A client is brought by ambulance to the ED after experiencing what the family thinks is a stroke. The nurse caring for this client is aware that which is an absolute contraindication for thrombolytic therapy?

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.

Reasoning:

Choice A reason: Weight loss is not a typical side effect of corticosteroid therapy for Addison’s disease. Corticosteroids mimic cortisol, promoting weight gain through increased appetite and fat redistribution. Weight loss is more common in untreated Addison’s disease due to cortisol deficiency and reduced appetite.

Choice B reason: Poor wound healing is a side effect of corticosteroids, as they suppress immune responses and inhibit collagen synthesis. This impairs fibroblast activity and tissue repair, increasing infection risk and delaying wound closure, a significant concern for patients on long-term therapy for Addison’s disease.

Choice C reason: Hypertension is a common side effect of corticosteroids due to their mineralocorticoid effects, which increase sodium and water retention, elevating blood volume and pressure. This is particularly relevant in Addison’s disease treatment, where corticosteroids restore deficient aldosterone and cortisol, potentially causing fluid overload.

Choice D reason: Hypotension is not a side effect of corticosteroid therapy but a symptom of untreated Addison’s disease due to aldosterone deficiency, causing sodium loss and hypovolemia. Corticosteroid therapy corrects this, so hypotension is unlikely unless under-dosed or during acute crisis.

Choice E reason: Alterations in glucose metabolism are a side effect of corticosteroids, which induce insulin resistance and increase gluconeogenesis, leading to hyperglycemia. In Addison’s disease, corticosteroids replace deficient cortisol, but excess dosing can mimic Cushing’s syndrome, causing elevated blood glucose and requiring careful monitoring.