Adrenal Gland Flashcards
adrenal medulla
neuronal tissue
cortisol
suppresses neuron formation
promotes Epinephrine production
blood flow from cortex to medulla
action of cortisol on NE?
increases PNMT activity
NE > E
ACTH
stimulates production of DOPA
ACh
stimulates secretion of stored catecholamines
from preganglionic sympathetics
catecholamines
secreted into blood as hormones
80% E
20% NE
cathecholamine synthesis pathway
tyrosine > L-dopa > dopamine > E > NE
action of catecholamines
brief with fast degradation
GPCR - on adrenergic receptors
alpha 1 receptors
increase vascular smooth muscle contraction
alpha 2 receptors
inhibit NE and insulin release
beta 1 receptors
increase cardiac output
beta 2 receptors
increase hepatic glucose output, decrease contraction of vessels and uterus
beta 3 receptors
increase hepatic glucose output, increase lipolysis
degradation of catecholamines
COMT and MAO
to measure catecholamine production
catecholamine
metanephrine
vanillylmandelic acid (VMA)
mineralocorticoids
21 carbons
glucocorticoids
21 carbons
androgens
19 carbons
zona glomerulosa
lacks 17 alpha hydroxylase - only produces mineralocorticoids
action of aldosterone
increase Na reabsorption
increase K and H secretion
low aldosterone
hyperkalemia
hypotension
metabolic acidosis
high aldosterone
hypokalemia
HTN
metabolic alkalosis
kidneys and cortisol
convert it to cortisone - low affinity for aldosterone receptors
aldosterone regulation
major is RAAS
not under control of ACTH like cortisol
renin
released with low blood volume
stimulates angiotensinogen to ANG I
ACE
in lung
ANG I to ANG II
ANG II
increased Ca levels and triggers aldosterone synthesis
increased potassium
triggers aldosterone synthesis
influx of Ca bc of depolarized cells
ACTH
controls conversion of cholesterol to pregnenolone
induces secretion of cortisol, corticosterone, and DOC
- mineralcorticoids
- HTN with too high ACTH
cortisol
binds nuclear receptors - promotes gene transcription
actions of cortisol
increased gluconeogenesis, protein catabolism, lipolysis, decreased insulin sensitivity
anti-inflammatory
immune suppression
vascular response to catecholamines
inhibit bone formation
increased GFR
decreased REM
acute high cortisol
low I:G ratio
give body energy in times of stress
chronic high cortisol
high I:G ratio
ex/ cushings
cortisol release
diurnal
lowest before sleep
highest before awakening
decreased ACTH
atrophy in zona fasciculata and reticularis
excess ACTH
hyperpigmentation
-cross-reaction with MCR-1 on melanocytes with excess MSH
androgens in male and female
female - majority from adrenal
male - majority from testes
CRH
from paraventricular hypothalamus to anterior pituitary
increases ACTH secretion from corticotrophs
cortisol feedback
negative feedback on CRH from hypothalamus
cortisol deficiency
high ACTH
cortisol excess
decreased ACTH
dexamethasone suppression test
administer synthetic cortisol
-used to determine if hypercortisolism is from ACTH tumor or cortisol tumor
ACTH tumor
DST - only high dose suppresses cortisol
cortisol tumor
DST - neither low or high dose suppress cortisol
11-beta hydroxysteroid DH
converts cortisol to cortisone
in kidney
overproduction of adrenal androgens
increased urinary 17-ketosteroids
excess cortisol
hyperglycemia
excess aldosterone
hypokalemia
hirsutism
masculinization in females
addisons disease
adrenocortical insufficiency
- autoimmune destructon all adrenal cortex
- decreased cortisol, aldosterone, androgens
hypoglycemia, anorexia, weight loss, N/V, hypotension, hyperkalemia, hyperpigmentation**
secondary adrenocortical insufficiency
low CRH or ACTH
-decreased cortisol
low ACTH levels, no hyperpigmentation, aldosterone normal
cushings
excess cortisol
hyperglycemia, muscle wasting, central obesity, round face, osteoporosis
cushings disease
hypersecretion ACTH (pituitary tumor)
cushings syndrome
defect in adrenal cortex
-low ACTH
conns syndrome
primary hyperaldosteronism
-aldosterone secreting tumor
HTN, hypokalemia, metabolic alkalosis
decreased renin levels
21 hydroxylase deficiency
increased 17 ketosteroids in urine
high ACTH
17 alpha hydroxylase deficiency
cannot produce cortisol or androgens
overproduction of mineralocorticoids
hypertension, hypokalemia, metabolic alkalosis
pheochromocytoma
tumor of chromaffin tissue
-produce excess catcholamines
HA, sweating, palpitations** triad
HTN and orthostatic hypotension
pounding heart
beta 1
increased HR
beta 1
increase BP
alpha 1
cold hands and feet
alpha 1
to control high BP
alpha 1 antagonist
ACTH dependent
tumor ACTH
responds to DST
ACTH independent
tumor cortisol
no response to DST
factitious cushings
overreplacement of cortisol
approach to cortisol diagnosis
exclude exogenous steroid use
DST test - synthetic cortisol
24 hour cortisol
findings with cushings
central obesity, muscle wasting, striae in skin
decreased bone density
increased glucose - insulin resistance
increased BP - increased PNMT > increased E
other cortisol effects
decreased LH, FSH = female menstrual abnormal
decreased TSH
decreased GH
11beta hydroxysteroid DH
cortisol > cortisone
breaks cortisol down in kidney so it won’t act as a mineralocorticoid
this is why you get metabolic alkalosis with hypercortisolism
addisons disease
primary adrenal insufficiency
-mainly autoimmune - 21 hydroxylase
primary vs. secondary adrenal insufficiency
primary - problem adrenal gland
secondary - problem pituitary
primary has hyperpigmentation - high ACTH causes MSH rxn (MRC-1 in skin**)
secondary has no hyperpigmentation
MCR2
adrenal glands
-bind ACTH
primary hyperaldosteronism
HTN
hypokalemia
hypomagnesemia
metabolic alkalosis
aldosterone:renin ratio
to determine aldosterone levels
infusion of saline and aldosterone assay
to try to suppress it
sodium escape
chronic aldosterone
- sodium lost (mechanism not important)
- not as elevated as you may think**
