Cardiac Pathology — MCQs

Cardiac Pathology Indian Medical PG Practice Questions and MCQs

Question 11: Vegetations on the undersurface of A.V. valves are found in which condition?

A. Acute rheumatic fever
B. Libman-Sack's endocarditis (Correct Answer)
C. Non-bacterial thrombotic endocarditis
D. Chronic rheumatic carditis

Explanation: **Explanation:** The correct answer is **Libman-Sacks Endocarditis (LSE)**. This condition is a form of non-infective endocarditis associated with **Systemic Lupus Erythematosus (SLE)**. [1] **1. Why Libman-Sacks Endocarditis is correct:** The hallmark of LSE is the presence of small, sterile, pinkish vegetations (verrucae) that can occur **anywhere** on the valve surface [3]. Uniquely, these vegetations are found on the **undersurface** of the valves, the chordae tendineae, and the endocardial surfaces (mural endocardium) [1]. This "random" distribution, particularly on the undersurface of Atrioventricular (A.V.) valves, is a classic pathognomonic feature. **2. Why other options are incorrect:** * **Acute Rheumatic Fever:** Vegetations (verrucae) are small, sterile, and friable, but they occur strictly along the **lines of closure** on the atrial surface of A.V. valves [2]. * **Non-Bacterial Thrombotic Endocarditis (NBTE):** Also known as marantic endocarditis, these sterile vegetations are found along the **lines of closure** [2]. They are associated with hypercoagulable states or advanced malignancies (e.g., Trousseau sign). * **Chronic Rheumatic Carditis:** This stage is characterized by valve thickening, commissural fusion ("fish-mouth" deformity), and calcification rather than active vegetations [4]. **High-Yield Clinical Pearls for NEET-PG:** * **Location Summary:** * *Rheumatic:* Lines of closure (Atrial surface of A.V. valves) [2]. * *Infective Endocarditis:* Large, friable vegetations on the flow surface; can cause perforation [2]. * *Libman-Sacks:* Both surfaces (including undersurface) and chordae [1]. * **LSE Pathology:** Histologically shows intense valvulitis with **fibrinoid necrosis** and often contains hematoxylin bodies (LE cells). * **Most common valve involved in LSE:** Mitral valve [3]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, p. 570. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, p. 568. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 232-233. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 566-567.

Question 12: Which of the following is NOT a cause of myocarditis?

A. Trichinosis
B. Mycobacterium tuberculosis (Correct Answer)
C. Corynebacterium diphtheriae
D. Systemic lupus erythematosus

Explanation: **Explanation:** The correct answer is **B. Mycobacterium tuberculosis**. While *Mycobacterium tuberculosis* (TB) frequently involves the heart, it characteristically affects the **pericardium** (causing chronic constrictive pericarditis), not the myocardium [2]. Myocarditis is defined as inflammation of the heart muscle, and TB is an extremely rare cause of primary myocardial inflammation. **Analysis of Options:** * **A. Trichinosis:** *Trichinella spiralis* is the most common helminthic cause of myocarditis worldwide. It typically presents with eosinophilic infiltration of the myocardium. * **C. Corynebacterium diphtheriae:** This is a classic bacterial cause of myocarditis. The damage is mediated by the **diphtheria exotoxin**, which inhibits protein synthesis (via ADP-ribosylation of EF-2), leading to fatty change and necrosis of myocytes in up to 25% of patients. * **D. Systemic Lupus Erythematosus (SLE):** SLE is a well-known non-infectious cause of myocarditis [2]. It can cause inflammation across all layers of the heart (pancarditis), though **Libman-Sacks endocarditis** (sterile vegetations) is its most characteristic cardiac manifestation. **NEET-PG High-Yield Pearls:** * **Most common cause of myocarditis:** Viral infections, specifically **Coxsackievirus B** [1]. * **Chagas Disease:** Caused by *Trypanosoma cruzi*; it is a major cause of myocarditis in South America [1]. * **Giant Cell Myocarditis:** A rare, rapidly fatal form characterized by multinucleated giant cells and extensive necrosis [1]. * **Hypersensitivity Myocarditis:** Often drug-induced (e.g., sulfonamides, diuretics) and histologically marked by **eosinophils** [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 578-579. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 581-582.

Question 13: Antishkow's cells are seen in which condition?

A. Rheumatic heart disease (Correct Answer)
B. Rheumatic arthritis
C. Bacterial endocarditis
D. Marantic endocarditis

Explanation: **Explanation:** **Anitschkow cells** (also known as "caterpillar cells") are pathognomonic for **Acute Rheumatic Heart Disease (RHD)**. They are specialized activated macrophages found within **Aschoff bodies**, which are the characteristic granulomatous lesions of RHD [1]. 1. **Why Rheumatic Heart Disease is correct:** In the acute phase of RHD, the body mount an immune response against Group A Streptococcal antigens that cross-reacts with cardiac tissue (molecular mimicry). This leads to the formation of Aschoff bodies. Anitschkow cells within these bodies have abundant cytoplasm and a central nucleus with chromatin condensed into a slender, wavy ribbon, resembling a **caterpillar** under light microscopy [1]. When viewed in cross-section, they may look like "owl eyes." 2. **Why other options are incorrect:** * **Rheumatoid arthritis:** While it can cause pericarditis or rheumatoid nodules, it does not feature Anitschkow cells or Aschoff bodies. * **Bacterial endocarditis:** Characterized by large, friable, destructive vegetations containing bacteria and fibrin, not granulomatous Aschoff bodies. * **Marantic endocarditis (NBTE):** Involves sterile, small thrombi on valves typically seen in wasting diseases (cancer); it lacks the specific inflammatory cellular infiltrate of RHD. **High-Yield Clinical Pearls for NEET-PG:** * **Aschoff Bodies:** Pathognomonic for RHD; they represent foci of fibrinoid necrosis surrounded by lymphocytes, plasma cells, and Anitschkow cells [1]. * **Aschoff Giant Cells:** When Anitschkow cells become multinucleated, they are termed Aschoff giant cells. * **Pancarditis:** RHD is a pancarditis (affects endo-, myo-, and pericardium). * **McCallum Patch:** A map-like area of subendocardial thickening, usually in the left atrium, caused by regurgitant jets in RHD. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 566-567.

Question 14: The commonest type of pericarditis in acute rheumatic fever is?

A. Serous
B. Fibrinous (Correct Answer)
C. Serofibrinous
D. Purulent

Explanation: **Explanation:** **1. Why Fibrinous Pericarditis is Correct:** Acute Rheumatic Fever (ARF) is characterized by **pancarditis**, involving the endocardium, myocardium, and pericardium. The pericardial involvement typically manifests as **fibrinous or serofibrinous pericarditis** [1]. In this condition, the pericardium loses its glistening appearance and becomes opaque and granular due to the deposition of fibrin [2]. This creates a rough, shaggy surface traditionally described as the **"Bread and Butter" appearance** (where the visceral and parietal layers resemble two slices of buttered bread pulled apart) [2]. **2. Analysis of Incorrect Options:** * **A. Serous:** This involves a thin, watery exudate (e.g., in early viral infections or uremia). While ARF can have a serous component, the predominant and characteristic feature is the fibrin deposit [1]. * **C. Serofibrinous:** While many sources use "fibrinous" and "serofibrinous" interchangeably, **Fibrinous** is the classic textbook description for the specific inflammatory reaction in ARF [2]. If both are present, "Fibrinous" is the preferred primary descriptor for the pathology. * **D. Purulent:** Also known as suppurative pericarditis, this is caused by bacterial or fungal infections (e.g., Staphylococci or Pneumococci) and involves pus formation, which is not a feature of the sterile inflammatory response in ARF [1]. **3. High-Yield Clinical Pearls for NEET-PG:** * **Pathognomonic Lesion:** The **Aschoff body** (granuloma) is the hallmark of ARF, found most commonly in the myocardium. * **Anitschkow Cells:** Found within Aschoff bodies, these are modified macrophages with "caterpillar-like" chromatin. * **MacCallum Patch:** A subendocardial thickening, usually in the left atrium, caused by regurgitant jets. * **Clinical Sign:** A **pericardial friction rub** is the classic physical exam finding for fibrinous pericarditis. * **Valve Involvement:** The **Mitral valve** is most commonly affected in ARF, followed by the Aortic valve. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 581-582. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 101-103.

Question 15: Which statement is false regarding Non-Bacterial Thrombotic Embolism (NBTE)?

A. Marantic endocarditis
B. Thrombi on the leaflets of the cardiac valves
C. Vegetations elicit an inflammatory reaction (Correct Answer)
D. Non-invasive in nature

Explanation: Non-Bacterial Thrombotic Endocarditis (NBTE), also known as **Marantic Endocarditis**, is characterized by the deposition of small, sterile thrombi on the leaflets of cardiac valves [1]. **Why Option C is the correct (False) statement:** The hallmark of NBTE is that the vegetations are **non-inflammatory**. Unlike infective endocarditis, there is no significant infiltration of neutrophils or organization by granulation tissue. The thrombi consist of bland fibrin and platelets loosely attached to the valve surface. Because there is no underlying inflammation or destruction of the valve tissue, the vegetations do not cause structural damage to the leaflets [1]. **Analysis of other options:** * **Option A (Marantic endocarditis):** This is a synonymous term derived from "marasmus" (wasting), as it is frequently seen in patients with debilitating diseases like advanced cancer or chronic sepsis. * **Option B (Thrombi on leaflets):** NBTE involves the formation of small (1–5 mm) friable vegetations, typically along the line of closure of the valves (most commonly the mitral valve) [1]. * **Option D (Non-invasive):** The vegetations are superficial and do not invade or erode the underlying endocardium or valve substance. **NEET-PG High-Yield Pearls:** 1. **Association:** Strongly associated with **hypercoagulable states** and **mucinous adenocarcinomas** (Trousseau syndrome/migratory thrombophlebitis) [2]. 2. **Clinical Significance:** While the vegetations are non-destructive to the valve, they are highly friable and prone to **systemic embolization**, often leading to strokes or infarcts in the spleen and kidneys. 3. **Comparison:** Unlike Libman-Sacks endocarditis (SLE), which can occur on both sides of the valve, NBTE vegetations typically occur only on the atrial surface of AV valves or ventricular surface of semilunar valves [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, p. 568. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, p. 570.

Question 16: Antitschkow cells in acute rheumatic fever are derived from which cell type?

A. Lymphocytes
B. Histiocytes
C. Macrophages (Correct Answer)
D. Neutrophils

Explanation: **Explanation:** **Anitschkow cells** (also known as "caterpillar cells") are the pathognomonic cellular component of the **Aschoff body**, which is the hallmark granulomatous lesion of **Acute Rheumatic Fever (ARF)** [1]. **Why Macrophages are the correct answer:** Anitschkow cells are specialized, activated **cardiac histiocytes (macrophages)** [2]. Under the microscope, they are characterized by an abundant cytoplasm and a central nucleus containing a wavy, ribbon-like chromatin pattern that resembles a caterpillar [1]. When viewed in cross-section, they may appear as "owl-eye" cells. These cells are derived from the mononuclear phagocyte system (macrophages) that migrate to the site of myocardial inflammation [2]. **Why other options are incorrect:** * **Lymphocytes:** While T-lymphocytes and plasma cells are present within the Aschoff body, they do not transform into Anitschkow cells [2]. * **Histiocytes:** While "histiocyte" is often used interchangeably with macrophage, modern pathology and NEET-PG conventions specifically identify the **macrophage** as the definitive precursor. (Note: If "Macrophages" were not an option, Histiocytes would be the next best choice). * **Neutrophils:** These are markers of acute bacterial inflammation. ARF is an immune-mediated delayed hypersensitivity reaction (Type II) where granulomatous inflammation (macrophages/giant cells) predominates rather than a neutrophilic infiltrate [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Aschoff Bodies:** Found in all three layers of the heart (pancarditis), but most common in the **myocardium** (interstitium) [1]. * **Aschoff Giant Cells:** Formed by the fusion of multiple Anitschkow cells (multinucleated). * **Evolution:** Aschoff bodies eventually undergo fibrosis, leaving behind a small collagenous scar. * **MacCallum Patch:** A subendocardial thickening, usually in the **left atrium**, caused by regurgitant jets in ARF. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 566-567. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, p. 566.

Question 17: Fibrous scar in myocardial infarction is well established by which time frame?

A. 6 weeks (Correct Answer)
B. 6 months
C. 6 days
D. 30 days

Explanation: The healing process of Myocardial Infarction (MI) follows a predictable chronological sequence of inflammation, repair, and remodeling [1]. **Explanation of the Correct Answer:** **Option A (6 weeks)** is correct because the replacement of necrotic myocardium with a **dense, fibrous collagenous scar** is typically well-established by the end of the 6th to 8th week [1]. By this stage, the highly vascularized granulation tissue has been replaced by relatively acellular, white collagenous tissue, marking the completion of the healing phase [1]. **Analysis of Incorrect Options:** * **Option C (6 days):** At this stage, the heart is characterized by **early granulation tissue** at the edges, extensive macrophage infiltration, and the beginning of collagen deposition [1]. The tissue is soft and structurally weak, making this the peak period for myocardial rupture [1]. * **Option D (30 days):** By one month, the scar is forming and maturing, but the process of collagen cross-linking and contraction is still ongoing [1]. It is not considered "well-established" until the 6-week mark. * **Option B (6 months):** While the scar may undergo further thinning or remodeling over months, the definitive fibrous scar is already fully formed much earlier (by 6–8 weeks) [1]. **High-Yield Clinical Pearls for NEET-PG:** * **0–24 hours:** Coagulative necrosis and wavy fibers [1]. * **1–3 days:** Peak neutrophilic infiltration (Yellow-tan center) [1]. * **3–7 days:** Peak macrophage activity; highest risk of **free wall rupture**, VSD, or papillary muscle rupture [1]. * **1–2 weeks:** Maximum granulation tissue formation [1]. * **Modification:** Factors like large infarct size, advanced age, or steroid use can delay this healing timeline. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 552-554.

Question 18: Occlusion of the anterior descending branch of the left coronary artery will lead to infarction of which area?

A. Posterior wall of the interventricular septum
B. Anterior wall of the left ventricle (Correct Answer)
C. Lateral wall of the heart
D. Inferior surface of the right ventricle

Explanation: **Explanation:** The **Left Anterior Descending (LAD) artery**, often referred to as the "widow-maker," is the most common site of coronary artery occlusion (40–50%). It primarily supplies the **anterior wall of the left ventricle**, the **anterior 2/3rd of the interventricular septum**, and the cardiac apex [1]. Therefore, an occlusion in this branch directly results in an anteroseptal or anterior wall myocardial infarction [2]. **Analysis of Incorrect Options:** * **Option A (Posterior wall of the interventricular septum):** This area, along with the posterior wall of the left ventricle, is typically supplied by the **Posterior Descending Artery (PDA)**. In 85% of individuals (right dominance), the PDA arises from the Right Coronary Artery (RCA) [1]. * **Option C (Lateral wall of the heart):** The lateral wall of the left ventricle is supplied by the **Left Circumflex Artery (LCX)**. Occlusion here leads to a lateral wall MI. * **Option D (Inferior surface of the right ventricle):** The right ventricular wall and the inferior (diaphragmatic) surface of the heart are supplied by the **Right Coronary Artery (RCA)** [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Frequency of Occlusion:** LAD (40-50%) > RCA (30-40%) > LCX (15-20%). * **ECG Correlations:** * LAD occlusion: ST elevation in leads **V1–V4**. * LCX occlusion: ST elevation in leads **I, aVL, V5, V6**. * RCA occlusion: ST elevation in leads **II, III, aVF**. * **Papillary Muscle Rupture:** The posteromedial papillary muscle has a single blood supply (RCA), making it more prone to rupture than the anterolateral muscle (dual supply from LAD/LCX). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 550-552. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Cardiovascular Disease, pp. 286-288.

Question 19: Flat vegetations in pockets of valves are due to?

A. Rheumatic heart disease
B. Rheumatic heart disease (Correct Answer)
C. Non-bacterial thrombotic endocarditis (NBTE)
D. Infective endocarditis

Explanation: The correct answer is **Rheumatic Heart Disease (RHD)**. In **Acute Rheumatic Fever**, the vegetations (verrucae) are characteristically small (1–2 mm), firm, and sterile. They are typically found along the **lines of closure** of the valve leaflets [1]. However, a unique pathological feature of RHD is the involvement of the endocardial surface beyond the leaflets, leading to **flat vegetations in the pockets of the valves** (the angles where the leaflets meet the wall) and the formation of **MacCallum patches** (subendocardial thickenings, usually in the left atrium) [2]. **Analysis of Options:** * **Rheumatic Heart Disease (Correct):** Features small, friable, row-like verrucae along lines of closure and within valve pockets [1]. * **Non-Bacterial Thrombotic Endocarditis (NBTE):** Characterized by small, sterile, bland vegetations (marantic endocarditis) occurring in wasted states (cancer/cachexia). These occur strictly along the lines of closure and do not typically involve the valve pockets or cause significant inflammation [1]. * **Infective Endocarditis (IE):** Features **large, bulky, friable, and destructive** vegetations that often contain bacteria [5]. They can lead to valve perforation or chordae rupture, unlike the "flat" nature of RHD verrucae [1]. * **Libman-Sacks Endocarditis (SLE):** These vegetations are unique because they occur on **both sides** of the valve leaflets (undersurfaces) and on the endocardial surfaces, but they are typically described as "mulberry-like" rather than flat pocket vegetations [4]. **High-Yield Pearls for NEET-PG:** * **MacCallum Patch:** Most common in the **Posterior wall of the Left Atrium**. * **Aschoff Bodies:** Pathognomonic focal inflammatory lesions found in all three layers of the heart (pancarditis) in RHD [2]. * **Anitschkow Cells:** "Caterpillar cells" (activated macrophages) found within Aschoff bodies [2]. * **Most common valve involved:** Mitral > Aortic > Tricuspid > Pulmonary [3]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, p. 568. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, p. 566. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 566-567. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, p. 570. [5] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 568-570.

Question 20: All of the following are causes of myocarditis except:

A. Trichinosis
B. Mycobacterium tuberculosis (Correct Answer)
C. Borrelia
D. CMV

Explanation: **Explanation:** The correct answer is **B. Mycobacterium tuberculosis**. In pathology, **myocarditis** is defined as an inflammation of the heart muscle (myocardium) that causes injury without an underlying ischemic cause [1]. While *Mycobacterium tuberculosis* (TB) frequently involves the cardiovascular system, it characteristically causes **pericarditis** (specifically chronic constrictive pericarditis) rather than primary myocarditis. While rare myocardial tuberculomas can occur, TB is not classified as a standard cause of infectious myocarditis in medical literature or standard textbooks like Robbins Pathology. **Analysis of Incorrect Options:** * **A. Trichinosis:** *Trichinella spiralis* is the most common helminthic cause of myocarditis worldwide. * **C. Borrelia:** *Borrelia burgdorferi* (Lyme disease) is a well-known cause of "Lyme Carditis," which often manifests as conduction blocks (AV blocks) due to myocardial inflammation. * **D. CMV:** Cytomegalovirus is a significant viral cause of myocarditis, particularly in immunocompromised patients and post-transplant recipients [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Most common cause overall:** Viral infections, specifically **Coxsackievirus B** [1]. * **Chagas Disease:** Caused by *Trypanosoma cruzi*; it is the most common cause of myocarditis in endemic areas (South America) [1]. * **Diphtheritic Myocarditis:** Caused by the *Corynebacterium diphtheriae* exotoxin; it is a major cause of death in diphtheria patients. * **Hypersensitivity Myocarditis:** Characterized by an **eosinophilic infiltrate**, usually due to drug reactions (e.g., sulfonamides) [1]. * **Giant Cell Myocarditis:** A rare, aggressive form with a poor prognosis, characterized by multinucleated giant cells and extensive necrosis [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 578-581.

Practice by Chapter

Congenital Heart Disease

Practice Questions

Ischemic Heart Disease

Practice Questions

Hypertensive Heart Disease

Practice Questions

Valvular Heart Disease

Practice Questions

Myocarditis and Cardiomyopathies

Practice Questions

Pericardial Disease

Practice Questions

Cardiac Tumors

Practice Questions

Heart Failure Pathophysiology

Practice Questions

Cardiac Transplantation Pathology

Practice Questions

Endocarditis

Practice Questions

Want unlimited practice?

Get full access to all questions, explanations, and performance tracking.

Start For Free