A patient with Addison disease presents with hyperpigmentation.
What is the cause?
Increased ACTH stimulating melanocytes.
Increased thyroid hormone production.
Decreased aldosterone levels.
Increased melanin due to high cortisol.
The Correct Answer is A
Choice A rationale
In Addison disease, the primary adrenal insufficiency leads to a profound decrease in cortisol production. This loss of cortisol removes the negative feedback inhibition on the hypothalamus and the anterior pituitary gland. Consequently, there is a compensatory increase in the secretion of adrenocorticotropic hormone (ACTH). ACTH is derived from pro-opiomelanocortin (POMC), which also produces melanocyte-stimulating hormone (MSH). High levels of ACTH directly bind to melanocortin receptors on skin melanocytes, leading to increased melanin synthesis and hyperpigmentation.
Choice B rationale
Thyroid hormone production is not the underlying cause of hyperpigmentation in Addison disease. While patients with autoimmune Addison disease may also have concurrent autoimmune thyroiditis as part of polyglandular autoimmune syndromes, the specific mechanism of skin darkening is unique to the ACTH pathway. Normal thyroid hormone levels (T3: to 205 ng/dL; T4: to 12 mcg/dL) do not stimulate melanocytes. Therefore, increased thyroid activity would not explain the generalized bronzing of the skin observed in primary adrenal failure.
Choice C rationale
Decreased aldosterone levels are a hallmark of Addison disease, leading to significant electrolyte imbalances such as hyponatremia (normal: 135 to 145 mEq/L) and hyperkalemia (normal: 3.5 to 5.0 mEq/L). While hypoaldosteronism causes dehydration and hypotension, it does not possess the biochemical properties necessary to stimulate melanocytes or alter skin pigment distribution. The hyperpigmentation is specifically a result of the pituitary gland's response to low cortisol, not the mineralocorticoid deficiency that occurs within the adrenal cortex itself.
Choice D rationale
This statement is physiologically incorrect because Addison disease is characterized by a deficiency, not an increase, of cortisol. High cortisol levels, as seen in Cushing syndrome, do not typically cause hyperpigmentation unless the condition is ACTH-dependent. In Addison disease, cortisol levels are consistently below the normal morning range of 5 to 23 mcg/dL. The hyperpigmentation is a direct consequence of the lack of cortisol, which triggers the massive release of ACTH and its precursors that act on skin cells.
Nursing Test Bank
Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is A
Explanation
Choice A rationale
Administering 2 tablets is the correct action because the ordered dose is 500 mg and each available tablet contains 250 mg. By providing two of these tablets, the nurse delivers the exact amount prescribed. This calculation is a basic nursing competency used to ensure medication safety. Giving the correct number of tablets prevents underdosing, which would result in subtherapeutic levels of the medication, and overdosing, which could lead to toxicity or adverse reactions for the patient.
Choice B rationale
Administering 1 tablet would only provide 250 mg of the medication, which is exactly half of the 500 mg dose that was ordered by the healthcare provider. Providing only one tablet would result in a medication error categorized as underdosing. This would fail to meet the therapeutic needs of the patient and could lead to a worsening of the condition being treated, as the drug concentration in the bloodstream would not reach the necessary level for effectiveness.
Choice C rationale
Administering 1.5 tablets would provide a total dose of 375 mg, as 250 mg multiplied by 1.5 equals 375 mg. This amount is still 125 mg short of the required 500 mg dose. While closer than a single tablet, it remains an incorrect dosage that would not fulfill the prescriber's order. Nursing practice requires precise calculation to ensure that the patient receives the specific amount of active ingredient necessary to produce the desired physiological response without error.
Choice D rationale
Administering 0.5 tablets would only provide 125 mg of the medication, which is significantly less than the 500 mg dose required for the patient. Such a small amount would be entirely insufficient for treating the patient's condition. In clinical practice, the nurse must always verify the dose on hand against the dose ordered. Using a half tablet in this scenario would be a clear mathematical error and a violation of the rights of medication administration.
Correct Answer is D
Explanation
Choice A rationale
A stable blood pressure helps maintain the integrity of the blood-brain barrier. The barrier consists of tight junctions between endothelial cells, astrocytes, and a basement membrane. These structures are designed to regulate the movement of substances into the brain parenchyma. When blood pressure remains within a normal autoregulatory range, the physical pressure against these tight junctions is controlled, preventing the mechanical "stretching" or leaking of fluids and solutes into the delicate neural tissue.
Choice B rationale
Normal oxygen saturations, typically maintained above 95 percent, ensure that the endothelial cells of the blood-brain barrier receive adequate oxygen for metabolic processes. Hypoxia, or low oxygen, is what actually threatens the barrier. Under hypoxic conditions, the tight junction proteins can degrade, and inflammatory mediators are released, leading to increased permeability. Therefore, maintaining high oxygen levels is a protective factor that keeps the barrier sealed and functioning as a selective filter for the CNS.
Choice C rationale
A glucose level of 90 mg/dL is within the normal fasting range of 70 to 99 mg/dL. The brain requires a constant supply of glucose, which is transported across the blood-brain barrier via specific GLUT1 transporters. Normal physiological levels of glucose do not disrupt the structural integrity of the barrier. It is chronic hyperglycemia, seen in uncontrolled diabetes, that eventually damages the microvasculature and increases permeability through the formation of advanced glycation end products.
Choice D rationale
Inflammation and infection are primary causes of increased blood-brain barrier permeability. During an infection such as meningitis, pathogens and immune cells trigger the release of proinflammatory cytokines like tumor necrosis factor and interleukins. These substances cause the tight junctions between endothelial cells to loosen. This increased permeability allows white blood cells and antibiotics to enter the brain, but it also permits the entry of toxins and excess fluid, leading to potentially dangerous cerebral edema.
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