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Immunology
I.
II.
Function of the immune system:
a.
To produce cells that travel through the body as well as into and out of lymphoid tissue, selectively
seeking out and destroying foreign antigens and materials while recognizing and sparing host cells
i.
Must be able to distinguish self from non-self and threatening vs. non-threatening
b.
Approaches threats in 3 fundamental ways:
i.
Killing them
ii.
Consuming them
iii.
Outnumbering them
c.
Two divisions of immune system:
i.
Innate immunity
ii.
Acquired immunity
Innate Immunity
a.
Present at birth, immediately available, non-specific
b.
Uses PRRs expressed by leukocytes to bind molecules on microbial cells & damaged or infected host
cells
i.
When activated, WBCs attack & clear infection
c.
Involves:
i.
Physical/structural barriers
1.
Skin: epidermis, keratinocytes, sebaceous glands
2.
Mucosa: GI, respiratory, urogenital, eye/ear mucous membranes (saliva, HCl, tears)
ii.
Competitive exclusion: bacteria already present in body prevents infection
iii.
Leukocytes & macrophages
1.
Neutrophils
a.
↑ level= bacterial infection; involved in inflammation
2.
Eosinophils
a.
Phagocytize antigen-antibody complexes, allergens & large parasites
b.
↑level= parasitic infection, allergies
3.
Basophils
a.
Secrete histamine & heparin when bound by IgE; related to mast cells; mediators
of allergic reactions
4.
Lymphocytes
a.
Natural killer cells; recognize & kill cells with ↓ levels of MHC-1 (cancerous or
invaded by virus)
b.
Involved in viral infections (shift to right)
iv.
Inflammation: redness, swelling, heat, pain, impaired function
v.
Fever: ↑cytokine activity;↑ metabolic rate; ↑tissue repair; ↓microbial reproduction
vi.
Antimicrobial proteins
1.
Cytokines: protein hormones acting as mediators by stimulating inflammation &
enhancing function of phagocytic cells
2.
Interferon: diffuse to neighbor cells, activate NK cells & macrophages
3.
Complement: enzymes & plasma proteins activated by cascade reaction to destroy
microbes
d.
Macrophages
i.
Ag-presenting cells- most important immune cell
ii.
Monocytes
1.
Immature macrophages in blood with migratory, chemotaxic & phagocytic properties
iii.
Macrophages: normal & inflammatory macrophages
1.
Normal: Kupffer cells, Histiocytes & langerhans cells, alveolar macrophages, pleural &
peritoneal macrophages, mesangial macrophages, microglial cells, fre & fixed
macrophages in lymph nodes, spleen & bone marrow
e.
Leukocyte deployment
i.
III.
IV.
At sites of inflammation, chemical messengers are released by basophils, mast cells and damages
tissue.
ii.
Chemicals stimulate this leukocyte process:
1.
Marginationà diapedesis à chemotaxis à phagocytosis
Acquired Immunity
a.
Developed over time; conveys specific resistance; involves specificity to a particular antigen & memory
b.
Two divisions:
i.
Passive immunity
1.
Acquired from antibodies or lymphocytes of another person; lasts 2-3 weeks
2.
From mom à fetus; immunoglobulin transfer
ii.
Active immunity
1.
Production of own antibodies or lymphocytes against antigen by vaccine or natural
exposure
Immune system
a.
Components:
i.
Central or primary lymphoid tissue: bone marrow & thymus
ii.
Peripheral or secondary lymphoid tissue: accumulation & concentration of B and T cells- lymph
nodes, spleen, MALT, GALT, BALT
b.
B-cells: plasma cells, memory cells
c.
T-cells: involves “training” of T-cells in thymus
i.
Helper T cells (CD4)- secrete cytokines & lymphokines; activate entire immune system
ii.
Cytotoxic T cells (CD8)- kill cells infected with virus that are recognized by CD8 cells
iii.
Suppressor T cells (CD8)- inhibit activity of other immune system cells
d.
Antigens
i.
Molecules that trigger immune response; have determinants (epitope)
ii.
3 types:
1.
Immunogens, haptens, tolerogens
e.
Major Histocompatibility complex (MHC)
i.
Soluble protein surface receptor used to identify self vs. non-self; cell “fingerprint”
ii.
MHC-I:
1.
labels cells as self & presents foreign matter inside cells to CD8 cells
2.
present endogenous proteins like viral proteins
iii.
MHC-II:
1.
present in Ag-presenting cells (macrophages, dendritic cells & B-cells) to present foreign
material to CD4 cells to that helper T cells can plan attack
2.
present exogenous proteins like bacteria
f.
Antigen presentation:
i.
Step 1: Antigen processing
1.
MHC-II- APCs engulf & break down foreign particles. MHC-II pick up small peptide
fragment & present it on cell surface
2.
MHC-I- pathogens become intracellular so particles are in cytoplasm. Particle binds to
MHC-I, then complex sent to cell surface
ii.
Step 2: APC-CD4 Interaction
1.
CD4 recognize non-self MHC-II peptide complexà activates cytokines (IL-1, IL-6, TNFα)àsend activation signal to B cells, macrophages & T cells
2.
CD8 recognize non-self MHC-1 peptide complex & kills it
iii.
Step 3: T-cell- B cell Cooperation
1.
Memory cell binds Agà Ag presentation- MHC-II peptide complex bound to B cell
surface à active CD4 binds to thisà CD4 cell releases cytokines needed for B cell division
& production of plasma cells to produce antibodies
g.
Immunoglobulin
i.
Made by B (plasma) cells; 4 main chains (2 heavy, 2 light)- Y shaped, tips called variable region
interact with antigen: Tips of Y (Fab portion)= Ag binding site, bottom of Y (Fc
portion)=activates complement
ii.
V.
VI.
VII.
VIII.
Functions: very specific, agglutination, neutralize toxins, opsonization, signal increased
phagocytosis, serve as cell surface receptors, activate complement
iii.
5 classes: (GAMED)
1.
IgG: dominant in body; crosses placenta; lifelong immunity formed in 2° response
2.
IgA: dominant outside body; in external secretions; neutralizes bacterial exotoxins,
viruses & prevents adherence to mucosal epithelium
3.
IgM: on B cell surface; in early response; efficient at agglutination (10 binding sites)
4.
IgE: attached to mast cells; cause degranulation of mast cells à inflammatory response
when interacts with pollen, allergens or parasite
5.
IgD: on B cell surface; B cell Ag receptor & marker for mature B cells
h.
Two types of immunity:
i.
Humoral: Ab-mediated immunity (made by B cells); extracellular infections
1.
Primary response: IgM
2.
Secondary response: IgG
ii.
Cell-mediated: cytotoxic T cells, NK cells & macrophages; intracellular infections
i.
Hypersensitivity Reactions:
i.
Type I- immediate IgE mediated
ii.
Type II- IgG or IgM Ab mediated; mismatch blood transfusion, Rh incompatibility
iii.
Type III-immune complex mediated; Ab-Ag activation à tissue damage
iv.
Type IV- T-cell mediated; injury is cell mediated or delayed & induced by cytokines (poison Ivy)
j.
Dysfunction in Autoimmune Disease
i.
Exogenous mechanisms: molecular mimicry, superantigenic stimulation
ii.
Endogenous mechanisms: neoantigens
Transplants
a.
Sibling is best transplant option besides twin
b.
Host-versus-graft disease
i.
Chronic rejection- graft heals normally for weeks to years the forms scar tissue infiltrates &
replaces graft tissue
ii.
Acute rejection- T cell mediated; graft heals for 7-12 days then total destruction within 2 weeks
iii.
Hyperacute rejection- Ab mediated; in patients with preexisting high levels of Ab specific for
graft Ag; Graft never heals, no blood supply
c.
Graft-versus-host disease
Immunocompromised state/co-morbid illness
a.
Primary causes:
i.
lymphoid stem cells, T-cells, B-cells
b.
Secondary causes:
i.
viral, bacterial infections, DM, malignancy, chemotherapy, steroids, splenectomy, malnutrition
Microfloral Relationships
a.
Commensalism: symbiotic interaction where one organism benefits without harm or benefit to the host
i.
Disruption to commensal-host relationshipà colonization & opportunistic infection
b.
Mutualism: symbiotic interaction where both derive benefits from the other
i.
Can be obligatory or non-obligatory
c.
Parasitism: symbiotic interaction where symbiont benefits while causing harm to host
Pathogen Entry
a.
Sites of relative sterility: larynx, trachea, lungs, esophagus, jejunum, anterior urethra, bladder, kidney,
cervix, ovaries, fallopian tubes, uterus, prostate, testes, epididymis
b.
Sterile body fluids: blood, urine, cerebrospinal fluid, synovial fluid, bile, pleural, pericardial and
peritoneal fluid
c.
Portals of entry:
i.
Penetration
1.
Includes infectious processes
ii.
Direct contact
1.
STDs, Vertical transmission (TORCHS)
iii.
Ingestion
1.
Causes of infectious bloody diarrhea: SECSY
Inhalation
1.
Pathogens must overcome respiratory defense mechanisms (mucociliary escalator,
BALT)
d.
Pathogens:
i.
Prions: proteins without a genome capable of causing nervous system disease, the spongiform
encephalopathies
ii.
Viruses: smallest obligate intracellular pathogens; have a protein coat (capsid); some also have a
lipoprotein envelope
iii.
Bacteria: self-replicating unicellular organism lacking an organized nucleus (prokaryote) and
organelles; contain peptidoglyan cell wall, cytoplasmic membrane, cytoplasm & genome; may
have pili, fimbriae or flagella; reproduce by binary fission
1.
Growth requirements:
a.
Fastidious: strict growth requirement
b.
Obligate anaerobe
c.
Obligate aerobe
d.
Facultative anaerobe: can utilize fermentation when O2 is absent; can utilize
aerobic cellular respiration when O2 is present to make ATP
iv.
Spirochetes: helical-shaped, gram -, move in corkscrew; anaerobic
v.
Mycoplasmas: smallest, free living unicellular organism; have small genome, cytoplasm & cell
membrane; lack peptidoglycan cell wall
vi.
Rickettsiae: small, obligate intracellular parasites; host cell dependent, transmission via
arthropods
vii.
Chlamydiae: small, obligate intracellular coccoid bacteria
viii.
Fungi: large, free-living eukaryotic organisms
1.
Yeasts (reproduce by budding)
2.
Molds (produce hyphae)
ix.
Parasites: largest pathogenic organisms
1.
Protozoa: unicellular eukaryote with organized nucleus; transmitted through sexual
contact, contaminated food/water, arthropod vector
2.
Helminths: wormlike parasitic organisms: nematodes, cestodes and trematodes
Characteristics of Infectious Disease
a.
Characteristics:
i.
Epidemic: disease rate that exceeds what is expected in a period of time
ii.
Endemic: disease that occurs in a predictable and regular manner (2 cases of flu in 1 month)
iii.
Pandemic: worldwide epidemic
iv.
Prevalence: number of total cases per time
v.
Incidence: number of new cases over a specific time interval
vi.
Vector: an organism that does not cause disease itself but spreads infection by transferring
pathogens from one host to another
vii.
Reservoir: a host that is chronically infected with the causative agent of a disease, and can infest
other potential hosts
b.
Stages
i.
Classical:
1.
Incubation: active replication without symptoms
2.
Prodromal: constitutional symptoms
3.
Acute: high point of disease process
4.
Convalescent period: defeat of pathogen with healing of damaged tissue
5.
Resolution
ii.
Nonclassical:
1.
Subclinical infectious disease, subacute infectious disease, latent infection, chronic
infectious disease, chronic carrier state, fulminant infection, death
iv.
IX.
Bacteria
Staphylococcus
aureus
Gram +/
Gram Gram +
Aerobic/
Disease
Anaerobic
Skin and soft tissue infections,
abscesses, endocarditis,
gastroenteritis, TSS
Pharyngitis, cellutis and skin
infections, rheumatic fever,
glomerulonephritis
Neonatal meningitis and sepsis
Coccus
clusters
coccus
Chains
Coccus
Chains
Gram +
Gram +
Coccus
Coccus
Gram +
Coccus
Chains
Diplococci or
short chains
Chains
Urinary tract and biliary tract
Otitis media, sinusitis,
pneumonia and meningitis
Endocarditis
Gram -
Coccus
Diplococci
Gram -
Coccus
Meningitis and
meningococcemia
Gonorrhea
Gram +
Gram +
Spore
forming rod
Spore
forming rod
rod
Streptococcus
Gram +
pyogenes (group A
strep)
Streptococcus
Gram +
agalactiae
(Group B strep)
Enterococcus
Streptococcus
pneumonia
Viridians group
streptococci
Neisseria
meningitides
Neisseria
gonorrhoeae
Clostridium tetani
Shape
Anaerobic
Tetanus
Anaerobic
Botulism
Clostridium
botulinum
Clostridium
difficile
Listeria
monocytogenes
Gram +
Gram +
rod
Escherichia coli
Gram -
Rod
Salmonella species
Shigella species
Campylobacter
jejuni
Klebsiella
pneumonia
Proteus species
Pseudomonas
aeruginosa
Hemophilus
influenza
Legionella
Gram Gram Gram -
Rod
Rod
Rod
Meningitis and sepsis in
newborns and
immunocompromised
UTI, sepsis, neonatal mengitis
and traveler’s diarrhea
Enterocolitis
enterocolitis
Enterocolitis
Gram-
Rod
Pneumonia, UTI and sepsis
Gram Gram -
Rod
Rod
Gram -
Coccobacilli,
rod
Rod
UTI and sepsis
Wound infection, UTI,
pneumonia and sepsis
Meningitis, ptitis media,
sinusitis, pneumonia
Legionnaires’ disease
Gram -
Pseudomembranous colitis
pneumonophilia
Mycoplasm
pneumonia
(pneumonia)
Pneumonia
No cell
wall, no
gram
staining
Chlamydia
Not seen
trachomatis
on gram
stain
Rickettsia rickettsii Not seen
on gram
stain
Urethritis, cervicitis,
conjunctivitis,
lymphogranuloma venereum
Rocky mountain spotted fever
Dermatology
Patients history
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It is often helpful to examine lesion before obtaining any history- nature of lesion may be apparent by observation
before we begin with a history.
Focused history for dermatology
o When and where did the rash or lesion start?
o Single or multiple lesions?
o Major locations or regions of involvement?
 On trunk
 Sun- exposed areas
 Back or lower legs
o Characteristics of rash
 Pruritic ie: chicken pox
 Rusting
 Blistering
 Painful
 Scaling
 Weeping
 Thickening ie hyperkeratosis in Verruca ; Lichenification
 Burning ie : prodromal stage of herpes zoster
o Describe lesions as they initially appear and evolution
o Evolution: is it healing or spread and developed/changed over time?
Describing skin lesions
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Locations and distributions
o Symmetrical vs. asymmetrical
o Sun-exposed areas
o Flexor vs. extensor surfaces
 Flexor – Atopic Dermatitis
 * in children found in extensor surfaces
 Extensor – Psoriasis
o Involvement of palms and soles
Type
o Cyst, macule, papule, pustule, ulcer, vesicle
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Color
o
o
o
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Erythematous/non-erythematous lesions or bases
Blue, brown, pink, white
Hyperpigmented vs. hypopigmented lesions
Surface features
o Crusting, rough, smooth, scaly, or verrucous
Arrangement
o Single or multiple
o Unilateral, bilateral, generalized, disseminated
o Grouped, annular, dermatomal, linear
Border and shape
o Well or poorly defined
o Active edge** ( as in tinea corporus)
o Round, oval irregular or pedunculated
Psoriasis
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Common chronic recurrent inflammatory skin disease
Etiology: genetic and environmental factors
Abnormal epidermal differentiation - hyperproliferation
Initiated and maintained primarily by t-cells
H&P:
o well demarcated, mildly pruritic, erythematous plaques
o Usually involving elbows, knees, scalp, and hair, margin
o Over plaques Silvery or white waxy, scales, bleeds when detached = Auspitz sign
Nail Changes: pitting, thickening, oil-spot, onycholysis
Koebnerization: new lesions at site of skin trauma ( also seen in lichen planus and vitiligo)
***Guttate Psoriasis: acute symmetrical eruption of drop like lesions usually on trunk and limbs of adolescents
after strep throat ( must present as above)
Tx: topical steroids, coal tar, retinoid, emollients, systemic immunosuppressants, phototherapy
Complications: arthritis
Atopic Dermatitis – “ The Itch that RASHES”
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Common chronic recurrent inflammatory skin disease
Etiology cutaneous immune dysfunction IgE mediated
Strong genetic link family and personal history atopy
H&P:
o prutritis the itch that rashes
o Aggravated by sweat contact, sensitivity, wool, food, allergy stress
o Erythematous excoriated scaling plaques and patches
Tx: elimination of precipitating irritants skin, care, cotton clothing, emollients, topical steroids, oral antihistamines
Complications: secondary infections
Contact dermatitis
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Irritants contact dermatitis non immunologic inflammatory reaction to toxic chemical
No previous exposure is necessary
Ex: water soap detergents solvents alcohol
Allergic contact dermatitis follows exposure to chemicals previously sensitized to
Appearance: erythema, scaling, papulovesicular, lesions
Tx: avoid exposure topical moisturizers and steroids
o Oral antihistamines
Seborrheic dermatitis
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Common chronic recurrent inflammatory skin disease
Etiology: common in sebum rich skin areas
Genetic link overgrowth of endogenous yeast
H&P:
o burning, pruritis, and scaling
o Excessive dandruff
o Orange, erythematous, patches, loose dry, or grease scale
o Excoriated, scaling, plaques, and patches
Distribution: face, eyebrows, blepharitis, nasolabia, folds, scalp
Infant: cradle cap
Tx: topical, anti-fungals, medicated shampoo
Lichen Planus
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Acute or chronic inflammatory dermatitis
Etiology: immune mediated or autoimmune disease
o Associated with Hepatitis C
H&P:
o symmetrical, Pruritic, eruption
o Flat-topped Planar, polygonal violaceous purple papulus
o Plygonal, Purple Papules, Penis, Prolonged course
Pityriasis Rosasia
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Acute self limiting disorder
Etiology suspected herpes virus infection HHV7
H&P:
o Herald patch- single lesion 2-5 cm precedes rash
o Eruption of many smaller scaling oval plaques
o Christmas tree distributed parallel to ribs radiating away from the spine
o Fades spontaneously 4-8 weeks
Tx: antihistamine
Pityriasis versicolor
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Chronic often asymptomatic superficial fungal infection
Etiology: malassezia furfur, pityrosporum
H&P:
o most common in hot humid environment
o Round to oval macules patches on the trunk
o Don’t tan in sun exposed areas
o Very fine scale
o Variable color white orange brown
Tx: topical antifungal shampoo
Recurrences are common
Impetigo
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Superficial skin infection
Etiology: staphyloccocus or strept (GABHS)
Can be primary or secondary
H&P: most common in children
o Spread by direct contact contagious
o Superficial pustule covered by honey colored crusts
o Lesions may be localized or extensive
o Face and extremities are most commonly involved
Bullous impetigo: 80% caused by staph aureus
Tx: topical antibiotic mupirocin***, oral keflex or erythomycin for generalized infection
Removal of crusts with saline soaks
Complications post streptococcal
Folliculitis
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Inflammation of hair follicles
Etiology: infection physical or chemical irritation
o Staph aureus pseudomonas (hot tub)
H&P: Follicular pustules seen in hair bearing areas
Distribution: face, scalp, chest, back, thighs, buttocks
Risks include shaving, waxing, hairs, occlusion
Tx: topical antibiotic (mupirocin)
Furuncle
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Furuncle acute abscess formation in adjacent hair follicles
Carbuncle deep abscess formed in a group of follicles causing a painful supportive mass
H&P: follicular pustules seen in hair bearing areas
TX: topical antibiotics mupirocin + oral keflex, clocacillin or erythmoycin
Prompt incision and drainage
Cellulitis
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Soft tissue and subcutaneous infection and inflammation
Etiology: streptococcus pyogenes styaphyloccocus aureus
H&P: precede by local trauma abrasion dermatoses
o Risks impaired lymphatic drainage IVDA
o Localized pain swelling erythema
o Area of spreading erythema warmth tenderness
o Fever chills malaise increase WBC
o Dx: CHC blood cultures electrolytes wound cultures
TX: local wound care, oral cephalasporin, Cloxacillin
Verruca
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Cutaneous intraepidermal viral infection
Etiology: HPV
Transmission: direct contact sexual contact
Types:
o Vulgaris: common most common on hand
o Plantar: painful calloused seen in children and adolescents on soles of feet pressure causes them to grow
into the dermis
H &P: papules or nodules
o Flesh colored hyperkeratotic firm papules
o Disrupt normal fingerprint lines
o Small black dots
TX: conservative, pare down warts, cryotherapy, salicylic acid, podophyllin, electrodessication, and curettage
Condyloma acuminatum
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Cutaneous intraepidermal viral infection
Etiology: HPV
Transmission: sexual contact
H&P:
o Males affects the penis
o Homosexuals perennial area
o Females vulva perineum
Tx: cryotherapy**, podophyllin
o Oncogenic- HPV 16, 18, 31 development cervical cancer
o Vaccine now available, papsmear
Herpes simplex type 1 and 3
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Common acute recurrent self limiting vesicular eruption
Etiology: HSV 1- facial, nongenital HSV 2- gential
Transmission: sexual contact
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Primary infection --> Recrudescent lesions
H&P:
o HSV-1: primary infection, gingivostomatitis, fever ,malaise, local LAD lasts about 2 weeks
o HSV-2: primary infections, vulvaginitis, penile or perennial lesions, fever, local LAD lasts about 2 weeks
TX: acyclovir topical or oral prophylaxis
o Herpetic whitlow painful vesicle on finger
o Culture positive HSV at delivery = c-section
Shingles
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Acute self limiting dermatomal vesicular eruption**
Etiology: varicella zoster
H&P:
o previous history of chicken pox
o Pain, tenderness, and parenthesias in dermatome
o Usually unilateral may involve adjacent dermatomes
o Thoracic most common in elderly opthalmic of CNV
o May cause contacts to develop chicken pox
o Erythema grouped vesicles pustules and crusts
TX: oral acylovir, prophylaxis
Complications: post-herpetic neuralgia, ophthalmic disease, Ramsey-hunt syndrome
Fungal infections
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Etiology: dermatophytes (microsporum, trichophyton, epidermphyon) or yeasts
Dermatophytes digest keratin- skin hair and nails
Transmission human to human animal or soil contact
Risks heat humidity sweating occlusion DM **oclucive footwear
H&P: often annular lesions asymptomatic or pruritic
o Tinea capitis: alopecia with scale and inflammation
o Tinea corporis: single or mutlti[le plaques scaling serythema active borders central clearing
o Tinea cruris: inner thighs and inguinal folds
o Tinea pedis: interdigital dry or macerated 'moccasin'
o Tinea manum: dryneess hyperkaratosis of palms 'one hand two feet disease'
o Tinea unguim: change of color in nail brittleness subungual debris
Distal subungul onchomycosis- most common
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Dx: KOH prep, wood's lamp, fungal culture biopsy
Tx: topical antifungals for tinea corporis cruris pedis
o Systemic antifungals for tinea capitis= griseofulvin
Candida
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Cutaneous or mucous membrane infection
Etiology: varicella zoster virus recrudesence
Risk moisture humid obesity DM immunosuppression skin folds HX antibiotics use
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H&P
o
o
o
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Genital: pruritic, painful, vulvovaginitis with adherent white plaques
Interrigo: macerated appearance to submammary
Oral thrush- white plaques adhere to erythematous buccal mucosa tongue
TX: topical or oral antifungals
Infestations
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Pediculosis (LICE)
Pediculosis wingless 6 legged insect spread by direct fomites
Pediculus humanus head and body
Phthirus pubis pubic lice
Dx observation of nits and mature lice
Tx pyrethrin permethrin lindane
Scabies sarcoptes scabiee mite
Transmitted via direct contact or sexual contact
Distribution palpules pruritus and burrows in finger webs wrists elbows buttocks genitalia ankles
Dx observation microscopic evaluation of burrow
Tx permethrin ivermectin
Repeat treatment after 1 week hygiene recommendation for BOTH
Hidradenitis suppurativa
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Chronic recurrent inflammatory conditions wherein hair follicles and apocrine gland ducts are occulded and
become secondarily infected
Associations obesity DM smoking genetic and hormonal
H&P
o Pain odor and drainiange affeecting the axilla and groin
o Double open comedones** pustules nodules
o Absecces and sinus tract formation
Tx topical and systemic antibiotics (clindamycin tetracyclin) intralesional steroids isotretinoin surgery
Pemphigus vulagaris
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Serious uncommon autoimmun blistering disease
IgG produced aginst proteins in the skin and mucus membranes*** leading to acantholysis and intraepidermal
bulla
H&P recurrent painful and oral mucosa
Flaccid blisters or bulla** residual erosions
Hyperpigmentaiton
Positive nikolsky's sign
Dx biopsy of tissue with immunofluoresncens
TX may be treated in burn unit or ICU
Iv fluids, electrolyte balance, wound care
Bullous pemphigoid
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Chronic autoimmune bullous disease may reoccur
igG produced agianst antigens in the dermal epidermal basement membrane__ leading to subepidermal tense
bulla**
H&P
o Lesions begin as pruritic hives
Dx biopsy of tissue with immunofluoresence
Molluscum contagiousum
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Self limited viral infections of the skin affecting children and sexually active adults
Iummunocompromised patients may develop more widespread and larger lesions
Etiology: pox virus (MCV)
H&P
o Asymptomatic occasionally pruritic lesions
o Dome shaped** umblicated pearly papules
o Flesh colored
o Affects trunk and face of children
TX: resolve sponataneously in 9-12 months cryotherapy curettage
Acne







Inflammatory disorder of pilosebaceous follicles with a 90% prevalense in adolsencets and young adults
Etiology abnormal follicular keratinization incerased sebum
Associations genetics make up PCOs
Medications steroids ACTH androgens OCP
H&P affect face neck chest and back
o Often asymptomatic comedcomes may be tender nodules
Tx topical salicylic acid retinoids benzoyl peroxid
Topical antibiotic (clindamycin)
Rosacia




Common chronic inflammatory disorder of pilosebaceous units and vasculature of the face
Etiology suspected fungal or mite component
H&P easy and recurrent flushing
Tx avoid triggers, topical antibiotics
Seborrheic keratosis




Common idiopathic benign epidermal growth in middle aged and elderly patients
H&P gradual develp[ment occasionally pruritic
Verrucous or crusted surface **
Stuck on appearance**
Paronychia







Inflammation of proximal or lateral nail fodls
Etiology: staph aureus, candida albicans
Associations trauma water immersion
H&P
Painful tender nail folds
Periungual swelling and erythema purlent discharge
TX topical and systemic antibiotics
Erthyma multiforme





A self limited skin reaction pattern to a variety of stimulus
Association HSV mycoplasma drugs
H&P
o Classic iris or target- shaped lesions in a symmetrical and acral distribution affects palms and soles
o Malaise, arthalgia
TX antipyretics antihistamines analgesics topical steroid
If reccurent consider HSV prohylactic therapy
SJS-TEN



Spectrum of mucocutaneous drug induced or idopathic reaction associated with impaired capacity to detoxify
intermediated drugs metabolites
H&P skin tenderness erythema necrosis desquamation
o Assosiation genetic susceptibility drugs
TX remove offending drug supportive care ophto assesment ICU or burn unit woud care
o Steroids and IVIG still controversial becoming standard
o High mortality rate
Skin Cancer



(Melanoma number one cause of death metastasis to the brain)
The predecessor lesion to squamous cell carcinoma is actinic keratosis
Nevastic levi is predecessor to melanoma
Basal cell carcinoma






Most common form of skin cancer
Arising in sun exposed area
Association chronic UV damage
H&P
o ulcerates **
o Pearly papule rolled border**
Dx biopsy
Metastasis and death rare
Squamous cell





2nd most common form o f skin cancer
Metastatic potential**
Associations chronic uv damage immunosuppression
Dx: biopsy
Tx: excision, crytherapy
Melanoma








Melanocyte derived skin cancer
Hyper-pigamented macule or plaque with AMCDE: asymmetry irregular borders color variation diameter >6
evolutional change
Types based on histopathology
Superficial spreading malignant melanoma 60-70
Acral lengetiginous melanoma: most common form in africans asians and hispacins palms and soles
Dx: biopsy most important prognostic indicator
Tx: excision sentinel lymph node biopsy radiation chemo
Metastsis local to adjacent skin and lympnodes systemic to lung liver brain bone GI
Felon- preceded by puncture womb infection is in a closed space, treat by incision and drainage and tetanus
Erythema nodosum- painful because of subcutaneous forniculitis, no scaring
Peutz jeghers syndrome- polyposis of the intestine and the stomach, lentignies, hyperpigmented, high rates of
surveilence
Black widow spider- neurotoxin, lactrotoxin causes muscle spasms because it blocks acth
Pagets disease of the breast- introductal cancer, treat by excision, plaques that eroded the nipple
Vitilgo- melanocytes are absent, give steroids, phototherapy
Brown recluse spider- tissue toxin, sphingomylinase D, undergo necrosis, surgical debridement, local wound care,
SLE Systemic lupus- butterfly rash
Ophthalmology
I.
II.
III.
IV.
Causes of vision loss
a.
Sudden vision loss:
i.
In non-inflamed eye- vitreous hemorrhage, retinal detachment, macular degeneration, retinal
artery or vein occlusions, optic neuritis
ii.
In inflamed eye- acute anterior uveitis, acute glaucoma, corneal ulcer
b.
Gradual vision loss: cataracts, chronic glaucoma, chronic uveitis
Disorders found on inspection
a.
Ptosis-drooping of eyelid
b.
Ectropion- lower lid turned outward
c.
Entropion- inward turning of eyelid; lashes scratch sclera & cornea
d.
Proptosis- eyeball protrudes from socket
e.
Epicanthus- vertical fold of skin that lies over the medial canthus
f.
Hordeolum- aka stye; tender abscess caused by staphylococcus
g.
Chalazion- hard non-tender inflammation of a meibomian gland
h.
Blepharitis- chronic bilateral inflammation of lid margins; caused by staph or seborrhea
i.
Pinguecula- yellow nodule on either side of the cornea
j.
Pterygium- fleshy triangular intrusion of conjunctiva onto nasal side of cornea
Refractive errors
a.
Emmetropia- perfect vision, light focused perfectly on retina
b.
Myopia- near sightedness, globe too long, light rays focus in front of retina, need lens for distance
c.
Hyperopia- far sightedness, globe too short, need lens for close up
d.
Astigmatism- corneal surface not spherical, refractive errors in horizontal and vertical axis differ
e.
Presbyopia- lens becomes unable to increase refractive power to accommodate upon near objects due to
loss of elasticity of lens with advancing age
Eye emergencies
a.
Acute angle closure glaucoma
i.
Pathophysiology: increased intraocular pressure that occurs from the occlusion of the anterior
chamber angle by the iris
ii.
Epidemiology: ↑ incidence in Far-Eastern, Asian, Inuit (Eskimo)
iii.
Symptoms: ocular pain, iridescent vision, halos around lights, peripheral vision loss
iv.
Signs: enlarged, fixed (non-responsive), mid-dilated pupil, steamy/cloudy/hazy cornea, “angry”
appearing eye
v.
Diagnosis: tonometry
vi.
Treatment: *laser or incisional iridotomy, acetazolamide, pilocarpine
b. Herpes Simplex Keratitis
i.
Etiology: HSV-1 (primary herpetic eye infection)
ii.
Symptoms: irritation, photophobia, tearing, redness, visual deficits
iii.
Signs: corneal opacities and *dendritic lesions
iv.
Treatment: Trifluridine, Vidarabine (*topical corticosteroids are CI!)
c. Varicella Zoster Ophthalmicus
i.
Etiology: Herpes Zoster that is reactivated in ganglia of *trigeminal nerve- ophthalmic branch
(V1)
ii.
Signs: vasicular, pustular, crusting lesions. *tip of nose involvement (Hutchinson’s sign)
iii.
Treatment: oral antivirals (Acyclovir, Valacyclovir) and corticosteroids
d. Bacterial Keratitis
i.
Etiology: extended contact wear, Pseudomonas, moraxella, staph, strep
ii.
Symptoms: purulent discharge
iii.
Signs: hazy cornea, center ulceration, hypopyon (pus in anterior chamber)
iv.
Treatment: depends on etiology- Tobramycin, cipro, cefazolin
e. Protozoan: Acanthamoeba
i.
Found in patients after swimming in contaminated water with contacts
f.
Corneal ulcer
i.
Etiology: a complication of infectious keratitis; noninfectious causes are severe dry eyes, severe
allergic eye disease and ocular inflammatory or systemic vasculitis disease
ii.
Symptoms: pain, photophobia, tearing, foreign body sensation, ↓ vision
iii.
Signs: circumcorneal injection, purulent/watery discharge
iv.
Treatment: antibiotic therapy, underlying cause
g. Blunt and Penetrating Trauma with Ruptured/Lacerated Globe
i.
Symptoms: severe conunctival hemorrhage, bloody chemosis, extrusion of globe contents,
shallow anterior chamber
ii.
Signs: Pear-shaped or teardrop pupil- points to site of rupture or laceration
iii.
Diagnosis: orbital thin-slice CT scan
iv.
Treatment: emergent ophthalmologic referral; protect with Fox shield
h. Hyphema
i.
Etiology: hemorrhage in anterior chamber
ii.
Symptoms: ocular pain, photophobia
i.
Foreign body
i.
Signs: may form rust ring
ii.
Diagnosis: fluorescein & cobalt blue slit-lamp exam; **MRI CI!!
iii.
Treatment: evert lid & remove object
j.
Orbital blowout fracture
i.
Etiology: fracture of inferior & medial wall resulting from blunt trauma
ii.
Symptoms: ocular pain, diplopia
iii.
Signs: loss of upward gaze, palpable bony step-offs
iv.
Diagnosis: Water’s View x-ray
k. Chemical Burns
i.
*alkali burns are much more damaging
ii.
Signs: conjunctival injection & blanching, corneal edema, ↑ IOP
iii.
Diagnosis: pH evaluation by litmus paper
iv.
Treatment: immediate copious irrigation with saline by Morgan lens
l.
Orbital Cellulitis
i.
Etiology: infection of soft tissues behind orbital septum; commonly an extension of ethmoid
sinusitis; *MCC is Staphylococcus aureus
ii.
Symptoms: fever, painful/decreased ocular movement
iii.
Signs: proptosis, lid edema & erythema, skin feels warm
iv.
Treatment: *IV Cefuroxime
m. Retinal detachment
i.
Symptoms: painless unilateral vision loss, *dark curtain pulled over visual field, photopsia,
sparks & floaters
ii.
Signs: ophthalmoscopic exam shows tear flapping
iii.
Treatment: laser or cryosurgery to seal tear
n. Central retinal artery occlusion
i.
Etiology: complete occlusion of central retinal artery
ii.
Symptoms: *painless, unilateral vision loss
iii.
Signs: *pale retina with cherry-red spot at fovea
o. Papilledema
i.
Etiology: caused by optic venous stasis, *malignant hypertension, indicates increased intracranial
pressure
ii.
Symptoms: asymptomatic
iii.
Signs: swollen optic disc with blurred margins & obliterated vessels
p. Transient Ischemia Attack (TIA)
i.
Etiology: ischemia of retina or focal ischemia of cerebrum
ii.
Symptoms: sudden painless, usually unilateral vision loss
iii.
Treatment: naturally reversible within 24 hours
q. Central retinal vein occlusion
i.
Stormy sunset appearance
V.
Diabetic Retinopathies
a.
Nonproliferative Diabetic Retinopathy
i.
Etiology: thickening of retinal capillary walls
ii.
Epidemiology: **Leading cause of adult blindness
iii.
Symptoms: asymptomatic, decreased visual acuity
iv.
Physical findings: microaneurysms, macular edema, hard exudates, “flame shaped”
hemorrhages, dot & blot hemorrhages, cotton-wool spots, venous loops, dilation & beading
v.
Diagnosis: fluorescein angiography
vi.
Treatment: *strict blood glucose control, laser photocoagulation
b. Proliferative Diabetic Retinopathy
i.
Etiology: neovascularization from prolonged retinal ischemia & hypoxia
ii.
Epidemiology: DM1 > DM2
iii.
Risk factors: *nonproliferative diabetic retinopathy
iv.
Symptoms: asymptomatic, ↓visual acuity or frank blindness
v.
Physical findings: *neovascularization, “boat-shaped” hemorrhages, sectional retinal
detachments, findings of NPDR
vi.
Diagnosis: fluorescein angiography, B-scan ultrasound
vii.
Treatment: *laser photocoagulation
c. Hypertensive Retinopathy
i.
Etiology: prolonged systemic hypertension & arterial wall thickening causing microaneurysms
ii.
Risk factors: hypertension, diabetic retinopathy
iii.
Symptoms: asymptomatic
iv.
Physical findings: blurred optic disc, papilledema, retinal streak hemorrhages/ boat shaped
hemorrhages, *macular star
v.
Retinal vessels: copper wiring, A-V nicking, tapering & banking, silver wiring
vi.
Diagnosis: fluorescein angiography, blood pressure reading
vii.
Treatment: treat underlying HTN & DM
VI.
Differential Diagnosis of Red Eye
a.
Viral Conjunctivitis
i.
Etiology: Adenovirus type 3 associated with URI
ii.
Symptoms: no pain, no photophobia, no blurred vision
iii.
Signs: edema & hyperemia of one or both eyes, conjunctival injection, *watery discharge
iv.
Treatment: topical vasoconstrictors & steroids, sulfonamide drops
v.
*highly contagious
b.
Bacterial conjunctivitis
i.
Etiology: Staph aureus, H. flu, strep pneumo & pseudomonas aeruginosa
ii.
Symptoms: copious purulent discharge
iii.
Diagnosis: gram stain
iv.
Treatment: broad spectrum topical antibiotics (Polytrim, gentamicin or tobramycin)
c. Chlamydial/ Gonococcal Conjunctivitis
i.
ii.
iii.
iv.
Symptoms: eye infection greater than 3 weeks, mucopurulent discharge, conjunctival injection,
possible uveitis
Sings: palpable preauricular node, conjunctival papillae, chemosis
Diagnosis: fluorescent antibody stain, enzyme immunoassay tests, Giemsa stain
Treatment: oral azithromycin with topical erythromycin, tetracycline or sulfacetamide;
Gonococcal: ceftriaxone
d. Allergic Conjunctivitis
i.
Symptoms: thin, watery discharge, photophobia & visual loss, lids swollen &red
ii.
Signs: large cobblestone papillae, large preauricular lymph nodes
iii.
Treatment: NSAIDs, topical antihistamines, mast cell stabilizers
e. Keratoconjunctivitis sicca
i.
Symptoms: dryness, redness, scratchy feeling of the eyes, ocular irritation
ii.
Signs: mucous plaques & discharge, corneal epithelial defects or ulceration
iii.
Diagnosis: slit lamp exam shows abnormalities of tear film stability, reduced tears, Schirmer test
iv.
Treatment: lubricating drops & ointments
f.
Dacryocystitis
i.
Cyst in lacrimal duct area
ii.
Etiology: acute: S. aureus, chronic: mucosal degeneration, ductile stenosis
iii.
Symptoms: pain, redness of tear-sac, swelling, purulent material, tenderness
iv.
Treatment: Keflex, Augmentin with topical antibiotic drops
g. Blepharitis
i.
Anterior: affects outside lids where lashes attach; caused by S. aureus
1. Remove scales with baby shampoo
ii.
Posterior: inner eyelid (meibomian glands), seborrheic
1. Expression of meibomian gland on regular basis
h. Hordeolum
i.
Etiology: Staph aureous, blockage of meibomian & sebaceous glands
ii.
Treatment: topical bacitracin
i. Uveitis
i.
Intraocular inflammation of iris, ciliary body and choroid
ii.
Symptoms: deep eye pain, photophobia, conjunctiva Bessel dilation, *ciliary flush, small
irregular pupil
iii.
Treatment: mydriatics, corticosteroids
ENT
Clues to Diagnosis of Conductive Hearing Loss
History
Physical Finding
Sudden painless loss of
Cerumen
hearing
Narrow canal with debris
Sudden painful loss of
Normal canal with red, immobile TM
hearing
Immobile TM
Normal mobile TM
Gradual painless loss of
Reddish-blue pulsating mass behind intact
hearing
TM
Retracted/ perforated TM with chronic
drainage
Clues to Diagnosis of Sensorineural Hearing Loss
History
Physical Findings
Gradual hearing loss, noise
exposure, tobacco use
Gradual hearing loss, tinnitus,
noise exposure
Rapidly progressive hearing
loss, possibly fluctuating,
bilateral loss
Sudden, fluctuating, unilateral
hearing loss, tinnitus, episodic
vertigo
Gradual unilateral hearing loss,
tinnitus
Suggested Cause
Complete canal occlusion
Otitis Externa
Chronic otitis media
Middle ear effusion
Otosclerosis
Glomus tumor or vascular
anomaly
cholesteatoma
Audiogram
Elderly patients with normal
TM
Normal TM
Normal TM, with possible,
vertigo, or disequilibrium
Suggested
Cause
Presbycusis
Bilateral, symmetric highfrequency loss
Bilateral, symmetric loss
Noise-induced
centered at 4 kHz
Any abnormal hearing with Autoimmune
poor speech discrimination
Normal TM
Unilateral low-frequency
loss
Meniere’s
disease
Normal TM, possible facial
nerve weakness &
unsteadiness
Any unilateral abnormal
configuration
Acoustic
neuroma
Pulmonology
I.
Restrictive/ Interstitial Lung Disease
a.
Idiopathic Pulmonary Fibrosis
i.
Definition: stiffening of alveolar & perialveolar tissue resulting in reduced O2 perfusion
ii.
Etiology: continuous, unknown pulmonary inflammatory process
iii.
Symptoms: DOE then resting dyspnea, nonproductive cough, tachypnea
iv.
Signs: cyanosis, finger clubbing, inspiratory crackles
v.
Diagnosis: CXR: *honeycombing, ground glass haziness, ↓lung volume; *surgical lung biopsy
(gold standard)
vi.
Treatment: corticosteroids
b. Sarcoidosis
i.
Collections of noncaseating granulomas
ii.
Etiology: unknown
iii.
Symptoms: nonproductive cough, hemoptysis, bilateral blurry vision, eye pain & redness
iv.
Signs: lymphadenopathy, erythema nodosum, lupus pernio, parotid gland enlargement, uveitis
v.
Diagnosis: CXR- bilateral hilar adenopathy
vi.
Treatment: corticosteroids, cyclosporine, methotrexate, hydroxychloroquine
c. Silicosis
i.
Restrictive lung disease caused by inhalation of inorganic dust silica
ii.
Symptoms: DOE, productive cough
iii.
Signs: rales, cyanosis, cor pulmonale
iv.
Diagnosis: CXR- Eggshell calcifacations
v.
Treatment: TB prophylaxis
d. Coal Miner’s Lung
i.
Symptoms: DOE
ii.
Signs: cor pulmonale & symptoms
iii.
Diagnosis: CXR- nodular opacities in upper lung fields
e. Asbestosis
i.
*only pneumonconiosis associated with an increased bronchogenic carcinoma
ii.
*associated with mesothelioma
iii.
Symptoms: DOE
iv.
Signs: rales, cor pulmonale
v.
Diagnosis: CXR- lateral & lower lung/diaphragm level calcifications
f.
II.
Berylliosis
i.
Symptoms: DOE & weight loss
ii.
Signs: crackles, rales
iii.
Diagnosis: blood beryllium lymphocyte proliferation test
iv.
Treatment: methotrexate
Anion Gap
a.
Metabolic Acidosis
i.
Normal anion gap: diarrhea, renal tubular acidosis
ii.
Anion gap: (La Mudpie) lactic acidosis, aspirin, methanol, uremia, DKA, paraldehyde, propylene
glycol, isopropyl alcohol, INH, ethylene glycol
b.
Metabolic alkalosis
i.
H+ ion loss: vomiting, renal loss (Conn’s & Cushing syndrome), ↓chloride intake, diuretic use,
hypokalemia
ii.
HCO3 ion retention: oral/IV bicarbonate, milk-alkali syndrome
III.
Solitary Pulmonary Nodule
a.
*most are benign
b.
Benign causes: hamartoma, infective granuloma, cyst, pulmonary embolus
c.
Malignant causes: primary lung cancer, metastasis
d.
Diagnosis: serial/comparative CXR
e.
Treatment:
i.
Low probability: serial CXRs every 3 months for 1st year
ii.
Intermediate probability: CT & PET scan, sputum cytology, biopsy
iii.
High probability: surgical resection
IV.
Bronchiolitis
a.
Etiology: *RSV, influenza, adenovirus
b.
Diagnosis: nasal smear for RSV, CXR: hyperinflation, mild interstitial infiltrates, focal atelextasis, air
trapping, flat diaphragm
c.
Treatment: *racemic epinephrine
d.
*can lead to BOOP
V.
Bronchiolitis obliterans with organizing pneumonia (BOOP)
a.
Granulation tissue in distal airway
b.
Etiology: toxic fumes, infection, connective tissue disease
c.
Signs: CXR- patchy masses of intra-alveolar granulation tissue in small airway lumen & alveolar ducts
d.
Epidemiology: 50-60 year old without bronchiolitis
e.
Diagnosis: CXR: patchy, bilateral ground glass or alveolar infiltrates
f.
Treatment: steroid
VI.
Pneumonia
a.
Diagnosis: CXR:
i.
Interstitial: bilateral markings with occasional patchy consolidation
ii.
Segmental/Lobar: focal consolidation
iii.
Bronchopneumonia: diffuse bilateral pattern, small fluffy infiltrates
b.
Treatment: PO macrolide
Pneumonia Bacterial Pathogens
Organism
Clinical Setting
Strep pneumo
MCC of CAP in adults
Antimicrobial Therapy
Penicillin G
Gram + diplococcic
H flu
Rust colored sputum
Cardiopulmonary disease or precedent URI
2/3 gen cephalosporin
Pleomorphic gram –
coccobaccili
Staph aureus
Chronic care facility, nosocomial, cystic fibrosis, Naf, Ox, Clox, Diclox +
IV drug abusers
rifampin
Gram + cocci in clusters
Klebsiella pneumonia
DM, alcoholics
3 gen cephalosporin +
aminoglycoside
Gram – rod
Escherichia coli
Currant jelly sputum- hemoptysis
Nosocomial infection
3 gen cephalosporin +
aminoglycoside
Gram – rod
Pseudomonas aeruginosa Nosocomial, bronchiectasis, cystic fibrosis
Pipericillin + aminoglycoside
Gram – rod
Anaerobes
AMS, poor dental hygiene
Clindamycin
Mycoplasma pneumonia
Foul smelling sputum
Young adults, summer & fall
Erythromycin or doxycyclin
Legionella pneumophila
DX: cold agglutinin tites
Contaminated water, AC
Doxycycline
Triad: hyponatremia, AMS, diarrhea
Chlamydia psittaci
Moraxella catarrhalis
DX: urinary antigen assay
Exotic birds
Elderly & immunosuppression
Doxycycline
TMP-SMZ
Gram – diplococcic
Pneumocystis carinii
Immunosuppression and malignancy
TMP-SMZ
DX silver sputum stain
Pneumonia Fungal Pathogens
Coccidioides immitis
Travel to Southwest US
Histoplasma capsulatum Travel to Mississippi River Valley
Aspergillus
Neutropenia & immunocomp.
Cryptococcus
AIDS & immunocomp.
Blastomyces dermatitidis Travel to mid-western US
VII.
Amphotericin B
Pleuritis
a.
Inflammation of parietal pleura
b.
Symptoms: localized, sharp & momentary pain made worse by exercise, coughing, sneezing, deep
breathing & movement
c.
Etiology: in young otherwise healthy patients caused by pneumonia, viral URI, rib fracture
d.
Diagnosis: pleural friction rub, CXR effusion
e.
Treatment: treat underlying disease
VIII.
IX.
Pleural effusion
a.
Abnormal accumulation of fluid in pleural space
b.
Etiology: MCC is congestive heart failure, pneumonia, cancer
c.
Symptoms: SOB, dyspnea, cough, pleuritic chest pain, ipsilater shoulder pain (Kehr sign)
i.
*chest pain usually means exudative effusion
d.
Signs: ↓ tactile fremitus, dullness to percussion, decreased breath sounds; Hoover sign; contralateral shift
of the trachea & bulging intercostal spaces
e.
Transudative:
i.
Causes: left ventricular failure, pulmonary embolism, cirrhosis
ii.
Caused by systemic factors: decreased oncotic pressure, increase in hydrostatic pressure
f.
Exudative:
i.
Causes: bacterial pneumonia, malignancy, viral infection & pulmonary embolism
ii.
Occurs when local factors that influence the formation & absorption of pleural fluid are altered
g.
Pleural effusion analysis:
i.
Malignant effusion: turbid to bloody
ii.
Uncomplicated pneumonia: clear to turbid
iii.
Empyema: turbid to purulent
iv.
Tuberculosis: serous to serosanguineous
v.
Pulmonary infarction: serous to grossly bloody
vi.
Pancreatitis: turbid to serosanguineous
h.
Treatment: Treat specific cause or thoracentesis
Pneumothorax
a.
Accumulation of air in pleural space which may lead to pulmonary collapse on the affected side
b.
Types:
i.
Primary spontaneous pneumonthorax: affects tall, thin boys b/w 10-30y.o.; family hx and
cigarette smoking may be factors; occurs are rest, patients don’t seek medical attention right away
1.
Symptoms: tachypnea, hypoxia
2.
Treatment:
a.
If small & asymptomatic- observe
b.
If small & symptomatic- aspiration w/ needle catheter
ii.
Secondary spontaneous pneumonthorax: affects older patients with preexisting lung disease;
present with life-threatening respiratory failure w/ underlying COPD
1.
Symptoms: tachypnea, hypoxia, tachycadira, cyanosis, hypotension
2.
Treatment: *TOC- chest tube; pleurodesis
iii.
Pneumomediastinum: free air in mediastinal structures from acute elevation of intrathoracic
pressure (asthma, coughing, vomiting, childbirth, seizures)
1.
Symptoms: subcutaneous emphysema, Hamman sign
iv.
Traumatic pneumothorax: results from penetrating trauma
v.
Iatrogenic pneumothorax: follows procedure
1.
Treatment: *TOC- aspiration
*if pneumothorax is large: ↓breath sounds, hyperresonance, ↓tactile fremitus, positive Hoover sign
vi.
Tension pneumonthorax: results from penetrating or blunt trauma, lung infection, CPR; air enters
pleural space on inspiration & can’t exit on expiration
1. Signs: unilateral chest expansion, ↓ tactile fremitus, hyperresonance, ↓ breath sounds,
mediastinal shift, tachycardia & hypotension, hemodynamically unstable
2. Treatment: immediate needle decompression, then chest tube. Don’t wait for CXR!
c. Diagnosis for all types:
vi.
Demonstration of a visceral pleural line is diagnostic and may only be seen on an expiratory film
vii.
Arterial blood gas- hypoxia, acute respiratory alkalosis
X.
XI.
Tuberculosis
a.
Etiology: mycobacterium tuberculosis (Mtb)- an acid fast aerobic rod-shaped bacteria
b.
Pathophysiology: occurs in those without previous contact with Mtb à gain access to terminal alveoli
(upper lobe/apex) & multiplyà engulfed by macrophagesà T-lymphocytes develop cell-mediated response
à develop granulomatous lesionà 2-3 weeks later, central part of Ghon’s focus undergoes caseous necrosis
c.
Primary TB:
i.
Asymptomatic, + PPD, radiographic calcific lung lesions
ii.
*NOT contagious
iii.
Receive prophylactic INH & B6 for 9 months
d.
Secondary TB:
i.
Fever, *night sweats, weight loss, malaise, hemoptysis, apical rales
e.
Diagnosis: 0.1ml PPD (doesn’t distinguish between active & latent), CXR- upper lobe infiltrate w/
cavitations, sputum culture (definitive dx w/ + cultures)
i.
Positive PPD sizes:
1.
>5mm- housemate/inmate contact
2.
>10mm- persons at risk
3.
>15mm- persons at low risk
f.
Treatment (active TB):
i.
First-line therapy (2 months)- INH, Rifampin, PZA, Ethambutol, B6
ii.
Second-line (4 months)- INH, Rifampin, B6
iii.
Monitoring: cultures from posà neg.= most reliable indicator of Tx response
COPD
a.
Chronic Bronchitis
i.
Chronic productive cough for 3 months in 2 successive years; increased airway resistance
ii.
“Blue bloater”
iii.
Symptoms: chronic cough, mucopurulent sputum, overweight, cyanotic & comfortable at rest,
rhonchi & rales
iv.
Signs: CXR- ↑interstitial markings at bases, diaphragm NOT flattened
b. Emphysema
i.
Abnormal permanent enlargement of airspaces distal to terminal bronchioles with destruction of
their walls and bulla or blebs, and without obvious fibrosis; decreased elastic recoil of lungs
ii.
Types:
1. Centriacinar emphysema: focal destruction limited to respiratory bronchioles; most
severe in upper lobes, *MC form in smokers
2. Panacinar emphysema: involves entire alveolus distal to terminal bronchioles; most
severe in lower lobes, *MC in patients w/ homozygous α1 anti-tripson deficiency
a. *α1 anti-tripson deficiency: liver glycoprotein that inhibits serine proteases,
neutrophil elastase
3. Distal acinar emphysema: least common, localized to fibrous septa or pleura, formation
of bulla
iii.
“Pink puffer”
iv.
v.
Symptoms: SOB, cough is RARE, clear mucoid sputum, patient thin, weight loss, use of
accessory muscles, chest quiet, pursed lip at expiration
Signs: CXR- hyperinflation, flat diaphragm, vascular markings diminished
c. Diagnosis of COPD: Pulmonary function tests (can’t distinguish between emphysema & chronic
bronchitis)
i.
Forced expiratory spirometry & FEV1
ii.
↑total lung capacity,↑residual volume, ↓vital capacity & FEV1/FVC
d. Treatment of COPD:
i.
*smoking cessation
ii.
O2 therapy
iii.
Bronchodilators: *ipratropium, β2 agonists
iv.
Theophylline
v.
Steroids
XII.
Pulmonary Hypertension
a.
Resistance to pulmonary blood flow is only 1/12th the resistance across the systemic bed
b.
Etiology: conditions which affect pulmonary arteries, pulmonary parenchyma, thoracic cage &
neuromuscular system, cause left atrial or pulmonary HTN
c.
Diagnosis: EKG- left axis deviation
d.
Treatment: Nitric Oxide, Warfarin, calcium channel blocker
XIII.
Cor Pulmonale
a.
Right ventricular hypertrophy & eventual right-sided heart failure in the absence of left-sided heart failure
b.
Etiology: MCC is COPD; chronic hypoxia
c.
Symptoms: DOE, effort syncope, angina pectoris, weakness, palpitations, cough, pulmonic ejection
murmur
d.
Signs: hepatomegaly, JVD, peripheral edema, ascites, right ventricular heave, pulmonary & tricuspid
regurgitation
e.
Diagnosis:
i.
EKG- right ventricular hypertrophy, right axis deviation, inverted T waves, *tall peaked P waves
ii.
CXR- RV hypertrophy, enlargement of cardiac silhouette
iii.
Doppler echocardiography/ cardiac catheterization
f.
Treatment: *O2, Na, fluid restriction & diuretics, cardiac glycosides (Digoxin)
XIV.
Asthma
a.
Etiology: MC-environmental allergens, URI, aspirin/ NSAID drug hypersensitivity, environmental
pullutants, tobacco smoke
i.
EIA factors: MC-exposure to cold/dry air, coexisting URI
b.
Pathophysiology: Triad: (1)airway inflammation (2) intermittent airflow obstruction (3) bronchial
hyperresponsiveness
c.
Types:
d.
e.
f.
g.
XV.
XVI.
XVII.
i.
Allergic asthma: extrinsic, bronchospasm from allergens
ii.
Idiosyncratic asthma: intrinsic, bronchospasm S/P URI
iii.
EIA: intrinsic
Symptoms: wheezing, dyspnea, cough, fever, chest tightness, sputum production, *usually worse at night
Signs: respiratory distress, *end-expiratory wheezing or prolonged expiratory phase
Diagnosis: *spirometry, methacholine/histamine challenge testing
Treatment: acute emergency management (in this order): supplemental O2, inhaled β2 agonists, inhaled
ipratropium bromide, methylprednisolone, theophylline
i.
EIA tx: prophylactic sodium cromolyn & nedocromil; leukotriene antagonists
Acute Respiratory Distress Syndrome (ARDS)
a.
State of diffuse pulmonary parenchymal injury associated with noncardiogenic pulmonary edema
b.
Etiology: results from disease that causes diffuse inflammation in body, *MCC sepsis
c.
Pathophysiology: Exudative phase à fibroproliferative phaseà fibrosis phase
d.
Symptoms: DOEà severe dyspnea at rest, tachypnea, anxiety, agitation
e.
Signs: febrile or hypothermic, hypotension, cold extremities, bilateral rales, cyanosis of lips, lethargy
f.
Diagnosis: clinical diagnosis; PaO2/FiO2 ratio of less than 200 and ALI by a ratio of less than 300;
CXR-*white out appearance
g.
Treatment: supplemental O2 (won’t help), *treat underlying cause
Respiratory Failure
a.
PaO2 value of less than 60mmHg while breathing air or a PaCO2 of more than 50mmHg
b.
Types:
i.
Hypoxic (Type 1): PaO2 < 60mmHg w/ normal PaCO2
ii.
Hypercapnic (Type 2): PaCO2 > 50mmHg
c.
Etiology: *MCC of hypoxemia- V/Q mismatch, shunting
d.
Signs:
i.
Hypoxemia: dyspnea, cyanosis, anxiety, confusion
ii.
Hypercapnia: dyspnea & headache
e.
Diagnosis: ABG analysis
f.
Treatment: reverse and/or prevent tissue hypoxia
Pulmonary Embolism
a.
Etiology: DVT usually involves formation of a large clot in deep veins in lower legs & thighs
b.
Pathophysiology: *Virchow Triad:
i.
(1)stasis of blood flow
ii.
(2)hypercoagulability
iii.
(3) damage to endothelial lining of veins
c.
Symptoms: *Triad
i.
(1) hemoptysis
ii.
(2) dyspnea
iii.
(3) chest pain
d.
Diagnosis: *Gold standard- Pulmonary angiography; V/Q scan
e.
Treatment: Fibrinolytic therapy, Heparin