A 65-year-old woman is diagnosed who "angina pectoris”. What causes this condition?
Bacterial endocarditis
ischemic heart disease
Left ventricular hypertrophy
Marantic endocarditis
Mural thrombosis
The Correct Answer is B
A. Bacterial endocarditis: Bacterial endocarditis involves infection of the heart valves, leading to vegetations, fever, and potential embolic events. It does not typically present with exertional chest pain relieved by rest, which is characteristic of angina pectoris caused by myocardial ischemia.
B. Ischemic heart disease: Angina pectoris results from transient myocardial ischemia due to reduced coronary blood flow, most commonly from atherosclerotic narrowing of coronary arteries. The imbalance between myocardial oxygen supply and demand produces chest pain without myocardial necrosis, defining stable angina in ischemic heart disease.
C. Left ventricular hypertrophy: Left ventricular hypertrophy develops in response to chronic pressure overload, such as from hypertension. Although it may increase myocardial oxygen demand, it is not the primary cause of angina; the underlying issue is usually compromised coronary perfusion.
D. Marantic endocarditis: Marantic (nonbacterial thrombotic) endocarditis is associated with hypercoagulable states and malignancy, leading to sterile vegetations on valves. It does not directly cause the exertional chest pain typical of angina pectoris.
E. Mural thrombosis: Mural thrombosis refers to clot formation along the endocardial surface, often after myocardial infarction. While it can lead to embolic complications, it is not the underlying mechanism responsible for angina, which stems from transient coronary artery insufficiency.
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Related Questions
Correct Answer is D
Explanation
A. Congestive heart failure:Congestive heart failure can cause dyspnea and pulmonary congestion, but hemoptysis and sudden pleuritic chest pain are not classic presenting features. CHF-related pulmonary edema usually produces pink, frothy sputum rather than frank blood and develops in the context of volume overload rather than acute embolic events.
B. Cor pulmonale:Cor pulmonale refers to right ventricular hypertrophy and failure secondary to chronic pulmonary hypertension. It develops gradually in patients with chronic lung disease and presents with peripheral edema and fatigue, not sudden chest pain and hemoptysis.
C. Phlebothrombosis:Phlebothrombosis refers to thrombus formation in a vein, often in the lower extremities, especially in patients with varicose veins. While it is the underlying source of emboli, it does not directly cause chest pain or hemoptysis unless a clot dislodges and travels to the lungs.
D. Pulmonary thromboembolism:Pulmonary thromboembolism occurs when a thrombus, often originating from deep leg veins, embolizes to the pulmonary arteries. Sudden chest pain and hemoptysis result from pulmonary infarction and pleural irritation. Varicose veins increase venous stasis, predisposing to thrombosis and subsequent embolism.
E. Pulmonary edema:Pulmonary edema involves fluid accumulation in the alveoli, most commonly due to left-sided heart failure. It causes dyspnea and crackles but does not typically present with sudden pleuritic chest pain and hemoptysis linked to venous thromboembolic risk factors.
Correct Answer is D
Explanation
A. Cryptococcus sp.:Cryptococcusspecies are fungi that primarily affect immunocompromised individuals, causing meningitis and pulmonary infections. They are not associated with post-infectious autoimmune reactions like rheumatic fever.
B. Neisseria sp.:Neisseriaspecies, such as N. meningitidisor N. gonorrhoeae, cause meningitis or urogenital infections, respectively. These infections do not trigger the autoimmune response leading to rheumatic fever.
C. Plasmodium sp.:Plasmodiumspecies are protozoa responsible for malaria. Malaria is not linked to autoimmune sequelae like rheumatic fever following infection.
D. Streptococcus sp.:Rheumatic fever is a delayed autoimmune complication of infection with Streptococcus pyogenes(group A beta-hemolytic streptococcus). Molecular mimicry between bacterial M proteins and host tissues triggers inflammation affecting the heart, joints, skin, and central nervous system.
E. Treponema sp.:Treponema pallidumcauses syphilis. While it can have cardiovascular and neurologic effects in later stages, it does not induce post-infectious autoimmune reactions like rheumatic fever.
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