Thrombolytic therapy should be initiated within what time frame of an ischemic stroke to achieve the best functional outcome?
12 hours
9 hours
3 hours
6 hours
The Correct Answer is C
Reasoning:
Choice A reason: Initiating thrombolytic therapy within 12 hours is too late for optimal ischemic stroke outcomes. Beyond 4.5 hours, the risk of hemorrhage outweighs benefits, as ischemic tissue becomes necrotic, reducing the effectiveness of thrombolytics like tPA in restoring blood flow and improving function.
Choice B reason: A 9-hour window for thrombolytic therapy exceeds the recommended time frame for ischemic stroke. After 4.5 hours, the risk of hemorrhagic transformation increases, and neuronal salvage is less likely due to prolonged ischemia, making this time frame ineffective for achieving optimal functional recovery.
Choice C reason: Thrombolytic therapy within 3 hours of ischemic stroke onset maximizes functional outcomes. Tissue plasminogen activator (tPA) dissolves clots, restoring blood flow to viable brain tissue. Early administration minimizes neuronal damage, reduces disability, and improves recovery, with guidelines supporting a 3–4.5-hour window for eligible patients.
Choice D reason: A 6-hour window for thrombolytics is beyond the optimal 3–4.5-hour period for ischemic stroke. While some patients may benefit up to 4.5 hours, delays increase hemorrhage risk and reduce the likelihood of salvaging ischemic tissue, leading to poorer functional outcomes compared to earlier intervention.
Nursing Test Bank
Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is B
Explanation
Reasoning:
Choice A reason: An increased number of erythrocytes is not indicative of iron-deficiency anemia, which is characterized by reduced red blood cell production due to low iron availability for hemoglobin synthesis. Increased erythrocytes suggest compensatory mechanisms or polycythemia, not the reduced erythropoiesis seen in iron deficiency.
Choice B reason: Microcytic and hypochromic erythrocytes are hallmarks of iron-deficiency anemia. Low iron impairs hemoglobin synthesis, leading to smaller (microcytic) and paler (hypochromic) red blood cells. This matches the client’s low hemoglobin and hematocrit, confirming iron deficiency as the cause of the anemia.
Choice C reason: Clustering of platelets with sickled red blood cells is specific to sickle cell anemia, not iron-deficiency anemia. Sickle cell disease involves hemoglobin S, causing cell deformation, not iron deficiency. Platelet clustering is unrelated to the microcytic, hypochromic cells of iron deficiency.
Choice D reason: Macrocytic and hyperchromic erythrocytes suggest megaloblastic anemia, typically from vitamin B12 or folate deficiency, not iron deficiency. Iron-deficiency anemia produces microcytic, hypochromic cells due to impaired hemoglobin synthesis, making macrocytic, hyperchromic cells inconsistent with the client’s laboratory findings.
Correct Answer is D
Explanation
Reasoning:
Choice A reason: Bundle branch block affects ventricular conduction but does not typically cause emboli. It may lead to dyssynchrony but lacks the stasis in the atria that promotes clot formation, making it less associated with cardiogenic embolic strokes compared to atrial fibrillation’s thrombus-forming mechanism.
Choice B reason: Ventricular tachycardia is a life-threatening arrhythmia affecting the ventricles, causing hemodynamic instability but not typically embolic strokes. It does not promote atrial stasis or clot formation, which are necessary for cardiogenic emboli to travel to the brain, unlike atrial fibrillation.
Choice C reason: Supraventricular tachycardia causes rapid heart rates above the ventricles but is less likely to form atrial clots than atrial fibrillation. It does not typically cause the prolonged stasis needed for thrombus formation, making it less associated with embolic strokes in the brain.
Choice D reason: Atrial fibrillation is strongly associated with cardiogenic embolic strokes. It causes irregular atrial contractions, leading to blood stasis in the atria, promoting thrombus formation. These clots can embolize to the brain, causing ischemic stroke, making it a key risk factor requiring anticoagulation.
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