Lecture 61 "Adrenal Gland"
Terms
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- 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