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24 Cards in this Set

  • Front
  • Back
type of nerve cells that comprise the adrenal medulla
post-ganglionic sympathetic nerve cells
sources of cholesterol (2)
extracted from LDL-cholesterol (major)

de novo synthesis from acetate (minor)
______ enzyme is absent in the zone glomerulosa resulting in the inability to synthesize _____ and _____
17α-hydroxylase

cortisol

androgens
______ enzyme is absent in the zone fasciculata and zone reticularis resulting in the inability to synthesize _____
aldosterone synthase

aldosterone
21α-hydroxylase deficiency causes
decreased production of aldosterone and cortisol and increased synthesis of androgens (due to increased levels of ACTH)
characteristics of 21α-hydroxylase deficiency (5)

*net effect
lack of feedback inhibition to anterior pituitary (because of low aldosterone and cortisol)

increased ACTH production (due to lack of feedback inhibition to anterior pituitary)

stimulation of growth of adrenal gland = congenital hyperplasia (due to increased ACTH production)

stimulation of synthetic pathways for androgens (due to congenital hyperplasia)

ambiguous genitalia in females at birth (due to stimulation of adrogen synthesis)

net effect: salt-losing (no aldosterone), virilizing (increased androgens), congenital adrenal hyperplasia (increased ACTH)
cortisol transport in plasma (3)
90% bound to cortisol binding globulin (CBG)

7% bound to albumin

3% circulates "free"
cortisol's metabolic effects (5)
stimulates gluconeogenesis in the liver

enhances protein breakdown in skeletal muscle cells (making amino acids available for gluconeogensis)

stimulates lipolysis in adipose tissue of extremities (stimulates deposition centrally)

permits actions of catecholamines (e.g., vasoconstriction)

decreases osteoblastic activity in trabecular bone and interferes with Ca absorption from the gut (long-term cortisol use results in fragile bones)

*stress/fasting hormone*
cortisol's anti-inflammatory effects (4)
inhibits production of cytokines (e.g., interleukins, prostaglandins, leukotrienes)

inhibits production of chemoattractant molecules which bring leukocytes (e.g., neutrophils, macrophages) to the site of inflammation

stabilizes lysosomal membranes

contributes to vasoconstriction and decreased capillary permeability (decreased blood flow)
cortisol's immunosuppressive effect (2)
decreases lymphocyte proliferation

inhibits hypersensitivity reactions (allergic reactions) due to cell-mediated processes
cortisol levels are elevated during times of (2)
stress

fasting
targets of cortisol negative feedback (2)
anterior pituitary (major)
-inhibits release of ACTH

hypothalamus (minor)
-inhibits release of CRH
cortisol levels:

*highest at
*lowest at
*highest at 8 AM

*lowest at midnight
ACTH levels

*highest at
*lowest at
*highest at 8 AM

*lowest at midnight
aldosterone secretion is controlled by (3)
angiotensin II (secondary to decrease in effective circulating volume)

plasma [K] (aldosterone is low during times of hypokalemia)

ACTH (minor)
sex drive in females is maintained by
androgens (especially DHEA)
side effects of OTC DHEA (4)
virilization (in females)

cessation of menstrual periods

decreased HDL-cholesterol

stimulation of prostate cancer cells (maybe)
characteristics of hyperadrenal function (8)
change in body fat distribution
-moon face
-buffalo hump

skin thinning and fragility

osteopenia (high cortisol level - obsteoblastic activity inhibited)

increased frequency and severity of infections

muscle wasting and weakness

glucose intolerance (high cortisol level)

hypokalemia (high aldosterone level)

HTN (high aldosterone level)
characteristsics of hypoadrenal function (6)
decreased cardiac output and hypotension (due to absence of aldosterone)

inability to regulate blood glucose (due to absence of cortisol)

hyperpigmentation over extensor surfaces, mucous membranes, areolae and surgical scars (due to increased levels of ACTH)

anorexia and weight loss

nausea

diarrhea
ACTH stimulates synthesis of these Epi precursors (2)
dopa

NE
cortisol upregulates
PNMT enzyme

(converts NE to Epi)
catecholamines vs. cortisol

*rate of release
*half life
catecholamines:
*rate of release: rapidly (peptide hormones, stored in secretory granules)
*half life: short

cortisol:
*rate of release: slow (has to be synthesized from cholesterol)
*half life: long
catecholamines vs. cortisol

*profile during prolonged exercise
catecholamines:
-rise quickly and continue to increase for the duration of prolonged exercise

cortisol:
-rise slowly, peak after 30-45 minutes, and decrease along the duration of prolonged exercise
actions of growth hormone (2)
stimulates FFA mobilization in adipose tissue

stimulates gluconeogenesis in the liver