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Session 4 Pharm- 5
Pharm -5- Steroids
| Question | Answer |
|---|---|
| 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) |
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smaxsmith
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