Gastroenterology — MCQs

A 7-year-old girl from Bihar presented with three episodes of massive hematemesis and melena. There is no history of jaundice. On examination, she had a large spleen, non-palpable liver, and mild ascites. Portal vein was not visualized on ultrasonography. Liver function tests were normal and endoscopy revealed esophageal varices. The most likely diagnosis is –

Q1018

A decrease in which of the following is the most likely cause of peripheral edema in a patient with long-term alcoholism and liver disease?

Q1019

Which of the following is not used for diagnosing celiac disease?

Q1020

Post hepatic Portal Hypertension is caused by

Gastroenterology Indian Medical PG Practice Questions and MCQs

Question 1011: Initial treatment for management of mild to moderate Crohn's disease is:

A. Mesalamine
B. Infliximab
C. Sulfasalazine
D. Budesonide (Correct Answer)

Explanation: ***Budesonide*** - **Budesonide** is a **steroid** with high first-pass metabolism, meaning it works locally in the gastrointestinal tract with minimal systemic effects, making it suitable for mild to moderate Crohn's disease. - It is effective in inducing remission for mild to moderate ileocolonic Crohn's disease, with a better safety profile than systemic corticosteroids. *Mesalamine* - **Mesalamine (5-ASA)** is primarily used for **ulcerative colitis** and has limited efficacy in Crohn's disease, especially for moderate disease. - While it can be considered for very mild Crohn's disease, its role is often debated and not a first-line agent for moderate cases. *Infliximab* - **Infliximab** is a **biologic agent (anti-TNF-α)** used for moderate to severe Crohn's disease or for patients who have failed conventional therapy. - It works by blocking a key inflammatory cytokine and is not typically used as initial treatment for mild disease due to its potency and potential side effects. *Sulfasalazine* - **Sulfasalazine** is more effective in **colonic Crohn's disease** and **ulcerative colitis**, and its efficacy in small bowel Crohn's disease is limited [1]. - Many patients experience side effects such as **nausea**, **headaches**, and **allergic reactions**, limiting its use as a first-line agent.

Question 1012: Gold standard method of diagnosing celiac disease is

A. Blood picture
B. Small bowel biopsy (Correct Answer)
C. Anti-endomysial antibodies
D. Biochemical test

Explanation: ***Small bowel biopsy*** - A **small bowel biopsy** is considered the **gold standard** for diagnosing celiac disease as it directly visualizes the characteristic damage to the intestinal lining. - The biopsy reveals histologic changes like **villous atrophy**, crypt hyperplasia, and increased intraepithelial lymphocytes, which are pathognomonic for celiac disease [1]. *Blood picture* - A blood picture (complete blood count) might show **anemia** (often iron-deficiency anemia) due to malabsorption, but this is a non-specific finding and not diagnostic for celiac disease [1]. - It does not provide direct evidence of intestinal damage caused by gluten. *Anti-endomysial antibodies* - **Anti-endomysial antibodies (EMA)** are highly specific for celiac disease, but they are still a serological test, not the definitive diagnostic method. - Serological tests like EMA and **tissue transglutaminase (tTG) antibodies** are used for screening and monitoring but require biopsy confirmation. *Biochemical test* - Biochemical tests might show abnormalities related to **malabsorption**, such as low iron, calcium, or vitamin D levels, but these are secondary effects and not diagnostic of celiac disease itself [1]. - These tests indicate nutritional deficiencies but do not identify the underlying cause.

Question 1013: Abdominal pain, fever and jaundice. This triad is known as;

A. Renault's triad
B. Charcot's triad (Correct Answer)
C. Virchow triad
D. Saint's triad

Explanation: ***Charcot's triad*** - **Charcot's triad** consists of **abdominal pain**, **fever**, and **jaundice**, indicating **acute cholangitis** [1]. - This triad is a hallmark of **biliary tract obstruction** with concurrent infection [1]. *Renault's triad* - This is a **distractor** name; there is no recognized medical triad called "Renault's triad." - It does not describe any specific clinical presentation or set of symptoms. *Virchow triad* - **Virchow triad** describes factors that predispose to **thrombus formation**: **endothelial injury**, **stasis**, and **hypercoagulability**. - It is associated with conditions like **deep vein thrombosis (DVT)** and **pulmonary embolism**, not cholangitis. *Saint's triad* - **Saint's triad** refers to the co-occurrence of **gallstones**, **hiatal hernia**, and **diverticulosis**. - This triad describes three unrelated gastrointestinal conditions and is distinct from the symptoms of cholangitis.

Question 1014: Which of the following is a type of inflammatory bowel disease primarily affecting the small intestine? a) Coeliac disease b) Tropical sprue c) Regional ileitis d) Cystic fibrosis e) Ulcerative colitis

A. Ulcerative colitis
B. Cystic fibrosis
C. Tropical sprue
D. Regional ileitis (Correct Answer)
E. Coeliac disease

Explanation: ***Regional ileitis*** - **Regional ileitis** is another name for **Crohn's disease** when it primarily affects the **ileum**, which is part of the small intestine [1]. - Crohn's disease is a type of **inflammatory bowel disease (IBD)** [1] characterized by **transmural inflammation** that can affect any part of the gastrointestinal tract, but most commonly involves the small intestine. *Ulcerative colitis* - **Ulcerative colitis** is an **inflammatory bowel disease** that exclusively affects the **large intestine (colon and rectum)** [2]. - Unlike Crohn's disease, it involves continuous inflammation of the mucosa and submucosa, usually starting in the rectum and extending proximally [2]. *Cystic fibrosis* - **Cystic fibrosis** is a **genetic disorder** that affects the lungs, pancreas, liver, and intestine, leading to the production of **thick, sticky mucus**. - While it can cause malabsorption and intestinal issues due to pancreatic insufficiency, it is not primarily an inflammatory bowel disease in itself. *Tropical sprue* - **Tropical sprue** is a malabsorption syndrome thought to be caused by **environmental factors and microbial changes** in the small intestine, typically affecting individuals in tropical regions [3]. - It results in abnormal small intestinal architecture and nutrient malabsorption, but it is not classified as an inflammatory bowel disease like Crohn's or ulcerative colitis. *Coeliac disease* - **Coeliac disease** is an **immune-mediated condition** triggered by the ingestion of **gluten**, leading to damage of the small intestinal villi [3]. - While it affects the small intestine and involves an immune response, it is distinct from inflammatory bowel diseases which are characterized by chronic, relapsing inflammation of the GI tract.

Question 1015: The obstruction of two or more major hepatic veins is seen in:

A. Crigler-Najjar syndrome
B. Reye's syndrome
C. Budd-Chiari syndrome (Correct Answer)
D. Rotor syndrome

Explanation: ***Budd-Chiari syndrome*** - This syndrome is defined by **obstruction of hepatic venous outflow**, typically affecting two or more major hepatic veins or the inferior vena cava [2]. - The obstruction leads to **hepatic congestion**, liver enlargement, and potentially liver failure [2]. *Crigler-Najjar syndrome* - This is a rare genetic disorder characterized by a deficiency of the enzyme **uridine diphosphate glucuronosyltransferase (UGT1A1)**, leading to unconjugated hyperbilirubinemia [1]. - It primarily affects **bilirubin metabolism** and is not associated with obstruction of hepatic veins [1]. *Reye's syndrome* - Reye's syndrome is a rare but severe condition causing **fatty liver with encephalopathy**, commonly seen in children who have taken aspirin during a viral infection. - It involves **mitochondrial dysfunction** and liver damage, but not direct obstruction of hepatic veins. *Rotor syndrome* - This is a rare, benign autosomal recessive disorder characterized by **chronic, conjugated hyperbilirubinemia** due to a defect in hepatic excretion of conjugated bilirubin into bile. - It results from impaired transport of bilirubin within the liver cells and does not involve mechanical obstruction of hepatic veins.

Question 1016: All of the following are true about Crohn's disease except.

A. Cobble stone appearance
B. Perianal fistula is seen
C. Skip lesions seen
D. It is superficial inflammation involving mucosa (Correct Answer)

Explanation: ***It is superficial inflammation involving mucosa*** - Crohn's disease is characterized by **transmural inflammation**, meaning it affects all layers of the bowel wall, not just the superficial mucosa [1]. - This **full-thickness inflammation** contributes to complications like **fistulas** and **strictures** [2]. *Cobble stone appearance* - The **cobblestone appearance** on endoscopic examination is a classic finding in Crohn's disease, resulting from deep longitudinal ulcers and intervening edematous mucosa. - This is a direct consequence of the **transmural inflammation**. *Perianal fistula is seen* - **Perianal fistulas** are common manifestations of Crohn's disease, occurring due to the transmural inflammation extending into the perianal tissues [2]. - These are formed when an inflamed crypt gland ruptures into the perianal tissue, creating a tract. *Skip lesions seen* - **Skip lesions** refer to discontinuous areas of inflammation, where segments of diseased bowel are separated by healthy, uninvolved segments [1]. - This **patchy pattern** is a hallmark feature distinguishing Crohn's disease from ulcerative colitis [1].

Question 1017: A 7-year-old girl from Bihar presented with three episodes of massive hematemesis and melena. There is no history of jaundice. On examination, she had a large spleen, non-palpable liver, and mild ascites. Portal vein was not visualized on ultrasonography. Liver function tests were normal and endoscopy revealed esophageal varices. The most likely diagnosis is –

A. Chronic liver disease with portal hypertension
B. Portal hypertension of unknown etiology
C. Kala azar with portal hypertension
D. Portal hypertension due to extrahepatic obstruction (Correct Answer)

Explanation: ***Portal hypertension due to extrahepatic obstruction*** - The patient presents with **massive hematemesis and melena** due to **esophageal varices**, indicating **portal hypertension** [1]. - The **non-palpable liver**, **normal liver function tests**, and **non-visualization of the portal vein** on ultrasound strongly suggest an **extrahepatic cause** like **portal vein thrombosis**, rather than intrinsic liver disease [1]. *Portal hypertension of unknown etiology* - While portal hypertension is present, the specific findings, such as the non-visualization of the portal vein and normal LFTs, provide crucial clues that allow for a more precise diagnosis than simply "unknown etiology." - This option is too broad and does not account for the specific diagnostic indicators provided. *Chronic liver disease with portal hypertension* - **Normal liver function tests (LFTs)** and a **non-palpable liver** make chronic liver disease highly unlikely. - Patients with chronic liver disease (e.g., cirrhosis) typically present with **abnormal LFTs** and often a **palpable, nodular liver**. *Kala azar with portal hypertension* - While Kala-azar (visceral leishmaniasis) is endemic in Bihar and can cause **splenomegaly** and **portal hypertension**, it is usually associated with **fever**, **weight loss**, and **pancytopenia**, which are not mentioned. - Furthermore, the specific finding of a **non-visualized portal vein** on ultrasound points more directly to a mechanical obstruction of the portal vein itself rather than diffuse liver involvement as seen in Kala-azar.

Question 1018: A decrease in which of the following is the most likely cause of peripheral edema in a patient with long-term alcoholism and liver disease?

A. Interstitial colloid osmotic pressure
B. Interstitial hydrostatic pressure
C. Capillary hydrostatic pressure
D. Plasma colloid osmotic pressure (Correct Answer)

Explanation: ***Plasma colloid osmotic pressure*** - **Liver disease** leads to decreased synthesis of **albumin**, the primary protein responsible for maintaining **plasma colloid osmotic pressure** [2]. - A reduction in this pressure allows fluid to extravasate from the capillaries into the interstitial space, causing **edema** [1], [3]. *Interstitial colloid osmotic pressure* - An increase, rather than a decrease, in interstitial colloid osmotic pressure would pull more fluid into the interstitial space, contributing to edema. - However, in liver disease with reduced albumin production, the primary issue is reduced plasma, not interstitial, colloid osmotic pressure [4]. *Interstitial hydrostatic pressure* - An increase in interstitial hydrostatic pressure would tend to drive fluid back into the capillaries, thus *reducing* edema. - A decrease would allow more fluid to accumulate in the interstitium, but this is not the primary mechanism in liver disease-related edema. *Capillary hydrostatic pressure* - An increase in **capillary hydrostatic pressure** can cause edema (e.g., in heart failure) [1]. - While liver disease can lead to conditions like **portal hypertension** (an increase in pressure within the portal venous system), this primarily causes ascites and not directly peripheral edema, which is more directly linked to decreased plasma colloid osmotic pressure [4].

Question 1019: Which of the following is not used for diagnosing celiac disease?

A. Anti-endomysial antibody
B. Anti-gliadin antibody
C. Anti-tissue transglutaminase antibody
D. Anti-nuclear antibody (Correct Answer)

Explanation: ***Anti-nuclear antibody*** - **Anti-nuclear antibodies (ANAs)** are primarily associated with **systemic autoimmune diseases** like systemic lupus erythematosus (SLE), not celiac disease. - While a patient with celiac disease might coincidentally have a positive ANA, it is not a diagnostic marker for **celiac disease** itself. *Anti-endomysial antibody* - **Anti-endomysial antibodies (EMA)** are highly specific and sensitive for **celiac disease**, especially in IgA-sufficient individuals. - They target the same antigen as anti-tissue transglutaminase antibodies. *Anti-gliadin antibody* - **Anti-gliadin antibodies (AGA)** were historically used for celiac diagnosis but are less specific and sensitive than other serological markers. - Their use has largely been replaced by **anti-tissue transglutaminase (tTG)** and **anti-endomysial antibodies (EMA)**. *Anti-tissue transglutaminase antibody* - **Anti-tissue transglutaminase (tTG) IgA antibodies** are the **primary screening test** recommended for celiac disease due to their high sensitivity and specificity. - A positive result often leads to endoscopic biopsy for confirmation.

Question 1020: Post hepatic Portal Hypertension is caused by

A. Portal vein thrombosis
B. Budd-Chiari syndrome (Correct Answer)
C. Veno occlusive disease
D. Congenital hepatic fibrosis
E. Chronic hepatic venous congestion
F. Right heart failure

Explanation: ***Budd-Chiari syndrome*** - This syndrome involves **hepatic vein obstruction**, leading to **outflow blockade** from the liver, causing blood to back up into the sinusoids and portal system. - The obstruction occurs **distal to the hepatic sinusoids** but **proximal to the inferior vena cava**, classifying it as a post-hepatic cause of portal hypertension. *Portal vein thrombosis* - This condition involves a **clot in the portal vein**, which is located **before the liver sinusoids**. - It consequently causes **pre-hepatic portal hypertension**, as the blockage occurs upstream from the liver itself. [1] *Veno occlusive disease* - This condition affects the **small intrahepatic venules**, often caused by **toxins or chemotherapy**. [2] - It is considered a **sinusoidal** or **intrahepatic cause** of portal hypertension, not a post-hepatic cause affecting the main hepatic veins. [2] *Congenital hepatic fibrosis* - This is a developmental disorder characterized by **malformed portal tracts** and **fibrosis** within the liver. - It causes **intrahepatic portal hypertension** due to increased resistance to blood flow within the liver parenchyma. *Chronic hepatic venous congestion* - This refers to a general state of sustained high pressure in the hepatic veins, often due to **systemic causes**. - While it reflects impaired outflow, Budd-Chiari syndrome is the specific, acute or chronic **obstruction of the hepatic veins** themselves, making it a more precise and direct cause of post-hepatic portal hypertension. *Right heart failure* - **Right heart failure** causes systemic venous congestion, leading to increased pressure in the **inferior vena cava (IVC)** and, subsequently, the hepatic veins. [2] - This is an **extrinsic cause** of increased pressure transmitted to the hepatic veins, but the primary pathology lies within the heart, rather than an intrinsic obstruction of the hepatic veins as seen in Budd-Chiari syndrome. [2]

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)

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Gastrointestinal Bleeding

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Liver Diseases and Cirrhosis

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Viral Hepatitis

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Biliary Tract Disorders

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Gastrointestinal Motility Disorders

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Gastrointestinal Malignancies

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