Gastroenterology Practice Questions

Q: Which one of the following causes intestinal pseudo-obstruction?

All the above. Intestinal pseudo-obstruction (Ogilvie’s syndrome when acute) is a clinical syndrome characterized by signs and symptoms of mechanical bowel obstruction (distension, pain, vomiting) without an actual physical lesion blocking the lumen. It results from **impaired gastrointestinal motility** due to disturbances in the enteric nervous system, smooth muscles, or autonomic nerve supply [1]. **Analysis of Options:** * **Hypothyroidism:** Low thyroid hormone levels lead to generalized slowing of metabolic processes, including decreased gut peristalsis [1]. Severe hypothyroidism (myxedema) is a classic metabolic cause of paralytic ileus and chronic pseudo-obstruction. * **Tricyclic Antidepressants (TCAs):** These drugs possess potent **anticholinergic properties**. By blocking acetylcholine (the primary neurotransmitter for gut contraction), they inhibit smooth muscle activity, leading to delayed transit and pseudo-obstruction. * **Parkinsonism:** This is a neurodegenerative disorder affecting the autonomic nervous system [1]. Both the disease pathology (degeneration of enteric neurons) and the medications used to treat it (e.g., anticholinergics, levodopa) contribute to severe colonic dysmotility. **High-Yield Clinical Pearls for NEET-PG:** * **Common Causes:** Electrolyte imbalances (Hypokalemia, Hypercalcemia), Diabetes Mellitus (autonomic neuropathy), Scleroderma (smooth muscle atrophy), and Narcotics/Opioids. * **Diagnosis:** Abdominal X-ray shows dilated bowel loops with air-fluid levels, but **CT scan** is essential to rule out mechanical obstruction (the

Q: Which of the following is not a feature of Crohn’s disease?

Continuous lesions. **Explanation:** The correct answer is **A. Continuous lesions**. This is a hallmark feature of **Ulcerative Colitis (UC)**, not Crohn’s Disease (CD). In Crohn’s disease, the inflammation is characterized by **"skip lesions,"** where areas of diseased bowel are separated by segments of healthy, normal mucosa [1]. **Analysis of Options:** * **A. Continuous lesions:** In UC, the disease starts in the rectum and extends proximally in a continuous, symmetrical fashion [1]. CD is patchy and asymmetrical. * **B. Non-caseating granulomas:** These are a pathognomonic histological feature of Crohn’s disease (found in about 40-60% of cases). Their presence helps differentiate CD from UC, as UC does not form granulomas. * **C. Backwash ileitis:** While primarily associated with UC (where inflammation from the colon "washes back" into the terminal ileum), it is a trick option. However, the question asks for a feature that is *not* characteristic of CD. Since CD primarily affects the terminal ileum (Ileocolic distribution), ileal involvement is a core feature, whereas "continuous lesions" is an absolute contraindication for a CD diagnosis [2]. * **D. Cobblestone appearance:** This occurs in CD due to deep longitudinal and transverse ulcers intersecting with islands of edematous, normal mucosa. **NEET-PG High-Yield Pearls:** * **Transmural Inflammation:** CD affects all layers of the bowel wall (leading to fistulas/strictures); UC is limited to the mucosa and submucosa [1]. * **Smoking:** Smoking is a risk factor for **Crohn’s** but is actually **protective** against Ulcerative Colitis. * **ASCA vs. p-ANCA:** CD is associated with **ASCA** (Anti-Saccharomyces cerevisiae antibodies), while UC is associated with **p-ANCA**. * **Creeping Fat:** The presence of mesenteric fat wrapping around the bowel is specific to Crohn’s disease.

Q: Which of the following is NOT a feature of Zollinger-Ellison syndrome?

Large gastric ulcer. Explanation: Zollinger-Ellison Syndrome (ZES) is caused by a gastrin-secreting tumor (gastrinoma), leading to profound gastric acid hypersecretion [3]. Why "Large gastric ulcer" is the correct answer: In ZES, ulcers typically occur in the duodenum (over 75% of cases), often in atypical locations like the distal duodenum or jejunum. While ulcers in ZES are often multiple or refractory, they are predominantly duodenal, not gastric [1]. Gastric ulcers are less common because the gastric mucosa is relatively more resistant to the high acid levels compared to the small intestine. Analysis of incorrect options: * Diarrhea non-responsive to fasting: This is a classic feature. The massive acid load enters the small bowel, inactivating pancreatic enzymes and malabsorbing fat. Since the diarrhea is driven by hormonal (gastrin) hypersecretion rather than oral intake, it persists during fasting (secretory diarrhea). * Epigastric pain: This is the most common presenting symptom (75-90% of patients) due to peptic ulcer disease. * Secretin study: This is the investigation of choice (most sensitive and specific provocative test). In ZES, intravenous secretin paradoxically increases serum gastrin levels (>200 pg/mL), whereas it inhibits gastrin in normal individuals. Clinical Pearls for NEET-PG: * Location: Most gastrinomas are found in the "Gastrinoma Triangle" (confluence of cystic/common bile duct, junction of 2nd/3rd parts of duodenum, and neck/body of pancreas). * Association: 25% of cases are associated with MEN-1 syndrome (3Ps: Parathyroid, Pancreas, Pituitary) [2]. * Diagnosis: Initial screening is by Fasting Serum Gastrin (>1000 pg/mL is diagnostic). If borderline, perform the Secretin Stimulation Test. * Treatment: High-dose PPIs are the mainstay for symptom control; surgical resection is required for localized tumors.

Q: Which of the following is NOT a precipitating factor for hepatic encephalopathy?

Diarrhea. Hepatic Encephalopathy (HE) is a reversible neuropsychiatric syndrome caused by liver failure or portosystemic shunting, leading to the accumulation of neurotoxins (primarily ammonia) [1]. Precipitating factors are triggers that either increase ammonia production or decrease its clearance. **Why Diarrhea is the Correct Answer:** Diarrhea is generally **not** a precipitating factor. In fact, inducing diarrhea (osmotic laxation) using **Lactulose** is the standard treatment for HE. Lactulose works by acidifying the gut lumen, converting ammonia ($NH_3$) into non-absorbable ammonium ($NH_4^+$), and promoting its excretion through frequent bowel movements. **Analysis of Incorrect Options:** * **High Protein Intake:** Protein is broken down by gut bacteria into ammonia [1]. Excessive intake increases the nitrogenous load, overwhelming the liver's ability to detoxify it. * **Hematemesis (GI Bleed):** Upper GI bleeding is a major trigger. Blood in the gut acts as a massive "protein meal" (hemoglobin is protein-rich). Bacterial breakdown of this blood significantly spikes ammonia levels. * **Infection:** Sepsis or Spontaneous Bacterial Peritonitis (SBP) increases tissue catabolism and impairs renal function, both of which elevate blood ammonia levels. **NEET-PG High-Yield Pearls:** * **Most common precipitant:** Infections and GI bleeding. * **Metabolic triggers:** Hypokalemia and Metabolic Alkalosis (often caused by diuretics) are high-yield precipitants. Alkalosis shifts the equilibrium toward $NH_3$, which crosses the blood-brain barrier more easily. * **Constipation:** This is a classic precipitant (opposite of diarrhea) because it increases the transit time for bacterial ammonia production. * **Drug of choice:** Lactulose (first-line) and Rifaximin (add-on). **Clinical Grading:** The severity of HE is assessed using clinical signs ranging from poor concentration (Grade 1) to unconsciousness (Grade 4) [2].

Q: Which statement is not true regarding erosive gastritis?

Barium meal may clinch the diagnosis.. **Explanation:** Erosive gastritis (also known as hemorrhagic gastritis) is characterized by superficial mucosal lesions that do not penetrate the muscularis mucosa. **Why Option D is the correct (false) statement:** Barium meal is **not** useful for diagnosing erosive gastritis. Because the erosions are superficial and do not result in significant contour changes or deep craters, they are typically invisible on contrast radiography. Barium studies are better suited for detecting deep chronic ulcers or structural abnormalities like strictures. **Analysis of other options:** * **Option A:** **Upper GI Endoscopy (UGIE)** is the investigation of choice. It allows direct visualization of the gastric mucosa, showing multiple small, superficial erosions, petechiae, and friability. * **Option B:** Pain is often **absent** or minimal. Unlike peptic ulcer disease, erosive gastritis is frequently asymptomatic until it presents as painless hematemesis or melena. If symptoms occur, they are usually vague dyspepsia or epigastric discomfort. * **Option C:** It is commonly **drug-induced**, most notably by NSAIDs (which inhibit protective prostaglandins) and alcohol [1]. Other causes include severe physiological stress (Curling’s or Cushing’s ulcers) and portal hypertension [1]. **NEET-PG High-Yield Pearls:** * **Most common clinical presentation:** Upper GI bleeding (hematemesis/melena). * **Stress Gastritis:** Occurs in critically ill patients (burns, sepsis, trauma). Prophylaxis with PPIs or H2 blockers is standard in ICU settings [1]. * **NSAID Gastropathy:** The risk is systemic; even parenteral or rectal NSAIDs can cause erosions due to systemic COX-1 inhibition [1]. * **Management:** Removal of the offending agent (NSAIDs/Alcohol) and acid suppression with PPIs.

Q: What is the most specific antibody for celiac disease in patients with IgA deficiency?

Anti-gliadin antibodies. ### Explanation **Concept Overview:** Celiac disease is strongly associated with **selective IgA deficiency** (occurring in 2–3% of patients). Standard screening tests, such as IgA anti-tissue transglutaminase (tTG) and IgA anti-endomysial antibodies (EMA), will yield **false-negative** results in these individuals because they cannot produce sufficient IgA [2]. In such cases, IgG-based versions of these tests must be used. **Why Option D is Correct:** While IgA-tTG is the overall best screening test for the general population, **Deamidated Gliadin Peptide (DGP) IgG antibodies** are highly sensitive and specific for diagnosing celiac disease in patients with IgA deficiency [1]. In the context of this specific question, "Anti-gliadin antibodies" (specifically the IgG subtype) remains the classic answer for this subset of patients. **Why Other Options are Incorrect:** * **A & B (Anti-endomysial and Anti-tTG):** These are typically measured as **IgA** antibodies. In a patient with IgA deficiency, these tests will be negative regardless of whether the disease is present. While IgG-tTG exists, it is generally considered slightly less specific than IgG-DGP in this specific clinical scenario. * **C (Anti-reticulin):** This is an older antibody test with low sensitivity and specificity; it is no longer used in modern clinical practice. **NEET-PG High-Yield Pearls:** * **Best Initial Screening Test:** IgA anti-tissue transglutaminase (tTG). * **Most Specific Test:** IgA anti-endomysial antibody (EMA). * **Gold Standard Diagnosis:** Small bowel biopsy showing villous atrophy, crypt hyperplasia, and increased intraepithelial lymphocytes (Marsh Classification) [1]. * **Mandatory Step:** Always check **Total Serum IgA levels** if celiac disease is suspected but serology is negative. * **HLA Association:** HLA-DQ2 (95%) and HLA-DQ8 [1].

Question 1

A 50-year-old man became dizzy while passing stool and noticed fresh blood in the stool. Previous two concurrent colonoscopic examinations done for routine screening of carcinoma colon were normal. What is the most likely cause of the bleed?

Accepted Answer

Dilatation of veins of the colon

Answer

Early carcinoma of the colon

Answer

Sigmoid diverticulitis

Answer

Microscopic colitis

Question 2

Autosomal Dominant Familial Nonhemolytic Hyperbilirubinemia occurs in all except?

Accepted Answer

Dubin-Johnson syndrome

Answer

Crigler-Najjar syndrome

Answer

Gilbe syndrome

Answer

Cryoglobulinemia

Question 3

Which one of the following causes intestinal pseudo-obstruction?

Accepted Answer

All the above

Answer

Hypothyroidism

Answer

Tricyclic antidepressant

Answer

Parkinsonism

Question 4

Which of the following is not a feature of Crohn’s disease?

Accepted Answer

Continuous lesions

Answer

Non-caseating granulomas are present

Answer

Backwash ileitis may be associated with Crohn’s disease

Answer

Cobblestone appearance

Question 5

Which of the following is NOT a feature of Zollinger-Ellison syndrome?

Accepted Answer

Large gastric ulcer

Answer

Diarrhea non-responsive to fasting

Answer

Epigastric pain

Answer

Secretin study is the investigation of choice

Question 6

A 25-year-old man presents with low-grade fever, weight loss, fatigue, crampy abdominal pain, episodic diarrhea, and postprandial bloating. Right lower quadrant tenderness is elicited on palpation of the abdomen. Capsule endoscopy reveals thickening of the terminal ileum, edema, marked luminal narrowing, and a cobblestone appearance of the mucosa. Which of the following is a characteristic of this condition?

Accepted Answer

It can cause fistula formation between loops of affected bowel.

Answer

Additional typical findings include crypt abscesses and pseudopolyps.

Answer

Inflammation and ulceration limited to mucosa and submucosa with sparing of deeper layers.

Answer

It can affect any portion of the gastrointestinal tract, but the proximal jejunum is the most common site of involvement.

Question 7

An elderly patient presents with a prolonged history of weakness and lethargy. On examination, the patient is found to be anemic and stool is positive for occult blood. Which of the following is the investigation of choice?

Accepted Answer

Colonoscopy

Answer

Barium meal

Answer

Barium enema

Answer

CT abdomen

Question 8

Which of the following is NOT a precipitating factor for hepatic encephalopathy?

Accepted Answer

Diarrhea

Answer

High protein intake

Answer

Hematemesis

Answer

Infection

Question 9

Which statement is not true regarding erosive gastritis?

Accepted Answer

Barium meal may clinch the diagnosis.

Answer

Endoscopy is the investigation of choice.

Answer

Pain is absent.

Answer

It may be drug induced.

Question 10

What is the most specific antibody for celiac disease in patients with IgA deficiency?

Accepted Answer

Anti-gliadin antibodies

Answer

Anti-endomysial antibodies

Answer

Anti-tissue transglutaminase antibodies

Answer

Anti-reticulin antibodies

Gastroenterology — MCQs

Gastroenterology — MCQs

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