A client who has experienced an initial transient ischemic attack (TIA) states: “I’m glad it wasn’t anything serious.” Which is the best nursing response to this statement?

Reasoning:

Choice A reason: Sickle cell disease is a hemolytic anemia caused by a hemoglobin mutation, not low iron. Laboratory findings show normal or elevated iron due to hemolysis, not low serum iron, transferrin saturation, or ferritin, which are specific to iron deficiency, ruling out sickle cell anemia.

Choice B reason: Pernicious anemia results from vitamin B12 deficiency, impairing DNA synthesis and red blood cell maturation. It is not associated with low serum iron, transferrin saturation, or ferritin, which reflect iron stores. Pernicious anemia typically shows megaloblastic changes, not microcytic anemia, unlike iron deficiency.

Choice C reason: Hemolytic anemia involves red blood cell destruction, often increasing iron levels due to hemoglobin breakdown. Low serum iron, transferrin saturation, and ferritin are not typical, as hemolysis does not deplete iron stores. These findings point to iron deficiency, not hemolytic processes.

Choice D reason: Iron deficiency anemia is characterized by low serum iron, transferrin saturation, and ferritin, reflecting depleted iron stores. Iron is essential for hemoglobin synthesis, and its deficiency causes microcytic, hypochromic anemia, leading to fatigue, matching the client’s laboratory findings and clinical presentation accurately.

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.