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28 Cards in this Set

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key for regulation of the function of the adrenal glands:
hypothalamic-pituitary-adrenal axis
Where is CRH produced
in the paraventricular nucleus of the hypothalamus, parvocellular neurons produce CRH

41 aa neuropeptide.
vasopressin and CRH can act synergistically to:
stimulate max release of ACTH from the corticotrophs of the anterior pituitary.
CRH secretion can influence

(behavioral functions)
fear
anxiety
depression
sympathetic nervous system activation
when CRH reaches the pituitary:
it binds to receptors on the corticotrophs, and stimulates ACTH synthesis and secretion -> ACTH travels to the adrenal cortex -> stimulate production of hormones (primarily glucocorticoids)
glucocorticoids are so named because:
they have a hyperglycemic effect on blood sugar levels.
during a stress response:
when CRH and ACTH are released, there will be enough fuel released into the bloodstream by action of glucocorticoids to provide substrates for active tissues.
when cortisol is released into the bloodstream:
it provides negative feedback action on the pituitary, hypothalamus and hippocampus.

neurons of the hoppocampus communicate with the hypothalamus to help regulate hormone output.

if there's too much cortisol in the body for too long -> neurons in the hippocampus can be damaged
pro-opiomelanocortin (POMC)
- precursor protein of ACTH
- first product made in the corticoptrophs when CRH interacts with receptor
- protease cleave the POMC -> variety of substances including ACTH (39aa).
alpha - melanocyte stimulating hormone

(alpha-MSH)
ACTH can be cleaved to make this. since the first 13 aa of ACTH are homologous to the 13aa alpha-MSH molecule.
high levels of ACTh and pigmentation:
ACTH can bind to the MSH receptors found in skin cell -> high levels of ACTH -> skin pigmentation
beta-endorphin:
- cleavage of POMC can produce beta-endorphin
- not the same molecule that is active in the CNS (that one's produced in the arcuate nucleus and is used for pain perception)
- beta-endorphin produced in the pituitary has no effect on pain perception
histology of the adrenal cortex:
adrenal gland is surrounded by a capsule. Deep to this capsule is the adrenal cortex (3 distinct layers)

Zona glomerulosa (outer most layer): mineralocorticoids (aldosterone)
Zona Fasciculata (middle layer): glucocorticoids (cortisol)
zona reticularis (deepest layer): weak androgens (DHEA, androsteinedione, bit of testosterone)

deepest: adreal medulla, produce epinephrine and norepinephrine.
17-alpha hydroxyprogesterone -> 11-deoxycortisol
21 alpha hydroxylase
11 deoxycortisol -> cortisol
11 beta hydroxylase
deficiencies of 21-alpha hydroxylase and 11beta hydroxylase:
prevents the synthesis of both cortisol and aldosterone

but there i sa backup of precursor molecules, which are eventually shuttled into androgen synthesizing pathways instead, resulting in virilizing effects on the body.
factors stimulating ACTH secretion:

cortisol
- decrease in cortisol - body removes negative feedback. Also lead to secretion of CRH. Sometimes occur by removing an adrenal gland, or adrenalectomy. Can also occur by giving a cortisol synthesis inhibitor like Metyrapone
factors stimulating ACTH secretion:

sleep
sleep-wake transition

an hour before waking up, large spontaneous rise in cortisol in the body -> raises blood sugar levels and gets the body ready to get up.

CRH and cortisol are subsequently secreted in a pulsatile fashion throughout the rest of the day.
factors stimulating ACTH secretion:

stress
stress -> CRH secretion -> cortisol synthesis

different kinds of stressors that cna trigger this release:
- hypoglycemia
- surgery/anesthesia: cortisol and aldosterone can interact with each other's receptors, the cortisol can activate the mineralocorticoid receptors resulting in Na and water retention -> edema. Vasopressin is also released as a stress hormone -> edema
- trauma, infection and pyrogens
psychiatric disturbances
stimulate cortisol release -> ACTH increase
alpha-adrenergic agonists
and ACTH level
- stimulate release for CRH -> increase in cortisol -> increase ACTH
Serotonin and ACTH level
- key stimulator for CRH release because there are serotonin receptors present on the CRH neurons.
- selective serotonin reuptake inhibitors (SSRIs)
- first few weeks of taking this, make symptoms worse because serotonin stimulate CRH neurons -> increase in cortisol and stress responses. over time, serotonin receptors on the CRH neurons are deownregulated -> resolution of symptoms and control of anxiety
GABA and ACTH
stimulator of cortisol released
Enkephalins and ACTH
inhibitory

- fragments from the breakdown of POMC -> slight negative feedback effect on the pituitary
in the liver, cortisol promotes:
development of enzymes for gluconeogenesis and glycogen synthesis

but once cortisol levels rise -> switch to catabolism, and glucose is released.
renin is secreted from the kidney in response to:
drop in sodium levels or fluid volume

rise in potassium
cushing's syndrome:
- similar symptoms to Cushings's disease
- presence of an adreanl gland tumor rather than a pituitary tumor
- remove the offending adreanl gland neoplasm
Congenital adrenal hyperplasia
adrenogenital syndrome

deficiency in either 21-alpha hydroxylase or 11 beta hydroxylase

- don't synthesize glucocorticoids or mineralocorticoids
- precursors substances are shuttled to the androgen synthesis pathway -> overproduction of DHEA and testosterone -> virilization -> clitoromegaly

- treat with cortisol -> reinstate negative feedback on the pituitary and hypothalamus -> decrease CRH and ACTH.