A patient who has been receiving IV heparin infusion and oral warfarin (Coumadin) for a deep vein thrombosis (DVT) is diagnosed with heparin-induced thrombocytopenia (HIT) when the platelet level drops to 80,000/uL. Which action will the nurse take first?

Choice A reason: This statement is incorrect because the combination of heparin and warfarin does not dissolve the blood clot faster. Instead, these medications have different mechanisms of action. Heparin works quickly to prevent further clot formation, while warfarin takes several days to reach therapeutic levels and maintain anticoagulation over the long term.
Choice B reason: While the risk of a blood clot in the lungs (pulmonary embolism) is a concern, the necessity of using both heparin and warfarin is not because of the need for multiple blood thinners but rather due to their complementary pharmacokinetics. Heparin provides immediate anticoagulation, whereas warfarin requires time to become effective.
Choice C reason: This statement is also incorrect. Heparin does not dissolve clots but works to prevent the extension of existing clots and the formation of new ones. Warfarin, likewise, does not dissolve clots but prevents further clot formation by inhibiting vitamin K-dependent clotting factors.
Choice D reason: This is the accurate response. Heparin works immediately, providing rapid anticoagulation, which is essential for acute management of venous thromboembolism. On the other hand, warfarin takes several days to achieve its anticoagulant effect because it works by inhibiting the synthesis of vitamin K-dependent clotting factors. Therefore, the patient is initially placed on heparin to provide immediate protection against clotting while warfarin is started simultaneously. Once warfarin reaches a therapeutic level, heparin can be discontinued, and warfarin can maintain long-term anticoagulation.

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.