Cholesterol gallstones are made up of:-
McCallum patches/plaques are usually seen in which chamber of the heart?
False statement about Barrett esophagus is:
Glanzmann thrombasthenia is due to defect in:-
Which of the following features distinguishes Crohn's disease from Ulcerative colitis?
Hemolysis is predominantly intravascular in which of the following conditions?
Which of the following is positive in Follicular lymphoma?
Bellini duct cancer is seen in which of the following?
Which type of necrosis is characterized by deposition of immune complexes and fibrin in the walls of blood vessels?
NEET-PG 2019 - Pathology NEET-PG Practice Questions and MCQs
Question 11: Cholesterol gallstones are made up of:-
- A. Amorphous cholesterol dihydrate
- B. Amorphous cholesterol monohydrate
- C. Crystalline cholesterol monohydrate (Correct Answer)
- D. Crystalline cholesterol dihydrate
Explanation: ***Crystalline cholesterol monohydrate*** - **Cholesterol gallstones** primarily consist of **crystalline cholesterol monohydrate**, which forms when the bile becomes supersaturated with cholesterol [1]. - The **crystallization** of cholesterol leads to the formation of visible stones within the gallbladder. *Amorphous cholesterol dihydrate* - This form of cholesterol is not typically found as the primary component of **gallstones**. - **Amorphous** structures lack a defined crystalline lattice and are less stable for forming solid stones. *Amorphous cholesterol monohydrate* - While **cholesterol monohydrate** is the core component, it is in a **crystalline** rather than amorphous state in gallstones [1]. - **Amorphous** forms are generally transient intermediates and do not constitute the bulk of the stones. *Crystalline cholesterol dihydrate* - **Dihydrate** forms of cholesterol are not the main constituent of gallstones; the **monohydrate** form is the predominant type [1]. - The specific hydration state of **cholesterol monohydrate** makes it the primary compound found in the solid, crystalline structure of gallstones [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Liver and Gallbladder, p. 882.
Question 12: McCallum patches/plaques are usually seen in which chamber of the heart?
- A. Right atrium
- B. Left ventricle
- C. Left atrium (Correct Answer)
- D. Right ventricle
Explanation: Left atrium - **McCallum patches** are typically found in the **left atrium**, predominantly on the left atrial endocardium [1]. - They are associated with the regurgitant jet of **rheumatic mitral valve disease**, leading to endocardial thickening and fibrosis [1]. Right atrium - While rheumatic heart disease can affect the right side of the heart, particularly the tricuspid valve, **McCallum patches have a specific association with the left atrium** due to mitral valve involvement [1]. - Endocardial changes in the right atrium are less commonly described as McCallum patches. Left ventricle - The left ventricle is primarily a pumping chamber; while it can undergo hypertrophy or dilation in rheumatic heart disease, **McCallum patches are specific endocardial lesions of the atrium** [1]. - **Jet lesions** can occur in the ventricle due to aortic regurgitation, but these are distinct from atrial McCallum patches. Right ventricle - The right ventricle is also a pumping chamber, and endocardial changes here are not typically referred to as McCallum patches. - Rheumatic involvement of the tricuspid valve can cause right heart strain, but **McCallum patches are characteristic of left atrial involvement** [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, p. 566.
Question 13: 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 14: Glanzmann thrombasthenia is due to defect in:-
- A. Gp VI
- B. Thromboxane A2
- C. Gp Ia/IIa
- D. Gp IIb/IIIa (Correct Answer)
Explanation: ***Gp IIb/IIIa*** - Glanzmann thrombasthenia is a **rare, inherited bleeding disorder** characterized by a defect or deficiency in the **glycoprotein IIb/IIIa (Gp IIb/IIIa) complex** on the platelet surface [1]. - This complex is crucial for platelet aggregation as it acts as the receptor for **fibrinogen**, which links activated platelets together [1]. *Gp VI* - **Glycoprotein VI (Gp VI)** is a collagen receptor on platelets, important for initial **platelet adhesion and activation** at sites of vascular injury. - Defects in Gp VI are associated with milder bleeding disorders, not Glanzmann thrombasthenia. *Thromboxane A2* - **Thromboxane A2 (TXA2)** is a potent **vasoconstrictor** and **platelet aggregator** synthesized by platelets. - Disorders in TXA2 synthesis or response, such as aspirin-induced platelet dysfunction, cause bleeding but are biochemically distinct from Glanzmann thrombasthenia. *Gp Ia/IIa* - The **glycoprotein Ia/IIa (Gp Ia/IIa) complex** (also known as integrin ̡2̢1) is another **collagen receptor** on platelets, mediating platelet adhesion to collagen. - Defects in Gp Ia/IIa lead to a different type of mild bleeding disorder, affecting initial adhesion rather than aggregation. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 668-669.
Question 15: 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 16: Hemolysis is predominantly intravascular in which of the following conditions?
- A. Paroxysmal nocturnal hemoglobinuria (Correct Answer)
- B. Warm autoimmune hemolytic anemia
- C. Cold autoimmune hemolytic anemia
- D. Spherocytosis
Explanation: ***Paroxysmal nocturnal hemoglobinuria*** - **PNH** is characterized by a defect in the **PIG-A gene**, leading to a deficiency of **GPI-anchored proteins** like CD55 and CD59 on red blood cells [1]. - This deficiency makes the red blood cells susceptible to complement-mediated lysis, predominantly occurring **intravascularly** [1]. *Warm autoimmune hemolytic anemia* - This condition involves **IgG autoantibodies** binding to red blood cells, which are then primarily removed by **macrophages in the spleen** and liver (extravascular hemolysis) [2]. - The presence of **spherocytes** and a positive direct **antiglobulin test (DAT)** are characteristic [2]. *Cold autoimmune hemolytic anemia* - Involves **IgM autoantibodies** that bind to red blood cells at colder temperatures, often causing agglutination in the peripheral circulation. - While some complement activation and lysis can occur intravascularly, the primary mechanism involves **macrophages in the liver** clearing antibody-coated red cells (extravascular), or red cell destruction in the cooler acral areas. *Spherocytosis* - This is a condition of abnormal red blood cell shape due to defects in **cytoskeletal proteins** (e.g., spectrin, ankyrin), making them less deformable. - These rigid spherocytes are primarily trapped and destroyed by the **phagocytic cells in the spleen**, indicating an **extravascular hemolytic process** [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 650-651. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 602-603.
Question 17: Which of the following is positive in Follicular lymphoma?
- A. Cyclin D1 (Bcl-1)
- B. Bcl-2 protein (Correct Answer)
- C. Bcl-10 signaling protein
- D. Bcl-6 transcription factor
Explanation: ***Bcl-2 protein*** - The characteristic **t(14;18) chromosomal translocation** in follicular lymphoma leads to the **overexpression of the Bcl-2 protein**, which promotes cell survival by inhibiting apoptosis [1], [4]. - This constitutive activation makes the tumor cells resistant to programmed cell death, contributing to their accumulation [2]. - **Bcl-2 positivity is highly specific for follicular lymphoma** among lymphomas, making it the most diagnostically useful marker [3]. *Cyclin D1 (Bcl-1)* - **Cyclin D1** overexpression is characteristic of **Mantle Cell Lymphoma**, typically due to a **t(11;14) translocation**. - It plays a role in cell cycle progression rather than directly inhibiting apoptosis in the same manner as Bcl-2. *Bcl-10 signaling protein* - **Bcl-10** is involved in **NF-ΙB activation**, particularly in certain types of **MALT lymphoma** and other lymphoid neoplasms. - It is not a primary diagnostic marker for follicular lymphoma. *Bcl-6 transcription factor* - **Bcl-6** is a germinal center marker and is **positive in most follicular lymphomas** since they are germinal center-derived B-cell neoplasms. - However, Bcl-6 is also expressed in other germinal center-derived lymphomas like **DLBCL of germinal center subtype**, making it **less specific** than Bcl-2 [3], [5]. - While both Bcl-2 and Bcl-6 can be positive in follicular lymphoma, **Bcl-2 overexpression due to t(14;18) is the defining molecular hallmark** and most diagnostically specific feature [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, pp. 602-604. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 310-311. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, p. 604. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 561-562. [5] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 563-564.
Question 18: Bellini duct cancer is seen in which of the following?
- A. Liver
- B. Spleen
- C. Heart
- D. Kidney (Correct Answer)
Explanation: ***Kidney*** - Bellini duct carcinoma is a **rare and aggressive subtype of renal cell carcinoma (RCC)**, originating from the collecting ducts of Bellini in the kidney. [1] - It accounts for a very small percentage of all RCCs and is characterized by a **poor prognosis**. *Liver* - The liver is affected by primary cancers like **hepatocellular carcinoma** and **cholangiocarcinoma**, or by metastatic disease, none of which arise from Bellini ducts. - Bellini ducts are structures **exclusive to the kidney**, not found in the liver. *Spleen* - Primary cancers of the spleen are **extremely rare**, with most malignant lesions being **lymphomas** or metastases. [2] - The spleen is a **lymphoid organ** and does not contain Bellini ducts. *Heart* - Primary cardiac tumors are uncommon, with the majority being **benign myxomas**. Malignant tumors include **sarcomas**. - The heart's anatomy is distinct and **does not contain any structures analogous to Bellini ducts**. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 959-961. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, pp. 605-606.
Question 19: Which type of necrosis is characterized by deposition of immune complexes and fibrin in the walls of blood vessels?
- A. Liquefactive necrosis
- B. Coagulative necrosis
- C. Caseous necrosis
- D. Fibrinoid necrosis (Correct Answer)
Explanation: ***Fibrinoid necrosis*** - This type of necrosis is classically associated with **immune-mediated vascular damage**, where antigen-antibody complexes are deposited in arterial walls [2]. - The microscopic appearance is characterized by bright pink, amorphous material composed of **fibrin and immune complexes**, giving a fibrin-like staining pattern [1]. *Liquefactive necrosis* - Characterized by the **dissolution of dead cells into a viscous liquid mass**, often seen in bacterial infections or brain infarcts. - The necrotic tissue is replaced by inflammatory cells and fluid, rather than immune complex deposits. *Coagulative necrosis* - Occurs due to **ischemia**, leading to protein denaturation and preservation of cell outlines for a period. - It does not involve the deposition of immune complexes or fibrin in vessel walls. *Caseous necrosis* - A form of coagulative necrosis associated with **tuberculosis**, characterized by a friable, "cheese-like" appearance. - It primarily involves granulomatous inflammation and macrophage accumulation, not immune complex deposition in blood vessels. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 514-518. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 214-242.