Cardiac Pathology Practice Questions

Q: A 65-year-old man dies due to myocardial infarction. Which stains can be used to see the infarct in the heart while conducting an autopsy?

Triphenyl tetrazolium chloride. ***Triphenyl tetrazolium chloride***- This stain is used to macroscopically identify **acute myocardial infarction** during autopsy, typically within the first few hours up to 2 weeks post-infarct [1].- It detects the activity of **dehydrogenase enzymes** (like LDH); viable myocardium reacts with TTC to form a **brick red** color, while the necrotic (infarcted) tissue lacks these enzymes and remains **pale** or *gray-yellow* [1].*Oil red O*- **Oil red O** is a lipid stain primarily used to demonstrate neutral lipids and **triglycerides**, often used for conditions like steatosis or fat emboli.- It is not specific for the cellular necrosis defining an acute infarct and is generally used on frozen sections.*Sudan black B*- **Sudan black B** is a lipid stain used to visualize phospholipids, neutral lipids, and lipoproteins.- It is more commonly employed in hematopathology (e.g., staining **myeloblasts**) or for demonstrating specific lipid storage, not for defining the boundaries of an acute myocardial infarct in gross pathology examination.*Masson trichrome*- This is a differential stain used to distinguish between muscle (red) and **collagen** (blue or green), used to highlight **fibrosis**.- While crucial for identifying **old, healed myocardial infarcts** (scar tissue), it is ineffective for rapid visualization of a fresh, acute infarct where significant collagen deposition has not yet taken place [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 552-554.

Q: An athlete collapsed suddenly during exercise and died on the field. Postmortem heart is shown in the figure. There is family history of heart disease. What is the diagnosis?

Hypertrophic cardiomyopathy. ***Hypertrophic cardiomyopathy*** - **Sudden cardiac death** in young athletes, especially with a family history, is a classic presentation of **hypertrophic cardiomyopathy (HCM)** [2][3]. - Postmortem examination typically reveals **asymmetric septal hypertrophy** and **myocardial fiber disarray**, which are characteristic of HCM [1]. *Mitral regurgitation* - While mitral regurgitation can lead to heart failure, it is less commonly associated with **sudden death in athletes** without prior symptoms. - The primary finding would be **valvular abnormalities** and **left atrial/ventricular dilation**, not typically isolated hypertrophy. *Mitral stenosis* - Mitral stenosis primarily causes **left atrial enlargement** and **pulmonary hypertension**, leading to symptoms like dyspnea and fatigue. - It is not a common cause of **sudden cardiac death** in athletes and would not typically present with the gross hypertrophy seen in HCM. *Aortic stenosis with left ventricular hypertrophy* - Aortic stenosis can cause **left ventricular hypertrophy** due to increased pressure overload. - However, sudden death in athletes due to aortic stenosis is less common than HCM, and the hypertrophy in aortic stenosis is typically **concentric** and symmetrical, unlike the asymmetric hypertrophy often seen in HCM [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 577-578. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 576-577. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Cardiovascular Disease, pp. 303-304.

Q: All are true regarding the heart specimen shown except:

Spade-shaped cavity of left ventricle. ***Spade-shaped cavity of left ventricle*** - The heart specimen in **hypertrophic cardiomyopathy (HCM)** typically shows a **banana-shaped or crescentic left ventricular cavity** due to the hypertrophied septum bulging into the outflow tract [1]. - A **spade-shaped cavity** is characteristic of **apical hypertrophic cardiomyopathy**, which is a specific, less common variant of HCM. *Asymmetrical septal hypertrophy* - This is a hallmark feature of **hypertrophic cardiomyopathy (HCM)**, where the **interventricular septum** is disproportionately thicker than the free wall of the left ventricle [1][2]. - It is the most common morphological pattern seen in HCM [2]. *Left ventricular outflow tract obstruction* - This occurs in a significant proportion of HCM patients due to the **hypertrophied septum** and **systolic anterior motion (SAM)** of the mitral valve [1]. - The obstruction leads to a **pressure gradient** across the left ventricular outflow tract, causing symptoms like dyspnea and syncope [1]. *Diastolic dysfunction* - **Diastolic dysfunction** is a universal finding in HCM due to the **stiff, non-compliant hypertrophied left ventricle** [1]. - This impaired relaxation and filling of the ventricle leads to elevated **diastolic pressures** and contributes to symptoms of heart failure [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 577-578. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Cardiovascular Disease, pp. 303-304.

Q: A patient presented with mitral valve stenosis, identify the diagnosis from the mitral valve histopathology depicted below. (AIIMS Nov 2017)

Rheumatic heart disease. ***Rheumatic heart disease*** - **Rheumatic heart disease** is the most common cause of **mitral valve stenosis** and is characterized by **fibrosis** and **calcification** of the valve leaflets, often with **commissural fusion** [1]. - Histopathology would show features like **Aschoff bodies** (granulomas with Anitschkow cells) in the acute phase [3], and later **fibrous thickening** and **neovascularization** of the valve [1]. *Tuberculosis* - While tuberculosis can affect the heart (tuberculous pericarditis or myocarditis), it is an **extremely rare cause of isolated valvular stenosis**. - Histopathology would show **caseating granulomas** with **Langhans giant cells**, which are not typical findings in primary valvular stenosis. *Myxomatous degeneration* - **Myxomatous degeneration** primarily affects the **mitral valve**, leading to **mitral valve prolapse** and **regurgitation**, not stenosis. - Histopathology shows **accumulation of proteoglycans** and **disruption of collagen fibers** within the valve, making it floppy. *Viral myocarditis* - **Viral myocarditis** is an inflammation of the **myocardium** (heart muscle) and typically leads to **dilated cardiomyopathy** and **heart failure**, not primary valvular stenosis. - Histopathology would reveal **inflammatory infiltrates** (lymphocytes) and **myocyte necrosis**, not changes specific to valve stenosis. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 566-567. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Cardiovascular Disease, pp. 293-294. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, p. 566.

Q: Which of the following is the most common cause of death in this condition?

Cardiac failure. ***Cardiac failure*** - The image reveals **myocarditis** with **inflammatory infiltrates** and **myocyte necrosis**, indicative of direct myocardial injury. - Severe myocarditis can lead to significant impairment of cardiac function, resulting in **dilated cardiomyopathy** and ultimately **heart failure**, which is the most common cause of death. *Bacterial endocarditis* - This condition involves **vegetations on heart valves**, often leading to **valvular insufficiency** or **embolism**, but it is not primarily a disease of the myocardium itself causing widespread failure as depicted. - The image does not show evidence of valvular vegetations or bacterial colonies typical of endocarditis. *Ball thrombus in left atria* - A ball thrombus typically forms in the **left atrium** due to conditions like **mitral stenosis** or atrial fibrillation, potentially causing **embolic events** or sudden obstruction. - This is a sequela of other cardiac diseases and not a primary myocardial pathology leading to widespread inflammation and necrosis as seen. *Acute coronary insufficiency* - Acute coronary insufficiency is characterized by **ischemia** due to reduced blood flow through the **coronary arteries**, usually caused by **atherosclerotic plaque rupture** and thrombosis. - The histological features of myocarditis, with diffuse inflammatory cells and scattered myocyte damage in the image, are distinct from the typical pattern of **ischemic necrosis** found in myocardial infarction.

Q: The following image shows presence of:

Anitschkow cell. ***Anitschkow cell*** - Anitschkow cells are characteristic **caterpillar cells** or **owl-eye cells** seen in the **Aschoff bodies** of **rheumatic fever** [1]. - They are **enlarged macrophages** with a central, wavy, chromatin-rich nucleus [1]. *Aschoff cell* - Aschoff cells are a type of **modified macrophage** or **Anitschkow cell** that are part of the **Aschoff body**, not a distinct cell type on their own [1]. - The term "Aschoff cell" is often used interchangeably with Anitschkow cell, but Anitschkow cell refers to the specific morphology. *Kulchitsky cell* - Kulchitsky cells are **neuroendocrine cells** found in the **gastrointestinal tract** and **bronchi**. - They are associated with **carcinoid tumors** and produce various hormones. *Langhan cell* - Langhan cells are a type of **multinucleated giant cell** formed from fused **epithelioid macrophages**. - They are characteristic of **granulomatous inflammation**, particularly seen in **tuberculosis**. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, p. 566.

Q: The image shows infarcted tissue of the heart that develops after

3 days. ***3 days*** - Grossly, an **infarcted area** of the heart typically appears **yellow-tan** and soft by **3-7 days** due to the onset of **coagulative necrosis** and early inflammatory response [1]. - This time frame allows for significant **neutrophilic infiltration** and the beginning of **macrophage activity** to clear necrotic debris, leading to the characteristic appearance [1]. *3 hours* - Within **3 hours** of infarction, the gross appearance of the myocardium is usually **normal** or shows only subtle changes like slight pallor [1]. - Microscopic changes like **wavy fibers** and early **edema** might be present, but gross discoloration is not yet evident [1]. *3 weeks* - By **3 weeks**, the infarcted area would typically be replaced by a **dense, gray-white scar** composed primarily of **collagen** [1]. - The initial yellow-tan appearance of necrotic tissue would have been largely reabsorbed and replaced by **fibrosis** [1]. *3 months* - At **3 months**, the infarct would be a **well-established, firm, white fibrous scar**, indicating complete healing and remodeling [1]. - There would be no remaining yellow-tan necrotic tissue, as the process of **fibrosis** would be complete [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 552-554. [2] 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. 147-148.

Q: The following is the Hematoxylin and Eosin stained section from the heart of a patient after myocardial infarction. What can you say about the age of the infarction?

1-2 days. ***1-2 days*** - At 1-2 days post-MI, **neutrophilic infiltration** is prominent, and **coagulative necrosis** of cardiomyocytes is well-established, leading to loss of nuclei and striations [1]. - This time frame is characterized by the peak inflammatory response to the necrotic tissue [1,2]. *6 hour* - Within 6 hours of MI, there might be early signs of **coagulative necrosis**, such as **wavy fibers** and **hypereosinophilia**, but significant inflammatory infiltrate is usually not yet present [1]. - **Neutrophilic infiltration** is minimal or absent at this very early stage [1]. *1 week* - By 1 week, **macrophages** become the predominant inflammatory cells, clearing necrotic debris [1]. - **Granulation tissue** begins to form, characterized by new blood vessels and fibroblasts, indicating the start of repair [1]. *3 week* - At 3 weeks, the infarcted area is largely replaced by **dense fibrous scar tissue** [1]. - There is minimal inflammatory infiltrate, and the area is composed primarily of **collagen** [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, p. 552. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 552-554.

Q: In a patient, Mitral valve vegetations are seen along the lines of closure along with fusion of commissures. What is the likely diagnosis?

Rheumatic endocarditis. ***Rheumatic endocarditis*** - **Rheumatic fever** is a common cause of **mitral valve disease**, leading to **vegetations along the lines of closure** [2] and characteristic **fusion of commissures** [1]. - This chronic inflammation results in **fibrosis** and **calcification**, causing **mitral stenosis** [3] or regurgitation. *Libman-Sacks endocarditis* - Characterized by **sterile vegetations** typically found on **both sides of the valve leaflets** (atrial and ventricular surfaces) [2], often associated with **Systemic Lupus Erythematosus (SLE)**. - It does not typically cause **commissural fusion** or significant valvular stenosis. *Marantic endocarditis* - Also known as **nonbacterial thrombotic endocarditis (NBTE)**, it involves **sterile vegetations** composed of fibrin and platelets, usually found on the **lines of closure** [2]. - It is associated with **debilitating illnesses** like cancer or sepsis, but **does not cause commissural fusion**. *Bacterial endocarditis* - Involves **large, destructive vegetations** that can be found on any part of the valve [2], often associated with **valve destruction**, **abscess formation**, and **septic emboli**. - While it causes vegetations, it typically **does not lead to commissural fusion** as a primary feature; fusion is more characteristic of chronic rheumatic heart disease. **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. 568. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Cardiovascular Disease, pp. 293-294.

Question 1

A 65-year-old man dies due to myocardial infarction. Which stains can be used to see the infarct in the heart while conducting an autopsy?

Accepted Answer

Triphenyl tetrazolium chloride

Answer

Oil red O

Answer

Sudan black B

Answer

Masson trichrome

Question 2

An athlete collapsed suddenly during exercise and died on the field. Postmortem heart is shown in the figure. There is family history of heart disease. What is the diagnosis?

Accepted Answer

Hypertrophic cardiomyopathy

Answer

Mitral regurgitation

Answer

Mitral stenosis

Answer

Aortic stenosis with left ventricular hypertrophy

Question 3

All are true regarding the heart specimen shown except:

Accepted Answer

Spade-shaped cavity of left ventricle

Answer

Asymmetrical septal hypertrophy

Answer

Left ventricular outflow tract obstruction

Answer

Diastolic dysfunction

Question 4

A patient presented with mitral valve stenosis, identify the diagnosis from the mitral valve histopathology depicted below. (AIIMS Nov 2017)

Accepted Answer

Rheumatic heart disease

Answer

Tuberculosis

Answer

Myxomatous degeneration

Answer

Viral myocarditis

Question 5

A 5-year-old child presents with fever with chest pain. On auscultation, pericardial friction rub was heard with bilaterally clear lung fields. The Histopathological finding shows presence of:

Accepted Answer

Aschoff bodies

Answer

Granulomas with caseation

Answer

Anitschkow cells

Answer

Fibrinous exudate

Question 6

Which of the following is the most common cause of death in this condition?

Accepted Answer

Cardiac failure

Answer

Bacterial endocarditis

Answer

Ball thrombus in left atria

Answer

Acute coronary insufficiency

Question 7

The following image shows presence of:

Accepted Answer

Anitschkow cell

Answer

Aschoff cell

Answer

Kulchitsky cell

Answer

Langhans cell

Question 8

The image shows infarcted tissue of the heart that develops after

Accepted Answer

3 days

Answer

3 hours

Answer

3 weeks

Answer

3 months

Question 9

The following is the Hematoxylin and Eosin stained section from the heart of a patient after myocardial infarction. What can you say about the age of the infarction?

Accepted Answer

1-2 days

Answer

6 hours

Answer

1 week

Answer

3 weeks

Question 10

In a patient, Mitral valve vegetations are seen along the lines of closure along with fusion of commissures. What is the likely diagnosis?

Accepted Answer

Rheumatic endocarditis

Answer

Libman-Sacks endocarditis

Answer

Marantic endocarditis

Answer

Bacterial endocarditis

Cardiac Pathology — MCQs

Cardiac Pathology — MCQs

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