A 67-year-old woman develops sudden, substernal chest pain. Laboratory studies and ECG confirm acute myocardial infarct of the left ventricle. Despite vigorous therapy, the patient cannot maintain her blood pressure and expires. Autopsy reveals occlusion of the left main coronary artery. What is the most important underlying cause of coronary artery thrombosis in this patient?
Acute inflammation
Coronary artery atherosclerosis
Cystic medial necrosis
Mycotic aneurysm
Systemic hypertension
The Correct Answer is B
A. Acute inflammation: While inflammation can contribute to plaque instability, acute inflammation alone is not the primary cause of coronary artery thrombosis. It may play a role in plaque rupture but does not directly cause occlusion in the absence of atherosclerosis.
B. Coronary artery atherosclerosis: Coronary atherosclerosis is the most common underlying cause of thrombosis leading to acute myocardial infarction. Plaque formation narrows the arterial lumen, and rupture or erosion of an atherosclerotic plaque triggers platelet aggregation and thrombus formation, resulting in sudden vessel occlusion and infarction.
C. Cystic medial necrosis: Cystic medial necrosis affects the aortic wall and predisposes to aneurysms or dissections, not coronary thrombosis. It does not directly narrow or occlude coronary arteries.
D. Mycotic aneurysm: Mycotic aneurysms result from infectious weakening of an arterial wall, usually in larger arteries. They are rare and do not commonly cause coronary artery thrombosis or acute myocardial infarction.
E. Systemic hypertension: Chronic hypertension contributes to vascular injury and accelerates atherosclerosis but is not the immediate cause of thrombotic occlusion. It is a risk factor rather than the direct etiologic agent of coronary thrombosis.
Nursing Test Bank
Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is A
Explanation
A. Asbestos:Asbestos exposure is strongly associated with pleural diseases, including pleural plaques, pleural thickening, and malignant mesothelioma. Inhaled asbestos fibers cause chronic inflammation and fibrosis, leading to interstitial lung disease with alveolar septal fibrosis and honeycomb changes, as described in this patient. Occupational exposure in mining or construction is a classic risk factor.
B. Cigarette smoke:Cigarette smoke is primarily linked to chronic bronchitis, emphysema, and lung carcinoma. While it can exacerbate lung damage in combination with asbestos, it does not cause pleural plaques or diffuse pleural encasement.
C. Coal:Coal dust exposure causes coal workers’ pneumoconiosis, which leads to nodular lung fibrosis, mainly in the upper lobes. It does not typically cause pleural plaques or mesothelioma, nor does it produce honeycomb changes throughout the lung.
D. Beryllium:Chronic beryllium disease leads to noncaseating granulomatous inflammation and interstitial fibrosis. It is not associated with pleural plaques or mesothelioma, making asbestos the more likely causal agent in this scenario.
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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