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Session 4 Pharm- 5

Pharm -5- Steroids

What is the signal that stimulates the anterior pituitary to synthesize and release ACTH CRH released by hypothalamus
What is the signal that stimulates the adrenal gland to synthesize and release cortisol it is released by the anterior pituitary ACTH
What zone of the adrenal cortex synthesizes cortisol Zona Fasciculata
What zone of the adrenal cortex synthesizes aldosterone Zona Glomerulosa
What is the role of cortisol in the body impacts regulation of metabolism, stress response, CNS functions, immunity
What is the role of aldosterone in the body regulate Na+ and K+ concentrations (decreases K and Increases NA)
What type of secretion rhythm does the adrenal cortex hormones follow Circadian Rhythm (peak early in morning and after meals)
Pt has hypercortisolism what is this also known as Cushing's syndrome
What are the s/sx of Cushing's syndrome Weight Gain, High B/P, Facial Plethora (moon face), muscle weakness, Fat redistribution (buffalo hump), osteoporosis, gonadal dysfunction
What is Iatrogenic Cushing's Exogenous administration of glucocorticoids that causes symptoms
If a pt has an excess of cortisol and it is not responding to feedback inhibition what are the 2 likely causes pituitary adenomas and adrenal adenomas
What test can be administered to determine if Cushing's syndrome is pituitary related or not Dexamethasone Suppression test
If the Cushing's is from an adenoma outside of the pituitary what should the results be from the dexamethasone suppression test No change in cortisol levels
If the Cushing's syndrome is from a pituitary tumor what should the results be from a dexamethasone suppression test cortisol levels should decrease
When should you administer the dexamethasone at night before pt goes to bed
What effect does glucocorticoids have on Gluconeogenesis, Protein catabolism, Glucose utilization increases hepatic gluconeogenesis, increases protein breakdown into amino acids (muscle wasting), decreases glucose utilization all of this increases blood glucose
What effect does glucocorticoids have on lipids increases deposition back of neck and face (buffalo hump and moon face), decreases deposition in extremities, over all increases lipolysis and free fatty acids
T/F glucocorticoids increases fat deposition and decreases fat lipolysis F overall increases fat deposition in the face and back of neck but decreases in the rest of body and actually has a net increase in lipolysis
What effect does glucocorticoids have on bone decreases osteoblast activity and increases osteoclast formation
What effect does glucocorticoids have on Ca++ decreases intestinal absorption and increases renal excretion
T/F glucocorticoids are an effective tx for osteoporosis F- they actually can exacerbate and cause osteoporosis
Where do the mineral corticoids exert their effect distal tubules and collecting duct of kidney
What is the effect of the mineral corticoids urinary retention of Na+ and Increases ECF volume but increases excretion of K+ and H+
What is the major system to regulate mineral corticoid activity Renin-Angiotensin system
What is the effect on the cardiovascular system if you have excess corticosteroids Hypertension exacerbating arteriosclerosis, cardiomyopathy, enhanced vascular response to vasoconstrictors (nor epi and angiotensin)
What are the effects if you have a deficiency of corticosteroids on the cardiovascular system hypotension- unresponsive to vasoconstrictors
What drug can you give to inhibit all gonadal and adrenal steroid hormone synthesis Ketoconazole
What s/e can you have from ketoconazole Hypersensitivity rxn and GI disturbances
What is the MOA of Metyrapone inhibits enzyme 11beta hydroxylase increasing levels of 11 deoxycorticosteroids increases levels of adrenal androgens
When would you use metyrapone pregnant women with Cushing's syndrome
What are the s/e of metyrapone salt and water retention, hirsutism, transient dizziness
Why do you see salt and water retention with metyrapone it inhibits 11beta hydroxylase and causes an increase in 11 deoxycorticosteroids which have potent mineral corticoid activity
What is the MOA of Aminoglutethimide Blocks initial conversion of cholesterol to pregnenolone (initial step to make adrenal cortex steroids) this will lower adrenal cortex steroids (all of them cortisol and Mineral corticoids and androgens)
When should you use Aminoglutethimide Cushing syndrome caused by adrenal carcinoma, ectopic ACTH producing tumors and adrenal hyperplasia
What are the s/e of aminoglutethimide lethargy, drowsiness, HA, N/V
What is the MOA of Mifepristone Antagonist at the Glucocorticoid receptor and progestin receptor
What use does mifepristone play in Cushing's syndromes Cushing's syndrome caused by adrenal carcinoma, ectopic ACTH producing tumors
What is the MOA of spironolactone Antagonist at mineral corticoid receptors (antagonist of aldosterone)
What is the use for spironolactone hyperaldosteronism
T/F most cortisol is excreted unchanged by the kidney F most cortisol is metabolized in the liver by reduction of double bonds and conjugation with sulfate and glucuronate
T/F only about 5-10% of the cortisol in the blood stream is free and active T 90-95% is bound to plasma albumin and corticosteroid binding globulin (CBG) and is inactive
What effect do corticosteroids have on the immune system they suppress it decrease transcription/translation of pro-inflammatory mediators IL-2, TNF alpha and others and increases anti inflammatory factors I kappa B alpha, IL-10
T/F giving glucocorticoids decreases a pts chance of getting an infection F they inhibits proliferation, activation and chemotaxis of leukocytes and increase risk of infection
What is the role of IL-2 in the immune system plays a role in activation of many immune system responders, Activates Monocytes, NK cells, Stimulates division of B cells and T cells and TH cells
T/F glucocorticoid binds a G protein couple cell surface receptor F binds to a glucocorticoid receptor inside of the cell
What is the Direct Type 1 mechanism of glucocorticoids action on cells enters cell because of lipophilic cholesterol base binds glucocorticoid receptor (GR) and forms GR/S complex that dimerizes and enters the nucleus binds directly to DNA at he glucocorticoid response element altering mRNA translation
What is alternate day therapy of glucocorticoids you give 48hrs worth of steroid every other day for maintenance of steroid levels
T/F you can stop the steroid tx immediately after the condition is fixed F if you give exogenous steroids you need to taper the dose to allow body to resume normal function and control
What is the protocol for a rapid withdrawal of exogenous steroid administration reduce dose 50% every day
What is the protocol for a slow withdrawal of exogenous steroid administration lower dose 2.5-5mg every 2-3 days
Pt has been on high dose steroids or has been on long term therapy how should you taper them halve dose weekly until 25mg is reached then reduce by 1mg every 3-7days
What is Addison's disease Primary Adrenal Insufficiency defective adrenal function get low cortisol, low aldosterone and high ACTH
How is the dose of exogenous steroid split for tx of Addison's disease give 2/3 in the morning and 1/3 in the afternoon
T/F pts with Addison's typically only need to have replacement of cortisone no the mineral corticoids F they often need both Hydrocortisone for glucocorticoid replacement and Fludrocortisone for mineral corticoid activity
Pt has secondary adrenal insufficiency what is the problem The brain is not either creating enough CRH or ACTH due to defective pituitary or hypothalamic function
What is a major cause of secondary adrenal insufficiency Exogenous corticosteroid it may cause atrophy of the anterior pituitary or hypothalamus this is why you taper withdrawal of steroids to allow hypothalamus and pituitary to recover and resume secretion
What conditions are classically tx with glucocorticoids Inflammatory bowel disease, Asthma, Eczema
What is the drug of choice for systemic/oral inflammation (IBD and Severe Asthma) Prednisolone
What is the steroid of choice for inhalation therapy (asthma) Beclomethasone and Budesonide
What is the steroid of choice for topical therapy (eczema, dermatitis, distal UC and Crohn's) Triamcinolone, Hydrocortisone
What is the tx given to mothers delivering premature babies that helps reduce incidence of respiratory distress syndrome of the infant Beclomethasone 48hrs prior to birth
What is the most common enzyme deficiency in the adrenal cortex that results in increased androgen secretion and decreased mineral corticoid secretion Lack of 21 hydroxylase
What are the effects of a 17hydroxylase deficiency decreases androgens and increases mineral corticoids (decreased vascularization in males and hypertension)
What are the effects of a deficiency in 11-hydroxylase deficiency increased androgens, Increased mineral corticoids (Masculinization and Hypertension)
What is the tx for congenital adrenal hyperplasia suppress release of CRH and ACTH to decrease production of androgens (give dexamethasone and Hydrocortisone) Replace deficient hormone depending on enzyme deficiency (hydrocortisone, Fludrocortisone, dexamethasone), Prevent aromatization of androgens
What two drugs can you give to prevent aromatization of androgens to estrogens aromatase inhibitors (anastrozole, letrozole) and Flutamide (anti-androgen)
Created by: smaxsmith