NEET-PG 2012 — Pediatrics
42 Previous Year Questions with Answers & Explanations
What is the most common presentation of tuberculosis (TB) in children?
What is the venous hematocrit level at which you will diagnose polycythemia in a newborn?
What is the RDA (Recommended Dietary Allowance) for vitamin A in infants aged 0-6 months?
Congenital varicella infection causes all except:
Neonatal conjunctivitis is caused by all of the following except:
Rubella is known to cause all of the following conditions except:
Double aortic arch is associated with which syndrome?
A 3-month-old infant presents with an abdominal palpable mass and non-bilious vomiting. What is the most likely diagnosis?
What is the PRIMARY pathophysiological mechanism underlying the most common cause of neonatal hyperbilirubinemia?
Most common site of extramedullary relapse of ALL in a 6-year-old boy is
NEET-PG 2012 - Pediatrics NEET-PG Practice Questions and MCQs
Question 1: What is the most common presentation of tuberculosis (TB) in children?
- A. Abscess
- B. Consolidation
- C. Hilar adenopathy (Correct Answer)
- D. CNS tuberculosis
Explanation: ***Hilar adenopathy*** - **Hilar adenopathy** is the most common radiographic finding in children with **primary tuberculosis**, reflecting lymph node involvement. - This is often accompanied by a small parenchymal lesion, forming the **Ghon complex**. *Abscess* - While TB can cause abscesses (e.g., cold abscesses in bone or soft tissue), it's not the **most common initial presentation** of primary childhood TB. - Abscess formation suggests a more **advanced or extrapulmonary** manifestation. *Consolidation* - **Consolidation** can be seen in adult-type or progressive primary TB, but it is less frequent than hilar adenopathy as the **initial presentation** in children. - It indicates **pneumonia-like changes** due to parenchymal inflammation. *CNS tuberculosis* - **Central Nervous System (CNS) tuberculosis** (e.g., tuberculous meningitis or tuberculoma) is a severe, extrapulmonary form of TB. - It is a **serious complication** rather than the most common initial presentation in children.
Question 2: What is the venous hematocrit level at which you will diagnose polycythemia in a newborn?
- A. 55%
- B. 60%
- C. 65% (Correct Answer)
- D. 70%
Explanation: ***Correct: 65%*** - **Polycythemia** in a newborn is typically diagnosed when the **venous hematocrit** is **≥65%**. - This threshold indicates an abnormally high concentration of **red blood cells**, increasing blood viscosity. *Incorrect: 55%* - A venous hematocrit of 55% is generally considered within the **normal range** for a newborn, especially within the first few hours of life. - It does not meet the criteria for diagnosing **polycythemia**. *Incorrect: 60%* - While 60% is elevated compared to adult norms, it is still generally within the higher end of the **normal range** for an infant. - This level alone is usually **not sufficient** to diagnose **polycythemia** or warrant intervention without other clinical signs. *Incorrect: 70%* - A venous hematocrit of 70% definitely indicates **polycythemia** and significant **hyperviscosity**. - However, the diagnostic threshold for polycythemia is **65%**, meaning the condition is identified earlier.
Question 3: What is the RDA (Recommended Dietary Allowance) for vitamin A in infants aged 0-6 months?
- A. 400 mcg
- B. 600 mcg
- C. 800 mcg
- D. 350 mcg (Correct Answer)
Explanation: ***350 mcg*** - The **Recommended Dietary Allowance (RDA)** for vitamin A in infants aged 0-6 months is specifically set at **350 micrograms (mcg)** of **retinol activity equivalents (RAE)**. - This level is based on the **average vitamin A intake from human milk** during this period, assuming adequate maternal nutrition. *600 mcg* - This value is higher than the recommended intake for infants aged 0-6 months and is closer to the RDA for **older infants** or **young children**. - Excessive vitamin A intake can be **toxic**, making adherence to age-specific RDAs crucial. *800 mcg* - This amount is significantly higher than the RDA for infants 0-6 months and approaches the RDA for **adults**. - Providing such a high dose to an infant could lead to **vitamin A toxicity**, with symptoms including irritability, increased intracranial pressure, and desquamation of the skin. *400 mcg* - While closer to the correct answer, **400 mcg** is still slightly above the established RDA of 350 mcg for this specific age group. - The precise RDA values are determined based on **extensive research** to ensure optimal health outcomes without risk of deficiency or toxicity.
Question 4: Congenital varicella infection causes all except:
- A. Macrocephaly (Correct Answer)
- B. Cortical atrophy
- C. Cicatrix
- D. Limb hypoplasia
Explanation: ***Macrocephaly*** - **Macrocephaly** is generally not a direct consequence of congenital varicella infection; rather, **microcephaly** due to brain damage is more commonly observed. - Congenital varicella typically causes destructive lesions leading to tissue loss, not increased head circumference. *Cortical atrophy* - **Cortical atrophy** results from the destructive effects of the virus on the developing brain, leading to **neuronal loss** and reduced brain volume. - This can manifest as **microcephaly**, an indirect but common finding associated with congenital varicella. *Cicatrix* - **Cicatrix** (zig-zag scarring) is a classic dermatological manifestation of congenital varicella, resulting from the virus's impact on developing skin. - These characteristic **skin lesions** are one of the most identifiable features of the syndrome. *Limb hypoplasia* - **Limb hypoplasia**, involving underdeveloped limbs, is a hallmark feature of congenital varicella, often due to **viral damage** to limb buds and associated neural structures. - This can lead to **bone shortening** and muscle atrophy in affected limbs.
Question 5: Neonatal conjunctivitis is caused by all of the following except:
- A. Chlamydia
- B. Pseudomonas
- C. Aspergillus (Correct Answer)
- D. Gonococcus
Explanation: ***Aspergillus*** - **Fungal infections** of the eye, particularly by *Aspergillus*, are extremely rare in neonates and typically present as **keratitis** rather than conjunctivitis. - While *Aspergillus* can cause severe infections in immunocompromised individuals, it is not a common cause of neonatal conjunctivitis. *Gonococcus* - **_Neisseria gonorrhoeae_** is a well-known cause of **ophthalmia neonatorum** (gonococcal conjunctivitis), presenting as severe, purulent discharge usually within the first 2-5 days of life. - This infection can lead to **corneal ulceration** and blindness if untreated. *Chlamydia* - **_Chlamydia trachomatis_** is the most common bacterial cause of **neonatal conjunctivitis**, typically appearing 5-14 days after birth. - It causes a **mucopurulent discharge** and can be associated with **chlamydial pneumonia** in infants. *Pseudomonas* - **_Pseudomonas aeruginosa_** can cause severe and rapidly progressive **neonatal conjunctivitis** and **keratitis**, especially in premature infants or those exposed to contaminated solutions. - It is a highly aggressive pathogen that can lead to significant ocular morbidity.
Question 6: Rubella is known to cause all of the following conditions except:
- A. Conduction defects
- B. VSD
- C. Microcephaly
- D. Glaucoma (Correct Answer)
Explanation: ***Glaucoma*** - While rubella can cause **ocular defects** such as **cataracts** and **pigmentary retinopathy**, glaucoma is not a typical congenital manifestation of rubella syndrome. - **Congenital glaucoma** is more commonly associated with other genetic syndromes or developmental anomalies. *Microcephaly* - **Microcephaly** is a recognized neurological complication of congenital rubella syndrome, resulting from impaired brain development due to viral infection. - The rubella virus can interfere with the **proliferation and migration** of neuronal cells during fetal development. *VSD* - **Ventricular septal defect (VSD)** is a common congenital heart defect associated with congenital rubella syndrome. - Other cardiac anomalies seen include **patent ductus arteriosus (PDA)** and **pulmonary artery stenosis**. *Conduction defects* - **Conduction defects** and other **cardiac arrhythmias** can occur in congenital rubella syndrome due to direct viral damage to the developing cardiac conduction system. - This can manifest as **bradyarrhythmias** or various degrees of **heart block**.
Question 7: Double aortic arch is associated with which syndrome?
- A. DiGeorge syndrome (Correct Answer)
- B. CATCH 22 syndrome
- C. Shprintzen syndrome
- D. None of the options
Explanation: ***DiGeorge syndrome*** - **DiGeorge syndrome** is caused by a **22q11.2 deletion** affecting the development of the third and fourth pharyngeal pouches, leading to **thymic hypoplasia**, **parathyroid hypoplasia**, and **cardiac anomalies**. - Common cardiac defects include **interrupted aortic arch type B**, **truncus arteriosus**, **tetralogy of Fallot**, and **VSD**. - **Double aortic arch** can occur in 22q11.2 deletion syndrome, though it is less common than other cardiac anomalies; however, among the syndromes listed, this represents the most appropriate association. - The question tests recognition that various cardiac arch anomalies, including double aortic arch, may be seen in this genetic syndrome. *CATCH 22 syndrome* - This is an **acronym** for DiGeorge syndrome: **C**ardiac defects, **A**bnormal facies, **T**hymic hypoplasia, **C**left palate, **H**ypocalcemia, and **22q11 deletion**. - It is **essentially the same condition** as DiGeorge syndrome, just using different nomenclature. - While technically correct, "DiGeorge syndrome" is the more standard medical terminology currently used. *Shprintzen syndrome* - **Shprintzen syndrome** (also called **velocardiofacial syndrome or VCFS**) is caused by the **same 22q11.2 deletion** as DiGeorge syndrome. - It represents a **phenotypic variant within the 22q11.2 deletion syndrome spectrum**, with more emphasis on palatal and facial features. - Since it shares the same genetic basis, it can also present with similar cardiac anomalies, but "DiGeorge syndrome" is the more commonly recognized term for this genetic disorder. *None of the options* - This is incorrect because the three syndromes listed above (DiGeorge, CATCH 22, and Shprintzen) all refer to **22q11.2 deletion syndrome** or its variants, which can be associated with various cardiac anomalies including double aortic arch. - Among the listed options, **DiGeorge syndrome** is the most appropriate and widely recognized answer.
Question 8: A 3-month-old infant presents with an abdominal palpable mass and non-bilious vomiting. What is the most likely diagnosis?
- A. Hypertrophic pyloric stenosis (Correct Answer)
- B. Tracheoesophageal fistula
- C. Duodenal atresia
- D. Intussusception
Explanation: ***Hypertrophic pyloric stenosis*** - The classic presentation includes **projectile non-bilious vomiting** and a palpable **olive-shaped mass** in the epigastrium of an infant typically between 3 weeks and 6 months of age. - The vomiting is non-bilious because the obstruction is proximal to the ampulla of Vater. *Intussusception* - While it can present with an **abdominal mass** and vomiting, the vomiting is often **bilious** and the classic stool is **'currant jelly'**, which is not mentioned here. - It usually presents with sudden onset of severe, **colicky abdominal pain** and occurs more commonly in slightly older infants (6-12 months). *Tracheoesophageal fistula* - This condition presents at birth with symptoms such as **choking, coughing**, and **cyanosis** during feeding. - It usually causes respiratory distress and feeding difficulties from the first days of life, not a palpable abdominal mass and non-bilious vomiting at 3 months. *Duodenal atresia* - This is a congenital obstruction that typically presents with **bilious vomiting** (as the obstruction is distal to the ampulla of Vater) within the first 24-48 hours of life. - Imaging usually shows a **“double bubble” sign** on abdominal X-ray, and an abdominal mass is not typically palpable.
Question 9: What is the PRIMARY pathophysiological mechanism underlying the most common cause of neonatal hyperbilirubinemia?
- A. Inefficient erythropoiesis
- B. Immature liver enzyme (Correct Answer)
- C. RBC hemolysis
- D. Decreased bilirubin excretion
Explanation: ***Immature liver enzyme*** - The most common cause of neonatal hyperbilirubinemia is **physiological jaundice**, and its PRIMARY pathophysiological mechanism is **immature hepatic conjugation** due to deficiency of **UDP-glucuronosyltransferase (UGT1A1)**. - While neonates do produce more bilirubin from RBC breakdown, the **rate-limiting step** is the liver's inability to conjugate unconjugated bilirubin efficiently for excretion. - This immaturity causes accumulation of unconjugated bilirubin, which peaks at **3-5 days of life** and resolves as the enzyme system matures by **7-10 days**. - Key clinical feature: **Unconjugated (indirect) hyperbilirubinemia** in an otherwise healthy term neonate. *RBC hemolysis* - Neonates do have a **shorter RBC lifespan** (70-90 days vs. 120 days in adults) and higher hematocrit, leading to increased bilirubin production (~2-3 times adult rate). - However, this is a **contributory factor**, not the primary mechanism—a normal liver can handle this load easily. - **Pathological hemolysis** (ABO/Rh incompatibility, G6PD deficiency, spherocytosis) causes jaundice through a different mechanism with earlier onset (<24 hours) and more severe hyperbilirubinemia. *Inefficient erythropoiesis* - Ineffective erythropoiesis (abnormal RBC production with intramedullary destruction) is seen in conditions like **thalassemia** and **megaloblastic anemia**. - This can contribute to increased bilirubin load but is not the mechanism in physiological jaundice. - In neonates, erythropoiesis is typically transitioning from fetal to adult hemoglobin but is not pathologically inefficient. *Decreased bilirubin excretion* - Decreased excretion of **conjugated bilirubin** occurs in **cholestatic conditions** (biliary atresia, neonatal hepatitis, choledochal cyst). - This results in **direct (conjugated) hyperbilirubinemia**, not the indirect hyperbilirubinemia seen in physiological jaundice. - While neonates do have relatively decreased enterohepatic circulation clearance, the primary bottleneck is conjugation, not excretion.
Question 10: Most common site of extramedullary relapse of ALL in a 6-year-old boy is
- A. Testes
- B. Liver
- C. CNS (Central Nervous System) (Correct Answer)
- D. Lung
Explanation: ***CNS (Central Nervous System)*** - The **central nervous system** is the **most common site of extramedullary relapse** in pediatric acute lymphoblastic leukemia (ALL), accounting for the majority of extramedullary relapses. - CNS is an immunologically privileged sanctuary site where chemotherapy penetration is limited due to the blood-brain barrier. - CNS relapse presents with symptoms like headache, vomiting, cranial nerve palsies, or signs of increased intracranial pressure and requires intrathecal chemotherapy and cranial irradiation. - Prophylactic CNS therapy is a standard component of ALL treatment protocols to prevent CNS relapse. *Testes* - **Testes** are the **second most common** site of extramedullary relapse and the most common **solid organ** site in boys with ALL. - Like the CNS, testes are immunologically privileged sites with limited chemotherapy penetration. - Testicular relapse presents as painless testicular enlargement (unilateral or bilateral) and requires testicular radiation plus systemic therapy intensification. *Liver* - While **hepatic infiltration** can occur in ALL, the liver is not a common site for **isolated extramedullary relapse**. - Hepatic involvement typically indicates widespread systemic disease rather than a primary relapse site. *Lung* - **Pulmonary involvement** in ALL is rare as an isolated extramedullary relapse site. - Lung findings in ALL patients are more commonly due to infection, leukostasis in hyperleukocytosis, or disseminated disease.