Gastroenterology — MCQs

Gastroenterology Indian Medical PG Practice Questions and MCQs

Question 1021: 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]

Question 1022: Which of the following is the right choice of treatment for portosystemic encephalopathy?

A. Diuretics
B. Emergency portosystemic shunt surgery
C. Lactulose (Correct Answer)
D. High protein diet

Explanation: ***Lactulose*** - **Lactulose** is a non-absorbable disaccharide that is metabolized by gut bacteria, producing a laxative effect and acidifying the colon. - This acidification traps **ammonia** (a neurotoxin) in its ionized form (NH4+), preventing its absorption and facilitating its excretion in feces, thereby reducing systemic ammonia levels [1]. *Diuretics* - **Diuretics** are primarily used to manage fluid overload, ascites, and edema in liver cirrhosis, but they do not directly treat the high ammonia levels characteristic of portosystemic encephalopathy. - While they can improve some symptoms of liver disease, they are not a specific treatment for **encephalopathy**. *Emergency portosystemic shunt surgery* - **Portosystemic shunt surgery** is typically performed to decompress the portal system and reduce bleeding risk from varices, but it can worsen portosystemic encephalopathy by increasing shunting of portal blood (and toxins) into the systemic circulation [1]. - It is generally contraindicated specifically for the treatment of **encephalopathy** and is reserved for specific cases like refractory variceal bleeding. *High protein diet* - **High-protein diet** can actually precipitate or worsen portosystemic encephalopathy by increasing the production of ammonia from protein metabolism [1]. - Patients with portosystemic encephalopathy often require **protein restriction** as part of their management, though complete restriction is typically avoided to prevent malnutrition.

Question 1023: A young girl presents with abdominal pain and a recent change in bowel habit, with passage of mucus in stool. There is no associated blood in stool and symptoms are increased with stress. The most likely diagnosis is:

A. Amebiasis
B. Irritable bowel syndrome (Correct Answer)
C. Crohn's disease
D. Ulcerative Colitis

Explanation: ***Irritable bowel syndrome*** - **Irritable bowel syndrome (IBS)** typically presents with **abdominal pain**, altered bowel habits (constipation, diarrhea, or mixed), and **mucus in stool** without blood [1]. - The symptoms are often exacerbated by **stress** and there is no evidence of structural or biochemical abnormalities [1]. *Amebiasis* - **Amebiasis** is an infection caused by *Entamoeba histolytica*, usually leading to **bloody diarrhea** (dysentery), abdominal pain, and fever. - The absence of blood in the stool and the presence of stress-related symptom exacerbation make amebiasis less likely. *Crohn's disease* - **Crohn's disease** is a type of inflammatory bowel disease characterized by **transmural inflammation** that can affect any part of the gastrointestinal tract. - Symptoms often include **abdominal pain**, diarrhea (which can be bloody), weight loss, and fatigue, and it does not typically show a direct correlation with stress as the primary exacerbating factor. *Ulcerative Colitis* - **Ulcerative colitis (UC)** is an inflammatory bowel disease characterized by **continuous inflammation** of the colon, typically starting in the rectum. - Key symptoms include recurrent **bloody diarrhea**, abdominal pain, and tenesmus, which are not described in this case, particularly the absence of blood.

Question 1024: The gold standard investigation for gastro-esophageal reflux disease is:

A. Measurement of length of lower esophageal sphincter
B. Esophageal manometry
C. 24-hour pH recording (Correct Answer)
D. Endoscopy

Explanation: ***24-hour pH recording*** - This is considered the **gold standard** because it directly measures the frequency and duration of **acid reflux** into the esophagus. - It correlates symptoms with reflux episodes, providing objective evidence for the diagnosis of **GERD**. *Measurement of length of lower esophageal sphincter* - While the **lower esophageal sphincter (LES)** dysfunction is central to GERD, simply measuring its length is not a diagnostic gold standard. - Reduced LES pressure or transient relaxations are more significant than static length measurement. *Esophageal manometry* - This test measures the **pressure and coordination** of esophageal muscle contractions and LES pressure. - It is primarily used to evaluate **motility disorders** and locate the LES, not as a primary diagnostic for GERD itself. *Endoscopy* - **Endoscopy** is useful for assessing complications of GERD such as esophagitis, strictures, or Barrett's esophagus, and to **rule out other pathologies**. - However, many patients with GERD symptoms have a normal endoscopic examination, making it less specific for the diagnosis of reflux itself.

Question 1025: A 12 year old boy presents with hematemesis, melena and mild splenomegaly. There is no obvious jaundice or ascites. The most likely diagnosis is:

A. NCPF
B. Malaria with DIC
C. Cirrhosis
D. EHPVO (Correct Answer)

Explanation: EHPVO - **Extrahepatic portal vein obstruction (EHPVO)** in children commonly presents with upper GI bleeding due to **esophageal varices** caused by portal hypertension, alongside **splenomegaly**. [1] - The absence of jaundice and ascites, paired with the patient's age, is highly suggestive of EHPVO since it primarily affects the portal vein before it reaches the liver, sparing hepatic function initially. NCPF - **Non-cirrhotic portal fibrosis (NCPF)** also causes portal hypertension, splenomegaly, and GI bleeding. However, it is more commonly seen in older adults and is a diagnosis of exclusion. - While it fits some symptoms, EHPVO is a more common cause of portal hypertension in children without underlying liver disease. [1] Malaria with DIC - **Malaria** can cause splenomegaly and, in severe cases, DIC leading to bleeding, but it would typically present with **fever, chills**, and other systemic signs of infection, which are not mentioned. - DIC would also likely present with more diffuse bleeding manifestations beyond hematemesis and melena, and not typically without other signs of severe malaria. Cirrhosis - **Cirrhosis** leads to portal hypertension, splenomegaly, and GI bleeding from varices. However, it is usually accompanied by overt signs of **liver dysfunction** such as **jaundice, ascites**, and encephalopathy, which are reportedly absent in this case. [1] - In a 12-year-old, childhood cirrhosis causes are typically distinct from adult causes and would still manifest with more significant liver compromise.

Question 1026: Which of the following findings is characteristic of Mallory-Weiss syndrome?

A. Hematemesis (Correct Answer)
B. Melena
C. Epigastric pain
D. Vomiting

Explanation: ***Hematemesis*** - **Hematemesis** (vomiting blood) is the hallmark symptom of Mallory-Weiss syndrome, resulting from longitudinal tears in the distal esophagus or gastric cardia [1]. - These tears are typically caused by sudden increases in **intra-abdominal pressure**, often due to forceful retching or vomiting, leading to bleeding [1]. *Melena* - **Melena** indicates bleeding from the upper gastrointestinal (GI) tract, but it signifies digested blood, resulting in black, tarry stools, and is not the primary presentation of acute Mallory-Weiss tears. - While melena can occur if the bleeding from a Mallory-Weiss tear is slow or prolonged, **frank hematemesis** is the more immediate and characteristic sign. *Epigastric pain* - **Epigastric pain** can be present in Mallory-Weiss syndrome due to the forceful vomiting and the tears themselves, but it is a non-specific symptom found in many GI conditions. - It is not as specific or diagnostically crucial as hematemesis for identifying Mallory-Weiss tears. *Vomiting* - **Vomiting** or retching is often the precipitating event that causes Mallory-Weiss tears, but it is the cause, not the characteristic finding of the syndrome itself [1]. - The key diagnostic feature is the **subsequent bleeding** (hematemesis) that results from the tears, differentiating it from simple vomiting [1].

Question 1027: Post-hepatic portal hypertension is caused by?

A. Congenital hepatic fibrosis
B. Banti Syndrome
C. Portal vein thrombosis
D. Budd-Chiari Syndrome (Correct Answer)

Explanation: ***Budd-Chiari Syndrome*** - **Budd-Chiari Syndrome** is characterized by obstruction of the **hepatic veins** or **inferior vena cava**, leading to blood backing up into the liver and causing **post-hepatic portal hypertension** [1]. - This obstruction prevents proper blood outflow from the liver, increasing pressure in the **hepatic sinusoids** and consequently the **portal venous system** [1]. *Congenital hepatic fibrosis* - This is a **pre-sinusoidal cause** of portal hypertension, often associated with developmental abnormalities of the **bile ducts**. - It leads to increased resistance to blood flow within the **portal tracts** before the sinusoids. *Banti Syndrome* - **Banti Syndrome** is an older term for **splenomegaly** with associated **pancytopenia** and **portal hypertension**, primarily caused by splenic vein thrombosis or increased splenic blood flow. - While it involves portal hypertension, the primary site of obstruction is typically **pre-hepatic** or **intra-hepatic sinusoidal**, not post-hepatic. *Portal vein thrombosis* - **Portal vein thrombosis** causes **pre-hepatic portal hypertension** due to obstruction of the **portal vein** before it enters the liver [2]. - This blockage prevents normal blood flow into the liver, increasing pressure in the **splenic** and **mesenteric venous systems**.

Question 1028: Which of the following is NOT included in the Child-Pugh criteria for assessing liver disease severity?

A. ALT / AST (Correct Answer)
B. S. albumin
C. Serum Bilirubin
D. Ascites

Explanation: ***ALT / AST*** - The Child-Pugh score primarily assesses the synthetic and excretory functions of the liver, not necessarily the degree of **hepatocellular inflammation** reflected by transaminases [3]. - While ALT/AST levels are crucial for diagnosing acute liver injury and monitoring chronic liver diseases, they are **not direct components** of the Child-Pugh class, which focuses on prognosis [1]. *S. albumin* - **Serum albumin** reflects the synthetic function of the liver, as albumin is exclusively produced by hepatocytes [2]. - Low albumin levels indicate significant **hepatic dysfunction**, which is directly incorporated into the Child-Pugh scoring system. *Serum Bilirubin* - **Serum bilirubin** measures the liver's ability to conjugate and excrete bilirubin, a key excretory function [2]. - Elevated bilirubin levels signify impaired liver function and are a critical parameter in the **Child-Pugh classification**. *Ascites* - The presence and severity of **ascites** are clinical signs of decompensated liver disease, reflecting portal hypertension and fluid retention [2]. - Ascites is a **clinical parameter** directly included in the Child-Pugh score, contributing to the assessment of disease severity.

Question 1029: A 25-year-old obese woman who denies any history of alcohol abuse presents with severe abdominal pain radiating to the back. Laboratory results indicate an increase in serum amylase and lipase, with a marked decrease in calcium. Which of the following likely has caused this condition?

A. Abetalipoproteinemia
B. Cholelithiasis (Correct Answer)
C. Cystic fibrosis
D. Alcohol

Explanation: **Cholelithiasis** - **Obesity** is a significant risk factor for gallstone formation [2], which can obstruct the pancreatic duct and lead to **pancreatitis** [1]. - The classic presentation of severe abdominal pain radiating to the back, elevated **amylase** and **lipase**, and **hypocalcemia** (due to fat saponification in severe pancreatitis) is highly consistent with pancreatitis secondary to gallstones [1]. *Abetalipoproteinemia* - This is a rare genetic disorder characterized by the inability to synthesize apolipoprotein B, leading to severe **malabsorption** and **neurological deficits**, not pancreatitis. - While it involves lipid abnormalities, it typically presents with steatorrhea, growth failure, and ataxia, not acute abdominal pain. *Cystic fibrosis* - Individuals with **cystic fibrosis** can develop pancreatic insufficiency and chronic pancreatitis due to thick secretions blocking pancreatic ducts, but **acute severe pancreatitis with hypocalcemia** is less typical as an initial presentation in a 25-year-old without a prior diagnosis. - Features like **recurrent respiratory infections** and **failure to thrive** would usually precede or accompany pancreatic issues. *Alcohol* - Although **alcohol abuse** is a very common cause of pancreatitis, the patient explicitly **denies any history of alcohol abuse**, making this etiology less likely in this specific case. - Clinically, alcohol-induced pancreatitis presents similarly, but the absence of positive history rules it out as the primary cause.

Question 1030: Toxic megacolon is seen in -

A. Crohn's disease
B. Colonic diverticulosis
C. Hamartomatous polyp
D. Chronic nonspecific ulcerative colitis (Correct Answer)

Explanation: ***Chronic nonspecific ulcerative colitis*** - **Toxic megacolon** is a severe complication of **ulcerative colitis**, characterized by acute toxic symptoms and **colonic dilation**. [1] - It results from inflammation extending into the **muscularis propria**, leading to colonic dysfunction and paralysis. *Crohn's disease* - While Crohn's disease can affect any part of the gastrointestinal tract and cause severe inflammation, **toxic megacolon is rarer** in Crohn's than in ulcerative colitis. [1] - Crohn's disease is more commonly associated with **strictures**, **fistulas**, and **skip lesions**. [1] *Colonic diverticulosis* - **Colonic diverticulosis** refers to the presence of small outpouchings in the colon wall, which can become inflamed (diverticulitis). - It does not typically lead to direct **toxic megacolon**, although severe diverticulitis can rarely cause a localized form of colonic distension. *Hamartomatous polyp* - A **hamartomatous polyp** is a non-neoplastic growth that results from an abnormal mixture of normal tissues. - These polyps are associated with various syndromes (e.g., Peutz-Jeghers syndrome) but are **not a cause of toxic megacolon**.

Practice by Chapter

Esophageal Disorders

Practice Questions

Peptic Ulcer Disease

Practice Questions

Inflammatory Bowel Disease

Practice Questions

Irritable Bowel Syndrome

Practice Questions

Malabsorption Syndromes

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Pancreatitis (Acute and Chronic)

Practice Questions

Gastrointestinal Bleeding

Practice Questions

Liver Diseases and Cirrhosis

Practice Questions

Viral Hepatitis

Practice Questions

Biliary Tract Disorders

Practice Questions

Gastrointestinal Motility Disorders

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Gastrointestinal Malignancies

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