Adrenal Gland Flashcards
What is secreted in the different parts of the adrenal gland?
cortex = corticoids and androgens
medulla = catecholamines
In which CAH are sex hormones decreased?
defect in 17-alpha
How does the cortisol affect the liver, muscle, fat, and skin?
liver = increased gluconeogenesis
muscle = breakdown of protein
fat = lipolysis in extremeties, central fat deposition
skin = breakdown of collagen –> thin skin, easy bruising
How does cortisol affect the immune system, endocrine, and GI?
immune = depression
endocrine = insulin resistance, down regulates pituitary hormones
GI = interferes w/ Ca absorption –> risk of osteoporosis long-term
How is cortisol regulated by hypothalamus and pit?
CRH released from paraventricular nucleus of hypothalamus –> CRF1 receptor in pituitary –> ACTH –> cortisol
cortisol does negative feedback to both hypothalamus and ant pit
What is the ACTH molecule derived from and what is its significance to pigment?
derived from POMC –> ACTH in ant pit –> in non pituitary tissues, breaks down, contains MSH
MSH = melanocyte-stimulating hormone
excess ACTH –> hyperpigmentation
How do CRH and ACTH affect each other?
CRH –> ACTH
ACTH has negative feedback to CRH
CRH also inhibits itself
How do glucocorticoids specifically affect CRH and ACTH?
inhibit POMC transcription –> no ACTH
inhibit mRNA synthesis of CRH and ACTH
What is the difference btw a low and high dose DST?
low dose = determines whether a problem is present; normal = suppression of ACTH and cortisol
high dose = determines the source of the problem
What are the the results of high dose DST for pituitary cushing, adrenal cushing, and ectopic ACTH?
pituitary: supression of ACTH
adrenal: no suppression of cortisol
ectopic: no supression
What is the Cosyntropin stim test?
Admin ACTH –> see what happens
healthy = cortisol should increase
adrenal insuffiency = no response
dramatic increase in cortisol –> could be secondary adrenal insufficieny
What is the difference btw Cushing syndrome and Cushing Disease?
Cushing syndrome = umbrella term for high cortisol; non-pituitary cause
Cushing disease = pituitary tumor causing high cortisol
What would the results be of a low dose ONDST for cushing syndrome and disease?
syndrome = ACTH suppressed, cortisol not suppressed
disease = ACTH not suppressed, cortisol suppressed
What is Addison’s disease?
primary adrenal insufficiency
progressive destruction of adrenal gland
High ACTH but low cortisol
will fail cosyntropin stim test
What is secondary adrenal insufficiency?
usually a pituitary problem
sometimes too much steriods –> decreases ACTH
see low ACTH and low cortisol
On cosyntropin stim test: cortisol will rise dramatically
In what diseases would you see hyperpigmentation?
cushing disease (secondary cortisol excess)
Addison’s (primary adrenal insuficieny)
How does Aldosterone affect the kidneys?
increases synthesis and activity of Na channels in apical membrane
Increases synthesis and activity of Na/K ATPase in the basolateral membrane of the distal tubule
overall = increased K excretion, increased sodium reabsorption
What is Conn syndrome?
primary hyperaldosteronism = adrenal problem
usually neoplasm
see high BP and Na, low K
won’t change ACTH very much
low renin
What is secondary hyperaldosteronism?
hypersecretion of renin by juxtaglomerular cells of kidney –> too much aldosterone
high BP and Na, low K
little change in ACTH
What is hypoaldosteronism?
adrenal problem –> little aldosterone
low Na, high K
high renin (trying to raise aldosterone)
low BP
What is secondary hypoaldosteronism?
Hyposecretion of renin –> not enough aldosterone
Low Na, high K
low BP
How does ACTH affect cortisol and aldosterone?
affects cortisol much more
ACTH deficiency –> low cortisol, but little change in aldosterone
What are the adrenal androgens and where are they from?
from zona reticularis –> DHEA and DHEAS –> precursors to sex hormones
rely on 3beta-HSD to exert activities
How does the body stimulate catecholamine production?
Sympathetics –> ACh –> nicotinic receptors in adrenal medulla –> increased synthesis of tyrosine hydroxylase and activity of dopamine
What is the rate limiting step of catecholamine synthesis?
tyrosine – tyr hydroxylase –> L-DOPA
What is the general formation of catecholamines and where does it occur?
in cytoplasm: Tyr –> DOPA –> dopamine
in granule: Dopamine –> NE
cytoplasm: NE –> epi -> to granule again for release
What does VMAT do?
moves Epi into specialized storage vesicles for release
How are chromaffin granules released?
via exocytosis after sympathetic stimulation
How are catecholamines broken down?
NE/E –> thru MAO –> thru COMT –> VMA
*VMA measurement can determine catecholamine production
What is MAO?
oxidizes stuff
breaks down catecholamines
used to treat neuropsychiatric disorders
What is COMT?
methylates stuff
primary enzyme that inactivates catecholamines released from the adrenal gland
What do you see in pheochromocytoma?
usually benign and unilateral adrenal tumor
excess catecholamines
symptoms wax and wane (high bp, headaches, sweating)