Gastroenterology Practice Questions

Q: Which statement is false regarding Crohn's disease?

No recurrence after surgery. The correct answer is **A (No recurrence after surgery)** because this statement is false. Unlike Ulcerative Colitis (UC), which is limited to the colon and can be "cured" by a total proctocolectomy [1], **Crohn’s Disease (CD)** is a chronic, transmural inflammatory condition that can affect any part of the gastrointestinal tract from the mouth to the anus [2]. Surgery in CD is reserved for complications (e.g., strictures, fistulae, or perforation) and is **not curative**. Post-surgical recurrence at the site of anastomosis is extremely common. **Analysis of other options:** * **B. Aphthous ulcers:** These are the earliest macroscopic signs of Crohn’s disease. They often coalesce to form deep, linear "rake-like" ulcers, contributing to the characteristic "cobblestone" appearance. * **C. Skip lesions:** CD is characterized by discontinuous involvement of the bowel, where areas of active disease are separated by segments of normal-appearing mucosa (skip lesions) [2]. * **D. Fistula formation:** Because CD involves **transmural inflammation** (affecting all layers of the bowel wall), it frequently leads to penetrating complications such as sinus tracts, abscesses, and fistulae (entero-enteric, entero-vesical, or perianal). **High-Yield Clinical Pearls for NEET-PG:** * **Most common site:** Terminal ileum (Ileocolic region). * **Microscopy:** Non-caseating granulomas (pathognomonic but seen in only ~50% of cases). * **Smoking:** A major risk factor that worsens CD (conversely, it appears "protective" in UC). * **Serology:** ASCA (Anti-Saccharomyces cerevisiae antibodies) is positive in CD, whereas p-ANCA is associated with UC. * **Radiology:** "String sign of Kantor" (due to terminal ileum stricture).

Q: What is the most common cause of gastric varices?

Cirrhosis. **Explanation:** **1. Why Cirrhosis is the Correct Answer:** While gastric varices are often associated with splenic vein thrombosis, **Cirrhosis** is the most common cause overall [1]. In cirrhosis, portal hypertension (defined as a portal venous pressure gradient >5 mmHg) leads to the development of collateral circulation to bypass the liver [1]. These collaterals manifest as esophageal and gastric varices [1]. Gastric varices occur in approximately 20% of patients with cirrhosis, usually as an extension of esophageal varices (Gastro-esophageal varices or GOV). **2. Analysis of Incorrect Options:** * **Splenic Vein Thrombosis (SVT):** This is the most common cause of **isolated** gastric varices (IGV). It leads to "left-sided" or "sinusoidal" portal hypertension. While a classic textbook association, it is statistically less frequent than cirrhosis in the general population. * **Splenectomy:** This is actually a *treatment* for isolated gastric varices caused by splenic vein thrombosis, not a cause of varices. * **Mesenteric Thrombosis:** This typically leads to bowel ischemia or congestion but does not primarily manifest as gastric varices. **3. NEET-PG High-Yield Pearls:** * **Classification:** Gastric varices are classified by the **Sarin Classification**. GOV1 (extension along the lesser curvature) is the most common type. * **Management:** For acute bleeding from gastric varices, **Endoscopic Cyanoacrylate injection** (glue) is the treatment of choice, unlike esophageal varices where band ligation is preferred [1]. * **Isolated Gastric Varices (IGV):** If you see varices in the fundus *without* esophageal varices, always suspect **Splenic Vein Thrombosis** (often secondary to chronic pancreatitis).

Q: What is the first sign of non-cirrhotic portal fibrosis?

Upper GI bleeding. **Non-Cirrhotic Portal Fibrosis (NCPF)**, also known as Idiopathic Portal Hypertension (IPH), is a clinical syndrome characterized by portal hypertension in the absence of cirrhosis, extrahepatic portal vein obstruction, or Budd-Chiari syndrome [1]. **Why Upper GI Bleeding is the first sign:** In NCPF, the primary pathology involves obliterative venopathy of the small portal vein branches, leading to increased portal pressure. Unlike cirrhosis, **liver synthetic function remains preserved** for a long time. Therefore, the disease remains asymptomatic until the portal hypertension becomes severe enough to cause esophageal varices [1]. **Upper GI bleeding (hematemesis)** is typically the first clinical presentation in over 70-80% of cases. **Why other options are incorrect:** * **Splenomegaly (Option C):** While splenomegaly is almost always present at the time of diagnosis, it is usually an incidental finding or discovered during the evaluation of the initial bleed. Patients rarely seek medical attention for an enlarged spleen alone. * **Ascites (Option B):** Ascites is rare in NCPF because hepatic synthetic function (albumin production) is maintained [1]. If it occurs, it is usually transient and follows a massive variceal bleed. * **Jaundice (Option D):** Jaundice is a sign of hepatocellular failure. Since the liver parenchyma is healthy in NCPF, jaundice is not a feature of this condition. **NEET-PG High-Yield Pearls:** * **Classic Triad:** Massive splenomegaly, preserved liver function, and variceal bleeding. * **Histology:** Shows "obliterative portal venopathy" and portal fibrosis, but **no nodules** (distinguishing it from cirrhosis). * **Prognosis:** Much better than cirrhosis because the liver is "bystander" to the vascular pathology. * **Common Association:** Chronic exposure to arsenic or recurrent umbilical sepsis in neonates.

Q: Which type of ulcer is commonly associated with burns and hematemesis?

Curling ulcer. **Explanation:** **Curling Ulcers** are acute gastric erosion/ulcers that occur as a complication of **severe burns**. The underlying pathophysiology involves systemic hypovolemia and hypotension following a major burn, which leads to reduced mucosal blood flow (ischemia). This ischemia compromises the protective mucosal barrier, allowing gastric acid to cause acute ulceration, often presenting with **hematemesis** (coffee-ground emesis) or melena. **Analysis of Options:** * **Curling Ulcer (Correct):** Classically associated with burns. *Mnemonic: "Curling" sounds like "Curling iron," which causes burns.* * **Cushing Ulcer (Incorrect):** These are stress ulcers associated with **increased intracranial pressure** (e.g., tumors, trauma, or surgery). They are caused by overstimulation of the vagus nerve, leading to excessive gastric acid secretion. *Mnemonic: "Cushing" is for "Cushioning the brain."* * **Malignant Ulcer (Incorrect):** These are cancerous lesions (e.g., Gastric Adenocarcinoma) characterized by heaped-up, irregular margins. They are not acutely triggered by burns. * **Intracranial Tumor (Incorrect):** This is a clinical condition that leads to a Cushing ulcer, not the name of the ulcer itself. **High-Yield NEET-PG Pearls:** 1. **Location:** Curling ulcers are most commonly found in the **fundus and body** of the stomach, but can occur in the duodenum. 2. **Prophylaxis:** In clinical practice, patients with severe burns or ICU stress are started on **Proton Pump Inhibitors (PPIs)** or H2 blockers to prevent these stress-induced ulcers. 3. **Cameron Ulcers:** These are linear erosions found in a large hiatal hernia (another common PG exam distractor).

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

Rotor syndrome. ### Explanation The correct answer is **Rotor syndrome**. To answer this question, one must distinguish between pre-hepatic, hepatic, and post-hepatic causes of jaundice based on the type of bilirubin that accumulates [2]. **1. Why Rotor Syndrome is the Correct Answer:** Rotor syndrome is an autosomal recessive condition characterized by **conjugated hyperbilirubinemia**. It results from a defect in the hepatic storage capacity of bilirubin and a deficiency in the organic anion transporting polypeptides (OATP1B1 and OATP1B3), which are responsible for the re-uptake of conjugated bilirubin into hepatocytes. Unlike unconjugated causes, the liver successfully conjugates the bilirubin, but it leaks back into the blood [3]. **2. Analysis of Incorrect Options (Causes of Unconjugated Hyperbilirubinemia):** * **Hemolytic Anemia:** Excessive breakdown of RBCs leads to an overproduction of heme, overwhelming the liver's conjugation capacity [2], [3]. * **Large Hematoma:** As a large collection of blood resolves, the breakdown of hemoglobin releases massive amounts of unconjugated bilirubin into the circulation. * **Megaloblastic Anemia:** This causes **ineffective erythropoiesis**, where RBC precursors are destroyed within the bone marrow (intramedullary hemolysis), releasing unconjugated bilirubin. **3. High-Yield Clinical Pearls for NEET-PG:** * **Unconjugated Hyperbilirubinemia:** Think of Overproduction (Hemolysis), Impaired Uptake (Drugs like Rifampicin), or Impaired Conjugation (Gilbert’s and Crigler-Najjar syndromes) [1], [3]. * **Conjugated Hyperbilirubinemia:** Think of Dubin-Johnson and Rotor syndromes (asymptomatic) or Biliary Obstruction [3], [4]. * **Differentiating Dubin-Johnson vs. Rotor:** * **Dubin-Johnson:** Black liver (melanin-like pigment), normal total urinary coproporphyrin but >80% is Coproporphyrin I. * **Rotor:** Normal color liver, high total urinary coproporphyrin (<80% is Coproporphyrin I).

Q: What is the usual maximum dose of furosemide and spironolactone in patients with cirrhosis and portal hypertension?

Furosemide 160 mg and spironolactone 400 mg. In patients with cirrhosis and portal hypertension, ascites develops due to secondary hyperaldosteronism and sodium retention. The standard medical management involves a combination of **Spironolactone** (an aldosterone antagonist) and **Furosemide** (a loop diuretic). **1. Why Option A is Correct:** The goal of therapy is to maintain a **100:40 ratio** of Spironolactone to Furosemide. This specific ratio is clinically proven to maintain normokalemia by balancing the potassium-sparing effect of spironolactone with the potassium-wasting effect of furosemide. * **Starting Dose:** 100 mg Spironolactone and 40 mg Furosemide. * **Maximum Dose:** The doses are titrated every 3–5 days if weight loss is inadequate, up to a maximum of **400 mg Spironolactone and 160 mg Furosemide**. **2. Why Other Options are Incorrect:** * **Options B & C:** These violate the established 100:40 ratio. Using disproportionate doses increases the risk of electrolyte imbalances (hyperkalemia if spironolactone is too high, or hypokalemia if furosemide is too high). * **Option D:** While 200 mg/80 mg is a common intermediate step in titration, it is not the "maximum" dose defined by clinical guidelines (AASLD/EASL). **Clinical Pearls for NEET-PG:** * **Weight Loss Goal:** Aim for 0.5 kg/day in patients without edema and 1.0 kg/day in those with peripheral edema. * **Side Effect:** Gynecomastia is a common side effect of spironolactone; if it occurs, it can be switched to **Amiloride**. * **Refractory Ascites:** Defined when ascites cannot be mobilized despite the maximum doses (400mg/160mg) or when diuretic-induced complications (e.g., encephalopathy, creatinine >2.0 mg/dL) occur. Note: Although references discuss portal hypertension and sodium retention [1][2], they do not explicitly define the 400mg/160mg dosage maximum in the provided snippets.

Question 1

Which of the following management procedures of acute upper gastrointestinal bleed should possibly be avoided?

Accepted Answer

Intravenous vasopressin

Answer

Intravenous b-blockers

Answer

Endoscopic sclerotherapy

Answer

Balloon tamponade

Question 2

Which statement is false regarding Crohn's disease?

Accepted Answer

No recurrence after surgery

Answer

Aphthous ulcer

Answer

Skip lesions

Answer

Fistula formation

Question 3

Which of the following statements are true about Budd-Chiari syndrome?

Accepted Answer

Ascites may be present and hepatic vein thrombosis is associated

Answer

Cirrhosis may occur and ascites may be present

Answer

Hepatic vein thrombosis is associated and good prognosis

Question 4

What is the investigation of choice in upper GI bleeding?

Accepted Answer

Endoscopy

Answer

Barium swallow

Answer

X-ray

Answer

Ultrasound

Question 5

What is the most common cause of gastric varices?

Accepted Answer

Cirrhosis

Answer

Splenic vein thrombosis

Answer

Splenectomy

Answer

Mesenteric thrombosis

Question 6

A 22-year-old woman presents with a 3-day history of dark urine and abdominal distension. On examination, she is alert with icterus and normal heart and lung sounds. Laboratory findings include: Hematocrit: 26%, Reticulocytes: 5%, Platelets: 1.3 lakhs, Alkaline Phosphatase: 30 units/L, ALT: 110 units/L, AST: 220 units/L, Total Bilirubin: 13 mg% (Direct: 4 mg). HBsAg is positive, while Hepatitis A and C are negative. Urine drug screen is negative. Abdominal ultrasound shows a nodular liver and an enlarged spleen. What is the most likely diagnosis?

Accepted Answer

Wilson disease

Answer

Acetaminophen intoxication

Answer

Acute viral hepatitis

Answer

Primary biliary cirrhosis

Question 7

What is the first sign of non-cirrhotic portal fibrosis?

Accepted Answer

Upper GI bleeding

Answer

Ascites

Answer

Splenomegaly

Answer

Jaundice

Question 8

Which type of ulcer is commonly associated with burns and hematemesis?

Accepted Answer

Curling ulcer

Answer

Cushing ulcer

Answer

Malignant ulcer

Answer

Intracranial tumor

Question 9

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

Accepted Answer

Rotor syndrome

Answer

Hemolytic anemia

Answer

Large hematoma

Answer

Megaloblastic anemia

Question 10

What is the usual maximum dose of furosemide and spironolactone in patients with cirrhosis and portal hypertension?

Accepted Answer

Furosemide 160 mg and spironolactone 400 mg

Answer

Furosemide 80 mg and spironolactone 400 mg

Answer

Furosemide 160 mg and spironolactone 200 mg

Answer

Furosemide 80 mg and spironolactone 200 mg

Gastroenterology — MCQs

Gastroenterology — MCQs

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