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28 Cards in this Set
- Front
- Back
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key for regulation of the function of the adrenal glands:
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hypothalamic-pituitary-adrenal axis
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Where is CRH produced
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in the paraventricular nucleus of the hypothalamus, parvocellular neurons produce CRH
41 aa neuropeptide. |
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vasopressin and CRH can act synergistically to:
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stimulate max release of ACTH from the corticotrophs of the anterior pituitary.
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CRH secretion can influence
(behavioral functions) |
fear
anxiety depression sympathetic nervous system activation |
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when CRH reaches the pituitary:
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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)
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glucocorticoids are so named because:
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they have a hyperglycemic effect on blood sugar levels.
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during a stress response:
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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.
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when cortisol is released into the bloodstream:
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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 |
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pro-opiomelanocortin (POMC)
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- 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). |
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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.
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high levels of ACTh and pigmentation:
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ACTH can bind to the MSH receptors found in skin cell -> high levels of ACTH -> skin pigmentation
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beta-endorphin:
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- 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 |
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histology of the adrenal cortex:
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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. |
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17-alpha hydroxyprogesterone -> 11-deoxycortisol
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21 alpha hydroxylase
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11 deoxycortisol -> cortisol
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11 beta hydroxylase
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deficiencies of 21-alpha hydroxylase and 11beta hydroxylase:
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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. |
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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
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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. |
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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 |
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psychiatric disturbances
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stimulate cortisol release -> ACTH increase
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alpha-adrenergic agonists
and ACTH level |
- stimulate release for CRH -> increase in cortisol -> increase ACTH
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Serotonin and ACTH level
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- 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 |
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GABA and ACTH
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stimulator of cortisol released
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Enkephalins and ACTH
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inhibitory
- fragments from the breakdown of POMC -> slight negative feedback effect on the pituitary |
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in the liver, cortisol promotes:
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development of enzymes for gluconeogenesis and glycogen synthesis
but once cortisol levels rise -> switch to catabolism, and glucose is released. |
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renin is secreted from the kidney in response to:
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drop in sodium levels or fluid volume
rise in potassium |
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cushing's syndrome:
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- similar symptoms to Cushings's disease
- presence of an adreanl gland tumor rather than a pituitary tumor - remove the offending adreanl gland neoplasm |
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Congenital adrenal hyperplasia
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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. |
