Cardiac Pathology — MCQs

Cardiac Pathology Indian Medical PG Practice Questions and MCQs

Question 261: Heart failure cells are

A. Lipofuscin granules in cardiac cells
B. Pigmented alveolar macrophages (Correct Answer)
C. Pigmented pancreatic acinar cells
D. Pigment cells seen in liver

Explanation: ***Pigmented alveolar macrophages*** - These macrophages engulf **hemosiderin** (iron-rich pigment from degraded red blood cells) that leaks into the alveoli due to increased capillary pressure in left-sided **heart failure**. - The presence of **hemosiderin-laden macrophages** in the sputum or lung tissue is diagnostic for chronic pulmonary congestion caused by heart failure. *Lipofuscin granules in cardiac cells* - **Lipofuscin** is a "wear-and-tear" pigment that accumulates in aging cells, including cardiac cells. - While present in older hearts, its presence does not specifically indicate **heart failure** or represent "heart failure cells" in the described context. *Pigmented pancreatic acinar cells* - Pancreatic acinar cells primarily produce digestive enzymes and are not typically associated with **pigment accumulation** in the context of heart failure. - Pigmentation in pancreatic cells would suggest other pathologies, such as **hemochromatosis** affecting the pancreas. *Pigment cells seen in liver* - The liver can accumulate various pigments, such as **hemosiderin** in hemochromatosis or **bilirubin** in cholestasis. - While liver congestion can occur in right-sided heart failure, the specific "heart failure cells" refer to the **pulmonary macrophages**.

Question 262: Dense collagen deposition replacing inflammatory infiltrate and debris in myocardial tissue is characteristically seen at what duration following myocardial infarction?

A. Immediate MI
B. 2 days
C. 2 weeks (Correct Answer)
D. Postmortem infarct effect

Explanation: ***2 weeks*** - At **2 weeks** post-myocardial infarction, gross changes include the presence of granulation tissue and **neovascularization**, indicating healing [1]. - Viable cardiac muscle can often be observed, along with ongoing inflammatory response and gradual replacement of necrotic tissue [1]. *Immediate MI* - During the **immediate phase**, the myocardium shows early signs of necrosis with no significant healing or granulation tissue formation yet [1]. - Changes such as **pallor** of the myocardium can be seen, but gross changes indicating structural recovery are not present [1]. *Postmortem infarct aefact* - This term relates to changes observed after death; it's not a valid timeframe regarding acute infarction recovery. - This option lacks relevance to the healing process following **myocardial infarction**. *2 days* - At **2 days**, the myocardium primarily exhibits **coagulative necrosis**, without significant signs of healing like granulation tissue [1]. - Inflammatory changes are present, but gross tissue appearance is still largely characterized by necrosis and not recovery [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, p. 552.

Question 263: Amyloidosis shown in cardiac muscle is mainly due to which fibril?

A. AA (Amyloid A Protein Amyloidosis)
B. AL (Immunoglobulin Light Chain Amyloidosis) (Correct Answer)
C. ATTR (Transthyretin Amyloidosis)
D. Atrial Natriuretic Peptide Amyloidosis (Theoretical Form)

Explanation: ***ATTR*** - Cardiac amyloidosis is mainly associated with **transthyretin amyloidosis** (ATTR), which is related to the deposition of **transthyretin fibrils** in the heart tissue [1]. - This type of amyloidosis often presents in patients with **senile systemic amyloidosis** or familial cases linked to mutations in the transthyretin gene [1]. *AA* - **AA amyloidosis** is usually secondary to chronic inflammatory conditions and does not primarily affect the cardiac muscle. - It is derived from **serum amyloid A protein**, differing from the fibrils associated with cardiac involvement. *AL* - **AL amyloidosis** results from the deposition of **light chain immunoglobulins**, typically related to plasma cell dyscrasias rather than the transthyretin fibrils affecting the heart. - This form of amyloidosis is distinguished by its systemic effects primarily in the kidneys and nervous system. *AANF* - **AANF amyloidosis** is not a recognized type of amyloidosis in medical literature related to cardiac involvement. - The primary fibrils associated with cardiac amyloidosis are either **transthyretin (ATTR)** or **light chain (AL)**, making this option misleading [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, p. 266. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 580-581.

Question 264: Dilated cardiomyopathy is caused by which gene alteration?

A. Titin (Correct Answer)
B. Mitochondrial genes
C. Dystrophin mutations
D. Lamin A/C mutations

Explanation: ***Titin*** - **Titin** gene mutations are a well-known cause of **dilated cardiomyopathy**, affecting the structural integrity of cardiac myocytes [1]. - These mutations lead to **disruption in sarcomere architecture**, resulting in impaired cardiac function [1]. *Dystrophin* - Primarily associated with **Duchenne muscular dystrophy** and **Becker muscular dystrophy**, not directly causing dilated cardiomyopathy. - Deficiency of dystrophin typically affects skeletal muscle more than cardiac muscle. *Sarcomere* - While sarcomere protein mutations can cause cardiomyopathies, they are less specific than titin mutations for dilated cardiomyopathy. - Sarcomere mutations are often linked to **hypertrophic cardiomyopathy** rather than dilated types. *Mitochondrial genes* - Mutations in mitochondrial genes result in **metabolic disorders** like **mitochondrial myopathy** but are not a direct cause of dilated cardiomyopathy. - Mitochondrial dysfunctions typically present with multi-system involvement rather than isolated cardiac symptoms. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, p. 574.

Practice by Chapter

Congenital Heart Disease

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Ischemic Heart Disease

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Hypertensive Heart Disease

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Valvular Heart Disease

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Pericardial Disease

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Cardiac Tumors

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Heart Failure Pathophysiology

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Cardiac Transplantation Pathology

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Endocarditis

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