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15 Cards in this Set
- Front
- Back
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What is the rate limiting step in steroid synthesis? What stimulates this step?
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cholesterol --> pregnenolone
ACTH via a cAMP signalling system. |
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When DDx for suspected SIADH, what must be ruled out?
In which sex is adrenal androgen deficiency sometimes unnoticeable? why? |
cortisol deficiency
men; b/c they have another source of androgens. |
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Hyperpigmentation is a sx of (primary/secondary) cortisol deficiency?
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primary adrenal dz only.
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Deficiency of which hormone can give you non-anion gap metabolic acidosis?
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aldosterone deficiency.
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Does failure of the HPA (a type of secondary adrenal insufficiency) structures usually result in hypoaldosteronism? why?
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No, because the adrenal glands are fine and aldo secretion is largely dependent on K+ lvls and Renin-angII axis.
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If a pt is on chronic high doses of corticosteroids and pulled off of them quickly, what can happen?
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the tx has caused a selective suppression of CRH and ACTH production, and it can take the body awhile to catch up (cortisol deficiency [and maybe others] until it does catch up)
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Explain what happens with the rapid ACTH test in Normal adrenal gland, secondary insufficiency, and primary insufficiency.
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normal will see a v. fast and large cortisol plasma spike.
secondary will see a blunted increase (gland atrophy) primary will see no increase/ v.small increase. |
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Walk through the steps in eval of adrenal insufficiency.
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ACTH infusion (cosyntropin)
(1) peak cortisol > 20 w/ increment > 5mcg/dl = normal adrenal fx (2) <20, <5 - baseline ACTH < 20 = 2ndary insuffic. - baseline ACTH > 200 = primary |
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A deficiency in 21-hydroxylase will block which avenues of steroid synthesis?
- what lab levels will show in this deficiency? - clinical sx? |
blocks glucoC and mineraloC, the former
- hyperkalemia, hyponatremia, vol depletion, high urine Na wasting --> death unless dx'ed and tx'ed. - hypocortisol sx, hypoaldo sx, adrenal androgen excess (hirsutism, masculization, isosexual precocity) |
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A deficiency in 11-hydroxylase will result in what avenues being blocked?
- what will build up to excess? |
11-deoxycorticosterone (the aldosterone precursor) cannot be turned into corticosterone... 11-deoxycortisol also can't be converted into cortisol. Like 21-OHase def, this leads to increased weak adrenal androgens
- Importantly though, the mineralocorticoid precursor is ACTIVE on most mineraloC receptors... so this buildup actually leads to sx of mineralocorticoid EXCESS. |
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Do our synthetic steroids cross-react b/t glucocorticoid and mineralcorticoids?
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Yes, the cross reactivity varies. Cortisone is pretty evenly potent on both. Dexamethasone is SOLELY GlucoC. Fludrocortisone is 10:1 mineraloC.
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Cushing's syndrome is due to what?
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excess of all adrenal steroids.
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Pt presents w/ muscle wasting, weakness, and multiple fracture (bone weakness). Pt is centrally obese, and is markedly intolerant of glucose. Pt also reports that they bruse easily and that their wounds take longer to heal. On exam, their skin is found to be thin.
What endocrine problem do they have? |
hypercortisolism
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Walk through the steps in eval of Cushing's syndx.
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Urine 24hr cortisol is high --> do a lose-dose dexa test:
(1) normal suppression EXCLUDES cushing's (2) no change --> take plasma ACTH lvls and do a *high* dose Dexa test. (a)ACTH undetect; no dexa suppress = adrenal tumor (b) ACTH elevated; no suppression = ectopic ACTH syndrome (c) ACTH wnl or high; suppression to <50% of baseline = Cushing's dz (pituitary tumor) |
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What drugs can be used for effective palliative tx of those with intractable Cushing's? where do they act in the steroid synth chain?
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ketoconazole blocks lanosterol --> cholesterol as well as *any* adrenal downstream path to the androgens.
aminoglutethemide blocks cholesterol --> prenenolone as well as testosterone to Estrogen in the Gonads. |
