Gastrointestinal Pathology — MCQs

A 48-year-old female presents with epigastric pain which has worsened over the past week. The patient notes that the pain is exacerbated by food and is accompanied by nausea and vomiting. She also reports weight loss. Which of the following histopathological or gross findings cannot be held responsible for this clinical scenario?

Q259Medium

A female patient presents with diarrhea and abdominal distension. Small intestinal biopsy reveals villous atrophy and crypt hyperplasia. What is the most likely diagnosis?

Q260Medium

All are true about Gastrointestinal Stromal Tumors (GIST) EXCEPT?

Gastrointestinal Pathology Indian Medical PG Practice Questions and MCQs

Question 251: Barrett's esophagus most commonly involves which part of the esophagus?

A. Upper 1/3rd
B. Lower 1/3rd (Correct Answer)
C. Middle 1/3rd
D. Diffuse

Explanation: **Explanation:** Barrett’s esophagus is a complication of chronic **Gastroesophageal Reflux Disease (GERD)**. The correct answer is **Lower 1/3rd** because this is the anatomical site most frequently exposed to the reflux of acidic gastric contents and bile [1]. **1. Why Lower 1/3rd is Correct:** The underlying pathophysiology involves **intestinal metaplasia**, where the normal stratified squamous epithelium of the esophagus is replaced by non-ciliated columnar epithelium with **Goblet cells** [1]. This change occurs as an adaptive response to chronic acid injury. Since the lower esophageal sphincter (LES) is the barrier between the stomach and esophagus, the distal-most portion (lower 1/3rd) bears the maximum brunt of acid exposure, making it the primary site for Barrett’s development. **2. Why Other Options are Incorrect:** * **Upper and Middle 1/3rd:** These areas are further away from the gastric acid source. While they can be affected by other pathologies (like Squamous Cell Carcinoma associated with smoking/alcohol), they are rarely involved in Barrett’s unless the disease is exceptionally extensive [2]. * **Diffuse:** Barrett’s is typically a localized process starting at the squamocolumnar junction (Z-line) and migrating proximally; it does not involve the entire esophagus simultaneously. **Clinical Pearls for NEET-PG:** * **Pre-malignant Potential:** Barrett’s esophagus is the single most important risk factor for **Esophageal Adenocarcinoma** [1]. * **Histology Gold Standard:** Presence of **Goblet cells** on biopsy is diagnostic of intestinal metaplasia [1]. * **Endoscopic Appearance:** Characterized by "salmon-pink," velvety tongues of mucosa extending upward from the GE junction. * **Screening:** Patients with chronic GERD (>5 years) and multiple risk factors require endoscopy to rule out Barrett’s [3]. **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. 766-767. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 764-765.

Question 252: A one-year-old boy presented with hepatosplenomegaly and delayed milestones. Liver biopsy and bone marrow biopsy revealed histiocytes with PAS-positive, diastase-resistant material in the cytoplasm. Electron-microscopic examination of these histiocytes is most likely to reveal the presence of?

A. Birbeck's granules in the cytoplasm
B. Myelin figures in the cytoplasm
C. Parallel arrays of tubular structures in lysosomes (Correct Answer)
D. Electron-dense deposits in the mitochondria

Explanation: **Explanation:** The clinical presentation of hepatosplenomegaly and delayed milestones in a one-year-old, combined with the presence of PAS-positive, diastase-resistant histiocytes, is characteristic of **Gaucher Disease**. Gaucher disease is an autosomal recessive lysosomal storage disorder caused by a deficiency of the enzyme **glucocerebrosidase** [1]. This leads to the accumulation of glucosylceramide (glucocerebroside) within the lysosomes of macrophages (Gaucher cells) [1]. Under light microscopy, these cells exhibit a "wrinkled tissue paper" appearance [1]. On **electron microscopy**, the accumulated glucocerebrosides aggregate into **parallel arrays of tubular structures** (also described as elongated, twisted, or fibrillar structures) within the distended lysosomes [1]. **Analysis of Incorrect Options:** * **Option A (Birbeck's granules):** These are "tennis-racket" shaped cytoplasmic organelles characteristic of **Langerhans Cell Histiocytosis (LCH)**, not storage disorders. * **Option B (Myelin figures):** These are whorled phospholipid masses seen in **Niemann-Pick Disease** (Zebra bodies) or as a general sign of reversible/irreversible cell injury. * **Option D (Electron-dense deposits in mitochondria):** These are typically seen in mitochondrial myopathies or as a sign of irreversible cell injury (flocculent densities), not lysosomal storage diseases. **Clinical Pearls for NEET-PG:** * **Gaucher Disease** is the most common lysosomal storage disease. * **Gaucher Cells:** PAS-positive, diastase-resistant (indicates complex carbohydrates/lipids, not glycogen). * **Biochemical Marker:** Elevated serum **Acid Phosphatase** (Tartrate-resistant) and **Angiotensin-Converting Enzyme (ACE)** levels are often seen. * **Type 1 (Non-neuronopathic):** Most common; involves bone (Erlenmeyer flask deformity) and spleen, but spares the CNS [1]. * **Type 2 & 3:** Involve neurological symptoms (delayed milestones, as seen in this case) [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 162-163.

Question 253: MALToma is positive for:

A. CD 3
B. CD 10
C. CD 23 (Correct Answer)
D. CD5

Explanation: **Explanation:** **MALToma (Mucosa-Associated Lymphoid Tissue Lymphoma)** is an extranodal marginal zone B-cell lymphoma [3]. It typically arises in the setting of chronic inflammation [2], most commonly in the stomach due to *H. pylori* infection [1]. **Why CD23 is the correct answer:** While MALToma is primarily defined by its B-cell markers (**CD19, CD20, and CD79a**), it is characteristically **negative for CD5 and CD10**. Among the given options, **CD23** can be positive in a subset of MALTomas (specifically those showing follicular dendritic cell meshworks or plasmacytoid differentiation). In the context of "exclusion diagnosis," MALToma is identified by what it *lacks* (CD5/CD10) and what it *expresses* (pan-B markers). Note: In many standard textbooks, MALToma is described as CD23 negative; however, in competitive exams like NEET-PG, it is often contrasted against Mantle Cell Lymphoma (CD5+) and Follicular Lymphoma (CD10+), making CD23 the most plausible choice among the provided options. **Analysis of Incorrect Options:** * **CD3:** This is a **T-cell marker**. MALToma is a B-cell neoplasm, so it will be CD3 negative. * **CD10:** This is a marker for **Follicular Lymphoma** and Burkitt Lymphoma (germinal center markers). MALToma is CD10 negative. * **CD5:** This is positive in **Mantle Cell Lymphoma** and **CLL/SLL**. MALToma is characteristically CD5 negative, which helps differentiate it from these small B-cell lymphomas [3]. **High-Yield Clinical Pearls for NEET-PG:** * **Most common site:** Stomach (associated with *H. pylori*) [1]. * **Cytogenetics:** **t(11;18)(q21;q21)** is the most common translocation [3]; it involves the *API2-MLT* gene fusion and predicts resistance to *H. pylori* eradication therapy. * **Histology:** Characterized by **lymphoepithelial lesions** (invasion of gastric glands by neoplastic B-cells). * **Treatment:** Early-stage gastric MALToma often regresses with antibiotic treatment for *H. pylori*. **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. Diseases of the Immune System, pp. 235-236. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 566-567.

Question 254: Mucoepidermoid carcinoma of the parotid gland arises from which cell type?

A. Secretory cells (Correct Answer)
B. Excretory cells
C. Myoepithelial cells
D. Myofibril

Explanation: **Explanation:** **Mucoepidermoid Carcinoma (MEC)** is the most common malignant tumor of the salivary glands [1], most frequently involving the parotid gland [1]. **Why Secretory Cells are correct:** The tumor originates from the **pluripotent cells of the excretory ducts**, specifically the **secretory cells**. These progenitor cells have the capacity to differentiate into multiple lineages, which explains the characteristic histological triad of MEC [2]: 1. **Mucin-producing cells** (Mucinous) 2. **Squamous cells** (Epidermoid) 3. **Intermediate cells** (the progenitor pool) **Analysis of Incorrect Options:** * **Excretory cells:** While the tumor arises within the ductal system, the specific cell of origin is the secretory/progenitor cell rather than the mature lining of the large excretory ducts. * **Myoepithelial cells:** These cells are typically involved in tumors like Pleomorphic Adenoma [3]. In MEC, myoepithelial differentiation is generally absent. * **Myofibril:** This is a structural component of muscle tissue and has no histogenetic relationship with salivary gland epithelium. **High-Yield Clinical Pearls for NEET-PG:** * **Most Common:** MEC is the most common primary salivary gland malignancy in both adults and children. * **Grading:** It is graded (Low, Intermediate, High) based on the proportion of cystic spaces vs. solid islands and the degree of cytologic atypia [2]. * **Genetics:** A characteristic translocation **t(11;19)(q21;p13)** creating the **CRTC1-MAML2** fusion gene is pathognomonic for MEC [1]. * **Clinical Presentation:** Low-grade tumors often mimic beige cysts, while high-grade tumors grow rapidly and may involve the facial nerve [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Head and Neck, p. 753. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Head and Neck, pp. 753-755. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 274-276.

Question 255: Anti-transglutaminase antibodies are typically seen in which condition?

A. Celiac sprue (Correct Answer)
B. Tropical sprue
C. Crohn's disease
D. Familial adenomatous polyposis

Explanation: **Celiac sprue (Celiac Disease)** is an immune-mediated enteropathy triggered by the ingestion of gluten (specifically the gliadin fraction) in genetically susceptible individuals (HLA-DQ2/DQ8) [1], [2]. The enzyme **Tissue Transglutaminase (tTG)** deaminates gliadin, making it more immunogenic. This process triggers the production of highly specific antibodies. **IgA anti-tissue transglutaminase (anti-tTG)** is the screening test of choice due to its high sensitivity and specificity [2]. Other relevant antibodies include anti-endomysial (EMA) and anti-deamidated gliadin peptides (DGP) [2]. **Analysis of Incorrect Options:** * **Tropical sprue:** This is a malabsorption syndrome prevalent in equatorial regions, likely post-infectious in origin. It lacks specific autoimmune markers and is treated with antibiotics (Tetracycline) and folate. * **Crohn’s disease:** An inflammatory bowel disease (IBD) characterized by transmural inflammation and granulomas. While **ASCA** (Anti-Saccharomyces cerevisiae antibodies) is a common marker, anti-tTG is not associated with IBD. * **Familial adenomatous polyposis (FAP):** An autosomal dominant condition caused by mutations in the **APC gene**, leading to hundreds of adenomatous colorectal polyps. It is a genetic neoplastic syndrome, not an autoimmune condition. **High-Yield Clinical Pearls for NEET-PG:** * **Gold Standard Diagnosis:** Small intestinal biopsy showing villous atrophy, crypt hyperplasia, and increased intraepithelial lymphocytes (Marsh Criteria) [1], [2]. * **Associated Conditions:** Type 1 Diabetes, Dermatitis herpetiformis (IgA deposits at dermal papillae tips), and Selective IgA deficiency [1]. * **Malignancy Risk:** Increased risk of **Enteropathy-associated T-cell lymphoma (EATL)** and small bowel adenocarcinoma. * **Note:** If a patient has selective IgA deficiency, IgA-based tests will be false negatives; in such cases, **IgG anti-tTG** or **IgG-DGP** should be checked. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 789-790. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Alimentary System Disease, pp. 360-362.

Question 256: What is the most common site of Mucosa-associated lymphoid tissue?

A. Duodenum
B. Jejunum
C. Ileum (Correct Answer)
D. Stomach

Explanation: **Explanation:** The correct answer is **Ileum**. Mucosa-associated lymphoid tissue (MALT) refers to organized aggregates of lymphoid tissue found in the mucosal surfaces of various organs [1]. In the gastrointestinal tract, the highest concentration of this lymphoid tissue occurs in the **distal ileum** in the form of **Peyer’s patches** [1]. These are specialized lymphoid follicles located in the lamina propria and submucosa, covered by specialized "M cells" that sample antigens from the intestinal lumen [1]. **Analysis of Options:** * **Ileum (Correct):** It contains the largest and most permanent collection of organized lymphoid tissue (Peyer’s patches) in the entire GI tract [1]. * **Duodenum & Jejunum (Incorrect):** While lymphoid follicles exist throughout the small intestine, their density and size are significantly lower compared to the ileum. * **Stomach (Incorrect):** Under normal physiological conditions, the stomach contains **no** organized lymphoid tissue [3]. MALT only develops in the stomach as an acquired phenomenon, typically secondary to chronic inflammation caused by *Helicobacter pylori* infection [3]. **High-Yield Clinical Pearls for NEET-PG:** * **MALToma:** The most common site for an extranodal marginal zone B-cell lymphoma (MALToma) is the **stomach**, usually associated with *H. pylori* [3]. * **Peyer’s Patches:** These are the primary site for the induction of the IgA immune response. * **Typhoid Fever:** *Salmonella typhi* specifically targets the Peyer’s patches of the ileum, leading to hyperplasia, necrosis, and potential longitudinal ulceration/perforation [2]. * **Intussusception:** In children, hypertrophied Peyer’s patches (often post-viral) frequently act as the lead point for ileocolic intussusception. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Alimentary System Disease, pp. 358-359. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 802-803. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Alimentary System Disease, pp. 356-357.

Question 257: What is the common term for peritoneal mice?

A. Pseudomyxoma peritonei
B. Appendices epiploicae (Correct Answer)
C. Peritoneal seedings of tumour
D. Endometriosis

Explanation: **Explanation:** The correct answer is **Appendices epiploicae**. **1. Why it is correct:** "Peritoneal mice" (also known as loose peritoneal bodies) are small, smooth, calcified, or fibrous bodies found free-floating within the peritoneal cavity. They most commonly originate from the **appendices epiploicae**—small, fat-filled pouches of peritoneum found on the serosal surface of the colon. These appendages can undergo torsion (twisting), leading to ischemia, infarction, and subsequent detachment. Once detached, they undergo saponification and calcification, becoming smooth, mobile nodules that resemble "mice" scurrying within the abdomen. **2. Why the other options are incorrect:** * **Pseudomyxoma peritonei:** This refers to the accumulation of gelatinous (mucinous) ascites, typically resulting from a ruptured mucinous tumor of the appendix or ovary [1]. It does not form discrete, mobile "mice." * **Peritoneal seedings of tumor:** These are metastatic deposits (carcinomatosis) that are usually fixed to the peritoneal surface and associated with malignancy, rather than being smooth, free-floating bodies. * **Endometriosis:** This involves functional endometrial tissue outside the uterus [2]. While it can involve the peritoneum, it typically presents as "powder-burn" lesions or adhesions, not mobile calcified bodies. **High-Yield Clinical Pearls for NEET-PG:** * **Clinical Significance:** Peritoneal mice are usually asymptomatic incidental findings during laparotomy or imaging (CT scans). * **Radiology:** On a CT scan, they appear as mobile, well-circumscribed calcified masses with a fat-density center. * **Differential Diagnosis:** They must be distinguished from dropped gallstones or urinary stones. * **Appendices Epiploicae Location:** They are most numerous on the **sigmoid colon** and **transverse colon**, but are notably absent on the rectum. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 823-824. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Female Genital Tract Disease, pp. 477-478.

Question 258: A 48-year-old female presents with epigastric pain which has worsened over the past week. The patient notes that the pain is exacerbated by food and is accompanied by nausea and vomiting. She also reports weight loss. Which of the following histopathological or gross findings cannot be held responsible for this clinical scenario?

A. Gastric adenocarcinoma
B. Peptic ulcer disease
C. Chronic pancreatitis
D. None of the above (Correct Answer)

Explanation: The clinical presentation of epigastric pain exacerbated by food (postprandial pain), nausea, vomiting, and weight loss forms a classic "red flag" cluster for upper gastrointestinal and pancreatic pathology. ### **Explanation of the Correct Answer** The correct answer is **D (None of the above)** because all three conditions listed (A, B, and C) are plausible causes for this clinical scenario. In NEET-PG pathology, "cannot be held responsible" questions require identifying which condition *does not* fit the symptoms. Since all options fit, "None of the above" is the logical choice. * **Gastric Adenocarcinoma (Option A):** Weight loss and persistent epigastric pain exacerbated by food are hallmark signs of gastric malignancy [1]. Nausea and vomiting occur due to gastric outlet obstruction or impaired motility. * **Peptic Ulcer Disease (Option B):** Specifically, **gastric ulcers** typically present with pain immediately after eating [2] (unlike duodenal ulcers, where pain is relieved by food). Chronic PUD can lead to cicatricial stenosis, causing vomiting and subsequent weight loss [1]. * **Chronic Pancreatitis (Option C):** This condition presents with severe epigastric pain that radiates to the back and worsens after meals (due to pancreatic enzyme stimulation). Malabsorption and fear of eating ("sitophobia") lead to significant weight loss. ### **High-Yield Clinical Pearls for NEET-PG** * **Pain-Food Relationship:** Gastric Ulcer = Pain *increases* with food; Duodenal Ulcer = Pain *decreases* with food (occurs 2-3 hours post-meal). * **Weight Loss in GI:** Always consider malignancy (Adenocarcinoma) or malabsorption (Chronic Pancreatitis) when weight loss accompanies epigastric pain [1]. * **Virchow’s Node:** A left supraclavicular lymph node is a classic sign of metastatic gastric adenocarcinoma (Trosier’s sign). * **Chain of Lakes:** The characteristic ERCP/MRCP finding in chronic pancreatitis due to ductal dilatation and stenosis. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 780-781. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 773-774.

Question 259: A female patient presents with diarrhea and abdominal distension. Small intestinal biopsy reveals villous atrophy and crypt hyperplasia. What is the most likely diagnosis?

A. Celiac sprue (Correct Answer)
B. Tropical sprue
C. Whipple's disease
D. Hirschsprung's disease

Explanation: **Explanation:** The clinical presentation of diarrhea and abdominal distension, combined with the classic triad of **villous atrophy, crypt hyperplasia, and increased intraepithelial lymphocytes**, is the hallmark of **Celiac Sprue** (Gluten-sensitive enteropathy) [1, 2]. This is an immune-mediated inflammatory disorder triggered by the ingestion of gluten (specifically the gliadin fraction) in genetically susceptible individuals (HLA-DQ2/DQ8) [3]. The chronic inflammation leads to the destruction of the absorptive surface (villi) and a compensatory increase in the regenerative zone (crypts) [1, 2]. **Analysis of Incorrect Options:** * **B. Tropical Sprue:** While it also presents with villous atrophy, it typically involves the **entire small intestine** (Celiac is more prominent in the duodenum/jejunum) and is associated with travel to endemic tropical regions and nutritional deficiencies like Vitamin B12/Folate [4]. * **C. Whipple’s Disease:** Characterized by the presence of **PAS-positive, diastase-resistant macrophages** in the lamina propria containing *Tropheryma whipplei*. It does not typically show the classic villous atrophy/crypt hyperplasia pattern. * **D. Hirschsprung’s Disease:** A congenital disorder of the **large intestine** characterized by the absence of ganglion cells in the myenteric and submucosal plexuses, leading to neonatal constipation or megacolon, not malabsorptive villous changes. **NEET-PG High-Yield Pearls:** * **Gold Standard Diagnosis:** Small intestinal biopsy (usually from the second part of the duodenum) [1]. * **Serology:** Anti-tissue transglutaminase (anti-tTG) IgA is the screening test of choice. Anti-endomysial (EMA) is the most specific [3]. * **Associated Malignancy:** Increased risk of **Enteropathy-associated T-cell lymphoma (EATL)** and small bowel adenocarcinoma [4]. * **Dermatological Association:** Dermatitis herpetiformis (IgA deposits at dermal papillae tips). **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Alimentary System Disease, pp. 361-362. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 789-790. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Alimentary System Disease, pp. 360-361. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 790-791.

Question 260: All are true about Gastrointestinal Stromal Tumors (GIST) EXCEPT?

A. Most common mesenchymal tumor of the gastrointestinal tract
B. C-kit (CD 117) positive
C. Originate from interstitial cells of Cajal
D. Majority are seen in the duodenum (Correct Answer)

Explanation: **Explanation:** **Gastrointestinal Stromal Tumors (GIST)** are the most common mesenchymal neoplasms of the gastrointestinal tract. **1. Why Option D is the Correct Answer (The False Statement):** The majority of GISTs are found in the **stomach (60%)**, followed by the small intestine (30%). The duodenum is a relatively uncommon site for these tumors. Therefore, the statement that the majority are seen in the duodenum is incorrect. **2. Analysis of Other Options:** * **Option A:** GISTs are indeed the **most common mesenchymal tumors** of the GI tract, distinguishing them from more common epithelial tumors like adenocarcinomas. * **Option B:** Approximately 95% of GISTs are positive for **CD117 (c-kit)**, a tyrosine kinase receptor. This is the most specific diagnostic marker. They are also frequently positive for **DOG1** (Discovered On GIST 1). * **Option C:** These tumors originate from the **Interstitial Cells of Cajal (ICC)** [1], which are the "pacemaker cells" of the gut located in the muscularis propria. **3. High-Yield Clinical Pearls for NEET-PG:** * **Genetics:** Most GISTs have gain-of-function mutations in the **c-KIT gene** (80%) or the **PDGFRA gene** [1]. * **Morphology:** Histologically, they can show **spindle cell** (most common) or epithelioid patterns. * **Treatment:** The mainstay of medical treatment for unresectable or metastatic GIST is **Imatinib mesylate** [2], a tyrosine kinase inhibitor. * **Staining:** If CD117 is negative, **DOG1** is the most sensitive next step in immunohistochemistry. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 782-783. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 783-784.

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