Adrenal Flashcards
Outermost layer of the adrenal cortex where aldosterone is produced
zona glomerulosa
Middle layer of the adrenal cortex where cortisol is produced
zona fasciculata
Inner layer of the adrenal cortex where androgens are produced
zona reticularis
Rate-limiting step of adrenocortical hormone synthesis from cholesterol
conversion of cholesterol to pregnenolone by cholesterol desmolase
location of the type I adrenocorticoid receptor
predominantly expressed in the kidneys
location of the type II adrenocorticoid receptor
expressed in most tissues
Enzyme that oxidizes the C-11 hydroxyl group of adrenocorticoids
11BHSD2
Enzyme that reduces the C-11 position of adrenocorticoids
11BHSD1
Transcription factor in all cell types that is involved in cellular responses to stress, cytokines, free radicles, UV and antigens and acts as the 1st responder to harmful stimuli
NFkB
3 important inducers of NFkB
TNF-alpha, IL-1, LPS
4 factors that contribute to potency/duration of actions of glucocorticoid analogues
- affinity for transcortin (globulin) and albumin
- Affinity for 11BHSD2
- Lipophilicity
- Affinity for receptor
Structural feature of prednisolone that causes it to have a higher affinity for GR over MR
C1-C2 double bond
Structural feature of aldosterone that causes it to be protected from inactivated by 11BHSD2
C11-C18 hemiacetyl group
Glucocorticoid analogue that has a much higher affinity for MR
fludrocortisone
Name for hypercortisolism
Cushing’s disease
Normal AM serum cortisol
16-20 mcg/dL
Normal PM cortisol
6-10 mcg/dL
1st line therapy for glucose control in Cushing’s pt
Metformin
Synthetic inhibitor of glucocorticoid and progesterone receptors approved for control of hyperglycemia secondary to hypercortisolism in older adult pts with endogenous Cushing’s syndrome who have either failed surgery or are not candidates for surgery
mifepristone
Black box warning associated with mifepristone
Termination of pregnancy
The most prevalent cause of Cushing’s symptoms in North America
exogenous glucocorticoids
Avg. endogenous cortisol production by the adrenal glands per day
15-30 mgq
Equivalent prednisone dose of hydrocortisone 20 mg
5 mg
Equivalent methylprednisone dose of hydrocortisone 20 mg
4 mg
Equivalent dexamethasone dose of hydrocortisone 20 mg
0.75 mg
autoimmune adrenal insufficiency
Addison’s disease
Initial hydrocortisone dose in acute adrenal insufficiency
high dose hydrocortisone at 300 mg IV in divided doses
Baseline dosing of fludrocortisone in chronic adrenal insufficiency
0.1 mg/day
Baseline dosing of hydrocortisone (or equivalent) in chronic adrenal insufficiency
15-20 mg QAM and 5 mg QPM
glucocorticoid dose if minor stress occurs (flue, broken arm, ect)
Double dose for a short time (days-wks)
hydrocortisone dose if major stress occurs (ex. surgery)
150-300 mg PO or IV daily in divided doses
Portion of adrenal gland that synthesizes and secretes steroids responsible for salt balance, metabolism and adrogenic actions
Adrenal cortex
Structural feature of dexamethasone and betamethasone that makes them have weak affinity for transcortin/albumin
Flourine group
4 typical lab values in a Cushing’s patient
- high BG
- high BP
- low K (due to mineralcorticoid activity)
- high ACTH if tumor is in pituitary
5 unavoidable s/s to manage in glucocorticoid excess
- glucose control
- mood stabilization
- control HTN
- protect against opportunistic infection
- protection against osteoporosis
Glucose reading that is affected the most by glucocorticoids
Post-prandial glucose
Mechanism for hyperpigmentation in chronic adrenal insufficiency
Pituitary tries to overcompensate by producing more ACTH, which drives melanin production
3 indications of glucocorticoid overtreatment
- weight gain/ abnormal fat distribution
- osteopenia
- hyperglycemia
4 indications of glucocorticoid undertreatment
- myalagias
- flu-like symptoms
- fever
- hypoglycemia
4 indications of mineralocorticoid overtreatment
- HTN
- low plasma renin
- low serum K
- high serum Na (less likely)
5 indications of mineralocorticoid undertreatment
- orthostasis
- fatigue
- high plasma renin
- high serum K
- low serum Na (less likely)
Mechanism by which long-term glucocorticoid treatment for other conditions leads to secondary adrenal insufficiency
HPA axis suppress, leading to decreased ACTH production
Amount of time that glucocorticoids can be given before causing HPA axis suppression
10-14 days
Rational behind tapering short steroid courses, such as in a Medrol dose pack
Prevent rebound flair up of the problem being treated
Test that can evaluate if HPA axis suppression has occured
Cosyntropin stimulation test
Baseline AM cortisol measurement that indicates HPA axis suppression
Post-cosyntropin cortisol level that indicates HPA axis suppression
Once HPA axis suppression has occurred, the amount of time it takes for adrenal cortex to resume cortisol production in response to ACTH
2-3 months
Once HPA axis suppression has occurred, the amount of time it takes for the pituitary ACTH secretion to resume
1 month
Once HPA axis suppression has occurred, the amount of time it takes for the stress response the reengage reliably
up to 1 year
How glucocorticoid therapy should be tapered down after a long course of therapy
Decrease dose by 25-50% every few days to 1 week
3 steps to take to protect from osteoporosis due to glucocorticoid use
- maintain adequate calcium and Vit D
- BMD screening
- treatment with bisphosphonate if indicated
Maximum value that WBC should be during glucocorticoid therapy
13,000 (normal= 4000-1000)
Infection that patients need to have prophylaxis against if taking >10mg prednisone/day
Pneumocystis jeroveci (PCP) pneumonia
Standard prophylaxis for PCP pneumonia
Bactrim DS 1 tab every 3 days of Bactrim single-strength 1 qd
