Gastrointestinal Pathology — MCQs

Gastrointestinal Pathology Indian Medical PG Practice Questions and MCQs

Question 471: Skip lesions with non-caseating granulomas is characteristic of

A. Hodgkin's lymphoma
B. Ulcerative colitis
C. Sarcoidosis
D. Crohn's disease (Correct Answer)

Explanation: ***Crohn's disease*** - **Skip lesions** involve discontinuous areas of inflammation in the GI tract, which is a hallmark of Crohn's disease, unlike the continuous inflammation seen in ulcerative colitis [2], [3]. - The presence of **non-caseating granulomas** (often referred to as tuberculoid granulomas due to their resemblance to tuberculosis granulomas) is a characteristic histological finding in approximately 50% of Crohn's disease cases [1], [2]. *Hodgkin's lymphoma* - This is a type of cancer originating from lymphocytes and typically presents with **lymphadenopathy** and systemic symptoms. - While granulomas can sometimes be found in association with Hodgkin's lymphoma (secondary granulomas due to immune response), **skip lesions** in the GI tract and primary tuberculoid granulomas are not characteristic diagnostic features. *Ulcerative colitis* - Ulcerative colitis is characterized by **continuous inflammation** that starts in the rectum and can extend proximally through the colon, contrasting with the skip lesions of Crohn's [3]. - It primarily affects the **mucosa and submucosa** and typically does not feature transmural inflammation or the formation of granulomas [3]. *Sarcoidosis* - Sarcoidosis is a systemic inflammatory disease characterized by the formation of **non-caseating granulomas** in multiple organs, most commonly the lungs and lymph nodes [4]. - Although it can rarely affect the GI tract, **skip lesions** specific to the patterns seen in inflammatory bowel disease are not a defining feature; its granulomas are found within affected organs generally rather than as discontinuous intestinal lesions. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 806-807. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Alimentary System Disease, pp. 366-367. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Alimentary System Disease, pp. 365-366. [4] 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. 198-200.

Question 472: In celiac disease, all are true EXCEPT:

A. Gliadin is the cause
B. Increased brush border (Correct Answer)
C. Decreased villi to crypt ratio
D. Associated with HLA-DQ2 and HLA-DQ8

Explanation: ***Increased brush border*** - Celiac disease is characterized by **atrophy of the intestinal villi**, leading to a **decreased surface area** for absorption, not an increased brush border [1], [2]. This leads to malabsorption and its associated symptoms. - The inflammatory process in celiac disease causes destruction of the enterocytes and their microvilli, which constitute the brush border, thus reducing its integrity and function [2]. *Gliadin is the cause* - **Gliadin**, a component of gluten found in wheat, barley, and rye, is the primary trigger for the immune response in genetically predisposed individuals with celiac disease [1], [2]. - Digested gliadin peptides are recognized by immune cells, leading to an inflammatory reaction in the small intestine [2]. *Decreased villi to crypt ratio* - One of the hallmark histological findings in celiac disease is **villous atrophy**, which results in a significant **decrease in the villi to crypt ratio**, indicating loss of the absorptive surface and compensatory crypt hyperplasia [2]. - This architectural change is crucial for the diagnosis of celiac disease and reflects the damage to the small intestine lining. *Associated with HLA-DQ2 and HLA-DQ8* - Celiac disease is strongly associated with specific **HLA (Human Leukocyte Antigen) class II alleles**, primarily **HLA-DQ2 and HLA-DQ8**, which are found in over 95% of affected individuals [1]. - These genetic markers are essential for disease susceptibility, with **HLA-DQ2** present in approximately 90-95% of patients and **HLA-DQ8** in the remaining 5-10% [1]. **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. 789-790.

Question 473: A male infant presented with distension of abdomen shortly after birth with delayed passage of meconium. Subsequently a full-thickness biopsy of the rectum was performed. The rectal biopsy is likely to show:

A. Lack of ganglion cells (Correct Answer)
B. Fibrosis of submucosa
C. Thickened muscularis propria
D. Hyalinization of the muscular coat

Explanation: ***Lack of ganglion cells*** - The clinical presentation of **abdominal distension** and **delayed meconium passage** in a neonate is highly suggestive of **Hirschsprung disease** [1]. - **Hirschsprung disease** is characterized by the **absence of ganglion cells** in the myenteric (Auerbach's) and submucosal (Meissner's) plexuses of the distal bowel, starting from the anus and extending proximally to varying degrees [1], [2]. *Fibrosis of submucosa* - While some chronic inflammatory conditions can lead to submucosal fibrosis, it is **not the primary histopathological feature** of Hirschsprung disease. - Submucosal fibrosis is more typically seen in conditions like **Crohn's disease** or chronic infectious colitis. *Thickened muscularis propria* - A **thickened muscularis propria** can be an indirect finding in Hirschsprung disease, occurring as a result of **hypertrophy** of the muscle layers proximal to the aganglionic segment, due to increased effort to propel stool past the obstructed area. - However, the **primary diagnostic feature** on biopsy is the absence of ganglion cells, not muscle thickening, which is a secondary change [2]. *Hyalinization of the muscular coat* - **Hyalinization** refers to a glassy, eosinophilic appearance of tissue, often due to protein accumulation or degeneration. - This is **not a characteristic finding** in Hirschsprung disease and is typically associated with conditions like vascular injury or aging changes. **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. 94-95. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, p. 759.

Question 474: The histological features of celiac disease include all of the following EXCEPT:

A. Crypt hyperplasia
B. Increase in intraepithelial lymphocytes
C. Increase in inflammatory cells in lamina propria
D. Increase in thickness of the mucosa (Correct Answer)

Explanation: ***Increase in thickness of the mucosa*** - Celiac disease typically causes **villous atrophy**, leading to a **thinner intestinal mucosa**, not an increase in thickness [1]. - The architectural changes in celiac disease primarily involve blunting or absence of villi [2]. *Crypt hyperplasia* - This is a characteristic feature of celiac disease, where the **crypts of Lieberkühn** become elongated and hyperplastic to compensate for the damaged villi [1]. - It reflects increased cell turnover in response to mucosal injury. *Increase in intraepithelial lymphocytes* - An increase in **intraepithelial lymphocytes (IELs)** is a hallmark histological finding in celiac disease, often seen even before significant villous atrophy [1]. - These lymphocytes are typically CD3+ T-cells that infiltrate the epithelial layer. *Increase in inflammatory cells in lamina propria* - The lamina propria in celiac disease shows an increased infiltration of **chronic inflammatory cells**, including plasma cells and lymphocytes [2]. - This reflects the ongoing immune response to gluten peptides in the intestinal wall. **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 475: Which of the following features distinguishes Crohn's disease from Ulcerative colitis?

A. Lymphocyte infiltrate
B. Mucosal edema
C. Pseudopolyps
D. Transmural involvement (Correct Answer)

Explanation: ***Transmural involvement*** - **Crohn's disease** is characterized by **transmural inflammation**, meaning the inflammation extends through all layers of the bowel wall [1]. This deep inflammation can lead to complications like **fistulas**, **strictures**, and **abscesses** [1], [3]. - In contrast, **Ulcerative colitis** typically involves inflammation limited to the **mucosa and submucosa** [4]. *Lymphocyte infiltrate* - Both Crohn's disease and Ulcerative colitis involve a **lymphocyte infiltrate** as part of the chronic inflammatory process [2]. This feature is not specific enough to differentiate between the two conditions. - The presence of lymphocytes, plasma cells, and other inflammatory cells is common in any chronic inflammatory bowel condition. *Mucosal edema* - **Mucosal edema** can be found in both Crohn's disease and Ulcerative colitis due to the inflammatory process. It is a general sign of inflammation rather than a specific differentiating feature. *Pseudopolyps* - **Pseudopolyps** are characteristic of **Ulcerative colitis**, forming as islands of regenerating mucosa in areas of severe inflammation and ulceration [4]. - While they can occasionally be seen in chronic Crohn's disease, they are much more common and prominent in Ulcerative colitis, representing a reparative process rather than primary disease activity. **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, p. 809.

Question 476: False statement about Barrett esophagus is:

A. Chronic GERD is the predisposing factor
B. May lead to malignancy after few years
C. Goblet cells seen on histology
D. Columnar to squamous metaplasia (Correct Answer)

Explanation: ***Columnar to squamous metaplasia*** - Barrett esophagus is characterized by the replacement of the normal **squamous epithelium** of the distal esophagus with **columnar epithelium** [1]. - Therefore, the statement "Columnar to squamous metaplasia" is incorrect as it describes the opposite process, making it the false statement. *Chronic GERD is the predisposing factor* - **Chronic gastroesophageal reflux disease (GERD)** causes repeated exposure of the esophageal lining to stomach acid, leading to cellular damage [1][2]. - This chronic irritation is the primary risk factor for the development of Barrett esophagus [1]. *May lead to malignancy after few years* - Barrett esophagus is a significant risk factor for the development of **esophageal adenocarcinoma** [1][3]. - The metaplastic columnar epithelium can undergo further dysplastic changes, which can progress to invasive cancer over time [2]. *Goblet cells seen on histology* - The distinctive histological feature of Barrett esophagus is the presence of **intestinal metaplasia**, which includes the identification of **goblet cells** within the columnar epithelium [1]. - These goblet cells are a key diagnostic marker for Barrett esophagus [1]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Alimentary System Disease, pp. 348-349. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 764-765. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 765-766.

Question 477: Which is TRUE about granulomas in Crohn's disease?

A. Caseating
B. Non-caseating (Correct Answer)
C. Foreign body type
D. Suppurative

Explanation: ***Non-caseating*** - **Granulomas** in **Crohn's disease** are typically composed of aggregates of **macrophages**, epithelioid cells, and giant cells without central necrosis [1]. - Their presence is a key **histological feature**, though they are only found in a minority of Crohn's disease cases (about 50%) [1]. *Caseating* - **Caseating granulomas** are characterized by a central area of **necrotic cellular debris** resembling cheese. - They are a hallmark of **tuberculosis** and certain fungal infections, not Crohn's disease [2]. *Foreign body type* - **Foreign body granulomas** form in response to inert foreign material and contain **foreign body giant cells** engulfing the material [3]. - While observed in various conditions, they are not the characteristic type of granuloma seen in Crohn's disease. *Suppurative* - **Suppurative granulomas** feature a central collection of **neutrophils** (pus) surrounded by epithelioid cells. - These are typically associated with certain bacterial or fungal infections and are not characteristic of Crohn's disease. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Alimentary System Disease, pp. 365-367. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 109. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 196-197.

Question 478: Which microscopic finding is characteristic of Crohn's disease but not of ulcerative colitis?

A. Granulomas (Correct Answer)
B. Crypt abscesses
C. Pseudopolyps
D. Mucosal atrophy

Explanation: ***Granulomas*** - The presence of **non-caseating granulomas** is a classic histological feature found in Crohn's disease, distinguishing it from ulcerative colitis [1][2][3]. - Granulomas indicate a **chronic inflammatory process** and are often seen in segments of the intestine affected by Crohn's [2][3]. *Mucosal atrophy* - Mucosal atrophy is more commonly associated with **ulcerative colitis**, characterized by surface epithelial damage and loss of crypts. - In contrast, Crohn's disease often retains normal mucosal architecture, despite deeper inflammation [1]. *Pseudopolyps* - Pseudopolyps occur as a result of **regeneration** following mucosal ulceration and are primarily associated with **ulcerative colitis**. - They represent areas of **regrowth** in the inflamed mucosa, not a feature of Crohn's disease. *Crypt abscesses* - Crypt abscesses, characterized by the presence of **neutrophils** in the crypts, are typical of **ulcerative colitis** rather than Crohn's disease. - Crohn's disease is more likely to show **transmural inflammation** without the formation of crypt abscesses [1][2]. **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.

Question 479: A patient with ulcerative colitis has a colonic biopsy that reveals pseudopolyps. Which finding, if present, would most specifically suggest Crohn's disease rather than ulcerative colitis?

A. Transmural inflammation (Correct Answer)
B. Crypt abscesses
C. Mucosal atrophy
D. Pseudopolyps

Explanation: ***Transmural inflammation*** - This finding is **characteristic of Crohn's disease** [1,2,3], significantly differentiating it from ulcerative colitis, which primarily involves the mucosa and submucosa [4]. - In Crohn's disease, the **inflammation extends through the entire bowel wall** [2,3], leading to complications like strictures and fistulas [1]. *Mucosal atrophy* - Mucosal atrophy can be **seen in both ulcerative colitis** and Crohn's disease [3], making it not specific to either condition. - It generally refers to a **thinning** of the mucosal layer, which does not distinctly differentiate the two diseases. *Pseudopolyps* - While pseudopolyps are present in ulcerative colitis [4], they also **can occur in Crohn's disease**, particularly during healing phases. - Their presence does not provide a definitive distinction, as both conditions may exhibit similar histological features. *Crypt abscesses* - Crypt abscesses are a hallmark of ulcerative colitis [4] and are typically absent in Crohn's disease. - However, their presence does not help in **differentiating** the two diseases as they are a common feature associated with ulcerative colitis. **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, p. 809.

Question 480: A man presents with severe abdominal pain. His biopsy shows transmural inflammation, fissures, and cobblestone mucosa. Which condition is consistent with these findings?

A. Ulcerative colitis
B. Celiac disease
C. Irritable bowel syndrome
D. Crohn disease (Correct Answer)

Explanation: ***Crohn disease*** - **Transmural inflammation**, **fissures**, and **cobblestone mucosa** are classic histological and endoscopic features of Crohn disease, distinguishing it from other inflammatory bowel conditions [1]. - These findings indicate deep, discontinuous inflammation that can affect any part of the gastrointestinal tract from mouth to anus [1], [2]. *Ulcerative colitis* - Characterized by **superficial inflammation** limited to the mucosa and submucosa, primarily affecting the colon, without transmural involvement or fissures [1]. - Presents with **crypt abscesses** and continuous inflammation often starting in the rectum and extending proximally. *Celiac disease* - An autoimmune disorder triggered by **gluten**, characterized histologically by **villous atrophy**, crypt hyperplasia, and increased intraepithelial lymphocytes. - Does not involve transmural inflammation, fissures, or cobblestone mucosa. *Irritable bowel syndrome* - A **functional bowel disorder** characterized by abdominal pain and altered bowel habits without any specific inflammatory or structural changes seen on biopsy. - Biopsy results in IBS are typically normal, lacking any signs of inflammation or mucosal damage. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Alimentary System Disease, pp. 365-367. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 806-807.

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