Gastrointestinal Pathology Practice Questions

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

Increase in thickness of the mucosa. ***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.

Q: A newborn baby presented with a failure to pass meconium in the immediate postnatal period. The pediatrician also notices visible yet ineffective peristalsis, and abdominal distention. A radiological contrast enema demonstrated a narrow conical segment and a dilated proximal bowel. A diagnosis of Hirschsprung disease was made. Which of the following is a cause of the condition in the patient?

Failure of migration of neural crest cells. ***Failure of migration of neural crest cells*** - Hirschsprung disease is characterized by the **absence of ganglion cells** (specifically **Auerbach's and Meissner's plexuses**) in the distal bowel. - This aganglionosis results from the **failure of neural crest cells to migrate** completely into the intestinal wall during embryonic development. *Persistence of embryonic structures in the bowel wall* - This mechanism is associated with conditions like **Meckel's diverticulum**, where a remnant of the **vitelline duct** persists. - It does not explain the absence of ganglion cells or the functional obstruction seen in Hirschsprung disease. *Congenital obstruction due to external factors* - This would involve conditions such as an **annular pancreas**, **bands**, or **malrotation with volvulus**, creating a physical barrier. - Hirschsprung disease is a **functional obstruction** due to neuromuscular dysfunction, not an external compression or blockage. *Abnormal peristalsis due to neural dysfunction* - While there is abnormal peristalsis, the underlying cause is not just **"neural dysfunction"** in a general sense, but specifically the **absence of entire ganglion cell plexuses** within the bowel wall. - This option is too broad and doesn't pinpoint the precise developmental defect.

Q: Patient presented with diarrhoea, poor appetite and malabsorption. His duodenal biopsy was taken which showed crypt hyperplasia, villi atrophy and infiltration of CD8+ T cells in the epithelium. What is the likely diagnosis of the patient?

Celiac disease. ***Celiac disease*** - The combination of **diarrhoea**, **malabsorption**, **villi atrophy**, **crypt hyperplasia**, and **CD8+ T-cell infiltration** in the duodenal epithelium is pathognomonic for celiac disease [1]. - This condition is triggered by **gluten ingestion**, leading to an immune-mediated enteropathy [1], [3]. *Whipple disease* - Characterized by **malabsorption**, fever, arthralgia, and neurological symptoms [2]. - Histologically, it shows **foamy macrophages** containing PAS-positive material (Tropheryma whipplei) in the lamina propria, not primarily CD8+ T-cell infiltration [2]. *Environmental enteropathy* - Also known as tropical enteropathy, it causes **villi atrophy** and malabsorption, particularly in individuals living in areas with poor sanitation. - However, the prominent feature is often a diffuse inflammatory infiltrate, and specific **CD8+ T-cell infiltration** in the epithelium is not as specific as in celiac disease. *Pancreatitis* - Presents with **abdominal pain**, nausea, and vomiting, and can lead to malabsorption due to pancreatic enzyme insufficiency. - Histology of the duodenum would typically be normal, as the pathology primarily involves the **pancreas**, not the duodenal mucosa itself.

Q: Which of the following features distinguishes Crohn's disease from Ulcerative colitis?

Transmural involvement. ***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.

Q: Which of the following is the most common epithelial tumor of the stomach?

Gastric adenocarcinoma. ***Gastric adenocarcinoma*** - This is the **most common** malignant epithelial tumor of the stomach, accounting for over 90% of all gastric cancers [1], [2]. - It arises from the **glandular epithelial cells** lining the stomach [1]. *GIST* - **Gastrointestinal Stromal Tumors (GISTs)** are mesenchymal tumors, originating from the interstitial cells of Cajal, not epithelial cells [2]. - While they are common **non-epithelial** tumors of the stomach, they are far less frequent than gastric adenocarcinoma [2]. *Sarcoma* - **Sarcomas** are rare **mesenchymal tumors** of the stomach, arising from connective tissues like muscle or fat, not epithelial cells. - They constitute a very small percentage of gastric malignancies. *Carcinoid tumor* - **Carcinoid tumors** are **neuroendocrine tumors** that originate from enterochromaffin-like cells in the stomach. - While they are epithelial in origin, they are much less common than gastric adenocarcinoma. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, p. 779. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Alimentary System Disease, pp. 354-355.

Q: Which of the following is a cause of Hirschsprung disease in a patient?

Failure of migration of neural crest cells. ***Failure of migration of neural crest cells*** - Hirschsprung disease is characterized by the absence of **ganglion cells** (Auerbach and Meissner plexuses) in the distal colon [1]. - This aganglionosis results from the failure of **neural crest cells** to migrate completely from the esophagus to the anus during embryonic development [1]. *Failure of involution of vitelline duct* - This condition is associated with **Meckel's diverticulum**, which is a remnant of the vitelline duct, not Hirschsprung disease. - **Meckel's diverticulum** can cause symptoms like GI bleeding or obstruction, but it does not involve aganglionosis of the colon. *Excessive peristalsis of the affected part of the gut* - Hirschsprung disease is characterized by a **lack of peristalsis** in the aganglionic segment, leading to functional obstruction [1]. - The healthy, proximal colon may show increased peristalsis in an attempt to overcome the obstruction, but the affected segment itself is aperistaltic. *Obstruction secondary to an infectious agent* - Obstruction due to an infectious agent is typically related to **inflammatory processes** or strictures caused by infections (e.g., severe colitis). - This mechanism of obstruction does not involve the **developmental anomaly** of missing ganglion cells, which is central to Hirschsprung disease. **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.

Q: False statement about Barrett esophagus is:

Columnar to squamous metaplasia. ***Columnar to squamous metaplasia*** - Barrett esophagus involves the conversion of the normal stratified **squamous epithelium** to **intestinalized columnar epithelium** (metaplasia) due to acid injury. - Describing it as "columnar to squamous" is the reverse of the actual pathological process, making this the **false statement**. *Chronic GERD is the predisposing factor* - Persistent **reflux of gastric contents** into the lower esophagus induces the adaptive change from squamous to columnar cells to better resist acid. - Long-standing **GERD** is the strongest clinical predictor for the development of Barrett esophagus. *May lead to malignancy after few years* - Barrett esophagus is a clinically significant **premalignant condition** that follows a progression of metaplasia-dysplasia-carcinoma. - Patients have a significantly increased risk of developing **esophageal adenocarcinoma** compared to the general population. *Goblet cells seen on histology* - The presence of **intestinal metaplasia**, specifically characterized by **mucin-containing goblet cells**, is required for the diagnosis of Barrett esophagus. - These cells are identifiable on H&E stains and are often highlighted with **Alcian blue** stain to confirm the diagnosis.

Q: Most common type of gastric cancer is:

Adenocarcinoma. ***Adenocarcinoma*** - **Gastric adenocarcinoma** accounts for over 90% of all gastric cancers, making it overwhelmingly the most common type. - It arises from the glandular cells of the stomach lining. *Lymphoma* - **Gastric lymphoma** is a less common type of gastric malignancy, often originating from mucosa-associated lymphoid tissue (MALT). - While it can occur in the stomach, it represents a small percentage compared to adenocarcinoma. *GIST* - **Gastrointestinal stromal tumors (GISTs)** are mesenchymal tumors that arise from the interstitial cells of Cajal in the GI tract, including the stomach. - They are rare compared to adenocarcinoma. *Carcinoid* - **Gastric carcinoids**, or neuroendocrine tumors, originate from specialized hormone-producing cells in the stomach lining. - They are generally slow-growing and represent a very small fraction of all gastric neoplasms.

Q: Most common genetic alteration in colorectal carcinoma?

APC mutation. ***APC mutation*** - **APC (adenomatous polyposis coli)** is a tumor suppressor gene, and its inactivation is the **earliest and most common genetic event** in colorectal carcinoma development [1]. - Mutations in APC lead to **uncontrolled cell proliferation** by disrupting the Wnt signaling pathway, which is crucial for colon crypt regeneration [1]. *BRAF mutation* - **BRAF mutations** are associated with a subset of colorectal cancers, particularly those with **microsatellite instability (MSI)** and poor prognosis, but are not the most common overall [2]. - They occur in approximately **5-10% of colorectal cancers** and are primarily found in the sporadic, right-sided tumors. *KRAS mutation* - **KRAS mutations** are found in about 30-50% of colorectal cancers and are important in predicting resistance to anti-EGFR therapies [1]. - While common, they typically occur **later** in the progression from adenoma to carcinoma than APC mutations [1]. *p53 mutation* - **p53 (TP53)** is a tumor suppressor gene, and mutations in p53 are very common in many cancers, including colorectal carcinoma. - However, p53 mutations usually occur in the **later stages** of colorectal cancer development, often associated with the transition from adenoma to carcinoma and metastasis [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, p. 819. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Alimentary System Disease, pp. 373-374.

Question 1

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:

Accepted Answer

Lack of ganglion cells

Answer

Fibrosis of submucosa

Answer

Thickened muscularis propria

Answer

Hyalinization of the muscular coat

Question 2

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

Accepted Answer

Increase in thickness of the mucosa

Answer

Crypt hyperplasia

Answer

Increase in intraepithelial lymphocytes

Answer

Increase in inflammatory cells in lamina propria

Question 3

A newborn baby presented with a failure to pass meconium in the immediate postnatal period. The pediatrician also notices visible yet ineffective peristalsis, and abdominal distention. A radiological contrast enema demonstrated a narrow conical segment and a dilated proximal bowel. A diagnosis of Hirschsprung disease was made. Which of the following is a cause of the condition in the patient?

Accepted Answer

Failure of migration of neural crest cells

Answer

Persistence of embryonic structures in the bowel wall

Answer

Congenital obstruction due to external factors

Answer

Abnormal peristalsis due to neural dysfunction

Question 4

Patient presented with diarrhoea, poor appetite and malabsorption. His duodenal biopsy was taken which showed crypt hyperplasia, villi atrophy and infiltration of CD8+ T cells in the epithelium. What is the likely diagnosis of the patient?

Accepted Answer

Celiac disease

Answer

Whipple disease

Answer

Environmental enteropathy

Answer

Pancreatitis

Question 5

Which of the following features distinguishes Crohn's disease from Ulcerative colitis?

Accepted Answer

Transmural involvement

Answer

Lymphocyte infiltrate

Answer

Mucosal edema

Answer

Pseudopolyps

Question 6

Which of the following is the most common epithelial tumor of the stomach?

Accepted Answer

Gastric adenocarcinoma

Answer

GIST

Answer

Sarcoma

Answer

Carcinoid tumor

Question 7

Which of the following is a cause of Hirschsprung disease in a patient?

Accepted Answer

Failure of migration of neural crest cells

Answer

Failure of involution of vitelline duct

Answer

Excessive peristalsis of the affected part of the gut

Answer

Obstruction secondary to an infectious agent

Question 8

False statement about Barrett esophagus is:

Accepted Answer

Columnar to squamous metaplasia

Answer

Chronic GERD is the predisposing factor

Answer

May lead to malignancy after few years

Answer

Goblet cells seen on histology

Question 9

Most common type of gastric cancer is:

Accepted Answer

Adenocarcinoma

Answer

Lymphoma

Answer

GIST

Answer

Carcinoid

Question 10

Most common genetic alteration in colorectal carcinoma?

Accepted Answer

APC mutation

Answer

BRAF mutation

Answer

KRAS mutation

Answer

p53 mutation

Gastrointestinal Pathology — MCQs

Gastrointestinal Pathology — MCQs

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