Adrenal Pharm [TRH] Flashcards
(41 cards)
How helpful are basal cortisol levels as Diagnostic tools?
not very…they oscillate w/ACTH levels
What is the Short ACTH stimulation test?
tests if the adrenal gland is functioning! [if yes, stop test]
- compares cortisol levels b4 & after 250 mcg of tetracosactide [synthetic ACTH]
- if 1 hr later: cortisol is 2x > normal = normal 1’ adrenal fxning
What is the Long ACTH stimulation test?
if short test is abnormal
- possible that hypopituitarism = hypofxn but still responds to cortisol
- used to differentiate b/w 1’ & 2’ adrenal insufficiency
- 1 mg tetracosactide multiple administrations & measure blood at 1, 4, 8, & 24 hours later
- in 1’ addison’s= cortisol low @ all times
- 2’ corticoadrenal insufficiency [small adrenal but still responds (just delayed)] = eventually cortisol ^^
After a long ACTH stimulation test…
what would a pt with addison’s test results be?
a pt w/ 2’ corticoadrenal insufficiency’s results?
- in 1’ addison’s= cortisol low @ all times
- 2’ corticoadrenal insufficiency [small adrenal but still responds (just delayed)] = eventually cortisol ^^
What does a 24hr Urine cortisol measure?
-what Dx can it confirm?
free cortisol!!!
- shouldnt be affected by conditions or medications that alter corticotropin binding protein
- HIGH LEVELS: confirms hypercortisolism
- 11B-hydroxylase2 is overwhelmed & thus inactivation of cortisol–> cortisone doesnt happen
**need to have similar results >2 times? or in correlation w/ other Dx tests?
What does a late night salivary cortisol test tell us?
shows loss of circadian rhythm & absence of late night nadir
= indicates cushings syn!!
***also need 2+ tests of this
What tests can you do on pregnant ppl?
Which tests can be used on epileptics?
prego: urine free cortisol
epileptics: NOT dexamethasone [antiepileptic drugs ^^dexaM clearance]
- use urine or salivary cortisol tests
What should you do once hypercortisolism has been established?
Do a baseline ACTH level!
- LOW: ACTH independent disease
- HIGH: ACTH dependent
What is a LOW dose Dexamethasone Challenge Test?
-
1mg DEX test or 2 mg/day over 48 hrs
- GOLD STANDARD screening test for cushings
- if blood cortisol > normal after test = failure to suppress [ACTH] cortisol w/ DEX –> ^^cushings suspicion
- abnormal test should be followed up with a High dose DEX test
What is the high test DEX test?
give 8 mg DEX overnight
- even pit. ACTH secreting tumor will show a decrease in cortisol prodxn with this high dose
- distinguishes pit. ACTH secreting tumor CUshings from ectopic cells
How do we interpret the following results:
- low dose DEX= no change in cortisol levels
- ACTH level= low
Cushings caused by an adrenal tumor
How do we interpret the following tests:
- low dose DEX test: no change [cortisol still ^^]
- ACTH= high
- High dose DEX= no change [cortisol still ^^]
Cushings related to ectopic tumor/cells secreting ACTH
How do we interpret these labs:
- low dose DEX: no change [cortisol still ^^]
- high dose DEX: normal suppression [cortisol decreases]
Cushings Syndrome caused by a pituitary tumor aka Cushings DIsease
What test do we use if Cushings Syndrome has already been Dx’d?
CRF/H stimulation test:
- distinguishes Cushings disease [pit. origin] from ectopic ACTH-secreting tumors
- pit tumors are responsive to CRH= ACTH/cortisol^^
- >2.5x^^ in ACTH = cushings
- ectopic tumors & adrenal tumors show NO response
- pit tumors are responsive to CRH= ACTH/cortisol^^
How do glucoC’s effect the CV system?
- positive inotropic effect
- ^^BP [Na/h20 retention]
- maintains sensitivity of small BV’s to catecholamines in order to retain tone & BP
How do glucoC’s effect the CNS?
- lower seizure threshold [^^risk of seizure]
- behavioral changes: mood depression/^^ is MC, euphoria, restlessness, anxiety & psychosis possible
How do glucoC’s effect the GI system?
- increase gastric acid & pepsin
- may suppress local immune response against h. pylori –> ulcer formation
- decreased Ca++ absorption from the gut
How do glucoC’s effect bone metabolism?
- direct inhibition of osteoblasts
- 2’ stimulation of PTH which stimul8s osteoclasts
- net absorption of bone matrix ==> osteoporosis [long use]
How do glucoC’s effect the M.Sk. system?
- hypoK+
- muscle wasting –> loss of protein
- may result in greater disability than original inflammation?
How do glucoC’s effect hematology aspects?
- lympho’s decrease–> ^^ susceptibility to infxn
- T cells decrease more than B cells
- eos & baso-phils decrease
- neutros & erythrocyte levels ^^
- inhibits leukocyte extravasation
What are the 3 main therapeutic effects of glucoC medication?
- anti-inflammatory
- immunosuppressant
- anti-allergic
How are the anti-inflammatory effects of glucoC medication potentiated?
- ArachA metabolites decrease–> COX2 express decrease
- decrease in peripheral leuko & tissue mac [] –> depression of immune factor prodxn such as:
- platelet activating factor, TNF, interleukins
- reduce edema [leukos only allowed to extravasate to injured tissue] = cap wall integrity maintained
- lysosomal membranes stabilized so proteases not released = less fibrosis [tissue break down and scarring]
- reduce vasoactive factor release promoting vasoD & shock
- max effect 6 hrs after Tx, gone after 24hrs
HOw are the immunosuppressant effects of glucoC’s potentiated?
- inflammation occurs @ boundary of donated tissue
- inhibit the axn of immune factors
- Ag release 4m grafted/donor tissue may be inhibited
–can result in increased susceptibility to infxn
HOw are the anti-allergic effects of glucoC’s potentiated?
- inhibits mast cell synthesis of Histamine–> limits allergic attack duration
- NO affect on HistamineR or axn of already released Histamine
