Flashcards in Endocrine - Online MedEd - Adrenals Deck (31):
Adrenal gland sits on top
Of the kidney
Adrenal medulla is in the middle. Produces...
Adrenal sits on kidney - has GFR... zones of adrenal
Glomerulosa - salt - aldosterone
Fasciculata - sugar - cortisol
Reticularis - sex - testosterone
Cushing's syndrome - pathophys (4 ways)
1) Lung tumour secretes ACTH (small cell)
2) Cushing's disease - tumour on anterior pituitary that secretes ACTH
3) Ingesting steroids - i.e. treat autoimmune diseases (maybe taking too much)
4) Primary tumour of adrenal gland - produce cortisol
(ACTH driven will have elevated ACTH driving cortisol; those that are cortisol driven will have excess cortisol and low ACTH)
Cushing's syndrome cause by...
Some ACTH dependent, some ACTH independent
Cortisol is responsible for
Cortisol excess causes
Look for: really bad acne, moon facies, truncal obesity (buffalo hump), stretch marks and purple striae on abdomen
Work up of Cushing's syndrome...
Need biochemical evidence of Cushing's
Remember "low then high"!*
1) Do a low dose dexamethasone suppression test. First measure cortisol --> then give dexamethasone --> dexamethasone should suppress cortisol
*In this case, will fail to suppress --> gives you Cushing' syndrome.
*Will also need to be sure it is excess cortisol - so get a 24 hour urine cortisol or a late night salivary cortisol
2) Next measure ACTH --> if ACTH is normal --> then the excess cortisol is coming from the adrenals --> do a CT/MRI and resect it.
But if ACTH is elevated --> now ACTH dependent, but not sure which one. NOW get high dose dexamethasone suppression
If got a pituitary tumour --> there will be some suppression --> so then it is Cushing's disease --> resect it
IF fails to suppress --> now it is ectopic tumour --> go find it! very rare - do a pan scan (CT of chest and pelvis)
Too little Cortisol is
Addison's disease.... what is it a problem of
Adrenal - Will also lose aldosterone!
Pituitary - RAS is intact
*Treatment is different
Addison's disease - what are the most common causes?
Adrenal destruction - autoimmune or TB related
Can also have dysfunctional anterior pituitary
Patient presentation of addison's
Acute - lose both cortisol (blood vessels) and aldosterone (hold onto Na) - will be hypotensive and N/V/coma - definitely ill!
Chronic - infiltrative, autoimmune, malignancy, orthostatic hypotension (not frank), hyper pigmentation (due to ACTH being made!), low Na and high K (no aldosterone)
Diagnostic work up of Addison's
2) Sufficient cortisol - do not do a random, want an early AM cortisol - if normal, then rule out; if Addison's, low cortisol
3) Confirmatory - is it a deficient pituitary or adrenal. Do a cosyntropin stimulation test (give ACTH) - if cortisol rises, then problem is in the anterior pituitary --> now into pan hypo-pit --> do an MRI --> adrenal gland is intact, so just replace cortisol
Expect in Addison's disease --> that the problem is in the adrenal gland --> so cortisol will not rise with administration of cosyntropin/ACTH --> do CT imaging/MRI of adrenal gland --> if adrenal gland is lost --> must replace both cortisol and aldosterone --> give cortisol and fludrocortisone
Too much aldosterone is called
RAS axis is independent of HPA axis... what is JG apparatus
Renin turns on
ANGI to ANGII
ANGII turns on
Channels in CD to reabsorb Na and excrete K
Which causes aquaporins to be inserted to reabsorb water
Esp with low flow through kidney system
There could be a tumour that secretes too much aldosterone. Focus on which axis?
Not the HPA axis
Pathology of Conn's
1) Primary tumour is Conn
2) There could also be Renovascular hypertension/problem of renal artery - 1) Fibromuscular dysplasia in Female; 2) Atherosclerotic disease in old man
(Renovascular hypertension is considered appropriate response, but tumour is inappropriate)
What is the presentation of Conn's
HTN and hypoK*
Though not so much in real life...
Secondary hypertension (refractory to 3 or more meds)
What is the first test to order for Conn's
If neither is elevated, there is a mimicker --> congenital adrenal hyperplasia and licorice ingestion
-If Aldo is elevated and so is renin --> renin is driving the aldo production so that aldo/renin<10 --> have renovascular hypertension --> fibromuscular dysplasia (stent), atherosclerotic disease (no stent, just deal with hypertension)
-If Aldo is elevated and renin is not! --> so autonomous secretion of aldo, so aldo/renin ratio > 30 --> now have Conn's --> confirmatory test is salt supression
For dx of Conn's
Start with Aldo to renin ratio --> should be high (>30)
Next do a salt suppression test
Give a salt load --> what should happen is aldosterone is that aldosterone should decrease --> get MRI and cut it out
*Regardless, must get adrenal vein sampling before you go to resection
-Side without the mass is often hyper functioning so need to sample adrenal vein
Pheochromocytoma - pathology
Catecholamine secreting tumour
Presentation of pheo
Diagnostic step of pheo
Plasma free catecholamines - for pheo crisis now
Or get 24 hour urine metanephrines - more sensitive, but not in crisis
Once dx of pheo is confirmed... what to do?
Adrenal vein sampling
Pre-operative preparation of pheo...
Why? Because if poke pheo, can get massive release of catecholamines
Treatment is: Alpha blockade first, then beta blockade, then resect!
Mass on adrenal gland is called