Cardiac Pathology Practice Questions

Q: What is the histopathological finding 12 hours after ischemic injury to heart?

Hyper-eosinophilia of myocytes. ***Hyper-eosinophilia of myocytes*** - Within **4-12 hours** of myocardial ischemia, the most characteristic histological finding is the development of **hypereosinophilia** in the sarcoplasm of myocardial cells [1]. - This is due to the loss of **glycogen** and an increase in **cytoplasmic protein binding** to eosin, indicating early irreversible cell injury [1], [2]. *Neocapillary invasion of myocytes* - **Neocapillary invasion** is a feature of **healing** and **repair** processes, usually observed much later, typically days to weeks after the initial injury, to facilitate scar formation [1]. - This process involves the growth of **new blood vessels** into the damaged tissue. *Karyorrhexis of myocytes* - **Karyorrhexis**, the fragmentation of the cell nucleus, is a later stage of necrosis, usually becoming apparent **12-24 hours post-infarction** [1]. - In the initial 12 hours, nuclear changes like **pyknosis** (nuclear shrinkage and increased basophilia) might be observed, but karyorrhexis is not prominent [1]. *Coagulation necrosis of myocytes* - While myocardial infarction is characterized by **coagulation necrosis**, the classic histological signs of full-blown coagulation necrosis, such as loss of striations and nuclear changes, become prominent at **12-24 hours and beyond** [1]. - In the first 12 hours, **hypereosinophilia** is the primary early indicator of this necrotic process, preceding the more overt classical features [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. 548-550.

Q: Which of the following has the most friable vegetations:

Infective endocarditis. ***Infective endocarditis*** - The vegetations in infective endocarditis are composed of **fibrin**, **platelets**, and **microorganisms**, making them typically very **friable** and prone to embolization [1]. - This friability is a key factor in the pathogenesis of **septic emboli**, which can lead to complications such as stroke, organ infarction, and systemic infections [1]. *Libman Sack's endocarditis* - Characterized by sterile vegetations, predominantly on the **mitral and aortic valves**, in patients with **Systemic Lupus Erythematosus (SLE)** [1]. - While these vegetations can be a source of emboli, they are generally **less friable** than those seen in infective endocarditis, as they lack the aggressive bacterial component. *SLE* - SLE itself is a **systemic autoimmune disease** that can cause various cardiac manifestations, including pericarditis, myocarditis, and endocarditis (Libman-Sacks). - The term "SLE" refers to the underlying disease, not directly to the friability of vegetations, though it is associated with Libman-Sacks endocarditis which has relatively less friable vegetations. *Rheumatic heart disease* - Results from **acute rheumatic fever**, leading to chronic valvular damage, most commonly affecting the **mitral valve** [2]. - The vegetations, when present during acute rheumatic fever, are small, sterile, and composed primarily of **fibrin and platelets**, making them generally **less friable** and less likely to embolize compared to infective endocarditis [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 568-570. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, p. 566.

Q: In rheumatic heart disease, infective endocarditis is detected by echocardiogram and the largest vegetations seen are due to -

Staphylococcus aureus. Staphylococcus aureus - Staphylococcus aureus is well-known for causing aggressive infective endocarditis with large, destructive vegetations due to its virulence factors [1]. - These large vegetations are easily detectable by echocardiogram and are associated with a higher risk of embolic events and valve destruction [1]. Candida albicans - While Candida albicans can cause endocarditis, often in immunocompromised individuals or IV drug users, its vegetations are typically larger and more friable than most bacterial causes but S. aureus still produces larger bacterial vegetations due to its rapid colonization and biofilm formation. - Fungal endocarditis generally has a poorer prognosis and requires prolonged antifungal therapy. Salmonella typhi - Salmonella typhi is a less common cause of infective endocarditis; when it does occur, it is often associated with immunocompromised states or pre-existing cardiac lesions. - The vegetations caused by Salmonella are generally not as large or rapidly destructive as those seen with S. aureus. Streptococcus viridans - Streptococcus viridans is a frequent cause of subacute infective endocarditis, particularly on previously damaged valves [1]. - The vegetations are typically small to medium-sized and less destructive than those caused by S. aureus, leading to more indolent disease [1].

Q: Vegetations on under surface of cusps are found in:

Libman-Sacks endocarditis. ***Libman-Sacks endocarditis*** - This condition is characterized by **sterile vegetations** composed of immune complexes and fibrin, typically found on the **undersurface of the mitral and aortic valve cusps**. [1] - It is a prominent cardiac manifestation of **systemic lupus erythematosus (SLE)**. *SABE* - **Subacute bacterial endocarditis (SABE)** refers to infection of an already damaged heart valve, causing slowly progressive vegetations. - While it causes vegetations, they are typically on the **closure line** or ventricular side of the valve, and are not sterile but contain bacteria. [1] *Rheumatic fever* - Acute rheumatic fever causes **small, verrucous vegetations** primarily along the **closure lines of the valve leaflets (especially mitral)**, due to fibrin deposition. [1] - These are caused by an autoimmune reaction to streptococcal infection and are not found on the undersurface of the cusps. *Infective endocarditis* - **Infective endocarditis** involves vegetations formed from thrombus and microorganisms on heart valves, typically on the **atrial surface of the mitral valve** or the **ventricular surface of the aortic valve**. [1] - These vegetations are large and destructive, containing active infection, unlike the sterile vegetations of Libman-Sacks endocarditis. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, p. 568.

Q: All of the following arteries are common sites of occlusion by a thrombus except:

Marginal. ***Marginal*** - The **marginal arteries** are typically small and supply a smaller portion of the right ventricle, making them less likely sites for **major clinical occlusion** compared to larger, more critical coronary vessels. - While occlusion can occur, it usually causes less extensive damage and is therefore **less common** as a primary site of acute thrombus-related myocardial infarction. *Posterior interventricular* - The **posterior interventricular artery (PDA)** is a major coronary artery, responsible for supplying the posterior walls of the ventricles and the posterior one-third of the interventricular septum. - Occlusion of the PDA, often a branch of the right coronary artery (RCA) or circumflex artery, can lead to **significant infarction** in these critical areas, making it a common site of thrombus formation. *Circumflex* - The **circumflex artery (Cx)** is a major branch of the left main coronary artery that supplies the left atrium and the posterior and lateral walls of the left ventricle. - Occlusion of the circumflex artery can result in **lateral or posterior myocardial infarction**, making it a frequent site for thrombus formation. *Anterior interventricular* - The **anterior interventricular artery (LAD)**, also known as the left anterior descending artery, is the most common site of coronary artery occlusion. - It supplies the anterior wall of the left ventricle and the anterior two-thirds of the interventricular septum, and its occlusion is often referred to as the **"widowmaker"** due to the extensive damage and high mortality associated with it.

Q: A patient presents with acute rheumatic carditis with fever. The true statement is:

Signs of inflammation and necrosis. ***Signs of inflammation and necrosis*** - Acute rheumatic carditis involves a systemic inflammatory response, leading to **inflammation of the heart muscle (myocarditis)**, which can involve cellular necrosis. [1] - The inflammatory process in rheumatic carditis is mediated by an autoimmune response to streptococcal antigens, causing damage to cardiac tissues. [1] *Reduced myocardial contractility* - While severe inflammation and damage in rheumatic carditis can ultimately lead to **reduced myocardial contractility**, this is a consequence rather than the primary, true underlying pathological process described. - The initial and primary pathological finding during acute rheumatic carditis is the **inflammation and formation of Aschoff bodies**, not necessarily immediate and direct, macroscopic reduction in contractility. [1] *Increase in troponin T* - An increase in **troponin T** indicates myocardial damage, which can occur in severe cases of acute rheumatic carditis due to extensive inflammation and myocardial cell necrosis. - However, **troponin elevation** is a biomarker of injury, not a direct pathological description of the tissue changes themselves, and may not be present in all forms or stages of acute rheumatic carditis where inflammation is the predominant feature. *Valve replacement will ameliorate C.C.F.* - **Valve replacement** addresses severe valvular damage that often develops as a **long-term complication of rheumatic fever (chronic rheumatic heart disease)**, which can lead to congestive cardiac failure (CCF). - During the acute phase of **rheumatic carditis**, the primary issue is inflammation of all layers of the heart (pericarditis, myocarditis, endocarditis), and valve replacement is not the immediate treatment for acute CCF resulting from acute myocarditis. [1]

Q: Features of rheumatic carditis are all except:

Intramyocardial microemboli. ***Intramyocardial microemboli*** - **Intramyocardial microemboli** are not a characteristic feature of rheumatic carditis. Microemboli are typically associated with conditions like infective endocarditis or other hypercoagulable states, leading to obstruction of small coronary arteries. - Rheumatic carditis involves an inflammatory, autoimmune response to cardiac tissues, not embolic events. *Myocardial fibrosis* - **Myocardial fibrosis** can occur in chronic rheumatic heart disease as a reparative process following episodes of acute inflammation and damage to the myocardium. - This fibrosis often leads to stiffening and dysfunction of the cardiac muscle. *Lymphocytic infiltration* - **Lymphocytic infiltration** of the myocardium is a hallmark of acute rheumatic carditis, indicating the inflammatory and autoimmune nature of the disease as immune cells target cardiac tissue [1]. - This cellular infiltration contributes to myocardial damage and dysfunction. *Aschoff nodule* - **Aschoff bodies (or nodules)** are pathognomonic granulomatous lesions found in the myocardium during acute rheumatic carditis [1]. - These nodules consist of fibrinoid necrosis and inflammatory cells, including activated macrophages (Anitschkow cells), reflecting the autoimmune inflammatory process [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 566-567.

Q: True about Rheumatic carditis –

Pancarditis. ***Pancarditis*** - **Rheumatic carditis** is characterized by inflammation of all three layers of the heart: the **pericardium** (pericarditis), **myocardium** (myocarditis), and **endocardium** (endocarditis) [1]. - This widespread inflammation explains why it is termed **pancarditis**, affecting the heart comprehensively [1]. *Only Pericarditis* - While **pericarditis** can occur in rheumatic fever, it is rarely the sole manifestation of cardiac involvement and is usually accompanied by inflammation of other heart layers. - Isolated pericarditis without signs of myocarditis or endocarditis would not be classified as rheumatic carditis. *Only myocarditis* - **Myocarditis**, or inflammation of the heart muscle, is a significant component of rheumatic carditis, often leading to impaired heart function. - However, rheumatic carditis typically involves the endocardium (specifically the heart valves) and can also involve the pericardium, making "only myocarditis" an incomplete description [1]. *Only endocarditis* - **Endocarditis**, especially of the heart valves, is a hallmark feature of rheumatic carditis, leading to characteristic **valvular lesions** [1]. - Although critical, endocarditis in rheumatic fever is almost always accompanied by some degree of myocardial and/or pericardial involvement, classifying it as part of a pancarditis [1].

Question 1

A 30-year-old football player presented to the emergency department with sudden cardiac arrest/collapse. Based on the histological image provided, what is the most likely cause of his death?

Accepted Answer

Hypertrophic Obstructive Cardiomyopathy (HOCM)

Answer

Dilated Cardiomyopathy (DCM)

Answer

Restrictive Cardiomyopathy (RCM)

Answer

Arrhythmogenic cardiomyopathy

Question 2

An athlete collapsed and expired while playing school basketball. Histology of the cardiac specimen is most likely to indicate which of the following conditions?

Accepted Answer

Hypertrophic cardiomyopathy (HCM)

Answer

Dilated cardiomyopathy (DCM)

Answer

Restrictive cardiomyopathy (RCM)

Answer

Arrhythmogenic right ventricular dysplasia (ARVD)

Question 3

What is the histopathological finding 12 hours after ischemic injury to heart?

Accepted Answer

Hyper-eosinophilia of myocytes

Answer

Neocapillary invasion of myocytes

Answer

Karyorrhexis of myocytes

Answer

Coagulation necrosis of myocytes

Question 4

Which of the following has the most friable vegetations:

Accepted Answer

Infective endocarditis

Answer

SLE

Answer

Rheumatic heart disease

Answer

Libman Sack's endocarditis

Question 5

In rheumatic heart disease, infective endocarditis is detected by echocardiogram and the largest vegetations seen are due to -

Accepted Answer

Staphylococcus aureus

Answer

Candida albicans

Answer

Salmonella typhi

Answer

Streptococcus viridans

Question 6

Vegetations on under surface of cusps are found in:

Accepted Answer

Libman-Sacks endocarditis

Answer

SABE

Answer

Rheumatic fever

Answer

Infective endocarditis

Question 7

All of the following arteries are common sites of occlusion by a thrombus except:

Accepted Answer

Marginal

Answer

Posterior interventricular

Answer

Circumflex

Answer

Anterior interventricular

Question 8

A patient presents with acute rheumatic carditis with fever. The true statement is:

Accepted Answer

Signs of inflammation and necrosis

Answer

Reduced myocardial contractility

Answer

Increase in troponin T

Answer

Valve replacement will ameliorate C.C.F.

Question 9

Features of rheumatic carditis are all except:

Accepted Answer

Intramyocardial microemboli

Answer

Myocardial fibrosis

Answer

Lymphocytic infiltration

Answer

Aschoff nodule

Question 10

True about Rheumatic carditis –

Accepted Answer

Pancarditis

Answer

Only Pericarditis

Answer

Only myocarditis

Answer

Only endocarditis

Cardiac Pathology — MCQs

Cardiac Pathology — MCQs

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