Adrenal Cortex: Glucocorticoid Flashcards
plasma profile of glucocorticoids
increased blood glucose, increased FFA, increased AA
what releases glucocorticoids
zona fasiculata
what hormones are released by the zona fasiculata
progesterone and cortisol
what makes progesterone into 17 hydroxyprogesterone
17a hydroxylase
what makes 17 hydroxyprogesterone into 11 deoxycortisol
21 beta hydroxylase
what makes deoxycortisol into cortisol
11 beta hydroxylase
what are the glucocorticoids
cortisol, cortisone, corticosterone
how does cortisol circulate
bound to transcortin and albumin
half life of glucocortisol
70min aka long
when are glucocorticoids released
in response to stress
major function of glucocorticoids
increase plasma glucose via gluconeogenesis
where are glucocorticoids metabolized
liver and kidney
what does cortisol do
- decrease bone formation, increase bone resorption
- decrease CT
- inhibit inflammatory and immune response
- maintain CO, increase arteriolar tone, decrease endothelial permeability
- facilitate maturation of the fetus
- increase glomerular filtration and free water clearance
- modulate emotional tone and wakefulness
- maintain muscle function, decrease muscle mass
when is cortisol released
increases with waking, possibly increased sensory input and visual processing
what chemical is on cortisol
hydroxy group on C11
cortisol to cortisone
11b hydroxysteroid dehydrogenase
what chemical is one cortisone
ketone on c11
regulation of cortisol
CRH–>AP–>ACTH–>adrenal cortex–>cortisol
negative feedback to AP and hypothalamus
how is ACTH released in the blood
CRH binds to Gs–>AC–>cAMP–>PKA–>P proteins–>POMC mRNA–>POMC–>ACTH, beta LPH into the blood
how are the steroid enzymes released from adrenal gland
ACTH binds to adrenal gland Gs–>cAMP–>PKA–>p proteins–>mRNA–>steroidigenic enzymesto mito–>pregnenolone–>to SER–>back to mito–>glucocorticoids and androgens in blood
what steroidogenic enzymes are made when ACTH binds
17 alpha and 21 beta hydroxylase
what increases ACTH secretion
- decreased cortisol levels
- sleep wake transition
- stress, hypoglycemia, surgery, trauma
- psychiatric disturbances
- ADH
- alpha adrenergic agonists
- beta adrenergic antagonist
- serotonin
what decreases ACTH secretion
- increased blood cortisol
- opioids
- somatostatin
what is the diabetogenic effect of glucocorticoids
cortisol increases glucose production from non carb sources and increases glucose utilization
action of insulin
decrease glycogenolysis, gluconeogenesis, ketogenesis and lipolysis
action of glucagon and epinephrine
increase glycogenolysis, gluconeogenesis, ketogenesis, lipolysis
what is the effect of glucocorticoids on AA production in the plasma
unbranched AA (alanine) are taken up into tissues faster than branched (leucine) and used more readily so there are increased numbers in the plasma
what is the primary metabolic action of cortisol
gluconeogenesis
what other actions does cortisol do
increased lipolysis, increased FFA and AA mobilization, decrease fat synthesis, inhibit glucose storage
blood effect of glucocorticoids
increased FFA, increased ketone bodies, increased glucose, increase AA
what does cortisol inhibit
cyclooxygenase (decreases prostaglandins, thromboxanes)
what is cushings disease
excessive long term cortisol exposure
sx of cushings
protein depletion, muscle weakness, fat redistribution into central obesity, increased glucose (may be confused with DM), increased Na retention, osteoporosis, suppressed immune system, insomnia
normal response of dexamethasone suppression test
ACTH and cortisol will be depressed by low dose of dexamethasone
what does the dexamethasone suppression test test
pathophysiology of anterior pituitary and adrenal
ACTH secreting neoplasm of pituitary dexamethasone suppression test
low dose of dexamethasone will have little or no effect on ACTH and cortisol, high dose depress ACTH and cortisol
ACTH secreting neoplasm of ectopic foci or cortisol secreting tumor of adrenal cortex dexamethasone suppression test
neither low or high dose will have any affect on ACTH or cortisol
sx of adrenocortical insufficiency
weight loss, poor appetite, malaise, n/v, abdominal pain, fever, poor stress response, hypoglycemia, skin hyperpigmentation (addisons disease), low bp, vascular collapse, increased K
what is cushings disease
hypercortisol, decreased ACTH if cortisol increased
what is addisons disease
hypocortisol
what is seen in 21b hydroxylase or 17a hydroxylase deficiency
increased ACTH because of decreased/absent cortisol
plasma profile in primary addisons disease?
decreased cortisol, increased ACTH, and decreased plasma glucose
plasma profile in cushings disease
ACTH, cortisol and plasma glucose all increased
secondary disorder
plasma profile in 21 b hydroxylase deficiency
increased ACTH, decreased deoxycorticosterone, decreased aldosterone, decreased cortisol, increased dihydroepiandosterone (shunted toward adrenal androgens), increased urinary 17 ketosteroids
plasma profile in 17 a hydroxylase deficiency
excess production of deoxycorticosterone and cortisone, causing high blood pressure.
cortisol and adrenal androgens (DHEA) are suppressed.
aldosterone indirectly suppressed bc high BP (inactivated RAAS)
