A client with hypothyroidism was prescribed levothyroxine (Synthroid), a T4 replacement. The client was reading about hypothyroidism and asked the nurse why they are receiving only T4 replacement when hypothyroidism causes low T3 and T4 levels. What is the best response by the nurse?
T4 replacement does not require any TSH monitoring as is required with T3
Your body effectively converts T4 into T3 so replacing T3 is unnecessary
T3 and T4 cannot be administered together because they will become inactive
Drug therapy does not replace T3 because it is the inactive precursor to T4
The Correct Answer is B
Reasoning:
Choice A reason: Levothyroxine (T4) replacement requires TSH monitoring to ensure adequate dosing, as TSH reflects thyroid function. T3 replacement also requires monitoring, but T3 is less commonly used due to its short half-life. This statement is inaccurate, as TSH monitoring is essential for T4 therapy.
Choice B reason: The body converts levothyroxine (T4) to triiodothyronine (T3) via deiodinase enzymes in peripheral tissues, restoring both hormone levels. T3 replacement is unnecessary, as T4 provides a stable precursor for T3 production, making this statement accurate for explaining hypothyroidism treatment rationale.
Choice C reason: T3 and T4 can be administered together in specific cases (e.g., combination therapy) without becoming inactive. However, T4 alone is standard due to its longer half-life and conversion to T3. This statement is inaccurate, as it falsely claims biochemical incompatibility between the hormones.
Choice D reason: T3 is the active thyroid hormone, not an inactive precursor to T4. T4 is converted to T3, which binds receptors to regulate metabolism. This statement is inaccurate, as it reverses the roles of T3 and T4 in thyroid hormone physiology and therapy.
Nursing Test Bank
Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is C
Explanation
Choice A reason: Bladder cancer primarily affects the bladder, causing hematuria or obstruction, leading to post-renal injury, not intra-renal. Intra-renal damage involves nephron injury, which is less likely with bladder cancer unless advanced metastasis affects kidneys, making this patient less at risk than one on nephrotoxic chemotherapy.
Choice B reason: Benign prostatic hyperplasia causes urinary obstruction, leading to post-renal kidney injury from backpressure, not intra-renal damage. The kidneys’ nephrons are not directly harmed by BPH, making this 65-year-old male less at risk for intra-renal injury compared to a patient receiving nephrotoxic drugs.
Choice C reason: Chemotherapy, especially agents like cisplatin, is nephrotoxic, causing intra-renal acute kidney injury by damaging renal tubules. This 25-year-old female faces high risk due to direct tubular toxicity, leading to acute tubular necrosis, making her the most likely to develop intra-renal injury among the options.
Choice D reason: Renal artery stenosis causes pre-renal kidney injury by reducing renal perfusion, not intra-renal damage. The nephrons remain intact unless chronic ischemia leads to secondary damage. This 36-year-old female has a lower risk of intra-renal injury compared to the chemotherapy patient’s direct nephrotoxic exposure.
Correct Answer is D
Explanation
Choice A reason: Chronic kidney disease (CKD) does not primarily cause anemia by leaking red blood cells (RBCs) into urine. While hematuria may occur in some renal conditions, anemia in CKD results mainly from reduced erythropoietin production, not RBC loss. This statement is inaccurate, as it misrepresents the primary mechanism of anemia in CKD.
Choice B reason: Inflammation in CKD may contribute to anemia by suppressing erythropoiesis through cytokine release, but it does not directly attack RBCs. The primary cause is erythropoietin deficiency due to impaired renal function. This statement is inaccurate, as it overstates inflammation’s role and ignores the key hormonal mechanism in CKD-related anemia.
Choice C reason: High vascular pressure in CKD can damage kidneys but does not directly cause RBCs to burst (hemolysis). Anemia in CKD stems from reduced erythropoietin, not mechanical RBC destruction. This statement is inaccurate, as it incorrectly links hypertension’s renal effects to direct RBC damage, misrepresenting the anemia’s cause.
Choice D reason: CKD causes anemia due to reduced erythropoietin synthesis by damaged kidneys. Erythropoietin stimulates RBC production in bone marrow. In CKD, impaired renal function decreases erythropoietin, leading to anemia. This statement is accurate, as it correctly identifies the hormonal deficiency as the primary cause of low RBC counts in CKD.
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