Gastroenterology Practice Questions

Q: Which of the following is the least likely manifestation of acute Budd-Chiari syndrome?

Venous collaterals. **Explanation:** The core concept in this question is the differentiation between **acute** and **chronic** presentations of Budd-Chiari Syndrome (BCS). BCS results from the obstruction of hepatic venous outflow, leading to post-sinusoidal portal hypertension. **Why "Venous Collaterals" is the correct answer:** Venous collaterals (such as caput medusae or prominent abdominal wall veins) are signs of **chronic** portal hypertension [1]. They require weeks to months to develop as the body attempts to bypass the venous obstruction. In an **acute** presentation, the sudden blockage leads to rapid hepatic congestion and pressure buildup before collateral pathways have time to form. Therefore, they are the least likely finding in the acute phase. **Analysis of Incorrect Options:** * **Enlarged tender liver:** In acute BCS, the sudden venous outflow obstruction causes massive hepatic congestion and stretching of Glisson’s capsule, leading to painful hepatomegaly [2]. * **Ascites:** The rapid increase in sinusoidal pressure leads to the transudation of fluid into the peritoneal cavity. Ascites in BCS is typically high-protein (SAAG >1.1 g/dL). * **Jaundice:** While often mild, jaundice occurs in acute BCS due to centrizonal (Zone 3) congestion and subsequent hepatocellular damage. **NEET-PG High-Yield Pearls:** * **Classic Triad:** Abdominal pain, hepatomegaly, and ascites. * **Imaging:** Doppler Ultrasound is the initial investigation of choice; "Spider-web" appearance on venography is characteristic. * **Pathology:** The **Caudate lobe** often undergoes compensatory hypertrophy because its venous drainage (directly into the IVC) is frequently spared. * **Most common cause (Global):** Thrombosis (often associated with polycythemia vera or prothrombotic states). In Asia, membranous webs of the IVC are more common.

Q: Ileocecal tuberculosis is associated with which type of anemia?

Megaloblastic anemia. **Explanation:** The correct answer is **Megaloblastic anemia**. **Pathophysiology:** Ileocecal tuberculosis primarily involves the terminal ileum, which is the specific site for the absorption of the **Vitamin B12-Intrinsic Factor complex**. Chronic inflammation, ulceration, or stricture formation in the ileum leads to malabsorption of Vitamin B12 [1]. Furthermore, the development of strictures can cause stasis of intestinal contents, leading to **Small Intestinal Bacterial Overgrowth (SIBO)**; these bacteria compete for and consume Vitamin B12. A deficiency in Vitamin B12 impairs DNA synthesis, resulting in ineffective erythropoiesis and the characteristic megaloblastic changes in the bone marrow and peripheral blood [1]. **Analysis of Incorrect Options:** * **Iron deficiency anemia:** While chronic blood loss from intestinal ulcers can occasionally cause this, the classic association with ileal pathology is B12 malabsorption. * **Sideroblastic anemia:** This is typically due to defects in heme synthesis (e.g., lead poisoning, isoniazid use, or hereditary causes), not malabsorption. * **Normocytic normochromic anemia:** While common in many chronic inflammatory diseases (Anemia of Chronic Disease), the specific anatomical involvement of the ileum makes megaloblastic anemia the more definitive and high-yield association for this condition. **NEET-PG High-Yield Pearls:** * **Most common site of GI TB:** Ileocecal region (due to increased lymphoid tissue/Peyer's patches and physiological stasis). * **Classic X-ray findings:** Stierlin’s sign (rapid emptying of the cecum) and Kantor’s string sign. * **Differential Diagnosis:** Crohn’s disease (also involves the terminal ileum and causes megaloblastic anemia). * **Gold Standard Diagnosis:** Colonoscopy with biopsy showing caseating granulomas.

Q: A 48-year-old alcoholic male presents with bilateral gynecomastia. Which physical finding in cirrhosis shares the same pathogenesis as gynecomastia?

Spider angioma. The correct answer is **Spider angioma**. **Pathogenesis:** In patients with cirrhosis, the liver’s ability to metabolize steroid hormones is significantly impaired. This leads to **hyperestrogenism** (increased serum estradiol levels) due to two main factors: 1. Decreased hepatic clearance of estrogen. [1] 2. Increased peripheral conversion of androgens (androstenedione) to estrogens. Both **gynecomastia** and **spider angiomata** (vascular spiders) are direct clinical manifestations of this hyperestrogenic state [2]. Estrogen causes the dilation of terminal arterioles, leading to the characteristic central red dot with radiating "legs" seen in spider angiomata. **Analysis of Incorrect Options:** * **A. Caput medusa:** This is a result of **portal hypertension** [2]. It occurs due to the recanalization of the paraumbilical vein, which shunts blood from the portal system to the systemic epigastric veins. * **B. Asterixis:** This "flapping tremor" is a sign of **hepatic encephalopathy** [3]. It is caused by the accumulation of neurotoxins (primarily ammonia) that the failing liver cannot detoxify. * **C. Ascites:** This is multifactorial but primarily driven by **portal hypertension** and **hypoalbuminemia** (leading to decreased oncotic pressure), along with secondary sodium and water retention [1], [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Hyperestrogenism** in cirrhosis also leads to **palmar erythema**, testicular atrophy, and loss of axillary/pubic hair [2]. * **Spider angiomata** are typically found in the distribution of the **superior vena cava** (face, neck, upper chest, and arms). * The presence of multiple spider angiomata is highly specific for cirrhosis and correlates with the severity of liver disease and the risk of esophageal varices.

Q: Before starting Infliximab in a 65-year-old gentleman for Inflammatory bowel disease, which of the following tests is mandatory?

Mantoux test. **Explanation:** **1. Why Mantoux Test is Correct:** Infliximab is a potent **TNF-alpha (Tumor Necrosis Factor) inhibitor**. TNF-alpha plays a crucial role in the formation and maintenance of **granulomas**, which are the body’s primary mechanism for sequestering *Mycobacterium tuberculosis*. By inhibiting TNF-alpha, Infliximab can lead to the breakdown of these granulomas, causing the **reactivation of Latent Tuberculosis Infection (LTBI)** into active, often disseminated, disease. Therefore, screening for TB using a **Mantoux test (TST)** or an Interferon-Gamma Release Assay (IGRA), along with a Chest X-ray, is mandatory before initiating any anti-TNF therapy, especially in TB-endemic regions like India [1]. **2. Why Other Options are Incorrect:** * **Colonoscopy (A):** While essential for the initial diagnosis and monitoring of IBD, it is not a specific safety requirement "mandatory" immediately before starting a biologic agent. * **ERCP (C):** This is an invasive procedure used for biliary or pancreatic duct pathologies (e.g., Primary Sclerosing Cholangitis associated with UC) and has no role in the pre-biologic screening protocol. * **Liver Biopsy (D):** This is not required. While baseline Liver Function Tests (LFTs) are checked, a biopsy is an invasive procedure reserved for specific diagnostic dilemmas, not routine screening. **Clinical Pearls for NEET-PG:** * **Pre-Infliximab Screening Checklist:** TB screening (Mantoux/IGRA + CXR), Hepatitis B Surface Antigen (HBsAg), and Hepatitis C serology [1]. * **Vaccination:** Patients should receive inactivated vaccines (e.g., Flu, Pneumococcal) before starting; **Live vaccines** (e.g., BCG, Yellow Fever) are **contraindicated** once therapy begins. * **Side Effects:** Infliximab increases the risk of serious infections, reactivation of Hepatitis B, and potentially worsens Heart Failure (NYHA Class III/IV).

Q: Wilson's disease is characterized by all of the following except?

The defective gene is ATP7A. **Explanation:** Wilson’s Disease (Hepatolenticular Degeneration) is an autosomal recessive disorder of copper metabolism. **1. Why Option A is the Correct Answer (The Exception):** The defective gene in Wilson’s disease is **ATP7B**, located on **Chromosome 13**. This gene encodes a copper-transporting P-type ATPase responsible for transporting copper into the bile and incorporating it into ceruloplasmin. * **ATP7A** is the defective gene in **Menkes Disease** ("Kinky Hair Syndrome"), which leads to systemic copper deficiency rather than overload. **2. Analysis of Other Options:** * **Option B:** Copper deposition in the basal ganglia (especially the putamen) leads to extrapyramidal symptoms [1]. Common features include **Parkinsonian signs** (tremors, rigidity), dystonia, ataxia, and a characteristic "wing-beating" tremor [1]. * **Option C:** **Kayser-Fleischer (KF) rings** (copper deposition in the Descemet’s membrane of the cornea) are present in 95% of neurological cases. **Sunflower cataracts** (copper in the lens) are also classic, though less common. * **Option D:** While initial screening involves serum ceruloplasmin and 24-hour urinary copper, a **liver biopsy** showing a copper content **>250 µg/g dry weight** remains the gold standard and confirmatory test for diagnosis. **Clinical Pearls for NEET-PG:** * **Screening Test:** Serum Ceruloplasmin (usually 100 µg/day). * **MRI Brain Finding:** "Face of the Giant Panda" sign in the midbrain. * **Treatment:** Chelators like **D-Penicillamine** (first-line) or Trientine [1]; Zinc is used for maintenance as it inhibits intestinal copper absorption.

Question 1

In a patient with Wilson disease-related compensated cirrhosis, without evidence of neurologic or psychiatric symptoms, what is the best treatment option?

Accepted Answer

Zinc

Answer

Trientine

Answer

Tetrathiomolybdate

Answer

d-penicillamine

Question 2

Which of the following is the least likely manifestation of acute Budd-Chiari syndrome?

Accepted Answer

Venous collaterals

Answer

Enlarged tender liver

Answer

Ascites

Answer

Jaundice

Question 3

Diarrhea associated with acanthocytes in a blood smear suggests which of the following conditions?

Accepted Answer

Abetalipoproteinemia

Answer

Whipple's disease

Answer

Celiac sprue

Answer

Ulcerative colitis

Question 4

Ileocecal tuberculosis is associated with which type of anemia?

Accepted Answer

Megaloblastic anemia

Answer

Iron deficiency anemia

Answer

Sideroblastic anemia

Answer

Normocytic normochromic anemia

Question 5

A 48-year-old alcoholic male presents with bilateral gynecomastia. Which physical finding in cirrhosis shares the same pathogenesis as gynecomastia?

Accepted Answer

Spider angioma

Answer

Caput medusa

Answer

Asterixis

Answer

Ascites

Question 6

A 30-year-old chronic alcoholic presents with sudden onset of epigastric pain radiating to the back. Which of the following findings is NOT typically seen in this patient's presentation?

Accepted Answer

Low serum lipase

Answer

Increased LDL

Answer

Hypocalcemia

Answer

Increased serum amylase

Question 7

Which of the following is NOT true regarding Gilbert's syndrome?

Accepted Answer

Conjugated hyperbilirubinemia

Answer

Fasting hypoglycemia

Answer

Normal liver histology

Answer

Normal liver enzymes

Question 8

Before starting Infliximab in a 65-year-old gentleman for Inflammatory bowel disease, which of the following tests is mandatory?

Accepted Answer

Mantoux test

Answer

Colonoscopy

Answer

ERCP

Answer

Liver biopsy

Question 9

A young female with a known myeloproliferative disorder presents with a 3-day history of progressive abdominal discomfort and ascites. What is the most likely diagnosis?

Accepted Answer

Budd-Chiari syndrome

Answer

Hepatitis A

Answer

Perforation peritonitis

Answer

Acute pancreatitis

Question 10

Wilson's disease is characterized by all of the following except?

Accepted Answer

The defective gene is ATP7A

Answer

Neurological features include Parkinsonian features and ataxia

Answer

Kayser-Fleischer rings and sunflower cataracts are typical eye findings

Answer

Liver biopsy is confirmatory for the diagnosis

Gastroenterology — MCQs

Gastroenterology — MCQs

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