Pharm -5- Steroids
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| What is the signal that stimulates the anterior pituitary to synthesize and release ACTH | CRH released by hypothalamus
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| What is the signal that stimulates the adrenal gland to synthesize and release cortisol it is released by the anterior pituitary | ACTH
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| What zone of the adrenal cortex synthesizes cortisol | Zona Fasciculata
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| What zone of the adrenal cortex synthesizes aldosterone | Zona Glomerulosa
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| What is the role of cortisol in the body | impacts regulation of metabolism, stress response, CNS functions, immunity
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| What is the role of aldosterone in the body | regulate Na+ and K+ concentrations (decreases K and Increases NA)
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| What type of secretion rhythm does the adrenal cortex hormones follow | Circadian Rhythm (peak early in morning and after meals)
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| Pt has hypercortisolism what is this also known as | Cushing's syndrome
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| 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
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| What is Iatrogenic Cushing's | Exogenous administration of glucocorticoids that causes symptoms
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| 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
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| What test can be administered to determine if Cushing's syndrome is pituitary related or not | Dexamethasone Suppression test
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| 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
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| If the Cushing's syndrome is from a pituitary tumor what should the results be from a dexamethasone suppression test | cortisol levels should decrease
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| When should you administer the dexamethasone | at night before pt goes to bed
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| 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
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| 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
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| 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
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| What effect does glucocorticoids have on bone | decreases osteoblast activity and increases osteoclast formation
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| What effect does glucocorticoids have on Ca++ | decreases intestinal absorption and increases renal excretion
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| T/F glucocorticoids are an effective tx for osteoporosis | F- they actually can exacerbate and cause osteoporosis
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| Where do the mineral corticoids exert their effect | distal tubules and collecting duct of kidney
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| What is the effect of the mineral corticoids | urinary retention of Na+ and Increases ECF volume but increases excretion of K+ and H+
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| What is the major system to regulate mineral corticoid activity | Renin-Angiotensin system
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| 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)
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| What are the effects if you have a deficiency of corticosteroids on the cardiovascular system | hypotension- unresponsive to vasoconstrictors
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| What drug can you give to inhibit all gonadal and adrenal steroid hormone synthesis | Ketoconazole
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| What s/e can you have from ketoconazole | Hypersensitivity rxn and GI disturbances
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| What is the MOA of Metyrapone | inhibits enzyme 11beta hydroxylase increasing levels of 11 deoxycorticosteroids increases levels of adrenal androgens
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| When would you use metyrapone | pregnant women with Cushing's syndrome
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| What are the s/e of metyrapone | salt and water retention, hirsutism, transient dizziness
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| 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
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| 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)
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| When should you use Aminoglutethimide | Cushing syndrome caused by adrenal carcinoma, ectopic ACTH producing tumors and adrenal hyperplasia
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| What are the s/e of aminoglutethimide | lethargy, drowsiness, HA, N/V
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| What is the MOA of Mifepristone | Antagonist at the Glucocorticoid receptor and progestin receptor
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| What use does mifepristone play in Cushing's syndromes | Cushing's syndrome caused by adrenal carcinoma, ectopic ACTH producing tumors
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| What is the MOA of spironolactone | Antagonist at mineral corticoid receptors (antagonist of aldosterone)
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| What is the use for spironolactone | hyperaldosteronism
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| 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
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| 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
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| 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
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| 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
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| 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
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| T/F glucocorticoid binds a G protein couple cell surface receptor | F binds to a glucocorticoid receptor inside of the cell
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| 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
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| What is alternate day therapy of glucocorticoids | you give 48hrs worth of steroid every other day for maintenance of steroid levels
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| 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
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| What is the protocol for a rapid withdrawal of exogenous steroid administration | reduce dose 50% every day
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| What is the protocol for a slow withdrawal of exogenous steroid administration | lower dose 2.5-5mg every 2-3 days
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| 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
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| What is Addison's disease | Primary Adrenal Insufficiency defective adrenal function get low cortisol, low aldosterone and high ACTH
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| 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
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| 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
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| 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
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| 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
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| What conditions are classically tx with glucocorticoids | Inflammatory bowel disease, Asthma, Eczema
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| What is the drug of choice for systemic/oral inflammation (IBD and Severe Asthma) | Prednisolone
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| What is the steroid of choice for inhalation therapy (asthma) | Beclomethasone and Budesonide
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| What is the steroid of choice for topical therapy (eczema, dermatitis, distal UC and Crohn's) | Triamcinolone, Hydrocortisone
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| 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
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| 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
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| What are the effects of a 17hydroxylase deficiency | decreases androgens and increases mineral corticoids (decreased vascularization in males and hypertension)
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| What are the effects of a deficiency in 11-hydroxylase deficiency | increased androgens, Increased mineral corticoids (Masculinization and Hypertension)
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| 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
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| 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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