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three layers of the adrenal cortex
zona glomerulosa, zona fasciculata, zona reticularis
zona glomerulosa
outer most layer of the adrenal cortex
secretes mineralcorticoids (aldosterone)
aldosterone
regulates [Na+], [K+] and blood volume (since water follows salt)
specifically Na reabsorption, K secretion
zona fasciculata
middle layer of adrenal cortex
secretes glucocorticoids/glucosteroids (cortisol)
zona reticularis
innermost layer of the adrenal cortex
secretes mostly sex steroids (androgens)
DHEA
androgen
contributes to pubertal growth spurt in both sexes and important in inducing secondary sex characteristics in females
steroid hormone synthesis
the production of a specific adrenal steroid hormone in each zone is determined by which enzymes are present in each zone (which alter the chemical structure of cholesterol)
production of cortisol from cholesterol
cholesterol --> prenenolone --> 17-hydroxyprogesterone--> cortisol
cortisol is considered
the main stress hormone
3 hormone cascade for cortisol
neural inputs cause hypothalamus to secrete CRH
CRH causes anterior pituitary to release ACTH
ACTH causes adrenal cortex to release cortisol
cortisol causes target cells to produce response
CRH
produced by the hypothalamus
corticotropin releasing hormone
tropic hormone
ACTH
released by the anterior pituitary gland (corticotropes)
Adrenocorticotropic hormone
tropic hormone
what cells in the anterior pituitary release ACTH
corticotropes
what part of the 3 hormone cascade for cortisol results in a negative feedback
increased plasma levels of cortisol negatively feedback on the hypothalamus and the anterior pituitary
stimuli that can enhance cortisol secretion
anxiety
pain
trauma
hypovolemia (low blood volume)
hypoglycemia (low blood sugar)
hypothermia (low body temp)
what other hormones are enhanced by the same stimuli as cortisol
catecholamines (epinephrine and norepinephrine)
epinephrine is released from
adrenal medulla (hormone)
Norepinephrine is released from
sympathetic neurons (neurotransmitter)
functions of basal or nonstress levels of cortisol
1. metabolic effects
2. permissive
3. anti-inflammatory/anti-immune
4. fetal/neonatal development
functions of basal or nonstress levels of cortisol: metabolic effects
liver glucose production between meals
provides substrates and maintain enzymes involved in metabolic homeostasis to keep plasma glucose concentrations regular
functions of basal or nonstress levels of cortisol: permissiveness
cortisol is permissive to adrenergic receptors of the cardiovascular system (# of alpha and beta-1 receptors increases to maintain adequate BP)
functions of basal or nonstress levels of cortisol: anti-inflammatory/ anti-immune
prevent hyper-response
functions of basal or nonstress levels of cortisol: fetal/neonatal development
fetal development of brain, intestines, lungs, glands
turns on surfactant late in gestation to help inflate lungs
functions of cortisol in stress
1. metabolic effects
2. bone resorption
3. support sympathetic
4. stimulates erythropoietin
5. anti-inflammatory/ immunosuppression
6. inhibition of non-essential functions
functions of cortisol in stress: metabolic effects
catabolizes body stores of nutrients thereby mobilizing glucose, fatty acids, amino acids for energy and tissue repair
can cause tissue wasting, muscle loss, elevated blood glucose
functions of cortisol in stress: bone resorption
Ca+2 mobilization for possible bone repair
results in osteoporosis with prolonged exposure
functions of cortisol in stress: support sympathetic
supports sympathetic responses related to vasoconstriction
high BP with prolonged exposure
functions of cortisol in stress: stimulates erythropoietin
replaces RBC's if bleeding out
polycythemia with prolonged exposure (too many cells, blood becomes thick)
functions of cortisol in stress: anti-inflammatory/immunosuppression
helps in treatment and prevent rejection of transplanted organs
increased susceptibility for infection with prolonged exposure
functions of cortisol in stress: inhibition of non essential functions
reproduction and growth
adrenal insufficiency results in
cortisol hypo-secretion
primary adrenal insufficiency
Addison's disease
primary adrenal insufficiency is caused by
-destructive tumors
-infection
-autoimmune destruction (most common)
to the adrenal cortex
primary adrenal insufficiency results in
hypotension
low blood glucose
high plasma ACTH and CRH (no negative feedback)
secondary adrenal insufficiency is caused by
anterior pituitary dysfunction = loss of ACTH
secondary adrenal insufficiency results in
similar symptoms as primary adrenal insufficiency, but with low ACTH
hypotension
low blood glucose
high CRH
cortisol hypersecretion
cushing's syndrome/disease
Cushing's syndrome
hypercortisolism and all of its effects, regardless of original cause
when cortisol is HIGH (any scenario)
Cushing's disease
a case of Cushing's syndrome when the cause is identified as an ACTH-secreting tumor (anterior pituitary affected)
cortisol hypersecretion is caused by
hyper-secreting tumors (on adrenal gland or anterior pituitary)
glucocorticoid therapy for other conditions
hypersecretion of cortisol results in
osteoporosis
thin skin
muscle weakness
immunosuppression
high blood glucose
hypertension
decreased fertility
stunted growth
redistribution of fat
redistribution of fat when cortisol levels are high
obesity in trunk and face yet wasting of arms and legs with unusual deposition of fat on back/shoulders
what are other hormones released during stress
aldosterone
vasopressin
growth hormone
glucagon
beta-endorphin
epinephrine
aldosterone
increases Na+ retention and BP
vasopressin
increases water retention and BP
growth hormone
breaks down fat, mobilizes blood glucose
glucagon
mobilizes glucose from liver stores
beta-endorphin
pain relief and mood elevator
stress can decrease the levels of
insulin
insulin
storage hormone
with less insulin during stress, levels of glucose, fatty acids, and amino acids in the plasma increase