Gastroenterology — MCQs
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Which of the following is the site of venous thrombosis in Budd-Chiari syndrome?
A 40-year-old woman with Crohn's disease reports multiple bowel movements with frequent stools. She was previously treated with a mesalamine derivative "Pentasa" and in the latest episode of the disease flare-up, she didn't tolerate the oral steroid therapy with budesonide. What is the next appropriate step in her treatment?
Which of the following is a complication of gallstones?
Which of the following statements about ulcerative colitis is correct?
The drug used in steroid-refractory acute severe ulcerative colitis is:
Which of the following is not typically used in the management of pneumatosis cystoides intestinalis?
Which condition is associated with the highest risk of colorectal cancer?
Ramu, an 8-year-old boy, presents with upper gastrointestinal bleeding. On examination, he is found to have splenomegaly, with no signs of ascites or hepatomegaly, and esophageal varices are detected on upper gastrointestinal endoscopy. What is the most likely diagnosis?
Most effective medication in Gastroesophageal Reflux Disease (GERD) is:
Which of the following statements about Helicobacter pylori is true?
Gastroenterology Indian Medical PG Practice Questions and MCQs
Question 1281: Which of the following is the site of venous thrombosis in Budd-Chiari syndrome?
- A. Infrahepatic inferior vena cava
- B. Infrarenal inferior vena cava
- C. Hepatic vein (Correct Answer)
- D. Portal vein
Explanation: ***Hepatic vein*** - **Budd-Chiari syndrome** is specifically defined by **thrombosis of the hepatic veins** [3] or the suprahepatic inferior vena cava, obstructing venous outflow from the liver. - This obstruction leads to **hepatic congestion** [2], liver enlargement, abdominal pain, and ascites. *Infrahepatic inferior vena cava* - While thrombosis can occur in the inferior vena cava, if it is located **below the liver**, it would not directly cause the classic features of Budd-Chiari syndrome. - Obstruction at this level would primarily lead to **lower extremity edema** and potentially renal vein thrombosis. *Infrarenal inferior vena cava* - Thrombosis in the **infrarenal portion of the IVC** would cause symptoms in the lower body, such as leg swelling [3], but not the hepatic congestion characteristic of Budd-Chiari syndrome. - This condition is distinct and typically presents with symptoms localized to the **inferior vena cava drainage area below the kidneys**. *Portal vein* - **Portal vein thrombosis** causes **portal hypertension** but does not directly involve the hepatic veins [1]. - While it can lead to ascites, it does not typically cause the acute, severe hepatic necrosis and sinusoidal congestion seen in Budd-Chiari syndrome as liver outflow is not obstructed.
Question 1282: A 40-year-old woman with Crohn's disease reports multiple bowel movements with frequent stools. She was previously treated with a mesalamine derivative "Pentasa" and in the latest episode of the disease flare-up, she didn't tolerate the oral steroid therapy with budesonide. What is the next appropriate step in her treatment?
- A. Sulfasalazine
- B. Prednisolone (oral)
- C. Hydrocortisone (IV)
- D. Azathioprine (Correct Answer)
Explanation: ***Azathioprine*** - This patient has **moderate-to-severe Crohn's disease** (based on frequency and previous treatment failures with mesalamine and budesonide), indicating a need for **immunosuppressive therapy**. [1] - **Azathioprine** is a thiopurine, an **immunomodulator** used for maintaining remission and reducing the need for corticosteroids in Crohn's disease. [1] Its delayed onset of action (weeks to months) makes it suitable for long-term management after initial symptom control. *Hydrocortisone (IV)* - While intravenous corticosteroids like **hydrocortisone** are effective for inducing remission in severe Crohn's disease, the question implies a flare-up that didn't tolerate *oral* steroid therapy with budesonide, suggesting a need for a **steroid-sparing agent** or a different class of medication for long-term management. - The use of IV steroids would be for initial severe flare management, but for a patient with repeated flares and steroid intolerance, a **maintenance immunomodulator** is the next step. *Prednisolone (oral)* - Similar to budesonide, **oral prednisolone** is a corticosteroid used to induce remission. [1] However, the patient's history of not tolerating oral steroid therapy (budesonide) suggests that another oral corticosteroid might also be poorly tolerated or not effective for sustained remission. - Long-term use of systemic corticosteroids like prednisolone carries significant **side effects**, making a steroid-sparing agent a more appropriate next step in chronic management. [1] *Sulfasalazine* - **Sulfasalazine** is an aminosalicylate derivative, similar to mesalamine, and is primarily effective in **mild-to-moderate ulcerative colitis** or Crohn's colitis, but **not as effective for Crohn's disease affecting the small bowel**. [1] - The patient has already failed **mesalamine** (a 5-ASA derivative), making another 5-ASA derivative like sulfasalazine an unlikely effective option for this flare-up, especially since it's typically used for milder disease.
Question 1283: Which of the following is a complication of gallstones?
- A. Cholangitis (Correct Answer)
- B. Acute pancreatitis
- C. Hemobilia
- D. Biliary enteric fistula
Explanation: ***Cholangitis*** [2] - **Cholangitis** refers to an infection of the **biliary tree**, most commonly caused by obstruction of the bile ducts by gallstones, leading to bacterial overgrowth. [2] - The obstruction (often due to choledocholithiasis) allows bacteria from the duodenum to ascend into the biliary system, causing inflammation and infection. *Hemobilia* - **Hemobilia** is bleeding into the **biliary tract**, typically caused by trauma, iatrogenic injury (e.g., biopsy), or vascular anomalies, not directly from gallstones. - While gallstones can cause inflammation, they do not typically lead to the direct arterial or venous bleeding characteristic of hemobilia. *Acute pancreatitis* [1] - **Acute pancreatitis** can be caused by gallstones if a stone temporarily obstructs the **ampulla of Vater**, blocking both the common bile duct and the pancreatic duct. [1] - However, it's considered a complication of **choledocholithiasis** (gallstones in the common bile duct), not a direct complication of gallstones themselves. *Biliary enteric fistula* [1] - **Biliary enteric fistula** is an abnormal connection between the biliary tree and the gastrointestinal tract, usually caused by chronic inflammation and erosion by a gallstone (e.g., a **gallstone ileus**). [1] - While a direct complication of gallstones, the question asks for *a* complication, and cholangitis is a more immediate and common infectious complication directly arising from biliary obstruction.
Question 1284: Which of the following statements about ulcerative colitis is correct?
- A. Can involve the perianal region
- B. Most commonly involves the colon (Correct Answer)
- C. Affects only the mucosal layer of the colon
- D. Skip lesions are commonly seen
Explanation: ***Most commonly involves the colon*** - **Ulcerative colitis** is a chronic inflammatory disease primarily affecting the **colon** and rectum [1]. - Inflammation typically starts in the rectum and extends proximally in a continuous fashion [1]. *Affects only the mucosal layer of the colon* - While ulcerative colitis primarily affects the **mucosal and submucosal layers**, severe cases can extend deeper into the muscularis propria, distinguishing it from Crohn's disease which is transmural [1]. - This statement is too absolute as inflammation can infrequently extend beyond just the mucosal layer. *Can involve the perianal region* - **Perianal involvement**, such as **fistulas, abscesses**, and **skin tags**, is characteristic of **Crohn's disease**, not ulcerative colitis [1]. - Ulcerative colitis inflammation is contiguous and limited to the colon. *Skip lesions are commonly seen* - **Skip lesions**, defined as areas of inflammation separated by segments of healthy tissue, are a hallmark feature of **Crohn's disease**. - **Ulcerative colitis** is characterized by **continuous inflammation** that starts in the rectum and extends upwards [1].
Question 1285: The drug used in steroid-refractory acute severe ulcerative colitis is:
- A. Steroids
- B. Infliximab
- C. Cyclosporine (Correct Answer)
- D. Sulfasalazine
Explanation: ***Cyclosporine*** - **Cyclosporine** is an effective **calcineurin inhibitor** used in cases of **acute severe ulcerative colitis** that are refractory to steroid therapy [1]. - It acts by suppressing the immune system and reducing inflammation in the colon, thereby preventing colectomy [1]. *Sulfasalazine* - **Sulfasalazine** is an **aminosalicylate** commonly used for mild to moderate ulcerative colitis, particularly for maintaining remission [1]. - It is not considered a primary treatment for **acute severe, steroid-refractory** disease [1]. *Steroids* - The question explicitly states "steroid-refractory," meaning the patient has already failed **steroid therapy** [1]. - Therefore, using **steroids** again as the primary intervention for this specific clinical scenario would not be appropriate. *Infliximab* - **Infliximab**, an **anti-TNF-α agent**, is also used in steroid-refractory acute severe ulcerative colitis [1]. - However, **cyclosporine** has a **more rapid onset of action** which makes it a preferred initial option in severe cases; Infliximab is often considered after cyclosporine failure or in scenarios where cyclosporine is contraindicated.
Question 1286: Which of the following is not typically used in the management of pneumatosis cystoides intestinalis?
- A. Albendazole (Correct Answer)
- B. Sulfasalazine
- C. Metronidazole
- D. High flow oxygen
Explanation: ***Albendazole*** - **Albendazole** is an **anti-parasitic medication** used to treat helminthic infections [2]. - While parasitic infections can sometimes cause gastrointestinal symptoms, it is not a standard treatment for **pneumatosis cystoides intestinalis**, which primarily involves gas cysts in the bowel wall. *High flow oxygen* - **High flow oxygen** is a common and effective treatment for pneumatosis cystoides intestinalis. - It works by increasing the partial pressure of nitrogen in the blood, creating a **diffusion gradient** that promotes the absorption of nitrogen gas from the cysts in the bowel wall. *Metronidazole* - **Metronidazole** is an antibiotic that is often used in the management of pneumatosis cystoides intestinalis, especially when bacterial overgrowth or infection is suspected. - It can help to reduce gas production by **anaerobic bacteria** in the gut, which may contribute to the formation of gas cysts. *Sulfasalazine* - **Sulfasalazine** is an anti-inflammatory drug used in the treatment of inflammatory bowel diseases (IBD) like ulcerative colitis and Crohn's disease [1]. - In cases where pneumatosis cystoides intestinalis is secondary to an **inflammatory bowel condition**, sulfasalazine may be used to address the underlying inflammation that might be contributing to the gas cysts [1].
Question 1287: Which condition is associated with the highest risk of colorectal cancer?
- A. Crohn's disease
- B. Ulcerative colitis
- C. Familial polyposis (Correct Answer)
- D. Infantile polyp
Explanation: ***Familial polyposis*** - Familial polyposis, particularly **Familial Adenomatous Polyposis (FAP)**, is associated with a nearly **100% risk of colorectal cancer** if untreated due to the development of numerous adenomatous polyps [1]. - Patients with FAP typically require **prophylactic colectomy** due to this high risk [1]. *Crohn's disease* - While Crohn's disease does increase the risk of colorectal cancer, the risk is **lower** compared to conditions like familial polyposis. - Colorectal cancer develops more commonly in long-standing cases and with **persistence of inflammation**. *Ulcerative colitis* - Ulcerative colitis also carries an increased risk for colorectal cancer, but it requires a longer duration of disease (often **over 8 years**) to significantly increase risk. - Cancer risk in ulcerative colitis is related to the extent of **colonic involvement**, making it less severe than familial polyposis. *Infantile polyp* - Infantile polyps are benign growths occurring in children and are generally **not associated with increased colorectal cancer risk** [1]. - These polyps usually **do not progress** to malignancy and are often discovered incidentally.
Question 1288: Ramu, an 8-year-old boy, presents with upper gastrointestinal bleeding. On examination, he is found to have splenomegaly, with no signs of ascites or hepatomegaly, and esophageal varices are detected on upper gastrointestinal endoscopy. What is the most likely diagnosis?
- A. Budd chiari syndrome
- B. Cirrhosis
- C. Veno-occlusive disease
- D. Non cirrhotic portal hypertension (Correct Answer)
Explanation: ***Non cirrhotic portal hypertension*** - The presence of **splenomegaly** and **esophageal varices** with **no signs of ascites or hepatomegaly** strongly suggests **portal hypertension** that is not due to cirrhosis. [1] - This condition involves increased portal venous pressure due to obstructions *before* (pre-hepatic) or *within* (intra-hepatic, non-cirrhotic) the liver, or *after* (post-hepatic) the liver, leading to splenomegaly and collateral circulation. [2] *Budd chiari syndrome* - Characterized by **hepatic vein outflow obstruction**, manifesting with **hepatomegaly**, ascites, and abdominal pain, which are not described in the patient. - While it can cause portal hypertension and esophageal varices, the lack of hepatomegaly and ascites makes it less likely in this case. *Cirrhosis* - Marked by diffuse **hepatic fibrosis** and **nodule formation**, leading to impaired liver function, **hepatomegaly** (initially), and often **ascites**, which are absent. [3] - While it causes portal hypertension and varices, the absence of liver dysfunction symptoms or signs of chronic liver disease makes this less probable. *Veno-occlusive disease* - This condition primarily affects the **small intrahepatic venules**, leading to **hepatomegaly**, ascites, and jaundice, especially after hematopoietic stem cell transplantation. - The patient's presentation lacks the typical features of acute liver damage and hepatomegaly associated with veno-occlusive disease.
Question 1289: Most effective medication in Gastroesophageal Reflux Disease (GERD) is:
- A. PPI (Correct Answer)
- B. Antacids
- C. Prokinetic drugs
- D. H2 blockers
Explanation: ***PPI*** - **Proton pump inhibitors (PPIs)** are considered the most effective medications for GERD because they **irreversibly block the H+/K+-ATPase pump** in gastric parietal cells, leading to substantial and prolonged reduction in acid secretion. [1] - This profound acid suppression promotes **healing of esophageal erosions** and provides superior symptom relief compared to other drug classes. [1] *Antacids* - **Antacids** neutralize existing stomach acid, providing **rapid but temporary symptomatic relief**. [1] - They do not inhibit acid production and are **ineffective for long-term management** or healing of esophageal damage in GERD. *Prokinetic drugs* - **Prokinetic agents** enhance esophageal motility and gastric emptying, which can be beneficial in some GERD patients by reducing acid exposure. - However, they do **not reduce acid secretion** and are generally less effective than PPIs for primary GERD treatment. *H2 blockers* - **H2-receptor antagonists (H2 blockers)** reduce stomach acid production by blocking histamine H2 receptors on parietal cells, leading to a moderate decrease in acid secretion. - While effective for mild GERD, they are generally **less potent and provide less sustained acid suppression** than PPIs [1], and patients can develop **tachyphylaxis** (tolerance) to their effects.
Question 1290: Which of the following statements about Helicobacter pylori is true?
- A. It is a gram-positive bacterium.
- B. It causes hypergastrinemia.
- C. It is involved in the causation of peptic ulcer disease. (Correct Answer)
- D. All of the options.
Explanation: ***It is involved in the causation of peptic ulcer disease.*** - *Helicobacter pylori* is a major cause of **peptic ulcer disease**, significantly increasing the risk of both gastric and duodenal ulcers [1]. - Its presence leads to chronic inflammation and damage to the gastric and duodenal mucosa, predisposing to ulcer formation [2]. *It is a gram-positive bacterium.* - *Helicobacter pylori* is a **gram-negative** spiral-shaped bacterium, not gram-positive. - Its gram staining property is a key characteristic used for its identification in microbiology. *It causes hypergastrinemia.* - While *H. pylori* can affect gastrin levels, it typically leads to **hypochlorhydria** and **low gastrin levels** due to inflammation of the gastric antrum, not hypergastrinemia. [Note: Text correction based on evidence] Chronic *H. pylori* infection can lead to an increase in gastrin (hypergastrinaemia) due to depletion of somatostatin from D cells, which stimulates increased acid production [1]. - Chronic *H. pylori* infection can sometimes lead to an increase in gastrin, but this is usually due to reduced somatostatin inhibition rather than direct gastrin stimulation [1]. *All of the options.* - This option is incorrect because the statement that it is a gram-positive bacterium is false. - Therefore, not all the listed options are true.
Practice by Chapter
Esophageal Disorders
Practice Questions
Peptic Ulcer Disease
Practice Questions
Inflammatory Bowel Disease
Practice Questions
Irritable Bowel Syndrome
Practice Questions
Malabsorption Syndromes
Practice Questions
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
Practice Questions
Gastrointestinal Malignancies
Practice Questions
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