B5.034 Prework 2 Endogenous Steroids and Adrenal Insufficiency Flashcards
what is adrenal insufficiency (AI)
hypofunction of the adrenal cortex (production of cortisol)
why does AI arise?
destruction of the adrenal gland itself (primary AI, Addisons disease (AD))
lack of ACTH (secondary AI)
most common cause of AD
autoimmune destruction of the adrenal gland (80%)
infectious causes of AI
viral, mycobacterial, fungal
AIDs the most common
hemorrhagic causes of AI
anticoagulants/ coagulopathy, sepsis, thrombosis
metastatic cancers causing AI
brast, lung, GI, renal
infiltrative causes of AI
amyloidosis, sarcoidosis, hemochromatosis, demyelination
what causes secondary AI
adrenal gland atrophy from ACTH deficiency
most often results from:
-pituitary corticotroph atrophy owing to previous exogenous glucocorticoid use (prednisone)
-panhypopituitarism
-isolated ACTH deficiency
diagnosis of AI
demonstrate diminished responsiveness of the hypothalamic-pituitary-adrenal axis to stimulation
- morning cortisol value less than 4 mg
- cosyntropic (ACTH) stimulation test usually required and is the gold standard
describe the cosyntropin stimulation test
rise in cortisol level to 18, or a change in 9 in 30-60 min after 250 mg of cosyntropin (ACTH) administration is normal response
what causes hyperpigmentation in primary AI
excess ACTH can interact with melanocytes
usually occurs in areas exposed to light and pressure
acute therapy for AI
IV fluid
high dose IV glucocorticoids
chronic therapy for AI
physiologic oral glucocorticoid replacement
mineralocorticoid replacement (for primary)
patient education
-medic alert bracelet
-dosage increases for stress and surgery
-parenteral admin is oral not an option
agents used for oral glucocorticoid replacement
prednisone
agent for IV glucocorticoids
hydrocortisone
mineralocorticoid activity
maintains BP
general rule of AI during sickness
double current steroid for 3 days
if major surgery or critical illness change to IV steroids
physiologic effects of cortisol
affects vascular and bronchial smooth muscles with the relationship to catecholamines
in absence of cortisol there is vasodilation and hypotension
physiologic effect of glucocorticoids
stimulate gluconeogenesis and glycogen synthesis in the fasting state
increase serum glucose by inhibiting uptake of glucose in the muscle
stimulates hormone sensitive lipase and lipolysis (minor effect)
action of short acting steroids
hydrocortisone
may mimic diurnal rhythm best, 100% bioavailability
short half life, generally recommended once in the morning and once in the early afternoon
action of long acting steroids
dexamethasone and prednisone provide longer duration of action
better for noncompliance
greater inter individual variability
what is fludrocortisone
potent steroid which is mainly a mineralocorticoid
dose 0.1 mg per day
given to individuals with primary AI that have little or no mineralocorticoid steroids
function of fludrocortisone
helps sodium retention at the level of the kidney
has a side effect of hypokalemia due to excessive mineralocorticoid activity
steroid side effects
immunosuppression hypertension weight gain osteoporosis insomnia mood swings peptic ulcers redistribution of fat
