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Questions and Answers
What is the most common viral cause of myocarditis?
What is the most common viral cause of myocarditis?
Which type of myocarditis is characterized by a widespread inflammatory infiltrate and poor prognosis?
Which type of myocarditis is characterized by a widespread inflammatory infiltrate and poor prognosis?
What is a potential result of myocarditis when healing occurs?
What is a potential result of myocarditis when healing occurs?
What is a common symptom of chronic heart failure that may develop due to heart enlargement?
What is a common symptom of chronic heart failure that may develop due to heart enlargement?
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What type of infiltrate is typically seen in hypersensitivity myocarditis?
What type of infiltrate is typically seen in hypersensitivity myocarditis?
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What leads to the 'apical ballooning' commonly seen in the left ventricular apex?
What leads to the 'apical ballooning' commonly seen in the left ventricular apex?
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What role does aldosterone play in heart failure progression?
What role does aldosterone play in heart failure progression?
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Which complication is likely to arise from left atrial dilation due to mitral regurgitation?
Which complication is likely to arise from left atrial dilation due to mitral regurgitation?
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Which of the following is NOT a typical clinical feature of dilated cardiomyopathy (DCM)?
Which of the following is NOT a typical clinical feature of dilated cardiomyopathy (DCM)?
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What is one of the most common etiologies of dilated cardiomyopathy?
What is one of the most common etiologies of dilated cardiomyopathy?
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What is a characteristic feature of dilated cardiomyopathy?
What is a characteristic feature of dilated cardiomyopathy?
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Which of the following best describes hypertrophic cardiomyopathy?
Which of the following best describes hypertrophic cardiomyopathy?
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Which of the following applies to arrhythmogenic right ventricular cardiomyopathy?
Which of the following applies to arrhythmogenic right ventricular cardiomyopathy?
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In the context of dilated cardiomyopathy, which is a potential etiology?
In the context of dilated cardiomyopathy, which is a potential etiology?
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What histological finding is most commonly associated with hypertrophic cardiomyopathy?
What histological finding is most commonly associated with hypertrophic cardiomyopathy?
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What sequence of events leads to impaired myocardial perfusion in hypertrophic cardiomyopathy (HCM)?
What sequence of events leads to impaired myocardial perfusion in hypertrophic cardiomyopathy (HCM)?
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How does lightheadedness relate to cardiovascular dynamics when standing?
How does lightheadedness relate to cardiovascular dynamics when standing?
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What is a consequence of increased physical exertion in individuals with HCM?
What is a consequence of increased physical exertion in individuals with HCM?
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What effect do arrhythmias have on HCM symptoms?
What effect do arrhythmias have on HCM symptoms?
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What is the relationship between increased left ventricular (LV) obstruction and preload during lightheadedness?
What is the relationship between increased left ventricular (LV) obstruction and preload during lightheadedness?
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What is one of the primary characteristics of dilated cardiomyopathy (DCM)?
What is one of the primary characteristics of dilated cardiomyopathy (DCM)?
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Which compensatory mechanism is activated due to decreased renal perfusion in DCM?
Which compensatory mechanism is activated due to decreased renal perfusion in DCM?
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What is the likely outcome of severe myocyte contractility impairment in DCM?
What is the likely outcome of severe myocyte contractility impairment in DCM?
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How do the heart chambers typically change in DCM?
How do the heart chambers typically change in DCM?
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What is the role of angiotensin II in the pathophysiology of DCM?
What is the role of angiotensin II in the pathophysiology of DCM?
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What histological finding is observed in DCM?
What histological finding is observed in DCM?
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What does the increased stretch of myofibers in DCM lead to?
What does the increased stretch of myofibers in DCM lead to?
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Which mechanism is involved in compensating for decreased cardiac output in DCM?
Which mechanism is involved in compensating for decreased cardiac output in DCM?
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What is a potential consequence of chronic elevations in aldosterone and angiotensin II in DCM?
What is a potential consequence of chronic elevations in aldosterone and angiotensin II in DCM?
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What clinical feature may indicate left atrial dilation in a patient with DCM?
What clinical feature may indicate left atrial dilation in a patient with DCM?
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Which symptom reflects pulmonary venous congestion in DCM?
Which symptom reflects pulmonary venous congestion in DCM?
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Which condition is a potential complication of dilated cardiomyopathy related to cardiac remodeling?
Which condition is a potential complication of dilated cardiomyopathy related to cardiac remodeling?
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What is a characteristic sign of heart failure in a patient with dilated cardiomyopathy?
What is a characteristic sign of heart failure in a patient with dilated cardiomyopathy?
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What type of myocarditis may lead to chronic immune-mediated cardiac insufficiency years after the initial attack?
What type of myocarditis may lead to chronic immune-mediated cardiac insufficiency years after the initial attack?
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Which type of infiltration is commonly observed in giant cell myocarditis?
Which type of infiltration is commonly observed in giant cell myocarditis?
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Which of the following viruses is NOT commonly associated with myocarditis?
Which of the following viruses is NOT commonly associated with myocarditis?
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Which underlying mechanism is suggested to potentially cause apical ballooning in the left ventricular apex?
Which underlying mechanism is suggested to potentially cause apical ballooning in the left ventricular apex?
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Which type of myocarditis is characterized by perivascular interstitial infiltrates primarily consisting of eosinophils?
Which type of myocarditis is characterized by perivascular interstitial infiltrates primarily consisting of eosinophils?
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What is a direct consequence of increased wall stress in hypertrophic cardiomyopathy (HCM)?
What is a direct consequence of increased wall stress in hypertrophic cardiomyopathy (HCM)?
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How does standing affect preload and consequently left ventricular (LV) performance?
How does standing affect preload and consequently left ventricular (LV) performance?
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What characterizes the occurrence of syncope in individuals with HCM during physical exertion?
What characterizes the occurrence of syncope in individuals with HCM during physical exertion?
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Which factor primarily contributes to lightheadedness when a person stands up?
Which factor primarily contributes to lightheadedness when a person stands up?
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What impact do aberrant myocytes have on arrhythmias in HCM?
What impact do aberrant myocytes have on arrhythmias in HCM?
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What is the primary treatment for patients with Hypertrophic Cardiomyopathy (HCM) to manage their symptoms?
What is the primary treatment for patients with Hypertrophic Cardiomyopathy (HCM) to manage their symptoms?
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What clinical feature is best associated with the physical examination of Hypertrophic Cardiomyopathy?
What clinical feature is best associated with the physical examination of Hypertrophic Cardiomyopathy?
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Which of the following is a common consequence of Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC)?
Which of the following is a common consequence of Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC)?
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What is a critical consideration in the management of patients with HCM concerning physical activity?
What is a critical consideration in the management of patients with HCM concerning physical activity?
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What is a characteristic pathophysiological alteration in the myocardium of patients with HCM?
What is a characteristic pathophysiological alteration in the myocardium of patients with HCM?
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Which mutation is most likely responsible for the sudden collapse of the 19-year-old basketball player?
Which mutation is most likely responsible for the sudden collapse of the 19-year-old basketball player?
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What is the main characteristic finding on an echocardiogram in a patient with hypertrophic cardiomyopathy?
What is the main characteristic finding on an echocardiogram in a patient with hypertrophic cardiomyopathy?
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Which of the following cardiac conditions is most associated with ventricular tachycardia due to abnormalities in right ventricular activation?
Which of the following cardiac conditions is most associated with ventricular tachycardia due to abnormalities in right ventricular activation?
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What imaging technique can reveal abnormal right ventricular morphology in ARVC?
What imaging technique can reveal abnormal right ventricular morphology in ARVC?
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What type of wave may indicate abnormal right ventricular activation in an EKG reading?
What type of wave may indicate abnormal right ventricular activation in an EKG reading?
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Which cardiomyopathy is characterized primarily by a defect in energy transfer from mitochondria to the sarcomere?
Which cardiomyopathy is characterized primarily by a defect in energy transfer from mitochondria to the sarcomere?
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Which of the following is a common genetic cause of dilated cardiomyopathy?
Which of the following is a common genetic cause of dilated cardiomyopathy?
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Which condition is NOT a typical associated factor in dilated cardiomyopathy?
Which condition is NOT a typical associated factor in dilated cardiomyopathy?
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Study Notes
Dilated Cardiomyopathy (DCM)
- Definition: DCM is a heart muscle disease characterized by enlarged, weakened heart chambers that struggle to pump blood effectively.
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Etiology:
- Idiopathic (most common)
- Familial/Genetic
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Inflammatory:
- Infectious (Viral): Coxsackievirus A & B, parvovirus B19, adenovirus, ECHO, HIV, CMV, influenza
- Nonviral: Trypanasoma cruzi (Chagas Disease), Trichinella spiralis (Trichinosis), Toxoplasma gondii (Toxoplasmosis), Borrelia burgdorferi (Lyme Disease), Corynebacterium diphtheriae (Diptheria)
- Noninfectious: Hypersensitivity myocarditis, Giant cell myocarditis
- Toxic: Chronic alcohol ingestion, chronic cocaine use, chemotherapeutic agents
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Pathological Features:
- Gross Appearance: Heavy, large, flabby heart with dilation of all chambers. May be limited to one side.
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Microscopic Appearance:
- Enlarged nuclei and irregular hypertrophy of myocytes
- Attenuated, stretched, irregular, degenerated, and atrophic myocytes
- Interstitial, endocardial, and perivascular fibrosis
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Pathophysiology:
- ** Impaired myocyte contractility:** Decreases ventricle stroke volume (SV) and cardiac output (CO)
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Compensatory mechanisms:
- Frank-Starling Mechanism: Increased end-diastolic volume (EDV) leads to increased myofiber stretch, which increases contractile force and SV.
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Neurohormonal Activation:
- Decreased CO results in decreased renal perfusion, triggering the renin-angiotensin-aldosterone system (RAAS) activation.
- Sympathetic stimulation increases heart rate and contractility, further increasing CO.
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RAAS Activation:
- Angiotensin II increases systemic vascular resistance (SVR), making it difficult for a weakened LV to pump.
- Aldosterone increases intravascular/EDV, leading to fluid backup and pulmonary/systemic congestion.
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Clinical Features:
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Slow, progressive signs/symptoms of congestive heart failure (CHF):
- Cool extremities, low arterial pressure, tachycardia
- Pulmonary venous congestion leading to auscultatory crackles
- Left and upward displacement of the point of maximal impulse (PMI)
- Enlarged heart
- Third heart sound (S3)
- Complications: Mitral/Tricuspid regurgitation, atrial fibrillation, mural thrombus/thromboembolism
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Slow, progressive signs/symptoms of congestive heart failure (CHF):
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Prognosis:
- High mortality rate
- Death typically occurs from progressive cardiac failure or arrhythmia
Hypertrophic Cardiomyopathy (HCM)
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A heart muscle disease characterized by thickening of the heart muscle, particularly in the left ventricle.
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Etiology: Primarily genetic, caused by mutations in genes responsible for cardiac proteins.
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Pathogenesis:
- Increased wall stress: Due to increased myocardial oxygen demand.
- Hypertrophy: Squeezes down on small coronary branches, impairing myocardial perfusion.
- Outflow obstruction: The thickened heart muscle can obstruct blood flow from the left ventricle, leading to a reduction in CO.
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Pathological Features:
- Gross Appearance: Enlarged heart, particularly the left ventricle
- Microscopic Appearance: Hypertrophic myocytes with disorganized arrangement.
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Pathophysiology:
- Aberrant myocytes: Within the conduction system, leading to abnormal conduction and arrhythmias.
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Clinical Features:
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Symptoms:
- Chest pain
- Dyspnea
- Syncope
- Arrhythmias
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Physical exam findings:
- Hyperdynamic precordium
- A fourth heart sound (S4)
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Symptoms:
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Treatment:
- Medical: Beta-blockers, calcium channel blockers, antiarrhythmics
- Surgical: Septal myectomy, alcohol septal ablation
- Devices: Implantable cardioverter-defibrillator (ICD)
Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC)
- A rare heart muscle disease characterized by the replacement of heart muscle with fat and fibrous tissue.
- Etiology: Primarily genetic, associated with mutations in genes involved in desmosome formation.
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Pathogenesis:
- Genetic: Leads to abnormalities in the cell-to-cell connections of heart muscle cells, making them more prone to damage and death.
- Replacement of muscle with fat and fibrosis: This disrupts the normal electrical activity of the heart, leading to arrhythmias.
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Clinical Features:
- Symptoms: Arrhythmias, palpitations, syncope, sudden cardiac death
- Physical exam findings: May have a heart murmur.
Comparison of Dilated and Hypertrophic Cardiomyopathy
Feature | Dilated Cardiomyopathy | Hypertrophic Cardiomyopathy |
---|---|---|
Heart muscle | Weak, stretched, and thin | Thick, stiff |
Heart chambers | Enlarged | Normal or slightly enlarged |
Blood flow | Reduced due to weak pumping | Obstructed due to thickened heart muscle |
Symptoms | Congestive heart failure, fatigue, shortness of breath | Syncope, chest pain, arrhythmias |
Treatment | Medications, heart transplant | Medications, surgical myectomy, alcohol septal ablation |
Hypertrophic Cardiomyopathy
- 19-year-old college student with a family history of sudden death, collapses suddenly during basketball
- EKG shows ventricular tachycardia and ventricular fibrillation
- Patient resuscitated and hospitalized, but dies suddenly 3 years later
- Echocardiogram reveals thickened left ventricular wall and small chamber
- Interventricular septum markedly thickened
- Most likely mutation in a sarcomeric protein, causing hypertrophic cardiomyopathy
Hypertrophic Cardiomyopathy Pathophysiology
- Genetic condition, often inherited
- Mutation in sarcomeric proteins leads to impaired energy transfer from mitochondria to the sarcomere
- Results in excessive hypertrophy of the left ventricle muscle
- Thickened ventricular septum can obstruct blood flow out of the left ventricle.
- Impaired muscle function and blood flow can lead to arrhythmias like ventricular tachycardia and fibrillation.
- Sudden death is a major risk due to cardiac arrhythmias.
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Description
This quiz covers the essential aspects of Dilated Cardiomyopathy (DCM), a condition where the heart chambers become enlarged and weakened. It includes information about its definition, etiology, pathological features, and various infectious and non-infectious causes. Test your knowledge of this significant heart disease.