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34 Cards in this Set

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what are the 3 layers of the adrenal gland and what does each produce?

outer zone = cortisol and glucocorticoids.


inner zone = aldosterone and mineralocorticoids


medulla = adrenaline & DHEA.

what cells do pheochromocytomas affect?


classic pheochromocytoma triad?



chromaffin cells.


PST


paroxysmal headaches, sweating & tachycardia.





Paragangliomas are what?

primary extra-adrenal pheo's. can be located on sympathetic chain, thorax, bladder and brain.

Other S&S of pheochromocytoma?

drug resistant HTN.


sense of impending doom.


mottled cyanosis.


pallor.


abdominal px.


postural tachycardia and hypotension.


vomiting.


increased anxiety, hunger and weight loss.


angina.

pheochromocytoma test findings?


thyroid?


BG?


ESR?


Leukocytes?


plasma renin?

thyroid= normal.


BG + or - mild


ESR + or -


Leukocytes - common


plasma renin increased

how to test for pheochromocytoma?

plasma fractionated free metanephrines (most sensitive).


Urinary catecholamines and metanephrines for 24 hours.



when a patient has HTN before 45 or 50 years old think what?

pheochromocytoma

tx of choice for pheochromocytoma?


post op considerations?

laproscopic resection


could become hypotensive, because no more hypersecretion of epi.

survival rates of pheochromocytoma with tx?

with surgery 44& 5 year survival.


with surgery and radiation 75% survival rate

neurofibromatosis type 1.


Classic features?

first described pheochromocytoma syndrome.


multiple neurofibromas.


cafe au lait spots.


axillary freckling.


lisch nodule on iris.


pheochromocytomas occur in about 1% of these patients.

how does addison's develope?


results in what?

develops from bilateral adrenal cortex destruction. 90% destruction occurs for addisons.


decreased adrenocortical hormones.


autoimmune most common cause.


aldosterone can be affected.

common S&S with addisons ds?


Tx?

hypotension. especially orthostatic.


hyperpigmentation in areas of friction like hands. hyperpigmentation also occurs in the mouth and face.


High ACTH and low cortisol levels found.


Tx with hydrocortisone. aldosterone maybe.

who gets addisons ds?

all ages, but mostly old.


dx in 2nd or 3rd decade of life. stupid way to list it, but that's what you get for copy and paste....


clinically apparent during metabolic stress or trauma.

Adrenoleukodystrophy is a random thing you should probably know. what is it?

accumulationof very long-chain fatty acids in the adrenal cortex, testes, brain, and spinalcord. Itmay present at any age and accounts forone-third of cases of Addison disease in boys.

other causes of addisons are?

congenital.


idiopathic atrophy of adrenal cortex.


bilateral adrenal hemorrhage.


drugs that suppress corticosteroid synthesis.


amyloidosis.


tumors.

most frequent then Odd S&S for addisons's ds?

Most frequent S&S


orthostatic hypotension.


hyperpigmentation.


new scars.




Odd S&S


craving salty foods.


intolerance of temperature extremes.


n, v, d, weight loss, dizziness.

addisonian crisis S&S

fever of unknown etiology.


sharp sudden px in abdomen.


hypoglycemia.


loss of consciousness.


other S&S same as with addison's ds.

DX tests?

cortisol level in morning if possible. < 3mcg is dx. Especially if ACTH is >200.


cortisol <8 mcg at any other time.



dx of addisons ds

give ACTH called cosytropin.


Little or no change in cortisol levels post injection have primary adrenal insufficiency.

Acute tx of addisons ds.

volume replacment.


correct hypoglycemia.


corticosteroid tx with dexamethasone.



addisons ds daily tx?

presnisone and hydrocortisone. May need to doulbe in times of stress (illness, surgery, traumatic, heat, . Not emotional)

conn syndrome

primary hyperaldosteronism from increaased aldosterone secretion.


suppressed plasma renin activity.


hypertension and hypokalemia.

what causes primary hyperaldosteronism?

APA's or aldosterone producing adenomas.


bilateral adrenal hyperplasia.


primary adrenal hyperplasia

GRA or glucocorticoid remediable aldosteronism defintion and tx?

RAS is suppressed and aldosterone is regulated by ACTH..


tx = dexamethasone to suppress the ACTH and thereby the aldosterone.

what is the normal life cycle of aldosterone?


what conditions would alter its life cycle?

RAS system stimulates synthesis. Liver normally metabolizes it.


In CHF the aldo is not metabolized as well and this induces HTN.

who gets primary hyperaldosteronism?

AA.


women more commonly in IAH and APA's.


APA's 30 to 50


IAH (bilateral adrenal hyperplasia) peaks in 6th decade

Tx for aldosteromas vs IAH?

aldosteroma's get resected. pre-op = spiralactone and post op = manage BP.




IAH gets aldosterone antagonists like CCB or AVE inhibitors or mineralocorticoids or triamterene or amiloride. The last 2 suck.

most common cause of cushings ds?


endogenous and exogenous?

Endogenous pituitary tumor secreting ACTH.


exogenous steroids.

what is cushings?

hypercortisol secretion.



what can cause ectopic ACTH secretion?

small cell lung cancer


pancreatic carcinoma


adrenal carcinoma

who gets cushings?

primarily 25 to 45 year olds.


increasing rapidity after 50 years old.

Cushings S&S

weakness.


lower back px.


depressed mood.


frank psychosis.


polyuria and polydipsia.


central weight gain.


stretch marks.


easy bruising.


buffalo hump.


abdominal striae.


Moon facies.


HTN.


oily skin.


glucose intolerance.


amenorrhea.


ED in men.


hyperpigmentation.


osteopenia.



cushings dx?

24 hour urine collection over 3 days to get cortisol levels.


give dexamethasone and if symptoms suppressed then it is cushings.

what should be done with an alcoholic who is not sober who is showing signs of cushings?

wait until they are sober and abstinent from alcohol.