MCQ NO 1: Diarrhea & Shock
An 8-year-old girl is brought to the emergency department with profuse watery diarrhea for 5 days, persistent vomiting, and progressive lethargy. She has a history of chronic abdominal distension, poor weight gain, and intermittent loose stools for the past year. On examination, she appears dehydrated, tachycardic, and hypotensive. She has pedal edema and muscle wasting.
Laboratory investigations reveal:
Serum sodium: 124 mEq/L
Serum potassium: 2.6 mEq/L
Serum bicarbonate: 14 mEq/L
Serum albumin: 2.2 g/dL
Tissue transglutaminase (tTG-IgA): markedly elevated
Which of the following is the most appropriate immediate management step in this patient?
A. Aggressive intravenous fluid resuscitation with correction of electrolyte imbalance
B. Initiation of gluten-free diet alone
C. Intravenous corticosteroids and parenteral nutrition
D. Oral zinc supplementation and probiotics
E. Rapid correction of hyponatremia with hypertonic saline
Correct answer & Explanation
The correct answer is A. Aggressive intravenous fluid resuscitation with correction of electrolyte imbalance.
Discussion: celiac crisis (celiac disease)
This child has features of a celiac crisis, a rare but life-threatening presentation of untreated or poorly controlled celiac disease. Celiac crisis is characterized by severe diarrhea, vomiting, dehydration, profound electrolyte disturbances, metabolic acidosis, hypoalbuminemia, and hemodynamic instability. The markedly elevated tissue transglutaminase IgA (tTG-IgA) level, together with the history of chronic abdominal distension, poor weight gain, and intermittent diarrhea, strongly supports the diagnosis of underlying celiac disease.
In the acute setting, the patient’s hypotension, tachycardia, severe dehydration, hyponatremia (124 mEq/L), hypokalemia (2.6 mEq/L), metabolic acidosis (bicarbonate 14 mEq/L), and hypoalbuminemia (2.2 g/dL) indicate a medical emergency. Therefore, the priority is stabilization with intravenous fluids and careful correction of electrolyte abnormalities. Once the patient is hemodynamically stable, a gluten-free diet can be initiated and long-term nutritional rehabilitation planned.
Why the Other Options Are Incorrect
B. Initiation of gluten-free diet alone
Although a gluten-free diet is the definitive treatment for celiac disease, it does not address the immediate life-threatening complications of dehydration, shock, and electrolyte imbalance. Stabilization must precede dietary therapy.
C. Intravenous corticosteroids and parenteral nutrition
Corticosteroids may occasionally be considered in severe refractory cases of celiac crisis, but they are not the first-line intervention. Initial management focuses on fluid resuscitation and correction of metabolic abnormalities. Parenteral nutrition is reserved for selected patients who cannot tolerate enteral feeding.
D. Oral zinc supplementation and probiotics
These measures may provide supportive benefits in some diarrheal illnesses but are inadequate for a critically ill child with severe dehydration, electrolyte disturbances, and shock.
E. Rapid correction of hyponatremia with hypertonic saline
Hypertonic saline is indicated only for severe symptomatic hyponatremia with manifestations such as seizures or impending cerebral herniation. Rapid correction of sodium can lead to osmotic demyelination syndrome and should be avoided. The hyponatremia in this patient is best corrected gradually during fluid and electrolyte replacement.
Key Learning Point
Celiac crisis is a pediatric emergency characterized by severe diarrhea, dehydration, metabolic acidosis, electrolyte disturbances, and hypoalbuminemia in a patient with celiac disease. The immediate management priority is aggressive fluid resuscitation and correction of electrolyte abnormalities before initiating a gluten-free diet and other definitive therapies.
MCQ NO 2: Watery Diarrhea
An 18-month-old previously healthy boy is brought to the emergency department with 3 days of profuse watery diarrhea and multiple episodes of non-bilious vomiting. He has low-grade fever and decreased oral intake. There is no blood or mucus in stools. On examination, he is irritable, has sunken eyes, dry mucous membranes, delayed capillary refill (3 seconds), and tachycardia.
Laboratory findings:
Serum sodium: 150 mEq/L
Serum potassium: 3.4 mEq/L
Serum bicarbonate: 16 mEq/L
Stool microscopy shows no leukocytes or red blood cells.
Which of the following best explains the primary mechanism of diarrhea in this patient?
A. Direct enterocyte invasion causing mucosal ulceration
B. Enterotoxin-mediated activation of adenylate cyclase
C. Osmotic diarrhea due to lactase deficiency secondary to villous injury
D. Secretory diarrhea due to activation of enteric nervous system by viral NSP4 protein
E. Systemic cytokine-mediated intestinal hypermotility
Correct answer & Explanation:
Item #1
CORRECT Answer: D. Secretory diarrhea due to activation of enteric nervous system by viral NSP4 protein
Discussion: Rotavirus gastroenteritis:
This presentation is typical of rotavirus gastroenteritis:
Age: 6–24 months (most common)
Profuse watery diarrhea
Vomiting prominent
No blood or fecal leukocytes
Metabolic acidosis from bicarbonate loss
Hypernatremic dehydration possible
Pathophysiology (PG concept):
Rotavirus produces NSP4, a viral enterotoxin that:Stimulates chloride secretion
Activates the enteric nervous system
Causes secretory diarrhea
Also leads to villous blunting → secondary lactose malabsorption (osmotic component)
Thus, diarrhea is primarily secretory, with a secondary osmotic component.
Why others are incorrect:
Direct invasion → seen in Shigella, Salmonella
Adenylate cyclase activation → typical of cholera
Pure osmotic mechanism → not the primary mechanism
Cytokine-mediated hypermotility → not the main mechanism
MCQ NO 3: Diarrhea & milk intake
A 6-year-old boy presents with recurrent abdominal pain, bloating, flatulence, and watery diarrhea for the past 3 months. His symptoms typically occur 1–2 hours after consuming milk or ice cream and improve when dairy is avoided. There is no weight loss, no blood in stool, and growth parameters are normal. Physical examination is unremarkable.
Stool examination shows acidic pH (5.0) and positive reducing substances. Tissue transglutaminase IgA is negative.
Which of the following is the most appropriate diagnostic test to confirm the suspected condition?
A. Duodenal biopsy demonstrating villous atrophy
B. Hydrogen breath test after oral lactose load
C. Measurement of fecal elastase
D. Serum anti-endomysial antibody testing
E. Sweat chloride test
Correct answer & Explanation:
Correct answer: Hydrogen breath test after lactose load
Discussion: Lactose Intolerance
Lactose intolerance is characterized by:
Post-dairy abdominal symptoms
Normal growth (rules out chronic malabsorption)
Acidic stool with reducing substances (carbohydrate malabsorption)
The hydrogen breath test is the gold standard non-invasive diagnostic test. In lactose intolerance, undigested lactose is fermented by colonic bacteria, producing hydrogen, which is measured in expired air.
Why others are incorrect:
Duodenal biopsy → for celiac disease
Fecal elastase → for pancreatic insufficiency
Anti-endomysial antibodies → for celiac disease
Sweat chloride test— cystic fibrosis
MCQ no 4: Diarrhea & rickets
A 4-year-old boy is evaluated for progressive bowing of the legs and difficulty walking. He received two courses of therapeutic vitamin D over the past year with minimal improvement. His weight and height are both below the 3rd percentile. On examination, he has pallor, severe genu varum, widened wrists, muscle wasting, and a distended abdomen. His mother reports that he passes bulky, foul-smelling stools 3–4 times daily. Laboratory investigations show:
Hemoglobin: 8.2 g/dL
Serum calcium: 7.9 mg/dL
Serum phosphate: 2.7 mg/dL
Alkaline phosphatase: 1650 IU/L
Serum albumin: 2.8 g/dL
What is the most likely underlying diagnosis responsible for his rickets?
A. Celiac disease
B. Hereditary vitamin D–resistant rickets
C. Hypophosphatemic rickets
D. Nutritional vitamin D deficiency
Correct Answer: A. Celiac disease
Discussion: Celiac disease
The key clues are:
Severe rickets not responding to vitamin D therapy
Failure to thrive
Pallor (iron deficiency anemia)
Hypoalbuminemia
Distended abdomen
Bulky, foul-smelling stools (steatorrhea)
These findings indicate chronic intestinal malabsorption, and the most likely cause is celiac disease.
The intestinal villous atrophy of celiac disease causes malabsorption of calcium and vitamin D, leading to secondary hyperparathyroidism and severe rickets. Iron deficiency anemia and hypoalbuminemia are additional clues suggesting malabsorption rather than isolated nutritional deficiency.
Why the other options are incorrect
B. Hereditary vitamin D–resistant rickets
Causes refractory rickets but does not explain steatorrhea, anemia, or hypoalbuminemia.
C. Hypophosphatemic rickets
Typically presents with short stature and lower-limb deformities.
Gastrointestinal symptoms and malnutrition are absent.
D. Nutritional vitamin D deficiency
Usually responds to appropriate vitamin D replacement.
Does not typically cause hypoalbuminemia and steatorrhea.
Key learning point:
In a child with refractory rickets, the combination of growth failure, iron deficiency anemia, hypoalbuminemia, and steatorrhea should immediately suggest celiac disease as the underlying diagnosis. Screening should begin with anti-tTG IgA antibodies and total serum IgA levels.
MCQ NO 5: Chronic constipation
A 10-year-old boy is brought to the pediatric gastroenterology clinic with a 3-year history of chronic constipation. He passes hard stools every 4–5 days and has been receiving regular laxatives with only partial improvement. There is no history of chronic diarrhea, blood in stools, abdominal pain, fever, nocturnal symptoms, or perianal discharge. On examination, his height is below the 3rd percentile and weight is at the 10th percentile. He appears pale and has grade II digital clubbing. There are no perianal abnormalities. Laboratory investigations reveal:
- Hemoglobin: 9.8 g/dL
- MCV: 70 fL
- Serum ferritin: Low
- ESR: Normal
- CRP: Normal
Which of the following is the most likely diagnosis?
A. Celiac disease
B. Crohn disease
C. Functional constipation
D. Hirschsprung disease
E. Hypothyroidism
Correct Answer: A. Celiac disease
Discussion: Atypical celiac disease
This child has chronic constipation, but several alarm features suggest an organic etiology:
- Short stature
- Iron deficiency anemia
- Digital clubbing
- Poor response to conventional constipation treatment
Although diarrhea is the classic manifestation of celiac disease, many older children present with non-classical disease, including:
- Chronic constipation
- Short stature
- Iron deficiency anemia
- Delayed puberty
- Isolated growth failure
The presence of clubbing may initially raise concern for Crohn disease, but the absence of diarrhea, abdominal pain, weight loss, perianal disease, and elevated inflammatory markers makes inflammatory bowel disease less likely.
The combination of constipation, growth failure, iron deficiency anemia, and clubbing should prompt testing for celiac disease with anti-tTG IgA and total IgA levels.
Why the Other Options Are Incorrect
B. Crohn disease
- Clubbing may occur, but Crohn disease typically presents with chronic diarrhea, abdominal pain, weight loss, elevated inflammatory markers, or perianal disease.
C. Functional constipation
- Does not explain short stature, iron deficiency anemia, or clubbing.
D. Hirschsprung disease
- Usually presents in infancy with delayed passage of meconium and longstanding severe constipation from birth.
E. Hypothyroidism
- Can cause constipation and growth failure, but iron deficiency anemia and clubbing are not typical features.
Key Learning Point
In a child with treatment-resistant constipation, the presence of short stature, iron deficiency anemia, or clubbing should prompt evaluation for celiac disease, even in the absence of diarrhea. Non-classical celiac disease is increasingly recognized in school-aged children and adolescents.
MCQ no 6: Bloody diarrhea
A 13-year-old boy is admitted with a 6-week history of progressively worsening diarrhea. He is passing 10–12 bloody stools daily, including nocturnal stools, associated with urgency and tenesmus. He has lost 6 kg over the past two months and complains of fatigue. Examination reveals pallor, tachycardia (HR 118/min), and mild diffuse abdominal tenderness. His BMI is below the 5th percentile.
Investigations:
Hemoglobin: 8.5 g/dL
ESR: 65 mm/hr
CRP: 48 mg/L
Serum albumin: 2.6 g/dL
Stool cultures: Negative
Fecal calprotectin: >2000 μg/g
Colonoscopy demonstrates continuous circumferential inflammation extending from the rectum to the splenic flexure with spontaneous mucosal bleeding and multiple deep ulcerations.
He is started on intravenous hydrocortisone. After 5 days of therapy, he continues to pass 9–10 bloody stools daily and his Pediatric Ulcerative Colitis Activity Index (PUCAI) score remains 75.
What is the most appropriate next step in management?
A. Azathioprine
B. Infliximab
C. Mesalamine (oral and rectal)
D. Methotrexate
E. Oral prednisolone
Correct Answer: B. Infliximab
Discussion: Ulcerative colitis
This child has Acute Severe Ulcerative Colitis (ASUC) as suggested by:
Frequent bloody diarrhea (>6/day)
Nocturnal stools
Urgency and tenesmus
Significant weight loss
Anemia and hypoalbuminemia
Elevated inflammatory markers
Colonoscopy showing continuous disease beginning from the rectum without skip lesions
The patient was appropriately started on intravenous hydrocortisone, which is first-line treatment for ASUC.
A PUCAI score ≥65 after 5 days of intravenous corticosteroids indicates steroid-refractory acute severe colitis. In such patients, escalation to rescue therapy is required.
Infliximab is currently the preferred rescue therapy in most pediatric centers and is highly effective in avoiding urgent colectomy.
Why the Other Options Are Incorrect
A. Azathioprine
Slow onset of action (several weeks to months).
Used for maintenance of remission, not induction in acute severe disease.
C. Mesalamine (oral and rectal)
Appropriate for mild-to-moderate ulcerative colitis.
Inadequate for steroid-refractory ASUC.
D. Methotrexate
Limited role in ulcerative colitis and not recommended as rescue therapy.
E. Oral prednisolone
Failure of IV corticosteroids indicates need for escalation, not continuation of steroid therapy by another route.
Key Examination Pearl
A child with acute severe ulcerative colitis who has a PUCAI ≥65 after 3–5 days of intravenous hydrocortisone has steroid-refractory disease, and the single best next treatment is infliximab. Azathioprine should never be chosen as rescue therapy because of its delayed onset of action.
MCQ NO 7: Abdominal pain
A 14-year-old boy presents with a 9-month history of intermittent abdominal pain, chronic diarrhea, poor appetite, and a 7-kg weight loss. He reports waking up at night to pass stools and has noticed increasing fatigue. Over the past 3 months, he has developed painful swelling around the anus with occasional purulent discharge.
On examination, his weight and height are both below the 5th percentile. He appears pale and has digital clubbing. Abdominal examination reveals mild right lower quadrant tenderness. Perianal examination demonstrates a skin tag and a draining fistula.
Investigations show:
Hemoglobin: 9.2 g/dL
ESR: 78 mm/hr
CRP: 62 mg/L
Serum albumin: 2.9 g/dL
Stool cultures: Negative
Fecal calprotectin: >1800 μg/g
Colonoscopy reveals patchy areas of inflammation with intervening normal mucosa. Multiple deep linear ulcers are seen in the terminal ileum and ascending colon.
Which of the following is the most likely diagnosis?
A. Abdominal tuberculosis
B. Crohn disease
C. Intestinal Behçet disease
D. Ulcerative colitis
E. Yersinia enterocolitica infection
Correct Answer: B. Crohn disease
Discussion: Crohn disease
This scenario contains several classic features of Crohn disease:
Chronic diarrhea with nocturnal symptoms
Weight loss and growth failure
Elevated inflammatory markers
Hypoalbuminemia
Perianal disease (skin tags and fistula)
Right lower quadrant pain
Patchy (“skip”) lesions on colonoscopy
Deep linear ulcers
Terminal ileal involvement
Among these findings, perianal fistulizing disease is particularly suggestive of Crohn disease and is uncommon in ulcerative colitis.
Why the Other Options Are Incorrect
A. Abdominal tuberculosis
May mimic Crohn disease but perianal fistulas are less common.
Usually associated with TB exposure, fever, and characteristic histological findings.
C. Intestinal Behçet disease
Can cause deep ulcers but is usually accompanied by recurrent oral and genital ulcers and other systemic manifestations.
D. Ulcerative colitis
Typically causes continuous colonic inflammation beginning in the rectum.
Perianal fistulas and terminal ileal deep ulceration strongly favor Crohn disease.
E. Yersinia enterocolitica infection
Usually presents as an acute or subacute illness rather than a 9-month progressive course with growth failure and fistulizing disease.
Key Learning Points
Growth failure may precede gastrointestinal symptoms in pediatric Crohn disease.
Perianal fistula, skin tags, and abscesses are hallmark features of Crohn disease.
Terminal ileal involvement and skip lesions differentiate Crohn disease from ulcerative colitis.
Chronic diarrhea, weight loss, anemia, and elevated fecal calprotectin should prompt evaluation for inflammatory bowel disease.
Examination Pearl
In a child with chronic diarrhea, growth failure, and perianal fistula, Crohn disease should be considered until proven otherwise. The presence of skip lesions and terminal ileal disease makes Crohn disease the most likely diagnosis.
MCQ no 8: Fever & jaundice
A 9-year-old previously healthy boy is brought to the emergency department with a 7-day history of fever, malaise, anorexia, nausea, and vomiting. Three days later, his parents noticed yellow discoloration of the eyes and dark-colored urine. Today, he became increasingly drowsy and irritable and had difficulty recognizing family members.
On examination:
Temperature: 37.8°C
Heart rate: 90/min
Blood pressure: 100/60 mmHg
He is confused and disoriented to time and place.
Scleral icterus is present.
Liver is palpable 2 cm below the costal margin and tender.
No splenomegaly or ascites.
Asterixis is present.
Investigations:
Total bilirubin: 12.8 mg/dL
ALT: 1850 IU/L
AST: 1620 IU/L
INR: 2.4
Serum ammonia: Elevated
Blood glucose: 68 mg/dL
Serum creatinine: 0.7 mg/dL
Which of the following is the most appropriate diagnosis?
A. Acute liver failure secondary to acute viral hepatitis
B. Acute-on-chronic liver failure
C. Hepatic encephalopathy due to Wilson disease
D. Septic encephalopathy
E. Reye syndrome
Correct Answer: A. Acute liver failure secondary to acute viral hepatitis
Discussion: Acute viral hepatitis leading to acute liver filure
This child has classical features of acute viral hepatitis complicated by acute liver failure (ALF):
Prodrome of fever, malaise, anorexia, nausea, and vomiting
Development of jaundice
Altered sensorium and asterixis (hepatic encephalopathy)
Markedly elevated transaminases
Coagulopathy (INR >1.5)
No evidence of pre-existing chronic liver disease
The diagnosis of acute liver failure in children is based on:
No known chronic liver disease.
Biochemical evidence of acute liver injury.
Coagulopathy (INR ≥1.5 with encephalopathy, or INR ≥2 without encephalopathy).
This patient fulfills all criteria.
Why the Other Options Are Incorrect
B. Acute-on-chronic liver failure
Requires underlying chronic liver disease, which is absent.
C. Hepatic encephalopathy due to Wilson disease
Usually presents with Coombs-negative hemolytic anemia, low alkaline phosphatase, Kayser-Fleischer rings, or chronic liver disease features.
D. Septic encephalopathy
Does not explain severe jaundice, markedly elevated transaminases, and significant coagulopathy.
E. Reye syndrome
Typically follows aspirin exposure during a viral illness and presents with hyperammonemia but usually without marked jaundice.
Key Learning Point
Any child with acute hepatitis who develops altered mental status and coagulopathy should be considered to have acute liver failure until proven otherwise. Hepatic encephalopathy in acute viral hepatitis is a medical emergency requiring intensive monitoring and early referral to a liver transplant center.