Gastrointestinal Pathology — MCQs

A clinical study of adult patients with chronic bloody diarrhea is performed. One group of these patients is found to have a statistically increased likelihood for antibodies to Saccharomyces cerevisiae but not anti-neutrophil cytoplasmic autoantibodies, NOD2 gene polymorphisms, TH1 and TH17 immune cell activation, vitamin K deficiency, megaloblastic anemia, and gallstones. Which of the following diseases is this group of patients most likely to have?

Q296Medium

Which of the following is FALSE about Barrett's esophagus?

Q297Medium

What is true about intestinal lymphoma?

Q298Medium

What is the characteristic histological finding in solitary rectal ulcer syndrome?

Q299Medium

Histologic examination of a gastric lesion reveals fat-laden cells. What is the likely cause?

Q300Easy

Which of the following is false about celiac disease?

Gastrointestinal Pathology Indian Medical PG Practice Questions and MCQs

Question 291: Colon carcinogenesis is associated with all of the following genetic mutations, EXCEPT:

A. APC
B. kRAS
C. B-catenin
D. HER2 gene (Correct Answer)

Explanation: The pathogenesis of colorectal carcinoma (CRC) follows a well-defined molecular pathway, primarily the **Adenoma-Carcinoma Sequence** [1]. **Explanation of the Correct Answer:** * **D. HER2 gene:** This is the correct answer because HER2 (ERBB2) amplification is primarily associated with **breast and gastric carcinomas**, not the standard pathogenesis of colon cancer [3]. While it may be explored as a minor therapeutic target in metastatic cases, it is not a driver mutation in the classic colon carcinogenesis models. **Explanation of Incorrect Options:** * **A. APC (Adenomatous Polyposis Coli):** Known as the "gatekeeper" of colonic neoplasia. Mutations in the APC gene are the earliest event in the chromosomal instability (CIN) pathway, occurring in both sporadic CRC and Familial Adenomatous Polyposis (FAP) [2]. * **B. kRAS:** This is a downstream signaling oncogene. Mutations in kRAS typically occur after APC loss, promoting the transition from a small adenoma to a larger, more dysplastic polyp [1]. * **C. β-catenin:** In the absence of functional APC, β-catenin accumulates and translocates to the nucleus, where it activates genes (like *MYC* and *Cyclin D1*) that promote proliferation [1]. It is a central component of the WNT signaling pathway involved in CRC. **High-Yield Clinical Pearls for NEET-PG:** * **Vogelstein Model:** The sequence is: Loss of APC → Mutation of kRAS → Loss of SMAD2/4 → Loss of TP53 [4]. * **Microsatellite Instability (MSI) Pathway:** Associated with DNA Mismatch Repair (MMR) gene mutations (*MLH1, MSH2*); characteristic of Lynch Syndrome [4]. * **"Gold Standard" Screening:** Colonoscopy remains the most effective screening tool for identifying these precursor adenomas. **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] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Breast, pp. 1059-1060. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Alimentary System Disease, pp. 373-374.

Question 292: Total capacity of the stomach is markedly reduced in which of the following conditions?

A. Cauliflower growth of the stomach
B. Hourglass stomach
C. Pyloric stenosis
D. Linitis plastica (Correct Answer)

Explanation: **Explanation:** The correct answer is **Linitis plastica**, also known as "Leather Bottle Stomach." **1. Why Linitis Plastica is correct:** Linitis plastica is a morphological variant of **diffuse-type gastric adenocarcinoma** (Lauren classification). It is characterized by an infiltrative growth pattern where malignant cells (often **Signet ring cells**) spread extensively through the submucosa and muscularis propria [1]. This triggers a massive **desmoplastic reaction** (fibrosis), causing the gastric wall to become extremely thick, rigid, and non-distensible. Consequently, the stomach loses its ability to expand, leading to a **marked reduction in total gastric capacity** [1]. On barium swallow, it presents with the classic "leather bottle" appearance. **2. Why the other options are incorrect:** * **Cauliflower growth:** This refers to an **intestinal-type** adenocarcinoma that grows as a bulky, fungating mass into the lumen [1]. While it occupies space, it does not cause global rigidity or a significant reduction in the total volume of the stomach wall itself. * **Hourglass stomach:** This is a structural deformity typically caused by scarring from a chronic gastric ulcer on the lesser curvature. It divides the stomach into two interconnected pouches but does not involve a circumferential reduction in total capacity. * **Pyloric stenosis:** This causes an obstruction at the gastric outlet. Rather than reducing capacity, it leads to **gastric dilatation** as food and secretions accumulate behind the narrowed pylorus. **Clinical Pearls for NEET-PG:** * **Genetics:** Linitis plastica is frequently associated with the loss of **E-cadherin** (CDH1 gene mutation) [1]. * **Microscopy:** Look for **Signet ring cells** (nucleus pushed to the periphery by a large mucin vacuole) [1]. * **Virchow’s Node:** Left supraclavicular lymphadenopathy is a common sign of metastasis in gastric cancers. * **Krukenberg Tumor:** Gastric cancer (especially diffuse type) often metastasizes bilaterally to the ovaries. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 779-780.

Question 293: Which one of the following types of stomach cancers carries the best prognosis?

A. Superficial spreading (Correct Answer)
B. Ulcerative types
C. Linitis plastica type
D. Polypoidal type

Explanation: ### Explanation The prognosis of gastric carcinoma is primarily determined by the **depth of invasion** and the **presence of nodal involvement** at the time of diagnosis [1, 4]. **Why "Superficial Spreading" is correct:** Superficial spreading carcinoma is a subtype of **Early Gastric Cancer (EGC)**. By definition, EGC is confined to the **mucosa and submucosa**, regardless of lymph node status [2]. Because the tumor has not penetrated the muscularis propria, the risk of distant metastasis is significantly lower. Patients with superficial spreading lesions have a 5-year survival rate exceeding **90-95%**, making it the variant with the best prognosis [1, 3]. **Analysis of Incorrect Options:** * **B. Ulcerative types:** These are usually advanced gastric cancers (Bormann Type II or III) that have penetrated deep into the gastric wall [2]. They carry a much higher risk of lymphatic and hematogenous spread compared to superficial types. * **C. Linitis plastica:** Also known as "leather bottle stomach" (Bormann Type IV), this is a diffuse-type adenocarcinoma characterized by signet-ring cells and marked desmoplasia [3]. It infiltrates the entire stomach wall, leading to rigidity [3]. It carries the **worst prognosis** among all gastric cancers. * **D. Polypoidal type:** While these are often well-differentiated (Bormann Type I), they are typically bulky, advanced masses by the time they are symptomatic [4]. While better than linitis plastica, their prognosis does not match the excellent outcomes of superficial/early gastric cancer. **NEET-PG High-Yield Pearls:** * **Early Gastric Cancer (EGC):** Defined by depth (Mucosa/Submucosa), NOT by lymph node status [2]. * **Virchow’s Node:** Left supraclavicular lymph node involvement (Trosier’s sign). * **Krukenberg Tumor:** Bilateral ovarian metastasis from gastric cancer (Signet-ring cells). * **Sister Mary Joseph Nodule:** Periumbilical metastasis. * **Lauren Classification:** Divides gastric cancer into **Intestinal** (associated with H. pylori/metaplasia) and **Diffuse** (associated with CDH1 mutation/E-cadherin loss) [4]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Alimentary System Disease, pp. 349-350. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Alimentary System Disease, pp. 355-356. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 779-780. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, p. 779.

Question 294: What is a littoral cell angioma?

A. A tumor of the spleen (Correct Answer)
B. An angiomatous lesion of the skin
C. An angioblastic tumor of the cerebellum
D. A congenital vascular anomaly at the base of the brain

Explanation: **Explanation:** **Littoral Cell Angioma (LCA)** is a rare, primary vascular neoplasm arising exclusively from the **spleen**. It originates from the "littoral cells" that line the splenic sinuses of the red pulp. These cells are unique because they possess both endothelial and histiocytic properties. 1. **Why Option A is Correct:** LCA is a spleen-specific tumor. Pathologically, it presents with anastomosing vascular channels lined by tall, plump cells (littoral cells) that often show hemophagocytosis. A key diagnostic feature is the **dual immunohistochemical profile**: they express both endothelial markers (CD31) [1] and histiocytic markers (CD68). 2. **Why Other Options are Incorrect:** * **Option B:** Angiomatous lesions of the skin include entities like cherry hemangiomas or pyogenic granulomas [1], but not LCA. * **Option C:** An angioblastic tumor of the cerebellum refers to a **Hemangioblastoma**, which is classically associated with Von Hippel-Lindau (VHL) syndrome. * **Option D:** A congenital vascular anomaly at the base of the brain typically refers to a **Berry Aneurysm** (Circle of Willis) or an Arteriovenous Malformation (AVM). **High-Yield Clinical Pearls for NEET-PG:** * **Clinical Presentation:** Most patients present with splenomegaly, hypersplenism (anemia/thrombocytopenia), or are asymptomatic. * **Imaging:** Often shows multiple nodular lesions on CT/MRI (hypodense). * **Nature:** Usually benign, though rare malignant variants (Littoral cell angiosarcoma) exist. * **Key Marker:** CD68 positivity differentiates it from other splenic vascular tumors like splenic hemangioma. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 523-528.

Question 295: A clinical study of adult patients with chronic bloody diarrhea is performed. One group of these patients is found to have a statistically increased likelihood for antibodies to Saccharomyces cerevisiae but not anti-neutrophil cytoplasmic autoantibodies, NOD2 gene polymorphisms, TH1 and TH17 immune cell activation, vitamin K deficiency, megaloblastic anemia, and gallstones. Which of the following diseases is this group of patients most likely to have?

A. Angiodysplasia
B. Crohn disease (Correct Answer)
C. Diverticulitis
D. Ischemic enteritis

Explanation: **Explanation:** The clinical presentation of chronic bloody diarrhea combined with specific serological and genetic markers points toward **Crohn Disease (CD)**. **Why Crohn Disease is Correct:** * **ASCA vs. pANCA:** Anti-*Saccharomyces cerevisiae* antibodies (**ASCA**) are highly specific for Crohn disease (found in 60-70% of cases), whereas perinuclear anti-neutrophil cytoplasmic antibodies (**pANCA**) are more characteristic of Ulcerative Colitis. * **Genetics:** **NOD2** (CARD15) gene polymorphisms are the strongest genetic risk factors for CD, particularly ileal disease. * **Pathogenesis:** CD is driven by a **TH1 and TH17** immune response (producing IFN-γ and IL-17), unlike UC, which is more TH2-mediated [4]. * **Complications:** Because CD often involves the terminal ileum, it leads to malabsorption of fat-soluble vitamins (e.g., **Vitamin K deficiency**), Vitamin B12 (**Megaloblastic anemia**), and disruption of the enterohepatic circulation of bile salts, which increases the risk of **Gallstones** [1]. **Why the other options are incorrect:** * **Angiodysplasia:** Presents as painless hematochezia in the elderly; it is a vascular malformation, not an inflammatory or autoimmune condition. * **Diverticulitis:** Typically presents with acute left lower quadrant pain and fever; it does not involve ASCA or ileal malabsorption. * **Ischemic Enteritis:** Usually presents with acute abdominal pain out of proportion to physical findings or post-prandial "intestinal angina" in patients with atherosclerosis [5]. **NEET-PG High-Yield Pearls:** * **Transmural inflammation** and **Non-caseating granulomas** are hallmark pathological features of CD [2], [3]. * **String sign of Kantor** (barium study) and **Creeping fat** (gross appearance) are classic CD findings [2]. * **Skip lesions** occur in CD, whereas UC involves continuous colonic involvement starting from the rectum [1]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Alimentary System Disease, pp. 365-366. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Alimentary System Disease, pp. 366-367. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 806-807. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 803-805. [5] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Alimentary System Disease, pp. 368-369.

Question 296: Which of the following is FALSE about Barrett's esophagus?

A. In short-segment Barrett's, there is less than 3 cm of columnar epithelium.
B. Barrett's ulcer occurs just above the squamocolumnar junction. (Correct Answer)
C. If a peptic stricture occurs in Barrett's esophagus, it always occurs at the new squamocolumnar junction.
D. It is a premalignant condition.

Explanation: ### Explanation **Barrett’s Esophagus (BE)** is a complication of chronic GERD where the normal stratified squamous epithelium of the esophagus is replaced by metaplastic columnar epithelium (containing goblet cells) [1]. **Why Option B is the Correct (False) Statement:** A **Barrett’s ulcer** is a deep, chronic peptic ulcer that occurs **within the metaplastic columnar segment** itself, not above the squamocolumnar junction (SCJ). Ulcers occurring *at* or *above* the SCJ are typically standard reflux esophagitis erosions. Barrett’s ulcers are clinically significant because they can lead to strictures, perforation, or significant hemorrhage. **Analysis of Other Options:** * **Option A (True):** BE is classified by length. **Short-segment BE** involves <3 cm of columnar metaplasia, while **Long-segment BE** involves ≥3 cm. Long-segment carries a higher risk of malignancy. * **Option C (True):** Peptic strictures in the context of BE characteristically occur at the **new (proximal) squamocolumnar junction**. This is because the acid-resistant columnar epithelium protects the distal part, while the vulnerable squamous epithelium at the transition zone bears the brunt of the acid insult, leading to fibrosis. * **Option D (True):** BE is a well-established **premalignant condition** [1]. It follows the metaplasia → dysplasia → adenocarcinoma sequence [2]. The risk of esophageal adenocarcinoma is increased 30–40 fold in these patients [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Diagnosis:** Requires both endoscopic evidence of "salmon-pink" mucosa and histological evidence of **Intestinal Metaplasia (Goblet cells)** [1]. * **Stain:** **Alcian Blue** at pH 2.5 is used to highlight the acidic mucin in goblet cells. * **Surveillance:** Patients with BE require regular endoscopic surveillance to monitor for high-grade dysplasia [2]. **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.

Question 297: What is true about intestinal lymphoma?

A. It is involved in non-Hodgkin's lymphoma. (Correct Answer)
B. It is made up of predominantly T cells.
C. It is C-kit positive.
D. It is most common at the ileocecal junction.

Explanation: Primary gastrointestinal (GI) lymphoma is the most common site for extranodal lymphomas, accounting for approximately 1–4% of all GI malignancies. [1] **Explanation of the Correct Option:** * **Option A:** Almost all primary gastrointestinal lymphomas are **Non-Hodgkin Lymphomas (NHL)**. Hodgkin lymphoma involving the GI tract is extremely rare and usually occurs as part of systemic disease. The most common histological subtype is Diffuse Large B-Cell Lymphoma (DLBCL), followed by MALT lymphoma. [1] **Explanation of Incorrect Options:** * **Option B:** The vast majority (approx. 85–90%) of primary GI lymphomas are of **B-cell origin** (e.g., MALToma, DLBCL) [1]. T-cell lymphomas (like Enteropathy-associated T-cell lymphoma) are much rarer and typically associated with Celiac disease. * **Option C:** **C-kit (CD117)** is the hallmark marker for **Gastrointestinal Stromal Tumors (GIST)**, not lymphomas. Lymphomas express lymphoid markers like CD20 (B-cell) or CD3 (T-cell). * **Option D:** The **stomach** is the most common site for primary GI lymphoma (50–60%), followed by the small intestine (20–30%). [1] While the ileocecal region is a common site within the intestine, it is not the most common site in the GI tract overall. **High-Yield Clinical Pearls for NEET-PG:** 1. **MALToma:** Strongly associated with *H. pylori* infection. [1] Treatment of the infection often leads to regression of the tumor. 2. **IPSID (Immunoproliferative Small Intestinal Disease):** A variant of MALT lymphoma seen in the Mediterranean, associated with Alpha-heavy chain disease. 3. **Burkitt Lymphoma:** Often involves the ileocecal region in children (sporadic form). 4. **EATL (Enteropathy-associated T-cell lymphoma):** High-yield association with refractory Celiac disease and HLA-DQ2/DQ8. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Alimentary System Disease, pp. 356-358.

Question 298: What is the characteristic histological finding in solitary rectal ulcer syndrome?

A. Thick collagen band under the endothelial layer
B. Intraepithelial collection of lymphocytes
C. Crypt hypoplasia
D. Increased muscle layer proliferation (Correct Answer)

Explanation: **Explanation:** **Solitary Rectal Ulcer Syndrome (SRUS)** is a chronic, non-neoplastic inflammatory condition often associated with pelvic floor dyssynergia and chronic straining. The core pathophysiology involves repeated mucosal prolapse and ischemia, leading to a characteristic histological pattern known as **fibromuscular obliteration**. **Why Option D is correct:** The hallmark of SRUS is the **proliferation of smooth muscle fibers** from the muscularis mucosae into the lamina propria [1]. This is accompanied by the replacement of the normal lamina propria with collagen (fibrosis). This "fibromuscular hyperplasia" is a diagnostic feature that distinguishes it from other inflammatory bowel diseases. **Analysis of Incorrect Options:** * **Option A:** A thick subepithelial collagen band (typically >10 μm) is the classic finding in **Collagenous Colitis**, a type of microscopic colitis, not SRUS. * **Option B:** Intraepithelial lymphocytosis is characteristic of **Lymphocytic Colitis** or Celiac disease. While some inflammation exists in SRUS, it is not the defining feature. * **Option C:** SRUS typically shows **crypt architectural distortion** (hyperplasia, branching, or "diamond-shaped" crypts) rather than hypoplasia. **High-Yield Clinical Pearls for NEET-PG:** * **Clinical Triad:** Rectal bleeding, mucoid discharge, and a feeling of incomplete evacuation [1]. * **Endoscopy:** Despite the name, the lesion can be an ulcer, a polypoid mass, or simply erythematous mucosa; it is not always "solitary" or an "ulcer." * **Location:** Usually located on the **anterior rectal wall**, approximately 5–10 cm from the anal verge [1]. * **Key Histology Keyword:** "Fibromuscular obliteration of the lamina propria." **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 811-813.

Question 299: Histologic examination of a gastric lesion reveals fat-laden cells. What is the likely cause?

A. Lymphoma
B. Post-gastrectomy changes
C. Signet-cell carcinoma of the stomach
D. Atrophic gastritis (Correct Answer)

Explanation: ### Explanation The presence of fat-laden cells (lipid-containing macrophages) in the gastric mucosa is a characteristic feature of **Gastric Xanthelasma** (also known as Lipid Island). **1. Why Atrophic Gastritis is Correct:** Gastric xanthelasma consists of clusters of foamy macrophages (histiocytes) containing cholesterol and neutral fats within the lamina propria. While the exact pathogenesis is debated, it is strongly associated with chronic inflammatory states and mucosal injury. **Atrophic gastritis**, particularly when associated with *H. pylori* infection or bile reflux, is the most common underlying condition where these lesions are incidentally found [1]. The chronic inflammation leads to cell membrane breakdown, providing the lipids that are subsequently phagocytosed by macrophages. **2. Why Incorrect Options are Wrong:** * **Lymphoma:** Gastric lymphoma (like MALToma) presents with a dense infiltrate of atypical lymphocytes and "lymphoepithelial lesions," not lipid-laden macrophages [2]. * **Post-gastrectomy changes:** While bile reflux post-surgery can cause reactive gastropathy, the specific finding of "fat-laden cells" is a hallmark of xanthelasma, which is more broadly linked to the underlying chronic atrophic process. * **Signet-cell carcinoma:** This is a common distractor. Signet-ring cells contain **mucin**, which pushes the nucleus to the periphery [3]. While they may appear "clear" or "vacuolated," they do not contain fat/lipids and stain positive for PAS or Mucicarmine, not oil red O [3]. **3. NEET-PG High-Yield Pearls:** * **Gastric Xanthelasma:** Most common in the antrum; appears endoscopically as yellow-white, well-demarcated plaques. * **Signet Ring Cell vs. Xanthelasma:** Signet ring cells are malignant and contain mucin; Xanthelasma cells are benign histiocytes and contain lipids. * **Clinical Significance:** Xanthelasma is considered a marker for chronic mucosal damage and is often seen alongside intestinal metaplasia. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Alimentary System Disease, pp. 351-352. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Alimentary System Disease, pp. 356-357. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, p. 779.

Question 300: Which of the following is false about celiac disease?

A. Crypt hyperplasia
B. Infiltration of lymphocytes
C. Villous hyperplasia (Correct Answer)
D. Villous atrophy

Explanation: In Celiac disease, the fundamental pathology is a T-cell mediated immune response to gluten, leading to characteristic structural changes in the small intestinal mucosa [1]. **Explanation of the Correct Answer:** **Option C (Villous hyperplasia)** is the false statement because Celiac disease is characterized by **villous atrophy**, not hyperplasia [1], [2]. The chronic inflammatory process leads to the destruction and flattening of the finger-like projections (villi), which significantly reduces the surface area for absorption. **Analysis of Incorrect Options:** * **Option A (Crypt hyperplasia):** As the surface villi are destroyed, the intestinal stem cells in the crypts of Lieberkühn proliferate rapidly to compensate for the loss [1]. This results in elongated, deepened crypts. * **Option B (Infiltration of lymphocytes):** An increase in **Intraepithelial Lymphocytes (IELs)**—specifically CD8+ T cells—is the earliest histological marker of Celiac disease (Marsh Stage 1) [1]. * **Option D (Villous atrophy):** This is the hallmark of advanced Celiac disease (Marsh Stage 3) [2]. The villi become blunted and eventually disappear, leading to a "flat" mucosal appearance. **High-Yield Clinical Pearls for NEET-PG:** * **Marsh Classification:** Used to grade the severity of histological changes (Stage 0 to 4). * **Serology:** **Anti-tissue Transglutaminase (anti-tTG) IgA** is the screening test of choice. **Anti-Endomysial Antibody (EMA)** is the most specific [2]. * **Genetics:** Strongly associated with **HLA-DQ2** (95%) and **HLA-DQ8** [1], [2]. * **Site:** Most severe in the **distal duodenum and proximal jejunum** (areas with highest gluten exposure) [2]. * **Complications:** Increased risk of **Enteropathy-associated T-cell lymphoma (EATL)** and small bowel adenocarcinoma. **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.

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Malabsorption Syndromes

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Vascular Disorders of Intestine

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Diverticular Disease

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Intestinal Obstruction

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Gastrointestinal Infections

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Polyps and Neoplasms

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Appendiceal Pathology

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