Valvular Heart Disease — MCQs

10 questions

The severity of mitral stenosis can be judged by-

274. A young athlete was found to have hypertrophic cardiomyopathy during testing for a competitive sport. Which of the following maneuvers will increase the murmur?

Murmur heard in aortic stenosis

A 60-year-old lady presents with shortness of breath (SOB) and episodes of angina pectoris. Work-up reveals aortic stenosis. Which of the following is the most likely reason behind these chest pain episodes?

All of the following are true about rheumatic fever/rheumatic heart disease except:

Which of the following describes aortic regurgitation murmur?

About carey coombs murmur which is false –

Which of the following conditions is LEAST likely to cause peripheral edema?

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

Q10

Which of the following has the most friable vegetations:

Valvular Heart Disease Indian Medical PG Practice Questions and MCQs

Question 1: The severity of mitral stenosis can be judged by-

A. Duration of murmur
B. Intensity of murmur
C. Presence of left ventricular S3
D. Loud S1 (Correct Answer)

Explanation: ***Loud S1*** - A **loud S1** in mitral stenosis indicates that the **mitral valve leaflets are still mobile** and able to snap shut forcefully, which is characteristic of early to moderate stenosis [2]. - As mitral stenosis becomes more severe and the valve becomes calcified and rigid, the S1 sound may become diminished or even absent due to reduced leaflet mobility [1]. *Intensity of murmur* - The **intensity (loudness)** of the diastolic murmur in mitral stenosis **does not directly correlate with the severity** of the stenosis. - A loud murmur can be heard with mild stenosis, while a soft murmur in severe stenosis may be due to reduced cardiac output or left atrial pressure. *Duration of murmur* - While a **longer duration of the diastolic murmur** can coincide with more severe mitral stenosis, it is not as reliable a single indicator as other findings. - The duration is influenced by the pressure gradient across the valve and the length of diastole [2]. *Presence of left ventricular S3* - A **left ventricular S3** is typically associated with **left ventricular dysfunction** and volume overload, as seen in conditions like mitral regurgitation or dilated cardiomyopathy [3]. - It is **not a feature of mitral stenosis**, where the primary issue is obstruction to left ventricular filling.

Question 2: 274. A young athlete was found to have hypertrophic cardiomyopathy during testing for a competitive sport. Which of the following maneuvers will increase the murmur?

A. Handgrip
B. Valsalva maneuver (Correct Answer)
C. Squatting
D. Leaning forward
E. Passive leg raise

Explanation: **Valsalva maneuver** - The **Valsalva maneuver** reduces **preload** by decreasing venous return to the heart. - A decrease in preload reduces the left ventricular chamber size, which in turn exacerbates the **left ventricular outflow tract (LVOT) obstruction** characteristic of hypertrophic cardiomyopathy (HCM), thereby **increasing the intensity of the murmur**. *Handgrip* - **Handgrip** is an isometric exercise that leads to an increase in **afterload** and **peripheral vascular resistance**. - Increased afterload causes the left ventricle to eject blood against higher pressure, which **enlarges the left ventricular chamber** and **reduces the LVOT obstruction**, thus **decreasing the intensity of the murmur** in HCM. *Squatting* - **Squatting** increases both **preload** (due to increased venous return) and **afterload** (due to increased peripheral vascular resistance). - The increased preload and afterload lead to an **increased left ventricular volume**, which **reduces the LVOT obstruction** and therefore **decreases the intensity of the murmur** in HCM. *Passive leg raise* - **Passive leg raise** increases **preload** by increasing venous return to the heart from the lower extremities. - The increased preload leads to an **increased left ventricular chamber size**, which **reduces the LVOT obstruction** and therefore **decreases the intensity of the murmur** in HCM. *Leaning forward* - Leaning forward during auscultation is typically used to better hear **aortic regurgitation murmurs**, as it brings the aorta closer to the chest wall. - This maneuver does not significantly alter **cardiac preload or afterload** in a way that would consistently increase the murmur of hypertrophic cardiomyopathy.

Question 3: Murmur heard in aortic stenosis

A. Apex, low pitch murmur associated with mitral valve issues
B. Pan-systolic murmur, high pitch murmur associated with mitral regurgitation
C. Left Sternal area, murmur indicating mitral regurgitation
D. Right 2nd intercostal, high pitch systolic ejection murmur (Correct Answer)

Explanation: ***Right 2nd intercostal, high pitch systolic ejection murmur*** - The murmur of **aortic stenosis** is classically heard loudest at the **right second intercostal space** (aortic area) due to turbulent flow through the stenosed aortic valve. - It is a **high-pitched, systolic ejection murmur** with a crescendo-decrescendo pattern, often radiating to the carotid arteries [2]. *Apex, low pitch murmur associated with mitral valve issues* - A murmur heard at the **apex** that is low-pitched typically suggests **mitral stenosis**, which is a diastolic rumble, not an aortic stenosis murmur [1]. - This option refers to characteristics associated with **mitral valve disease**, not aortic stenosis. *Pan-systolic murmur, high pitch murmur associated with mitral regurgitation* - A **pan-systolic murmur** is characteristic of conditions like **mitral regurgitation** or tricuspid regurgitation, where blood flows throughout the entire systole [3]. - While it can be high-pitched, its pan-systolic nature and association with mitral regurgitation make it distinct from aortic stenosis. *Left Sternal area, murmur indicating mitral regurgitation* - Murmurs heard primarily at the **left sternal area** can indicate various conditions, but this option specifically points to **mitral regurgitation**. - **Mitral regurgitation** is better heard at the apex and usually radiates to the axilla, and the description does not fit the typical presentation of aortic stenosis [3].

Question 4: A 60-year-old lady presents with shortness of breath (SOB) and episodes of angina pectoris. Work-up reveals aortic stenosis. Which of the following is the most likely reason behind these chest pain episodes?

A. Increased pressure in aorta
B. Decreased pressure in aorta
C. Increased oxygen consumption in the heart (Correct Answer)
D. Increase in volume overload of the heart
E. Decreased coronary blood flow

Explanation: ***Increased oxygen consumption in the heart*** - In **aortic stenosis**, the left ventricle must generate significantly higher pressures to eject blood through the narrowed aortic valve, leading to **left ventricular hypertrophy**. This increased workload significantly raises the **myocardial oxygen demand**. - Angina pectoris occurs when this increased oxygen demand surpasses the oxygen supply, leading to **myocardial ischemia**. - This is the **primary mechanism** of angina in aortic stenosis. *Increased pressure in aorta* - While there is **increased pressure within the left ventricle** to overcome the stenotic valve, the pressure in the aorta *distal* to the stenosis is often normal or even slightly reduced due to the obstruction. - Increased aortic pressure itself is not the primary direct cause of angina in aortic stenosis; rather, it's the compensatory ventricular workload. *Decreased pressure in aorta* - A **decreased pressure in the aorta** could actually worsen coronary perfusion, but the primary reason for angina in aortic stenosis is the vastly **increased myocardial demand**, not necessarily a critical drop in aortic pressure. - The elevated left ventricular pressure required to overcome the stenosis is the key factor driving the angina. *Increase in volume overload of the heart* - **Aortic stenosis primarily causes pressure overload**, not volume overload, on the left ventricle due to the obstruction to outflow. - Volume overload typically occurs in conditions like **aortic regurgitation** or **mitral regurgitation**, which have different pathophysiological mechanisms for angina. *Decreased coronary blood flow* - While **decreased coronary perfusion** can be a contributing factor in aortic stenosis (due to reduced aortic pressure and shortened diastolic filling time), it is a **secondary mechanism**. - The **primary cause** of angina in aortic stenosis is the markedly **increased myocardial oxygen demand** from left ventricular hypertrophy and increased workload, rather than a primary reduction in coronary blood flow.

Question 5: All of the following are true about rheumatic fever/rheumatic heart disease except:

A. Presence of Anitschkow cells is pathognomonic
B. MacCallum plaques are commonly seen in left atrium
C. Mitral stenosis is evident in the early stage of the disease (Correct Answer)
D. Mitral valve is most commonly affected

Explanation: ***Mitral stenosis is evident in the early stage of the disease*** - **Mitral stenosis** is typically a **late complication** of rheumatic heart disease [1], developing **years or even decades** after the initial acute rheumatic fever. - The **early stages** of rheumatic heart disease are characterized by **mitral regurgitation** (and sometimes aortic regurgitation) due to **acute inflammation** and **valvulitis** causing incomplete valve closure. - Stenosis develops only after **repeated inflammatory episodes** lead to **fibrosis, calcification**, and **fusion of commissures** [1]. - This is clearly **FALSE** and is the correct answer to this "except" question. *Presence of Anitschkow cells is pathognomonic* - **Anitschkow cells** (caterpillar cells) are highly **characteristic histiocytes** with elongated nuclei seen in **Aschoff bodies** of rheumatic fever [1]. - They are considered **virtually pathognomonic** in the appropriate clinical context of rheumatic carditis [1]. - While theoretically they might be seen in other conditions, their presence in myocardial Aschoff bodies is **diagnostically specific** for rheumatic fever. - This statement is considered **TRUE** for examination purposes. *MacCallum plaques are commonly seen in left atrium* - **MacCallum plaques** are areas of **fibrous thickening** of the left atrial endocardium, typically on the **posterior wall** near the mitral valve. - These result from **regurgitant jet lesions** from the damaged mitral valve. - This is a **TRUE** statement and a classic pathological finding in rheumatic heart disease. *Mitral valve is most commonly affected* - The **mitral valve** is the most frequently affected valve in **rheumatic heart disease** (75-80% of cases) [1]. - The **aortic valve** is second most common, while tricuspid and pulmonary valves are rarely affected [1]. - This is a **TRUE** statement. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 566-567.

Question 6: Which of the following describes aortic regurgitation murmur?

A. Ejection systolic murmur
B. Diastolic murmur (Correct Answer)
C. Ventricular contraction
D. Systolic murmur

Explanation: ***Diastolic murmur*** - Aortic regurgitation occurs when the **aortic valve does not close completely**, leading to blood flowing back into the **left ventricle during diastole** [1]. - This backflow of blood during the **relaxation phase** of the heart creates the characteristic diastolic murmur [1]. *Ejection systolic murmur* - This murmur type is typically heard during **systole** and is associated with conditions like **aortic stenosis**, where there is turbulent flow across a narrowed aortic valve during ejection [3]. - It does not describe the sound of blood flowing back into the ventricle during **diastole**, which characterizes aortic regurgitation. *Ventricular contraction* - **Ventricular contraction** occurs during **systole** and is the mechanism by which blood is ejected from the ventricles [2]. - While related to cardiac cycle, it does not directly describe the timing or nature of the murmur caused by aortic regurgitation. *Systolic murmur* - A **systolic murmur** is heard when the ventricles contract, such as in conditions like **aortic stenosis** or **mitral regurgitation** [3]. - Aortic regurgitation is specifically a **diastolic event** as blood leaks back into the left ventricle during ventricular relaxation [1].

Question 7: About carey coombs murmur which is false –

A. Mid-diastolic murmur
B. Can be associated with AR (Correct Answer)
C. Seen in rheumatic fever
D. Low pitched murmur

Explanation: *Carey Coombs murmur can be associated with AR* - The Carey Coombs murmur is caused by inflammation and thickening of the mitral valve in **acute rheumatic fever**, leading to increased flow velocity across the valve during diastole [3]. - It is **not directly associated with aortic regurgitation (AR)**; instead, AR can occur concurrently as part of the overall rheumatic heart disease aetiology, but the murmur itself is mitral in origin [1], [3]. *Mid-diastolic murmur* - The Carey Coombs murmur is indeed a **mid-diastolic murmur**, heard at the apex [2]. - This timing is due to the turbulent flow of blood across the inflamed **mitral valve** during the middle part of ventricular diastole [2]. *Seen in rheumatic fever* - The Carey Coombs murmur is a classic sign specifically associated with **acute rheumatic fever** [3]. - It results from inflammation of the mitral valve causing relative **mitral stenosis** and turbulence during diastole. *Low pitched murmur* - This murmur is typically described as **low-pitched and rumbling**, heard best with the bell of the stethoscope [2]. - Its low pitch is characteristic of turbulent flow caused by relative mitral stenosis [2].

Question 8: Which of the following conditions is LEAST likely to cause peripheral edema?

A. Nephrotic syndrome
B. Venous insufficiency (Correct Answer)
C. Congestive heart failure
D. Hyperthyroidism

Explanation: Venous insufficiency - **Venous insufficiency** is a common cause of peripheral edema due to impaired venous return leading to fluid accumulation in the lower extremities. - It is characterized by **pitting edema**, skin changes, and often associated with varicose veins. *Nephrotic syndrome* - **Nephrotic syndrome** causes generalized edema, including peripheral edema, due to significant **proteinuria** [1] leading to hypoalbuminemia and decreased plasma oncotic pressure. - The reduced oncotic pressure causes fluid to shift from the intravascular space into the interstitial space. *Congestive heart failure* - **Congestive heart failure** leads to peripheral edema primarily due to increased hydrostatic pressure in the capillaries as a result of the heart's inability to pump blood effectively. - This results in fluid extravasation into the interstitial tissues, often presenting as **pitting edema** in the ankles and legs. *Hyperthyroidism* - While **hyperthyroidism** is not a classic cause of significant peripheral edema, some patients can develop **pretibial myxedema**, which is a condition associated with autoimmune thyroid disease. - This form of edema is typically non-pitting and localized, and it is not a direct result of increased hydrostatic or decreased oncotic pressure in the same way as conditions like CHF or nephrotic syndrome.

Question 9: 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.

Question 10: 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.

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