A 66-year-old man comes to the office with nausea, loss of appetite, fatigue, and marked weakness. Medical history is significant for hypertension treated with amlodipine. The patient also has polymyalgia rheumatica, for which he was prescribed daily prednisone 12 months ago, but he stopped taking it 7 days ago because he was unhappy with the associated weight gain. Temperature is 36.7 C (98.1 F), blood pressure is 100/70 mm Hg without orthostatic changes, pulse is 100/min, and respirations are 18/min. The patient's face is round and plethoric, and there is excess supraclavicular fat deposition. Laboratory results are as follows: Chest x-ray is unremarkable. Which of the following biochemical abnormalities is most likely to be present in this patient?

Question

A 66-year-old man comes to the office with nausea, loss of appetite, fatigue, and marked weakness.  Medical history is significant for hypertension treated with amlodipine.  The patient also has polymyalgia rheumatica, for which he was prescribed daily prednisone 12 months ago, but he stopped taking it 7 days ago because he was unhappy with the associated weight gain.  Temperature is 36.7 C (98.1 F), blood pressure is 100/70 mm Hg without orthostatic changes, pulse is 100/min, and respirations are 18/min.  The patient's face is round and plethoric, and there is excess supraclavicular fat deposition.  Laboratory results are as follows:  Chest x-ray is unremarkable.  Which of the following biochemical abnormalities is most likely to be present in this patient?

Quizplus · Accepted Answer

11ec25c8_d3c3_9612_bc81_6311b2a0f6e3_MD0003_00 This patient, who has nausea, weakness, and fatigue following abrupt discontinuation of chronic glucocorticoid therapy, most likely has secondary (central) adrenal insufficiency (AI), which results from disruption of the hypothalamic-pituitary axis (HPA). Chronic use of exogenous glucocorticoids (eg, prednisone) suppresses the secretion of both corticotropin-releasing hormone from the hypothalamus and ACTH from the anterior pituitary gland. On abrupt discontinuation of exogenous glucocorticoids, the pituitary gland may be unable to increase ACTH secretion to meet metabolic demands for up to 6-12 months, resulting in secondary AI. hypothalamic-pituitary axis Any patient who receives chronic glucocorticoids for ≥3 weeks is at risk for developing secondary AI, with the risk increasing in those who have had a longer treatment duration and those who have cushingoid features (eg, facial plethora, supraclavicular fat pad). The diagnosis of secondary AI is confirmed by the measurement of low levels of both morning cortisol and ACTH. Because aldosterone secretion from the adrenal cortex is mediated primarily by angiotensin II rather than ACTH, aldosterone levels are normal in secondary AI. Mild hyponatremia may be present because cortisol deficiency can increase antidiuretic hormone (ADH) secretion, but otherwise, electrolyte abnormalities in secondary AI are typically minimal. adrenal cortex (Choices A, B, and D) Primary AI results from the destruction of all 3 layers of the bilateral adrenal cortex (eg, autoimmune adrenalitis). There are low levels of both cortisol and aldosterone, and ACTH levels are increased due to the absence of cortisol-induced negative feedback on the HPA. The low aldosterone levels cause hyperkalemia and hypovolemia, with hypovolemia inducing a more prominent increase in ADH secretion and more pronounced hyponatremia than occurs in secondary AI. In addition, the increased ACTH levels cause hyperpigmentation via increased levels of the precursor of ACTH, proopiomelanocortin. (Choice E) Increased ACTH and cortisol levels can be seen physiologically in response to stress or pathologically in ACTH-dependent Cushing syndrome (ie, Cushing disease, ectopic ACTH production). Educational objective: Chronic use of exogenous glucocorticoids can cause secondary (central) adrenal insufficiency (AI) due to disruption of the hypothalamic-pituitary axis. Laboratory studies show low ACTH and cortisol levels and a normal aldosterone level. In contrast, patients with primary AI have elevated ACTH, low aldosterone and cortisol, and significant electrolyte abnormalities (eg, hyperkalemia, hyponatremia). References: Predisposing factors for adrenal insufficiency. (http://www.ncbi.nlm.nih.gov/pubmed/19474430)

A 66-Year-Old Man Comes to the Office with Nausea, Loss