Gastroenterology Practice Questions

Q: Which of the following is NOT associated with acute pancreatitis?

Steatorrhea. **Explanation:** **1. Why Steatorrhea is the Correct Answer:** Steatorrhea (fatty, foul-smelling stools) is a hallmark of **exocrine pancreatic insufficiency**. This occurs when more than 90% of the pancreatic parenchyma is destroyed or non-functional. It is a classic feature of **Chronic Pancreatitis**, where there is permanent structural damage [1]. In **Acute Pancreatitis**, the inflammation is sudden and usually reversible; the gland typically retains enough functional capacity to prevent malabsorption during the acute phase. **2. Analysis of Incorrect Options:** * **Upper Abdominal Pain:** This is the most common presenting symptom (95% of cases). It is typically steady, boring, and severe, located in the epigastrium or periumbilical region [1]. * **Epigastric Tenderness:** Physical examination usually reveals significant tenderness in the upper abdomen, often accompanied by guarding and distension [1]. * **Cullen’s Sign:** This refers to periumbilical ecchymosis (bluish discoloration) caused by the tracking of hemoperitoneum from the retroperitoneum. While rare, it is a specific sign of **severe necrotizing pancreatitis**. **3. Clinical Pearls for NEET-PG:** * **Grey Turner’s Sign:** Ecchymosis in the flanks (associated with severe/hemorrhagic pancreatitis). * **Fox’s Sign:** Ecchymosis over the inguinal ligament. * **Most Common Cause:** Gallstones (overall), followed by Alcohol. * **Diagnosis:** Requires 2 out of 3: (1) Typical abdominal pain, (2) Serum Amylase/Lipase >3x upper limit, (3) Characteristic findings on imaging (CECT is the gold standard) [1]. * **Lipase vs. Amylase:** Lipase is more specific and remains elevated longer than amylase.

Q: All are features of Plummer-Vinson syndrome except?

Achalasia cardia. **Explanation:** **Plummer-Vinson Syndrome (PVS)**, also known as Paterson-Brown-Kelly syndrome, is characterized by a classic clinical triad. The correct answer is **Achalasia cardia** because it is a primary esophageal motility disorder involving the failure of the lower esophageal sphincter (LES) to relax, which is pathophysiologically unrelated to PVS [1]. **Breakdown of Options:** * **Iron deficiency (Option B):** This is the primary underlying metabolic derangement. Chronic iron deficiency leads to mucosal atrophy and is thought to predispose the upper esophagus to web formation. * **Esophageal web (Option A):** These are thin, mucosal folds typically located in the **post-cricoid region** (upper esophagus). They are a hallmark structural finding in PVS. * **Dysphagia (Option D):** The dysphagia in PVS is typically painless, intermittent, and specifically for solids, caused by the physical obstruction of the esophageal web. **High-Yield Clinical Pearls for NEET-PG:** * **Epidemiology:** Most commonly seen in middle-aged Caucasian women. * **Physical Exam Signs:** Look for features of iron deficiency like **koilonychia** (spoon-shaped nails), glossitis (smooth red tongue), and cheilosis. * **Diagnosis:** The investigation of choice for visualizing the web is a **Barium Swallow** (lateral view). * **Malignant Potential:** PVS is a **premalignant condition**. It significantly increases the risk of **Squamous Cell Carcinoma** of the post-cricoid region and upper esophagus. * **Treatment:** Iron supplementation often improves the dysphagia; however, mechanical dilation may be required for persistent webs.

Q: Which of the following is true regarding Gilbert syndrome?

Improves with phenobarbitone administration.. **Explanation:** Gilbert syndrome is a common, benign condition characterized by a reduction in the activity of the enzyme **UDP-glucuronosyltransferase (UGT1A1)** [1]. This enzyme is responsible for the conjugation of bilirubin in the liver [3]. **Why Option C is correct:** Phenobarbitone is a potent inducer of microsomal enzymes, including UGT1A1 [3]. Administration of phenobarbitone increases the expression of the enzyme, thereby enhancing bilirubin conjugation and effectively lowering serum bilirubin levels [2]. This is a classic pharmacological response used to differentiate Gilbert syndrome from more severe types of Crigler-Najjar syndrome [1]. **Analysis of Incorrect Options:** * **Option A:** Gilbert syndrome is characterized by **unconjugated (indirect) hyperbilirubinemia**, as the defect lies in the conjugation process [4]. * **Option B:** The condition actually **worsens with starvation**, fasting, dehydration, stress, or intercurrent illness. Caloric restriction leads to an increase in unconjugated bilirubin levels [4]. * **Option D:** It is a **benign, non-life-threatening** condition [1]. Most patients are asymptomatic, and the liver architecture and other liver function tests (ALT, AST, ALP) remain perfectly normal. **High-Yield Clinical Pearls for NEET-PG:** * **Genetic Defect:** Most commonly due to a TATAA box mutation in the *UGT1A1* gene [4]. * **Diagnosis:** Suggested by isolated unconjugated hyperbilirubinemia (<3 mg/dL) in the absence of hemolysis (normal reticulocyte count and hemoglobin) [4]. * **Rifampicin Test:** Administration of Rifampicin can provoke an increase in bilirubin in these patients, aiding diagnosis. * **Prognosis:** Excellent; no specific treatment is required other than reassurance.

Q: Primary sclerosing cholangitis is associated with which of the following conditions?

Ulcerative colitis. **Primary Sclerosing Cholangitis (PSC)** is a chronic cholestatic liver disease characterized by inflammation, fibrosis, and stricturing of the intrahepatic and extrahepatic bile ducts [1]. **Why Option A is correct:** There is a profound association between PSC and **Inflammatory Bowel Disease (IBD)**, specifically **Ulcerative Colitis (UC)** [1]. Approximately **70-80%** of patients with PSC have underlying UC [2]. Conversely, about 2-5% of UC patients develop PSC. Interestingly, PSC can be diagnosed before, during, or years after the onset of colitis, and even after a total proctocolectomy. **Why the other options are incorrect:** * **B. Celiac Sprue:** This is an autoimmune-mediated intolerance to gluten affecting the small intestine. While it is associated with other autoimmune conditions (like Type 1 Diabetes or Dermatitis Herpetiformis), it has no specific link to PSC. * **C. Wilson’s Disease:** This is a genetic disorder of copper metabolism. While it causes liver cirrhosis, the pathology involves copper deposition in hepatocytes, not the biliary tree. * **D. Whipple’s Disease:** Caused by *Tropheryma whipplei*, this is a systemic infectious disease primarily affecting the small bowel and joints, unrelated to the biliary destruction seen in PSC. **High-Yield Clinical Pearls for NEET-PG:** * **Imaging Gold Standard:** MRCP/ERCP shows a characteristic **"Beaded Appearance"** (multifocal strictures and dilations). * **Antibody Marker:** **p-ANCA** is positive in 60-80% of cases (though not specific) [1]. * **Biopsy:** May show pathognomonic **"Onion-skin fibrosis"** around bile ducts. * **Malignancy Risk:** PSC significantly increases the risk of **Cholangiocarcinoma** and Colorectal Cancer. * **Gender Predilection:** Unlike Primary Biliary Cholangitis (PBC), PSC is more common in **males** (M:F ratio 3:1) [1].

Q: Hyperamylasemia is seen in all of the following conditions except:

Cystic fibrosis. The correct answer is **Cystic Fibrosis (B)**. **1. Why Cystic Fibrosis is the correct answer:** In Cystic Fibrosis (CF), the mutation in the CFTR gene leads to thick, inspissated secretions that obstruct the pancreatic ducts [1]. Over time, this causes progressive **acinar atrophy** and extensive **fibrotic replacement** of the pancreatic parenchyma. Because the enzyme-producing cells (acinar cells) are destroyed, the pancreas becomes "burned out," leading to pancreatic insufficiency. Consequently, serum amylase levels are typically **low or undetectable**, rather than elevated. **2. Analysis of Incorrect Options:** * **Pancreatic Pseudocyst (A):** High amylase levels are a hallmark of pseudocysts [2]. Amylase remains elevated or persistently rises following an episode of acute pancreatitis if a pseudocyst develops. * **Macroamylasemia (C):** This is a benign condition where amylase binds to high-molecular-weight proteins (like IgA or IgG). The resulting complex is too large to be filtered by the renal glomeruli, leading to **persistent hyperamylasemia** despite normal pancreatic function and low urinary amylase. * **Parotitis (D):** Amylase has two main isoenzymes: P-type (pancreatic) and S-type (salivary). Inflammation of the salivary glands (e.g., Mumps, sialadenitis) increases S-type amylase [2], causing hyperamylasemia. **Clinical Pearls for NEET-PG:** * **Amylase vs. Lipase:** Lipase is more specific for acute pancreatitis and remains elevated longer (7–14 days) than amylase (3–5 days). * **Hypertriglyceridemia:** Can cause "falsely normal" amylase levels due to interference with the laboratory assay. * **Other causes of Hyperamylasemia:** Ectopic pregnancy, intestinal perforation, renal failure (decreased clearance), and diabetic ketoacidosis.

Q: Which of the following is a poor prognostic factor in a patient with acute pancreatitis?

Leukocytosis > 20000/µL. **Explanation:** The prognosis of acute pancreatitis is determined by the severity of the systemic inflammatory response and the extent of pancreatic necrosis [1]. To predict outcomes, clinicians use scoring systems like **Ranson’s Criteria**, APACHE II, and the BISAP score. **Why Option A is Correct:** According to **Ranson’s Criteria**, a White Blood Cell (WBC) count **> 16,000/µL** at the time of admission is a significant indicator of severity. A leukocytosis of **> 20,000/µL** (as given in the option) reflects a profound systemic inflammatory response syndrome (SIRS), which correlates with a higher risk of multi-organ failure and pancreatic necrosis, thus indicating a poor prognosis [1]. **Why the Other Options are Incorrect:** * **Options B & C (Decreased Amylase/Lipase):** The absolute levels of serum amylase and lipase are diagnostic but **not prognostic**. A very high level does not mean the disease is severe, and a decrease does not necessarily mean the patient is worsening (though it may occur in end-stage chronic pancreatitis or massive necrosis, it is not a standard prognostic marker). * **Option D (Diastolic BP > 90 mmHg):** Hypertension is not a poor prognostic sign. In fact, **hypotension** (Systolic BP 200 mg/dL, **A**ge >55 yrs, **L**DH >350 IU/L, **A**ST >250 IU/L, **W**BC >16,000/µL [1]. * **Most sensitive marker for prognosis:** C-Reactive Protein (CRP) > 150 mg/L at 48 hours. * **Single best predictor of mortality:** Rising Blood Urea Nitrogen (BUN) or persistent SIRS. * **Imaging:** Contrast-Enhanced CT (CECT) is the gold standard for assessing necrosis (best done after 72 hours) [1].

Question 1

What is the best test for determining the eradication of H. pylori infection?

Accepted Answer

Breath urea test

Answer

Urease test

Answer

Tissue biopsy

Answer

Serum ELISA

Question 2

Which of the following is NOT associated with acute pancreatitis?

Accepted Answer

Steatorrhea

Answer

Epigastric tenderness

Answer

Upper abdominal pain

Answer

Cullen's sign

Question 3

All are features of Plummer-Vinson syndrome except?

Accepted Answer

Achalasia cardia

Answer

Esophageal web

Answer

Iron deficiency

Answer

Dysphagia

Question 4

What is true about the early stages of GERD?

Accepted Answer

Increased number of transient lower esophageal sphincter relaxations (TLOSRs)

Answer

Increased lower esophageal sphincter (LOS) pressure

Answer

Shortening of the lower esophageal sphincter (LOS)

Answer

Loss of intra-abdominal esophagus

Question 5

Which of the following is true regarding Gilbert syndrome?

Accepted Answer

Improves with phenobarbitone administration.

Answer

Characterized by conjugated hyperbilirubinemia.

Answer

Worsens with starvation.

Answer

Is a life-threatening condition.

Question 6

Primary sclerosing cholangitis is associated with which of the following conditions?

Accepted Answer

Ulcerative colitis

Answer

Celiac sprue

Answer

Wilson's disease

Answer

Whipple's disease

Question 7

Hyperamylasemia is seen in all of the following conditions except:

Accepted Answer

Cystic fibrosis

Answer

Pancreatic pseudocyst

Answer

Macroamylasemia

Answer

Parotitis

Question 8

Which of the following statements about achalasia cardia are TRUE?

Accepted Answer

Statements 1, 2, and 4 are true; statements 3 and 5 are false.

Answer

Statements 1, 2, and 3 are true; statements 4 and 5 are false.

Answer

Statements 1, 2, 3, and 4 are true; statement 5 is false.

Answer

Statements 1, 2, 4, and 5 are true; statement 3 is false.

Question 9

Which of the following is a poor prognostic factor in a patient with acute pancreatitis?

Accepted Answer

Leukocytosis > 20000/µL

Answer

Decreased serum amylase

Answer

Decreased serum lipase

Answer

Diastolic BP > 90 mmHg

Question 10

Which of the following statements regarding primary sclerosing cholangitis associated with ulcerative colitis is FALSE?

Accepted Answer

Primary sclerosing cholangitis resolves after total colectomy.

Answer

Biliary cirrhosis is a known complication.

Answer

There is an increased risk of hilar cholangiocarcinoma.

Answer

Levels of alkaline phosphatase may be elevated.

Gastroenterology — MCQs

Gastroenterology — MCQs

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