Gastrointestinal Pathology — MCQs

A 35-year-old man undergoes gastrectomy for gastric carcinoma. Gross examination of the resected stomach reveals diffuse thickening without a discrete mass lesion. Microscopic examination shows an infiltration of signet-ring cells dispersed singly. Family history reveals that his father had a similar cancer at a young age. What gene is most likely to be mutated in this patient and his father?

Q24Medium

Osteomas, adenomatous polyps of the intestine, and periampullary carcinomas are characteristically seen in which of the following conditions?

Q25Easy

Barrett's esophagus is diagnosed by which of the following histological findings?

Q26Medium

All of the following statements about Menetrier's disease are true EXCEPT?

Q27Easy

Barrett's esophagus is a precursor to which type of esophageal cancer?

Q28Easy

Which of the following organs is the most common site of origin of the tumor associated with Zollinger-Ellison syndrome?

Q29Easy

Familial polyposis coli is associated with which of the following?

Q30Medium

In Crohn's disease, which of the following findings is NOT typically seen?

Gastrointestinal Pathology Indian Medical PG Practice Questions and MCQs

Question 21: Ectopic tissue in the stomach is most commonly of what organ's origin?

A. Spleen
B. Pancreas (Correct Answer)
C. Liver
D. Kidney

Explanation: **Explanation:** The presence of histologically normal tissue in an abnormal anatomical location (without vascular or neural connection to the parent organ) is known as **Ectopia** or **Heterotopia** (a form of Choristoma) [2]. **1. Why Pancreas is Correct:** The **pancreas** is the most common organ to exhibit ectopia within the gastrointestinal tract [1]. Ectopic pancreatic tissue is most frequently found in the **stomach** (usually the antrum), followed by the duodenum and jejunum [2]. It typically presents as a small, firm, yellow-white submucosal nodule. While often asymptomatic, it can occasionally lead to inflammation (pancreatitis), ulceration, or even mimic a gastrointestinal stromal tumor (GIST) on imaging [2]. **2. Why Other Options are Incorrect:** * **Spleen (Splenosis/Accessory Spleen):** While accessory spleens are common, they are usually found near the splenic hilum, tail of the pancreas, or greater omentum, rather than within the gastric wall. * **Liver:** Ectopic liver tissue is rare and most commonly found on the gallbladder surface or near the suspensory ligaments of the liver. * **Kidney:** Ectopic kidney tissue is extremely rare in the GI tract and is usually associated with complex developmental malformations in the retroperitoneum. **3. High-Yield Clinical Pearls for NEET-PG:** * **Meckel’s Diverticulum:** The most common ectopic tissue found here is **Gastric mucosa** (leading to peptic ulceration/bleeding), followed by pancreatic tissue [1]. * **Zenker’s Diverticulum:** This is a "false" pulsion diverticulum occurring at **Killian’s dehiscence**. * **Inlet Patch:** This refers specifically to ectopic gastric mucosa in the upper third of the **esophagus** [2]. * **Histology:** Ectopic pancreas in the stomach often contains all components: acini, ducts, and occasionally Islets of Langerhans [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Pancreas, p. 889. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 757-759.

Question 22: A 50-year-old female patient complains of difficulty in swallowing. The patient has a history of multiple diagnostic CT-scans of the head and neck region. Which of the following salivary gland tumors is more likely in this patient?

A. Pleomorphic adenocarcinoma
B. Mucoepidermoid carcinoma (Correct Answer)
C. Adenoid cystic carcinoma
D. Acinic cell carcinoma

Explanation: **Explanation:** The correct answer is **Mucoepidermoid carcinoma (MEC)**. **1. Why Mucoepidermoid Carcinoma is correct:** The key clinical clue in this case is the history of **multiple diagnostic CT scans** (ionizing radiation) to the head and neck region. Mucoepidermoid carcinoma is the most common malignant salivary gland tumor in both adults and children. Crucially, it is the salivary gland malignancy most strongly associated with **prior exposure to ionizing radiation**. Pathologically, it is characterized by a mixture of three cell types: squamous (epidermoid) cells, mucus-secreting cells, and intermediate cells [1]. **2. Why the other options are incorrect:** * **Pleomorphic Adenoma (Option A):** While this is the most common *benign* tumor of the salivary glands [2], the question asks for a tumor likely triggered by radiation. Furthermore, "Pleomorphic adenocarcinoma" is not a standard primary classification; the malignant counterpart is "Carcinoma ex pleomorphic adenoma" [1]. * **Adenoid Cystic Carcinoma (Option C):** This tumor is known for its "Swiss-cheese" appearance (cribriform pattern) and a high propensity for **perineural invasion**, causing pain. It is not specifically linked to radiation history as strongly as MEC [1]. * **Acinic Cell Carcinoma (Option D):** This is a low-grade malignancy that resembles serous acinar cells [1]. While it is the second most common childhood salivary malignancy, it lacks the classic association with radiation exposure described in the vignette. **3. NEET-PG High-Yield Pearls:** * **Most common overall salivary tumor:** Pleomorphic Adenoma (Benign) [2]. * **Most common malignant salivary tumor:** Mucoepidermoid Carcinoma [1]. * **Most common site:** Parotid gland (but the smaller the gland, the higher the chance of malignancy). * **Genetic Hallmark of MEC:** Translocation **t(11;19)** resulting in the *CRTC1-MAML2* fusion gene. * **Warthin’s Tumor:** Associated with smoking; presents as bilateral/multifocal cystic lesions in the parotid. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Head and Neck, pp. 751-755. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Alimentary System Disease, pp. 345-346.

Question 23: A 35-year-old man undergoes gastrectomy for gastric carcinoma. Gross examination of the resected stomach reveals diffuse thickening without a discrete mass lesion. Microscopic examination shows an infiltration of signet-ring cells dispersed singly. Family history reveals that his father had a similar cancer at a young age. What gene is most likely to be mutated in this patient and his father?

A. APC
B. CDH1 (Correct Answer)
C. PMS2
D. p53

Explanation: ### Explanation The clinical presentation describes **Diffuse-type Gastric Adenocarcinoma**, characterized by a "leather bottle" appearance (**Linitis Plastica**) due to diffuse thickening of the stomach wall without a discrete mass [1]. The hallmark microscopic finding is **signet-ring cells** (cells with large mucin vacuoles pushing the nucleus to the periphery) that infiltrate the stroma individually [1]. **Why CDH1 is correct:** The **CDH1 gene** encodes **E-cadherin**, a cell-surface protein responsible for intercellular adhesion. A germline mutation in *CDH1* leads to **Hereditary Diffuse Gastric Cancer (HDGC)** syndrome. The loss of E-cadherin causes cells to lose their cohesiveness, allowing them to infiltrate the gastric wall as single cells (signet-ring morphology) [1]. This patient’s young age and positive family history strongly point toward this autosomal dominant syndrome. **Analysis of Incorrect Options:** * **APC:** Mutations in the *APC* gene are associated with **Familial Adenomatous Polyposis (FAP)** [2]. While FAP increases the risk of intestinal-type gastric cancer, it does not typically present with diffuse signet-ring cell morphology. * **PMS2:** This is a DNA mismatch repair (MMR) gene. Mutations in *PMS2* (or *MLH1, MSH2, MSH6*) cause **Lynch Syndrome**, which is associated with **Intestinal-type** gastric cancer, not the diffuse type [2]. * **p53:** While *TP53* mutations are common in many sporadic cancers (including gastric), they are not the primary driver for the specific hereditary diffuse signet-ring cell pattern described. **High-Yield Clinical Pearls for NEET-PG:** * **Lauren Classification:** Divides gastric cancer into **Intestinal** (bulky, glandular, associated with H. pylori/metaplasia) and **Diffuse** (signet-ring cells, E-cadherin loss, younger patients) [1]. * **Virchow’s Node:** Left supraclavicular lymph node involvement in gastric CA. * **Sister Mary Joseph Nodule:** Periumbilical metastasis. * **Krukenberg Tumor:** Bilateral ovarian metastasis from a gastric primary (signet-ring cells). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, p. 779. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, p. 817.

Question 24: Osteomas, adenomatous polyps of the intestine, and periampullary carcinomas are characteristically seen in which of the following conditions?

A. Cowden syndrome
B. Peutz-Jeghers syndrome
C. Familial adenomatous polyposis (FAP)
D. Gardner syndrome (Correct Answer)

Explanation: The correct answer is **Gardner syndrome**, which is a phenotypic variant of **Familial Adenomatous Polyposis (FAP)**. Both conditions are caused by a germline mutation in the **APC gene** on chromosome 5q21 [1]. **Why Gardner Syndrome is Correct:** Gardner syndrome is characterized by the classic triad of: 1. **Intestinal Polyposis:** Hundreds to thousands of adenomatous polyps (identical to FAP) with a 100% risk of progression to colorectal carcinoma [1]. 2. **Extra-colonic Bone/Soft Tissue Tumors:** Specifically **osteomas** (commonly of the mandible or skull), epidermal cysts, and desmoid tumors. 3. **Periampullary Carcinoma:** Patients have a significantly increased risk of duodenal and periampullary adenocarcinoma. **Why Other Options are Incorrect:** * **Cowden Syndrome:** Caused by **PTEN mutations**. It features hamartomatous polyps, trichilemmomas, and an increased risk of breast, thyroid (follicular), and endometrial cancers [2]. * **Peutz-Jeghers Syndrome:** Caused by **STK11 mutations** [2]. It is characterized by **hamartomatous polyps** (with a "Christmas tree" branching pattern of smooth muscle) and mucocutaneous hyperpigmentation (melanotic macules on lips/buccal mucosa) [2]. * **Familial Adenomatous Polyposis (FAP):** While FAP includes the polyps and periampullary risk, the presence of **osteomas** specifically defines the **Gardner variant** [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Turcot Syndrome:** FAP/Lynch syndrome + CNS tumors (Medulloblastoma/Glioblastoma). *Mnemonic: TUrcot = Turban (Head).* * **CHRPE:** Congenital Hypertrophy of Retinal Pigment Epithelium is a highly specific screening marker for FAP/Gardner syndrome. * **APC Gene:** A negative regulator of the Wnt signaling pathway; it normally promotes the degradation of β-catenin [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 821-822. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, p. 813.

Question 25: Barrett's esophagus is diagnosed by which of the following histological findings?

A. Squamous metaplasia
B. Intestinal metaplasia (Correct Answer)
C. Squamous dysplasia
D. Intestinal dysplasia

Explanation: **Barrett’s Esophagus (BE)** is a complication of chronic Gastroesophageal Reflux Disease (GERD). It is defined as the replacement of the normal stratified squamous epithelium of the lower esophagus with **columnar epithelium** containing **goblet cells** [1]. 1. **Why Intestinal Metaplasia is Correct:** The hallmark of Barrett’s esophagus is **intestinal metaplasia**. Under the stress of chronic acid reflux, the esophageal squamous cells undergo a phenotypic shift to a more acid-resistant columnar phenotype [1]. The presence of **Goblet cells** (which contain acidic mucins that stain with Alcian blue) is the definitive histological requirement for the diagnosis of Barrett’s in many clinical guidelines, as this specific change carries the risk of progression to adenocarcinoma [1]. 2. **Analysis of Incorrect Options:** * **Squamous metaplasia:** This is the replacement of another cell type *with* squamous cells (e.g., in the lungs of smokers) [3], [4]. In Barrett’s, the process is the opposite: squamous cells are replaced by columnar cells. * **Squamous dysplasia:** This refers to precancerous changes in squamous cells, typically leading to Squamous Cell Carcinoma. Barrett’s is a precursor to Adenocarcinoma [1]. * **Intestinal dysplasia:** While dysplasia can occur *within* Barrett’s esophagus, it is a secondary progression/complication, not the defining histological finding for the initial diagnosis of Barrett’s itself [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Gross Appearance:** Appears as "velvety red/salmon-pink" tongues or patches extending upward from the GE junction (contrasting with the pale-pink squamous mucosa). * **Risk:** It is a major risk factor for **Esophageal Adenocarcinoma** [1]. * **Stain:** **Alcian Blue** at pH 2.5 is used to highlight the goblet cells. * **Molecular Marker:** CDX2 is a transcription factor often expressed in intestinal metaplasia. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Alimentary System Disease, pp. 348-349. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 764-765. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 91-92. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, p. 49.

Question 26: All of the following statements about Menetrier's disease are true EXCEPT?

A. It is a premalignant condition
B. Usually decreased acid secretion (Correct Answer)
C. May be confused with Zollinger Ellison Syndrome
D. Associated with protein-losing enteropathy

Explanation: **Explanation:** Ménétrier’s disease is a rare, acquired hypertrophic gastropathy characterized by massive enlargement of gastric rugal folds [1]. The underlying pathophysiology involves over-expression of **Transforming Growth Factor-alpha (TGF-α)**, which leads to selective hyperplasia of surface mucous cells (foveolar cells) and atrophy of deep glandular cells [1]. **Why Option B is the "Except" (Correct Answer):** The question asks for the "Except" statement. Option B states "Usually decreased acid secretion" is the correct answer, which implies it is a false statement. However, in standard medical literature, Ménétrier’s disease is classically associated with **hypochlorhydria or achlorhydria** (decreased acid) because the expansion of mucous cells replaces the acid-producing parietal cells [1]. *Note: If the provided key marks "decreased acid" as the incorrect statement, it may be due to a specific examiner's focus on the fact that acid is "markedly" absent rather than just "decreased," or a potential error in the provided key, as decreased acid is a hallmark of the disease.* **Analysis of Other Options:** * **Option A (Premalignant):** True. There is an increased risk of gastric adenocarcinoma in adults (approx. 10%) [1]. * **Option C (Confused with ZES):** True. Both present with giant gastric folds. However, ZES shows parietal cell hyperplasia (high acid), while Ménétrier shows foveolar hyperplasia (low acid). * **Option D (Protein-losing enteropathy):** True. Excessive mucus production and leaky intercellular junctions lead to significant albumin loss, resulting in peripheral edema and hypoproteinemia. **NEET-PG High-Yield Pearls:** * **Classic Triad:** Giant rugal folds (resembling cerebral convolutions), hypoproteinemia (edema), and achlorhydria. * **Histology:** "Corkscrew" appearance of elongated, dilated foveolar glands [1]. * **Pediatric cases:** Often associated with **CMV infection** and are usually self-limiting [1]. * **Treatment:** Cetuximab (anti-EGFR antibody) is 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.

Question 27: Barrett's esophagus is a precursor to which type of esophageal cancer?

A. Adenocarcinoma (Correct Answer)
B. Squamous cell carcinoma
C. Carcinoid tumor
D. Esophageal leiomyoma

Explanation: **Barrett’s Esophagus** is a condition defined by **intestinal metaplasia** within the esophageal squamous mucosa [1]. It occurs due to chronic Gastroesophageal Reflux Disease (GERD), where the normal stratified squamous epithelium is replaced by non-ciliated columnar epithelium with **goblet cells** to better withstand gastric acid [1]. This metaplastic columnar epithelium is inherently unstable and can progress through a sequence of low-grade dysplasia to high-grade dysplasia, and ultimately to **Adenocarcinoma** [1][2]. This is the most common type of esophageal cancer in the Western world and typically involves the distal third of the esophagus [2]. **Analysis of Incorrect Options:** * **B. Squamous cell carcinoma:** This is the most common esophageal cancer worldwide, but it arises from the native squamous lining [3]. Major risk factors include alcohol, smoking, and achalasia, rather than Barrett’s. * **C. Carcinoid tumor:** These are neuroendocrine tumors arising from enterochromaffin cells. While they can occur in the GI tract, they are not associated with Barrett’s metaplasia. * **D. Esophageal leiomyoma:** This is the most common *benign* mesenchymal tumor of the esophagus, arising from smooth muscle cells, and has no relationship with epithelial metaplasia. **High-Yield Clinical Pearls for NEET-PG:** * **Histology Gold Standard:** Presence of **Goblet cells** on biopsy is essential for the diagnosis of Barrett’s Esophagus [1]. * **Endoscopic Appearance:** Described as "salmon-pink" velvety tongues of mucosa extending upwards from the GE junction. * **Molecular Marker:** Progression to adenocarcinoma is often associated with mutations in **TP53** and **p16/INK4a**. * **Surveillance:** Patients with Barrett’s require periodic endoscopic surveillance to detect dysplasia early [1]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Alimentary System Disease, pp. 348-349. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 765-766. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 766-767.

Question 28: Which of the following organs is the most common site of origin of the tumor associated with Zollinger-Ellison syndrome?

A. Duodenum (Correct Answer)
B. Lymph nodes
C. Spleen
D. Pancreas

Explanation: **Explanation:** **Zollinger-Ellison Syndrome (ZES)** is characterized by the triad of hypergastrinemia, severe peptic ulcer disease, and gastrin-secreting tumors known as **gastrinomas** [1]. **1. Why Duodenum is Correct:** Historically, the pancreas was thought to be the primary site. However, recent surgical and pathological data confirm that the **duodenum** is the most common site of origin for gastrinomas (approx. 50–88% of cases). These tumors are typically found within the **"Gastrinoma Triangle"** (bounded by the confluence of the cystic and common bile ducts, the junction of the second and third portions of the duodenum, and the neck and body of the pancreas) [1]. Duodenal gastrinomas are often small, multicentric, and slower to metastasize compared to pancreatic ones. **2. Why Other Options are Incorrect:** * **Pancreas:** While the pancreas is the second most common site and often hosts larger, more aggressive gastrinomas, it is no longer considered the most frequent primary site. * **Lymph Nodes:** Gastrinomas are frequently found in peripancreatic or duodenal lymph nodes [1]. However, debate exists whether these represent primary "nodal gastrinomas" or early metastases from an occult duodenal primary. * **Spleen:** The spleen is not a primary site for gastrinomas. **NEET-PG High-Yield Pearls:** * **Association:** ~25% of ZES cases are associated with **Multiple Endocrine Neoplasia Type 1 (MEN1)**. * **Clinical Presentation:** Refractory peptic ulcers (often in distal duodenum/jejunum) and chronic **secretory diarrhea** (due to high acid inactivating pancreatic lipase) [2]. * **Diagnosis:** Best initial test is **fasting serum gastrin levels** (>1000 pg/mL is diagnostic). The confirmatory test is the **Secretin Stimulation Test** (paradoxical rise in gastrin). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1124-1125. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Alimentary System Disease, pp. 353-354.

Question 29: Familial polyposis coli is associated with which of the following?

A. Intussusception
B. Toxic megacolon
C. Cancer (Correct Answer)
D. Ulcerative colitis

Explanation: **Explanation:** **Familial Adenomatous Polyposis (FAP)**, or polyposis coli, is an autosomal dominant condition caused by a germline mutation in the **APC (Adenomatous Polyposis Coli) gene** on chromosome 5q21 [1]. It is characterized by the development of hundreds to thousands of adenomatous polyps throughout the colon [2]. **Why 'Cancer' is the correct answer:** FAP follows the classic **"adenoma-to-carcinoma sequence."** Because the number of polyps is so vast, the risk of at least one polyp progressing to adenocarcinoma is **virtually 100%** by the age of 40-50 years [2]. Prophylactic colectomy is the standard management to prevent this inevitable malignancy. **Why other options are incorrect:** * **Intussusception:** While large solitary polyps (like Peutz-Jeghers hamartomas) can act as lead points for intussusception, it is a rare complication in FAP compared to the absolute certainty of malignancy. * **Toxic Megacolon:** This is a life-threatening complication of inflammatory bowel diseases (IBD), specifically Ulcerative Colitis, and is not associated with polyposis syndromes. * **Ulcerative Colitis:** This is an idiopathic inflammatory bowel disease. While it also increases colon cancer risk, it has a completely different pathophysiology (inflammatory vs. genetic mutation) and is not etiologically linked to FAP. **High-Yield Clinical Pearls for NEET-PG:** * **Gardner Syndrome:** FAP + Osteomas (mandible), Epidermoid cysts, and Desmoid tumors. * **Turcot Syndrome:** FAP + CNS tumors (Medulloblastoma). *Mnemonic: **T**urcot = **T**urban (Head).* * **Diagnosis:** Requires >100 polyps for a classical FAP diagnosis [2]. * **Extra-colonic manifestation:** Congenital Hypertrophy of Retinal Pigment Epithelium (CHRPE) is a highly specific early screening marker. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, p. 817. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 821-822.

Question 30: In Crohn's disease, which of the following findings is NOT typically seen?

A. Hyperplastic polyps
B. Diverticulosis (Correct Answer)
C. Fissuring ulcer
D. Epithelioid granuloma

Explanation: **Explanation:** The correct answer is **B. Diverticulosis**. **1. Why Diverticulosis is the correct answer:** Diverticulosis is a structural condition characterized by the herniation of the mucosa and submucosa through muscular defects in the colonic wall, primarily due to high intraluminal pressure and low-fiber diets [1]. It is **not** a pathological feature of Crohn’s disease. In fact, Crohn’s disease is characterized by transmural inflammation and fibrosis, which leads to thickening of the bowel wall—a process that would generally oppose the formation of thin-walled diverticula [2]. **2. Analysis of Incorrect Options:** * **Hyperplastic/Inflammatory Polyps:** In Crohn’s, chronic cycles of ulceration and regeneration lead to the formation of "pseudopolyps" or inflammatory polyps. These are common findings in both major types of Inflammatory Bowel Disease (IBD). * **Fissuring Ulcers:** A hallmark of Crohn’s is the presence of deep, knife-like "fissures" that extend through the mucosa into the muscularis and serosa [2]. These can lead to fistula formation or perforation. * **Epithelioid Granuloma:** Non-caseating epithelioid granulomas are a highly specific diagnostic feature of Crohn’s disease (seen in ~40-60% of cases) [3]. Their presence helps distinguish Crohn’s from Ulcerative Colitis, where granulomas are absent. **3. NEET-PG High-Yield Pearls for Crohn’s Disease:** * **Distribution:** "Skip lesions" (segmental involvement); most common site is the **terminal ileum** [2]. * **Morphology:** "Cobblestone" appearance of mucosa, "Creeping fat" (mesenteric fat wrapping), and "String sign of Kantor" on barium studies due to strictures [2]. * **Microscopy:** Transmural inflammation (involving all layers) and lymphoid aggregates [3]. * **Clinical:** Often presents with malabsorption (Vitamin B12 deficiency) and perianal fistulae [2]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Alimentary System Disease, pp. 370-371. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Alimentary System Disease, pp. 365-367. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 806-807.

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