Cardiac Pathology — MCQs

Cardiac Pathology Indian Medical PG Practice Questions and MCQs

Question 221: An elderly woman is found dead in her home with frothy discharge from her nose and mouth. An autopsy reveals extensive pink frothy fluid in the lungs. What is the most likely cause of death?

A. Sudden cardiac arrest
B. Choking
C. Drowning
D. Congestive heart failure (Correct Answer)

Explanation: ***Congestive heart failure*** - The presence of **frothy discharge** from the nose and mouth, along with extensive **pink frothy fluid in the lungs**, is a classic sign of **pulmonary edema**, often caused by acute decompensation in **congestive heart failure** [1]. - This fluid accumulation in the alveoli impairs oxygen exchange, leading to rapid death. *Sudden cardiac arrest* - While *sudden cardiac arrest* can lead to death, it doesn't typically present with the specific findings of **profuse frothy fluid** from the nose and mouth or significant **pulmonary edema** on autopsy unless it's a consequence of an underlying condition like severe heart failure. - The primary findings in sudden cardiac arrest are usually related to a **fatal arrhythmia** or **myocardial infarction**, not necessarily prominent pulmonary fluid [2]. *Choking* - **Choking** is caused by an obstruction of the airway, leading to **asphyxia**. - Autopsy findings would typically show evidence of an **obstructing foreign body** in the airway and signs of asphyxia (e.g., cyanosis), not extensive frothy fluid in the lungs. *Drowning* - **Drowning** involves aspiration of fluid into the lungs, which can cause frothy discharge. - However, in typical drowning cases, the frothy discharge is usually **white** or stained brown from debris, and the presence of **pink frothy fluid** more specifically points to **pulmonary edema** from a cardiogenic cause rather than water aspiration. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 536-538. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Cardiovascular Disease, pp. 290-291.

Question 222: Considering the effects of chronic hypertension on the heart, which pathological change is primarily observed?

A. Ventricular dilation
B. Myocardial infarction
C. Ventricular hypertrophy (Correct Answer)
D. Valvular regurgitation

Explanation: ***Ventricular hypertrophy*** - Chronic hypertension increases the **afterload** on the left ventricle, causing the heart muscle to work harder to eject blood [1]. - This sustained increased workload leads to **compensatory thickening of the ventricular walls**, primarily the left ventricle (concentric left ventricular hypertrophy), to maintain cardiac output [1]. - This is the **primary and earliest pathological change** in chronic hypertension affecting the heart [2]. *Ventricular dilation* - While ventricular dilation can occur in later stages of hypertension-induced heart disease (dilated cardiomyopathy), it is generally a sign of **decompensation** and not the primary pathological change [2]. - **Ventricular hypertrophy** is initially a compensatory mechanism, while dilation signifies pump failure. *Myocardial infarction* - A myocardial infarction is primarily caused by **atherosclerotic plaque rupture** and subsequent coronary artery occlusion. - While hypertension is a significant **risk factor** for atherosclerosis and MI, it does not directly cause the primary pathological change within the heart muscle cells to be an infarction itself, but rather hypertrophy [2]. *Valvular regurgitation* - Valvular regurgitation is typically caused by **damage or disease of the heart valves** (e.g., rheumatic fever, endocarditis, congenital defects). - Although hypertension can contribute to processes like **aortic root dilation** which might lead to aortic regurgitation, it is not the primary or most common direct pathological effect on the heart chambers themselves. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, p. 536. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 560-562.

Question 223: A 45-year-old female presents with dyspnea and fatigue. An echocardiogram reveals a large pericardial effusion. A biopsy of the pericardium shows fibrous thickening with dense collagen bundles, scattered lymphocytes, and caseating granulomas. What is the most likely diagnosis?

A. Bacterial pericarditis
B. Viral pericarditis
C. Tuberculous pericarditis (Correct Answer)
D. Uremic pericarditis

Explanation: ***Tuberculous pericarditis*** - The presence of **fibrous thickening** with **dense collagen bundles** and **scattered lymphocytes** in the biopsy is characteristic of tuberculous pericarditis, often due to **Mycobacterium tuberculosis** infection [2]. - **Large pericardial effusion** and notable **dyspnea** in this patient aligns with the typical presentation of tuberculous involvement of the pericardium. - The fibrous thickening observed results from organization of fibrinous exudates, which leads to opaque fibrous thickening of the pericardium [1]. *Bacterial pericarditis* - Generally presents with **purulent effusion** and is commonly linked to **acute bacterial infections** which are less likely to show dense collagen in biopsies. - Would typically exhibit a more **acute onset** of symptoms, often with fever and other signs of systemic infection. *Viral pericarditis* - Usually associated with **viral infections** like **Coxsackievirus**, often shows inflammatory changes but lacks the dense fibrous thickening observed here. - Generally leads to a **transudative effusion** rather than the dense fibrosis found in this case. *Uremic pericarditis* - Occurs in patients with **chronic kidney disease**, typically presenting with **serous effusions** rather than fibrous thickening. - The biopsy findings do not correlate as uremic pericarditis shows **non-specific inflammation** with little or no lymphocytic infiltration. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 101-103. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 582-583.

Question 224: A 48-year-old male presents with progressive shortness of breath. Echocardiography reveals a large mass in the left atrium, and the biopsy shows myxomatous tissue. Which feature is characteristic of this tumor?

A. Myxoid stroma (Correct Answer)
B. Fibroblastic activity
C. Necrosis
D. Differentiation into squamous cells

Explanation: ***Myxoid stroma*** - Cardiac myxomas are characterized by a gelatinous, myxoid stroma rich in acid mucopolysaccharides [1] - This distinctive histological feature confirms the diagnosis of cardiac myxoma, which is the most common primary cardiac tumor in adults and typically presents as a left atrial mass [2] - The abundant mucoid matrix gives the tumor its characteristic gelatinous appearance on gross examination [1] *Fibroblastic activity* - While some fibrous elements may be present, prominent fibroblastic activity is not the defining characteristic of cardiac myxoma - Tumors like cardiac fibromas would show more significant fibroblast proliferation and dense collagenous stroma *Necrosis* - Necrosis is generally not a prominent feature of benign cardiac myxomas - Extensive necrosis is more indicative of malignant tumors or rapid growth with insufficient blood supply - Myxomas are typically slow-growing and well-vascularized *Differentiation into squamous cells* - Myxomas are derived from mesenchymal cells and do not show squamous differentiation - Squamous differentiation would be characteristic of carcinomas or other epithelial tumors, which is inconsistent with the mesenchymal origin of cardiac myxomas **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 583-584. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Cardiovascular Disease, pp. 304-306.

Question 225: In the context of myocardial infarction, which cellular change primarily contributes to damage in heart muscle?

A. Hypertrophy of surviving cells
B. Infiltration by inflammatory cells
C. Loss of contractile proteins
D. Necrosis of myocardial cells (Correct Answer)

Explanation: ***Necrosis of myocardial cells*** - Myocardial infarction is defined by the **death of heart muscle cells (cardiomyocytes)** due to prolonged ischemia, which is a key characteristic of necrosis [1]. - **Necrosis** leads to the irreversible loss of cell structure and function, directly contributing to heart damage and impaired pumping ability [3]. *Hypertrophy of surviving cells* - This is a compensatory mechanism where remaining healthy heart muscle cells enlarge to handle the increased workload, occurring **after** the infarct, not as a primary cause of damage. - While it can lead to maladaptive remodeling long-term, it is a response to injury rather than the initial injury itself. *Infiltration by inflammatory cells* - **Inflammatory cells** (e.g., neutrophils, macrophages) infiltrate the infarcted area as part of the healing process to clear dead tissue, which occurs **after** the initial cellular damage [2]. - This process can contribute to secondary tissue damage and remodeling but is not the primary mechanism of cell death during the acute ischemic event. *Loss of contractile proteins* - The **loss or degradation of contractile proteins** (actin, myosin) occurs *as a consequence* of cell death during necrosis, not as the primary initiating event of damage [3]. - While the cell's ability to contract is lost, this is downstream from the crucial event of cell death itself. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, p. 550. [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. 548-550.

Question 226: All of the following are characteristic features of Tricuspid Atresia except for -

A. Decreased pulmonary vascularity
B. Left axis deviation
C. Right ventricular hypoplasia
D. Split S2 (Correct Answer)

Explanation: ***Splitting of S2 is present in Tricuspid Atresia*** - In **tricuspid atresia**, the S2 heart sound is typically **single** rather than split because there is no blood flow through the tricuspid valve to the right ventricle, and pulmonary blood flow is often reduced, leading to a diminished or absent P2. - Absence of blood flow to the right ventricle prevents normal mechanisms of S2 splitting [1]. *Left axis deviation* - **Left axis deviation** on an EKG is a common finding in tricuspid atresia due to the **underdevelopment of the right ventricle** and the increased prominence of the left ventricle. - The electrical activity is predominantly directed towards the left side of the heart. *Right ventricular hypoplasia* - **Right ventricular hypoplasia** is a defining characteristic of tricuspid atresia [1], as the absence of the tricuspid valve prevents blood flow into, and thus proper development of, the right ventricle. - The right ventricle can range from a *small, non-functional chamber* to being almost absent. *Decreased pulmonary vascularity* - **Decreased pulmonary vascularity** is observed in tricuspid atresia because the pulmonary blood flow is significantly reduced, usually depending on a **patent ductus arteriosus (PDA)** or a **ventricular septal defect (VSD)** for blood to reach the lungs [1]. - The lack of direct flow from the right atrium to the right ventricle limits the amount of blood ejected into the pulmonary arteries. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 545-546.

Question 227: Characteristic histopathological feature of rheumatic heart disease is -

A. McCallum's patch
B. Bread and butter pericarditis
C. Shaggy vegetations
D. Aschoff's nodule (Correct Answer)

Explanation: ***Aschoff's nodule*** - Aschoff's nodules are characteristic histopathological findings in **rheumatic heart disease**, indicating granulomatous inflammation [1]. - These nodules contain **pathognomonic** multinucleated giant cells and lymphocytic infiltrate commonly seen in the myocardium [1]. *Shaggy vegetation* - Shaggy vegetations are associated with **infective endocarditis**, not rheumatic heart disease. - They appear as irregular, fibrinous masses on valvular surfaces and are not specific to rheumatic heart failure. *Bread & butter pericarditis* - This describes the appearance of pericardial surfaces in **pericarditis** rather than rheumatic heart disease specifically. - It typically results from inflammation but is not a characteristic feature of rheumatic heart failure. *Mc Callum patch* - McCallum's patch refers to scars on the left atrial wall due to rheumatic fever but is not a definitive histopathological feature. - While relevant to rheumatic heart disease, it does not represent a specific histological finding like Aschoff's nodules do. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 566-567.

Question 228: Which of the following protein mutations is associated with restrictive cardiomyopathy?

A. Myosin regulatory proteins
B. Myosin binding protein-C
C. Tropomyosin
D. Troponin I (Correct Answer)

Explanation: ***Troponin I*** - Mutations in **cardiac troponin I (TNNI3)** are a well-established genetic cause of **familial restrictive cardiomyopathy (RCM)**. - These mutations often lead to an increased affinity of **troponin C for calcium**, impairing myocardial relaxation and hence restrictive filling. *Myosin regulatory proteins* - Mutations in **myosin regulatory light chain (MYL2)** are more commonly associated with **hypertrophic cardiomyopathy (HCM)** due to their role in regulating the contractile force [1]. - While they can indirectly affect cardiac function, they are not the primary genetic cause of restrictive phenotypes. *Myosin binding protein-C* - Mutations in **cardiac myosin-binding protein C (MYBPC3)** are a leading cause of **hypertrophic cardiomyopathy (HCM)**, not restrictive cardiomyopathy [1], [3]. - These mutations lead to disorganized myofibrillar structure and enhanced contractility, ultimately causing **ventricular hypertrophy** [1]. *Tropomyosin* - Mutations in **alpha-tropomyosin (TPM1)** can be associated with both **hypertrophic (HCM)** and **dilated cardiomyopathy (DCM)**, depending on the specific mutation [2]. - While tropomyosin plays a role in regulating muscle contraction, its mutations are less commonly linked to the primary genetic cause of **restrictive cardiomyopathy (RCM)** phenotypes compared to troponin I. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 576-577. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, p. 574. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Cardiovascular Disease, pp. 303-304.

Question 229: In patients with hypertrophic cardiomyopathy, which gene is most commonly associated with mutations?

A. β - myosin heavy chain (Correct Answer)
B. Elastin
C. α - tropomyosin
D. Troponin T

Explanation: ***β - myosin heavy chain*** - Mutations in the **β-myosin heavy chain (MYH7)** gene are the most common cause of **hypertrophic cardiomyopathy (HCM)**, accounting for approximately 30-50% of identifiable genetic causes [1]. - The **MYH7 gene** encodes a key component of the cardiac sarcomere, and its mutations lead to dysfunctional contractile proteins, causing myocardial hypertrophy and disarray [1]. *Elastin* - **Elastin mutations** are primarily associated with conditions like **Williams syndrome**, which involves cardiovascular abnormalities such as **supravalvular aortic stenosis**, but not HCM. - Elastin is a protein that provides elasticity to tissues, not directly involved in myocardial contraction leading to HCM. *α - tropomyosin* - While mutations in **α-tropomyosin (TPM1)** can cause **HCM**, they are much less common than mutations in the **β-myosin heavy chain** gene, accounting for a smaller percentage of cases [1]. - **α-tropomyosin** is also a component of the cardiac sarcomere, involved in regulating muscle contraction [1]. *Troponin T* - Mutations in **cardiac troponin T (TNNT2)** are another known genetic cause of **HCM**, but they are less prevalent than MYH7 mutations [1]. - **Troponin T** is part of the troponin complex, which regulates calcium-dependent muscle contraction in the heart [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, p. 574.

Question 230: Which of the following will be seen on cardiac biopsy of a patient who had a post MI reperfusion injury?

A. Waviness of fibres
B. Eosinophilic contraction bands (Correct Answer)
C. Neutrophils in cardiac cells
D. Swelling of cells

Explanation: ***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.

Practice by Chapter

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