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NBME Step 2 CK Form 8 Answers

step2ck_form8/Block 4/Question#3 (reveal difficulty score)
A 42-year-old woman comes to the physician ...
Resistant of kidneys to ADH (vasopressin) ๐Ÿ” / ๐Ÿ“บ / ๐ŸŒณ / ๐Ÿ“–
tags: renal endo repeat inc

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 +8  upvote downvote
submitted by โˆ—jlbae(159)
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DI, PP, SIADH, etc are all the fucking worst I swear I learned them at least 8 times but can never get the shit to stick

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mycoplasma  same here. +

 +1  upvote downvote
submitted by โˆ—step_prep2(66)
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  • Patient taking lithium (which is known to cause nephrogenic diabetes insipidus) who has developed polydipsia and polyuria who on water deprivation test is found to have very minimal increase in urine osmolality, most consistent with diabetes insipidus
  • Key idea: To formally differentiate between nephrogenic and central diabetes insipidus, you would give patient desmopressin (increased urine osmolality = central DI // No change in urine osmolality = nephrogenic DI), but in this case the history with lithium is suggestive of nephrogenic
  • Nephrogenic diabetes insipidus: Hereditary, hyperkalcemia, hypokalemia, lithium, demeclocycline
  • Central diabetes insipidus: Pituitary damage (tumor, autoimmune, trauma, surgery, ischemic encephalopathy)

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beans123  treatment for lithium associated nephrogenic DI is amiloride vs nephrogenic DI not from lithium, treatment is a thiazide +1

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submitted by โˆ—akjs16(4)
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For anybody thinking about polydipsia like me: water deprivation will take urine osmolality straight to 600 mOsm/kg H20. Furthermore, when plasma osmolality >295 or plasma Na > 145, it's time to administer desmopression to differentiate central and nephrogenic DI.

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submitted by โˆ—namesthegame22(13)
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Central diabetes insipidus may result from head trauma and is characterized by inadequate secretion of ADH.

Lack of ADH leads to decreased free water reabsorption from collecting tubules, resulting in an abnormally increased serum osmolality.

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