Gastroenterology — MCQs
On this page
Which of the following statements is FALSE about Budd-Chiari syndrome?
A middle-aged man presents with congestive heart failure with elevated liver enzymes. His skin has a grayish pigmentation. Liver enzyme levels are higher than typically seen in congestive heart failure, suggesting an inflammatory process (hepatitis) with scarring (cirrhosis) of the liver. A liver biopsy discloses a marked increase in iron storage. In humans, how is molecular iron primarily handled?
All are features of Irritable Bowel Syndrome except?
What is the most likely precipitating cause for acute hepato-cellular failure?
A 30-year-old patient has high fat content in the stool. The D-xylose test is normal. Where is the pathology suspected?
In a patient with acute severe colitis on day 3 of hospitalization, what is the best predictor of colectomy?
A 78-year-old man presents to the emergency department with acute onset of bright red blood per rectum. Symptoms started 2 hours earlier, and he has had three bowel movements since then with copious amounts of blood. He denies prior episodes of rectal bleeding. He notes dizziness with standing but denies abdominal pain. He has had no vomiting or nausea. A nasogastric lavage is performed and shows no coffee-ground material or blood. Lab evaluation reveals hemoglobin of 10.5 g/dL. What is the most likely source of the bleeding?
Which of the following is NOT a risk factor for carcinoma of the stomach?
Which of the following is NOT a feature of obstructive jaundice?
Which of the following conditions is typically not diagnosed via intestinal biopsy?
Gastroenterology Indian Medical PG Practice Questions and MCQs
Question 481: Which of the following statements is FALSE about Budd-Chiari syndrome?
- A. It is associated with coagulopathy.
- B. Cirrhosis may occur.
- C. Ascites may be present.
- D. The hepatic artery is involved. (Correct Answer)
Explanation: **Explanation:** **Budd-Chiari Syndrome (BCS)** is defined as an obstruction of the hepatic venous outflow, occurring at any level from the small hepatic veins to the junction of the inferior vena cava (IVC) and the right atrium. **Why Option D is the Correct (False) Statement:** The primary pathology in BCS involves the **hepatic veins** or the **IVC**, not the hepatic artery. In contrast to hepatic vein obstruction, conditions like veno-occlusive disease involve the terminal hepatic venules while the larger veins remain patent [1]. The hepatic artery remains patent and often undergoes compensatory hypertrophy to maintain liver perfusion as the venous drainage is compromised. **Analysis of Other Options:** * **Option A (Coagulopathy):** BCS is strongly associated with hypercoagulable states. In the West, myeloproliferative neoplasms (e.g., Polycythemia vera) and Factor V Leiden mutations are common causes. In Asia, membranous webs in the IVC are more frequent. * **Option B (Cirrhosis):** Chronic venous congestion leads to centrizonal pressure necrosis and fibrosis (cardiac cirrhosis), eventually progressing to frank cirrhosis and portal hypertension [1]. * **Option C (Ascites):** This is a hallmark clinical feature. The post-sinusoidal obstruction increases sinusoidal pressure, leading to the transudation of fluid into the peritoneal cavity. The ascitic fluid typically has a high serum-ascites albumin gradient (SAAG >1.1 g/dL). **NEET-PG High-Yield Pearls:** * **Classic Triad:** Abdominal pain, hepatomegaly, and ascites. * **Imaging Gold Standard:** Doppler Ultrasound is the initial test; "Spider-web" collateral vessels are characteristic on venography. * **Caudate Lobe Hypertrophy:** The caudate lobe often enlarges because its venous drainage enters the IVC directly, bypassing the obstructed main hepatic veins. * **Nutmeg Liver:** Chronic congestion gives the liver a mottled appearance on gross pathology [1].
Question 482: A middle-aged man presents with congestive heart failure with elevated liver enzymes. His skin has a grayish pigmentation. Liver enzyme levels are higher than typically seen in congestive heart failure, suggesting an inflammatory process (hepatitis) with scarring (cirrhosis) of the liver. A liver biopsy discloses a marked increase in iron storage. In humans, how is molecular iron primarily handled?
- A. Stored primarily in the spleen.
- B. Stored in combination with ferritin. (Correct Answer)
- C. Excreted in the urine as Fe2+.
- D. Absorbed in the intestine by albumin.
Explanation: ### Explanation The clinical presentation of congestive heart failure, "bronze" skin pigmentation, and cirrhosis (the "bronze diabetes" triad) is classic for **Hereditary Hemochromatosis**. This condition involves excessive iron accumulation leading to multi-organ damage [1]. **Why Option B is Correct:** Iron is highly reactive and can generate toxic free radicals via the Fenton reaction [2]. To prevent this, the body stores intracellular iron in a non-toxic, soluble form by binding it to **ferritin** [2]. Ferritin acts as a hollow shell that can sequester up to 4,500 iron atoms. When ferritin stores are overwhelmed, it aggregates into insoluble **hemosiderin**, which is what is typically seen on a liver biopsy using Prussian Blue stain [2]. **Why Other Options are Incorrect:** * **Option A:** While the spleen (part of the reticuloendothelial system) does store iron from recycled RBCs, the **liver** is the primary storage organ for excess systemic iron in hemochromatosis [1]. * **Option C:** Humans have **no active physiological mechanism for iron excretion**. Iron is lost only through desquamation of skin/mucosal cells or blood loss (menstruation). It is not excreted in the urine. * **Option D:** Intestinal absorption of iron occurs via **Divalent Metal Transporter 1 (DMT1)** and is regulated by **hepcidin** [3]. Albumin is a general transport protein but is not the primary mechanism for iron absorption or specific transport (which is the role of **transferrin**). ### NEET-PG High-Yield Pearls * **Gene Mutation:** Most commonly the **HFE gene** (C282Y mutation) on Chromosome 6 [1], [3]. * **Pathophysiology:** Deficiency in **Hepcidin** leads to unregulated ferroportin activity and excessive iron absorption [3]. * **Diagnosis:** Best initial test is **Transferrin Saturation** (>45%); Gold standard for quantification is **MRI (T2*)** or Liver Biopsy [1]. * **Treatment:** Therapeutic phlebotomy is the mainstay; Deferoxamine is used for secondary iron overload [1].
Question 483: All are features of Irritable Bowel Syndrome except?
- A. Vomiting (Correct Answer)
- B. Pain abdomen
- C. Diarrhoea
- D. Constipation
Explanation: Irritable Bowel Syndrome (IBS) is a **functional gastrointestinal disorder** characterized by chronic abdominal pain and altered bowel habits in the absence of demonstrable organic pathology [1]. **1. Why "Vomiting" is the correct answer:** Vomiting is considered a **"Red Flag" or "Alarm Symptom"** in gastroenterology. Its presence suggests an organic cause (such as intestinal obstruction, malignancy, or inflammatory bowel disease) rather than a functional one. According to the **Rome IV Criteria**, the diagnosis of IBS relies on the absence of alarm features like persistent vomiting, unexplained weight loss, gastrointestinal bleeding, or nocturnal diarrhea [2]. **2. Why other options are incorrect:** * **Pain Abdomen:** This is the hallmark of IBS [1]. The pain is typically related to defecation and is often associated with a change in stool frequency or form. * **Diarrhoea & Constipation:** These are the primary manifestations of altered bowel habits in IBS [1]. Patients are categorized into subtypes based on these symptoms: **IBS-D** (Diarrhea predominant), **IBS-C** (Constipation predominant), or **IBS-M** (Mixed). **Clinical Pearls for NEET-PG:** * **Rome IV Criteria:** Recurrent abdominal pain (at least 1 day/week in the last 3 months) associated with 2 or more of: 1) Related to defecation, 2) Change in stool frequency, 3) Change in stool form (appearance). * **Epidemiology:** More common in females and younger patients (<50 years). * **Pathophysiology:** Involves visceral hypersensitivity and gut-brain axis dysregulation. * **High-Yield Fact:** IBS does **not** cause nocturnal symptoms or anemia [2]. If these are present, look for an alternative diagnosis.
Question 484: What is the most likely precipitating cause for acute hepato-cellular failure?
- A. Oral lactulose
- B. Large IV albumin infusion
- C. Large carbohydrate meal
- D. Upper GI bleeding (Correct Answer)
Explanation: **Explanation:** In patients with chronic liver disease, the transition to **acute-on-chronic liver failure (ACLF)** or hepatic encephalopathy is typically triggered by a specific precipitating event [1]. **Upper GI Bleeding (Correct Answer):** Upper GI bleeding (e.g., esophageal varices) is the most potent precipitant [3]. It induces liver failure through two main mechanisms: 1. **Hypoperfusion:** Massive blood loss leads to hypotension and decreased oxygen delivery to hepatocytes, causing ischemic injury. 2. **Nitrogen Load:** Blood in the gastrointestinal tract is a massive protein load. Bacteria break down this blood into ammonia and other nitrogenous toxins, which are absorbed into the portal circulation, overwhelming the liver's detoxification capacity and precipitating encephalopathy [2]. **Analysis of Incorrect Options:** * **Oral Lactulose:** This is a **treatment**, not a cause. Lactulose acidifies the gut, converting ammonia ($NH_3$) to non-absorbable ammonium ($NH_4^+$), and acts as an osmotic laxative to clear nitrogenous waste. * **Large IV Albumin Infusion:** Albumin is used therapeutically in cirrhosis to manage ascites and prevent Hepatorenal Syndrome [4]. While it increases oncotic pressure, it does not precipitate hepatocellular failure. * **Large Carbohydrate Meal:** High-protein meals can trigger encephalopathy, but carbohydrate-rich meals are generally well-tolerated and do not impose a metabolic stressor significant enough to cause acute failure. **NEET-PG High-Yield Pearls:** * **Most common precipitants of Hepatic Encephalopathy:** Infections (SBP), GI Bleed, Diuretics (hypokalemia/alkalosis), and Constipation. * **Mechanism of Hypokalemia:** Diuretic-induced hypokalemia stimulates renal ammoniagenesis, worsening the condition. * **TIPS (Transjugular Intrahepatic Portosystemic Shunt):** A common iatrogenic cause of encephalopathy due to bypassing the liver's filtration [2].
Question 485: A 30-year-old patient has high fat content in the stool. The D-xylose test is normal. Where is the pathology suspected?
- A. Pancreas (Correct Answer)
- B. Intestine
- C. Both
- D. None of the above
Explanation: **Explanation:** The clinical presentation of high fat content in the stool (steatorrhea) indicates **malabsorption**. To differentiate the cause, the **D-xylose test** is the gold standard diagnostic tool. [1] 1. **Why Pancreas is correct:** D-xylose is a monosaccharide that is absorbed directly by the proximal small intestinal mucosa without requiring pancreatic enzymes (lipase, amylase, or proteases) for digestion. * In **Pancreatic Insufficiency** (e.g., Chronic Pancreatitis), there is a deficiency of lipase leading to fat malabsorption (steatorrhea), but the intestinal mucosa remains intact. [1] Therefore, D-xylose is absorbed normally, resulting in a **Normal D-xylose test**. 2. **Why Intestine is incorrect:** If the pathology were in the small intestine (e.g., Celiac disease, Tropical sprue, or Whipple’s disease), the damaged mucosa would be unable to absorb the D-xylose. [1], [2] This would result in an **Abnormal (Low) D-xylose test**. 3. **Why "Both" is incorrect:** If both were involved, the intestinal component would still cause a low D-xylose result, contradicting the findings in the question. **NEET-PG High-Yield Pearls:** * **D-xylose Test:** Used specifically to differentiate **maldigestion** (Pancreatic cause) from **malabsorption** (Mucosal/Intestinal cause). * **Normal Values:** After a 25g oral dose, a 5-hour urinary excretion of **>4g** is considered normal. * **False Positives:** Low urinary D-xylose (mimicking intestinal disease) can occur in patients with **renal insufficiency**, ascites, or Small Intestinal Bacterial Overgrowth (SIBO), as bacteria metabolize the xylose before absorption. [1] * **Treatment of Steatorrhea in Pancreatitis:** Managed with oral pancreatic enzyme replacement therapy (PERT) taken with meals.
Question 486: In a patient with acute severe colitis on day 3 of hospitalization, what is the best predictor of colectomy?
- A. CRP > 45 mg/L and 3-8 stools per day (Correct Answer)
- B. ESR > 60 mm/Hg and abdominal pain
- C. Rectal bleeding and abdominal distention
- D. Tachycardia and fever
Explanation: ### Explanation The correct answer is **A: CRP > 45 mg/L and 3-8 stools per day.** This question tests the application of the **Oxford Criteria** (also known as the Travis Criteria), which is the gold standard for predicting the failure of medical therapy in patients with acute severe ulcerative colitis (ASUC). [1] **1. Why Option A is Correct:** According to the Oxford study, patients assessed on **Day 3** of intensive intravenous corticosteroid therapy who have **more than 8 stools per day** OR **3–8 stools per day combined with a CRP > 45 mg/L** have an 85% probability of requiring a colectomy during that admission. These objective markers are highly predictive of "steroid-refractory" disease, signaling the need for rescue therapy (Infliximab/Cyclosporine) or surgical intervention. **2. Why Other Options are Incorrect:** * **Option B:** While ESR is an inflammatory marker, it is slower to respond than CRP and is not part of the validated predictive indices for acute surgical risk in ASUC. * **Option C:** Rectal bleeding and distention are signs of severity (and potential toxic megacolon), but they are less precise than the stool frequency/CRP combination for predicting the specific need for colectomy on Day 3. * **Option D:** Tachycardia and fever are components of the **Truelove and Witts criteria** used to define the *severity* of an attack upon admission, but they are not the primary predictors of *steroid failure* on Day 3. **3. NEET-PG High-Yield Pearls:** * **Truelove and Witts Criteria:** Used for initial classification of ASUC (≥6 bloody stools/day + at least one sign of systemic toxicity: Fever >37.8°C, HR >90 bpm, Hb <10.5 g/dL, or ESR >30 mm/hr). * **Management Timeline:** If Oxford criteria are met on Day 3, do not delay; initiate rescue therapy or consult surgery. [1] * **Toxic Megacolon:** Defined as transverse colon diameter **>6 cm** on X-ray; it is an absolute indication for urgent surgery.
Question 487: A 78-year-old man presents to the emergency department with acute onset of bright red blood per rectum. Symptoms started 2 hours earlier, and he has had three bowel movements since then with copious amounts of blood. He denies prior episodes of rectal bleeding. He notes dizziness with standing but denies abdominal pain. He has had no vomiting or nausea. A nasogastric lavage is performed and shows no coffee-ground material or blood. Lab evaluation reveals hemoglobin of 10.5 g/dL. What is the most likely source of the bleeding?
- A. Internal hemorrhoids
- B. Dieulafoy lesion
- C. Diverticulosis (Correct Answer)
- D. Mallory-Weiss tear
Explanation: ### Explanation **1. Why Diverticulosis is the Correct Answer:** Diverticulosis is the **most common cause of painless, massive hematochezia** (bright red blood per rectum) in the elderly. The bleeding occurs because a nutrient artery (vasa recta) stretched over the dome of a diverticulum becomes thin and eventually ruptures into the colonic lumen. * **Clinical Presentation:** Typically presents as sudden, painless, large-volume bleeding. * **Localization:** While diverticula are more common in the left colon, **diverticular bleeding** more frequently originates from the **right colon**. * **Exclusion of Upper GI Source:** The negative nasogastric (NG) lavage (no blood/coffee grounds) significantly decreases the likelihood of an Upper GI bleed (like a peptic ulcer) presenting as hematochezia [1]. **2. Why Other Options are Incorrect:** * **Internal Hemorrhoids:** While common, they typically cause "streaks" of blood on stool or dripping into the toilet bowl. They rarely cause the massive, hemodynamically significant bleeding (dizziness, Hb drop) seen in this patient. * **Dieulafoy Lesion:** This is a dilated submucosal artery that erodes the overlying epithelium. While it causes brisk bleeding, it is most commonly found in the **lesser curvature of the stomach** (Upper GI). * **Mallory-Weiss Tear:** This involves a mucosal tear at the gastroesophageal junction, usually following **forceful vomiting or retching**. This patient denied vomiting and had a negative NG lavage [1]. **3. NEET-PG High-Yield Pearls:** * **Most common cause of Lower GI Bleed (LGIB):** Diverticulosis. * **Most common cause of LGIB in children:** Meckel’s Diverticulum. * **Diagnostic Gold Standard:** Colonoscopy (after stabilization). If bleeding is too brisk to visualize, **99mTc-labeled RBC scan** or **CT Angiography** is used. * **Management:** 70–80% of diverticular bleeds stop spontaneously with supportive care.
Question 488: Which of the following is NOT a risk factor for carcinoma of the stomach?
- A. Blood group A
- B. Atrophic gastritis
- C. Duodenal peptic ulcer (Correct Answer)
- D. Partial gastrectomy
Explanation: ### Explanation The development of gastric adenocarcinoma is a multifactorial process involving chronic mucosal inflammation, environmental triggers, and genetic predisposition [2]. **Why Duodenal Peptic Ulcer is the Correct Answer:** Patients with **duodenal ulcers (DU)** are generally considered to be at a **decreased risk** for gastric cancer. This is because DU is typically associated with *H. pylori* infection limited to the antrum, leading to **hyperchlorhydria** (increased acid secretion) [1]. In contrast, gastric cancer thrives in an environment of **hypochlorhydria** and pangastritis [2]. Therefore, while *H. pylori* causes both, the physiological state associated with DU is protective against malignancy. **Analysis of Incorrect Options:** * **Blood Group A:** There is a well-documented genetic association between Blood Group A and the **diffuse type** of gastric cancer. (Note: Blood Group O is associated with Peptic Ulcer Disease). * **Atrophic Gastritis:** This is a precursor lesion [2]. Chronic inflammation leads to the loss of parietal cells (achlorhydria) and intestinal metaplasia, significantly increasing the risk of the **intestinal type** of gastric cancer. * **Partial Gastrectomy:** Patients who have undergone a Billroth II reconstruction are at higher risk (after 15–20 years) due to **alkaline reflux** of bile and pancreatic secretions, which causes chronic inflammation of the gastric remnant (Stump Cancer) [3]. **High-Yield NEET-PG Pearls:** * **Lauren Classification:** Divides gastric cancer into **Intestinal** (associated with environmental factors like H. pylori, smoking, nitrates) and **Diffuse** (associated with genetics/E-cadherin mutations). * **Nitrosamines:** Found in smoked and salted foods; they are potent dietary carcinogens for the stomach. * **Protective Factors:** Fresh fruits and vegetables (Vitamin C and Beta-carotene).
Question 489: Which of the following is NOT a feature of obstructive jaundice?
- A. Pruritus
- B. Elevated serum bilirubin level
- C. Raised alkaline phosphatase
- D. Raised urinary urobilinogen (Correct Answer)
Explanation: **Explanation:** In obstructive (post-hepatic) jaundice, the flow of conjugated bilirubin from the liver to the duodenum is blocked (e.g., due to gallstones or pancreatic head cancer) [2], [3]. **Why "Raised urinary urobilinogen" is the correct answer:** Normally, conjugated bilirubin reaches the intestine and is converted by gut bacteria into **urobilinogen**. Most urobilinogen is excreted in feces, but a small portion is reabsorbed and excreted in urine. In complete biliary obstruction, bilirubin cannot reach the gut; therefore, no urobilinogen is formed [1]. Consequently, **urinary urobilinogen is absent or significantly decreased**, not raised [1], [3]. **Analysis of Incorrect Options:** * **A. Pruritus:** Obstruction leads to the systemic accumulation of bile salts and other pruritogens in the skin, making itching a hallmark feature. * **B. Elevated serum bilirubin level:** Obstruction prevents the excretion of conjugated bilirubin, leading to its regurgitation into the bloodstream (conjugated hyperbilirubinemia) [2]. * **C. Raised alkaline phosphatase (ALP):** ALP is synthesized by biliary canalicular cells. Pressure from obstruction induces increased synthesis and release of ALP, typically >3 times the upper limit of normal. **NEET-PG High-Yield Pearls:** * **Stool color:** Because no stercobilin (derived from urobilinogen) is formed, patients present with **pale/clay-colored stools** [3]. * **Urine color:** Conjugated bilirubin is water-soluble and excreted by the kidneys, resulting in **dark "tea-colored" urine** [1], [3]. * **Vitamin Deficiency:** Lack of bile in the gut leads to malabsorption of fat-soluble vitamins (A, D, E, **K**). A prolonged Prothrombin Time (PT) that corrects with parenteral Vitamin K is characteristic of obstructive jaundice.
Question 490: Which of the following conditions is typically not diagnosed via intestinal biopsy?
- A. Abetalipoproteinemia
- B. Tropical sprue (Correct Answer)
- C. Intestinal lymphangiectasia
- D. Agammaglobulinemia
Explanation: **Explanation:** The diagnosis of **Tropical Sprue** is primarily clinical and based on a combination of travel history to endemic areas, symptoms of malabsorption (chronic diarrhea, weight loss), and megaloblastic anemia (Vitamin B12/Folate deficiency). While an intestinal biopsy in Tropical Sprue shows abnormalities like blunted villi and increased intraepithelial lymphocytes, these findings are **non-specific** and mimic Celiac disease. Therefore, a biopsy is not diagnostic on its own; the diagnosis is confirmed by the clinical response to antibiotics (Tetracycline) and Folate. **Analysis of Incorrect Options:** * **Abetalipoproteinemia:** Biopsy is diagnostic, showing pathognomonic **clear, lipid-laden enterocytes** (vacuolated appearance) because the body cannot export triglycerides as chylomicrons. * **Intestinal Lymphangiectasia:** Biopsy reveals characteristic **dilated mucosal and submucosal lymphatic vessels**, which is the gold standard for diagnosis. * **Agammaglobulinemia:** Biopsy is diagnostic as it shows a complete **absence of plasma cells** in the lamina propria, often accompanied by Giardia infection or nodular lymphoid hyperplasia [1]. **NEET-PG High-Yield Pearls:** * **Whipple’s Disease:** Biopsy shows PAS-positive macrophages containing *Tropheryma whipplei* [1]. * **Celiac Disease:** Characterized by villous atrophy, crypt hyperplasia, and increased intraepithelial lymphocytes (Marsh Criteria) [1]. * **Amyloidosis:** Diagnosed via biopsy showing apple-green birefringence under polarized light with Congo Red stain. * **Key Distinction:** If a biopsy shows "flat mucosa" but the patient has a history of living in the Caribbean or India, think Tropical Sprue; if they have HLA-DQ2/DQ8, think Celiac Disease [1].
Practice by Chapter
Esophageal Disorders
Practice Questions
Peptic Ulcer Disease
Practice Questions
Inflammatory Bowel Disease
Practice Questions
Irritable Bowel Syndrome
Practice Questions
Malabsorption Syndromes
Practice Questions
Pancreatitis (Acute and Chronic)
Practice Questions
Gastrointestinal Bleeding
Practice Questions
Liver Diseases and Cirrhosis
Practice Questions
Viral Hepatitis
Practice Questions
Biliary Tract Disorders
Practice Questions
Gastrointestinal Motility Disorders
Practice Questions
Gastrointestinal Malignancies
Practice Questions
Want unlimited practice?
Get full access to all questions, explanations, and performance tracking.
Start For Free