A 55-year-old male was admitted 1 week ago for a left lower leg venous thromboembolism, confirmed by ultrasound. He started to work from home 4 months ago and reports that his activity level has significantly decreased. When admitted, his left lower leg had 3+ edema and was warm and reddened over the calf area. He was immediately started on intravenous heparin therapy, with warfarin (Coumadin) on the same day. The patient asks the nurse why two medications are necessary. Which response by the nurse is accurate?

Choice A reason: Decreasing blood glucose levels are not an indicator of effective therapy in patients with acute adrenal insufficiency. In fact, hypoglycemia is a common symptom of Addison's Disease due to insufficient cortisol production, and effective therapy would aim to normalize blood glucose levels, not decrease them further.
Choice B reason: Increasing serum potassium levels would indicate worsening of the condition rather than improvement. Hyperkalemia is a hallmark of Addison's Disease due to aldosterone deficiency, and effective therapy should decrease serum potassium levels, not increase them.
Choice C reason: Increasing serum sodium levels would indicate that the therapy is effective for acute adrenal insufficiency. Addison's Disease is characterized by hyponatremia due to aldosterone deficiency, and effective treatment aims to normalize sodium levels in the blood. An increase in serum sodium levels indicates that the treatment is correcting the underlying electrolyte imbalance.
Choice D reason: Decreasing serum chloride levels are not a specific indicator of effective therapy for Addison's Disease. Chloride levels are generally less affected and not a primary marker for assessing treatment efficacy. The main focus should be on correcting sodium and potassium imbalances.

Choice A reason:
Increasing serum potassium levels would not indicate effective therapy for a patient with Addison's disease. In Addison's disease, the adrenal glands do not produce enough aldosterone, which is responsible for regulating sodium and potassium balance. As a result, patients with Addison’s disease often experience hyperkalemia (high potassium levels). Effective therapy typically aims to normalize potassium levels, so an increase would suggest inadequate treatment or worsening of the condition.
Choice B reason:
Decreasing blood glucose levels would not typically be seen as a positive indicator in a patient with Addison's disease. The body’s ability to maintain normal blood glucose levels is compromised in Addison’s disease due to a deficiency in cortisol. Cortisol plays a key role in regulating glucose metabolism, and its deficiency can lead to hypoglycemia (low blood glucose levels). If blood glucose levels are decreasing, it may indicate inadequate glucocorticoid replacement therapy, suggesting the therapy is not fully effective.
Choice C reason:
Decreasing serum chloride levels would not be expected in a patient with Addison’s disease who is receiving proper treatment. Chloride is regulated alongside sodium and is influenced by aldosterone. In Addison's disease, aldosterone deficiency leads to a decreased ability to retain sodium, which in turn can affect chloride levels. However, a decrease in chloride levels alone is not a clear sign of effective therapy. Normalization of serum sodium levels is a better indicator of treatment success.
Choice D reason:
Increasing serum sodium levels is the correct finding that indicates effective therapy in a patient with Addison’s disease. In this condition, aldosterone deficiency results in sodium loss through the kidneys, leading to hyponatremia (low sodium levels). Effective therapy, which typically involves the administration of glucocorticoids and mineralocorticoids (such as fludrocortisone), helps to correct this imbalance by increasing sodium retention and normalizing serum sodium levels. This would demonstrate that the current therapies are working to restore the electrolyte balance.