A client has a history of sickle cell anemia with several sickle cell crises over the past 10 years. What blood component results in sickle cell anemia?
Hemoglobin A
Hemoglobin S
Hemoglobin M
Hemoglobin F
The Correct Answer is B
Reasoning:
Choice A reason: Hemoglobin A is the normal adult hemoglobin, comprising two alpha and two beta chains. In sickle cell anemia, a mutation in the beta-globin gene produces hemoglobin S, not hemoglobin A, which does not cause sickling or the vaso-occlusive crises characteristic of the disease.
Choice B reason: Hemoglobin S is the abnormal hemoglobin in sickle cell anemia, resulting from a point mutation in the beta-globin gene. This causes red blood cells to sickle under stress, leading to hemolysis and vaso-occlusion, resulting in pain, organ damage, and the clinical features of sickle cell crises.
Choice C reason: Hemoglobin M is a rare hemoglobin variant causing methemoglobinemia, not sickle cell anemia. It results from mutations affecting heme iron, leading to cyanosis, not the sickling and vaso-occlusion seen with hemoglobin S, making it irrelevant to the client’s condition.
Choice D reason: Hemoglobin F, or fetal hemoglobin, is present in newborns and persists in small amounts in adults. In sickle cell anemia, increased hemoglobin F can reduce sickling, but it is not the cause. Hemoglobin S drives the disease’s pathophysiology, not hemoglobin F.
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Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is D
Explanation
Reasoning:
Choice A reason: DIC is not primarily an autoimmune disease complication. While autoimmune conditions may trigger inflammation, DIC results from widespread activation of coagulation pathways due to conditions like sepsis or trauma, leading to microthrombi and factor consumption, not direct autoimmune attack on body cells.
Choice B reason: Hemolytic processes destroying erythrocytes cause hemolytic anemia, not DIC. While hemolysis may contribute to inflammation, DIC is driven by systemic activation of coagulation, forming microthrombi that consume platelets and clotting factors, leading to bleeding, not primarily erythrocyte destruction.
Choice C reason: Immune-mediated platelet destruction occurs in conditions like immune thrombocytopenia, not DIC. DIC involves systemic clotting activation, consuming platelets and factors, causing both thrombosis and bleeding. The immune system does not directly target platelets in DIC’s pathophysiology, making this explanation inaccurate.
Choice D reason: DIC is caused by abnormal activation of the clotting pathway, triggered by conditions like sepsis or trauma, leading to excessive microthrombi formation in organs. This consumes platelets and clotting factors, causing bleeding tendencies.
Correct Answer is C
Explanation
Reasoning:
Choice A reason: Addison disease results from adrenal insufficiency, causing deficient cortisol and aldosterone production. This leads to symptoms like hypotension, hyponatremia, and hyperkalemia, opposite to the cortisol excess seen in Cushing syndrome, which involves weight gain, hypertension, and hyperglycemia due to elevated adrenal cortex activity.
Choice B reason: Hashimoto disease is an autoimmune thyroiditis causing hypothyroidism, with low thyroid hormone levels leading to fatigue, weight gain, and cold intolerance. It does not involve adrenal cortex cortisol excess, unlike Cushing syndrome, which is characterized by hypercortisolism and distinct metabolic and physical symptoms.
Choice C reason: Cushing syndrome is defined by excess free circulating cortisol from the adrenal cortex, due to pituitary tumors, adrenal hyperplasia, or exogenous steroids. This causes weight gain, moon face, hypertension, and hyperglycemia, reflecting cortisol’s effects on metabolism, fat distribution, and fluid balance, making it the correct disorder.
Choice D reason: Graves disease is an autoimmune condition causing hyperthyroidism, with excess thyroid hormone leading to weight loss, tachycardia, and heat intolerance. It does not involve adrenal cortex cortisol production, unlike Cushing syndrome, which is specifically related to hypercortisolism and its systemic metabolic effects.
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