Gastrointestinal Pathology — MCQs

A 24-year-old woman gives birth to a term infant after an uncomplicated pregnancy. Apgar scores are 9 and 10 at 1 and 5 minutes after birth. The infant's length and weight are at the 55th percentile. There is no significant passage of meconium. Three days after birth, the infant vomits all oral feedings. On physical examination, the infant is afebrile, but the abdomen is distended and tender, and bowel sounds are reduced. An abdominal ultrasound scan shows marked colonic dilation above a narrow segment in the distal sigmoid region. A biopsy specimen from the narrowed region shows an absence of ganglion cells in the muscle wall and submucosa. Which of the following is most likely to produce these findings?

Q275Easy

Mutation of the STK11 and LKB1 gene is associated with which of the following conditions?

Q276Easy

Gluten-sensitive enteropathy is most strongly associated with which HLA haplotype?

Q277Medium

Which of the following features is NOT seen in Crohn's disease?

Q278Medium

Which of the following is produced by argentaffinoma of the ileum?

Q279Easy

Adenocarcinoma in the esophagus most commonly occurs in which region?

Q280Easy

Which of the following is NOT important in the definition of ulcerative colitis?

Gastrointestinal Pathology Indian Medical PG Practice Questions and MCQs

Question 271: All of the following are true about diffuse gastric cancer according to Lauren's classification except?

A. Familial
B. More common in males (Correct Answer)
C. Undifferentiated
D. More common in the proximal part of the stomach

Explanation: Lauren’s classification divides gastric adenocarcinoma into two main histological types: **Intestinal** and **Diffuse** [1]. **Why Option B is the correct answer (The Exception):** Unlike the intestinal type, which shows a strong male predominance (2:1 ratio), the **diffuse type occurs equally in males and females** [1]. In some younger age cohorts, it may even show a slight female preponderance. Therefore, the statement "More common in males" is incorrect for the diffuse type. **Analysis of other options:** * **A. Familial:** Diffuse gastric cancer is strongly associated with genetic factors, most notably germline mutations in the **CDH1 gene** (encoding E-cadherin) [1]. This is the hallmark of Hereditary Diffuse Gastric Cancer (HDGC) syndrome. * **C. Undifferentiated:** Histologically, the diffuse type is poorly differentiated. It lacks gland formation and consists of discohesive cells that infiltrate the gastric wall individually or in small clusters [1]. The classic finding is the **Signet ring cell** [1]. * **D. More common in the proximal part:** While the intestinal type is often associated with distal locations (antrum) and chronic gastritis, the diffuse type is more frequently found in the **proximal stomach** (cardia/body) and can involve the entire stomach (*Linitis Plastica*) [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Intestinal Type:** Associated with environmental factors (H. pylori, smoking, nitrates), precursor lesions (atrophic gastritis/metaplasia), and older age [1]. * **Diffuse Type:** Not associated with H. pylori or precursor lesions; characterized by a "leather bottle" appearance (**Linitis Plastica**) due to a desmoplastic reaction [1]. * **Virchow’s Node:** Left supraclavicular lymphadenopathy (Trosier sign) is a classic sign of gastric cancer metastasis. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 779-780.

Question 272: Which type of colonic polyp has the maximum chance of malignant change?

A. Hyperplastic polyp
B. Adenomatous polyp (Correct Answer)
C. Juvenile polyp
D. Polyp of Peutz-Jeghers syndrome

Explanation: **Explanation:** The malignant potential of a colonic polyp depends on its histological nature. **Adenomatous polyps** are true neoplastic proliferations of the colonic epithelium and are considered precursors to colorectal adenocarcinoma (the adenoma-carcinoma sequence) [1]. The risk of malignancy within an adenoma increases with **size** (>2 cm), **histological type** (villous > tubulovillous > tubular), and the degree of **dysplasia** [1], [2]. **Analysis of Options:** * **Adenomatous Polyp (Correct):** These are dysplastic by definition. Among these, **Villous adenomas** have the highest risk of malignancy (up to 40%) compared to tubular adenomas (approx. 5%) [2]. * **Hyperplastic Polyp:** These are non-neoplastic proliferations resulting from decreased cell turnover. They are the most common type of polyp in the colon but generally have **no malignant potential** (except for the "sessile serrated" subtype, which is distinct) [3]. * **Juvenile Polyp:** These are **hamartomatous** polyps (malformations of normal tissue). Solitary juvenile polyps are benign and carry no increased risk of cancer [4]. * **Peutz-Jeghers Polyp:** These are also **hamartomatous**. While Peutz-Jeghers Syndrome significantly increases the lifetime risk of various cancers (pancreas, breast, ovary), the individual polyps themselves are not considered pre-malignant [4]. **High-Yield Pearls for NEET-PG:** 1. **Size is the most important predictor:** Polyps <1 cm have <1% risk; >2 cm have a >40% risk of containing cancer [1]. 2. **Architecture:** "Villous is Villainous"—Villous adenomas are more likely to be sessile, large, and harbor invasive carcinoma [2]. 3. **Familial Adenomatous Polyposis (FAP):** Caused by a mutation in the **APC gene** (Chromosome 5q21). Malignancy is 100% by age 40 if the colon is not removed [3]. 4. **Gardner Syndrome:** FAP + Osteomas + Soft tissue tumors (Desmoid tumors). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 815-817. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Alimentary System Disease, pp. 371-373. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 821-822. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, p. 813.

Question 273: Creeping fat is a characteristic feature of which of the following conditions?

A. Crohn's disease (Correct Answer)
B. Ulcerative colitis
C. Celiac disease
D. Tropical sprue

Explanation: **Explanation:** **Crohn's Disease (Correct Answer):** "Creeping fat" (also known as fat wrapping) is a pathognomonic gross morphological feature of **Crohn's disease**. It occurs when mesenteric adipose tissue extends from the mesenteric attachment and wraps around the antimesenteric convexity of the serosal surface of the bowel. This phenomenon is driven by transmural inflammation and the release of pro-inflammatory cytokines (like TNF-α) from the mesenteric fat, which undergoes hyperplasia and fibrosis. It is often associated with stricture formation and bowel wall thickening [1]. **Why other options are incorrect:** * **Ulcerative Colitis:** This condition is characterized by mucosal and submucosal inflammation only [2]. Since it does not involve the full thickness of the wall (transmural) or the serosa, creeping fat and strictures are typically absent [1]. * **Celiac Disease:** This is an immune-mediated enteropathy of the small interior characterized by villous atrophy, crypt hyperplasia, and intraepithelial lymphocytosis. It does not involve gross serosal changes. * **Tropical Sprue:** Similar to Celiac disease, this involves malabsorption and histological changes in the mucosa, but it lacks the transmural inflammatory profile required to produce creeping fat. **High-Yield NEET-PG Pearls:** * **Transmural Inflammation:** Crohn’s is transmural; UC is limited to mucosa/submucosa [1]. * **Skip Lesions:** Characteristic of Crohn’s; UC is continuous and starts from the rectum [1]. * **String Sign of Kantor:** Radiological finding in Crohn's due to terminal ileal narrowing [1]. * **Granulomas:** Non-caseating granulomas are seen in 35% of Crohn’s cases [2]; they are absent in UC. * **Cobblestone Appearance:** Seen in Crohn's due to linear ulcerations and edematous intervening mucosa [1]. **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.

Question 274: A 24-year-old woman gives birth to a term infant after an uncomplicated pregnancy. Apgar scores are 9 and 10 at 1 and 5 minutes after birth. The infant's length and weight are at the 55th percentile. There is no significant passage of meconium. Three days after birth, the infant vomits all oral feedings. On physical examination, the infant is afebrile, but the abdomen is distended and tender, and bowel sounds are reduced. An abdominal ultrasound scan shows marked colonic dilation above a narrow segment in the distal sigmoid region. A biopsy specimen from the narrowed region shows an absence of ganglion cells in the muscle wall and submucosa. Which of the following is most likely to produce these findings?

A. Colonic atresia
B. Hirschsprung disease (Correct Answer)
C. Intussusception
D. Necrotizing enterocolitis

Explanation: ### Explanation **Correct Answer: B. Hirschsprung disease** **Mechanism and Pathophysiology:** Hirschsprung disease (congenital aganglionic megacolon) results from the **failure of neural crest cells to migrate** cranio-caudally from the cecum to the rectum during embryonic development [1]. This leads to a functional obstruction because the affected segment lacks both the **Meissner (submucosal)** and **Auerbach (myenteric)** nerve plexuses [1]. The aganglionic segment remains permanently contracted (narrowed), while the proximal normal colon undergoes massive compensatory dilation (megacolon) [1]. **Why it fits the clinical picture:** * **Delayed meconium passage:** 90% of cases fail to pass meconium within 48 hours. * **Obstruction symptoms:** Abdominal distension and bilious vomiting. * **Histopathology:** The gold standard for diagnosis is a rectal suction biopsy showing the **absence of ganglion cells** and presence of hypertrophied nerve bundles [2]. **Analysis of Incorrect Options:** * **A. Colonic atresia:** This is a structural (not functional) defect where the lumen is physically closed. While it causes obstruction, it would not specifically show aganglionosis on biopsy. * **C. Intussusception:** This involves the "telescoping" of one bowel segment into another. It typically occurs in infants aged 6–18 months and presents with "currant jelly" stools and a sausage-shaped mass, not neonatal aganglionosis. * **D. Necrotizing enterocolitis (NEC):** This is an ischemic/inflammatory necrosis of the bowel, most common in **premature** infants. It presents with pneumatosis intestinalis (gas in the bowel wall) on X-ray, not a congenital lack of ganglia. **NEET-PG High-Yield Pearls:** * **Genetic Association:** Strongly associated with **RET proto-oncogene** mutations and **Down Syndrome** (Trisomy 21) [1], [2]. * **Diagnosis:** Initial screening is via Anorectal Manometry (failure of internal anal sphincter to relax); definitive diagnosis is **Rectal Suction Biopsy** [2]. * **Staining:** Acetylcholinesterase (AChE) staining shows increased activity/hypertrophied nerve fibers in the lamina propria [2]. * **Location:** Always involves the rectum (starts distally and extends proximally). **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 275: Mutation of the STK11 and LKB1 gene is associated with which of the following conditions?

A. Familial adenomatous polyposis
B. Hereditary nonpolyposis colorectal cancer
C. Peutz-Jeghers syndrome (Correct Answer)
D. Neurofibromatosis

Explanation: **Explanation:** **Peutz-Jeghers Syndrome (PJS)** is an autosomal dominant condition characterized by the development of multiple gastrointestinal hamartomatous polyps and mucocutaneous hyperpigmentation (melanotic macules on lips and oral mucosa) [1]. The molecular hallmark of PJS is a germline mutation in the **STK11 (Serine/Threonine Kinase 11)** gene, also known as **LKB1**, located on chromosome 19p13 [1]. This gene acts as a tumor suppressor that regulates cell polarity and energy metabolism; its loss leads to uncontrolled cellular growth and an increased risk of various malignancies (colorectal, breast, pancreatic, and gynecological) [1]. **Analysis of Incorrect Options:** * **A. Familial Adenomatous Polyposis (FAP):** Caused by mutations in the **APC gene** (Chromosome 5q21) [2]. It is characterized by hundreds to thousands of adenomatous polyps and a 100% risk of colorectal cancer if untreated. * **B. Hereditary Nonpolyposis Colorectal Cancer (HNPCC/Lynch Syndrome):** Caused by mutations in **DNA Mismatch Repair (MMR) genes** (primarily *MSH2, MLH1, MSH6, PMS2*), leading to microsatellite instability (MSI) [2]. * **D. Neurofibromatosis:** NF1 is caused by mutations in the **NF1 gene** (neurofibromin) on chromosome 17, while NF2 involves the **merlin gene** on chromosome 22. **High-Yield Clinical Pearls for NEET-PG:** * **PJS Polyps:** These are **hamartomatous**, showing a characteristic "Christmas tree" branching pattern of smooth muscle (arborization) on histology [1]. * **Intussusception:** The most common physical complication of PJS polyps. * **Cancer Risk:** While the polyps themselves are non-neoplastic, patients have a significantly elevated lifetime risk of extra-intestinal cancers (especially breast and pancreas) [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 813-814. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, p. 817.

Question 276: Gluten-sensitive enteropathy is most strongly associated with which HLA haplotype?

A. HLA-DQ2 (Correct Answer)
B. HLA-DR4
C. HLA-DQ3
D. None of the above

Explanation: **Explanation:** Gluten-sensitive enteropathy (Celiac Disease) is an immune-mediated enteropathy triggered by the ingestion of gluten in genetically susceptible individuals [1]. The pathogenesis involves the deamidation of gliadin peptides by the enzyme **tissue transglutaminase (tTG)**. These negatively charged peptides are then presented by antigen-presenting cells to CD4+ T-cells [2]. **1. Why HLA-DQ2 is correct:** The susceptibility to Celiac Disease is strongly linked to specific Class II Major Histocompatibility Complex (MHC) molecules. Approximately **95% of patients carry the HLA-DQ2 haplotype**, while the remaining 5% usually carry **HLA-DQ8** [1]. These specific HLA molecules have a high affinity for binding deamidated gliadin peptides, initiating the inflammatory cascade that leads to villous atrophy. **2. Why other options are incorrect:** * **HLA-DR4:** This haplotype is most classically associated with **Rheumatoid Arthritis** and Type 1 Diabetes Mellitus, not Celiac Disease. * **HLA-DQ3:** This is not a primary genetic driver for Celiac Disease. While HLA-DQ3 is a broad category that includes DQ7, DQ8, and DQ9, it is specifically the **DQ8** subtype (not DQ3 generally) that is associated with the disease. **Clinical Pearls for NEET-PG:** * **Negative Predictive Value:** The absence of HLA-DQ2/DQ8 has a nearly 100% negative predictive value; if a patient lacks these, Celiac Disease is extremely unlikely. * **Gold Standard Diagnosis:** Small intestinal biopsy showing **villous atrophy, crypt hyperplasia, and increased intraepithelial lymphocytes (Marsh Criteria)** [2]. * **Serology:** Anti-tissue transglutaminase (anti-tTG) IgA is the screening test of choice [1]. * **Associated Malignancy:** Increased risk of **Enteropathy-associated T-cell lymphoma (EATL).** **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 277: Which of the following features is NOT seen in Crohn's disease?

A. Granulomas
B. Fissuring ulcers
C. Pyloric gland hyperplasia (Correct Answer)
D. Paneth cell metaplasia

Explanation: **Explanation:** In Crohn’s Disease (CD), the inflammatory process is **transmural** [2], [3] and can affect any part of the GIT [3], leadng to specific histological adaptations. **Why Pyloric Gland Hyperplasia is the Correct Answer:** Pyloric gland hyperplasia is **not** a characteristic feature of Crohn’s disease. Instead, Crohn’s disease is associated with **Pyloric Gland Metaplasia** (also known as pseudopyloric metaplasia) [1]. This occurs when the specialized mucosa of the small or large intestine undergoes transformation into mucus-secreting glands resembling those of the gastric antrum (pyloric glands) as a response to chronic mucosal injury and ulceration. **Analysis of Incorrect Options:** * **Granulomas:** Non-caseating granulomas are a hallmark of CD (seen in ~40-60% of cases) [2], [4]. They can occur in any layer of the bowel wall and even in uninvolved segments or regional lymph nodes [2]. * **Fissuring Ulcers:** CD is characterized by deep, knife-like "fissures" that penetrate through the mucosa into the muscularis propria, often leading to fistula formation [3], [4]. * **Paneth Cell Metaplasia:** This is a common feature of chronic inflammatory bowel disease (IBD), particularly in the distal colon (where Paneth cells are normally absent), representing a reactive change to chronic inflammation. **NEET-PG High-Yield Pearls:** * **Distribution:** Skip lesions (discontinuous involvement) are classic for CD [3]. * **Gross Appearance:** "Cobblestone" mucosa, "creeping fat" (mesenteric fat wrapping), and "string sign of Kantor" on barium studies [4]. * **Microscopy:** Transmural inflammation with lymphoid aggregates (Crohn’s Rosettes) [4]. * **Serology:** ASCA (Anti-Saccharomyces cerevisiae antibodies) is positive in CD, whereas p-ANCA is more common in Ulcerative Colitis. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, p. 809. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 806-807. [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. Common Clinical Problems From Alimentary System Disease, pp. 366-367.

Question 278: Which of the following is produced by argentaffinoma of the ileum?

A. GABA
B. Serotonin (Correct Answer)
C. Epinephrine
D. Norepinephrine

Explanation: **Explanation:** **Argentaffinoma** is a historical term for a **Carcinoid tumor**, a well-differentiated neuroendocrine tumor [3]. These tumors arise from enterochromaffin (EC) cells, which are part of the diffuse neuroendocrine system [3]. 1. **Why Serotonin is Correct:** Enterochromaffin cells in the gastrointestinal tract (especially the ileum) are specialized to synthesize, store, and secrete **Serotonin (5-Hydroxytryptamine)** [1]. These cells are called "argentaffin" because they possess the ability to reduce silver salts to metallic silver. When these tumors metastasize to the liver, serotonin bypasses hepatic metabolism and enters the systemic circulation, leading to **Carcinoid Syndrome** (flushing, diarrhea, and right-sided heart failure) [2]. 2. **Why Other Options are Incorrect:** * **GABA:** This is the primary inhibitory neurotransmitter in the central nervous system, not a product of ileal neuroendocrine cells. * **Epinephrine & Norepinephrine:** These catecholamines are primarily produced by the adrenal medulla (chromaffin cells) and sympathetic postganglionic fibers. Tumors producing these are called Pheochromocytomas or Paragangliomas, not argentaffinomas. **High-Yield Clinical Pearls for NEET-PG:** * **Most Common Site:** The most common site for carcinoid tumors is the **appendix**, but the most common site for those that metastasize and cause syndrome is the **ileum** [3]. * **Diagnostic Marker:** The gold standard for diagnosis is the measurement of **5-HIAA** (a serotonin metabolite) in a 24-hour urine sample. * **Histology:** Characterized by "salt and pepper" chromatin and nests of uniform polygonal cells [2]. * **Rule of 1/3rds:** 1/3 are multicentric, 1/3 are metastatic, and 1/3 are associated with a second malignancy. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 94-95. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 781-782. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 780-781.

Question 279: Adenocarcinoma in the esophagus most commonly occurs in which region?

A. Middle esophagus
B. Upper esophagus
C. Barrett's esophagus (Correct Answer)
D. None of the above

Explanation: **Explanation:** **1. Why Barrett’s Esophagus is the Correct Answer:** Adenocarcinoma of the esophagus typically arises in the background of chronic gastroesophageal reflux disease (GERD). The persistent acid reflux leads to **Barrett’s Esophagus**, a metaplastic change where the normal stratified squamous epithelium is replaced by intestinal-type columnar epithelium (containing goblet cells) [1]. This metaplasia is a premalignant condition that progresses through low-grade and high-grade dysplasia to invasive **Adenocarcinoma** [3]. Since GERD affects the distal portion of the esophagus, Adenocarcinoma is most commonly found in the **lower third** of the esophagus [2]. **2. Why Other Options are Incorrect:** * **Upper and Middle Esophagus:** These regions are the most common sites for **Squamous Cell Carcinoma (SCC)** [3]. SCC is associated with risk factors like smoking, alcohol, and achalasia cardia, rather than acid reflux. While SCC was historically the most common esophageal cancer globally, Adenocarcinoma is now more prevalent in Western countries and is rising in incidence elsewhere due to obesity and GERD. **3. High-Yield Clinical Pearls for NEET-PG:** * **Location:** Adenocarcinoma = Lower 1/3rd [2]; Squamous Cell Carcinoma = Middle 1/3rd (most common) and Upper 1/3rd [3]. * **Microscopic Hallmark:** Barrett’s esophagus is identified by the presence of **Goblet cells** on H&E stain (confirmed by Alcian Blue stain) [1]. * **Risk Factors for Adenocarcinoma:** Obesity, GERD, Barrett’s esophagus, and tobacco use. Interestingly, *H. pylori* infection is associated with a *decreased* risk of esophageal adenocarcinoma due to gastric atrophy reducing acid production. * **Molecular Pathogenesis:** Progression involves mutations in **TP53** and **CDKN2A (p16)**. **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. 765-766. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 766-767.

Question 280: Which of the following is NOT important in the definition of ulcerative colitis?

A. It is a chronic inflammatory condition.
B. It involves continuous mucosal inflammation.
C. Granulomas are found in the biopsy. (Correct Answer)
D. It affects the rectum and a variable extent of the colon.

Explanation: **Explanation:** Ulcerative Colitis (UC) is a chronic, idiopathic inflammatory bowel disease (IBD) characterized by a specific set of clinical and pathological features. **Why Option C is the correct answer:** The presence of **non-caseating granulomas** is a hallmark histological feature of **Crohn’s Disease**, not Ulcerative Colitis [1]. In UC, the inflammation is limited to the mucosa and submucosa [2], and while you may see crypt abscesses and crypt distortion, granulomas are characteristically absent. Their presence in a biopsy strongly suggests a diagnosis of Crohn’s [1]. **Analysis of Incorrect Options:** * **Option A:** UC is indeed a **chronic inflammatory condition** marked by periods of relapse and remission. * **Option B:** A defining feature of UC is **continuous mucosal inflammation** [2]. Unlike Crohn’s, which has "skip lesions," UC begins in the rectum and spreads proximally without interrupted areas of healthy tissue [2]. * **Option C:** UC characteristically **starts in the rectum** (proctitis) and extends proximally to involve a variable length of the colon (e.g., left-sided colitis or pancolitis) [2]. **NEET-PG High-Yield Pearls:** * **Depth of Involvement:** UC is mucosal/submucosal; Crohn’s is transmural [2]. * **Lead Pipe Appearance:** Seen on barium enema in chronic UC due to loss of haustrations. * **Pseudopolyps:** Common in UC due to regenerating islands of mucosa amidst ulceration. * **Smoking Paradox:** Smoking is a risk factor for Crohn’s but appears to be **protective** against Ulcerative Colitis. * **Complication:** UC has a higher risk of **Toxic Megacolon** and **Primary Sclerosing Cholangitis (PSC)** compared to Crohn’s. **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. 367-368.

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