Gastrointestinal Pathology — MCQs
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A biopsy of the antrum of the stomach of an adult who presents with epigastric pain reveals numerous lymphocytes and plasma cells within the lamina propria, which is of normal thickness. There are also scattered neutrophils within the glandular epithelial cells. A Steiner silver stain from this specimen is positive for a small, curved organism. What is the most likely diagnosis?
Which condition is characterized by mucosal melanosis and hamartomatous polyps?
Which of the following colonic polyps has no risk for malignancy?
Pseudomyxoma peritonei is typically seen in association with which of the following ovarian neoplasms?
Which of the following conditions is characterized by villous atrophy?
What is true regarding carcinoid of the appendix?
Ulcerative colitis involves which layer of the intestinal wall?
All of the following are true regarding Menetrier's disease, EXCEPT:
The "adenoma-carcinoma sequence" is characteristic of which of the following malignancies?
Which of the following is FALSE regarding Peutz-Jeghers syndrome?
Gastrointestinal Pathology Indian Medical PG Practice Questions and MCQs
Question 11: A biopsy of the antrum of the stomach of an adult who presents with epigastric pain reveals numerous lymphocytes and plasma cells within the lamina propria, which is of normal thickness. There are also scattered neutrophils within the glandular epithelial cells. A Steiner silver stain from this specimen is positive for a small, curved organism. What is the most likely diagnosis?
- A. Enteroinvasive Escherichia coli
- B. Enterotoxigenic E. coli
- C. Helicobacter pylori (Correct Answer)
- D. Salmonella typhi
Explanation: ### Explanation The clinical and histological presentation points directly to **Chronic Gastritis** caused by **_Helicobacter pylori_** [1], [2]. **Why the correct answer is right:** * **Location:** *H. pylori* typically involves the **antrum** of the stomach [1]. * **Histology:** The presence of **lymphocytes and plasma cells** in the lamina propria indicates chronic inflammation, while **neutrophils** within the glandular epithelium (active inflammation) signify "active chronic gastritis" [1], [2]. * **Microscopy:** *H. pylori* is a **small, curved, Gram-negative rod**. It is best visualized using special stains like **Steiner silver stain**, Warthin-Starry stain, or Giemsa stain [1]. The organism resides in the superficial mucus layer [1]. **Why the incorrect options are wrong:** * **Enteroinvasive (EIEC) and Enterotoxigenic (ETEC) *E. coli*:** These primarily affect the small or large intestines, causing diarrhea (inflammatory and watery, respectively). They do not cause chronic antral gastritis or show positivity on silver stains in gastric biopsies. * **Salmonella typhi:** This is the causative agent of Typhoid fever. It primarily involves the **Peyer’s patches** of the ileum (causing hyperplasia and ulceration) and the reticuloendothelial system (liver/spleen), not the gastric mucosa. **High-Yield Clinical Pearls for NEET-PG:** * **Virulence Factors:** *H. pylori* uses **Urease** (to neutralize gastric acid) and **CagA** (associated with increased risk of gastric cancer). * **Gold Standard Diagnosis:** Endoscopic biopsy followed by Histopathology. * **Non-invasive Screening:** Urea Breath Test (UBT) is the most reliable for checking eradication. * **Complications:** It is the most common cause of Peptic Ulcer Disease (PUD) and is strongly associated with **Gastric Adenocarcinoma** and **MALT Lymphoma** [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 770-771. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Alimentary System Disease, pp. 356-357.
Question 12: Which condition is characterized by mucosal melanosis and hamartomatous polyps?
- A. Peutz-Jeghers syndrome (Correct Answer)
- B. Cronkhite-Canada syndrome
- C. Familial adenomatous polyposis
- D. Hereditary nonpolyposis colorectal cancer
Explanation: ### Explanation **1. Why Peutz-Jeghers Syndrome (PJS) is Correct:** Peutz-Jeghers Syndrome is an autosomal dominant disorder caused by a germline mutation in the **STK11 (LKB1)** gene on chromosome 19 [1]. It is classically defined by the triad of: * **Hamartomatous polyps:** These are non-neoplastic "arborizing" polyps (smooth muscle fibers extending into the lamina propria) found most commonly in the small intestine [1]. * **Mucosal Melanosis:** Characteristic mucocutaneous hyperpigmentation (melanotic macules) found on the lips, buccal mucosa, palms, and soles [1]. * **Increased Cancer Risk:** While the polyps themselves are hamartomatous, patients have a significantly high risk of developing gastrointestinal and extra-intestinal malignancies (breast, pancreas, ovary, and testis) [1]. **2. Why the Other Options are Incorrect:** * **Cronkhite-Canada Syndrome:** This is a **non-hereditary** (sporadic) syndrome. While it features hamartomatous polyps, it is distinguished by ectodermal changes like alopecia, nail atrophy, and hyperpigmentation of the skin, but *not* the specific oral melanosis seen in PJS [1]. * **Familial Adenomatous Polyposis (FAP):** Caused by **APC gene** mutations [2]. It is characterized by hundreds to thousands of **adenomatous** polyps (premalignant), not hamartomatous ones [2]. It lacks mucosal melanosis. * **Hereditary Nonpolyposis Colorectal Cancer (HNPCC/Lynch Syndrome):** Caused by mutations in **DNA mismatch repair genes** (MLH1, MSH2) [2]. It is characterized by early-onset colorectal cancer without a significant preceding polyp burden [2]. **3. High-Yield Clinical Pearls for NEET-PG:** * **PJS Polyp Histology:** Look for the **"Christmas Tree"** appearance (branching smooth muscle bundles). * **Most Common Site:** Small intestine (Jejunum > Ileum > Duodenum) [1]. * **Intussusception:** The most common surgical complication of PJS polyps in children. * **Sex Cord Tumors:** PJS is associated with "Sertoli cell tumors" of the testis and "SCTAT" (Sex Cord Tumors with Annular Tubules) in the ovary. **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, pp. 821-822.
Question 13: Which of the following colonic polyps has no risk for malignancy?
- A. Juvenile polyps (Correct Answer)
- B. Hamartomatous polyps associated with Peutz-Jeghers syndrome
- C. Juvenile polyposis syndrome
- D. Familial adenomatous polyposis syndrome
Explanation: The risk of malignancy in colonic polyps depends on whether the lesion is a sporadic inflammatory/hamartomatous growth or part of a genetic syndrome involving germline mutations. **1. Why Option A is Correct:** **Sporadic Juvenile Polyps** are focal, hamartomatous malformations of the mucosal epithelium and lamina propria [1]. They are typically solitary, found in children (under age 5), and located in the rectum. Because they are simple malformations without underlying dysplasia or significant genetic mutations, they have **no malignant potential** [1]. **2. Why the Other Options are Incorrect:** * **Option B (Peutz-Jeghers Syndrome):** While the individual hamartomatous polyps themselves are not pre-malignant, the syndrome is associated with a significantly increased risk of developing various carcinomas (colorectal, pancreatic, breast, and ovarian) due to the **STK11 mutation** [1]. * **Option C (Juvenile Polyposis Syndrome):** Unlike solitary juvenile polyps, this autosomal dominant syndrome involves hundreds of polyps. The constant epithelial turnover and associated mutations (SMAD4 or BMPR1A) lead to a **10–50% risk** of developing colorectal adenocarcinoma [1]. * **Option D (FAP):** This is caused by a mutation in the **APC gene**. It is characterized by thousands of adenomatous polyps, with a **100% risk** of malignancy by age 40 if the colon is not removed [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Most common polyp in children:** Juvenile polyp (presents with painless rectal bleeding). * **Histology of Juvenile Polyp:** Characterized by "dilated, cystically enlarged glands" filled with mucin and inflammatory debris [1]. * **Peutz-Jeghers Syndrome Triad:** Mucocutaneous pigmentation (lips/buccal mucosa), hamartomatous polyps (arborizing smooth muscle pattern), and increased risk of visceral cancers [1]. * **Hyperplastic polyps:** Generally considered non-neoplastic (no malignant potential) if located in the left colon and small in size [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 811-822.
Question 14: Pseudomyxoma peritonei is typically seen in association with which of the following ovarian neoplasms?
- A. Serous cystadenoma
- B. Pseudomucinous cyst
- C. Mucinous cystadenoma (Correct Answer)
- D. Teratoma
Explanation: **Explanation:** **Pseudomyxoma peritonei (PMP)** is a clinical condition characterized by the accumulation of abundant gelatinous, mucinous material within the peritoneal cavity, often referred to as "jelly belly." [1] **Why Mucinous Cystadenoma is Correct:** The condition is most commonly associated with **mucinous tumors**. While historically thought to arise primarily from the ovary, current evidence suggests that the vast majority of PMP cases originate from a primary **appendiceal mucinous neoplasm** that metastasizes to the peritoneum and ovaries [1], [2]. When associated with an ovarian primary, it is almost exclusively seen with **Mucinous Cystadenoma** or its borderline/malignant counterparts. The mucin-secreting cells implant on peritoneal surfaces, leading to progressive bowel obstruction [1]. **Analysis of Incorrect Options:** * **A. Serous Cystadenoma:** These are the most common ovarian tumors but secrete thin, watery fluid rather than thick mucin; they are associated with psammoma bodies, not PMP [2]. * **B. Pseudomucinous cyst:** This is an archaic term sometimes used for mucinous tumors, but "Mucinous Cystadenoma" is the standard pathological nomenclature used in exams. * **D. Teratoma:** While specialized teratomas (like Struma ovarii) exist, they do not typically produce the diffuse peritoneal mucin characteristic of PMP. **NEET-PG High-Yield Pearls:** * **Primary Site:** If both the appendix and ovary have mucinous tumors in a case of PMP, the **appendix** is usually the primary site (Mnemonic: Appendix > Ovary) [1]. * **Characteristic Sign:** "Scalloping" of the liver surface on CT scan due to pressure from mucinous deposits. * **Treatment:** Cytoreductive surgery 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 15: Which of the following conditions is characterized by villous atrophy?
- A. Celiac disease
- B. Giardiasis
- C. Tropical sprue
- D. All of the above (Correct Answer)
Explanation: **Explanation:** Villous atrophy refers to the flattening or blunting of the intestinal villi, leading to a decreased surface area for absorption. This pathological finding is a hallmark of several malabsorptive disorders. 1. **Celiac Disease:** This is an immune-mediated enteropathy triggered by gluten. Histology typically shows a "triad" of **villous atrophy**, crypt hyperplasia, and increased intraepithelial lymphocytes (IELs) [1]. 2. **Tropical Sprue:** This is a chronic diarrheal syndrome seen in tropical regions, likely post-infectious. It presents with similar histological features to Celiac disease, including **villous atrophy**, but it involves the entire small intestine (distal > proximal) and responds to antibiotics and folate [2]. 3. **Giardiasis:** While *Giardia lamblia* usually causes a normal mucosal pattern, heavy infestations can lead to **partial villous atrophy**, epithelial damage, and inflammation, especially in immunocompromised patients (e.g., IgA deficiency). **Why "All of the above" is correct:** Villous atrophy is not pathognomonic for a single disease [4]; it is a shared morphological response to various types of mucosal injury, including autoimmune (Celiac), infectious (Giardiasis, Whipple’s), and environmental (Tropical sprue) causes [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Celiac Disease Gold Standard:** Small intestinal biopsy (usually from the second part of the duodenum). * **Marsh Classification:** Used to grade the severity of villous atrophy in Celiac disease. * **Differentiating Feature:** Celiac disease primarily affects the **proximal** small intestine (duodenum) [3], whereas Tropical sprue often involves the **distal** ileum, leading to Vitamin B12 deficiency. * **Other causes of villous atrophy:** Common Variable Immunodeficiency (CVID), Autoimmune enteropathy, and HIV enteropathy. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 789-790. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 790-791. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Alimentary System Disease, pp. 361-362. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Alimentary System Disease, pp. 360-361.
Question 16: What is true regarding carcinoid of the appendix?
- A. Most commonly occurs at the base of the appendix.
- B. Is the most common neoplasm of the appendix. (Correct Answer)
- C. Most cases require right hemicolectomy.
- D. Metastases are quite common.
Explanation: **Explanation:** **Correct Answer: B. Is the most common neoplasm of the appendix.** Carcinoid tumors (now classified as Neuroendocrine Tumors or NETs) are the most frequent primary neoplasms of the appendix, accounting for approximately 80% of all appendiceal tumors [3]. They are typically discovered incidentally during appendectomies performed for suspected acute appendicitis. **Analysis of Incorrect Options:** * **Option A:** Carcinoid tumors most commonly occur at the **tip of the appendix** (70-75% of cases), not the base. When located at the base, they may cause luminal obstruction leading to appendicitis. * **Option C:** Most appendiceal carcinoids are small (<1 cm) and are cured by a **simple appendectomy** [1]. A right hemicolectomy is only indicated if the tumor is >2 cm, involves the resection margin (base), or shows evidence of mesoappendiceal invasion [1]. * **Option D:** Metastases are **extremely rare** (less than 2%) for appendiceal carcinoids, especially those under 2 cm [1]. Consequently, Carcinoid Syndrome is also very rare unless there is extensive hepatic metastasis [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Origin:** Derived from subepithelial neuroendocrine cells (Kulchitsky cells). * **Staining:** Positive for **Chromogranin A** and **Synaptophysin**. * **Histology:** Characterized by "salt and pepper" chromatin and nests of uniform polygonal cells [2]. * **Prognosis:** Appendiceal carcinoids have an excellent prognosis, with a 5-year survival rate exceeding 95%. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Alimentary System Disease, pp. 375-376. [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 17: Ulcerative colitis involves which layer of the intestinal wall?
- A. Serosa
- B. Lamina propria
- C. Mucosa (Correct Answer)
- D. Muscularis externa
Explanation: **Explanation:** **Ulcerative Colitis (UC)** is a chronic inflammatory bowel disease characterized by continuous, diffuse inflammation that starts in the rectum and extends proximally [2]. 1. **Why Option C is Correct:** The hallmark of Ulcerative Colitis is that the inflammatory process is **superficial**, primarily limited to the **mucosa** and the **submucosa** [1], [2]. Histologically, it presents with "crypt abscesses" (neutrophils in crypt lumens) and "crypt distortion" [1]. Because the inflammation does not typically penetrate deeper, the intestinal wall remains thin, unlike the thickened wall seen in Crohn’s disease. 2. **Why Other Options are Incorrect:** * **Option A (Serosa) & D (Muscularis externa):** These are the outermost and middle layers of the bowel wall. Involvement of these layers indicates **transmural inflammation**, which is the defining feature of **Crohn’s disease**, not UC. In UC, the serosa remains normal unless a complication like toxic megacolon occurs [2]. * **Option B (Lamina propria):** While the lamina propria (a component of the mucosa) is indeed involved, the standard anatomical description for the extent of UC is the "Mucosa" as a whole. **High-Yield Clinical Pearls for NEET-PG:** * **Distribution:** Continuous involvement (no skip lesions) starting from the rectum (rectal sparing is a feature of Crohn's) [2]. * **Gross Appearance:** "Lead pipe" appearance on barium enema due to loss of haustra; Pseudopolyps (regenerating islands of mucosa). * **Complications:** Toxic megacolon and a significantly higher risk of **Adenocarcinoma** of the colon compared to Crohn’s. * **Serology:** Associated with **p-ANCA** (Crohn’s is associated with ASCA). * **Smoking Paradox:** Smoking is protective in UC but a risk factor for 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 18: All of the following are true regarding Menetrier's disease, EXCEPT:
- A. Protein loss
- B. Exophytic growth (Correct Answer)
- C. Hypertrophy of gastric mucosa
- D. Premalignant condition
Explanation: **Explanation:** **Menetrier’s Disease** is a rare, acquired hypertrophic gastropathy characterized by massive enlargement of the gastric rugae [1]. The correct answer is **Option B (Exophytic growth)** because Menetrier’s disease is characterized by **diffuse mucosal thickening** (resembling cerebral convolutions) rather than a localized, discrete exophytic or polypoid mass. **Analysis of Options:** * **Hypertrophy of gastric mucosa (Option C):** This is the hallmark of the disease. There is profound hyperplasia of surface mucous cells (foveolar cells), leading to the characteristic "giant rugal folds" that typically involve the body and fundus while sparing the antrum [1]. * **Protein loss (Option A):** The excessive secretion of mucus and the leakage of serum proteins across the altered epithelial junctions lead to **protein-losing enteropathy**. This clinically manifests as hypoalbuminemia and peripheral edema. * **Premalignant condition (Option D):** Menetrier’s disease is associated with an increased risk of developing **gastric adenocarcinoma** in adults (estimated risk is roughly 2–15%), necessitating regular endoscopic surveillance [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Pathogenesis:** Driven by excessive secretion of **TGF-α** (Transforming Growth Factor-alpha), which leads to overstimulation of the **EGFR** (Epidermal Growth Factor Receptor). * **Histology:** Shows "corkscrew" appearance of foveolar glands and **atrophy of parietal cells**, leading to **hypochlorhydria** (reduced acid production) [1]. * **Triad:** Giant rugal folds + Hypoalbuminemia + Hypochlorhydria. * **Pediatric cases:** Often associated with **CMV infection** and are usually self-limiting, unlike the chronic progressive course in adults [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 775-776.
Question 19: The "adenoma-carcinoma sequence" is characteristic of which of the following malignancies?
- A. Follicular thyroid carcinoma
- B. Carcinoma of the gallbladder
- C. Carcinoma of the stomach
- D. Carcinoma of the colon (Correct Answer)
Explanation: **Explanation:** The **adenoma-carcinoma sequence** refers to the stepwise progression of normal colonic epithelium to invasive adenocarcinoma through a series of accumulated genetic mutations [1]. This is the most common pathway for **Colorectal Carcinoma (Option D)** [2]. The sequence typically follows a predictable molecular timeline: 1. **APC Gene Mutation:** Loss of the APC tumor suppressor gene (the "gatekeeper") leads to decreased intercellular adhesion and increased proliferation, forming an early adenoma [3]. 2. **KRAS Mutation:** Activation of the KRAS oncogene promotes further growth and the formation of a larger, more dysplastic polyp [3]. 3. **TP53 and DCC Loss:** Final loss of tumor suppressor genes (TP53 on chromosome 17p and DCC on 18q) leads to malignant transformation [2]. **Analysis of Incorrect Options:** * **A. Follicular thyroid carcinoma:** Arises from follicular cells, often associated with RAS mutations or PAX8-PPAR-gamma rearrangements, but does not follow a defined adenoma-to-carcinoma progression. * **B. Carcinoma of the gallbladder:** Usually arises from flat dysplasia or chronic inflammation (porcelain gallbladder) rather than a pre-existing adenomatous polyp. * **C. Carcinoma of the stomach:** Most commonly follows the **Correa pathway** (Chronic gastritis → Atrophy → Intestinal metaplasia → Dysplasia → Adenocarcinoma), particularly in the intestinal type. **High-Yield NEET-PG Pearls:** * **APC Gene:** Located on chromosome **5q21**. * **Microsatellite Instability (MSI) Pathway:** An alternative pathway for colon cancer (e.g., Lynch Syndrome) involving DNA mismatch repair (MMR) genes like MLH1 and MSH2 [4]. * **Villus Architecture:** Among adenomas, **villous adenomas** have the highest malignant potential compared to tubular adenomas ("Villous is Villainous") [2]. **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. 224-225. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Alimentary System Disease, pp. 372-374. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, p. 819. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 821-822.
Question 20: Which of the following is FALSE regarding Peutz-Jeghers syndrome?
- A. Autosomal recessive inheritance (Correct Answer)
- B. Presence of hamartomatous polyps
- C. Presence of cutaneous pigmentation
- D. Increased risk of developing breast, lung, and ovarian cancers
Explanation: **Explanation:** **Peutz-Jeghers Syndrome (PJS)** is a rare polyposis syndrome characterized by the triad of hamartomatous polyps, mucocutaneous hyperpigmentation, and an increased risk of various malignancies [1]. **1. Why Option A is the Correct (False) Statement:** Peutz-Jeghers Syndrome follows an **Autosomal Dominant** inheritance pattern, not recessive [1]. It is primarily caused by a germline mutation in the **STK11 (LKB1)** gene located on chromosome 19p13.3, which encodes a serine/threonine kinase that regulates cell polarity and metabolism [1]. **2. Analysis of Other Options:** * **Option B (Hamartomatous polyps):** These are the hallmark of PJS. They are most commonly found in the small intestine (jejunum) [2]. Histologically, they show a characteristic **"Christmas tree" branching pattern** of smooth muscle (arborization) extending into the lamina propria [2]. * **Option C (Cutaneous pigmentation):** Patients develop pathognomonic **melanotic macules** (dark brown to blue-gray spots) on the lips, buccal mucosa, perioral area, palms, and soles [2]. These often appear in infancy and may fade after puberty (except for those on the buccal mucosa). * **Option D (Increased cancer risk):** PJS is a cancer predisposition syndrome. While the polyps themselves have low malignant potential, patients have a significantly high lifetime risk of extra-intestinal cancers, including **breast, pancreas, lung, ovary (Sertoli cell tumors), and uterus [1], [2].** **High-Yield Clinical Pearls for NEET-PG:** * **Most common site of polyps:** Small intestine (Jejunum > Ileum > Duodenum) [2]. * **Common complication:** Intussusception (the polyp acts as a lead point). * **Diagnostic Gene:** *STK11/LKB1* [1]. * **Differentiating Feature:** Unlike Familial Adenomatous Polyposis (FAP), the polyps in PJS are hamartomatous, not adenomatous [2]. **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. 813.
Practice by Chapter
Oral Cavity and Esophageal Pathology
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Gastritis and Peptic Ulcer Disease
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Inflammatory Bowel Disease
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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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