
Primary sclerosing cholangitis: what disease is this associated with?
Ulcerative Colitis
Primary sclerosing cholangitis: What can prim. Scl. Cholangitis lead to?
2° biliary cirrhosis/sclerosis
Biliary sclerosis : what is the cause of Primary Biliary Sclerosis (PBS)?
(compare the name/disease of PBS vs. PSC: primary sclerosing cholangitis)
autoimmune disorder with antimitochondrial antibodies
Biliary sclerosis : name 3 signs associated with PBS:
1) severe obstructive jaundice 2) itching 3) hypercholesterolemia (xanthoma)
Biliary sclerosis : What is the cause of SBS: secondary biliary sclerosis?
EXTRA-hepatic biliary obstruction → ↑ pressure in INTRA-hepatic ducts →
↑ injury/sclerosis
Biliary sclerosis : what is 2° biliary sclerosis associated with (name 3 things)?
ascending cholangitis (bacterial infection), bile stasis, and bile lakes
Heptocellular carcinoma = hepatoma: in liver cancers, is this common?
yes, #1 most common!
Heptocellular carcinoma = hepatoma: there is an ↑ incidence of hepatoma
due to what diseases/exposures (name 7)
1) hep B, 2) hep C, 3) Wilson's disease, 4) hemochromatosis, 5) a-antitrypsin
def 6) EtOH cirrhosis 6) carcinogens (e.g. aflatoxin B1)
Heptocellular carcinoma = hepatoma: How do hepatomas spread? How does
this differ with renal cell ca. spread?
They BOTH commonly spread hematogenously!
Heptocellular carcinoma = hepatoma: What is major lab finding with
hepatocelluar ca?
↑ AFP (alpha fetoprotein)
Reye's syndrome = rare!!! But…: What is this syndrome?
Hepato-encephalopathy: fatal: occurs in childhood
Reye's syndrome = rare!!! But…: name 3 findings:
1) fatty liver w/ microvesicular fatty change 2) hypoglycemia, 3) coma
Reye's syndrome = rare!!! But…: is this associated with any outside
factors/triggering factors?
yes: 1) viral infection (esp. VZV or influenza B) 2) salicylates!!!
Reye's syndrome = rare!!! But…: if baby/child has fever what do you use in
place of aspirin?
use acetaminophen (but with caution): i.e. acetaminophen OD hepato-toxicity
Gallstones: name 3 types of stones and tell me how they show up on CT scan:
1) cholesterol stone (radiolucent but 10-20% opaque due to calcification) 2)
mixed stone = cholesterol + pigment (radiolucent) 3) pigment stone
(radio-opaque)
Gallstones: Which is the most common type of gall stone?
mixed stone
Gallstones: name at least 5 out 9 risk factors for Cholesterol stones: is there a
mnemonic?
1) obesity 2) Crohn's D 3) Cystic fibrosis 4) elderly 5) clofibrate 6) estrogens
7) multiparity 8) rapid weight loss 9) native American origin mnemonic = 4
F's fat, female….
Gallstones: name 4 risk factors for pigment stones:
1) pts with chronic RBC hemolysis 2) alcoholic cirrhosis 3) elderly 4) biliary
infection
Gallstones: What is a good way to diagnosis stones?
ultrasound
Gallstones: What is CHARCOT'S TRIAD
1) epigastric/RUQ pain 2)fever 3) jaundice
Acute pancreatitis: this is what our US attorney general had. :
pathophysiology mechanism?
activation and thus autodigestion by pancreatic enzymes
Acute pancreatitis: this is what our US attorney general had. : Causes? (good
mnemonic)
Get Smashed (EtOH will can lead to AP) = 1) Gallstones 2) EtOH 3) Trauma
4) Steroids 5) Mumps 6) autoimmune disease 7) scorpion sting of all things!
8) hyperlipidemia 9) drugs
Acute pancreatitis: this is what our US attorney general had. : clinically
presents with?
intense epigastric pain radiating to back
Acute pancreatitis: this is what our US attorney general had. : labs(name 2):
which of the two has a higher specificity?
↑ amylase + ↑lipase (higher specificity) "li is hi"
Acute pancreatitis: this is what our US attorney general had. : Name 5 nasty
complications that can result from AP?
1) DIC 2) ARDS 3) diffuse fat necrosis 4) hypocalcemia 5) pseudocyst
formation
Acute pancreatitis: this is what our US attorney general had. : if you have
CHRONIC pancreatitis: what do we think of your life habits?
Chronic Pancr. Is strongly associated w/ alcoholism
Pancreatic cancer: what is a common and fatal pancreatic cancer?
pancreatic adenocarcinoma
Pancreatic cancer: what is the prognosis?
6 months: very aggressive: usually has mets when pt. presents
Pancreatic cancer: where are tumors most commonly located? And what does
this lead to?
pancreatic head → obstructive jaundice.
Pancreatic cancer: PATHOLOGY-RESPIRATORY SECTION
0
COPD = also known as OLD: obstructive lung disease: why is it called
obstructive?
obstruction of AIR FLOW → air traping in lungs
COPD = also known as OLD: obstructive lung disease: what is the major
PFT finding?
FEV1 / FVC ration is ↓ (hallmark finding)
COPD = also known as OLD: obstructive lung disease: name the 4 types of
COPD
1) Chronic Bronchitis (Blue Bloater) 2) emphysema (pink puffer) 3) asthma
4) bronchietasis
COPD = also known as OLD: obstructive lung disease: what is the definition
of Chronic Bronchitis
productive cough for >3 consecutive months in two or more years.
COPD = also known as OLD: obstructive lung disease: what do you expect
on lung histology?
hypertrophy of mucus-secreting glands in the bronchioles (Reid index of
>50%)
COPD = also known as OLD: obstructive lung disease: leading cause is
smoking: what are the physical findings for Chronic Bronchitis? (name 3)
1)cyanosis 2) wheezing 3) crackles
COPD = also known as OLD: obstructive lung disease: what is the
pathophysiological mechanism of EMPHYSEMA?
destruction of fibrous septa/alveolar walls → enlargement of air space and ↓
total surface area for gas exchange
COPD = also known as OLD: obstructive lung disease: if the cause is
smoking, what kind of emphysema would you see on histo slide?
centri-acinar emphysema
COPD = also known as OLD: obstructive lung disease: what else can cause
emphysema: (also may work synergistically with smoking): What kind of
findings do you see in lung histo and name another organ affected?
alpha 1-antitrypsin deficiency → panacinar emphysema + liver cirrhosis
COPD = also known as OLD: obstructive lung disease: what causes the
emphysema in this disorder?
↑ elastase activity to damage lung tissue.
COPD = also known as OLD: obstructive lung disease: name 4 findings of
emphysema (in general)
1) dyspnea; 2) ↓ breath sounds 3) tachycardia 4) ↓ I/E ratio
COPD = also known as OLD: obstructive lung disease: What is mechanism
of asthma
BRONCHIAL hypersensitivity/hyperresponsiveness → REVERSIBLE
bronchoconstriction
COPD = also known as OLD: obstructive lung disease: name 3 common
triggers
1) viral URI 2) allergens 3) stress!!
COPD = also known as OLD: obstructive lung disease: name 7 findings
1) cough 2) wheezing 3) dyspnea 4) hypoxemia 5)↓ I/E ratio 6) tachypnea 7)
pulsus paradoxus
COPD = also known as OLD: obstructive lung disease: BRONCHIECTASIS:
what is its mechanism??
chronic necrotizing infection of BRONCHI → dilated airways, purulent
sputum, recurrent infections, hemoptysis (see Robbins for a good discussion
of this)
COPD = also known as OLD: obstructive lung disease: what disorders is
bronchietasis commonly associated with?
1) bronchial obstruction 2) cystic fibrosis 3) poor ciliary motility
Restrictive Lung Disease (RLD): What are classic PFT findings for RLD?
↓ VC ↓TLC ; FEV1/FVC ration > 80%
Restrictive Lung Disease (RLD): Name the two MAJOR types of RLD
1) poor breathing mechanics (EXTRA-pulmonary) 2) Interstitial lung
diseases
Restrictive Lung Disease (RLD): cover up various parts of the
text/table/outline to test yourself on the following: 1) 2 types of poor
breathing mechanics 2) 8 types of interstitial disease that give you a
restrictive picture.
0
Lung Physical Findings: cover up parts of the very good table to test yourself
on various findings.
0
Lung Physical Findings: Obstructive vs. Restrictive findings
0
Lung Physical Findings: Name 3 lung volumes that are increased in COPD
↑TLC, ↑FRC, ↑RV
Lung Physical Findings: What 2 values are BOTH reduced in COPD and
RLD?
1) FEV1 and 2) FVC (think FEV1/FVC ratio) NOTE! in COPD, FEV1 is
more dramatically reduced and thus the FEV1/FVC ratio is ↓
Asbestosis = long latency = think shipbuilders and plumbers: what is the
main pathology resulting from asbestosis?
DIFFUSE, interstitial fibrosis caused by inhaled asbestos Fibers.
Asbestosis = long latency = think shipbuilders and plumbers: What cancers
are increased in pts with asbestosis?
1) pleural mesothelioma 2) bronchogenic carcinoma (BC)
Asbestosis = long latency = think shipbuilders and plumbers: Major finding
in lung?
Ferruginous bodies: asbestos fibers coated with hemosiderin also 2) ivory
white pleural plaques
Neonatal respiratory distress syndrome: What is the main cause
surfactant deficiency --> to increased surface tension --> alveolar collapse
Neonatal respiratory distress syndrome: surfactant is made by which cells?
After when?
type 2 pneumocytes after 35th gestational week
Neonatal respiratory distress syndrome: what do you measure? Where do you
get this fluid?
lecithin-to-sphingomyelin ratio in the amniotic fluid = measure of lung
maturation <1.5 in neonatal distress syndrome
Neonatal respiratory distress syndrome: what is surfactant made of (chemical
name)
dipalmitoyl phosph-tidyl-choline (DP-PTC)
Neonatal respiratory distress syndrome: treatment for poor maturation of
lungs
1) before birth = maternal steroids 2) after= artificial surfactant
Karta-gener's syndrome: what is this?
immotile cilia due to dynein arm defect
Karta-gener's syndrome: results in what in female and male? (4 things)
1) sterility (in male sperm also immotile) 2)bronchietasis 3)recurrent sinusitis
(bacteria & particles not pushed out) 4) associated with situs inversus (e.g.
dextro-cardia)
Lung Cancer: name the 3 main classes of cancers that affect parts of the lung
1) bronchogenic carcinoma (with different subtypes) 2) carcinoid tumor 3)
metastasis
Lung Cancer: list the 5 types of major bronchogenic carcinomas
CENTRAL 1) squamous cell ca 2)small cell ca PERIPHERAL 3)
adenocarcinoma 4) bronchoalveolar ca 5) large cell ca
Lung Cancer: mnemonic: what is meant by SPHERE of symptoms?
S= superior vena cava syndrome; P= pancoast tumor; H= Horner's syndrome;
E= Endocrine (paraneoplastic); Recurrent laryngeal / hoarseness; E =
Effusions (pleural OR pericardial)
Lung Cancer: What can a CARCINOID tumor cause?
Carcinoid Syndrome = flushing, diarrhea, wheezing, and salivation
Lung Cancer: Metastases to lung is very common, LUNG cancer also prone
to metastasize to what other parts?
1) brain (epilepsy) 2) bone (fracture) 3)liver (jaundice + hepatomegaly)
Pancoast tumor: What is it?
it's a carcinoma of the apex of lung
Pancoast tumor: what may it affect?
may affect CSP= cervical sympathetic plexus causing Horner's syndrome
Pancoast tumor: what is Horner's syndrome?
P.A.M. is Horny = Ptosis, Anhydrosis, Miosis
Pneumonia: 1st AID breaks it down into TYPE/ ORGANISM/
CHARACTERISTICS = cover parts of this table and fill in the blanks
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Pneumonia: Lobar Pneumonia; Organism(s) and characteristics
Pneumococcus; intraalveolar exudate -> consolidation, may involve entire
lung
Pneumonia: Bronchopneumonia: Organism and characteristics
S aureus, H flu, Klebsiella, S pyogenes; Acute inflammatory infiltrates from
bronchioles into adjacent alveoli; patchy distribution involving >= 1 lobes
Pneumonia: Interstitial pneumonia; Organism(s) and characteristics
Viruses, mycoplasma, legionella; diffuse patchy inflammation localized to
interstitial areas at alvolar walls; distribution involving >= 1 lobes
Pneumonia: PATHOLOGY - NEUROLOGIC
0
Degenerative diseases: name two diseases that affect the CEREBRAL
CORTEX
1) Alzheimer's disease 2) Pick's disease
Degenerative diseases: name two diseases that affect BASAL GANGLIA &
BRAIN STEM:
1) Huntington's disease 2) Parkinson disease
Degenerative diseases: name 5 diseases that affect SPINOCEREBELLAR
MOTOR NEURON
1) Olivo-ponto-cerebellar atrophy 2) Friedreich's ataxia 3)ALS =
amyotrophic lateral sclerosis 4)Werdnig-Hoffmann disease 5) Polio
Degenerative diseases: what is the most common cause of elderly dementia?
Alzheimer's
Degenerative diseases: name two pathological findings characteristic of
Alzheimer's
1) senile plaques = intracytoplasmic inclusion bodies 2) neurofibrillary
tangles (abnormally phosphorylated tau protein)
Degenerative diseases: what is the 2nd most common cause of dementia in
elderly?
multi-infarct dementia in elderly\
Degenerative diseases: How can Alzheimer also affect intracranial
vasculature?
amyloid angiopathy --> intracranial hemorrhage
Degenerative diseases: The familial form of Alzheimer's is associated with
what chromosomes (name 4) and (name the allele's name in 2 of the 4)
chromosome 1, 14, 19 (APO-E4 allele), 21 (p-Ap gene)
Degenerative diseases: What is pathognemomic with Pick's disease upon
histology?
Pick bodies = intra-cytoplasmic inclusion bodies
Degenerative diseases: What cortical areas does Pick's disease affect
Frontal and temporal lobes (remember; sharp, atrophic apearance of gross
specimen)
Degenerative diseases: What is the inheritance pattern of Huntington's
Auto Dominant
Degenerative diseases: What are some symptoms?
1) chorea 2) dementia
Degenerative diseases: Huntington's is due to atrophy of _____ what? Loss of
___ ergic neurons.
atrophy of caudate nucleus = loss of GABA-nergic neurons
Degenerative diseases: what is the genetic abnormality of Huntington's?
1) Chr. 4 - expansion of CAG repeats
Degenerative diseases: Parkinson disease is associated with what pathology
findings?
1) Lewy bodies 2) depigmentation of substantia nigra (loss of dopaminergic
neurons)
Degenerative diseases: rare cases of Parkinson's have been linked to what
contaminant of certain illicit drugs?
MPTP = contaminant to street drug
Degenerative diseases: Parkinson's can make you feel in a "TRAP" = ?
T = tremor at rest; R = cogwheel rigidity; A = akinesia ; Postural instability
Degenerative diseases: ALS = Lou Gehrig's disease (the Iron Horse of the
Yankees, hero of Joe DiMaggio) = what signs is ALS associated with?
Both UMN and LMN deficits
Degenerative diseases: Werdnig-Hoffman disease - presents as birth as?
1) flopy baby syndrome 2) note tongue fasciculations as well (also seen in
ALS)
Degenerative diseases: for Polio, what kind of signs to you see?
predominantly LMN deficits.
Intracranial Hemorrhage/Hemotomas: name 4 types of cranial related
hemorrhages (think of layers that could possibly be involved)
1) epidural hemorrhage 2) subdural h 3) subarachnoid h 4) parenchymal h
Intracranial Hemorrhage/Hemotomas: what is a common site of epidural
hematoma/hemorrhage
1) rupture of MMA: middle meningeal artery, often 2ndary to fracture of
temporal bone
Intracranial Hemorrhage/Hemotomas: what does CT show for epidural h?
biconcave disc NOT crossing suture lines
Intracranial Hemorrhage/Hemotomas: what else do you see?
lucid interval
Intracranial Hemorrhage/Hemotomas: How do subdural h. most often occur?
rupture of bridging veins (think, elderly being jolted in roller coaster)
Intracranial Hemorrhage/Hemotomas: this is venous bleeding so how would
this influence symptomatic findings?
venous = less pressure = delayed onset of symptoms
Intracranial Hemorrhage/Hemotomas: what types of people do you see
subdural h.?
1) elderly, 2) alcoholics 3) blunt trauma/sudden change in velocity injuries
Intracranial Hemorrhage/Hemotomas: for SUBDURALs what do you see
upon CT?
1) crescent-shaped hemorrhage instead 2) YES IT does cross the suture lines
Intracranial Hemorrhage/Hemotomas: subarachnoid hemorrhage is often seen
where (name 2 types
rupture of 1) aneurysm (usually Berry aneurysm) or an 2)AVM
Intracranial Hemorrhage/Hemotomas: symptoms?
the worst headache of my life
Intracranial Hemorrhage/Hemotomas: since its subarachnoid, what do you
see on what test?
bloody or xanthochromic CSF on spinal tap
Intracranial Hemorrhage/Hemotomas: name 4 risk factors for parenchymal
hematoma
1) HTN 2) amyloid angiopathy 3) diabetes mellitus 4) tumor
Intracranial Hemorrhage/Hemotomas: AUTHOR
Hilcias Duran
Berry aneurysms: most common site for Berry aneurysms
bifurcation of the anterior communicating artery (Circle of Willis)
Berry aneurysms: berry aneurysms are associated with
adult polycystic disease, Ehlers-Danlos s., and marfan's
Berry aneurysms: Classic triad of Multiple Sclerosis
SIN: Scanning speech, intention tremor, nystagmus (affect woman 20-30s)
Berry aneurysms: Prevalence of MS
increase prevalence w/ increased distance from the equator
Berry aneurysms: Clinical s/s of MS
periventricular plaques, preservation of axons, loss of oligodentrocytes,
reactive astrocystic gliosis, increased protein in csf(IgG) in CSF, relapsing
course, optic neuritis, MLF syndrome, hemiparesis, bladder/bowel
incontinence)
Berry aneurysms: Progressive multifocal leukoencephalopathy (PML) is
associated w/
JC virus and seen in 2-4 % of AIDS pts (reactivation or latent infect)
Berry aneurysms: pathogenesis of Guillian-Barre syndrome
Berry aneurysms: s/s of Guillian-Barre syndrome
Berry aneurysms: association between G-B syndrome and…
Inflammation and demyelination of peripheral nerves and motor fibers of the
ventral roots (sensory effec less severe than motor)
symmetrical ascending muscle weakness beginning in the distal lower
extremities. Autonomic fxn may be severely affected (eg. Cardiac
irregularities, HTN, or hypoTN) Findings: inc. csf protein w/ normal cell
count ("albumino-cytologic dissociation") elevated protein may lead to
papilledema
herpesvirus or camplobacter jejuni infection, inoculations, and stress but no
definitive link to a pathogen
Poliomyelitis: organism causing polio and mechanism of action
poliovirus, transmitted via fecal oral route and enters blood stream then into
CNS where it causes destruction of the anterior horn of S.C. leading in turn to
LMN destruction
Poliomyelitis: s/s of polio
malaise, HA, fever, nausea, abd. Pain, sore throats, signs of LMN signs
Poliomyelitis: finding of polio
csf w/ lymphocytic pleocytosis w/ slight elevation of protein, virus recovered
from stool or throat
Aphasia : describe Broca's (expressive) aphasia
confluent aphasia w/ intact comprehension broca's is broken speech
Aphasia : describe Wernicke's (aphasia)
Fluent aphasia w/ impaired concentration Wernick's ="What?" W area
located in superior temperal gyrus
seizures : describe two types of partial seizures
1.simple partial (awareness is intact)--motor, sensory, autonomic, psychic
2.Complex partial (impaired awareness)
seizures : describe types of Generalized seizure ( diffuse)
1.absence- blank stare (petit mal) 2.myoclonic- quick repetitive jerks
3.tonic-clonic- alternating stiffening and mvmt (grand mal) 4. Tonicstiffening 5.atonic-"drop" seizures
seizures : what are the causes of seizures in children?
genetic, infection, trauma, congenital, metabolic
seizures : adults?
tumors, trauma, stroke, infection
seizures : elderly?
stroke, tumor, trauma, metabolic, infection
Horner's syndrome: what is Horner's syndrome?
sympathectomy of face (lesion above T1) 1.Ptosis 2.anhidrosis and flushing
of affected side 3.miosis [PAM is horny]
Horner's syndrome: Horner's syndrome is associated w/ what type of tumor?
pancoast tumor
syringomyelia: what is syringomyelia?
enlargement of the central canal of the S.C. Crossing fibers of spinothalamic
tract are damaged.
syringomyelia: what are the s/s of syringomyelia?
b/l loss of pain and temp sensation in the uper extremities w/ the touch
sensation. Most common at C8-T1
syringomyelia: commonly seen in what pts?
pts w/ Arnold-Chiari malformation
Tabes dorsalis : what infection is tabes dorsalis associated w/?
teriary syphilis
Tabes dorsalis : what happens in the CNS?
degeneration of dorsal columns and dorsal root
Tabes dorsalis : dorsalis also is associated with what s/s?
charcot's joint, shooting (lightning) pain, Argyll Robertson pupils, and
absence of DTRs
Osteoarthritis : what occurs in OA?
mechanical wear and tear of the joints, leads to destruction of the articular
cartilage, subchondral bone formation, sclerosis, osteophytes, eburnation,
Herberden's nodes (DIP), and Bouchard's nodes (PIP)
Osteoarthritis : classical presentation of OA?
pain in weight bearing joints after use (worse at the end of the day0 improves
w/ rest. No systemic symptoms
Rheumatoid Arthritis : what happens in in RA?
autoimmune inflammatory proccess which affects synovial joints, w/ pannus
formation in joints (MCP, PIP), S-Q rheumatoid nodules, ulnar
deviation,subluxation
Rheumatoid Arthritis : classical presentation of RA?
female, 80% pts Rf positive (anti-IgG Ab) morning stiffness improving w/
use, symmetrical joint involvement, and systemic symptoms (fever, fatigue,
pleurtis, pericarditis)
Rheumatoid Arthritis : AUTHOR
Jason Portnof
Sjogren's Syndrome: What is the classic triad of Sjogren’s syndrome?
dry eyes (conjunctivitis, xeropthalmia), dry mouth (dysphagia, xerostomia),
arthritis
Sjogren's Syndrome: What is SICCA syndrome?
dry eyes, dry mouth, nasal and vaginal dryness, chronic bronchitis, reflux
esophagitis
Sjogren's Syndrome: T/F Sjogren’s syndrome predominantly affects males
between 40 and 60 years of age.
False. Females between 40 and 60 y.o are predominantly affected in
Sjogren’s syndrome.
Gout: T/F Gout is the precipitation of monosodium urate crystals into joints
due to hyperuricemia.
TRUE
Gout: What is the favored manifestation of gout?
Podagra. (painful MTP joint)
Gout: The crystals of gout are:
needle shaped and negatively bifringent
Pseudogout: T/F Pseudogout is the precipitation of calcium pyrophosphate
crystals within the joint space.
TRUE
Pseudogout: The crystals of psuedogout are:
basophilic, rhomboid crystals
Pseudogout: Psudogout usually affects:
Large joints (classically the knee)
Pseudogout: T/F Both gout and psuedogout predominantly affect men.
False. Gout is more common in men. Pseudogout affects both sexes equally,
most pts are >50 years old.
Pseudogout: T/F The treatment for both pseudogout and gout is allopurinol,
probenecid, colchicines, and NSAIDS.
False. That is the tx for gout. However, there is no tx for pseudogout.
Celiac sprue: Celiac sprue is the autoimmune-mediated intolerance of what
substance, leading to steatorrhea?
gliadin (wheat)
Celiac sprue: T/F Findings in Celiac sprue include blunting of villi,
neutrophils in the lamina propria, and abnormal D-xylose test.
False. lymphocytes, not neutrophils are found in the lamina propria.
Systemic Lupus Erythematosus: What drugs can produce a SLE-like
syndrome that is commonly reversible?
HIp: Hydralazine, INH, Phenytoin, Procainamide
Systemic Lupus Erythematosus: SLE causes LSE. What is LSE?
Libman Sacks Endocarditis. Valvular vegetations found on both sides of
valve (Mitral Valve Stenosis) and do not embolize.
Systemic Lupus Erythematosus: T/F 90% Systemic lupus erythematousus pts
are female between ages 14 and 45. SLE is most common and severe in black
females.
Both statements are true
Systemic Lupus Erythematosus: What are 4 lab tests in SLE? Which test,
when positive is predictive of a poor prognosis?
1. ANA (antinuclear antibodies)- sensitive, not specific for SLE, 2. anti-ds
DNA (antibodies to double stranded DNA)- very specific, poor prognosis, 3.
Anti-Smith antibodies (anti-Sm)- very specific, but not prognostic, 4.
Antihistone antibodies- drug induced lupus
Systemic Lupus Erythematosus: In what organ are wire loop lesions found in
SLE?
kidney (with immune complex deposition and nephrotic syndrome)
Systemic Lupus Erythematosus: What causes death commonly in SLE?
Renal failures and infections
Systemic Lupus Erythematosus: What are symptoms of SLE?
fever, fatigue, wt loss, joint pain, malar rash, photosensitivity. Also: pleuritis,
pericarditis, nonbacterial verrucous endocarditis, Raynaud’s phenomenon
Sarcoidosis: What disease is characterized by gamaglobulinemia, rheumatoid
arthritis, ace increase, interstitial fibrosis, and noncaseating granulomas?
Sarcoidosis
Seronegative spondyloarthropathies: Name 2 seronegative
spondyloarthropathies.
ankylosing spondylitis, reiters’ syndrome
Seronegative spondyloarthropathies: What is a seronegative
spondyloarthropathy?
Arthritis without rheumatoid factor (no anti-IgG Ab). Strong association with
HLA-B27 (gene that codes for HLA MHC1)
Seronegative spondyloarthropathies: T/F seronegative spondyloarthropahties
occur more often in males
TRUE
Seronegative spondyloarthropathies: What is the classic triad for Reiter’s
syndrome?
Urethritis, conjunctivitis and anterior uveitis, arthritis. “Can’t see, can’t pee,
can’t climb a tree”
Seronegative spondyloarthropathies: T/F reiter’s syndrome occurs commonly
post respiratory or chlamydia infections.
False. Post-GI or chlamydia infections
Seronegative spondyloarthropathies: Describe ankylosing spondylitis
Chronic inflammatory disease of spine and sacroiliac joints. Ankylosis (stiff
spine), uveitis and aortic regurg.
Scleroderma: T/F Crest syndrome is wider-spread than diffuse scleroderma.
False. Diffuse scleroderma has widespread skin involvement, rapid
progression, early visceral involvement. CREST syndrome has limited skin
involvement, often confined to fingers and face. More benign clinical course.
Scleroderma: T/F Crest syndrome occurs in male pts that have allergic rxn to
toothpaste.
False. CREST= calcinosis, raynaud’s phenomenon, esophageal dysmotility,
sclerodactyly, telangiectasia.
Scleroderma: What antibodies are associated with scleroderma (progressive
systemic sclerosis- PSS)?
"diffuse scleroderma- anti-Scl-70 antibody, Crest syndrome- anticentromere
antibody
Skin disorders: T/F Pemphigus vulgaris is described as an autoimmune
disorder with IgG antibody against epidural basement membrane (linear
immunofluorescence). Affects skin but spares oral mucosa.
False. That description is for Bullous pemphigoid (less severe disease than
Pemphigus vulgaris). Pemphigus vulgaris is a potentially fatal autoimmune
skin disorder. Intradermal bullae involve the oral mucosa and skin. Findings
include acantholysis, IgG ab against epidermal cell surface.
Skin disorders: T/F Dermatitis is a group of inflammatory pruritic skin
disorders. The etiology is allergy (usually type IV hypersensitivity), chemical
injury, or infection.
TRUE
Skin disorders: What HLA groups are associated with psoriasis?
HLA-B27, HLA-13, HLA-17
Skin disorders: What is psoriasis? Where is it most commonly found?
Psoriasis is nonpruritic chronic inflammation of the skin, particularly on the
knees and elbows.
Goodpasture's: T/F Goodpasture’s syndrome affects the lungs and liver.
False. Lungs and Kidneys. (Pulmonary hemorrhagesà hemoptysis, renal
lesionsà hematuria, anemia, crescentic glomerulonephritis)
Goodpasture's: What type of Abs are associated with Goodpastures?
anti-glomerular basement membrane abs produce linear staining on
immunofluorescence.
Goodpasture's: Who commonly gets Goodpastures?
Men between 20-40 years.
Cushing's syndrome: What are etiologies of Cushing’s syndrome? Is ACTH
always elevated?
Cushing's syndrome: Describe the clinical picture of Cushings.
increased cortisol due to:, 1. Cushing’s disease (primary pituitary adenoma)
increased ACTH, 2. Primary adrenal (hyperplasia/neoplasia) decreased
ACTH, 3. Ectopic ACTH production (ie- small cell lung ca) increased
ACTH, 4. Iatrogenic, decreased ACTH
HTN, wt gain, moon facies, truncal obesity, buffalo hump, hyperglycemia
(insulin resistance), skin change (thinning, striae), osteoporosis, immune
supression
Hyperaldosteronism: T/F Conn’s syndrome is secondary hyperaldosteronism.
False. Conn’s syndrome is primary hyperaldosteronism, caused by an
aldosterone-secreting tumor. Results in HTN, hypokalemia, metabolic
alkalosis, low plasma renin.
Hyperaldosteronism: Which hyperaldosteronism is associated with high
plasma renin?
Secondary hyperaldosteronism. It is due to renal artery stenosis, chronic renal
failure, CHF, cirrhosis, or nephrotic syndrome. Kidney perception of low
intravascular volume results in an overactive renin-angiotensin sysem.
Hyperaldosteronism: What is the tx for hyperaldosteronism?
Spironolactone, a diuretic that works by acting as a aldosterone antagonist.
Addison's Disease: What characterizes addison’s disease? (which hormones
are elevated or deficient)? Is it associated with HTN or hypotension?
Primary deficiency of aldosterone and cortisol due to adrenal atrophy,
causing hypotension and skin hyperpigmentation. Adrenal atrophy, absence
of hormone production, involves all 3 cortical divisions.
Addison's Disease: T/F In primary insufficiency decreased pituitary ACTH
production is characterized by skin hyperpigmentation.
False: increased ACTH causes MSH activity & hyperpigmentation
Tumors of adrenal medulla: T/F Neuroblastoma is the most common tumor of
adrenal medulla in adults.
False. Pheochromocytoma is the most common tumor of adrenal medulla in
adults. It is derived from chromaffin cells (arise from neural crest). It is
associated with neurofibromatosis MEN types II and III.
Tumors of adrenal medulla: Where does neuroblastoma occur?
Neuroblastoma is the most common tumor of adrenal medulla in children. It
can occur anywhere along the sympathetic chain.
Tumors of adrenal medulla: AUTHOR
Jason Lee
Pheochromocytoma: secrete combination of two molecules
epinephrine and norepinephrine
Pheochromocytoma: epidemiology (rule of 10's)
10% malignant, 10% bilateral, 10% extra-adrenal, 10% calcify, 10% kids,
10% familial
Pheochromocytoma: symptoms - 5 P's
(elevated blood) Pressure, Pain (headache), Perspiration, Palpitations,
Pallor/diaphoresis --> relapsing and remittant
Pheochromocytoma: elevations in two lab values
urinary VMA and serum catecholamines
Pheochromocytoma: association with two other endocrine diseases
MEN II and III
Pheochromocytoma: treatment
alpha-antagonists
Multiple Endocrine Neoplasia: type I (Wermer's syndrome) - 3 P's
Pancreas, Pituitary, and Parathyroid tumors
Multiple Endocrine Neoplasia: type II (Sipple's syndrome)
medullary carcinoma of thyroid, pheochromocytoma, parathyroid tumor, or
adenoma
Multiple Endocrine Neoplasia: type III
medullary carcinoma of thyroid, pheochromocytoma, oral/intestinal
ganglioneuromatosis
Hypothyroidism and hyperthyroidism: myxedema is prominent in which one
hypothyroidism
Hypothyroidism and hyperthyroidism: chest pain, palpitations, arrhythmias
hyperthyroidism
Hypothyroidism and hyperthyroidism: TSH is (increased/decreased) in
primary hyperthyroidism? In primary hypothyroidism?
hyper - decreased, hypo - increased
Hypothyroidism and hyperthyroidism: Graves' disease involves
autoantibodies with what mechanism of action?
stimulation of TSH receptors
Hypothyroidism and hyperthyroidism: three symptoms of Graves'
ophthalmopathy, pretibial myxedema, diffuse goiter
Hypothyroidism and hyperthyroidism: Graves' is a type __ hypersensitivity
type II
Hashimoto's thyroiditis: thyroid is (enlarged/not enlarged) and
(tender/nontender)
enlarged, nontender
Hashimoto's thyroiditis: autoimmune antibodies directed against ---
microsomes
Hashimoto's thyroiditis: histology shows (type of cell) infiltrate
lymphocytes (with germinal centers)
Subacute thyroiditis (de Quervain's): self-limited (hyper/hypo)thyroidism
following ---
hypothyroidism following flu-like illness
Subacute thyroiditis (de Quervain's): symptoms include
jaw pain, tender thyroid gland, early hyperthyroidism
Thyroid cancer: most common, good prognosis, "ground glass" nuclei,
psammoma bodies
papillary carcinoma
Thyroid cancer: poor prognosis, uniform follicles
follicular carcinoma
Thyroid cancer: calcitonin producing (C cells), sheets of cells
medullary carcinoma (MEN II and III)
Thyroid cancer: older patients, horrible prognosis
undifferentiated/anaplastic
Cretinism: caused by a lack of dietary --- or defect in --- formation
iodine (endemic), T4 (sporadic)
Cretinism: symptoms include
pot-belly, paleness, puffy face, protuberant tongue, protruding umbilicus
Acromegaly: caused by excess --- in adults
growth hormone
Acromegaly: symptoms include
large furrowed tongue, deep voice, large hands and feet, coarse facial features
Acromegaly: in children, leads to ---
gigantism
Diabetes mellitus: acute symptoms common to both types
polydipsia, polyuria, polyphagia, weight loss
Diabetes mellitus: match: (DKA/hyperosmolar coma) with (type I/type II)
DKA=type I, hyperosmolar coma=type II
Diabetes mellitus: effects (increased/decreased) of insulin deficiency and
glucagon excess on 1) glucose uptake, 2) protein catabolism, 3) lipolysis
1) decreased, 2) increased, 3) increased
Diabetes mellitus: increased plasma free fatty acids leads to
ketogenesis
Diabetes mellitus: hyperglycemia has what effect on blood volume and
electrolytes
decreased volume (osmotic diuresis), electrolyte depletion
Diabetes mellitus: three chronic manifestations
retinopathy (hemorrhage, exudate, microaneurysm), nephropathy (nodular
sclerosis), neuropathy (sensory, motor, autonomic)
Diabetes mellitus: sorbitol accumulation leads to what sequelae in the eye
cataracts, glaucoma
Diabetes mellitus: three tests - what are they? which one measures long-term
glucose control?
fasting glucose, glucose tolerance test, HbA1c
Diabetes mellitus: AUTHOR
Jacob Pugsley
Type 1 - juvenile onset: % of diabetes
0.15
Type 1 - juvenile onset: Insulin necessary in treatment
Always
Type 1 - juvenile onset: Age
<30
Type 1 - juvenile onset: Association with obesity
No
Type 1 - juvenile onset: Genetic predisposition
weak, polygenic
Type 1 - juvenile onset: Association with HLA system
Yes (HLA-DR3 & 4)
Type 1 - juvenile onset: Glucose intolerance
Severe
Type 1 - juvenile onset: Ketoacidosis
Common
Type 1 - juvenile onset: B-cell numbers in the islets
decreased
Type 1 - juvenile onset: Serum insulin levels
decreased
Type 1 - juvenile onset: Classic symptoms of polyuria, polydipsia, thirst,
weight loss
Common
Type 1 - juvenile onset: Theorized cause
viral or immune destruction of B cells
Type 2 - adult onset: % of diabetes
0.85
Type 2 - adult onset: Insulin necessary in treatment
Sometimes
Type 2 - adult onset: Age
>40
Type 2 - adult onset: Association with obesity
Yes
Type 2 - adult onset: Genetic predisposition
Strong, polygenic
Type 2 - adult onset: Association with HLA system
No
Type 2 - adult onset: Glucose intolerance
mild to moderate
Type 2 - adult onset: Ketoacidosis
Rare
Type 2 - adult onset: B-cell numbers in the islets
Variable
Type 2 - adult onset: Serum insulin levels
Variable
Type 2 - adult onset: Classic symptoms of polyuria, polydipsia, thirst, weight
loss
Sometimes
Type 2 - adult onset: Theorized cause
increased resistance to insulin
Diabetic Ketoacidosis (type 1): What precipitates this
Increase in insulin requirements from increase in stress (e.g. infection)
Diabetic Ketoacidosis (type 1): Ketone bodies from where
Excess fat breakdown, increase ketogenesis from increased free fatty acids
which are made into ketone bodies
Diabetic Ketoacidosis (type 1): Signs/Symptoms
Kussmaul respirations (rapid/deep breathing), hyperthermia,
nausea/vomiting, abdominal pain, psychosis/dementia, dehydration, fruity
breath odor
Diabetic Ketoacidosis (type 1): Labs
Hyperglycemia, high H+, low HCO3- (anion gap metabolic acidosis), high
blood ketone levels, leukocytosis
Diabetic Ketoacidosis (type 1): Complications
Life threatening mucormycosis, Rhizopus infection, cerebral edema, cardiac
arrhythimias, heart failure
Diabetic Ketoacidosis (type 1): Treatment
Fluids, insulin, and potassium; glucose if necessary to prevent hypoglycemia.
Diabetes insipidus: summary
intensive thirst, polyuria, inability to concentrate urine with fluid constriction
owing to lack of ADH (central DI) or to lack of renal response to ADH
(nephrogenic DI). Caused by lithium or demeclocycline
Diabetes insipidus: Findings
Urine specific gravity < 1.006; serum osmolality > 290 mOsm/L
Diabetes insipidus: Treatment
adequate fluid intake; Central DI - intranasal desmopressin (ADH analog);
nephrogenic DI - hydrochlorothiazide, indomethacin, or amiloride
SIADH: what does it stand for
Syndrome of inapropriate ADH
SIADH: finds
1) excess water retention 2) hyponatremia [may lead to seizures - correct
slowly] 3) urine osmolarity > serum osmolarity
SIADH: causes
1) Ectopic ADH [small cell lung cancer] 2) CNS disorders/head trauma 3)
pulmonary disease 4) Drugs
Hyperparathyroidism: What causes primary hyperparathyroidism?
Usually an adenoma
Hyperparathyroidism: What are the findings of primary disease?
hypercalcemia, hypercalciuria, hypophosphatemia, high parathyroid
hormone, high cAMP in urine; often asymptomatic, may present with
weakness and constipation
Hyperparathyroidism: what is osteitis fibrosa cystica? (von Recklinghausen's
syndrome)
cystic bone spaces filled with non-neoplastic fibrous tissue
Hyperparathyroidism: What causes secondary hyperparathyroidism?
low serum Ca++, most often chronic renal disease.
Hyperparathyroidism: What are the findings of secondary
hyperparathyroidism?
hypocalcemia, hyperphosphatemia, high parathyroid hormone
Hypoparathyroidism: findings
hypocalcemia, tetany.
Hypoparathyroidism: causes
accidental surgical excision (thyroid surgery) or DiGeorge syndrome
Hypoparathyroidism: note: pseudohypoparathyroidism
autosomal recessive kidney unresponsiveness to PTH. Hypocalcemia,
shortened 4th/5th digits, short stature
Carcinoid syndrome: frequency
rare
Carcinoid syndrome: cause
carcinoid tumors (neuroendocrine cells), especially those of the small bowel;
they secrete high levels of serotonin (5-HT) that does not get metabolized by
the liver due to liver metastases.
Carcinoid syndrome: symptoms
recurrent diarhea, cutaneous flushing, asthmatic wheezing, and right-sided
valvular disease.
Carcinoid syndrome: most common tumor of what?
apendix
Carcinoid syndrome: lab
high 5-HIAA in urine
Carcinoid syndrome: Rule of 1/3s:
1/3 metastasize; 1/3 present with second malignancy; 1/3 multiple
Carcinoid syndrome: Treatment?
Octreotide
Carcinoid syndrome: What is this medication?
synthetic octapeptide analog of somatostatin (growth hormone-inhibiting
hormone)
Zollinger-Ellison syndrome: What kind of tumor causes this?
Gastrin secreting tumor (usually) of the pancreas
Zollinger-Ellison syndrome: what does it cause?
recurrent ulcers
Zollinger-Ellison syndrome: may be associated with what?
MEN type I
Osteoporosis: what is this?
reduction in bone mass in spite of normal bone mineralization
Osteoporosis: what characterizes type 1?
Postmenopausal (10-15 years after menopause); increased bone reabsorption
due to low estrogen levels. Treated with estrogen replacement
Osteoporosis: what characterizes type 2?
Senile osteoporosis - affects men and women > 70 y/o
Osteoporosis: what races are affected most?
whites>blacks>asians
Osteoporosis: symptoms of vertebral crush fractures
acute back pain, loss of height, kyphosis
Osteoporosis: other
distal radius (Colles') fracures, vertebral wedge fracures.
Osteoporosis: see picure
0
Osteoporosis: PATHOLOGY - REPRODUCTIVE
(end of endocrine)
Benign prostatic hyperplasia: who gets BPH?
common in men > 50 y/o
Benign prostatic hyperplasia: what might cause it?
may be due to age-related increase in estradiol with possible sensitization of
the prostate to the growth promoting effects of DHT.
Benign prostatic hyperplasia: findings
nodular enlargement of the periurethral (lateral and middle) lobes of the
prostate gland, compressing the urethra to a vertical slit.
Benign prostatic hyperplasia: symptoms
increased frequency of urination, nocturia, difficulty in starting and stoping
the stream of urine, dysuria.
Benign prostatic hyperplasia: complications
may lead to distention and hypertrophy of the bladder, hydronephrosis, UTIs
Benign prostatic hyperplasia: premalignant lesion?
No
Hydatidiform mole: What is it?
pathologic ovum (empty egg - ovum with no DNA) resulting in a cystic
swelling of chorionic villi and proliferation of chorionic epithelium
(trophoblast).
Hydatidiform mole: Most common precursor of what?
choriocarcinoma
Hydatidiform mole: what happens to B-hCG?
elevated
Hydatidiform mole: findings
honeycombed uterus, cluster of grapes apearance
Hydatidiform mole: genotype
complete mole is 46,xx and is completely paternal in origin (no maternal
chromosomes); no associated fetus. PARTial mole is made up of 3 or more
PARTS (triploid or tetraploid)
Pregnancy-induced hypertension (preeclampsia-eclampsia): what is the triad?
hypertension, proteinuria, edema
Pregnancy-induced hypertension (preeclampsia-eclampsia): what makes it
eclampsia?
addition of seizures to the triad
Pregnancy-induced hypertension (preeclampsia-eclampsia): what % of
pregnant women?
0.07
Pregnancy-induced hypertension (preeclampsia-eclampsia): when does it
present?
20 weeks gestation to 6 weeks postpartum
Pregnancy-induced hypertension (preeclampsia-eclampsia): what increases
the likelihood?
preexisting hypertension, diabetes, chronic renal disease, autoimmune
disorders
Pregnancy-induced hypertension (preeclampsia-eclampsia): what is HELLP
syndrome?
Hemolysis, Elevated LFTs, Low Platelets
Pregnancy-induced hypertension (preeclampsia-eclampsia): Clinical features
headache, blurred vision, abdominal pain, edema of face and extremeties,
altered mentation, hyperreflexia
Pregnancy-induced hypertension (preeclampsia-eclampsia): Lab findings
thrombocytopenia, hyperuricemia
Pregnancy-induced hypertension (preeclampsia-eclampsia): Treatment
Delivery of fetus as soon as viable. Otherwise, bedrest, salt restriction,
monitoring and treatment of hypertension
Pregnancy-induced hypertension (preeclampsia-eclampsia): Treatment for
eclampsia (a medical emergency)
IV Magnesium sulfate, diazepam
Pregnancy complications: Abruptio placentae
premature separation of the placenta. Painful uterine bleeding (usually 3rd
trimester). Fetal death. May be associated with DIC
Pregnancy complications: Placenta accreta
defective decidual layer allows placenta to attach directly to myometrium.
Predisposed by prior C-section or inflamation. May have massive
hemorrhage after delivery.
Pregnancy complications: Placenta previa
attachment of the placenta to lower uterine segment. May occlude cervical os.
Painless bleeding in any trimester.
Pregnancy complications: Ectopic pregnancy
most often in fallopian tubes, predisposed by salpingitis (PID).
Cervical Pathology: Dysplasia and carcinoma in situ
Disordered epithelial growth; begins at basal layer and extends outward.
Classified as CIN 1, CIN 2, or CIN 3 (carcinoma in situ), depending on extent
of dysplasia. Associated with HPV. May progress to invasive carcinoma.
Cervical Pathology: Invasive carcinoma
Often squamous cell carcinoma. Pap smears can catch cervical dysplasia
(koilocytes) before it progresses to invasive carcinoma.
Cervical Pathology: AUTHOR
Gabi Rizzuto
Uterine pathology: most common tumor in female (hint - has increased
incidence in blacks)? Do they progress to malignancy?
leiomyoma; no.
Uterine pathology: endometriosis - most common site?
ovary
Uterine pathology: endometriosis in the myometrium = ?
adenomyosis
Uterine pathology: most common gyn malignancy? (hint - causes vaginal
bleeding in a postmenopausal women)
endometrial carcinoma
Uterine pathology: Leiomyosarcoma: does it arise de novo or from
leiomyoma?
de novo
PCOS (Stein-Leventhal syndrome): Major clinical manifestations include:
amenorrhea, infertility, obesity, and ----?
hirsutism
Ovarian cysts: the four types of ovarian cysts
follicular, corpus luteum, theca-lutein, chocolate
Ovarian cysts: blood containing cyst from ovarian endometriosis
chocolate cyst
Ovarian cysts: cyst that is associated with choriocarcinoma and moles
theca-lutein cyst
Ovarian cysts: cyst defined by hemorrhage into persistent corpus luteum
corpus luteum cyst
Ovarian cysts: cyst defined by distention of unruptured graafian follicle
follicular cyst
Ovarian germ cell tumors : that which is analagous to male seminoma
dysgerminoma
Ovarian germ cell tumors : produces alpha-fetoprotein
yolk sac tumor
Ovarian germ cell tumors : associated with elevated hCG
choriocarcinoma
Ovarian germ cell tumors : monodermal teratoma made up of only thyroid
tissue
struma ovarii
Ovarian germ cell tumors : most common germ cell tumor of ovary (90%)
teratoma
Ovarian germ cell tumors : True or False: immature teratomas are benign
False. Mature ("dermoid cyst") ones are benign, immature ones are
aggressively malignant
Ovarian non-germ cell tumors: bilateral non germ cell tumor with fallopian
tube like epithelium
serous cystadenoma
Ovarian non-germ cell tumors: Pseudomyxoma peritonei (intraperitoneal
accumulation of mucinous material) may be a consequence of which ovarian
non germ cell tumor?
mucinous cystadenocarcinoma
Ovarian non-germ cell tumors: tumor resembling bladder epithelium
brenner tumor
Ovarian non-germ cell tumors: triad of ovarian fibroma, ascites, and
hydrothorax = ?
Meigs' syndrome
Ovarian non-germ cell tumors: Pathology term for the small follicles filled
with eosinophilic secretions that are seen in granulosa cell tumors
Call-Exner bodies
Breast disease: Which one of the following does NOT put an individual at
increased risk for breast disease? Gender, age, early 1st menarche, late 1st
pregnancy, late menopause, family history, fibroadenoma/non-hyperplastic
cysts
fibroadenoma/hyperplastic cysts
Breast disease: Eczematous patches on the nipple w/ corresponding large
cell's with clear halo on histology are indicative of --?
Paget's disease & most likely an underlying ductal carcinoma
Breast disease: Fibrosis, cystic, sclerosing, & epithelial hyperplasia are all
histologic subtypes of what breast disease?
Fibrocystic disease (note: no increase risk of developing carcinoma)
Breast disease: Most common breast tumor in women < 25 years of age? is it
malignant or a precursor to malignancy?
Fibroadenoma. No, no.
Breast disease: A benign tumor of the breast that presents with nipple
discharge
Intraductal papilloma
Breast disease: Are malignant breast tumors more common pre or post
menopause
post
Hypertension: True of false: 50% is classified as secondary HTN (usually
resulting from renal disease)
false. (90% essential/primary, 10% secondary)
Hypertension: "read the questioner's mind": HTN predisposes individuals to
this disease (the one John Ritter died of)
aortic dissection
Hypertension: Pathology changes associated with HTN
hyaline thickening & atherosclerosis
Arteriosclerosis: This awful term refers to a stiffening of the arteries that
invovles the media. Particularly likely to occur at the radial & ulnar arteries.
Monckeberg arteriosclerosis
Atherosclerosis: True or false: atherosclerosis is a disease of small sized
arteries
false. affects elastic, large & medium muscular arteries.
Atherosclerosis: Earliest sign of atherosclerotic disease
fatty streak
Atherosclerosis: most likely location
abdominal aorta. (then coronary artery, popliteal artery, and carotid artery)
Ischemic heart disease: Type of angina resulting from coronary artery spasm
Prinzmetal's variant
Ischemic heart disease: This coronary artery branch is most commonly
implicated in myocardial infarction
LAD (left anterior descending)
Ischemic heart disease: most common cause of sudden cardiac death
(lethal) arrhythmia
Infarcts: red vs. pale: Solid tissues like the heart, brain, kidney and spleen
have only a single blood supply (not so good collaterals). Therefore infarcts
are more likely to be --?
pale
Infarcts: red vs. pale: 2 instances where red infarct is likely
(1) reperfusion (2) loose tissues with good collaterals - like the lungs or
intestine
Evolution of MI: Rank the following vessels from most to least commonly
occluded: RCA, LAD, circumflex
LAD>RCA>circumflex
Evolution of MI: Histologic changes on day 1 of an MI?
pallor of infarcted area; coagulative necrosis
Evolution of MI: days 2-4?
dilated vessels (hyperemia); neutrophil invasion; extensive coagulative
necrosis
Evolution of MI: days 5-10?
yellow-brown softening of infarcted region; macrophages present;
granulation tissue begins to grow in
Evolution of MI: after 7 weeks?
infarct is gray-white; scar complete
Diagnosis of MI: True or false: ECG is not diagnostic during the first 6 hours
following an MI
False; it is the gold standard within this time period
Diagnosis of MI: What is the test of choice within the first 24 hours?
CK-MB
Diagnosis of MI: This enzyme is elevated from 4 hours up to 10 days after an
MI and is the most specific protein marker
cardiac troponin I
Diagnosis of MI: on ecg, transmural infarction causes ______
ST elevation, Q wave changes
MI complications: Most common (90% of patients)
arryhthmias, esp. 2 days after infarct
MI complications: automimmune phenomen several weeks post-MI that
results in fibrinous pericarditis
Dressler's syndrome
MI complications: high risk of mortality
cardiogenic shock (large infarcts)
MI complications: seen about a week after the infarction
rupture of ventricular wall, septum, or papillary muscle
Cardiomyopathies: Most common
dilated (congestive) cardiomyopathy; heart looks like a ballon on X-ray
Cardiomyopathies: True or False: substance abuse is a common cause of
dilated cardiomyopathy
True; cocaine and alcohol especially
Cardiomyopathies: These two infectious diseases are associated with dilated
myopathy
coxsackievirus B and Chagas' disease
Cardiomyopathies: True or false: hypertrophic cardiomyopathy causes
systolic dysfunction
False; dilated myopathy causes systolic dysfunction, hypertrophic causes
diastolic
Cardiomyopathies: Half of hypertrophic myopathies are inherited as an
_________ trait (x-linked, dominant, etc.)
autosomal dominant; major cause of sudden death in young athletes
Cardiomyopathies: On echo in hypertrophic disease, the LV thickens and the
chamber looks how?
like a banana
Cardiomyopathies: These "-osis" diseases are major causes of
restrictive/obliterative cardiomyopathy
sarcoidosis, amyloidosis, hemochromatosis, endocardial fibroelastosis,
endomyocardial (Loffler's) fibrosis….also, scleroderma but it's not an -osis
Heart murmurs: Name two causes of holosystolic murmurs
1) VSD, 2) mitral regurg, and 3) tricuspid regurg
Heart murmurs: Widened pulse pressure seen with this diastolic murmur
aortic regurg
Heart murmurs: Describe the murmur associated with the most common
valvular lesion
Mitral prolapse; late systolic murmur following mid-systolic click
Heart murmurs: True or false: aortic stenosis causes a decrescendo-crescendo
murmur following an ejection click
False; ejection click is followed by a crescendo-decrescendo systolic murmur
Heart murmurs: cause of a continuous murmur loudest at time of S2?
patent ductus artieriosis
Heart murmurs: opening snap followed by late diastolic rumbling?
mitral stenosis
Cardiac tumors: most common heart tumor?
metastasis
Cardiac tumors: primary cardiac tumor in 1) adults and 2) children
adults=myxoma (almost always in left atrium); children=rhabdomyoma
CHF: fun gross pathologic term for changes in liver with CHF?
nutmeg
CHF: what are "heart failure cells"?
hemosiderin-laden macrophages in lung
CHF: dyspnea on exertion, pulmonary edema, and paroxysmal nocturnal
dyspnea are symptoms of?
left heart failure
CHF: patient says "I have to sleep upright." the clinical term for this is?
orthopnea
embolus types: most pulmonary emboli arise from?
DVT
embolus types: True or false: Amniotic fluid can lead to DIC
TRUE
deep vein thrombosis: what are the component of virchow's triad?
stasis, hypercoagulability, endothelial damage
cardiac tamponade: what is pulsus paradoxus?
greater than 10 mmHg drop in systolic on inspiration
cardiac tamponade: what is electrical alternans?
characteristic of tamponade on ECG in which QRS complex height varies
beat-to-beat
cardiac tamponade: AUTHOR
James Rosoff / Flora Waples-Trefil
Bacterial Endocarditis: What valve is usually involved in endocarditis?
Mitral
Bacterial Endocarditis: What valve indicated drug use if it is involved?
Tricuspid
Bacterial Endocarditis: Can endocarditis be non-bacterial?
Yes. It can be secondary to metastasis, renal failure (maranctic or
thrombotic), fungal
Bacterial Endocarditis: What type of endocarditis does s. Aureus cause?
rapid onset, high virulence, tends to occur secondary to infection elsewhere
Bacterial Endocarditis: What do the vegetations look like
Large.
Bacterial Endocarditis: What type of endocarditis does s. viridians cause?
subacute. Tends to have smaller vegetations.
Bacterial Endocarditis: What predisposes you to s.viridins endocarditis?
tends to occur on previously damaged valves, so rheumatic fever. It is
commonly seen after dental work.
Bacterial Endocarditis: What are the 8 sings of endocarditis?
JR=NO FAME Janeway lesions, Roth's spots, Nail-bed hemorrhages, Osler's
nodes, Fever, Anemia, Murmur (new), Emboli
Bacterial Endocarditis: What do Janeway Lesions look like?
multiple small flat erythematous lesions on palms and soles
Bacterial Endocarditis: What are roth spots?
round white spots on the retina surrounded by hemorrhage.
Bacterial Endocarditis: What are osler's nodes?
Tender raised lesions on the fingers and toes.
Bacterial Endocarditis: What is the etiology of these lesions?
Bacterial vegetations fliping off the heart valve and lodging in the periphery.
Rheumatic Fever/Rheumatic Heart Disease: What type of bacteria causes
rheumatic fever?
Group A beta-hemolytic strep
Rheumatic Fever/Rheumatic Heart Disease: when does it occur?
Children 5-15 years, four weeks after a bacterial infection
Rheumatic Fever/Rheumatic Heart Disease: Is the bacteria responsible for the
symptoms?
No. RF is an autoimmune reaction of a cross-reactive protein that is found in
the initial bacterial infection.
Rheumatic Fever/Rheumatic Heart Disease: What are the non cardiac clinical
signs of rheumatic fever?
FEVERSS - Fever, Erythema marginatum, valve damage, Elevated ESR,
Red-hot joints (migratory polyarthritis), Subcutaneous nodules, and St. Vitus
dance (chorea)
Rheumatic Fever/Rheumatic Heart Disease: What hear valves are effected?
Mitral (most frequent), Aortic, Tricuspid (5%) - high pressure valves mainly.
Rheumatic Fever/Rheumatic Heart Disease: What is an Aschoff body?
classic histological sign of RF, found in the myocardium, contained fibrinoid
material, fragmented collages, surrounded by giant cells.
Rheumatic Fever/Rheumatic Heart Disease: What are the cardiac signs of
RF?
Verrucious vegetations on the valve, pancarditis, possible pericardial
effusions and myocarditis (most common cause of death)
Pericarditis: Name four causes of serous pericarditis.
RAIL - Rheumatic Arthritis, Infection, Lupus, and Uremia
Pericarditis: What is serous pericarditis?
straw colored, protein rich exudates - non-purulent, and acute
Pericarditis: What are three causes of fibirnous exudates?
MI, Rheumatic fever, and Uremia
Pericarditis: Cloudy pericardial exudates indicated what?
Bacterial infection
Pericarditis: What are two causes of Hemorrhagic pericarditis?
malignancy and TB
Pericarditis: What is hemorrhagic pericarditis?
Bloody and inflammatory exudates
Pericarditis: What are the clinical signs of pericardial exudates?
pericardial pain, friction rub, decreased heart sounds, ST elevation
throughout, and pulses paradoxes (like cardiac tamponade)
Pericarditis: What are the long term sequela of pericarditis?
chronic adhesive or constrictive pericarditis
Pericarditis: What is constiricit pericadritis
Fibrous scarring in the pericardium obliterates the space and constrict the
right side of the heart (because it is less able to withstand the pressure)
Pericarditis: What types of pericaditis lead to this?
TB and pyrogenic staph infections
Syphilitic Heart Disease: What part of the heart does syphilis damage?
The vaso vasorum of the aorta
Syphilitic Heart Disease: What does this lead to?
Dilation of the aorta and valve ring
Syphilitic Heart Disease: What clinical results does this have?
it can cause an aortic aneurysm or valvular incompetence
Syphilitic Heart Disease: What parts of the aorta are effected
ascending and arch
Syphilitic Heart Disease: What is the appearance or the aorta?
Called a "tree-bark" apearance.
Buerger's Disease: Buerger's disease is also known as?
smoker's disease, thromboangiitis obliterans
Buerger's Disease: What are the Sx (5)?
intermittent claudication, superficial nodular phlebitis, cold sensitivity, severe
pain in affected part, may lead to gangrene
Buerger's Disease: What is the Tx?
Quit smokng
Takayasu's arteritits: Also known as ?
pulseless disease
Takayasu's arteritits: What is it?
thickening of aortic arch and/or proximal great vessels
Takayasu's arteritits: ESR elevated?
yes
Takayasu's arteritits: Primarily affects whom?
Young Asian Females
Takayasu's arteritits: Mnemomic
FAN MY SKIN On Wednesday
Takayasu's arteritits: Sx (7)
Fever, Arthritis, Night Sweats, Myalgia, Ocular Disturbances, Weak pulses in
uper extremities (FAN MY SKIN On Wednesday)
Temporal Arteritis: Also known as?
Giant Cell Arteritis
Temporal Arteritis: Affects what vessels?
medium and small arteries (usually carotid branches)
Temporal Arteritis: ESR elevated?
yes
Temporal Arteritis: Primarily affects whom?
Elderly Females
Temporal Arteritis: Sx (3)
Unilateral Headache, Jaw claudication, impaired vision
Temporal Arteritis: Many patients are also affected with this syndrome
Polymalgia Rheumatica
Temporal Arteritis: Tx (?)
Steroids
Polyarteritis Nodosa: How would you describe the inflammation in this
disease?
necrotizing, caused by immune complex deposition
Polyarteritis Nodosa: In which vessels?
small to medium-sized muscular arteries, renal and visceral vessels
Polyarteritis Nodosa: ESR elevated?
yes
Polyarteritis Nodosa: Sx (7) … and they are SO specific
fever,weight loss,malaise,abdominal pain,headache ,myalgia,hypertension
Polyarteritis Nodosa: Other findings
cotton-wool spots, microaneurysms, pericarditis, myocarditis, palpable
purpura
Polyarteritis Nodosa: What viral infection is found in 30% of PN patients?
Hepatitis B
Polyarteritis Nodosa: what antibody is associated with this disease?
P-ANCA
Polyarteritis Nodosa: What two ways can you remember the assoc Ab?
P-ANCA --> PAN (PolyArteritis Nodosa)
Polyarteritis Nodosa: What does P-ANCA refer to?
Perinuclear pattern of Antineutrophil Cytoplasmic Antibodies
Polyarteritis Nodosa: Primarily affects whom?
Young males
Polyarteritis Nodosa: Tx
Corticosteroids, Azathioprine, Cyclophosphamide
Wegener's Granulomatosis: What are three major findings (hint: they are
necrotizing)
Focal Necrotizing Vasculitis, Necrotizing granulomas of the lung and uper
airway, Necrotizing glomerulonephritis
Wegener's Granulomatosis: Sx (7)
Perforated nasal septum, Chronic Sinusitis, Otitis Media, Mastoiditis, Cough ,
Dyspnea, Hemoptysis
Wegener's Granulomatosis: What antibody is associated with this disease
C-ANCA
Wegener's Granulomatosis: What should you look for on CXR?
large nodular densities
Wegener's Granulomatosis: Tx
Corticosteroids, Azathioprine, Methotrexate
Kawasaki Disease: Who gets it?
infants, kids
Kawasaki Disease: What is the disease course?
acute, self-limiting
Kawasaki Disease: What vessels are involved?
small and medium sized
Kawasaki Disease: What does CRASH stand for
Conjunctivitis, Rash (truncal), Aneurysms of Coronary Arteries, Strawberry
tongue, changes in lips/oral mucosa, Hands and Feet show induration and
desquamation
Kawasaki Disease: Glomerular Pathology
275
Kawasaki Disease: What is prerenal azotemia?
selective rise in BUN during early renal failure
Kawasaki Disease: Define segmental.
involving part of the glomerular tuft
Kawasaki Disease: Nephritic Syndrome
0
Kawasaki Disease: hematuria, hypertension, oliguria, azotemia = ?
Nephritic Syndrome, "I" = inflammation
Kawasaki Disease: LM findings in post-strep glomerulonephritis?
lumpy bumpy and hypercellular w/ neutrophils
Kawasaki Disease: EM findings in post-strep glomerulonephritis?
subepithelial humps (from deposition of cationic antigen)
Kawasaki Disease: IF findings in post-strep glomerulonephritis?
granular
Kawasaki Disease: Goodpasture's is what type of hypersensistivity?
type II (IgG binding directly to BM)
Kawasaki Disease: Goodpasture's IF?
linear
Kawasaki Disease: Symptoms of Goodpasture's?
hemoptysis, hematuria
Kawasaki Disease: Membranoproliferative glomerulonephritis EM?
subendothelial humps; "tram track"
Kawasaki Disease: Course of crescentic glomerulonephritis?
rapid (the Red Crescent is the Islamic Red Cross, an organization that
provides relief during emergencies, like crescentic glomerulonephritis)
Kawasaki Disease: Course of Membranoproliferative glomerulonephritis?
slow
Kawasaki Disease: IgA nephropathy IF and EM?
mesangial deposits of IgA (Mes"A"ngium)
Kawasaki Disease: Which can be post infectious, IgA nephropathy or
Goodpasture's?
IgA nephropathy
Kawasaki Disease: Nephrotic Syndrome
0
Kawasaki Disease: Signs of nephrotic syndrome?
massive proteinuria, hypoalbuminemia, generalized edema, hyperlipidemia
(think "erotic" = an erection(edema) and ejaculate(massive proteinuria)
Kawasaki Disease: LM of membranous glomerulonephritis?
diffuse capillary and basement membrane thickening
Kawasaki Disease: IF of membranous glomerulonephritis?
granular
Kawasaki Disease: EM of membranous glomerulonephritis?
spike and dome ("if you have a spike in your dome, you must be insane in the
"membran"e," -Chirag)
Kawasaki Disease: Minimal change disease EM?
foot process effacement
Kawasaki Disease: Most common cause of childhood nephrotic syndrome?
minimal change disease
Kawasaki Disease: Focal segmental glomerular sclerosis LM?
segmental sclerosis and hyalinosis
Kawasaki Disease: Diabetic nephropathy LM?
Kimmelstiel-Wilson lesions
Kawasaki Disease: SLE (5 patterns of renal involvement) LM?
wire-loop apearance w/ extensive granular BM depsits in membranous
glomerulonephritis pattern
Kidney Stones: What is the most common kidney stone?
Calcium (with either oxalate of phosphate)
Kidney Stones: What kidney stone is associated with a bacterial infection?
Ammonium magnesium phosphate (struivte) stones are associated with urase
positive bugs that make ammonium
Kidney Stones: What are the two most common stone-forming bacteria?
proteus vulgaris and Staph.
Kidney Stones: What stones are associated with gout?
Uric acid stones
Kidney Stones: What else can cause uric acid stones?
Any disease with high cell turnover (remember that uric acid is a by-product
of DNA formation), so leukemia and myeloproliferative disease
Kidney Stones: What stones are associated with cystineuria?
cystine stones
Kidney Stones: What two stones are radiolucent?
Uric acid and cystine (the two purely metabolic causes)
Kidney Stones: What are the complications of stones?
Hydronephrosis and pyelonephritis
Kidney Stones: What causes calcium stones?
Anything that increases calcium in the blood, so high PTH, malignancy (bone
breakdown, PTH production), vitamin D overdose.
Renal Cell Carcinoma: Is this a common renal cancer?
Yes, the most common
Renal Cell Carcinoma: Who is prone to this?
males, ages 50-70, smokers, gene deletions on chromosome 3
Renal Cell Carcinoma: This is a cancer of what cell type?
renal tubule cells, histologically they apear clear.
Renal Cell Carcinoma: What are the clinical signs of this cancer?
flank pain, fever, hematuria, palpable mass, secondary polycythemia
Renal Cell Carcinoma: How does it spread?
It invades the renal veins and IVC, to spread hematogenously
Renal Cell Carcinoma: What hormones can it produce?
ACTH, prolactin, Parathyroid-like hormone, gonadotropins and renin.
Wilm's Tumor: Who gets this cancer?
Children 2-4 years
Wilm's Tumor: Is it common?
The most common renal cancer in children
Wilm's Tumor: What is the chromosomal abnormality that leads to this?
deletion of tumor supressor gene WT1 on chromosome 11
Wilm's Tumor: What tetrad is it associated with?
WAGR - Wilm's, Anirida (lack of an iris), Genitourinary malformation, and
Retardation
Wilm's Tumor: How does it present?
huge palpable mass and hemihypertrophy
Wilm's Tumor: What is the histological appearance?
mixed - with stromal, mesenchymal, tubular, glomerular and fibrous elements
Transitional Cell Carcinoma: Where does this cancer occur?
Urinary spaces (tract, calyces, pelvis, bladder)
Transitional Cell Carcinoma: Does it recur?
yes, often
Transitional Cell Carcinoma: How does it spread?
Local invasion
Transitional Cell Carcinoma: What can predispose you to it?
Pee SAC toxins - Phenacetin, Smoking, Aniline dye (benezenes), and
Cyclophsophimide.
Transitional Cell Carcinoma: How does it present?
Hematuria
Acid-Base Physiology: What is the primary disturbance in Metabolic
acidosis?
a decrease in bicarbonate
Acid-Base Physiology: What is the compensation?
A drop in CO2 by hyperventilation
Acid-Base Physiology: What are common causes?
diabetic ketoacidosis (production of ketone acids), diarrhea (loss of GI
bicarb), salisylate overdose, acetazoleamide (diuretic) OD, lactic acidosis,
renal failure (can't excrete organic acids), ethylene glycol ingestion
Acid-Base Physiology: What is the primary disturbance in respiratory
acidosis?
A build-up in CO2
Acid-Base Physiology: What is the compensation?
Increased bicarb reabosrobtion from the kidney
Acid-Base Physiology: What are some common causes?
COPD, airway obstruction, opiates and sedatives, guillan-barr or ALS,
Acid-Base Physiology: What is the primary disturbance in metabolic
alkalosis?
increased bicarbonate
Acid-Base Physiology: What is the compensation?
Increased CO2 by decreased respiration
Acid-Base Physiology: What are some common causes?
Vomiting, hyperaldosteronism (increased H+ secretion), loop or thiazide
diuretics (volume contraction)
Acid-Base Physiology: What is the primary disturbance in respiratory
alkalosis?
A drop in CO2
Acid-Base Physiology: What is the compensation?
increased excretion of bicarb by the kidney
Acid-Base Physiology: What are some common causes?
hyperventilation, high altitude, pneumonia and pulmonary embolus
(hypoxemia causes hyperventilation_
Acid-Base Physiology: What is the Henderson Haselbach equation?
pH = pKa + Log (HCO3-)/(.03*pCO2)
Acid Base Nomogram: Is there an awesome graph on page 277 that you
should know?
Yes
Acid Base Nomogram: basically four cases
0
Acid Base Nomogram: Low pH, low pCO2 (low HCO3-)
metabolic acidosis
Acid Base Nomogram: Low pH, high pCO2 (high HCO3-)
chronic respiratory acidosis
Acid Base Nomogram: High pH, low pC02 (low HC03-)
acute respiratory alkalosis
Acid Base Nomogram: High pH, high pCO2 (high HCO3-)
metabolic alkalosis
Acidosis/Alkalosis: Check arterial pH
0
Acidosis/Alkalosis: pH < 7.4
acidosis
Acidosis/Alkalosis: pH > 7.4
alkalosis
acidosis: P (CO2) > 40
Respiratory acidosis
acidosis: P (CO2) > 40, Hypoventilation or Hyperventilation
HYPO
acidosis: Causes
Acute lung disesae, chronic lung disease, Drugs (opioids, narcotics,
sedatives), Weakening of Resp. muscles
acidosis: P (CO2) < 40
0
acidosis: What should you do next?
Check Anion Gap
acidosis: What is the normal anion gap?
8-12 mEq/L
acidosis: Increased Anion Gap - 4 Causes
Renal Failure, lactic acidosis, ketoacidosis, aspirin ingestions
acidosis: Normal anion gap metabolic acidosis (4)
Diarrhea, sniffin glue, renal tubular acidosis, hyperchloremia
acidosis: pH > 7.4
alkalosis
acidosis: pCO2 < 40
Respiratory alkalosis
acidosis: respiratory acidosis Causes (2)
HYPERventilation, aspirin ingestion (early)
acidosis: pCO2 > 40
metabolic alkalosis w/ compensation
acidosis: metabolic alkalosis Causes (4)
vomiting, diuretic use, antacids, hyperaldosteronism
Anion gap acidosis: How do you calculate it
Na - Cl - HCO3
Anion gap acidosis: What is normal?
8-12 mEq/L
Anion gap acidosis, MUDPILES: M
Methanol
Anion gap acidosis, MUDPILES: U
Uremia
Anion gap acidosis, MUDPILES: D
DKA
Anion gap acidosis, MUDPILES: P
Paraldehyde or Phenformin
Anion gap acidosis, MUDPILES: I
Iron tablets or INH
Anion gap acidosis, MUDPILES: L
Lactic Acidosis
Anion gap acidosis, MUDPILES: E
Ethanol, Ethylene Glycol
Anion gap acidosis, MUDPILES: S
Salicylates
Acid Base Compensations: Metabolic acidosis
pCO2 = 1.5(HCO3) + 8 +/- 2
Acid Base Compensations: Metabolic alkalosis
pCO2 increases 0.7 mm Hg per 1 mEq/L HCO3 increase
Acid Base Compensations: Respiratory acidosis (acute)
HCO3 increases by 1 mEq/L for every 10 mmHg increase of pCO2
Acid Base Compensations: Respiratory acidosis (chronic)
HCO3 increases by 3.5 mEq/L for every 10 mmHg increase of pCO2
Acid Base Compensations: Respiratory alkalosis (acute)
HCO3 decreases by 2 mEq/L for every 10 mmHg decrease of pCO2
Acid Base Compensations: Respiratory alkalosis (chronic)
HCO3 decreases by 5 mEq/L for every 10 mmHg decrease of pCO2
Acute Pyelonephritis: Affects _______ of kidney
cortex
Acute Pyelonephritis: Spares ____________
glomeruli/vessels
Acute Pyelonephritis: _______ _______ in urine are pathognomonic
WBC casts
Chronic Pyelonephritis: Tubules may contain __________ casts
Eosinophilic
Chronic Pyelonephritis: Coarse ________, _________ scarring
Asymmetric corticomedullary
Diffuse Cortical Necrosis: infarction of _________ of both kidneys
cortex (cortices)
Diffuse Cortical Necrosis: due to combination of _________ and _________
vasospasm and DIC
Diffuse Cortical Necrosis: associated with _________ and _________
obstetric catastrophes and septic shock
Acute Tubular Necrosis: Most common cause of
renal failure
Acute Tubular Necrosis: reversible or irreversible
reversible
Acute Tubular Necrosis: fatal or non-fatal
fatal, if left untreated
Acute Tubular Necrosis: associated with (3)
renal ischemia (shock), crush injury (myoglobulinuria), toxins
Acute Tubular Necrosis: Death occurs most often during initial oliguric
phase; T or F
TRUE
Renal Papillary Necrosis: Associated with (3)
Diabetes mellitus, Acute pyelonephritis, Chronic phenacetin use
Acute Renal Failure: Definition
abrupt decline in renal function over a period of days
Acute Renal Failure: Will see increase in _______ & _______
BUN & Creatinine
Acute Renal Failure: Prerenal is due to decreased ______
RBF
Acute Renal Failure: Renal is due to
ATN, Ischemia, toxins
Acute Renal Failure: Post renal is due to
outflow obstruction
Acute Renal Failure: 3 causes of above
renal stones, BPH, neoplasia
Acute Renal Failure: bilateral or unilateral
bilateral
Pre or post renal failure: Urine osmolality > 500
prerenal
Pre or post renal failure: Urine osmolality < 350
renal or postrenal
Pre or post renal failure: urine Na < 10
prerenal
Pre or post renal failure: urine Na > 40
postrenal
Pre or post renal failure: urine Na > 20
renal
Pre or post renal failure: FE(Na) >4%
postrenal
Pre or post renal failure: FE(Na) <1%
prerenal
Pre or post renal failure: FE(Na) >2%
renal
Pre or post renal failure: BUN/Cr ratio <15
renal
Pre or post renal failure: BUN/Cr ratio >15
postrenal
Pre or post renal failure: BUN/Cr ratio > 20
prerenal
Pre or post renal failure: Chronic renal failure due to (2)
diabetes, hypertension
Pre or post renal failure: Consequences of Renal Failure (8) p.279
Why?
Pre or post renal failure: Anemia
lack of EPO
Pre or post renal failure: Renal osteodystrophy
lack of active Vit D
Pre or post renal failure: Arrythmia
hyperkalemia
Pre or post renal failure: Metabolic acidosis
decreased acid secretion
Pre or post renal failure: Uremia
increase in BUN and Cr
Pre or post renal failure: CHF/Pulmonary Edema
retention of Na and H20
Pre or post renal failure: Chronic Pyelonephritis
0
Pre or post renal failure: Hypertension
0
Pre or post renal failure: AUTHOR
Aaron Goldberg
Alcoholism: tremor, tachcardia, hypertension, malaise, nausea, delirium
tremens are symtpoms of what?
alcohol withdrawal
Alcoholism: when do you get symptoms of alcohol withdrawal?
in case of physiological tolerance and dependence when intake is interrupted
Alcoholism: what is disulfiram and how does it work?
disulfiram is a pharmacological treatment of alcoholism - negatively
conditions patient against EtOH
Alcoholism: a good possible referral to sustain EtOH abstinence in alcoholics
Alcoholics Anonymous and other peer groups
Alcoholism: 3 mechanisms of EtOH action
1) interpolates into membranes --> toxic effects, partic. in brain 2) alcohol
dehydrogenase converts EtOH to acetaldehyde, forms adducts with proteins
and nucleic acids, converted to acetate, Ac-CoA, FA synthesis, fatty liver 3)
increased NADH/NAD ratio
Complications of alcoholism: Condition in which these are seen: hepatitis and
cirrhosis, pancreatitis, dilated cardiomyopathy, peripheral neuropathy,
cerebellar degeneration, Wernicke-Korsakoff syndrome, testicular atrophy
and hyperestrinism, and Mallory-Weiss syndrome
alcoholism
Complications of alcoholism: name histological type of cirrhosis in
alcoholism
micronodular cirrhosis
Complications of alcoholism: accompanying symptoms of alcoholic cirrhosis
jaundice, hypoalbuminemia, coagulation factor deficiences, portal
hypertension
Complications of alcoholism: list clinical findings in alcoholic cirrhosis
besides jaundice
peripheral edema and ascites, encephalopathy, neurologic manifestations
(asterixis, flaping tremor of hands)
Complications of alcoholism: What is the cause of Wernicke-Korsakoff
syndrome?
thiamine (B1) deficiency, particularly in alcoholics
Complications of alcoholism: what is the presenting triad of Wernicke's
encephalopathy?
psychosis, ophthalmoplegia, and ataxia
Complications of alcoholism: distinguishing features of Korsakoff's from
Wernicke's
in Korsakoff, also *memory loss*, confabulation,confusion.
Complications of alcoholism: is Korsakoff's syndrome reversible?
No.
Complications of alcoholism: Tx for Wernicke-Korsakoff syndrome
IV Vitamin B1 (thiamine)
Complications of alcoholism: What is Mallory-Weiss syndrome?
longitudinal lacerations at the gastroesophageal junction caused by excessive
vomiting (for ex., in alcoholism) with failure of LES relaxation that could
lead to fatal hematemesis
Argyll Robertson pupil: name for a pupil that constricts with accomodation
but is not reactive to light, and what is it pathognomonic for?
Argyll Robertson pupil. Pathognomonic for 3' syphilis. "Prostitute's pupil"
accomodates but does not react.
Amyloidosis: detect what using apple green biorefringence on Conco red
stain?
amyloid
Amyloidosis: most common cause of amyloidosis?
primary light chain deposition seen with multiple myeloma.
Amyloidosis: another cause of primary amyloidosis?
Waldenstrom's macroglobulinemia.
Amyloidosis: Secondary amyloidosis can cause what in the kidney?
nephrotic syndrome
Amyloidosis: disease associated with beta amyloid deposition in cerebral
cortex
Alzheimer's
Amyloidosis: islet cell amyloid deposition characteristic of what
diabetes mellitus type 2
Aschoff body: "-------- body" found in rheumatic heart disease
Aschoff body (granuloma with giant cells)
Aschoff body: "------- cells" found in rheumatic heart disease
Anitschkow's cells (activated histiocytes) "Aschoff and Anitschow" -- two
RHussians with RHeumatic heart disease
Auer bodies (rods): peroxidase-positive cytoplasmic inclusions in
granulocytes and myeloblasts, name and primary association
Auer rods; primarily seen in acute promyelocytic leukemia (M3)
Auer bodies (rods): treatment of AML M3 can release what, leading to what?
release Auer rods, leading to DIC
Casts: RBC casts indicate
glomerular inflammation (nephritic syndromes), ischemia, or malignant
hypertension
Casts: how to determine if hematuria/pyuria is of renal origin
presence of casts
Casts: WBC casts indicate
inflammation in renal interstitium, tubules, and glomeruli
Casts: casts often seen in normal urine
hyaline casts
Casts: casts seen in chronic renal failure
waxy casts
Erythrocyte sedimentation rate: ESR elevated in
dramatically in infection, malignancy, connective tissue disease; also in
pregnancy, inflammatory disease, and anemia
Erythrocyte sedimentation rate: ESR lowered in
sickle cell anemia, CHF, and polycythemia
Erythrocyte sedimentation rate: Should ESR be used for asymptomatic
screening
No
Erythrocyte sedimentation rate: ESR used to monitor course of -----
temporal arteritis and polymyalgia rheumatica
Erythrocyte sedimentation rate: ESR is expensive and specific. T/F
false. Cheap and nonspecific.
Ghon complex: indicates TB granulomas with lobar or perihilar lymph node
involvement
Ghon focus and lymph node involvement, Ghon complex.
Ghon complex: Does a Ghon complex reflect primary or secondary TB?
primary.
Hyperlipidemia signs: plaque in blood vessel wall
atheromata
Hyperlipidemia signs: plaque or nodule composed of lipid-laden histiocytes
in skin, especially eyelids
xanthoma
Hyperlipidemia signs: lipid deposit in tendon, especially Achilles
tendinous xanthoma
Hyperlipidemia signs: lipid deposit in cornea, nonspecific (arcus senilis)
corneal arcus
Psammoma bodies: laminated, concentric, calcific spherules in tumor
Psammoma bodies
Psammoma bodies: Psammoma bodies seen in:
1. papillary adenocarcinoma of thyroid 2. serous papillary cystadenoma of
ovary 3. meningioma 4. malignant mesothelioma "PSaMMoma" Papillary
(thyroid), Serous (ovary), Meningioma, Mesothelioma
RBC forms: Biconcave RBC
normal
RBC forms: Spherocytes
hereditary spherocytosis, autoimmmune hemolysis
RBC forms: Elliptocyte
hereditary elliptocytosis
RBC forms: Macro-ovalocyte
megaloblastic anemia, marrow failure
RBC forms: Helmet cell, schistocyte
DIC, traumatic hemolysis
RBC forms: Sickle cell
obviously sickle cell anemia
RBC forms: Teardrop cell
myeloid metaplasia with myelofibroblasts
RBC forms: Acanthocyte
spiny apearance in abetalipoproteinemia
RBC forms: Target cell
Thalassemia, liver disease, HbC
RBC forms: Poikilocyte
Nonuniform shapes in TTP/HUS, microvascular damage, DIC
RBC forms: Burr cell
TTP/HUS
HLA subtypes!: HLA B27
Psoriasis, Ankylosing spondylitis, Inflammatory bowel disease, Reiter's
syndrome ("PAIR")
HLA subtypes!: HLA 13,17
Psoriasis
HLA subtypes!: HLA DR2
Multiple sclerosis, hay fever
HLA subtypes!: HLA DR3, DR4
Diabetes mellitus type I
HLA subtypes!: HLA DR5
Pernicious anemia -- B12 deficiency
HLA subtypes!: HLA DR7
Steroid-responsive nephrotic syndrome
Reed-Sternberg cells: Distinctive giant cell in blood; binucleate or bilobed
with 2 halves as mirror images ("owl's eyes"); name and disease association
Reed-Sternberg cells, necessary but not sufficient for dx of Hodgkin's
disease. Variants include lacunar cells in nodular sclerosis variant.
Reed-Sternberg cells: How many types of Hodgkin's disease?
4 - see also p. 241
Reed-Sternberg cells: Only variant of Hodgkin's seen more in women than
men
nodular sclerosis
Reed-Sternberg cells: prognosis of nodular sclerosis variant of Hodgkin's
excellent
Virchow's (sentinel) node: firm supraclavicular lymph node, often on left
side, easily palpable (ie, by medical students), also known as "jugular gland"
- name and association
Virchow's node - presumptive evidence of malignant visceral neoplasm
(classically stomach)
Peripheral blood smears: most common cause of microcytic hypochromic
anemia
iron deficiency
Peripheral blood smears: ferritin levels in microcytic hypochromic anemia
low
Peripheral blood smears: serum iron-binding capacity in microcytic
hypochromic anemia
elevated
Peripheral blood smears: lead poisoning gives what appearance on peripheral
smear
microcytic hypochromic
Peripheral blood smears: causes of megaloblastic anemia
folate or B12 deficiency
Peripheral blood smears: 5-7 lobes (hypersegmented) PMNs in
megaloblastic anemia
Peripheral blood smears: large RBCs (MCV >100) in
megaloblastic anemia
Peripheral blood smears: do you give folate to pt. deficient in B12?
Never
Peripheral blood smears: autoimmune disease that causes B12 deficiency;
what does it deplete?
pernicious anemia, depletes intrinsic factor
Peripheral blood smears: where is B12 absorbed in gut?
terminal ileum, with intrinsic factor from stomach
Peripheral blood smears: Target cells mnemonic
HALT (Hemoglobin C disease, Asplenia, Liver disease, Thalassemia)
Peripheral blood smears: Hemoglobin SS in what disease?
sickle cell anemia
Peripheral blood smears: molecular change B-globin GLU->VAL at #6
HbS
Peripheral blood smears: 8% of US african-americans carry what Hb
HbS
Peripheral blood smears: conditions in which HbSS cells sickle
hypoxia, dehydration, increased blood viscosity
Peripheral blood smears: vaso-occlusive crises with chest pain in young
african-americanl; consider
sickle cell anemia
Peripheral blood smears: aplastic crises in sickle cell anemia associated with
which virus
B19 virus
Peripheral blood smears: manifestation of sickle cell anemia in spleen
splenic sequestration crisis
Peripheral blood smears: increased risk of CVA in sickle cell anemia?
yes
Enzyme markers: AST or ALT used for MI?
AST only
Enzyme markers: AST or ALT more elevated in viral hepatitis
ALT>AST in viral hepatitis ("virALT")
Enzyme markers: AST or ALT more elevated in alcholic hepatitis
AST>ALT in alcoholic hepatitis ("ToAST")
Enzyme markers: Amylase elevation
acute pancreatitis, mumps
Enzyme markers: Low ceruloplasmin
Wilson's disease
Enzyme markers: Creatine phosphokinase elevated in
muscle disorders (Duchenne's muscular dystrophy), and MI
Enzyme markers: subtype of CPK elevated in MI
CPK-MB
Enzyme markers: GGT stands for and elevated in
gamma glutamyl transferase, various liver diseases
Enzyme markers: Lipase elevated in
acute pancreatitis
Enzyme markers: Alkaline phosphatase elevated in
Bone disease (Paget's disease of bone), obstructive liver disease
(hepatocellular carcinoma)
Immunohistochemical stains: Vimentin stains what
connective tissue
Immunohistochemical stains: Desmin stains what
muscle
Immunohistochemical stains: Cytokeratin stains what
epithelial cells
Immunohistochemical stains: Glial fibrillary acid proteins (GFAP) stains
what
neuroglia
Immunohistochemical stains: Neurofilament stains what
neurons
Immunohistochemical stains: AUTHOR
Shailen Sehgal
Enzyme Kinetics: _______ is elevated in a myocardial infarction. (AST,
ALT, or both)
AST
Enzyme Kinetics: In viral hepatitis, is ALT or AST more elevated?
ALT
Enzyme Kinetics: In alcoholic hepatitis, is ALT or AST more elevated?
AST
Enzyme Kinetics: ________ can be elevated in mumps or acute pancreatitis,
while _________ elevation is more specific for acute pancreatitis.
amylase, lipase
Enzyme Kinetics: What enzyme is elevated in Duchenne's muscular
dystrophy, and after a myocardial infarction?
CPK
Enzyme Kinetics: _______ can be elevated in Paget's disease and
hepatocellular carcinoma.
alkaline phosphatase
Enzyme Kinetics: Elevated GGT is seen in various diseases of which organ?
liver
Enzyme Kinetics: True or False? In a myocardial infarction, serum
LDH-1>LDH-2
TRUE
Enzyme Kinetics: Decreased serum ceruloplasmin is seen in _______
Wilson's Disease
Immunohistochemical Stain Corresponding cell type: (Match the stain with
the corresponding cell type)
0
Immunohistochemical Stain Corresponding cell type: Vimentin
connective tissue
Immunohistochemical Stain Corresponding cell type: Cytokeratin
Epithelial cells
Immunohistochemical Stain Corresponding cell type: Neurofilaments
neurons
Immunohistochemical Stain Corresponding cell type: Glial Fibrillary acid
proteins (GFAP)
neuroglia
Immunohistochemical Stain Corresponding cell type: Desmin
muscle
Pharmacokinetics: amount of drug in body/_______ = Vd
plasma drug concentration (note: Vd is Volume of Distribution)
Pharmacokinetics: rate of elimination of drug/[plasma drug] = ?
CL (Clearance)
Pharmacokinetics: (.7)(Vd)/CL = ?
T 1/2
Pharmacokinetics: A drug infused at a constant rate reaches about 94% of
steady state after _______ t 1/2s.
4
Dosage Calculations: A loading dose is calculated using this formula.
(Cp)(Vd)/F (note: Cp = target plasma concentration, and F = bioavailability)
Dosage Calculations: A maintenance dose is calculated using this formula.
(Cp)(CL)/F
Elimination of Drugs: Rate of elimination is proportional to _______ ______
in 1st order elimination.
drug concentration
Elimination of Drugs: In the case of EtOH, which is elimated by _____ order
elimination, a constant amount of drug is eliminated per unit time.
zero
Phase I vs. Phase II metabolism: Phase ____ (I or II) reactions yield slightly
polar metabolites that are often _____ (active or inactive)
I, active
Phase I vs. Phase II metabolism: Phase ____ (I or II) reactions yield very
polar metabolites that are often _____ (active or inactive) and are excreted by
the _______.
II, inactive, kidney
Phase I vs. Phase II metabolism: Phase II reactions are often of this type.
conjugation
Phase I vs. Phase II metabolism: Cytochrome P-450 is involved in _____
phase (I or II) reactions.
I
Drug Development: A patent lasts for _____ years after filing for application.
20
Drug Development: How many phases are there in drug development?
4
Drug Development: Drugs are first tested in patients in phase _____ of
clinical testing, pharmacokinetic safety is determined in phase ______ of
clinical testing, double blind tests are done in phase ____ and post-market
surveillance is done in phase _____.
2,1,3,4
Pharmacodynamics: In a dose response curve, a competitive antagonist shifts
the curve _____, while a non-competitive antagonist shifts the curve ______.
right, down
Pharmacodynamics: AUTHOR
HiralShah
Pharmacodynamics (continued): What pharmacologic relationship would
determine the existence of spare receptors?
EC50 < Kd
Pharmacodynamics (continued): What does it mean if EC50 and Kd are
equal?
The system does not have spare receptors
Pharmacodynamics (continued): A partial agonist acts on the same receptor
system as a full agonist? T/F
TRUE
Pharmacodynamics (continued): What's the main difference between a partial
agonist and a full agonist?
A partial agonist has a lower maximal efficacy.
Pharmacodynamics (continued): Is a partial agonist less potent than a full
agonist?
Not necessarily. It can be less, more or equally potent as a full agonist.
Antimicrobial Tx -- Mechanism of Action: The penicillin type drugs work by
blocking ------ synthesis, specifically by inhibiting this molecule from
cross-linking?
blocks bacterial cell wall synthesis by inhibition of peptidoglycan synthesis.
Antimicrobial Tx -- Mechanism of Action: Which other drugs (aside from
penicillin) have this same mechanism of action?
Imipenem, aztreonam and cephalosporins
Antimicrobial Tx -- Mechanism of Action: Bacitracin, vancomycin and
cycloserine block the synthesis of this molecule, preventing cell wall
synthesis
peptidoglycans
Antimicrobial Tx -- Mechanism of Action: These drugs block the 50s
ribosomal subunit
clindamycin, chloramphenicol, erythromycin, lincomycin, linezolid,
streptogramins "Buy AT 30, CELL at 50"
Antimicrobial Tx -- Mechanism of Action: These drugs block the 30s
ribosomal subunit
Aminoglycosides and tetracyclines "Buy AT 30, CELL at 50"
Antimicrobial Tx -- Mechanism of Action: These drugs block nucleotide
synthesis by interfering with the folate pathway
Sulfonamides (e.g. Bactrim), trimethoprim
Antimicrobial Tx -- Mechanism of Action: These drugs block DNA
topoisomerases
Quinolones (e.g. Cipro)
Antimicrobial Tx -- Mechanism of Action: Which drug blocks mRNA
synthesis
rifampin
Antimicrobial Tx -- Mechanism of Action: Which are the bacteriacidal Abx
Penicillin, cephalosporin, vancomycin, aminoglycosides, fluoroquinolones,
metronidazole
Antimicrobial Tx -- Mechanism of Action: These drugs disrupt the
bacterial/fungal cell membranes
polymyxins
Antimicrobial Tx -- Mechanism of Action: These specific disrupt fungal cell
membranes
amphotericin B, nystatin, fluconazole/azoles (FAN the fungal cell
membranes)
Antimicrobial Tx -- Mechanism of Action: What is the mechanism of action
of Pentamidine
Unknown
Penicillin: Which is the IV form and which is the oral form
G = IV, V=oral
Penicillin: Which of these is not a mechanism of penicillin action: (1) binds
penicillin-binding protein, (2) blocks peptidoglycan synthesis, (3) blocks
transpeptidase catalyzed cross-linking of cell wall and (4) activates autolytic
enzymes
Penicillin does not block peptioglycan synthesis, bacitracin, vancomycin and
cycloserine do that
Penicillin: T or F: penicillin is effective against gram pos and gram neg rods
False: penicillin is used to treat common streptococci (but not staph),
meningococci, gram pos bacilli and spirochetes (i.e. syphilis, treponema). Not
used to treat gram neg rods.
Penicillin: What should you watch out for when giving penicillin?
Hypersensitivity rxn (urticaria,severe pruritus) and hemolytic anemia
Methicillin, nafcillin, dicloxacillin: These drugs are used mainly for what
type of infection
Staphlococcal infection (hence very narrow spectrum)
Methicillin, nafcillin, dicloxacillin: T or F: these drugs have the same
mechanism of action as penicillin
TRUE
Methicillin, nafcillin, dicloxacillin: Are these drugs penicillinase resistant? If
so why?
Bulkier R group makes these drugs resistant to penicillinase
Methicillin, nafcillin, dicloxacillin: What should you watch out for when
giving these drugs?
Hypersensitivity rxn (urticaria,severe pruritus); methicillin can cuase
interstitial nephritis
Ampicillin and amoxicillin: T or F: these drugs have the same mechanism of
action as penicillin
TRUE
Ampicillin and amoxicillin: Which has greater oral bioavailability?
amOxicillin (O for Oral)
Ampicillin and amoxicillin: What do you use these for?
Ampicillin/amoxicillin HELPS to kill enterococci (H. influenzae, E. coli,
Listeria monocytogenes, Proteus mirabilis, Salmonella)
Ampicillin and amoxicillin: Can penicillinase effect these drugs efficacy?
Yes, they are penicillinase sensitive
Ampicillin and amoxicillin: Why not give these drugs with a penicillinase
inhibitor. Name one.
clavulanic acid
Ampicillin and amoxicillin: What should you watch out for when giving
these drugs?
Hypersensitivity rxn (ampicillin rash), pseudomembranous colitis
Carbenicillin, piperacillin, ticarcillin: Why are these considered to have an
extended spectrum?
Because they are effective against pseudomonas and other gram neg rods
(enterobacter and some species of klebsiella)
Carbenicillin, piperacillin, ticarcillin: What should you watch out for when
giving these drugs?
Hypersensitivity rxn
Carbenicillin, piperacillin, ticarcillin: Why does concomitant administration
with clavulanic acid increase the efficacy of these drugs?
Because they are penicillinase sensitive. (only piperacillin and ticarcillin)
Cephalosporins: What is the mechanism of action of Cephalosporins?
inhibit cell wall synthesis
Cephalosporins: How are they similar/different from penicillin?
both have a beta-lactam ring structure but cephalosporins are less susceptible
to penicillinases
Cephalosporins: What are the main similarities/difference between 1st and
2nd generation cephalosporins?
2nd gen has extensive gram neg coverage but weaker gram pos coverage
Cephalosporins: 1st gen covers what bugs?
gram positives (staph and strep), Proteus mirabilis, E. coli, Klebsiella (PEcK)
Cephalosporins: 2nd gen covers what bugs?
gram positives (staph and strep) though less so, H. influenzae, Enterobacter
aerogenes, Neisseria, Proteus mirabilis, E. coli, Klebsiella (HEN PEcK)
Cephalosporins: What can 3rd generation drugs do that 1st and 2nd
generation can't?
Cross the blood brain barrier
Cephalosporins: What are some other benefits of 3rd gen?
better activity against gram neg bugs resistant to beta-lactam drugs.
Ceftazidime for Pseudomonas and ceftriaxone for N. gonorrhea
Cephalosporins: What are the benefits of 4th gen (e.g. Cefipime)?
increased activity against Pseudomonas, gram pos organisms and more
beta-lactamase resistant (i.e. 4th gen combines 1st gen and 3rd gen
characteristics into super drug)
Cephalosporins: What drugs should you avoid taking with cephalosporins?
Aminoglycosides (increases nephrotoxicity) and ethanol (causes a
disulfiram-like rxn -- headache, nausea, flushing, hypotension)
Aztreonam: When would you use aztreonam?
Only to treat Klebsiella, Pseudomonas and Serratia sp.
Aztreonam: Is it beta-lactamase resistant?
Yes, this is one of the huge benefits of the drug, and it is not cross-reactive
with PCN!
Aztreonam: Which population of pt. is this drug good for?
The PCN-allergic patient that can't take aminoglycosides b/c of renal
insufficiency
Aztreonam: Are there any toxicity issues with this drug?
Not really. Generally well tolerated with occasional GI upset. Vertigo,
Headache and rare hepatotoxicity have been reported.
Imipenem/cilastatin: What is imipenem?
broad spectrum beta-lactamase-resistant abx
Imipenem/cilastatin: What do you always administer it with and why?
cilastatin -- it decreases inactivation of imipenem in renal tubules
Imipenem/cilastatin: What do you use it for?
Gram pos cocci, gram neg rods and anaerobes (broad spectrum)
Imipenem/cilastatin: What bug is it the drug of choice for?
Enterobacter
Imipenem/cilastatin: What are its side-effects
GI distress, skin rash, seizures at high conc.
Vancomycin: Is it bactericidal or bacteriastatic and why?
Bactericidal because it blocks cross linkage and elongation of peptidoglycan
by binding D-ala D-ala protion of cell wall.
Vancomycin: How does resistance to Vanco occur?
D-ala D-ala is replaced with D-ala D-lactate which vanco does not block
Vancomycin: What is it used for?
Used for serious infection that is resistant to other drugs (e.g. gram pos
multi-drug resistant organisms like S. aureus and C. difficile, methicillin
resistant staph (MRSA))
Vancomycin: What are the important toxicities of vanco?
generally NOT many problems except, Nephrotoxicity, Ototoxicity and
Thrombophlebitis
Vancomycin: What can happen with rapid infusion of vanco?
Red man's syndrome. Diffuse flushing which can be controlled by
pretreatment with anti-histamines and with slow infusion rate
Protein Synthesis Inhibitors: Which drugs target bacterial protein synthesis by
blocking the 30S unit vs 50S unit?
Buy AT 30, CELL at 50
Protein Synthesis Inhibitors: What does AT stand for?
A = Aminoglycosides (streptomycin, gentamicin, tobramycin an damikacin.
And T = Tetracyclines
Protein Synthesis Inhibitors: What does CELL stand for?
C = Chloramphenicol, E= Erythromycin, L= Lincomycin and L=
cLindamycin
Protein Synthesis Inhibitors: Which of the above are bactericidal?
Only the aminoglycosides are, the rest are bacteriostatic
Aminoglycosides: Name some aminoglycosides?
Gentamicin, neomycin, amikacin, tobramycin and streptomycin
Aminoglycosides: How do these drugs work?
They inhibit formation of the initiation complex in mRNA translation
Aminoglycosides: Why are they ineffective against anaerobes?
They require oxygen for uptake into bacteria
Aminoglycosides: When would you use aminoglycosides?
against severe gram-negative rod infections
Aminoglycosides: What drugs can you use aminoglycosides with for
synergy?
the drugs that inhibit cell wall synthesis (e.g. penicillin and cephalosporins -the beta-lactam antibiotics). Presumably this allows the drug to get in with
out reliance on oxygen transport
Aminoglycosides: What drug in this class is commonly used for bowel
surgery?
Neomycin
Aminoglycosides: What are the two major toxicities?
Nephrotoxicity (esp. when used with cephalosporins) and Ototoxicity (esp.
when used with loop diuretics). amiNOglycosides
Tetracyclines: Name some tetracylcines
Tetracycline, doxycycline, demeclocycline, minocycline
Tetracyclines: How does it work?
Blocks t-RNA attachment to 30S subunit
Tetracyclines: Which tetracycline can you use in patients with renal failure
and why?
Can use doxycycline because its elimination is fecal
Tetracyclines: Should you take these drugs with a glass of milk?
NO, because it intereferes with absorption in the gut as does antacids and
iron-containing preparations
Tetracyclines: What are tetracyclines used for?
VACUUM your Bed Room -- Vibrio cholerae, Acne, Chlamydia,
Ureaplasma, Urealyticum, Mycoplasma pneumoniae, Borrelia burgdorferi,
Rickettsia, tularemia
Tetracyclines: What are the common toxicities
GI distress, teeth discoloration, inhibition of bone growth in children,
Fanconi's syndrome and photosensitivity
Macrolides: Name some macrolides?
Erythromycin, azithromycin, clarithromycin
Macrolides: How do these drugs work?
inhibit protein synthesis
Macrolides: What are they used for?
URIs, pneumonias, STDs -- gram pos cocci in patients that are allergic to
PNC --- Mycoplasm, Legionella, Chlamydia, Neisseria.
Macrolides: Pneumonic for macrolide use?
Eryc's Niple is at his Mid Clavicular Line (Eryc is brand name for
erythromycin). Mycoplasm, Legionella, Chlamydia, Neisseria.
Macrolides: What are the major toxicities?
GI discomfort, acute cholestatic hepatitis, eosinophilia, skin rashes
Macrolides: What is the most common cause for non-compliance to
macrolides?
GI discomfort
Chloramphenicol: How does this drug work?
inhibits 50S peptidyltransferase
Chloramphenicol: Main use?
Meningitis (H. influenzae, N. meningitides, S. pneumo). Used conservatively
b/c of toxicity
Chloramphenicol: What are the main toxicities?
Anemia and aplastic anemia (both dose dependent), gray baby syndrome (in
premes b/c they lack UDP-glucoronyl transferase)
Clindamycin: How does it work?
blocks peptide bond formation at 50S
Clindamycin: When do you use it?
Anaerobic infections (e.g. Bacteroides fragilis and C.perfringens)
Clindamycin: Toxicities?
Pseudomembranous colitis, fever, diarrhea
Sulfonamides: Name some sulfonamides
Sulfamethoxazole (SMX), sulfisoxazole, triple sulfa and sulfadiazine
Sulfonamides: How does it work?
Inhibits bacterial folic acid synthesis from PABA by blocking
dihydropteroate synthase.
Sulfonamides: What are its uses?
Gram-positive, gram-negative, Nocardia, Chlamydia. Triple sulfas and SMX
for simple UTIs
Sulfonamides: Toxicities?
hypersensitivity rxn, hemolysis if G6PD deficient, nephorotoxicity
(tubulointerstitial nephritis), kernicterus in infants, displace other drugs from
albumin (e.g. warfarin)
Trimethoprim: How does it work?
inhibits folic acid pathway by blocking dihydrofolate reductase which
humans have as well
Trimethoprim: What are its uses?
used in combo with Sulfamethoxazole (TMP-SMX) causing a sequential
block of folate synthesis. Used for recurrent UTIs, Shigella, Salmonella, and
prophylaxis for PCP in AIDS patients
Trimethoprim: Toxicities?
Megaloblastic anemia, pancytopenia (may be alleviated with suplemental
folinic acid)
Fluoroquinolones: What the most famous floroquinolone?
Ciprfloxacin (treatment for Anthrax)
Fluoroquinolones: How does it work?
inhibits DNA gyrase (topoisomerase II)
Fluoroquinolones: What are its uses?
Gram neg rods or urinary and GI tract (incl. pseudomonas), Neisseria, some
gram pos sp
Fluoroquinolones: What population is contraindicated for use?
pregnancy and children
Fluoroquinolones: What are its toxicities?
GI upset, superinfection, skin rashes, headache, dizziness and tendonitis and
tendon rupture in adults. FluoroquinoLONES hurt attachment to BONES.
Metronidazole: How does it work?
forms toxic metabolites in the bacteria. Bactericidal.
Metronidazole: What are its uses?
anti-protozoal: Giardia, Entamoeba, Trichomonas, Gardnerella vaginalis,
anaerobes (bacteroides, clostridium)
Metronidazole: What is the role of Metronidazole in H. pylori infection?
Used as part of triple therapy: bismuth, amoxicillin and metronidazole
Metronidazole: Main toxicity?
disulfiram-like (antabuse) reaction to alcohol and headache
Metronidazole: Which drug do you use to treat anaerobic infections above the
diaphram and below the diaphram
anaerobes above diaphram: Clindamycin, and anaerobes below diaphram:
metronidazole
Polymyxins: How does it work?
disrupts osmotic properties of bacteria, acts like a detergent
Polymyxins: What is it used for?
resistant gram negative infections
Polymyxins: Toxicities?
neurotoxicity, ATN
Isoniazid: How does it work?
decreases synthesis of mycolic acid
Isoniazid: What is it used for?
MTB (mycobacterium tuberculosis). The only agent used as solo prophylaxis
against TB
Isoniazid: Toxicities?
Hemolysis if G6PD deficient, neurotoxicity, hepatotoxicitiy, drug induced
SLE. INH, Injures Neurons and Hepatocytes
Isoniazid: What vitamin prevents neurotoxicity
Vitamin B6 (pyridoxine)
Isoniazid: Why are toxicities particularly important to monitor in patients
taking INH?
INH half-lives are different in fast versus slow acetylators!
Rifampin: How does it work?
inhibits DNA-dependent RNA polymerase
Rifampin: What is it used for?
MTB, meningococcal prophylaxis
Rifampin: Toxicities?
Minor hepatotoxicity and increases P-450
Rifampin: How can it be used for leprosy?
rifampin delays resistance to dapsone when used for leprosy
Rifampin: What would happen if you used rifampin alone?
get rapid resistance
Rifampin: What does it do to bodily fluids?
makes them red/orange in color
Rifampin: What are the 4 R's of Rifampin
RNA polymerase inhibitor, Revs up microsomal p-450, Red/Orange body
fluids, Resistance is rapid
Anti-TB Drugs: What are the anti-TB drugs?
Rifampin, Ethambutol, Streptomycin, Pyrazinamide, Isoniazid (INH) -RESPIre
Anti-TB Drugs: What do you use for TB prophylaxis?
INH
Anti-TB Drugs: What toxicity is common to all?
hepatotoxicity
Anti-TB Drugs: AUTHOR
Michael Shino
Resistance mechanisms for various antibiotics: Most common resistance
mechanism for penicillins / cephalosporins.
Beta-lactamase cleavage of beta-lactam ring.
Resistance mechanisms for various antibiotics: Most common resistance
mechanism for aminoglycosides.
Modification via acetylation, adenylation, or phosphorylation.
Resistance mechanisms for various antibiotics: Most common resistance
mechanism for vancomycin.
Terminal D-ala of cell wall component replaced with D-lac; decrease affinity.
Resistance mechanisms for various antibiotics: Most common resistance
mechanism for Chlorampenicol.
Modification via acetylation.
Resistance mechanisms for various antibiotics: Most common resistance
mechanism for macrolides.
Methylation of rRNA near erythromycin's ribosome-binding site.
Resistance mechanisms for various antibiotics: Most common resistance
mechanism for tetracycline.
Decrease uptake or increase transport out of cell.
Resistance mechanisms for various antibiotics: Most common resistance
mechanism for sulfonamides.
Altered enzyme (bacterial dihydropteroate synthetase), decrease uptake, or
increase PABA synthesis.
Nonsurgical antimicrobial prophylaxis: Drug of choice for meningococcal
infection.
Rifampin (drug of choice), minocycline.
Nonsurgical antimicrobial prophylaxis: Drug of choice for gonorrhea.
Cefriaxone.
Nonsurgical antimicrobial prophylaxis: Drug of choice for syphilis.
Benzathine penicillin G.
Nonsurgical antimicrobial prophylaxis: Drug of choice for history of
recurrent UTIs.
TMP-SMX.
Nonsurgical antimicrobial prophylaxis: Drug of choice for Pneumocystis
carinii pneumonia.
TMP-SMX (drug of choice), aerosolized pentamindine.
Anti-fungal therapy: Mechanism of action of the anti-fungal therapy
polyenes.
Form artificial pores in the cytoplasmic membrane.
Anti-fungal therapy: Mechanism of action of the anti-fungal therapies
terbinafine and azoles.
Terbinafine blocks the conversion of squalene to lanosterol. Azoles block the
conversion of lanosterol to ergosterol.
Anti-fungal therapy: Mechanism of action of the anti-fungal therapy
flucytosine.
Blocks the production of purines from the precurors.
Anti-fungal therapy: Mechanism of action of the anti-fungal therapy
griseofulvin.
Disrupts microtubles.
Amphotericin B: Mechanism of action of Amphotericin B.
Binds ergosterol (unique to fungi); forms membrane pores that allow leakage
of electrolytes and disrupt homeostasis. "Amphotericin 'tears' holes in the
fungal membrane by forming pores."
Amphotericin B: Clinical uses of Amphotericin B.
Used for a wide spectrum of sytemic mycoses. Cryptococcus, Blastomyces,
Coccidioides, Aspergillus, Histoplasma, Candida, Mucor (systemic mycoses).
Intrathecally for fungal meningitis; does not cross blood-brain barrier.
Amphotericin B: Symptoms of Amphotericin B toxicity.
Fever/chills ("shake and bake"), hypotension, nephrotoxicity, arrhythmias
("amphoterrible").
Nystatin: Mechanism of action of Nystatin.
Binds to ergosterol, disrupting fungal membranes.
Nystatin: Clinical use of Nystatin.
Swish and swallow for oral candidiasis (thrush).
Fluconazole, ketoconazole, clotrimazole, miconazole, itraconazole,
voriconazole.: Mechanism of action for fluconazole, ketoconazole,
clotrimazole, miconazole, itraconazole, voriconazole.
Inhibits fungal steroid (ergosterol) synthesis.
Fluconazole, ketoconazole, clotrimazole, miconazole, itraconazole,
voriconazole.: Clinical uses of fluconazole, ketoconazole, clotrimazole,
miconazole, itraconazole, voriconazole.
Systemic mycoses. Fluconazole for cryptococcal meningitis in AIDS patients
and candidal infections of all types (i.e., yeast infections). Ketoconazole for
Blastomyces, coccidioides, Histoplasma, Candida albicans; hypercortisolism.
Fluconazole, ketoconazole, clotrimazole, miconazole, itraconazole,
voriconazole.: Symptoms of fluconazole, ketoconazole, clotrimazole,
miconazole, itraconazole, voriconazole toxicity.
Hormone synthesis inhibition (gynecomastia), liver dysfunction (inhibits
cytochrome P-450), fever, chills.
Flucytosine: Mechanism of action of Flucytosine.
Inhibits DNA synthesis byconversion to fluorouracil, which competes with
uracil.
Flucytosine: Clinical uses of Flucytosine.
Used in sytemic fungal infections (e.g. Candida, Cryptococcus).
Flucytosine: Symptoms of Flucytosine toxicity.
Nausea, vomitting, diarrhea, bone marrow supression.
Caspofungin: Mechanism of action for Caspofungin.
Inhibits cell wall synthesis.
Caspofungin: Clinical use of Caspofungin.
Invasive aepergillosis.
Caspofungin: Symptoms of Caspofungin toxicity.
GI upset, flushing.
Terbinafine: Mechanism of action of Terbinafine.
Inhibits the fungal enzyme squalene epoxidase.
Terbinafine: Clinical use of Terbinafinel.
Used to treat dermatophytoses (especially onychomycosis).
Griseofulvin: Mechanism of action of Griseofulvin.
Interfers with microtubule function; disrupts mitosis. Deposits in
keratin-contianing tissues (e.g. nails).
Griseofulvin: Clinical use of Griseofulvin.
Oral treatment of superficial infections; inhibits growth of dermatophytes
(tinea, ringworm).
Griseofulvin: Symptoms of Griseofulvin toxicity.
Teratogenic, carcinogenic, confusion, headaches, increase warfarin
metabolism.
Antiviral chemotherapy: Viral adsorption and penetration into the cell is
blocked by ---------.
Gama-globulins (non-specific).
Antiviral chemotherapy: Uncoating of the virus after its penetration into the
cell is blocked by --------.
Amantadine (influenza A).
Antiviral chemotherapy: Early viral protein synthesis is blocked by --------.
Fomivirsen (CMV).
Antiviral chemotherapy: Viral nuclei acid synthesis is blocked by --------.
Purine, pyrimidine analogs; reverse transcriptase inhibitors.
Antiviral chemotherapy: Late viral protein synthesis and processing is
blocked by --------.
Methimazole (variola); protease inhibitors.
Antiviral chemotherapy: Packaging and assembly of new viron is blocked by
--------.
Rifampin (vaccinia).
Amantadine: Mechanism of action of Amantadine.
Blocks viral penetration/uncoating; may buffer pH of endosome. Also causes
the release of dopamine from intact nerve terminals. "Amantadine blocks
influenza A and rubellA and causes problems with the cerebellA."
Amantadine: Clinical uses of Amantadine.
Prophylaxis for influenza A; Parkinson's disease.
Amantadine: Symptoms of Amantadine toxicity.
Ataxia, dizziness, slurred speech. (Rimantidine is a derivative with fewer
CNS side effects.)
Zanamivir: Mechanism of action of Zanamivir.
Inhibits influenza neuraminidase.
Zanamivir: Clinical use of Zanamivir.
Both influenza A and B.
Ribavirin: Mechanism of action of Ribavirin.
Inhibits synthesis of guanine nucleotides by competitively inhibiting IMP
dehydrogenase.
Ribavirin: Clinical use of Ribavirin.
RSV (respiratory syncytial virus).
Ribavirin: Symptoms of Ribavirin toxicity.
Hemolytic anemia. Severe teratogen.
Acyclovir: Mechanism of aciton of Acyclovir.
Perferentially inhibits viral DNA polymerase when phosphorylated by viral
thymidine kinase.
Acyclovir: Clinical use of Acyclovir.
HSV, VZV, EBV. Mucocutaneous and genital herpes lesions. Prophylaxis in
immunocompromised patients.
Acyclovir: Symptoms of Acyclovir toxicity.
Delirium, tremor, nephrotoxicity.
Ganciclovir (DHPG dihydroxy-2-propoxymethyl guanine): Mechanism of
action of Ganciclovir.
Phosphorlation by viral kinase; perferentially inhibits CMV DNA
polymerase.
Ganciclovir (DHPG dihydroxy-2-propoxymethyl guanine): Clinical use of
Ganciclovir.
CMV, especially in immunocompromised patients.
Ganciclovir (DHPG dihydroxy-2-propoxymethyl guanine): Symptoms of
Ganciclovir toxicity.
Leukopenia, neutropenia, thrombocytopenia, renal toxicity. More toxic to
host enzymes than acyclovir.
Foscarnet: Mechanism of action of Foscarnet.
Viral DNA polymerase inhibitor that binds to the pyrophophate binding site
of the enzyme. Does not require activation by viral kinase. "FOScarnet =
pyroFOSphate analog."
Foscarnet: Clinical use of Foscarnet.
CMV retinitis in immunocompromised patients when ganciclovir fails.
Foscarnet: Symptoms of Foscarnet toxicity.
Nephrotoxicity.
HIV therapy: Saquinavir, ritonavir, indinavir, nelfinavir, amprenavir are
example of this type of anti-HIV drug.
Protease inhibitor.
HIV therapy: Mechanism of action of protease inhibitors.
Inhibit assembly of new virus by blocking protease enzyme.
HIV therapy: Symptoms of protease inhibitor toxicity.
GI intolerance (nausea, diarrhea), hyperglycemia, lipid abnormalities,
thrombocytopenia (indinavir).
HIV therapy: Reverse transcriptase inhibitors:
0
HIV therapy: Zidovudine (AZT), didanosine (ddI), zalcitabine (ddC),
stavudine (d4T), lamivudine (3TC), and abacavir are examples of --------reverse transcriptase inhibitors.
Nucleoside.
HIV therapy: Nevirapine, delavirdine, and efavirenz are examples of --------reverse transcriptase inhibitors.
Non-nucleoside.
HIV therapy: Mechanism of action of reverse transcriptase inhibitors.
Preferentially inhibit reverse transcriptase of HIV; prevent incorporation of
viral genome into host DNA.
HIV therapy: Symptoms of reverse transcriptase inhibitor toxicity.
Bone marrow supression (neutropenia, anemia), periphral neuropathy, lactic
acidosis (nucleosides), rash (non-nucleosides), megaloblastic anemia (AZT).
HIV therapy: Highly active antiretroviral therapy (HAART) generally entails
combination therapy with ---------- and -----------.
Protease inhibitors, reverse transcriptase inhibitors.
HIV therapy: When should HIV therapy be initiated?
When patients have low CD4 counts (<500 cells/mm3) or high viral load.
HIV therapy: -------- is used during pregnancy to reduce risk of fetal
transmission.
AZT.
Interferons: Mechanism of action of Interferons.
Glycoproteins from human leukocytes that block various stages of viral RNA
and DNA synthesis.
Interferons: Clinical use of Interferons.
Chronic hepatitis B and C, Kaposi's sarcoma.
Interferons: Symptoms of Interferon toxicity.
Neutropenia.
Antiparasitic drugs: Clinical uses of Ivermectin.
Onchocerciasis "rIVER blindness treated with IVERmectin".
Antiparasitic drugs: Clinical uses of Mebendazole / thiabendazole.
Nematode/roundworm (e.g., pinworm, whipworm) infections.
Antiparasitic drugs: Clinical uses of Pyrantel pamoate.
Giant roundworm (Ascaris), hookworm (Necator/Ancylostoma), pinworm
(Enterobius).
Antiparasitic drugs: Clinical uses of Praziquantel.
Trematode/fluke (e.g., schistosomes, Paragonimus, Clonorchis) and
cysticercosis.
Antiparasitic drugs: Clinical uss of Niclosamide
Cestode/tapeworm (e.g., Diphyllobothrium latum, Taenia species) infections
except cysticercosis.
Antiparasitic drugs: Clinical uses of Pentavalent antimony.
Leishmaniasis.
Antiparasitic drugs: Clinical uses of Chloroquine, quinine, mefloquine,
atovaquone, proguanil.
Malaria.
Antiparasitic drugs: Clinical uses of Primaquine.
Latent hypnozoite (liver) forms of malaria (Plasmodium vivax, P.ovale).
Antiparasitic drugs: Clinical uses of Metronidazole.
Giardiasis, amebic dysentery (Entamoeba histolytica), bacterial vaginitis
(Gardnerella vaginalis), Trichomonas.
Antiparasitic drugs: Clinical uses of Pentamidine.
Pneumocystis carinii pneumonia prophylaxis.
Antiparasitic drugs: Clinical uses of Nifurtimox.
Chagas' disease, American trypanosomiasis (Trypanosoma cruzi).
Antiparasitic drugs: Clinical uses of Suramin.
African trypanosomiasis (sleeping sickness).
Pharmacology - CNS / Neurologic drugs: Parasympathetic preganglionic
neurons release the neurotransmitter -------- which act on -------- receptors.
Ach, nicotinic.
Pharmacology - CNS / Neurologic drugs: Parasympathetic postganglionic
neurons release the neurotransmitter -------- which act on ------- receptors.
Ach, muscarinic.
Pharmacology - CNS / Neurologic drugs: Sympathetic preganglionic neurons
to sweat glands release the neurotransmitter ------- which act on ------receptors.
Ach, nicotinic.
Pharmacology - CNS / Neurologic drugs: Sympathetic postganglionic
neurons to sweat glands release the neurotransmitter ------- which act on
------- receptors.
Ach, muscarinic.
Pharmacology - CNS / Neurologic drugs: Sympathetic preganglionic neurons
to glands, cardiac and smooth muscles release the neurotransmitter ------which act on ------- receptors.
Ach, nicotinic.
Pharmacology - CNS / Neurologic drugs: Sympathetic postganglionic
neurons to glands, cardiac and smooth muscles release the neurotransmitter
------- which act on ------- receptors.
NE, alpha and beta
Pharmacology - CNS / Neurologic drugs: Sympathetic preganglionic neurons
to renal vascular smooth muscle release the neurotransmitter ------- which act
on ------- receptors.
Ach, nicotinic.
Pharmacology - CNS / Neurologic drugs: Sympathetic postganglionic
neurons to renal vascular smooth muscle release the neurotransmitter ------which act on ------- receptors.
Dopamine, D1
Pharmacology - CNS / Neurologic drugs: Sympathetic preganglionic neurons
to the adrenal medulla release the neurotransmitter ------- which act on ------receptors.
Ach, nicotinic.
Pharmacology - CNS / Neurologic drugs: Sympathetic preganglionic neurons
to the adrenal medulla synapse directly on ------- cells of the adrenal medulla.
Chromaffin.
Pharmacology - CNS / Neurologic drugs: Somatic neurons synapse directly
on -------- muscle and release the neurotransmitter ------- which act on ------receptors.
skeletal muscle, Ach, nicotinic.
Autonomic drugs: Cholinergic:
0
Autonomic drugs: Ach is synthesized from acetyl-CoA and choline by the
enzyme ---------.
Choline acetyltransferase.
Autonomic drugs: The transport of choline into the nerve terminal can be
inhibited by --------.
Hemicholinium.
Autonomic drugs: The release of transmitter from vesicles in the nerve
ending require the entry of ------ into the neuron.
Calcium.
Autonomic drugs: --------- inhibits the release of the stored Ach.
Botulinum toxin.
Autonomic drugs: The action of Ach in the synapse is terminated by its
metabolism to acetate and choline by the enzyme ---------.
Acetylcholinesterase.
Noradrenergic:: In the noradrenergic nerve terminal, tyrosine is hydroxylated
to -------, which is decarboxylated to --------, which is finally hydroxylated to
NE.
DOPA, dopamine.
Noradrenergic:: Dopamine is transported into vesicles for hydroxylation to
NE. This transport can be blocked by the drug --------.
Reserpine.
Noradrenergic:: The action of NE and DA is terminated by --------- and
----------.
Reuptake, diffusion (different than for Ach).
Noradrenergic:: --------- inhibits the release of the stored NE.
Guanethidine.
Noradrenergic:: The --------- drugs promote catecholamine release.
Amphetamine.
Noradrenergic:: The drugs --------- and ---------- inhibit the reuptake of NE.
Cocaine, TCA.
Noradrenergic:: The release of NE from a sympathetic nerve ending is
modulated by ---------, --------- and ---------.
NE, Ach, angiotensin II.
Noradrenergic:: NE inhibits its own release at the noradrenergic nerve
terminal through --------- receptors.
Alpha 2.
Noradrenergic:: Angiotensin II --------- (inhibits / stimulates) the release of
NE from the noradrenergic nerve terminal.
Stimulates.
Noradrenergic:: Ach inhibits the release of NE from the noradrenergic nerve
terminal by binding to --------- receptors.
M1.
Direct agonists:: Clinical application and action of Bethanechol.
Postoperative and neurogenic ileus and urinary retention. / Activates bowel
and bladder smooth muscle.
Direct agonists:: Clinical application and action of Carbachol and
Pilocarpine.
Glaucoma. / Activates ciliary muscle of eye (open angle), pupillary sphincter
(narrow angle).
Indirect agonists (anticholinesterases):: Clinical application / action of
Neostigmine.
Postoperative and neurogenic ileus and urinary retention, myasthenia gravis,
reversal of neuromuscular junction blockade (postoperative). / Increase
endogenous Ach.
Indirect agonists (anticholinesterases):: Clinical application / action of
Pyridostigmine.
Myasthenia gravis. / Increase Ach; increase strength.
Indirect agonists (anticholinesterases):: Clinical application / action of
Edrophonium.
Diagnosis of myasthenia gravis (extremely short acting). / Increase
endogenous Ach.
Indirect agonists (anticholinesterases):: Clinical application / action of
Physostigmine.
Glaucoma (crosses blood-brain barrier) and atropine overdose. / Increase
endogenous Ach.
Indirect agonists (anticholinesterases):: Clinical application / action of
Echothiophate.
Glaucoma. / Increase endogenous Ach.
Indirect agonists (anticholinesterases):: Symptoms of cholinesterase inhibitor
poisoning.
Diarrhea, Urination, Miosis, Bronchospasm, Bradycardia, Excitation of
skeletal muscle and CNS, Lacrimation, Sweating, Salivation (also abdominal
cramping). "DUMBBELSS".
Indirect agonists (anticholinesterases):: Cholinesterase inhibitor poisoning
may be caused by ---------.
Parathion and other organophosphates.
Indirect agonists (anticholinesterases):: The cholinesterase regenerator ------can be used as an antidote for cholinesterase inhibitor poisoning.
Pralidoxime.
Indirect agonists (anticholinesterases):: Mechanism of action of Pralidoxime.
Cholinoreceptor blockers:: Clinical uses of the muscarinic antagonist
Atropine.
Cholinoreceptor blockers:: Side effects of Atropine.
Regenerates active cholinesterase, chemical antagonist, used to treat
organophosphate exposure.
Dilate pupils, decrease acid secretion in peptic ulcer disease, decrease
urgency in mild cystitis, decrease GI motility, reduce airway secretions, and
treat organophosphate poisoning. "Blocks SLUD: Salivation, Lacrimation,
Urination, Defecation."
Increase body temp, rapid pulse, dry mouth, dry/flushed skin, disorientation,
mydriasis with cycloplegia, and constipation. "Atropine parasympathetic
block side effects: Blind as bat, Red as a beet, Mad as a hatter, Hot as a hare,
Dry as a bone."
Cholinoreceptor blockers:: Hexamethonium (ganglionic blocker) blocks
-------- receptors.
Nicotinic.
Cholinoreceptor blockers:: AUTHOR
Tzivia Moreen
antimuscarinic drugs: "tropi" are anti-muscarinic
while vacationing in the tropics you lie on a beach and your muscles waste
away!
antimuscarinic drugs: benztropine is used to treat
Parkinson's disease
antimuscarinic drugs: scopolamine is used to treat
motion sickness
antimuscarinic drugs: scopolamine is an antimuscarinic that does not convert
to the mnemonic!
0
antimuscarinic drugs: name 2 antimuscarinic drugs that act on the CNS
benztropine, scopolamine
antimuscarinic drugs: name a muscarinic used to treat motion sickness
scopolamine
antimuscarinic drugs: name a muscarinic used to treat Parkinson's disease
benztropine
antimuscarinic drugs: mechanism of action of benztropine
antimuscarinic
antimuscarinic drugs: mechanism of action of scopolamine
antimuscarinic
antimuscarinic drugs: name three antimuscarinics that act on eye
atropine, homatropine, tropicamide
antimuscarinic drugs: the action of atropine is ______
produce mydriasis, cycloplegia
antimuscarinic drugs: mechanism of atropine is
antimuscarinic
antimuscarinic drugs: the action of homatropine is ______
produce mydriasis, cycloplegia
antimuscarinic drugs: mechanism of homatropine is
antimuscarinic
antimuscarinic drugs: the action of tropicamide is
produce mydriasis, cycloplegia
antimuscarinic drugs: mechanism of tropicamide is
antimuscarinic
antimuscarinic drugs: ipatropium is used to treat
asthma, COPD
antimuscarinic drugs: mechanism of ipatropium is
antimuscarinic
antimuscarinic drugs: name an antimuscarinic used to treat asthma and COPD
ipatropium
neuromuscular blocking drugs: neuromuscular blocking drugs are used for
muscle paralysis in surgery or mechanical ventilation
neuromuscular blocking drugs: name a depolarising neurmuscular blocking
drug
succinylcholine
neuromuscular blocking drugs: name 6 nondepolarizing neuromuscular
blocking drugs
tubocurarine
neuromuscular blocking drugs: *mnemonic -- the "cur" drugs are
nondepolarizing neuromuscular blocking agents
atracurium
neuromuscular blocking drugs: is succinylcholine depolarizing or
nondepolarizing?
depolarizing
neuromuscular blocking drugs: is tubocurarine depolarizing or
nondepolarizing?
nondepolarizing
neuromuscular blocking drugs: is atracurium depolarizing or
nondepolarizing?
nondepolarizing
neuromuscular blocking drugs: is mivacurium depolarizing or
nondepolarizing?
nondepolarizing
neuromuscular blocking drugs: is pancuronium depolarizing or
nondepolarizing?
nondepolarizing
neuromuscular blocking drugs: is vacuronium depolarizing or
nondepolarizing?
nondepolarizing
neuromuscular blocking drugs: is rapacuronium depolarizing or
nondepolarizing?
nondepolarizing
neuromuscular blocking drugs: what is tubocurarine used for
nondepolarizing neuromuscular blockade
neuromuscular blocking drugs: what agents are used to reverse
neuromuscular blockade by succinylcholine?
cholinesterase inhibitors in phase II (ex -- neostigmine)
neuromuscular blocking drugs: what phase of succinylcholine neuomuscular
bloackade is reversible?
phase II (repolarized but blocked)
neuromuscular blocking drugs: what agents are used to reverse pahse I
neuromuscular blockade by succinylcholine?
phase I Succinylcholine neuromuscular blockade cannot be reversed
neuromuscular blocking drugs: what phase of succinylcholine neuomuscular
bloackade is irreversible?
phase I Succinylcholine neuromuscular blockade cannot be reversed
neuromuscular blocking drugs: what is atracurium used for
nondepolarizing neuromuscular blockade
neuromuscular blocking drugs: what is the effect of cholinesterase inhibitors
on succinylcholine neuromuscular blockade?
phase I: cholinesterase inhibitors potentiates the blockade phase II:
cholinesterase inhibitors reverse the blockade
neuromuscular blocking drugs: what cholinesterase inhibitor is used to
reverse phase II of succinylcholine neuromuscular blockade?
neostigmine
neuromuscular blocking drugs: what is mivacurium used for
nondepolarizing neuromuscular blockade
Dantrolene: what is dantrolene used for
treat malignant hyperthermia
Dantrolene: what causes malignant hyperthermia
use inhalation anesthetics and succinylcholine together
Dantrolene: what inhalation anesthetic DOES NOT cause malignanat
hyperthermia?
N2O
Dantrolene: what is dantrolene used for
neuroleptic malignant syndrome
Dantrolene: what is neuroleptic malignant syndrome
a toxicity of antipsychotic drugs
Dantrolene: what drug is used to treat malignant hyperthermia
dantrolene
Dantrolene: what is the mechanism of dantrolene
prevents release of Ca++ from saarcoplasmic reticulum of skeletal muscle
Sympathomimetics: epinephrine, NE, isoproterenol, dopamine, and
dobutamine are all________________
catecholamines
Sympathomimetics: catecholamines are_____________________
sympathomimetics
Sympathomimetics: name 5 catecholamines
EPI, NE, Isoproterenol, dopamine, dobutamine
Sympathomimetics: what receptors does epinephrine act on?
alpha-1, alpha-2, beta-1, beta-2 adrenergics
Sympathomimetics: what receptors does NE work on?
alpha-1, alpha-2, beta-1 adrenergics
Sympathomimetics: what receptors does isoproterenol work on?
beta-1 = beta-2 adrenergics
Sympathomimetics: what receptors does dopamine work on?
D1 = D2, D1 and D2 more than beta, beta more than alpha
Sympathomimetics: what receptors does dobutamine work on?
beta-1 > beta-2
Sympathomimetics: which catecholamines are agonists to alpha-adrenergic
receptors
EPI, NE > dopamine
Sympathomimetics: which catecholamines are agonists to beta-1 adrenergic
receptors
EPI, NE, Isoproterenol, dopamine, dobutamine
Sympathomimetics: which catecholamines are agonists to beta-2 adrenergic
receptors
EPI, isoproterenol, dopamine and dobutamine (less)
Sympathomimetics: what is epinephrine used to treat?
anaphylaxis, open-angle glaucoma, asthma, hypotension
Sympathomimetics: what is norepinephrine used to treat?
hypotension (but decreases renal perfusion)
Sympathomimetics: what is isoproterenol used to treat?
AV block
Sympathomimetics: what is dopamine used to treat
shock with renal failure, heart failure
Sympathomimetics: what is dobutamine used to treat
shock, heart failure
Sympathomimetics: what catecholamine is used to treat anaphylaxis
epinephrine ("EPI-pen")
Sympathomimetics: what catecholamines are used to treat hypotension
EPI, NE
Sympathomimetics: what catecholamine is used to treat asthma
epinephrine
Sympathomimetics: what catecholamine is used to treat AV block
isoproterenol
Sympathomimetics: what catecholamines are used to treat shock
doapmine, dobutamine
Sympathomimetics: what is the action of amphetamine
indirect general adrenergic agonist, releases stored catecholamines
Sympathomimetics: what is the action of ephedrine
indirect general adrenergic agonist, releases stored catecholamines
Sympathomimetics: what is amphetamine used to treat
narcolepsy, obesity, attention deficit disorder
Sympathomimetics: what is ephedrine used to treat
nasal decongestion, urinary incontinence, hypotension
Sympathomimetics: name three sympathomimetic drugs used to treat
hypotension
epinephrine, norepinephrin, ephedrine
Sympathomimetics: what is the action of phenylephrine
adrenergic agonist, alpha-1 > alpha-2
Sympathomimetics: what is the action of albuterol
adrenergic agonist, beta-2 >beta-1
Sympathomimetics: what is the action of terbutaline
adrenergic agonist, beta-2 >beta-2
Sympathomimetics: what is phenylephrine used for?
pupil dilator, vasoconstriction, nasal decongestion
Sympathomimetics: what sympathomimetics are used to treat nasal
congestion
ephedrine, phenylephrine
Sympathomimetics: what is the mechanism of cocaine
indirect general adrenergic agonist, catecholamine uptake inhibitor
Sympathomimetics: what is the action of cocaine
vasoconstriction, local anesthesia
Sympathomimetics: what is the mechanism of clonidine
centrally acting alpha-adrenergic agonist, decreases central adrenergic
outflow
Sympathomimetics: what drug has the same mechanism as amphetamine
ephedrine
Sympathomimetics: what is the mechanism of alpha-methyldopa
centrally acting alpha-adrenergic agonist, decreases central adrenergic
outflow
Sympathomimetics: what drug has the same mechanism as clonidine
alpha-methyldopa
Sympathomimetics: what are clonidine and alpha-methyldopa used to treat
hypertension, especially in renal disease because they do not decreased blood
flow to the kidney
Sympathomimetics: what sympathomimetic is used to treat urinary
incontinence
ephedrine
Sympathomimetics: what sympathomimetic is used to treat attention deficit
disorder
amphetamine
Sympathomimetics: what sympathomimetic is used to treat narcolepsy
amphetamine
alpha-blockers: name a nonselective irreversible alpha blocker
phenoxybenzamine
alpha-blockers: name a nonselective reversible alpha blocker
phentolamine
alpha-blockers: what is the mechanism of phenoxybenzamine
nonselective irreversible alpha blocker
alpha-blockers: what is the mechanism of phentolamine
nonselective reversible alpha blocker
alpha-blockers: what are phenoxybenzamine and phentolamine used for
pheochromocytoma
alpha-blockers: what are the side effects of nonselective alpha blockers
orthostatic hypotension, reflex tachycardia
alpha-blockers: name 3 alpha-1 selective adrenergic blockers
prazosin, terazosin, doxazosin
alpha-blockers: what is the mechanism of prazosin
alpha-1 selective adrenergic blocker
alpha-blockers: what is the mechanism of terazosin
alpha-1 selective adrenergic blocker
alpha-blockers: what is the mechanism of doxazosin
alpha-1 selective adrenergic blocker
alpha-blockers: what are alpha-1 selective adrenergic alpha blockers used for
hypertension, urinary retention in BPH
alpha-blockers: what are the side effects of alpha-1 blockers
orthostatic hypotension, dizziness, headache
alpha-blockers: what is prazosin used for?
hypertension, urinary retention in BPH
alpha-blockers: what drugs have the same action as prazosin
terazosin, doxazosin
alpha-blockers: what are the side effects of terazosin?
orthostatic hypotension, dizziness, headache
alpha-blockers: what selective alpha blockers cause orthostatic hypotension
phenoxybenzamine, phentolamine, terazosin, prazosin, doxazosin
alpha-blockers: name an alpha-2 selective adrenergic blocker
yohimbine
alpha-blockers: what is yohimbine used for
impotence (effectiveness controversial)
alpha-blockers: what alpha blockers are used to treat pheochromocytoma
phenoxybenzamine, phentolamine
beta-blockers ("lol"s): name some beta-blockers
propranolol, metoprolol, atenolol, nadolol, timolol, pindolol, esmolol,
labetalol
beta-blockers ("lol"s): what is the mechanism of propanolol
selective beta-adrenergic blocker
beta-blockers ("lol"s): what is the mechanism of metoprolol
selective beta-adrenergic blocker
beta-blockers ("lol"s): what is the mechanism of esmolol
selective beta-adrenergic blocker
beta-blockers ("lol"s): what is the mechanism of pindolol
selective beta-adrenergic blocker
beta-blockers ("lol"s): what are beta-blockers used to treat
hypertension, angina, MI, SVT, CHF, glaucoma
beta-blockers ("lol"s): how do beta blockers treat hypertension
decrease cardiac output, decrease renin secretion
beta-blockers ("lol"s): how do beta blockers treat angina
decrease heart rate, decrease cardiac contractility, decreased O2 consumption
beta-blockers ("lol"s): why are beta blockers used to treat MI
decrease MI mortality
beta-blockers ("lol"s): which beta blockers are used to treat SVT
propanolol, esmolol
beta-blockers ("lol"s): how do propanolol and esmolol treat SVT
decrease AV conduction velocity
beta-blockers ("lol"s): how do beta blockers treat CHF
slow progression of chronic failure
beta-blockers ("lol"s): which beta blocker is used to treat glaucoma
timolol
beta-blockers ("lol"s): what is timolol used to treat glaucoma
decrease secretion of aqueous humor
beta-blockers ("lol"s): what are the toxic effects of beta blockers
impotence, exacerbation of asthma, caution in diabetes
beta-blockers ("lol"s): what are the cardiovascular toxic effects of beta
blockers
bradychardia, AV block, CHF
beta-blockers ("lol"s): what are the CNS adverse effects of beta blockers
sedation, sleep alterations
beta-blockers ("lol"s): which beta blockers are beta-1 selective
acebutolol, betaxolol, esmolol, atenolol, metaprolol (A BEAM of beta-1
blockers)
beta-blockers ("lol"s): which beta-1 blocker is short-acting
esmolol
beta-blockers ("lol"s): which beta blockers are non-selective
propanolol, timolol, pindolol, nadolol, labetalol
beta-blockers ("lol"s): which beta blocker also blocks alpha receptors
labetalol (all others are spelled "olol")
glaucoma drugs: which alpha agonists are used to treat glaucoma
epinephrine, brimonidine
glaucoma drugs: which beta blockers are used to treat glaucoma
timolol, betxolol, carteolol
glaucoma drugs: which cholinomimetics are used to treat glaucoma
pilocarpine, carbachol, physostigmine, echothiophate
glaucoma drugs: which diuretics are used to treat glaucoma
acetazolamide, dorzolamide, brinzolamide
glaucoma drugs: which prostaglandin is used to treat glaucoma
latanoprost
glaucoma drugs: what classes of drugs are used to treat glaucoma
alpha agonists, beta blockers, cholinomimetics, diuretics, prostaglandins
(*mnemonic -- treating glaucoma is easy as ABCD)
glaucoma drugs: what is the effect of epinephrine in glaucoma
increase outflow of aqueous humor
glaucoma drugs: what are the side effects of epinephrine treatment in
glaucoma
mydriasis, stinging
glaucoma drugs: what glaucoma should epinephrine NOT be used for
closed-angle glaucoma
glaucoma drugs: what is the effect of brimonidine in glaucoma
decreased aqueous humor synthesis
glaucoma drugs: what are the side effects of brimonidine treatment in
glaucoma
no pupillary or vision changes
glaucoma drugs: what is the effect of beta-blocker treatment in glaucoma
decrease aqueous humor secretion
glaucoma drugs: what are the side effects of beta blocker treatment in
glauzoma
no pupillary or vision changes
glaucoma drugs: what is the effect of cholinomimetics in glaucoma
ciliary muscle contraction, opening of trabecular meshwork, increase outflow
of aqueous humor
glaucoma drugs: what are the side effects of cholinomimetics in glaucoma
miosis, cyclospasm
glaucoma drugs: what is the effect of diuretic treatment in glaucoma
inhibition of carbonic anhydrase --> decrease HCO3 secretion --> decrease
aqueous humor secretion
glaucoma drugs: what are the side effects of diuretics in glaucoma
no pupillary or vision changes
glaucoma drugs: what is the effect of prostaglandin (latanoprost) treatment in
glaucoma
increase outflow of aqueous humor
glaucoma drugs: what is the side effect of prostaglandin treatment in
glaucoma
darkens color of iris (browning)
glaucoma drugs: which drugs used to treat glaucoma increase outflow of
aqueous humor
cholinomimetics, prostaglandin, epinephrine
glaucoma drugs: can you use epinephrine in closed-angle glaucoma
NO
glaucoma drugs: brimonidine is used to treat what eye disease
glaucoma
glaucoma drugs: what kind of drug is latanoprost
prostaglandin
glaucoma drugs: latanoprost is used to treat what eye disease
glaucoma
glaucoma drugs: which glaucoma drugs decrease aqueous secretion
beta blockers, diuretics
L-dopa/carbidopa: what does L-dopa stand for
levodopa
L-dopa/carbidopa: what is the mechanism of action of L-dopa/carbidopa
increase dopamine level in brain
L-dopa/carbidopa: what is L-dopa/carbidopa used to treat
Parkinson's disease
L-dopa/carbidopa: how is L-dopa different from dopamine
L-dopa can cross the blood-brain barrier, dopamine cannot
L-dopa/carbidopa: what happens to L-dopa after it crosses the BBB
converted to dopamine by dopa decarboxylase
L-dopa/carbidopa: what enzyme convertes L-dopa to dopamine
dopa decarboxylase
L-dopa/carbidopa: what is the function of carbidopa
peripheral decarboxylase inhibitor
L-dopa/carbidopa: why is carbidopa given with L-dopa
increase L-dopa availability in CNS by inhibiting decarboxylase in periphery,
also limits peripheral side effects
L-dopa/carbidopa: what are the side effects of L-dopa.carbidopa treatment
arrhythmias, dyskinesias
L-dopa/carbidopa: why do patients taking L-dopa get arrhythmias
peripheral effects of dopamine
L-dopa/carbidopa: why do patients taking L-dopa get dyskinesias
excess dopamine stimulation in CNS
Parkinson's disease drugs: what drugs are used to treat Parkinson's disease
dopamine agonists, MAO inhibitors, antimuscarinics
Parkinson's disease drugs: specifically, which drugs are used to treat
Parkinson's
Bromocriptine, Amantadine, Levodopa, Selegiline, Antimuscarinics
(BALSA)
Parkinson's disease drugs: which dopamine agosts are used to treat
Parkinson's
L-dopa/carbidopa, bromocriptine, pramipexole, ropinirole, amantadine
Parkinson's disease drugs: what is the action of bromocriptine in Parkinson's
ergot alkaloid, partial dopamine agonist
Parkinson's disease drugs: what is the action of amantadine in Parkinson's
enhances dopamine release
Parkinson's disease drugs: what MAOI is used to treat Parkinson's
selegiline
Parkinson's disease drugs: what is the mechanism of selegiline
selective MAO type B inhibitor
Parkinson's disease drugs: what antimuscarinic is used to treat Parkinson's
benztropine
Parkinson's disease drugs: what is the effect of benztropine in Parkinson's
improves tremor, rigidity, little effect on bradykinesia
Sumatriptan: what is sumatriptan used for
acute migraine, cluster headache attacks
Sumatriptan: what is the mechanism of sumatriptan
5-HT1D agonist
Sumatriptan: what is the half life of sumatriptan
less than 2 hours
Sumatriptan: what are the side effects of sumatriptan
chest discomfort, mild tingling
Sumatriptan: what are the contraindications for sumatriptan
patients with CAD or Prinzmetal's angina
Epilepsy drugs: which drugs are used for simple and complex partial seizures
phenytoin, carbamazapine, lamotrigine, gabapentin, topiramate,
phenobarbital
Epilepsy drugs: what types of seizures is phenytoin indicated for
simple and complex partial, tonic-clonic, status epilepticus
Epilepsy drugs: what types of seizures is carbamazepine indicated for
simple and complex partial, tonic-clonic
Epilepsy drugs: what types of seizures is lamotrigine indicated for
simple and complex partial, tonic-clonic
Epilepsy drugs: what types of seizures is gabapentin indicated for
simple and complex partial, tonic-clonic
Epilepsy drugs: what types of seizures is topiramate indicated for
simple and complex partial
Epilepsy drugs: what types of seizures is phenobarbital indicated for
simple and complex partial, tonic-clonic
Epilepsy drugs: what drugs can be used for tonic-clonic seizures
phenytoin, carbamazapine, lamotrigine, gabapentin, phenobarbital, valproate
Epilepsy drugs: what drugs can be used for absence seizures
valproate, ethosuximide
Epilepsy drugs: what drugs can be used for status epilepticus
phenytoin, benzodiazapines (diazepam, lorazepam)
Epilepsy drugs: what types of seizure is valproate indicated for
tonic-clonic, absence
Epilepsy drugs: what types of seizure is ethosuximide inidcated for
absence
Epilepsy drugs: what type of seizure are benzodiazepines indicated for
status epilepticus
Epilepsy drugs: other than anti-seizure, what else is phenytoin used for
class 1B anti-arrhythmic
Epilepsy drugs: how should a patient taking carbamazepine be followed
monitor LFT's weekly
Epilepsy drugs: which seizure drugs have adjunct use
gabapentin, topiramate
Epilepsy drugs: which seizure drug is safest in pregnant women
phenobarbital
Epilepsy drugs: which seizure drug is used in Crigler-Najjar II
phenobarbital
Epilepsy drugs: what are the advantages of phenobarbital
can be used in pregnant women, Crigler Najjar II
Epilepsy drug toxicities: what are the side effects of benzodiazepines
sedation, tolerance, dependence
Epilepsy drug toxicities: what are the side effects of carbamazepine
diplopia, ataxia, CYP induction, blood dyscrasias, liver toxicity
Epilepsy drug toxicities: what are the side effects of ethosuximide
GI distress, lethargy, headache, urticaria, Stevens-Johnson syndrome
Epilepsy drug toxicities: what are the side effects of phenobarbital
sedation, CYP induction, tolerance, dependence
Epilepsy drug toxicities: what are the side effects of phenytoin
nystagmus, diplopia, ataxia, sedation, ginigival hyperplasia, hirsutism,
anemias, teratogenic
Epilepsy drug toxicities: what are the side effects of valproate
GI distress, rare by fatal hepatotoxicity, neural tube defects (spina bifida)
Epilepsy drug toxicities: what are the side effects of lamotrigine
life-threatening rash, Stevens-Johnson syndrome
Epilepsy drug toxicities: what are the side effects of gabapentin
sedation, movement disorders
Epilepsy drug toxicities: what are the side effects of topiramate
sedation, mental dulling, kidney stones, weight loss
Epilepsy drug toxicities: which anti-epileptic drug is teratogenic
phenytoin
Epilepsy drug toxicities: which anti-epileptic drug can cause dependence
benzodiazepines, phenobarbital
Epilepsy drug toxicities: which anti-epileptic drug can cause neural tube
defects
valproate
Epilepsy drug toxicities: which anti-epileptic drugs can cause GI distress
valproate, ethosuximide
Epilepsy drug toxicities: it is necessary to check LFT's with which
anti-epileptic drugs
carbamazepine, valproate
Epilepsy drug toxicities: which anti-epileptic drugs cause CYP induction
phenobarbital, carbamazepine
Epilepsy drug toxicities: which anti-epileptic drugs can cause blood problems
carbamazepine, phenytoin
Epilepsy drug toxicities: which anti-epileptic drugs can cause
Stevens-Johnson syndrome
lamotrigine, ethosuximide
Epilepsy drug toxicities: which anti-epileptic drugs can cause diplopia
carbamazepine, phenytoin
Phenytoin: what is the mechanism of phenytoin action
use-dependent blockade of Na+ channels
Phenytoin: what is the clinical application of phenytoin
grand mal seizures
Phenytoin: what are the toxicities of phenytoin
nystagmus, ataxia, diplopia, lethargy
Phenytoin: what are the chronic toxicities of phenytoin
gingival hyperplasia in children, peripheral neuropathy, hirsutism,
megaloblastic anemia, malignant hyperthermia (rare)
Phenytoin: should pregnant women take phenytoin
NO -- teratogenic
Phenytoin: why does phenytoin cause megaloblastic anemia
causes decreased vitamin B-12
Barbiturates: name 4 barbiturates
phenobarbital, pentobarbital, thiopental, secobarbital
Barbiturates: what is the mechanism of barbiturate action
increase duration of Cl channel opening --> decreased neuron firing -->
facilitate GABA-A action
Barbiturates: how do barbiturates facilitate GABA-A action
increase duration of Cl channel opening which decreases neuron firing
(Barbidurate increases duration
Barbiturates: is barbiturate action on the CNS stimulatory or inhibitory
inhibitory
Barbiturates: what is the clinical application of barbiturates
sedative for anxiety, seizures, insomnia, anesthesia induction (thiopental)
Barbiturates: which barbiturate is used for anesthesia induction
thiopental
Barbiturates: what are the side effects of barbiturates
dependence, additive CNS depression effects with alcohol, respiratory or CV
depression (death), drug interactions due to CYP induction
Barbiturates: what should you find out before giving a patient barbiturates
what other medications they take, because of CYP induction and many drug
interactions
Barbiturates: what happens if you give barbiturates to a patient in
alcohol-induced coma or DT's
they might DIE!! Because of additive effect of barbiturates and alcohol -->
respiratory depression
Barbiturates: when are barbiturates contra-indicated
porphyria
Barbiturates: can barbiturates cause dependence
Barbiturates: My friend Barb was very anxious so her doctor gave her
barbiturates to increase the duration of the time she could speak in public
without freaking out and having a seizure. She became so dependent on it that
she recommended it to her friend Portia who couldn't take it because of
porphyria. One day Barb drank too much alcohol and took her barbiturates
and never woke up! THE END
Benzodiazepines: name a bunch of benzodiazepines
YES
clinical pharmacology made ridiculous. Period
diazepam, lorazepam, triazolam, temazepam, oxazepam, midazolam,
chlordiazepoxide (all have ZZZ in them)
Benzodiazepines: what is the mechanism of benzodiazepines
increase frequency of Cl channel opening --> facilitate GABA-A action
(Frenzodiazepines increase frequency)
Benzodiazepines: which GABA receptors are facilitated by barbiturates and
bezodiazepines
GABA-A
Benzodiazepines: what are the clinical applications of benzodiazepines
anxiety, spasticity, status epilepticus (diazepam), detoxification (alcohol
withdrawal, DT's)
Benzodiazepines: which benzodiazepine can be used for status epilepticus
diazepam
Benzodiazepines: what drugs can be used to treat alcohol withdrawal
benzodiazepines
Benzodiazepines: which benzodiazepines are short-acting
TOM thumb: Triazolam, Oxazepam, Midazolam
Benzodiazepines: what are the toxic effects of benzos
dependence, additive CNS depression effects with alcohol
Benzodiazepines: how are benzos better than barbiturates
less respiratory depression and coma risk
Benzodiazepines: how do you treat benzo overdose
flumazenil
Benzodiazepines: what is flumzenil used for
benzo overdose
Benzodiazepines: how does flumazenil work
competitive antagonist at GABA receptor
Benzodiazepines: can a patient become benzodiazepine dependent
YES
Benzodiazepines: are barbiturates or benzodiazepines used for alcohol
withdrawal
benzodiazepines
Antipsychotics (neuroleptics): what is another name for antipsychotics
neuroleptics
Antipsychotics (neuroleptics): name 4 antipsychotic drugs
thioridazine, haloperidol, fluphenazine, chlorpromazine
Antipsychotics (neuroleptics): how do you keep benzos straight from
antipsychotics
Benzos help 3rd year Jon Kazam be less anxious around patients: Shazam
Kazam! Without antipsychotics patients talk like a crazy 'zine (well, not
perfect, but I'm working on it)
Antipsychotics (neuroleptics): what is the mechanism of most antipsychotics
block dopamine D2 receptors
Antipsychotics (neuroleptics): what is the clinical application of
antipsychotics
schizophrenia, psychosis
Antipsychotics (neuroleptics): what are the side effects of antipsychotics
extrapyramidal side effects (EPS), sedation, endocrine, muscarinic blockade,
alpha blockade, histamine blockade
Antipsychotics (neuroleptics): what is a long-term effect of antipsychotic use
tardive dyskinesia
Antipsychotics (neuroleptics): what is neuroleptic malignant syndrome
a side effect of antipsychotics; rigidity, autonomic instability, hyperpyrexia
Antipsychotics (neuroleptics): how do you treat neuroleptic malignant
syndrome
dantrolene, dopamine agonists
Antipsychotics (neuroleptics): what is tardive dyskinesia
side effect of neuroleptics; stereotypic oral-facial movements, may be due to
dopamine receptor sensitization
Antipsychotics (neuroleptics): what is the "rule of 4" with EPS side effects
from antipsychotic drugs
evolution of EPS side effects: 4 hours -- acite dystonia, 4 days -- akinesia, 4
weeks -- akasthesia, 4 months -- tardvie dyskinesia
Antipsychotics (neuroleptics): is tardvie dyskinesia reversible
often irreversible
Antipsychotics (neuroleptics): what is fluphenazine used for
schizophrenia, psychosis
Atypical antipsychotics: name 3 atypical antipsychotics
clozapine, olanzapine, risperidone
Atypical antipsychotics: what type of antipsychotic is clozapine
atypical
Atypical antipsychotics: what type of antipsychotic is olanzapine
atypical
Atypical antipsychotics: what type of antipsychotic is risperidone
atypical
Atypical antipsychotics: what is the mechanism of atypical antipsychotics
block 5-HT2 and dopamine receptors
Atypical antipsychotics: what is the mechanism of clozapine
block 5-HT2 and dopamine receptors
Atypical antipsychotics: what is the mechanism of olanzapine
block 5-HT2 and dopamine receptors
Atypical antipsychotics: what is the mechanism of risperidone
block 5-HT2 and dopamine receptors
Atypical antipsychotics: what is the clinical application of clozapine
schizophrenia positive and negative symptoms
Atypical antipsychotics: what is the clinical application of olanzapine
schizophrenia positive and negative symptoms, OCD, anxiety disorder,
depression
Atypical antipsychotics: what is the clinical application of risperidone
schizophrenia positive and negative symptoms
Atypical antipsychotics: how are atypical antipsychotics different from
classic ones
atypicals treat positive and negative symptoms of schizophrenia, fewer
extrapyramidal and anticholinergic side effects than classic antipsychotics
Atypical antipsychotics: which antipsychotics should be used to treat positive
and negative symptoms of schizophrenia
atypical ones -- clozapine, olanzapine, risperidone
Atypical antipsychotics: which antipsychotics should be used for fewer side
effects
atypical ones -- clozapine, olanzapine, risperidone
Atypical antipsychotics: what is a potential toxicity of clozapine
agranulocytosis
Atypical antipsychotics: which antipsychotic drug can cause agranulocytosis
clozapine
Atypical antipsychotics: what test must be done weekly on patients taking
clozapine
WBC count because of potential agranulocytosis
Lithium: what is the mechanism of action of lithium
unknown; may be related to inhibition of phosphoinositol cascade
Lithium: what is the clinical application of lithium
mood stabilizer for bipolar disorder
Lithium: how does lithium help people with bipolar disorder
prevents relapse and acute manic episodes
Lithium: what are the side effects of lithium
tremor, hypothyroidism, polyuria, teratogenic
Lithium: is it OK for women taking lithium to get pregnant
NO -- teratogenic
Lithium: what does lithium cause polyuria
ADH antagonist --> nephrogenic diabetes insipidus
Lithium: AUTHOR
Hina Talib
Antidepressants: What do the following drugs inhibit: 1. MAO inhibitors, 2.
Desipramine/maprotilline, 3. Mirtazapine and 4. Fluoxetine/trazodone?
1. MAO 2. NE reuptake 3. Alpha 2-R 4. 5HT reuptake
Antidepressants: All of the above actions are ------synaptic
PRE
List the Tricyclic Antidepressants: What are the three C's of their toxicity?
Convulsions, Coma, Cardiotoxicity (arrythmias). Also respiratory depression,
hypyrexia.
List the Tricyclic Antidepressants: How about toxicity in the eldery?
confusion and hallucinations due to anticholinergic SE
List the Tricyclic Antidepressants: What is the mechanism of TCA?
block reuptake of NE and 5HT
List the Tricyclic Antidepressants: What is the clinical uses of TCAs?
Endogenous depresion. Bed wetting - imipramine. OCD- clomipramine.
List the Tricyclic Antidepressants: How are tertiary TCA's different than
secondary in terms of side effects?
Amitriptyline (tertiary) has more anti-cholinergic effects than do secondary
(nortriptyline). Desipramine is the least sedating.
List the Tricyclic Antidepressants: what are the SE of TCAs?
sedation, alpha blocking effects, atropine-like anti cholinergic side effects
(tachycardia, urinary retention)
List the Tricyclic Antidepressants: Fluoxetine, sertraline, paroxetine,
citalopram are what class of drugs?
pg 311 SSRI's for endogenous depression
List the Tricyclic Antidepressants: How long does it take an anti-depressant
to have an effect?
2-3weeks
List the Tricyclic Antidepressants: How does the toxicity differ fromTCA's
and what are they?
Fewer than TCA's. CNS stimulation - anxiety, insomnia, tremor, anorexia,
nausea, and vomiting.
List the Tricyclic Antidepressants: What toxicity happens with SSRI's and
MAO inhibitors given together?
Seratonin Syndrome! Hyperthermia, muscle rigidity, cardiovascular collapse
List the Tricyclic Antidepressants: What are heterocyclics?
pg 312 2nd and 3rd generation antidepressants with varied and mixed
mechanisms of action. Used major depression.
List the Tricyclic Antidepressants: Examples of heterocyclics?
trazodone, buproprion, venlafaxine, mirtazapine, maprotiline
List the Tricyclic Antidepressants: Which one is used for smoking cessation?
Buproprion. Mechanism not known. Toxicity - stimulant effects, dry mouth,
aggrevation of pyschosis
List the Tricyclic Antidepressants: Which one used in GAD?
Venlafaxine - inhibits 5HT and DA reuptake. Toxicity - stimulant effects
List the Tricyclic Antidepressants: which one blocks NE reuptake
maprotiline
List the Tricyclic Antidepressants: Which one increases release of NE and
5HT via alpha 2 antagonism?
mirtazapine. Also potent 5HT Rantagonist. Toxicity - sedation, increase
serum cholesterol, increase apetite
List the Tricyclic Antidepressants: What is trazodone and it' SE?
primarily inhibits seratonin reuptake. Toxicity - sedation, nausea, priapism,
postural hypotension
Give 2 examples of MAO: Mechanism and Clinical Uses?
non selevtive MAO inhibition. Atypical antidepressant, anxiety,
hypochondriasis
Give 2 examples of MAO: What is the toxicity with tyramine ingestion (in
foods) and meperidine?
Hypertensive crisis
Give 2 examples of MAO: Other toxicities?
CNS stimulation, contraindicated with SSRI's or B-agonists
What is the mechanims of selgiline (deprenyl)?: what is the clinical use and
toxicity?
adjunctive agent to L-dopa for Parkinsons. May enhance adverse effects of
L-dopa
General principles: What is the significance of drugs with decreased
solubility in blood?
rapid induction and recovery times . Ie. N20
General principles: What is the significance of drugs with increased solubility
in blood?
increased potency = I/ MAC. Ie. Halothane
Inhaled Anesthetics: list them
halothane, enflurane, isoflurane, sevoflurane, methoxyflurane, nitrous oxide
Inhaled Anesthetics: What is good about lower solubility?
the quicker the anesthetic response, and the quicker the recovery
Inhaled Anesthetics: What are these drug's effects?
myocardial depression, respiratory depression, nausea/emesis, increase
cerebral blood flow
Inhaled Anesthetics: What toxicity mactches the following drugs 1.
Halothane 2. Methoxyflurane 3. Enflurane 4. Rare
1. Hepatotoxcity 2. Nephrotoxicty 3. Proconvulsant 4. Malignant
hyperthermia
IV anesthetics: What do barbituates, benzodiazepines, arylcyclohexylamines
and narcotic analgesics have in common?
they are IV anesthetics
IV anesthetics: What the pharmacokinetics and uses of thiopental?
high lipid solubility, rapid entry into brain. Used for induction of anesthesia
for short surgical procedures. Terminated by redistribution from brain.
Decreased cerebral blood flow
IV anesthetics: Give an example of a benzo and what is this class's
shortcoming?
midazolam used for endoscopy. Used with gaseous anesthetics and narcotics.
May cause severe post-op respiratory depressio and amnesia
IV anesthetics: What does Ketamine (PCP analog and an
arylcyclohexylamine) do?
dissociative anesthetic. Cardiovascular stimulant. Causes disorientation,
hallucination, bad dreams. Increases cerebral blood flow.
IV anesthetics: How are narcotic analgesics used? Examples?
Morphone and fentanyl are used with CNS depressant during general
anesthesia.
IV anesthetics: What is the advantage of propofol
used for rapid anesthesia induction and short procedures. Less post-op nausea
than thiopental
Local anesthetics: Name some esters?
procaine, cocaine, tetracaine,
Local anesthetics: Name some amides?
lidocaine, bupivacaine, (amides have two I's in name!)
Local anesthetics: What is the mechanism and clinical use?
bind receptor and block Na channels. Tertiary amine local anesthetics
penetrate membrane in uncharge form, then bind charged form. Use for minor
surgical procedures, spinal anesthesia.
Local anesthetics: How do you decide to use ester or amides?
if allergic to esters, give amides
Local anesthetics: what is the toxicity
CNS excitation, severe cardiovascular toxicity (bupivacaine), hypertension,
arrhythmias (cocaine)
Local anesthetics: In infected ________ tissue, anesthetics are charged and
cannot penetrate membrane. Therefore, ______ anesthetics are needed.
acidic; more
Local anesthetics: What is the order of nerve blockade for size and
myelination? Which factor predominates?
small diameter> large diameter. Myelinated fibers> unmyelinated fibers. Size
factor predominates
Local anesthetics: what is the order of loss of sensation?
pain first, then temp, then touch, then pressure
Local anesthetics: Why would you give these drugs with vasoconstrictors?
to enhance local action
Opiod analgesics: List as many as you can.
morphine, fentanyl, codeine, heroin, methadone, meperidine,
dextromethorphan
Opiod analgesics: Mechanism: They act as _____ for opiod receptors to
modulate synaptic transmission
agonists
Opiod analgesics: which drugs act at the mu, delta, kappa receptors?
morphine enkephalin, dynorphin
Opiod analgesics: Clinical use?
pain, cough supression (dex), diarrhea (loperamide), acute pulmonary edema,
methadone maintenance programs
Opiod analgesics: What are the major toxicities?
addiction, respiratory depression, constipation, miosis, additive CNS
depression wth other drugs
Opiod analgesics: Tolerance does not develop to __________and ______
miosis and constipation
Opiod analgesics: How would you treat toxicity?
naloxone, naltrexone (opiod R antagonist)
Other NSAIDS: List three NSAIDS?
ibuprofen, naproxen, indomethacin
Other NSAIDS: What is their mechanism?
reversibly inhibit COX 1 and 2. Blocks PG synthesis
Other NSAIDS: What is their clinical use (3As)?
Antipyretic, analgesic, anti-inflammatory. Indomethacin is used to close a
PDA.
Other NSAIDS: What are common toxicities?
renal damage, aplastic anemia, GI distress, ulcers
COX 2 Inhibitors: Where is cox2 found?
in inflammatory cells and mediates inflammation and pain
COX 2 Inhibitors: Why is cox2 inhibition better than cox1?
cox1 helps to maintain gastric mucosa, thus, should not have the corrosive
effects of other NSAIDs on the GI lining (less incidence of ulcers and
bleeding)
COX 2 Inhibitors: Clinical Use?
RA and osteoarthritis
Acetaminophen: What is its mechanism and where does it work?
reversibly inhibits cox, mostly in CNS. Inactivated peripherally.
Acetaminophen: What are its 2 As?
antipyretic, analgesic but NOT anti-inflammatory.
Acetaminophen: Overdose effects?
hepatic necrosis, acetaminophen metabolites depletes glutathine and forms
toxic tissue adducts in the liver
cardiovascular therapy: Changes in CO affect two major pathways?
1. Carotid sinus firing, sympa discharge 2. Renal blood flow, renin-ang
pathway
cardiovascular therapy: What is the effect of the following drugs: 1. Positive
inotropic drugs 2. Beta blockers 3. Ace inhibitors 4. AII antagonists 5.
Vasodilators and 6. Diuretics
1. Increases cardiac output. 2. Inhibit renin release. 3. Inhibit ACE 4. Inhibits
effects of AngII including increasing the preload, increasing the afterload and
remodelling. 5. Decrease the preload and afterload. 6. Decrease the preload
and afterload
antihypertensive drugs: What are the adverse effects of these two diueretics:
hydrochlorothiazide, loop diuretics
1. Hypokalemia, hyperlipidemia, hyperuricemia, lassitude, hypercalcemia,
hyperglycemia 2. Hypokalemia, met alk, hypotension, ototoxicity
antihypertensive drugs: These are wahat class of drugs: clonidine,
methyldopa, ganglionic blockers, reserpine, guanethidine, prazosin, beta
blockers?
sympathoplegics
antihypertensive drugs: Adverse effects of clonidine?
dry mouth, sedation, severe rebound HTN
antihypertensive drugs: Adverse effects of methyldopa?
sedation, positive coombs test
antihypertensive drugs: Adverse effects of ganglionic blockers?
orthostatic HTN, blurred vision, constitpation, sexual dysfuncction
antihypertensive drugs: Adverse effects of reserpine?
sedation, depression, nasal stuffiness, diarrhea
antihypertensive drugs: adverse effects of beta blockers?
impotence, asthma, cardiovascular, cns
antihypertensive drugs: Adverse effects of guanethidine?
orthostatic and exercise Hypotension, sex dysfxn, diarrhea
antihypertensive drugs: Adverse effects of prazosin?
1st dose orthostatic hypotension, dizzy, headache
antihypertensive drugs: The following are what class: hydralazine, minoxidil,
nifedipine, verapamil, nitroprusside
vasodilators
antihypertensive drugs: which one causes lupus like syndrome? Other
toxicities?
hydralazine, nausea, headache, reflex tachycardia, angina, salt retention
antihypertensive drugs: adverse effets of minoxidil?
hypertrichosis (hair growth - think Rogaine with minoxidil!), pericardial
effusion, reflex tachycardia, angina, salt retention
antihypertensive drugs: Side effects of nifedipine, verapamil?
dizziness, flushing, constipation, nausea
antihypertensive drugs: which one causes cynide toxicity?
nitroprusside
antihypertensive drugs: Adverse effects of ACE-I Captorpil? Think
CAPTOPRIL
C: cough, A: angioedema, P: proteinuria, T: taste changes, O: hypOtension,
P: pregnancy problems like fetal renal damage, R: rash, I: increased renin, L:
lower angiotensin. Also hyperkalemia.
antihypertensive drugs: Losartan is a ----------- R-Inhibitor? With
____-toxicity and ____kalemia
angiotensin II, fetal renal, hyper
Hydralizine: Which two anti-htn drugs do you use with B blockers to prevent
reflex tachycardia, diuretic to block salt retention?
hydralizine, minoxidil
Hydralizine: What is hydralizine's mechanims and clinical use?
increase cGMP --> smooth muscle relaxation. Vasodilates arteries > veins.
Reduces afterload. Used for severe HTN or CHF
Calcium channel blockers, name three: Mechanism: block _____ chanels of
cardiac and smooth muscles to reduce contractility
voltage dependednt L type Ca
Calcium channel blockers, name three: Rank their effects on vascular smooth
muscle ad on the heart.
smooth muscle nifed> diltia > verapamil heart: vera> diltia> nifedepine
Calcium channel blockers, name three: What is the calcium channel blockers
use?
HTN, angina, arrythmias (not nifedipine)
Calcium channel blockers, name three: ACE -I, name three
captopril, enalapril, lisinopril
Calcium channel blockers, name three: Mechanim considering bradykinin
and renin release?
reduce lvels of ang II, prevent inactivation of bradykinin, renin release is
increased to to loss of feedback inhibition
Calcium channel blockers, name three: what is the clinical use of these?
HTN, CHF, diabetic renal disease
Diuretics- site of action: What is the site of action of 1. Acetazolamide, 2.
Osmotic agents, 3. Loop agents, 4. Thiazides, 5. Potassium sparing, 6. ADH
antagonists
1. PCT 2. PCT, thin desc limb, CD 3. Thick ascending limb 4. Distal conv
tubule 5. DCT a bit later 6. CD in inner medulla
Diuretics- site of action: How does mannitol an osmotic diuretic work?
increase tubular fluid osmolarity, producing increased urine flow
Diuretics- site of action: what is the use and toxicity?
Use: shock, drug overdose, decrease intracranial pressure. Toxicity pulmonary edema, dehydration. Contraindicated in anuria, CHF
Acetazolamide: Is a ______inhibitor. Causes ______diuresis and _____ in
total body HC03 stores.
Carbonic anhydrase, self-limited NaHCO3, reduction.
Acetazolamide: What electrolye disturbace does it treat? Does it cause?
treats met alk, causes in toxicity hyperchloremic met acidosis.
ACIDazolamide caues ACIDosis.
Acetazolamide: Other toxicity?
neuropathy, NH3 toxicity, sulfa allergy
Acetazolamide: uses?
glaucoma, urinary alk, met alk, altitude sickeness
Furosemide: This sulfonamide loop diuretic inhibits _______cotransport
NA, K, 2CL
Furosemide: Furosemide also works by?
abolishes hypertonicit y of medulla, prevent concentration of urine. Increase
Caexcertion. Loops Lose calcium
Furosemide: The three uses for this loop diuretic?
edematous states, htn, hypercalcemia
Furosemide: Toxicity using the OH DANG?
ototoxicity, hypokalemia, dehydration, allergy, nephritis interstitial, gout
Ethacrynic Acid: How is this drug different from furosemide? And how does
that affect its use?
Although both have the same action, ethacrynic is a phenoxyacetic acid
derivative not a sulfonamide. Therefore use this drug when you are allergic to
sulfa.
Ethacrynic Acid: What drug can be used to treat acute gout?
ethacrynic acid
Ethacrynic Acid: AUTHOR
Stacy Ugras
Hydrochlorothiazide: Hydrochlorothiazide is a thiazide diuretic that inhibits
the reabsorption of ----- in the ---- tubule
NaCl; early distal tubule
Hydrochlorothiazide: Does hydrochlorothiazide increase or decrease the
excretion of calcium ion?
decrease
Hydrochlorothiazide: A toxic dose of hydrochlorathiazide will do what to the
blood levels of these electrolites: potassium, sodium, glucose, lipid, uric acid,
calcium
hypokalemic metabolic alkalosis, hyponatremia, hyperGlycemia,
hyperLipidemia, hyperUricemia, hyperCalcemia (hyperGLUC)
K+-sparing diuretics: Spironolactone is a competitive antagonist to the --receptor in the ---- tubule
aldosterone; cortical collecting tubule
K+-sparing diuretics: Name two K+-sparing diuretics that block Na+
channels in the cortical collecting duct
Triamterine and amiloride
K+-sparing diuretics: Besides causing hyperkalemia, a toxic dose of
spironolactone will cause this endocrine effect
Gynecomastia (antiandrogen effect)
K+-sparing diuretics: Name three K+-sparing diuretics
Spironolactone, Triamterene, Amiloride (The K+ STAys.)
Diuretics: electrolye exchange: Diuretics are classified as carbonic anhydrase
inhibitors, loop diuretics, thiazides, and K+-sparing diuretics. Which of these
causes in increase in urine NaCl?
All of them!
Diuretics: electrolye exchange: Which types of diuretucs increase urine K+?
All except K+-sparing diuretics. Carbonic anhydrase inhibitors, loop
diuretics, thiazides.
Diuretics: electrolye exchange: Do carbonic anhydrase inhibitors increase or
decrease blood pH?
Decrease, cause acidosis
Diuretics: electrolye exchange: Do K+-sparing diuretics cause acidosis or
alkalosis?
Acidosis, decreases pH
Diuretics: electrolye exchange: Do loop diuretics cause acidosis or alkalosis?
Alkalosis, increases pH
Diuretics: electrolye exchange: Do thiazide diuretics cause an increase or
decrease in blood pH?
Increase, cause alkalosis
Diuretics: electrolye exchange: Do loop diuretics increase or decrease levels
of urine calcium ion?
Increase
Diuretics: electrolye exchange: Do thiazide diuretics increase or decrease
levels of urine calcium ion?
Decrease
Antianginal therapy: Name four determinants of the level of myocardial
oxygen consumption
There are five: end diastolic volume, blood pressure, heart rate, contractility,
ejection time
Antianginal therapy: Do nitrates affect preload or afterload?
preload
Antianginal therapy: Do Beta-blockers affect preload or afterload?
afterload
Antianginal therapy: What is the effect of nitrates on: diastolic volume, blood
pressure, contractility, heart rate, ejection time?
decrease EDV, decrease BP, increase contractility (reflex response), increase
HR (reflex response), decrease ejection time
Antianginal therapy: What is the effect of Beta-blockers on: diastolic volume,
blood pressure, contractility, heart rate, ejection time?
Antianginal therapy: The effects of using nitrates and Beta-blockers together
will: a) decrease myocardial oxygen demands by the same amount as using
either alone, b) decrease myocardial oxygen demands by an amount greater
than if each were used alone, or c) have no effect on myocardial oxygen
demand
increase EDV, decrease BP, decrease contractility, decreased HR, increase
ejection time
b) Decrease myocardial oxygen demands by an amount greater that if each
were used alone
Antianginal therapy: Nifedipine blocks -- channels
calcium
Antianginal therapy: In its effects on myocardial oxygen consumption, is
Nifedipine similar to Nitrates or B-blockers?
Nitrates (Nifedipine is similar to Nitrates)
Antianginal therapy: In its effects on myocardial oxygen consumption, is
Verapamil similar to Nitrates or B-blockers?
B-blockers
Nitroglycerine, isosorbide dinitrate: Dose nitroglycerin dilate arteries or veins
more?
Veins>>arteries
Nitroglycerine, isosorbide dinitrate: Does nitroglycerin increase or decrease
cGMP in smooth muscle?
Increase
Nitroglycerine, isosorbide dinitrate: In industrial exposure to nitroglycerine,
weekend withdrawal is characterized by which three symptoms?
Tachycardia, dizziness , and headache ("Monday disease")
Nitroglycerine, isosorbide dinitrate: Toxic dosage of nitroglycerine causes
which three symptoms?
Tachycardia, hypotension, headache
Cardiac drugs: sites of action: Digitalis has its action on which cell membrane
transporter?
Na/K ATPase
Cardiac drugs: sites of action: Ryanodine has its action on which channel?
Calcium release channel in the sarcoplasmic receptor
Cardiac drugs: sites of action: Calcium enters cardiac cells through which
channel?
Voltage-gated calcium channel
Cardiac drugs: sites of action: Cytoplasmic calcium concentrations in cardiac
cells can be decreased by sequestering calcium in the sarcoplasmic reticulum.
Calcium enters the SR through which transporter?
Calcium pump in the wall of the SR
Cardiac drugs: sites of action: Calcium channel blockers have their effect on
which calcium transporters?
Voltage-gated calcium channel
Cardiac Glycosides: What is digoxin's effect on the intracellular Na+ level?
Increase
Cardiac Glycosides: What is digoxin's effect on the intracellular calcium
level?
Increase
Cardiac Glycosides: Name two ECG changes ellicited by digoxin
administration
There are 4: increase PR, decrease QT, scooping of ST segment, T-wave
inversion
Cardiac Glycosides: Name three symptoms of digoxin toxicity
Nausea, vomiting, diarrhea, blurry vision, arrhythmia
Cardiac Glycosides: Which potentiates the effects of digoxin- hypo- or
hyperkalemia?
hypokalemia
Antiarrhythmics- Na+ channel blockers (classI): Which phase of the cardiac
action potential do antiarrhythmics decrease the slope of?
Phase 4 depolarization
Antiarrhythmics- Na+ channel blockers (classI): What type of antiarrhythmic
is Amiodarone?
Class 1A (Class 1A includes Quinidine, Amiodarone, Procainamide,
Disopyramide, "Queen Amy Proclaims Diso's pyramid."
Antiarrhythmics- Na+ channel blockers (classI): Do class 1A antiarrhythmics
increase or decrease the effective refractory period, AP duration, and QT
interval?
Increase ERP, increase AP duration, increase QT interval
Antiarrhythmics- Na+ channel blockers (classI): What do class 1B
antiarrhythmics do to the AP duration?
Decrease AP duration
Antiarrhythmics- Na+ channel blockers (classI): What type of antiarrhythmic
is mexiletine?
Class 1B (includes Lidocaine, mexiletine, tocainide)
Antiarrhythmics- Na+ channel blockers (classI): What type of antiarrhythmic
is encainide?
Class IC (includes flecainide, encainide, propafenone)
Antiarrhythmics- Na+ channel blockers (classI): What effect do class 1C
antiarrhythmics have on the AP duration?
No effect!
Antiarrhythmics- Beta-blockers (classII): What does esmolol do to the cAMP
in cardiac cells?
decreases cAMP (a beta-blocker)
Antiarrhythmics- Beta-blockers (classII): What does atenolol do the calcium
currents in cardiac cells?
decreases calcium current (beta-blocker)
Antiarrhythmics- Beta-blockers (classII): Timolol decreases the slope of
which phase of the cardiac AP cycle?
Phase 4 (a beta-blocker)
Antiarrhythmics- Beta-blockers (classII): What does propanolol do the the PR
interval?
Increases interval (beta-blocker)
Antiarrhythmics- Beta-blockers (classII): Is esmolol a short- or long-acting
beta blocker?
short-acting
Antiarrhythmics- K+ channel blockers (class III): Does amiodarone increase
or decrease AP duration?
Increase (K+ channel blocker)
Antiarrhythmics- K+ channel blockers (class III): Does sotalol increase or
decrease the effective refractory period?
Increase (K+ channel blocker)
Antiarrhythmics- K+ channel blockers (class III): Does bretylium increase or
decrease the QT interval?
Increase (K+ channel blocker)
Antiarrhythmics- K+ channel blockers (class III): Name a symptom of sotalol
toxicity.
Torsades de pointes (K+ channel blocker)
Antiarrhythmics- K+ channel blockers (class III): Name three of the
symptoms of amiodarone toxicity.
Pulmonary fibrosis, corneal deposits, hepatoxicity, skin deposits resulting in
photodermatitis, neurologic effects, constipation, bradychardia, heart block,
CHF, hypothyroidism/hyperthyroidism. (Therefore, should check PFTs,
LFTs, and TFTs)
Antiarrhythmics- Ca2+ channel blockers (class IV): Does verapamil increase
or decrease the conduction velocity of the AV nodal cells?
Decrease (calcium channel blocker)
Antiarrhythmics- Ca2+ channel blockers (class IV): How does diltiazem
affect the effective refractory period and the PR interval?
Increases ERP, increases PR (calcium channel blocker)
Other antiarrhythmics: Name a potential use of Mg+ to treat arrhythmias.
To treat torsades de pointes and digoxin toxicity
Other antiarrhythmics: Name a potential use of K+ to treat arrhythmias.
Depress ectopic pacemakers, especially in digoxin toxicity
Other antiarrhythmics: Name a use of adenosine in treating arrhythmias.
To diagnose and abolish AV nodal arrhythmias.
Lipid-lowering agents: What is the effect of cholestyramine on the serum
triglyceride level?
Slight increase (cholestyramine is a bile acid resin)
Lipid-lowering agents: What is the effect of colestipol on HDL?
No effect! (colestipol is a bile acid resin)
Lipid-lowering agents: What is the effect of lovastatin on HDL?
Increase (lovastatin is an HMG-CoA reductase inhibitor)
Lipid-lowering agents: Name 2 side effects of pravastatin.
Increase LFTs and cause myositis (prevastatin is an HMG-CoA reductase
inhibitor)
Lipid-lowering agents: What is the effect of Niacin on HDL?
Increase
Lipid-lowering agents: What are the side effects of clofibrate?
Incease LFTs and cause myositis (Clofibrate is a "Fibrate")
Lipid-lowering agents: Which increases HDL most: simvastatin, niacin, or
gemfibrozil?
Niacin
Lipid-lowering agents: Which decreases triglyceride level most: colestipol,
Atorvastatin, niacin, or bezafibrate?
Bezafibrate
Lipid-lowering agents: What is the main effect of ezetimibe?
decrease serum LDL (a cholesterol absorption inhibitor)
Lipid-lowering agents: Gemfibrozil increases the activity of which enzyme?
Lipoprotein lipase (which converts VLDL to IDL)
Lipid-lowering agents: AUTHOR
Rafael Vazquez
Arachidonic acid products: What enzyme breaks down membrane lipid into
arachidonic acid?
Phospholipase A2
Arachidonic acid products: What two enzymes are responsible for the
production of Hydroperoxides (HPETEs) and Endoperoxidases, respectively
from arachidonate?
Lipoxygenase= HPETE, Cyclooxygenases=endoperoxidases
Arachidonic acid products: What major class of products do HPETEs give
rise to?
Leukotrienes
Arachidonic acid products: What are the 3 major products of
Endoperoxidases?
Prostacyclin (PGI), Prostaglandins (PGE, PGF), Thromboxane (TXA)
Arachidonic acid products: In general what effect do leukotrienes have on
bronchial tone?
Leukotrienes in general increase bronchial tone
Arachidonic acid products: In the arachodonic acid pathway, what two
enzymes do corticosteroids block?
Phospholipase A2, COX-2
Arachidonic acid products: NSAIDs, Acetaminophen and COX-2 inhibitors
block which arachadonic acid pathway enzymes
NSAIDs-non-selectively block COX-1 and COX-2, acetaminophen doesn't
block COX-1 or COX-2, but instead it may block COX-3 in found in the
brain, COX-2 inhibitors block COX-2
Arachidonic acid products: What are the 4 major effects of Prostacyclin
decrease platelet aggregation, decrease vascular tone, decrease bronchial
tone, decrease uterine tone
Arachidonic acid products: What are the 3 major effects of Prostaglandins
increased uterine tone, decrease vascular tone, decrease bronchial tone
Arachidonic acid products: What are the 3 major effects of Thromboxane
increase platelet aggregation, increase vascular tone, increase bronchial tone
Arachidonic acid products: Zileuton is a ________ pathway inhibitor?
Lipoxygenase
Arachidonic acid products: Zariflukast is associated with what enzymes?
Lekukotrienes
Asthma drugs: Bronchodilation is mediated by what molecule
cAMP
Asthma drugs: Bronchoconstriction is mediated by _________ and
___________
Ach and adenosine
Asthma drugs: How many asthma drug categories are there?
7- (1) nonspecific B-agonists, (2) B2 agonists, (3) Methylxanthines, (4)
muscarinic antagonist, (5) cromolyn, (6) corticosteroids, (7) Antileukotrienes
Asthma drugs: What is the only nonspecific B-agonist drug and what are its
effects?
Isoprotenerol-relaxes bronchial smooth muscle (B2) and tachycardia (B1)
(adverse effect).
Asthma drugs: What are the two B2 selective agonist asthma drugs?
Albuterol- relaxes bronchial smooth muscle (B2), Salmetrol
Asthma drugs: What are the indications for Albuterol and Salmetrol,
respectively?
Albuterol- use during acute exarcebation, Salmetrol- long-acting agent for
prophylaxis
Asthma drugs: what are the notable adverse effects of B2 agonist?
arythmias and tremor
Asthma drugs: B2-agonists activate this enzyme in bronchial smooth muscle
that leads to an increase in ________ = bronchodilation
B2 agonists activate adenylate cyclase and increase conversion of ATP to
cAMP
Asthma drugs: What are the likely mechanism of action theophylline?
bronchodialation by inhibition phosphodiesterase (PDE), decreasing cAMP
hydrolysis and antagnonizing adenosine action
Asthma drugs: Why is usage of theophylline limited?
limited b/c narrow therapeutic index (cardiotoxicity, neurotxicity)
Asthma drugs: What kind of drug is Ipratropium?
muscarinic antagonist
Asthma drugs: How does mechanism of action of Ipratropium?
competitive block of muscarinic receptors= prevention of
bronchoconstriction
Asthma drugs: cromolyn works by inhibiting the release of _______ from
______ cell?
prevents release of medicators from mast cells
Asthma drugs: Cromolyn is mainly used for the ______ of athsma and it is
not indicated for _______ treatment of athsma?
Used only for prophylaxis, not effective during acute episode. Also, toxicity
rare
Asthma drugs: __________and ________ are two major corticosteroids used
for treatment of what kind of asthma?
Beclomethasone and prednisone are 1st line therapy for chronic asthma
Asthma drugs: What is the mechanism of action of corticosteroids?
inhibits the synthesis of virtually of cytokines-->inactivates NF-KB, the
transcription factor that induces the production of TNF-a, amonth other
inflammatory agents.
Asthma drugs: Zileuton blocks the conversion of _______ to ________.
zileuton is a 5-lipoxygenase pathway inhibitior. Blocks the conversion of
arachidonic acti to leukotrienes
Asthma drugs: Zafirlukast works by_______ ________ ________
bloking leukotriene receptors
Asthma drugs: What the most basic asthma treatment strategy?
avoidance of exposure to antingen (dust, pollen, etc)
Asthma drugs: After exposure to antigen crosslinks IgE on mast cells. This is
prevented by the following drugs: _________ and ________
cromolyn and steroids
Asthma drugs: Following allergen exposure mediators are released (ex.
_______ and _________). This triggers an ______ asthmatic response
characterized by ________ and may be treated with the following 3 asthmatic
drug categories to treat the symptoms.
examples of mediators are leukotrienes and histamine. Following allergen
exposure an early asthmatic response characterized by bronchoconstriction
that can be treated with B-agonsists, methylxanthines, and muscarinic
antagonists.
Asthma drugs: Also, mediators elicit a ________ response is which leads to
bronchial __________ and is treated with __________.
mediators elicit a late response and this leads to bronchial hyperactivity. This
is best treated with steroids.
GI therapy: the following questions are from the diagram at the top of the
page
0
GI therapy: _____ cells are predominatly found in the antrum and _________ Gastrin cells are predominant in the antrum and parietal cells are predominant
cells are predominatly found in the fundus.
in the fundus.
GI therapy: What are the 3 main stimuli of acid secretion?
Ach, histamine, gastrin
GI therapy: Gastrin stimulates the ECL cells to secrete histamine that
stimulates ______ cells. Gastrin also activate the ______ cells to increase
expression of _______ that increases ______secretion.
Gastrin stimulates the ECL cells to secrese histamine that stimulates parietal
cells. Parietal cells are also activated by gastrin to increase the expression of
the H,K ATPase that increases acid secretion.
GI therapy: This type of drug acts by inhibiting M1 and M3 receptors on ECL
cells and Parietal cells, respectively.
muscarinic antagonists block M1 receptors in ECL cells and M3 receptors in
parietal cells.
GI therapy: This type of drug inhibits the ability of the ECL cell to stimulate
acid secretion by interfering with the _____ receptor.
H2 blocker inhibits the ability of the ECL cell to stimulate acid secretion by
interfering with the parietal H2 receptor.
GI therapy: The most direct way of inhibiting acid secretion is by using this
type of drug which acts on this enzyme.
the most direct way of inhibiting acid secretion is by using proton pump
blockers which inhibit the H,K ATPase on parietal cells.
GI therapy: ____________ acts by binding to the ulcer and increasing its
healing. It may interfere with drug absorption in the stomach.
sucralfate binds to the ulcer base and provides physical protection. It allows
HCO3- secretion to reestablish pH gradient in the mucus layer.
GI therapy: What hormone binds ECL cells and decreases acid secretion?
somatostatin
GI therapy: These type of drugs used to decrease pH in the stomach.
antacids….duh….jk. (I was instructed to make a question of every word)
GI therapy: questions not from the diagram
0
GI therapy: ____________, ___________, ___________, and ___________
are examples of H2 blockers and they act by (reversibly/irreversibly)
cimetedine, ranitidine, famotidine, nizatidine reversilbly block H2 receptors.
GI therapy: This H2 blocker is the only one that has many side effects which
cimetedine is a potent inhibitor of P450, it has antiandrogenic effect and
include potent inhibition of ______, _____ effects, and _____ renal excretion decrease renal excretion of creatinine. Other H2 blockers are relatively free of
of creatinine.
these effects.
GI therapy: _________ and _________ (reversibly/irreversibly) inhibit the
H/K ATPase in the stomach _______cells.
Omeprazole and Iansoprazole irreversibly inhibit the H/K ATPase in stomach
parietal cells
GI therapy: Proton pump inhibitors are indicated for peptic ulcer, ________,
_______, and _________ syndrome
peptic ulcer, gastritis, esophageal reflux, and Zollinger-Ellison syndrome
GI therapy: T/F: Bismuth and sucralfate allow HCO3- secretion.
True: bismuth and sucralfate bind to ulcer base and provide physical
protection, and allow HCO3- secretion to reestablish pH gradient in the
mucus layer=increased ulcer healing
GI therapy: T/F: misoprostol is a PGE2 analog and increases the production
and secretion of gastric mucous barrier.
False: misoprostol is a PGE1 analog and it increases the production and
secretion of gastric mucous barrier.
GI therapy: What are the 3 indications for misoprosol?
prevention of NSAID-induced peptic ulcers, maintains a PDA and used to
induce labor
GI therapy: In what population is misoprostol contraindicated?
women of childbearing potential (abortifacient). It also casues diarrhea
GI therapy: Infliximab is ___________ against ______.
monoclonal antibody to TNFa
GI therapy: The clinical indication for Infliximab is:
Crohn's, along with fistula healing
GI therapy: T/F: Infliximab can cause respiratory infection, fever,
hypotension
TRUE
GI Drugs (cont.): This drug offers both anitbacterial action and
anti-inflamatory effects. It is used for 2 inflammatory GI diseases ______ and
_______.
sulfasalazine: combination of sulfapyridine (antibacterial) and mesalamine
(anti-inflammatory effects). It is used for Ulcerative colitis and remission of
Crohn's.
GI Drugs (cont.): T/F: Side effects of the above include: malaise, sulfonamide
toxicity, neutropenia
false: side effects: malaise, nausea, sulfonamide toxicity
GI Drugs (cont.): ___________ is a powerful central-acting antiemetic. It acts
by antagonizing the______ receptor.
Ondansetron: is a powerful antiemetic. Think: you will not vomit with
ondansetron, so you can go on dancing.
GI Drugs (cont.): T/F used to treat vomiting preoperatively and for cancer
chemo therapy pts.
False: it is used to treat vomiting postoperatively.
GI Drugs (cont.): Headache and __________ are side effects
constipation (can't vomit or poop)
GI Drugs (cont.): Antacid overuse can affect:_________, __________, or
______ excretion of other drugs by altering ______ and ______ pH or by
delaying gastric _________.
Antacid overuse can affect absorption, bioavailability, or urinary excretion of
other drugs by altering gastric and urinary pH or by delaying gastric
emptying.
GI Drugs (cont.): Constipation and (hypo/hyper) phosphatemia is seen with
overuse of ________________
aluminum hydroxide - Aluminimum amt. of feces
GI Drugs (cont.): Magnesium hydroxide overuse = ___________
diarhea; Mg = Must go to the bathroom
GI Drugs (cont.): Calicium carbonate= hypercalcemia and
(increase/decreased) acid
causes hypercalcemia and increased acid.
GI Drugs (cont.): T/F: hyperkalemia can be seen with AlOH, MgOH, CaCO2
False! hypokalemia
heparin: Catalyzes activation of ____________, decreases ________ and
__________. It has a ____t1/2. check PTT
catalyzes the activation of antithrombin III, decreases thrombin and Xa. It has
a short t1/2
heparin: It is used for immediated anticoagulation for pulmonary
embolism,_______, _______, MI, and ________. Follow PTT
used for pulmonary embolism, stroke, angina, MI, and DVT.
heparin: T/F: Is used during pregnancy
true: it is used during pregnancy because it does not cross the placenta.
heparin: It can cause bleeding,___________, and drug-drug interactions.
thrombocytopenia
heparin: ___________ is used for rapid reversal of heparization (it is a
_______ charged molecule that binds the ________ charged heparin)
protamine sulfate is used for rapid reversal of heparinization (it is a positively
charged molecule that binds the negatively charged heparin).
heparin: Newer________________ (enoxaparin) act more on _____, have
better bioavailability and 2-4 times longer t1/2. Can be administered subcut
and (with/without) lab monitoring.
lower-molecular-weight heparins (enoxaparin) act more on Xa, have better
bioavailabitlity and 2-4 times longer half-life. Can be adm. Subcut and
without lab monitoring.
warfirin (coumandin): Interferes with normal synthesis and
Interferes with normal synthesis and gamma-carboxylation of vitamin
gamma-carboxylation of vitamin K-dependent factors ___, ___, ___, and ___, K-dependent clotting factors II, VII, IX, and X, protein C and S via vitamin K
also, ___ and ___ via ______ antagonism.
antagonism.
warfirin (coumandin): t1/2 (short/long)
long
warfirin (coumandin): Used for _______ anticoagulation. Follow PT
WEPT - Warfirin affects the Extrinsic pathway and prolongs PT
warfirin (coumandin): T/F: is used during pregnacy
False! (warfarin, unlike heparin, can cross the placenta).
warfirin (coumandin): Toxicity: bleeding, _________, drug-drug interactions
teratogenic
heparin vs. warfarin: Heparin is a (large/small) _____charged acicid polymer
while Warfarin is (large/small) (charged/neutral) molecule
Heparin is a large negatively charged acidic polymer while Warfarin is a
small neutral charged lipid-soluble molecule
heparin vs. warfarin: T/F: Heparin is given orally while warfarin is given
SC/IV
False! Heparin is given IV/SC and warfarin is give oral
heparin vs. warfarin: Site of action: heparin _________, warfarin ______
heparin's site of action is the blood; warfarin's site of action is the liver
(synthesises clotting factors)
heparin vs. warfarin: Onset of action of _________ is slow; the onset of
action of ______ is rapid
onset of action of heparin is rapid (secs) and the onset of action of warfarin is
slow, limitd by t1/2 of normal clotting factors.
heparin vs. warfarin: Warfarin works by imparing the synthesis of _______
dependent factors __, ___, ___, and ___ also _____, and ____; heparin
activates _____, ____ and ___
Warfarin works by imparing the synthesis of vitamin K dependent factors II,
VII, IX, and X also protein S and protein C; heparin activates ATIII, Iia
(thrombin) and Xa.
heparin vs. warfarin: Heparin 's duration of action is (acute/chronic);
warfarin's duration of action is (actue/chronic)
Heparin's duration of action is actute and warfarin's duration of action is
chronic.
heparin vs. warfarin: Tx of acute OD: Heparin = _________;
warfarin=______
Tx of heparin OD is protamine sulfate; Tx of warfarin= IV vit. K and fresh
frozen plasma.
heparin vs. warfarin: Warfarin is monitored by _________ while Heparin is
monitored by ___________.
Warfrin is monitored by PT (extrinsic pathway) (WEPT) and heparin is
monitored by PTT (intrinsic pathway)
Thrombolytics: questions from diagram at bottom of page
0
Thrombolytics: plasmin is the major ___________ enzyme. It breaks down
both _______ and _______
fibrinolytic enzyme. It accelerates breaks down of both fribin and fibrinogen
yielding fibrin splip products and degradation products, respectively.
Thrombolytics: Fibrinogen is converted to fibrin by _________
thrombin
Thrombolytics: tPA and urokinase promote the converson of ______ to
________ thereby increasing fibrinolysis.
plasminogen to plasmin
Thrombolytics: Various stimuli activate a blood proactivator to a blood
activator that promotes conversion of _________ to blank thereby increasing
fibrinolysis
plasminogen to plasmin
Thrombolytics: Streptokinase and anistreplase both activate and Activator
that increases convesion of plasminogen to plasmin.
0
Thrombolytics: Aminocaproic acid:____________ fibrinolysis.
inhibits fibrinolysis by inhibition of plasminogen conversion to plasmin.
Thrombolytics: 4 examples of thrombolytics include: ________, _________,
_____________, and ___________
Streptokinase, urokinase, tPA(altepalse), APSAC (anistreplase)
Thrombolytics: work by directly or indirectly aiding the conversion of
___________ to __________, which cleaves ______ and ________ clots.
tPA specifically coverts _______________ to plasmin
Directly or indirectly aid conversion of plaminogen to plasmin, which cleaves
thrombin and fribrin clots. It is claimed that tPA specifically coverts
fribrin-bound plasminogen to plasmin.
Thrombolytics: T/F: clinical use is for DVTs
False: used for early MI
Thrombolytics: pts. receiving this medication are at most risk for: ______
bleeding
Hematologic Drugs: mechanism of antiplatelet interaction
0
Hematologic Drugs: questions from diagram at top of page
0
Hematologic Drugs: When a break in the endothelium occurs _________ and
_________ are exposed.
collagen and vWF
Hematologic Drugs: Platelets are activated by binding to the above
Platelets bind to collagen and vWF. The two structures expressed by platelets
macromolecules. The two structures expressed by the platelets involved in
that are involved in this process are GP 1a and GP 1b. GP 1a and GP 1b bind
this process are __________ and _________ and they bind to _________ and
to collagen and vWF, respectively.
__________, repectively
Hematologic Drugs: After platelet activation _________ is expressed on their
surface. What is the role of this structure?
after platelets are activated they express GP IIb/IIIa. This molecule is
important in platlelet-platelet aggregation.
Hematologic Drugs: _________ and _________ interaction is needed in order
for platelet aggregation to occur.
GP IIb/IIIa and fribinogen
Hematologic Drugs: 5-HT, _______, and ________ are molecules that play a
role in the glycoprotein expression of activated platelets.
5-HT, ADP, and TxA2 are molecules that play a role in the glycoprotein
expression of activated platelets.
Hematologic Drugs: Aspirin acts by inhibiting production of ________ that
in turn inhibits glycoprotein expression in activated platelets.
TxA2
Hematologic Drugs: ADP production is inhibited by the drug _________.
ticlopidine
Hematologic Drugs: This antibody drug targets the _______ on platelets.
Abciximab
Copidogrel, ticlopidine: T/F: inhibits platele aggregation by irreversibly
inhibiting the ADP pathway involved in the binding of fibrinogen
TRUE
Copidogrel, ticlopidine: It is used for ______ ________ syndrome, coronary
_______, and it has been shown to decrease the incidence or recurrence of___
____.
it is used for acute coronary syndrome, coronary stenting. Decreases
incidence or recurrence of thrombotic stroke
Copidogrel, ticlopidine: Ticlopidine is associated with_________ as a side
effect.
Ticlopidine causes neutropenia and it is reserved for those who cannot
tolerate aspirin.
Abciximab: This drug binds to __________ on activated platelets.
gp IIb/Iia
Abciximab: It is used for ___________ and ________ _________
___________ ___________
acute coronary syndromes and percutanous transluminal coronary angioplasty
Abciximab: toxiciites are _______ and ________
bleeding and thrombocytopenia
Aspirin: It ________ and (reversibly/irreversibly) inhibits COX1 and COX2
to prevent the conversion of _______ to prostaglandins.
acetilates and irreversably inhibits COX-1 and COX-2
Aspirin: T/F: aspirin has an effect of PT, PTT
false it has no effect
Aspirin: What are the 4 A's of aspirin and NSAIDS in general
Antipyretic, Analgesic, Anti-inflam, antiplatelet
Aspirin: Important toxicities include _________, bleeding, hyperventilation,
__________- in children, and CN ____ toxicity
gastric ulceration, bleeding, hyperventilation, Reyes syndrome and tinnitus
(CNVIII).
diabetes drugs: AUTHOR
Marc Waase
Endocrine Drugs: Hydrocortisone, prednisone, triamcinolone, dexamtasone,
bleclomethasone are examples of what kind of drugs?
Glucocorticoid
Endocrine Drugs: Glucocorticoids decrease the production of ___ and ____
Leukotrienes and prostanglandins
Endocrine Drugs: To treat Addison's disease, inflammation, immune
suppression, asthma, use ____
Glucocorticoids
Endocrine Drugs: An important side-effect of Glucocortioid usage is ____
Iatrogenic Cushing's Syndrome
Endocrine Drugs: Buffalo hump, moon facies, truncal obesity, muscles
wasting, thin skin, easy bruisability, osteoporosis, adrenocortical atrophy,
peptic ulcers characterize what syndrome?
Cushing's Syndrome
Reproductive Drugs: Which two drugs inhibit cGMP phosphodiesterase,
leading to smooth muscle relaxation in the corpus cavernosum and penile
erection?
Sildenafil and Verdenafil --they fill the penis
Reproductive Drugs: What class of drugs are used tto treat erectile
dysfunction
cGMP Inhibitors
Reproductive Drugs: CGMP inibitors taken with ____have a high risk of
liofe-threeatening hypotension
nitrates
Reproductive Drugs: Which drugs is a partial agonist of estrogen recpetors in
the pituitary gland, stimulating increase in LH and FSH, which stimulates
ovulation to treat infertility
clomiphene
Reproductive Drugs: Clomiphene's side effects include:
Hotflashes, ovarian enlargment, multiple simultaneous pregnancies, visual
disturbances
Reproductive Drugs: What abortifacient is a competitite inhibitor of
preogestins at progesterone recpetor and may lead to heavy menstrual-like
bleeding?
Reproductive Drugs: The advantage of this drug is that it is reliable,
decreases incidence of ectopic pregnancy, decreases risk of pelvic infections,
and regulates menses; however it also puts you in a hypercoagulable stat and
may increase your trigylcerides, weight, and blood pressure
Mifepristone (RU486)
Oral Contracpetices - syntheitc progestins/estrogen
Rheumatologic Drugs: ____is converted to uric acid which leads to gout
Xanthine (converted from excess purines)
Rheumatologic Drugs: This drug depolymerizes microtubules, impairing
leukocyte chemotaxis and degranulation, and used to treat acute gout
Colchicine
Rheumatologic Drugs: This drugs inhibits reabsorption of uric acid and used
to treat chronic gout
Probenecid
Rheumatologic Drugs: This drug is used to treat chronic gout, but also inhbits
secretion of penicillin
Probenecid
Rheumatologic Drugs: This drugs inhibits xanthine oxidase decreasing the
conversion fo xanthine to uric acid
Allopurinol
Oncologic Drugs: What are the cell cycle specific oncologic drugs
antimetabolites, plant alkaloids, stroid hormones, bleomycin, paclitaxel,
etoposide
Oncologic Drugs: What are the cell cycle Nonspecific oncologic drugs?
alkylating agents and antibiotics
Oncologic Drugs: ____is an S-phase-specific anti-metabolite that is an folic
acid analog that inhibits dihydrofolate reducate decreasing dTMP(thymidine
and purines) and decreaing DNA/prtein synthesis.
Methotrexate
Oncologic Drugs: ____is an S-phase-specific anti-metabolite that is a
pyrmidine analog which complexed to folic acid, inhibiting thymidylate
synthase, decreasing dTMP and decreasing DNA/protein synthesis
5-Fluorouracil (5-FU)
Oncologic Drugs: Myelosuppression by methotrxate is reversible with ____
leucovorin (folinic acid) rescue
Oncologic Drugs: Which drug blocks purine synthesis and is used to treat
leukemias, lymphomas (not CLL or Hodgkins)
6-mercaptopurine (6-MP)
Oncologic Drugs: Which drug alkylates DNA and is used to treat CML?
Busulfan
Oncologic Drugs: Which drug inhibits DNA polymerase and is used to treat
AML?
cytarabine
Oncologic Drugs: This drug used to treat Leukemias and Lymphomas is
metaboilized by xanthine oxidase
6-mercaptopurine (6-MP)
Oncologic Drugs: Used to treat leukemias, lymphomas, choricarcinoma,
sacromas, rheumatoid arthritis, psoriasis, and can be an abortifacient; it may
lead to myelosuppression
Methotrexate
Oncologic Drugs: Used to treat colon cancer and other solid tumors, basal
cell carcinoma (topically)
5-Fluorouracil (5-FU)
Oncologic Drugs: Myelosuppression by 5-FU is ______
Not reversible
Oncologic Drugs: This drug used to treat AML may lead to leukopenia,
thrombocytopenia, megaloblastic anemia?
cytarabine
Oncologic Drugs: This drugs used to treat CML may lead to pulmonary
fibrosis and hyperpigmentation?
Busulfan
Oncologic Drugs: ____is an alkylating agent acivated by liver that covalently
x-links DNA at guanine N-7, and is used to treat non-hodgkin's lymphoma,
breast/ovarian carcinomas
cyclophosphamides
Oncologic Drugs: ____ alkylates DNA after bioactivation and can cross the
BBB and treats brain tumors (glioblastoma multiforme)
Nitrosoureas (Carmustine, lomustine, semustine, streptozocin)
Oncologic Drugs: ____acts like an alkylating agent, x-linking via hyrdolysis
of Cl and platinum; used to treat testicular, bladder, lung carcinomas
Cisplatin
Oncologic Drugs: This alkylating agent can cause myelosuppression and
hemorhagic cystitis
cyclophosphamides
Oncologic Drugs: This combination of drugs is used to treat Hodgkin's and
myelomas, sarcomas, and solid tumors (breast, ovary, lung)
ABVD: Adriamycin, Bleomycin, Vinblastine, Dacarbazine
Oncologic Drugs: ____noncovalently intercalates in DNA, creating breaks to
decrease replication and transcription
Doxorubicin (adriamycin)
Oncologic Drugs: ____intercalates DNA strands and induces free radical
fromation which causes strand breaks
Bleomycin, Dactinomycin
Oncologic Drugs: Which drugs causes cardiotoxicity, alopecia, and
myelosuppression?
Doxorubicin (adriamycin)
Oncologic Drugs: Which drug is used to trat oat cell carcinoma of the lung
and prostate/testicular carcinoma?
Etoposide
Oncologic Drugs: This combination of drugs is used to treat lymphoma, CLL,
Hodgkin's, Wilm's tumor, choriocarcinoma
MOp (Mustargen, Oncovin (Vincristine), Procarbazine (Matulane),
Prednisone)
Oncologic Drugs: Which glucocorticoid may trigger apoptosis and may even
work on nondividing cells
Prednisone
Oncologic Drugs: This drug is a G2-phase specific inhibitor of Topisiomerase
II, leaving double strand breaks in DNA following DNA replication
Etoposide
Oncologic Drugs: This drug used to treat testicular cancer and lymphomas
may cayse pulmonary fibrosis, skin chnages, and myelosuppression
Bleomycin, Dactinomycin
Oncologic Drugs: This drugs used as an immunosuppressant and in
lymphomas may cause acne, osteoporosis, hypertension, peptic ulcers,
hyperglycemia, psychosis?
Prednisone
Oncologic Drugs: ____is an estrogen receptor mixed agonist/antagonist that
blocks the binding of estrogen to ER+ cells.
Tomoxifen/Raloxifene
Oncologic Drugs: ____is n M-phase-specific alkaloid that binds to tubulin
and blocks polymerization of microtubules, preventing spindle formation
Vincristine and Vinblastine
Oncologic Drugs: ____is an M-phase-specific agen that binds to tubulin and
hyperstabilizes the polymerized microtubules, so that the mitotic spindle
cannot break down
Paclitaxel
Oncologic Drugs: What drugs is used to treat breast cancer, but may increas
the risk of endometrial carcinomas and hot flashes
Tomoxifen
Oncologic Drugs: Side-effects of Vinblastine include….
VinBASTine BLASTs Bone Morraow, causing myelosupression, as well as
neurotoxicity and paralutic ileus.
Oncologic Drugs: Side effects of Paclitaxel include….
Myelosupression and hypersensitivity
Immunosuppressants and Cytokine Therapy: This drug binds to cyclophilins,
blocking differentiation and activation of T cells mainly by inhibiting IL2
production
cyclosporine
Immunosuppressants and Cytokine Therapy: This antimetabolite derivative of
6-mercaptopurine interferes with the metabolism and synthesis of nucleic
acid, therefore toxic to proliferating lymphocytes
azathioprine
Immunosuppressants and Cytokine Therapy: This potent immunosuppressive
drug binds to the FK-binding protein and inhibits secretion of IL2 and other
cytokines
tacrolimus (FK506)
Immunosuppressants and Cytokine Therapy: This drug is used to suppress
organ rejection after transplantation, but may predispose patient to viral
infections and lymphoma
cyclosporine
Immunosuppressants and Cytokine Therapy: Azaothioprine is used to in what
setting?
Kidney transplants, autoimmune disorders (glomerulonephritis, hemolytic
anemia)
Immunosuppressants and Cytokine Therapy: Recombinant CytokineAldesleukin (interleukin-2) is used for?
Renal cell carcinoma, metastatic melanoma
Immunosuppressants and Cytokine Therapy: Recombinant CytokineErythropoietin (epoetin) is used for?
anemia
Immunosuppressants and Cytokine Therapy: Recombinant CytokineFilgrastim is used for?
Recovery of Bone Marrow; it is a granulocyte colony stimulating factor
Immunosuppressants and Cytokine Therapy: Recombinant Cytokine- alpha
interferon is used for?
Hep B/C, Kaposi's sarcoma, leukemia, malgnant melanoma
Immunosuppressants and Cytokine Therapy: Recombinant Cytokine- beta
interferon is used for?
Multiple Sclerosis
Immunosuppressants and Cytokine Therapy: Recombinant Cytokine- gamma
interferon is used for?
Chronic Granulomatous disease
Immunosuppressants and Cytokine Therapy: Recombinant Cytokineoprelvekin (interleukin2) is used for?
Thrombocytopenia
Immunosuppressants and Cytokine Therapy: Recombinant Cytokinesargamostim is used for?
Recovery of Bone Marrow (it is a granulocyte-macrophage colony
stimulating factor)
Immunosuppressants and Cytokine Therapy: Recombinant Cytokinethrombopoietin is used for?
Thrombocytopenia
Toxicology: What is the antidote for acetaminophen toxicity/overdose
N-acetylcysteine
Toxicology: What is the antidote for salicylates toxicity/overdose
Alkanize urine/dialysis
Toxicology: What is the antidote for antichoinesterase toxicity/overdose
Atropine, pralidoxime
Toxicology: What is the antidote for antimuscarinic/anticholinergic agents
toxicity/overdose
physostigimine salicylate
Toxicology: What is the antidote for Beta-blockers toxicity/overdose
glucagon
Toxicology: What is the antidote fordigitalis toxicity/overdose
Stop digitalis, Normalize K+, lodpcaine, anti-digitialis Fab Fragments,
Magnesium
Toxicology: What is the antidote for lead toxicity/overdose
CaEDTA, dimercaprol, succimer, penicillamine
Toxicology: What is the antidote for iron toxicity/overdose
Deferoxamine
Toxicology: What is the antidote for aresnic/mercury/gold toxicity/overdose
Dimercaprol (BAL), succimer
Toxicology: What is the antidote for copper, arsenic, gold toxicity/overdose
Penicillamine
Toxicology: What is the antidote N-acetylcysteine used to treat?
Acetaminophen toxicity/overdose
Toxicology: What is the antidote for cyanide toxicity/overdose
nitrite, hydroxocobalamin, thiosoulfate
Toxicology: What is the antidote for methemoglobin toxicity/overdose
methylene blue
Toxicology: What is the antidote glucagon used to treat?
Beta-blocker toxicity/overdose
Toxicology: What is the antidote for carbon monoxide toxicity/overdose
100% oxygen, hyperbaric oxygen
Toxicology: What is the antidote atropine used to treat?
anticholinesterase toxicity/overdose
Toxicology: What is the antidote for methanol toxicity/overdose
Ethanol, dialusis, fomepizole
Toxicology: What is the antidote for opiods toxicity/overdose
Nalozone/naltrexone
Toxicology: What is the antidote for ethylene glycol toxicity/overdose
Ethanol, dialusis, fomepizole
Toxicology: What is the antidote for benzodiazepines toxicity/overdose
Flumazenil
Toxicology: What is the antidote for (TCA) Tricyclic Antidepressants
toxicity/overdose
NaHCO3
Toxicology: What is the antidote for Heparin toxicity/overdose
Protamine
Toxicology: What is the antidote Deferoxamine used to treat?
Iron toxicity/overdose
Toxicology: What is the antidote for warfarin toxicity/overdose
vitamin K, fresh frozen plasma
Toxicology: What is the antidote Naloxone/naltrexone used to treat?
opioid toxicity/overdose
Toxicology: What is the antidote for tPA/streptokinase toxicity/overdose
aminocaproic acid
Toxicology: What is the antidote Physostigmine salicylate used to treat?
Antimuscarinic/anticholinergic agents toxicity/overdose
Toxicology: What is the antidote Flumazenil used to treat?
Benzodiazepine toxicity/overdose
Toxicology: What is the antidote Protamine used to treat
Heparin toxicity/overdose
Toxicology: Children living in old houses might eat the paint chips which
could cause ____
Lead Poisoning
Toxicology: Signs of Lead poisoning include:
Lead Lines on gingivae and epiphyses of Long bones, Encephalopathy and
Erythrocyte Basophilic stipling, Abdominal colic and sideroblastic Anemia,
Wrist and Foot Drop
Toxicology: 1st line of Treatment for Lead Poisoning include
Dimercaprol and EDTA
Toxicology: Weak acids, such as phenobarbitol, methotreaxate, aspirin,
alkanize urine with ____ to increase clearance
bicarbonate
Toxicology: Weak bases, such as amphetamines, acidify urine with NH4Cl to
____ clearance
increase
Toxicology: AUTHOR
Lakshmi Swamy
Drug reactions: For each drug reaction, give the pharmacological agents
responsible. The number of drugs you should list are given in parentheses.
You could also quiz yourself in reverse by going down the list of drugs on the
right.
0
Drug reactions: Pulmonary fibrosis (3)
bleomycin, amiodarone, busulfan
Drug reactions: Hepatitis (2)
isoniazid, halothane
Drug reactions: Focal to massive hepatic necrosis (4)
halothane, valproic acid, acetaminophen, amanita phalloides
Drug reactions: Anaphylaxis (1)
penicillin
Drug reactions: SLE-like syndrome (4). [mnemonic: it's not HIPP to have
lupus]
hydralazine, INH, procainamide, phenytoin
Drug reactions: Hemolysis in G6PD-deficient patients (8)
sulfonamides, INH, aspirin, ibuprofen, primaquine, nitrofurantoin,
pyrimethamine, chloramphenicol
Drug reactions: Thrombotic complications (1 class)
OCPs (e.g. estrogens and progestins)
Drug reactions: Adrenocortical insufficiency (withdrawal of what class of
drugs causes adrenocortical insufficiency?)
withdrawal of glucocorticoids causes hypothalamic-pituitary-axis supression
Drug reactions: Photosensitivity reactions (3) [mnemonic: SAT for a photo]
Sulfonamides, amiodarone, tetracycline
Drug reactions: Induce P-450 system (6)
barbiturates, phenytoin, carbamazepine, rifampin, griseofulvin, quinidine
Drug reactions: Inhibit P-450 system (6, including one fruit)
cimetidine, ketoconazole, grapefruit, erythromycin, INH, sulfonamides
Drug reactions: Tubulointerstitial nephritis (5)
sulfonamides, furosemide, methicillin, rifampin, NSAIDs (except aspirin)
Drug reactions: Hot flashes (1)
Tamoxifen
Drug reactions: Cutaneous flushing (4)
niacin, Ca++ channel blockers, adenosine, vancomycin
Drug reactions: Cardiac toxicity (2)
doxorubicin (adriamycin), daunorubicin
Drug reactions: Agranulocytosis (3, all start with letter C)
clozapine, carbamazepine, colchicine
Drug reactions: Stevens-Johnson syndrome (3)
ethosuximide, sulfonamides, lamotrigine
Drug reactions: Cinchonism (2)
quinidine, quinine
Drug reactions: Tendonitis, tendon rupture and cartilage damage (kids) (1)
fluoroquinolones
Drug reactions: Disulfiram-like reaction (4)
metronidazole, certain cephalosporins, procarbazine, sulfonylureas
Drug reactions: Otoxicity and nephrotoxicity (3)
aminoglycosides, loop diuretics, cisplatin
Drug reactions: Drug-induced Parkinson's (4)
haloperidol, chlorpromazine, resperine, MPTP
Drug reactions: Torsades de pointes (two subclasses of antiarrhythmics)
Class III (sotalol), class IA (quinidine) antiarrhythmics
Drug reactions: Aplastic anemia (3)
chloramphenicol, benzene, NSAIDs
Drug reactions: Neuro/nephrotoxicity (1)
polymyxins
Drug reactions: Pseudomembranous colitis (2)
clindamycin, ampicillin
Drug reactions: Gynecomastia (5) [mnemonic: Some Drugs Create Awesome
Knockers]
spironolactone, digitalis, cimetidine, chronic Alcohol use, estrogens,
ketoconazole
Drug reactions: Atropine-like side effects (1)
tricyclics
Drug reactions: Cough (1)
ACE inhibitors (losartan --> no cough)
Drug reactions: Gingival hyperplasia (1)
phenytoin
Drug reactions: Diabetes insipidus (1)
lithium
Drug reactions: Tardive dyskinesia (1)
antipsychotics
Drug reactions: Fanconi's syndrome (1)
tetracycline
Drug reactions: Gray baby syndrome (1)
chloramphenicol
Drug reactions: Extrapyramidal side effects (3)
chlorpromazine, thioridazine, haloperidol
Drug reactions: Osteoporosis (2)
corticosteroids, heparin
Alcohol toxicity: Ethylene glycol is converted to ------- ------ by alcohol
dehydrogenase. This product can lead to acidosis and nephrotoxicity.
oxalic acid.
Alcohol toxicity: Alcohol dehyrogenase also converts methanol to
formaldehyde and formic acid, which can cause severe ----- and damage to
the -------.
acidosis. retina
Alcohol toxicity: Ethanol competes with ethylene glycol and methanol (if
present) for alcohol dehydrogenase. ADH action on EtOH produces -------.
acetaldehyde
Alcohol toxicity: What symptoms does acetaldehyde cause?
nausea, vomiting, headache, hypotension
Alcohol toxicity: Acetaldehyde itself can be metabolized by acetaldehyde
dehydrogenase to ----- -----.
acetic acid.
Alcohol toxicity: Acetaldehyde dehydrogenase is inhibited by what drug?
disulfiram.
Herbal agents: Give the clinical uses for the following herbal agents.
0
Herbal agents: echinacea clinical use
common cold
Herbal agents: ephedra clinical use
as for ephedrine
Herbal agents: feverfew clinical use
migraine
Herbal agents: ginko clinical use
intermittent claudication
Herbal agents: kava clinical use
chronic anxiety
Herbal agents: milk thistle clinical use
viral hepatitis
Herbal agents: saw palmetto clinical use
benign prostatic hyperplasia
Herbal agents: St. John's wort clinical use
mild to moderate depression
Herbal agents: dehyroepiandrosterone clinical use
symptomatic improvement in females with SLE or AIDS
Herbal agents: Melatonin clinical use
jet lag, insomnia
Herbal agents: Give the toxicities for the following herbal agents.
0
Herbal agents: echinacea toxicity
GI distress, dizziness, and headache
Herbal agents: ephedra toxicity
CNS and cardiovascular stimulation; arrhythmias, stroke and seizures at high
doses.
Herbal agents: feverfew toxicity
GI distress, mouth ulcers, antiplatelet actions
Herbal agents: ginko toxicity
GI distress, anxiety, insomnia, headache, and antiplatelet actions
Herbal agents: kava toxicity
GI distress, sedation, ataxia, hepatotoxicity, phototoxicity, dermatotoxicity
Herbal agents: milk thistle toxicity
loose stools
Herbal agents: saw palmetto toxicity
GI distress, decreased libido, hypertension
Herbal agents: St. John's wort toxicity
GI distress and phototoxicity; serotonin syndrome with SSRIs
Herbal agents: dehyroepiandrosterone toxicity
Androgenization (premenopausal women), estrogenic effects
(postmenopausal), feminization (young men)
Herbal agents: Melatonin toxicity
Sedation, supresses midcycle LH, hypoprolactinemia
Drug category: For each drug name ending, give the general category of drug
it indicates and an example of a drug in that category.
0
Drug category: -ane
inhalational general anesthetic. Halothane
Drug category: -azepam
benzodiazepine. Diazepam
Drug category: -azine
phenothiazine (neuroleptic, antiemetic). Chlorpromazine
Drug category: -azole
antifungal. Ketoconazole
Drug category: -barbital
barbiturate. Phenobarbital
Drug category: -caine
local anesthetic. Lidocaine
Drug category: -cillin
penicillin. Methicillin
Drug category: -cycline
antibiotic, protein synthesis inhibitor. Tetracycline
Drug category: -ipramine
tricyclic antidepressant. Imipramine
Drug category: -navir
protease inhibitor. Saquinavir
Drug category: -olol
beta antagonist. Propranolol
Drug category: -operidol
butyrophenone (neuroleptic). Haloperidol
Drug category: -oxin
cardiac glycoside (inotropic agent). Digoxin
Drug category: -phylline
methylxanthine. Theophylline
Drug category: -pril
ACE inhibitor. Captopril
Drug category: -terol
beta-2 agonist. Albuterol
Drug category: -tidine
H2 antagonist. Cimetidine
Drug category: -triptyline
tricyclic antidepressant. Amitriptyline
Drug category: -tropin
pituitary hormone. Somatotropin
Drug category: -zosin
alpha-1 antagonist. Prazosin
Drug category: AUTHOR
Lakshmi Swamy
Drug category: PHYSIOLOGY
0
Bacterial Strucutre & Cell Walls: Where is beta-lactamase in bacteria? What
does it do?
Beta-lactamases are found in the periplasm of gram negative bacteria. The
enzyme hydrolyzes beta-lactam antibiotics, conferring resistance.
Bacterial Strucutre & Cell Walls: Which gram-positive organism lacks a
polysaccharide capsule and has a capsule made of something else?
Bacillus anthracis - has D-glutamate instead of polysaccharide
Bacterial Strucutre & Cell Walls: What are spores made of and what do they
do?
Keratin-like coat, dipicolinic acid. Provide resistanceto dehydration, heat and
chemicals
Bacterial Strucutre & Cell Walls: What helps organisms adhere to indwelling
catheters?
The glycocalyx (composed of polysaccharide)
Bacterial Strucutre & Cell Walls: What is the major surface antigen of
gram-positive cell walls and what does it do?
Teichoic acid - unique to gram-positive bacteria. Induces TNF and IL-1
Bacterial Strucutre & Cell Walls: What is specific to gram-negative bacterial
cell membranes?
Endotoxin/LPS (lipopolysaccharide)
Bacterial Growth Curve: Describe the four phases of bacterial growth.
1) Lag phase of metabolic activity without division. 2) Log phase of rapid
cell division. 3) Stationary phase in which nutrient depletion slows growth. 4)
Death due to prolonged nutrient depletion and buildup of waste products.
Main Exotoxin and Endotoxin Features: What are exotoxins and endotoxin
chemically?
Exotoxins are polypeptides, while endotoxins are lipopolysaccharides.
Main Exotoxin and Endotoxin Features: Where do bacteria keep their
exotoxin or endotoxin genes?
Exotoxin genes on plasmids or bacteriophages; endotoxin genes on bacterial
chromosomes.
Main Exotoxin and Endotoxin Features: Which is more fatal – exotoxin or
endotoxin?
Exotoxin is highly fatal (~1 microgram), while you need 100’s of micrograms
for endotoxin to prove lethal.
Main Exotoxin and Endotoxin Features: Which has greater heat stability –
endotoxin or exotoxin?
Endotoxin – stable at 100°C for 1 hour, while endotoxin is rapidly destroyed
at 60°C (EXCEPT Staph enterotoxin)
Main Exotoxin and Endotoxin Features: True or False: We can vaccinate
against exotoxins and endotoxins.
False: We do have toxoids vaccines against exotoxins for diseases like
tetanus, botulism and diphtheria, but there are no vaccines against endotoxins.
Bugs with Exotoxins: Which bugs have Exotoxin that acts by ADP
ribosylation?
Corynebacterium diphtheriae (which then inactivates EF-2). Also Escherichia
coli, Vibrio cholerae, and Bordetalla pertussis (all these then stimulate
adenylate cyclase).
Bugs with Exotoxins: Which bug has exotoxin that blocks the release of
acetylcholine? What symptoms does that cause?
Clostridium botulinum. Anticholinergic symptoms, CNS paralysis, flopy
baby, and a wrinkle-free forehead if injected!!
Bugs with Exotoxins: Which bug has exotoxin that blocks glycine release?
What does that cause?
Clostridium tetani. Causes “lockjaw”.
Bugs with Exotoxins: How does Staph aureus cause toxic shock syndrome?
The toxin is a superantigen that binds to MHC II protein and T-cell receptor à
induces IL-1 and IL-2 à TSS
Endotoxin (especially lipid A): How could bacterial infection cause
disseminated intravascular coagulation?
Endotoxin can activate Hageman factor --> initiates coagulation cascade -->
DIC
Endotoxin (especially lipid A): How could bacterial infection cause
hypotension?
Endotoxin activates macrophages to release nitric oxide (--> vasodilationà
hypotension); can also activate alternate complement pathway C3a, -->
hypotension (N.B. also edema).
Endotoxin (especially lipid A): How does bacterial infection cause fever?
Endotoxin activates macrophages to release IL-1 and TNF --> fever.
Gram Stain Limitations: --- are too thin to be visualized. Use darkfield
microscopy and fluorescent antibody staining instead.
Treponema
Gram Stain Limitations: --- lack a cell wall
Mycoplasma
Gram Stain Limitations: --- stain with silver
Legionella pneumophila
Fermentation patterns of Neisseria: What are the two Neisseria species?
N. meningitidis, N. gonorrhoeae
Fermentation patterns of Neisseria: How are the Neisseria species
differentiated?
MeninGococci ferment Maltose & Glucose; Gonococci ferment only Glucose
Pigment-producing Bacteria: --- produces a yellow pigment
Staphylococcus aureus (Latin aureus = gold)
Pigment-producing Bacteria: --- produces a blue-green pigment
Pseudomonas aeruginosa
Pigment-producing Bacteria: --- produces a red pigment
Serratia marcescens (think red marachino cherry)
IgA Proteases: IgA proteases allow organisms to…
… colonize mucosal surfaces
IgA Proteases: Name 4 organisms with IgA proteases
Strep pneumoniae, N. meningitidis, N. gonorhoeae, H. influenzae
Gram-positive Lab Algorithm: What are the lab steps for ID'ing
Staphylococcus aureus?
1st gram stain --> get purple/blue cocci (= positive); 2nd catalase test -->
positive (staphylococcus clusters); 3rd coagulase test --> positive
(differentiates S. aureus from the coagulase-negative S. epidermidis and S.
saprophyticus)
Gram-positive Lab Algorithm: What are the 4 types of gram-postive rods?
Corynebacterium, Listeria, Bacillus, Clostridium
Gram-positive Lab Algorithm: When do you test for bacitracin sensitivity or
resistance?
For beta-hemolytic strep. Bacitracin-sensitive --> Group A beta-hemolytic
Strep pyogenes. Bacitracin-resistant --> Group B (Bad!) beta-hemolytic Strep
agalactiae
Gram-positive Lab Algorithm: Name 4 laboratory features of Streptococcus
pneumoniae
alpha hemolytic (green – partial hemolysis), positive Quellung reaction,
optochin-sensitive, and bile-soluble
Gram-positive Lab Algorithm: When would you do the optochin test?
When you have alpha hemolytic strep
Gram-negative Lab Algorithm: Once you see gram-negative rods under the
microscope, what is your next diagnostic test?
test lactose fermentation
Gram-negative Lab Algorithm: What are the 3 fast lactose fermenters:
Klebsiella, E. coli, and Enterobacter
Gram-negative Lab Algorithm: How do you distinguish among lactose
non-fermenters?
Perform an oxidase test
Gram-negative Lab Algorithm: Which are oxidase-positive?
Pseudomonas
Gram-negative Lab Algorithm: Which are oxidase-negative?
Shigella, Salmonella, or Proteus
Gram-negative Lab Algorithm: What are the gram-negative cocci?
Neisseria
Gram-negative Lab Algorithm: What are the gram-negative coccoid rods?
H. influenzae, Pasteurella, Brucella, Bordetella pertussis
Gram-negative Lab Algorithm: Which gram negative coccoid requires factors
V and X for growth?
H. flu
Special Culture Requirements: Use chocolate agar and factors V & X for ---
Hemophilus influenzae
Special Culture Requirements: Factor V has --- and Factor X has ---
NAD, hematin
Special Culture Requirements: Thayer-Martin (VCN) media to culture ---
Neisseria gonorrhoeae
Special Culture Requirements: Bordet-Gengou (potato) agar to culture ---
Bordetella pertussis
Special Culture Requirements: Tellurite plate, Loffler's medium, blood agar
for ---
Corynebacterium diphtheriae
Special Culture Requirements: Lowenstein-Jensen agar for growing ---
Mycobacterium tuberculosis
Special Culture Requirements: Pink colonies on MacConkey's agar are ---
Lactose-fermenting enterics (Klebsiella, Eschericihia, or Enterobacter
Special Culture Requirements: Charcoal yeast extract agar buffered with
increased iron and cysteine to grow ---
Legionella pneumophila
Special Culture Requirements: Sabouraud's agar to culture ---
Fungi
Stains: Stain used to diagnose Whipple's disease
PAS (Periodic Acid Schiff)
Stains: PAS stains ---
glycogen, mucopolysaccharides
Stains: Ziehl-Neelsen stains ---
Acid-fast bacteria
Stains: India ink stains ---
Cryptococcus neoformans
Stains: Congo red stains -- and exhibits ---
Amyloid, aple-green birefringence in polarized light
Stains: Giemsa's stains what 4 organisms?
Borrelia, Plasmodium, trypanosomes, Chlamydia (intracellular inclusions on
Giemsa)
Conjugation, Transduction, Transformation: Which process can involve
eukaryotic DNA?
Transformation
Conjugation, Transduction, Transformation: DNA transferred from 1
bacterium to another through a sex pilus is
Conjugation
Conjugation, Transduction, Transformation: DNA transferred by a virus from
1 cell to another
Transduction
Conjugation, Transduction, Transformation: Generalized transduction can
transfer --
Any gene
Conjugation, Transduction, Transformation: Specialized transduction
transfers ---
only certain genes (that's why it's special!)
Obligate Aerobes: "Nagging Pests Must Breathe" helps you remember what?
obligate aerobes: Nocardia, Pseudomonas aeruginosa, Mycobacterium
tuberculosis, Bacillus
Obligate Aerobes: Aerobic bacteria commonly found in burn wounds,
nosocomial pneumonia, and pneumonias in cystic fibrosis patients?
Pseudomonas aeruginosa (an obligate aerobe)
Obligate Aerobes: What bug likes the lungs’ apices and why?
Mycobacterium tuberculosis – because the apices have the highest partial
pressure of oxygen
Obligate Anaerobes: If you hear crepitus, indicating gas in tissue, what type
of infection do you suspect?
Anaerobic bacterial infection, such as Clostridium, Bacteroides, or
Actinomyces (CBA)
Obligate Anaerobes: Which bugs are anaerobic and why?
Clostridium, Bacteroides, and Actinomyces. Air causes them oxidative
damage, because they lack catalase and/or superoxide dismutase.
Obligate Anaerobes: Why are aminoglycoside antibiotics ineffective against
anerobic bacteria?
AminO2glycosides require O2 to enter into bacterial cells; anaerobic bacteria
aren't where the oxygen is
Intracellular Bugs: Name the 2 obligate intracellular organisms
Rickettsia, Chlamydia - "They stay inside (cells) when it's Really Cold"
Intracellular Bugs: Why do they need the host's cell?
They can't make ATP
Intracellular Bugs: Name 7 facultative intracellular organisms
Mycobacterium, Brucella, Francisella, Listeria, Yersinia, Legionella,
Salmonella
Intracellular Bugs: AUTHOR
Olga Kulinets
Encapsulated Bacteria: List 4 examples of encapsulated bacteria
Streptococcus Pneumoniae, Haemophilus influenzae, Neisseria meningitidis,
Klebsiella pneumoniae
Encapsulated Bacteria: What is the main virulence factor of encapsulated
bacteria and why?
Polysacharide capsule is antiphagocytic
Encapsulated Bacteria: What is a necessary component of humoral immune
response to encaps. Bacteria?
IgG2
Encapsulated Bacteria: What vaccines are available for encapsulated
bacteria?
Pneumovax, H. influenzae, meningococcal
Encapsulated Bacteria: What serves as vaccine antigen?
Capsule
Encapsulated Bacteria: What laboratory test can be used to detect the
presence of encapsulated bacteria?
Quellung reaction - capsule swells when specific anticapsular antisera are
added - "Quellung = capsular swellung"
Encapsulated Bacteria: What complications/clinical signs is pneumococcus
associated with?
Rusty sputum, sepsis in sickle cell anemia, and splenectomy
Spores: Bacterial: What kind of bacteria form spores and when?
Certain gram-positive rods when nutrients are limited
Spores: Bacterial: Name 3 spore-formers
Bacillus anthracis, C. perfringens, C. tetani = gram positive soil bugs
Spores: Bacterial: T or F: Spores are highly resistant to destruction by heat
and chemicals
TRUE
Spores: Bacterial: Spores have ___ acid in their core
dipicolinic
Spores: Bacterial: T or F: Spores are metabolically active
False. Spores have no metabolic activity
Spores: Bacterial: What disinfecting procedure kills spores?
Autoclaving (ex/ surgical equipment)
Alpha-hemolytic Bacteria: What organisms are alpha-hemolytic?
Pneumococci, viridans strep
Alpha-hemolytic Bacteria: Pneumococci are catalase ___ and optochin ___
Pneumococci are catalase negative and optochin sensitive
Alpha-hemolytic Bacteria: Viridans strep are catalase ___ and optochin ___
Viridans strep are catalase sensitive and optochin resistant
Beta-hemolytic Bacteria: What organisms are beta-hemolytic?
Staph aureus, strep pyogenes, strep agalactiae, lysteria monocytogenes
Beta-hemolytic Bacteria: Staph aureus is catalase ___ and coagulase ___
Positive, positive
Beta-hemolytic Bacteria: Strep pyogenes is catalase ___ and bacitracin __
negative, sensitive
Beta-hemolytic Bacteria: Strep agalactiae is catalase __ and bacitracin__
negative, resistant
Beta-hemolytic Bacteria: Where is Lysteria monocytogenes found, and what
is its characteristic pathology and laboratory appearance?
Unpausterized milk, miningitis in newborns, tumbling motility
Catalase/Coagulase: What are catalase and coagulase tests used for?
Catalase is used to distinguish staph (+) from strep (-), coagulase is used to
distinguish S. aureus (+) from S. epidermis (-) and S. saprophyticus(-)
Catalase/Coagulase: How is catalase a virulence factor?
It degrades H2O2, an antimicrobial product of PMNs that is a substrate for
myeloperoxidase
Staph aureus: What is the function of protein A?
Virulence factor - binds to Fc-IgG and inhibits complement fixation and
phagocytosis
Staph aureus: TSST is a ___ (type of virulence factor) that binds to ___ (2
types of receptor) and causes ___ of ___ (type of cells) leading to ___
(disease)
TSST is a superantigen that binds to MHC II and T-cell receptor and causes
polyclonal activation of T-cells leading to toxic shock syndrome
Staph aureus: 3 toxins of S. aureus and a syndrome caused by each
TSST- 1 - toxic shock syndrome, exfoliative toxin - scalded skin syndrome,
enterotoxins - rapid-onset food poisoning
Staph aureus: T/F - S. aureus causes acute bacterial endocarditis
TRUE
Staph aureus: T/F - S. aureus causes skin disease and organ abscesses, but not
pneumonia
False - causes all 3
Staph aureus: T/F - S. aureus food poisoning is due to bacterial infiltration of
the intestinal wall
False - it is due to ingestion of preformed enterotoxin
Strep Pyogenes: T/F: strep pyogenes is catalase negative and bacitracin
sensitive
TRUE
Strep Pyogenes: 3 pyogenic manifestations of strep pyogenes
pharyngitis, cellulitis, impetigo
Strep Pyogenes: Which is not a toxigenic manifestation of strep pyogenes:
scarlet fever, rheumatic fever, TSS, acute glomerulonephritis
Rheumatic fever and acute glomerulonephritis are immune-mediated
Strep Pyogenes: List 5 signs and symptoms characteristic of rheumatic fever
PECCS: polyarthritis, erythema marginatum, chorea, carditis, subcutaneous
nodules
Enterococci: T/F: Enterococci are penicillin G sensitive and show variable
hemolysis
F - they are resistant, but do have variable hemolysis
Enterococci: Lancefield group D includes ___ and ___, which can be
differentiated through ___ (lab test)
Enterococci and non-enterococcal Group D strep. Enterococci can grow on
6.5% NaCl, and non-enterococci cannot.
Enterococci: Lancefield grouping is based on ___ on the bacterial cell wall
C carbohydrate
Viridans Strep: Viridans Strep are ___ hemolytic
alpha
Viridans Strep: Strep mutans causes ___
dental caries
Viridans Strep: S. sanguis causes ___
bacterial endocarditis
Viridans Strep: How do you differentiate viridans strep from S. pneumoniae
in the laboratory?
Both are alpha-hemolytic, but viridans strep is resistant to optochin (live in
the mouth, not afraid of-the-chin)
Clostridia: T/F: Clostridia are gram-positive, spore-forming, microaerophilic
bacteria
False - they are obligate anaerobes
Clostridia: Name 4 types of Clostridia and disease caused by each
Tetanus - tetanic paralysis, Botulinum - flaccid paralysis, Perfringens gangrene, Difficile - diarrhea
Clostridia: How does Clostridia cause tetanic paralysis?
Exotoxin blocks glycine (inhibitory neurotransmitter) release from Renshaw
cells in spinal chord leading to tetanic paralysis
Clostridia: How does C. botulinum cause flaccid paralysis?
Preformed, heat - labile toxin inhibits ACh release
Clostridia: T/F: C. perfringens produces alpha-toxin, a globulin that causes
myonecrosis, gas gangrene, or hemolysis
False - alpha-toxin is a lecithinase
Clostridia: What causes pseudomembranous colitis? How is it treated?
Cytotoxin, an alpha toxin produced by C. diff, usu after antibiotic use
(clindamycin ar ampicillin). Treat with metronidazole.
Diphtheria: Exotoxin is encoded by ___ and ihibits ___ by ADP-ribosylation
of ___
beta-prophaage, protein synthesis, EF-2
Diphtheria: T/F: Symptoms of diphtheria include pseudomembranous
pharyngitis, lymphadenopathy, and hematuria
Does not cause hematuria
Diphtheria: Lab tests for Diphtheria
Gram-positive, club-shaped rods with metachromatic granules; grow on
tellurite agar
Diphtheria: ABCDEFG of diphtheria
ADP ribosylation, Beta-prophage, Corynebacterium, Diphtheriae, EF-2,
Granules
Anthrax: Anthrax is caused by ___ (bacteria)
Bacillus anthracis
Anthrax: T/F: Bacillus anthracis is spore-forning and gram negative rod
FALSE - it is a gram-positive rod
Anthrax: What is the progression of anthrax?
Contact leads to malignant pustule (painless ulcer) which can progress to
bacteremia and death
Anthrax: What is woolsorter's disease?
Life-threatening pneumonia caused by inhalation of spores
Anthrax: Characteristic lesion of anthrax
Black skin lesions - vesicular papules covered by black eschar
Actinomycis Vs. Nocardia: Actinomycis, Nocardia are gram___ rods that
form long-branching filaments resembling fungi
positive
Actinomycis Vs. Nocardia: What air requirement do actinomysis and
nocardia have?
Actinomyces is an anaerobe and nocardia is an aerobe
Actinomycis Vs. Nocardia: A vs. N (pick one): pulmonary infection in
immunocompromized
nocardia
Actinomycis Vs. Nocardia: A vs. N (pick one): oral/facial abscess with sulfur
granules that may drain through sinus tracts in skin
actinomyces
Actinomycis Vs. Nocardia: A vs. N (pick one): Normal oral flora
actinomyces
Actinomycis Vs. Nocardia: A vs. N (pick one): Weakly acid fast
nocardia
Actinomycis Vs. Nocardia: What treatment do you use for actinomycis? For
nocardia?
SNAP - sulpha for nocardia; actinomyces use penicillin
Penicillin and gram-neg bacteria: Gram negative bugs are ___ to benzyl
penicillin G and ____ to penicillin derivatives such as ampicillin
resistant, may be susceptible
Penicillin and gram-neg bacteria: T/F: Vancomycin can enter gram-negative
bacteria
False - gram-negative outer membrane layer inhibits entry of penicillin G and
vancomycin
Name bacteria associated with food poisoning from the following sources::
Reheated rice
Bacillus cereus
Name bacteria associated with food poisoning from the following sources::
Contaminated seafood
Vibrio parahemolyticus and vulnificus
Name bacteria associated with food poisoning from the following sources::
Meats, mayonaise, custard
S. aureus
Name bacteria associated with food poisoning from the following sources::
Reheater meat dishes
C. perfringens
Name bacteria associated with food poisoning from the following sources::
Improperly canned food
C. botulinum
Name bacteria associated with food poisoning from the following sources::
Undercooked meat
E. coli 0157:H7
Name bacteria associated with food poisoning from the following sources::
Poultry, meat, eggs
Salmonella
Name diarrheal organism associated with the following:: Ferments lactose
and causes non-bloody diarrhea
enterotoxigenic E. coli
Name diarrheal organism associated with the following:: Comma-shaped
organism
Vibrio cholerae
Name diarrheal organism associated with the following:: Does not ferment
lactose, motile, bloody diarrhea
Salmonella
Name diarrheal organism associated with the following:: Does not ferment
lactose, nonmotile, very low ID50, bloody diarrhea
Shigella
Name diarrheal organism associated with the following:: Comma or
S-shaped, growth at 42 degrees, bloody diarrhea
Campylobaxter jejuni
Name diarrheal organism associated with the following:: Transmitted by
seafood
Vibrio parahemolyticus
Name diarrheal organism associated with the following:: Transmitted through
pet feces (puppies), bloody diarrhea
Yersenia enterocolitica
Name diarrheal organism associated with the following:: Rice-water stools
Vibrio cholerae
Name diarrheal organism associated with the following:: 4 non-bacterial
causes of non-bloody diarrhea
Virus - rotavirus, norwalk virus; protozoan - Cryptosporidium and Giardia
Name diarrheal organism associated with the following:: Ferments lactose
and causes bloody diarrhea
E. coli 0157:H7
Name diarrheal organism associated with the following:: Protozoan cause of
bloody diarrhea
Entamoeba histolytica
Enterobacteriaceae: Lab tests for enterobacteriaceae
Ferment glucose, oxidase negative
Enterobacteriaceae: T/F: Enterobacteriaceae includes E.coli, Salmonella,
Klebsiella, Enterobacter, Serratia, Proteus, and Pseudomonas
False - does not include Pseudomona
Enterobacteriaceae: Describe O, K, and H antigens
O - somatic, polysacharide of endotoxin; K - capsular, related to virulence; H
- flagellar, found in motile species
Haemophilus Influenzae: Name 4 diseases caused by H. influenzae
epiglottitis, meningitis, otitis media, pneumonia
Haemophilus Influenzae: T/F - H. influenzae is a large gram-negative rod
False - it is a small (coccobacillary) gram-negative rod
Haemophilus Influenzae: H. influenzae is transmitted by ____ and invasive
disease is caused by capsular type ___. It produces ___ protease.
aerosol, B, IgA
Haemophilus Influenzae: Culture on ___ agar requires ___ and ___
Chocolate agar, Factor V (NAD), X (hematin)
Haemophilus Influenzae: T/F: H. influenzae causes the flu.
False - influenza virus causes flue
Haemophilus Influenzae: Use ___ to treat H. influenzae meningitis and ___
for prophylaxis of close contacts.
Ceftriaxone, rifampin
Haemophilus Influenzae: T/F: H. influenzae vaccine contains type D capsular
polysacharide conjugated to enterotoxin
False: vaccine contains type B capsular polysacharide conjugated to
diphtheria toxoid or other protein
Haemophilus Influenzae: When is the H. influenzae vaccine given?
Btw 2 and 18 months of age
Legionella Pneumophilia: Legionella Pneumophilia is a gram___ rod
negative
Legionella Pneumophilia: It will grow on ___ yeast extract with ___ and ___,
and should be treated with ___
Charcoal, iron, cysteine, erythromycin
Legionella Pneumophilia: T/F: Legionella pneumophilia is transmitted
through environmental water source habitat.
TRUE
Legionella Pneumophilia: T/F: Legionella is transmitted person to person.
False - no person to person transmission
Pseudomonas Aerugenosa: T/F: Pseudomonas Aerugenosa is anaerobic
gram-negative rod found in water sources
False - it is AERobic (AERuginosa)
Pseudomonas Aerugenosa: Name 5 infections commonly caused by
Pseudomonas
Pneumonia (esp. in CF), sepsis, external otitis, UTI, hot tub folliculitis
Pseudomonas Aerugenosa: T/F: Pseudomonas Aerugenosa ferments lactose
and is oxidase-negative
False - P. Aurugenosa does not ferment lactose and is oxidase negative
Pseudomonas Aerugenosa: Blue-green pigment produced by P. Aerugenosa
pyocyanin
Pseudomonas Aerugenosa: What 2 toxins does P. Aerugenosa produce?
Endotoxin (causes fever and shock), exotoxin A (inactivated EF-2)
Pseudomonas Aerugenosa: What is the treatment for P. aeruginosa
Aminoglycoside plus extended-spectrum penicillin (piperacillin, ticarcillin)
Pseudomonas Aerugenosa: What kind of injury makes a person especially
susceptible to P. aeruginosa infection?
Burns
Helicobacter Pylori: What conditions does H. pylori cause and is a risk factor
for?
Causes gastriti and 90% of duodenal ulcers, risk of peptic ulcer, gastric
carcinoma
Helicobacter Pylori: T/F: H. pylori is a gram-negative rod that creates an
alkaline environment
TRUE
Helicobacter Pylori: What is a test for H. pylori?
Urease breath test
Helicobacter Pylori: What is the treatment for H. pylori?
Triple therapy - bismuth, metronidazole, and tetracycline or amoxicyclin OR
more expensive metronidazole, omeprazole, and clarithromycin
Helicobacter Pylori: What 2 bacteria are urease positive?
H. pylori and Proteus
Lactose - fermenting enteric bacteria: What culture technique differentiates
lactose fermenting from non-fermenting bacteria?
Lactose fermenters grow pink colonies on MacConkey's agar (Lactose is
KEE)
For the following, state if they ferment lactose:: Klebsiella
Ferments lactose
For the following, state if they ferment lactose:: Salmonella
Does not ferment
For the following, state if they ferment lactose:: E.coli
Ferments lactose
For the following, state if they ferment lactose:: Staph Aureus
Does not ferment
For the following, state if they ferment lactose:: Enterobacter
Ferments lactose
For the following, state if they ferment lactose:: Citrobacter
Ferments lactose
Salmonella Vs. Shigella: Select salmonella, shigella, or both:
0
Salmonella Vs. Shigella: Non-lactose fermenter
both
Salmonella Vs. Shigella: Motile
SalMOnella
Salmonella Vs. Shigella: Invades futher, disseminates hematogenously
Samonella
Salmonella Vs. Shigella: More virulent
Shigella (10e1 innocumlum compared to 10e5 innoculum for Salmonella)
Salmonella Vs. Shigella: Symptoms prolonged with antibiotic treatment
Samonella
Salmonella Vs. Shigella: Has an animal resevoir
Samonella
Salmonella Vs. Shigella: Invade intestinal mucosa causing bloody diarrhea
both
Salmonella Vs. Shigella: What immune cell type predominantly responds to
Salmonella?
Monocytes
Salmonella Vs. Shigella: How is Shigella transmitted?
4 f's: food, fingers, feces, and flies
Cholera and Pertussi toxins: How does Vibrio Cholerae toxin work?
Permanently activates Gs causing rice-water diarrhea
Cholera and Pertussi toxins: How does Pertussis toxin work?
Permanently disables Gi, causing whooping cough, also promotes
lymphocytosis by inhibiting chemokine receptors
Cholera and Pertussi toxins: What do Pertussis toxin and Choleratoxin have
in common?
Act via ADP ribosylation that permanently activates adenyl cyclase, resulting
in increased cAMP
Zoonotic Bacteria: Name 5 common zoonotic bacteria
Bugs from your pet: Borrelia burgdorferi, Brucella, Francisella tularensis,
Yersinia pestis, Pasteirella multocida
Name the disease, mode of transmission, and source associated with the
following:: Borrelia burgdorferi
Lyme disease; tick bite; Ixodes ticks that live on deer and mice
Name the disease, mode of transmission, and source associated with the
following:: Brucella
Brucellosis/undulant fever; dairy products, contact with animals -- "Undulate
and Unpasteurized products give you Undulant fever"
Name the disease, mode of transmission, and source associated with the
following:: Francisella tularensis
Tularemia; tick bite; rabbits, deer
Name the disease, mode of transmission, and source associated with the
following:: Yersenia pestis
Plague, flea bite; rodents, esp. prarie dogs
Name the disease, mode of transmission, and source associated with the
following:: Pasteurella multocida
Cellulitis; animal bite; cats, dogs
Gardnerella vaginalis: What symptoms are associated with G. vaginalis
infection?
Vaginosis - greenish vaginal discharge, fishy smell, not painful
Gardnerella vaginalis: What is Mobiluncus?
An anaerobe commonly involved in G. vaginalis infections
Gardnerella vaginalis: G. vaginallis should be treated with ___
Metronidazole
Gardnerella vaginalis: What are the laboratory characteristics of G. vaginalis?
Pleiomorphic, gram-variable rod; clue cells - vaginal epithelial cells covered
with bacteria are visible under a microscope
Identify as associated with Meningococci, Gonococci, or both::
Gram-negative cocci
both
Identify as associated with Meningococci, Gonococci, or both:: Polysacharide
capsule
Meningococci
Identify as associated with Meningococci, Gonococci, or both:: Neonatal
conjunctivitis
Gonococci
Identify as associated with Meningococci, Gonococci, or both:: Vaccine
available
Meningococci
Identify as associated with Meningococci, Gonococci, or both:: Gonorrhea
Gonococci
Identify as associated with Meningococci, Gonococci, or both:: Meningitis w/
septicemia
Meningococci
Identify as associated with Meningococci, Gonococci, or both:: Waterhouse Friederichsen syndrome
Meningococci
Identify as associated with Meningococci, Gonococci, or both:: Septic
arthritis
Gonococci
Identify as associated with Meningococci, Gonococci, or both:: PID
Gonococci
Identify as associated with Meningococci, Gonococci, or both:: Maltose
fermentation
Meningococci
Primary and Secondary TB (figure): What is primary TB?
Primary and Secondary TB (figure): What are possible outcomes of primary
TB?
Primary and Secondary TB (figure): What is secondary TB?
Reponse to TB infection by a non-immune host, consists of hilar node
involvement and Ghon focus
Healing by fibrosis (characterized by hypersensitivity w/ pD+), progressive
lung disease (ass. W/ HIV, malnutrition), severe bacteremia (leading to
miliary TB and death), preallergic lymphatic or hematogenous dissemination
(leads to dormant tubercle bacilli in several organs and reactivation in adult
life)
Response to reinfection by a partially immune hypersensitized host (usu
adult) OR reactivation of dormant tubercle bacilli from primary infection -consists of fibrocaseous cavitary lesion
Primary and Secondary TB (figure): What organs are commonly effected by
extrapulmonary TB?
CNS (parenchymal tuberculoma or meningitis), vertebral body (Pott's
disease), lymphadenitis, renal, GI
Mycobacteria: What are common symptoms of TB?
Fever, night sweats, weight loss, hemoptysis
Mycobacteria: T/F: All mycobacteria are acid-fast
TRUE
Mycobacteria: T/F: M. Tuberculosis and M. avium-intracellulare can be
resistant to multiple drugs
TRUE
Mycobacteria: T/F: M. kansasii is asymptomatic
False: causes pulmonary TB-like symptoms
Mycobacteria: T/F: M. scrofulaceum commonly causes cervical
lymphadenitis in the elderly
False: usually causes cervical lymphadenitis in kids
Leprosy (Hansen's disease): What organism causes leprosy?
Mycobacterium leprae
Leprosy (Hansen's disease): T/F: M. leprae is an acid-fast bacterium that
grows well in vitro
False - M. leprae does not grow in vitro
Leprosy (Hansen's disease): M. leprae likes ___ temperatures and infects ___
and ___ (tissues)
cool, skin, superficial nerves
Leprosy (Hansen's disease): What are the two forms of Hansen's disease?
Which form is worse?
Lepromatous and tuberculoid, tuberculoid is self-limited, lepromatous is
worse (failed cell-mediated immunity) "LEpromatous = LEthal"
Leprosy (Hansen's disease): What is wrong with armadillos?
Resevoir of leprosy in U.S.
Leprosy (Hansen's disease): What is treatmet for leprosy and associated
toxicities?
Long-term oral dapsone, toxicity = hemolysis and methemoglobinemia.
Alternate treatments include rifampin and combination of clofazimine and
dapsone.
Leprosy (Hansen's disease): AUTHOR
Adam Weitzman, et al.
Ricketsia: What is the classic triad of Rickettsial infection?
headache, fever, rash
Ricketsia: True/False: Ricketsia are facultative intracellular parasites
False, they are obligate parasites and need CoA and NAD
Ricketsia: Most Ricketsia are transmitted by what?
arthropod vector
Ricketsia: Why is Coxiella an atypical ricketsia?
It is transmitted by aerosol and causes pneumonia and no rash. Has negative
Weil-Felix test.
Ricketsia: What is the treatment of choice for rickettsial infection?
Tetracycline
Rickettsial diseases and vectors: What bug causes Rocky Mountain spotted
fever? What is the vector?
Rickettsia rickettsii, tick vector
Rickettsial diseases and vectors: What bug causes Endemic typhus? What is
the vector?
Rickettsia typhi, flea vector
Rickettsial diseases and vectors: What bug causes Epidemic typhus? What is
the vector?
Rickettsia prowazeckii, human body louse
Rickettsial diseases and vectors: What bug causes Q fever? What is the
vector?
Coxiella burnetii, only rickettsial disease without a vector
Rocky Mountain spotted fever: What three diseases have characteristic palm
and sole rash?
Rocky Mountain spotted fever, syphilis, and coxsackievirus A16 (hand, foot,
and mouth disease)
Rocky Mountain spotted fever: How does the rash of Rocky Mountain
spotted fever progress?
centripetally, starting on palms and soles, migrating to wrists/ankles, then
trunk
Rocky Mountain spotted fever: What are the symptoms of Rocky Mountain
spotted fever? What is the causative agent?
Classic triad of rickettsial disease-headache, fever, rash. Rickettsia rickettsii
Rocky Mountain spotted fever: Where is Rocky Mountain spotted fever
common?
Endemic to EAST coast
Weil-Felix reaction: What does the Weil-Felix reaction assay for?
antirickettsial antibodies using cross reactivity with Proteus antigen.
Weil-Felix reaction: Which rickettsia test positive with Weil-Felix? Which
test negative?
typhus (R. typhi and R. prowazekii) and Rockey Mountain spotted fever (R.
rickettsii) are usually positive. Q fever (C. burnetii, the weird one) is usually
negative.
Mycoplasma pneumonia: Mycoplasma pneumonia causes what type of
infection? Describe the symptoms. Which age group is it most common in?
Classic cause of atypical "walking" pneumonia. Insidious onset, headache,
nonproductive cough, diffuse interstitial infiltrate. More common in patients
under 30.
Mycoplasma pneumonia: How does an X-ray appear in a Mycoplasma
infection?
Streaky, much worse than the patient apears.
Mycoplasma pneumonia: What is special about the mycoplasma cell wall?
Only bacterial membrane containing cholesteral
Mycoplasma pneumonia: What can you test for in the blood of patient with
Mycoplasma?
They have high titers of cold agglutinins (IgM)
Mycoplasma pneumonia: Why can't you treat Mycoplasma infection with
penecillin? What can you use?
Mycoplasma has no cell wall. Use tetracycline or erythromycin
Mycoplasma pneumonia: What agar is Mycoplasma grown on?
Eaton's
Chlamydiae: True/False: Chlamydia is an obligate intracellular parasite.
TRUE
Chlamydiae: Chlamydiae infects which type of surface?
Mucosal
Chlamydiae: How many forms does Chlamydia have? Describe them.
Two: Elementary body, small/dense (Enters cell) and Initial/Reticulate body
(Replicates by fusion)
Chlamydiae: What is unusual about Chlamydia's cell wall?
The peptidoglycan wall lacks muramic acid.
Chlamydiae: What 4 things does Chlamydia cause?
arthritis, conjunctivitis, pneumonia, and nongonococcal urethritis
Chlamydiae: How do you diagnose a chlamydial infection? How do you treat
it?
cytoplasmic inclusions seen on Giemsa or fluorescent antibody-stained
smear. Use erythromycin or tetracyclin
Chlamydiae: Why is Chlamydia psittaci notable?
Has an avian reservoir
Chlamydiae: What species of animals do Chlamydia trachomatis and
Chlamydia pneumonia infect? What do they cause?
They only infect humans. C. trachomatis causes arthritis. C. pneumonia
causes atypical pneumonia; transmitted by aerosol.
Chlamydia trachomatis serotypes: What are the serotypes of chlamydia?
A - K, L1 - 3
Chlamydia trachomatis serotypes: What do types A, B, C cause?
chronic infection; blindness in Africa (Africa/Blindness/Chronic infection
Chlamydia trachomatis serotypes: What do L1 - L3 cause?
L = Lymphogranuloma venereum (acute lymphadenitis - positive Frei test)
Chlamydia trachomatis serotypes: What do type D - K cause?
everything else!! --> urethritis/PID, ectopic pregnancy, neonatal pneumonia,
or neonatal conjunctivitis
Chlamydia trachomatis serotypes: How is neonatal chlamydia aquired?
passage through infected birth canal
Chlamydia trachomatis serotypes: How is neonatal chlamydia treated?
erythromycin eye drops
Spirochetes: Describe the shape of a spirochete.
Spiral shaped bacteria with axial filaments
Spirochetes: Name the three major spirochetes.
Borrelia (big size), Leptospira, Treponema (BLT. B is Big)
Spirochetes: Which can be identified by light microscopy using aniline dyes
(Wright or Giemsa)?
Borrelia (big size)
Spirochetes: How is Treponema visualized?
dark-field microscopy
Lyme disease: What is the classic symptom of Lyme dz and how is it
characterized?
erythema chronicum migricans (an expanding "bull's eye" red rash with
central clearing.
Lyme disease: What else does Lyme dz affect?
joints, CNS, heart
Lyme disease: What are the Sx of Stage 1 Lyme dz?
erythema chronicum migricans, flu-like sx
Lyme disease: What are the Sx of Stage 2 Lyme dz?
neurologic and cardiac manifestations
Lyme disease: What are the Sx of Stage 3 Lyme dz?
autoimmune migratory polyarthritis
Lyme disease: What causes Lyme disease and how is it transmitted?
Borrelia burgdorferi, by the Ixodes tick.
Lyme disease: What are important reservoirs?
Mice
Lyme disease: What animal is required for the life cycle?
Deer
Lyme disease: How do you treat Lyme disease?
Tetracycline
Lyme disease: Where in the US is Lyme disease common?
northeast (named after Lyme, Connecticut)
Lyme disease: During what time of year is transmission most common?
summer months
Treponemal disease: Treponemes are what type of organism?
spirochetes
Treponemal disease: What causes syphillis?
Treponema pallidum
Treponemal disease: What causes yaws?
Treponema pertenue
Treponemal disease: What is yaws?
a tropical infection that is not an STD (although, VDRL test is positive)
Syphilis: What causes syphilis?
Treponema pallidum, a spirochete
Syphilis: What is characteristic of primary syphilis?
A painless chancre (localized disease)
Syphilis: What is characteristic of secondary syphilis?
Constitutional symptoms, maculopapular rash, and condylomata lata.
Syphilis: What is characteristic of end state syphilis?
Gummas, aortitis, neurosyphilis (tabes dorsalis), Argyll Robertson pupil.
Syphilis: What do you treat syphilis with?
Penicillin G
VDRL vs. FTA-ABS: What do VDRL and FTA-ABS test for? Which is
better and why?
treponemes (syphilis), FTA-ABS is more specific, turns positive earlier and
stays positive longer.
VDRL false posititves: What does VDRL detect? What disease is it used for?
Nonspecific antibody that reacts with beef cardiolipin. Used for diagnosis of
syphilis.
VDRL false posititves: What false positives are detected with VDRL?
viral infection (mononucleosis, hepatitis), some drugs, rheumatic fever,
rheumatoid arthritis, SLE, and leprosy.
Spores: fungal: Most fungal spores are sexual or asexual?
asexual
Spores: fungal: How are coccidioidomycosis and histoplasmosis transmitted?
inhalation of asexual spores
Spores: fungal: What are asexual spores called?
conidia (e.g. blastoconidia, arthroconidia)
Candida albicans: Is c. albicans infection local, systemic, or both?
both
Candida albicans: What is the morphology of c. albicans in culture at 20 deg
C?
budding yeast with pseudohyphae
Candida albicans: What is the morphology of c. albicans in culture at 37 deg
C?
germ tubes
Candida albicans: What does "alba" mean?
White
Candida albicans: What disease does c. albicans cause in
immunocompromised patients?
thrush in throat (neonates, steroids, diabetes, AIDS)
Candida albicans: What disease does c. albicans cause in IV drug users?
endocarditis
Candida albicans: What disease does c. albicans cause s/p antibiotic tx?
vaginitis
Candida albicans: What disease does c. albicans cause in people who wear
diapers (i.e. babies)?
diaper rash
Candida albicans: What is the treatment for superficial c. albicans infection?
nystatin
Candida albicans: What is the treatment for serious systemic c. albicans
infection?
amphotericin B
Systemic Mycoses: Name 4 types of systemic mycoses.
Coccidioidomycosis, Histoplasmosis, Paracoccidioidomycosis,
Blastomycosis
Systemic Mycoses: Name the Endemic location of Coccidioidomycosis.
Southwestern United States, California.
Systemic Mycoses: Why is the disease caused by Coccidioidomycosis called
“valley fever?”
Common in the San Joaquin Valley or desert (desert bumps) "valley fever"
Systemic Mycoses: Name the Endemic location of Histoplasmosis.
Mississipi and Ohio river valleys.
Systemic Mycoses: What is a common form of transmission of
Histoplasmosis.?
Bird or bat dropings
Systemic Mycoses: Is Histoplasmosis found intracellularly or extracellularly?
Intracellular (frequently seen inside macrophages)
Systemic Mycoses: Name the Endemic location of Paracoccidioidomycosis.
Rural Latin America.
Systemic Mycoses: What is special about Paracoccidioidomycosis’
appearance?
Captain's wheel apearance.
Systemic Mycoses: Name the Endemic location of Blastomycosis.
States east of Mississipi River and Central America.
Systemic Mycoses: How does Blastomycosis reproduce?
Big, Broad-Based Budding.
Systemic Mycoses: What is a dimorphic fungus?
Mold in soil (at lower temperature) and yeast in tissue (at higher/body
temperature: 37°C) Cold=Mold; Heat=Yeast
Systemic Mycoses: Which of the following are dimorphic:
Coccidioidomycosis, Histoplasmosis, Paracoccidioidomycosis,
Blastomycosis ?
All except coccidioidomycosis, which is a spherule in tissue.
Systemic Mycoses: What is the appropriate treatment for local infection with
the systemic mycoses?
Treat with fluconazole or ketoconazole for local infection
Systemic Mycoses: What is the appropriate treatment for systemic infection
with the systemic mycoses?
Treat with amphotericin B for systemic infection.
Systemic Mycoses: What acid fast bacterial disease can the systemic mycoses
mimic?
TB (granuloma formation)
Systemic Mycoses: What is the appropriate agar to use for culturing of
systemic mycoses?
Culture on Sabouraud's agar.
Cutaneous Mycoses: What organism causes Tinea versicolor?
Malassezia furfur. Causes hypopigmented skin lesions.
Cutaneous Mycoses: What organism causes Tinea nigra?
Cladosporium werneckii
Cutaneous Mycoses: How do you treat Tinea versicolor?
miconazole, selenium sulfide
Cutaneous Mycoses: What part of the skin is infected by tinea nigra and how
does it present?
Infection of keratinized layers of skin. Apears as brownish spots
Cutaneous Mycoses: How do you treat tinea nigra?
sialicylic acid
Cutaneous Mycoses: Concerning Tinea pedis, cruris, corporis, capitis, what
does the lesion look like?
Pruritic lesion wit central clearing resembling a ring.
Cutaneous Mycoses: What organisms cause Tinea pedis, cruris, corporis, &
capitis?
Dermatophytes: Microsporum, Trichophyton, Epidermophyton
Cutaneous Mycoses: Concerning Tinea pedis, cruris, corporis, capitis, what
do you see in a KOH prep?
Mold hyphae, not dimorphic
Cutaneous Mycoses: Concerning Microsporium, what is the reservoir for this
organism
Pets
Cutaneous Mycoses: How is Microsporum infetction treated?
topical azoles
Opportunistic fungal infections: What organism is the cause of thrush in
immunocomprornised?
Candida albicans
Opportunistic fungal infections: Other than thrush and vulvovaginitis, what
other diseases can Candida albicans cause?
Disseminated candidiasis (to any organ) & chronic mucocutaneous
candidiasis
Opportunistic fungal infections: What is the morphology of Candida
albicans?
Pseudohyphae + budding yeasts or Germ tubes at 37 degrees C
Opportunistic fungal infections: What pulmonary disease is caused by
Aspergillus fumigatus?
lung cavity aspergilloina ("fungus ball"), invasive aspergillosis.
Opportunistic fungal infections: What is the morphology of Aspergillus
fumigatus?
Mold with septate hyphae that branch at a V-shaped (45°) angle.
Opportunistic fungal infections: Is Aspergillus fumigatus dimorphic?
NO
Opportunistic fungal infections: What diseases does the yeast Cryptocuccus
neoformans cause?
Cryptococcal meningitis, cryptococcosis.
Opportunistic fungal infections: What is the morphology of Cryptocuccus
neoformans?
Heavily encapsulated yeast.
Opportunistic fungal infections: Is Cryptocuccus neoformans dimorphic?
No
Opportunistic fungal infections: What type of budding pattern is seen in
Cryptocuccus neoformans?
Narrow-based unequal budding
Opportunistic fungal infections: What natural environment is Cryptocuccus
neoformans usually found?
Found in soil, pigeon dropings.
Opportunistic fungal infections: What do you culture Cryptocuccus
neoformans on?
Culture on Sabouraud's agar.
Opportunistic fungal infections: What special stain is used for Cryptocuccus
neoformans ?
Stains with India ink.
Opportunistic fungal infections: What special test does the capsule of
Cryptocuccus neoformans allow you to do?
Latex agglutination test detects polysaccharide capsular antigen
Opportunistic fungal infections: What is the morphology of Mucor?
Mold with irregular nonseptate hyphae branching at wide angles (> 90°).
Opportunistic fungal infections: What immune modifying diseases (2) state is
commonly associated with infection with Mucor?
Disease mostly in ketoacidotic diabetic and leukemic patients.
Opportunistic fungal infections: How does infection with Mucor lead to
sympotms (pathogensis)?
Fungi proliferate in the walls of blood vessels and cause infarction of distal
tissue.
Pneumocystis carinii: What disease does Pneumocystis carinii cause?
Causes pneumonia (PCP).
Pneumocystis carinii: What class of organism is Pneumocystis carinii?
Yeast (originally classified as protozoan)
Pneumocystis carinii: How is Pneumocystis carinii transmitted to caused
disease?
Inhaled
Pneumocystis carinii: What predisposes to disease with Pneumocystis carinii?
Most infections asymptomatic. Immunosupression (e.g., AIDS) predisposes
to disease.
Pneumocystis carinii: How do you stain for Pneumocystis carinii?
Silver stain of lung tissue.
Pneumocystis carinii: How do you treat infection with Pneumocystis carinii?
Treat with TMP-SMX, pentamidine.
Pneumocystis carinii: With regards to P. carinii, what should you do for an
AIDS patient with CD4 below 200 cells/mL to prevent PCP?
Start prophylaxis when CD4 drops below 200 cells/mL in HIV patients.
Sporothrix schenckii: Where is Sporothrix schenckii normally found and how
is it transmitted?
Found on vegetation and transmitted by trauma to the skin, typically by a
thorn ("rose gardener's" disease)
Sporothrix schenckii: What are the symptoms of Sporcitrichosis?
Local pustule or ulcer with nodules along draining lymphatics. Little systemic
illness.
Sporothrix schenckii: How do you treat Sporcitrichosis?
Treat with itraconazole or potassium iodide.
Entamoeba histolytica: What disease(s) does it cause?
Amebiasis: bloody diarrhea, (dysentery), liver abscess, RUQ pain
Entamoeba histolytica: How is it transmitted?
Cysts in water
Entamoeba histolytica: How is it diagnosed?
Serology and/or trophozoites or cysts in stool
Entamoeba histolytica: How it is treated?
Metronidazole and iodoquinol
Giardia lamblia: What disease(s) does it cause?
Giardiasis: bloating, flatulence, foul-smelling diarrhea
Giardia lamblia: How is it transmitted?
Cysts in water
Giardia lamblia: How is it diagnosed?
Trophozoites or cysts in stool
Giardia lamblia: How it is treated?
Metronidazole
Cryptosporidium: What disease(s) does it cause?
Severe diarrhea in AIDS. Mild disease (watery diarrhea) in non-HIV
Cryptosporidium: How is it transmitted?
Cysts in water
Cryptosporidium: How is it diagnosed?
Cysts in water
Cryptosporidium: How it is treated?
None
Toxoplasma: What disease(s) does it cause?
Brain abscess in HIV, birth defects
Toxoplasma: How is it transmitted?
Cysts in meat or cat feces
Toxoplasma: How is it diagnosed?
Serology, biopsy
Toxoplasma: How it is treated?
Sulfadiazine + pyrimethamine
What are the different species?: What disease(s) does it cause?
Malaria: cyclic fever, headache, anemia, splenomegaly; Malaria - severe
(cerebral)
What are the different species?: How is it transmitted?
Mosquito (Anopheles)
What are the different species?: How is it diagnosed?
Blood smear
What are the different species?: How it is treated?
Chloroquine (primaquine for P. vivax, P. ovale), sulfadoxine +
pyrimethamine, mefloquine, quinine
Trichomonas vaginalis: What disease(s) does it cause?
Vaginitis: foul-smelling, greenish discharge; itching and burning
Trichomonas vaginalis: How is it transmitted?
Sexual
Trichomonas vaginalis: How is it diagnosed?
Trophozoites on wet mount
Trichomonas vaginalis: How it is treated?
Metronidazole
Trypanosoma cruzi: What disease(s) does it cause?
Chagas' disease (heart disease)
Trypanosoma cruzi: How is it transmitted?
Reduviid bug
Trypanosoma cruzi: How is it diagnosed?
Blood smear
Trypanosoma cruzi: How it is treated?
Nifurtimox
Trypanosoma gambiense & rhodesiense: What disease(s) does it cause?
African sleeping sickness
Trypanosoma gambiense & rhodesiense: How is it transmitted?
Tsetse fly
Trypanosoma gambiense & rhodesiense: How is it diagnosed?
Blood smear
Trypanosoma gambiense & rhodesiense: How it is treated?
Suramin for blood-borne disease or melarsoprol for CNS penetration
Leishmania donovani: What disease(s) does it cause?
Visceral leishmaniasis (kala-azar)
Leishmania donovani: How is it transmitted?
Sandfly
Leishmania donovani: How is it diagnosed?
Macrophages containing amastigotes
Leishmania donovani: How it is treated?
Sodium stibogluconate
Babesia: What disease(s) does it cause?
Babesiosis
Babesia: How is it transmitted?
Ixodes tick
Babesia: How is it diagnosed?
Blood smear, no RBC pigment, apears as "maltese cross"
Babesia: How it is treated?
Quinine, clindamycin
Naegleria: What disease(s) does it cause?
Rapidly fatal meningoencephalitis
Naegleria: How is it transmitted?
Swimming in fresh water lakes
Naegleria: How is it diagnosed?
Amebas in spinal fluid
Naegleria: How it is treated?
None
Naegleria: AUTHOR
Nomi Levy
Medically important helminths: Which Cestode (tapeworm) can cause brain
cysts and seizures?
Taenia solium
Medically important helminths: Echinococcus granulosus (a cestode) can
cause cysts in the ____when ingested in dog feces; and _____ if antigens are
released from cysts
liver, anaphylaxis
Medically important helminths: What is the standard treatment for trematodes
(flukes)?
Praziquantel
Medically important helminths: Which fluke penetrates human skin, forming
granulomas, fibrosis, and inflammation of the spleen & liver?
Schistosoma
Medically important helminths: Larvae of the nematode (roundworm) ___ are
known to penetrate skin of feet & cause anemia if infect intestine.
Ancylostoma duodenale (hookworm)
Medically important helminths: Echinococcus granulosus (a cestode) can
cause cysts in the ____when ingested in dog feces; and _____ if antigens are
released from cysts.
liver, anaphylaxis
Medically important helminths: Which nematode causes anal pruritis?
Enterobius vermicularis (pinworm)
Medically important helminths: Lavae of the nematode ___ are found in the
soil, penetrate the skin, and cause intestinal infection.
Strongyloides stercoralis
Medically important helminths: Trichinella spiralis (a nematode) is usually
found in what food?
undercooked meat, usually pork
Medically important helminths: Which nematode can be seen crawling in the
conjunctiva?
Loa loa
Medically important helminths: Treatment for river blindness, caused by
onchocerca volvulus, is ___
Ivermectin
Medically important helminths: Wuchereria bancrofti cause blockage of
lymphatic vessels in a condition known as:
elephantiasis
Medically important helminths: Three nematodes treated with
Diethylcarbamazine:
Loa loa, Toxocara canis, and Wucheria bancrofti
Parasite hints: Perianal pruritis caused by:
Enterobius
Parasite hints: Microcytic anemia a result of infection with
Ancylostoma, Necator
Parasite hints: Schistosoma mansoni is known to result in
portal hypertension
Parasite hints: Schistosoma haematobium can cause ___ cancer and
hematuria
bladder
Parasite hints: A trematode that causes hemoptysis is:
Paragonimus westernani
Parasite hints: Clonorchis sinensis causes disease in the:
biliary tract
Virology: All DNA viruses are dsDNA except:
parvoviridae
Virology: All DNA viruses are linear except these two:
papoviruses, hepadnavirus (circular)
Virology: All RNA viruses are ssRNA except
Reoviridae ("repeato-virus" (reovirus) is dsRNA)
Virology: Do hepadnavirus, herpesviruses, and poxvirus have an envelope?
Yes
Virology: Which virus is often responsible for "pink eye" (conjunctivitis)?
adenovirus
Virology: Which SS-linear(-) DNA virus is responsible for "slapped cheeks"
rash?
Parvovirus
Virology: Which is the smallest DNA virus?
Parvovirus
Virology: Which DNA virus can cause aplastic crises in sickle cell disease?
Parvovirus (B19 virus)
Virology: Name 3 "naked" DNA virsuses (no envelope)
Parvo, Adeno, and Papovirus (you have to be naked for a PAP smear…)
Virology: The largest DNA virus, one which can cause "milkmaid's blisters"
or molluscum contagiosum (and could be used in germ warfare), is:
poxvirus
DNA virus characteristics: Papovirus is not linear, but rather ____
circular, supercoiled
DNA virus characteristics: The only DNA virus that is not icosahedral is
Pox (complex)
DNA virus characteristics: All DNA viruses replicate in the nuclear except
Pox (carries own DNA-dependent RNA polymerase)
RNA viruses: Poliovirus, Echovirus,Rhinovirus, Coxsackievirus, and HAV
are all members of which viral family?
Picornaviruses ("PERCH")
RNA viruses: Picorna-, Calci-, Flavi-, Toga-, Retro-, and Coronaviruses all
share which RNA structure?
SS + linear
RNA viruses: Which SS-linear, nonsegmented RNA virus family is
responsible for measles, mumps, and croup?
PaRaMyxovirus (Parainfluenza-croups; RSV-bronchiolitis in babies;
Measles, Mumps)
RNA viruses: Hantavirus, Sanfly/Rift Valley fevers, and California
encephalitis are all part of this SS-circular RNA viral family.
Bunyaviruses
RNA viruses: Orthomyxoviruses include which ubiquitous virus?
Influenza virus
RNA viruses: HIV and HTLV are both ____ with ____capsid symmetry.
retroviruses; icosahedral
RNA viruses: What is the #1 cause of fatal diarrhea in children?
Rotavirus (a reovirus)
RNA viruses: Rabies is caused by this viral family.
Rhabdoviruses
RNA viruses: Virus family credited with the "common cold"
Coronaviruses
RNA viruses: Ebola/Marburg hemorrhagic fever are caused by which viral
family?
Filoviruses
More virology: Three naked (nonenveloped) RNA viruses are:
Calcivirus, Picornavirus, Reovirus (Naked CPR)
More virology: From where to herpesviruses aquire their envelopes?
nuclear membrane
More virology: From where do enveloped viruses usually acquire their
envelopes?
plasma membranes
More virology: This is the only virus that is not haploid:
retrovirus (which has 2 identical ssRNA molecules, so considered diploid)
More virology: The only DNA viruses that does not replicate in the nucleus
is:
poxvirus
More virology: The two RNA viruses which do not replicate in the cytoplasm
are:
Influenza virus and retroviruses
Viral Vaccines: Live attenuated vaccines induce humoral and cell-mediated
immunity, while killed viruses induce only ____ immunity.
humoral
Viral Vaccines: Are MMR (measles, mumps, rubella) vaccines live or killed?
Live attenuated
Viral Vaccines: Rabies, influenza, HAV, and Salk polio vaccines are of
which type (live or killed)?
Killed (SalK=killed)
Viral Vaccines: A recombinant viral vaccine exists for which virus?
HBV (antigen=HBsAg)
Viral Vaccines: Worldwide pandemics of influenza virus are in part
attributable to which type of viral genetics?
Reassortment (viruses with segmented genomes exchange segments)
Viral Pathogens: What structural similarity is shared by herpesviruses, HBV,
and smallpox virus?
They are DNA enveloped viruses.
Viral Pathogens: RNA nucleocapsid enteroviruses include which pathogens?
poliovirus, coxsackievirus, echovirus, HAV
Viral Pathogens: The viral pathogens adenovirus, papillomaviruses, and
parvoviruses are all what type of viral pathogens?
DNA nucleocapsid viruses
Viral Pathogens: Bunyaviruses, Orthomyxoviruses (influenza viruses),
Arenaviruses, and Reoviruses are all what type of RNA virus?
segmented (BOAR)
Viral Pathogens: Aseptic (viral) meningitis can be caused by which small
RNA viruses?
poliovirus, coxsackievirus, echovirus (and not by two other picoRNAviruses,
rhinovirus and HIV)
Viral Pathogens: Reovirus considered the most important global cause of
infantile gastroenteritis
Rotavirus (ROTA=Right Out The Anus)
Viral Pathogens: All paramyxoviruses have 1 serotype with this exception:
parainfluenza virus (4 serotypes)
Viral Pathogens: Parotitis can be caused by this paramyxovirus:
mumps virus ("mumps gives you bumps")
Viral Pathogens: Triad of mumps symptoms are:
asceptic Meningitis, Orchitis, and Parotitis (MOP)
Viral Pathogens: AUTHOR
Connie Chang
Measles virus: What virus type causes measles?
paramyxovirus
Measles virus: What bluish-gray spots on the buccal mucosa are diagnostic of
measles
Koplik spots
Measles virus: 3 Cs of measles
Cough, Coryza, Conjunctivitis
Measles virus: 3 possible sequellae
SSPE, encephalitis, giant cell pneumonia. SSPE = subacute sclerosing
panencephalitis
Influenza viruses: Five facts about Influenza: enveloped/nonenveloped,
nuclear material, antigens, infection --> what risk?, protection.
1. Enveloped 2. ssRNA with segmented genome 3. Hemagglutinin and
neuraminidase antigens 4. Risk of fatal bacterial superinfection 5. Protection
= killed viral vaccine
Influenza viruses: Treatment for influenza A?
Amantadine, rimantadine, zanamivir, and oseltamivir
Influenza viruses: Treatment for influenza B?
Zanavir and oseltamivir (neuraminidase inhibitors)
Rabies virus: Rabies -- _______ (cytoplasmic inclusion) in _______(cell
type)
Negri bodies in neurons
Rabies virus: Rabies -- incubation period
weeks to 3 months
Rabies virus: Rabies -- most common sources in US
bat, raccoon, skunk (>dog)
Rabies virus: Rabies travels to the CNS by…
retrograde migration up nerve axons
Rabies virus: Rabies - Si/Sx
hydrophobia and fatal encephalitis with seizures
Arboviruses: Arbovirus -- mode of transmission
Transmitted by arthropods (mosquitoes, ticks)
Arboviruses: Arbovirus -- classic illnesses
Dengue fever (in SE Asia = hemorrhagic shock syndrome) and yellow fever
Arboviruses: Arbovirus -- members of the family
flavivirus, togavirus, bunyavirus
Yellow fever: Yellow fever is transmitted by ____________
the Aedes mosquito (flavivirus)
Yellow fever: Symptoms of yellow fever
high fever, black vomitus, and jaundice.
Yellow fever: Yellow fever -- histology
Liver: councilman bodies (acidophilic inclusions)
Name the diseases caused by the following Herpesviridae:: HSV-1
Gingivostomatitis, keratoconjunctivitis, temporal lobe encephalitis, herpes
labialitis
Name the diseases caused by the following Herpesviridae:: HSV-2
Herpes genitalis, neonatal herpes
Name the diseases caused by the following Herpesviridae:: VSV
Varicella-zoster (shingles), encephalitis, pneumonia
Name the diseases caused by the following Herpesviridae:: EBV
Infecious mononuelosis, Burkitt's lymphoma
Name the diseases caused by the following Herpesviridae:: CMV
Cogenital infection, mononucleosis, pneumonia
Name the diseases caused by the following Herpesviridae:: HHV-8
Karposi's sarcoma
Name the routes of transmission for the following Herpesviridae:: HSV-1
respiratory secretions and saliva
Name the routes of transmission for the following Herpesviridae:: HSV-2
sexual contact, perinatal
Name the routes of transmission for the following Herpesviridae:: VSV
respiratory secretions
Name the routes of transmission for the following Herpesviridae:: EBV
respiratory secretions, saliva
Name the routes of transmission for the following Herpesviridae:: CMV
congenital, transfusion, sexual contact, saliva, urine, transplant
Name the routes of transmission for the following Herpesviridae:: HHV-8
sexual contact
Mononucleosis: Mononucleosis is caused by _______
EBV
Mononucleosis: symptoms of mono
fever, hepatosplenomegaly, pharyngitis, and lymphadenopathy (esp posterior
auricular nodes)
Mononucleosis: how do you test for mono?
heterophil antibody test
Mononucleosis: what do you see in the peripheral blood (mono)?
atypical lymphocytes (cytotoxic T cells)
Tzank test: What's a Tzanck test?
A smear of an opened skin vesicle to detect multinucleated giant cells (seen
in HSV-1, HSV-2, VSV)
Hepatitis transmission: Name the type of nucleic acid and the virus type for
the following hepatitis viruses:
0
Hepatitis transmission: Name the type of nucleic acid and the virus type for
the following hepatitis viruses: Hepatitis A
RNA picornavirus
Hepatitis transmission: Name the type of nucleic acid and the virus type for
the following hepatitis viruses: Hepatitis B
DNA hepadnavirus
Hepatitis transmission: Name the type of nucleic acid and the virus type for
the following hepatitis viruses: Hepatitis C
RNA flavivirus
Hepatitis transmission: Name the type of nucleic acid and the virus type for
the following hepatitis viruses: Hepatitis D
deta agent -- requires HBsAG as its envelope (coinfection only)
Hepatitis transmission: Name the type of nucleic acid and the virus type for
the following hepatitis viruses: Hepatitis E
RNA calcivirus
Hepatitis transmission: Name the mode of transmission for the following
hepatitis viruses
0
Hepatitis transmission: Mode of transmission: Hepatitis A
fecal-oral
Hepatitis transmission: Mode of transmission: Hepatitis B
parenteral, sexual, maternal-fetal
Hepatitis transmission: Mode of transmission: Hepatitis C
blood (IV drug users)
Hepatitis transmission: Mode of transmission: Hepatitis D
coinfection with HBV!
Hepatitis transmission: Mode of transmission: Hepatitis E
enterically; water-borne epidemics
Hepatitis transmission: which Hepatitis virus causes a high mortality rate in
pregnant women?
E
Hepatitis transmission: which hepatitis virus has a short incubation period?
A (3 weeks)
Hepatitis transmission: which Hep virus has a long incubation period?
B (3 months)
Hepatitis transmission: which Hep virus has a DNA-dependent DNA
polymerase?
B; reverse transcription also occurs
Hepatitis transmission: which pairs of viruses are similar in course, severity,
and incubation?
HAV & HEV; HBV & HCV
Hepatitis transmission: Which virus type infection leads to
chronic-carrier-status?
B, C, and D
Hepatitis serologic markers: If I got a Hepatitis B vaccine (no infection), for
what Ab would I have a positive serology?
HBsAb
Hepatitis serologic markers: If I recently had a Hepatitis B infection, for what
Ab would I have a positive serology
HBsAb and HBcAb (positive during window period)
Hepatitis serologic markers: What test tells you either that I have a current
infection or that I am a chronic Hep B carrier?
HBsAg
Hepatitis serologic markers: What test demands that you(the doctor) to tell
me to stop having sex with my spouse lest I give them Hep B?
HBeAg
Hepatitis serologic markers: What test tells you(the doctor) that I can resume
sex with my spouse because I'm not likely to give them Hep B?
HBeAb (indicates low transmissibility)
Hepatitis serologic markers: What is the "window period"?
after the actue infection is cleared and before the humoral response produces
lots and lots of Ab (HBsAg AND anti-HBs negative; HBcAb positive)
Hepatitis serologic markers: How big is the Hep B virus
42 nm
Hepatitis serologic markers: When can I detect HBV particles by DNA
polymerase?
during the incubation period and the acute disease period
Hepatitis serologic markers: How can I distniguish between complete
recovery from Hep B infection and the chronic carrier state?
Complete recovery: HBsAg-neg, HBsAb-pos; Chronic carrier: HBsAb-neg.
HBsAb-pos; HBcAb is positive in BOTH states
HIV: HIV has a ________ genome with __<#>__ molecules of __<nucleic
acid>____
HIV has a diploid genome with 2 molecules of RNA
HIV: name the "rectangular nucleocapsid protein": HIV: name the envelope
proteins
gp41 and gp 120
HIV: name the matrix protein: HIV: what other important protein hangs out
inside the nucleocapsid?
reverse transcriptase
HIV: name the matrix protein: Does HIV integrate into the host genome?
YES. HIV syntehsizes dsDNA from RNA and integrates the dsDNA into the
host genome
HIV diagnosis: How do I make a diagnosis of HIV?
ELISA --> confirmed by Western blot
HIV diagnosis: T or F: HIV testing is always positive 1-2 weeks after
infection
FALSE. ELISA/Western blot look for viral PROTEINS and can be falsely
negative for the first 1-2 months of HIV infection
HIV diagnosis: How can I monitor the effect of HIV drug therapy?
HIV PCR/viral load
HIV immunity: Who is immune to HIV?
homozygous for CCR5 mutation
HIV immunity: What % of US caucasians have a slower course of HIV
infection because of heterozygosity for the above allele?
0.2
HIV immunity: Persons with ______________ have a rapid progression to
AIDS
CXCR1 mutation
Time course of HIV infection: HIV become symptomatic _____ after
infection
3-10 years
Time course of HIV infection: Anti-p 24 and anti-gp120 increase between
_______ after initial infection; after the onset of immunodeficiency, they
___________(increase or decrease)
1-2 months; decrease
Name the opportunistic infections seen in the following categories: (for AIDS
patients): bacterial
TB, Mycobacterium avium-intercellulare complex
Name the opportunistic infections seen in the following categories: (for AIDS
patients): viral
HSV, VAV, CMV, PML (JC virus)
Name the opportunistic infections seen in the following categories: (for AIDS
patients): fungal
Thrush (Candida albicans), cryptococcosis (cryptococcal meningitis),
histoplasmosis, Pneumocystis pneumonia
Name the opportunistic infections seen in the following categories: (for AIDS
patients): protozoan
toxoplasmosis, cryptosporidiosis
Prions: Multiple choice: Prions are -- 1) infectious proteins ONLY 2)
infectious RNA 3) infectious DNA 4) infectious proteins occasionally mixed
with nucleic acids
1) infectious proteins
Prions: Name examples of prion diseases
CJD, kuru, scrapie, "mad cow"
Prions: Jeopardy style: pathologic prions take on this conformation
What is beta-pleated sheet
Prions: Prions are associated with ___________ encephalopathy
spongiform
Name the dominant normal flora in each of these areas:: skin
Staph epidermidis
Name the dominant normal flora in each of these areas:: nose
Staph aureus
Name the dominant normal flora in each of these areas:: oropharynx
Strep viridans
Name the dominant normal flora in each of these areas:: dental plaque
Strep mutans
Name the dominant normal flora in each of these areas:: colon
Bacteroides fragilis > E. coli
Name the dominant normal flora in each of these areas:: vagina
Lactobacillus, colonized by E. coli and group B strep
Common causes of pneumonia: Name the common causes of pneumonia in
the following age groups:
0
Common causes of pneumonia: Name the common causes of pneumonia in
the following age groups: Children (6 weeks to 18 yrs)
Virus (RSV), Mycoplasma, Chlamydia pneumoniae, Strep pneumoniae
Common causes of pneumonia: Name the common causes of pneumonia in
the following age groups: Adults (18-40 yrs)
Mycoplasma, Chlamydia pneumoniae, Strep pneumoniae
Common causes of pneumonia: Name the common causes of pneumonia in
the following age groups: Adults (40-65 yrs)
Strep pneumoniae, H. influenze, Anaerobes, Viruses, Mycoplasma
Common causes of pneumonia: Name the common causes of pneumonia in
the following age groups: Elderly
Strep pneumoniae, viruses, anerobes, H. Influenzae, Gram-negative rods
Common causes of pneumonia: An AIDS patient comes into your office with
symptoms of pneumonia. What organisms are you considering?
Staphylococcus, gram-negative rods, fungi, viruses, Pneumocystis carinii
Common causes of pneumonia: A patient in the CCU gets pneumonia. What
organisms are you thinking?
Nosocomial infections are usually Staphylococcus and gram-negative rods
Common causes of pneumonia: The same patient also aspirated some peas
prior to getting sick. What organisms do you add to your list?
Anaerobes
Common causes of pneumonia: His domineering wife of this same patient is
mad because he also had a viral infection last week. What infectious agents
would you now consider?
add H. influenzae; another common postviral pneumonia bug is Staph
Common causes of pneumonia: The wife is so distressed she goes into labor
and gives birth to a 10 lb baby girl, who also gets pneumonia. Does she have
the same bug as her dad in the CCU?
Neonatal pneumonia is usually due to Group B streptococci or E. coli -- the
dad could have the latter.
Common causes of pneumonia: Of course, the wife get sick too, but her
pneumonia is classified as "atypical." What might she have?
Mycoplasma, Legionella, Chlamydia
Name the causes of meningitis in the following age groups:: Newborn (0-6
months)
Group B strep, E. coli, Listeria
Name the causes of meningitis in the following age groups:: Children (6 mo
to 6 years)
Strep pneumoniae, Neisseria meningitidis, Haemophilus influenze type B,
Enteroviruses
Name the causes of meningitis in the following age groups:: 6-60 years
N. meningitidis, Enteroviruses, S. pneumoniae, HSV
Name the causes of meningitis in the following age groups:: 60+ years
Gram-negative rods, Listeria
Name the causes of meningitis in the following age groups:: An AIDS patient
comes to you with high fevers, stiff neck, and mental status changes. What
organisms might be causing his meningitis?
Cryptococcus, CMV, toxoplasmosis (brain abscess), JC virus (PML)
CSF findings in meningitis: You do a spinal tap on your patient. The CSF
pressure appears to be increased. What type of infectious agent have you
eliminated?
none. It could be bacterial, TB, fungal, or viral (in viral, CSF pressure is
normal to increased)
CSF findings in meningitis: You do a quick smear of the spinal tap under the
microscope and see increased polys. What type of infectious agent does this
suggest?
bacterial. In fungal, TB, and viral, you see increased lymphocytes.
CSF findings in meningitis: The lab tests show an increase in protein and a
decrease in sugar in the CSF. Does that confirm your previous guess or
confuse you?
Confirms. These findings are seen in bacterial, fungal, and TB infections. In
viral infections the protein and sugar concentrations of the CSF are normal.
Osteomyelitis: What population is most likely to get osteomyelitis?
children
Osteomyelitis: What lab test is elevated in osteomyelitis?
ESR
For each of the following groups of persons, name the organism that is most
likely to cause osteomyelitis: Most people (nonspecific)
S aureus -- assume S aureus if no other information
For each of the following groups of persons, name the organism that is most
likely to cause osteomyelitis: sexually active
Neisseria gonorrhea (rare -- septic arthritis is more common)
For each of the following groups of persons, name the organism that is most
likely to cause osteomyelitis: drug addicts
Pseudomonas aeruginosa
For each of the following groups of persons, name the organism that is most
likely to cause osteomyelitis: Sickle cell Px
Salmonella
For each of the following groups of persons, name the organism that is most
likely to cause osteomyelitis: Prosthetic replacement
S. aureus and S. epidermidis
For each of the following groups of persons, name the organism that is most
likely to cause osteomyelitis: Vertebral
Mycobacterium tuberculosis
Urinary tract infections: What 2 groups of males are likely to get UTIs?
old men with enlarged prostates and baby boys with congenital defects
Urinary tract infections: What are symptoms of pyelonephritis?
fever, chills, flank pain, CVA tenderness
Urinary tract infections: What are symptoms of a UTI?
dysuria, frequency, urgency, suprapubic pain
Urinary tract infections: The 2nd most common cause of UTI in young,
ambulatory women is __________________
Staphylococcus saprophyticus
Urinary tract infections: Your patient gets a UTI while in the hospital. What
organisms do you want to make sure his antibiotics cover while his urine
culture is growing?
E. coli, Proteus, Klebsiella, Serratia, Pseudomonas
Urinary tract infections: What are predisposing factors for UTIs?
female gender (10:1; short urethra colonized by fecal flora), flow obstruction,
kidney surgery, catheterization, gynecologic abnormalities, diabetes,
pregnancy
Urinary tract infections: AUTHOR
Sharyn Miskovitz
UTI Bugs: Has a blue-green pigment and fruity odor
Pseudomonas aeruginosa
UTI Bugs: Two UTI bugs that are nosocomial and drug resistant
Pseudomonas aeruginosa and Serratia marcescens
UTI Bugs: Leading cause of UTIs
Escherichia coli
UTI Bugs: What does Proteus mirabilis produce?
Urease
UTI Bugs: Serratia marcescens produce what color pigment?
red
UTI Bugs: Large mucoid capsule and viscous colonies
Klebsiella pneumoniae
UTI Bugs: What do E. coli colonies show on EMB agar?
metallic sheen
UTI Bugs: 2nd leading cause of UTIs in sexually active women
Staphylococcus saprophyticus
UTI Bugs: Associated with struvite stones and swarming on agar
Proteus mirabilis
Sexually transmitted diseases: What are the three clinical stages of syphilis
1st degree, 2nd degree, and thrid degree
Sexually transmitted diseases: Lymphogranuloma venereum is caused by
what organism?
Chlamydia trachomatis
Sexually transmitted diseases: A painless chancre is a sign of what disease?
1st degree syphilis
Sexually transmitted diseases: What organism causes chlamydia?
Chlamydia trachomatis
Sexually transmitted diseases: What are the clinical features of Gonorrhea?
Urethritis, cervicitis, PID, prostatitis, epididymitis, arthritis
Sexually transmitted diseases: What serotypes of Chlamydia trachomatis
cause chlamydia?
D-K
Sexually transmitted diseases: What are the features of AIDS?
Oportunistic infections, Kaposi's sarcoma, lymphoma
Sexually transmitted diseases: The clinical feature of Trichomoniasis is what?
Vaginitis
Sexually transmitted diseases: Chancroid is caused by what organism?
Haemophilus ducreyi
Sexually transmitted diseases: Gummas, tables dorsalis, general paresis,
aortitis, Argyll Robertson pupil are clinical features of what STD?
3rd degree syphilis
Sexually transmitted diseases: HSV-2 causes what disease with what
features?
Genital herpes with painful penile,vulvar, or cervical ulcers
Sexually transmitted diseases: Ulcers, lymphadenopathy, and rectal strictures
are signs of what disease?
Lymphogranuloma venereum
Sexually transmitted diseases: Which organisms cause Condylomata
acuminata?
HPV 6 and 11
Sexually transmitted diseases: Hepatitis B causes what clinical feature?
Jaundice
Sexually transmitted diseases: What are the clinical features of 2nd degree
syphilis?
Fever, lymphadenopathy, skin rashes, condylomata lata
Sexually transmitted diseases: Chancroid has what clinical feature?
Painful genital ulcers
Sexually transmitted diseases: What serotypes of Chlamydia trachomatis
cause Lymphogranuloma venereum?
L1-L3
Sexually transmitted diseases: Trichomonas vaginalis causes what disease?
Trichomoniasis
Sexually transmitted diseases: Urethritis, cervicitis, conjunctivities, Reiter's
syndrome, and PID are features of what diesease?
Chlamydia
Sexually transmitted diseases: Koilocytes are characteristic of what diease?
Condylomata acuminata
Sexually transmitted diseases: What organism causes 1st, 2nd, and 3rd degree
syphilis?
Treponema pallidum
Pelvic inflammatory disease: What are the top bugs that cause PID?
Chlamydia trachomatis (subacute, often undiagnosed), Neisseria gonorrheae
(acute, high fever)
Pelvic inflammatory disease: What is a risk factor for ectopic pregnancy,
infertility, chronic pelvic pain, and adhesions?
Salpingitis
Pelvic inflammatory disease: What is the most common STD in the US?
Chlamydia trachomatis (3-4 million cases per year)
Pelvic inflammatory disease: What type of abscesses can occur in PID?
Tubo-ovarian abscesses
Pelvic inflammatory disease: What does the chandelier sign test for?
Cervical motion tenderness
Pelvic inflammatory disease: What are some of the manifestations of PID?
Purulent cervical discharge, salpingitis, endometriosis, and hydrosalpinx
Pelvic inflammatory disease: What STDs other than C. trachomatis and N,
gonorrhea cause PID?
Gardnerella (clue cells) and Trichomonas (motile on wet prep)
Nosocomial infections: What are 2 of the most common causes of nosocomial
infections?
E. Coli (UTI) and S. aureus (wound infection)
Nosocomial infections: When in a renal dialysis unit which pathogen should
you be concerned about?
HBV
Nosocomial infections: What is the most likely pathogen when a water source
(water aerosols) is involved?
Legionella
Nosocomial infections: What pathogen is often found on respiratory therapy
equiptment?
Pseudomonas aeruginosa (AIRuginosa when AIR or burns are involved?
Nosocomial infections: What are the two pathogens most commonly
associated with urinary catheterization?
E. coli and Proteus mirabilis
Nosocomial infections: Being in a newborn nursery is a risk factor for what
pathogens?
CMV and RSV
Nosocomial infections: Which pathogen would most associated with
hyperalimentation (total parenteral nutrition)
Candida albicans
Infections dangerous in pregnancy: What are the organisms that can cross the
blood-placenta barrier and be dangerous in pregnancy?
ToRCHcS=Toxoplasma, Rubella, CMV, HSV/HIV, Syphilis
Infections dangerous in pregnancy: Bug hints (if all else fails)
Name the associated bug
Infections dangerous in pregnancy: Branching rods in oral infection
Actinomyces israelii
Infections dangerous in pregnancy: Surgical wound
S. aureus
Infections dangerous in pregnancy: Pus, empyema, abscess
S. aureus
Infections dangerous in pregnancy: Pediatric Infection
Haemophilus influenzae (including epiglottis)
Infections dangerous in pregnancy: Sepsis/meningitis in newborn
Group B strep
Infections dangerous in pregnancy: Dog or cat bite
Pasteurella multocida
Infections dangerous in pregnancy: Pneumonia in cystic fibrosis, burn
infection
Pseudomonas aeruginosa
Infections dangerous in pregnancy: Currant jelly sputum
Klebsiella
Infections dangerous in pregnancy: Traumatic open wound
Clostridium perfringens
Antibody structure and function: Which part of the light and heavy chain
recognizes the antigen?
Variable part
Antibody structure and function: The interchain and intrachain bonds in the
antibody are of what type?
Disulfide bonds
Antibody structure and function: What is the term called when the antibody
prevents bacterial adherence?
Neutralization
Antibody structure and function: The amino terminal is part of which
fragment of the antibody?
Fab fragment
Antibody structure and function: The fab fragment of the antibody is
composed of which chain(s)?
Light and heavy chains
Antibody structure and function: Describe the Fc fraction of the B cell
receptor.
Constant, Carboxy terminal, Complement-binding (IgG + IgM only),
Carbohydrate side chains
Antibody structure and function: What is the purpose of opsonization?
The antibody promotes phagocytosis
Antibody structure and function: The hypervarible region is a compontent of
which fragment of the antibody?
Fab fragment
Antibody structure and function: Only the heavy chain contributes to which
fraction of the antibody?
Fc
Antibody structure and function: Why does an antibody activate
complement?
To enhance opsonization and lysis
Antibody structure and function: The constant part of the heavy chain of IgM
and IgG does what?
Fixes complement
Immunogloblulin isotypes: Which isotype has an unclear function?
IgD
Immunogloblulin isotypes: What is the main anitbody in a second response to
an antigen?
IgG
Immunogloblulin isotypes: When is IgM produced?
Primary response to an antigen
Immunogloblulin isotypes: Which isotype induces the release of mediators
from mast cells and basophils when exposed to an antigen?
IgE
Immunogloblulin isotypes: Where is IgD found?
On the surface of many B cells and in serum
Immunogloblulin isotypes: Which isotype fixes complement, crosses the
placenta, opsonizes bacteria, and neutralizes bacterial toxins and viruses ?
IgG
Immunogloblulin isotypes: Which isotype that guards the mucous membranes
from attachement of bacteria and viruses?
IgA
Immunogloblulin isotypes: IgE stimulates which type of hypersensitivity
reaction?
Type I
Immunogloblulin isotypes: IgE mediates immunity to what?
Worms
Immunogloblulin isotypes: Which isotype fixes complement but does not
cross the placenta?
IgM
Immunogloblulin isotypes: Which isotype has the lowest concentration in the
serum?
IgE
Immunogloblulin isotypes: Which isotype found in secretions?
IgA
Immunogloblulin isotypes: Which isotype crosses the placenta?
IgG
Ig epitopes: Which Ig epitope is common to a single class of Ig (5 classes,
determined by the heavy chain)?
Isotype (IgG, IgA, IgM, IgE, IgD) Isotype=iso (same). Common to same
class.
Ig epitopes: Which Ig epitope is determined by antigen-binding site?
Idiotype (specific for a given antigen) Idiotype=idio (unique). Hypervariable
region is unique.
Ig epitopes: Which Ig epitope differs among members of the same species
and can be on the light or heavy chain?
Allotype (polymorphism)
MHC I and II: Antigen presenting cells have which type(s) of MHC protein?
MHC I and MHC II
MHC I and II: Which class MHC proteins is the main determinants of organ
rejection?
MHC II
MHC I and II: How many class I genes does the MHC consist of?
3 (A, B, C)
MHC I and II: What class of MHC antigen loading occurs in acidified
endosomes?
MHC II
MHC I and II: All nucleated cells have which type of MHC protein(s)?
MHC I
MHC I and II: Which class MHC protein has 1 polypeptide with beta 2
microglobin?
MHC I
MHC I and II: Where does MHC I antigen loading occur in the cell?
RER (viral antigens)
MHC I and II: What are the 3 MHC II genes?
DP, DQ, DR
MHC I and II: Which class MHC protein has 2 polypeptides and and alpha
and beta chain?
MHC II
Differentiation of B and T cells: Which helper T cell is involved in
antibody-mediated immunity?
Th2 cell
Differentiation of B and T cells: In an environment with a lot of IL-12, naïve
helper T cells will mature to which helper T cell?
Th1 cell
Differentiation of B and T cells: Why do Th2 cells produce IL-4 and IL-5?
To help B cells make antibody (B=2nd letter of alphabet)
Differentiation of B and T cells: Gamma interferon is secreted by what cell to
activate macrophages?
Th1 cell
Differentiation of B and T cells: Which growth factor induces the maturation
from naïve helper T cell to Th2 cell?
IL-4
Differentiation of B and T cells: Th1 secretes what growth factor to activate
CD8 cells?
IL-2
Differentiation of B and T cells: IL-4 and IL-5 are released from Th2 to
activate what type of cell?
B cell
Differentiation of B and T cells: Why do Th1 cells produce IL-2 and
gamma-interferon?
To activate macrophages (increase killing efficiency of intracellular bacteria)
and CD8 cells
Differentiation of B and T cells: Which helper T cell is involved in
cell-mediated immunity?
Th1 cell
Differentiation of B and T cells: Major function of B cells and T cells
Choose either B (antibody-mediated immunity) or T cell (cell-mediated
immunity)
Differentiation of B and T cells: Allergy (hay fever)
B cell
Differentiation of B and T cells: Regulation of antibody response (help and
suppression)
T cell
Differentiation of B and T cells: Autoimmunity
B cell
Differentiation of B and T cells: Allergy (poison oak)
T cell
Differentiation of B and T cells: Host defense against infection (opsonize
bacteria, neutralize toxins and viruses)
B cell
Differentiation of B and T cells: Host defense against infection (especially
Mycobacterium uberculosis, viruses, and fungi)
T cell
Differentiation of B and T cells: Graft and tumor rejection
T cell
Adjuvant definition: What is the short definition of an adjuvant?
That which aids another
Adjuvant definition: Human vaccines contain aluminum hydroxide or what?
Lipid adjuvants
Adjuvant definition: Adjuvants are ________ stimulators of the immune
response but are not immunogenic by themselves.
Nonspecific
Adjuvant definition: What are adjuvants given with to enhance response?
Weak immunogen
T-cell glycoproteins: Cytotoxic T cells have which type of co-receptor?
CD8
T-cell glycoproteins: CD4 cell secretes which 3 cytokines to activate B cells?
IL-2, IL-4, IL-5
T-cell glycoproteins: What is the CD3 complex?
A cluster of polypeptides associated with a T-cell receptor. It is important in
signal transduction
T-cell glycoproteins: When a cell first gets infected with a virus which three
cells respond?
APC, B cell (through IgM BCR), and CD8 (through TCR and MHC I on
infected cell)
T-cell glycoproteins: Name three antigen-presenting cells.
Macrophage, dendritic cell, and B cell
T-cell glycoproteins: CD4 are on which type of T cells?
Helper T cells
T-cell glycoproteins: CD4 cell secretes which growth factor to activate the
CD8 cells?
IL-2
T-cell glycoproteins: CD4 on helper T cells bind to what?
MHC II on antigen-presenting cells. Product of CD and MHC=8
T-cell glycoproteins: CD8 on cytotoxic T cells bind to what?
MHC I on virus-infected cells. Product of CD and MHC=8
T cell activation: What recognizes the foreign antigen that is presented by
MHC II?
TCR on the Th cell
T cell activation: IL-2 from the helper T cell activates which cell to kill
virus-infected cells?
Cytotoxic T cell
T cell activation: A foreign body is phagocytosed by what type of cell?
APC
T cell activation: The helper T cell is activated to produce which two
cytokines in cell-mediated immunity?
IL-2 and gamma-interferon
T cell activation: What recognizes endogenously synthesized (viral or self)
proteins that are presented by MHC I?
TCR on cytotoxic T cell
T cell activation: What is the costimulatory signal needed for a helper T cell
to be activated by MHC II on an APC?
B7 (protein on APC) and CD28 (receptor on helper T cell)
T cell activation: AUTHOR
Flora Waples-Trefil
Anergy: The state when an immune cell matures but does not respond to
antigens, this process is called…..
Anergy
Anergy: Anergy in both T and B cells is caused by…
Their response to a self-antigen
Anergy: Where are B cells exposed to self-antigen
bone marrow
Anergy: Which type of cell is more sensitive to anergic stimulus?
T cells
Important Cytokines: What cytokine is an endogenous pyrogen?
IL-1
Important Cytokines: Which major cytokines are produced by Macrophages?
IL-1, IL-6, and TNF-alpha
Important Cytokines: What are the effects of the cytokines produced by
macrophages?
(1) causes the liver to make more complement, (2) fever, (3) mobilizes
neutrophils from bone marrow, (4)helpts T-cells migrate to lymph nodes and
mature, therefore, helps acute phase reaction
Important Cytokines: IL-1 by itself causes what effects?
Fever, stimulates the growth and differentiation of T and B cells, neutrophils,
fibroblasts and epithelial cells
Important Cytokines: What cytokine stimulates the growth of helper T and
NK cells
IL-2
Important Cytokines: What cells secrete IL-2
Helper T cells
Important Cytokines: What cytokine has the same effect as GM-CSF
IL-3
Important Cytokines: What cytokines promote the growth and differentiation
of B cells
IL-4, IL-5, TNF-alpha
Important Cytokines: What cytokine stimulates the synthesis of IgE and IgG?
IL-4
Important Cytokines: What cytokine stimulates eosinophil production?
IL-5
Important Cytokines: T-helper cells secrete which cytokines?
IL-2, IL-4, IL-5, gamma interferon
Important Cytokines: What cytokine stimulates the synthesis of IgA?
IL-5
Important Cytokines: What cytokine acts to attract neutrophils?
IL-8 (major) and TNF-alpha (minor)
Important Cytokines: What cytokine stimulates macrophages?
gamma-interferon
Important Cytokines: What is the difference between TNF-alpha and
TNF-beta?
TNF-alpha is secreted by macrophages, and TNF-beta is secreted by T
lymphocytes. Their functions are similar.
Important Cytokines: What do TNF-alpha and TNF-beta do?
increase IL-2 output and B-cell proliferation, attracts neutrophils
Cell Surface Proteins: What markers identify T cells
TCR and CD3
Cell Surface Proteins: what cells have receptors for MHC I
NK cells
Cell Surface Proteins: What does MHC I do?
presents self-antigens, in viral infections the molecules presented by MHC I
will change, which is why NK cells respond to viral infections best.
Cell Surface Proteins: What cells have MHC I on their surface?
all cells except RBCs
Cell Surface Proteins: what does MHC II do?
Presents non-self antigens
Cell Surface Proteins: What cells have MHC II?
macrophages, monocytes, dendritic cells (called professional antigen
presenting cells)
Cell Surface Proteins: What markers are specific for B cells?
CD20, CD19, IgM
Cell Surface Proteins: What marker disappears when B cells become anergic?
IgM is internalized in anergic cells
Cell Surface Proteins: What is a marker for Macrophages?
CD14
Cell Surface Proteins: What is a marker for NK cells?
receptors for MHC I, CD 16
Acute Phase Response: What cytokines are responsible for the Acute Phase
Response?
IL-1, IL-6, TNF-alpha
Acute Phase Response: How does the acute Phase Reaction cause a fever?
IL-1 acts on the hypothalamus to increase body temp, fat is mobilized to
increase energy, and muscle mass is used to create heat
Acute Phase Response: The Acute Phase Reaction involves the mobilization
of which cells?
B cells, T cells, Neutrophils
Acute Phase Response: Why is fever useful in an infection?
Viruses and bacteria divide less in higher temperatures, it increases antigen
production, and increases parts of the immunes response
Acute Phase Response: What does the liver do in the Acute Phase Reaction?
Creates acute phase proteins (ex: C-reactive) which then activate complement
and help in opsinization
Acute Phase Response: What does bone marrow do in the Acute Phase
Reaction?
Releases CSF which causes leukocytosis
Acute Phase Response: What do Dendritic cells do in the Acute Phase
Reaction?
the Professional antibody presenting cells migrate to the lymph nodes to
initiate the adaptive response.
Complement: What kind of bacteria does complement act against?
Gram negative
Complement: Why does complement act preferentially against gram bacteria?
Complement initiators like to behind to carbohydrates, so gram- bacteria or
noticed more than others.
Complement: The classic pathway is initiated by….?
IgM or IgG (remember, GM makes Classic cars) antibody-antigen complexes
Complement: The alternate pathway is initiated by….?
basically, everything else - endotoxins, microbial surfaces, IgA, etc.
Complement: C1, C2, C3, C4 do what?
Viral neutralization
Complement: C3b does what?
think B for Binding - anything that ends in b acts to opsinize bacteria
Complement: What does C3a do?
Think A for Inflame - anything that ends in a acts to increase the
inflammatory response. C3a leads to anaphylaxis, along with C5a
Complement: What is MC5b6,7,8,9?
This is the name for the membrane attack complex that punches holes in
membranes and actually kills the bacteria.
Complement: What does a lack of C1 esterase cause and why?
causes angioedema - which is basically overactive complement. This is
because C1 is the initial step in the classic pathway, and if it cannot be
limited, you over-react.
Complement: What does a lack of C3 cause?
sever and recurrent pyrogenic infections of the sinuses and UR tract, because
C3 is the first common step in both pathways, and without it both pathways
are cripled.
Complement: Lack of C6, C7, and C8 cause what?
Nisseria bacteremia. I have no idea why.
Complement: Lack of decay accelerating factor (DAF) leads to what?
Paroxysmal nocturnal hemaoglobinuria because the complement attacks the
RBCs. DAF stops C3.
Complement: What is the first step in the complement cascade that combines
the two pathways?
C3 activation
Complement: What is the first step to bind to the cell membrane?
C5a (after C5 is cleaved by C3 products)
Interferon Mechanism: What is the purpose of interferons?
Interferons interfere is viral infection of cells and replication. They also
activate NK cells to kill infected cells
Interferon Mechanism: What do Alpha and beta interferon do?
degrade viral mRNA, thereby inhibiting viral protein synthesis.
Interferon Mechanism: what does gamma interferon do?
upregulates MHC I and II in all cells
Hypersensitivity: What is another name for Type I hypersensitivity
anaphylactic or atpoic
Hypersensitivity: What do type I, II, and III have in common?
they all use antibodies
Hypersensitivity: What cells are involved in Type I?
Mast cell and Basophils
Hypersensitivity: What Ig triggers Type one reactions?
IgE
Hypersensitivity: What molecule acts as a mediator of this reaction?
IgE causes the release of histamine. This is a very fast reaction. Think First is
Fast.
Hypersensitivity: What are some examples of Type I reactions?
Anaphylactic shock, asthma, hives, local wheal and flare reactions.
Hypersensitivity: What is another name for Type II Hypersensitivity?
Cytotoxic (think Cy-2-toxic)
Hypersensitivity: What happens in this reaction?
antibodies bind to a perceived "enemy" cell and use complement and
phagocytosis to kill it.
Hypersensitivity: What antibodies are common in this reaction?
IgM and IgG
Hypersensitivity: What are some examples of Type II reactions?
Goodpasture's, autoimmune hemolytic anemia, graves disease, rheumatic
fever, etc.
Hypersensitivity: What do Type II and Type III have in common
They both use complement MAC (Membrane attack complexes) to do some
of the work.
Hypersensitivity: What is different between Type II and Type III reactions
Type III reactions involve neutrophils and the release of a large number of
cytokines and inflammatory mediators. Type II also hapens to specific cells
or tissues, while type III is soluble.
Hypersensitivity: What is the mechanism of a Type III Hypersensitivity
Reaction?
Soluble antibody-antigen complexes activate complement and attract
inflammatory cells
Hypersensitivity: What are some examples of this?
SLE, rheumatoid arthritis, etc
Hypersensitivity: What is serum sickness
When you have a type III reaction to a foreign protein, such as an injected
drug. It takes about 5-10 days, and you present with fever, utricara, arthralgia,
and proteinuria
Hypersensitivity: What is Arthus Reaction?
A local, subacute reaction to injected antibodies. Hapens in the skin.
Hypersensitivity: Examples of the Arthus reaction?
hypersensitivity pnemonitis and thermophilic actinomycetes
Hypersensitivity: What is the mechanism of a Type IV reaction?
This is T-cell mediated and therefore delayed. Think that 4 is last.
Hypersensitivity: What are examples of this type of reaction?
TB skin test, poison ivy, transplant rejection
Immune Deficiencies: Lack of B cells lead to what kind of disorders?
Lack of Ig
Immune Deficiencies: Give two examples of this…..
Burton's Agammaglobulinemia, Selective Immunoglobin deficiency
Immune Deficiencies: Burton's agammaglobulinemia is caused by what?
X-linked defect that cause low levels in all Igs. Causes all kinds of bacterial
infects. Think Boys and Bacteria for Burton's
Immune Deficiencies: At what age do the infections start in Burton's?
6 months, because that is when the maternal IgG declines.
Immune Deficiencies: What is the defect in Selective immunoglobulin
deficiency?
A lack of a certain class of Ig, probably caused by a defect in iostype
switching.
Immune Deficiencies: What Ig is most likely to be lacking?
IgA, which results in sinus and lung bacterial infections
Immune Deficiencies: What are three diseases that involve B and T cells?
Wiscott-Aldrich syndrome, and Ataxia-telangiactasia
Immune Deficiencies: What is SCID?
Stem cell defect (can be anything, no one gene), leads to total lack of an
immune system.
Immune Deficiencies: How do the patients present?
patients present early with viral, bacterial, fungal, and protazoal infections
Immune Deficiencies: What is Wiskott-Aldritch Syndrome
an X-linked defect that results in depressed cellular immunity and IgM
formation
Immune Deficiencies: How does it present?
Triad of Eczema, thrombocytopenia, and pyogenic infections. There is a
specific inability to fight off encapsulated bacteria
Immune Deficiencies: What are the Ig titers in a patient like this?
IgA is elevated, IgE is normal, and IgM is depressed
Immune Deficiencies: What is ataxia-telangiactasia?
Defect in DNA repair that leads to neurologic problems (ataxia) and spider
angiomas (telangiectasia) and IgA deficiency
Immune Deficiencies: Name six phagocytotic disorders.
Il-12 receptor deficiency, Hyper IgM syndrome, Job's syndrome,
Chediak-Higashi disease, Chronic granulomatous disease, Leukocyte
adhesion syndrome. (Use: In Heaven Jesus Can Contemplate Love, use Job to
remember the biblical link)
Immune Deficiencies: What does Il-12 receptor deficiency cause?
Mycobacterial infections
Immune Deficiencies: What does Hyper IgM syndrome cause?
Because the cells can't class switch, you have only IgM, and nothing else,
resulting is never pyogenic infections at 6 months
Immune Deficiencies: What will the titers look like in Hyper IgM?
High IgM, low IgA, IgE, and IgG
Immune Deficiencies: What causes Job's disease?
T-cells fail to make interferon gamma and therefore neutrophils are not
attracted to sites of infection
Immune Deficiencies: What is the clinical picture in Job's disease?
recurrent "cold" staph abscesses, eczema, and high levels of IgE
Immune Deficiencies: What is Chronic Granulomatous Disease?
a group of disorders that result in impaired neutrophils function
Immune Deficiencies: How does CGD present?
multiple oportunistic infections with bacteria
Immune Deficiencies: What is the test for CGD?
negative nitoblue tertraolium dye reduction test
Immune Deficiencies: What is Chediak-Higashi disease?
autosomal recessive disease of microtubule dysfunction, leading to impaired
phagocytosis
Immune Deficiencies: How does Chediak-Higashi disease present?
Multiple pyrogenic Staph and strep infections
Immune Deficiencies: What is Leukocyte Adhesions deficiency syndrome?
deficiency of LFA-1 in phagocytotic cells, presents with pyrogenic infections
Immune Deficiencies: Of the phagocytotic disorders, which two do not
present with pyogenic bacterial infections?
Job's disease (no neutrophils action leads to "cold" abcesses) and IL-12
(mycobacterial infections)
Passive vs. Active Immunity: What is active immunity?
slow onset, leads to long-lasting memory, hapens after you are exposed to an
antigen, basis for vaccines
Passive vs. Active Immunity: What is passive immunity?
When you receive pre-formed antibodies, limited by the lifespan of the
antibodies, rapid onset
Passive vs. Active Immunity: What diseases are treated by using passive
immunity?
Tetanus, Botulism, HBV, Rabies (To Be Healed Rapidly)
Passive vs. Active Immunity: What Igs are used for this treatment?
high-affinity IgA and IgG
Passive vs. Active Immunity: What is another scenario in which Igs are
transferred from host to patient?
Maternal Igs are transferred to the infant.
Antigen Variation: What is antigenic variation?
When pathogens change their proteins (surface, flagellar, etc) so that they can
escape the immune system's antibodies.
Antigen Variation: What are two mechanisms of antigenic shift?
DNA re-arrangement, and RNA segment re-arrangement
Antigen Variation: What type of antigenic shift does Borrelia have?
It changes it's surface proteins and causes relapsing fevers - each new fever
corresponds to new growth of the bacteria due to new antigens.
Antigen Variation: What bacteria has antigenic shift in its flagella?
Salmonella has two types of flagella, and it can shift between them.
Antigen Variation: What type of shifting does n. Gonorrhea undergo?
There is DNA recombinations that cause its pillus to be hypervariable.
Antigen Variation: African sleeping sickness is caused by what bacteria?
Trypanosome gabiense and T. rhodesiense
Antigen Variation: What kind of antigen shift do Trypanosomes have?
The Trypanosomes shift the proteins on their membranes in a cyclic,
pre-programmed manner, leading to cyclic fevers.
Antigen Variation: Influenza has both antigenic shift and antigenic drift.
What is the difference between the two?
Drift is a minor change in surface glycoproteins that allows new stains of flu
to avoid host defense. Shift is a major change where new surface proteins are
created.
Antigen Variation: What is the mechanism of antigenic shift in influenza?
when two types of flu infect the same cell and trade pieces of RNA new
proteins are made.
Autoantibodies: ANA is associated with?
SLE
Autoantibodies: What is specific for SLE
anti ds-DNA, anti-Smith
Autoantibodies: What is associated with drug-induced lupus?
antihistone
Autoantibodies: What is Rheumatoid Factor
anti-IgG, associated with Rhematoid arthritis
Autoantibodies: What is Anti-neutrophil associated with?
vasculitis
Autoantibodies: What indicates CREST scleroderma?
Anti-centromere antibody
Autoantibodies: what is anti-mitochondrial associated with?
primary billiary cirrhosis
Autoantibodies: What indicates celiac sprue?
anti-gliaden antibodies
Autoantibodies: What is anti-basement membrane associated with?
Goodpasture's syndrome
Autoantibodies: What indicates pemphigus vulgaris?
anti-epithelial antibodies
Autoantibodies: What is anti-microsomal associated with?
Hashimoto's thryroiditis
Transplant Rejection: What is hyperacute rejection?
This occurs when the host has pre-formed antibodies to the donor
Transplant Rejection: How fast does this occur?
Within minutes of the transplant
Transplant Rejection: Can it be controlled?
No. IT is innate because the antibodies are already into the blood.
Transplant Rejection: What is acute rejection?
a cell mediated type II cytotoxic response that occurs in the weeks following
the rejection
Transplant Rejection: What molecule causes this reaction?
the foreign MHC on the transplant
Transplant Rejection: Is it reversible?
Yes, with immunosupressive drugs (cyclosporin, OKT3).
Transplant Rejection: What is chronic rejection?
Antibody mediated vascular necrosis that hapens over months/years
Transplant Rejection: Is it reversible?
No - the damage is permenant.
Transplant Rejection: What is graft-versus-host disease?
This occurs when graft T-cells proliferate in the immune-supressed host and
attack the host cells as foreign.
Transplant Rejection: What are symptoms of GVHD?
maculopapular rash, jaundice, hepatosplenomegaly, diarrhea
Transplant Rejection: AUTHOR
Marc Otten
Blood Cell Differentiation: True/False: Myeloblast --> Promyelocyte -->
Metamyelocyte --> Myelocyte --> Stab cell --> Neutrophil, Eosinophil or
Basophil
False, Metamyelocyte is after myelocyte (Greek tip - 'meta' means after)
Blood Cell Differentiation: A megakaryoblast becomes a ------------- then
----------------
Megakaryocyte then platelet
Blood Cell Differentiation: A reticulocyte is an immature -------------
erythrocyte
Blood Cell Differentiation: Monoblasts are progenitors of
monocytes
Blood Cell Differentiation: What is the progenitor of plasma cells and active
T cells?
Lymphoblasts
Erythrocyte: Describe the shape of rbc's
Anucleate, biconcave, large SA:V ratio
Erythrocyte: What is the rbc's source of energy?
C2
Erythrocyte: Why purpose does the large SA:V ratio serve in an rbc?
easy gas exchange of O2 and CO2
Erythrocyte: Define erythrocytosis
Increased number of red cells
Erythrocyte: Define poikilocytosis
Varying shapes
Erythrocyte: How is glucose metabolized in an rbc?
90% anaerobic and 10% HMP shunt
Erythrocyte: What is the lifetime of the rbc?
120 days
Erythrocyte: Importance of "physiologic chloride shift"?
Membrane contains chloride-bicarbonate antiport which allows rbc to
transport CO2 from the periphery to the lungs for elimination
Leukocyte: Name three types of granulocytes
Neutrophils, eosinophils, basophils
Leukocyte: Name two mononuclear cells
lymphocytes and monocytes
Leukocyte: Purpose of leukocytes?
Defense against infections
Leukocyte: Normal levels of leukocytes?
4.000 - 10,000/ul
Basophil: What % of all leukocytes do basophils comprise?
<1%
Basophil: True/False: Nucleus of basophil is trilobed
False, bilobed
Basophil: Granules of a basophil are ------------ and stain with -------------stains
basophilic, basic (wow, tough one)
Basophil: Granules of a basophil contain
heparin (anticoagulant), histamine (vasodilator), other vasoactive amines and
SRS-A
Mast Cell: Function of mast cell?
Mediates allergic reactions
Mast Cell: Upon degranulation, mast cells release
histamine, heparin, and eosinophil chemotactic factors
Mast Cell: Mast cells bind which class of globulin
IgE
Mast Cell: True/False: Mast cells are the same cell type as basophils
False, they are the same structurally and functionally, but are not the same
cell type
Mast Cell: Mast cells are involved in which type of hypersensitivity
reactions?
Type 1
Mast Cell: Which pharmacologic agent is used to prevent mast cell
degranulation and what is it used to treat?
Cromolyn sodium/asthma
Eosinophil: What % of all leukocytes do eosinophils comprise?
1-6%
Eosinophil: The nucleus of an eosinophil is ------------
bilobed
Eosinophil: Function of an eosinophil?
Defend against helminthic and protozoan infections
Eosinophil: Eosinophils are highly phagocytic for ---------------
Antigen-antibody complexes
Eosinophil: What are the causes of eosinophilia?
Neoplastic, Asthma, Allergic Processes, Collagen Vascular Diseases,
Parasites (NAACP = mnemonic)
Eosinophil: What substances do eosinophils produce?
histaminase and arylsulfate
Neutrophil: Function of neutrophil?
Acute inflammatory response cell, phagocytosis
Neutrophil: What percentage of WBC's do neutrophils comprise?
40-75%
Neutrophil: Nucleus of a neutrophil is ----------------
multilobed
Neutrophil: Primary granules in a neutrophil are called -------------
lysosomes
Neutrophil: Describe primary granules of a neutrophil.
Large, spherical, azurophilic
Neutrophil: Primary granules in a neutrophil contain --------------
hydrolytic enzymes, lysozyme, myeloperoxidase and lactoferrin
Neutrophil: In what pathologic conditions do you see hypersegmented
neutrophils?
B12/folate deficiency
Monocyte: Shape of monocyte nucleus
kidney shaped
Monocyte: Cytoplasm of monocyte looks like --------------
frosted glass
Monocyte: In the tissues, monocytes differentiate into --------------
macrophages
Monocyte: Monocytes comprise what percent of all leukocytes?
2-10%
Lymphocyte: Describe nucleus of lymphocyte
small, round, densely staining
Lymphocyte: True/False: A lymphocyte has a large amount of dark
cytoplasm
False, small amount of pale cytoplasm
Lymphocyte: What to B lymphocytes produce?
antibodies
Lymphocyte: Function of T lymphocytes?
Cellular immune response and regulation of B lymphocytes and macrophages
B Lymphocyte: B lymphocytes are part of the -------------- immune response.
humoral
B Lymphocyte: Where do B lymphocytes mature?
Bone marrow (B = Bone marrow)
B Lymphocyte: What markers are present on B lymphocytes?
CD19 and CD20
B Lymphocyte: B lymphocytes migrate to
peripheral lymphoid tissue (follicles of lymph nodes, white pulp of spleen,
unencapsulated lymphoid tissue)
B Lymphocyte: When B cells encounter antigen, they differentiate into
--------- and produce ---------
plasma cells/antibodies
B Lymphocyte: B cells function as antigen presenting cells (APC) via
------------
MHC II
Plasma Cell: Nucleus of plasma cell is ----------- and has a -------------chromatin distribution
off-center/clock-face
Plasma Cell: True/False: Plasma cells have abundant RER and
well-developed Golgi apparatus
TRUE
Plasma Cell: Plasma cell neoplasm
multiple myeloma
Plasma Cell: Plama cells differentiate from --------- to produce large amounts
of ---------- specific to a particular antigen
B cells/antibody
T Lymphocyte: Function of T cells?
Mediate cellular immune response
T Lymphocyte: T cells mature in the -------------
Thymus
T Lymphocyte: What does CD stand for?
Cluster of Differentiation
T Lymphocyte: Name four types of cells that T cells differentiate into?
cytotoxic, helper, supressor, delayed hypersensitivity
T Lymphocyte: Markers present on T helper cells?
CD3, CD4
T Lymphocyte: Markers present on cytotoxic T cells?
CD3, CD8
T Lymphocyte: Class ----- MHC molecules present antigen to CD--- positive
T helper cells
2, 4
T Lymphocyte: Class ----- MHC molecules present antigen to CD--- positive
cytotoxic T cells
1, 8
Macrophage: Function of macrophages
phagocytize bacteria, cell debris and senescent red cells, and scavenges
damaged cells and tissues
Macrophage: Macrophages differentiate from circulating ---------------
monocytes
Macrophage: Macrophages are activated by
gamma interferon
Macrophage: Macrophages function as APC via ------------
MHC II
Airway cells: Ciliated cells extend to -------------------
respiratory bronchioles
Airway cells: Goblet cells extend to ------------------
terminal bronchioles
Airway cells: Type ----- cells line the alveoli and take up what % of the
alveolar surface?
Type 1, 97%
Airway cells: Type ----- cells secrete pulmonary surfactant and take up what
% of the alveolar surface?
Type 2, 3%
Airway cells: Pulmonary surfactant is made up of ----------------
dipalmitoylphosphatidylcholine
Airway cells: What is the purpose of pulmonary surfactant?
Decrease alveolar surface tension
Airway cells: Which type of cells serve as precursors to both type 1 and type
2 cells?
Type 2
Airway cells: In amniotic fluid, what ratio is indicative of fetal lung maturity?
lecithin:sphingomyelin ratio >2.0
Airway cells: Function of ciliated cells?
To sweep mucus secretions out of the lungs toward the mouth
Microglia: Microglia are CNS --------------
phagocytes
Microglia: Embryonic origin of microglia?
mesodermal
Microglia: True/False: Microglia are readily seen with Nissl stain
FALSE
Microglia: Describe nucleus and cytoplasm of microglia
small irregular nuclei, little cytoplasm
Microglia: In response to tissue damage, microglia transform into ------------
large, ameboid phagocytic cells
Microglia: HIV-infected microglia form ----------------------- in the CNS
multinucleated giant cells
Oligodendroglia: Function of oligodendroglia?
To myelinate multiple CNS axons
Oligodendroglia: In Nissl stain, oligodendroglia appear as -------------
small nuclei with dark chromatin and relatively little cytoplasm
Oligodendroglia: Oligodendroglia are the predominant type of glial cell in
--------- matter
white
Oligodendroglia: Oligodendroglia are destroyed in --------------------
Multiple sclerosis
Schwann Cells: Each Schwann cell functions to myelinate how many PNS
axons?
One
Schwann Cells: What is the function of Schwann cells?
To promote axonal regeneration
Schwann Cells: Name an example of a schwannoma
acoustic neuroma
Schwann Cells: Location of acoustic neuroma commonly associated with
what anatomical landmark?
internal acoustic meatus (CN VII and CN VIII)
Gas Exchange Barrier: See p. 73 for Gas exchange barrier diagram
0
Fetal landmarks: Implantation of blastocyst is present in which week?
1
Fetal landmarks: The bilaminar disk is formed within which week?
2
Fetal landmarks: Gastrulation, primitive streak, notochord, neural plate begin
to form
Within week 3
Fetal landmarks: Neural tube formed, organogenesis, extremely susceptible to
teratogens
Weeks 3-8
Fetal landmarks: Heart begins to beat, Upper and lower limb buds begin to
form
Week 4
Fetal landmarks: When do genitalia begin to have male/female
characteristics?
Week 10
Fetal landmarks: From day 0 to implantation at end of week 1, name stages of
embryogenesis
Fertilization (day 0), zygote (day 2), morula (day 3), blastocyst (day 5),
implantation (day 6)
Teratogens: Example
Effect on fetus
Teratogens: ACE Inhibitors
Renal damage
Teratogens: Cocaine
Abnormal fetal development, fetal addiction
Teratogens: DES
vaginal clear cell adenocarcinoma
Teratogens: Iodide
congenital goiter or hypothyroidism
Teratogens: 13-cis-retinoic acid
extremely high risk for birth defects
Teratogens: thalidomide
limb defects ("fliper" limbs)
Teratogens: warfarin, x-rays
multiple anomalies
Teratogens: fetal infections
congenital malformations
Umbilical cord: how many umbilical arteries?
2
Umbilical cord: what kind of blood do the umbilical arteries carry?
deoxygenated blood from fetus
Umbilical cord: how many umbilical veins?
1
Umbilical cord: what kind of blood is carried by umbilical vein?
suplies oxygenated blood from placenta to the fetus
Umbilical cord: a single umbilical artery is associated with what anomalies?
congenital and chromosomal
Embryologic derivatives: surface ectoderm
adenohypophysis, lens of eye, epithelial linings, epidermis
Embryologic derivatives: neuroectoderm
neurohypophysis, CNS neurons, oligodendrocytes, astrocytes, pineal gland
Embryologic derivatives: neural crest
ANS, dorsal root ganglia, melanocytes, chromaffin cells of adrenal medulla,
enterochromaffin cells, pia, celiac ganglion, Schwann cells, odontoblasts,
parafollicular - C cells of thyroid, laryngeal cartilage
Embryologic derivatives: mesoderm
dura connective tissue, muscle, bone, cardiovascular structures, lymphatics,
blood urogenital structures, serous linings of body cavities (peritoneal),
spleen, adrenal cortex
Embryologic derivatives: endoderm
gut tube epithelium and derivatives (lungs, liver, pancreas, thymus, thyroud,
parathyroid)
Embryologic derivatives: what induces ectoderm to form neuroectoderm
(neural plate)?
notochord
Embryologic derivatives: what is the postnatal derivative of the notochord?
nucleus pulposus of the intervertebral disk
Early Develpoment: Name the precursor for the ectoderm and its purpose
epiblast, invaginates to form primitive streak
Early Develpoment: Cells from the primitive streak give rise to
intraembryonic mesoderm and endoderm
Early Develpoment: How many germ layers in second week and what are
they?
2, epiblast and hypoblast (remember rule of 2's for second week)
Early Develpoment: How many cavities in second week and what are they?
2, amniotic cavity and yolk sac (remember rule of 2's for second week)
Early Develpoment: How many components to placenta in second week and
what are they?
2, cytotrophoblast and syncytiotrophoblast (remember rule of 2's for second
week)
Early Develpoment: How many germ layers in third week and what are they?
3, (gastrula): ectoderm, mesoderm, endoderm (Rule of 3's for third week)
Fetal Erythropoiesis: In the 3-8th weeks, fetal erythropoiesis occurs in
Yolk sac
Fetal Erythropoiesis: In the 6-30th weeks, fetal erythropoiesis occurs in
Liver
Fetal Erythropoiesis: In the 9-28th weeks, fetal erythropoiesis occurs in
Spleen
Fetal Erythropoiesis: Erythropoiesis occurs in the Bone marrow from the ---week onward
28th
Fetal Erythropoiesis: Mnemonic for remembering fetal erythropoiesis?
Young Liver Synthesizes Blood
Heart Embryology: Embryonic structure
Gives rise to
Heart Embryology: Truncus arteriosus
Ascending aorta and pulmonary trunk
Heart Embryology: Bulbus cordis
Smooth parts of left and right ventricle
Heart Embryology: Primitive ventricle
trabeculated parts of left and right ventricle
Heart Embryology: Primitive atria
trabeculated left and right atrium
Heart Embryology: Left horn of sinus venosus (SV)
coronary sinus
Heart Embryology: Right horn of sinus venosus (SV)
smooth part of right atrium
Heart Embryology: Right common cardinal vein and right anterior cardinal
vein
SVC
Twinning: Monozygotic twins have ---- amniotic sacs, ----- placentas, ---chorions
2,1,1
Twinning: Dizygotic (fraternal) twins have ---- amniotic sacs, ----- placentas,
---- chorions
2,2,2
Twinning: AUTHOR
Alex Arriaga
Fetal Circulation: Do you want to see a high yield diagram?
Then go to page 76!
Fetal Circulation: Saturation level of blood in umbilical vein?
0.8
Fetal Circulation: Foramen ovale: its function in fetal circulation?
Most oxygenated blood reaching the heart via the IVC is diverted through the
foramen ovale and pumped out the aorta to the head.
Fetal Circulation: Ductus Arteriosus: its function in fetal circulation?
Deoxygenated blood from the SVC is expelled into the pulmonary artery and
ductus arteriosus to the lower body of the fetus.
Fetal Circulation: What happens at birth, when infant takes a breath?
Decreased resistance in pulmonary vasculature causes increased left atrial
pressure vs right atrial pressure; foramen ovale closes; increase in O2 leads to
decrease in prostaglandins, causing closure of ductus arteriosus.
Fetal Circulation: What drug can be given to close a patent ductus arteriosus?
Indomethacin
Fetal Circulation: What drug can be given to keep a patent ductus arteriosus
open?
Prostaglandins
Fetal-postnatal derivatives: Umbilical vein becomes the:
ligamentum teres hepatis
Fetal-postnatal derivatives: umbilical arteries become the:
medial umbilical ligaments
Fetal-postnatal derivatives: ductus Arteriosus becomes the:
ligamentum arteriosum
Fetal-postnatal derivatives: ductus venosus becomes the:
ligamentum venosum
Fetal-postnatal derivatives: foramen ovale becomes the:
fossa ovalis
Fetal-postnatal derivatives: allantois - urachus becomes the:
median umbilical ligament
Fetal-postnatal derivatives: notochord becomes the:
nucleus pulposus
Fetal-postnatal derivatives: urachal cyst or sinus is a remnant of the:
allantois (urine drainage from the bladder)
Aortic Arch Derivatives: 1st arch:
part of maxillary artery (1st is MAXimal)
Aortic Arch Derivatives: 2nd arch:
stapedial artery and hyoid artery (Second = Stapedial)
Aortic Arch Derivatives: 3rd arch:
common Carotid artery and proximal part of internal carotid artery (C is the
3rd letter of the alphabet)
Aortic Arch Derivatives: 4th arch:
on left, aortic arch; on right, proximal part of right subclavian artery 4th arch
(4 limbs) = systemic
Aortic Arch Derivatives: 6th arch:
proximal part of pulmonary arteries and (on left only) ductus arteriosus. 6th
arch = pulmonary and the pulmonary-to-systemic shunt (ductus arteriosus)
Aortic Arch Derivatives: diagram of aortic arch derivatives:
see page 76!
Branchial apparatus: branchial clefts are dervied from:
ectoderm
Branchial apparatus: branchial arched are derived from:
mesoderm and neural crests
Branchial apparatus: branchial pouches are derived from:
endoderm
Branchial apparatus: mnemonic to remember branchial apparatus derivation:
CAP covers outside from inside (Clefts = ectoderm, Arches = mesoderm,
Pouches = endoderm)
Branchial arch 1 derivatives: Meckel's cartilage:
Mandible, Malleus,incus,sphenoMandibular ligament
Branchial arch 1 derivatives: Muscles:
Muscles of Mastication (temporalis, Masseter, lateral and Medial pterygoids),
Mylohyoid, anterior belly of digastric, tesnsor tympani, tensor veli palatini
Branchial arch 1 derivatives: Nerve:
CN V3
Branchial Arch 2 derivatives: Reichert's cartilage:
Stapes, Styloid process, lesser horn of hyoid, Stylohyoid ligament
Branchial Arch 2 derivatives: Muscles:
muscles of facial expression, Stapedius,Stylohyoid, posterior belly of
digastric.
Branchial Arch 2 derivatives: Nerve:
CN VII
Branchial arch 3 derivatives: Cartilage:
greater horn of hyoid
Branchial arch 3 derivatives: Muscle:
stylopharyngeus (Think of pharnx: stylopharyngeus is innervated by
glossopharyngeal nerve.
Branchial arch 3 derivatives: Nerve:
CN IX
Branchial arch 4 to 6 derivatives: Cartilages:
thyroid, cricoid, arytenoids, cornicuate, cuneiform
Branchial arch 4 to 6 derivatives: Muscles (4th arch):
mostly pharyngeal constrictors, cricothyroid, levator veli palatini.
Branchial arch 4 to 6 derivatives: 5th arch:
makes no major developmental contributions
Branchial arch 4 to 6 derivatives: Muscles (6th arch):
all intrinsic muscles of larynx except cricothyroid
Branchial arch 4 to 6 derivatives: Nerve (4th arch):
CN X
Branchial arch 4 to 6 derivatives: Nerve (6th arch):
CNX (recurrent laryngeal branch)
Branchial arch innervation: Arch 1 derviatives are supplied by:
CN V2 and V3
Branchial arch innervation: Arch 2 derivatives are supplied by:
CN VII
Branchial arch innervation: Arch 3 derivatives are supplied by:
CN IX
Branchial arch innervation: Arch 4 and 6 derivatives supplied by:
CNX
Branchial arch innervation: For diagram:
see p. 77
Branchial cleft derivatives: 1st cleft develops into
external auditory meatus
Branchial cleft derivatives: 2nd through 4th clefts form:
temporary cervical sinuses, which are obliterated by proliferation of 2nd arch
mesenchyme.
Branchial cleft derivatives: Persistent cervial sinus can lead to a:
branchial cyst in the neck
Ear development:: Bone: Incus/Malleus come from:
1st arch
Ear development:: Bone: Stapes comes from:
2nd arch
Ear development:: Muscle: Tensor tympani (V3) comes from:
1st arch
Ear development:: Muscle: Stapedius (VII) comes from:
2nd arch
Ear development:: External auditory meatus comes from:
1st cleft
Ear development:: Eardrum, eustacian tube comes from:
1st pharyngeal membrane
Branchial pouch derviatives:: 1st pouch develops into:
middle ear cavity, eustacian tube, mastiod air cells (1st pouch contributes to
endoderm-lined structures of ear)
Branchial pouch derviatives:: 2nd pouch develops into:
epithelial lining of palatine tonsil
Branchial pouch derviatives:: 3rd pouch (dorsal wings) develops into:
inferior parathyroids (3rd pouch contributes to 3 structures: thymus, left and
right inferior parathyroids)
Branchial pouch derviatives:: 3rd pouch (ventral wings) develops into:
thymus
Branchial pouch derviatives:: 4th pouch develops into:
superior parathyroids
Branchial pouch derviatives:: Aberrant development of 3rd and 4th pouches
-->
DiGeorge's syndrome --> leads to T-cell deficiency (thymic hypoplasia) and
hypocalcemia (parathyroid glands)
Thymus: Site of:
T-cell maturation
Thymus: Encapsulated or unencapsulated?
encapsulated
Thymus: which branchial pouch?
from epithelium of 3rd branchial pouches
Thymus: Lymphocyte origin?
lymphocytes are of mesenchymal origin
Thymus: cortex is dense with:
immature T cells
Thymus: medulla is pale with:
mature T cells and epithelial reticular cells and contains Hassall's corpuscles.
(think of the Thymus as "finishing school" for T cells. They arrive immature
and "dense" in the cortex; they are mature in the medulla.
Thymus: What occurs at the corticomedullary junction?
Positive and negative selection
Thyroid Development: Thyroid diverticulum arises from:
floor of primitive pharnyx, descends into neck.
Thyroid Development: Connected to tongue by
thyroglossal duct, which normally disapears but may persist as a pyramidal
lobe of thyroid.
Thyroid Development: Formen cecum is:
a normal remnant of the thyroglossal duct
Thyroid Development: The most common ectopic thyroid tissue site is the:
Tongue!
Tongue development: 1st branchial arch forms the
anterior 2/3 of the tongue (thus sensation via CN V3, taste via CNVII)
Tongue development: 3rd and 4th branchial arches form:
posterior 1/3 of the tongue (thus sensation and taste mainly via CN IX,
extreme posterior via CN X).
Tongue development: Cranial nerves for taste?
CN VII, IX, X (solitary nucleus)
Tongue development: Motor innervation is via CN?
CN XII
Tongue development: For diagram:
see p. 78
Cleft lip and cleft palate:: define cleft lip
failure of fusion of the maxillary and medial nasal processes
Cleft lip and cleft palate:: define cleft palate
failure of fusion of the lateral palatine processes, the nasal septum, and/or the
median palatine process.
Cleft lip and cleft palate:: For diagram:
see p. 78
Diaphragm embryology: diaphragm is derived from:
Septum transversarium, Pleuroperitoneal folds, Body wall, Dorsal mesentery
of esophagus (Several Parts Build Diaphragm. Diaphragm descends during
develpoement but maintains innervation from above C3-C5. "C3, 4, 5 keeps
the diaphragm alive."
Diaphragm embryology: hiatial hernia
abdominal contents may herniate into the throax due to incomplete
development of the diaphragm.
Diaphragm embryology: For diagram:
see p. 79
Bone Formation: Intramembranous
spontaneous bone formation without preexisting cartilage.
Bone Formation: Endochondral
ossification of carilaginous molds. Long bones form by this type of
ossification at 1o and 2o centers
Meckel's Diverticulum: definition
persistence of the vitelline duct or yolk stalk. May contain ectopic
acid-secreting gastric muscosa and/or pancreatic tissue.
Meckel's Diverticulum: What is the most common congenital anomaly of the
GI tract?
Meckel's diverticulum
Meckel's Diverticulum: Complications of Meckel's Diverticulum?
can cause bleeding or obstruction near the terminal ileum.
Meckel's Diverticulum: Comparison of Meckel's Diverticulum to
Omphalomesenteric cyst?
Cystic dilatation of the vitelline duct.
Meckel's Diverticulum: Associated with
intussusception and volvulus
Meckel's Diverticulum: Mnemonic to remember Meckel's diverticulum
The five 2's: 2 inches long, 2 feet from the ileocecal valve, 2% of population,
commonly presents in first 2 years of life, may have 2 epithelia.
Meckel's Diverticulum: For diagram:
see p. 79
Pancreas and Spleen embryology: Parcreas is derived from the
foregut
Pancreas and Spleen embryology: ventral pancreatic bud becomes the
pancretic head, uncinate process (lower half of head), and main pancreatic
duct.
Pancreas and Spleen embryology: dorsal pancreatic bud becomes:
everything else (body, tail, isthmus, and accessory pancreatic duct).
Pancreas and Spleen embryology: Spleen arises from
dorsal mesentery but is suplied by artery of foregut.
Pancreas and Spleen embryology: For diagram:
see p 79
Genital ducts: Mesonephric (wolffian) duct
Develops into Seminal vesicles, Epididymis, Ejaculatory duct, and Ductus
deferens (SEED)
Genital ducts: Paramesonephric (mullerian) duct
Develops into fallopian tube, uterus, and part of vagina.
Genital ducts: Mullerian inhibiting substance is secreted by:
the testes to supress development of paramesonephric ducts in males.
Genital ducts: For diagram:
see p. 80
Bicornuate uterus:: results from
incomplete fusion of the paramesonephric ducts.
Bicornuate uterus:: Associated with
urinary tract abnormalities and infertility
Bicornuate uterus:: For diagram:
see p. 80
Male/female genital homologues:: Genital tubercle (male) -->
glans penis via dihydrotestosterone
Male/female genital homologues:: genital tubercle (female) -->
glans clitoris via estrogen
Male/female genital homologues:: urogenital sinus (male) -->
corpus spongiosum, bulbourethral glands (of Cowper), prostate gland: via
dihydrotestosterone
Male/female genital homologues:: urogenital sinus (female) -->
vestiubular bulbs, greater vestibular glands (of Bartholin), Urethral and
paraurethral glands (of Skene): via estrogen
Male/female genital homologues:: urogenital folds (male) -->
ventral shaft of penis (penile urethra) via dihydrotestosterone
Male/female genital homologues:: urogenital folds (female) -->
labia minora via estrogen
Male/female genital homologues:: labioscrotal swelling (male) -->
scrotum via dihydrotestosterone
Male/female genital homologues:: labioscrotal swelling (female) -->
labia majora via estrogen
Male/female genital homologues:: For diagram:
see p. 80
Congenital penile abnormalities: Hypospadia
abnormal opening of the penile urethra on inferior (ventral) side of penis due
to failure of urethral folds to close.
Congenital penile abnormalities: Epispadia
abnormal opening of the penile urethra on superior (dorsal) side of penis due
to faulty positioning of the genital tubercle.
Congenital penile abnormalities: epispadia is associated with
exstrophy of the bladder
Congenital penile abnormalities: Which is more common, hypospadia or
epispadia?
Hypospadial; fix hypospadias to prevent UTI's
Sperm Development: Spermatogenesis begins with
spermatogonia (type A and type B; type A forms both type A and type B
spermatogonia)
Sperm Development: full development takes how long?
2 months
Sperm Development: where does spermatogenesis occur?
Spermatogenesis occurs in Seminiferous tubules.
Sperm Development: For diagram:
see p. 81
Derivation of sperm parts:: acrosome is derived from
the golgi aparatus and flagellum (tail) from one of the centrioles.
Derivation of sperm parts:: what does the neck of the sperm have?
Middle piece (neck) has Mitochondria.
Derivation of sperm parts:: Sperm food supply is:
fructose
Derivation of sperm parts:: For diagram:
see p. 81
Meiosis and Ovulation:: 1o oocytes begin and complete meiosis I when?
begin: during fetal life; complete: just prior to ovulation. Meiosis I is arrested
in prOphase for years until Ovulation.
Meiosis and Ovulation:: What phase is Meiosis II arrested in?
Meiosis II is arrested in METaphase until fertilization. -- "An egg MET a
sperm."
Meiosis and Ovulation:: AUTHOR
Anna Awdankiewicz
Amniotic Fluid Abnormalities: What is polyhydramnios?
high amount of amniotic fluid (>1.5-2L)
Amniotic Fluid Abnormalities: What is polyhydramnios clinically associated
with?
esophageal/duodenal atresis and anencephaly both of which impair the ability
of the fetus to swallow amniotic fluid
Amniotic Fluid Abnormalities: What is the condition leading to low amniotic
fluid (<0.5L) called?
Oligohydramnios
Amniotic Fluid Abnormalities: What 2 conditions is oligohydramnios
associated with?
Bilateral renel agenesis or posterior urethral valves (in males) which results in
the failure of the fetus to excrete urine into the amniotic fluid.
Amniotic Fluid Abnormalities: What syndrome can oligohydramnios result
in?
Potter's Syndrome
Amniotic Fluid Abnormalities: What does the term Potter's syndrom
describe?
Bilateral renal agenesis leading to oligohydramnios which results in fetal
limb and facial deformaties and pulmonary hypoplasis
Amniotic Fluid Abnormalities: What causes Potter's syndrome?
Malformation of the ureteric bud
Amniotic Fluid Abnormalities: What results when the poles of both kidneys
fuse during development?
Horseshoe kidney
Amniotic Fluid Abnormalities: What arrests the ascend of the fused kidneys?
The horseshoe kidneys get traped under the inferior mesenteric artery.
Landmark Dermatomes: What dermatome is found at the posterior half of the
skull?
C2
Landmark Dermatomes: Where is the C3 dermatome?
neck (high turtleneck shirt)
Landmark Dermatomes: Where is the C4 dermatome?
lower neck (low-collar shirt)
Landmark Dermatomes: Where is the T4 dermatome?
At the niple
Landmark Dermatomes: Which dermatome can be found at the level of the
xiphoid process?
T7
Landmark Dermatomes: Which dermatome is important for early appendicitis
pain refferl to the umbilicus?
T10
Landmark Dermatomes: Where is the L1 dermatome?
At the inguinal ligament
Landmark Dermatomes: What dermatome is found at the knee caps?
L4
Landmark Dermatomes: Which dermatomes are associated with erection and
sensation of penile and anal zones?
S2, S3, S4 (S2, 3, 4 keeps the man begging for more)
Landmark Dermatomes: Gallbladder pain can be reffered to the right
shoulder via which nerve?
Phrenic nerve
Landmark Dermatomes: Which dermatome is found at the level of the belly
butten?
T10
Rotator Cuff Muscles: Which muscles form the rotator cuff?
Supraspinatus, Infraspinatus, Teres minor, and Subscapularis (SItS)
Rotator Cuff Muscles: Which muscle helps the deltoid abduct the arm?
Supraspinatus
Rotator Cuff Muscles: What function does the Infraspinatus muscle have?
laterally rotates the arm at the shoulder joint
Rotator Cuff Muscles: What is the function of the Teres minor muscle?
to adduct and laterally rotate the arm (Possible mistake in First Aid)
Rotator Cuff Muscles: Which muscle medically rotates and adducts the arm?
Subscapularis
Thenar-hypothenar Muscles: Name the thenar muscles.
Oponens pollicis, Abductor pollicis brevis, Flexor pollicic brevis
Thenar-hypothenar Muscles: Name the hypothenar muscles.
Oponens digiti minimi, Abductor digiti minimi, Flexor digiti minimi
Thenar-hypothenar Muscles: What functions do the thenar and hypothenar
muscles preform?
opose, abduct and flex (OAF)
Unhappy triad/Knee injury: What structures can be injured when a football
player's cleated shoe is planted firmly in the turf and the knee is struck from
the lateral side?
medial collateral ligament (MCL), medial meniscus, and anterior cruciate
ligament (ACL) (unhapy triad on the knee joint)
Unhappy triad/Knee injury: What does a anterior drawer sign indicate?
Tearing of the Anterior cruciate ligament (ACL)
Unhappy triad/Knee injury: What does abnormal passive abduction indicate?
A torn Medial collateral ligament (MCL)
Recurrent Laryngeal nerve: The recurrent laryngeal nerve is a branch of
which cranial nerve?
CN X
Recurrent Laryngeal nerve: Which muscles does it supply?
intrinsic muscles of the larynx except the cricothyroid muscle
Recurrent Laryngeal nerve: What structure does the right recurrent laryngeal
nerve wrap around?
right subclavian artery
Recurrent Laryngeal nerve: What structure does the left recurrent laryngeal
nerve wrap around?
arch of the aorta and the ligamentum arteriosum
Recurrent Laryngeal nerve: In what kind of surgery can this nerve be
damaged in?
thyroid surgery
Recurrent Laryngeal nerve: What happens when this nerve gets damaged?
hoarseness
Scalp and meninges: layers: Name the layers of the scalp
skin, connective tissue, aponeurosis, loose connective tissue, pericranium
(SCALP)
Scalp and meninges: layers: Name the meninges.
Dura, arachnoid, and pia (DAP)
Scalp and meninges: layers: What space is found between the dura and
arachnoid?
subdural space
Scalp and meninges: layers: Between what meninges is the subarachnoid
space located?
between the arachnoid and the pia
Scalp and meninges: layers: What is found in the subarachnoid space?
CSF
Scalp and meninges: layers: In which scalp layer are the emissary veins
found?
loose connective tissue
Mastication Muscles: Which 3 muscles are responsible for closing the jaw?
Masseter, temporalis, and medial pterygoid (M's munch)
Mastication Muscles: Which muscles opens the jaw?
Lateral pterygoid
Mastication Muscles: Which nerve innervates the muscles that are
responsible for jaw opening and closing?
Trigeminal nerve V3
Mastication Muscles: Name the nerve that supplies the muscles of the tounge
except palatoglossus.
Hypoglossal nerve
Mastication Muscles: What nerve innervates the palatoglossus muscle?
Vagus nerve
Mastication Muscles: The muscles with the root "palat" (except tensor veli
palatini) are innervated by what nerve?
vagus nereve
Mastication Muscles: What nerve innervates tensor veli palatini?
mandibular branch of CN V
Carotid Sheath: List the structures found in the carotid sheath (in the order
from lateral, medial, posterior)
Internal jugular vein, common carotid artery, and vagus nerve (VAN)
Diaphragm Structures: What structure crosses the diaphragm at T8?
IVC (I 8 10 EGG's AT 12)
Diaphragm Structures: At what T level does the esophagus and vagus nerve
cross the diaphragm?
T10 (I 8 10 EGG's AT 12)
Diaphragm Structures: What structure crosses the diaphragm at T12?
aorta, thoracic duct, and azygous vein (I 8 10 EGG's AT 12)
Diaphragm Structures: Name the innervation of the diaphragm
C3, 4, and 5 (phrenic nerve)
Diaphragm Structures: Where can the pain from the diaphragm be reffered
to?
shoulder
Coronary artery anatomy: What artery supplies the SA and AV nodes?
RCA right coronary artery
Coronary artery anatomy: The inferior portion of the left ventricle is supplied
by what artery 80% of the time?
RCA via the PD posterior descending artery
Coronary artery anatomy: In which artery does coronary artery occlusion
most sommonly occur?
LAD left anterior descending artery
Coronary artery anatomy: What artery supplies the anterior interventricular
septum?
LAD left anterior descending artery
Coronary artery anatomy: When do coronary arteries fill?
during diastole
Coronary artery anatomy: What is the most posterior part of the heart?
left atrium
Coronary artery anatomy: What can the enlargement of the left atrium cause?
dysphagia
Bronchopulmonary segments: What does each bronchopulmonary segment
contain?
3º (segmental) bronchus and 2 arteries (bronchial and pulmonary) in the
center
Bronchopulmonary segments: What drains along the borders of the
bronchopulmonary segments?
veins and lymphatics
Bronchopulmonary segments: What runs with the airways?
arteries
Lung Relations: How many lobes does the right lung has?
3 lobes
Lung Relations: Which lung lobe has 2 lobes?
left
Lung Relations: What is the homologue of the right middle lobe in the left
lobe?
lingula
Lung Relations: Which lung is the more common site for inhaled foregin
body?
right lung?
Lung Relations: Why is 1 lung a more common site for inhaled foregin body?
Because of the lessvacute angle of the right main stem bronchus
Lung Relations: What is the relation of the pulmonary artery to the bronchus
in each lung hilus?
RALS - right lung anterior and left lung superior
Femoral Triangle: What does the femoral sheath contain?
femoral artery, femoral vein, and femoral canal (containing deep inguinal
lymph node)
Femoral Triangle: Does the femoral nerve lie within the femoral sheath?
no, it lies outside the sheath
Femoral Triangle: What do you call the entrance of abdominal contents
through the femoral canal?
femoral hernia
Femoral Triangle: What does the femoral triangle contain?
femoral vein, aretery and nerve (VAN)
Femoral Triangle: Where does the femoral hernia protrude to?
below and lateral to the pubic tubercle
Abdominal Hernias: What are abdominal hernias?
protrusions of peritoneum through an opening - usually sites of weakness
Abdominal Hernias: What is the name of the hernia in which abdominal
structures enter the thorax?
diaphragmatic hernia
Abdominal Hernias: What is the most common diaphragmatic hernia?
hiatal hernia
Abdominal Hernias: What happens in this type of hernia?
the stomach herniates upward through the esophageal hiatus
Abdominal Hernias: What can result from a defective development of
pleuroperitoneal membrane in infants?
diaphragmatic hernias
Abdominal Hernias: From where does a direct hernia protrude?
from the inguinal (Hesselbach's) triangle - bulges directly through the
abdominal wall medial to the inferior epigastric artery
Abdominal Hernias: Which inguinal ring does it go through?
external inguinal ring only
Abdominal Hernias: Who usually gets a direct hernia?
older men
Abdominal Hernias: What does the indirect hernia go through?
the internal (deep) inguinal ring and external (superficial) inguinal ring and
into the scrotum
Abdominal Hernias: On which side of the inferior epigastric artery does the
indirect hernia enter the internal inguinal ring?
lateral to the inferior epigastric artery
Abdominal Hernias: Who usually get an indirect hernia and why?
infants, because of the failure of processus vaginalis to close
Abdominal Hernias: Which structures make up Hesselbach's triangle?
inferior epigastric artery, lateral border of rectus abdominis, and inguinal
ligament
Inguinal canal: Where does the inguinal canal start and end?
begins at the deep inguinal ring and terminates at the superficial ring
Inguinal canal: What does the inguinal canal transmit?
the spermatic cord or the round ligament of the uterus and the genital branch
of the genitofemoral nerve
Inguinal canal: What structures make up the anterior wall of the inguinal
canal?
aponeuroses of the external oblique and internal oblique muscles
Inguinal canal: What structures make up the posterior wall of the inguinal
canal?
aponeurosis of the transverse abdominal muscle and transversalis fascia
Inguinal canal: What structures make up the superior wall of the inguinal
canal?
arching fibers of the internal oblique and transverse muscles
Inguinal canal: What structures make up the inferior wall (floor) of the
inguinal canal?
inguinal and lacunar ligaments
Arterial supply of stomach: From where does the stomach receive its main
blood supply?
from the branches of the celiac trunk
Arterial supply of stomach: From where does the celiac trunk arise?
from the front of the abdominal artery immediately below the aortic hiatus of
the diaphragm
Arterial supply of stomach: What arteries does the celiac trunk divide into?
left gastric, splenic, and common hepatic arteries
Arterial supply of stomach: What does the left gastric artery run along?
lesser curvature of the stomach
Arterial supply of stomach: What artery does the left gastric artery
anastomose with?
the right gastric artery
Arterial supply of stomach: What does the splenic artery run along?
runs along the superior boarder of the pancrease
Arterial supply of stomach: What arteries does the splenic artery give rise to?
(dorsal pancreatic artery), short gastric arteries and left gastroepiploic artery
Arterial supply of stomach: What does the left gastroepiploic artery run
along?
the greater curvature of the stomach
Arterial supply of stomach: What does the common hepatic artery divide
into?
hepatic artery proper, right gastric artery, and gastroduodenal artery
Arterial supply of stomach: AUTHOR
Neeti Bathia
portal system anastamoses: esophageal varices results at the anastamosis of
which veins?
left gastric vein (portal) and azygous (systemic)
portal system anastamoses: manifestation of portal hypertension at the
anastamosis of the superior rectal with the middle/inferior rectal veins
hemorrhoids
portal system anastamoses: caput medusae is at anastamosis of which veins
paraumbilical (portal) and inferior epigastric (systemic)
portal system anastamoses: the two other sites of portal system anastamosis
retroperitoneal vein (portal) with renal vein (systemic) and retroperitoneal
vein with paravertebral vein (systemic)
portal system anastamoses: 3 manifestations seen in alcoholic cirrhosis
esoph. Varices, hemorrhoids, caput medusae "Gut, butt and caput"
lymph drainage: drains right arm and right half of head
right lymphatic duct
lymph drainage: what thoracic duct drains
everything that right lymphatic duct does not
pectinate line: location of pectinate line
where hindgut meets ectoderm
pectinate line: innervation, hemorrhoid type, aterial supply and venous
drainage above pectinate line
visceral innervation(not painful), internal hemorrhoids (think of
adenocarcinoma association), superior rectal artery(branch of IMA), and
superior rectal vein to inferior mesenteric vein to portal system
pectinate line: innervation, hemorrhoid type, aterial supply and venous
drainage below pectinate line
somatic innervation(painful!), external hemorrhoids (think of squamous cell
carcinoma association), inferior rectal artery, inferior rectal vein to internal
pudendal vein to internal iliac vein to IVC
retroperitoneal structures: parts of duodenum that are retroperitoneal
2nd, 3rd and 4th parts
retroperitoneal structures: parts of colon that are retroperitoneal
descending and ascending colon
retroperitoneal structures: 2 big organs that are retroperitoneal
pancreas (except tail) and kidneys
retroperitoneal structures: 2 major vessels that are retroperitoneal
aorta and IVC
digestive tract anatomy: two big nerve plexuses in digestive tract and what
they do
Submucosal (Meissners) controls Secretions; Myeneteric (Auerbach's)
controls Motility
digestive tract anatomy: Layers of digestive tract from inside to out
villi, lamina propria, muscularis mucosae, submucosa, serosa
Gonadal venous drainage : drainage of left ovary/testis
left gonadal vein to left renal vein to IVC
Gonadal venous drainage : drainage of right ovary/testis
right gonadal vein to IVC
Enteric plexuses: location of myenteric plexus
b/w inner and outer layers of GI smooth muscle
Enteric plexuses: location of submucosal plexus
b/w mucosa and inner layer of GI smooth muscle
GI blood supply: region and structures supplied by celiac artery
foregut: stomach to duodenum, liver, gallbladder, pancreas
GI blood supply: hindgut is supplied by which artery
inferior mesenteric artery
GI blood supply: superior mesenteric artery supplies ---
midgut: duodenum to proximal 2/3 of transverse colon
Kidney anatomy and glomerular structure: grossly, the collecting system is
made up of --
papillae, medullary pyramids, renal pelvis and ureter
Kidney anatomy and glomerular structure: which structures are in the renal
medulla?
proximal and distal straight tubules, loop of Henle, vasa recta
Kidney anatomy and glomerular structure: location of macula densa
part of DCT next to afferent arteriole
Juxtaglomerular apparatus (JGA): two components of JGA
JG cells (afferent arteriole) and macula densa (DCT, senses Na)
Juxtaglomerular apparatus (JGA): three factors leading to renin secretion
decreased renal blood pressure, decreased sodium in distal tubule, increased
sympathetic tone
Juxtaglomerular apparatus (JGA): what secretes erythropoeitin?
JG cells
Ureters: course: two structures under which ureters pass
uterine artery and ductus deferens "water under bridge"
Ligaments of the uterus : which ligament contains ovarian vessels?
suspensatory ligament of uterus
Ligaments of the uterus : what does round ligament of uterus contain?
nothing!
Ligaments of the uterus : which ligament contains uterine vessels?
transverse cervical (cardinal) ligament
Ligaments of the uterus : what does broad ligament contain?
round ligaments of uterus and ovaries and uterine tubules and vessels
Autonomic innervation of male sexual response: erection is mediated by ---while emission is mediated by ----.
Parasympathetics; Sympathetics "Point and Shoot"
Autonomic innervation of male sexual response: which nerves mediate
ejaculation?
visceral and somatic
Clinically important landmarks: McBurney's point
site of apendix, 2/3 of way from umbilicus to ASIS
Clinically important landmarks: significance of ischial spine
site of pudendal nerve block
Clinically important landmarks: site of lumbar puncture
iliac crest
Peripheral nerve layers: what is covered by endoneurium?
single nerve fiber
Peripheral nerve layers: what must be rejoined in microsurgery for limb
reattachment?
Perineurium: the Permeability barrier
Peripheral nerve layers: what surrounds the entire nerve?
epineurium
Corpuscles : sites of meissner's corpuscles and their function
dermis of palm, soles, and digits; involved in light discriminatory touch of
hairless skin
Corpuscles : Sites of Pacinian corpuscles and their function
deep skin at ligaments joint capsules, serous membranes and mesenteries;
involved in Pressure, coase touch, vibration and tension
Inner ear: 3 components of bony labyrinth
cochlea, vestibul and semicircular canals
Inner ear: Site and composition of endolymph
membranous labyrinth, high potassium (like ICF)
Inner ear: site and composition of perilymph
bony labyrinth, high sodium (like ECF)
Inner ear: site of cochlear duct, utricle, saccule, and semicircular canals
membranous labyrinth
Inner ear: what frequency does base of cochlea pick up?
high-frequency
Inner ear: site and function of ampullae
in semicircular canals, for angular acceleration
Inner ear: site and function of maculae
in utricle and saccule, for linear acceleration
Inner ear: which frequency is lost first in hearing loss in elderly
high-frequency
Inner ear: site of endolymph production
stria vascularis
Inner ear: what part of the cochlea picks up low frequency sound?
the apex
Collagen types: most abundant protein in human body
collagen
Collagen types: collagen primarily found in basement membrane and basal
lamina
type IV. "under the floor"
Collagen types: collagen type primarily found in cartilage
type II. "carTWOlage"
Collagen types: collagen type primarily found in bone
type I. "bONE"
Collagen types: Reticulin found in skin, blood vessels, uterus, fetal tissue, and
granulation tissue
type III.
Collagen types: Collagen type X is found primarily in -----.
epiphyseal plate
Epidermis layers: What are the layers of the epidermis from surface to base?
stratum corneum, stratum lucidum (in thick skin), stratum granulosum,
stratum spinosum, stratum basalis. "Californians Like Girls in String Bikinis"
Epithelial cell junctions: This type of junction is also called the zona
occludens. (occludes diffusion across intracellular space)
tight junction
Epithelial cell junctions: Forming a perimeter just below the tight junction,
the zona adherens (intermediate junction) is composed of ------ and -----filaments.
e-cadherin & actin filaments
Epithelial cell junctions: Desmoplakin and ----- filaments are a part of the
desmosome, also called the ----- ------.
keratin. Macula adherens
Epithelial cell junctions: Structures that allow adjacent cells to communicate
for electric and metabolic purposes.
gap junction
Epithelial cell junctions: These structures connect cells to underlying
extracellular matrix. Integrins are found in these structures.
hemidesmosome
Glomerular basement membrane: The glomerular basement membrane is
formed from fused endothelial and podocyte basement membranes and coated
with ---- (pos / neg) charged ------ ------.
negatively charged heparan sulfate
Glomerular basement membrane: Responsible for filtering plasma according
to ----- and ----.
charge & size.
Glomerular basement membrane: In Nephrotic syndrome, Negative charge is
lost. That's why plasma -----, which are negatively charged, are lost in the
urine as a consequence.
protein
Glomerular basement membrane: Principle antigen presenting cell of
epidermis
Langerhans cell
Cilia structure: what is the arrangement of microtubules?
9+2
Cilia structure: what is dynein?
An ATPase that links peripheral 9 doublets and causes bending of cilium by
differential sliding of doublets
Cilia structure: what happens in Kartagener's syndrome?
due to a dynein arm defect, resulting in immotile cilia
Nissl bodies: What are nissl bodies?
RER in neurons, not found in axon or axon hillock
Nissl bodies: What do nissl bodies synthesize?
enzymes (i.e. ChAT) and peptide neurotransmitters
Nissl bodies: AUTHOR
Nick Bernthal
Functions of Golgi/RER/SER: What is I-Cell Disease
Failure of golgi to add mannose-6-phos to lysosome proteins, causing their
secretion outside the cell (defect of golgi)
Functions of Golgi/RER/SER: name organelle of protein synthesis
Rough ER
Functions of Golgi/RER/SER: name organelle of protein transport
Golgi
Functions of Golgi/RER/SER: name organelle of N-oligodsaccharide addition
Rough ER
Functions of Golgi/RER/SER: name organelle of N-oligodsaccharide
modification
Golgi
Functions of Golgi/RER/SER: name organelle of proteoglycan assembly
Golgi
Functions of Golgi/RER/SER: name organelle of steroid synthesis and
detoxification of drugs and poisons
Smooth ER
Functions of Golgi/RER/SER: Mucus-secreting goblet cells of small intestine
and antibody secreting plasma cells are rich in ______ (organelle)
Rough ER
Functions of Golgi/RER/SER: Liver hepatocytes and steroid producing cells
of the adrenal cortex are rich in ______ (organelle)
Smooth ER (look at function two questions above)
Sinusoids: T or F: Liver sinusoids have basement membranes?
C2
Sinusoids: T or F: Spleen sinusoids have basement membranes?
True -- "barrel hoop" basement membranes line sinusoids
Sinusoids: Spleen sinusoids traverse the _______ pulp
Red
Sinusoids: Match: T-cells are in the red or white pulp
Red
Sinusoids: Match: B-cells are in the red or white pulp
White (within the follicles)
Pancreatic Cell Types: T or F: alpha cells make glucagon
True
Pancreatic Cell Types: T or F: B cells make somatostatin
False -- beta cells make insulin
Pancreatic Cell Types: T or F: delta cells make somatostatin
TRUE
Pancreatic Cell Types: Islet cells arise from what primordial structure
Pancreatic Buds
Adrenal Cortex and Medulla : Zona Glomerulosa makes ________
Aldosterone
Adrenal Cortex and Medulla : What zona makes the sex hormones
Zona reticularis
Adrenal Cortex and Medulla : What zona makes cortisol
Zona Fasciculata (remember GFR and "The Deeper you go, the sweeter it
gets" -- i.e. salt, sugar, sex
Adrenal Cortex and Medulla : What is the primary regulator of the zona
fasciculata
ACTH (direct) and CRH (indirect)
Adrenal Cortex and Medulla : What is the primary regulator of the zona
glomerulosa
Renin-Angiotensin
Adrenal Cortex and Medulla : what is the primary regulator of the zona
reticularis
ACTH (direct) and CRH (indirect)
Adrenal Cortex and Medulla : What is the most common tumor of the adrenal
medulla in adults
Pheochromocytoma
Adrenal Cortex and Medulla : What is the most common tumor of the adrenal
medulla in children
Neuroblastoma
Adrenal Cortex and Medulla : What is the main secretory product of the
medulla
Catecholamines
Adrenal Cortex and Medulla : What is the main secretory product of
Brunner's Glands and where do they reside
Secrete alkaline mucus and live in the submucosa of the duodenum
Lymph Nodes: Is a lymph node a primary or secondary lymphoid organ
Secondary
Lymph Nodes: What part of the lymph node is the site of B-cell localization
and proliferation
Follicle
Lymph Nodes: What is the function of the medulla
Communicate with efferent lymphatics and contain lymphocytes, plasma
cells, macs, and reticular cells
Lymph Nodes: The paracortex is the home of ____ cells
T-cells
Lymph Nodes: What is the name of the syndrome associated with
disfunctional paracortex
DiGeorge's Syndrome
Lymph Nodes: What tissue is responsible for IgA secretion in the gut?
Peyer's patch (Think IgA -- Intra-Gut Antibody) -- Stimulated B-cells from
Peyer's secrete IgA into the lumen
Lumbar Puncture: At what level should one perform a lumbar puncture?
Between L4 and L5 (to keep the cord alive, keep the needle between L3 and
L5)
Lumbar Puncture: What structures are pierced?
Skin, Ligaments, Epidural space, Dura, Subdural Space, Arachnoid,
Subarachnoid (CSF) (NOTE: pia is NOT pierced)
Nerve Injury: Injury to what nerve causes loss of dorsiflexion of foot
common peroneal (L4-S2) (PED = Peroneal Everts and Dorsiflexes)
Nerve Injury: Injury to what nerve causes loss of plantar flexion
tibial (L4-S3) (TIP = Tibial Inverts and Plantarflexes; if injured, can't stand
on TIPtoes)
Nerve Injury: Loss of Knee Jerk?
Femoral (L2-L4)
Nerve Injury: Loss of hip adduction?
Obturator (L2-L4)
Nerve Injury: In adults, where does the spinal cord end?
L1-L2
Nerve Injury: Where does the subarachnoid space end?
S2
Nerve Injury: divide the 31 spinal nerves into their divisions
8Cs, 12Ts, 5Ls, 5Ss, 1 coccygeal
CNS/PNS Supportive Cells: What cell is responsible for physical support and
repair, as well as K+ metabolism
astrocytes
CNS/PNS Supportive Cells: what are the phagocytic cells of the nervous
system
microglia
CNS/PNS Supportive Cells: what cells produce myelin in the CNS
oligodendricytes
CNS/PNS Supportive Cells: what cells produce myelin in the PNS
Schawnn cells
Blood Brain Barrier : What three structures form the BBB
Choroid plexus epithelium, Intracerebral capillary endothelium, Arachnoid
(remember CIA)
Blood Brain Barrier : Do nonpolar/lipid soluble substances or polar,
water-soluble substances pass through the BBB more easily?
Nonpolar/lipid soluble
Blood Brain Barrier : Why is L-dopa, not dopamine, the treatment of choice
in Parkinson's Disease
L-dopa crosses the BBB
Hypothalamus: What are the functions of the hypothalamus (7)
Thirst, Adenohypophysis control, Neurohypophysis hormone synthesis,
Hunger, Autonomic regulation (including circadian rhythms), Temperature
regulation, Sexual urges (TAN HATS)
Hypothalamus: Does the anterior hyporthalamus control cooling when hot?
Yes, think Anterior Cooling = A/C
Hypothalamus: Does the posterior hypothalamus control heat conservation?
Yes, think no Posterior hypothalamus = poikilotherm (cold blooded snake)
Hypothalamus: Which nucleus is responsible for hunger?
Lateral nucleus
Hypothalamus: Which nucleus is responsible for satiety?
ventromedial nucleus (without which you grow ventrally and medially
Posterior Pituitary: Which nuclei of the hypothalamus project axons into the
posterior pituitary?
supraoptic nuclei (ADH) and paraventricular nuclei (oxytocin)
Functions of Thalamic Nuclei: What is the function of the lateral geniculate
nucleus?
Visual pathway (remember Lateral is needed to Look)
Functions of Thalamic Nuclei: What is the function of the medial geniculate
nucleus?
Auditory pathway (remember Medial is to hear Music)
Functions of Thalamic Nuclei: Function of the ventral posterior nucleus,
lateral part (VPL)?
receives body senses (proprioception, pressure, pain, touch, vibration)
Functions of Thalamic Nuclei: Function of the ventral posterior nucleus,
medial part (VPM)?
receives facial sensations, including pain
Functions of Thalamic Nuclei: Ventral Nuclei (VA/VL) functions?
Motor
Limbic System: What are the functions of the limbic system?
Feeding, Fighting, Feeling, Flight, and Sex (the five Fs)
Limbic System: What two areas does the hippocampus project to?
the subiculum (mammillary nuclei) and the septal area
Limbic System: Trace the pathway from Mammillary body to hippocampus.
Mammillary body, anterior nucleus of thalamus, cyngulate gyrus, entorhinal
cortex, hipocampus
Limbic System: AUTHOR
Conor Liston
Basal ganglia: Describe the primary function fo the basal ganglia.
The basal ganglia mediates voluntary movements and postural adjustments
Basal ganglia: What are the roles of the direct and indirect pathways?
Indirect pathway inhibits movement; Direct pathway facilitates movement.
Basal ganglia: Delineate the flow of processing in the direct pathway.
Putamen (inhibitory) => Gpi (inhibitory) => Thalamus: inhibition of Gpi =>
activation of thalamus
Basal ganglia: Delineate the flow of processing in the indirect pathway.
Putamen (inhibitory) => GPe (inhibitory) => STN (excitatory)=>GPi
(inhibitory) =>Thalamus; induces excitation of Gpi => inhibition of thalamus
Basal ganglia: What is the anatomical defect in Parkinson's Dz?
Loss of substantia nigra pars compacta (SNc) dopamine output to putamen
=> activation of indirect pathway and inhibition of direct pathway
Chorea: What is the clinical presentation and cause of chorea?
sudden, jerky, purposeful movements; caused by basal ganglia lesionChorea=
dancing, think choreography
Athetosis: What is the clinical presentation and cause of athetosis?
slow, writhing movements, especially of fingers; caused by basal ganglia
lesion
Hemiballismus: What is the clinical presentation of hemiballismus?
sudden, wild flailing of 1 arm; half ballistic= as in throwing a baseball
Hemiballismus: What is the anatomical defect in hemiballismus?
contralateral subthalamic nucleus lesion
Cerebral cortex functions: Where is the primary sensory cortex (S1) located?
anterior aspect of parietal lobe
Cerebral cortex functions: Where is the primary motor cortex (M1) located?
posterior aspect of frontal lobe
Cerebral cortex functions: Where is the primary visual cortex (V1) located?
most posterior aspect of occipital lobe
Cerebral cortex functions: What are the Brodman's Area designations for S1,
M1, V1?
S1: 3, 1, 2; M1: 4; V1: 17
Cerebral cortex functions: What is the role of Broca's area? where is it
located?
inferior aspect of frontal lobe; mediates motor speech (production)
Cerebral cortex functions: What is the role of Wernicke's area? Where is it
located?
superior temporal gyrus; mediates speech comprehension
What is a consequence of a lesion in:: Broca's area?
motor (expressive, nonfluent) aphasia; BROca's BROken speech
What is a consequence of a lesion in:: Wernicke's area?
sensory (fluent, receptive) aphasia; Wernicke is Wordy but makes no sense
What is a consequence of a lesion in:: Arcuate fasciculus?
conduction aphasia: poor repetition w/ good comprehension and fluent speech
What is a consequence of a lesion in:: Amygdala?
Kluver-Bucy syndrome: hyperorality, hypersexuality
What is a consequence of a lesion in:: Right parietal lobe?
spatial neglect syndrome (contralateral)
What is a consequence of a lesion in:: Mammillary bodies?
Wernicke-Korsakoff's encephalopathy: anterograde amnesia (think
alcoholism)
What is a consequence of a lesion in:: Cerebellar vermis?
Truncal ataxia and dysarthria
What is a consequence of a lesion in:: Cerebellar hemisphere?
Limb ataxia and intention tremor
What is a consequence of a lesion in:: Reticular activating system?
Coma
Cavernous sinus: Name five nerves and one vessel that pass through the
cavernous sinus.
CN III, IV, V1, V2, VI; internal carotid artery
Foramina: middle cranial fossa (CN II-VI): Name three structures passing
through optic canal (one nerve, two vessels).
CN II, ophthalmic artery, central retinal vein
Foramina: middle cranial fossa (CN II-VI): Name five structures passing
through superior orbital fissure (four nerves, one vessel).
CN III, IV, V1, VI; ophthalmic vein
Foramina: middle cranial fossa (CN II-VI): Name the foramina of exit for
each division of the trigeminal nerve (CN V).
Standing Room Only: V1 = Superior orbital fissure; V2 = foramen
Rotundum; V3 = foramen Ovale
Foramina: posterior cranial fossa (CN VII-XII): Name four structures passing
through the jugular foramen (three nerves, one vessel).
CN IX, X, XI; jugular vein
Foramina: posterior cranial fossa (CN VII-XII): Name structures passing
through foramen magnum.
brain stem, vertebral arteries, spinal roots of CN XI
Foramina: posterior cranial fossa (CN VII-XII): Name two nerves passing
through internal auditory meatus.
CN VII, VIII
Extraocular muscles and nerves: Describe the innervation of the extraocular
muscles.
LR6SO4R3 : Lateral Rectus = CN VI, Superior Oblique = CN IV, and the
Rest are CN III
Pupillary light reflex: List in sequence the nerves, brain structures, and
muscles involved in the pupillary light reflex from illumination of one eye to
bilateral pupillary constriction.
Light => retina => optic nerve => optic chiasm => optic tract => prectectal
nuclei (synapse) => Edinger-Westphal nuclei (synapse) => oculomotor nerve
=> ciliary ganglion (synapse) => pupillary constrictor muscles
Internuclear ophthalmoplegia: What is the characteristic lesion in internuclear
ophthalmoplegia?
destruction of the medial longitudinal fasciculus (MLF) => medial rectus
palsy on attempted lateral gaze
Internuclear ophthalmoplegia: Name three characteristic clinical features of
internuclear ophthalmoplegia.
1. On attempted lateral gaze, contralateral eye fails to abduct past midline; 2.
Contralateral nystagmus on attempted lateral gaze; 3. Normal convergence
Internuclear ophthalmoplegia: What neurologic disease is commonly
associated with internuclear ophthalmoplegia (aka MLF syndrome)?
multiple sclerosis; think MLF = MS
Visual field deficit with lesion: Name the visual field defect associated with a
lesion of each of the following structures:
0
Visual field deficit with lesion: Right optic nerve
Right anopsia
Visual field deficit with lesion: Optic chiasm
Bitemporal hemianopsia
Visual field deficit with lesion: Rigth optic tract
Left homonymous hemianopsia
Visual field deficit with lesion: Right Meyer's loop (temporal lesion)
Left uper quadrantic anopsia
Visual field deficit with lesion: Right Meyer's loop (parietal lesion)
Left lower quadrantic anopsia
Visual field deficit with lesion: Dorsal optic radiation
Left hemianopsia with macular sparing
Cranial nerves: Classify each cranial nerve (1-12) according to its function as
a sensory nerve, a motor nerve, or both.
Mnemonic: Some Say Marry Money But My Brother Says Big Brains Matter
Most
Cranial nerves: Name the cranial nerves that innervate the eye muscles.
Oculomotor (III), Trochlear (IV), and Abducens (VI)
Cranial nerves: Name the cranial nerves that innervate the facial muscles
(extraocular muscles excluded).
Trigeminal (V): mastication; Facial (VII): facial movement
Cranial nerves: Name the cranial nerves associated with sight, smell, hearing,
and taste.
sight: optic (II); smell: olfactory (I); hearing: vestibulocochlear (VIII); taste:
facial (VII) for ant. 2/3 of tongue and glossopharyngeal (IX) for post 1/3
Cranial nerves and passageways: Which cranial nerves pass through the
superior orbital fissure?
III, IV, V1, VI
Cranial nerves and passageways: Which cranial nerves pass through the
internal auditory meatus?
VII, VIII
Cranial nerves and passageways: Which cranial nerves pass through the
jugular foramen?
IX, X, XI
Brain stem anatomy: Which cranial nerves exit the brainstem caudal to the
pons?
Cranial nerves VI through XII
Brain stem anatomy: Which cranial nerves exit the brainstem rostral to the
pons?
Cranial nerves I through V
Brain stem anatomy: Which cranial nerves are associated with the
cerebellopontine angle?
CN VII, VIII, and IX
Dural venous sinuses: What is the main location of CSF return via the
arachnoid granulations?
superior sagittal sinus
Dural venous sinuses: Describe the route of CSF from the superior sagittal
sinus to the internal jugular vein.
superior sagittal sinus => confluence of sinuses => transverse sinus =>
sigmoid sinus => internal jugular vein (via jugular foramen)
Dural venous sinuses: Which three sinuses combine to form the confluence of
sinuses?
superior sagittal sinus, straight sinus, occipital sinus
Dural venous sinuses: AUTHOR
Steve Dong
Homounculus : Homunculus is the topographical representation of the body
that exists in what 2 areas of the cerebral cortex?
Sensory and Motor areas
Homounculus : Sensation for ____(What part of the body) is generally
located superior medially on the primary sensory cortex while ____ is located
more laterally
Lower limbs, Head and neck
Homounculus : Lesion at the anterior cerebral artery will canse deficit in
sensation or movement in which part of the body?
Lower limbs
Circle of Willis : Which artery supplies the medial surface of the brain,
leg-foot area of motor and sensory cortices?
Anterior cerebral artery
Circle of Willis : If you suspect a lesion in both Broca's and Wernecke's
areas, a lesion in which artery could be the cause?
Middle cerebral artery
Circle of Willis : At which artery in the circle of willis is the most common
place of aneurysm? You often see visual symptoms
Anterior communicating artery
Circle of Willis : This is also another common area of aneurysm. aneurysm
causes CN III palsy
Posterior communicating artery
Circle of Willis : This artery comes off of middle cerebral artery and supply
internal capsule, caudate, putamen, globus pallidus
Lateral Striate
Circle of Willis : In general, in stroke of anterior circle you would see what
kind of deficits?
Sensory and motor dysfunction, aphasias
Circle of Willis : how will a stroke of posterior circle will manifest?
Cranial nerve deficits, (vertigo, visual deficit), coma, cerabellar deficints
(ataxia).
Sounds : You would ask the patient to say this to test CN X (vagus)
Kuh-kuh-kuh
Sounds : "La la la" tests which CN?
XII - Hypoglossal (innervation of the tongue)
Sounds : "Mi mi mi" tests which CN?
VII - Facial (innervation of lips)
Vagal nuclei : This nuclei confers visceral Sensory information (eg: taste, gut
distension)
Nucleus Solitarius (VII, IX, X)
Vagal nuclei : Nucleus aMbiguus confers Motor innervation of what part of
the body?
pharynx, larynx, and uper esophagus (IX, X, XI)
Vagal nuclei : This nucleus sends parasympathetic fibers to the heart, lungs,
and upper GI
Dorsal motor nucleus
Play this game: Where is the Lesion?? : patient's tongue deviates to the left
left CN XII
Play this game: Where is the Lesion?? : Patient's jaw deviates toward the left
left CN V
Play this game: Where is the Lesion?? : patient tends to fall toward the left
side
left lesion of the cerebellum
Play this game: Where is the Lesion?? : Patient's uvula deviate to the left
right CN X lesion
Play this game: Where is the Lesion?? : Patient's shoulder droop on the left
left CN XI lesion
Play this game: Where is the Lesion?? : Patient has weakness turning head to
the left
right CN XI lesion
Herniation syndromes: Which of the following herniations can cause
compression on the brain stem that can result in coma and death? 1. Cingulate
herniation 2. Transtentorial herniation 3. Uncal herniation 4. Cerebellar
tonsillar herniation
1 herniates under the falx cerebri and does not cause coma and death. 2.
Transtectoral, 3. Uncal, and 4. tonsillar herniations can
Uncal herniation can cause the following clinical signs, name their causes: 1.
Ipsilateral dilated pupil, ptosis
Stretching of CN III
Uncal herniation can cause the following clinical signs, name their causes: 2.
Contralateral homonymous hemianopsia
Compression of ipsilateral posterior cerebral artery
Uncal herniation can cause the following clinical signs, name their causes: 3.
Ipsilateral paresis
Compression of contralateral crus cerebri (Kernohan's notch)
Uncal herniation can cause the following clinical signs, name their causes: 4.
Duret hemorrhage
Caudal displacement of brain stem
Spinal Cord : The dorsal columns have 2 tracts. The Fasciculus ____ carries
nerve fibers for _____(part of the body). The fasciculus ____ carries tract
from ____ (part of the body)
Cuneatus, uper body and extremities. Gracilis, lower body and extremities
Spinal Cord : The lateral cortical spinal tract carries what type of fibers, and
how are they arranged in the spinal cord?
motor fibers, arms medially, legs laterally
Spinal Cord : What tract carries pain and temperature sensation? Where is it
located on the spinal cord?
Spinal Thalamic tract, ventral part
Play this game: Where is the Lesion?? Pt II Ill name its common location on
the spinal cord, you name the disease: in grey matter, affect lower motor
neuron only, cause flaccid paralysis
Poliomyelitis / Werdnig-Hoffmann disease
Play this game: Where is the Lesion?? Pt II Ill name its common location on
the spinal cord, you name the disease: Mostly white matter of Cervical
region, lesion are asymmetric and random
Multiple sclerosis
Play this game: Where is the Lesion?? Pt II Ill name its common location on
the spinal cord, you name the disease: grey matter, and motor tracts: upper
and lower motor neuron deficits
Amyotrophic Lateral Sclerosis
Play this game: Where is the Lesion?? Pt II Ill name its common location on
the spinal cord, you name the disease: everywhere, but spares the dorsal
columns
Ventral artery occlusion
Play this game: Where is the Lesion?? Pt II Ill name its common location on
the spinal cord, you name the disease: dorsal column, impairs propioception
and causes locomotor ataxia
Tabes dorsalis (tertiary syphilis)
Play this game: Where is the Lesion?? Pt II Ill name its common location on
the spinal cord, you name the disease: Dorsal column, lateral corticospinal
tracts and spinocerebellar tracts
Vitamin B12 Neuropathy/Friedreich's ataxia
Play this game: Where is the Lesion?? Pt II Ill name its common location on
the spinal cord, you name the disease: central white commisure and ventral
horns
Syringomyelia
Brown Sequard Syndrome, UMN, LMN, Facial Lesions : Mr.
Brown-Sequard was struck on the spinal cord that resulted in the hemisection
of the spinal cord at T3 level. Give me 4 symptoms that you may find in him
1. Ipsilateral motor paralysis 2. Ipsilateral loss of tactile, vibration,
proprioception senses 3. Contralateral pain and temperature loss 4. Ipsilateral
loss of ALL sensation at the T3 level
Brown Sequard Syndrome, UMN, LMN, Facial Lesions : What are the signs
of Lower Motor neuron lesion?
everything lowered: ↓ muscle mass, ↓ muscle tone, ↓ reflexes, downgoing
toes
Brown Sequard Syndrome, UMN, LMN, Facial Lesions : What are the signs
of Upper Motor neuron lesion?
Uper = everything up (tone, DTRs, toes)
Brown Sequard Syndrome, UMN, LMN, Facial Lesions : Upper motor
neuron lesion of the face motor deficit
causes contralateral weakness of lower face only
Brown Sequard Syndrome, UMN, LMN, Facial Lesions : Lower motor
neuron lesion of the facial nerve
weakness of both uper and lower face seen
Brown Sequard Syndrome, UMN, LMN, Facial Lesions : A patient comes in
with facial paralysis and inability to close the eye on one side of the face,
suggesting Bell's Palsy. What diseases might you see in him that could have
caused his condition?
ALexanger Bell with STD: AIDS, Lyme, Sarcoid, Tumors, Diabetes
Brown Sequard Syndrome, UMN, LMN, Facial Lesions : Upper motor
neuron lesion coming from the facial nucleus result in what?
contralateral paralysis of lower quadrant
Spinal muscle control : What is the difference between alpha and gamma
motor neurons?
alpha fibers participates in the reflex arc and cause extrafusal contraction.
Gamma neurons are stimulated by CNS to contract intrafusal fiber to increase
sensitivity of reflex arc
Brachial Plexus : What are the 5 divisions/parts of the bracial plexus?
Roots Trunks Divisions Cords Branches (Randy Travis Drinks Cold Beer)
Play this game: Where is the Upper Limb nerve Lesion??: Claw hang
Trunk of C8 and T1
Play this game: Where is the Upper Limb nerve Lesion??: Wingled Scapula
Long thoracic nerve
Play this game: Where is the Upper Limb nerve Lesion??: Decreased thumb
function, Pope's blessing
Play this game: Where is the Upper Limb nerve Lesion??: Patient comes into
the ER with trauma injury that broke his humerus bone. Two weeks later
when you examined him, you noticed that his wrist is dropped. Neuro exam
showed that the triceps and brachioradialis reflexes of the same arm are
absent.
What
wasLimb
the injured
nerve? Patient has lost
Play this game: Where
is the
Upper
nerve Lesion??:
power of his arm muscles. He could not longer flex his wrist or fingers, and
has trouble with thumb movements. History showed that he broke his had a
suprecondylar fracture (of the humerus) What was the injured nerve?
Play this game: Where is the Upper Limb nerve Lesion??: Patient has clawed
hand. Exam showed that he has imparied wrist flexion and adduction,
impaired adduction of thumb and last 2 fingers. He also has lost of sensation
over medial palm and pinky finger. What was the injured nerve?
Play this game: Where is the Upper Limb nerve Lesion??: Patient dislocates
his shoulder and could no longer use his deltoid.
Play this game: Where is the Upper Limb nerve Lesion??: Patient could no
longer flex at his elbow joint and supination of his forearm is weakened.
Exam shows loss of biceps reflex and variable sensory loss of his forearm
Play this game: Where is the Upper Limb nerve Lesion??: Following a blow
to his shoulders, the patient presents with limb hanging by side (paralysis of
abductors), medially rotated (paralysis of lateral rotators), and protonated
forearm (loss of biceps)
median nerve
radial nerve (innervates BEST!) Brachioradialis, Extensors of wrist and
fingers, Supinator, and Triceps
median nerve
ulnar nerve
axillary nerve
musculocutaneous nerve
C5 and C6 roots. Known as Erb-Duchenne palsy
Thoracic Outlet Syndrome : Thoracic outlet syndrome leads to loss of the
compression of ____ artery and ____ trunk of brachial plexus
Subclavian, inferior (C8. T1)
Thoracic Outlet Syndrome : In thoracic outlet syndrome, when the patient
turn his head toward the opposite side, you notice the dissapearance of _____
(what physical finding?)
radial pulse
Thoracic Outlet Syndrome : What muscles would you expect to be atrophied
as a result of thoracic outlet syndrome?
thenar and hypothenar eminences, innterosseous
Thoracic Outlet Syndrome : What neurological symptoms would you see?
sensory deficits of medial side of forearm and hand
Clinical Reflexes: What nerve root do you test for if you illecit the following
reflexes?
0
Clinical Reflexes: nerve root: Biceps
C5
Clinical Reflexes: nerve root: Triceps
C7
Clinical Reflexes: nerve root: Patella
L4
Clinical Reflexes: nerve root: Achilles
S1
Clinical Reflexes: What is the Babinski reflex a sign of? When is it normal?
UMN lesion, its normal during 1st year of life
Intelligence testing: BIOCHEMISTRY
0
Chromatin: In mitosis, the negatively charged DNA condenses by wrapping
around…
nucleosomes
Chromatin: name the proteins nucleosomes are made of:
Histones: H2A, H2B, H3, H4
Chromatin: the structure that ties nucleosomes together to form chromatin:
H1 (another histone)
Chromatin: how long is a chromatin fiber?
30 nm
Chromatin: which one is transcriptionally active, heterochromatin or
euchromatin?
Euchromatin = true, active, less condensed, open Heterochromatin =
condensed, darker/more color, inactive (less open)
Nucleotides: the purines are
A and G -- Pure As Gold = Purines
Nucleotides: the pyrimidines are:
C, U, T -- CUT the PY -rimidines
Nucleotides: Which pair is stronger, G-C or A-T?
GC has 3 H bonds. AT has 2 bonds. (AT = 2 points in Scrabble, GC = 6
points -- GC wins!)
Nucleotides: significance of # of H bonds?
higher GC content, more H bonds, higher melting temperature
Nucleotides: guanine has this side group:
ketone
Nucleotides: thymine has this side group:
methyl -- thymine has methyl
Nucleotides: deamination of cytosine gives -->
Uracil -- remember U before C in CUT (see above)
Nucleotides: Nucleotides are held together by these bonds:
3'-5' phosphodiesterase bond
Transition vs. Transversion: substituting purine for purine, pyrimidine for
pyrimidine is call:
transition - staying inside the same class
Transition vs. Transversion: substituting purine for pyrimidine, vice versa
transversion - change from 1 type to another, 1 version to another version of
nucleotide
Genetic Code features: each codon specifies only 1 amino acid:
Unambiguous
Genetic Code features: more than 1 codon can code for the same amino acid:
Degenerate
Genetic Code features: all organisms have nonoverlapping, commaless
nucleotides except for:
viruses (are they really organisms? …)
Genetic Code features: name 4 organisms/structures where a different genetic
code is used:
mitochondria, archaeobacteria, Mycoplasma, some yeasts
Mutations in DNA: A silent mutation is…
when the base change (usually @ 3rd codon) does not change the aa, thanks
to the degenerate feature of the genetic code!
Mutations in DNA: what's worse, nonsense, missense, or silent?
nonsense > missense > silent
Mutations in DNA: what is a conservative mutation?
new amino acid is similar in structure (e.g. small vs. bulky, linear side chain
vs. rings)
Mutations in DNA: what is a missense mutation?
changed amino acid - e.g. Glu-->Val in sickle cell anemia
Mutations in DNA: what is a nonsense mutation?
early stop codon. Nonsense = No meaning, no aa.
Mutations in DNA: what happens if a frameshift mutation occurs?
the open reading frame is shifted so that all the nucleotides are misread -->
result is usually a truncated protein
Prokaryotic DNA replication and DNA polymerases: how many origins of
replications does a prokaryote (bacteria, viruses, plasmids) have?
1
Prokaryotic DNA replication and DNA polymerases: a primase makes…
RNA primer on which DNA polymerase initiate replication
Prokaryotic DNA replication and DNA polymerases: what is needed to
replicate DNA on the lagging strand?
Okazaki fragments
Prokaryotic DNA replication and DNA polymerases: DNA polymerase III action?
has 5'-->3' synthesis ability -- reaches the primer of preceding "O" fragment.
Also has 3'-->5' exonuclease proofreading ability!
Prokaryotic DNA replication and DNA polymerases: RNA primers are
degraded by:
DNA polymerase I
Prokaryotic DNA replication and DNA polymerases: the DNA fragments are
sealed by:
DNA ligase
Prokaryotic DNA replication and DNA polymerases: proofreading of the
DNA is done by:
DNA polymerase III
Prokaryotic DNA replication and DNA polymerases: What happens if there is
a supercoil of the DNA, ready to snap?
DNA topoisomerases -- create nick in the helix to relieve supercoils
Eukaryoyic DNA polymerases:: DNA polymerase alpha
replicates lagging strand and synthesizes RNA primers
Eukaryoyic DNA polymerases:: DNA repair is done by:
DNA polymerase beta and epsilon
Eukaryoyic DNA polymerases:: When mitochondria divide we need this to
replicate the mitochondrial DNA
DNA polymerase gamma
Eukaryoyic DNA polymerases:: This DNA polymerase replicates the leading
strand:
DNA polymerase delta
DNA repair : single strand: to remove a damaged base:
single-strand, excision repair-specific glycosylase
DNA repair : single strand: Endonuclease - action?
cleaves the DNA several bases to the 5' side
DNA repair : single strand: Exonuclease - action?
remove short stretches of nucleotide
DNA repair : single strand: What can happen if both strands are damaged?
repair --> recombination!
DNA repair defects: defective uvr ABC endonuclease --> thymidine dimers
seen in:
Xeroderma pigmentosum -- autosomal recessive, inability to repair thymidine
dimers which form when exposure to UV light
Directions: Direction of transcription and translation?
5' --> 3' ! (please BYOPhosphate from 5 to 3)
Directions: Direction of protein synthesis?
N to C - also 5 to 3
types of RNA: what is the largest RNA?
mRNA ( m = massive)
types of RNA: what is the most abundant RNA?
rRNA -- in ribosomes! R = Rampant
types of RNA: what is the smallest RNA?
tRNA -- T = Tiny
RNA polymerases: Whose RNA is all made with one enzyme, prokaryote or
eukaryote?
Prokaryote! RNA polymerase makes all 3 RNAs
RNA polymerases: RNA polymerases I, II, III (1, 2, 3) make (respectively):
RMT -- rRNA, mRNA, tRNA
RNA polymerases: RNA polymerase II has another talent with DNA:
can initiate chain by opening DNA at promoter site (AT rich upstream
sequences: TATA, CAAT)
RNA polymerases: alpha-amanitin - action?
inhibit RNA polymerase II
Start and Stop Codons: start codon:
AUG -- AUG inaugurates protein synthesis!
Start and Stop Codons: What does the start codon code for?
Methionine -- removed in eukaryotes; formyl-methionine in prokaryotes
Start and Stop Codons: Stop codons - how to remember?
UGA: U Go Away; UAA = U Are Away; UAG = U Are Gone
Regulation of gene expression: What happens if a promoter is mutated?
reduction in amount of gene transcribed -- this is where RNA polymerase and
other transcription factors bind to DNA upstream from gene locus
Regulation of gene expression: a stretch of DNA, far or near, that can alters
gene expression by binding transcription factors is called:
Enhancer
Regulation of gene expression: AUTHOR
Sarah Goldman
Introns vs. Exons: Which part of DNA is transcribed to mRNA?
Exons
Introns vs. Exons: _______ are intervening noncoding segments of DNA
Introns (INtrons stay IN the nucleus; EXons Exit and are EXpressed
Splicing of mRNA: ________ facilitate splicing by binding to primary
mRNA transcripts and forming spliceosomes
Small nuclear ribonucleoprotein particles (snRNP)
RNA processing (eukaryotes): Where does RNA processing occur?
In the nucleus
RNA processing (eukaryotes): What are the 3 steps of RNA processing,
following transcription?
1) caping on 5' end (7-methyl-G); 2) Polyadenylation on 3' end (200 A's); 3)
Splicing out of introns
RNA processing (eukaryotes): The initial transcript is called_________. The
capped and tailed transcript is called_______.
Heterogeneous nuclear RNA (hnRNA); mRNA
tRNA structure: True or false: The anticodon end of tRNA is opposite the 5'
end
False. The anticodon end is oposite the 3' aminoacyl end
tRNA structure: What codon is at the 3' end of all tRNAs?
CCA and chemically modified bases
tRNA structure: The amino acid is covalently bound to which end of the
tRNA?
3' end
tRNA charging: What enzyme scrutinizes the amino acid before and after it
binds to tRNA?
Aminoacyl-tRNA-sythetase (1 per amino acid, uses ATP)
tRNA charging: What happens if a tRNA is mischarged?
It reads the usual codon, but inserts the wrong amino acid.
tRNA Wobble: True or false: codons that differ in the 3rd position may code
for the same tRNA/amino acid
True. Accurate base pairing is required only in the first 2 nucleotide positions
of an mRNA codon; the 3rd position is the "wobble" position.
Protein synthesis: ATP vs. GTP: (a) ATP or (b) GTP is used in tRNA
charging?
(a) ATP (tRNA Activation)
Protein synthesis: ATP vs. GTP: What energy form is required for binding of
tRNA to the ribosome and for translocation?
GTP (tRNA Griping and Going places)
Polymerase chain reaction (PCR): What is the laboratory procedure used to
synthesize many copies of a desired fragment of DNA?
PCR
Polymerase chain reaction (PCR): What are the 3 steps of PCR?
Molecular biology techniques: Match the following techniques with the
appropriate interaction: Techniques: a) Southern blot; b)Northern blot;
c)Western blot; d)Southwestern blot Interactions: 1) DNA-RNA
hybridization; 2)Antibody-protein hybridizaton; 3) DNA-protein interaction;
4)DNA-DNA hybridization
Enzyme-linked immunosorbent assay (ELISA): What interaction is tested by
ELISA?
1) DNA denatured by heating into 2 separate strands; 2) Annealing of
premade DNA primers to a specific seqence of each strand, during cooling;
3)Heat-stable DNA polymerase replicates the DNA sequence following each
primer
a) Southern blot---4)DNA-DNA (Southern-Same) b)Northern
blot---1)DNA-RNA c)Western blot---2)Antibody-protein d)Southwestern
blot---3)DNA-protein interaction
antigen-antibody reactivity
Enzyme-linked immunosorbent assay (ELISA): What indicates a positive test
result?
An intense color reaction in the test solution
Modes of inheritance: What percentage of offspring from two carrier parents
are affected by an autosomal recessive trait?
0.25
Modes of inheritance: Which mode of inheritance is often due to defects in
structural genes, and affects many generations?
Autosomal dominant
Modes of inheritance: If a woman is heterozygous for an X-linked recessive
disorder, what is the chance that her son will be affected?
0.5
Modes of inheritance: True or False: Females heterozygous for an X-linked
trait may be affected by the disorder.
TRUE
Modes of inheritance: What mode of inheritance is transmitted only through
the mother? What are some examples of such disorders?
Mitochondrial inheritance; examples include Leber's hereditary optic
neuropathy and mitochondrial myopathies
Modes of inheritance: AUTHOR
Lee Kiang
Genetic Terms: Distinguish between variable expression and incomplete
penetrance
In variable expression, NATURE and SEVERITY of PHENOTYPE VARIES
amongst individuals. In incomplete penetrance not all individuals with mutant
GENOTYPE show mutant PHENOTYPE
Genetic Terms: Define pleiotropy
1 gene has > 1 effect on individual's phenotype
Genetic Terms: Angelman's syndrome is an example of _______.
Maternal imprinting. In imprinting, phenotype differs based on whether
mutation is maternal or paternal.
Genetic Terms: Give an example of Paternal imprinting
Prader-Willi syndrome
Genetic Terms: In Huntington's disease, severity worsens or age of onset
becomes earlier with successive generations. This phenomenon is
called________.
Anticipation
Genetic Terms: What is Loss of Heterozygosity, and in what situation does it
not apply?
With congenital or acquired mutation of tumor supressor gene, the
completement allele must be deleted/mutated before the development of Ca.
NOT TRUE with ONCOGENES.
Genetic Terms: When the body cannot produce enough normal gene product
with only one functional allele, there is a ______mutation. An example is the
mutation COL1A1 in the disease _________.
Dominant negative mutation; Osteogenesis Imperfecta.
Genetic Terms: Define Linkage Disequilibrium
Tendency for certain alleles at 2 linked loci to occur together more often than
expected by chance. Measured in a population, not within a family; varies
among pops.
Genetic Terms: When cells in the body have a different genetic makeup, this
is ________.
Mosaicism
Hardy-Weinberg population genetics: For a population in Hardy-Weinberg
equilibrium, where p and q are separate alleles, what is the heterozygote
prevalence?
Hardy-Weinberg equation for alleles p and q: p^2 + 2pq + q ^ = 1; p+q=1.
The heterozygote prevalence is 2pq
Hardy-Weinberg population genetics: The Hardy-Weinberg law assumes 4
criteria. List them.
1. No mutation at the locus; 2. No selection for any genotypes at the locus; 3.
Mating completely random; 4. No migration into/out of population being
considered
Genetic Errors: What is a main risk factor for Trisomy 21?
Down syndrome=Trisomy 21. Prevalence 1:800, increased risk with
advanced maternal age.
Genetic Errors: Name 3 genetic diseases that involve mental retardation
Down Syndrome, Fragile-X, Phenylketonuria
Genetic Errors: The mechanism of this disease involves failure to express
gene-encoding RNA binding protein, due to progressive expansion of
unstable DNA
Fragile X-associated mental retardation
Genetic Errors: A single missense mutation in beta globin, conferring
susceptibility to infections, painful crises
Sickle Cell anemia, 1:400 African-Americans
Genetic Errors: Name 3 characteristics of the CF phenotype
Recurrent pulmonary infection, exocrine pancreatic insufficiency, infertility.
Genetic Errors: Characterized by café-au-lait spots, neurofibromas, increased
tumor susceptibility- what is this, and what is the inheritance?
Neurofibromatosis, prevalence 1:3000. AD, with 50% new mutations
Genetic Errors: Name two X-linked genetic errors
Fragile X, Duchenne's muscular dystrophy
Genetic Errors: Characterized by increased susceptibility to fractures,
connective tissue fragility:
Osteogenesis Imperfecta
Genetic Errors: Phenotype of Phenylketonuria
Mental and growth retardation.
Trinucleotide repeat expansion diseases: Name 4 trinucleotide repeat
expansion diseases
Freidreich's ataxia, Huntington's chorea, mytotonic dystrophy, fragile X
syndrome
Lysosomal Storage Diseases: What are the two categories of lysosomal
storage diseases?
1. Sphingolipidoses; 2. Mucopolysaccharidoses
Lysosomal Storage Diseases: In _______disease, a deficiency of
alpha-galactosidase A results in the clinical finding of _____.
Fabry's disease; Renal Failure.
Lysosomal Storage Diseases: What are the manifestations of the AR disease
leading to accumulation of galactocerebroside in the brain?
Krabbe's disease. Optic Atrophy, spasticity, early death.
Lysosomal Storage Diseases: This disease leads to glucocerebroside
accumulation in 4 sites, and has characteristic "crinkled paper" cells.
Gaucher's disease. Glucocerebroside accumulation in brain, liver, spleen,
bone marrow. Gaucher's cells have "crinkled paper" apearance with enlarged
cytoplasm.
Lysosomal Storage Diseases: Match: Galactocerebroside accumulation,
Glucocerebroside accumulation to Gaucher's, Krabbe's
galaKto = Krabbe. GlUco=GaUcher's.
Lysosomal Storage Diseases: AR disease with buildup of sphingomyelin and
cholesterol in reticuloendothelial and parenchymal cells and tissues
Niemann-Pick disease. "NoMAN PICKs his nose with his sphinger"
Lysosomal Storage Diseases: In _______disease, a deficiency of the enzyme
_______results in a cherry-red spot on the macula and death by age 3.
Tay-Sachs disease. "Tay-saX lacks heXoaminidase"
Lysosomal Storage Diseases: Carrier rate for Tay-Sachs in Jews of European
Descent
1 in 30
Lysosomal Storage Diseases: What is Metachromatic Leukodystrophy?
Deficiency of arylsulfatase A results in accumulation of sulfatide in brain,
kidney, liver and peripheral nerves.
Lysosomal Storage Diseases: What are the two mucopolysaccharidoses?
Hurler's and Hunter's syndromes
Lysosomal Storage Diseases: Inheritance of Hurler's syndrome, clinical
manifestation:
AR, alpha-L-iduronidase results in corneal clouding, mental retardation.
Lysosomal Storage Diseases: Inheritance of Hunter's, clinical manifestation:
X-linked Recessive. "Hunters aim for the X" Deficiency of iduronate
sulfatase- a milder form of Hurler's with no corneal clouding and with MILD
mental retardation.
Lysosomal Storage Diseases: AUTHOR
Ronnie Gurevich
Enzyme kinetics: Km = ___ at 1/2 Vmax
[S]
Enzyme kinetics: what is the relationship between affinity and Km?
inverse correlation (lower Km = higher affinity)
Enzyme kinetics: when adding a competitive inhibitor: what happens to
Vmax and Km
Vmax is unchanged; Km is increased
Enzyme kinetics: when adding a non-competitive inhibitor: what happens to
Vmax and Km
Vmax is decreased; Km is unchanged
Enzyme regulation methods: name 5 methods by which enzyme activity is
regulated
1. concentration alteration; 2. covalent modification; 3. proteolytic
modification; 4. allosteric regulation; 5. transcriptional regulation
Cell cycle phases: name the 5 phases of the cell cycle
G1= growth, S = DNA synthesis, G2 = growth, Go = quiescent G1 stage, M=
mitosis "G stands for Gap/Growth, S stands for synthesis"
Cell cycle phases: which parts of the cell cycle are considered INTERPHASE
G1, S, G2
Cell cycle phases: what phase is usually the shortest? what phase is shortened
in rapidly dividing cells?
M; G1 (duration varies)
Cell cycle phases: what phase are most cells in
G0
Plasma membrane composition: what is the percentage of cholesterol in the
cell membrane? Phospholipids?
~ 50% each
Plasma membrane composition: which side of the membrane are glycosylated
lipids on?
the noncytoplasmic
Phosphatidylcholine function: phosphatidylcholine (lecithin) is a major
component of___ (list 4)
RBC membranes, myelin, bile, surfactant (DpC).
Phosphatidylcholine function: what does phosphatidylcholine esterify
cholesterol
Na-K-ATP pump: on what side of the cell membrane is the ATP pump
phosphorylated (by ATP)
the cytoplasmic
Na-K-ATP pump: what is the ion exchange that goes on?
3 Na out; 2 K in
Na-K-ATP pump: what is a pump inhibitor that binds to the K site?
Ouabain
Na-K-ATP pump: how do cardiac glycosides work?
(digoxin, digitoxin). They bind to the Na-K-ATP pump and increase cardiac
contractility
G protein linked 2nd messengers : what is the G protein class and main
function of the alpha1 receptor
class q; increase smooth muscle contraction
G protein linked 2nd messengers : what is the G protein class and main
function of the alpha 2 receptor
class i; decrease sympathetic outflow, decrease insulin release
G protein linked 2nd messengers : what is the G protein class and main
function of the beta1 receptor
class s; increase: heart rate, contractility, renin release, lipolysis, aqueous
humor production
G protein linked 2nd messengers : what is the G protein class and main
function of the beta 2 receptor
class s; vasodilation, bronchodilation, increase glucagon release
G protein linked 2nd messengers : what is the G protein class and main
function of the M1 receptor
class q; CNS
G protein linked 2nd messengers : what is the G protein class and main
function of the M2 receptor
class i; decrease heart rate
G protein linked 2nd messengers : what is the G protein class and main
function of the M3 receptor
class q; increase exocrine gland production
G protein linked 2nd messengers : what is the G protein class and main
function of the D1 receptor
class s; relax renal vascular smooth muscle
G protein linked 2nd messengers : what is the G protein class and main
function of the D2 receptor
class i; modulates transmitter release, especially in the brain
G protein linked 2nd messengers : what is the G protein class and main
function of the H1 receptor
class q; increase nasal and bronchial mucous production, contraction of
bronchioles, pruritis, pain
G protein linked 2nd messengers : what is the G protein class and main
function of the H2 receptor
class s; increase gastric acid secretion
G protein linked 2nd messengers : what is the G protein class and main
function of the V1 receptor
class q; increase vascular smooth muscle contraction
G protein linked 2nd messengers : what is the G protein class and main
function of the V2 receptor
class s; increase water permeability and reabsorption in the collecting tubules
G protein linked 2nd messengers : how does Gq work?
stimulates phospholipase C which causes cleavage of PIp 2.
G protein linked 2nd messengers : how does Gs work?
binds to adenylcyclase which converts ATP--> cAMP
G protein linked 2nd messengers : how does Gi work?
by inhibiting adenylcyclase
G protein linked 2nd messengers : what do the 2 products of PIp 2 do?
Ip 3 increases intracellular [Ca] DAG activates protein kinase C
arachadonic acid products: name the enzyme that liberates AA from the cell
membrane
phospholipase A2
arachadonic acid products: what does the lipoxygenase pathway yield
leukotrienes (L for Lipoxygenase and Leukotrienes)
arachadonic acid products: LTB4 is a____
neutrophil chemotactic agent
arachadonic acid products: which leukotrienes are involved in
bronchoconstriction, vasoconstriction, smooth muscle contraction, and
increased vascular permeability
LT C4, D4, E4 (SRS-A)
arachadonic acid products: what are the 3 products of the cyclooxygenase
pathway?
thromboxane, prostacyclin, prostaglandin
arachadonic acid products: what are the 2 functions of TxA2
platelet aggregation, vasoconstricion
arachadonic acid products: what are the 2 functions of PGI2
inhibition of platelet aggregation; vasodilation (Platelet Gathering Inhibitor)
microtubule: what are the shape and dimensions of a microtubule?
cylindrical, 24 nm in diameter, variable length.
microtubule: what are the components of a microtubule
polymerized dimers of alpha and beta tubulin (+2 GTPs per dimer)
microtubule: where are microtubules found
cilia, flagella, mitotic spindles, neuronal axons (slow axoplasmic transport)
microtubule: antihelminthic drug that acts on microtubules
mebendazole/thiabendazole
microtubule: anti breast cancer drug that acts on microtubules (prevent
disassembly)
taxol
microtubule: antifungal drug that acts on microtubules
griseofluvin
microtubule: anti cancer drug that acts on microtubules (prevent assembly)
vincristine/vinblastine
microtubule: anti gout drug that acts on microtubules
cholchicine
collagen synthesis and structure: hydroxylation of specific prolyl and lysyl
residues in the ER requires ____
vitamin C
collagen synthesis and structure: how is collagen synthesized form
procollagen
procollagen is exocytosed into the EC space, and cleaved by procollagen
peptidase to make tropocollagen which aggregates to form collagen fibrils.
collagen synthesis and structure: what is the function of lysine-hydroxylysine
in collagen
it cross links tropocollagen and reinforces the fibrillar structure of collagen
collagen synthesis and structure: a collagen fibril is made of many stagggered
collagen molecules. What is a collagen molecule made of?
3 collagen alpha chains, usually Gly-X-Y. X and Y- proline, hydroxyproline,
hydroxylysine)
Ehlers-Danlos syndrome: in this disease, faulty collagen synthesis causes
what 3 things
1. Hyperextensible skin; 2, tendency to bleed; 3. Hypermobile joints
Ehlers-Danlos syndrome: what is the genetic inheritance of type IV EDS
autosomal dominant
Ehlers-Danlos syndrome: what is the genetic inheritance of type VI EDS
autosomal recessive
Ehlers-Danlos syndrome: what is the genetic inheritance of type IX EDS
x linked
Ehlers-Danlos syndrome: what type of cerebral vascular disorder is EDS
associated with
berry aneurysms
Osteogenesis imperfecta: brittle bone disease causes____
multiple fractures w/ minimal trauma
Osteogenesis imperfecta: blue sclera is due to ______
translucency of the connective tissue over the choroid
Osteogenesis imperfecta: what is the main pathology in OI
genetic defect in collagen synthesis
Osteogenesis imperfecta: what is the most common form of OI
autosomal dominant with abnormal type I collagen
Osteogenesis imperfecta: the presentation of a child with OI may be confused
with_____
child abuse
ATP: what are the units comprising ATP
adenine base; ribose sugar; 3 phosphoryls
ATP: what type of high energy bonds does ATP have
2 phosphoanhydride bonds, 7 kcal/mol each
ATP: how many ATPs are produced in aerobic glucose metabolism?
38 via malate shuttle; 36 via G3P shuttle
ATP: how many ATPs are produced in anaerobic glycolysis?
2
activated carriers: what is the active carrier of phosphoryls
ATP
activated carriers: what is the active carrier of electrons
NADH, NADPH, FADH2
activated carriers: what is the active carrier of acyl
coenzyme A, lipoamide
activated carriers: what is the active carrier of CO2
biotin
activated carriers: what is the active carrier of 1-C units
THF
activated carriers: what is the active carrier of methyl groups
SAM
activated carriers: what is the active carrier of aldehydes
Tp
activated carriers: what is the active carrier of glucose
UDP-glucose
activated carriers: what is the active carrier of choline
CDP-choline
S-adenosyl-methionine (SAM): what are the 2 components of SAM
ATP + methionine
S-adenosyl-methionine (SAM): what vitamin is SAM dependent on for
regeneration
B-12 (regenerates met)
S-adenosyl-methionine (SAM): what is the function of SAM
transfer methyl units ("SAM, the methyl donor man")
signal molecule precursors: what enzyme converts ATP --> cAMP
adenylate cyclase
signal molecule precursors: what enzyme converts GTP --> cGMP
guanylate cyclase
signal molecule precursors: what enzyme converts glutamate --> GABA
glutamate decarboxylase (with vit B 6)
signal molecule precursors: what enzyme converts choline --> ACh
choline acetyltransferase (ChAT)
signal molecule precursors: what enzyme converts arachidonic acid -->
prostaglandins, leukotrienes, thromboxanes
cyclooxygenase/lipoxygenase
signal molecule precursors: what enzyme converts fructose-6-P-->
Fructose-1,6-bis-P
phosphofructokinase (rate limiting step of glycolysis)
signal molecule precursors: what enzyme converts 1,3-BPG --> 2,3-BPG
bisphosphoglycerate mutase
NAD+/NADPH: it is used in catabolic processes to carry reducing
equivalents
NAD+ (--> NADH)
NAD+/NADPH: NADPH is used in (name 3)
1. anabolic process (suply reducing equivalents); 2. respiratory burst; 3.
P-450
NAD+/NADPH: the HMP shunt and the malate dehydrogenase reaction
produce_____
NADPH
oxygen dependent respiratory burst: what enzyme converts O2--> O2■
NADPH oxidase (with NADPH)
oxygen dependent respiratory burst: what enzyme converts O2■--> H2O2
superoxide dismutase
oxygen dependent respiratory burst: what enzyme converts H2O2 --> HOCl■
myeloperoxidase
oxygen dependent respiratory burst: what enzyme converts H2O2 --> H2O
catalase (also requires GSH--> GSSG)
hexokinase vs glucokinase: where is hexokinase found
throughout the body
hexokinase vs glucokinase: where is glucokinase found
mainly in the liver
hexokinase vs glucokinase: the affinity (Km) and capacity (Vm) of
glucokinase (compared to hexokinase) is
lower affinity (higher Km) and higher capacity (higher Vmax)
glycolysis regulation, irreversible enzymes: what is the irreversible enzyme
and the regulator of the reaction: D-glucose ---> Glucose-6-phosphate
hexokinase (glucokinase in the liver);hexokinase is negatively regulated by
G6P
glycolysis regulation, irreversible enzymes: what is the irreversible enzyme
and the regulator of the reaction: fructose-6-P ---> fructose-1,6-BP
phosphofructokinase (rate limiting step of glycolysis); up-regulated by AMP,
fructose-2,6-BP; down-regulated by ATP, citrate
glycolysis regulation, irreversible enzymes: what is the irreversible enzyme
and the regulator of the reaction: PEP ---> pyruvate
pyruvate kinase; up regulated by fructose-1,6-BP; down-regulated by ATP,
alanine
glycolysis regulation, irreversible enzymes: what is the irreversible enzyme
and the regulator of the reaction: pyruvate ---> acetyl-CoA
pyruvate dehydrogenase. Down-regulated by ATP, NADH, acetyl CoA
glycolytic enzyme deficiency: what are the 7 glycolytic enzyme deficiencies
associated with hemolytic anemia
hexokinase, glucose phosphate isomerase, aldolase, triosephosphate
isomerase, phosphate glycerate kinase, enolase, pyruvate kinase
glycolytic enzyme deficiency: how do RBCs metabolize glucose
anaerobically (depend solely on glycolysis)
pyruvate dehydrogenase complex: this complex contains 3 enzymes. What
are the 5 cofactors it requires?
the first 4 B vitamins +lipoic acid [B1(thiamine, Tp); B2 (FAD); B3 (NAD);
B5(pantothenate-->acetyl CoA) ]
pyruvate dehydrogenase complex: what is another complex that works in a
similar way
alpha ketoglutarate dehydrogenase
pyruvate dehydrogenase complex: what is the reaction it catalyzes
pyruvate + NAD + CoA ---> acetyl-CoA + CO2 + NADH
pyruvate dehydrogenase deficiency: what are the only purely ketogenic
amino acids
Leucine, Lysine
pyruvate dehydrogenase deficiency: lactic acidosis in this condition is due to
backup of _____
alanine and pyruvate (can be seen in alcoholics)
pyruvate dehydrogenase deficiency: what is the Tx for this condition
intake of ketogenic nutrients (high fat content)
pyruvate dehydrogenase deficiency: what is one of the most important
findings associated with this condition
neurological defects
pyruvate dehydrogenase deficiency: AUTHOR
Flora Waples-Trefil
Pyruvate Metabolism: Pyruvate can be metabolized into four compounds.
Name them.
Lactate, Acetyl-coA, Oxaloacetate, and Alanine - remember, if you Love
pyruvate, you'l be AOA.
Pyruvate Metabolism: When is pyruvate generated?
Anaerobic metabolism, mainly in muscles. Remember - lactic acid makes
muscles sore.
Pyruvate Metabolism: What role does Alanine play in transport?
Alanine carries nitrogen groups from muscles to liver.
Pyruvate Metabolism: How many ATP equivilnets are there between glucose
and pyruvate?
6
Pyruvate Metabolism: Where is Oxaloacetate used?
Oxaloacetate and Acetyl-CoA are both elements of the TCA cycle.
Oxaloacetate can alos be used in gluconeogenesis
Pyruvate Metabolism: How many ATP equivilents does ti take to turn
Pyruvate into Alanine?
Trick question. None. Alanine is the only pyruvate product that does not
require energy.
Cori Cycle: What is the Cori cycle?
The process that gets lactic acid from cells who burn glucose anaerobically to
the liver, where gluconeogenesis is preformed to send glucose back to those
cells.
Cori Cycle: What two types of tissue produce lactate most frequently?
Muscles working anaerobically, and RBCs (no mitochondria)
Cori Cycle: How many ATPs do cells get burning glucose to pyruvate?
2
Cori Cycle: How may ATP does it take to get glucose from pyruvate in the
liver?
6
Cori Cycle: Given that you lose 4 ATP in each cycle, why is this a useful
process?
Allows muscles to continue to function anaerobically if you need to and are
low on blood glucose.
TCA Cycle: Name the molcules in the TCA cycle.
Citrate, Isocitrate, Alpha-Ketogluterate, Succinyl CoA, Succinate, Fumerate,
Malate, Oxaloacetate.
TCA Cycle: How to remember this?
Cindy Is Kinky So She Fornicates More Often.
TCA Cycle: What is the net gain of ATP?
12 per cycle of the TCA, so 24 per glucose
TCA Cycle: What things are formed per pyruvate?
3 NADPH, 1 FADH2, 1 GTP, and 2CO2.
TCA Cycle: How is this cycle regulated?
unless there is suficient ADP it will not run
TCA Cycle: Which enzyme complex in the cycle requires co-factors?
The Alpha-ketogluterate dehydrogenase complex.
TCA Cycle: What factors does it require?
5 - the same ones that are required by the pyruvate dehyrodgenase complex
TCA Cycle: Which are….?
B1 (thiamine), B2 (riboflavin, FAD), B3 (Niacin, NAD), B5 (pantothenate)
and Lipopoic acid
Electron Transport Chain and Oxidative Phosphyrylation: What does the
electron transport chain do?
The ETC carries high energy electrons from NADH and FADH2 to oxegen
Electron Transport Chain and Oxidative Phosphyrylation: How does this
generate ATP?
Each cytochrome complex pumps H+ into the intermembrane space. ATP
generation is coupled to the H+ gradient
Electron Transport Chain and Oxidative Phosphyrylation: Where are these
enzymes located?
The inner mitochondrial membrane
Electron Transport Chain and Oxidative Phosphyrylation: What is the effect
of ETC inhibitors?
By stoping the ETC they cuase the loss of the H+ gradient, which stops ATP
syntesis
Electron Transport Chain and Oxidative Phosphyrylation: Name four ETC
inhibitors.
Cyanide, Anitmycin A, rotenone, and CO
Electron Transport Chain and Oxidative Phosphyrylation: What is the effect
of ATPase inhibitors?
By stoping the enzyme that uses the H+ gradient to produce ATP, the H+
gradient increases and the ETC stops.
Electron Transport Chain and Oxidative Phosphyrylation: Name one.
Oligomycin
Electron Transport Chain and Oxidative Phosphyrylation: What are the
effects of uncoupling agnest?
They increase membrnae permeabliity, so you lose the H+ gradient, so the
ETC works harder, and you use more oxegen, wihtout making more ATP.
Electron Transport Chain and Oxidative Phosphyrylation: What are the
clinical comsequences of this?
Since the by-product of the ETC chain is heat, when the ETC is uncoupled
and therefore unregulated, you get excess heat production and fever.
Electron Transport Chain and Oxidative Phosphyrylation: What common
drug overdose causes this?
Asprin and other salycilates
Gluconeogenesis, Irreversible Enzymes: What is gluconeognesis?
Since glycolysis is a very energetically favorable reaction, special enxymes
are required to get over the energy hump and make glucose from pyruvate.
Gluconeogenesis, Irreversible Enzymes: How many enzymes are unique to
this reaction?
4. The other 7 enzymes are the same ones used in glycolysis
Gluconeogenesis, Irreversible Enzymes: What are the four unique enzymes?
Pyruvate Carboxylase, PEP Carboxykinase, Fructose-1-6-bisphosphanate,
and Glucose-6-phospahte, Remember: Pathway Produces Fresch Glucose.
Gluconeogenesis, Irreversible Enzymes: What does Pyruvate Carboxylase
do?
Pyruvale into oxaloacetate
Gluconeogenesis, Irreversible Enzymes: Where does this reaction take place?
In the mitochondria. Remember, this is where the pyruvate is, asince
otherwise it would eb going into the TCA cycle
Gluconeogenesis, Irreversible Enzymes: What happens next?
Oxaloacetate is turned into malate, which is transferied into the cytosol
Gluconeogenesis, Irreversible Enzymes: Why is this imporntat?
If gluconeogneeis and glycolysis hapened int eh same space, they would
cancel each other out.
Gluconeogenesis, Irreversible Enzymes: Where does the rest of the cycle take
place?
In the cytosol
Gluconeogenesis, Irreversible Enzymes: What tissues have these enzymes?
liver, kidney, and intestinal epithlium.
Gluconeogenesis, Irreversible Enzymes: What happens if you lack one of
these?
Hypoglycemia if you do not eat frequently
Gluconeogenesis, Irreversible Enzymes: Give an example.
Von Gierke's Disease (lack of Glucose-6-phosphatase)
Pentose Phosphate Pathway (HMP Shunt): Is any ATP produced or
consumed in this?
No
Pentose Phosphate Pathway (HMP Shunt): Is it reverisble?
Yes. The direction of flwo is controled by the metablic needs of the cell.
Pentose Phosphate Pathway (HMP Shunt): What does this pathway produce?
Ribose-5-P for nucliotides synthesis and NADPH for RBC metabolism and
fatty acid production
Pentose Phosphate Pathway (HMP Shunt): Where does it take place?
In the cytosol.
Pentose Phosphate Pathway (HMP Shunt): What tissues have this pathway?
Places that make fatty acids or seteroids, so liver, mammary tissue, and
adrenal cortex, as well as RBC
Glucose-6-P Dehydrogenase Deficiency: G6PD is part of what pathway?
It is the rate limiting step in the pP (aka HMP) shunt.
Glucose-6-P Dehydrogenase Deficiency: What molecule is decreased if this
enzyme is inactive?
NADPH
Glucose-6-P Dehydrogenase Deficiency: What is this a problem?
NADPH is necissary to reduce glutathione, which is vital in detoxification of
free radicles and oxidizing agents.
Glucose-6-P Dehydrogenase Deficiency: What cells are most sensitive to this
kind o damage?
RBCs
Glucose-6-P Dehydrogenase Deficiency: What kind of disease is caused by a
lack of G6PD?
Hemolytic anemai, triggered by oxidative stress.
Glucose-6-P Dehydrogenase Deficiency: What consititues oxidative stress?
TB drugs, Fava beans, sulfonamides
Glucose-6-P Dehydrogenase Deficiency: How is this disorder passed on?
X- linked recessive.
Glucose-6-P Dehydrogenase Deficiency: Where is this prevelent?
Black and mediteranean populations
Glucose-6-P Dehydrogenase Deficiency: Histoligically, what will be seen?
Heinz bodies (clumped hemoglobin)
Disorders of Fructose Metabolism: Fructose is central in what pathways in
the liver?
Fructose is found in the glycolysis and gluconeognesis pathway.
Disorders of Fructose Metabolism: What is the first step in putting fructose
into each of these pathways?
Aldolase B splits fructose-1-P ito Glyceraldehye-3-P
Disorders of Fructose Metabolism: Therefore, a metabloic problem *before*
the aldolase will cuse whqat disorder?
Fructose will accumulate, and spill into the urine
Disorders of Fructose Metabolism: What is this called?
essential fructosuira
Disorders of Fructose Metabolism: What is the enzyme involved?
frucokinase (puts a P on fructose)
Disorders of Fructose Metabolism: Is this a dangerous disorder?
no, it is benign, you just have high levels of fructose in your blood and urine.
Asymptomatic.
Disorders of Fructose Metabolism: What will happen if Aldolase B is
impaired?
Fructose-1-P will build up in the liver
Disorders of Fructose Metabolism: Is this a problem?
Yes. Phophate is used up, and glycogenolysis and gluconeogensis are both
impaired.
Disorders of Fructose Metabolism: What are the symptoms?
Hypoglycemia, jaundice and cirrosis.
Disorders of Fructose Metabolism: What is the treatment?
Decrease fructose and sucrose intake
Disorders of Fructose Metabolism: What is the naem of this disorder?
Fructose intolerence
Disorders of Galactose Metabolism: What two steps does Galactose have to
go through to enter glycolysis?
Glactokinase turns galactose into galactose-1-P, and then Galactose-1-P
uridyl transferase turns that into glucose-1-P
Disorders of Galactose Metabolism: If galactokinase is imparied, what
happens?
Galactose builds up in the blood and spills in the urine, but there is no build
up of the toxic compound galactose-1-P
Disorders of Galactose Metabolism: Is this dangerous?
No
Disorders of Galactose Metabolism: What happens if Galactose-1-P uridyl
tranferase is impaired
Glactose builds up int eh blood, and spills into the urine. There is a build up
of the toxic metabolite glactose-1-P
Disorders of Galactose Metabolism: What is this disease called?
Galactosemia
Disorders of Galactose Metabolism: Is is dangerous?
Yes
Disorders of Galactose Metabolism: What are the symptoms?
cataracts, hepatoslenomegaly, and mental retardation
Disorders of Galactose Metabolism: What is the treatement?
reduceing galactose in diet
Disorders of Galactose Metabolism: How do you do this?
Galactose comes from lactose, so limit dairy
Lactase deficiency: Where is lactase normally found?
intestinal brush border
Lactase deficiency: Therefore, if it is missing, what is the main symptom?
gas, bloating, and osmitic diarrhea
Lactase deficiency: Is this common?
Yes.
Lactase deficiency: More in what populations?
Asians and black more than europeans
Esential Amino Acids: What is a neumonic for the essential amino acids?
PriVaTe TIM HALL - Phe, Val, Trp, Thr, Ile, Met, His, Arg, Leu and Lys.
Esential Amino Acids: Which amino acids are purely ketogenic?
Leu and Lys
Esential Amino Acids: Which amino acids are purely both ketogeneic and
glucogenic?
Tyrosine, Isoleucine, Phe and Try
Esential Amino Acids: What a.a.'s are purely glucogenic?
Anything that is not one of the six above.
Esential Amino Acids: Wath two amino acids are essential during growht, but
not he rest of the time?
Arg and His
Acidic and Basic Amino Acids: What two a.a.'s are acidic and negativly
charged at body pH?
Asp (asparatic acid) and Glu (glutamic acid)
Acidic and Basic Amino Acids: What two a.a.'s are basic and positivly
charged at body pH?
Arginine and Lysine (rememebr they are th two with NH3 groups.
Acidic and Basic Amino Acids: How does the body use the positive charge
on Arg and Lys?
Histones, which bind to negativly charged DAN are high in these a.a.
Transport of Amonium by Alanine and Glutamine: Whay does your body
produce amonium?
It comes from the NH3 group of amino acids which are being broken down
Transport of Amonium by Alanine and Glutamine: Where does this happen?
Everywhere in the body
Transport of Amonium by Alanine and Glutamine: What is the enzyme that
transfers the NH3 group
Amino transferases (ex:AST (asparatate amino trnasferase), ALT (alanine
amino transferase)
Transport of Amonium by Alanine and Glutamine: What two molecules is
NH3 transferred between?
It moves from an amino acid to alpha=ketogluterate, making it glutamate.
Transport of Amonium by Alanine and Glutamine: Is this reaction reversible?
Yes. Glutamate functions as a resevoir, so NH# can be made into urea, or is
can give NH3s for a.a. production
Transport of Amonium by Alanine and Glutamine: Where are these enzymes
found?
Inside the cells, so if they are in the blood that is a sign of tissue damage
(most in liver and muscle)
Transport of Amonium by Alanine and Glutamine: Once the NH3 has been
added to alpha-ketoglutamate and you have glutamate, what are two
pathways it can take from their?
The NH3 can be transferred to pyruvate to form alanine, which is then
trasfered int eh blood to the liver to join the urea cycle. Or, glutamate can,
with NADPH, release it directly into the blood as amonium.
Transport of Amonium by Alanine and Glutamine: What is the difference
between pyruvate and alanine?
an NH3 group.
Urea Cycle: What is the function of the urea cycle?
a molecule that hleps dispose of excess nitrogen.
Urea Cycle: What tissue does it occur in?
Liver
Urea Cycle: What part of the cell?
The first two reactions in mitochondria, the rest in cytoplasm
Urea Cycle: How many molecules of nitrogen are in urea?
Two
Urea Cycle: What molecules do they come from?
one if free amonium, the other from asparatate.
Urea Cycle: What is the immediate precursor of both moleulces?
Glutamate provides free amonium (see aboe), and is also converted into
aspartate.
Urea Cycle: What are the reactions?
Ornithine into Carbamoyl phosphate into citruline, add asparate becomes
arginosuccinate, fumerate leaves, leaving arginine, produces urea and
ornithing again.
Urea Cycle: Neumonic for this?
Ordinarrily Careless Crapers Are Also Frivolous About Urination.
Urea Cycle: Is this reversible?
No, highly irreversible
Urea Cycle: Which reactions happen in the mitochondria?
Carbamoyl phsophate is formed there, and added to ornithine to make
citruline.
Amino acid dervatives: What a.a. does Histamine come from?
Histadine
Amino acid dervatives: What a.a. does creatinine come from?
arginine
Amino acid dervatives: What a.a. does throxine come from?
Tyrosine (which comes from phenylalanine)
Amino acid dervatives: What a.a. does niacin come from?
Tryptophan
Amino acid dervatives: What a.a. does heme come from?
The porphyrin comes from glycine
Amino acid dervatives: What a.a. does melatonin come from?
Tryptophan
Amino acid dervatives: What a.a. does NE and Epi come from?
Dopamine, which comes from tyrosine
Amino acid dervatives: What a.a. does Urea come from?
arginine (the NH3 is donated by glutamate)
Amino acid dervatives: What a.a. does melanin come from?
Dopamine, which comes from tyrosine
Amino acid dervatives: What a.a. does dopamine come from?
Tyrosine (which comes from phenylalanine)
Amino acid dervatives: What a.a. does seratonin come from?
Tryptophan
Amino acid dervatives: What a.a. does Nitric oxide come from?
Arginine
Amino acid dervatives: What a.a. does NADP come from?
Niacin, which comes from tryptophan
Phenylketonuria: What is the primary problems in this disease?
Phenylalanine cannt be converted into tyrosine
Phenylketonuria: What does this cause?
Tyrosein becomes essentail and phenylalanine builds up in blood and spills
into urine.
Phenylketonuria: What are the clinical findings?
fair skin and eyes (no melanin), mental retardation (seratonin lack?) and a
musty odor.
Phenylketonuria: Treatement?
Restirction phenylalanine, ingest tyrosine
Alkaptonuria: What is the primary problems in this disease?
lack of an enzyme in the tyroine degradation pahtywa
Alkaptonuria: What enzyme?
homogentisic oxidase
Alkaptonuria: What are the clinical findings?
Dark urine and connective tissue
Alkaptonuria: Is the benign?
Yes. Can have arthralgias.
Albinism: What is the primary problems in this disease?
Inability to make melanin from tyrosine
Albinism: Causes?
Can be lack of tyrosinase or that nerual crest cels failed to migrate and you
have no melanocytes.
Albinism: Risks it causes?
Lack of melanin leads to risk of skin cancer
Homocystinuria: What is the primary problems in this disease?
two possible: Can't make homocysinte into cystine, or can't make
homocystine into methionine.
Homocystinuria: Results of this defect?
If it is homocystine to cystine that is impaired, cystine is essential. IT can
cause mental retardation, osteoperosis, and lens dislocation.
Homocystinuria: Treatment?
If it is homocystine to cystine, you give cystine. If it is homocystine to
methionine you give methionine.
Homocystinuria: What co-factor is used to change homocystine to
methionine?
Vitamine B12 and tetrahydrofolate
Homocystinuria: Can increased Vit B 12 be theraputic?
Yes, if the problem is the affinityof the enzyme for its co-factors
Cystinuria: What is the primary problem in this disease?
Lack of a.a. transporter in kidney
Cystinuria: What a.a. are effected?
COLA: Cystine, Ornithine, Lysine, and Arginine
Cystinuria: What are the clinical effects?
Kidney stones made of cystine (radiolucent)
Cystinuria: Treatment?
Acetazolamide
Cystinuria: How does it work?
alkalinizes the urine
Maple Syrup Urine Disease: What is the primary problem in this disease?
block in degredation of branches aa
Maple Syrup Urine Disease: Which are those?
I Love Vermont Maple Syrup: Ile, Leu, Val
Maple Syrup Urine Disease: What are the clinical signs?
Urine smells like maple syrup, leads to mental retardatrion, CNS defects, and
death.
Maple Syrup Urine Disease: AUTHOR
Peter Henderson
Purine salvage deficiencies: Adensoine deaminase deficiency leads to what
condition?
SCID
Purine salvage deficiencies: SCID affects T cells, B cells, or both?
Both
Purine salvage deficiencies: Lesch-Nyhan syndrone (LNS) results in inability
to salvage which nucleotide?
Purine
Purine salvage deficiencies: LNS has which inheritance pattern?
X-linked recessive
Purine salvage deficiencies: Result of LNS is excess production of
__________.
Uric acid (gout is one finding in LNS)
Fatty acid metabolism sites: Fatty acids are synthesized in the _________.
Cytosol
Fatty acid metabolism sites: Fatty acids are degraded in __________.
Mitochondria (where products will be consumed)
Fatty acid metabolism sites: Fatty acid entry into cystol is via ________.
Citrate shuttle
Fatty acid metabolism sites: Fatty acid entry into mitochondria is via
_______, which is inhibited by _________.
carnitine shuttle; cytoplasmic malonyl CoA
Liver: Fed state vs. fasting state: In fasting state, fatty acids are ultimately
converted to what?
Ketone bodies
Glycogen storage diseases: What is the end result of all glycogen storage
diseases?
Abnormal glycogen metabolism and accumulation of glycogen in cells
Glycogen storage diseases: Type I is also known as _______.
Von Gierke's disease
Glycogen storage diseases: What is the deficiency in type I/Von Gierke's
disease?
Glucose 6-phosphatase deficiency
Glycogen storage diseases: Findings in type I/Von Gierke's disease are
________ and _________.
Severe fasting hypoglycemia, excess glycogen in liver
Glycogen storage diseases: Type II is also known as ______.
Pompe's disease
Glycogen storage diseases: What is the deficiency in type II/Pompe's disease?
Lysosomal alpha-1,4 glucosidase deficiency
Glycogen storage diseases: Findings in type II/Pompe's disease are
_________ and _________.
Cardiomegaly, systemic findings (liver, muscle)
Glycogen storage diseases: Type III is also known as _____.
Cori's
Glycogen storage diseases: What is the deficiency in type III/Cori's?
Debranching enzyme alpha-1,6-glucosidase deficiency
Glycogen storage diseases: Type IV is also known as _______.
McArdle's disease
Glycogen storage diseases: What is the deficiency in type IV/McArdle's
disease?
Skeletal muscle glycogen phosphorylase deficiency (McArdle's = Muscle)
Glycogen storage diseases: Result of type IV/McArdle's disease is
_________.
Increased glycogen in muscle, but can't be broken down (results in cramps,
myoglobinuria)
Glycogen storage diseases: What is the pneumonic to remember types I
through IV?
Very Poor Carbohydrate Metabolism
Ketone bodies: What are two incidences when ketone bodies found in urine?
Prolonged starvation, diabetic ketoacidosis
Ketone bodies: Ketone bodies are made from _______.
HMG-CoA
Ketone bodies: Ketone bodies are metabolized by the brain to 2 molecules of
________.
Acetyl-CoA
Insulin: Where is insulin made?
Beta cells of pancreas
Insulin: Insulin does not affect glucose uptake in _____, ______, or _______.
Brain, RBCs, hepatocytes
Insulin: Required for uptake of glucose by ______ and _______.
Adipose tissue, skeletal muscle
Insulin: GLUT_ receptors are found in beta cells and GLUT_ receptors in
muscle and fat.
2, 4
Insulin: Inhibits glucagon release by what cells?
Alpha cells of pancreas
Insulin: True/False: Serum C-peptide is present with exogenous insulin
uptake.
FALSE
Insulin vs. Glucagon: Glucagon _______ stuff, turns glycogen synthase
_____, turns phosphorylase ___.
Phosphorylates, OFF, ON
Insulin vs. Glucagon: Insulin _______ stuff, turns glycogen synthase _____,
turns phosphorylase ___.
Dephosphorylates, ON, OFF
Cholesterol synthesis: Rate limiting step is catalyzed by what enzyme?
HMG-CoA reductase
Cholesterol synthesis: Lovastatin (inhibits/stimulates) HMG-CoA reductase.
Inhibits
Cholesterol synthesis: 2/3 of plasma cholesterol is esterified by
_____________.
Lecithin-cholesterol acyltransferase (LCAT)
Major apolipoproteins: A-I does what?
Activates LCAT
Major apolipoproteins: B-100 binds to _______ receptor.
LDL
Major apolipoproteins: C-II is a cofactor for what enzyme?
Lipoprotein lipase
Major apolipoproteins: E does what?
Mediates extra (remnant) uptake
Lipoprotein functions: Chylomicrons deliver dietary _____ to ________ and
dietary ______ to ______.
Triglycerides, peripheral tissues; Cholesterol, liver
Lipoprotein functions: Which cells secrete chylomicrons?
Intestinal epithelial cells
Lipoprotein functions: Secretion is mediated by apolipoprotein _______.
B-48
Lipoprotein functions: True/False: VLDL delivers hepatic triglycerides to
peripheral tissues.
TRUE
Lipoprotein functions: Where is VLDL secreted from?
Liver
Lipoprotein functions: LDL delivers hepatic cholesterol to _______.
Peripheral tissues
Lipoprotein functions: LDL is taken up by target cells via what process?
Receptor-mediated endocytosis
Lipoprotein functions: HDL mediates transport of cholesterol from where to
where?
Periphery to liver (reverse cholesterol transport)
Lipoprotein functions: HDL acts as a repository for ______ and _______.
apoC and apoE
Lipoprotein functions: HDL is secreted from which 2 places?
Liver and intestine
Familial dyslipidemias: Type I (hyperchylomicronemia) has elevated blood
levels of ______.
Triglycerides
Familial dyslipidemias: Type IIa (hypercholesterolemia) has increased levels
of what?
LDL
Familial dyslipidemias: What is the pathophysiology of type IIa?
Decreased number of LDL receptors
Familial dyslipidemias: Type IIb (combined hyperlipidemia) has increased
levels of ____ and _____.
LDL, VLDL
Familial dyslipidemias: Type III (dysbetalipoproteinemia) has altered
apolipoprotein __, and increased ____ and _____.
E, IDL, VLDL
Familial dyslipidemias: Type IV (hypertriglyceridemia) is caused by hepatic
overproduction of what?
VLDL
Familial dyslipidemias: True/False: Type V (mixed hypertriglyericdemia) has
only increased VLDL
False; Increased VLDL and chylomicrons
Identify the site of metabolism (Mitochondria, Cytoplasm, or Both): Fatty
acid oxidation (Beta-oxidation)
Mitochondria
Identify the site of metabolism (Mitochondria, Cytoplasm, or Both):
Glycolysis
Cytoplasm
Identify the site of metabolism (Mitochondria, Cytoplasm, or Both):
Gluconeogenesis
Both
Identify the site of metabolism (Mitochondria, Cytoplasm, or Both): Fatty
acid synthesis
Cytoplasm
Identify the site of metabolism (Mitochondria, Cytoplasm, or Both): Urea
cycle
Both
Identify the site of metabolism (Mitochondria, Cytoplasm, or Both):
Acetyl-CoA production
Mitochondria
Identify the site of metabolism (Mitochondria, Cytoplasm, or Both): Heme
synthesis
Both
Identify the site of metabolism (Mitochondria, Cytoplasm, or Both): HMP
Shunt
Cytoplasm
Identify the site of metabolism (Mitochondria, Cytoplasm, or Both): Protein
synthesis (RER)
Cytoplasm
Identify the site of metabolism (Mitochondria, Cytoplasm, or Both): Steroid
synthesis (SER)
Cytoplasm
Identify the site of metabolism (Mitochondria, Cytoplasm, or Both): krebs
cycle
Mitochondria
Aminolevulinate (ALA) synthesis: ALA synthesis is the rate-limiting step for
the produciton of what?
Heme
Aminolevulinate (ALA) synthesis: ALA is found in the ______
Mitochondria
Heme synthesis: Heme synthesis occurs in the ______ and ________.
Liver, bone marrow
Heme synthesis: Underproduction of heme causes ___________
___________ _________.
Microcytic hypochromatic anemia
Heme synthesis: Accumulation of intermediates causes what?
Porphyria
Porphyrias: This type of porphyria is marked by a deficiency in
uroporphyrinogen I synthetase
Acute intermittent porphyria
Porphyrias: How does lead affect iron incorporation into heme?
It prevents it
Porphyrias: This is the most common type of porphyria; a deficiency in
uroporphynogen decarboxylase)
Porphyria cutanea tarda
Heme catabolism: True/False: The progression of heme catabolism is heme
--> biliverdin --> bilirubin
TRUE
Heme catabolism: Bilirubin is (Toxic/Non-toxic) to CNS and transported by
_________.
Toxic, albumin
Heme catabolism: In the liver, heme is conjugated with __________.
Glucuronate
Heme catabolism: True/False: Urobilinogen is an intestinal intermediate that
is never found in the blood and urine.
False: a small amount is reabsorbed into blood and excreted in urine.
Hemoglobin: Hemoglobin is composed of how many polypeptide
subunits?+A105
4 (2 alpha, 2 beta)
Hemoglobin: Carbon monoxide has a 200x (higher/lower) affinity for
hemoglobin than does oxygen
Higher
Hemoglobin: T (taut) form of hemoglobin has a (high/low) affinity for
oxygen
Low
Hemoglobin: R (relaxed) form of hemoglobin has a (high/low) affinity for
oxygen
High
Hemoglobin: True/False: Myoglobin, like hemoglobin, has a sigmoid-shaped
O2 binding curve.
FALSE
Hemoglobin structure regulation: Increased Cl, H, CO2, DPG, and
temperature favor shift over curve to (left/right).
Right (unloads more O2)
Hemoglobin structure regulation: True/False: Shift to right is due to
preference for T form over R form.
TRUE
Methemoglobinemia: True/False: Methemoglobin is an oxidized form of
hemoglobin that binds O2 more readily.
False: it binds O2 less readily
CO2 transport in blood: CO2 binds to (heme/amino acids in globin chain).
Amino acids in globin chain
CO2 transport in blood: CO2 binding favors which form of hemoglobin? And
what sort of shift does it cause?
T. Right shift.
CO2 transport in blood: AUTHOR
Simi Gupta
Vitamins: fat soluble: What are the fat soluble vitamins?
A,D,E,K
Vitamins: fat soluble: The absorption of fat soluble vitamins depends on what
two organs?
small intestine (ileum) and pancreas
Vitamins: fat soluble: Is toxicity more common for fat or water soluble
vitamins?
fat soluble becauase the vitamins accumulate in the fat
Vitamins: fat soluble: What can cause fat-soluble vitamin deficiencies besides
just general lack of intake?
malabsorption syndromes and mineral oil intake
Vitamins: water soluble: What are the water soluble vitamins?
B1, 2, 3, 5, 6, 12, C, Biotin, Folate
Vitamins: water soluble: What do B complex deficiencies cause?
dermatitis, glossitis, and diarrhea
Vitamin A (retinol): What is the function of vitamin A?
constituent of visual pigments
Vitamin A (retinol): Match up the appropriate vitamin with these alternates
names? A.thiamine, B.riboflavin, C.niacin, D.retinol,
C2
Vitamin A (retinol): What does a deficiency of vitamin A cause?
night blindness and dry skin
Vitamin B1 (thiamine): What does a deficiency of vitamin B1 cause?
Ber1Ber1 and Wernicke-Korsakoff syndrome
Vitamin B1 (thiamine): What is the function of vitamin B1?
Cofactor for oxidative decarboxylation of alpha-keto acids and a
transketolase in the HMP shunt.
Vitamin B1 (thiamine): Beriberi is characterized by what 3 symptoms?
polyneuritis, cardiac pathology, and edema
Vitamin B2 (riboflavin): What does a deficiency of vitamin B2 cause?
angular stomatitis, cheilosis, corneal vascularization
Vitamin B2 (riboflavin): What is the function of vitamin B2?
cofactor in oxidation and reduction
Vitamin B3 (niacin): What is vitamin B3 a constituent of?
NAD+, NADP+
Vitamin B3 (niacin): What does a deficiency of vitamin B3 cause?
Pellagra
Vitamin B3 (niacin): What are the symptoms of pellagra?
Diarrhea, Dermatitis, Dementia
Vitamin B5 (pantothenate): What is vitamin B5 a constituent of?
CoA
Vitamin B5 (pantothenate): A deficiency in vitamin B5 causes what 4
problems?
dermatitis, enteritis, alopecia, adrenal insufficiency
Vitamin B6 (pyridoxine): When vitamin B6 is converted to ___, it is a
cofactor in what three processes?
pyridoxal phosphate; cofactor in transamination, decarboxylation, and
trans-sulfuration
Vitamin B6 (pyridoxine): What may induce a deficiency in vitamin B6?
INH and oral contraceptives
Biotin: Biotin is a cofactor in which 3 carboxylations?
pyruvate to oxaloacetate, acetyl-CoA to malonyl CoA, and proprionyl-CoA to
methylmalonylCoA
Biotin: The use of __ and ingestion of __ cause a deficiency in biotin?
antibiotics; raw eggs
Folic acid: What is the most common vitamin deficiency in the US?
folic acid
Folic acid: Neurologic symptoms with anemia are seen in folic acid or B12
deficiency?
B12
Folic acid: What is folic acid important in the synthesis of?
Nitrogenous bases in DNA and RNA
Folic acid: What two drugs are PABA analogues (the precursor of folic acid
in bacteria)?
sulfa drugs and dapsone
Vitamin B12 (cobalamin): Vitamin B12 is involved in which two
conversions?
Homocysteine to Methionine and Metholmalonyl CoA to SuccinylCoA
Vitamin B12 (cobalamin): Where is vitamin B12 stored
liver
Vitamin B12 (cobalamin): What are the 3 main causes of vitamin B12
defiiciency?
malabsorption, lack of intrinsic factor, and absence of terminal ileum
Vitamin B12 (cobalamin): What test is used to determine a deficiency of
vitamin B12
Schilling
Vitamin B12 (cobalamin): AUTHOR
Dan Jamieson
Vitamin C (ascorbic acid) : Deficiency of Vit C causes what?
Scurvy
Vitamin C (ascorbic acid) : Vit C is necessary for ________ of proline and
lysine in ________ synthesis
hydroxylation / collagen
Vitamin C (ascorbic acid) : Vit C also facilitates absorption of what?
Iron - by keeping iron in Fe2+ reduced state
Vitamin C (ascorbic acid) : Vit C is necessary as a cofactor for what?
Dopamine --> NE
Vitamin C (ascorbic acid) : What are the clinical findings of scurvy?
Swollen Gums, bruising, anemia, poor wound healing
Vitamin D: D2, also called _______ is consumed from what?
ergocalciferol, comsumed in milk
Vitamin D: Cholecalciferol, also called ____ is formed where?
D3, formed in sun-exposed skin
Vitamin D: 25-OH D3 is what form of Vit D
Storage form
Vitamin D: 1,25 (OH)2D3 is what form of Vit D
Active form
Vitamin D: Deficiency of Vit D in children causes? In adults?
Children - Rickets // Adults - Osteomalacia. Also can cause hypocalcemic
tetany
Vitamin D: Vit D functions to
Increase intestinal absorption of calcium and phosphate
Vitamin D: Too Much Vitamin D has three clinical effects. What are they?
Hypercalcemia, loss of apetite, stupor.
Vitamin D: The 6 causes of hypercalcemia are:
Vit D. Intoxication / Malignancy / Hyperparathyroidism / Milk-Alkali
syndrome / Sarcoidosis / Paget's disease of bone
Vitamin D: Excess Vit D is seen in what disease state?
Sarcoidosis - where epithelial macrophages convert vit D into its active form
Vitamin E: Deficiency in Vit E causes?
Increased fragility of erythrocytes (E is for erythrocytes)
Vitamin E: Vit E functions as an ______ to protect _______
Antioxidant, to protect erythrocytes from hemolysis
Vitamin K : T/F - Vitamin K deficiency causes neonatal thrombi and
pulmonary emboli.
False - Vit K deficiency causes - neonatal hemorrhage
Vitamin K : How does Vit K effect the PT, aPTT and Bleeding time?
Increased PT and aPTT but normal bleeding time.
Vitamin K : What coagulation factors require Vitamin K?
Factors II, VII, IX, X and protein C and S. (remember 1972).
Vitamin K : How does warfarin work?
It is a vitamin K antagonist.
Vitamin K : What does Vit K catalyze?
The gamma-carboxylation of glutamic acid residues on various proteins
concerned with blood clotting.
Vitamin K : Where is Vit K synthesized?
Vit K is synthesized by the normal intestinal flora.
Ethanol Metabolism : What are the two enzymes required to convert Ethanol
--> acetaldehyde --> acetate?
Alcohol dehydrogenase for the first reaction, and acetaldehyde
dehydrogenase for the second.
Ethanol Metabolism : What is the limiting reagent in the above reaction?
NAD+ is the limiting reagent for both reactions
Ethanol Metabolism : How does Disulfiram work?
Disulfiram (antabuse) - inhibits acetaldehyde dehydrogenase (acetaldehyde
accumulates, contributing to hangover symptoms)
Ethanol Metabolism : When I go out drinking with the class of 2006, why is
PBL so painful the next morning?
Because acetaldehyde accumulates in my system, and after 2 years, PBL is
always painful.
Ethanol Hypoglycemia : How does ethanol metabolism lead to
hypoglycemia?
Ethanol metabolism increases NADH/NAD+ ratio in the liver, causing
diversion of pyruvate to lactate and OAA to malate, thereby inhibiting
gluconeogenesis and leading to hypoglycemia.
Ethanol Hypoglycemia : What is hepatocellular steatosis, and how does it
occur?
Hepatocellular steatosis = hepatic fatty change… It occurs because of the
above pathway resulting in an increase in NADH/NAD+ ratio, which causes
a shunting away from glycolysis and toward fatty acid synthesis.
Kwashiorkor vs. marasmus : What is kwashiorkor?
Protein malnutrition resulting in skin lesions, edema, liver malfunction (fatty
change).
Kwashiorkor vs. marasmus : What is marasmus?
protein - calorie malnutrition resulting in tissue wasting.
Kwashiorkor vs. marasmus : The clinical picture of a small child with a
swollen belly is characteristic of kwashiorkor or marasmus?
Kwashiorkor
Kwashiorkor vs. marasmus : Kawashiorkor results from a protein-deficient
M.E.A.L. What does M.E.A.L. stand for?
Malabsorption, Edema, Anemia, Liver (fatty)
Summary of pathways : Glucose is first converted to what in the cell?
Glucose-6-phosphate
Summary of pathways : What are the three products that glucose-6-phosphate
is converted to in the cell?
Glucose-1-P (to glycogen pathway) // Fructose-6-P (To TCA) //
6-phosphogluconolactone (to Ribose-5 phosphate pathway)
Summary of pathways : What are the steps of the TCA?
Acetyl-CoA --> Citrate --> Isocitrate --> alpha-ketoglutarate -->
Succinyl-CoA --> Succinate --> Fumarate --> Malate --> Oxaloacetate
Summary of pathways : What are the steps of the Urea Cycle?
Aspartate --> Arginosuccinate --> Arginine --> Ornithine --> Citrulline -->
Arginosuccinate
Summary of pathways : Odd chain fatty acids enter the TCA through what
series of molecules?
Odd chain FA --> Propionyl-CoA --> Methylmalonyl-CoA -->
Succinyl-CoA… into TCA
Summary of pathways : Acetyl Co-A, aside from entering the TCA, can be
converted into what three molecules?
Mevalonic acid, Acetoacetyl-CoA, malonyl-CoA
Summary of pathways : Beta - hydroxybutyrate is formed from Acetyl-CoA
through what precursors?
Acetyl-CoA --> Acetoacetyl-CoA --> Acetoacetate --> Beta-hydroxybutyrate
Summary of pathways : Cholesterol is formed from acetyl co-A through what Acetyl-CoA --> Mevalonic Acid --> Isoprene --> Squalene --> Lanosterol -->
precursors?
Cholesterol
Summary of pathways : The conversion of Arginine to Ornithine creates as a
byproduct, what?
H20 --> Urea
Summary of pathways : NH4 + CO2, leads to _______, and enters the Urea
cycle where?
Leads to Carbamoyl Phosphate, enters at the conversion of ornithine -->
citrulline
Summary of pathways : Write the steps of conversion of glucose to
acetyl-CoA
Glucose --> Glucose -6-P --> Fructose-6-P --> fructose-1,6-bisphosphate -->
glyceraldehyde-3P --> 1,3-bis-phosphoglycerate --> 3-phosphoglycerate -->
2-phosphoglycerate --> phosphoenolpyruvate --> pyruvate --> acetyl-coA
Summary of pathways : AUTHOR
Stephanie Kemper
ethics: List 5 examples of exceptions to confidentiality.
1. Infectious diseases - physicians may have a duty to warn public officials
and identifiable people at risk. 2. The Tarasoff decision. 3. Child and/or elder
abuse. 4. Impaired atuomobile drivers. 5. Suicidal/homicidal patient
ethics: True or false. Physician may hold patient involuntarily for a period of
time if the patient is deemed suicidal or homicidal.
True.
ethics: AUTHOR
John Eifler
Prevalence vs. Incidence: Is prevalence greater than, less than, or equal to
incidence for acute disease?
equal to
Prevalence vs. Incidence: Is prevalence greater than, less than, or equal to
incidence in chronic disease?
greater than
Prevalence vs. Incidence: What is the name for the number of new cases in a
population at a given time?
Incidence
Sensitivity: Sensitivity is the number of ______ divided by the number of
_______.
true positives, all people with the disease
Sensitivity: What value is determined by 1- specificity
false positive ratio
Sensitivity: Is sensitivity more useful in ruling in a disease or ruling out a
disease?
ruling in a disease (SNOUT = SeNsitivity rules OUT)
Specificity: Specificity is the number of true _________ divided by the
number of all people without the disease
negatives
Predictive Value: Positive predictive value is the probability of having a
condition, given ________.
a positive test
Predictive Value: True or False: Predictive values are dependent on the
prevalence of the disease.
TRUE
Predictive Value: The higher the prevalence of a disease, the ______ the
positive predictive value of the test.
higher
Predictive Value: Negative predictive value is the number of _______
divided by the number of people who ________.
true negatives, tested negative for disease
Odds Ratio and relative risk: What is relative risk?
Relative risk is defined as the ratio: [disease risk in exposed group / disease
risk in unexposed group]
Odds Ratio and relative risk: When does the odds ratio approximate the
relative risk?
Only if the prevalence of disease is not too high
Odds Ratio and relative risk: For what type of study is the odds ratio used?
case-control (retrospective) study
Odds Ratio and relative risk: For what type of study is relative risk used?
cohort study
Odds Ratio and relative risk: If the _______ for OR or RR includes 1, the
study is inconclusive.
95% confidence interval
Odds Ratio and relative risk: What is attributable risk?
[disease risk in exposed group] – [disease risk in unexposed group]
Standard deviation vs. error: What is the formula for the standard error of the
mean?
standard deviation / square root of sample size
Standard deviation vs. error: As the sample size increases, does the standard
error of the mean increase or decrease?
decreases
Standard deviation vs. error: Is the standard error of the mean greater than or
less than the standard deviation?
SEM is less than standard deviation
Statistical Distributions: In a normal distribution, what are the relationships
between the mean, median, and mode?
mean = median = mode
Statistical Distributions: What are the relationships between mean, median,
and mode in the case of positive skew?
mean > median > mode
Precision vs. accuracy: What is the definition of precision?
consistency and reproducibility of test
Precision vs. accuracy: Does systemic error reduce a) accuracy or b)
precision?
accuracy
Reliability and validity: What is reliability?
reproducibility of a test
Reliability and validity: What is validity?
extent to which the test measures what it purports to measure
Correlation coefficient r: What does the correlation coefficient, r, indicate?
The strength of correlation between 2 variables
t-test vs. ANOVA vs. Chi-squared: What is the t-test?
It checks the difference between means of 2 groups (Mr. T is mean)
t-test vs. ANOVA vs. Chi-squared: ANOVA is used for what?
It checks the difference of means for 3 or more groups.
t-test vs. ANOVA vs. Chi-squared: The chi-squared test checks the difference
between 2 or more __________ of categorical outcomes.
percentages or proportions
Meta-analysis: Why pool data from several studies in a meta-analysis?
to increase statistical power
Meta-analysis: What limitations exist for meta-analyses?
They are limited by the limitations on the individual studies, and it has bias in
study selection
Case-control study: In a case-control study, the sample is chosen based on
____________.
presence or absence of disease
Case-control study: In a case-control study, information is collected about
___________.
Risk factors for disease
Cohort study: In a cohort study, the sample is chosen based on
_____________.
presence or absence of risk factors
Clinical Trial: A clinical trial needs what two characteristics to be
highest-quality?
randomized and double-blind
Bias: What type of bias results from subjects choosing their group in the
study?
Selection bias
Bias: What type of bias results from the subjects not being representative?
Sampling bias
Bias: Name 4 ways to reduce bias.
1) blind studies, 2) placebo responses, 3) crossover studies—each subject acts
as own control, and 4) randomization
Bias: What is late-look bias?
information gathered at an inapropriate time
Statistical Hypotheses: What is the null hypothesis?
Hypothesis is that there is no association between the disease and the risk
factor in the population
Statistical Hypotheses: What is a hypothesis that there is an association
between disease and the risk factor called?
Alternative hypothesis
Statistical Hypotheses: AUTHOR
Maya Shammas
Behavioral Science: Epidimiology : True or false. Another name for type I
error is beta error.
False. Type I error is alpha error and type II error is beta error.
Behavioral Science: Epidimiology : Define Type I error
Stating that there is an effect or difference when non exists.
Behavioral Science: Epidimiology : Define "alpha".
A preset level of significance. You "saw" a difference that did not exist.
Behavioral Science: Epidimiology : What does "p" refer to in context of
alpha error?
The probablity of making a type I error
Behavioral Science: Epidimiology : The preset level of significance is usually
set to p< ___?
p<0.05
Behavioral Science: Epidimiology : Define type II error
Stating that there is not an effect or difference when one exists.
Behavioral Science: Epidimiology : Define "beta"
Beta is the probability of making a type II error. You did not "see" a
difference that does exist.
Behavioral Science: Epidimiology : To mistakenly accept the experimental
hypothesis and reject the null hypothese is type I or II error?
Type I error
Behavioral Science: Epidimiology : To fail to reject the null hypothesis when
in fact it is false is type I or II error?
Type II error.
Behavioral Science: Epidimiology : Setting a guilty man free is an example
of alpha or beta error?
Beta error.
Behavioral Science: Epidimiology : Convicting an innocent man is an
example of alpha or beta error?
C2
Behavioral Science: Epidimiology : Define Power
Probability of rejecting null hypothesis when it is in fact false
Behavioral Science: Epidimiology : Name the two factors power depends on.
1. Total number of end points experienced by the population., 2. Difference
in compliance between treatment groups
Behavioral Science: Epidimiology : True or false: If you increase the sample
size, you increase power.
True. Increasing sample size increases power. "There is power in numbers."
Behavioral Science: Epidimiology : What is the equation to calculate power?
Power = 1 - beta
Reportable Diseases: True or False: HIV is reportable in all states.
False. It varies by state. AIDS is reportable in all states.
Reportable Diseases: List the 12 diseases that are reportable in all states
Hep B, Hep A, Salmonella, Shigella, Syphilis, Measles, Mumps, AIDS,
Rubella, Tuberculosis, Chickenpox, Gonorrhea
What are the Leading Causes of Death in:: Infants (name 5)
Congenital anomalies, short gestation/low birth weight, sudden infant death
syndrom, maternal complications of pregnancy, respiratory distress syndrome
What are the Leading Causes of Death in:: Age 1-14 (name 5)
Injuries, cancer, congenital anomalies, homicide, heart disease
What are the Leading Causes of Death in:: Age 15-24 (name 5)
Injuries, homicide, suicide, cancer, heart disease
What are the Leading Causes of Death in:: Age 25-64 (name 5)
Cancer, heart disease, injuries, suicide, stroke
What are the Leading Causes of Death in:: Age 65+ (name 5)
Heart disease, cancer, stroke, COPD, pneumonia, influenza
Disease Prevention: What is primary prevention? Give an example.
Prevent disease occurrence. Ex. Vaccination
Disease Prevention: What is secondary prevention? Give and example.
Early detection of disease. Ex. Pap smear.
Disease Prevention: What is tertiary prevention? Give an example.
Reduce disability from disease. Ex. Exogenous insulin for diabetes.
Additional services for Specific Groups:: What are the preventive services
need for Diabetes?
Eye, foot exams; urine test
Additional services for Specific Groups:: What are the preventive services
need for Drug abuse?
HIV, TB tests; hepatitis immunization
Additional services for Specific Groups:: What are the preventive services for
alcoholism?
Influenza, pneumococcal immunizations; TB test
Additional services for Specific Groups:: What are the preventive services for
overweight?
Blood sugar test
Additional services for Specific Groups:: What are the preventive services for
homeless, recent refugees or immigrant?
TB test
Additional services for Specific Groups:: What are the preventive services for
high-risk sexual behavior?
HIV, hep B, syphilis, gonorrhea, chlamydia tests
Suicide: Name nine risk factors for suicide completion.
SAD PERSONS= Sex (male), Age, Depression, Previous attempt, Ethanol
(alcohol or drug use), Rational thought, Sickness (medical illness +/- 3 or
more prescription medications), Organized plan (presence and lethality of
plan), No spouse (alone), Social suport lacking.
Suicide: Suicide attempts occur more often in women or men?
Women
Suicide: Suicide completion occur more often in women or men?
Men
Medicaid and Medicare: Medicaid provides assistance at the level of the
state, federal or both.
Medicaid is federal and state assistance.
Medicaid and Medicare: Medicaid provides assistance for what population of
people?
Very poor people. (MedicaisD is for Destitute).
Medicaid and Medicare: Medicare provides assistance at the level of the
state, federal or both.
Medicare is federal assistance.
Medicaid and Medicare: Medicare provides assistancefor what population of
people?
The elderly. (MedicarE is for Elderly)
Medicaid and Medicare: Medicare Part A covers doctor or hospital bills?
Hospital bills.
Medicaid and Medicare: Medicare Part B covers doctor or hospital bills?
Doctor bills.
Behavioral Sciences: Ethics: Define "autonomy".
Obligation to respect patients as individuals and to honor their preferences in
medical care.
Behavioral Sciences: Ethics: List the three legal requirements of informed
consent.
1. Discussion of pertinent information. (Patients must understand the risk,
benefits, and alternatives including no intervention), 2. Patient's agreement to
the plan of care., 3. Freedom from coercion.
Behavioral Sciences: Ethics: List the 4 exceptions to informed consent.
1. Patient lacks decision-making capacity (not legally competent.), 2. Implied
consent in an emergency., 3. Therepeutic privelege., 4. Waiver- patient
waives the right to informed consent.
Behavioral Sciences: Ethics: What is "therapeutic privelege"?
It is withholding information when disclosure would severly harm the patient
or undermine informed decision-making capacity.
Behavioral Sciences: Ethics: What are the 5 determinants of decision-making
capacity?
1. Patient makes and communicates a choice., 2. Patient is informed., 3.
Decision remains stable over time., 4. Decision is consistent with patient's
values and goals., 5. Decision not a result of delusions or hallucinations.
Behavioral Sciences: Ethics: True or false. The patient's family can require
that a doctor withhold information from the patient.
False. The patient's family cannot requires that a doctor withhold information
from the patient.
Behavioral Sciences: Ethics: What is an "oral advance directive"?
Incapacitated patient's prior oral statements is used as a guide in
decision-making.
Behavioral Sciences: Ethics: Name one problem associated with oral
advanced directive.
Interpretation of the directive varies.
Behavioral Sciences: Ethics: Name 4 factors that make an oral advanced
directive more valid.
1. The patient was informed., 2. The directive is specific., 3. The patient
makes a choice., 4. The decision was repeated over time.
Behavioral Sciences: Ethics: What is a "living will"?
Written advance directive in which the patient directs physician to withhold
or withdraw life-sustaining treatment if the patient develops a terminal
disease or enters a persistent vegetative state.
Behavioral Sciences: Ethics: What is a "durable power of attorney"?
Written advance directive in which the patient designates a surrogate to make
medical decisions in the event that the patient loses decision-making capacity.
Patient may also specify decisions in clinical situations.
Behavioral Sciences: Ethics: Can patient revoke surrogate power?
Yes.
Behavioral Sciences: Ethics: Is a living will or a durable power of attorney
more flexible?
Durable power of attorney.
Behavioral Sciences: Ethics: Define "nonmaleficence."
Do no harm.
Behavioral Sciences: Ethics: True or false. If benefits of an intervention
outweigh the risks, a patient may make an informed decision to proceed.
True.
Behavioral Sciences: Ethics: Define "beneficience."
Physicians have a special ethical responsibility to act in the patient's best
interest ("physician is a fiduciary").
Behavioral Sciences: Ethics: If patient autonomy conflicts with beneficence,
and the patient makes an informed decision, does the physician or the patient
have the right to decide?
Ultimately, the patient has the right to decide.
Behavioral Sciences: Ethics: Define "confidentiality."
Repecting patient privacy and autonomy.
Behavioral Sciences: Ethics: True or false. The physician should never
disclose information to family or friends.
False. Disclosing information should be guided by what the patient would
want.
Behavioral Sciences: Ethics: True or false. The patient may waive the right to
confidentiality.
True. Ex. Insurance companies.
Behavioral Sciences: Ethics: List the 4 exceptions to confidentiality.
1. Potential harm to others is serious., 2. Liklihood of harm to self is great., 3.
No alternative means exist to warn or to protect those at risk., 4. Physicians
can take steps to prevent harm.
Behavioral Sciences: Ethics: What is the "Tarasoff decision"?
It is an example of an exception to confidentiality. It is a law requiring
physicians to directly inform and protect potential vistim from harm.
Behavioral Sciences: Ethics: List 5 examples of exceptions to confidentiality.
1. Infectious diseases - physicians may have a duty to warn public officials
and identifiable people at risk., 2. The Tarasoff decision., 3. Child and/or
elder abuse., 4. Impaired atuomobile drivers., 5. Suicidal/homicidal patient
Behavioral Sciences: Ethics: True or false. Physician may hold patient
involuntarily for a period of time if the patient is deemed suicidal or
homicidal.
True.
Behavioral Sciences: Ethics: AUTHOR
Victor Esenwa
ETHICAL SITUATIONS (what is your response for each senario): Patient is
noncompliant
Work to improve physician-patient relationship
ETHICAL SITUATIONS (what is your response for each senario): Patient
with difficulty taking medications
Write instruction, try to simplify treatment regimens
ETHICAL SITUATIONS (what is your response for each senario): Family
member ask for information about patient's prognosis
Permission of the patient is required.
ETHICAL SITUATIONS (what is your response for each senario): 17yr old
girl asks for an abortion
Depending on state parental consent for abortion is required for minor. But
NOT for an emergency, STD treatment, prescription for contraceptive,
addiction management and medical care for pregnancy.
ETHICAL SITUATIONS (what is your response for each senario):
Terminally ill patient requests euthanasia?
Refuse involvement of any form of euthanasia. But may prescribe medically
apropriate analgesics that coincidentally shortens the patient's life
ETHICAL SITUATIONS (what is your response for each senario): Patient
states that he finds you attractive
Romantic relationships with patient are never apropriate. Use direct and
closed- ended question and use a chaperone (if necessary)
ETHICAL SITUATIONS (what is your response for each senario): Patient
refuses a necessary procedure or wants an unnecessary one
Try to understand why patient wants/doesn’t want a procedure. Never
perform Unnecessary procedures.
ETHICAL SITUATIONS (what is your response for each senario): Patient
angry about long waiting time
Apologize but stay away from efforts to explain the delay.
ETHICAL SITUATIONS (what is your response for each senario): Patient is
upset with treatment from another doctor.
Suggest tte patient address their issues with the physician. If it’s a member of
the office - tell the patient you will talk with the doctor.
ETHICAL SITUATIONS (what is your response for each senario): Child
request information about his illness.
Ask what the parents have told the child about his illness. Let the parents
decide what info about his illness that will be relayed to the kid..
ETHICAL SITUATIONS (what is your response for each senario): Patient
who is a smoker and believes cigarettes are good for him.
Ask how the patient feels about his smoking. Offer advice on cessation if the
patient seems willing to make an effort to quit
MALPRACTICE: What are the requirements of a civil suit under negligence?
Remember the 3 D's 1. Dereliction (physician breach duty of patient 2.
Damage (patient is harmed) 3. Direct (Breach of duty causes harm)
MALPRACTICE: What is the common factor leading to litigation between
physician and patient?
Poor communication
Apgar Score (at birth): List the Apgar score categories?
1. Color 2. Heart rate 3. Reflex irritability 4. muslce tone 5 Respiratory effort.
Apgar Score (at birth): Maximum Apgar score? Points for each category?
1. Max of 10 points 2. 0-2 (0,1,2)
Apgar Score (at birth): A.P.G.A.R mneumonic?
Aperance (blue, trunk pink, all pink) Pulse (0, <100, 100+) Grimace (0,
grimace, grimace with cough) Activity (limp, some, active) Respiration (0,
irregular, regular)
Low birth weight: Define low birth weight?
Less than 2500g
Low birth weight: Causes of Low birth weight?
Prematurity and intrauterine growth retardation
Low birth weight: Compilications of low birth weight?
Infections (poor immune system), Rrespiratory distress syndrome, necrotizing
entercolitis, intraventricular hemorrhage, and Pesistent fetal circulation
Infant deprivation effects: What are the effects of Infant deprivation(ID) ?
1. decreased muscle tone 2. poor language skills, 3.poor socialization 4 lack
of basic trust, 5. Anaclitic depression, 6. weight loss 7. physical illness
[Anaclitic: Psychological dependence on others]
Infant deprivation effects: The four W's are used to describe the effects of
infant deprivation?
Weak, Wordless, Wanting (socially), Wary
Infant deprivation effects: Complication of severe infant deprivation?
For longer than 6months - changes may be irreversible. Infant death is
possible with severe deprivation.
Anaclitic depression: What is Anaclitic depression?
Depression in an infant due to continued separation caregiver? Results in
withdrawal and unresponsiveness.
Regression in children: Cause of regression in a child?
common in children under stress. E.g toilet trained child who bedwets when
hospitalized
Child abuse: List evidence of physical abuse in a child.
Healed fractures(xray) Cigarette burns Hematoma, multiple bruises Retinal
hemorrhage or detachment
Child abuse: In physical child abuse - who is normally the abuser?
Usually female and the primary caregiver
Child abuse: Number of yearly child abuse related deaths?
3000/yr (USA)
Child abuse: List evidence of sexual abuse in a child.
Genital, anal trauma STDs, UTI
Child abuse: In sexual child abuse - who is normally the abuser?
Known to victim, usually male
Child abuse: What is the peak incidence of sexual abused (age range)?
9-12 years of age
Child abuse: DEVELOPMENTAL MILESTONES
p 124
Child abuse: (list motor and cognitive/social milestones for each age)
0
Child abuse: 3months
Motor: Holds head up, Moro reflex disapear Cog/Social: Social smile
Child abuse: 4-5mo
Motor: Rolls front to back, sits when proped Cog/social: Recognizes people
Child abuse: 7-9mo
Motor: sits alone Cog/social:Stranger anxiety,recognize voices
Child abuse: 12-14mo
Motor:Babinski disapears
Child abuse: 15mo
Motor: walks Cog/social:few words, separation anxiety
Child abuse: Toddler
0
Child abuse: 12-24mo
Motor: climbs stairs, stacks 3 blocks Cog/Social: Object permanence
Child abuse: 18-24
Motor: Stacks 6 blocks Cog/social: Raprochement
Child abuse: 24-48mo
Cog/social: parallel play
Child abuse: 24-36mo
Cog/social: Core gender identity
Child abuse: Preschool
0
Child abuse: 30-36mo
Cog/social: Toilet training
Child abuse: 3yrs
Motor: rides tricycle, copies line or circle drawing Cog/Social: Group play
Child abuse: 4yrs
Simple drawing (stick figure), hops on 1foot Cog/social: co-operative play
Child abuse: School age
0
Child abuse: 6-11yrs
Cog/Social: Development of conscience (superego), same-sex friends,
identification with same sex parent.
Child abuse: Adolescence (Puberty)
0
Child abuse: 11yrs(girls) , 13yrs(boys)
Abstract reasoning (formal operations), formation of personality.
Reflexs present at birth: Name 4 reflexes present at birth (that normally
disappear in 1st year)
1. Moro reflex - extension of limbs when startled 2. Rooting reflex - niple
seek 3. Palmar reflex - grasps objects to palm 4. Babinski reflex - large toe
dorsiflexes with plantar stimulation.
Changes in the elderly: What are the sexual changes in the elderly?
1. Sexual changes - sexual interest does not change with age - men (slower
ejaculation/erection), women: vaginal shortening, thinning and dryness
Changes in the elderly: What are the sleeping pattern changes in the elderly?
↓ REM sleep, ↓ slow-wave, increased sleep latency, increased awakening
during the night.
Changes in the elderly: What are the common medical conditions in the
elderly?
Arthritis, hypertension, heart disease
Changes in the elderly: Is there an increase - in Psychiatric problems e.g
depression in the elderly? Suicide rates?
Yes to both questions
Kubler-Ross dying stages: What are the Kubler-Ross dying stages?
Denial, Anger, Bargaining, Grieving, Acceptance. (not necessary in this
order. >1 can occur.
Kubler-Ross dying stages: Mneumonic for Kubler-Ross dying stages?
Death Arrives Bringing Grave Adjustments
Grief: What are common behaviors associated with breavement? How long
can they last?
1.Guilt, Shock, denial and somatic symptoms 2. 6mo-1yr
Neurotransmitter changes with Disease : Determine what NT increase or
decrease with listed disease.
0
Neurotransmitter changes with Disease : Anxiety?
increase NE, decrease serotonin (5'HT) decrease GABA
Neurotransmitter changes with Disease : Depression?
decrease NE, decrease serotonin
Neurotransmitter changes with Disease : Alzheimer's dementia?
decrease Ach
Neurotransmitter changes with Disease : Huntington's disease?
decrease GABA, decrease Ach
Neurotransmitter changes with Disease : Schizophrenia?
Increase dopamine
Neurotransmitter changes with Disease : Parkinson's disease
decrease dopamine
Frontal lope Functions: What is the functions of the frontal lobe?
Concentration, Orientation, Language Abstraction, Judgement, motor
regulation Mood, Lack of social judgment<--- most notable frontal lobe
lesion.
Sleep Stages: Mneumonic for Sleep Stage waveforms?
At night, BATS Drink Blood
Sleep Stages: Name the waveforms of sleeping?
Beta (highest freq., lowest amplitude) Alpha Theta Spindles and K complexes
Delta (lowest freq, highest amplitude) Beta
Sleep Stages: Below give the Description for each stage? % of total sleep
time spent the stage?
0
Sleep Stages: Beta
Awake(eyes open), alert, active mental concentration
Sleep Stages: Alpha
Awake (eyes closed)
Sleep Stages: Theta
Light sleep (stage 1 of sleep, 5%)
Sleep Stages: Sleep spindles and K complexes
Deeper sleep (stage 2 of sleep, 45%)
Sleep Stages: Delta
Deepest, Non REM sleep: sleepwalking, night terrors, bed wetting (slow
wave sleep) (Stage 3-4 of sleep, 25%)
Sleep Stages: Beta (REM sleep)
Dreaming, loss of motor tone, possibly a memory processing function,
erections, increase brain Oxygen use.
Sleep Stages: What waveform is Non-REM? REM?
Delta , Beta
Sleep Stages: The serotonergic predominance of ----------------- nucleus
initiates Sleep?
Raphe nucleus
Sleep Stages: What is the effect of NE on sleep?
Reduces REM sleep
Sleep Stages: Extraocular movements during REM is due to activity
---------------------
pRF (paramedian pontine reticular formation) /conjugate gaze center
Sleep Stages: What is "paradoxical sleep" and "desynchronized sleep"?
Terms to describe REM sleep because it has the same EEG pattern as while
awake and alert.
Sleep Stages: Why is Benzodiazepines useful for night terrors, and
sleepwalking?
it shortens stage 4 sleep (delta)
Sleep Stages: This tricyclic drug ---- is used to treat enuresis because it
shortens stage 4 drug?
Imipramine
REM Sleep: Mneumonic for remembering the characteristics of REM sleep?
REM is like Sex (increase pulse, penile/clitoral tumerscence, decreases with
age)
REM Sleep: How often does REM occur during sleep?Does it increase or
decrease through the night?
Every 90mins. Increases with the night
REM Sleep: % of REM sleep?
0.25
REM Sleep: Principal neurotransmitter in REM sleep?
Ach
Sleep apnea : In this type of apnea - there is no respiratory effort?
Central sleep apnea
Sleep apnea : In this type of apnea - there is respiratory effort? For at least
how long?
Obstructive sleep apnea. For atleast 10 seconds
Sleep apnea : Common effect of sleep apnea?
becoming chronically tired
Sleep apnea : Sleep apnea is associated with what health conditions?
Obesity , Loud snoring, Systemic/pulmonary hypertension, arrhythmias and
Possible sudden death
Sleep apnea : Treatment for sleep Apnea?
Weight loss (if obese), CPAP (continuous positive airway pressure), surgery.
Narcolepsy: What is Narcolepsy? Name two types?
Person falls alseep suddenly. Hypnagogic - have hallucinations just before
sleep Hypnopompic- have hallucinations just before awakening
Narcolepsy: What is the predominant wave form at the Narcolepsy onset?
REM sleep
Narcolepsy: What is Cataplexy?
Sudden collaspe while awake
Narcolepsy: How much of a role does genetics play in Narcolepsy?
Narcolepsy has a strong genetic component
Narcolepsy: Treatment for Narcolepsy?
Amphetamines
Sleep in Depressed Patient: What are the major changes in sleep pattern in
depressed patients?
decreased slow-wave (non REM - Delta), decreased REM latency, early
morning awakening (important screening question)
Stress effects: What metabolic products does stress induce in the body?
free fatty acids, 17-OH corticosteroids, lipids, cholesterol, catecholamines.
Stress effects: What are the some cellular and organ based effects of stress?
Affects water absorbtion, muscular tonicity, gastrocolic reflex, and mucosal
circulation
Sexual dysfunction: What is the differential for sexual dysfunction?
1. Drugs(antihypertensive,neuroleptics,SSRI, ETOH) 2.
Disease(diabetes,depression) 3. Psychological (performance anxiety)
BMI: What is Body mass index?
measure of weight adjusted for height
BMI: What is the BMI formula?
weight(kg)/height(m)^2
Orientation (Psychiatry) : How can you elicit if a patient is orientated?
1. Is the patient aware of himself as a person 2. Does the patient know his
own name?
Orientation (Psychiatry) : Arrange (Place, time, Person) from 1st to last - in
orientation loss?
1st Time - 2nd Place - Last Person
Orientation (Psychiatry) : What is Anosognosia?
Unaware that one is ill
Orientation (Psychiatry) : What is Autotopagnosia?
Unable to locate one's own body parts.
Orientation (Psychiatry) : What is Depersonalization?
Body seems unreal or dissociated
Amnesia types : What is Anterograde amnesia?
Inability of remember things that occurred after a CNS insult (no new
memory)
Amnesia types : What is Korsakoff's amnesia? Associated behaviours?
A classic anterograde amnesia - caused by thiamine deficiency. Is associated
with confabulations.
Amnesia types : In Korsakoff's amnesia - what CNS structure is destroyed?
Bilarteral destruction of Mammilary bodies
Amnesia types : What is Retrograde amnesia?
Inability to remember things that occurred before a CNS insult.
Amnesia types : What type of amnesia is a complication of ECT
(electroconvulsive therapy)?
Retrograde amnesia
Substance Dependence: List the maladaptive pattern of substance
dependence?
1. Tolerance, 2. Withdrawal, 3. Substance taken in larger amounts than
intended., 4. Persistent desire or attempts to cutdown, 5. Lots of energy spent
trying get substance, 6. Important socia, occupational or recreational
activities given up or reduced because of substance use., 7. Continued use in
spite of knowledge of the problems that it causes
Substance Dependence: What is the definition of substance dependence?
The presence of 3 or more maladaptive signs in 1year
Substance Abuse: Definition of substance abuse?
Maladaptive pattern leading to significant impairment or distress.
Substance Abuse: List 4 symptoms of substance abuse?
1. Recurrent use resulting in failure to fulfill major obligation at work, school
or home, 2. Recurrent use in physically harzardous situations?, 3. Recurrent
substance - related legal problems, 4. Continued use in spite of persistnent
problems caused by use., - Only 1 or more are reguired to met the criteria of
substance abuse.
Substance Abuse: AUTHOR
Rob Flavell
Substance abuse (p. 128): Disinhibition, emotional lability, slurred speech,
ataxia, coma, and blackouts are symptoms of which drug?
Alcohol
Substance abuse (p. 128): CNS depression, nausea and vomiting,
constipation, pupillary constriction, and seizures are the signs of which drug?
Opioids
Substance abuse (p. 128): Psychomotor agitation, impaired judgement,
pupillary dilation, hypertension, tachycardia, euphoria, prolonged
wakefullness and attention, cardiac arrhythmias, delusions, hallucianations,
and fever are side effects of which drug?
Substance abuse (p. 128): Euphoria, psychomotor agitation, impaired
judgment, tachycardia, pupillary dilation, hypertension, hallucinations,
paranoid ideations, angina, and sudden cardiac death are symptoms of which
drug?
Substance abuse (p. 128): Belligerance, impulsiveness, fever, psychomotor
agitation, vertical and horizontal nystagmus, tachycardia, ataxia,
homocidality, psychosis, and delerium are side effects of which drug?
Amphetamines
Cocaine
PCP
Substance abuse (p. 128): Anxiety, depression, del.usions, visual
hallucinations, flashbacks, and pupil dilation are side effects of which drug?
LSD
Substance abuse (p. 128): Euphoria, anxiety, paranoid delusions, perception
of slowed time, impaired judgement, social withdrawl, increased appetite, dry
mouth, and hallucinations are symptoms of which drug?
Marijuana
Substance abuse (p. 128): Low safety margin and respiratory depression are
characteristics of which drug?
Barbiturates
Substance abuse (p. 128): Amnesia, ataxia, somnolesence, minor respiratory
effects, and addictictive effects with alcohol are the characteristics of which
drug?
Benzodiazepines
Substance abuse (p. 128): Restlessness, insomnia, increased diuresis, muscle
twitching, cardiac arrhythmias are the side effects of which drug?
Caffeine
Substance abuse (p. 128): Restlessness, anxiety, insomnia, and arrhytmias are
the side effects of whicch drug?
C2
Substance abuse (p. 128): A craving for cheetos and the desire to watch "old
school" are the side effects of which drug?
marijuana
Substance abuse (p. 128): What are the symptoms of alcohol withdrawl?
Tremor, tachycardia, hypertension, malaise, nausea, seizures, DTs, agitation,
hallucinations
Substance abuse (p. 128): What are the symptoms of opioid withdrawl?
anxiety, insomnia, anorexia, sweating, dilated pupils, piloerection, fever,
rhinorrhea, nausea, stomach cramps, diarrhea, and yawning
Substance abuse (p. 128): What are the symptoms of amphetamine
withdrawl?
Post use crash of depression, lethargy, headache, stomach cramps, hunger,
hypersomnolence
Substance abuse (p. 128): What are the symptoms of cocaine withdrawl
Post use crash of suicidality, hypersomnolence, fatigue, malaise, severe
craving
Substance abuse (p. 128): What are the symptoms of PCP withdrawl
Recurrance of symptoms due to reabsorption, with sudden onsets of severe
random violence
Substance abuse (p. 128): What are the side effects of barbiturate withdrawl?
Anxiety, seizures, delerium, life threatening CV collapse.
Substance abuse (p. 128): What are the side effects of benzodiazepine
withdrawl?
Rebound anxieety, seizures, tremor, insomnia.
Substance abuse (p. 128): What are the side effects of caffeine withdrawl?
Headache, lethargy, depression, weight gain
Substance abuse (p. 128): What are the side effects of nicotine withdrawl?
Irritabilty, headache, anxiety, weight gain, craving, tachycardia?
Substance abuse (p. 128): When do DT's occur?
2-5 days after last drink
Substance abuse (p. 128): What is the treatment for DTs?
Benzodiazepines
Substance abuse (p. 128): What is the sequence of symptoms experienced in
DT's?
Autonomic hyperactivity --> psychotic symptoms --> confusion
Substance abuse (p. 128): What is a competetive inhibitor of heroin?
Naloxone
Substance abuse (p. 128): What diagnoses are associated with heroin
addiction?
hepatitis, abscesses, overdose, hemorrhoids, AIDS, right sided endocarditis.
Substance abuse (p. 128): What drug is used for long term maintinence or
heroin detox?
methadone
Delerium & Dementia (p. 129): What are the symptoms of delerium?
Decreased attention span and arousal, disorganized thinking, hallucinations,
illusions, misperceptions, disturbance in sleep-wake cycle, cognitive
dysfunction
Delerium & Dementia (p. 129): What is the pattern of onset of delerium?
Rapid onset, waxing and waning.
Delerium & Dementia (p. 129): What class of drugs is associated with
delerium?
anticholinergics
Delerium & Dementia (p. 129): What are the symptoms of dementia?
Multiple cognitive deficits- memory, aphasia, apraxia, agnosia, loss of
abstract thought, behavioral or personality changes, impaired judgement.
Delerium & Dementia (p. 129): What are the differences between delerium
and dementia?
Dementia: alert patient, gradual onset.
Delerium & Dementia (p. 129): Dementia may mimic what other illness in
the elderly?
Depression
Major depression (p. 129): What are the two main characteristics of major
depression?
Depressed mood, anhedonia
Major depression (p. 129): What are the nine symptoms of depression?
Sleep disturbances, loss of interest, guilt, loss of energy, loss of
concentration, change in apetite, psychomotor retardation, suicidal ideations,
depressed mood (SIG E CAPS)
Major depression (p. 129): How many of those symptoms do you need and
for how long?
5 symptoms for 2 weeks.
Major depression (p. 129): What is the definition of recurrant major
depressive disorder?
2 or more episodes with 2 month symptom free interval
Major depression (p. 129): What is the lifetime prevalence of major
depression in men?
5-12%
Major depression (p. 129): What is the lifetime prevalence of major
depression in women?
10-25%
Major depression (p. 129): How long must a mild depressive episode last to
be called dysthymia?
2 years.
Major depression (p. 129): ECT is painful, true or false?
FALSE
Major depression (p. 129): What are the side effects of ECT?
due to anesthesia, disorientation, anterograde and retrograde amnesia
Manic episodes (p. 130): How long must abnormally elevated mood be
present for to be called a manic episode?
1 week
Manic episodes (p. 130): What are the symptoms of a manic episode?
Distractability, insomnia, grandiosity, flight of ideas, increase in goal directed
activity or psychomotor agitation, pressured speech, thoughtlessness (DIG
FAST)
Manic episodes (p. 130): How many of those symptoms must be present to be
considered a manic episode?
3
Manic episodes (p. 130): True or false: A hypomanic episode does not cause
marked impairment in social or occupational function?
TRUE
Manic episodes (p. 130): What is the drug of choice for bipolar disorder?
lithium
Manic episodes (p. 130): How many manic episodes does it take to define
bipolar disorder?
1
Manic episodes (p. 130): How many hypomanic episodes does it take to
define bipolar disorder?
1
Manic episodes (p. 130): What type of bipolar disorder involves hypomanic
episodes?
Type II
Manic episodes (p. 130): How long must a milder form of bipolar disorder
last to be called cyclothymic disorder?
2 years.
Munchausen's (p. 130): Is munchausen's syndrome involve conscious or
unconscious motivation?
Unconscious.
Somatoform disorders (p. 130): What are the characteristics of conversion?
Symptoms suggest motor or sensory neurologic or physical disorder, but
physical exam and tests are negative
Somatoform disorders (p. 130): True or false, somatoform disorders are more
common in women?
TRUE
Somatoform disorders (p. 130): What is a prolonged pain that is not explained
by an illness?
Somatoform pain disorder
Somatoform disorders (p. 130): What is the misinterpretation of normal
physical findings leading to a persistent fear of serious illness in spite of
medical reassurance?
Hypochondriasis
Somatoform disorders (p. 130): What are the characteristics of somatization
disorder?
A variety of complaints involving multiple organ systems
Somatoform disorders (p. 130): What is the disorder where a patient believes
their own anatomy is malformed?
body dysmorphic disorder
Somatoform disorders (p. 130): What is the false belief of being pregnant
associated with objective physical signs of pregnancy?
pseudocyesis
Somatoform disorders (p. 130): What is primary gain?
What a symptom does for a patient's internal psychic economy
Somatoform disorders (p. 130): What is secondary gain?
What a symptom gets a patient (sympathy or attention)
Somatoform disorders (p. 130): What is tertiary gain?
What the caretaker gets.
Panic disorder (p. 131): How long does it take a panic attack to peak?
10 minutes
Panic disorder (p. 131): What are the symptoms of panic attack?
palpitations, abdominal distress, nausea, increased perspiration, chest pain,
chills, and choking (PANIC)
Panic disorder (p. 131): How many of those must be present to call it a panic
disorder?
4
Panic disorder (p. 131): What psychiatric disorder has a high prevalence
during the step 1 exam?
panic disorder
Phobia (p. 131): What is a phobia?
Excessive or unreasonable fear cued by presence or anticipation of a specific
object or entity.
Phobia (p. 131): True or false: a patient has insight into their own phobia
TRUE
Phobia (p. 131): Gamophobia is fear of what?
marriage
Phobia (p. 131): Algophobia is fear of what?
pain
Phobia (p. 131): Acrophobia is fear of what?
heights
Phobia (p. 131): Agoraphobia is fear of what?
open places
PTSD (p. 131): What are the symptoms of PTSD?
Traumatic event is persistently reexperienced, a person persistently avoids
stimuli associated with the traums, and experiences persistent increased
arousal
PTSD (p. 131): How long must the symptoms last to be called PTSD?
1 month
PTSD (p. 131): PTSD often follows which disorder?
Acute stress disorder
Other anxiety disorders (p.131): What is adjustment disorder
Emotional symptoms including anxiety or depression causing impairment
following a psychosocial stressor, lasting less than 6 months
Other anxiety disorders (p.131): True or false: general anxiety is related to a
specific person, situation, or event?
FALSE
Other anxiety disorders (p.131): What are the symptoms of generalized
anxiety disorder?
GI symptoms, fatigue, and difficulty concentrating
Personality (p.131): What is a personality trait?
an enduring pattern of perceiving, relating to, and thinking about the
environment and oneself.
Personality (p.131): True or false: a personality disorder does not cause
impairment of social or occupational functioning?
FALSE
Personality (p.131): True or false: a patient with a personality disorder is
aware of their problem
FALSE
Personality (p.131): What are the cluster A personality disorders?
Paranoid, schizoid, schizotypal (Weird)
Personality (p.131): What are the cluster B personality disorders?
Antisocial, borderline, histrionic, narcissistic (Wild)
Personality (p.131): What are the cluster C personality disorders?
Avoidant, obsessive compulsive, dependant (Worried)
Personality (p.131): What cluster has a genetic association with anxiety
disorders?
C (worried)
Personality (p.131): What cluster has a genetic association with mood
disorders?
B (Wild)
Personality (p.131): What cluster has a genetic association with
schizophrenia?
A (weird)
Personality (p.131): What are the characteristics of paranoid personality
disorder?
Distrust, suspiciousness, and projection as a defense mechanism
Personality (p.131): What personality disorder involves limited emotional
expression and voluntary social withdrawl?
Schizoid
Personality (p.131): What personality disorder involves interpersonal
awkwardness, odd thought patterns and appearance?
Schizotypal
Personality (p.131): What personality disorder involves a disregard for others,
crimality, and conduct disorders?
Antisocial
Personality (p.131): What personality disorder involves unstable mood and
behavior, impulsiveness, emptiness, and occurs more often in women?
Borderline
Personality (p.131): What personality disorder involves excessive
emotionality, somatization, attention seeking, and sexually provocative?
Histrionic
Personality (p.131): What PD involves grandiosity, a sense of entitlement?
Narcissistic
Personality (p.131): What PD is sensitive to rejection, socially inhibited,
timid, and has feelings of inadequacy?
Avoidant
Personality (p.131): What PD is preoccupied with order, perfectionism, and
control?
Obsessive-compulsive
Personality (p.131): What PD is submissive and clinging, excessively needs
to be taken care of, and has low self confidence?
Dependant
Childhood disorders (p. 133): What disorder is characterized by repetitive
behaviors, unusual abilities, and below normal intelligence?
Autism
Childhood disorders (p. 133): What is the treatment for autism?
Communication skill and social skill training
Childhood disorders (p. 133): What is the name of a mild form of autism?
Aspberger syndrome?
Childhood disorders (p. 133): True or false: Children with aspberger's
syndrome has normal intelligence and lack social or cognitive defects?
TRUE
Childhood disorders (p. 133): What is the only X-linked childhood
personality disorder?
Rett disorder
Childhood disorders (p. 133): Rett syndrome starts at which age?
4
Childhood disorders (p. 133): What are the symptoms fo rett disorder?
Loss of development, and mental retardation?
Childhood disorders (p. 133): Why does Rett disorder appear only in women?
Male fetuses die in utero.
Childhood disorders (p. 133): True or false: Children with ADHD have
normal intelligence
TRUE
Childhood disorders (p. 133): What is the treatment for ADHD
Methyphenidate (ritalin)
Childhood disorders (p. 133): What is the name given to continued behavior
violating social norms?
Conduct disorder
Childhood disorders (p. 133): What is oppositional defiant disorder?
A noncompliant child in the absence of criminality
Childhood disorders (p. 133): What is the age of onset of tourette's
syndrome?
Before 18
Childhood disorders (p. 133): What is the treatment for tourette's syndrome?
Haloperidol
Childhood disorders (p. 133): What is the name given to a fear of loss of
attachment figure leading to factitious physical complaints?
Seperation anxiety disorder
Childhood disorders (p. 133): What is the typical age for seperation anxiety
disorder?
7 or 8
Eating disorders (p.133): What are the symptoms of anorexia nervosa?
Excessive dieting, body image distortion, increase in exercise. Sever weight
loss, amenorrhea, anemia, and electrolyte disturbances.
Eating disorders (p.133): What are the symptoms of bulimia nervosa?
Binge eating followed by self-induced vomiting or use of laxatives. Parotitis,
enamel erosion, increase in amylase, and esophageal varices from vomiting
Eating disorders (p.133): True or false: Bulimia nervosa involves normal
body weight?
TRUE
Hallucination vs. illusion vs. delusion (p.133): What is a hallucination?
A perception in the absence of actual external stimuli.
Hallucination vs. illusion vs. delusion (p.133): What is an illusion?
A misinterpretation fo actual external stimuli
Hallucination vs. illusion vs. delusion (p.133): What is a delusion?
A false belief that is not shared with other members of culture or subculture,
which is firmly maintained in spite of evidence to the contrary
Hallucination vs. illusion vs. delusion (p.133): True or false: A delusion is a
disorder in the content of thought?
TRUE
Hallucination vs. illusion vs. delusion (p.133): True or false: A loose
association is a disorder in the form ot thought?
TRUE
Hallucinations (p. 133): True or false: Visual hallucinations are rare in
schizophrenia?
FALSE
Hallucinations (p. 133): What type of hallucination occurs as an aura of
psychomotor epilepsy?
Olfactory
Hallucinations (p. 133): What type of hallucination is rarest?
Gustatory
Hallucinations (p. 133): What type of hallucination is common in DT's and in
cocaine abusers?
Tactile
Hallucinations (p. 133): What type of hallucination occurs while going to
sleep?
Hypnagogic
Hallucinations (p. 133): What type of hallucination occurs while waking from
sleep?
Hypnopompic
Hallucinations (p. 133): AUTHORS
Carolyn Goh / Cindy Ku
Hallucinations (p. 133): BEHAVIORAL SCIENCE
0
Schizophrenia: periods of psychosis and disturbed behavior last how long?
6 months
Schizophrenia: 4 positive symptoms?
hallucinations, delusions, strange behavior, loose associations
Schizophrenia: 4 negative symptoms?
flat affect, social withdrawal, thought blocking, lack of motivation
Schizophrenia: 4 A's (described by Bleuler) + 1
1.ambivalence (uncertainty), 2. autism (self-preoccupation and lack of
communication), 3. affect (blunted), 4. associations (loose), 5. auditory
(hallucinations)
Schizophrenia: 5 subtypes
disorganized, catatonic, paranoid, undifferentiated, residual
Schizophrenia: etiology
genetic factors > environmental factors
Schizophrenia: lifetime prevalence
1.5%; males>females; blacks>whites
Schizophrenia: different presentation in men and women
presents earlier and more often in men
Schizophrenia: schizophrenia + mood disorder = ?
schizoaffective disorder
Schizophrenia: Structural theory of the mind
C2
Schizophrenia: how many structures?
Freud had 3
Schizophrenia: primal urges, sex, aggression - things you want
Id
Schizophrenia: moral values, conscience - you know you can't have it
Superego
Schizophrenia: bridge and mediator between unconscious mind and external
world - conflict mediator
Ego
Topographic theory of the mind: *also 3
0
Topographic theory of the mind: Name the components of this theory
CPU - Conscious, Preconscious, Unconscious
Topographic theory of the mind: Conscious
what you're aware of
Topographic theory of the mind: Preconscious
what you are able to make conscious with effort (like phone number or SSN)
Topographic theory of the mind: Unconscious
what you are not aware of (what you don't know you don't know)
Topographic theory of the mind: the central goal of Freudian psychoanalysis
to make the patient aware of what is hidden in his/her unconscious
Oedipus complex: define oedipus complex
repressed sexual feelings of a child for the oposite sex parent, accompanied
by rivalry with same-sex parent - described by Freud
Ego defenses: Your --- has many ---, or automatic and unconscious reactions
to psychological stress.
ego defenses
Ego defenses: Name the mature ego defenses
Mature women wear a SASH: Sublimation, Altruism, Supression, Humor
Ego defenses: using ---, one replaces an unacceptable wish with a course of
action similar but not conflicting with one's values
sublimation
Ego defenses: --- is unsolicited generosity toward others that alleviates guilty
feelings
altruism
Ego defenses: unlike other defenses, this is a voluntary withholding of an idea
or feeling from conscious awareness
supression
Ego defenses: one uses ---, or appreciates the amusing nature to alleviate
anxiety-provoking or adverse situations
humor
Ego defenses: Acting out, dissociation, denial, displacement, fixation,
identification, isolation, projection, rationalization, reaction formation,
regression, repression, splitting are all ---.
immature
Ego defenses: the three D's of immaturity
Dissociation, Denial, Displacement
Ego defenses: by --- --- or throwing a tantrum, unacceptable feelings and
thoughts are expressed through actions
acting out
Ego defenses: the extreme forms of these temporary, drastic changes in
personality memory, consciousness, or motor behavior can result in multiple
personalities, or --- --- ---.
dissociation; dissociative identity disorder
Ego defenses: this is a common reaction in which one avoids awareness of
some painful reality
denial
Ego defenses: a mother might transfer avoided anger at her husband by
yelling at her child
displacement
Ego defenses: partially remaining at a more childish level of development,
like men's fascination with sports games
fixation
Ego defenses: victim of child abuse becomes abuser
identification
Ego defenses: separation of feelings from ideas and events like describing
murder in graphic detail with no emotional response
isolation
Ego defenses: when a man who wants another woman thinks his wife is
cheating on him, he is ---.
projecting
Ego defenses: when one wants to avoid self-blame, one might say a job
wasn't important anyway after not getting it
rationalization
Ego defenses: this is described by someone with libidinous thoughts enters a
monastery
reaction formation
Ego defenses: --- occurs when one turns back the maturational clock, going
back to earlier modes of dealing with the world - like children in stress who
wet the bed
regression
Ego defenses: involuntary withholding of an idea or feeling from conscious
awareness
repression
Ego defenses: belief that people are either good or bad
splitting
Transference and countertransference: sometimes a patient projects feelings
stemming from personal life onto his or her physician, and sometimes the
physician projects feelings stemming from personal life onto the patient
transference and countertransference, respectively
Classical conditioning: salivation (a natural response) is elicited by a bell (a
--- stimulus) that has been associated with food (a natural stimulus), not
necessarily a reward
conditioned, or learned
Operant conditioning: a particular action is elicited because it produces a ---.
reward
Operant conditioning: an action (pressing a button) is produced because, for
example, a mouse wants food
positive reinforcement
Operant conditioning: an action (pressing a button) is produced because, for
example, a med student wants to avoid shock
negative reinforcement - NOT punishment
Reinforcement schedules: pattern of reinforcement determines what?
how quickly a behavior is learned and extinguished if not rewarded
Reinforcement schedules: how quickly is a behavior on a continuous
schedule (i.e., vending machine use) extinguished when not rewarded?
most rapidly
Reinforcement schedules: what schedule shows the slowest extinction when
not rewarded?
variable ratio (gambling)
Intelligence testing: How does the Stanford-Binet test calculate IQ?
mental age/chronological age * 100
Intelligence testing: How does the Wechsler Adult Intelligence Scale
calculate intelligence?
11 subtests - 6 verbal, 5 performance
Intelligence testing: What is the mean IQ?
100, standard deviation = 15
Intelligence testing: what are the IQ values for profound, severe, and
moderate to mild mental retardation?
<20, <40, and <70 (or two standard deviations below the mean)
Intelligence testing: What determines IQ scores - based on correlation?
most highly correlated with school achievement, also correlated with genetic
factors
Intelligence testing: Are intelligence tests objective or projective?
objective
Myocardial action potential: The following questions relate to the action
potential that occurs in atrial and ventricular myocytes and in Purkinje fibers.
0
Myocardial action potential: During phase 0 of the myocardial action
potential, -------- ------- ------ channels open.
voltage-gated Na+
Myocardial action potential: Initial repolarization, or phase 1, is when
voltage-gated ---- channels begin to open and when voltage-gated Na+
channels ---- (close OR inactivate?).
K+ begin to open. Na+ channels inactivate.
Myocardial action potential: Phase 2 is the plateau, when ------- influx
balances ------ efflux.
Ca++ influx balances K+ efflux.
Myocardial action potential: Ca++ influx triggers another Ca++ release from
the ------- --------, which leads to myocyte ------.
sarcoplasmic reticulum. contraction
Myocardial action potential: During what phase do the voltage-gated Ca++
channels close?
phase 3
Myocardial action potential: During phase 3, the rapid repolarization phase,
there is massive -------- efflux.
K+
Myocardial action potential: During resting potential, the myocyte membrane
is highly permeable to what ion?
K+
Pacemaker action potential: Where does the pacemaker action potential
normally occur?
SA and AV nodes.
Pacemaker action potential: The phase 0 stroke of the pacemaker AP differs
from that of the ventricular AP in that the pacemaker cells lack fast ------------ ------- channels.
voltage-gated Na+
Pacemaker action potential: By using Ca++ current for phase 0 upstroke, the
conduction velocity is slowed compared to the fast Na+ upstroke of the
ventricular AP. What purpose does this slowed conduction serve?
The AV node then prolongs trasmission from the atria to ventricles, allowing
for sufficient filling time.
Pacemaker action potential: Which phase of the ventricular AP is absent in
the pacemaker AP?
phase 2, during which there is Ca++ influx in the ventricular AP.
Pacemaker action potential: What ion is responsible for the slow
depolarization current in the pacemaker AP? This current accounts for the
automaticity of the SA and AV nodes.
Na+ (this is the If, or the funny current)
Pacemaker action potential: ACh and catecholemines alter the slope of phase
4, which determines the ------- ------.
heart rate
Pacemaker action potential: Phase 4 depolarization occurs during which
phase of the cardiac cycle?
diastole
Cardiac Output: During exercise, cardiac output (CO) increases as a result of
an increase in -----.
Stroke volume
Cardiac Output: After prolonged exercise, CO increases as a result of an
increase in ------.
heart rate
Cardiac Output: the product of ----- and ----- equals cardiac output.
stroke volume X heart rate
Cardiac Output: Fick principle for cardiac output :
CO = (rate of O2 consumption) / (arterial O2 content-venous O2 content)
Cardiac Output: Formula for mean arterial pressure
CO X TPR
Cardiac Output: What is pulse pressure?
systolic - diastolic
Cardiac Output: Pulse pressure correlates to what other measure?
stroke volume
Cardiac output variables: What three entities affect stroke volume?
(Mnemonic: SV CAP)
contractility, afterload, preload
Cardiac output variables: If afterload is decreased, what happens to stroke
volume?
increased
Cardiac output variables: What happens to stroke volume in pregnancy?
increases
Cardiac output variables: What does hypoxia/hypercapnea do to contractility?
decreases
Cardiac output variables: What does a decrease in extracellular Na+ do to
contractility?
increases
Cardiac output variables: Digitalis increases intracellular ---- ion.
Na+
Cardiac output variables: What does acidosis do to contractility?
decreases
Preload and afterload: Ventricular end diastolic volume is -----.
preload
Preload and afterload: What is afterload?
diastolic arterial pressure (proportional to peripheral resistance)
Preload and afterload: What class of drugs decreases preload?
venous dilators (nitroglycerine)
Preload and afterload: Drugs like hydralazine decrease ------.
afterload (they are vasodilators)
Starling curve: Force of contraction is proportional to -------.
initial length of cardiac muscle fiber (preload)
Starling curve: Sympathetic stimulation will shift the curve on a graph of CO
vs. preload up and toward the ---- (right / left).
left.
Ejection Fraction: Ejection fraction is stroke volume divided by -----.
end diastolic volume
Ejection Fraction: EF is an index of ventricular -------.
contractility
Ejection Fraction: What is normal EF?
greater than 55%
Resistance, pressure, flow: Viscosity of blood depends mostly on ------
hematocrit
Resistance, pressure, flow: name three conditions in which viscosity
increases.
(1) polycythemia (2) hyperproteinemic state (e.g. multiple myeloma) (3)
hereditary spherocytosis
Resistance, pressure, flow: Resistance is proportional to viscosisty and
inversely proportional to ---------.
radius to fourth power.
Cardiac and vascular function curves: Decreasing the volume of blood shifts
the venous pressure curve to the ------. (on a graph of venous return vs. RA
pressure)
left
Cardiac and vascular function curves: On a graph of CO vs. EDV, digitalis
(positive inotrope) will shift the curve ------.
up.
Cardiac cycle: Isovolumetric contraction is the period between ---- valve
closure and ----- valve opening.
mitral / aortic
Cardiac cycle: During which period is O2 consumption by the heart the
highest?
isovolumetric contraction
Cardiac cycle: For each heart sound, give the significance
0
Cardiac cycle: S1
mitral and tricuspid valve closure
Cardiac cycle: S2
aortic and pulmonic valve closure
Cardiac cycle: S3
at end of rapid ventricular filling
Cardiac cycle: S4
high atrial pressure/ stiff ventricle
Cardiac cycle: For each situation, give the corresponding heart sound.
0
Cardiac cycle: high atrial pressure/ stiff ventricle heart sound.
S4
Cardiac cycle: aortic and pulmonic valve closure heart sound.
S2
Cardiac cycle: mitral and tricuspid valve closure heart sound.
S1
Cardiac cycle: at end of rapid ventricular filling heart sound.
S3
Cardiac cycle: Dilated CHF is associated with which extra heart sound?
S3
Cardiac cycle: S4 is associated with what condition?
hypertrophic ventricle
Cardiac cycle: For each wave of the jugular venous pulse, give the
corresponding physiologic event.
0
Cardiac cycle: jugular venous pulse a wave
atrial contraction
Cardiac cycle: jugular venous pulse c wave
RV contraction (tricuspid valve bulging into atrium)
Cardiac cycle: jugular venous pulsev wave
increase in atrial pressure due to filling against closed tricuspid valve.
Cardiac cycle: Jugular venous distention is a sign of --- --- ----.
right heart failure.
Cardiac cycle: AUTHOR
Daniel Weisholtz
Cardiac cycle: Editor
Marc Waase
Cardiac cycle: PHYSIOLOGY
0
Conduction to Contraction (Cardiac Myocyte): What is the function of the T
tubule?
allows depolarization to travel down it, leading to muscle contraction
Conduction to Contraction (Cardiac Myocyte): This band in a skeltal muscle
contains myosin filaments (thick filaments)
H band/zone
Conduction to Contraction (Cardiac Myocyte): This band in a skeltal muscle
contains only actin filaments (thin filaments)
I band
Conduction to Contraction (Cardiac Myocyte): Which band in a muscle
remains the same size?
A band (dark bands)
Conduction to Contraction (Cardiac Myocyte): During muscle contraction,
which bands shrink?
H, I, and Z bands
Conduction to Contraction (Cardiac Myocyte): What is the function of the
ryanodine receptor?
voltage-sensing CA+2 channel protein in the sacroplasmic reticulum
Conduction to Contraction (Cardiac Myocyte): What is the function of the
dihydropyridine receptor?
voltage-sensing CA+2 channel protein in the T-tubule
Cardiact myocyte physiology: Where does the calcium come from that
stimulates cardiac muscle contraction?
extracellular calcium enters the cell during the plateau of the action potential
and stimulates release of calcium from the sarcoplasmic reticulum
(calcium-induced calcium release)
1. action potential has a plateau which is due to Ca++ influx. 2. Cardiac nodal
cells spontaneously depolarize, resulting in automaticity. 3. Cardiac myocytes
are electrically coupled to each other by gap junctions.
The smooth muscle membrane depolarizes, voltage-gated calcium channels
open, calcium rushes into the cell, calcium binds to calmodulin, calcium
Smooth muscle contraction: How does the action potential in smooth muscle
calmodulin complex activates myosin light chain kinase, MLCK
lead to contraction?
phosphorylates myosin light chain which crosslinks with actin and causes
contraction.
Smooth muscle contraction: How is myosin light chain phosphatase involved
It dephosphorylates myosin light chain, making it less able to cross-bridge
in relaxation.
with actin--allowing relaxation
Cardiact myocyte physiology: Name three ways that cardiac muscle differs
from skelatal muscle with regards to its electrophysiolopgy.
Skeletal Muscle Contraction: Muscle contraction is a result of cross-linking
between which two proteins?
actin and myosin
Skeletal Muscle Contraction: ____binds to myosin head during a skeletal
muscle contraction
ATP
Electrocardiogram: Identify the significance of each of the following:
0
Electrocardiogram: P wave
atrial depolarization
Electrocardiogram: PR segment
conduction delay through AV node
Electrocardiogram: QRS complex
ventricular depolarization
Electrocardiogram: QT interval
mechanical contraction of ventricles
Electrocardiogram: T wave
ventricular repolarization
Electrocardiogram: ST segment
isoelectric, ventricles depolarized
Electrocardiogram: U wave
caused by hypocalemia
Electrocardiogram: What is masked by the QRS complex?
atrial repolarization
Electrocardiogram: Where is the pacemaker of the heart?
SA node in right atrium
Electrocardiogram: ECG tracings
351-352
Electrocardiogram: Match the ECG finding with the description of the ECG
trace:
0
Electrocardiogram: 1. Progressive lengthening of the PR interval until a beat
is "dropped" (a pwave not followed by a QRS complex). Usually
asymptomatic.
B. 2nd degree AV block, (Mobitz type I) (wenckebach)
Electrocardiogram: 2. A rapid succession of identical, back-to-back atrial
depolarziation waves. "sawtooth appearance"
G. Atrial flutter
Electrocardiogram: 3. Dropped beats that are not preceded by a change in the
length of the PR interval . These abrupt, nonconducted P waves result in a
pathologic condition.
C. Mobitz Type II
Electrocardiogram: 3. PR interval is prolonged (>200 msec). Asymptomatic
A. AV block 1st degree
Electrocardiogram: 4. Chaotic and erratic baseline with no discrete p waves
in between irregularly spaced QRS complexes
F. Atrial Fibrillation
Electrocardiogram: 5. The atria and ventricles beat independently of each
other. Both P waves and QRS complexes are present, although the P waves
bear no relation to the QRS complexes. The atrial rate is faster than the
ventricular rate.
D. 3rd Degree, complete AV block
Electrocardiogram: 6. A completely erratic rhythm with no identifiable
waves.
E. Ventricular Fibrillation
Control of mean arterial Pressure (MAP): Name four compensatory
mechanisms that are activated when baroreceptors detect low MAP
Heart rate increases (beta1), contractility increases (beta1), venous
tone--venous return increases (alpha), TPR increases (alpha), kidneys retain
sodium and H20 (renin-angiotensin-aldosterone system)
Arterial Baroreceptors: Aortic Arch baroreceptor transmits via what nerve to
the medulla?
vagus (X)
Arterial Baroreceptors: Carotid Sinus baroreceptor transmits via what nerve
to the medulla?
glossopharyngeal (IX)
Arterial Baroreceptors: Decreasing the stretch on the baroreceptors leads to:
(increased/decreased) efferent sympathetic stimulation
Increased. Decreased stretch as a result of decreased MAP decreases the
afferent signal from the baroreceptor which leads to an increase in the
efferent sympathetic signal from the brain
Arterial Baroreceptors: Hypotension leads to vaso____(constriction/dilation)
vasoconstriction
Arterial Baroreceptors: What is the effect of a carotid massage?
It increases the pressure in the carotid artery, increases the stretch of the
baroreceptors, and leads to a decrease in heart rate.
Arterial Baroreceptors: Which receptor transmits to the medulla, responding
only to increase blood pressure
Aortic arch
Chemoreceptors: Name three physiological changes that are sensed by
peripheral chemoreceptors (carotid and aortic bodies).
1. decreased pO2 below 60 mmHg; 2. increased pCO2; 3. decreased pH of
blood
Chemoreceptors: Central chemoreceptors (in brain) respond to ____ and ____
but do not directly respond to _____.
pH; pCO2; pO2
Circulation Through Organs: Which organ has the largest share of systemic
cardiac output?
Liver
Circulation Through Organs: Which organ has the highest blood flow per
gram of tissue?
Kidney
Circulation Through Organs: Which organ has a large arteriovenous O2
difference
Heart
Normal Pressures: Match the normal pressures with a heart chamber or major
vessel: A. Right atrium/vena cava, B. Right Ventricle, C. Pulmonary Artery,
D. Left Atrium, E. Left Ventricle, F. aorta
0
Normal Pressures: <150/10
E. LV
Normal Pressures: <25/10
C. PA
Normal Pressures: <25/<5
B. RV
Normal Pressures: <5
A. RA
Normal Pressures: <150/90
F. aorta
Normal Pressures: <12
D. LA
Normal Pressures: What does the PWCP approximate?
Pulmonary capillary wedge pressure aproximates left atrial pressure.
Normal Pressures: How is PWCP measured?
Swan-Ganz catheter
Blood Flow Autoregulation: What factors regulate blood flow to the
following tissues?
0
Blood Flow Autoregulation: Heart
local metabolites: O2, adenosine, NO
Blood Flow Autoregulation: Brain
local metabolites: CO2 (pH)
Blood Flow Autoregulation: Kidneys
myogenic and tubuloglomerular feedback
Blood Flow Autoregulation: Lungs
hypoxia causes vasoconstriction (only organ in which hypoxia leads to
vasoconstriction)
Blood Flow Autoregulation: Skeletal muscle
local metabolites: lactate, adenosine, K+
Blood Flow Autoregulation: Skin
sympathetic stimulation in response to changes in body temperature
Blood composition: Plasma-clotting factors = what?
serum
Blood composition: Blood is ___% of body weight
0.08
Blood composition: Blood is ___% plasma.
55% The rest is formed elements (hematocrit)
Blood composition: Plasma is ____% proteins.
0.07
Blood composition: Plasma proteins are ___% albumin.
0.55
Blood composition: Plasma proteins are ___% globulins
0.38
Blood composition: Leukocytes are normally ____% PMNs, ___%
lymphocytes, ___% monocytes, ___% eosinophils, ___basophils.
40-70% PMNs, 20-40% lymphos, 2-10% monos, 1-6% eos, <1% basophils
Blood composition: AUTHOR
Chris Leander
Coagulation Cascade: Factor initiating intrinsic pathway?
XII
Coagulation Cascade: Factor(s) initiating extrinsic pathway?
VII and tissue factor
Coagulation Cascade: Function of factor XIII?
Forms cross-linked fibrin
Coagulation Cascade: Factors examined with prothrombin time (PT)?
VII, X, V, prothrombin, fibrinogen (Hoffbrand. Haematology. 247)
Coagulation Cascade: Factors examined with partial thromboplastin time
(PTT)?
VIII, IX, XI, XII, X, V, prothrombin, fibrinogen (Hoffbrand. Haematology.
247)
Coagulation Cascade: Vitamin K dependent factors?
II, VII, IX, X, protein C, protein S (243)
Coagulation Cascade: Factors requiring phospholipid surface for activation?
IX and X
Coagulation Cascade: Factor I also known as?
Fibrinogen
Coagulation Cascade: Factor II also know as?
Prothrombin
Convergence of coagulation, complement, and kinin pathways: Two
substrates of Factor XIIa?
Factor XI and Prekallikrein
Convergence of coagulation, complement, and kinin pathways: Components
involved in the activation of factor XII?
Collagen, basement membrane, activated platelets, HMWK (cofactor [high
molecular weight kallikrein])
Convergence of coagulation, complement, and kinin pathways: Two
substrates of kallikrein?
HMWK and Plasminogen
Convergence of coagulation, complement, and kinin pathways: Complement
protein on which plasminogen acts?
C3
Convergence of coagulation, complement, and kinin pathways: Three
functions of bradykinin?
Increase vasodilation, increase permeability, increase pain
Convergence of coagulation, complement, and kinin pathways: What
converts HMWK to bradykinin?
kallikrein
Convergence of coagulation, complement, and kinin pathways: What does
plasmin's action on fibrin produce?
fibrin split products
Capillary Fluid Exchange: Forces that move fluid out of capillary?
Capillary pressure (Pc) and Interstitial fluid colloid osmostic pressure
Capillary Fluid Exchange: Forces that move fluid into capillary?
Interstitial fluid pressure (Pi) and Plasma colloid osmotic pressure
Equation for net filtration pressure?: Conditions that cause edema by
increased capillary pressure?
heart failure
Equation for net filtration pressure?: Conditions that cause edema by
increased capillary permeability?
toxins, infections, burns
Equation for net filtration pressure?: Conditions that cause edema by
decreased plasma proteins?
nephrotic syndrome, liver failure
Equation for net filtration pressure?: Conditions that cause edema by
increased fluid colloid osmotic pressure?
lymphatic blockage
Fluid Compartments: Percentage of total body weight that is water?
0.6
Fluid Compartments: Relative amounts of water in extracellular and
intracellular fluid compartments, respectively?
1/3; 2/3
Fluid Compartments: Relative amounts of extracellular fluid in plasma and
interstitial space, respectively?
1/4; 3/4
Fluid Compartments: 60-40-20 rule (% body water)?
60% total body water, 40% ICF, 20% ECF
Renal Clearance: Equation for clearance?
Cx = UxV/Px; Cx = clearance of X; Ux = urine concentration of X; Px =
plasma concentration of X; V = urine flow rate
Renal Clearance: Significance of Cx < GFR?
net tubular reabsorption of X
Renal Clearance: Significance of Cx > GFR?
net tubular secretion of X
Renal Clearance: Significance of Cx = GFR?
no net secretion or absorption of X
Glomerular Filtration Barrier: The two determinants of filtration across the
glomerular filtration barrier are - and -.
size and charge
Glomerular Filtration Barrier: Components of filtration barrier?
Fenestrated capillary endothelium, fused basement membrane with heparin
sulfate, epithelial layer
Glomerular Filtration Barrier: What comprises epithelial layer?
podocyte foot processes
Glomerular Filtration Barrier: The charge on the fused basement membrane is
-.
Negative
Glomerular Filtration Barrier: The charge barrier is lost in - , characterized by
what four findings?
nephrotic syndrome, albuminuria, hypoproteinemia, generalized edema,
hyperlipidemia
Glomerular filtration rate: What substance is freely filtered and is neither
reabsorbed nor secreted?
inulin
Glomerular filtration rate: Clinically, - clearance is a good measure of GFR.
creatinine
Glomerular filtration rate: Equation for GFR
GFR = U(in) X V/P(in) = C(in)
PAH: Where in nephron is PAH secreted?
proximal tubule
PAH: By what mechanism is it secreted?
2■ active transport. Mediated by a carrier system for organic acids
PAH: What drug competively inhibits PAH's secretion?
probenecid.
Effective Renal Plasma Flow: What substance entering the nephron is filtered
AND secreted?
PAH
Effective Renal Plasma Flow: Equation for effective renal plasma flow?
ERPF = U(pah) X V/P(pah) = C(pah)
Effective Renal Plasma Flow: Equation for renal blood flow?
RBF = RPF/1-Hct
Filtration Fraction: Equation for filtration fraction?
FF = GFR/RPF
Filtration Fraction: Class of substances responsible for dilating afferent
arteriole?
Prostaglandins
Filtration Fraction: Class of drug that inhibits production of above
substances?
NSAIDS
Filtration Fraction: Substance responsible for constricting efferent arteriole?
angiotensin II
Filtration Fraction: Class of drugs that inhibits production of angiotensin II?
ACE inhibitors
Free Water Clearance: What factors do you need to know to calculate free
water clearance?
urine flow rate, urine osmolarity, plasma osmolarity
Free Water Clearance: Equation for free water clearance?
C(H2O) = v - C (osm)
Glucose Clearance: Where is glucose absorbed in the nephron?
proximal tubule
Glucose Clearance: At what plasma glucose level does glucosuria begin?
200 mg/dL
Glucose Clearance: At what plasma glucose level is the glucose threshold
mechanism (Tm) saturated?
350 mg/dL
Amino Acid Clearance: How many carrier systems involved in amino acid
reabsorption?
3
Amino Acid Clearance: Where does 2■ active transport occur?
proximal tubule
Nephron Physiology: Substances reabsorbed in the early proximal tubule?
all glucose and amino acids; most bicarbonate, sodium, and water
Nephron Physiology: - is secreted in the early proximal tubule, which acts as
a buffer for -.
ammonia, H+
Nephron Physiology: Section of the nephron that is impermeable to sodium?
thin descending loop of Henle
Nephron Physiology: Substances actively reabsorbed in the thick ascending
loop of Henle?
Na+, K+, Cl-
Nephron Physiology: - and - are indirectly reabsorbed in the thick ascending
loop of Henle.
Ca+2 and Mg+2
Nephron Physiology: Substances actively reabsorbed in the early distal
convoluted tubule?
Na+ and Cl-
Nephron Physiology: Reabsorption of - is under the control of - (hormone) in
the early distal convoluted tubule,
Ca+2, PTH
Nephron Physiology: Substances regulated by aldosterone in collecting
tubules?
Na+, K+
Nephron Physiology: Reabsorption of water is regulated by - in the collecting
tubules?
ADH
Nephron Physiology: Osmolarity of the medulla can reach a concentration of
-.
1200 mOsm
Relative Concentrations Along Renal Tubule: Relative concentration
equation for comparing concentrations of substances in renal tubule to
plasma?
[tubular fluid]/[plasma]; TF/P
Relative Concentrations Along Renal Tubule: Substance with highest TF/P?
PAH
Relative Concentrations Along Renal Tubule: Why does this substance have
the highest TF/P?
Its both filtered and secreted
Relative Concentrations Along Renal Tubule: Substances with lowest TF/P?
glucose and amino acids
Relative Concentrations Along Renal Tubule: Why do these substances have
the lowest TF/P's?
They are reabsorbed almost completely in the early proximal tubule
Relative Concentrations Along Renal Tubule: What substance has a TF/P =
1?
inulin
Renin-Angiotensin System: Where does renin come from in the kidney?
Cells in the juxta-glomerular aparatus
Renin-Angiotensin System: Mechanism stimulating renin release?
Decrease in blood pressure in kidneys
Renin-Angiotensin System: What does renin do?
Cleaves angiotensinogen to angiotensin I
Renin-Angiotensin System: Angiotensin I is then cleaved by -, primarily in
the -, to make -?
angiotensin converting enzyme, lung capillaries, angiotensin II
Renin-Angiotensin System: 4 actions of angiotensin II?
1) Potent vasoconstriction, 2) Release of aldosterone from adrenal cortex, 3)
release of ADH from the posterior pituitary, 4) Stimulates hypothalmus to
increase thirst.
Renin-Angiotensin System: Overall actions of angiotensin II?
Increase intravascular volume and blood pressure
Renin-Angiotensin System: - (hormone) released from the - may act as a
"check" on the renin-angiotensin system in such cases as heart failure.
ANP, atria
Kidney Endocrine Functions: Endothelial cells of peritubular capillaries
secrete - in response to hypoxia.
erythropoietin
Kidney Endocrine Functions: What is the enzyme responsible for converting
25-OH vitamin D to I,25-(OH)2?
1-alpha-hydroxylase
Kidney Endocrine Functions: What hormone activates this enzyme?
PTH
Kidney Endocrine Functions: What is the function of secreted prostaglandins
in the kidney?
Vasodilation of the afferent arterioles to increase GFR
Kidney Endocrine Functions: Class of drugs that can cause renal failure in
high vasoconstrictive states due to inhibition of prostaglandin production?
NSAIDS. Prostaglandins are keeping the afferent arterioles vasodilated to
maintain GFR. Inhibition of prostaglandin production leads to acute renal
failure.
Hormones Acting On the Kidney: Name two stimuli for ADH secretion?
Increased plasma osmolarity; decreased blood volume
Hormones Acting On the Kidney: Two actions of ADH other than increasing
water permeability in the collecting duct
Increase urea absorption in the collecting duct; Increase Na/K/2Cl activity in
thick ascending limb
Hormones Acting On the Kidney: Hormones stimulated to be released by a
decrease in blood volume?
ADH, aldosterone, angiotensin II (via renin)
Hormones Acting On the Kidney: Hormones that increase Na+ reabsorption?
Aldosterone (distal tubule); angiotensin II (proximal tubule
Hormones Acting On the Kidney: Three effects of PTH on the kidney?
1) Increase Ca+2 reabsorption, 2) Decrease phosphate reabsorption, 3)
Increase vitamin D production
Hormones Acting On the Kidney: Hormone that decreases sodium
reabsorption?
ANP
Pituitary Gland: Hormones released from the posterior pituitary?
ADH and oxytocin
Pituitary Gland: Where are they made?
hypothalamus
Pituitary Gland: Hormones released from the anterior pituitary?
FLAT PiG: FSH, LH, ACTH, TSH, prolactin, GH
Pituitary Gland: Embryological origin of anterior and posterior pituitary,
respectively.
oral ectoderm (anterior), neuroectoderm (posterior)
Pituitary Gland: Hormones derived from proopiomelanocortin?
ACTH, MSH
Pituitary Gland: hormones with common alpha subunit?
TSH, LH, FSH, hCG
Pituitary Gland: Subunit determining hormone specificity?
beta subunit
PTH: Cells in the parathyroid that secrete PTH.
Chief cells
PTH: Organs/tissue on which PTH acts.
Bone, small intestine (via 1, 25 dihydroxy vitamin D), kidney
PTH: Cells stimulated in bone by PTH.
osteoblasts (directly) AND osteoclasts (indirectly)
PTH: How does PTH affect phosphate levels?
Decreases them; it’s the Phosphate Trashing Hormone
PTH: What is the function of PTH on bone?
Increase bone resorption of calcium and phosphate
PTH: What stimulates PTH release?
Low free serum Ca+2
PTH: Three action of PTH on the kidney.
1) Increase vitamin D production, 2) Phosphate secretion, 3) Calcium
reabsorption (distal convoluted tubule)
PTH: AUTHOR
Amy Whittle / Flora Waples-Trefil
Viamine D: What are two sources of Vitamin D?
Plants, and sun exposire on skin
Viamine D: What are they converted to in the kidney?
1,25-OH-vitamin D (biologically active form)
Viamine D: What are three fucntions of Vitamin D?
Increases calcium and phosphate absorbtion from the gut, increases bone
resobtion of Calcium and phosphate.
Viamine D: If calcium or potasium in the blood drop, what effect does that
have on vitamin D procudtion?
They both act to increase it. Makes sens, if you think about its actions.
Viamine D: What effect does PTH have on vitamin D?
increases its formation - again, PTH wants to increase blood calcium levels,
so an increase in vitamin D would help that.
Viamine D: What effect do vitamin D levels have on vitamin D production?
negative feedback loop
Viamine D: If you lack vitamin D as a child you get:
Rickets
Viamine D: If you lack vitamin D as a adult you get :
osteomalacia
Calcium, Phosphate, and Alkaline Phosphatase Levels: What are som
common cuases of Hypercalcemia?
Malignancy, Intoxication with Vit. D, Sacroidosis, Hyperparathyroidism,
Alkalie syndrome, and Pagets (bone). Remember: MISHAP
Calcium, Phosphate, and Alkaline Phosphatase Levels: What is alkaline
phsphtase a measurement of?
It is an enzyme found in bone and liver. The bone specific enzyme indicates
attemtped growth in the bone.
Calcium, Phosphate, and Alkaline Phosphatase Levels: In
Hyperparathyroidism, what are the Ca levels?
Increased, remember, PTH acts to increase CA in the serum.
Calcium, Phosphate, and Alkaline Phosphatase Levels: In
Hyperparathyroidism, what are the Phosphate levels?
Decreased. TPH increases its secretion in the kidney to keep serum Ca high
Calcium, Phosphate, and Alkaline Phosphatase Levels: In
Hyperparathyroidism, what are the Alk Phos levels?
Elevated, because PTH actiavrse osetoblasts as well as osteoclasts
Calcium, Phosphate, and Alkaline Phosphatase Levels: In Paget's (bone) what
are the Ca levels?
Normal or elevated
Calcium, Phosphate, and Alkaline Phosphatase Levels: In Paget's (bone) what
are the Phosphate levels?
Normal
Calcium, Phosphate, and Alkaline Phosphatase Levels: In Paget's (bone) what
are the Alk Phos levels?
Elevated a lot, becxuase of all the bone formation going on.
Calcium, Phosphate, and Alkaline Phosphatase Levels: In Vit. D intoxication
what are the Ca levels?
High. Vit. D increase absorbtion in the gut.
Calcium, Phosphate, and Alkaline Phosphatase Levels: In Vit. D intoxication
what are the Phosphate levels?
High.
Calcium, Phosphate, and Alkaline Phosphatase Levels: In Vit. D intoxication
what are the Alk Phos levels?
Normal or high, as the calcium is incorperated
Calcium, Phosphate, and Alkaline Phosphatase Levels: In Osteoperosis what
are the Ca levels?
Normal
Calcium, Phosphate, and Alkaline Phosphatase Levels: In Osteoperosis what
are the Phosphate levels?
Normal
Calcium, Phosphate, and Alkaline Phosphatase Levels: In Osteoperosis what
are the Alk Phos levels?
Normal
Calcium, Phosphate, and Alkaline Phosphatase Levels: In renal insufficiency
what are the Ca levels?
Low - no vit. D means less abosorbtion
Calcium, Phosphate, and Alkaline Phosphatase Levels: In renal insufficiency
what are the Phosphate levels?
High - kideny can't excrete well
Calcium, Phosphate, and Alkaline Phosphatase Levels: In renal insufficiency
what are the Alk Phos levels?
Normal
Calcitonin: Where is calcitonin made?
Thyroid gland
Calcitonin: What cells?
Parafolliclular cells (C cells)
Calcitonin: What is it's function?
supresses osteoclasts
Calcitonin: What triggers its release?
Increases serum calcium and calcium secretion
Calcitonin: Is this important in humans?
No. It opses PTH, but in humans it is not vital to ca+ homeostasis.
Thyroid Hormones: What do T3 and T4 do, basically?
Control the body's metabolic rate
Thyroid Hormones: What are the four Bs that describe T3's function?
Brain maturation, bone growth, beta adrenergic effects, basal metabolic rate
increased
Thyroid Hormones: What is the mechanism by which metabolic rate is
increased?
Increased Na+/K+ ATPase activity: increased O2 consumption, increased
body temperature
Thyroid Hormones: What happens to glucose and lipid balance under T3's
effect?
Increased glycogenolysis, gluconeogenesis, lipolysis
Thyroid Hormones: What tells the thyroid to release T3?
Hypothalamus releases TRH which stimulates TSH from the pituitary which
stiumlates follicle cells
Thyroid Hormones: What prevents there from being too much thyroid
hormone?
Negative feedback of T3 to the anterior pituitary: decreases sensitivity to
TRH from hypothalamus
Thyroid Hormones: What also stimulates follicle cells (pathological)?
TSI - Grave's disease
Iodine enters follicle cells and is oxidized; goes into lumen as I2.
Thyroglobulin (made from tyrosine) enters lumen and combines with I2 to
Thyroid Hormones: Describe how T3 andd T4 are made?
form monoiodotyrosine and di-iodotyroside (2 of di makes T4 and one di and
one mono makes T3). The T3 and T4 re-enter the follicular cell and are
Binds
to a receptor
in the nucleus
or cytoplasm
and
to bloodstream
the nucleus; the
degraded
by proteolysis,
releasing
the T3 and
T4moves
into the
receptor transforms to expose the DNA binding domain and the
Steroid/Thyroid hormone mechanism: How doees a steroid hormone effect its
hormone/receptor complex binds to an enhancer-like element in DNA.
function?
Bottom line: steroids and thyroid hormone cause gene transcription and
protein formation
Steroid/Thyroid hormone mechanism: Why are the actions of steroid and
You have to wait for the gene transcription and protein synthesis to hapen.
thyroid hormones delayed?
Steroid/Thyroid hormone mechanism: What are the steroid hormones?
I had a PET CAT who was buff because she took steroids. Progesterone,
Estrogen, Testosterone, Cortisol, Aldosterone, Thyroxine
Steroid/Thyroid hormone mechanism: How do steroids circulate if they are
lipophilic?
Bound to binding globulins: increases their solubility and allows for
increased delivery to the target organ
Adrenal steroids: What enzyme does ACTH work on?
Desmolase: convesion of cholesterol to pregnenolone
Adrenal steroids: What does ketoconazole do?
Inhibits desmolase, see above
Adrenal steroids: What happens if you have a 17 alpha hydroxylase
deficiency?
Adrenal steroids: What happens in 21 beta hydroxylase deficiency?
You can't make sex hormones, cortisol but you can make mineralcorticoids.
You get hypertension and hypokalemia because you are wasting all the K in
your kidneys while retaining Na. You are phenotypically femal but have no
maturation.
This is the most common. You have decreased cortisol, increased ACTH,
decreased mineralcorticoids, and increased sex hormones. You are
masculinized and have female pseudohermaphroditism.
Adrenal steroids: What is blood pressure and electrolytes in 21 beta
hydroxylase deficiency?
Hypotension, hyponatremic, hyperkalemic, volume depleted and increased
renin activity to compensate
Adrenal steroids: What condition do you suspect if a newborn has
hypovolemic shock?
21 beta hydroxylase deficiency
Adrenal steroids: What happens if you don't have 11 beta hydroxylase?
Decreased cortisol, decreased aldosterone and corticosterone, increased sex
hormones
Adrenal steroids: What does angiotensin II work on?
Aldosterone synthase: creates more aldosterone from corticosterone
Adrenal steroids: What does DHT come from and how?
Testosterone via 5 alpha reductase
Adrenal steroids: What does estradiol come from?
Testosterone via aromatase
Adrenal steroids: What does estrone come from?
Androstenedione via aromatase
Adrenal steroids: What does DHEA lead to eventually?
Testosteron (and its byproducts)
Adrenal steroids: What can progesterone be enzymatically transformed to?
Glucocorticoids, Androgens and estrogens eventually
Insulin dependent organs : What cells can take in glucose regardless of
insulin levels? Via what receptoir?
Bran and RBC: GLUT-1 receptor
Insulin dependent organs : What does the brain use in starvation when there is
no glucose?
Ketone bodies
Prolactin regulation: What does prolactin have to do with dopamine?
Prolactin increases dopamine synthesis and secretion from the hypothalamus,
which then inhbits prolactin secretion
Prolactin regulation: What do dopamine agonists do to prolactin secretion?
Eg bromocriptine
Inhibit it
Prolactin regulation: What does prolactin do to GnRH and what does this
mean clinically?
Inhbitis synthesis and release: inhibits ovulation
Prolactin regulation: What is a common sign of prolactinoma?
Amenorrhea
Prolactin regulation: What causes prolactin releas?
TRH from hypothalamus works on anterior pituitary to cause prolactin
release
Estrogen: What is the order of potency for estrone, striol, estradiol?
Most to least: estradiol >estrone>estriol
Estrogen: Where does estradiol come from?
Ovary
Estrogen: Do the testes make estrogen?
Yes
Estrogen: Where does estriol come from?
Placenta
Estrogen: What are the benefits of hormone replacement therapy with
estrogen post-menopause?
Less hot flashes, less bone loss
Estrogen: What are the negative effects of unopposed estrogen?
Increased risk of endometrial cancer.
Estrogen: What can decrease the risks of giving estrogen?
Giving progesterone with it.
Estrogen: What does estrogen do to the follicle?
Makes it grow
Estrogen: What does estrogen do to the endometrium and the myometrium?
Growth and excitability
Estrogen: What does estrogen do to the genitalia?
Development
Estrogen: What does estrogen do to breasts?
Stromal development
Estrogen: What does estrogen do to fat distribution?
Female pattern
Estrogen: What does estrogen do to transport proteins?
Increases hepatic synthesis
Estrogen: What does estrogen do to FSH?
Feedback inhibition
Estrogen: What does estrogen do to LH?
Causes surge: feedback switches from negative to posititve just before LH
surge.
Progesterone: What does increased progesterone indicate?
Ovulation
Progesterone: What does progesterone come from?
Corpus luteum, placenta, adrenal cortex, testes.
Progesterone: What does progesterone do to the endometrial glands and
spinal artery development?
Increase secretions, increase artery growth
Progesterone: What does progesterone do for a pregnancy?
Maintains it
Progesterone: What doe progesterone do to myometrial excitability?
Decreases it
Progesterone: What does progesterone do to sperm travel?
Creates thick cervical mucus that inhibits sperm entry into uterus
Progesterone: What does progesterone do to body temperature?
Increases
Progesterone: What does progesterone do to gonadotropins?
Inhibits (LH, FSH)
Progesterone: What does progesterone do to uterine smooth muscle?
Relaxes
Progesterone: AUTHOR
Gabriel Brooks
Menstrual Cycle: Follicular grwoth is fastest when?
during the 2nd week of the proliferative phase
Menstrual Cycle: The grafian follicle matures when?
The proliferative phase day 0-14
Menstrual Cycle: What is the sequence of Hormone surges prior to
Ovulation?
Estrogen surge, then LH surge along with FSH surge.
Menstrual Cycle: When does Progesterone surge
During the Secreoty phase days 14-21
Menstrual Cycle: What hormone is associated with the Maintance of the
Endometrium
Progesterone
hCG: What is the sorce of hCG
The syncytiotrophoblasts
hCG: What is Function of hCG: 1- physiologic, 2-diagnostic, 3-diagnostic
1- maintains the corpus luteum throughout the 1st trimester (acts like LH) 2is useful for pregancy detection. Apears in urine 8 days post fertilization, 3hCG is elevated in wone with hydatidiform moles
Menopause: What is the average age of Menopause
51 (earlier in smokers)
Menopause: Wge linked decline in number of ovarian follicles is associeated
with decline in what hormone
Estrogen
Menopause: What are th hormoneal changes during menopause
decreased estrogen, increased FSH, increased LH (but no surge), increased
GnRH
Menopause: What are the si/sx of menopause
HAVOC: hot flashes, Atrophy of vagina, osteoprosis, coronary artery disease
Androgens: What are the androgens? Where are there sources?
Testosterone , dyhydrotestosterone (DHT), androstenedione: testis,
testis/adrenal, adrenal
Androgens: What are the potencies of the Andrognes?
DHT > testosterone > androstenedione
Androgens: What are the targets of androgens
skin prostate, seminal vescles, epididymis, liver, muscle, brain
Androgens: What active molecule is testosterone converted to? What
converts it? What Drug inhibits it's conversion?
Testosterone is converted to DHT bu 5 alpha reductase which is inhibited by
finasteride
Androgens: What are the functions of androgens: 1-, 2-, 3-, 4-, 5-
1- differentiation of wolffian duct system into internal gonadal structures, 2secondary sex characteristics and growth spurt, 2- required for normal
spermatogenesis, 4- anabolic effects (increase in muscle size, increase in
RBC production, 5- libido
Androgens: What is the fate of Testosterone and androstenedione in adipose
tissue?
testosterone and androstene dione are converted to estrogen in andipose tissue
by enzyme aromatase.
Male sperpatogeneis: What is the function of FSH?
Stimulates sertoli cells to produce ABP and inhibin, stimulates sperm
production.
Male sperpatogeneis: What is the function of LH?
stimulates testosterone release from Leydig cells.
Male sperpatogeneis: What is the function of ABP (androgen-binding
protien)?
ensures that testosterone in seminiferous tubule is high
Male sperpatogeneis: What is the function of Inhibin?
It inhibits FSH release from the anterior pituitary
Male sperpatogeneis: What is the function of testosterone?
Respiratory: Response to High Altiitude: What are the physiological
responses to high altitude: 1-, 2-, 3-, 4-, 5-, 6-, 7-
differentiates male genitalia, has anabolic effects on protein metabolisim,
maintains gametogenesis, maintains libido, inhibits Gn RH, fuses epiphyseal
in bone.
1- acute increase in ventilation,plates
2- chronic
increase in ventilation, 3- increase
in EPO leading to an increase in hematocrit and hemaglobin (chronic
hypoxia), 4- increase in 2,3-DPG, 5- Cellular changes (increase in
mitochondria), 6- increase in excretion of bicarbonates to compensate for
respiratory alkalosis, 7- chronic hypoxic pulmonary vasoconstriction results
in RVH
Respiratory: Response to High Altiitude: What is the action of 2,3-DPG?
binds to hemaglobin so that hemoglobin releases more O2
Respiratory: Response to High Altiitude: What does acetazolamide doe?
it increases the renal excretion of bicarbonates.
Important Lung Products: What are 5 important lung products?
Surfactant, prostaglandins, histamine, ACE, Kallikrein
Important Lung Products: What does surfactant do? What is Surfactant?
What makes Surfactant?
It decreases alveolar surface tension which increases complaince, it is made
of dipalmitoyl phosphatidylcholine (lecithin), it is produced by type II
pneumocytes
Important Lung Products: What pathologic process has a deficiency of
Surfactant?
Neonatal RDS
Important Lung Products: What are the funcitons of ACE
converst angiotensin I to Angiotensin II, inactivates bradyykinin (ACE
inhibitors yield increase bradykinin and cause cough, angioedema)
Important Lung Products: What is the colapsing pressure
2(tension)/Radius
Important Lung Products: What does Kallikrein do?
It activates bradykinin
Lung Volumes: What is the Residual volume (RV)?
air in lung at max expiration
Lung Volumes: What is the expiratory reserve volume (ERV)?
air that can still be breathed out after nl expiration
Lung Volumes: What is the tidal volume (TV)?
air that moves into lung with each quiet inspiration (nl = 500ml)
Lung Volumes: What is the inspiratory reserve volume (IRV)?
Air in excess of tidal volume that moves into lung on max inspiration
Lung Volumes: What is the vital capacity (VC)?
TV + IRV + ERV
Lung Volumes: What is the functional reserve capacity (FRC)?
RV + ERV (volume in lungs after normal espiration)
Lung Volumes: What is the inspiratory Capacity (IC)?
IRV+ TV
Lung Volumes: What is the total lung capacity (TLC)?
IRV+TV+ERV+RV
Lung Volumes: AUTHOR
Valerie Young
Oxygen-hemoglobin dissociation curve: Decreased affinity of hemoglobin for
O2 = shift ___
Right
Oxygen-hemoglobin dissociation curve: A right shift is caused by an increase
or decrase in each of the following factors: P50, metabolic needs, PCO2,
temperature, H+, pH, altitude, and 2,3-DPG
Increase in all but pH
Oxygen-hemoglobin dissociation curve: Fetal Hb curve is shifted ___
Left (increased affinity for O2)
Pulmonary circulation: T/F: Pulmonary circulation is normally a
low-resistance, low-compliance system
F - Low-resistance, high-compliance
Pulmonary circulation: Cor pulmonale and subsequent RV failure are a
consequence of pulmonary ______
Hypertension
Pulmonary circulation: Hypoxic vasoconstriction that shifts blood away from
poorly ventilated regions is caused by ______
Decrease in PAO2
Pulmonary circulation: In normal health, O2 is perfusion or diffusion limited?
Perfusion limited - gas equilibrates along the length of the capillary
Pulmonary circulation: Which of the following is diffusion limited: CO2,
N2O, or CO?
CO - gas does not equilibrate by the time the blood reaches the end of the
capillary
Pulmonary circulation: When is O2 diffusion limited?
Exercise, emphysema, fibrosis
Pulmonary circulation: Determination of physiological dead space
C2
Pulmonary circulation: What is the equation for Vd?
(Vt) x (PaCO2 -PeCO2)/PaCO2; Pa = arterial & Pe = expired air
V/Q mismatch: What is the ideal V/Q ratio?
V/Q = 1 (permits adequate oxygenation)
V/Q mismatch: At the base of the lung, there is greater ventilation, perfusion,
or both?
Both are greater
V/Q mismatch: What is V/Q at the apex of the lung?
V/Q = 3 (wasted ventilation)
V/Q mismatch: What is V/Q at the base of the lung?
V/Q = 0.6 (wasted perfusion)
V/Q mismatch: V/Q = 0 implies _____
Airway obstruction (shunt)
V/Q mismatch: V/Q = infinity implies ______
Blood flow obstruction (physiological dead space)
V/Q mismatch: Organisms such as TB that thrive in high O2 flourish in the
apex or base of the lung?
Apex
V/Q mismatch: During exercise (increased cardiac output), the vessels in the
apex of the lung ___-------_______
Vasodilate such that V/Q aproaches 1 (versus normal apex V/Q of 3)
CO2 transport: CO2 is transported from tissue to lungs in these 3 forms:
______
(1) Bicarbonate (2) Bound to hemoglobin (3) Dissolved CO2
CO2 transport: What percentage of CO2 is transported in the form of
bicarbonate?
0.9
CO2 transport: What is the intracellular enzyme that converts CO2 into
H2CO3?
Carbonic anhydrase
CO2 transport: H2CO3 is broken down into H+ and HCO3. What happens to
the H+?
H+ combines with Hb to form HHb
CO2 transport: H2CO3 is broken down into H+ and HCO3. What happens to
the HCO3?
HCO3 is pumped out of the red blood cell in exchange for Cl-
CO2 transport: What is the Haldane effect?
Oxygenation of hemoglobin promotes the dissociation of CO2 from
hemoglobin
Salivary secretion: What are the 3 glands involved in salivary secretion?
Parotid, submandibular, sublingual
Salivary secretion: What compound begins starch digestion?
Alpha-amylase
Salivary secretion: What does bicarbonate in the salivary solution do?
Neutralizes bacterial acids and maintains dental health
Salivary secretion: These compounds in saliva lubricate food
Mucins (glycoproteins)
Salivary secretion: T/F: Parasympathetic activity stimulates salivary secretion
while sympathetic activity does not
F - Both parasympathetic and sympathetic activity stimulate salivary
secretion
Stomach secretions: Mucus functions to:
1) Protect the stomach surface from H+, 2) Lubricant
Stomach secretions: Intrinsic factor is needed to absorb which vitamin?
B12
Stomach secretions: Which cells secrete intrinsic factor?
Parietal cells
Stomach secretions: What are 3 functions of H+ in stomach secretions?
Kills bacteria, breaks down food, activates pepsinogen
Stomach secretions: Chief cells secrete _____
Pepsinogen
Stomach secretions: G cells secrete _____
Gastrin
Stomach secretions: Gastrin stimulates parietal cells to secrete _____
Acid
GI secretory products: Autoimmune destruction of _____ leads to chronic
gastritis and/or pernicious anemia
Parietal cells
GI secretory products: Name 3 compounds that stimulate gastric acid
secretion
Histamine, Ach, gastrin
GI secretory products: Name 2 compounds that inhibit gastric acid secretion
Somatostatin, GIP, prostaglandin
GI secretory products: Absence of this product is not essential for digestion
but increases the risk of Salmonella infections
Gastric acid
GI secretory products: Optimal pH for protein degredation by pepsin is ___
pH 1.0 - 3.0
GI secretory products: G cells are located in which 2 places?
Antrum and duodenum
GI secretory products: T/F: Gastrin stimulates gastric motility
TRUE
GI secretory products: Name 4 things that stimulate gastrin secretion
Stomach distention, amino acids, peptides, vagus (via GRP)
GI secretory products: What 2 things inhibit gastrin secretion?
Secretin and stomach acid pH < 1.5
GI secretory products: What is hypersecreted in Zollinger-Ellison syndrome?
Gastrin
GI secretory products: Secretin stimulates secretion of ____ from surface
mucosal cells of stomach and duodenum
Bicarbonate
GI secretory products: I cells are located where?
Duodenum and jejunum
GI secretory products: What stimulates the release of CCK from I cells?
Fatty acids, amino acids
GI secretory products: Name 3 things CCK does
Stimulates gallbladder contraction, stimulates pancreatic enzyme secretion,
inhibits gastric emptying
GI secretory products: Why does pain worsen after eating in cholelithiasis?
CCK release
GI secretory products: S cells secrete _____
Secretin
GI secretory products: Where are S cells located?
Duodenum
GI secretory products: What 2 things does secretin do?
Stimulates pancreatic HCO3 secretion, inhibits gastric acid secretion (nature's
antacid)
GI secretory products: What stimulates the release of secretin?
Fatty acids and acid in the duodenum
GI secretory products: Somatostatin is secreted by __ cells located in
________
D cells; pancreatic islets & GI mucosa
GI secretory products: Somatostatin inhibits (name at least 4 things):
Gastric acid and pepsinogen secretion, pancreatic and small intestine fluid
secretion, gallbladder contraction, and release of insulin and glucagon
GI secretory products: What stimulates somatostatin release?
Acid
GI secretory products: What inhibits somatostatin release?
Vagus
GI secretory products: This GI secretory product has anti-GH effects
Somatostatin
GI secretory products: Name 4 types of secretory cells that are located in the
duodenum
G cells, mucosal cells, I cells, S cells
GI secretory products: AUTHOR
Grace Lau
GI secretory products (continued): function of nitrous oxide
causes smooth muscle relaxation (i.e. LES relaxation)
GI secretory products (continued): 3 things gastrin is secreted in response to
(1) gastric distention, (2) vagal stimulation and (3) amino acid entering
stomach
GI secretory products (continued): action of gastrin
causes gastric H+ secretion
GI secretory products (continued): secretin is secreted in response to
H+ and fatty acids entering duodenum
GI secretory products (continued): action of secretin
pancreatic secretion of HCO3- and inhibits gastric H+ secretion
GI secretory products (continued): VIP (vasoactive intestinal peptide) is
secreted by ---- and ----- of the -----
secreted by smooth muscle and nerves of the intestines
GI secretory products (continued): action of VIP
relaxes smooth muscle, causes pancreatic HCO3- secretion and inhibits
gastric H+ secretion
GI secretory products (continued): Sympathetic (NE) action on GI (4 actions)
(1) increases production of saliva, (2) decreases splanchnic blood flow in
fight or flight response (3) decreases motility (4) constricts sphincters
GI secretory products (continued): Parasympathetic (Ach) action on GI (5)
(1) increases production of saliva, (2) increases gastric H+ secretion (3)
increases pancreatic enzyme and HCO3- secretion (4) stimulates enteric
nervous system to create intestinal peristalsis (5) relaxes sphincters
GI secretory products (continued): Cholecystokinin is secreted in response to
--- and --- entering the ----
amino acids and fatty acids entering the duodenum
GI secretory products (continued): CCK action of GI
causes contraction of gallbladder, relaxation of sphincter of Oddi, and
pancreatic seccretion of enzymes and HCO3-
Regulation of gastric acid secretion: These are four receptors on the parietal
cell that are involved in the regulation of gastric acid secretion
(1) histamine receptor (H2); (2) Acetylcholine receptor (M3); (3) Gastrin
receptor; (4) Prostaglandin receptor
Regulation of gastric acid secretion: H2 receptor antagonists
ranitidine, cimetidine, famotidine
Regulation of gastric acid secretion: Gastrin is increased in this syndrome
Zollinger-Ellison Syndrome
Regulation of gastric acid secretion: Inhibitor of prostaglandin receptor
Misoprostol
Regulation of gastric acid secretion: agonists of prostaglandin receptors on
pariental cell
PGI2 and PGE2
Glucose absorption: glucose absorption occurs at these two places
duodenum and proximal jejunum
Glucose absorption: glucose absorption occurs across the membrane through
this mechanism
sodium-glucose cotransporter
Pancreatic exocrine secretion: Secretory acini of the pancreas secrete
zymogens when stimulated by ---- and ---
acetylcholine and CCK
Pancreatic exocrine secretion: Pancreatic ducts secrete ---- and ---- when
stimulated by ------
secrete mucus and allkaline fluid when stimulated by secretin
Pancreatic enzymes: enzyme for starch digestion that is secreted in active
form from the pancreas
alpha-amylase
Pancreatic enzymes: pancreatic enzymes for fat digestion
lipase, phospholipase A, colipase
Pancreatic enzymes: pancreatic enzymes for protein digestion
trypsin, chymotrypsin, elastase, and carboxypeptidases (secreted as
proenzymes)
Pancreatic enzymes: Proenzyme of trypsin
trypsinogen
Pancreatic enzymes: enzyme that cleaves trypsinogen
enterokinase
Pancreatic enzymes: enzyme that activates the other proenzymes and can also
activate its own proenzyme through positive-feedback
trypsin
Pancreatic enzymes: pancreatic insufficiency clinical presentation
malabsorption and steatorrhea
Pancreatic enzymes: recommendations for pancreatic insufficiency
limit fat intake, monitor for signs of fat-soluble vitamin deficiency
Stimulation of pancreatic functions: stimulates ductal cells to secrete
bicarbonate-rich fluid
secretin
Stimulation of pancreatic functions: major stimulus for secretion of enzyme
rich fluid by pancreatic acinar cells
cholecystokinin
Stimulation of pancreatic functions: major stimulus for zymogen release,
poor stimulus for bicarbonate secretion
acetylcholine
Stimulation of pancreatic functions: inhibits the release of gastrin and secretin
somatostatin
Carbohydrate digestion: this enzyme starts digestion, hydrolyzes alpha-1,4
linkages to give lmaltose, maltotriose, and alpha-limit dextrans
salivary amylase
Carbohydrate digestion: this enzyme has the highest concentration in
duodenal lumen, hydrolyzes starch to oligosaccharides, maltose and
maltotriose
pancreatic amylase
Carbohydrate digestion: these enzymes are at brush border of intestine, the
rate-limiteing step in carbohydrate difestion, produces monosaccarides
oligosaccharide hydrolases
Bilirubin : this product of heme metabolism is taken up by hepatocytes
bilirubin
Bilirubin : conjugated or unconjugated version of bilirubin is water soluble
conjugated version
Bilirubin : condition that results from elevated bilirubin levels
jaundice
Bilirubin : condition with yellow skin and sclerae
jaundice
Bilirubin : normal life span of red blood cells
120 days
Bilirubin : where red blood cells are made
bone marrow
Bilirubin : where do the substrates of heme catabolism in the
reticuloendothelial system come from
80%RBCs and immature erythroid cells; 20% from bilirubin produced from
nonerythroid enzymes in liver
Bilirubin : free bilirubin is complexed with ---- in circulation
albumin
Bilirubin : bilirubin is conjugated in this organ
liver
Bilirubin : renal excretion of this form of bilirubin
urobilirubin (4mg/day)
Bilirubin : conjugated bilirubin is also called ---
direct bilirubin
Bilirubin : form of bilirubin excreted in feces
stercobilin
Bilirubin : bacterial conversion to this form of bilirubin in the colon
urobilinogen
Bilirubin : form of bilirubin in enterohepatic circulation from colon to liver
urobilinogen
Bile: T/F: Blood and bile flow in the same direction
False - blood flows toward the central vein while bile flows in the oposite
direction
Bile: Sinusoids drain to the _____ vein
Central vein
Bile: What makes up the portal triad?
Bile ductule, branch of portal vein, branch of hepatic artery
Bile: What are the macrophage-like cells in the liver called?
Kupffer cells
Bile: Does the apical or basolateral surface of hepatocytes face the bile
canaliculi?
Apical
Bile: The basolateral surface of hepatocytes faces ____
Sinusoids
Bile: What drains into the Space of Disse?
Lymph
Anatomy Clinical Vignettes: Baby vomits milk when fed and has gastric air
bubble. What kind of fistula is present?
blind esophagus with lower segment of esophagus attached to trachea
Anatomy Clinical Vignettes: 20-year old dancer with decreased plantar
flexion and decreased sensation over the back of her thigh, calf, and lateral
half of foot. What spinal nerve?
Tibial (L4 to S3)
Anatomy Clinical Vignettes: Patient with decreased pain and temp sensation
over lateral aspects of both arms. Lesion?
syringomyelia
Anatomy Clinical Vignettes: Penlight in patient's right eye produces bilateral
pupillary constriction. In left eye, there is paradoxical bilateral pupillary
dilation. Defect?
atrophy of left optic nerve
Anatomy Clinical Vignettes: Patient with decreased prick sensation on lateral
aspect of leg and foot. A deficit in what muscular action can also be
expected?
dorsiflexion and eversion of foot (common peroneal nerve)
Anatomy Clinical Vignettes: Elderly woman with arthritis and tingling over
lateral digits of right hand. Diagnosis?
Carpal tunnel syndrome, median nerve compression.
Anatomy Clinical Vignettes: Woman in car accident cannot turn her head to
the left and has right shoulder droop. What structure is damaged?
Right CN XI (runs through jugular foramen with CN IX and X), innervating
sternocleidomastoid and trapezius muscles)
Anatomy Clinical Vignettes: Man with one wild, flailing arm. Where is
lesion?
contralateral subthalamic nucleus (hemiballismus)
Anatomy Clinical Vignettes: Pregnant woman in 3rd trimester has normal
blood pressure when standing and sitting. When supine, BP drops to 90/50.
Diagnosis?
compression of IVC
Anatomy Clinical Vignettes: Soccer player was kicked in leg and suffered a
damaged medial meniscus. What else is likely to be damaged?
anterior cruciate ligament (remember the "unhapy triad")
Anatomy Clinical Vignettes: Gymnast dislocates her shoulder anteriorly.
What nerve is most likely to have been damaged?
Axillary nerve (C5, C6)
Anatomy Clinical Vignettes: Patient with cortical lesion does not know that
he has a disease. Where is lesion?
Right parietal lobe.
Anatomy Clinical Vignettes: Child presents with cleft lip. Which
embryologic process failed?
Fusion of maxillary and medial nasal processes.
Anatomy Clinical Vignettes: Patient cannot protrude tongue toward left side
and has right sided spastic paralysis. Where is lesion?
left medulla, CN XII
Anatomy Clinical Vignettes: Teen falls while rollerblading and hurts his
elbow. He can't feel the medial part of his palm. Which nerve and what
injury?
Ulnar nerve due to broken medial condyle
Anatomy Clinical Vignettes: 24-year-old male develops testicular cancer.
Metastatic spread occurs by what route?
para-aortic lymph nodes (recal descent of testes during development)
Anatomy Clinical Vignettes: Field hockey player presents to ER after falling
on her arm during practice. X-ray shows mid-shaft break of humerus. Which
nerve and what artery are most likely damaged?
Radial nerve and deep brachial artery, which run together.
Anatomy Clinical Vignettes: Patient cannot blink his right eye or seal his lips
and has mild ptosis on the right side. What is diagnosis, and what nerve is
often affected?
Bell's palsy; CNVII
Anatomy Clinical Vignettes: Patient complains of pain, numbness, and
tingling sensation. On exam, she has wasting of thenar eminence. What is
diagnosis, and what nerve is often affected?
Carpal tunnel syndrome, median nerve
Behavioral Science Vignettes: Woman with anxiety about gyn exam is told to
relax and imagine going through steps of exam. What process does this
exemplify?
systematic desensitization
Behavioral Science Vignettes: 65-year-old man is diagnosed with incurable
metastatic pancreatic adenocarcinoma. His family asks you not to tell the
patient. What do you do?
Behavioral Science Vignettes: Man admitted for chest pain is medicated for
ventricular tachycardia. The next day he jumps out of bed and does 50
pushups to show the nurses he has not had a heart attack. What defense
mechanism?
Assess whether telling patient will negatively affect his health. If not, tell
him.
denial
Behavioral Science Vignettes: You are attracted to your 26-year-old patient.
What do you say?
Nothing! Tone must be professional. It is not acceptable to have romantic
relationship with patients. Invite a chaperone into room if you think your
actions may be misinterpreted.
Behavioral Science Vignettes: Large group of people followed over 10 years.
Every 2 years, it is determined who develops heart disease and who does not.
What type of study?
cohort study
Behavioral Science Vignettes: Girl can groom herself, can hop on one foot,
and has an imaginary friend. How old is she?
Four years old
Behavioral Science Vignettes: Man has flashbacks about his girlfriend's death
2 months ago following a hit-and-run accident. He often cries and wishes for
the death of the culprit. Diagnosis?
normal bereavement
Behavioral Science Vignettes: 36-year-old woman with strong family history
of breast cancer refuses a mammogram because she heard it hurts. What do
you do?
Discuss risks and benefits of not having mammogram. Patients must give
informed consent. If she refuses, you must abide by her wishes.
Behavioral Science Vignettes: During a particular stage of sleep, man has
variable blood pressure, penile tumescence, and variable EEG. What stage of
sleep is he in?
REM sleep
Behavioral Science Vignettes: 15-year-old girl of normal height and weight
for her age has enlarged parotid glands but no other complaints. The mother
confides that she found laxatives in the daughter's closet. Diagnosis?
bulimia
Behavioral Science Vignettes: 11-year-old girl exhibits Tanner stage 4
development (almost full breasts and pubic hair). Diagnosis?
advanced stage, early development.
Behavioral Science Vignettes: 4-year-old girl complains of burning feeling in
her genitalia; otherwise she behaves and sleeps normally. Smear of discharge
shows N. gonorrhoeae. How was she infected?
sexual abuse
Behavioral Science Vignettes: 72-year-old man insists on stopping treatment
for his heart condition because it makes him feel "funny." What do you do?
Although you want to encourage him to take his medication, the patient has
the final say. You should investigate the "funny" feeling and determine if
there are drugs available that don't elicit this side effect.
Behavioral Science Vignettes: Person demands only the best and most
famous doctor in town. Personality disorder?
Narcissism
Behavioral Science Vignettes: Nurse has episodes of hypoglycemia; blood
analysis reveals no elevation in C protein. Diagnosis?
Factitious disorder; self-scripted insulin.
Behavioral Science Vignettes: 55-year-old businessman complains of lack of
successful sexual contacts with women and lack of ability to reach full
erection. Two years ago he had a heart attack. What might be the cause of his
problem?
Fear of sudden death during intercourse.
Biochemistry Clinical Vignettes: Full-term neonate of uneventful delivery
becomes mentally retarded and hyperactive and has a musty odor. Diagnosis?
PKU
Biochemistry Clinical Vignettes: Stressed executive comes home from work,
consumes 7 or 8 martinis in rapid succession before dinner, and becomes
hypoglycemic. Mechanism?
NADH increase prevents gluconeogenesis by shunting pyruvate and
oxaloacetate to lactate and malate.
Biochemistry Clinical Vignettes: 2-year-old has increased abdominal girth,
failure to thrive, and skin and hair depigmentation. Diagnosis?
Kwashiorkor
Biochemistry Clinical Vignettes: Alcoholic develops rash, diarrhea, and
altered mental status. Vitamin deficiency?
Vitamin B3 (pellagra)
Biochemistry Clinical Vignettes: 20-year-old man presents with idiopathic
hyperbilirubinemia. Most common cause?
Gilbert's disease
Biochemistry Clinical Vignettes: 51-year-old man has black spots in his
sclera and has noted that his urine turns black when he is standing.
Diagnosis?
Alkaptonuria
Biochemistry Clinical Vignettes: 25-year-old male complains of severe chest
pain and has xanthomas of his Achilles tendons. What is the disease, and
where is the defect?
Familial hypercholesterolemia; LDL receptor
Biochemistry Clinical Vignettes: AUTHOR
Justin Paul
Microbiology Vignettes: An alcoholic vomits gastric contents and has foul
smelling sputum. What organisms are most likely?
Anaerobes
Microbiology Vignettes: Middle-age man has acute monoarticular joint pain
and bilateral Bell's palsy. What disease and how?
Lyme, Ixodes tick
Microbiology Vignettes: Pt with Mycoplasma pneumoniae, cryoagglutinins.
What Ig types?
IgM
Microbiology Vignettes: U/A with WBC casts. Dx?
Pyelonephritis
Microbiology Vignettes: Young child with tetany, candidiasis, hypocalcemia,
and immunosuppression. What cell is deficient?
Tcell (DiGeorge)
Microbiology Vignettes: Pt with "rose gardener's" (thorn prick, ulcers along
lymph drainage). What bug?
Sporothrix schenckii
Microbiology Vignettes: 25yr old med student has "burning" gut after meals.
Gram negative rods in Bx. What organism?
H. pylori
Microbiology Vignettes: 32yr old man w/ "cauliflower" skin lesions. Bx
shows broad-based budding yeasts. Organism?
Blastomyces
Microbiology Vignettes: Breast feeding woman w/ redness & swelling of
right breast. Fluctuant mass. Dx?
Mastitis by S. aureus
Microbiology Vignettes: Young child w/ recurrent lung infxns &
granulomatous lesions. What defect in neutrophils?
NADPH oxidase (chronic granulomatous disease)
Microbiology Vignettes: 20yr old college student w/ lymphadenopathy, fever,
hepatosplenomegaly. Serum agglutinates sheep RBCs. What cell infected?
B-cell (EBV; infectious mononucleosis)
Microbiology Vignettes: 1hr after eating custard at a picnic, whole family
vomits. After 10hrs all better. Organism?
S. aureus(produces preformed enterotoxin)
Microbiology Vignettes: Infant eats honey -> flaccid. Organism?
Mechanism?
Clostridium botulinum; inhibited release of Ach
Microbiology Vignettes: Man w/ squamous cell carcinoma, penis. what
virus?
HPV
Microbiology Vignettes: Pt w/ endocarditis 3wks after prosthetic heart valve.
Organism?
S. aureus or S. epidermis
Pathology Vignettes: Woman w/ previous C-section has scar in lower uterus
close to opening of the os. Risk for what?
Placenta previa
Pathology Vignettes: 35yr old man w/ hi BP in arms. Low in legs. Dx?
Coarctation of Aorta
Pathology Vignettes: Woman w/ diffuse goiter and hyperthyroidism. Values
of TSH and thyroid hormones?
Low TSH, and high thyroid hormones
Pathology Vignettes: Pt w/ extended expiratory phase. Disease process?
Obstructive Lung Disease
Pathology Vignettes: Woman w/ headache, visual disturbance, galactorrhea,
amenorrhea. Dx?
Prolactinoma
Pathology Vignettes: Baby has foul smelling stool and recurrent pulmonary
infxns. Dx? Test to confirm?
Cystic fibrosis. Chloride sweat test.
Pathology Vignettes: Obese woman w/ hirsutism and hi serum testosterone.
Dx?
Polycyctic ovarian syndrome
Pathology Vignettes: Man w/ pain and swelling in knees, subcutaneous
nodules around the joints and Achilles, exquisite pain in the
metatarsophalangeal join of right big toe. Bx shows needle-like crystals. Dx?
Gouty arthritis
Pathology Vignettes: 48yr old female w/ progressive lethargy and extreme
sensitivity to cold temp. Dx?
Hypothyroidism
Pathology Vignettes: Pt w/ elevated serum cortisol levels undergoes
dexamethasone supp. test. 1mg doesn't lower cortisol. 8mgs does. Dx?
Pituitary tumor.
Pathology Vignettes: During a football game, player collapses/dies
immediately. Likely Cardiac disease?
Hypertrophic cardiomyopathy
Pathology Vignettes: Child anemic since birth. Splenectomy -> increased Hct
in what disease.
Spherocytosis
Pathology Vignettes: 43yr old man experiences dizziness/tinnitus. CT shows
enlarged internal acoustic meatus. Dx?
Schwannoma
Pathology Vignettes: Child exhibits weakness and enlarges calves. Disease?
How inherited?
Duchenne's muscular dystrophy, X-linked recessive.
Pathology Vignettes: 25yr old female w/ sudden uniocular vision loss and
slightly slurred speech. Hx of weakness and pareshesias that have resolved.
Dx?
Multiple Sclerosis
Pathology Vignettes: Teenager w/ nephritic syndrome & hearing loss. Dx?
Alport's syndrome
Pathology Vignettes: Tall thin male teenager w/ abrupt-onset dyspnea &
left-sided chest pain. Hyperresonant percussion on the affected side &
diminished breath sounds. Dx?
Pneumothorax
Pathology Vignettes: Young man concerned about wife's URIs and inability
to conceive. Also dextrocardia. What protein?
Dynein (Kartagener's)
Pathology Vignettes: 55yr old man who smokes & drinks has cough &
flu-like Sx. Gram stain shows nothing. Silver shows gram-neg rods. Dx?
Legionellapneumonia
Pathology Vignettes: Pt has stoke after incurring multiple long bone fractures
in trauma stemming from MVA. Cause?
Fat emboli.
Pathology Vignettes: 25yr old woman w/ a low grade fever, rash across nose
from sun, widespread edema. Should be concerned about what disease?
SLE
Pathology Vignettes: 50yr old man w/ diarrhea, PE reveals plethoric face and
heart murmur. Dx?
Carcinoid syndrome
Pathology Vignettes: Elderly woman w/ a headache and jaw pain. Elevated
ESR. Dx?
Temporal arteritis.
Pathology Vignettes: Pregnant woman @16wks w/ an atypically large
abdomen. Blood test abnormality? Disorder?
High hCG, hydatidiform mole
Pathology Vignettes: 80yr old man w/ a systolic crescendo-decrescendo
murmur. Most likely cause?
Aortic stenosis
Pathology Vignettes: Woman of short stature w/ short 4th and 5th
metacarpals. Endocrine disorder?
Albright's hereditary osteodystrophy or pseudohypoparathyroidism
Pathology Vignettes: After stressful event, 30yr old man w/ diarrhea and
blood per rectum. Intestinal bx shows transmural inflamm. Dx?
Crohn's
Pathology Vignettes: Young man w' mental deterioration and tremors. Brown
pigmentation in a ring around periphery of cornea and altered LFTs. Tx?
Penicillamine for Wilson's disease.
Pathology Vignettes: Pt w/ fatigue, blood tests show macrocytic,
megaloblastic anemia. Why danger to give folate alone?
Masks signs of neural damage w/ vitamin B12 deficiency
Pathology Vignettes: 10yr old "spaces out" in class (stops talking
midsentence and then continues as if nothing had happened). During spells,
quivering of lips. Dx?
Absence seizure.
Pathology Vignettes: 85yr old man w/ knee pain and swelling. X-ray shows
increased joint space w/o erosion. Dx? What does aspirate show?
Pseudogout. Rhomboid calcium pyrophosphate crystals.
Pathology Vignettes: X-ray shows bilateral hilar lymphadenopathy. Dx?
Sarcoidosis.
Pathology Vignettes: 5yr old boy w/ systolic murmur and a wide, fixed split
S2. Dx?
ASD
Pharmacology Vignettes: 28yr old chemist w/ MPTP exposure.
Neurotransmitter depleted?
Dopamine
Pharmacology Vignettes: Woman taking tetracycline is photosensitive.
Clinical manifestations?
Rash on sun-exposed regions of body
Pharmacology Vignettes: Non-diabetic pt has hypoglycemia but low
C-peptide. Dx?
Surreptitious insulin injection
Pharmacology Vignettes: African-american man who goes to Africa develops
a hemolytic anemia after taking malarial prophylaxis. Enzyme deficiency?
Glucose-6-Phosphate Dehydrogenase
Pharmacology Vignettes: 27yr old female w/ hx of psych illness now has
urinary retention due to a neuroleptic. Tx?
Bethanechol
Pharmacology Vignettes: Farmer presents w/ dyspnea, salivation, miosis,
diarrhea, cramping, blurry vision. Cause & mechanism?
Insecticide poisioning; inhibition of AChE
Pharmacology Vignettes: Pt w/ recent kidney transplant is on cyclosporine
for immunosuppression. Requires antifungal agent for candidiasis. What
antifungal -> cyclosporine toxicity?
Ketoconazole
Pharmacology Vignettes: Man on several meds including antidepressants and
antihypertensives, has mydriasis and becomes constipated. Cause?
TCA
Pharmacology Vignettes: 55yr old postmenopausal woman is on tamoxifen
therapy. Risk?
Endometrial carcinoma
Pharmacology Vignettes: Woman on MAO inh has hypertensive crisis after a
meal. What did she eat?
Tyramine (wine/cheese)
Pharmacology Vignettes: After taking clindamycin, pt dev toxic megacolon
and diarrhea. Mechanism?
Clostridium difficileovergrowth
Pharmacology Vignettes: Man starts meds for hyperlipidemia. Then rash,
pruritus, and upset GI. Drug?
Niacin
Pharmacology Vignettes: Pt on carbamazepine. What routine workup should
always be done?
LFTs
Pharmacology Vignettes: 23yr old female who is on rifampin for TB
prophylaxis and on birth control (estrogen) gets pregnant. Why?
Rifampin augments estrogen metabolism in the liver, rendering it less
effective.
Pharmacology Vignettes: Pt develops cough and must discontinue captopril.
What is a good replacement? Why not same side effects?
Losartan, an angiotensin II receptor antagonist, does not increase bradykinin
as captopril does.
Pharmacology Vignettes: AUTHOR
Emelia Argyropolous