Cortisol Flashcards
3 layers to the adrenal cortex
outer: zona glomerulosa
middle: zona fasciculata
inner: zona retiularis
Glucocorticoids are produced where in the adrenal cortex
zona fasciculata
Glucocorticoids
CORTISOL- essential to life for protein and carbohydrate metabolism
Mineralcorticoids are produced where in the adrenal cortex
zona glomerulosa
Mineralcorticoids
Aldosterone
Precursore to corticoids?
Cholesterol; can be stored in endocrine cells as ester
StAR
transports cholesterol into mito
P450 (Rate-limiting)
hydroxylates cholesterol into pregnenolone
Rate of steroid hormone secretion can only be controlled by
hormone synthesis (steroids cannot by stored)
Cortisol binds __________ in blood
transport protein CORTICOSTEROID-BINDING GLOBULIN (CBG) or TRANSCORTIN
Estrogen effect on transcortin
increases its synthesis
Cortisol effect?
increased gluconeogenesis, protein degradation for aa substrates for gluconeogenesis, increased glucagon, decreased GLUT4
a fasting person without cortisol
CANNOT MOBILIZE PROTEINS
Cortisol is permissive for
EPI and GH lipolysis “glucose-sparing effect”
NE, EPI, ADH, and GH
Cortisol causes
lipolysis in some adipose tissues, while in trunk and neck causes lipogenesis (moon face and abdominal fat)
Cushing’s disease
chronic exposure to high levels of cortisol (moon face and abdominal fat)
Cardiovascular permissive effect of cortisol
cortisol is permissive to catecholamines and angiotensin for contraction of vascular smooth muscle and contraction to maintain MAP
Permissive cardiovascular effects of cortisol re due to
increased beta receptors and increased Ca channels
Cortisol is permissive for growth with
GH and EPI
Steroid/cortisol have ______________ properties and are used for treatment
anti-inflammatory and anti-immune effects (inhibit inflammation and leukotriene and prostaglandin synthesis)
Side effects of using cortisol treatment
causes general breakdown of proteins, thinning of skin, muscle wasting, bone breakdown, ACTH secretion is suppressed (must ease off treatment)
Metabolism of cortisol
slow, in liver
Release of Cortisol
Stress/trauma –> CRH (hypothalamus) –> ACTH (anterior pituitary) –> Cortisol (adrenal cortex)
Mechanism for ACTH to increase cortisol
LDL uptake, hydrolysis of cholesterol, transport StAR into mito, binding of P450 to cholesterol
ACTH chronic
hypertrophy of adrenal cortex
Negative feedback loop
cortisol inhibits anterior pituitary and hypothalamus
Diurnal pattern of ACTH-cortisol
greatest in the morning, lowest at night (highest when fasting)
Cortisol spikes are proportional to
the magnitude of the trauma (despite (-)feedback loop)
Addison’s Disease
diminished cortisol, despite high levels of CRH and ACTH
Pituitary adenoma
high ACTH and Cortisol, low CRH
Adrenal adenoma (cushings disease)
high cortisol, low CRH and ACTH
Ectopic production of ACTH (cushing’s syndrome)
ACTH high in plasma, low production in pituitary, high cortisol, low CRH
Iatrogenic Cushings SYNDROME
High cortisol from medication, low CRH, low ACTH, and low Cortisol from adrenal cortex
removal of cortisol treatment of resection of cortisol secreting tumor
must be done slowly to allow ACTH and adrenal cortex to gradually become functional again
Dexamethasone suppression test at low doses
normal ppl should have suppressed ACTH, cushings syndrome no suppression
Dexamethasone suppression test at high doses
Cushing’s disease of pituitary gland is suppressed but Cushing’s syndrome of ectopic location is NOT suppressed
