Myocarditis and Cardiomyopathies — MCQs
Myocarditis is a side effect of which drug(s)?
A man who is chronic alcoholic will develop which type of cardiomyopathy?
Which of the following statements is false regarding restrictive cardiomyopathy?
Epsilon waves are most specific for
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?
Which of the following is the most common late toxic manifestation of diphtheria in a child?
Perifascicular atrophy of muscle fibers is seen in?
A young athlete died of sudden cardiac arrest after athletic activity. Post-mortem findings revealed interventricular septal hypertrophy. What is the most probable diagnosis?
An athlete collapsed and expired while playing school basketball. Histology of the cardiac specimen is most likely to indicate which of the following conditions?
Dilated cardiomyopathy is caused by which gene alteration?
Myocarditis and Cardiomyopathies Indian Medical PG Practice Questions and MCQs
Question 1: Myocarditis is a side effect of which drug(s)?
- A. clozapine (Correct Answer)
- B. aripiprazole
- C. olanzapine
- D. chlorpromazine
Explanation: ***Clozapine*** - **Clozapine** is an atypical antipsychotic known to cause several serious side effects, including **myocarditis**, particularly during the initial weeks of treatment. - Patients on clozapine must be monitored for symptoms of myocarditis, such as **tachycardia**, **fever**, chest pain, and fatigue. *Aripiprazole* - **Aripiprazole** is generally considered to have a favorable cardiovascular safety profile compared to other antipsychotics. - While it can cause some cardiovascular side effects like **orthostatic hypotension**, **myocarditis** is not a commonly associated side effect. *Olanzapine* - **Olanzapine** is associated with metabolic side effects such as weight gain, dyslipidemia, and hyperglycemia. - Although it can rarely cause other cardiovascular issues like **QT prolongation**, **myocarditis** is not a characteristic adverse effect. *Chlorpromazine* - **Chlorpromazine** is a first-generation antipsychotic often linked to **QT prolongation** and **orthostatic hypotension**. - While it can have cardiovascular effects, **myocarditis** is not typically listed as one of its prominent or common adverse reactions.
Question 2: A man who is chronic alcoholic will develop which type of cardiomyopathy?
- A. Dilated cardiomyopathy (Correct Answer)
- B. Hypertrophic cardiomyopathy
- C. Myocarditis
- D. Pericarditis
Explanation: ***Dilated cardiomyopathy*** - Chronic alcohol abuse is a major cause of **dilated cardiomyopathy**, where the heart's pumping chambers (ventricles) become enlarged and weakened, leading to reduced cardiac output [1]. - This condition often called **alcoholic cardiomyopathy**, is characterized by **ventricular dilation** and **systolic dysfunction**. *Hypertrophic cardiomyopathy* - This condition involves thickening of the heart muscle, often genetic, and is not directly caused by **chronic alcoholism**. - While alcohol can worsen pre-existing heart conditions, it does not typically lead to primary **hypertrophic cardiomyopathy**. *Myocarditis* - **Myocarditis** is an inflammation of the heart muscle, usually caused by viral infections or autoimmune processes. - Although heavy alcohol use can weaken the immune system, it is not a direct cause of viral or primary inflammatory myocarditis. *Pericarditis* - **Pericarditis** is the inflammation of the pericardium, the sac surrounding the heart, most commonly due to viral infections or autoimmune conditions. - While alcohol abuse can have various systemic effects, it is not a recognized direct cause of **pericarditis**.
Question 3: Which of the following statements is false regarding restrictive cardiomyopathy?
- A. Left ventricular hypertrophy is present.
- B. Filling pressure is decreased. (Correct Answer)
- C. In the early phase, systolic function is impaired.
- D. Heart failure is predominantly right-sided.
Explanation: Filling pressure is decreased. - In restrictive cardiomyopathy, the ventricles become stiff and noncompliant, impairing filling. - This leads to increased filling pressures (e.g., elevated left and right atrial pressures) as the heart attempts to fill adequately. Left ventricular hypertrophy is present. - Left ventricular hypertrophy is common in restrictive cardiomyopathy, particularly in conditions like amyloidosis and sarcoidosis, where infiltrative processes thicken the ventricular walls. - While the chambers are not dilated, the walls can be abnormally thick due to underlying pathology. In the early phase, systolic function is impaired. - In the early stages of restrictive cardiomyopathy, systolic function is typically preserved. The primary defect is diastolic dysfunction—impaired ventricular filling. - Systolic dysfunction may develop in later stages as the underlying disease progresses or due to severe volume overload. Heart failure is predominantly right-sided. - Right-sided heart failure symptoms (e.g., peripheral edema, ascites, jugular venous distension) are often prominent in restrictive cardiomyopathy. - Due to the rigid and non-compliant ventricles inhibiting filling, both ventricles are affected, but systemic venous congestion often dominates the clinical picture.
Question 4: Epsilon waves are most specific for
- A. Arrhythmogenic RV Cardiomyopathy (Correct Answer)
- B. Hypokalemia
- C. Hypothermia
- D. PSVT
Explanation: ***Arrhythmogenic RV Cardiomyopathy*** - Epsilon waves are small, positive deflections seen at the end of the **QRS complex**, best observed in precordial leads (V1-V3), and are a characteristic ECG finding in **Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC)**. - They represent delayed and fragmented electrical activity due to fibrofatty replacement of the right ventricular myocardium in ARVC. *Hypokalemia* - **Hypokalemia** typically manifests on ECG with **U waves**, which are positive deflections following the T wave, not epsilon waves. - Other ECG changes in hypokalemia include flattened T waves and ST-segment depression. *Hypothermia* - **Hypothermia** is associated with the presence of **Osborn waves** (J waves), which are positive deflections at the junction of the QRS complex and the ST segment. - These waves are distinct from epsilon waves and represent slowed repolarization. *PSVT* - **Paroxysmal Supraventricular Tachycardia (PSVT)** is a type of arrhythmia characterized by a narrow QRS complex tachycardia with a regular rhythm. - It does not involve epsilon waves; its ECG features are related to abnormal conduction pathways in the atria or AV node.
Question 5: 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 6: Which of the following is the most common late toxic manifestation of diphtheria in a child?
- A. Polyneuritis (Correct Answer)
- B. Renal failure
- C. Myocarditis
- D. Septicemia
Explanation: ***Polyneuritis*** - **Polyneuritis** is the **most common late toxic manifestation** of diphtheria, typically appearing **2-6 weeks or more** after the onset of infection. - It results from the **diphtheria toxin's neurotoxic effects**, causing demyelination of peripheral nerves. - Clinical features include **cranial nerve palsies** (especially palatal and pharyngeal weakness), **limb weakness**, and **areflexia**. - It can persist for weeks to months and is the characteristic delayed complication. *Renal failure* - While diphtheria toxin can cause **acute tubular necrosis**, renal failure is **uncommon** and not a primary late toxic manifestation. - When kidney injury occurs, it is typically mild and occurs earlier in the acute phase rather than as a delayed complication. *Myocarditis* - **Myocarditis** is a serious complication of diphtheria occurring in **10-25% of cases**, typically appearing in **weeks 2-6**. - While it overlaps with the timing of late manifestations, it generally presents **earlier in that window** (often weeks 2-3) compared to polyneuritis. - It is a **major cause of mortality** in diphtheria, but **polyneuritis is more common as a late manifestation** presenting after week 3-4. - Clinical features include arrhythmias, heart failure, and conduction defects. *Septicemia* - **Septicemia** is not a direct toxic manifestation of *Corynebacterium diphtheriae*. - Diphtheria causes disease primarily through **localized infection and systemic toxin effects**, not through bloodstream invasion. - Secondary bacterial superinfection is possible but is not a characteristic manifestation of diphtheria toxicity.
Question 7: Perifascicular atrophy of muscle fibers is seen in?
- A. Myopathy due to corticosteroids
- B. Dermatomyositis (Correct Answer)
- C. Inclusion body myositis
- D. Nemaline myopathy
Explanation: ***Dermatomyositis*** - Characterized by **perifascicular atrophy** of muscle fibers, which is a distinct histological feature seen in dermatomyositis [1]. - Additionally associated with **skin manifestations** such as a heliotrope rash and Gottron's papules. *Inclusion body myositis* - Features **rimmed vacuoles** and **inflammatory infiltrate**, but does not show perifascicular atrophy as seen in dermatomyositis. - Typically affects older adults and has a different clinical presentation compared to dermatomyositis. *Nemaline myopathy* - Characterized by **nemaline bodies** on muscle biopsy, not perifascicular atrophy, which is specific to dermatomyositis. - Generally presents with **congenital muscle weakness**, distinctly different from the autoimmune nature of dermatomyositis. *Steroid myopathy* - Results from **chronic corticosteroid use**, leading to muscle weakness but does not feature perifascicular atrophy. - Primarily affects **proximal muscles** and is linked to medication rather than a specific myopathy like dermatomyositis. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, pp. 1240-1241.
Question 8: A young athlete died of sudden cardiac arrest after athletic activity. Post-mortem findings revealed interventricular septal hypertrophy. What is the most probable diagnosis?
- A. Dilated Cardiomyopathy (DCM)
- B. Ventricular Septal Defect (VSD)
- C. Aortic Stenosis (AS)
- D. Hypertrophic Obstructive Cardiomyopathy (HOCM) (Correct Answer)
Explanation: ***Hypertrophic Obstructive Cardiomyopathy (HOCM)*** - **HOCM** is a common cause of **sudden cardiac death in young athletes** due to arrhythmogenic potential associated with **marked interventricular septal hypertrophy** [1]. - The **interventricular septal hypertrophy** observed post-mortem is a hallmark of HOCM, often leading to dynamic **left ventricular outflow tract obstruction** and myocardial ischemia [1], [2]. *Dilated Cardiomyopathy (DCM)* - DCM is characterized by **ventricular dilation** and **impaired systolic function**, not primarily septal hypertrophy [4]. - While DCM can cause sudden death, the primary post-mortem finding would be a **thinned, enlarged heart**, not isolated septal thickening [4]. *Aortic Stenosis (AS)* - Severe AS can cause **left ventricular hypertrophy**, but the hypertrophy would be **concentric** across the entire left ventricle, not specifically isolated to the interventricular septum [3]. - A definitive diagnosis of AS would also involve findings of a **stenotic aortic valve**, which is not mentioned as a post-mortem finding. *Ventricular Septal Defect (VSD)* - VSD is a **congenital heart defect** involving a hole in the ventricular septum, leading to shunting of blood. - While large VSDs can lead to complications, they are not typically characterized by isolated **septal hypertrophy** as the cause of sudden cardiac death in this context, nor would a defect itself cause the described hypertrophy. **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. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, p. 536. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, p. 576.
Question 9: An athlete collapsed and expired while playing school basketball. Histology of the cardiac specimen is most likely to indicate which of the following conditions?
- A. Dilated cardiomyopathy (DCM)
- B. Restrictive cardiomyopathy (RCM)
- C. Arrhythmogenic right ventricular dysplasia (ARVD)
- D. Hypertrophic cardiomyopathy (HCM) (Correct Answer)
Explanation: ***Hypertrophic cardiomyopathy (HCM)*** - The image shows **myocardial disarray and hypertrophy**, characterized by haphazardly arranged and abnormally branched cardiac muscle cells with large, irregular nuclei, which is a classic histologic finding in HCM [1]. - HCM is the most common cause of **sudden cardiac death in young athletes**, often during exertion, due to ventricular arrhythmias arising from the disarrayed myocardium [1]. *Dilated cardiomyopathy (DCM)* - Histology for DCM typically shows **myocyte atrophy**, thinning of the ventricular walls, and interstitial fibrosis, not the marked disarray and hypertrophy seen here [3]. - DCM leads to **progressive cardiac enlargement and systolic dysfunction**, and while it can cause sudden death, it is less common in athletes than HCM [4]. *Restrictive cardiomyopathy (RCM)* - RCM is characterized by **stiff, non-compliant ventricles** with impaired diastolic filling, often due to conditions like amyloidosis or sarcoidosis, showing interstitial infiltration or fibrosis. - The image does not show evidence of significant **interstitial infiltration or severe fibrosis** characteristic of RCM; instead, it highlights myocyte pathology. *Arrhythmogenic right ventricular dysplasia (ARVD)* - ARVD is characterized by the **replacement of right ventricular myocardium with fibrofatty tissue**, which would be evident histologically as fat and fibrous infiltration [2]. - While ARVD can cause sudden death in athletes, the displayed image primarily shows **myocyte hypertrophy and disarray**, not extensive fibrofatty replacement [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 577-578. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 576-577. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, p. 576. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 559-560.
Question 10: Dilated cardiomyopathy is caused by which gene alteration?
- A. Titin (Correct Answer)
- B. Mitochondrial genes
- C. Dystrophin mutations
- D. Lamin A/C mutations
Explanation: ***Titin*** - **Titin** gene mutations are a well-known cause of **dilated cardiomyopathy**, affecting the structural integrity of cardiac myocytes [1]. - These mutations lead to **disruption in sarcomere architecture**, resulting in impaired cardiac function [1]. *Dystrophin* - Primarily associated with **Duchenne muscular dystrophy** and **Becker muscular dystrophy**, not directly causing dilated cardiomyopathy. - Deficiency of dystrophin typically affects skeletal muscle more than cardiac muscle. *Sarcomere* - While sarcomere protein mutations can cause cardiomyopathies, they are less specific than titin mutations for dilated cardiomyopathy. - Sarcomere mutations are often linked to **hypertrophic cardiomyopathy** rather than dilated types. *Mitochondrial genes* - Mutations in mitochondrial genes result in **metabolic disorders** like **mitochondrial myopathy** but are not a direct cause of dilated cardiomyopathy. - Mitochondrial dysfunctions typically present with multi-system involvement rather than isolated cardiac symptoms. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, p. 574.
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