Gastroenterology Practice Questions

Q: What is the "string sign" of Kantor seen in?

Crohn's disease. The **"String sign of Kantor"** is a classic radiological finding seen on a barium meal follow-through (BMFT) in patients with **Crohn’s disease** [1]. It represents a thin, string-like appearance of the barium column in the terminal ileum [1]. This occurs due to severe narrowing of the intestinal lumen caused by transmural inflammation, thickening of the bowel wall, and intense spasms . **Why the other options are incorrect:** * **Ulcerative colitis:** This condition typically involves the colon and rectum (sparing the small intestine). The characteristic radiological finding is the **"Lead pipe appearance"** (loss of haustrations) due to chronic inflammation and fibrosis. * **Cholecystitis:** This is inflammation of the gallbladder, usually diagnosed via ultrasound (showing wall thickening or pericholecystic fluid) or HIDA scan, not by signs of intestinal luminal narrowing. * **Appendicitis:** While it can cause ileal irritation, it is primarily diagnosed clinically or via CT/Ultrasound. A specific radiological sign associated with it is the "inverted 3 sign" or "cecal bar," but not the string sign. **High-Yield Clinical Pearls for NEET-PG:** * **Kantor’s String Sign:** Terminal ileum narrowing in Crohn’s [1]. * **Stierlin’s Sign:** Rapid emptying of the cecum due to irritability (seen in Ileocecal TB and Crohn's). * **Cobblestone Appearance:** Seen on endoscopy in Crohn's due to deep longitudinal ulcers and intervening normal mucosa. * **Creeping Fat:** Mesenteric fat wrapping around the bowel, pathognomonic for Crohn’s disease. * **Skip Lesions:** Discontinuous areas of involvement, a hallmark of Crohn's .

Q: A patient with antral carcinoma repeatedly vomits. Which of the following is NOT typically seen?

Acidosis. **Explanation:** Antral carcinoma causing gastric outlet obstruction (GOO) leads to repeated vomiting of gastric contents. The characteristic metabolic derangement in this scenario is **Metabolic Alkalosis**, not acidosis. **1. Why Acidosis is the Correct Answer (The "NOT" seen feature):** Gastric juice is rich in hydrochloric acid (HCl). Repeated vomiting results in a massive loss of hydrogen ions ($H^+$). To compensate, the body shifts towards an alkaline state, leading to **Metabolic Alkalosis** (specifically, hypochloremic hypokalemic metabolic alkalosis). Therefore, acidosis is not typically seen. **2. Why the other options are wrong (Features that ARE seen):** * **Hypochloremia (D):** Gastric juice contains high concentrations of chloride ($Cl^-$). Vomiting leads to direct depletion of chloride, which is the primary driver of the alkalosis. * **Hyponatremia (C):** Sodium is lost both in the vomitus and through the kidneys. As the body becomes dehydrated, ADH is secreted, which retains water and further dilutes serum sodium. * **Hypokalemia (B):** This occurs due to three reasons: direct loss in vomitus, renal loss (as the kidney exchanges $K^+$ for $H^+$ to conserve acid), and the "aldosterone effect" triggered by volume depletion. **Clinical Pearls for NEET-PG:** * **Paradoxical Aciduria:** In severe GOO, despite systemic alkalosis, the urine becomes acidic. This happens because the kidney, faced with severe volume depletion, prioritizes sodium reabsorption in exchange for $H^+$ ions (via the $Na^+/H^+$ pump) once $K^+$ stores are exhausted. * **Treatment of Choice:** The initial management for this metabolic state is **0.9% Normal Saline** (to correct volume and chloride) with **Potassium supplementation**. * **Classic Triad:** Hypochloremic, hypokalemic, metabolic alkalosis with paradoxical aciduria.

Q: All of the following statements about primary sclerosing cholangitis are true, EXCEPT:

Increased risk associated with smoking. Explanation: Primary Sclerosing Cholangitis (PSC) is a chronic cholestatic liver disease characterized by inflammation and obliterative fibrosis of the intrahepatic and extrahepatic bile ducts, leading to a "beaded" appearance on imaging. **Why Option A is the Correct Answer (The Exception):** Unlike many other inflammatory conditions, **smoking is actually associated with a decreased risk** of developing Primary Sclerosing Cholangitis. This "protective" effect of smoking is also famously observed in Ulcerative Colitis (UC). Therefore, the statement that there is an *increased* risk associated with smoking is false. **Analysis of Other Options:** * **Option B:** Approximately 70-80% of patients with PSC have concomitant **Ulcerative Colitis** [1]. This association is a classic high-yield fact; however, only about 4-5% of UC patients develop PSC. [1] * **Option C:** PSC is a cholestatic disorder. **GGT and Alkaline Phosphatase (ALP)** elevations are typically the earliest biochemical markers, often rising significantly before bilirubin levels increase [1]. * **Option D:** The clinical presentation is often insidious. **Pruritus and fatigue** are the most common presenting symptoms, followed by jaundice as the disease progresses [1]. **NEET-PG High-Yield Pearls:** * **Gold Standard Investigation:** MRCP (shows "beaded appearance" or multifocal strictures). * **Antibody Marker:** **p-ANCA** is positive in about 60-80% of cases (though not specific) [1]. * **Biopsy Finding:** "Onion-skin" fibrosis (periductal concentric fibrosis). * **Malignancy Risk:** Significantly increased risk of **Cholangiocarcinoma** and Colorectal Cancer. * **Treatment:** Liver transplantation is the only definitive cure for end-stage disease.

Q: In acute pancreatitis, which of the following findings is NOT typically observed?

Hypercalcemia. In acute pancreatitis, the hallmark biochemical findings involve the elevation of pancreatic enzymes and specific electrolyte disturbances. ### **Why Hypercalcemia is the Correct Answer** **Hypercalcemia** is not a finding *caused* by acute pancreatitis; rather, it is a potential **etiology** (cause) of the condition [1]. In the setting of established acute pancreatitis, the body typically experiences **Hypocalcemia** (Option C). This occurs due to **saponification**: activated lipases break down peripancreatic fat into free fatty acids, which then bind (chelate) calcium ions to form "calcium soaps" in the retroperitoneum [1]. ### **Analysis of Other Options** * **Raised Amylase (Option A):** Serum amylase rises within 6–12 hours of onset. While sensitive, it is less specific than lipase and may return to normal within 3–5 days despite ongoing inflammation. * **Increased Serum Lipase (Option D):** Lipase is the **preferred biochemical marker** for diagnosis. It rises earlier, stays elevated longer (8–14 days), and is more specific to the pancreas than amylase. * **Hypocalcemia (Option C):** As explained above, this is a common finding and is a component of the **Ranson Criteria** and **Modified Glasgow Score**, where a significant drop in calcium indicates severe disease and a poor prognosis [1]. ### **NEET-PG High-Yield Pearls** * **Diagnosis:** Requires 2 out of 3: (1) Characteristic abdominal pain, (2) Serum amylase/lipase >3x upper limit of normal, (3) Characteristic findings on imaging (CECT is the gold standard but not usually needed in the first 48 hours) [1]. * **Most Common Cause:** Gallstones (Worldwide/India), followed by Alcohol. * **Sentinel Loop:** A localized ileus of the jejunum seen on X-ray. * **Cullen’s Sign:** Periumbilical ecchymosis indicating hemoperitoneum (severe necrotizing pancreatitis).

Q: Pseudoachalasia is associated with all of the following conditions EXCEPT?

Rosary esophagus. **Explanation:** **Pseudoachalasia** (also known as secondary achalasia) is a clinical condition that mimics the clinical, manometric, and radiographic features of primary achalasia (e.g., failure of LES relaxation and aperistalsis) [1]. However, unlike primary achalasia, which is idiopathic, pseudoachalasia is caused by an underlying secondary process—most commonly a malignancy [2]. **Why "Rosary Esophagus" is the correct answer:** **Rosary esophagus** (or "corkscrew esophagus") is the classic radiographic finding on a barium swallow for **Diffuse Esophageal Spasm (DES)** [1]. DES is a primary motility disorder characterized by high-amplitude, non-peristaltic contractions. It is a distinct entity and is not a cause or feature of pseudoachalasia. **Analysis of incorrect options:** * **Esophageal tumor & Carcinoma of the gastric fundus:** These are the most common causes of pseudoachalasia. Malignant infiltration of the esophageal wall or the myenteric (Auerbach’s) plexus at the gastroesophageal junction leads to mechanical obstruction and impaired relaxation of the LES [2]. * **Paraneoplastic syndrome:** Certain malignancies (notably small cell lung cancer) can cause pseudoachalasia via a paraneoplastic mechanism, where antibodies (like anti-Hu) attack the esophageal neurons, mimicking the idiopathic disease [2]. **Clinical Pearls for NEET-PG:** * **Red Flags for Pseudoachalasia:** Age >60 years, rapid weight loss, and short duration of symptoms (<6 months). Primary achalasia usually presents in younger patients with a more chronic course. * **Diagnostic Clue:** If an endoscope cannot pass through the LES easily ("pop" sensation), it suggests primary achalasia; if there is a fixed, rigid narrowing, suspect pseudoachalasia (malignancy) [2]. * **Chagas Disease:** Caused by *Trypanosoma cruzi*, this is another cause of secondary achalasia (common in South America).

Question 1

What is the "string sign" of Kantor seen in?

Accepted Answer

Crohn's disease

Answer

Ulcerative colitis

Answer

Cholecystitis

Answer

Appendicitis

Question 2

A patient with antral carcinoma repeatedly vomits. Which of the following is NOT typically seen?

Accepted Answer

Acidosis

Answer

Hypokalemia

Answer

Hyponatremia

Answer

Hypochloremia

Question 3

Chronic pancreatitis is seen in all the following conditions EXCEPT:

Accepted Answer

None of the above

Answer

Chronic renal failure

Answer

Intraductal mucinous carcinoma

Answer

Alcohol

Question 4

Which of the following is NOT a cause of acute pancreatitis?

Accepted Answer

Hypercalcemia

Answer

Increased amylase level

Answer

Subcutaneous fat necrosis

Answer

Hyperlipidemia

Question 5

All of the following statements about primary sclerosing cholangitis are true, EXCEPT:

Accepted Answer

Increased risk associated with smoking

Answer

Associated with Ulcerative colitis

Answer

GGT elevation occurs early

Answer

Pruiritis is a common presenting symptom

Question 6

In acute pancreatitis, which of the following findings is NOT typically observed?

Accepted Answer

Hypercalcemia

Answer

Raised amylase

Answer

Hypocalcemia

Answer

Increased serum lipase

Question 7

Which of the following statements regarding peptic ulcer disease is true?

Accepted Answer

Helicobacter pylori infection is known to increase the incidence of gastric ulcers.

Answer

Anterior ulcers bleed more commonly than posterior ulcers.

Answer

Posteriorly perforated ulcers always require conservative management.

Answer

Anti-Helicobacter pylori drugs must always be included in the treatment regimen for peptic ulcer disease.

Question 8

Pseudoachalasia is associated with all of the following conditions EXCEPT?

Accepted Answer

Rosary esophagus

Answer

Esophageal tumor

Answer

Paraneoplastic syndrome

Answer

Carcinoma of the gastric fundus

Question 9

Which of the following statements regarding the management of ileocecal Crohn's disease is true?

Accepted Answer

5-ASA agents can reduce the risk of small bowel obstruction.

Answer

Antibiotics should be avoided.

Answer

Steroids should be avoided in the first week.

Answer

Cholestyramine improves diarrhea but worsens steatorrhea.

Question 10

Duodenal ulcer is most commonly caused by:

Accepted Answer

H. pylori

Answer

GERD

Answer

NSAID therapy

Answer

Stress ulcer

Gastroenterology — MCQs

Gastroenterology — MCQs

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