hypothalamic pituitary relationshops 2 Flashcards
name the regions of the adrenal medulla in order
Zona glomerulosa
zona fasciculata
zona reticularis
medulla
what class of hormone is aldosterone, what secretes it, what does it do?
mineralocorticoid
zona glomerulosa
regulates salt and volume homesotasis
what class of hormone is norepi and epi, what secretes it, what does it do?
catecholamine
medulla
respond to stress rapidly
what class of hormone is cortisol, what secretes it, what does it do?
glucocorticoid
zona reticularis
longer acting stress response
regulates glucose use, immune and inflammation
what class of hormone is DHEAS, what secretes it, what does it do?
steroid
zona fasciculata and reticularis
makes androgens
HPA axis is under negative feedback control of what?
cortisol
what causes CRH to be released?
what does it then cause to be released?
emotional stress, metabolic stress, physical stress
causes ACTH to be released from anterior pituitary
causes cortisol to be released
what are the actions of cortisol on organ systems?
immune suppression
gluconeogenesis in liver
protein catabolism in muscle
lipolysis in adipose tissue
how do circadian rhythms control cortisol?
cortisol high in the morning,
low in evening
what affect does aldosterone have?
water/na+ reabsorption by kidneys, BP goes up
how is aldosterone secretion regulated? list the steps
liver makes angiotensinogen
becomes angiotensin 1 via
renin (made in kidney due to low BP)
becomes angiotensin 2 due to ACE
goes to adrenal cortex
becomes aldosterone
targets kidney tubules
what effect does ACTH have on zona glomerulosa
increased secretion of aldosterone
what causes cushing syndrome(CS)? symptoms?
too much cortisol over time
truncal obesity moon face hump osteoporosis hirsutism cognitive defects edema
what does the dexamethasone suppression test low dose show?
differentiates CS patients of any cause from patients who do not have CS
NO ACTH suppression shows CS
but doesnt show where ACTH is coming from
what does the dexamethasone suppression test high dose show?
when is it used
what does it show
distinguishes patients of CS caused by pituitary ACTH tumor and non pituitary ACTH tumor
used after diagnosis of CS is made
decrease in ACTH shows pituitary tumor
(feedback)
no change in ACTH shows ectopic tumor
(no feedback)
what does an excess of glucocorticoid do?
diabetogenic effect
visceral obesity
osteoporosis
thinning of skin, muscle atrophy
immunosuppression
water retention
decrease in growth
what is acth dependent cushing disease caused by?
acth secreting tumors (pituitary)
ectopic tumors
crh secreting tumors
what is acth independent cushing disease caused by?
adrenal carcinoma
adrenal adenoma
what is pseudo cushing syndrome?
major depression
anxiety
caused by illness or alcoholism rarely
what is the negative effect of exogenous glucocorticoids?
can atrophy adrenal cells that produce cortisol
whats the process by which aldosterone works?
combines with cytoplasmic receptor
initiates transcription in nucleus
new protein channels and pumps made
aldosterone induced proteins modulate channels and pumps
na reabsorption increased
k secretion decreased
where does ACTH come from? what does it make?
peptide from anterior pituitary, by POMC
makes cortisol
also MELANIN!
addisons disease causes what? by what?
hyperpigmentation, overproduction of ACTH
what is cosyntropin stimulation test used for?
detect adrenal gland insufficiency
cosyntropin in synthetic ACTH
what are the symptoms of a primary adrenal insufficiency?
adrenal gland not working
aldosterone and cortisol not produced
what are the symptoms of a secondary adrenal insufficiency?
aldosterone produced
cortisol not produced
what can cause primary adrenal insufficiency?
called addisons disease
can be autoimmune
can be hemhorrage
(waterhousefriedrichsen syndrome due to meningitidis)
infections such as tuberculosis
tumors going to adrenal gland
how is adrenal insufficiency treated?
replacing hormones adrenal glands are not making
cortisol replaced with corticosteroid
aldosterone replaced by mineralocorticoid
primary adrenal excess:
what happens to
plasma cortisol
CRH
ACTH
Hyperpigmentation
up
down
down
no hyper
secondary pituitary excess:
what happens to
plasma cortisol
CRH
ACTH
Hyperpigmentation
up
down
up
yes hyper
primary adrenal deficiency:
what happens to
plasma cortisol
CRH
ACTH
Hyperpigmentation
down
up
up
yes hyper
secondary deficiency:
what happens to
plasma cortisol
CRH
ACTH
Hyperpigmentation
down
up
down
yes hyper
steroid administration:
what happens to
plasma cortisol
CRH
ACTH
Hyperpigmentation
down (symptoms of excess)
down
down
no hyper
what does primary hyperaldosteronism entail?
give an example
too much aldosterone from adreanl cortex
conns syndrome for example: adenoma of adrenal cortex
what does secondary hyperaldosteronism entail?
too much renin secreted by kidney
what does hypoaldosteronism entail?
destruction of adrenal cortex
defects in making aldosterone
inadequate stimulation to make aldosterone
addisons disease causes what?
how is it treated
hypotension, hyponatremia
steroid replacement therapy for life
primary hyperaldosteronism causes what?
how is it treated
hypertension, hypokalemia, low plasma renin
solved with surgery or spironolactone
how do we test PAC-PRA ration to detect primary hyperaldosteronism?
PAC-PRA ration greater than 20
PAC greater or equal to 15
test for primary aldosteronism
describe how aldosterone is made by adrenal cortex?
zona glomerulosa
cholesterol to pregnenolone to progesterone (3b hydroxysterois dehydrogenase) to 11-deocycorticosterone (21b hydroxylase) to corticosterone (11b hydroxyalase) to aldosterone
describe how cortisol is made by adrenal cortex?
zona fasciculata and reticularis
cholesterol to pregnenolone to progesterone (3b hydroxysterois dehydrogenase) to 17OH progesterone (17a hydroxylase) to 11 deoxycortisol (21b hydroxyalase) to cortisol (11b hydroxylase)
describe how androgens is made by adrenal cortex?
zona fasciculata and reticularis
cholesterol
to
17OH pregnenolone (17a hydroxylase)
to
androgens
what prevents activation of mineralocortoid receptor by cortisol?
enzyme 11b-HSD2
what are all congenital adrenal enzyme deficiencies marked by?
bot adrenal glands are enlarged due to high acth
not enough cortisol to stop it
17 a deficiency, what happens to:
mineralocorticoids
cortisol
sex hormones
blood pressure
K+
labs
other presentations
up
down
down
up
down
down androstenedione
lack of sexual development
21 b deficiency, what happens to:
mineralocorticoids
cortisol
sex hormones
blood pressure
K+
labs
other presentations
down
down
up
down
up
up renin, up 17 hydroxyprogesterone
salt wasting, precocious puberty
11b deficiency, what happens to:
mineralocorticoids
cortisol
sex hormones
blood pressure
K+
labs
other presentations
down aldosterone, up DOC
down
up
up
down
down renin
viriliation
what is a pheochromocytoma, what happens?
adrenal gland tumor, too much ep and norepi released
activate a and b adrenergic receptors
causes hypertension
what are the catecholamine, what do they respond to?
what do they influence
epi and nor epi
respond to stress such as hypoglycemia or exercise
influences metabolism and cardiac output
what controls synthesis of catecholamines?
how is it upregulated?
sympathetic activity and CRH-ACTH-Cortisol Axis
upregulated by cortisol via PNMT
what signals catecholamine release from adrenal medulla?
AcH
whats the rate limiting step of norepi and epi production?
tyrosine hydroxylase, tyrosine to dopa
name the steps of norepi production?
tyrosine to dopa, to DA to chromaffin granule
norepi diffuses out
how is epi made from norepi?
norepi diffuses out of granule,
made into E via PNMT
E goes back to granule via VMAT
how are E stored?
in chromaffin granules with ATP, Ca and proteins
as chromogranins
what tumors do circulating chromogranins signal?
paragangliomas
what breaks down catecholamines
COMT mostly
what signals total catecholamine production?
catecholamines, metanephrines, VMA
pheochromocytoma is signalled by what?
elevated levels of catecholamines and byproducts
a receptors and b3 receptors respond better to what?
what do they do
NE
a: increase vascular smooth muscle constriction
b3: increase hepatic glucose output , lipolysis
b1 receptors respond better to what?
what do they do
both norepi and epi
increase cardiac output
b2 receptors respond better to what?
what do they do
epi
decrease contraction of blood vessels
what mediates long term stress response?
what happens?
mineralocorticoids
-blood pressure rise, kidneys retain water
glucocorticoids
- immune system repressed
- blood glucose rises, protein and fats broken down
what mediates short term stress response?
what happens?
catecholamines
- heart rate rises
- blood pressure rises
- bronchioles dilate
- metabolic rate increases
- liver makes glucose
what does epinephrine do?
up glycogenolysis up gluconeogenesis up lipolysis up calorigenesis down glucose use up insuln and gucagon up cardiac contractlity up heart rate up arterior dilation up muscle relaxation
what does norepi do?
up gluconeogensis up glycogenolysis down insulin up cardiac contractility up artery vasoconstriction up sphincter contraction up platelet aggregation
