Download PPS Recall March 2011 Disclaimer: The following is only a recall of

PPS Recall March 2011
Disclaimer: The following is only a recall of the gist of the questions in the exam. Some of the details regarding the
patient/s may not be exactly the same as the exam. We highlighted the answers (which we deemed are correct) in
red font. The explanations and references for each answer are quoted after each item.
1. What organ does phenylalanine affect most?
a. brain
b. kidney
c. heart
d. lungs
From Nelson’s Chapter 85
Phenylalanine is an essential amino acid. Dietary phenylalanine not utilized for protein synthesis is
normally degraded by way of the tyrosine pathway (Fig. 85-1 ). Deficiency of the enzyme phenylalanine hydroxylase
or of its cofactor tetrahydrobiopterin causes accumulation of phenylalanine in body fluids and the central nervous
system (CNS).
The brain is the main organ affected by hyperphenylalaninemia. The CNS damage in affected patients is
caused by the elevated concentration of phenylalanine in brain tissue, which interferes with the cerebral transport
of other large neutral amino acids (tyrosine, tryptophan).
2. By how much does birth length increase at 1 y/o?
a. 50%
b. 75%
c. 100%
From Nelson’s Chapter 14 Table 14-2
Height at birth is 50 cm. Height at 1 yr is 75 cm. By computation, the percent difference between 50cm and
75cm is 50%.
3. Initial reaction in primary infection
a. encapsulation
b. Ghon focus  Mel sa pagkakaalala ko hindi ito Ghon’s focus. Ghon’s something siya. Hehehe  Sorry, iisipin ko

c. ulceration
d. endotoxin
4. At what age would the child’s height approximate his parents’ height
a. 1 y/o
b. 2 y/o
c. 3 y/o
From Nelson’s Chapter 14 – Assessment of Growth
For full-term infants, size at birth reflects the influence of the uterine environment; however, size at age 2
yr correlates with mean parental height, reflecting the influence of genes.
5. Hallmark radiographic finding of reactivation TB
a. Caseation
b. tuberculoma
c. Cavitation
d. Discrete shadows
From Nelson’s Chapter 212 Tuberculosis (Mycobacterium Tuberculosis)
Pulmonary tuberculosis that occurs more than 1 yr after the primary infection is usually caused by
endogenous regrowth of bacilli persisting in partially encapsulated lesions. This reactivation tuberculosis is rare in
children but is common among adolescents and young adults. The most common form is an infiltrate or cavity in
the apex of the upper lobes, where oxygen tension and blood flow are great.
Pulmonary tuberculosis in adults usually represents endogenous reactivation of a site of tuberculosis
infection established previously in the body. This form of tuberculosis is rare in childhood but may occur in
adolescence. Children with a healed tuberculosis infection acquired at <2 yr of age rarely develop chronic
reactivation pulmonary disease, which is more common in those who acquire the initial infection at >7 yr of age.
The most frequent pulmonary sites are the original parenchymal focus, lymph nodes, or the apical seedings (Simon
foci) established during the hematogenous phase of the early infection. This form of disease usually remains
localized to the lungs because the established immune response prevents further extrapulmonary spread. The most
common radiographic presentations of this type of tuberculosis are extensive infiltrates or thick-walled cavities in
the upper lobes.
6. Not included in the WHO red flag milestone? Signs  May ages ito eh
a. sit without support
b. crawl
c. stand alone
d. walk alone
7. 1 month old patient was exclusively breastfed, had good weight gain. Patient came in with pallor Hgb 7.9, other
PE normal
a. Physiologic anemia
b. IDA
c. Transient Erythroblastopenia of Childhood
8. Baby born with apgar 9, 9, fell asleep and went into respiratory distress. Nurse suctioned the nose however she
could not insert the nasogastric tube.
a. choanal atresia
b. TEF
From Nelson’s Chapter 373 – Congenital Disorders of the Nose
Although children and adults preferentially breathe through their nose unless nasal obstruction interferes,
most newborn infants are obligate nasal breathers and significant nasal obstruction presenting at birth, such as
choanal atresia, may be a life-threatening situation for the infant unless an alternative to the nasal airway is
established.
Newborn infants have a variable ability to breathe through their mouths, so nasal obstruction does not
produce the same symptoms in every infant. When the obstruction is unilateral, the infant may be asymptomatic
for a prolonged period, often until the 1st respiratory infection, when unilateral nasal discharge or persistent nasal
obstruction may suggest the diagnosis. Infants with bilateral choanal atresia who have difficulty with mouth
breathing make vigorous attempts to inspire, often suck in their lips, and develop cyanosis. Distressed children then
cry (which relieves the cyanosis) and become calmer, with normal skin color, only to repeat the cycle after closing
their mouths. Those who are able to breathe through their mouths at once experience difficulty when sucking and
swallowing, becoming cyanotic when they attempt to feed.
Diagnosis: This is established by the inability to pass a firm catheter through each nostril 3–4 cm into the
nasopharynx. The atretic plate may be seen directly with fiberoptic rhinoscopy. The anatomy is best evaluated by
using high-resolution CT ( Fig. 373-1 )
9. Pt presents with arm adducted and internally rotated
a. Erb’s palsy
b. Erb Duchenne paralysis
c. Klumpke paralysis
d. Sciatica
From Nelson’s Chapter 99.7 Peripheral Nerve Injuries
Brachial plexus injury is a common problem, with an incidence of 0.6–4.6 per 1,000 live births. Injury to the
brachial plexus may cause paralysis of the upper part of the arm with or without paralysis of the forearm or hand
or, more commonly, paralysis of the entire arm. These injuries occur in macrosomic infants and when lateral
traction is exerted on the head and neck during delivery of the shoulder in a vertex presentation, when the arms are
extended over the head in a breech presentation, or when excessive traction is placed on the shoulders.
Approximately 45% of brachial plexus injuries are associated with shoulder dystocia. In Erb-Duchenne paralysis, the
injury is limited to the 5th and 6th cervical nerves. The infant loses the power to abduct the arm from the shoulder,
rotate the arm externally, and supinate the forearm. The characteristic position consists of adduction and internal
rotation of the arm with pronation of the forearm. Power to extend the forearm is retained, but the biceps reflex is
absent; the Moro reflex is absent on the affected side ( Fig. 99-6 ). The outer aspect of the arm may have some
sensory impairment. Power in the forearm and hand grasp are preserved unless the lower part of the plexus is also
injured; the presence of hand grasp is a favorable prognostic sign. When the injury includes the phrenic nerve,
alteration in diaphragmatic excursion may be observed fluoroscopically. Klumpke paralysis is a rare form of
brachial palsy; injury to the 7th and 8th cervical nerves and the 1st thoracic nerve produces a paralyzed hand and
ipsilateral ptosis and miosis (Horner syndrome) if the sympathetic fibers of the 1st thoracic root are also injured.
Mild cases may not be detected immediately after birth. Differentiation must be made from cerebral injury; from
fracture, dislocation, or epiphyseal separation of the humerus; and from fracture of the clavicle. MRI demonstrates
nerve root rupture or avulsion
10. Patient who has history of URTI or diarrhea (basta it was a viral infection) presents with symmetric lower
extremity paralysis, DTR absent on ankle, (+) on knees, no sensory deficit.
a. transverse myelitis
b. GBS
From Nelson’s Chapter 605.6 and Chapter 615
Transverse myelitis is characterized by abrupt onset of progressive weakness and sensory disturbances in
the lower extremities. (Take note that the patient in the case did not have sensory deficits) A history of a preceding
viral infection accompanied by fever and malaise is documented in most cases. Clinical manifestations: Low back or
abdominal pain and paresthesias of the legs are prominent symptoms in the early stages. The leg muscles are weak
and flaccid, and a sensory level is present, usually in the midthoracic region. Pain, temperature, and light touch
sensation are affected, but joint position and vibration sense may be preserved. Sphincter disturbances are
common, in which case catheterization of the bladder is necessary. Fever and nuchal rigidity are present early in
most cases. The neurologic deficit evolves for 2–3 days and then plateaus, with flaccidity gradually changing to
spasticity and with the concomitant development of upper motor neuron signs in the lower extremities.
Guillain-Barré syndrome is a postinfectious polyneuropathy involving mainly motor but sometimes also
sensory and autonomic nerves. This syndrome affects people of all ages and is not hereditary. The disorder closely
resembles experimental allergic polyneuritis in animals. Most patients have a demyelinating neuropathy, but
primarily axonal degeneration is documented in some cases. Clinical manifestations: The paralysis usually follows a
nonspecific viral infection by about 10 days. The original infection may have caused only gastrointestinal (
especially Campylobacter jejuni, but also Helicobacter pylori) or respiratory tract (especially Mycoplasma
pneumoniae) symptoms. West Nile virus also may cause Guillain-Barré–like syndrome, but more frequently causes
motor neuron disease similar to poliomyelitis. Guillain-Barré syndrome is reported following administration of
vaccines against rabies, influenza poliomyelitis (oral), and possibly the conjugated meningococcal vaccine.
Weakness begins usually in the lower extremities and progressively involves the trunk, the upper limbs, and finally
the bulbar muscles, a pattern known as Landry ascending paralysis. Proximal and distal muscles are involved
relatively symmetrically, but asymmetry is found in 9% of patients. The onset is gradual and progresses over days or
weeks. Particularly in cases with an abrupt onset, tenderness on palpation and pain in muscles is common in the
initial stages. Affected children are irritable. Weakness may progress to inability or refusal to walk and later to
flaccid tetraplegia. Paresthesias occur in some cases. Bulbar involvement occurs in about half of cases. Respiratory
insufficiency may result. Dysphagia and facial weakness are often impending signs of respiratory failure. They
interfere with eating and increase the risk of aspiration. The facial nerves may be involved. Some young patients
may exhibit symptoms of viral meningitis or meningoencephalitis. Extraocular muscle involvement is rare, but in an
uncommon variant, oculomotor and other cranial neuropathies are severe early in the course. Miller-Fisher
syndrome consists of acute external ophthalmoplegia, ataxia, and areflexia. Papilledema is found in some cases,
although visual impairment is not clinically evident. Urinary incontinence or retention of urine is a complication in
about 20% of cases but is usually transient. Miller-Fisher syndrome overlaps with Bickerstaff brainstem
encephalitis, which also shares many features with Guillain-Barré syndrome with lower motor neuron involvement
and may indeed be the same basic disease. Tendon reflexes are lost, usually early in the course, but are sometimes
preserved until later. This variability may cause confusion when attempting early diagnosis. The autonomic nervous
system may also be involved in some cases. Lability of blood pressure and cardiac rate, postural hypotension,
episodes of profound bradycardia, and occasional asystole occur. Cardiovascular monitoring is important. A few
patients require insertion of a temporary venous cardiac pacemaker.
11. Patient came in with frontal bossing, maxillary hypoplasia, hepatosplenomegaly, PBS showed nucleated RBC
a. Cooley anemia
b. aplastic anemia
c. Sickle cell anemia
From Nelson’s Chapter 462.9 and 462.1
HOMOZYGOUS β-THALASSEMIA (THALASSEMIA MAJOR, COOLEY ANEMIA) (It is important to know the
aliases of the diseases, just like this, we were baffled by what Cooley anemia was, only to find out from no less than
Tin Arombo that Cooley is the same with beta thalassemia) Clinical manifestations: The classic findings in children
with severe thalassemia, including typical facies (maxillary hyperplasia, flat nasal bridge, frontal bossing),
pathologic bone fractures, marked hepatosplenomegaly, and cachexia, are primarily seen in developing countries.
The spleen may become so enlarged that it causes mechanical discomfort and secondary hypersplenism. Features
of ineffective erythropoiesis include expanded medullary spaces (with massive expansion of the marrow of the face
and skull), extramedullary hematopoiesis, and a huge caloric need ( Fig. 462-7 ). Hepatosplenomegaly may
interfere with nutritional support. Pallor, hemosiderosis, and jaundice may combine to produce a greenish brown
complexion. As a result of the anemia, there is also an increase in iron absorption from the gastrointestinal tract,
with toxicity leading to further complications.
SICKLE CELL ANEMIA (HOMOZYGOUS HEMOGLOBIN S) OR S β-THALASSEMIA Clinical Manifestations:
Infants with sickle cell anemia have abnormal immune function. As early as 6 mo of age, some children, and by 5 yr
of age, most children have functional asplenia. Bacterial sepsis is one of the greatest causes of morbidity and
mortality in this patient population. Children with sickle cell anemia also have deficient levels of serum opsonins of
the alternate complement pathway against pneumococci. Regardless of age, all patients with sickle cell anemia are
at increased risk for infection and death as a result of bacterial infection, particularly with encapsulated organisms,
such as Streptococcus pneumoniae (see Chapter 181 ) and Haemophilus influenzae type B (see Chapter 192 ).
Dactylitis, often referred to as hand-foot syndrome, is frequently the 1st manifestation of pain in children with
sickle cell anemia, occurring in 50% of children by 2 yr of age. Dactylitis often presents with symmetric swelling of
the hands and/or feet (Fig. 462-1). Acute splenic sequestration is a life-threatening complication occurring
primarily in infants, and may occur as early as 5 wk of age. Approximately 30% of children with sickle cell anemia
have significant splenic sequestration episodes; although the presentation may be variable, a significant
percentage of cases can be fatal. The etiology of splenic sequestration episodes is unknown. Clinically, these events
are associated with engorgement of the spleen, with a subsequent increase in spleen size, evidence of hypovolemia,
and a decline in hemoglobin of at least 2.0 g/dL from baseline. Reticulocytosis and a decrease in the platelet count
may be present. These events can be accompanied by upper respiratory tract infections, bacteremia, or viral
infection.
12. Mother Rh (-) gave birth with a baby Rh (+), the mother should receive
a. Anti-D gamma globulin
b. transfusion
c. Corticosteroids
From Nelson’s Chapter 103.2
The risk of initial sensitization of Rh-negative mothers has been reduced to less than 1% by the
intramuscular injection of 300 μg of human anti-D globulin (1 mL of RhoGAM) within 72 hr of delivery of an Rhpositive infant, ectopic pregnancy, abdominal trauma in pregnancy, amniocentesis, chorionic villus biopsy, or
abortion. This quantity is sufficient to eliminate ≈ 10 mL of potentially antigenic fetal cells from the maternal
circulation. Large fetal-to-maternal transfers of blood may require proportionately more RhoGAM. RhoGAM
administered at 28–32 wk and again at birth (40 wk) is more effective than a single dose. The use of this technique,
combined with improved methods of detecting maternal sensitization and measuring the extent of fetal-tomaternal transfusion, plus the use of fewer obstetric procedures that increase the risk of such fetal-to-maternal
bleeding (version, manual separation of the placenta), should further reduce the incidence of erythroblastosis
fetalis.
13. Cheapest prophylaxis for malaria
a. Mefloquine
b. Doxycycline
14. Patient with Turner syndrome and chylous ascites
a. intestinal lymphangiectasia
b. abetalipoproteinemia
c. bile duct stasis (or probably bile duct aplasia or hypoplasia accdg to che)
d. chylomicron
From Nelson’s Chapter 335.3
Obstruction of the lymphatic drainage of the intestine can be due to congenital defects in lymphatic duct formation
or to secondary causes. The congenital form is often associated with lymphatic abnormalities elsewhere in the
body, as occur with Turner, Noonan, and Klippel-Trenaunay-Weber syndromes. Causes of secondary
lymphangiectasia include constrictive pericarditis, heart failure, retroperitoneal fibrosis, abdominal tuberculosis,
and retroperitoneal malignancies. Lymph rich in proteins and lymphocytes leaks into the bowel lumen, resulting in
protein-losing enteropathy and lymphocyte depletion. Hypoalbuminemia, hypogammaglobulinemia, edema,
lymphocytopenia, fat and fat-soluble vitamin malabsorption, and chylous ascites often occur. Intestinal
lymphangiectasia can also present with ascites, peripheral edema, and a low serum albumin.
15. DMSA showed photopenic areas
a. hydronephrosis
b. VUR
c. chronic pyelonephritis
d. chronic glomerulonephritis
From Nelson’s Chapter 538 Urinary Tract Infections
When the diagnosis of acute pyelonephritis is uncertain, renal scanning with technetium-labeled DMSA or
glucoheptonate is useful. The presence of photopenia supports the diagnosis of pyelonephritis, and experienced
radiologists can differentiate between an acute and a chronic process. In approximately 50% of children with a
febrile UTI, irrespective of age, the DMSA scan demonstrates parenchymal involvement. Among children with grade
III, IV, or V reflux and a febrile UTI, 80–90% show acute pyelonephritis. If the DMSA scan shows acute
pyelonephritis, approximately 50% of children will acquire a scar in that site over the following 5 mo. However, if
the DMSA scan is normal during a febrile UTI, no scarring will result from that particular infection.
A DMSA scan ( Fig. 538-4 ) often is performed in the presence of vesicoureteral reflux to assess whether renal
scarring is present. The DMSA is the most sensitive and accurate study for demonstrating scarring. Excretory
urography is not as sensitive as the DMSA scan in demonstrating renal scarring; in addition, visualization of the
collecting system in infants and young children often is suboptimal, there is a slight risk of a contrast allergy, and it
can take 1–2 yr for a renal scar to appear on the urogram.
16. What is the first sign of puberty in boys corresponding to SMR 2?
a. testicular enlargement
b. penile enlargement
From Nelson’s Chapter 12 Adolescence
In boys, the first visible sign of puberty and the hallmark of SMR2 is testicular enlargement, beginning as early as
9½ yr. This is followed by penile growth during SMR3. Peak growth occurs when testis volumes reach approximately
9–10 cm3 during SMR4.
In girls, the first visible sign of puberty and the hallmark of SMR2 is the appearance of breast buds, between 8 and
12 yr of age. Menses typically begins 2–2½ yr later, during SMR3–4 (median age, 12 yr; normal range, 9–16 yr),
around the peak height velocity (see Fig. 12-4 ).
17. Handedness
a. 3 y/o
From Nelson’s Chapter 10
Handedness is usually established by the 3rd yr. Frustration may result from attempts to change children's hand
preference. Variations in fine motor development reflect both individual proclivities and different opportunities for
learning. Children who are seldom allowed to use crayons, for example, develop a mature pencil grasp later.
18. Osteosarcoma would present with signs in the
a. metaphysis of bones
b. epiphysis
c. diaphysis
From Nelson’s Chapter 501
TABLE 501-1 -- Comparison of Features of Osteosarcoma and the Ewing Family of Tumors
FEATURE
OSTEOSARCOMA
EWING FAMILY OF TUMORS
Age
Second decade
Second decade
Race
All races
Primarily whites
Sex (M : F)
1.5 : 1
1.5 : 1
Cell
Spindle cell–producing osteoid
Undifferentiated small round cell, probably of
neural origin
Predisposition
Retinoblastoma, Li-Fraumeni syndrome,
Paget disease, radiotherapy
None known
Site
Metaphyses of long bones
Diaphyses of long bones, flat bones
Presentation
Local pain and swelling; often, history of
injury
Local pain and swelling; fever
Radiographic
findings
Sclerotic destruction (less commonly lytic);
sunburst pattern
Primarily lytic, multilaminar periosteal reaction
(“onion skinning”)
Differential
diagnosis
Ewing sarcoma, osteomyelitis
Osteomyelitis, eosinophilic granuloma,
lymphoma, neuroblastoma, rhabdomyosarcoma
Metastasis
Lungs, bones
Lung, bones
Treatment
Chemotherapy
Chemotherapy
Ablative surgery of primary tumor
Radiotherapy and/or surgery of primary tumor
FEATURE
OSTEOSARCOMA
EWING FAMILY OF TUMORS
Outcome
Without metastases: 70% cured; with
metastases at diagnosis, ≤20% survival
Without metastases: 60% cured; with metastases
at diagnosis, 20–30% survival
19. Ibuprofen has the following side effects except:
a. Gastric ulceration
b. Aggravate bleeding
c. metabolic alkalosis
d. reduced renal blood flow
20. PDA closes due to
a. increase PO2
b. decrease PCO2
c. increased PCO2
d. Increased pulmonary pressure
From Nelson’s Chapter 421 The Fetal to Neonatal Circulatory Transition
At birth, mechanical expansion of the lungs and an increase in arterial PO2 result in a rapid decrease in pulmonary
vascular resistance. Concomitantly, removal of the low-resistance placental circulation leads to an increase in
systemic vascular resistance. The output from the right ventricle now flows entirely into the pulmonary circulation,
and because pulmonary vascular resistance becomes lower than systemic vascular resistance, the shunt through
the ductus arteriosus reverses and becomes left to right. In the course of several days, the high arterial PO2 signals
constriction of the ductus arteriosus and it closes, eventually becoming the ligamentum arteriosum. The increased
volume of pulmonary blood flow returning to the left atrium increases left atrial volume and pressure sufficiently to
close the foramen ovale functionally, although the foramen may remain probe patent.
21. According to WHO Z scores, a Z score of Above 1 indicates
a. Normal
b. Possible risk
c. Overweight
d. Obese
22. Delayed tooth eruption may be considered at what age
a. 13 months
b. 10 months
c. 12 months
From Nelson’s Chapter 14 – Assessment of Growth
Delayed eruption is usually considered when there are no teeth by approximately 13 mo of age (mean + 3 standard
deviations). Common causes include hypothyroid, hypoparathyroid, familial, and (the most common) idiopathic.
Individual teeth may fail to erupt because of mechanical blockage (crowding, gum fibrosis).
23. A case on pt with gray white exudates on tonsils. What would your prophylaxis be?
a. Erythromycin
24. Not included in the printed 2011 immunization schedule
a. rotavirus
b. HPV
c. pneumococcal
d. meningococcal
25. Crawl
a. 6 mos
b. 8 mos
c. 10 mos
d. 12 mos
From Nelson’s Chapter 8
TABLE 8-2 -- Emerging Patterns of Behavior During the 1st Year of Life [*]
NEONATAL PERIOD (1ST 4 WK)
Prone:
Lies in flexed attitude; turns head from side to side; head sags on ventral suspension
Supine:
Generally flexed and a little stiff
Visual:
May fixate face on light in line of vision;“doll's-eye” movement of eyes on turning of the body
Reflex:
Moro response active; stepping and placing reflexes; grasp reflex active
Social:
Visual preference for human face
AT 1 MO
Prone:
Legs more extended; holds chin up; turns head; head lifted momentarily to plane of body on ventral
suspension
Supine:
Tonic neck posture predominates; supple and relaxed; head lags when pulled to sitting position
Visual:
Watches person; follows moving object
Social:
Body movements in cadence with voice of other in social contact; beginning to smile
AT 2 MO
Prone:
Raises head slightly farther; head sustained in plane of body on ventral suspension
Supine:
Tonic neck posture predominates; head lags when pulled to sitting position
Visual:
Follows moving object 180 degrees
Social:
Smiles on social contact; listens to voice and coos
AT 3 MO
Prone:
Lifts head and chest with arms extended; head above plane of body on ventral suspension
Supine:
Tonic neck posture predominates; reaches toward and misses objects; waves at toy
Sitting:
Head lag partially compensated when pulled to sitting position; early head control with bobbing
motion; back rounded
Reflex:
Typical Moro response has not persisted; makes defensive movements or selective withdrawal
reactions
Social:
Sustained social contact; listens to music; says “aah, ngah”
AT 4 MO
Prone:
Lifts head and chest, with head in approximately vertical axis; legs extended
Supine:
Symmetric posture predominates, hands in midline; reaches and grasps objects and brings them to
mouth
Sitting:
No head lag when pulled to sitting position; head steady, tipped forward; enjoys sitting with full truncal
support
Standing: When held erect, pushes with feet
Adaptive: Sees pellet, but makes no move to reach for it
Social:
Laughs out loud; may show displeasure if social contact is broken; excited at sight of food
AT 7 MO
Prone:
Rolls over; pivots;crawls or creep-crawls (Knobloch)
Supine:
Lifts head; rolls over; squirms
Sitting:
Sits briefly, with support of pelvis; leans forward on hands; back rounded
Standing: May support most of weight; bounces actively
Adaptive: Reaches out for and grasps large object; transfers objects from hand to hand; grasp uses radial palm;
rakes at pellet
Language: Forms polysyllabic vowel sounds
Social:
Prefers mother; babbles;enjoys mirror; responds to changes in emotional content of social contact
AT 10 MO
Sitting:
Sits up alone and indefinitely without support, with back straight
Standing: Pulls to standing position;“cruises” or walks holding on to furniture
Motor:
Creeps or crawls
Adaptive: Grasps objects with thumb and forefinger; pokes at things with forefinger; picks up pellet with assisted
pincer movement; uncovers hidden toy; attempts to retrieve dropped object; releases object grasped
by other person
Language: Repetitive consonant sounds (“mama,” “dada”)
Social:
Responds to sound of name; plays peek-a-boo or pat-a-cake;waves bye-bye
AT 1 YR
Motor:
Walks with one hand held (48 wk); rises independently, takes several steps (Knobloch)
Adaptive: Picks up pellet with unassisted pincer movement of forefinger and thumb; releases object to other
person on request or gesture
Language: Says a few words besides “mama,” “dada”
Social:
Plays simple ball game; makes postural adjustment to dressing
26. Photophobia, tooth enamel
a. Vitamin A
b. Vitamin C
c. Vitamin D
27. What vitamin is given with measles
a. Vitamin A
28. What vitamin is given with INH
a. Vitamin B6
29. Vitamin deficiency associated with Phenobarbital and phenytoin intake
a. Vitamin B
b. Vitamin D
From Nelson’s
The child's medication use is relevant because certain medications, such as the anticonvulsants phenobarbital and
phenytoin, increase degradation of vitamin D, and aluminum-containing antacids interfere with the absorption of
phosphate.
30. most common presenting sign (or first sign) of Retinoblastoma?
a. Strabismus
b. Leukocoria
c. Blindness
d. Corneal Abrasion
see Prev Med 2010
31. A teenager ingested large doses of Paracetamol, what should be given?
a. NAC
From Nelson’s Chapter 58
TABLE 58-6 -- Common Antidotes for Poisoning
ROUTE
ADVERSE
EFFECTS/WARNINGS/COMMENTS
ANTIDOTE
POISONING
DOSE
N-Acetylcysteine
(Mucomyst)
Acetaminophen;carbon
tetrachloride and
chloroform (experimental)
140 mg/kg loading, PO
followed by 70
mg/kg q4h for 17
doses
Nausea, vomiting
N-Acetylcysteine
(Acetodote)
Acetaminophen
150 mg/kg over
IV
30–60 min,
followed by 50
mg/kg over 4 hrs,
followed by 100
mg/kg over 16 hrs.
Nausea, vomiting, allergic reactions
Atropine
Organophosphate and
carbamate pesticides;
bradycardia due to
atrioventricular conduction
defects, β-blocking agents
0.05 mg/kg
IV/ET
repeated q5–10
min as needed;
dilute in 1–2 mL of
NS for ET
instillation
Tachycardia, dry mouth, blurred
vision, urinary retention
BAL in oil
(dimercaprol)
Arsenic, mercury, other
metals
3–5 mg/kg/dose
Deep IM
q4 hr, for the 1st
day; subsequent
dosing depends on
the toxin
Local injection site pain and sterile
abscess, nausea, vomiting, fever,
salivation, nephrotoxicity
Benztropine
(Cogentin)
Acute dystonic reactions
0.02–0.05
mg/kg/dose qd or
bid (max, 4 mg)
IV/PO
Sedation, blurred vision, dry mouth,
tachycardia
Cyanide antidote kit
Cyanide
Amyl nitrite: 1
crushable ampule;
inhale 30 sec of
each min
Inhalation
Methemoglobinemia
Hydrogen sulfide (nitrites
only)
Sodium nitrite:
0.33 mL/kg of 3%
IV
Methemoglobinemia
ANTIDOTE
POISONING
DOSE
ROUTE
ADVERSE
EFFECTS/WARNINGS/COMMENTS
solution if
hemoglobin level
is not known;
otherwise, based
on tables with
product
Sodium
IV
thiosulfate: 1.6 mL
(400 mg)/kg of
25% solution; may
be repeated every
30–60 min to max
of 50 mL
Deferoxamine
(Desferal)
Digoxin-specific
Fab antibodies
(Digibind)
Iron
Digitalis glycosides
(synthetic or natural)
Infusion of 15
mg/kg/hr (max, 6
g/24 hr)
IV(preferred) Hypotension (minimized by avoiding
rapid infusion rates)
IM:90 mg/kg/dose
q8h (max, 6 g/24
hr)
IM
1 vial binds 0.6 mg IV
of digitalis
glycoside; ingested
dose may be
estimated from
the serum level
(see table with
product)
Allergic reactions (rare), return of
condition being treated with digitalis
glycoside
Dimercaptosuccinic
acid (succimer,
DMSA, Chemet)
Lead and probably mercury, 10 mg/kg/dose
arsenic, and perhaps other q8h for 5 days,
metals
then 10 mg/kg
q12h for 14 days
PO
Nausea and vomiting; repeated
courses may be needed
Diphenhydramine
(Benadryl)
Extrapyramidal symptoms,
acute dystonic reactions,
allergic reactions
5 mg/kg divided
q8h;max, 300
mg/24 hr
IV/PO
Sedation or paradoxical agitation,
ataxia
EDTA, calcium
(calcium disodium,
Versenate)
Lead, manganese, nickel,
zinc, and perhaps
chromium
1–1.5 g/m2/24 hr
in divided doses
q12h for 5 days
IV
Nausea, vomiting, fever, hypertension,
arthralgias, allergic reactions, local
inflammation, nephrotoxicity
(maintain adequate hydration)
Ethanol (ethyl
alcohol)
Methanol, ethylene glycol
750 mg/kg loading IV/PO
dose followed by
80–150 mg/kg/hr
infusion of 5% or
10% ethanol
Nausea, vomiting, sedation, add folate
for methanol
Flumazenil
(Romazicon)
Benzodiazepines
0.2 mg over 30
IV
sec; if response is
inadequate, repeat
q1 min to 1 mg
max
Nausea, vomiting, facial flushing,
agitation, headache, dizziness,
seizures; do not use for unknown or
antidepressant ingestions
Note:May not reverse respiratory
depression
ANTIDOTE
POISONING
DOSE
ROUTE
Fomepizole (4methylpyrazole,
Antizole)
Ethylene glycol, methanol
15 mg/kg load; 10
mg/kg q12h for 4
doses; 15 mg/kg
q12h until level is
<20 mg/dL
IV
No specific dose
for children
ADVERSE
EFFECTS/WARNINGS/COMMENTS
Infuse slowly over 30 min; increase
doses to q4h if dialysis is concurrent
Thiamine and pyridoxine may be
helpful
Glucagon
β Blockers, calcium channel 0.05 mg/kg bolus
blockers, hypoglycemic
followed by
agents
infusion of 0.05
mg/kg/hr
Methylene blue
Methemoglobinemia
0.1–0.2 mL/kg of
IV
1% solution by
slow infusion; may
be repeated q30–
60 min
Nausea, vomiting, headache, dizziness
Naloxone (Narcan)
Narcotics
0.01 mg/kg;if no
effect, give 0.1
mg/kg;may be
repeated as
needed; may give
continuous
infusion
IV
Acute withdrawal symptoms if given
to addicted patients
Clonidine (inconsistent
response)
IV
Hyperglycemia, nausea, vomiting
Octreotide
Sulfonylureas
1–2 μg/kg q8 hr
IV/SC
Used in addition to high-dose glucose;
may add glucagon
Physostigmine
(Antilirium)
Anticholinergic agents
0.02 mg/kg by
slow push; may
repeat q5–10 min
to 2 mg max
IV/IM
Bradycardia, asystole, seizures,
bronchospasm, vomiting, headache
Pralidoxime (2-PAM, Organophosphate
Protopam)
insecticides
25–50 mg/kg over
5–10 min (max,
200 mg/min); can
be repeated after
1–2 hr, then q10–
12 hr as needed
IV/IM
Nausea, dizziness, headache,
tachycardia, muscle rigidity,
bronchospasm (rapid administration)
Pyridoxine (Vitamin
B6)
Isoniazid, Gyromitra
mushrooms
Isoniazid;dose =
dose of isoniazid
IV
Uncommon
Ethylene glycol
(investigational)
Mushrooms: 25
mg/kg
Oxygen
Carbon monoxide
100%, hyperbaric
Inhalation
Half-life of carboxyhemoglobin is 5 hr
in room air, but 1.5 hr in 100% O2 and
15–30 min in 3 atmospheres
hyperbaric
Vitamin K
Coumarin
5–10 mg
IV/SC
Monitor prothrombin time; give fresh
frozen plasma for acute bleeding;
repeat vitamin K for superwarfarin
Note:Do not use with cyclic
antidepressants
BAL, British antilewisite; DMSA, dimercaptosuccinic acid; EDTA, ethylene diamine tetraacetic acid; ET, endotracheal; IM,
intramuscular; IV, intravenous; max, maximum; NS, normal saline; PO, Oral.
32. Iron supplementation in the low birth weight starts at
a. 2 weeks
b. 4 weeks
c. 8 weeks
33. Patient was bitten by a dog on the face. What prophylaxis will you give
a. rabies IG
b. rabies vaccine and IG
34. Baby born 38 weeks HR 80, irregular respiration, sneeze, cyanotic palms and soles, some flexion. What is the
APGAR score for the pt
a. 6
b. 5
c. 4
d. 7
From Nelson’s Chapter 94
TABLE 94-2 -- Apgar Evaluation of Newborn Infants
SIGN
0
1
2
Heart rate
Absent
Below 100
Over 100
Respiratory effort
Absent
Slow, irregular
Good, crying
Muscle tone
Limp
Some flexion of
extremities
Active motion
Response to catheter in nostril (tested after oropharynx
is clear)
No
response
Grimace
Cough or
sneeze
Color
Blue, pale
Body pink, extremities
blue
Completely
pink
Sixty sec after complete birth of the infant (disregarding the cord and placenta), the five objective signs above are
evaluated, and each is given a score of 0, 1, or 2. A total score of 10 indicates an infant in the best possible
condition. An infant with a score of 0–3 requires immediate resuscitation. Modified from Apgar V: Res Anesth Analg
1953;32:260.
35. What is the predictor for morbidity in newborns
a. cord pH and age of gestation
b. age of gestation and apgar
c. ballard and apgar
d. cord pH and apgar
From Nelson’s Chapter 94
The Apgar score is a practical method of systematically assessing newborn infants immediately after birth to help
identify those requiring resuscitation and to predict survival in the neonatal period ( Table 94-2 ). The 1-min Apgar
score may signal the need for immediate resuscitation, and the 5-, 10-, 15-, and 20-min scores may indicate the
probability of successfully resuscitating an infant. A low score may be due to a number of factors, including drugs
given to the mother during labor and immaturity ( Table 94-3 ). The Apgar score was not designed to predict
neurologic outcome. Indeed, the score is normal in most patients in whom cerebral palsy subsequently develops,
and the incidence of cerebral palsy is low in infants with Apgar scores of 0–3 at 5 min (but higher than in infants
with Apgar scores of 7–10). The Apgar score and umbilical artery blood pH both predict neonatal death. An Apgar
score of 0–3 at 5 min is uncommon but is a better predictor of neonatal death (in both term and preterm infants)
than an umbilical artery pH of 7.0 or less; the presence of both variables increases the relative risk of neonatal
mortality in term and preterm infants.
36. Predictor of morbidity of pneumonia
a. tachypnea
b. retractions
37. Drug of choice for a 4 y/o with pneumonia with consolidation
a. IV Cefotaxime
b. IV Cefuroxime
c. IV Pen G
d. IV Ceftriaxone
38. CPR in neonate
a. 3:1
b. 15:1
c. 5:2
39. Small for gestational age is characterized as weight
a. weight below the 5th percentile
b. 2 SD below
40. Ballard score that corresponds to term gestation
a. 35
b. 37
Please see Nelson’s Chapter 97 Figure 97-5…Ballard Score of 30 corresponds to 36 weeks, and a ballard score or 35
corresponds to 38 weeks.
41. To what percent will we reduce the volume of iPOD to avoid hearing loss
a. 60%
b. 70%
c. 80%
d. 90%
42. Edematous child, irritable, skin lesions
a. edematous severe childhood undernutrition
b. marasmus
43. BMI > 40 after 6 months of diet modification and exercise, and you decide that you need drastic measures,
what would you do?
a. bariatric surgery
b. lipase inhibitors (Orlistat)
c. strict diet modification and exercise
44. When is the first dental visit.
a. 1st tooth eruption
b. 12 mos
45. How many days before do we start chloroquine prophylaxis
a. 5-7 days
b. 7-14 days
46. Mother contracted varicella while the she was pregnant. This is alarming when it occurs
a. 5 days before to 2 days after delivery
b. 5 days before and 5 days after delivery
c. 7 days before and 7 days after delivery
d. 7 days before and 5 days after delivery
From Nelson’s Chapter 250
Newborns have particularly high mortality in the circumstances of a susceptible mother contracting varicella
around the time of delivery. Infants whose mothers develop varicella in the period from 5 days prior to delivery to
2 days afterward are at high risk for severe varicella. The infant acquires the infection transplacentally as a result
of maternal viremia, which may occur up to 48 hr prior to the maternal rash. Depending on when virus crosses the
placenta, the infant's rash may occur toward the end of the 1st week to the early part of the 2nd week of life.
Because the mother has not yet developed a significant antibody response, the infant receives a large dose of virus
without the moderating effect of maternal anti-VZV antibody. If the mother develops varicella more than 5 days
prior to delivery, she still may pass virus to the soon-to-be-born child, but infection is attenuated due to
transmission of maternal antibody across the placenta. This moderating effect of maternal antibody occurs if
delivery occurs after 30 wk of gestation, when maternal immunoglobulin G (IgG) is able to cross the placenta. The
recommendations for human varicella-zoster immune globulin (VariZIG) reflect the differing risks to the exposed
infant. Newborns whose mothers develop varicella 5 days before to 2 days after delivery should receive 1 vial.
Although neonatal varicella may occur in about half of these infants despite administration of VariZIG, it is usually
mild. Every premature infant born at <28 wk of gestation to a mother with active chickenpox at delivery (even if the
maternal rash has been present for >1 wk) should receive VariZIG. Because perinatally acquired varicella may be life
threatening, the infant should be treated with acyclovir (10 mg/kg every 8 hr IV) when lesions develop. Neonatal
chickenpox can also follow a postpartum exposure of an infant delivered to a mother who was susceptible to VZV,
although the frequency of complications declines rapidly in the weeks after birth. Infants with community-acquired
chickenpox who develop severe varicella, especially those who develop a complication such as pneumonia,
hepatitis, or encephalitis, should also receive treatment with intravenous acyclovir (10 mg/kg every 8 hr IV).
47. Mother with miliary TB. What will you give her newborn
a. INH
b. BCG
c. INH + Rifampicin
48. Pt with fever, conjunctival suffusion, lymphadenopathy, desquamation, and rashes. What is the treatment?
a. IVIG
b. Corticosteroids
49. Rash that begins on the neck
a. Scarlet fever
b. Measles
Is this the same question as the kid with the strawberry tongue?
50. Patient presents with heliotrope rash, muscle weakness
a. Dermatomyositis
From Nelson’s Chapter 158
Juvenile dermatomyositis (JDM), the most common of the pediatric inflammatory myopathies, is distinguished by a
characteristic rash and proximal, symmetric muscle weakness that is often responsive to the immunosuppressive
therapy.
In the 3 mo before disease onset, presenting children who are <6 yr of age have more fever and upper respiratory
symptoms than older children, who have greater arthritis and musculoskeletal complaints, dysphagia, and
headaches. Weakness is frequently insidious, with a gradual increase of complaints of fatigue on walking and loss
of ability to perform activities of daily living.
The rash often has onset in sun-exposed areas and develops as the first symptom in 50% of cases, and
concomitantly with weakness in 25% of cases. The characteristic periorbital violaceous erythema (heliotrope) may
cross the bridge of the nose, in a masklike distribution, and involve the ears as well ( Fig. 158-1 ). Edema may be
limited to the periorbital area, or generalized, and may involve the scalp with inflammation sufficient to result in
partial baldness. The rash is often florid and is usually palpable over joints, especially the metacarpal phalangeal,
intercarpal phalangeal (Gottron papules), knees, elbows, and medial malleoli of the ankles ( Fig. 158-2 ). Cutaneous
involvement can spread to the extensor surfaces of the extremities, the torso in a shawl-like distribution, and be
generalized involving the trunk and buttocks. Children with an initial amyopathic form of JDM, with rash only, may
develop myositis and calcinosis later in their disease course if not appropriately treated. The severity of the rash is
reflected by a decreased number of nail-fold capillary loops, which is supporting evidence of a systemic
vasculopathy ( Fig 158-3 ). Diffuse severe vasculopathy may be manifest by infarction of the skin on the face in the
area of the medial canthi, oral epithelium, or digital or gastrointestinal ulceration. Healing may be accompanied by
hyperpigmentation or vitiligo.
51. According to the PPS policy statement, which is the most prevalent source of noise contributing to hearing
loss?
a. Street traffic
b. Recreation
c. Construction
d. Fireworks
52. Patient presents with drooling of saliva
a. Epiglotitis
b. Bacterial tracheitis
53. Stridor when lying supine
a. laryngomalacia
54. Policy statement regarding walkers
a. Helps develop strong legs
b. Prone to accidents and poisoning
c. Offers many advantages and wise to invest in one
* Available at pps.org.ph
55. Patient with VSD presented with fever, focal seizure, (+) dilated pupils on the right
a. brain abscess – (Mam Liz: although I’ve never seen a Left sided lesion na may brain abscess )
b. cerebral thrombosis
c. congestive heart failure
56. 14 year old with migraine – like right sided headache, sudden onset of decrease in sensorium
a. AVM
b. Intracranial mass
c. brain abscess
d. Meningitis
57. Patient born with Down syndrome translocation type. What test will you do
a. Chromosomal analysis of both parents
b. Chromosomal analysis of mother
c. Chromosomal analysis of siblings
d. don’t do anything
58. Of the orphan diseases which is the most common
a. galactosemia
b. maple syrup urine disease
c. pompe
d. gaucher
59. A pregnant woman presents to you, and on PE you hear fetal heart tones. Patient says she has felt the baby
move. What gestational age is the fetus?
a. 9 weeks
b. 12 weeks
c. 16 weeks
d. 18 weeks
From Nelson’s Chapter 96 – The Fetus
Fetal maturity is usually assessed by accurate ultrasonographic dating of gestational age, but it may also be
estimated by determining the surfactant content of amniotic fluid (Chapter 101.4 ). Determination of the extent of
calcification by ultrasound (placental maturity index), detection of the 1st audible fetal heart tones (16–18 wk),
and observation of the initial fetal movements (18–20 wk) may also aid in evaluating the maturity of a fetus. An
estimate of gestational age by dating of the last menstrual period should also be obtained.
60. 2 y.o. with hypoplastic iris, abdominal mass, smooth border
a. Wilms tumor – (Ma’am Liz: WAGR Syndrome)
b. Neuroblastoma
c. Hepatoblastoma
From Nelson’s Chapter 499 –Wilms tumor
Several syndromes and congenital abnormalities commonly are reported in patients with Wilms tumor ( Table 4992 ). WAGR syndrome is a contiguous gene deletion syndrome that consists of Wilms tumor, aniridia, genitourinary
abnormalities (cryptorchidism, streak ovaries, bicornate uterus, ambiguous genitalia), and mental retardation.
Patients with this syndrome have a constitutional deletion of chromosome 11p13 where the Wilms tumor gene,
WT1, and the aniridia gene, PAX6, are located. Denys-Drash syndrome is characterized by male
pseudohermaphrodism, early-onset renal failure characterized by mesangial sclerosis, and an increased risk of
Wilms tumor. Patients with this syndrome typically carry a missense mutation in the WT1 gene. BeckwithWiedemann syndrome is characterized by hemihypertrophy, macroglossia, and visceromegaly, with a 3–5% risk of
developing Wilms tumor. A variety of 11p15.5 abnormalities have been reported in patients with this syndrome,
and it is postulated that a second Wilms tumor gene, WT2, is located in this region. Loss of imprinting of the insulinlike growth factor 2 gene, an epigenetic process, also is associated with Wilms tumor. Other syndromes or
conditions with an increased risk of Wilms tumor include hemihypertrophy, sporadic aniridia, genitourinary
anomalies, Pearlman syndrome, Sotos syndrome, neurofibromatosis (von Recklinghausen disease), and von
Willebrand disease. The genitourinary anomalies most commonly associated with Wilms tumor are hypoplasia,
fusion and ectopia of the kidney, duplications of the collecting systems, hypospadias, and cryptorchidism.
TABLE 499-2 -- Syndromes Associated with Wilms Tumor and Their Clinical and Chromosomal Characteristics
SYNDROME
CLINICAL CHARACTERISTICS
CHROMOSOME OR OTHER ABNORMALITIES
WAGR
Aniridia, genitourinary abnormalities, mental
retardation
Del 11p13 (WT1 and PAX6 loci)
Denys-Drash
Early-onset renal failure with renal mesangial
sclerosis, male pseudohermaphrodism, increased
risk of Wilms tumor
WT1 mutations
SYNDROME
CLINICAL CHARACTERISTICS
CHROMOSOME OR OTHER ABNORMALITIES
BeckwithWiedemann
Organomegaly (liver, kidney, adrenal, pancreas),
macroglossia omphalocele, hemihypertrophy
Uniparental paternal disomy, duplication
11p15.5, loss of imprinting, mutation of
p57KIP57 have been described.
Del 11p15.5 (WT2 locus)
May also involve IGF2 and/or H19 genes
61. 15 month old with dyspnea and cyanosis especially when crying. has a Gr 2-3 soft blowing murmur on the 3rd4th ICS
a. TOF
b. Tricuspid atresia
c. TGA
d. TAPVR
62. 2 mos developed dyspnea CXR showed mild cardiomegaly (Ma’am Liz: I think they placed little cardiomegaly)
with diffuse reticular pattern (increased pulmonary blood flow)
a. TGA
b. Hypoplastic left heart syndrome
c. pulmonary valve atresia
d. TAPVR with venous obstruction
63. Inhibit protein synthesis except
a. capreomycin
b. ofloxacin – inhibit DNA gyrase
c. kanamycin
d. amikacin
64. Minimum age of employment
a. 12y
b. 15y
c. 18y
d. 20y
Also in the PPS policy statement: Children between 15 and 18 years old may be employed in undertakings not
hazardous or deleterious in nature, i.e. any kind of work in which the employee is not exposed to any risk that
constitutes an imminent danger to his or her life and limb, safety, and health. Still, children below 15 are not
allowed to work more than 4 hours per day, 5 days per week.
65. PPS policy on circumcision
a. Increased risk of HIV in uncircumscribed
b. Definite Health Benefits
c. No legal and ethical argument
d. Not routinely done
66. child of an OFW, presented with persistent diarrhea, hepatosplenomegaly, oral thrush
a. AIDS
67. case of a patient who presents with fever, swollen tonsils
a.Staphyloccal shock syndrome
b. streptococcal shock syndrome
68. Pt on Foley catheter develops fever. What is the most likely etiology
a. Enterococcus
b. Staph aureus
c. E. coli
69. For Staph Endocarditis what is added to vancomycin for synergism
a. rifampicin
b. amikacin
70. Pt develops diarrhea and vomiting. He was previously admitted and was given Ampicillin for 1 week
a. pseudomembranous colitis
71. Most commonly seen in Down syndrome Mel eto ba question dito? Parang case ata ito but not MC question
a. malrotation
b. duodenal atresia
c. volvulus
72. Innocent mumur can be differentiated by doing
a. change with positions –(Ma’am Liz: I think this should be the answer and not ECG which wont differentiate from
pathologic murmurs all the time)
b. ECG
73. Hematuria with dark brown casts
a. extraglomerular
b. glomerular
74. Patient presents with fever Temp 38.5, noted to have protein 1+ on urinalysis. The following day, patient was
afebrile and repeat UA showed negative proteinuria.
a. fixed proteinuria
b. orthostatic proteinuria
c. transient proteinuria
75. Portal venous gas
a. NEC
76. Pneumatosis intestinalis
a. NEC
From Nelson’s Chapter 102 (for numbers 75 and 76)
A very high index of suspicion in treating preterm at-risk infants is crucial. Plain abdominal x-rays are essential to
make a diagnosis of NEC. The finding of pneumatosis intestinalis (air in the bowel wall) confirms the clinical
suspicion of NEC and is diagnostic; 50–75% of patients have pneumatosis when treatment is started ( Fig. 102-4 ).
Portal venous gas is a sign of severe disease, and pneumoperitoneum indicates a perforation. Hepatic
ultrasonography may detect portal venous gas despite normal abdominal roentgenograms.
77. 4 yr old presented with cough and respiratory distress. He was admitted and given IV antibiotics and
terbutaline nebulizations and subsequently improved. On the 4th day, pt developed cough, sudden dyspnea,
chest pain and became cyanotic. What happened to the pt?
a. Pleural Effusion
b. Atelectasis
c. Pneumothorax
d. Bronchiectasis
78. First problem in drowning that you should give attention to
a. aspiration
b. hypothermia
c. hypoxia
d. Global hypoxic ischemic encephalopathy
79. Most common cause of intrauterine distress
a. placental insufficiency
b. Maternal drugs
c. Preterm
d. maternal illness
80. Patient with dyspnea and decreased breath sounds
a. pneumothorax
81. Which of the ff pathologic changes will cause tracheal deviations towards the same side?
a. Pleural Effusion
b. Atelectasis
c. Pneumothorax
d. Intrathoracic Mass
82. Pneumothorax caused by mechanical ventilator
a. barotrauma
b. volutrauma
83. A patient had gas poisoning (most likely carbon monoxide because of the presentation) and the ff symptoms,
cherry red lips and mucosa. What should be given?
a. 100% oxygen
b. Activated charcoal
From Nelson’s Chapter 58
CARBON MONOXIDE.
Although many industrial and naturally occurring gases pose a health risk by inhalation, the most common gas
involved in pediatric exposures is carbon monoxide (CO). CO is a colorless, odorless gas produced during the
combustion of any carbon-containing fuel. The less efficient the combustion, the greater the amount of CO
produced. Wood-burning stoves, old furnaces, and automobiles are potential sources.
Pathophysiology.
Toxicity develops through at least 3 mechanisms. First, it binds to hemoglobin, displacing oxygen-forming
carboxyhemoglobin (COHb), with an affinity for hemoglobin that is approximately 250 times that of oxygen.
Second, CO impairs the ability of hemoglobin to release oxygen to tissues. Finally, CO binds to cytochrome oxidase
in tissues, impeding oxygen use. Although the relative contribution of each of these mechanisms to CO toxicity is
unclear, the net result is tissue hypoxia.
Clinical and Laboratory Manifestations.
Symptoms of CO poisoning are usually proportional to the concentration of COHb in the blood. COHb
concentrations can be measured in almost all hospital laboratories. Early symptoms are nonspecific and include
headache, malaise, and nausea, which are often confused with the flu. At higher exposure levels, headaches
become severe, and dizziness, visual changes, and weakness may be present. Cherry-red mucosal coloring and
retinal hemorrhage may also be present. Children may experience syncopal episodes as a first symptom. At high
concentrations, coma, seizures, respiratory instability, and death may occur (see Chapter 74 ). Symptoms usually
appear at COHb levels of >15%, toxicity is present at levels of >20%, and severe neurologic effects are universal at
levels of >40%.
Treatment.
In addition to general supportive care, treatment of CO poisoning requires the administration of 100% oxygen.
High concentrations of oxygen shorten the COHb half-life in the blood and tissues. In healthy volunteers, the COHb
half-life averages 5–6 hr (range, 2–7 hr), which is dramatically reduced to approximately 40–60 min by the
administration of 100% oxygen at normal atmospheric pressures by a non-rebreathing face mask. In more severe
and/or chronic exposures, hyperbaric oxygen therapy may be required, which at 2.5–3.0 atm reduces the COHb
half-life to approximately 15–30 min. Severely poisoned patients benefit from hyperbaric oxygen therapy.
Indications for hyperbaric oxygen include neurologic symptoms compatible with CO poisoning and a COHb level of
>25% in children and pregnant women. After a significant exposure, some patients may experience delayed-onset
neurotoxicity, which may be permanent. Aggressive early treatment of patients with significant symptoms may
diminish the risk of neurologic sequelae.
84. Patient (<5 y/o) with asthma who is on daily short acting B2 agonist who still experience daily sxs and 2x a
week nighttime symptoms
a. med dose CS with SABA
b. leukotriene modifier + SABA
c. high dose CS
85. Urinary chloride low and metabolic alkalosis
a. gastric losses such as emesis
b. Bartter syndrome
c. CKD
86. Smith Lemli opitz with Hirchsprung what is the definite diagnostic modality
a. rectal manometry and biopsy
87. Patient with urinary protein of 1g/24 hr, hypertensive. You would advise
a. renal biopsy
b. repeat U/A
c. DMSA
d. ultrasound
88. Hypertension in a patient with acute nephritic syndrome is due to
a. hypoalbuminemia
b. decrease in renin
c. sodium and water retention
d. aldosterone
89. Pt has AGN and presents with seizures and hypertension
a. hypertensive encephalopathy
90. Dr. Frank has been having difficulty in managing the case of George who as end stage renal disease. George is
his patient since he was 10 yrs old and who is also being co-managed with another renal specialist. What should
Dr. Frank do?
a. Let the renal specialist handle the case
b. (Long sentence but the summary is…) The attending should sit down with the patient and parents and discuss
everything pertinent to the case.
91. Low incidence of developmental dysplasia of the hip seen in
a. Asians and Africans
b. Eastern European
c. White American
d. Native American
From Nelson’s Chapter 677.1
Although most newborn screening studies suggest that some degree of hip instability can be detected in one in 100
to one in 250 babies, actual dislocated or dislocatable hips are much less frequent, being found in 1–1.5 of 1000 live
births. The etiology of DDH is multifactorial, involving both genetic and intrauterine environmental factors. There is
marked geographic and racial variation in the incidence of DDH. The reported incidence based on geography ranges
from 1.7/1,000 babies in Sweden to 75/1,000 in Yugoslavia to 188.5/1,000 in a district in Manitoba, Canada. The
incidence of DDH in Chinese and African newborns is almost 0%, whereas it is 1% for hip dysplasia and 0.1% for
hip dislocation in white newborns. These differences may be due to environmental factors, such as child-rearing
practices, rather than to genetic predisposition. African and Asian caregivers have traditionally carried babies
against their bodies in a shawl so that a child's hips are flexed, abducted, and free to move. This keeps the hips in
the optimal position for stability and for dynamic molding of the developing acetabulum by the cartilaginous
femoral head. On the other hand, children in Native American and Eastern European cultures, which have a
relatively high incidence of DDH, have historically been swaddled in confining clothes that bring their hips into
extension. This position increases the tension of the psoas muscle–tendon unit and may predispose the hips to
displace and eventually dislocate laterally and superiorly.
92. Xray finding in primary TB
a. lymphadenopathy
b. infiltrates upper lobe
c. infiltrates lower lobe
93. Correct pair
a. Neonatal bleeding – ibuprofen
b. Mg SO4 – hyperactivity
both are correct!
94. Metoprolol is contraindicated in:
a. asthma
b. Glomerulonephritis
c. Renal failure
95. which is included in the New expanded EPI
a. OPV
b. DPT
c. hepatitis B
d. MMR
96. Antidote in organophosphate poisoning
a. atropine
*See previous table on antidotes
97. Deficiency of renin causes decrease in aldosterone and subsequently
a.hypercalcemia and metabolic acidosis
b. hypokalemia and metabolic alkalosis
c. hyperkalemia and metabolic acidosis
d. hypocalcemia and metabolic acidosis
98. Hib and PCV is advised in pts with asplenia because they are prone to infections due to
a. Streptococcus pneumoniae
99. 10 y.o. presents with worsening cough with whitish sputum, has not completed vaccination for Pneumococcal
and Hib  Tama ba Lols yung pagkakaalala ko rito?
a. Mycoplasma pneumoniae
b. Klebsiella pneumoniae
c. Streptococcal pneumonia
d. Haemophilus influenzae
100. ECG findings of peaked T waves, prolonged PR interval is suggestive of
a. Hyperkalemia
b. hypocalcemia
101. Pt presents with spastic movement of the corners of the mouth upon tapping at the zygomatic prominence
a. Hypocalcemia
102. Patient with atopic dermatitis with thrombocytopenia and ear discharge
a. Wiskott-Aldrich
b. Bruton
103. Contraindications in breastfeeding mother
a. chloramphenicol
b. cotrimoxazole
104. May also be given in bacterial meningitis if there is little evidence of resistance
a. Chloramphenicol
105. Hemophilia A bleeding what will you give if no factor VIII is available
a. FFP
b. cryoprecipitate
106. 6 yr old boy carrying a back pack to school. PPS policy statement on this
a. It is safe and helps carries books
b. Has no long term effect on spine function
c. Weight should not be more than 10% of body weight
d. Advise to carry over 1 shoulder only
107. Patient with lower left shoulder than the right. What will you advise the mother
a. advise consult to ortho
b. tell the mother that it is normal
108. 2 day old infant brought in for consult for bloody stools. Apt test was done and showed positive results
A. sepsis
B. GBS
C. swallowed blood
D. systemic illness
109. An 18 yo Female had acute chest pain, cyanosis and tachypnea. 1 week after giving birth. CXR was normal.
PO2 60 mmHg at FiO2 40%.
a. Pre eclampsia
b. Legionella Pneumonia
c. Pulmonary Embolism
d. Hysterical Hypoventilation
From Nelson’s
*Ch406: Commonly appreciated risk factors for thromboembolic disease in adults include immobility, malignancy,
pregnancy, infection, and hypercoagulability. Common symptoms and signs of PE include hypoxia (cyanosis),
tachypnea, dyspnea, cough, diaphoresis, and chest pain.
* Ch205:Legionella pneumonia exposure may occur through 2 general mechanisms: (1) aspiration of ingested
microorganisms, including those in gastric feedings, that are mixed with contaminated tap water; and (2) aerosols
from showers and sinks. Cause atypical pneumonia that was associated with extrapulmonary signs and symptoms
including diarrhea, hyponatremia, hypophosphatemia, abnormal results of liver function tests, confusion, and renal
dysfunction –not seen in our pt
110. Burn complication
a. DVT
b. neuropathic pain and itching
111. ABG which would indicate intubation
a. pH 7.2, pCO2 60, pO2 88
b. pH 7.2, pCO2 48, pO2 60
c. pH 7.0, pCO2 49, pO2 65
d. pH 7.0, pCO2 60, pO2 58
112. In dengue, best indicator of bleeding
a. PT
b. PTT
c. bleeding time
d. coagulation
113. Child presents with 2 week history of fever. On PE noted to be pale with hepatosplenomegaly with WBC of 56,
000 and on PBS showed atypical lymphocytes
a. typhoid/enteric fever
b. acute leukemia
c. Kawasaki disease
114. 5mm reading of PPD test is considered significant except
a. history of contact
b. CXR suggestive of PTB
c. loss of weight
d. hemoptysis
115. hypopigmented nonpruritic lesion
a. pityriasis alba
b. dishydrotic eczema
c. lichen simplex chronicus
d. candida
116. Which drink has the most caffeine content?
a. coke regular
b. pepsi
c. seven up
d. mountain dew
Believe it or not, it’s in the PPS policy statements
117. patient with pacemaker suddenly develops IE, which is the most likely causative organism?
a. Staphylococcus aureus
b. Streptococcus viridians
c. streptococcus pyrogenes
118. True about BCG except
a. It’s given twice – at birth and at school entry
119. red flag in psychosocial development
a. social smile at 1 month
b. stiffens when approached at 12 months
120. red flag in language parang iba choices?
a. coos at 2 months
b. mama and papa at 24 months
c. listens to music at 3 months
d. use of subject verb object at 24 months
121. metabolic disturbance in a newborn of a mother with diabetes mellitus except
a. hyponatremia
b. hypoglycemia
c. hypocalcemia
d. hypomagnesemia
122. Suspect TB if
a. cough 1 week
b. decrease appetite when milk is changed
c. failure to gain weight
d. cervical lymphadenopathy
123. In termination of end of life support, what should you consider
a. Best interest of the child
b. Parents’ preferences