Gastrointestinal Pathology Practice Questions

Q: Which of the following statements is not true regarding Menetrier's disease?

Overexpression of TGF-β. **Explanation:** Menetrier’s disease is a rare, acquired hypertrophic gastropathy characterized by the excessive secretion of **Transforming Growth Factor-alpha (TGF-α)**, not TGF-β. **1. Why Option B is the Correct Answer (The False Statement):** The pathogenesis of Menetrier’s disease involves the **overexpression of TGF-α**, which acts as a ligand for the **Epidermal Growth Factor Receptor (EGFR)**. This signaling pathway triggers the selective proliferation of mucous-secreting surface epithelial cells (foveolar cells) while inhibiting acid-producing parietal cells. TGF-β is generally involved in fibrosis and immune regulation, not the primary proliferative drive in this disease. **2. Analysis of Other Options:** * **Option A (Diffuse foveolar cell hyperplasia):** This is the hallmark histological feature. The gastric pits become elongated, corkscrew-shaped, and filled with mucus [1]. * **Option C (Protein-losing enteropathy):** The massive expansion of the surface epithelium and leakage through tight junctions lead to significant loss of albumin into the gastric lumen, resulting in **hypoalbuminemia** and peripheral edema. * **Option D (Hypertrophy of rugal folds):** Macroscopically, the disease presents with "cerebriform" enlargement of the gastric rugae (resembling brain gyri), primarily affecting the body and fundus while sparing the antrum [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Clinical Triad:** Giant gastric folds + Hypoalbuminemia + Achlorhydria (due to parietal cell atrophy). * **Risk:** Associated with an increased risk of **Gastric Adenocarcinoma** in adults [1]. * **Pediatric Association:** In children, it is often transient and associated with **CMV infection** [1]. * **Treatment:** EGFR inhibitors (e.g., Cetuximab) are used in severe cases. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 775-776.

Q: Tiger skin appearance of colonic mucosa is seen in which condition?

Melanosis coli. **Explanation:** **Melanosis coli** is the correct answer. This condition is characterized by a dark brown to black discoloration of the colonic mucosa, often described as a **"tiger skin," "leopard skin," or "alligator skin" appearance**. * **Pathophysiology:** It is caused by the chronic use of **anthraquinone laxatives** (e.g., senna, aloe, cascara). These substances cause apoptosis of colonic epithelial cells. The resulting apoptotic bodies are phagocytosed by macrophages in the *lamina propria*. * **Histology:** The dark pigment is actually **lipofuscin** (not melanin), stored within macrophages. It is a benign, reversible condition and is not associated with an increased risk of malignancy. **Why other options are incorrect:** * **Ulcerative colitis:** Characterized by diffuse mucosal inflammation, friability, and "pseudopolyps" [1]. In chronic cases, the colon may appear as a "lead pipe" due to loss of haustrations, but not tiger-skinned. * **Environmental enteropathy:** Primarily affects the small intestine (not colon), leading to villous atrophy and crypt hypertrophy, often seen in areas with poor sanitation. * **Carcinoid syndrome:** Associated with flushing, diarrhea, and right-sided heart failure. While carcinoid tumors can occur in the GI tract, they appear as firm, yellow submucosal nodules, not diffuse mucosal pigmentation. **High-Yield Pearls for NEET-PG:** * **Pigment:** Despite the name, the pigment is **Lipofuscin** (PAS positive), not melanin. * **Site:** Most prominent in the **cecum** and proximal colon. * **Association:** Strongly linked to **chronic constipation** and laxative abuse. * **Reversibility:** The appearance typically disappears within 6–12 months after stopping laxative use. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Alimentary System Disease, pp. 367-368.

Q: Which of the following is the earliest change in the intestine that occurs in Crohn's disease?

Aphthous ulcer. **Explanation:** In Crohn’s disease, the earliest macroscopic lesion is the **aphthous ulcer** [1]. These are small, shallow, punch-out ulcers that typically form over a lymphoid follicle (Peyer’s patch) [1]. As the disease progresses, these ulcers enlarge, coalesce, and extend deep into the wall to form linear, "serpentine" fissures [1]. **Analysis of Options:** * **Aphthous Ulcer (Correct):** This represents the initial stage of mucosal injury [1]. It is the precursor to the more extensive transmural inflammation characteristic of Crohn's. * **Cobblestone Appearance:** This is a **late/established feature**. It occurs when linear ulcers intersect, leaving islands of edematous, non-ulcerated mucosa between them. * **Stricture:** This is a **chronic complication** resulting from repeated cycles of transmural inflammation and subsequent fibrosis (healing by scarring), leading to luminal narrowing [1]. * **Perforation:** This is a **serious complication** of deep, penetrating ulcers. While Crohn’s is transmural, frank perforation is less common than in Ulcerative Colitis because the serosal inflammation often leads to adhesions or fistula formation first. **High-Yield NEET-PG Pearls:** * **Hallmark:** Transmural inflammation and **Non-caseating granulomas** (seen in 40-60% of cases) [1, 2]. * **Distribution:** "Skip lesions" (segmental involvement); most common site is the **terminal ileum** [1]. * **Radiology:** "String sign of Kantor" (due to strictures) and "Proud flesh" (separated bowel loops due to creeping fat) [1]. * **Microscopy:** Knife-like fissures and Paneth cell metaplasia. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Alimentary System Disease, pp. 365-367. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 806-807.

Q: Crohn's disease is associated with polymorphisms in which gene?

NOD2/CARD 15 gene. **Explanation:** **Correct Option: A. NOD2/CARD 15 gene** Crohn’s disease (CD) is a chronic inflammatory bowel disease (IBD) characterized by a dysregulated immune response to gut microbiota. The most strongly associated genetic risk factor is a polymorphism in the **NOD2 gene** (also known as **CARD15**), located on chromosome 16 [1]. * **Mechanism:** NOD2 encodes an intracellular receptor that recognizes bacterial peptidoglycans [1]. Mutations lead to defective innate immune sensing, impaired secretion of antimicrobial peptides (defensins) by Paneth cells, and subsequent chronic mucosal inflammation. **Incorrect Options:** * **B. P53 gene:** Known as the "guardian of the genome," mutations in *TP53* are associated with a wide array of sporadic cancers and Li-Fraumeni syndrome, but not the primary pathogenesis of IBD. * **C. Philadelphia chromosome:** This refers to the t(9;22) translocation resulting in the *BCR-ABL1* fusion gene, which is the hallmark of Chronic Myeloid Leukemia (CML). * **D. APC/Beta catenin:** This pathway is central to the "Adenoma-Carcinoma Sequence" in colorectal cancer. Mutations in the *APC* gene are responsible for Familial Adenomatous Polyposis (FAP). **High-Yield Clinical Pearls for NEET-PG:** * **Genetics:** NOD2/CARD15 has the strongest association with **ileal** Crohn’s disease [1]. * **Morphology:** Look for "creeping fat," "cobblestone appearance," "string sign of Kantor" on imaging, and **non-caseating granulomas** (pathognomonic, present in ~35% of cases). * **Transmurality:** Unlike Ulcerative Colitis (mucosal), Crohn’s is **transmural**, leading to fistulas and strictures. * **Smoking:** Smoking is a risk factor for Crohn’s but is paradoxically protective in Ulcerative Colitis. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 223-224.

Question 1

Which of the following statements is not true regarding Menetrier's disease?

Accepted Answer

Overexpression of TGF-β

Answer

Diffuse foveolar cell hyperplasia

Answer

Protein losing enteropathy

Answer

Hypertrophy of rugal folds

Question 2

Helicobacter pylori is implicated as a causative agent in which of the following conditions?

Accepted Answer

MALT Lymphoma

Answer

Hodgkin's Lymphoma

Answer

Non-Hodgkin's Lymphoma

Answer

Mantle cell Lymphoma

Question 3

Which is the most common neoplasm of the appendix?

Accepted Answer

Adenocarcinoma

Answer

Lymphoma

Answer

Leiomyosarcoma

Answer

Argentaffinoma

Question 4

Which of the following conditions has the highest malignant potential?

Accepted Answer

Familial polyposis

Answer

Crohn's disease

Answer

Ulcerative colitis

Answer

Infantile polyp

Question 5

Tiger skin appearance of colonic mucosa is seen in which condition?

Accepted Answer

Melanosis coli

Answer

Ulcerative colitis

Answer

Environmental enteropathy

Answer

Carcinoid syndrome

Question 6

Which of the following is the earliest change in the intestine that occurs in Crohn's disease?

Accepted Answer

Aphthous ulcer

Answer

Cobblestone appearance

Answer

Perforation

Answer

Stricture

Question 7

Mucosa associated lymphoid tumour (MALToma) is most commonly associated with which of the following microorganisms?

Accepted Answer

Helicobacter pylori

Answer

Candida albicans

Answer

Escherichia coli

Answer

Cytomegalovirus

Question 8

Crohn's disease is associated with polymorphisms in which gene?

Accepted Answer

NOD2/CARD 15 gene

Answer

P53 gene

Answer

Philadelphia chromosome

Answer

APC/Beta catenin

Question 9

According to the Vogelstein adenoma carcinoma theory, which of the following genes are mutated in the development of colon cancer?

Accepted Answer

All of the above

Answer

Beta catenin

Answer

K RAS

Answer

APC

Question 10

What is the metabolic abnormality seen in large colorectal villous adenoma?

Accepted Answer

Hypokalemic metabolic acidosis

Answer

Hypochloremic metabolic alkalosis

Answer

Chloride-sensitive metabolic acidosis

Answer

Chloride-sensitive metabolic alkalosis

Gastrointestinal Pathology — MCQs

Gastrointestinal Pathology — MCQs

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