Gastroenterology Practice Questions

Q: What is the drug of choice for an acute exacerbation of ulcerative colitis?

Steroids. **Explanation:** The management of Ulcerative Colitis (UC) is divided into two phases: **Induction of remission** (treating acute flares) and **Maintenance of remission** [2]. **Why Steroids are the Correct Answer:** Systemic corticosteroids (e.g., oral Prednisolone or IV Hydrocortisone/Methylprednisolone) are the **drugs of choice for inducing remission** in an acute moderate-to-severe exacerbation [1]. They possess potent anti-inflammatory properties that rapidly suppress the immune response. However, they have no role in maintenance therapy due to significant long-term side effects. **Analysis of Incorrect Options:** * **A & B (Sulfasalazine/Mesalazine):** These are 5-ASA (Aminosalicylates) compounds. While they are the drug of choice for **maintaining remission** and treating **mild** UC, they are insufficient as monotherapy for a significant acute exacerbation [1]. * **D (NSAIDs):** These are strictly **contraindicated** in patients with Inflammatory Bowel Disease (IBD) as they can precipitate or worsen an acute flare by inhibiting protective prostaglandins in the gut mucosa. **High-Yield Clinical Pearls for NEET-PG:** * **Route of Administration:** For severe cases (Truelove and Witts criteria), **IV steroids** are the initial treatment. If there is no response in 3–5 days, switch to "rescue therapy" with **Infliximab** or **Cyclosporine**. * **Distal Disease:** For proctitis or distal colitis, **topical (rectal) steroids or 5-ASAs** are preferred over systemic therapy [1]. * **Monitoring:** Always rule out *Clostridioides difficile* and CMV infection in a patient presenting with a refractory acute flare. * **Surgery:** Total proctocolectomy with Ileal Pouch-Anal Anastomosis (IPAA) is curative for UC [3].

Q: Which of the following is true about Mallory-Weiss syndrome?

Commonly seen in alcoholics. **Explanation:** **Mallory-Weiss Syndrome (MWS)** is characterized by non-transmural, longitudinal mucosal lacerations at the gastroesophageal junction or gastric cardia. **Why the correct answer is right:** The primary pathophysiology involves a sudden increase in intra-abdominal pressure, most commonly due to forceful retching, vomiting, or coughing. It is **commonly seen in alcoholics** because chronic alcohol consumption leads to frequent episodes of binge drinking followed by violent vomiting (retching). Additionally, alcohol-induced gastritis can sensitize the mucosa to injury. **Analysis of Incorrect Options:** * **A. Associated with gastrointestinal reflux:** While GERD causes mucosal inflammation (esophagitis), it is not a direct cause of the mechanical shearing forces required to produce Mallory-Weiss tears. * **B. Associated with obesity:** Obesity is a risk factor for Hiatal Hernia (which is often found in MWS patients), but it is not a direct causative factor for the syndrome itself [1]. * **C. Associated with a tumour:** MWS is a mechanical traumatic injury. While a tumor might cause obstruction or vomiting, the syndrome is defined by the tear itself, not by an underlying malignancy. **High-Yield Clinical Pearls for NEET-PG:** * **Presentation:** Typically presents as painless hematemesis following an initial bout of non-bloody vomiting. * **Diagnosis:** Gold standard is **Upper GI Endoscopy**, which reveals linear mucosal tears. * **Management:** Most cases (80-90%) stop bleeding spontaneously. Active bleeding is managed endoscopically (clips, epinephrine, or thermal cautery). * **Differentiate from Boerhaave Syndrome:** MWS is a **mucosal tear** (partial thickness), whereas Boerhaave is a **transmural rupture** (full thickness) leading to pneumomediastinum and surgical emergency.

Q: A 50-year-old male executive presents to the casualty department with hematemesis. He reports vomiting all the food he had consumed prior to the hematemesis, followed by forceful retching. He had consumed alcohol the previous day. What is the most probable diagnosis?

Mallory-Weiss tear. ### Explanation **Correct Option: C. Mallory-Weiss tear** **Reasoning:** The clinical hallmark of a **Mallory-Weiss tear (MWT)** is hematemesis following an initial episode of non-bloody vomiting or forceful retching [1]. The pathophysiology involves a longitudinal mucosal laceration at the **gastroesophageal junction** or distal esophagus, caused by a sudden increase in intra-abdominal pressure. This case is classic: the patient first vomited food, followed by forceful retching (increasing pressure), which then led to the tear and subsequent hematemesis. Alcohol consumption is a common predisposing factor as it induces gastric irritation and vomiting. **Why other options are incorrect:** * **Gastritis:** While alcohol can cause erosive gastritis, it typically presents with epigastric pain and coffee-ground emesis rather than brisk hematemesis following a specific sequence of non-bloody vomiting. * **Duodenal Ulcer:** This usually presents with chronic dyspepsia (relieved by food) and melena [2]. While it can cause hematemesis, it is not typically preceded by the "vomiting-then-retching" sequence. * **Esophageal Varices:** This usually presents as massive, painless hematemesis in a patient with signs of chronic liver disease (e.g., splenomegaly, jaundice). There is no characteristic preceding non-bloody vomit. **NEET-PG High-Yield Pearls:** * **Location:** Most tears (approx. 75%) occur just below the GE junction in the gastric mucosa. * **Diagnosis:** **Upper GI Endoscopy** is the gold standard (shows a linear mucosal tear). * **Management:** Most cases (80-90%) stop bleeding spontaneously with supportive care (PPIs, fluids) [1]. If persistent, endoscopic therapy (clips or epinephrine) is used. * **Distinction:** Do not confuse MWT with **Boerhaave Syndrome**, which is a *transmural* perforation of the esophagus (presents with Mackler’s triad: vomiting, chest pain, and subcutaneous emphysema).

Q: The amount of blood lost in the gastrointestinal tract to produce a single black stool is approximately?

60-70 ml. **Explanation:** The correct answer is **60-70 ml (Option C)**. **Medical Concept:** Melena is defined as the passage of black, tarry, foul-smelling stools. This characteristic appearance results from the degradation of hemoglobin by gastric acid and intestinal bacteria into **hematin** and other hemochromes. For melena to occur, two conditions must typically be met: 1. The blood must remain in the GI tract for at least **8 to 14 hours** to allow for degradation. 2. A minimum volume of blood must be lost. Clinical studies have shown that a single black stool can be produced with as little as **50 to 100 ml** of blood loss. Therefore, 60-70 ml is the most accurate range among the provided options. **Analysis of Options:** * **A (< 20 ml):** This volume is insufficient to cause visible melena. It may result in a positive Fecal Occult Blood Test (FOBT) but will not change the stool's color or consistency. * **B (30-40 ml):** While closer, this volume is generally below the threshold required to produce the classic "tarry" appearance of melena. * **D (100-110 ml):** While 100 ml can certainly cause melena, the question asks for the *approximate minimum* amount required to produce a single stool; 60-70 ml is the established physiological threshold. **NEET-PG High-Yield Pearls:** * **Site of Bleeding:** Melena usually indicates bleeding **proximal to the Ligament of Treitz** (Upper GI Bleed). However, bleeding from the small intestine or right colon can occasionally present as melena if transit is slow. * **Hematochezia:** Usually signifies Lower GI bleeding, but can occur in brisk Upper GI bleeds (loss of >1000 ml) due to rapid transit. * **False Melena:** Ingestion of iron supplements, bismuth (Pepto-Bismol), or charcoal can turn stools black, but they will lack the characteristic "tarry" consistency and foul odor [1].

Q: A patient presents with esophageal varices and a liver span of 19cm. What are the likely causes?

All of the above. The clinical presentation of **esophageal varices** indicates portal hypertension [1], while a **liver span of 19 cm** (normal is 12–15 cm) confirms **hepatomegaly**. In most cases of advanced cirrhosis, the liver becomes shrunken and nodular. However, certain etiologies of portal hypertension are classically associated with an enlarged liver [2]. 1. **Hemochromatosis:** Iron deposition in the hepatic parenchyma leads to both cirrhosis and significant hepatomegaly [2]. 2. **Alcoholic Liver Disease:** While late-stage alcoholic cirrhosis results in a small liver, the earlier stages of alcoholic hepatitis and fatty infiltration (steatosis) cause marked hepatomegaly alongside portal hypertension [2]. 3. **Budd-Chiari Syndrome:** This is caused by hepatic venous outflow obstruction [2]. The resulting severe congestive hepatopathy leads to a large, tender liver and rapid development of portal hypertension (varices) [3]. **Why "All of the Above" is correct:** All three conditions are high-yield causes of **"Cirrhosis with Hepatomegaly."** While cirrhosis usually implies a small liver, these specific pathologies maintain or increase liver volume despite the presence of portal hypertension [2], [3]. **NEET-PG High-Yield Pearls:** * **Causes of Cirrhosis with Hepatomegaly:** Remember the mnemonic **"HAAM"** — **H**emochromatosis, **A**lcoholic liver disease, **A**myloidosis, and **M**yeloproliferative disorders (or **M**alignancy/HCC). * **Budd-Chiari Triad:** Abdominal pain, ascites, and hepatomegaly [3]. * **Small Liver:** Classically seen in Post-necrotic cirrhosis (Viral Hepatitis B/C). * **Regenerative Nodules:** In Budd-Chiari, the caudate lobe often undergoes compensatory hypertrophy because it has independent venous drainage into the IVC [3].

Q: A 40-year-old female patient presented with dysphagia to both liquids and solids and regurgitation for 3 months. The dysphagia was non-progressive. What is the most likely diagnosis?

Achalasia cardia. ### Explanation **Correct Answer: C. Achalasia cardia** The clinical hallmark of **Achalasia cardia** is **simultaneous dysphagia to both liquids and solids** from the onset [1]. This occurs due to the failure of the Lower Esophageal Sphincter (LES) to relax and the absence of peristalsis in the distal esophagus (aperistalsis) [1]. The non-progressive nature and the presence of regurgitation in a middle-aged patient further support this diagnosis. **Analysis of Incorrect Options:** * **A. Carcinoma of the Esophagus:** Characterized by **progressive dysphagia**, initially starting with solids and later involving liquids [3]. It is typically associated with significant weight loss and occurs in older age groups. * **B. Lower Esophageal Mucosal Ring (Schatzki Ring):** Presents as **intermittent dysphagia** specifically to solids (the "steakhouse syndrome"). It does not typically cause liquid dysphagia [3]. * **D. Reflux Esophagitis with Stricture:** This is a mechanical obstruction resulting from chronic GERD. Like carcinoma, it presents with **progressive dysphagia** (solids followed by liquids) and usually has a long-standing history of heartburn [2]. **NEET-PG High-Yield Pearls:** * **Gold Standard Investigation:** Esophageal **Manometry** (shows incomplete LES relaxation and aperistalsis) [1]. * **Barium Swallow Finding:** "Bird’s beak" or "Rat-tail" appearance. * **Pathology:** Degeneration of the **Auerbach’s (myenteric) plexus** [1]. * **Treatment of Choice:** Laparoscopic Heller’s Myotomy with partial fundoplication or POEM (Peroral Endoscopic Myotomy). * **Chagas Disease:** A common secondary cause of achalasia (caused by *Trypanosoma cruzi*).

Q: Which of the following is NOT a cause of conjugated hyperbilirubinemia?

Gilbert syndrome. ### Explanation Hyperbilirubinemia is categorized into **unconjugated (indirect)** and **conjugated (direct)** based on whether the bilirubin has undergone glucuronidation in the liver [2]. **Why Gilbert Syndrome is the Correct Answer:** Gilbert syndrome is a common, benign autosomal recessive condition characterized by reduced activity of the enzyme **UDP-glucuronosyltransferase (UGT1A1)** [1]. This enzyme is responsible for conjugating bilirubin with glucuronic acid. A deficiency leads to impaired conjugation, resulting in isolated **unconjugated hyperbilirubinemia**, typically triggered by stress, fasting, or illness [1], [3]. **Analysis of Incorrect Options:** * **Dubin-Johnson Syndrome:** An autosomal recessive disorder caused by a defect in the **MRP2 gene**, which impairs the excretion of conjugated bilirubin into the bile canaliculi. This leads to conjugated hyperbilirubinemia and a characteristic **black liver** due to melanin-like pigment deposition. * **Rotor Syndrome:** Similar to Dubin-Johnson but involves defects in **OATP1B1 and OATP1B3** transporters. It results in conjugated hyperbilirubinemia without the dark liver pigmentation. * **Primary Biliary Cirrhosis (PBC):** An autoimmune destruction of intrahepatic bile ducts. This obstructive (cholestatic) process prevents the drainage of already conjugated bilirubin [2], leading to conjugated hyperbilirubinemia. **High-Yield Clinical Pearls for NEET-PG:** * **Crigler-Najjar Syndrome (Type I & II):** Also causes unconjugated hyperbilirubinemia due to UGT1A1 deficiency (Type I is total absence; Type II is severe deficiency) [1]. * **Urine Bilirubin:** Only conjugated bilirubin is water-soluble and can appear in urine (**bilirubinuria**) [3], [4]. Therefore, urine is dark in Dubin-Johnson and Rotor, but normal in Gilbert syndrome. * **Oral Cholecystography:** The gallbladder is visualized in Rotor syndrome but **not** in Dubin-Johnson syndrome.

Question 1

What is the drug of choice for an acute exacerbation of ulcerative colitis?

Accepted Answer

Steroids

Answer

Sulfasalazine

Answer

Mesalazine

Answer

NSAIDs

Question 2

Which of the following is true about Mallory-Weiss syndrome?

Accepted Answer

Commonly seen in alcoholics

Answer

Associated with gastrointestinal reflux

Answer

Associated with obesity

Answer

Associated with a tumour at the gastroesophageal junction

Question 3

A 50-year-old male executive presents to the casualty department with hematemesis. He reports vomiting all the food he had consumed prior to the hematemesis, followed by forceful retching. He had consumed alcohol the previous day. What is the most probable diagnosis?

Accepted Answer

Mallory-Weiss tear

Answer

Gastritis

Answer

Duodenal ulcer

Answer

Esophageal varices

Question 4

Gastroesophageal reflux disease (GERD) in the absence of endoscopic esophagitis is seen in which of the following conditions?

Accepted Answer

Partially treated cases with proton pump inhibitors (PPIs)

Answer

Scleroderma

Answer

Chronic renal failure (CRF)

Answer

Cirrhosis

Question 5

All of the following are true regarding carcinoid syndrome, EXCEPT:

Accepted Answer

Serotonin appears to be involved in the flushing symptoms.

Answer

Flushing associated with it affects the upper part of the body.

Answer

Tricuspid regurgitation is the most common cardiac lesion.

Answer

Midgut carcinoids account for 60-70% of cases of carcinoid syndrome.

Question 6

The amount of blood lost in the gastrointestinal tract to produce a single black stool is approximately?

Accepted Answer

60-70 ml

Answer

< 20 ml

Answer

30-40 ml

Answer

100-110 ml

Question 7

A patient presents with esophageal varices and a liver span of 19cm. What are the likely causes?

Accepted Answer

All of the above

Answer

Hemochromatosis

Answer

Alcoholic liver disease

Answer

Budd-Chiari syndrome

Question 8

Ascitic fluid with a Transudate Serum-Ascites Albumin Gradient (SAAG) and low albumin is found in which of the following conditions?

Accepted Answer

Congestive Heart Failure (CHF)

Answer

Tuberculosis

Answer

Cirrhosis

Answer

Pancreatitis

Question 9

A 40-year-old female patient presented with dysphagia to both liquids and solids and regurgitation for 3 months. The dysphagia was non-progressive. What is the most likely diagnosis?

Accepted Answer

Achalasia cardia

Answer

Carcinoma of the esophagus

Answer

Lower esophageal mucosal ring

Answer

Reflux esophagitis with esophageal stricture

Question 10

Which of the following is NOT a cause of conjugated hyperbilirubinemia?

Accepted Answer

Gilbert syndrome

Answer

Dubin-Johnson syndrome

Answer

Rotor syndrome

Answer

Primary biliary cirrhosis

Gastroenterology — MCQs

Gastroenterology — MCQs

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