A client who has experienced an ischemic stroke has been admitted to the medical unit. The client’s family is adamant that the client remain on bed rest to hasten recovery and to conserve energy. What principle of care should inform the nurse’s response to the family?
To prevent contractures and muscle atrophy, bed rest should not exceed 4 weeks
The client should mobilize as soon as physically able
The client should remain on bed rest until the client expresses a desire to mobilize
Lack of mobility will greatly increase the client’s risk of stroke recurrence
The Correct Answer is B
Reasoning:
Choice A reason: Limiting bed rest to 4 weeks to prevent contractures and atrophy is not the primary principle. While prolonged immobility causes these issues, early mobilization post-stroke improves recovery and prevents complications like thromboembolism, making immediate mobilization the key focus rather than a time limit.
Choice B reason: Mobilizing as soon as physically able is critical post-ischemic stroke to enhance recovery. Early mobilization improves circulation, prevents thromboembolism, maintains muscle strength, and promotes neuroplasticity, reducing disability. This principle counters the family’s insistence on bed rest, which increases complication risks and hinders recovery.
Choice C reason: Waiting for the client to express a desire to mobilize delays recovery. Stroke patients may lack initiative due to neurological deficits or depression. Early mobilization, guided by physical ability, prevents complications like deep vein thrombosis and supports rehabilitation, making patient desire a poor criterion.
Choice D reason: Lack of mobility does not directly increase stroke recurrence risk, which is more tied to vascular risk factors like hypertension or diabetes. However, immobility increases complications like thromboembolism, which could indirectly contribute to stroke. Early mobilization is the priority to enhance overall recovery.
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Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is C
Explanation
Reasoning:
Choice A reason: Thiazide diuretics reduce urine output in nephrogenic diabetes insipidus by increasing sodium excretion, which enhances water reabsorption indirectly. However, they are not the primary treatment for central diabetes insipidus, where ADH deficiency is the issue. Desmopressin, an ADH analog, directly addresses the hormonal deficiency, making thiazides less effective.
Choice B reason: Diabinese (chlorpropamide) is a sulfonylurea used for type 2 diabetes mellitus, not diabetes insipidus. It lowers blood glucose by stimulating insulin release, which is irrelevant to the water balance issue in diabetes insipidus caused by ADH deficiency. It does not address the underlying hormonal imbalance.
Choice C reason: Desmopressin (DDAVP) is a synthetic ADH analog used to treat central diabetes insipidus. It mimics ADH, promoting water reabsorption in the kidneys’ collecting ducts, reducing polyuria and thirst. This directly corrects the fluid imbalance caused by ADH deficiency, making it the primary and most effective treatment.
Choice D reason: Ibuprofen, a nonsteroidal anti-inflammatory drug, is used for pain and inflammation, not for fluid balance in diabetes insipidus. It has no effect on ADH or renal water reabsorption, making it irrelevant for treating the excessive urine output and dehydration associated with this condition.
Correct Answer is D
Explanation
Reasoning:
Choice A reason: Decreased pain tolerance may occur in chronic conditions, but it is not the primary mechanism of pain in a sickle cell crisis. Pain results from vaso-occlusion by sickled red blood cells, causing tissue ischemia, not a psychological or tolerance issue, making this explanation incorrect.
Choice B reason: Overhydration does not enlarge red blood cells or cause sickle cell crises. Dehydration can trigger sickling by increasing blood viscosity, but overhydration dilutes plasma, potentially reducing sickling. Pain in crises stems from vaso-occlusion, not cell size changes due to fluid status.
Choice C reason: Bone marrow in sickle cell anemia increases, not decreases, erythrocyte production to compensate for chronic hemolysis. Hypoxia results from vaso-occlusion, not reduced production, as sickled cells block vessels, impairing oxygen delivery, making this an incorrect explanation for crisis-related pain.
Choice D reason: Vascular occlusion in small vessels by sickled red blood cells is the primary mechanism of sickle cell crisis pain. Sickled cells obstruct microvasculature, reducing blood flow and oxygen delivery, causing tissue ischemia and severe pain, accurately explaining the client’s symptoms in the emergency department.
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