Paediatrics Oral Exam Topics With Complete
Solutions
Graded A+
QUESTIONS AND ANSWERS
Type I Diabetes - Definition, Etiology, Risk Factors, Presentation. ANSWER -
DEFINITION: Autoimmune Destruction of pancreatic b-cells - Permanent Insulin
Deficiency (3 types - transient neonatal, permanent neonatal, classic type I
ETIOLOGY: Genetic component, environmental (viral?)
RISK FACTORS: Genetic (HLA chromosome 6), environmental exposures (food Ag,
congenital rubella), autoantibodies (islet cell Ag, glutamic acid decarboxylase, insulin)
PRESENTATION: Polyuria, Polydipsia, Polyphagia and Wt loss + ABD pain, nausea,
increased appetite, Glycosuria (causes osmotic diuresis -polyuria/polydipsia), hyperglycemia
(fasting>126mg/dL or 2 hour postprandial>200), islet cell antibody to glutamic acid
decarboxylase positive (anti-insulin Ab), low C-Peptide
DKA - Cause, Presentation, Treatment. ANSWER -CAUSE: unregulated fatty acid
oxidation produces b-hydroxybutyrate, acetoacetate and acetone - arterial pH below 7.25,
serum bicarb < 15, Ketones elevated in serum/urine - metabolic acidosis, may be
precipitated by bacterial infection (think sepsis)
PRESENTATION: AMS, n/v, abd pain, kussmaul breathing(slow, deep), fruity breath,
seizures, dehydration (skin tenting, low capillary refill), tachycardia, Hx of recent wt
loss/polyuria/polydipsia, glucose >400, metabolic acidosis with anion gap, hyperketonemia
TREATMENT: slow fluids (risk of cerebral edema if rapid shifts in osmolality) - pt is 10%
dehydrated, 10-20cc/kg bolus, remaining fluid given slowly over 36-48 hours; fast acting
insulin IV, NO BICARB! (can increase CNS acidosis), monitor acidosis and glucose levels,
relative hyperkalemia (insulin drives K+ intracellularly), overall K+ depletion - give K+
unless > 6 mEq/L
CEREBRAL EDEMA TREATMENT: IV mannitol
Type II Diabetes - Definition, Types and Risk factors, Presentation. ANSWER -
DEFINITION: Non insulin dependent - can be relative insulin deficiency, peripheral
resistance to action of insulin or both
TYPES: Secondary (CF, Hemochromatosis, pancreatectomy, drugs - L-asparagine,
tacrolimus), Adult type (classic - Associated with obesity, insulin resistance, genetic
component), Maturity onset diabetes of youth (MODY - AD, onset before 25, not associated
,with diabetes or autoimmunity), Mitochondrial diabetes (associated with deafness and other
neuro deficits, maternal transmission - mtDNA pt mutation)
RISK FACTORS: genetic, obesity, diet, lack of exercise
PRESENTATION: Most asymptomatic, polyuria, polydipsia, acanthosis nigricans, wt loss,
HTN, Glycosuria, hyperglycemia (fasting>126, 2hr postprandial>200), Ketonuria
Diabetes - Complications, Treatment (I, II, Hypoglycemia), Insulin Types (Short,
Intermediate, Long). ANSWER -COMPLICATIONS: hypoglycemic crisis or
hyperglycemic crisis (DKA),
macrovascular (Atherosclerosis -> MI, CVA, poor wound healing)
microvascular (Retinopathy, nephropathy with microalbuminuria, neuropathy)
TYPE I TREATMENT - Prevent Complications (HBA1C, opthalmology, distal sensation
testing), Insulin Replacement - SC outpt, IV inpt (0.7 U/kg/24hrs); Fast with each meal and
long acting at bedtime
TYPE II TREATMENT - Prevent complications (HBA1C, opthalmology, distal sensation
testing), exercise + diet first, metformin only agent approved in kids, insulin if necessary
HYPOGLYCEMIA TREATMENT: if mild give oral glucose, severe at home (seizures)
give glucagon injection, IV glucose in hospital
SHORT: Regular, Lispro, Aspart, Glulisine
INTERMEDIATE: NPH, Lente
LONG: Glargine, Demeter
Neonatal Sepsis - Early vs Late, Signs and Symptoms, Risk Factors, Prevention, Evaluation,
Treatment. ANSWER -EARLY: Birth - 7 days - GBS, E. Coli, Listeria (transplacental), H.
Flu, Coag (-) staph/S. aureus (nosocomial), Klebsiella,
LATE: 8-28 days - GBS, E. Coli, H. Flu, Klebsiella, H. Flu, HSV, S. Pneumo, N.
Meningitidis, HSV, CMV, enteroviruses, coag neg staph/staph aureus (nosocomial
COMMON S+S: Deviation from infant's usual pattern of activity/feeding, temperature
instability, respiratory/GI/neuro abnormalities, fetal/neonatal distress during labor and
delivery (fetal tachycardia, mec stained amniotic fluid, low APGAR), Pneumonia
(respiratory distress), meningits (bulging fontanelle), hypoglycemia, metabolic acidosis,
DIC, hyperbilirubinemia
LESS COMMON S+S: Jaundice, respiratory distress (pneumonia), hepatomegaly, anorexia,
vomiting, lethargy, cyanosis, apnea, ABD distension, irritability, Diarrhea
RISK FACTORS: Delivery < 37 wks, 5 min APGAR < 6, fetal distress (tachycardia), mom
GBS+, ROM > 18 hours, meconium stained amniotic fluid, maternal fever/amnionitis
PREVENTION: Intrapartum ABX (PCN) at delivery reduces GBS sepsis
, EVALUATION: Vitals, PE, blood cultures, CBC (high neutrophils, WBC <5000 or >
19000, neutropenia), CRP, LP, Urine culture, other sites of infection (purulent eye
drainage), CXR if respiratory distress
TREATMENT: Culture/sensitivity specific - Empiric = Cephalosporins (cefotaxime
reaches CSF, treats GBS, E. Coli, G-'s) & Ampicillin (Listeria) OR Amp (G+ - Listeria,
staph, GBS, H. flu) & Gentamycin (E. coli, G-'s); H flu and pneumococcus show resistance to
Ampicillin Clinda/Flagyl for anaerobes, bactrim; Viral = acyclovir, zidovudine; Fungal =
fluconazole, Amphoteracin B
Neonatal Jaundice - Indirect (unconjugated) Hyperbilirubinemia - Causes. ANSWER -
INDIRECT = total > 1.5, direct <2 or <20%
Physiologic jaundice (decreased BUGT, decreased bacterial flora - reabsorb more bili,
higher bili production - decreased RBC life, increased RBC mass)
Hemolysis - Rh/ABO/Kell/Duffy incompatibility (type A or B w type O mom),
hemoglobinopathies (alpha-thal), RBC enzyme defects (G6PD, PKD), RBC membrane
(spherocytosis, ovalocytosis)
Infection!
Congenital hypothyroid,
Cephalohematoma
Breast milk jaundice (starts 4-7 days and can last for wks, enzyme inhibits BUGT)
Breast feeding Jaundice (1st week - inadequate feeding, volume contraction and relative
increase in bili - add formula supplementation)
Drugs (ASA, cephalosporins, sulfas - displace from albumin; Rifampin - inhibits uptake of
bili to liver)
Crigler-Najjar - type 1 absent BUGT (severe), type II decreased activity (treat with
phenobarbitol), Gilbert's (point mutation in BUGT - presents later)
Pyloric Stenosis
ITP
****Kernicterus - basal ganglia
Neonatal Jaundice - Direct (conjugated) Hyperbilirubinemia - Common and uncommon
causes. ANSWER -DIRECT = direct > 2mg/dL or >20% of total
COMMON - Hyperalimentation cholestasis, TORCHES infections, inspissated bile from
prolonged hemolysis, neonatal hepatitis, sepsis
Solutions
Graded A+
QUESTIONS AND ANSWERS
Type I Diabetes - Definition, Etiology, Risk Factors, Presentation. ANSWER -
DEFINITION: Autoimmune Destruction of pancreatic b-cells - Permanent Insulin
Deficiency (3 types - transient neonatal, permanent neonatal, classic type I
ETIOLOGY: Genetic component, environmental (viral?)
RISK FACTORS: Genetic (HLA chromosome 6), environmental exposures (food Ag,
congenital rubella), autoantibodies (islet cell Ag, glutamic acid decarboxylase, insulin)
PRESENTATION: Polyuria, Polydipsia, Polyphagia and Wt loss + ABD pain, nausea,
increased appetite, Glycosuria (causes osmotic diuresis -polyuria/polydipsia), hyperglycemia
(fasting>126mg/dL or 2 hour postprandial>200), islet cell antibody to glutamic acid
decarboxylase positive (anti-insulin Ab), low C-Peptide
DKA - Cause, Presentation, Treatment. ANSWER -CAUSE: unregulated fatty acid
oxidation produces b-hydroxybutyrate, acetoacetate and acetone - arterial pH below 7.25,
serum bicarb < 15, Ketones elevated in serum/urine - metabolic acidosis, may be
precipitated by bacterial infection (think sepsis)
PRESENTATION: AMS, n/v, abd pain, kussmaul breathing(slow, deep), fruity breath,
seizures, dehydration (skin tenting, low capillary refill), tachycardia, Hx of recent wt
loss/polyuria/polydipsia, glucose >400, metabolic acidosis with anion gap, hyperketonemia
TREATMENT: slow fluids (risk of cerebral edema if rapid shifts in osmolality) - pt is 10%
dehydrated, 10-20cc/kg bolus, remaining fluid given slowly over 36-48 hours; fast acting
insulin IV, NO BICARB! (can increase CNS acidosis), monitor acidosis and glucose levels,
relative hyperkalemia (insulin drives K+ intracellularly), overall K+ depletion - give K+
unless > 6 mEq/L
CEREBRAL EDEMA TREATMENT: IV mannitol
Type II Diabetes - Definition, Types and Risk factors, Presentation. ANSWER -
DEFINITION: Non insulin dependent - can be relative insulin deficiency, peripheral
resistance to action of insulin or both
TYPES: Secondary (CF, Hemochromatosis, pancreatectomy, drugs - L-asparagine,
tacrolimus), Adult type (classic - Associated with obesity, insulin resistance, genetic
component), Maturity onset diabetes of youth (MODY - AD, onset before 25, not associated
,with diabetes or autoimmunity), Mitochondrial diabetes (associated with deafness and other
neuro deficits, maternal transmission - mtDNA pt mutation)
RISK FACTORS: genetic, obesity, diet, lack of exercise
PRESENTATION: Most asymptomatic, polyuria, polydipsia, acanthosis nigricans, wt loss,
HTN, Glycosuria, hyperglycemia (fasting>126, 2hr postprandial>200), Ketonuria
Diabetes - Complications, Treatment (I, II, Hypoglycemia), Insulin Types (Short,
Intermediate, Long). ANSWER -COMPLICATIONS: hypoglycemic crisis or
hyperglycemic crisis (DKA),
macrovascular (Atherosclerosis -> MI, CVA, poor wound healing)
microvascular (Retinopathy, nephropathy with microalbuminuria, neuropathy)
TYPE I TREATMENT - Prevent Complications (HBA1C, opthalmology, distal sensation
testing), Insulin Replacement - SC outpt, IV inpt (0.7 U/kg/24hrs); Fast with each meal and
long acting at bedtime
TYPE II TREATMENT - Prevent complications (HBA1C, opthalmology, distal sensation
testing), exercise + diet first, metformin only agent approved in kids, insulin if necessary
HYPOGLYCEMIA TREATMENT: if mild give oral glucose, severe at home (seizures)
give glucagon injection, IV glucose in hospital
SHORT: Regular, Lispro, Aspart, Glulisine
INTERMEDIATE: NPH, Lente
LONG: Glargine, Demeter
Neonatal Sepsis - Early vs Late, Signs and Symptoms, Risk Factors, Prevention, Evaluation,
Treatment. ANSWER -EARLY: Birth - 7 days - GBS, E. Coli, Listeria (transplacental), H.
Flu, Coag (-) staph/S. aureus (nosocomial), Klebsiella,
LATE: 8-28 days - GBS, E. Coli, H. Flu, Klebsiella, H. Flu, HSV, S. Pneumo, N.
Meningitidis, HSV, CMV, enteroviruses, coag neg staph/staph aureus (nosocomial
COMMON S+S: Deviation from infant's usual pattern of activity/feeding, temperature
instability, respiratory/GI/neuro abnormalities, fetal/neonatal distress during labor and
delivery (fetal tachycardia, mec stained amniotic fluid, low APGAR), Pneumonia
(respiratory distress), meningits (bulging fontanelle), hypoglycemia, metabolic acidosis,
DIC, hyperbilirubinemia
LESS COMMON S+S: Jaundice, respiratory distress (pneumonia), hepatomegaly, anorexia,
vomiting, lethargy, cyanosis, apnea, ABD distension, irritability, Diarrhea
RISK FACTORS: Delivery < 37 wks, 5 min APGAR < 6, fetal distress (tachycardia), mom
GBS+, ROM > 18 hours, meconium stained amniotic fluid, maternal fever/amnionitis
PREVENTION: Intrapartum ABX (PCN) at delivery reduces GBS sepsis
, EVALUATION: Vitals, PE, blood cultures, CBC (high neutrophils, WBC <5000 or >
19000, neutropenia), CRP, LP, Urine culture, other sites of infection (purulent eye
drainage), CXR if respiratory distress
TREATMENT: Culture/sensitivity specific - Empiric = Cephalosporins (cefotaxime
reaches CSF, treats GBS, E. Coli, G-'s) & Ampicillin (Listeria) OR Amp (G+ - Listeria,
staph, GBS, H. flu) & Gentamycin (E. coli, G-'s); H flu and pneumococcus show resistance to
Ampicillin Clinda/Flagyl for anaerobes, bactrim; Viral = acyclovir, zidovudine; Fungal =
fluconazole, Amphoteracin B
Neonatal Jaundice - Indirect (unconjugated) Hyperbilirubinemia - Causes. ANSWER -
INDIRECT = total > 1.5, direct <2 or <20%
Physiologic jaundice (decreased BUGT, decreased bacterial flora - reabsorb more bili,
higher bili production - decreased RBC life, increased RBC mass)
Hemolysis - Rh/ABO/Kell/Duffy incompatibility (type A or B w type O mom),
hemoglobinopathies (alpha-thal), RBC enzyme defects (G6PD, PKD), RBC membrane
(spherocytosis, ovalocytosis)
Infection!
Congenital hypothyroid,
Cephalohematoma
Breast milk jaundice (starts 4-7 days and can last for wks, enzyme inhibits BUGT)
Breast feeding Jaundice (1st week - inadequate feeding, volume contraction and relative
increase in bili - add formula supplementation)
Drugs (ASA, cephalosporins, sulfas - displace from albumin; Rifampin - inhibits uptake of
bili to liver)
Crigler-Najjar - type 1 absent BUGT (severe), type II decreased activity (treat with
phenobarbitol), Gilbert's (point mutation in BUGT - presents later)
Pyloric Stenosis
ITP
****Kernicterus - basal ganglia
Neonatal Jaundice - Direct (conjugated) Hyperbilirubinemia - Common and uncommon
causes. ANSWER -DIRECT = direct > 2mg/dL or >20% of total
COMMON - Hyperalimentation cholestasis, TORCHES infections, inspissated bile from
prolonged hemolysis, neonatal hepatitis, sepsis
