hypothalamic pituitary relationshops 2 Flashcards by Mo Sarwar

name the regions of the adrenal medulla in order

Zona glomerulosa
zona fasciculata
zona reticularis

medulla

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what class of hormone is aldosterone, what secretes it, what does it do?

mineralocorticoid

zona glomerulosa

regulates salt and volume homesotasis

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what class of hormone is norepi and epi, what secretes it, what does it do?

catecholamine

medulla

respond to stress rapidly

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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

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what class of hormone is DHEAS, what secretes it, what does it do?

steroid

zona fasciculata and reticularis

makes androgens

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HPA axis is under negative feedback control of what?

cortisol

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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

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what are the actions of cortisol on organ systems?

immune suppression

gluconeogenesis in liver

protein catabolism in muscle

lipolysis in adipose tissue

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how do circadian rhythms control cortisol?

cortisol high in the morning,

low in evening

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what affect does aldosterone have?

water/na+ reabsorption by kidneys, BP goes up

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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

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what effect does ACTH have on zona glomerulosa

increased secretion of aldosterone

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what causes cushing syndrome(CS)? symptoms?

too much cortisol over time

truncal obesity
moon face
hump
osteoporosis
hirsutism
cognitive defects 
edema

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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

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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)

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what does an excess of glucocorticoid do?

diabetogenic effect

visceral obesity

osteoporosis

thinning of skin, muscle atrophy

immunosuppression

water retention

decrease in growth

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what is acth dependent cushing disease caused by?

acth secreting tumors (pituitary)

ectopic tumors

crh secreting tumors

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what is acth independent cushing disease caused by?

adrenal carcinoma

adrenal adenoma

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what is pseudo cushing syndrome?

major depression

anxiety

caused by illness or alcoholism rarely

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what is the negative effect of exogenous glucocorticoids?

can atrophy adrenal cells that produce cortisol

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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

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where does ACTH come from? what does it make?

peptide from anterior pituitary, by POMC

makes cortisol

also MELANIN!

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addisons disease causes what? by what?

hyperpigmentation, overproduction of ACTH

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what is cosyntropin stimulation test used for?

detect adrenal gland insufficiency

cosyntropin in synthetic ACTH

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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 ```