zianab
Forum Elite
Topics: 17
Posts: 282
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A 27-year-old woman comes to the physician because of muscle
weakness and cramps for 2 weeks. She has been taking
a ß-adrenergic blocking agent for hypertension for 2 years. She had
chronic lymphocytic thyroiditis (Hashimoto's disease) 1 year ago. Her
blood pressure is 160/108 mm Hg, and pulse is 60/min. Serum studies
show:
Na+ 140 mEq/L
Cl– 110 mEq/L
K+ 2.2 mEq/L
HCO3– 30 mEq/L
Urea nitrogen (BUN) 20 mg/dL
Creatinine 1 mg/dL
Magnetic resonance angiography of the abdomen shows
normal findings. Which organ created these findings?
A) Adrenal cortex
B) Adrenal medulla
C) Aorta
D) Renal arteries
E) Renal glomeruli
F) Thyroid gland
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| star1
Forum Guru
Topics: 93
Posts: 827
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D) Renal arteries
Why I choose this? According to the data we have two main problem
1- Hypertension, Muscle weakness, Hypokalemia
2-BUN/Creatinine ratio which is > 15:1 pointing to Prerenal Azotemia
When renal arteries have reduced lumen either due to atherosclerosis or due to vasospasm , blood flow to the kidney decreases and this trigger the Renin antiotension aldosterone system to increase Aldosternose which causes Na absortion, volume overload and hypokalemia.
this renal arteries problem also compromise the blood flow to kidney and causes ? Prerenal azotemia
GL
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| star1
Forum Guru
Topics: 93
Posts: 827
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HCO3– 30 mEq/L
why this HCO3 is elevated?
Secondary Hyperaldosteronism causes Metabolic Alkalosis and this lead to elevated Bicabonate.......
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| jvo_md
Forum Senior
Topics: 22
Posts: 189
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I'm cool with your answer, but in this case is not by artherosclerosis...Is most common by FIBRODYSPLASIA...Cause it's a young woman...
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| prathapdoctor
Forum Elite
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Posts: 406
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i think the answer is A,if it is because of renal artery involvement,the pathology would have been demonstrated in magnetic resonance angiography of adbomen whether its atherosclerosis or fibromuscular dysplasia,so the other condition that can produce this picture is conn syndrome caused by aldosterone producing tumor by adrenal cortex,so the answer is adrenal cortex only.
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| s2ckdeficient
Forum Newbie
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Schmidt's syndrome = Addison's disease and hypothyroidism secondary to Hashimoto's thyroiditis
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| s2ckdeficient
Forum Newbie
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uh its definitally not schmidts syndrome. what about beta blocker decreasing metabolism of aldosterone via dec. cardiac output and less flow to liver? Dont think it could be that because too acute. negative feedback would have compensated prolly.
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| doc_clotaire
Forum Guru
Topics: 159
Posts: 1,263
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That 's a very good question , Let 's go over it real quick !
CHIEF COMPLAINT : muscle weakness and cramp
BP : 160 /108
K : 2.2 ( N : 3.5-5) ,so she his hypokalemic ( muscle weakness , cramp )
HCO3 : 30 ( N : 28 ) so her bicabonate is increased ( metabolic alkalosis )
MR Angiography : normal finding(ruled out renovascular Hypertensiondue to fybrous dysplasia )
KEY WORD : Unresponsive to conventional treatment
DX : CONN SYNDROME ( Primary Aldosteronism ) characterised by HTA , hypokalemia , hypernatremia ( even though NA is kind of normal here but could be a TRICK ) and increased bicarbonate ( metabolic alkalosis )
THE ANSWER IS A
Adrenal cortex ( Adrenal adenoma whitch secrete ALDOSTERONE )
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| ssrpk
Forum Fanatic
Topics: 154
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I agree with A!
if it were renal artery stenosis, MRA wud have shown it!
HTN and hypokalemia means, hyperaldosteronism, as the vignette does'nt suggest any secondary cause, we have to assume tht its a primary one...
one thng confuses me here is the prsensce of hashimoto's [an autoimmune] does it have any relationship with hyperaldosteronism or is tht just a distractor!
and hypernatremia is very infrequently found in Conn's disease and it occurs probably due to concomitant polyuria tht the pateint has...usually serum Na+ remains in the normal range as the ater is equally absorbed!
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