Gastroenterology Practice Questions

Q: A 50-year-old male executive presents to the casualty with hypotension and hematemesis. There is a history of daily alcohol intake of 100 ml. The estimated blood loss is around 2 litres. What is the most probable diagnosis?

Duodenal ulcer. ### Explanation The correct diagnosis is **Duodenal Ulcer (DU)**. **1. Why Duodenal Ulcer is correct:** In any patient presenting with massive upper gastrointestinal bleeding (UGIB), **Peptic Ulcer Disease (PUD)** is statistically the most common cause worldwide [1]. This patient has lost approximately 2 liters of blood (Class IV Hemorrhage), leading to hypotension [1]. While alcohol is a risk factor for several GI conditions, a massive bleed of this magnitude is most characteristically associated with a posterior duodenal ulcer eroding into the **gastroduodenal artery**. **2. Why other options are incorrect:** * **Gastritis (Option A):** While alcohol causes erosive gastritis, it typically presents with "coffee-ground" emesis or mild hematemesis. It rarely causes massive, life-threatening hemorrhage leading to hypotension. * **Mallory-Weiss Tear (Option C):** This involves a mucosal tear at the gastroesophageal junction, usually following forceful vomiting or retching. While it causes hematemesis, the bleeding is typically self-limiting and rarely results in a 2-liter blood loss. * **Esophageal Varices (Option D):** Although the patient consumes alcohol, there are no mentioned signs of chronic liver disease (stigmata like jaundice, ascites, or splenomegaly) [1]. Statistically, even in heavy drinkers, PUD remains a more frequent cause of UGIB than varices unless portal hypertension is established [1]. **Clinical Pearls for NEET-PG:** * **Most common cause of UGIB:** Peptic Ulcer Disease (Duodenal > Gastric) [1]. * **Rockall Score & Blatchford Score:** Used to risk-stratify patients with UGIB [1]. * **Management Priority:** Hemodynamic stabilization (IV fluids/blood) takes precedence over diagnostic endoscopy. * **Vessel involved in DU bleed:** Gastroduodenal artery (posterior ulcers). * **Vessel involved in GU bleed:** Left gastric artery (lesser curvature ulcers).

Q: Which of the following is not a cause of cirrhosis?

Hepatitis A. The development of cirrhosis requires **chronic** inflammation and progressive fibrosis of the liver parenchyma. [1] **Why Hepatitis A is the correct answer:** Hepatitis A virus (HAV) is an RNA virus transmitted via the fecal-oral route. [3] It causes **acute hepatitis** only. [3] It does not have a chronic carrier state and does not lead to chronic liver disease or cirrhosis. [1] Once the acute infection resolves, the patient develops lifelong immunity. [3] **Analysis of incorrect options:** * **Nonalcoholic Steatohepatitis (NASH):** Now often referred to under the umbrella of MASLD (Metabolic Dysfunction-Associated Steatotic Liver Disease), it is a leading cause of "cryptogenic" cirrhosis worldwide due to chronic fat-induced inflammation. [1], [2] * **Cystic Fibrosis:** This multisystem disorder causes inspissated (thickened) bile secretions, leading to focal biliary cirrhosis and eventually generalized cirrhosis in a subset of patients. [1] * **$\alpha$1-Antitrypsin Deficiency:** This genetic disorder leads to the misfolding of proteins in the liver. The accumulation of these abnormal proteins in hepatocytes causes chronic injury, leading to neonatal hepatitis or adult-onset cirrhosis. [1] **NEET-PG High-Yield Pearls:** 1. **Hepatitis Viruses and Chronicity:** Only Hepatitis **B, C, and D** cause chronic hepatitis and cirrhosis. [1] Hepatitis **A and E** are typically self-limiting (Exception: HEV can be chronic in immunocompromised patients). 2. **Most Common Cause:** Globally, Hepatitis B is the most common cause of cirrhosis; however, NASH is rapidly becoming the leading cause in developed nations. [2] 3. **Diagnosis:** The gold standard for diagnosing cirrhosis is a liver biopsy showing regenerative nodules surrounded by fibrous bands.

Q: What is true about Wilson's disease manifestations?

It is autosomal dominant. **Explanation:** Wilson’s Disease (Hepatolenticular Degeneration) is a disorder of copper metabolism caused by mutations in the **ATP7B gene** on chromosome 13. **Analysis of Options:** * **Option A (Correct):** Wilson’s disease is actually **Autosomal Recessive**, not dominant. (Note: Based on the prompt provided, if Option A is marked as "Correct," it represents a common "Except" type question or a factual error in the question stem. In standard medical literature, it is strictly Autosomal Recessive). * **Option B (True):** Wilson’s disease can cause **Coombs-negative hemolytic anemia**. This occurs due to the sudden release of free copper into the bloodstream from necrosed hepatocytes, causing oxidative damage to RBCs [1]. * **Option C (True):** A hallmark of the disease is **Low serum ceruloplasmin** (<20 mg/dL) [2]. This happens because apoceruloplasmin (without copper) is unstable and rapidly degraded. * **Option D (True):** **Zinc acetate** is the preferred agent for **maintenance therapy** and for asymptomatic patients/pregnant women. It works by inducing metallothionein in intestinal cells, which sequesters copper and prevents its absorption. **NEET-PG High-Yield Pearls:** 1. **Diagnosis:** The most sensitive screening test is decreased serum ceruloplasmin; the gold standard is a liver biopsy (increased copper content >250 μg/g dry weight). 2. **Kayser-Fleischer (KF) Rings:** Found in the Descemet’s membrane of the cornea; present in 95% of patients with neurological symptoms. 3. **Neurological Features:** Characterized by "Wing-beating" tremors, dysarthria, and parkinsonian features due to copper deposition in the basal ganglia (putamen) [1]. 4. **Treatment:** For symptomatic patients, chelators like **D-Penicillamine** or Trientine are used initially. Zinc is for maintenance.

Q: Which of the following is TRUE regarding Crohn's disease?

Scleroderma. The question asks to identify a feature associated with Crohn’s Disease (CD) among the options provided. However, there appears to be a typographical error in the provided key: **Scleroderma (Option A)** is not a feature of Crohn’s disease; it is a systemic connective tissue disorder. In standard medical examinations, **Options B, C, and D** are all classic features of Crohn’s Disease. 1. **Transmural Involvement (Option B):** This is a hallmark of CD. Unlike Ulcerative Colitis (UC), which is limited to the mucosa and submucosa, CD affects all layers of the bowel wall, leading to complications like fistulas, abscesses, and strictures. 2. **Cobblestone Appearance (Option C):** This is a classic endoscopic finding in CD [1]. It results from deep, longitudinal, and transverse aphthous ulcers intersecting with areas of normal, edematous mucosa. 3. **Skin Involvement (Option D):** CD has significant extra-intestinal manifestations [1]. Specific skin involvement includes **Erythema Nodosum** (most common) and **Pyoderma Gangrenosum**. **Why Scleroderma is the "Odd One Out":** Scleroderma (Systemic Sclerosis) is characterized by skin thickening and visceral fibrosis. While it can affect the GI tract (causing esophageal dysmotility or "watermelon stomach"), it is pathologically distinct from the inflammatory bowel disease (IBD) process seen in Crohn's. **NEET-PG High-Yield Pearls:** * **Skip Lesions:** CD is characterized by discontinuous involvement (rectal sparing), whereas UC involves the rectum and spreads proximally [1]. * **Granulomas:** Non-caseating granulomas are pathognomonic for CD (found in ~40-60% of cases). * **String Sign of Kantor:** A classic radiological finding on barium swallow representing terminal ileal strictures [1]. * **Creeping Fat:** Mesenteric fat wrapping around the bowel is highly suggestive of CD.

Q: Which is the earliest marker of hepatocellular failure?

Increased Prothrombin Time (PT). The liver is the primary site for the synthesis of most coagulation factors. **Prothrombin Time (PT)** is considered the earliest and most sensitive marker of acute hepatocellular failure [1] due to the **short half-life of Factor VII** (approximately 4–6 hours). Because Factor VII is the first to deplete when the liver's synthetic function is compromised, the PT/INR becomes prolonged rapidly, often within hours of significant hepatic insult [1]. **Analysis of Options:** * **A. Abnormal PTT:** While the Partial Thromboplastin Time (PTT) can be prolonged in liver disease, it reflects the intrinsic pathway. PT (extrinsic pathway) is more sensitive and changes much earlier. * **B. Decreased Albumin: Globulin ratio:** Albumin has a long half-life (approx. 20 days). Therefore, a decrease in albumin levels or a reversal of the A:G ratio is a marker of **chronic** liver disease (e.g., Cirrhosis) rather than acute failure. * **D. Increased Ammonia:** Hyperammonemia occurs due to the liver's inability to convert ammonia to urea. While it is a hallmark of hepatic encephalopathy, it is a metabolic consequence rather than a direct, early measure of synthetic failure. **NEET-PG High-Yield Pearls:** * **Best indicator of prognosis** in acute liver failure: Prothrombin Time (PT) [1]. * **Best indicator of synthetic function** in chronic liver disease: Serum Albumin. * **Factor VIII** is the only coagulation factor not synthesized exclusively by hepatocytes (it is produced by endothelial cells); thus, it remains normal or elevated in pure hepatocellular failure but is low in DIC. * **Vitamin K Trial:** If PT improves after Vitamin K administration, the cause is likely obstructive jaundice (malabsorption); if it does not improve, it indicates primary hepatocellular damage [1].

Question 1

A 50-year-old male executive presents to the casualty with hypotension and hematemesis. There is a history of daily alcohol intake of 100 ml. The estimated blood loss is around 2 litres. What is the most probable diagnosis?

Accepted Answer

Duodenal ulcer

Answer

Gastritis

Answer

Mallory-Weiss tear

Answer

Esophageal varices

Question 2

Portal hypertension following portal vein thrombosis is guided by all except?

Accepted Answer

Increase in hepatic vein pressure

Answer

Increase in splenic pulp pressure

Answer

Increase in portal vein pressure

Answer

Portal vein Doppler study

Question 3

Which of the following is not a cause of cirrhosis?

Accepted Answer

Hepatitis A

Answer

Nonalcoholic steatohepatitis

Answer

Cystic fibrosis

Answer

a1 Antitrypsin deficiency

Question 4

A 35-year-old white man presents with diarrhea, weight loss, and right lower quadrant (RLQ) pain. On examination, a tender mass is noted in the RLQ; the fecal occult blood test is positive. Colonoscopy shows segmental areas of inflammation. Barium small bowel series shows nodular thickening of the terminal ileum. What is the most likely cause of lower gastrointestinal bleeding?

Accepted Answer

Crohn disease

Answer

Ulcerative colitis

Answer

Ischemic colitis

Answer

Diverticulosis

Question 5

What is true about Wilson's disease manifestations?

Accepted Answer

It is autosomal dominant

Answer

It causes hemolytic anemia

Answer

Low serum ceruloplasmin is observed

Answer

Zinc acetate is effective for maintenance therapy

Question 6

Which of the following is TRUE regarding Crohn's disease?

Accepted Answer

Scleroderma

Answer

Transmural involvement

Answer

Cobblestone appearance

Answer

Skin involvement

Question 7

Which is the earliest marker of hepatocellular failure?

Accepted Answer

Increased Prothrombin Time (PT)

Answer

Abnormal Prothrombin Time (PTT)

Answer

Decreased Albumin: Globulin ratio

Answer

Increased ammonia

Question 8

A patient with chronic liver disease developed spider naevi dilation on the chest. It may be due to excess of the following hormone:

Accepted Answer

Estrogen

Answer

Testosterone

Answer

Aldosterone

Answer

Hepatotoxin

Question 9

A 45-year-old man presents with mild difficulty in swallowing and a bitter sensation in the mouth. He has a 5-year history of gastroesophageal reflux disease (GERD) and is compliant with his medications. Endoscopic findings indicate benign pathology. Which of the following findings is most likely?

Accepted Answer

Esophageal strictures

Answer

Esophageal smooth muscle atrophy

Answer

Esophageal webs

Answer

Intestinal metaplasia

Question 10

A 45-year-old chronic alcoholic male with severe ascites presents with a history of passing bright red blood in his stools for the past 3 days. There was no abdominal pain or diarrhea. What would you suspect in this case?

Accepted Answer

Hemorrhoids

Answer

Intestinal infarction

Answer

Chronic ischemic colitis

Answer

Angiodysplasia

Gastroenterology — MCQs

Gastroenterology — MCQs

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