Hypertensive Heart Disease — MCQs

10 questions

Which of the following is not associated with pulmonary arterial hypertension?

The MOST COMMON cause of concentric hypertrophy of left ventricle is?

The chest radiograph shown below is from a 25-year-old male patient presenting with hypertension. The image demonstrates bilateral inferior rib notching. What is the most likely diagnosis?

Characteristic feature of hypertrophic obstructive cardiomyopathy is:

Which of the following cardiac complications may develop in a 33 year old woman with systemic lupus erythematosus (SLE) because of her underlying condition?

Which of the following murmurs increase with a Valsalva maneuver?

Which of the following has the most friable vegetations:

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, what is the most likely finding in this material?

A young female patient presents for a routine examination and is found to have a mid-systolic click on auscultation, with no history of rheumatic heart disease. The histopathological examination is most likely to show which of the following?

Q10

Fish mouth stenosis in rheumatic heart disease is due to which of the following mechanisms?

Hypertensive Heart Disease Indian Medical PG Practice Questions and MCQs

Question 1: Which of the following is not associated with pulmonary arterial hypertension?

A. Cor - pulmonale
B. Left ventricular hypertrophy (Correct Answer)
C. Mitral Stenosis
D. Interstitial lung disease

Explanation: ***Left ventricular hypertrophy*** - **Left ventricular hypertrophy** is typically caused by conditions that increase the workload on the left ventricle, such as **systemic hypertension** or **aortic stenosis** [1]. - Pulmonary arterial hypertension directly affects the **pulmonary vasculature**, leading to increased pressure in the pulmonary circuit and ultimately right heart strain, not left ventricular hypertrophy. *Cor pulmonale* - **Cor pulmonale** is defined as **right ventricular enlargement** secondary to lung disease or pulmonary vascular disease. - Pulmonary arterial hypertension increases the afterload on the right ventricle, causing it to dilate and hypertrophy, eventually leading to **right heart failure** (cor pulmonale) [2]. *Mitral Stenosis* - **Mitral stenosis** causes an obstruction to blood flow from the left atrium to the left ventricle, leading to increased pressure in the left atrium and pulmonary veins. - This elevated pressure can be transmitted backward into the pulmonary arteries, leading to **pulmonary arterial hypertension** [3]. *Interstitial lung disease* - **Interstitial lung disease** (ILD) can lead to destruction and remodeling of the pulmonary capillaries, increasing pulmonary vascular resistance [2]. - This increased resistance causes the pulmonary arterial pressure to rise, resulting in **pulmonary arterial hypertension**.

Question 2: The MOST COMMON cause of concentric hypertrophy of left ventricle is?

A. Hypertension (Correct Answer)
B. Aortic stenosis
C. Mitral stenosis
D. Aortic regurgitation

Explanation: ***Hypertension*** - Chronic **hypertension** is the most common cause of **pressure overload** on the left ventricle, leading to concentric hypertrophy [1]. - In response to the increased afterload, the ventricular wall thickens uniformly inward, reducing the chamber size while maintaining normal wall stress [2]. - Due to its high prevalence (30-40% of adults), hypertension is epidemiologically the most frequent cause of concentric LVH [1]. *Aortic stenosis* - While **aortic stenosis** is the classic pathological cause of **pressure overload** and concentric hypertrophy [2], **hypertension** is more prevalent in the population. - Aortic stenosis causes fixed outflow obstruction, leading to significant pressure work for the left ventricle. - This is the second most common cause but occurs in only 2-5% of elderly patients. *Mitral stenosis* - **Mitral stenosis** primarily causes pressure overload on the **left atrium** and **pulmonary circulation**, not the left ventricle. - It doesn't typically lead to **left ventricular hypertrophy** directly; instead, it causes left atrial enlargement and right ventricular hypertrophy. *Aortic regurgitation* - **Aortic regurgitation** results in **volume overload** of the left ventricle due to blood flowing back into the chamber during diastole. - This typically leads to **eccentric hypertrophy**, where the chamber dilates and the wall thickens proportionally, rather than concentric hypertrophy [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 560-562. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, p. 536.

Question 3: The chest radiograph shown below is from a 25-year-old male patient presenting with hypertension. The image demonstrates bilateral inferior rib notching. What is the most likely diagnosis?

A. Tetralogy of Fallot
B. Ebstein's Anomaly
C. TAPVC
D. Coarctation of Aorta (Correct Answer)

Explanation: ***Coarctation of Aorta*** - The chest radiograph shows findings consistent with **rib notching**, which is a classic sign of coarctation of the aorta due to increased collateral circulation through intercostal arteries. - The history of **hypertension** in a male patient, especially if presenting at a younger age or with differential blood pressures between upper and lower extremities, strongly suggests coarctation of the aorta. *Tetralogy of Fallot* - Characterized by a **boot-shaped heart** due to right ventricular hypertrophy and pulmonary outflow obstruction. - Would typically present with **cyanosis** and decreased pulmonary vascular markings, not rib notching or isolated hypertension. *Ebstein's Anomaly* - Involves apical displacement of the **tricuspid valve**, leading to atrialization of the right ventricle and severe tricuspid regurgitation. - Chest X-rays often show **severe cardiomegaly** (huge heart due to right atrial enlargement) and decreased pulmonary vascularity, which are not depicted here. *TAPVC* - Total anomalous pulmonary venous connection (TAPVC) involves all pulmonary veins draining into the systemic circulation. - The classic chest X-ray finding for supracardiac TAPVC is a **"snowman" or "figure of 8" sign** due to dilated anomalous vessels and superior vena cava, which is absent in this image.

Question 4: Characteristic feature of hypertrophic obstructive cardiomyopathy is:

A. Increased size of ventricle
B. Asymmetric septal hypertrophy (Correct Answer)
C. Normal myofiber arrangement
D. Increased size of atria

Explanation: ***Asymmetric septal hypertrophy*** - This is the hallmark feature of **hypertrophic obstructive cardiomyopathy (HOCM)**, where the **interventricular septum** thickens disproportionately more than the free wall of the left ventricle [1], [2]. - This septal thickening can lead to **left ventricular outflow tract obstruction**, particularly during systole, obstructing blood flow out of the heart [1]. *Increased size of ventricle* - While the left ventricle may appear enlarged in some dimensions due to hypertrophy, the primary characteristic is specifically **asymmetric thickening of the septum**, not a generalized increase in ventricular size [2]. - In other forms of cardiomyopathy, such as dilated cardiomyopathy, a global increase in ventricular size is observed, which is distinct from HOCM. *Normal myofiber arrangement* - A characteristic microscopic feature of HOCM is **myocardial disarray**, where cardiac muscle fibers are abnormally arranged instead of their usual parallel alignment [1]. - This disorganized arrangement contributes to the impaired function and electrical instability seen in HOCM. *Increased size of atria* - While **left atrial enlargement** can be a secondary finding in HOCM due to increased left ventricular end-diastolic pressure and impaired diastolic filling, it is not the primary or characteristic feature defining the condition [1]. - The fundamental pathology of HOCM lies in the specific hypertrophy of the ventricular myocardium, particularly the septum. **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.

Question 5: Which of the following cardiac complications may develop in a 33 year old woman with systemic lupus erythematosus (SLE) because of her underlying condition?

A. Mitral valve prolapse
B. Libman-Sacks endocarditis (Correct Answer)
C. Hemorrhagic pericarditis
D. Infective endocarditis

Explanation: ***Libman-Sacks endocarditis*** - Libman-Sacks endocarditis is a **non-infectious valvular vegetation** that is highly characteristic of **systemic lupus erythematosus (SLE)** [3]. - These vegetations can lead to **valvular incompetence** or **stenosis**, primarily affecting the **mitral and aortic valves** [1]. *Mitral valve prolapse* - While mitral valve prolapse can occur in SLE patients, it is a relatively common condition in the general population and is **not as specifically linked** to SLE pathology as Libman-Sacks endocarditis. - It involves the **leaflet(s) of the mitral valve bulging** back into the left atrium during systole, which causes a **mid-systolic click and late systolic murmur**, but does not represent the specific immune-mediated damage seen in SLE. *Hemorrhagic pericarditis* - Pericarditis is a common cardiac manifestation in SLE, leading to **inflammation of the pericardium**, but it is typically **serous or fibrinous**, not usually hemorrhagic. - **Hemorrhagic pericarditis** is more often associated with conditions like malignancy, tuberculosis, or trauma, and is not a typical presentation of SLE. *Infective endocarditis* - **Infective endocarditis** is caused by microbial infection of the heart valves, resulting in **vegetations containing bacteria or fungi** [2]. - While SLE patients can be at increased risk for infections due to immunosuppression, the vegetations of Libman-Sacks endocarditis are **sterile (non-infectious)** and distinct in their underlying pathophysiology [1].

Question 6: Which of the following murmurs increase with a Valsalva maneuver?

A. MR
B. VSD
C. AS
D. Hypertrophic cardiomyopathy (Correct Answer)

Explanation: ***Hypertrophic cardiomyopathy*** - The Valsalva maneuver decreases **preload**, leading to a reduction in left ventricular volume and an **increased outflow tract obstruction**. - This increased obstruction accentuates the murmur of hypertrophic cardiomyopathy, making it louder. *MR* - Mitral regurgitation (MR) murmur typically **decreases** or remains unchanged with the Valsalva maneuver due to reduced **venous return** and thus reduced left ventricular preload. - A decrease in preload lessens the volume of blood being regurgitated from the left ventricle into the left atrium. *VSD* - The murmur of a ventricular septal defect (VSD) usually **decreases** during the Valsalva maneuver because of the reduction in **venous return** and consequent decrease in left-to-right shunting. - Decreased systemic vascular resistance relative to pulmonary resistance also plays a role, reducing the pressure gradient for shunting. *AS* - Aortic stenosis (AS) murmur generally **decreases** during the Valsalva maneuver due to decreased **left ventricular volume** and reduced transvalvular flow. - The reduction in preload lessens the blood ejected through the stenotic aortic valve, thereby reducing the intensity of the murmur.

Question 7: Which of the following has the most friable vegetations:

A. SLE
B. Rheumatic heart disease
C. Libman Sack's endocarditis
D. Infective endocarditis (Correct Answer)

Explanation: ***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.

Question 8: 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, what is the most likely finding in this material?

A. Weber Palade bodies
B. Concentric whorls of lamellar structures
C. Non-branching filaments of indefinite length (Correct Answer)
D. Cross banded fibres with 67 nm periodicity

Explanation: ***Non branching filaments of indefinite length*** - The presence of **eosinophilic hyaline material** in restrictive heart disease suggests the deposition of **amyloid** [1][2], which is characterized by long, **non-branching filaments** [4]. - Transmission electron microscopy typically reveals **randomly oriented filaments** [3], confirming the diagnosis of amyloidosis. *Concentric whorls of lamellar structures* - Concentric whorls are more characteristic of **myxomatous degeneration** or **lipofuscin deposits**, not amyloid deposition. - This finding does not correlate with the **eosinophilic hyaline material** seen in the biopsy [2]. *Weber Palade bodies* - Weber Palade bodies are **granules found in endothelial cells**, related to the storage of von Willebrand factor, not heart tissue pathology. - Their presence does not explain the findings seen in **restrictive heart disease** or the specific biopsy results. *Cross banded fibres with 67 m periodicity* - Cross banded fibers are indicative of **collagen** or **muscle striations**, rather than amyloid. - Such fibers do not relate to the **eosinophilic hyaline material** revealed in this context [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 264-266. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 580-581. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 268-269. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 135-136.

Question 9: A young female patient presents for a routine examination and is found to have a mid-systolic click on auscultation, with no history of rheumatic heart disease. The histopathological examination is most likely to show which of the following?

A. Myxomatous degeneration of the mitral valve (Correct Answer)
B. Fibrinous deposition on the papillary muscle due to infective endocarditis
C. Aschoff nodule associated with rheumatic heart disease
D. Rupture of chordae tendineae leading to acute mitral regurgitation

Explanation: ***Myxomatous degeneration and prolapse of the mitral valve*** - The presence of a **mid-systolic click** in a young female patient is commonly linked to **mitral valve prolapse**, which is characterized by myxomatous degeneration. - Histologically, this condition involves **expansion of the spongiosa** layer due to accumulation of glycosaminoglycans, leading to valve redundancy. *Aschoff nodule on the mitral valve* - Aschoff nodules are associated with **rheumatic fever** [1], but this patient lacks a history of **rheumatic heart disease**. - These nodules are typically found in the myocardium and not specifically on the mitral valve in cases without rheumatic background. *Rupture of chordae tendinae* - While chordae rupture can cause acute mitral valve insufficiency, it is not a primary histopathological finding in an otherwise **asymptomatic young patient**. - This condition usually presents with acute symptoms and is related to **trauma** or severe mitral valve disease, unlike the findings here. *Fibrinous deposition on the tip of papillary muscle* - Fibrinous deposition typically indicates a **reactive process**, such as infective endocarditis, which does not correlate with a mere mid-systolic click. - This finding would not be expected in a routine examination of an otherwise healthy young female with no murmur indicating significant valvular disease. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 566-567.

Question 10: Fish mouth stenosis in rheumatic heart disease is due to which of the following mechanisms?

A. Calcification and fibrosis bridging across valvular commissures (Correct Answer)
B. Fibrinoid necrosis
C. Acute inflammation leading to valvular damage
D. Myxomatous degeneration of the valve, which can occur in rheumatic heart disease

Explanation: ***Calcification and fibrosis bridging across valvular commissures*** - In rheumatic heart disease, **calcification and fibrosis** occur as a result of chronic inflammation, leading to **stenosis** of the mitral valve, often described as "fish mouth" appearance [1]. - This mechanism is due to **post-inflammatory scarring** that restricts opening and closing of the valve, characteristic of chronic rheumatic changes [1][2]. *Myxomatous degeneration of the valve* - Myxomatous degeneration primarily affects the **mitral valve** and may cause **prolapse**, but it does not lead to **stenosis**. - This process involves **thinning and elongation** of the valve leaflets, contrasting with the fibrotic changes seen in rheumatic heart disease. *Acute inflammation leading to valvular damage* - Acute inflammation due to **rheumatic fever** typically causes **valvulitis**, not chronic stenosis, which is a late consequence of chronic damage. - This mechanism leads to **valvular regurgitation** rather than stenosis, hence it's not associated with "fish mouth" stenosis. *Fibrinoid necrosis* - Fibrinoid necrosis is seen in **acute rheumatic fever** but does not directly cause **valvular stenosis**; it represents an acute inflammatory response. - This is more related to **immune complex deposition** rather than the chronic fibrotic changes leading to fish mouth morphology in rheumatic heart disease. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 566-567. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Cardiovascular Disease, pp. 293-294.

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