A nurse is caring for a client who has a diagnosis of immune thrombocytopenic purpura (ITP). Despite medication therapy, the client's platelets are low. Which of the following procedures would reduce the destruction of platelets for a client who has ITP?
Transfusion of platelets
Replacement of ADAMTS-13
Administration of protamine sulfate
Laparoscopic splenectomy
The Correct Answer is D
A. While a platelet transfusion can temporarily increase platelet counts, it does not reduce the destruction of platelets in ITP and is generally not effective as a long-term solution.
B. Replacement of ADAMTS-13 is relevant in thrombotic thrombocytopenic purpura (TTP), not ITP. It is not used for reducing platelet destruction in ITP.
C. Protamine sulfate is an antidote for heparin overdose and does not address the platelet destruction in ITP.
D. A laparoscopic splenectomy is often considered for clients with ITP who do not respond to medication therapy. The spleen is a primary site for platelet destruction, and its removal can reduce the destruction of platelets, leading to increased platelet counts.
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Related Questions
Correct Answer is D
Explanation
A. Apixaban is an anticoagulant used to prevent clot formation and reduce stroke risk, not specifically to reduce bleeding risk.
B. Rate control is typically achieved with medications like beta-blockers or calcium channel blockers, not anticoagulants like apixaban.
C. Apixaban does not convert heart rhythm; it prevents blood clots.
D. The primary purpose of apixaban in patients with atrial fibrillation is to reduce the risk of stroke by preventing blood clot formation.
Correct Answer is D
Explanation
A. Romiplostim does not increase the production of ADAMTS-13; it is used to increase platelet counts.
B. Romiplostim does not prevent platelet destruction in the spleen; it works by stimulating platelet production.
C. Romiplostim does not prevent platelets from binding with heparin; it is not used for heparin-induced thrombocytopenia.
D. Romiplostim is a thrombopoietin receptor agonist that stimulates the bone marrow to increase platelet production, which is its primary mechanism of action in treating ITP.
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