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  #1  
Old 10-30-2012
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Arrow Billy Step 1 Questions # 61

A 32-year-old woman with systemic lupus erythematosus has been treated with corticosteroid therapy for several years
because of recurrent lupus nephritis. While on vacation, she undergoes an emergency appendectomy for acute
appendicitis. On postoperative day 2, she becomes somnolent and develops severe nausea and vomiting. She then
becomes hypotensive. Blood cultures are negative, and laboratory studies now show Na+ of 128 mmol/L, K+ of 4.9 mmol/L,
Cl− of 89 mmol/L, CO2 of 19 mmol/L, glucose of 52 mg/dL, and creatinine of 1.3 mg/dL. Which of the following morphologic
findings in the adrenal glands is most likely to be present in this patient?


□ (A) Bilateral caseating granulomas
□ (B) Bilateral cortical atrophy
□ (C) Bilateral hemorrhagic necrosis
□ (D) Bilateral cortical nodular hyperplasia
□ (E) Solitary 1-cm adenoma without atrophy of the contralateral adrenal cortex
□ (F) Solitary 2-cm adenoma with atrophy of the contralateral adrenal cortex
□ (G) Solitary 4-cm mass arising in the adrenal medullae
□ (H) Solitary 12-cm cortical mass with extensive necrosis and hemorrhage
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  #2  
Old 10-30-2012
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Will go with B. Is this from UW?
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No not from Uworld
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Old 10-30-2012
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It's B. Similar question in Uworld.
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Old 10-30-2012
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i'm also with B

thanks
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  #6  
Old 10-30-2012
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Default my answer :)

(B) Bilateral cortical atrophy
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Old 10-30-2012
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think its B. Bilateral cortical atrophy(h/o corticosteroid use)
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Old 10-30-2012
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Is it □ (B) Bilateral cortical atrophy
I remember doing this question but right now no idea.
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Old 10-31-2012
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steroids>>>>b/l cortical atrophy
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  #10  
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Correct Answer B is correct

This woman has findings of acute adrenocortical insufficiency (acute addisonian crisis). Long-term corticosteroid
therapy shuts off corticotropin stimulation to the adrenal glands, leading to adrenal atrophy. When this history is not
elicited, and the patient is not continued on the corticosteroid therapy, a crisis ensues, in this case made worse by the
stress of surgery. Many years ago, when tuberculosis was more prevalent and more severe without current drug therapy,
Addison disease from granulomatous destruction of the adrenals was more common. Hemorrhagic necrosis suggests
Waterhouse-Friderichsen syndrome, which can complicate septicemia with organisms such as Neisseria meningitidis.
Cortical nodular hyperplasia can be driven by an ACTH-secreting pituitary adenoma, or it can be idiopathic; in either case,
hypercortisolism ensues, not Addison disease. An adrenal cortical adenoma without atrophy of the contralateral adrenal
cortex could be a nonfunctioning adenoma or an aldosterone-secreting adenoma. If the contralateral cortex is grossly
atrophic, the adenoma on the opposite side is secreting excess glucocorticoids. An adrenal medullary mass in an adult is
most likely a pheochromocytoma, which secretes catecholamines. A large mass with hemorrhage and necrosis in the
adrenals suggests a cortical carcinoma.
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