A 69-year-old man Is brought to be Emergency Department because of the sudden-onset of left-sided chest pain that is exacerbated upon inspiration. Physical examination reveals dyspnea and hemoptysis. His temperature is 38’C (101”F), pulse is 110/min. respirations are 35/min. and blood pressure is 158/100 mm Hg. A lateral chest wall friction rub is present on auscultation. The left leg Is markedly edematous. A chest x-ray reveals a left pleural effusion. What is the most likely cause of this patient” s left-sided chest pain, pleural effusion. dyspnea, and hemoptysis?
Congestive heart failure Cor pulmonale
Diffuse alveolar damage
Pulmonary thromboembolism
Sub acute bacterial endocarditis
The Correct Answer is C
A. Congestive heart failure (Cor pulmonale): Congestive heart failure can cause pleural effusions and dyspnea, but the effusions are typically bilateral and not associated with acute pleuritic chest pain or hemoptysis. Cor pulmonale develops secondary to chronic pulmonary hypertension and presents more gradually, rather than with sudden-onset chest pain
B. Diffuse alveolar damage: Diffuse alveolar damage, seen in acute respiratory distress syndrome (ARDS), presents with severe hypoxemia and diffuse bilateral infiltrates on imaging. It does not typically cause unilateral pleuritic chest pain, hemoptysis, or a localized pleural effusion, nor is it associated with unilateral leg edema suggestive of deep vein thrombosis.
C. Pulmonary thromboembolism: Sudden pleuritic chest pain, dyspnea, tachycardia, hemoptysis, and low-grade fever strongly suggest pulmonary embolism. The markedly edematous leg indicates possible deep vein thrombosis, the most common source of emboli. Pulmonary infarction can cause pleural irritation, resulting in a friction rub and small pleural effusion visible on chest x-ray.
D. Subacute bacterial endocarditis: Subacute bacterial endocarditis presents with prolonged fever, heart murmurs, and embolic phenomena, but it is less likely to cause isolated pleuritic chest pain with hemoptysis and unilateral pleural effusion. The acute onset and presence of deep vein thrombosis signs make pulmonary embolism a far more probable cause.
Nursing Test Bank
Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is C
Explanation
A. Chronic obstructive pulmonary disease:COPD primarily causes hypoxia-induced pulmonary vasoconstriction, leading to right ventricular hypertrophy (cor pulmonale), not left ventricular enlargement. Left ventricular dilation in this patient is unlikely to be caused by COPD alone.
B. Coronary artery atherosclerosis:Coronary artery disease can lead to ischemic injury and myocardial infarction, which may cause localized wall thinning or remodeling. While it can contribute to heart failure, generalized left ventricular enlargement is more directly linked to chronic pressure or volume overload rather than focal ischemia.
C. Increased cardiac workload:Chronic increased workload, such as from systemic hypertension or valvular disease, causes the left ventricle to undergo hypertrophy and dilation to maintain cardiac output. Over time, these adaptive changes lead to left ventricular enlargement, which is commonly observed in patients with chronic congestive heart failure.
D. Pulmonary thromboembolism:Pulmonary embolism primarily increases right-sided pressures, leading to acute right ventricular strain or chronic cor pulmonale if recurrent. It does not directly cause left ventricular enlargement.
E. Viral myocarditis:Viral myocarditis can cause diffuse myocardial inflammation and sometimes dilated cardiomyopathy. However, in elderly patients with a long history of congestive heart failure, the more common mechanism for left ventricular enlargement is chronic increased workload rather than acute viral injury.
Correct Answer is C
Explanation
A. Chronic inflammation:Chronic inflammation involves infiltration of tissues by lymphocytes and macrophages and is seen in conditions such as chronic infections or autoimmune disorders. It is not the primary feature of varicose veins, esophageal varices, hemorrhoids, or varicoceles, which are structural vascular abnormalities.
B. Cystic medial necrosis:Cystic medial necrosis involves degeneration of the elastic and muscular components of arterial walls and is typically associated with aortic aneurysms or Marfan syndrome. It does not describe venous dilatation or tortuosity seen in varicosities.
C. Enlarged and tortuous blood vessels:Varicose veins, esophageal varices, hemorrhoids, and varicoceles are all characterized by dilated, elongated, and tortuous veins. These changes result from increased venous pressure, valve incompetence, or venous obstruction, leading to the visible or palpable vascular abnormalities.
D. Hyaline arteriosclerosis:Hyaline arteriosclerosis involves deposition of homogeneous hyaline material in small arteries and arterioles, usually from chronic hypertension or diabetes. It affects arterial walls rather than veins and is unrelated to varicosities.
E. Severe atherosclerosis:Atherosclerosis is a disease of arterial walls involving lipid deposition, fibrosis, and plaque formation. It affects arteries rather than veins and does not produce the tortuous dilatation characteristic of varicose veins or other venous varicosities.
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