Gastrointestinal Pathology — MCQs
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Which statement is false regarding familial adenomatous polyposis?
A 45-year-old woman presents with increasing abdominal girth over the past 2 years. Physical examination reveals abdominal distension. A CT scan shows multiple nodules on peritoneal surfaces along with low-attenuation mucinous ascites. Cytological examination after paracentesis showed well-differentiated columnar cells with minimal nuclear atypia. From which site did this pathology most likely originate?
Which of the following is NOT associated with colon carcinogenesis?
Barrett's esophagus is commonly associated with which of the following malignancies?
A segment of jejunum shows a nodular lesion in the submucosa. Histological examination reveals a tumor composed of uniform round cells arranged in trabeculae, with a "salt-and-pepper" chromatin pattern. Electron microscopy shows secretory granules, and immunohistochemistry is positive for serotonin. Which of the following parameters best correlates with the metastatic potential of this tumor?
Which of the following is NOT true regarding typhoid ulcer?
Which organism is associated with fish consumption and also causes carcinoma of the gallbladder?
Which of the following is NOT a complication of Helicobacter pylori?
Cribriform, honeycomb, or swiss cheese histology pattern is seen in which of the following tumors?
What is the characteristic microscopic finding in lymphocytic colitis?
Gastrointestinal Pathology Indian Medical PG Practice Questions and MCQs
Question 421: Which statement is false regarding familial adenomatous polyposis?
- A. Males are usually carriers. (Correct Answer)
- B. Autosomal dominant inheritance.
- C. If not treated, progresses to malignancy in 100% of cases.
- D. Males and females are affected equally.
Explanation: **Explanation:** **Familial Adenomatous Polyposis (FAP)** is an **autosomal dominant** disorder caused by a germline mutation in the **APC (Adenomatous Polyposis Coli) gene** located on chromosome **5q21** [1]. **Why Option A is the correct (False) statement:** In autosomal dominant (AD) disorders, the concept of a "carrier" (an individual who carries the gene but does not express the phenotype) generally does not apply in the same way it does for autosomal recessive traits. Because FAP has **high penetrance**, any individual (male or female) who inherits the mutated gene will express the disease. Therefore, males are not merely "carriers"; they are affected patients who will develop polyps. **Analysis of other options:** * **Option B (True):** FAP follows an **autosomal dominant** inheritance pattern. A child of an affected parent has a 50% chance of inheriting the mutation. * **Option C (True):** FAP is characterized by the development of hundreds to thousands of adenomatous polyps [1]. If a prophylactic total proctocolectomy is not performed, the risk of progression to colorectal carcinoma is **100%**, usually by age 40 [1]. * **Option D (True):** Since it is an autosomal (non-sex-linked) disorder, **males and females are affected equally**. **High-Yield Clinical Pearls for NEET-PG:** * **Diagnosis:** Requires at least **100 polyps** for a classical FAP diagnosis [1]. * **Gardner Syndrome:** FAP + Osteomas (mandible), epidermal cysts, and desmoid tumors. * **Turcot Syndrome:** FAP + CNS tumors (specifically **Medulloblastoma**; note: mismatch repair mutations lead to Glioblastoma). * **Screening:** Starts at age 10–12 years with annual sigmoidoscopy/colonoscopy. * **CHRPE:** Congenital Hypertrophy of Retinal Pigment Epithelium is a specific extra-intestinal marker for FAP. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 815-822.
Question 422: A 45-year-old woman presents with increasing abdominal girth over the past 2 years. Physical examination reveals abdominal distension. A CT scan shows multiple nodules on peritoneal surfaces along with low-attenuation mucinous ascites. Cytological examination after paracentesis showed well-differentiated columnar cells with minimal nuclear atypia. From which site did this pathology most likely originate?
- A. Pancreas
- B. Ileum
- C. Jejunum
- D. Appendix (Correct Answer)
Explanation: The clinical presentation of increasing abdominal girth, mucinous ascites (jelly-like fluid), and peritoneal nodules is classic for **Pseudomyxoma Peritonei (PMP)**. **1. Why Appendix is Correct:** The most common primary site for Pseudomyxoma Peritonei is the **Appendix**, specifically arising from a **Low-grade Appendiceal Mucinous Neoplasm (LAMN)** [1]. In this condition, the appendix ruptures or leaks, seeding the peritoneal cavity with mucus-secreting goblet cells. These cells continue to produce abundant extracellular mucin, leading to "gelatinous ascites" [1]. The cytological finding of well-differentiated columnar cells with minimal atypia is characteristic of the low-grade nature of LAMN-associated PMP. **2. Why Other Options are Incorrect:** * **Pancreas:** While mucinous cystic neoplasms of the pancreas can occur, they rarely cause generalized pseudomyxoma peritonei. Pancreatic involvement usually presents with localized masses or biliary obstruction. * **Ileum and Jejunum:** Primary mucinous tumors of the small intestine are extremely rare. While the small bowel may be involved secondary to peritoneal seeding, it is almost never the primary site of origin for PMP. **3. Clinical Pearls for NEET-PG:** * **The "Jelly Belly" Sign:** A classic descriptive term for the gross appearance of the abdomen in PMP due to massive mucin accumulation. * **Redistribution Phenomenon:** Mucin and neoplastic cells tend to accumulate at sites of peritoneal fluid resorption (e.g., greater omentum, undersurface of the diaphragm) while sparing the mobile small bowel loops initially. * **Differential Diagnosis:** In females, mucinous tumors of the **Ovary** were historically considered a primary cause; however, current evidence suggests most "ovarian" PMP cases are actually metastases from an occult appendiceal primary [1], [2]. * **Treatment:** The standard of care is Cytoreductive Surgery (CRS) combined with Hyperthermic Intraperitoneal Chemotherapy (HIPEC). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 823-824. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Female Genital Tract, pp. 1030-1032.
Question 423: Which of the following is NOT associated with colon carcinogenesis?
- A. APC
- B. k RAS
- C. B-catenin
- D. Mismatch repair (Correct Answer)
Explanation: **Explanation:** The question asks which factor is **NOT** associated with colon carcinogenesis. While it may seem counterintuitive, the correct answer is **Mismatch repair (D)** because it is the **deficiency** (loss) of mismatch repair (MMR) proteins, not the repair process itself, that leads to cancer. **1. Why Mismatch Repair is the Correct Answer:** Colon carcinogenesis occurs through two main pathways: the **Adenoma-Carcinoma sequence** (Chromosomal Instability) and the **Microsatellite Instability (MSI) pathway**. In the MSI pathway (associated with Lynch Syndrome), it is the **loss or mutation** of MMR genes (like *MLH1, MSH2*) that leads to the accumulation of errors [4]. Therefore, "Mismatch repair" as a functional process is a protective mechanism; its **absence** or **defect** is what causes cancer. **2. Analysis of Incorrect Options:** * **APC (A):** This is the "gatekeeper" of colonic neoplasia [2]. Mutations in the *APC* gene are the earliest event in the classic adenoma-carcinoma sequence (FAP syndrome). * **k-RAS (B):** Mutations in the *RAS* oncogene (specifically *KRAS*) follow *APC* mutations [1]. It promotes uncontrolled cell growth and is a key driver in the progression from a small adenoma to a large adenoma. * **B-catenin (C):** In the Wnt signaling pathway, when *APC* is mutated, it cannot degrade **β-catenin** [2]. High levels of β-catenin translocate to the nucleus and activate genes for cell proliferation [1]. **Clinical Pearls for NEET-PG:** * **Sequence of Mutations:** APC (Early) → KRAS (Intermediate) → p53/SMAD4 (Late) [3]. * **Vogelstein Model:** The classic name for the Adenoma-Carcinoma sequence. * **Microsatellites:** Short, repetitive DNA sequences that become unstable when MMR genes are defective [4]. * **Right vs. Left:** MSI pathway cancers are typically **right-sided** (proximal), while APC-pathway cancers are often **left-sided** (distal) [4]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, p. 819. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 304-305. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Alimentary System Disease, pp. 373-374. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 819-821.
Question 424: Barrett's esophagus is commonly associated with which of the following malignancies?
- A. Adenocarcinoma (Correct Answer)
- B. Squamous cell carcinoma
- C. Sarcoma
- D. Gastrointestinal stromal tumor
Explanation: **Explanation:** **Barrett’s Esophagus (BE)** is a condition where the normal stratified squamous epithelium of the lower esophagus undergoes **intestinal metaplasia** to non-ciliated columnar epithelium with goblet cells [3]. This change occurs as a protective response to chronic gastroesophageal reflux disease (GERD). **Why Adenocarcinoma is correct:** The metaplastic columnar epithelium in Barrett’s esophagus is inherently unstable. Over time, it can progress through a sequence of **low-grade dysplasia** to **high-grade dysplasia**, and finally to **invasive Adenocarcinoma** [1]. Barrett’s is considered the single most important precursor lesion for esophageal adenocarcinoma, increasing the risk by approximately 30 to 40-fold compared to the general population [3]. **Why other options are incorrect:** * **Squamous cell carcinoma (SCC):** This arises from the native squamous epithelium. Major risk factors include alcohol, smoking, and caustic injury. While SCC was historically more common, Adenocarcinoma is now more prevalent in Western countries due to the rise in obesity and GERD [2]. * **Sarcoma:** These are rare mesenchymal tumors (e.g., leiomyosarcoma) and do not arise from the epithelial metaplasia seen in Barrett’s. * **Gastrointestinal stromal tumor (GIST):** These arise from the Interstitial Cells of Cajal (pacemaker cells) in the muscularis propria, not the mucosal lining. **High-Yield Clinical Pearls for NEET-PG:** * **Gold Standard Diagnosis:** Endoscopy showing "salmon-pink" tongues of mucosa extending above the GE junction, confirmed by biopsy showing **Goblet cells** [3]. * **Molecular Marker:** Progression to malignancy is often associated with mutations in **TP53** and **p16/INK4a**. * **Location:** Adenocarcinoma typically involves the **distal third** of the esophagus, whereas SCC more commonly involves the middle third [1], [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 764-766. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 766-767. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Alimentary System Disease, pp. 348-349.
Question 425: A segment of jejunum shows a nodular lesion in the submucosa. Histological examination reveals a tumor composed of uniform round cells arranged in trabeculae, with a "salt-and-pepper" chromatin pattern. Electron microscopy shows secretory granules, and immunohistochemistry is positive for serotonin. Which of the following parameters best correlates with the metastatic potential of this tumor?
- A. Architectural pattern
- B. Cell pleomorphism
- C. Hormonal production
- D. Site and size (Correct Answer)
Explanation: **Explanation:** The clinical presentation and histological findings—specifically the **"salt-and-pepper" chromatin**, trabecular arrangement, and **serotonin positivity**—are pathognomonic for a **Neuroendocrine Tumor (NET)**, formerly known as a Carcinoid tumor [1]. **Why "Site and Size" is correct:** Unlike many epithelial malignancies where histological grade is the primary driver, the metastatic potential of neuroendocrine tumors is most reliably predicted by their **anatomic location** and **tumor diameter** [3]. * **Site:** Appendiceal and rectal NETs are usually benign, whereas ileal, gastric, and colonic NETs have a much higher risk of metastasis [2]. * **Size:** Tumors <1 cm rarely metastasize (<2%), while those >2 cm have a high probability (up to 70-80%) of nodal or distant spread [3]. **Why other options are incorrect:** * **Architectural pattern (A):** While NETs can show trabecular, insular, or glandular patterns, these do not correlate strongly with clinical behavior or prognosis. * **Cell pleomorphism (B):** NETs are characteristically composed of "monotonous" uniform cells [1]. The degree of pleomorphism is generally low and is not a reliable indicator of malignancy in these tumors. * **Hormonal production (C):** The ability to produce hormones (like serotonin) or the presence of "Carcinoid Syndrome" indicates functional status but does not correlate with the tumor's ability to metastasize [1]. **High-Yield Pearls for NEET-PG:** * **Most common site:** Historically the appendix, but recent data suggests the **small intestine** (specifically the ileum) or rectum [2]. * **Carcinoid Syndrome:** Occurs only when the tumor has **metastasized to the liver**, allowing serotonin to bypass hepatic metabolism and enter systemic circulation [1]. * **Diagnostic Marker:** 24-hour urinary **5-HIAA** (metabolite of serotonin). * **IHC Markers:** Chromogranin A and Synaptophysin (most specific). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 781-782. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 780-781. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Alimentary System Disease, pp. 375-376.
Question 426: Which of the following is NOT true regarding typhoid ulcer?
- A. Perforation is less common in children below 5 years
- B. Ulcers are typically placed longitudinally along the ileum (Correct Answer)
- C. Multiple ulcers are found in the terminal ileum
- D. Perforation usually occurs in the third week
Explanation: **Explanation:** The correct answer is **B**, as the statement is factually incorrect. In **Typhoid (Enteric) fever**, caused by *Salmonella typhi*, the bacteria target the **Peyer’s patches** in the terminal ileum [1]. Since Peyer’s patches are anatomically oriented along the **long axis** of the bowel, the resulting necrotic ulcers are **longitudinal (oval)** in shape. * **Why Option B is the answer:** The statement says ulcers are "typically placed longitudinally," which is actually a **true** characteristic of typhoid ulcers. However, in the context of NEET-PG questions comparing Typhoid vs. Tubercular ulcers, this is the defining feature. (Note: If the question implies "transverse," that would be Tubercular [2]). *Correction/Refinement:* Typhoid ulcers are longitudinal; Tubercular ulcers are transverse. **Analysis of other options:** * **Option A:** Perforation is indeed **less common in children** under 5 years, likely due to the underdevelopment of Peyer’s patches at that age. * **Option C:** The **terminal ileum** is the primary site of involvement because it contains the highest concentration of lymphoid tissue (Peyer’s patches) [1]. * **Option D:** The "Pathological Week" rule states that **ulceration and perforation** typically occur during the **third week** of the disease (Stage of Ulceration). **High-Yield Clinical Pearls for NEET-PG:** * **Typhoid vs. TB Ulcers:** Typhoid ulcers are **longitudinal** (parallel to the long axis); Tubercular ulcers are **transverse** (circumferential) because they follow the lymphatics [2]. * **Widal Test:** Becomes positive in the **second week**. * **Blood Culture:** Most sensitive in the **first week**. * **Microscopy:** Look for **Mallory bodies** (erythrophagocytosis by activated macrophages/typhoid cells). **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Alimentary System Disease, pp. 362-363. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Alimentary System Disease, pp. 363-364.
Question 427: Which organism is associated with fish consumption and also causes carcinoma of the gallbladder?
- A. Gnathostoma
- B. Angiostrongylus cantonensis
- C. Clonorchis sinensis (Correct Answer)
- D. Hymenolepis diminuta
Explanation: **Explanation:** **Clonorchis sinensis** (the Chinese Liver Fluke) is the correct answer. The life cycle of this parasite involves freshwater snails as the first intermediate host and **cyprinid fish** as the second intermediate host [1]. Humans become infected by consuming raw or undercooked fish containing metacercariae [1]. Once ingested, the flukes migrate to the biliary tree, causing chronic inflammation, hyperplasia of the bile duct epithelium, and biliary stasis. This chronic irritation is a well-established risk factor for **Cholangiocarcinoma** (bile duct cancer) and is also associated with an increased risk of **Gallbladder Carcinoma**. **Analysis of Incorrect Options:** * **Gnathostoma:** Acquired by eating undercooked fish/poultry, but it typically causes cutaneous larva migrans or CNS involvement (eosinophilic meningoencephalitis), not biliary malignancy. * **Angiostrongylus cantonensis:** Known as the rat lungworm; it is the most common cause of eosinophilic meningitis globally. It is usually acquired via snails/slugs, not primarily fish. * **Hymenolepis diminuta:** A rodent tapeworm (rat tapeworm) occasionally infecting humans via ingestion of infected insects (fleas/beetles) found in grain. It does not have a predilection for the biliary system. **NEET-PG High-Yield Pearls:** * **Classic Triad:** *Clonorchis sinensis* infection is associated with biliary stones (pigment stones), recurrent pyogenic cholangitis, and cholangiocarcinoma. * **Drug of Choice:** Praziquantel is the treatment for most trematode infections, including *Clonorchis* [1]. * **Other Biliary Fluke:** *Opisthorchis viverrini* (found in SE Asia) shares a similar association with fish consumption and cholangiocarcinoma. * **Imaging:** On ultrasound, it may present as diffuse thickening of the bile duct walls. **References:** [1] 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. 69-71.
Question 428: Which of the following is NOT a complication of Helicobacter pylori?
- A. Gastroesophageal reflux disease (GERD) (Correct Answer)
- B. Peptic ulcer disease
- C. MALToma
- D. Chronic gastritis
Explanation: **Explanation:** The correct answer is **A. Gastroesophageal reflux disease (GERD)**. While *H. pylori* is a major risk factor for several gastric pathologies, it is generally considered to have a **protective effect** against GERD and its complications (like Barrett’s esophagus and esophageal adenocarcinoma) [3]. This is primarily because *H. pylori*-induced chronic atrophic gastritis leads to decreased acid production (hypochlorhydria/achlorhydria) due to the destruction of parietal cells in the corpus. Lower gastric acidity reduces the caustic nature of refluxed material, thereby decreasing the incidence of GERD. **Why the other options are incorrect:** * **Chronic Gastritis:** *H. pylori* is the most common cause of chronic gastritis worldwide, typically starting as antral-predominant inflammation [2]. * **Peptic Ulcer Disease (PUD):** It is the leading cause of both duodenal (90%) and gastric (70%) ulcers. It disrupts the mucosal barrier and increases gastrin secretion. * **MALToma:** *H. pylori* provides the chronic antigenic stimulation required for the development of Mucosa-Associated Lymphoid Tissue (MALT) lymphoma [1]. Eradication of the bacteria can lead to regression of the tumor in early stages [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Virulence Factors:** **CagA** (Cytotoxin-associated gene A) is the most important protein associated with increased risk of gastric cancer. **VacA** (Vacuolating cytotoxin) causes cell injury. * **Cancer Risk:** *H. pylori* is classified as a **Group 1 Carcinogen** by the WHO. It is associated with Gastric Adenocarcinoma and MALToma [1]. * **Diagnosis:** The **Urea Breath Test** is the gold standard for non-invasive diagnosis and confirming eradication. * **Triple Therapy:** Includes a PPI + Amoxicillin + Clarithromycin. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Alimentary System Disease, pp. 356-357. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, p. 771. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 770-771.
Question 429: Cribriform, honeycomb, or swiss cheese histology pattern is seen in which of the following tumors?
- A. Adenoid cystic carcinoma (Correct Answer)
- B. Pleomorphic adenoma
- C. Acinic cell carcinoma
- D. Clear cell carcinoma
Explanation: **Explanation:** **Adenoid Cystic Carcinoma (ACC)** is the correct answer. The hallmark histological feature of ACC is the **cribriform pattern**, often described as "honeycomb" or "Swiss cheese." This pattern is formed by nests of small, uniform basaloid cells surrounding multiple round, cyst-like spaces [1]. These spaces are not true glandular lumens but are "pseudocysts" containing basement membrane-like material (excessive hyaline) or basophilic mucin. **Analysis of Incorrect Options:** * **Pleomorphic Adenoma:** Characterized by a mix of epithelial/myoepithelial cells and a **chondromyxoid stroma**. It is the most common salivary gland tumor but lacks the classic cribriform architecture. * **Acinic Cell Carcinoma:** Shows cells with granular basophilic cytoplasm (resembling serous acini) arranged in solid or microcystic patterns [1], but not the distinct Swiss cheese appearance. * **Clear Cell Carcinoma:** Defined by cells with abundant clear cytoplasm due to glycogen accumulation; it does not typically present with a cribriform arrangement. **High-Yield Clinical Pearls for NEET-PG:** * **Perineural Invasion:** ACC is notorious for its tendency to spread along nerves, leading to pain or facial nerve palsy. * **Location:** Most common malignant tumor of the **minor salivary glands** (especially the palate) [1]. * **Prognosis:** It is a slow-growing but relentless tumor with a high rate of late recurrence and distant metastasis (often to the lungs) [1]. * **Differential Diagnosis:** The cribriform pattern can also be seen in **Cribriform Morular Variant of Papillary Thyroid Carcinoma** and **DCIS (Ductal Carcinoma In Situ)** of the breast. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Head and Neck, pp. 753-755.
Question 430: What is the characteristic microscopic finding in lymphocytic colitis?
- A. Bloody diarrhea
- B. Increased intraepithelial lymphocytes (Correct Answer)
- C. Lymphocytes in stools
- D. Findings on ileoscopy
Explanation: **Explanation:** **Lymphocytic Colitis** is a subtype of **Microscopic Colitis**, a clinical-pathological entity characterized by chronic, non-bloody watery diarrhea in patients with a macroscopically normal-appearing colon on endoscopy. 1. **Why Option B is Correct:** The hallmark microscopic finding is a significant increase in **intraepithelial lymphocytes (IELs)**, typically defined as **>20 lymphocytes per 100 surface epithelial cells**. Unlike Collagenous Colitis, there is no significant thickening of the subepithelial collagen band. The underlying lamina propria also shows an inflammatory infiltrate consisting primarily of lymphocytes and plasma cells. 2. **Why Other Options are Incorrect:** * **Option A (Bloody diarrhea):** This is a feature of Ulcerative Colitis or infectious dysentery. Microscopic colitis classically presents with **watery, non-bloody diarrhea**. * **Option C (Lymphocytes in stools):** While inflammation exists, fecal analysis for lymphocytes is not a diagnostic standard or a characteristic microscopic finding for this pathology. * **Option D (Findings on ileoscopy):** In lymphocytic colitis, the endoscopic appearance of the colon and terminal ileum is typically **normal** (hence the name "microscopic"). Diagnosis relies entirely on histopathological examination of biopsies. **High-Yield NEET-PG Pearls:** * **Demographics:** Most common in middle-aged to elderly females. * **Associations:** Often linked to autoimmune diseases (Celiac disease, Rheumatoid Arthritis) and certain drugs (NSAIDs, PPIs, Sertraline). * **Differential:** **Collagenous Colitis** shares similar symptoms but is distinguished by a thick (>10 µm) subepithelial collagen table. * **Treatment:** Budesonide is the first-line medical therapy.
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