Flashcards in Adrenocorticosteriods Deck (12):
Moving on to the Adverse Effects of Glucocorticoids. The major undesirable effects are the result of their hormonal actions, which lead to a Cushing's like syndrome. What are the metabolic effects of glucocorticoids?
Rounding, puffiness, fat deposition, and plethora usually appear
Fat tends to be redistributed from the extremities to the trunk, the back of the neck and the supraclavicular fossae.
Increased growth of fine hair over the face, thighs and trunk
Breakdown of protein and diversion of AA to glucose production increase the need for insulin leads to
--weight gain, visceral fat deposition, myopathy and muscle wasting, thinning of the skin with striae and bruising, hyperglycemia and eventually osteoporosis, diabetes, and aseptic necrosis of the hip
Other serious adverse effects of glucocorticoids include?
Hypomania or acute psychosis
Depression (long term or long acting steroids)
Increased intraocular pressure is common
Glaucoma may be induced
Benign intracranial hypertension
bacterial and mycotic infections are masked
When corticosteroids are administered for more than 2 weeks what happens?
Adrenal suppression may occur
--if tx extends over weeks to months, the patients should be given appropriate supplementary therapy at times of minor stress such as accidental trauma or surgery
How should corticosteroid dosage be reduced?
--reduction process should be quite slow
May take 2-12 months for the hypothalamic-pituitary -adrenal axis to function acceptably and cortisol levels may not return to normal for another 6-9 months
What happens if dosage is reduced too rapidly?
Symptoms of the disorder in which they were using glucocorticoids for may reappear or increase in intensity.
--even with patients without an underlying disorder may develop symptoms with rapid reductions in corticosteroid levels
Symptoms: anorexia, nausea, vomiting, weight loss, lethargy, headache, fever, joint or muscle pain, and postural hypotension.
These symptoms appear either glucocorticoid deficiency or in the presence of normal or elevated plasma cortical levels indicating dependence
Patients receiving glucocorticoids must be monitored carefully for the development of what?
Sodium retention with edema
How can K loss and effects on bone be prevented in patients on chronic glucocorticoids?
Giving patient K, Ca and vitamin D supplements
The last set of drugs will go over the Antagonist of Adrenocortical Agents. First up is a mineralocorticoid antagonist called Spironolactone, what are features of this drug?
Reverses many of the manifestation of aldosteronism
--establish dx and ameliorating the signs and symptoms when surgical removal is delayed
AE: hyperkalemia, cardiac arrhythmia, menstrual abnormalities, gynecomastia, sedation, headache, GI disturbances, and skin rashes
Next are the synthesis inhibitors and Glucocorticoid Antagonists. First up is Aminogluthemide. What is the MOA and use of this drug?
Blocks the conversion of cholesterol and pregnenolone and causes a reduction in the synthesis of all hormonally active steroids
--tx of adrenal cancer along with hydrocortisone or dexamethasone
Next ketoconazole, an antifungal imidazole derivative is a potent and rather non selective inhibitor of adrenal and gonadal steroid synthesis. Effects only seen at high doses. What is it used for?
Tx of patients with Cushings Syndrome due to several causes.
Tx of prostate cancer
Next Metyrapone, a selective inhibitor of steroid 11-hydroxylation, interfering with cortisol and corticosteroid synthesis. What are the uses of this drug?
Only adrenal mediation that can be administered to pregnant women with Cushing's Syndrome
AE: salt and water retention and hirsutism resulting from diversion of the 11-deoxycortisol precursor to androgen synthesis