How do antiplatelet medications work?
Stimulate the plasmin system.
Alter the formation of the platelet plug.
Initiate the clotting cascade.
Interfere with the clotting cascade.
The Correct Answer is B
Choice A rationale
Antiplatelets do not stimulate the plasmin system, which is involved in breaking down clots.
Choice B rationale
Antiplatelet medications work by altering the formation of the platelet plug, preventing platelets from clumping together.
Choice C rationale
They do not initiate the clotting cascade, which is a separate process from platelet aggregation.
Choice D rationale
They do not interfere with the clotting cascade directly but affect platelet aggregation. .
Nursing Test Bank
Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is D
Explanation
Choice A rationale
Chronic Obstructive Pulmonary Disease (COPD) is a progressive disease characterized by obstructed airflow from the lungs. While related to respiratory health, it is distinct from tuberculosis.
Choice B rationale
Bronchiectasis is a condition involving the permanent enlargement of parts of the airways of the lung, often caused by infection or other lung conditions but is different from tuberculosis.
Choice C rationale
Emphysema is a chronic lung condition where the alveoli (air sacs) are damaged, leading to breathing difficulties. This condition is usually associated with smoking and is distinct from tuberculosis.
Choice D rationale
Consumption is an old term for tuberculosis, reflecting the wasting away (consuming) nature of the disease due to the progressive weight loss and weakness it causes.
Correct Answer is B
Explanation
Choice A rationale
Plaque formation in arteries does not start with platelets and fibrin.
Choice B rationale
Plaque begins with fatty streaks, which are the earliest signs of atherosclerosis and consist of lipid-laden cells in the arterial wall.
Choice C rationale
White blood cells are involved in the inflammatory process of atherosclerosis but do not represent the initial plaque formation.
Choice D rationale
Foam cells, which are lipid-laden macrophages, develop later in the process of plaque formation and contribute to the growth of atherosclerotic lesions. .
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