Gastroenterology — MCQs

A 25-year-old male presents with mild jaundice noticed during a recent febrile illness. He gives a history of similar episodes in the past following any illness or periods of fasting. Physical examination reveals mild icterus with no hepatosplenomegaly. Lab values are given below: Serum bilirubin: 2.4 mg/dL Unconjugated bilirubin: 2.1 mg/dL Conjugated bilirubin: 0.3 mg/dL Serum AST and ALT: Normal What is the most likely diagnosis?

Q950

A 20-year-old male presented with yellowish discoloration of his skin and sclera. He is otherwise normal. He gives a history of viral infection 10 days ago, which was resolved 2 days back. He also gives a history of similar episodes in the past following any illness. Lab values are given below. What is the most likely diagnosis? Serum bilirubin: 2.4 mg/dL Unconjugated bilirubin: 2.1mg/dL Conjugated bilirubin: 0.3mg/dL Serum AST and ALT: Normal

Gastroenterology Indian Medical PG Practice Questions and MCQs

Question 941: Which of the following is a recommended treatment for esophageal varices?

A. Transjugular intrahepatic portosystemic shunt (TIPS)
B. Endoscopic ligation (Correct Answer)
C. Intravenous labetalol
D. Oral amoxicillin

Explanation: ***Endoscopic ligation*** - This is a first-line endoscopic therapy for both actively bleeding esophageal varices and for the primary and secondary prevention of variceal hemorrhage [1]. - The procedure, also known as **variceal banding**, involves placing small rubber bands around the varices to ligate them, leading to thrombosis and eventual sloughing off [1]. *Transjugular intrahepatic portosystemic shunt (TIPS)* - TIPS is considered a second-line or salvage therapy for variceal bleeding that is refractory to endoscopic and pharmacological treatments [2]. - It is an invasive procedure that creates a shunt to reduce **portal pressure**, but it is reserved for uncontrolled bleeding due to risks such as **hepatic encephalopathy** [2]. *Intravenous labetalol* - While non-selective beta-blockers like **propranolol** or **nadolol** are used for the prophylaxis of variceal bleeding, they are not the treatment for an acute bleed. Vasoactive drugs like **terlipressin** or **octreotide** are used instead [1]. - Labetalol is a beta-blocker primarily used to manage **hypertension** and is not indicated for the acute management of variceal hemorrhage. *Oral amoxicillin* - Antibiotic prophylaxis (typically with intravenous third-generation cephalosporins like **ceftriaxone**) is recommended in patients with cirrhosis and variceal bleeding to prevent **spontaneous bacterial peritonitis (SBP)**. - Antibiotics do not treat the varices directly or stop the bleeding; they are given to reduce mortality associated with infections in this patient population.

Question 942: Which classification is used for Barrett esophagus?

A. Prague classification (Correct Answer)
B. Johnson classification
C. Forrest classification
D. Savary-Miller classification

Explanation: ***Prague classification***- This classification is specifically designed for the standardized endoscopic assessment and documentation of **Barrett esophagus** (BE).- It uses two main parameters: the maximal extent (M) and the circumferential extent (C) of the columnar-lined esophagus, ensuring consistent reporting for surveillance.*Savary-Miller classification*- This classification system is used to grade the severity of **reflux esophagitis** (erosive esophagitis), not Barrett esophagus.- It categorizes esophageal mucosal injury based on the extent and depth of erosions.*Johnson classification*- This classification is generally not a recognized standard system for classifying key GI pathology like Barrett esophagus, unlike established systems such as the **Prague classification** or **Los Angeles classification** for reflux esophagitis.- *Note: A Johnson classification exists for pediatric hip dysplasia, but it is unrelated to GI endoscopy.* *Forrest classification*- This system is used exclusively to classify the appearance of **peptic ulcer bleeding** (or other upper GI bleed sources) seen during endoscopy.- It helps predict the risk of rebleeding and guides interventions, such as those performed for ulcers with adherent clots or active oozing.

Question 943: A young male patient has the following serological status: HbsAg positive, IgM anti Hbc negative, IgG Anti-Hbc positive and HBeAg positive. Select the best treatment for this patient?

A. Ritonavir
B. Ombitasvir
C. Lamivudine (Correct Answer)
D. Abacavir

Explanation: Lamivudine - This serological profile (HBsAg+, IgM anti-HBc-, IgG anti-HBc+, HBeAg+) indicates HBeAg-positive chronic Hepatitis B with active viral replication [1] - Among the given options, Lamivudine is the only agent with anti-HBV activity as a nucleoside reverse transcriptase inhibitor (NRTI) that inhibits HBV DNA polymerase - Important Note: While Lamivudine was historically used for chronic HBV, current guidelines (WHO, AASLD, EASL) recommend Tenofovir or Entecavir as first-line therapy due to higher potency and lower resistance rates [2] - Lamivudine is now considered second-line due to high resistance rates (up to 70% after 5 years) Incorrect Option: Ombitasvir - Ombitasvir is an NS5A inhibitor used exclusively for Hepatitis C (HCV) treatment in combination regimens - Has no activity against HBV and is inappropriate for this patient Incorrect Option: Ritonavir - Ritonavir is an HIV protease inhibitor used primarily as a pharmacokinetic booster in antiretroviral therapy - Has no direct anti-HBV activity and is not used for HBV treatment Incorrect Option: Abacavir - Abacavir is an NRTI used for HIV treatment as part of combination ART - Despite being an NRTI class drug, it lacks significant anti-HBV activity and is not approved or effective for chronic Hepatitis B management

Question 944: A young female has episodes of binge eating followed by self-induced vomiting. Which of the following acid- base disturbance is she likely to have?

A. Respiratory acidosis
B. Metabolic acidosis
C. Respiratory alkalosis
D. Metabolic alkalosis (Correct Answer)

Explanation: ***Metabolic alkalosis***- Self-induced vomiting results in the significant loss of **gastric hydrochloric acid (HCl)**, leading to a net gain of bicarbonate (HCO3-) in the blood, causing metabolic alkalosis [1, 2].- This condition is often exacerbated by **volume depletion** (due to fluid loss), leading to a state known as "**contraction alkalosis**," where the kidneys attempt to conserve volume even at the expense of excreting bicarbonate [1].*Respiratory acidosis*- This condition is characterized by **hypoventilation** leading to the retention of **carbon dioxide (CO2)** and an increase in carbonic acid, lowering the pH [2].- It is typically seen in conditions compromising respiratory drive or function, such as COPD exacerbations, narcotic overdose, or severe pneumonia.*Respiratory alkalosis*- This disturbance is caused by **hyperventilation**, which results in excessive loss of **carbon dioxide (CO2)**, leading to low PCO2 and elevated pH [3].- While anxiety may be a component of eating disorders, the primary physiologic effect of vomiting is related to acid loss, not sustained hyperventilation causing respiratory alkalosis.*Metabolic acidosis*- This is caused by either the **addition of fixed acids** (e.g., lactic acidosis, diabetic ketoacidosis) or the **loss of bicarbonate** (e.g., severe diarrhea or renal tubular dysfunction) [2].- Vomiting directly causes loss of acid, which is the opposite mechanism needed to induce metabolic acidosis [2].

Question 945: A patient presented to the OPD with liver damage. The picture depicts the patient having their eyes examined. Which of the following substances is responsible for this condition?

A. Glucose
B. Galactose
C. Mannose
D. Copper (Correct Answer)

Explanation: ***Copper*** - The image displays a **Kayser-Fleischer ring**, a greenish-gold ring at the corneal limbus, which is a hallmark sign of **Wilson's disease**. This condition, combined with liver damage, points to an issue with copper metabolism. - Wilson's disease is an autosomal recessive disorder caused by a mutation in the **ATP7B gene**, leading to impaired biliary excretion and subsequent toxic accumulation of **copper** in the liver, brain, and cornea. *Glucose* - Elevated **glucose** levels, as seen in diabetes mellitus, can cause ocular complications such as **diabetic retinopathy** and **cataracts**, but not Kayser-Fleischer rings. - While diabetes can be associated with liver disease (e.g., **NAFLD**), the combination of this specific eye finding and liver damage is not characteristic of glucose-related pathology. *Galactose* - Excess **galactose** is characteristic of **galactosemia**, an inherited metabolic disorder that can cause liver failure and cirrhosis, similar to Wilson's disease. - However, the classic ocular finding in galactosemia is the formation of **"oil-droplet" cataracts**, not the Kayser-Fleischer rings shown in the image. *Mannose* - Disorders of **mannose** metabolism are typically classified as **congenital disorders of glycosylation (CDGs)**. - These rare genetic disorders present with a wide spectrum of multi-systemic symptoms, including neurological and developmental issues, but are not associated with the development of Kayser-Fleischer rings.

Question 946: A chronic alcoholic presents to the emergency room with acute abdominal pain in the epigastric region radiating to the back with nausea, anorexia, and occasional vomiting. Investigations showed elevated amylase levels and total count. Likely diagnosis is

A. a.Acute hepatitis
B. b.Acute pancreatitis (Correct Answer)
C. d.Acute appendicitis
D. c.Acute Cholecystitis

Explanation: ***Acute pancreatitis*** (Keep the correct option at the top and the incorrect options in the order they are provided in the input) - The clinical presentation of severe **epigastric pain radiating to the back**, associated with nausea and vomiting, is classic for **acute pancreatitis** [1]. - **Alcohol abuse** is a major risk factor, and the diagnosis is supported by findings of significantly elevated serum **amylase and/or lipase** levels [1]. *Acute hepatitis* - Typically presents with **jaundice**, fatigue, dark urine, and right upper quadrant discomfort, not the referred back pain seen here. - Key laboratory findings would include severely elevated **liver transaminases (AST/ALT)**, not primarily amylase. *Acute Cholecystitis* - Characterized by acute pain in the **right upper quadrant** or epigastrium, often radiating to the **right shoulder or scapula**, not the back [2]. - This condition is usually associated with gallstones and is diagnosed via imaging showing gallbladder wall thickening and pericholecystic fluid, though amylase can be mildly elevated secondarily. *Acute appendicitis* - Presents typically with periumbilical pain that migrates to the **right lower quadrant (RLQ)**, often associated with low-grade fever and localized tenderness. - The pain is not classically described as severe epigastric pain radiating to the back, and initial lab markers include leukocytosis but not specific elevation of amylase.

Question 947: Which of the following is not a component of Child-Pugh scoring?

A. LFT (Correct Answer)
B. Albumin
C. Bilirubin
D. Prothrombin Time

Explanation: ***LFT (Correct Answer)*** - **LFT (Liver Function Tests)** is a general term encompassing various biochemical tests such as AST, ALT, ALP, and GGT [1], [2] - These specific liver enzymes are **not components** of the Child-Pugh scoring system - The Child-Pugh score specifically uses only **5 parameters**: Albumin, Bilirubin, Prothrombin Time/INR, Ascites, and Hepatic Encephalopathy - These five components assess both **synthetic function** (albumin, PT/INR) and **clinical manifestations** (ascites, encephalopathy) of chronic liver disease [3] *Albumin (Incorrect)* - Serum **albumin** is one of the five specific components of the Child-Pugh score - It reflects the liver's **synthetic function** capacity - Scoring: >3.5 g/dL (1 point), 2.8-3.5 g/dL (2 points), <2.8 g/dL (3 points) - Lower albumin levels indicate more severe hepatic dysfunction and portal hypertension *Bilirubin (Incorrect)* - Total **bilirubin** is a core component used to assess the liver's **excretory and conjugating capacity** - Scoring: <2 mg/dL (1 point), 2-3 mg/dL (2 points), >3 mg/dL (3 points) - Elevated bilirubin indicates impaired hepatic clearance and correlates with severity of liver disease *Prothrombin Time (Incorrect)* - **Prothrombin Time (PT)** or **INR** measures the liver's ability to synthesize clotting factors [3] - It is a critical component reflecting hepatic **synthetic function** - Scoring: <4 sec prolonged or INR <1.7 (1 point), 4-6 sec or INR 1.7-2.3 (2 points), >6 sec or INR >2.3 (3 points) [4] - Prolonged PT/elevated INR indicates severely impaired synthesis of vitamin K-dependent clotting factors [3]

Question 948: Which of the following is a sensitive and specific marker of intestinal inflammation?

A. Procalcitonin
B. Fecal lactoferrin (Correct Answer)
C. High-sensitivity C-reactive protein
D. Tissue transglutaminase IgA

Explanation: ***Fecal lactoferrin***- This is an excellent proxy marker for active intestinal inflammation because **lactoferrin** is a highly concentrated protein released by **activated neutrophils** migrating into the gut lumen [1].- Elevated fecal levels often correlate well with endoscopic and histological evidence of mucosal inflammation [2], making it a sensitive and specific non-invasive test for conditions like **Inflammatory Bowel Disease (IBD)**.*Procalcitonin*- Primarily serves as a highly specific marker for diagnosing and monitoring **sepsis** and severe **systemic bacterial infection**.- It generally reflects systemic inflammatory responses and is not specific for inflammation localized to the **intestinal mucosa**.*Tissue transglutaminase IgA*- This is an autoantibody primarily used for screening and diagnosing **Celiac disease**, an autoimmune condition triggered by **gluten**.- It indicates underlying autoimmunity causing villous atrophy but is not used as a general marker of acute or chronic **intestinal inflammation** (like IBD).*High-sensitivity C-reactive protein*- It is a widely used, but **non-specific**, acute-phase reactant indicating **systemic inflammation** originating from any part of the body [1].- While elevated in IBD, its sensitivity and specificity for identifying isolated or localized intestinal inflammation are inferior to non-invasive **fecal markers** like lactoferrin or calprotectin.

Question 949: A 25-year-old male presents with mild jaundice noticed during a recent febrile illness. He gives a history of similar episodes in the past following any illness or periods of fasting. Physical examination reveals mild icterus with no hepatosplenomegaly. Lab values are given below: Serum bilirubin: 2.4 mg/dL Unconjugated bilirubin: 2.1 mg/dL Conjugated bilirubin: 0.3 mg/dL Serum AST and ALT: Normal What is the most likely diagnosis?

A. Dubin-Johnson syndrome
B. Gilbert syndrome (Correct Answer)
C. Rotor syndrome
D. Criggler-Najar type 1 syndrome

Explanation: ***Gilbert syndrome*** - It is characterized by isolated, mild, intermittent **unconjugated hyperbilirubinemia** (total bilirubin <4 mg/dL), often triggered by stress, fasting, illness, or dehydration, matching the patient's history of episodes following illness [1]. - The underlying cause is reduced activity (typically 30%) of the enzyme **uridine diphosphoglucuronate glucuronosyltransferase (UGT1A1)**, necessary for conjugating bilirubin, but liver function (AST/ALT) remains normal [1], [3]. *Dubin-Johnson syndrome* - This is characterized by **conjugated (direct) hyperbilirubinemia** due to defective excretion of bilirubin into the bile canaliculi, contrasting with the predominantly unconjugated pattern seen here [2]. - The liver tissue typically shows **black pigmentation** due to epinephrine metabolite accumulation, which is a key pathological feature. *Criggler-Najar type 1 syndrome* - This syndrome involves a severe or complete absence of the **UGT1A1 enzyme**, leading to very high levels of **unconjugated bilirubin** (often >20 mg/dL) that cause **kernicterus** and usually death in infancy, which is not consistent with a history of recurrent mild episodes in an adult [1]. - It requires lifelong treatment, typically with **phototherapy** and **liver transplantation**, due to the severe defect [1]. *Rotor syndrome* - Similar to Dubin-Johnson syndrome, Rotor syndrome also causes **conjugated (direct) hyperbilirubinemia** due to impaired hepatic storage and excretion of conjugated bilirubin, which contradicts the laboratory findings of mostly unconjugated bilirubin.

Question 950: A 20-year-old male presented with yellowish discoloration of his skin and sclera. He is otherwise normal. He gives a history of viral infection 10 days ago, which was resolved 2 days back. He also gives a history of similar episodes in the past following any illness. Lab values are given below. What is the most likely diagnosis? Serum bilirubin: 2.4 mg/dL Unconjugated bilirubin: 2.1mg/dL Conjugated bilirubin: 0.3mg/dL Serum AST and ALT: Normal

A. Criggler-Najar type 1 syndrome
B. Gilbert syndrome (Correct Answer)
C. Rotor syndrome
D. Dubin-Johnson syndrome

Explanation: ***Gilbert syndrome*** - This condition is characterized by **unconjugated hyperbilirubinemia** (as seen by 2.1 mg/dL unconjugated vs. 0.3 mg/dL conjugated) that is mild, typically <3 mg/dL, and intermittent. [1] The history of similar episodes following **stress**, **vigorous exercise**, or **illness** (like the recent viral infection) is a classic trigger for this condition, which is caused by reduced activity of the **UGT1A1 enzyme**. [1] *Dubin-Johnson syndrome* - This syndrome results in **conjugated (direct) hyperbilirubinemia** due to defective excretion of conjugated bilirubin (MRP2 transporter defect). *Criggler-Najar type 1 syndrome* - This is a severe congenital deficiency of the **UGT1A1 enzyme**, leading to markedly and persistently elevated **unconjugated bilirubin** (often >20 mg/dL) and usually resulting in **kernicterus** and death in infancy. [1] The patient presents later in life (20 years old) with only mild, fluctuating unconjugated hyperbilirubinemia, ruling out Type 1 severity. *Rotor syndrome* - Similar to Dubin-Johnson, Rotor syndrome causes **conjugated (direct) hyperbilirubinemia** due to hepatocyte storage and transport defects, which contradicts the patient's lab findings of predominantly unconjugated bilirubin. Unlike Dubin-Johnson, Rotor syndrome does **not** cause black pigmentation of the liver.

Practice by Chapter

Esophageal Disorders

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Peptic Ulcer Disease

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Inflammatory Bowel Disease

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Irritable Bowel Syndrome

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Malabsorption Syndromes

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Pancreatitis (Acute and Chronic)

Practice Questions

Gastrointestinal Bleeding

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Liver Diseases and Cirrhosis

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Viral Hepatitis

Practice Questions

Biliary Tract Disorders

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Gastrointestinal Motility Disorders

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Gastrointestinal Malignancies

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