Gastrointestinal Pathology — MCQs

Q: What is the most common site for leiomyoma in the gastrointestinal tract?

Stomach. **Explanation:** **Leiomyomas** are benign smooth muscle tumors that can occur anywhere in the gastrointestinal (GI) tract where smooth muscle is present. **Why the Stomach is Correct:** The **stomach** is the most common site for leiomyomas in the GI tract, followed by the esophagus. They typically arise from the *muscularis propria* or *muscularis mucosae*. While GISTs (Gastrointestinal Stromal Tumors) were historically misclassified as leiomyomas, true leiomyomas are still most frequently identified in the gastric wall during endoscopic or histological examinations. **Why Other Options are Incorrect:** * **Appendix:** Leiomyomas are extremely rare in the appendix; the most common mesenchymal tumor here is the neuroma, and the most common primary tumor is the carcinoid (neuroendocrine) tumor. * **Jejunum and Ileum:** While smooth muscle tumors occur in the small intestine, they are significantly less common than in the stomach. In the small bowel, GISTs are more prevalent than true leiomyomas [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Histology:** Leiomyomas consist of bundles of spindle-shaped cells with "cigar-shaped" nuclei and no significant atypia or mitotic activity. * **Immunohistochemistry (IHC):** True leiomyomas are **SMA (Smooth Muscle Actin) positive** and **Desmin positive**, but **CD117 (c-KIT) and DOG-1 negative** (this distinguishes them from GISTs) [1]. * **Most common mesenchymal tumor of the GI tract:** GIST (not leiomyoma) [1]. * **Most common site for GIST:** Stomach (60%) [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 783-784.

Gastrointestinal Pathology Indian Medical PG Practice Questions and MCQs

Question 1: What is the histopathological finding of gluten hypersensitivity?

A. Crypt hyperplasia (Correct Answer)
B. Increase in thickness of the mucosa
C. Distal intestine involvement
D. Villous hypertrophy

Explanation: **Explanation:** Gluten hypersensitivity, or **Celiac Disease**, is an immune-mediated enteropathy triggered by the ingestion of gluten in genetically predisposed individuals (HLA-DQ2/DQ8) [1]. The histopathological hallmark follows the **Marsh Classification** and is characterized by a "flat" mucosal profile. **Why Crypt Hyperplasia is Correct:** The chronic inflammatory response leads to increased enterocyte turnover. As the surface villi are destroyed (villous atrophy), the **crypts of Lieberkühn** undergo compensatory elongation and increased mitotic activity to replace the lost surface cells [1]. This is known as **crypt hyperplasia**. **Analysis of Incorrect Options:** * **B. Increase in thickness of the mucosa:** In Celiac disease, the total mucosal thickness usually **decreases or remains the same** because the loss of villous height is more significant than the gain from crypt hyperplasia. * **C. Distal intestine involvement:** Celiac disease primarily affects the **proximal small intestine** (duodenum and proximal jejunum) because these areas are exposed to the highest concentrations of dietary gluten [2]. * **D. Villous hypertrophy:** This is the opposite of what occurs. Celiac disease causes **villous atrophy** (blunting and flattening of villi), which reduces the surface area for absorption [2]. **High-Yield NEET-PG Pearls:** * **Gold Standard Diagnosis:** Small bowel biopsy (usually from the second part of the duodenum). * **Key Histology Triad:** Increased Intraepithelial Lymphocytes (IELs >25 per 100 enterocytes), Crypt Hyperplasia, and Villous Atrophy [1]. * **Serology:** Anti-tissue Transglutaminase (tTG) IgA is the screening test of choice; Anti-Endomysial Antibody (EMA) is the most specific. * **Associated Condition:** Dermatitis herpetiformis (itchy blisters on elbows/knees). * **Malignancy Risk:** Increased risk of Enteropathy-Associated T-cell Lymphoma (EATL). **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. 361-362.

Question 2: What is the most common site for leiomyoma in the gastrointestinal tract?

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

Explanation: **Explanation:** **Leiomyomas** are benign smooth muscle tumors that can occur anywhere in the gastrointestinal (GI) tract where smooth muscle is present. **Why the Stomach is Correct:** The **stomach** is the most common site for leiomyomas in the GI tract, followed by the esophagus. They typically arise from the *muscularis propria* or *muscularis mucosae*. While GISTs (Gastrointestinal Stromal Tumors) were historically misclassified as leiomyomas, true leiomyomas are still most frequently identified in the gastric wall during endoscopic or histological examinations. **Why Other Options are Incorrect:** * **Appendix:** Leiomyomas are extremely rare in the appendix; the most common mesenchymal tumor here is the neuroma, and the most common primary tumor is the carcinoid (neuroendocrine) tumor. * **Jejunum and Ileum:** While smooth muscle tumors occur in the small intestine, they are significantly less common than in the stomach. In the small bowel, GISTs are more prevalent than true leiomyomas [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Histology:** Leiomyomas consist of bundles of spindle-shaped cells with "cigar-shaped" nuclei and no significant atypia or mitotic activity. * **Immunohistochemistry (IHC):** True leiomyomas are **SMA (Smooth Muscle Actin) positive** and **Desmin positive**, but **CD117 (c-KIT) and DOG-1 negative** (this distinguishes them from GISTs) [1]. * **Most common mesenchymal tumor of the GI tract:** GIST (not leiomyoma) [1]. * **Most common site for GIST:** Stomach (60%) [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 783-784.

Question 3: Pseudomyxoma peritonei is most commonly associated with which of the following?

A. Mucinous cystadenocarcinoma of the ovary (Correct Answer)
B. Carcinoid tumor of the appendix
C. Endometrial carcinoma
D. Ileal carcinoid tumor

Explanation: **Explanation:** **Pseudomyxoma peritonei (PMP)** is a clinical condition characterized by the accumulation of abundant "gelatinous" or mucinous ascites within the peritoneal cavity [1]. This occurs due to the implantation of mucin-secreting tumor cells on the peritoneal surfaces [1]. **Why Option A is Correct:** Traditionally, **Mucinous cystadenocarcinoma of the ovary** was considered the most common cause of PMP in females. The tumor cells rupture or spread from the ovary, seeding the peritoneum and producing massive amounts of extracellular mucin. *Note on Modern Pathology:* While this question follows the classic teaching often tested in exams, current surgical pathology identifies the **Appendix** (specifically Low-grade Appendiceal Mucinous Neoplasms - LAMN) as the most frequent primary site for PMP [1], [2]. However, among the provided options, the ovarian mucinous tumor is the established classic association. **Why Incorrect Options are Wrong:** * **B & D (Carcinoid Tumors):** Carcinoid tumors (Neuroendocrine tumors) of the appendix or ileum typically present with symptoms of obstruction or "Carcinoid Syndrome" (flushing, diarrhea). They do not secrete mucin and therefore do not cause Pseudomyxoma peritonei. * **C (Endometrial Carcinoma):** This is a malignancy of the uterine lining. While it can spread to the peritoneum, it typically presents with vaginal bleeding and does not produce the characteristic gelatinous mucinous ascites associated with PMP. **NEET-PG High-Yield Pearls:** * **The "Jelly Belly":** A classic clinical descriptor for the appearance of the abdomen in PMP. * **Primary Source:** If both ovary and appendix show mucinous tumors, the **appendix** is now considered the primary source in the majority of cases (the ovary is usually a secondary site of spread) [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] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Female Genital Tract Disease, pp. 478-480.

Question 4: Skip lesions are seen in which of the following conditions?

A. Ulcerative colitis
B. Crohn's disease (Correct Answer)
C. Typhoid
D. Tuberculosis

Explanation: **Explanation:** **Crohn’s Disease (Correct Answer):** Skip lesions are a hallmark endoscopic and pathological feature of Crohn’s disease [1]. This refers to the **discontinuous** nature of the inflammation, where sharply demarcated areas of diseased bowel are separated by segments of normal-appearing mucosa [2]. This occurs because Crohn’s is a transmural inflammatory process that can affect any part of the gastrointestinal tract (from mouth to anus), most commonly the terminal ileum and cecum [2]. **Analysis of Incorrect Options:** * **Ulcerative Colitis:** Unlike Crohn’s, the inflammation in UC is **continuous and diffuse** [5]. It typically starts in the rectum (proctitis) and extends proximally without any "skipped" areas of healthy tissue [5]. * **Typhoid:** Caused by *Salmonella typhi*, it primarily affects the Peyer's patches of the terminal ileum, leading to longitudinal ulcers. It does not present with the characteristic skip distribution seen in IIBD. * **Tuberculosis (Intestinal):** While it can mimic Crohn’s (especially the ileocecal involvement), intestinal TB typically presents with transverse ulcers and circumferential involvement rather than the classic skip lesions [4]. **High-Yield Clinical Pearls for NEET-PG:** * **Crohn’s Disease:** Look for "Cobblestone appearance," "Creeping fat," "String sign of Kantor" on imaging [1], and **Non-caseating granulomas** (pathognomonic in 40-60% of cases) [3]. * **Ulcerative Colitis:** Look for "Lead pipe colon" (loss of haustrations), "Pseudopolyps," and "Crypt abscesses." * **Mnemonic:** **C**rohn’s = **C**ompletely transmural and **C**obblestoning; **U**lcerative **C**olitis = **U**ninterrupted **C**olonic involvement. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Alimentary System Disease, pp. 366-367. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Alimentary System Disease, pp. 365-366. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 806-807. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Alimentary System Disease, pp. 363-364. [5] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Alimentary System Disease, pp. 367-368.

Question 5: True about primary gastric lymphoma is

A. Affects young adults
B. Surgery is never indicated
C. T cell lymphoma
D. H. pylori infection increases the risk (Correct Answer)

Explanation: **Explanation:** **Primary Gastric Lymphoma** is the most common site for extranodal lymphomas, with the stomach accounting for approximately 20% of all cases. [1] **1. Why Option D is correct:** The strongest risk factor for primary gastric lymphoma, specifically **MALToma** (Mucosa-Associated Lymphoid Tissue lymphoma), is chronic **_H. pylori_ infection**. The infection triggers a chronic inflammatory response, leading to the recruitment of B-cells and the formation of organized lymphoid tissue (which is normally absent in the stomach). Over time, these B-cells can undergo malignant transformation. [1] Eradication of _H. pylori_ with antibiotics can lead to complete regression of early-stage MALTomas in up to 70-80% of cases. **2. Why the other options are incorrect:** * **Option A:** Gastric lymphoma typically affects **older adults**, usually in their 6th or 7th decade of life, rather than young adults. * **Option B:** While chemotherapy, radiotherapy, and antibiotic therapy are the mainstays, **surgery is indicated** in specific complications such as perforation, uncontrollable hemorrhage, or gastric outlet obstruction. [1] * **Option C:** The vast majority (>90%) of primary gastric lymphomas are of **B-cell origin** (Diffuse Large B-cell Lymphoma or MALToma). [1] Primary T-cell lymphomas of the stomach are extremely rare. **High-Yield Clinical Pearls for NEET-PG:** * **Most common type:** Diffuse Large B-cell Lymphoma (DLBCL) is the most common histological subtype, followed by MALToma. [1] * **Cytogenetics:** MALToma is frequently associated with the **t(11;18)(q21;q21)** translocation involving the *API2-MLT* gene. This translocation often predicts resistance to _H. pylori_ eradication therapy. * **Staging:** The **Lugano classification** is commonly used for staging gastrointestinal lymphomas. * **Endoscopy:** Often shows non-specific findings like thickened gastric folds, ulcers, or polypoid masses, necessitating deep biopsies. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Alimentary System Disease, pp. 356-358.

Question 6: Enteropathy-associated T-cell lymphoma is associated with which of the following conditions?

A. Malignant lymphoma
B. Celiac sprue (Correct Answer)
C. Menetrier disease
D. Crohn's disease

Explanation: **Explanation:** **Enteropathy-associated T-cell lymphoma (EATL)** is a rare but aggressive high-grade extranodal non-Hodgkin lymphoma that arises from the intraepithelial lymphocytes of the small intestine. **Why Celiac Sprue is correct:** EATL is a well-recognized, long-term complication of **Celiac disease** (gluten-sensitive enteropathy), particularly in patients with "refractory celiac disease" who fail to respond to a gluten-free diet [2]. Chronic antigenic stimulation by gluten leads to the clonal expansion of intraepithelial T-cells (typically CD3+, CD8-, CD56-), which eventually undergo malignant transformation [2]. It most commonly involves the proximal small bowel (jejunum). **Why the other options are incorrect:** * **Malignant lymphoma:** This is a general category of cancers. EATL is a specific subtype of T-cell lymphoma; therefore, "malignant lymphoma" is a classification rather than an associated pre-existing condition. * **Menetrier disease:** This is a hypertrophic gastropathy characterized by giant gastric folds and protein loss. It is associated with an increased risk of **gastric adenocarcinoma**, not T-cell lymphoma. * **Crohn’s disease:** While Crohn’s disease increases the risk of intestinal malignancy, it is more strongly associated with **adenocarcinoma** of the small bowel and colon, or occasionally B-cell lymphomas (especially if on immunosuppressants). **High-Yield NEET-PG Pearls:** * **Genetics:** Strongly associated with **HLA-DQ2 and HLA-DQ8** (same as Celiac disease) [1]. * **Morphology:** Characterized by "ulcerating mucosal masses" which can lead to intestinal perforation or obstruction. * **Immunophenotype:** Most cases are **CD3+ and CD103+** (a marker for intraepithelial lymphocytes) [3]. * **Prognosis:** Very poor, with a high rate of recurrence despite chemotherapy. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Alimentary System Disease, pp. 360-361. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 790-791. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 789-790.

Question 7: What is true about mucosa-associated lymphoid tissue (MALT) lymphoma?

A. Helicobacter pylori infection is a predisposing factor. (Correct Answer)
B. It is typically sensitive to chemotherapy.
C. Multiple distinct lymphomas are common.
D. It is characterized by stromal polyps.

Explanation: **Explanation:** **1. Why Option A is correct:** Gastric MALT lymphoma (Extranodal Marginal Zone B-cell Lymphoma) is the classic example of a malignancy arising from chronic inflammation [1]. *Helicobacter pylori* infection induces the formation of organized lymphoid tissue in the gastric mucosa (which normally lacks it) [1]. The chronic antigenic stimulation by *H. pylori* leads to the proliferation of B-cells [2]. In early stages, the tumor is "antigen-dependent," meaning that **eradication of *H. pylori* with antibiotics can lead to complete regression** of the lymphoma in approximately 70-80% of cases [1]. **2. Why the other options are incorrect:** * **Option B:** While sensitive to treatment, the primary and most effective initial therapy for localized gastric MALToma is **antibiotic eradication** of *H. pylori*, not systemic chemotherapy [1]. * **Option C:** MALTomas are typically **unifocal** (localized) at presentation [1]. While they can disseminate late in the disease, multiple distinct primary lymphomas are not a characteristic feature. * **Option D:** MALToma is characterized by **lymphoepithelial lesions** (invasion of gastric glands by neoplastic B-cells), not stromal polyps. **3. High-Yield Clinical Pearls for NEET-PG:** * **Cytogenetics:** The most common translocation is **t(11;18)(q21;q21)** involving the *API2-MLT* genes. Presence of this translocation usually predicts **resistance** to *H. pylori* eradication therapy. * **Morphology:** Look for "monocytoid" B-cells and the pathognomonic **lymphoepithelial lesions**. * **Immunophenotype:** Positive for **CD19, CD20, and CD79a**; Negative for CD5, CD10, and CD23 (helps differentiate from CLL/SLL and Follicular Lymphoma). * **Transformation:** Long-standing MALToma can transform into a high-grade **Diffuse Large B-cell Lymphoma (DLBCL)** [3]. **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] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Alimentary System Disease, pp. 357-358.

Question 8: What is seen in ulcerative colitis?

A. Cryptitis (Correct Answer)
B. Crypt loss
C. Crypt branching
D. Proliferating mucosa

Explanation: **Explanation:** **Ulcerative Colitis (UC)** is a chronic inflammatory bowel disease characterized by continuous, superficial mucosal inflammation limited to the colon and rectum [2]. **Why Cryptitis is the Correct Answer:** The hallmark of active Ulcerative Colitis is the infiltration of neutrophils into the mucosal layer. When neutrophils migrate into the epithelial lining of the intestinal crypts, it is termed **Cryptitis**. If these neutrophils accumulate within the lumen of the crypts, it leads to the formation of **Crypt Abscesses** [1]. These are classic histological markers of "active" disease in UC. **Analysis of Incorrect Options:** * **B. Crypt loss:** While chronic inflammation can lead to mucosal atrophy, crypt loss is more characteristic of long-standing, burnt-out disease or severe ulceration rather than the diagnostic acute inflammatory phase. * **C. Crypt branching:** This is a sign of **chronicity** (architectural distortion) rather than acute activity. While seen in UC, cryptitis is the more specific pathological descriptor for the inflammatory process itself. * **D. Proliferating mucosa:** In UC, the mucosa is typically friable, eroded, or ulcerated. While "pseudopolyps" (islands of regenerating mucosa) occur, "proliferating mucosa" is not a standard pathological term used to describe the primary lesion [2]. **NEET-PG High-Yield Pearls:** * **Extent:** Always involves the rectum and extends proximally in a **continuous** fashion (no skip lesions) [2]. * **Depth:** Inflammation is limited to the **Mucosa and Submucosa** (unlike Crohn’s, which is transmural) [1], [2]. * **Microscopy:** Cryptitis and Crypt Abscesses are the defining features of activity [1]. * **Gross Feature:** "Lead pipe" appearance on barium enema due to loss of haustra. * **Marker:** Strongly associated with **p-ANCA** positivity. * **Complication:** Higher risk of **Toxic Megacolon** and **Adenocarcinoma** compared to Crohn’s. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, p. 809. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Alimentary System Disease, pp. 367-368.

Question 9: Biopsy findings of celiac disease include all of the following except?

A. Crypt hyperplasia
B. Villous atrophy
C. Mucosal atrophy (Correct Answer)
D. Intraepithelial lymphocytes

Explanation: In Celiac disease, the characteristic histological changes are a result of an immune-mediated inflammatory response to gluten [1]. The correct answer is **Mucosal atrophy** because, while the villi disappear, the overall thickness of the mucosa remains relatively constant due to compensatory mechanisms. ### Why "Mucosal Atrophy" is the Exception: In Celiac disease, there is **Villous atrophy** (shortening/loss of villi), but this is accompanied by **Crypt hyperplasia** (elongation of the crypts) [1][2]. Because the crypts lengthen to compensate for the loss of villi, the total mucosal thickness does not significantly decrease. Therefore, "Mucosal atrophy" is a misnomer and technically incorrect in the context of Celiac disease. ### Explanation of Other Options: * **Villous atrophy (B):** This is a hallmark finding [1][2]. The blunting and eventual flattening of the finger-like projections (villi) lead to a decreased surface area for absorption. * **Crypt hyperplasia (A):** As the surface epithelium is damaged, the crypts (the "factory" of the epithelium) increase mitotic activity and elongate to replace lost cells [1]. * **Intraepithelial lymphocytes (D):** An increase in IELs (specifically CD8+ T cells) is the earliest histological marker of Celiac disease [1]. A count of >25 IELs per 100 enterocytes is considered diagnostic. ### NEET-PG High-Yield Pearls: * **Marsh Classification:** Used to grade the severity (Marsh 0: Normal; Marsh 1: IELs; Marsh 2: Crypt hyperplasia; Marsh 3: Villous atrophy). * **Gold Standard Diagnosis:** Duodenal biopsy (usually multiple samples from the second part of the duodenum and bulb). * **Serology:** Anti-tissue Transglutaminase (anti-tTG) IgA is the screening test of choice [2]. * **Site:** Most severe in the **distal duodenum** and **proximal jejunum** (areas with highest gluten exposure) [2]. **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 10: Helicobacter pylori is associated with which type of gastritis?

A. Type A Gastritis
B. Type B gastritis (Correct Answer)
C. Autoimmune Gastritis
D. Allergic Gastritis

Explanation: **Explanation:** Chronic gastritis is traditionally classified into two main types based on the etiology and the site of involvement: **Type A** and **Type B**. **1. Why Type B Gastritis is correct:** Type B gastritis is the most common form of chronic gastritis and is caused by **Helicobacter pylori** infection [1]. The "B" stands for **Bacterial**. It typically begins in the **Antrum** (Antral-predominant) but can progress to involve the entire stomach (pangastritis) [1]. *H. pylori* produces urease and induces a chronic inflammatory response, increasing the risk of peptic ulcer disease and gastric adenocarcinoma [1]. **2. Why other options are incorrect:** * **Type A Gastritis (Option A & C):** Type A stands for **Autoimmune**. It involves the **Body and Fundus** (sparing the antrum) [1]. It is characterized by antibodies against parietal cells and intrinsic factor, leading to Vitamin B12 deficiency (Pernicious anemia) and achlorhydria [1]. * **Allergic Gastritis (Option D):** This is a rare condition, often associated with eosinophilic infiltration of the gastric mucosa (Eosinophilic gastritis), usually triggered by food allergens or systemic allergic disorders, and is not related to *H. pylori*. **High-Yield Clinical Pearls for NEET-PG:** * **Location:** Type **A** affects the **A**cid-producing area (Body/Fundus); Type **B** affects the **B**ase (Antrum) [1]. * **H. pylori Stains:** Silver stains (Warthin-Starry), Giemsa, and Genta stains are used for visualization [1]. * **MALToma:** *H. pylori* is a major risk factor for Mucosa-Associated Lymphoid Tissue (MALT) lymphoma; eradication of the bacteria can lead to tumor regression [2]. * **Investigation of Choice:** Endoscopic biopsy with a Rapid Urease Test (RUT) is highly specific for diagnosis [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 770-772. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Alimentary System Disease, pp. 356-357.

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