INI-CET 2025 — Pediatrics
14 Previous Year Questions with Answers & Explanations
A 6-week-old infant presents with a history of non-bilious, non-projectile vomiting starting at 3 weeks of age. The infant's abdominal examination is normal. Which of the following is the most likely diagnosis?
A 3-year-old child is brought to the clinic with a history of cyanosis since infancy. Which of the following is a component of Tetralogy of Fallot (TOF)?
A neonate is found to have multiple hypopigmented macules and ash-leaf spots on Wood's lamp examination. Which of the following is the most likely diagnosis?
A child presents with hepatosplenomegaly & cherry red spots in the eye. He also has developmental regression with normal startle response. Likely enzyme deficiency?
Which of the following best explains the mechanism of breast milk jaundice?
Which of the following is/are incorrect regarding breastfeeding technique? 1. Infant's chin should be touching the breast 2. Infant's lower lip should be inverted during latching to the breast 3. A greater part of areola above the breast should be covered than below 4. Infant's cheeks should appear full during effective sucking.
Which of the following is not true regarding Marasmus in a child?
A 9-month-old child is brought to OPD with developmental concerns. The child cannot sit without support, says "dada" and "mama", and has stranger anxiety. What is the appropriate management?
A neonate delivered at 36-week gestation develops respiratory distress soon after birth. CXR is as shown. Likely diagnosis?
A young boy presented with petechiae and his platelet count was 10,000/cu mm. Bone marrow aspirate revealed normal cellularity with megakaryocyte hyperplasia. Most appropriate initial therapy?
INI-CET 2025 - Pediatrics INI-CET Practice Questions and MCQs
Question 1: A 6-week-old infant presents with a history of non-bilious, non-projectile vomiting starting at 3 weeks of age. The infant's abdominal examination is normal. Which of the following is the most likely diagnosis?
- A. Gastroesophageal reflux disease (GERD) (Correct Answer)
- B. Cow Milk Protein Allergy
- C. Intestinal obstruction
- D. Pyloric stenosis
Explanation: ***Gastroesophageal reflux disease (GERD)*** - This is the most common cause of non-bilious, **non-projectile** vomiting (regurgitation) in healthy infants, often starting early and peaking around 4-5 months of age. - The history is consistent with simple **physiologic reflux**, characterized by non-forceful spitting up and a **normal abdominal examination**. *Pyloric stenosis* - Classically involves **projectile** non-bilious vomiting that becomes progressively worse, which contradicts the non-projectile description. - A physical exam would typically reveal an **olive-like mass** (hypertrophied pylorus) or visible gastric peristalsis, which is stated to be absent. *Cow Milk Protein Allergy* - Although vomiting can occur, it is usually accompanied by other symptoms like **bloody stools**, severe irritability, or **eczema**, which are not mentioned. - Isolated, mild, non-projectile vomiting without systemic signs is less specific for a protein allergy than for GERD. *Intestinal obstruction* - Obstruction distal to the ampulla of Vater (e.g., malrotation, atresia) typically causes **bilious vomiting**, which is absent in this case. - Such conditions usually lead to an **abnormal abdominal examination** or signs of acute illness, which are not present here.
Question 2: A 3-year-old child is brought to the clinic with a history of cyanosis since infancy. Which of the following is a component of Tetralogy of Fallot (TOF)?
- A. Inter atrial septal defect
- B. Infundibular pulmonary stenosis (Correct Answer)
- C. Left ventricular hypertrophy (LVH)
- D. Transposition of the great arteries (TGA)
Explanation: ***Infundibular pulmonary stenosis*** - This is the most common anatomic type of **pulmonary stenosis** seen in TOF, caused by hypertrophy of the muscle below the pulmonary valve (infundibulum). - The degree of this stenosis dictates the direction of flow across the VSD and, consequently, the severity of **cyanosis**. *Inter atrial septal defect* - An ASD is not a primary component of TOF. When TOF is associated with an ASD, the condition is termed **Pentalogy of Fallot**. - ASD typically causes a **left-to-right shunt** and is usually an acyanotic or late-onset cyanotic condition, unlike classic TOF. *Left ventricular hypertrophy (LVH)* - The pressure overload due to **pulmonary stenosis** and the large **VSD** leads to **Right Ventricular Hypertrophy (RVH)**. - LVH suggests conditions like severe **aortic stenosis** or systemic overloading, not the typical hemodynamics of TOF. *Transposition of the great arteries (TGA)* - **TGA** is a separate, distinct cyanotic congenital heart disease where the great arteries are transposed (aorta from RV, pulmonary artery from LV). - The components of TOF involve a single great artery relationship but with a large **Ventricular Septal Defect (VSD)** and overriding aorta.
Question 3: A neonate is found to have multiple hypopigmented macules and ash-leaf spots on Wood's lamp examination. Which of the following is the most likely diagnosis?
- A. Tuberous Sclerosis (Correct Answer)
- B. Sturge-Weber Syndrome
- C. Neurofibromatosis Type 1
- D. Incontinentia Pigmenti
Explanation: ***Tuberous Sclerosis*** - **Ash-leaf spots** (hypopigmented macules shaped like an ash leaf) are the most common cutaneous manifestation of **Tuberous Sclerosis Complex (TSC)** and are best visualized under a **Wood's lamp**. - TSC is an autosomal dominant neurocutaneous disorder characterized by hamartomatous lesions in multiple organs, including the brain (**subependymal giant cell astrocytomas**), kidneys (**angiomyolipomas**), and heart (**rhabdomyomas**). *Sturge-Weber Syndrome* - Characterized by a **port-wine stain** (capillary malformation) typically in the distribution of the ophthalmic branch of the **trigeminal nerve (V1)**. - Associated features include **leptomeningeal angioma** (causing seizures) and ocular abnormalities like **glaucoma**. *Neurofibromatosis Type 1* - The characteristic pigmented lesions are **café-au-lait spots** (uniform, light-brown macules), typically six or more, along with **axillary or inguinal freckling**. - Associated with **Lisch nodules** (iris hamartomas) and **neurofibromas**. *Incontinentia Pigmenti* - A rare X-linked dominant disorder, usually lethal in males, presenting with characteristic skin lesions in phases (vesicular, verrucous, hyperpigmented, and atrophic). - The hyperpigmented phase consists of swirling, marble-cake patterns of brown-gray macules along the **Blaschko lines**, not ash-leaf spots.
Question 4: A child presents with hepatosplenomegaly & cherry red spots in the eye. He also has developmental regression with normal startle response. Likely enzyme deficiency?
- A. Sphingomyelinase (Correct Answer)
- B. Arylsulfatase A
- C. Glucocerebrosidase
- D. Hexosaminidase A
Explanation: ***Sphingomyelinase (Correct Answer)*** - The triad of **hepatosplenomegaly**, **developmental regression**, and **cherry red spots** in the eye is the classic presentation of **Type A Niemann-Pick disease (NPD A)**. - **NPD A** is caused by the deficient activity of the lysosomal enzyme **sphingomyelinase**, leading to the accumulation of **sphingomyelin** in the reticuloendothelial system and CNS. - The **normal startle response** is a key distinguishing feature from Tay-Sachs disease. *Hexosaminidase A (Incorrect)* - Deficiency of **Hexosaminidase A** causes **Tay-Sachs disease**, which presents with **cherry red spots** and severe neurodegeneration, but **lacks hepatosplenomegaly**. - The **exaggerated startle response** (hyperacusis) is a classic feature of Tay-Sachs, which is noted as **normal** in this specific clinical presentation—making it a key differentiator. *Arylsulfatase A (Incorrect)* - Deficiency of **Arylsulfatase A** causes **Metachromatic Leukodystrophy (MLD)**, characterized by progressive demyelination and neurological regression. - **MLD** does not typically present with **cherry red spots** or significant **hepatosplenomegaly**. *Glucocerebrosidase (Incorrect)* - Deficiency of **Glucocerebrosidase** causes **Gaucher's disease**, which is characterized by massive **hepatosplenomegaly** and bone crises. - **Gaucher's disease** does **not** typically present with **cherry red spots** or the unique pattern of early neurodegeneration seen here (except for the rare Type 2 form).
Question 5: Which of the following best explains the mechanism of breast milk jaundice?
- A. Increased RBC breakdown producing more unconjugated bilirubin
- B. Enhanced enterohepatic circulation due to beta-glucuronidase in breast milk deconjugating bilirubin (Correct Answer)
- C. Reduced intestinal absorption of bilirubin
- D. Hepatocellular injury by breast milk
Explanation: ***Enhanced enterohepatic circulation due to beta-glucuronidase in breast milk deconjugating bilirubin*** - Breast milk contains high levels of **beta-glucuronidase** which deconjugates conjugated bilirubin in the intestine back to unconjugated form, greatly increasing the pool available for reabsorption (enhanced **enterohepatic circulation**). - This is the **PRIMARY mechanism** of breast milk jaundice, leading to prolonged unconjugated hyperbilirubinemia in otherwise healthy breastfed infants. - High concentrations of **non-esterified free fatty acids** and pregnane-3α,20β-diol in breast milk may also inhibit the conjugation enzyme UDP-glucuronyl transferase (secondary mechanism). *Incorrect: Hepatocellular injury by breast milk* - Breast milk jaundice is a benign, physiological process and is **NOT** associated with hepatocellular necrosis or cytotoxic liver injury. - Liver function tests (LFTs) are typically **normal**, differentiating it from pathological liver disease. *Incorrect: Increased RBC breakdown producing more unconjugated bilirubin* - This mechanism is responsible for **hemolytic jaundice** (e.g., ABO incompatibility, G6PD deficiency), implying excessive bilirubin production from red cell destruction. - Breast milk jaundice occurs in neonates with **normal rates of erythrocyte destruction** and hemoglobin turnover. *Incorrect: Reduced intestinal absorption of bilirubin* - The mechanism involves **increased** intestinal absorption of bilirubin due to enhanced enterohepatic circulation. - Beta-glucuronidase breaks down conjugated bilirubin to the absorbable unconjugated form, leading to **excessive reabsorption**, not reduced absorption.
Question 6: Which of the following is/are incorrect regarding breastfeeding technique? 1. Infant's chin should be touching the breast 2. Infant's lower lip should be inverted during latching to the breast 3. A greater part of areola above the breast should be covered than below 4. Infant's cheeks should appear full during effective sucking.
- A. 1 & 4
- B. 2 & 3 (Correct Answer)
- C. 2, 3 & 4
- D. 1, 2, 3 & 4
Explanation: **Correct Answer: 2 & 3** Statements 2 and 3 describe **incorrect breastfeeding techniques**: ***Statement 2 (Incorrect)*** - The infant's lower lip should be **everted (rolled outward)**, not inverted - Proper latching requires lips to be wide open, resembling a 'fish mouth' - An inverted lower lip indicates **poor latch** and inadequate breast tissue in the mouth ***Statement 3 (Incorrect)*** - A **greater part of the areola below** the nipple should be covered, not above - This ensures the nipple points toward the roof of the mouth - Asymmetric latch with more lower areola covered is essential for effective milk transfer *Statement 1 (Correct)* - Infant's chin touching the breast is a sign of **proper positioning** - Helps achieve a deep latch and facilitates swallowing - Slightly extends the neck for optimal sucking mechanics *Statement 4 (Correct)* - **Full cheeks** during sucking indicate effective milk transfer - Shows proper seal of lips around the breast - Dimpled or hollow cheeks suggest **ineffective suction** or poor latch *Why other options are incorrect:* - **1 & 4**: Both are correct breastfeeding techniques - **2, 3 & 4**: Incorrectly includes statement 4, which describes proper technique - **1, 2, 3 & 4**: Incorrectly includes statements 1 and 4, which are both correct
Question 7: Which of the following is not true regarding Marasmus in a child?
- A. Protein loss is responsible for edema in this patient (Correct Answer)
- B. Weight-for-age is less than 60 % of expected
- C. Seen due to carbohydrate (caloric) deficiency
- D. Child appears emaciated with loss of subcutaneous fat
Explanation: ***Protein loss is responsible for edema in this patient*** - This statement is **false** because **marasmus** is primarily a **caloric-energy** deficiency, leading to severe wasting and **no edema**. - Edema is the characteristic feature of **Kwashiorkor**, which is primarily due to protein deficiency/loss, leading to decreased oncotic pressure. *Seen due to carbohydrate (caloric) deficiency* - Marasmus results from a severe deficiency of **calories** (energy), often due to inadequate intake of **carbohydrates** and fats. - This leads to the body breaking down its own stores, including muscle and fat, for energy. *Child appears emaciated with loss of subcutaneous fat* - The child with marasmus appears severely wasted, or **emaciated** (looks like 'an old man/woman' or 'skin and bones'). - There is visible loss of **subcutaneous fat** (pinching a fold of skin feels loose, without the layer of fat underneath). *Weight-for-age is less than 60% of expected* - Marasmus is a severe form of Protein Energy Malnutrition (PEM), traditionally documented when the **weight-for-age** is less than **60%** of the expected weight (compared to the standard reference). - The **Gomez classification** uses <60% weight-for-age to define **grade III** (severe) malnutrition, which corresponds to marasmus.
Question 8: A 9-month-old child is brought to OPD with developmental concerns. The child cannot sit without support, says "dada" and "mama", and has stranger anxiety. What is the appropriate management?
- A. Reassure the parents that it's normal development
- B. Order an immediate MRI
- C. Refer to neurologist for developmental assessment (Correct Answer)
- D. Advise parents to start exercises
Explanation: ***Refer to neurologist for developmental assessment*** - The milestone of **sitting without support** is generally expected by **8-9 months**. Failure to achieve this at 9 months, especially when it should have been emerging, is a **red flag for motor delay**. - Although language (saying 'dada'/'mama' non-specifically) and social milestones (stranger anxiety) are adequate, the gross motor delay warrants a **specialized developmental assessment** to rule out conditions like hypotonia, cerebral palsy, or neuromuscular disorders. - Early identification and intervention are crucial for optimal developmental outcomes. *Incorrect: Order an immediate MRI* - **Neuroimaging (like MRI)** is an expensive and invasive diagnostic step, usually reserved for cases where an underlying structural brain abnormality is strongly suspected *after* a thorough clinical and developmental assessment. - Initial management for suspected developmental delay involves detailed assessment by a specialist (pediatrician/neurologist) and screening tests, not immediate imaging. *Incorrect: Reassure the parents that it's normal development* - This reassurance is inappropriate because the child is demonstrating a **lag in gross motor milestones** (cannot sit without support at 9 months). - Some children may sit slightly later, but given this is at the upper limit of normal, further assessment is warranted rather than simple reassurance. - Failure to address a developmental delay early can lead to missed opportunities for timely **early intervention services**. *Incorrect: Advise parents to start exercises* - While physical therapy (exercises) will likely be part of the recommended intervention, simply advising exercises without a formal **developmental diagnosis** or proper assessment by a **physiotherapist/specialist** is insufficient and potentially incomplete management. - The priority is to **identify the cause** of the delay (e.g., hypotonia, cerebral palsy, muscular dystrophy) through specialist evaluation before initiating targeted therapy.
Question 9: A neonate delivered at 36-week gestation develops respiratory distress soon after birth. CXR is as shown. Likely diagnosis?
- A. Meconium Aspiration Syndrome
- B. Respiratory Distress Syndrome (Correct Answer)
- C. Transient Tachypnea of Newborn
- D. Neonatal Pneumonia
Explanation: ***Respiratory Distress Syndrome*** - The chest X-ray shows classic features of RDS, including a diffuse **reticulogranular pattern** (ground-glass appearance) and prominent **air bronchograms**, indicative of widespread alveolar atelectasis. - This condition is primarily caused by **surfactant deficiency** in preterm infants (like this 36-week neonate), leading to increased surface tension, alveolar collapse, and respiratory distress shortly after birth. ***Transient Tachypnea of Newborn*** - This is caused by delayed clearance of **fetal lung fluid** and is more common in term infants delivered by Caesarean section. - The chest X-ray typically shows **perihilar streaking**, fluid in the interlobar fissures, and hyperinflation, which are not the primary findings in the provided image. ***Neonatal Pneumonia*** - While it can present with respiratory distress, neonatal pneumonia typically shows **asymmetrical patchy infiltrates**, consolidation, or pleural effusions on chest X-ray. - The diffuse, symmetrical ground-glass appearance seen here is less characteristic of an infectious process like pneumonia, which is often more localized. ***Meconium Aspiration Syndrome*** - This condition occurs in term or post-term infants following aspiration of **meconium-stained amniotic fluid**, which is not mentioned in the history. - The characteristic X-ray findings are coarse, patchy opacities, **hyperinflation**, and potential air-leak syndromes (e.g., pneumothorax), which differ from the image.
Question 10: A young boy presented with petechiae and his platelet count was 10,000/cu mm. Bone marrow aspirate revealed normal cellularity with megakaryocyte hyperplasia. Most appropriate initial therapy?
- A. Bone Marrow Transplant
- B. Methotrexate
- C. Aspirin
- D. IVIG (Correct Answer)
Explanation: ***IVIG*** - The presentation (young patient, **petechiae**, extremely low platelet count of 10,000/cu mm, and **megakaryocyte hyperplasia** in bone marrow) is classic for **Immune Thrombocytopenia (ITP)**. - Given the severe thrombocytopenia (platelets <20,000/cu mm) and active bleeding risk (petechiae), the initial treatment of choice is typically **IVIG (Intravenous Immunoglobulin)** or corticosteroids to rapidly increase the platelet count. *Aspirin* - **Aspirin** is an antiplatelet agent that **inhibits platelet aggregation**; it is strictly contraindicated in severe thrombocytopenia like ITP as it would increase the risk of hemorrhage. - It is used for pain relief or secondary prevention of cardiovascular events, not for treating low platelet counts. *Bone Marrow Transplant* - **Bone marrow transplant** is a radical and highly risky procedure reserved for refractory, life-threatening hematological malignancies or severe aplastic anemia, or failed therapy for ITP. - It is never the appropriate **initial therapy** for acute ITP, which is predominantly an autoimmune disorder of peripheral platelet destruction. *Methotrexate* - **Methotrexate** is an immunosuppressive drug used typically in chronic inflammatory conditions (like rheumatoid arthritis) or malignancies. - It is considered a second or third-line treatment option, or part of a more aggressive immunosuppression regimen, for ITP that has failed initial therapy (steroids/IVIG), not the immediate first choice.