Cardiac Pathology Practice Questions

Q: Anitschkow cells are?

Modified macrophages. ***Modified macrophages*** - Antischkow cells are indeed **modified macrophages**, specifically found in the context of **rheumatic fever** [1]. - They are associated with **Aschoff bodies** and play a role in the **immune response** in the heart tissue [1]. *Modified neutrophils* - Neutrophils are primarily involved in **acute inflammatory responses**, not chronic conditions like those associated with Antischkow cells. - They do not exhibit the characteristic features or roles in **rheumatic fever** pathology that Antischkow cells do. *Modified B cells* - B cells primarily function in **humoral immunity** producing antibodies, whereas Antischkow cells are related to **macrophagic activity**. - They do not share the same histopathological significance in the context of rheumatic heart disease. *Modified RBCs* - Red blood cells (RBCs) lack nuclei and are not involved in the immune response, unlike macrophages. - Antischkow cells' characteristics are unrelated to any modifications related to RBCs' function or pathology. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, p. 566.

Q: Which condition causes large friable destructive vegetations containing microorganisms and inflammatory cells on the mitral valve?

Infective endocarditis. ***Infective endocarditis*** - **Infective endocarditis** is characterized by the formation of **vegetations** on heart valves, most commonly the mitral and aortic valves, due to microbial infection [1]. - These vegetations are composed of **platelets, fibrin, microorganisms, and inflammatory cells**, and can embolize to other parts of the body. *Libman-Sacks endocarditis* - **Libman-Sacks endocarditis** is a form of **non-bacterial verrucous endocarditis** seen in patients with **systemic lupus erythematosus (SLE)**. - While it also features vegetations on heart valves, these are **sterile**, small, and typically located on both sides of the valve leaflets (unlike infective endocarditis). *Non-bacterial thrombotic endocarditis (NBTE)* - **NBTE** involves the formation of **sterile vegetations** on heart valves, primarily due to hyper-coagulable states or chronic debilitating diseases like malignancy. - These vegetations consist of **fibrin and platelets** but lack microorganisms and are typically smaller and less destructive than those seen in infective endocarditis. *Rheumatic fever* - **Rheumatic fever** causes inflammatory lesions, known as **Aschoff bodies**, within the myocardium and can lead to **valvulitis**, primarily affecting the mitral valve [1]. - Acute rheumatic fever produces **small, sterile verrucous vegetations** along the lines of valve closure, which are far smaller and less destructive than those seen in infective endocarditis and do not contain microorganisms [1].

Q: Which of the following will be seen on cardiac biopsy of a patient who had a post MI reperfusion injury?

Eosinophilic contraction bands. ***Eosinophilic contraction bands*** - Seen on cardiac biopsy after **myocardial reperfusion injury**, where damaged muscle fibers exhibit bands due to contractile protein reorganization [1]. - These are indicative of **necrosis** and occur specifically in the setting of **reperfusion injury** [1]. *Neutrophils in cardiac cells* - While neutrophils may increase after myocardial injury [2], they are more indicative of **inflammation** rather than specific findings in reperfusion injury. - Their presence is **not a definitive feature** observed on biopsy in this context. *Waviness of fibres* - Waviness of myocardial fibers is typically associated with **ischemia** [2], not specifically a post-reperfusion injury finding. - This feature suggests **early necrosis**, but it lacks the specificity of contraction bands seen in reperfusion scenarios. *Swelling of cells* - Cell swelling is a general response to **cellular injury** but is not exclusive to reperfusion injury [3]. - It reflects **edematous changes** rather than the specific structural alterations seen in reperfusion injury like contraction bands. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, p. 554. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, p. 552. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 554-556.

Q: Fish mouth appearance of valve in RHD is due to-

Calcification & fibrosis. ***Calcification & fibrosis*** - The **fish mouth appearance** of the valve in rheumatic heart disease (RHD) is primarily due to **calcification and fibrosis** of the mitral valve [1]. - This results in **narrowing of the valve orifice**, which mimics the shape of a fish mouth during diastole [1]. *Rupture of valve* - Rupture of the valve typically leads to **acute severe valvular insufficiency** and does not explain the **gradual narrowing** characteristic of the fish mouth appearance. - It would generally be associated with **acute symptoms** rather than the chronic changes seen in RHD. *None of the above* - This option is incorrect as the fish mouth appearance is well-defined by **calcification and fibrosis**, making it a specific feature of RHD. - It also disregards the specific etiology associated with the valvular deformity in RHD. *Hypertrophy of ventricular wall* - While hypertrophy of the ventricular wall can occur in RHD due to increased workload, it does not directly lead to the **valvular deformity** known as fish mouth appearance. - This hypertrophy affects the **myocardium**, not the structure of the valves themselves which are primarily affected by fibrosis and calcification. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 566-567.

Q: Most common malignant tumor of the heart in adults

Cardiac Sarcoma. ***Cardiac Sarcoma*** - **Cardiac sarcomas** are the most common type of **primary malignant tumor** of the heart in adults, accounting for about 95% of primary malignant cardiac tumors. - **Angiosarcoma** is the most common subtype (approximately 33-50% of all cardiac sarcomas), typically originating from the **right atrium**. - These tumors are highly aggressive with rapid growth, early metastasis, and poor prognosis. - They commonly present with right-sided heart failure, pericardial effusion, or constitutional symptoms. *Rhabdomyoma* - **Rhabdomyomas** are the most common **primary cardiac tumors in infants and children** (60-80% of pediatric cardiac tumors), not adults. - These tumors are **benign** and strongly associated with tuberous sclerosis. - They often spontaneously regress after birth. *Lipoma* - **Lipomas** are **benign tumors** composed of mature adipocytes and account for about 10% of benign cardiac tumors. - They are typically asymptomatic and found incidentally. - They are not malignant and therefore not relevant to this question about malignant tumors. *Paraganglioma* - **Paragangliomas** (pheochromocytomas of the heart) are rare neuroendocrine tumors. - They are typically **benign** (though can be locally invasive) and may be hormonally active, causing catecholamine-related symptoms. - They represent less than 1% of cardiac tumors and are not the most common malignant cardiac tumor.

Q: Aetiology of Dressler Syndrome is

Autoimmune. ***Autoimmune*** - Dressler syndrome is a form of **pericarditis** that occurs several days to weeks after myocardial injury (e.g., myocardial infarction, cardiac surgery, trauma). [3] - It is considered an **autoimmune phenomenon** where the body's immune system attacks damaged cardiac tissue. [1] *Viral infection* - While viral infections can cause general pericarditis, Dressler syndrome specifically refers to **post-cardiac injury** inflammation, not direct viral involvement. [2], [3] - Viral pericarditis typically has a more acute presentation without a preceding cardiac event. [2] *Toxin mediated* - There is no evidence to suggest that Dressler syndrome is caused by **toxins** or toxic substances. - The pathogenesis is linked to an immune response to damaged myocardial cells. *Idiopathic cause* - While some forms of pericarditis are idiopathic, Dressler syndrome has a clear **triggering event** (cardiac injury) and a well-understood autoimmune mechanism. [3] - Therefore, it is not classified as idiopathic. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 214-215. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 581-582. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Cardiovascular Disease, pp. 297-298.

Q: What type of necrosis is associated with Myocardial Infarction (MI)?

Coagulative necrosis. ***Coagulative necrosis*** - Myocardial infarction (MI) typically results in **coagulative necrosis**, characterized by the preservation of the outline of the tissue despite cellular death [1]. - It is often associated with **ischemia**, where blood supply is obstructed, leading to cell death while maintaining tissue architecture for a time [1]. *Fat necrosis* - Fat necrosis is typically associated with **trauma** or **inflammation** in fat tissue, often seen in conditions like pancreatitis. - It is characterized by the presence of **necrotic adipocytes** and does not involve the myocardium directly or predominantly. *Caseous necrosis* - Caseous necrosis is often associated with **tuberculosis** infections, where tissue becomes crumbly and cheese-like. - It is not relevant to myocardial infarction, which does not present with the classical **granulomatous inflammation** of caseous necrosis. *Liquefactive necrosis* - Liquefactive necrosis typically occurs in conditions such as **brain infarcts** or bacterial infections leading to **pus formation**, not in MI. - It involves the transformation of tissue into a **liquid viscous mass**, which is not characteristic of myocardial tissue affected by infarction. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, p. 552.

Q: Which type of white blood cell plays a primary role in cardiac remodeling and chronic inflammation in heart failure?

Macrophages. ***Macrophages*** - **Macrophages** are increasingly recognized for their critical role in the pathogenesis and progression of **heart failure**, contributing to **cardiac remodeling**, chronic inflammation, and fibrosis - They infiltrate failing myocardium and play dual roles: promoting both **inflammation** and **tissue repair** - Their activation state (M1 vs M2 phenotypes) can significantly influence cardiac function and prognosis in heart failure patients - They secrete **cytokines**, **growth factors**, and **matrix metalloproteinases** that contribute to ventricular remodeling *Eosinophils* - **Eosinophils** are primarily involved in **allergic reactions** and defense against **parasitic infections** - While they can contribute to inflammation in specific cardiac conditions (e.g., **eosinophilic myocarditis**, **Loeffler endocarditis**), they are not primarily associated with the general pathophysiology of chronic heart failure *T cells* - **T cells** are central to **adaptive immunity**, including cell-mediated responses and modulation of immune reactions - Though T cells play a role in inflammatory processes in certain forms of heart disease, particularly **viral myocarditis**, they are not the predominant immune cell driving chronic cardiac remodeling in heart failure *B cells* - **B cells** are responsible for producing **antibodies** and are key players in humoral immunity - While B cells can contribute to autoimmune forms of heart disease and certain inflammatory processes, they are not typically the primary immune cell associated with the progression of chronic heart failure

Q: Which protein is defective in dilated cardiomyopathy?

Dystrophin. ***Dystrophin*** - **Dystrophin** is a crucial protein in the **muscle cell membrane** that anchors the cytoskeleton to the extracellular matrix. - Defects in dystrophin lead to sarcolemmal fragility, causing muscle damage and can result in **dilated cardiomyopathy**, especially in conditions like **Duchenne muscular dystrophy** [1]. *Myosin* - **Myosin** is a fundamental **motor protein** involved in muscle contraction, forming the thick filaments. - While mutations in myosin can cause various cardiac conditions, like hypertrophic cardiomyopathy, direct primary defects in myosin are not typically identified as the cause of dilated cardiomyopathy [2]. *Troponin* - **Troponin** is a protein complex that regulates muscle contraction by controlling the interaction between actin and myosin, particularly in response to calcium. - Although troponins are vital for cardiac function and are released during myocardial injury, their primary defect is not typically implicated in the etiology of dilated cardiomyopathy [2]. *Tropomyosin* - **Tropomyosin** is a protein that winds around actin filaments and, along with troponin, regulates the binding of myosin to actin. - While essential for muscle contraction, direct defects in tropomyosin are not a common genetic cause of dilated cardiomyopathy. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, pp. 1244-1245. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, p. 574.

Question 1

Anitschkow cells are?

Accepted Answer

Modified macrophages

Answer

Modified neutrophils

Answer

Modified B cells

Answer

Modified RBCs

Question 2

Which condition causes large friable destructive vegetations containing microorganisms and inflammatory cells on the mitral valve?

Accepted Answer

Infective endocarditis

Answer

Rheumatic fever

Answer

NBTE

Answer

Libman sacks

Question 3

Which of the following will be seen on cardiac biopsy of a patient who had a post MI reperfusion injury?

Accepted Answer

Eosinophilic contraction bands

Answer

Waviness of fibres

Answer

Neutrophils in cardiac cells

Answer

Swelling of cells

Question 4

Fish mouth appearance of valve in RHD is due to-

Accepted Answer

Calcification & fibrosis

Answer

Rupture of valve

Answer

Hypertrophy of ventricular wall

Answer

None of the options

Question 5

Most common malignant tumor of the heart in adults

Accepted Answer

Cardiac Sarcoma

Answer

Paraganglioma

Answer

Rhabdomyoma

Answer

Lipoma

Question 6

Aetiology of Dressler Syndrome is

Accepted Answer

Autoimmune

Answer

Toxin mediated

Answer

Viral infection

Answer

Idiopathic cause

Question 7

What type of necrosis is associated with Myocardial Infarction (MI)?

Accepted Answer

Coagulative necrosis

Answer

Liquefactive necrosis

Answer

Caseous necrosis

Answer

Fat necrosis

Question 8

Which type of white blood cell plays a primary role in cardiac remodeling and chronic inflammation in heart failure?

Accepted Answer

Macrophages

Answer

Eosinophils

Answer

T cells

Answer

B cells

Question 9

Concentric hypertrophy of left ventricle is seen in -

Accepted Answer

Congenital aortic stenosis due to bicuspid aortic valve

Answer

Mitral Stenosis

Answer

Aortic Regurgitation

Answer

Hypertrophic Obstructive Cardiomyopathy

Question 10

Which protein is defective in dilated cardiomyopathy?

Accepted Answer

Dystrophin

Answer

Tropomyosin

Answer

Myosin

Answer

Troponin

Cardiac Pathology — MCQs

Cardiac Pathology — MCQs

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