hormones of the Hypothalamic-Adenohypophyseal-Adrenocortical Axis
CRH (corticotropin releasing hormone), ACTH (adrenocorticotropic hormone), steroid hormones (corticosteroids)
CRH is secreted by this part of the brain
ACTH is secreted by this part of the brain
ACTH secretion is stimulated by this
CRH secretion is stimulated by this
stressful physical, chemical, and emotional stimuli such as trauma, exercise, hemorrhage, pain, hypoglycemia, LPS, overcrowding, extreme temps.
ACTH secretion is inhibited by this
steroid hormones are secreted by this part of the brain
the steroid hormones produced in the brain
aldosterone, cortisol, estradiol
aldosterone is produced in this part of the adrenal cortex
cortisol is produced in this part of the adrenal cortex
estradiol (sex steroids) is produced in this part of the adrenal cortex
cortisol inhibits the production of these hormones by negative feedback inhibition
CRH & ACTH
this causes too little production of ACTH
diminished blood flow to adenohypophysis
this causes too much production of ACTH
destruction of adrenal cortex (less cortisol to perform negative feedback inhibition)
ACTH promotes the uptake of this substance in all three zonae of the adrenal cortex so they can enzymatically convert it into aldosterone, cortisol, and estradiol
ACTH promotes mitosis/growth, overall health and integrity, but does not directly stimulate the pathway to make this
these substances do not influence the production of CRH or ACTH, only cortisol does
aldosterone & estradiol
Cushing's disease is an adenoma in the pituitary of these cells
in Cushing's, the adenohyphysis is not listening to cortisol negative inhibition feedback, so it keeps making this
in Cushing's, overproduction of ACTH causes this to happen
adrenal cortex overproduces cortisol which exerts excessive negative feedback inhibition on the hypothalamus to reduce production of CRH
in Cushing's, even though the hypothalamus's production of CRH is inhibited, ACTH is still being made because of this
only a small amount of CRH is needed to stimulate the adenohypophysis to make ACTH
in Addison's disease, an animal can't make adequate amounts of this
ACTH is not bound by these
ACTH causes increased glucose entry, glycogenolysis, and glycolysis at these zonae
fasciculata and reticularis
ACTH turns on enzymes but needs these 2nd messengers because it's stuck at the membrane
cAMP and PKA
ACTH is not actually needed at this zona because increased K+ and angiotensin II stimulate its pathway
essential enzyme in glucocorticoid pathway to produce cortisol
ACTH is degraded by these
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