Gastroenterology Practice Questions

Q: Which of the following statements about Wilson's disease is false?

Ceruloplasmin levels are elevated.. Wilson’s disease (Hepatolenticular degeneration) is a disorder of copper metabolism caused by a mutation in the **ATP7B gene** on chromosome 13 [1]. This defect impairs the biliary excretion of copper and its incorporation into ceruloplasmin. **Why Option D is the Correct (False) Statement:** In Wilson’s disease, **ceruloplasmin levels are characteristically low** (<20 mg/dL), not elevated [2]. The defect in the ATP7B protein prevents the binding of copper to apoceruloplasmin. Unbound apoceruloplasmin is unstable and rapidly degraded in the circulation, leading to reduced serum levels. **Analysis of Other Options:** * **Option A (True):** It is an **autosomal recessive** condition. A family history is often present, and screening of siblings is mandatory. * **Option B (True):** **Kayser-Fleischer (KF) rings** are caused by copper deposition in the Descemet’s membrane of the cornea. They are present in 95% of patients with neurological symptoms and are best seen via slit-lamp examination [1]. * **Option C (True):** While serum *total* copper may be low (due to low ceruloplasmin), the **free (non-ceruloplasmin bound) copper** and **tissue copper levels** (liver, brain) are significantly elevated, leading to organ toxicity [1]. **NEET-PG High-Yield Pearls:** * **Gold Standard Diagnosis:** Increased hepatic copper content on liver biopsy (>250 μg/g dry weight). * **Neurological Hallmark:** Wing-beating tremor and "Face of the Giant Panda" sign on MRI Brain [1]. * **Hematology:** Coombs-negative hemolytic anemia is a classic presentation [1]. * **Treatment:** Drug of choice is **Penicillamine** (chelator) or **Trientine**. Oral **Zinc** is used for maintenance as it interferes with intestinal copper absorption.

Q: According to Child-Pugh staging, what is the score for Class B?

7-9 points. The **Child-Pugh Score** (also known as the Child-Turcotte-Pugh score) is a clinical tool used to assess the prognosis of chronic liver disease, primarily cirrhosis. It predicts mortality and the necessity of liver transplantation. ### **Explanation of the Correct Answer** The Child-Pugh classification categorizes patients into three classes based on a cumulative score derived from five parameters (Bilirubin, Albumin, INR, Ascites, and Encephalopathy). [1] * **Class A (5–6 points):** Indicates well-compensated liver disease (1-year survival ~100%). * **Class B (7–9 points):** Indicates significant functional impairment and moderately decompensated disease (1-year survival ~80%). * **Class C (10–15 points):** Indicates severe decompensation (1-year survival ~45%). Therefore, **Option B (7–9 points)** is the correct classification for Class B. ### **Analysis of Incorrect Options** * **Option A (5–6 points):** This represents Class A (Mild/Compensated). * **Option C (10–12 points):** This is a subset of Class C; however, Class C extends up to 15 points. * **Option D (13–15 points):** This represents the most severe end of Class C, but does not encompass the entire class or the requested Class B range. ### **NEET-PG High-Yield Pearls** * **Mnemonic for Parameters:** **"A-B-C-D-E"** (Albumin, Bilirubin, Coagulation/INR, Distension/Ascites, Encephalopathy). * **Scoring:** Each parameter is scored from 1 to 3. The minimum possible score is 5, and the maximum is 15. [1] * **Clinical Utility:** Child-Pugh is excellent for bedside assessment, but the **MELD Score** (Model for End-Stage Liver Disease) is now preferred for transplant prioritization as it is more objective (uses Creatinine, Bilirubin, and INR). * **Surgical Risk:** Class C patients have an extremely high perioperative mortality rate (>80%) and are generally considered poor candidates for non-emergent surgery.

Q: What is the least useful diagnostic procedure in a case of acute hematemesis?

Gastric content aspiration. **Explanation:** In the management of acute hematemesis, the primary goals are hemodynamic stabilization followed by rapid identification of the bleeding source to initiate therapy [1]. **Why Gastric Content Aspiration is the least useful:** While a nasogastric (NG) aspirate was historically used to differentiate upper from lower GI bleeds, it is now considered the **least useful** diagnostic tool. A negative aspirate (clear fluid) does not rule out an upper GI bleed, as it may occur if the bleeding has stopped or if the source is post-pyloric (e.g., a duodenal ulcer) without bile reflux. It provides no information on the etiology and does not change the management plan, which invariably requires endoscopy. **Analysis of other options:** * **Endoscopy (Gold Standard):** This is the investigation of choice [1]. It is highly sensitive and specific, allowing for both diagnosis and immediate therapeutic intervention (e.g., banding, clipping, or adrenaline injection) [1]. * **Angiography:** Useful in cases of "obscure" or massive bleeding where endoscopy fails to visualize the source. It requires a bleeding rate of at least **0.5–1.0 mL/min** to be diagnostic. * **Barium Meal:** While largely replaced by endoscopy, it can still identify structural lesions like ulcers or tumors. However, it is contraindicated in the acute phase because residual barium interferes with subsequent endoscopy or angiography. **High-Yield Clinical Pearls for NEET-PG:** * **Investigation of choice:** Upper GI Endoscopy (UGIE), ideally performed within 24 hours [1]. * **Rockall Score & Glasgow-Blatchford Score:** Used to risk-stratify patients with acute GI bleeding [1]. * **Dieulafoy’s Lesion:** A rare cause of massive hematemesis caused by a dilated submucosal artery that erodes the overlying epithelium. * **Management:** Always prioritize "ABC" (Airway, Breathing, Circulation) and IV fluids before diagnostic procedures [1].

Q: Which is the most common complication of GERD?

Esophagitis. Explanation: Gastroesophageal Reflux Disease (GERD) occurs when the reflux of stomach acid into the esophagus causes troublesome symptoms or mucosal damage. [1] Why Esophagitis is the Correct Answer: Esophagitis (inflammation of the esophageal mucosa) is the most common complication of GERD. [1] Chronic exposure to gastric acid, pepsin, and bile salts leads to microscopic and eventually macroscopic damage to the squamous epithelium. While many patients have "Non-Erosive Reflux Disease" (NERD), among those who develop complications, erosive esophagitis is the most frequent finding on endoscopy. Analysis of Incorrect Options: * B. Strictures: Peptic strictures occur in approximately 10% of patients with untreated chronic GERD. [1] They are a result of deep fibrosis following chronic inflammation but are significantly less common than simple esophagitis. * C. Dental damage: This is an extra-esophageal complication caused by acid erosion of tooth enamel. While important, it occurs much less frequently than mucosal inflammation. * D. Vocal cord damage: Also known as reflux laryngitis, this is an extra-esophageal manifestation. While it causes hoarseness and chronic cough, it is not as common as direct esophageal injury. High-Yield Clinical Pearls for NEET-PG: * Barrett’s Esophagus: The most serious histological complication where squamous epithelium undergoes metaplasia to specialized columnar epithelium. [1] It is a precursor to Adenocarcinoma. * Gold Standard Diagnosis: 24-hour ambulatory pH monitoring (though clinical diagnosis or endoscopy is usually the first step). * Schatzki Ring: A mucosal ring at the squamocolumnar junction, often associated with hiatal hernia and GERD. [1] * Alarm Symptoms: Dysphagia, odynophagia, weight loss, and anemia—these necessitate immediate endoscopy to rule out malignancy.

Q: Which of the following conditions is characterized by an enlarged liver with hepatocellular dysfunction?

Wilson's disease. **Explanation:** The correct answer is **Wilson’s Disease**. This condition is an autosomal recessive disorder caused by a mutation in the **ATP7B gene**, leading to impaired biliary copper excretion and systemic copper accumulation. **Why Wilson's Disease is correct:** In Wilson’s disease, copper initially accumulates in the liver, causing oxidative stress and mitochondrial damage. This manifests as **hepatomegaly** (due to inflammation/steatosis) and **hepatocellular dysfunction** (ranging from asymptomatic transaminitis to acute liver failure or cirrhosis). It is a classic cause of liver disease in children and young adults. **Analysis of Incorrect Options:** * **Budd-Chiari Syndrome:** Characterized by hepatic venous outflow obstruction. While it causes massive hepatomegaly and ascites, the primary pathology is **vascular/congestive**, not primary hepatocellular dysfunction (though secondary damage occurs later). * **Alcoholic Hepatitis:** While it presents with hepatomegaly and dysfunction, the question asks for a condition "characterized" by this triad in a systemic context. Wilson’s is a more specific "textbook" answer for metabolic hepatocellular failure in exams. * **NASH (Non-Alcoholic Steatohepatitis):** Often presents with hepatomegaly, but hepatocellular *dysfunction* (jaundice, coagulopathy) is typically a very late finding seen only once cirrhosis develops. **High-Yield Clinical Pearls for NEET-PG:** * **Kayser-Fleischer (KF) rings:** Copper deposition in the Descemet membrane of the cornea (best seen on slit-lamp exam). * **Diagnosis:** Low serum Ceruloplasmin, increased 24-hour urinary copper, and increased hepatic copper content (Gold Standard). * **Neurological signs:** Basal ganglia involvement leading to tremors, dystonia, and parkinsonism. * **Treatment:** Chelating agents like **D-Penicillamine** or Trientine; Zinc for maintenance.

Q: What constitutes the classical triad of Budd-Chiari syndrome?

Hepatomegaly, abdominal pain, ascites. **Explanation** **Budd-Chiari Syndrome (BCS)** is a clinical condition caused by the obstruction of hepatic venous outflow, occurring anywhere from the small hepatic veins to the junction of the inferior vena cava (IVC) with the right atrium. **1. Why Option C is Correct:** The pathophysiology involves sudden venous congestion of the liver, leading to sinusoidal hypertension and ischemic injury. This manifests as the **classical triad**: * **Hepatomegaly:** Due to acute congestion and engorgement of the liver. * **Abdominal Pain:** Resulting from the stretching of Glisson’s capsule. * **Ascites:** Caused by high sinusoidal pressure forcing fluid into the peritoneal cavity [1]. **2. Analysis of Incorrect Options:** * **Option A & B (Fever/Jaundice):** Fever is not a primary feature of BCS; its presence suggests an underlying infection or inflammatory process. While jaundice can occur in acute liver failure, it is not a component of the "classical triad." Charcot's triad of jaundice, RUQ pain, and fever is associated with cholangitis [2]. * **Option D (Jaundice):** While hepatomegaly and pain are present, jaundice is often mild or absent in chronic cases, making it less characteristic than the rapid accumulation of ascites. **3. NEET-PG High-Yield Pearls:** * **Most Common Cause:** In the West, it is **thrombosis** (often associated with Polycythemia Vera or Factor V Leiden). In Asia, **membranous webs** in the IVC are more common. * **Imaging Gold Standard:** **Doppler Ultrasonography** is the initial investigation of choice. * **The Caudate Lobule:** Often undergoes **compensatory hypertrophy** because its venous drainage enters the IVC directly, bypassing the main hepatic veins. * **Charcot’s Triad:** Do not confuse the BCS triad with Charcot’s Triad (Fever, Jaundice, RUQ pain), which indicates **Acute Cholangitis** [2].

Q: Which of the following is true about celiac sprue?

Anti-gliadin antibodies are IgA/IgG. **Explanation:** Celiac sprue (Gluten-sensitive enteropathy) is an immune-mediated inflammatory disorder of the small intestine triggered by the ingestion of gluten in genetically predisposed individuals [1]. **Why Option C is Correct:** Diagnosis involves serological testing for various antibodies. **Anti-gliadin antibodies (AGA)** can be of both **IgA and IgG** subclasses. While AGA is less specific than newer tests, it remains a classic marker. In patients with selective IgA deficiency (which is more common in Celiac disease), IgG-based tests (like IgG-deamidated gliadin peptide) are essential for diagnosis. **Analysis of Incorrect Options:** * **A. Associated with HLA-DR4:** This is incorrect. Celiac disease is strongly associated with **HLA-DQ2** (95%) and **HLA-DQ8** (5%) [1]. HLA-DR4 is typically associated with Rheumatoid Arthritis. * **B. Antiendomysial antibodies (EMA):** While EMA is highly specific (nearly 100%), **Anti-tissue Transglutaminase (tTG) IgA** is the preferred initial screening test because it is equally sensitive, more cost-effective, and less observer-dependent than EMA. * **D. No predisposition to malignancy:** This is incorrect. Chronic untreated Celiac disease carries a significant risk of malignancies, most notably **Enteropathy-associated T-cell lymphoma (EATL)** and small bowel adenocarcinoma [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Gold Standard Diagnosis:** Small intestinal biopsy showing villous atrophy, crypt hyperplasia, and increased intraepithelial lymphocytes (Marsh Classification) [1]. * **Best Initial Test:** Anti-tTG IgA. * **Dermatological Association:** Dermatitis herpetiformis (intense pruritic vesicles on extensors). * **Site of Involvement:** Primarily the **duodenum** and proximal jejunum (where gluten concentration is highest).

Question 1

Which of the following statements about Wilson's disease is false?

Accepted Answer

Ceruloplasmin levels are elevated.

Answer

It is an autosomal recessive disorder.

Answer

Kayser-Fleischer rings are typically seen.

Answer

Copper levels are elevated.

Question 2

According to Child-Pugh staging, what is the score for Class B?

Accepted Answer

7-9 points

Answer

5-6 points

Answer

10-12 points

Answer

13-15 points

Question 3

What is the least useful diagnostic procedure in a case of acute hematemesis?

Accepted Answer

Gastric content aspiration

Answer

Barium meal

Answer

Endoscopy

Answer

Angiography

Question 4

Which is the most common complication of GERD?

Accepted Answer

Esophagitis

Answer

Strictures

Answer

Dental damage

Answer

Vocal cord damage

Question 5

Hypogonadism in cirrhosis is due to which of the following mechanisms?

Accepted Answer

All of the above

Answer

Direct effect of alcohol on the testes

Answer

Increased estrogen due to decreased hepatic catabolism

Answer

Increased peripheral conversion of androgens into estrogen

Question 6

Which of the following statements about Crohn's disease is true?

Accepted Answer

It can present with oral ulcerations resembling major aphthous ulcerations.

Answer

It is typically a self-limiting condition.

Answer

It is commonly observed in the Indian population.

Answer

Erythromycin is the usual treatment of choice.

Question 7

Which of the following conditions is characterized by an enlarged liver with hepatocellular dysfunction?

Accepted Answer

Wilson's disease

Answer

Budd-Chiari syndrome

Answer

Alcoholic hepatitis

Answer

NASH

Question 8

What constitutes the classical triad of Budd-Chiari syndrome?

Accepted Answer

Hepatomegaly, abdominal pain, ascites

Answer

Fever, jaundice, abdominal pain

Answer

Fever, ascites, jaundice

Answer

Abdominal pain, jaundice, hepatomegaly

Question 9

Large bowel (colonic) diarrhoea is associated with all of the following, except?

Accepted Answer

Large volume stool

Answer

Urgency

Answer

Tenesmus

Answer

Mucus

Question 10

Which of the following is true about celiac sprue?

Accepted Answer

Anti-gliadin antibodies are IgA/IgG

Answer

Associated with HLA-DR4

Answer

Antiendomysial antibodies are more specific and sensitive than other antibodies

Answer

No predisposition to malignancy

Gastroenterology — MCQs

Gastroenterology — MCQs

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