Cardiac Pathology Practice Questions

Q: Which of the following is not seen in Aschoff bodies?

Polymorphonuclear cells. ***Polymorphonuclear cells*** - **Aschoff bodies** are associated with rheumatic fever and typically contain **lymphocytes and macrophages**, not polymorphonuclear cells [1]. - The presence of **PMNs** would suggest an acute inflammatory response, which is not characteristic of Aschoff bodies. *Giant cells* - **Giant cells**, formed by the fusion of macrophages, can be found within Aschoff bodies. - They are indicative of **chronic inflammation**, presenting in conditions like rheumatic heart disease. *Aschoff cells* - **Aschoff cells** are a specific type of macrophage found within Aschoff bodies and are hallmark features of rheumatic fever [1]. - These cells are derived from activated macrophages and participate in **granulomatous inflammation**. *Fibroblasts* - **Fibroblasts** can also be present in Aschoff bodies, contributing to the **fibrous tissue** formation during the healing process. - They are involved in tissue repair and are found in various inflammatory conditions, including rheumatic fever. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, p. 566.

Q: Earliest light microscopic change in myocardial infarction is:

Waviness of the fibers. ***Waviness of the fibers*** - The earliest light microscopic change in myocardial infarction is **waviness of the fibers**, which occurs within **30 minutes** post-infarction [1]. - This change indicates an initial response to ischemic injury, manifesting as **disruption in the alignment** of muscle fibers. *Coagulative necrosis* - Coagulative necrosis appears later, typically **within a few hours** to days after the onset of infarction, indicating **tissue death** due to lack of blood supply [1]. - This change is characterized by **loss of cellular outlines** and preservation of the overall tissue architecture, which is not the earliest finding. *Phagocytic infiltration* - Phagocytic infiltration, involving macrophages, occurs **days later**, following neutrophilic infiltration, and reflects the body's **cleanup process** post-necrosis. - This response is not seen until the **acute phase** of myocardial injury has progressed further. *Neutrophilic infiltration* - Neutrophilic infiltration generally starts about **4 to 6 hours** after infarction, signifying an inflammatory response but is not the earliest light microscopic change [1]. - This process involves **recruitment of immune cells** to the site of injury, reflecting ongoing damage rather than initial changes [2]. **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. 548-550.

Q: Autopsy finding after 24 hours in a case of death due to myocardial infarction is

Coagulative necrosis.. ***Coagulative necrosis*** - Coagulative necrosis is the predominant histological finding after **myocardial infarction**, typically occurring within the first 12 hours [1]. - It results in preserved tissue architecture with **cellular outlines** remaining visible, indicating ischemic tissue damage [1,2]. *Liquefactive necrosis* - Commonly associated with **bacterial infections** or brain infarction, it leads to the transformation of tissue into liquid pus, which is not characteristic of myocardial infarction. - It occurs later and is not typically observed in heart tissue within 12 hours post-infarction. *Fat necrosis* - Primarily occurs due to damage to **adipose tissue**, as seen in cases of pancreatitis or trauma, and is not relevant to myocardial injury. - It is characterized by the release of **lipases** and fatty acids, a response not seen in myocardial infarction. *Caseous necrosis* - Often associated with **tuberculosis** or fungal infections, presenting as cheese-like necrotic tissue, it is not a feature of myocardial infarction. - This type of necrosis appears much later and reflects chronic granulomatous inflammation rather than acute ischemic damage. **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: Which of the following statements about atrial myxoma is true?

Most common in left atrium. *More common in males* - Atrial myxomas are actually **more commonly found in females**, not males. - The **gender ratio** shows a prevalence toward women, especially in younger populations. *Distant metastases are seen* - Atrial myxomas are benign tumors and do **not exhibit distant metastases**; they primarily cause local symptoms. - Unlike malignant conditions, they remain localized and do not spread beyond the heart. *Most common in left atrium* - While atrial myxomas typically arise in the **left atrium** [1][2], they can also occur in the right atrium and are not confined. - It's crucial to note that they can be found in other locations, thus making this statement misleading. *Reoccurs after excision* - Atrial myxomas do not usually **recur** after successful surgical excision, as they are singular lesions [2]. - Recurrence, if it occurs, is more related to incomplete resection rather than a characteristic behavior of tumor itself. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Cardiovascular Disease, pp. 304-306. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 583-584.

Q: What is the most common type of benign intracavitary cardiac tumor?

Myxoma. ***Myxoma*** - **Cardiac myxoma** is the **most common primary benign tumor of the heart**, accounting for approximately 50% of all primary cardiac tumors. - These tumors typically arise in the **atria, especially the left atrium**, and can cause symptoms due to obstruction of blood flow or embolization. *Leiomyoma* - **Leiomyomas** are benign tumors of **smooth muscle origin** and are most commonly found in the uterus (fibroids) or gastrointestinal tract, not typically in the heart. - While they can occur in the heart, they are exceedingly rare as primary cardiac tumors and are not the most common type. *Sarcoma* - **Sarcomas** are **malignant tumors** originating from mesenchymal tissues, and primary cardiac sarcomas are rare but are the most common type of primary malignant cardiac tumor. - The question specifically asks for a **benign intracavitary cardiac tumor**, ruling out sarcomas. *Lipoma* - **Lipomas** are benign tumors composed of **fat tissue** and can occur in various organs, including the heart. - While cardiac lipomas are found, they are far less common than myxomas and do not represent the most common benign intracavitary cardiac tumor.

Q: In myocardial infarction, which enzyme is raised within 4 to 6 hours and decreases within 3 to 6 days?

CPK. ***CPK*** - **Creatine phosphokinase (CPK)**, specifically the **CK-MB** isoenzyme, rises within 4-6 hours of myocardial infarction. - It typically peaks around 24 hours and decreases within 3 to 6 days, making it a good early marker. *SGOT* - **Serum glutamic oxaloacetic transaminase (SGOT)**, also known as **AST**, can be elevated in MI but is less specific as it's found in multiple tissues. - Its rise is usually observed later than CPK and it remains elevated for a shorter duration compared to the criteria given. *LDH* - **Lactate dehydrogenase (LDH)** rises later than CPK in MI, typically reaching peak levels around 3-6 days. - It stays elevated for a longer period (up to 10-14 days), making it useful for diagnosis of late-presenting MI but not early diagnosis within 4-6 hours. *Troponin* - **Cardiac troponins** (TnI and TnT) are highly specific and sensitive markers for myocardial injury, appearing in the blood as early as 3-6 hours. - However, troponins remain elevated for a much longer period than 3-6 days, often up to 10-14 days, differing from the specified decrease time.

Q: A young athlete died of sudden cardiac arrest after athletic activity. Post-mortem findings revealed interventricular septal hypertrophy. What is the most probable diagnosis?

Hypertrophic Obstructive Cardiomyopathy (HOCM). ***Hypertrophic Obstructive Cardiomyopathy (HOCM)*** - **HOCM** is a common cause of **sudden cardiac death in young athletes** due to arrhythmogenic potential associated with **marked interventricular septal hypertrophy** [1]. - The **interventricular septal hypertrophy** observed post-mortem is a hallmark of HOCM, often leading to dynamic **left ventricular outflow tract obstruction** and myocardial ischemia [1], [2]. *Dilated Cardiomyopathy (DCM)* - DCM is characterized by **ventricular dilation** and **impaired systolic function**, not primarily septal hypertrophy [4]. - While DCM can cause sudden death, the primary post-mortem finding would be a **thinned, enlarged heart**, not isolated septal thickening [4]. *Aortic Stenosis (AS)* - Severe AS can cause **left ventricular hypertrophy**, but the hypertrophy would be **concentric** across the entire left ventricle, not specifically isolated to the interventricular septum [3]. - A definitive diagnosis of AS would also involve findings of a **stenotic aortic valve**, which is not mentioned as a post-mortem finding. *Ventricular Septal Defect (VSD)* - VSD is a **congenital heart defect** involving a hole in the ventricular septum, leading to shunting of blood. - While large VSDs can lead to complications, they are not typically characterized by isolated **septal hypertrophy** as the cause of sudden cardiac death in this context, nor would a defect itself cause the described hypertrophy. **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. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, p. 536. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, p. 576.

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

2 weeks. ***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.

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

AL (Immunoglobulin Light Chain Amyloidosis). ***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.

Q: Dilated cardiomyopathy is caused by which gene alteration?

Titin. ***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.

Question 1

Which of the following is not seen in Aschoff bodies?

Accepted Answer

Polymorphonuclear cells

Answer

Aschoff cells

Answer

Fibroblasts

Answer

Giant cells

Question 2

Earliest light microscopic change in myocardial infarction is:

Accepted Answer

Waviness of the fibers

Answer

Neutrophilic infiltration

Answer

Phagocytic infiltration

Answer

Coagulative necrosis

Question 3

Autopsy finding after 24 hours in a case of death due to myocardial infarction is

Accepted Answer

Coagulative necrosis.

Answer

Fat necrosis.

Answer

Liquefactive necrosis.

Answer

Caseous necrosis.

Question 4

Which of the following statements about atrial myxoma is true?

Accepted Answer

Most common in left atrium

Answer

Does not cause distant metastases

Answer

Seldom recurs after excision

Answer

Predominantly affects males

Question 5

What is the most common type of benign intracavitary cardiac tumor?

Accepted Answer

Myxoma

Answer

Leiomyoma

Answer

Sarcoma

Answer

Lipoma

Question 6

In myocardial infarction, which enzyme is raised within 4 to 6 hours and decreases within 3 to 6 days?

Accepted Answer

CPK

Answer

SGOT

Answer

LDH

Answer

Troponin

Question 7

A young athlete died of sudden cardiac arrest after athletic activity. Post-mortem findings revealed interventricular septal hypertrophy. What is the most probable diagnosis?

Accepted Answer

Hypertrophic Obstructive Cardiomyopathy (HOCM)

Answer

Dilated Cardiomyopathy (DCM)

Answer

Ventricular Septal Defect (VSD)

Answer

Aortic Stenosis (AS)

Question 8

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

Accepted Answer

2 weeks

Answer

Immediate MI

Answer

2 days

Answer

Postmortem infarct effect

Question 9

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

Accepted Answer

AL (Immunoglobulin Light Chain Amyloidosis)

Answer

AA (Amyloid A Protein Amyloidosis)

Answer

ATTR (Transthyretin Amyloidosis)

Answer

Atrial Natriuretic Peptide Amyloidosis (Theoretical Form)

Question 10

Dilated cardiomyopathy is caused by which gene alteration?

Accepted Answer

Titin

Answer

Mitochondrial genes

Answer

Dystrophin mutations

Answer

Lamin A/C mutations

Cardiac Pathology — MCQs

Cardiac Pathology — MCQs

On this page

Practice by Chapter

Want unlimited practice?