Cardiac Pathology Practice Questions

Q: Flat vegetations in valve pockets due to deposition on previously normal valve surfaces are characteristic of:

Non-bacterial thrombotic endocarditis (NBTE). ***Rheumatic heart disease*** - Characterized by **flat vegetations** on heart valves, known as **Aschoff bodies**, which represent the sequelae of rheumatic fever [1]. - Vegetations in this condition occur due to **non-endothelial attachment**, leading to valve damage and dysfunction . *Rheumatic heart disease* - This is a repeat nd does not provide a different context, hence it is incorrect. - Must include distinguishing clinical features or findings that clearly differentiate it from other listed conditions. *Infective endocarditis* - Characterized by **irregular, bulky vegetations** on valves due to microbial infection, differentiating from the flatter vegetations seen in rheumatic heart disease [1]. - Often associated with **systemic symptoms** such as fever and embolic phenomena, which are not present here. *Non-bacterial thrombotic endocarditis (NBTE)* - Typically presents with **small vegetations** that may also be flat, but are usually found in the context of a malignancy or systemic disease [1]. - These vegetations are primarily **non-infectious**, i.e., not due to current infection, unlike in infective endocarditis. **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.

Q: What is the approximate time at which the quantity of ATP within ischemic cardiac myocytes is reduced to 10% of the original?

10 minutes. ***40 minutes*** - Research indicates that ATP levels in ischemic cardiac myocytes can be reduced to 10% of the original within approximately **40 minutes** of sustained ischemia. - This depletion directly leads to severe **metabolic dysfunction** and contributes to **cardiac cell injury**. *10 minutes* - Within this time frame, ATP levels have not yet dropped significantly, typically remaining above 50% of the original concentration. - Early ischemic changes may begin within minutes, but profound depletion occurs later. *20 minutes* - At 20 minutes of ischemia, ATP levels are still generally above **20-30%**, not yet reaching the critical depletion point of 10% [1]. - The heart can still sustain some function and viability during this period [1]. *<2 minutes* - Ischemia lasts too briefly for ATP levels to significantly decline; any effects at this stage are usually minimal. - Cells can maintain ATP levels and function quite well for several minutes before noticeable depletion occurs. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 554-556.

Q: The cells seen after 72 hours in the infarcted area in myocardial infarction are

Macrophages. ***Macrophages*** - After 72 hours in myocardial infarction, **macrophages** will infiltrate the infarcted area to clear cellular debris and promote healing [1][2]. - They play a crucial role in the later stages of **inflammation** and tissue repair following the initial neutrophilic response [1][2]. *Monocytes* - Monocytes circulate in the bloodstream and are different from the tissue-present macrophages, which are the ones actively involved in the healing process post-infarction. - While they do transform into macrophages during inflammation, they are **not the predominant cells** found in the infarcted area after 72 hours [2]. *Lymphocytes* - Lymphocytes are primarily involved in the **adaptive immune response** and are usually present later, after initial inflammation, rather than within the first few days post-infarction. - Their role is less significant in the acute phase of myocardial infarction compared to macrophages and neutrophils. *Neutrophils* - Neutrophils are typically the predominant cells in the early stages (within the first 24-48 hours) of myocardial infarction, responding to acute injury [1][2]. - By 72 hours, their numbers start to decline as macrophages become more prominent in the healing process [1][2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 89. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, p. 552.

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: 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: 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.

Question 1

Flat vegetations in valve pockets due to deposition on previously normal valve surfaces are characteristic of:

Accepted Answer

Non-bacterial thrombotic endocarditis (NBTE)

Answer

Infective endocarditis

Answer

Libman-Sacks endocarditis

Answer

Rheumatic heart disease

Question 2

A 50-year-old male presented with signs and symptoms of restrictive heart disease. A right ventricular endomyocardial biopsy revealed deposition of extracellular eosinophilic hyaline material. On transmission electron microscopy, this material is most likely to reveal the presence of:

Accepted Answer

Non-branching filaments of indefinite length

Answer

Weibel-Palade bodies

Answer

Concentric whorls of lamellar structures

Answer

Cross banded fibres with 67 nm periodicity

Question 3

What is the approximate time at which the quantity of ATP within ischemic cardiac myocytes is reduced to 10% of the original?

Accepted Answer

10 minutes

Answer

<2 minutes

Answer

20 minutes

Answer

40 minutes

Question 4

The cells seen after 72 hours in the infarcted area in myocardial infarction are

Accepted Answer

Macrophages

Answer

Neutrophils

Answer

Lymphocytes

Answer

Monocytes

Question 5

Which of the following is not seen in Aschoff bodies?

Accepted Answer

Polymorphonuclear cells

Answer

Aschoff cells

Answer

Fibroblasts

Answer

Giant cells

Question 6

Earliest light microscopic change in myocardial infarction is:

Accepted Answer

Waviness of the fibers

Answer

Neutrophilic infiltration

Answer

Phagocytic infiltration

Answer

Coagulative necrosis

Question 7

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 8

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 9

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 10

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

Cardiac Pathology — MCQs

Cardiac Pathology — MCQs

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