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23 Cards in this Set

  • Front
  • Back
What causes cushings syndrome?
overproduction of ACTH (inc. pituitary secretion from pituitary tumor, ectopic ACTH producing tissue pancreatic thryroid or lung tumors)
overproduction of Cortisol (adrenal tumors)
exogenous supraphysiologic corticoidsteroid administration
what is the clinical presentation of cushings syndrome?
obesity, HTN, facial plethora(moon facies), glucose intolerance, striae, fat redistribution (buffalo hump), myopathy, osteoporosis, psychiatric changes, females: menstrual irregularity, hirsutism
How do you diagnose cushings syndrome?
laboratory abnormalitites, dexamethasone supression test
how do you treat cushings syndrome?
primary tx is surgery if caused by tumor, drugs can be used until surgery can be done, or use drugs if tumor is in place where it cant be removed
what classes of drugs can be used to treat cushings syndrome?
steroid synthesis inhibitors
adrenolytic agents
neuromodulators of ACTH release
glucocorticoid receptor blockers
what is metyrapone?
steroid synthesis inhibitor
11-beta-hydroxylase inhibitor, blocks conversion of 11-deoxycortisol to cortisol
poorly tolerated due to nausea, vomiting, HA, dizzines, abdominal discomfort, rash
what is aminoglutethimide?
steroid synthesis inhibitor
blocks conversion of XOL to pregnenolone (1st step in pathway, so blocks all downstream hormones)
poorly tolerated: severe sedation, nausea, atacia, rash
what is ketoconozole?
oral antifungal, steroid synthesis inhibitor, potent inhibitor of many CYP enzymes, inhibits 11-beta-hydroxylase and 17 hydroxylase
when are steroid synthesis inhibitors use?
usually used together to reduce side effects and improve tolerance
used until surgery can be performed or in inoperable patients
What is primary adrenal insufficiency?
Addisons disease results from destruction of all adrenal cortical zones, deficiency in aldosterone, cortisol, and testosterone
ususally chronic but may be acute following trauma to adrenals
what are symptoms of addisons disease?
weakness, wieght loss, hyperpigmentation, hypotension, nausea, vomiting, vitiligo
how is addisons disease treated?
replacement of glucocoticoids and mineralocorticoids
hydrocortisone 20mg or prednisone 5mg in the morning plus 33 to 50% of the am dose in the evening and fludrocortisone 0.05 to 0.2 mg/day
adjust dose as needed
What is mitotane (lysodren)?
adrenolytic agent, cytotoxic agent resembles DDT, inhibits conversion of 11-hydroxycortisol to 11-desoxycorticosterone in the cortex, causes degradation of cells in zona fasiculata and reticularis resulting in atrophy of cortex and dec. cortisol and testosterone production, short term use has little effects on aldosterone production in zona glomerulosa
what are some adverse effects of mitotane?
production of cortisol is ususally reduced to point that corticosteroid suppplementation will be required, causes severe lethargy adn somnolence in 40% of patients, causes significant hypercholesterolemia
What is the mechanism of neuromodulator and give some examples?
decrease ACTH secretion, none are consistently effective, response rates are low
cyporheptadine (periactin)
bromocriptine (parlodel)
valproic acid (depakote)
octreotide (sandostatin)
what is mifepristone?
RU-486, progesterone and glucocorticoid receptor antagonist, primarily used to terminate pregnancy, limited experience in cushing's syndrome but appears to be highly effective
what causes exogenous hypercortisolemia?
occurs from chronic administration of glucocorticoid in excess of physiological amounts, produces cushings syndrome effects, tx by tapering glucocorticoids and d/c if possible, abrupt d/c results in adrenal insufficiency (secondary addisons dz)
What is secondary adrenal insufficiency?
results from too rapid d/c of therapeutic corticosteroids in doses greater than normal physiologic excretion, aldo secretion is no affected, can be avoided by gradually tapering the dose of corticosteroid over time
how do you taper corticosteroids?
rate and time depends on what is being treated and need for d/c, slow taper is preferred while wathcing for dz exacerbation, if rapid D/C is required then decrease dose by 50% per day, once normal physiological levles are neared (20-30mg cortisol, 5-7.5mg prednisone) must go very slowly, testing may be performed to evaluate axis function
example of corticosteroid taper
pt has been on 40mg prednisone per day for several months, dec. to 30mg/day for 1 week, then 20mg/day for 1 week, then 10mg/day for 1 week while observing for dz exacerbation, further dec. should be slower 9mg/day x 1wk, 8mg/day x1wk, 7mg/day x1wk, 6mg/day x1wk, etc. until patients is off teh drug
what is acute adrenal crisis?
occurs when the adrenal requirements of pt. exceed the ability to respond, most common cause is axis suppression from therapeutic corticosteroid use, may occur in situations of physica stress, such as: suergery, infection, trauma
what are the symptoms of adrenal crisis?
myalgias, anorexia, fever, weight loss, vomiting, fever, hypotension, shock, hyponatremia, hypoglycemia, hypercalcemia
how is acute adrenal crisis managed?
pts on corticosteroids who undergo physical stress should be put on "stress dose" of corticosteroids, hydrocortisone preferred due to mineralocorticoid and glucocorticoid activity, give hydrocortisone 100mg IV q 6-8hrs x 24-48hrs or constant infusion of 10-15mg/hrx24-48 hr or until stress is alleviated
then 50mg po q 8hr x48hr then taper patient back to dose of steroid they were on prior to event
if hyperkalemia is present add 0.1mg fludrocortisone po daily