Pharm Final: Adrenocortical Hormones

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choward04
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Pharm Final: Adrenocortical Hormones
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2013-04-06 18:57:16
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  1. HPA axis controls body processes, DIMES. Define.
    • D-Digestion
    • I-Immune
    • M- Mood
    • E-Energy stores
    • S- sexuality
  2. Which stress response is RAPID?
    SNS (NE/Epi) versus HPA (fast not rapid)
  3. What are the ultimate effects of glucocorticoids, mineralcorticoids, & androgens?
    • Glucocorticoids: immune system/ metabolism (cortisol)
    • -Mineralocorticoids: salt retaining (aldosterone)
    • -Androgen: DHEA
  4. List 7 effects of gluco-corticoids (acute)?
    • 1. ⇑ gluconeogenesis
    • 2. ⇑ Lipolysis
    • 3. ⇑ arousal
    • 4. ⇑ BP
    • 5.⇑ fuel from skeletal muscle
    • 6. ⇓ wound healing
    • 7. ⇓ inflammation
  5. 8 effects of chronic stress
    • 1. lymphocyte suppression--> infection
    • 2. glucose alteration --> DM
    • 3. HTN
    • 4. Bone resorption
    • 5. Ca+ absorption inhibition
    • 6. Gonadotropin inhibition
    • 7. Fat accumulation/redistribution
    • 8. Increase renal vasopressin activity
  6. What are 4 effects of cortisol?
    • 1. metabolism
    • 2. CV
    • 3. growth
    • 4. immunity
  7. When does ACTH pulses peak?
    Early AM & after meals
  8. T or F.  During fight or flight, catecholamines effects are "blunted" without cortisol.
    True because cortisol enhances the response. Also enhances lipolytic response of fat cells to catecholamines
  9. T or F. Cortisol counteracts insulin.
    True. causing insulin resistance (increasing available glucose)
  10. T or F.  Cortisol has an anabolic effect of protein synthesis.
    False--> catabolic--> stimulates protein synthesis in liver BUT degrades proteins in lymph, connective tissue, muscle, peripheral, fat & skin
  11. How does cortisol have an anti-inflammatory effect?
    • -Decrease leukocyte function
    • -Decrease cytokines, chemokines, & mediators
    • -Inhibits macrophages
    • -Decrease COX-2
    • -Decrease prostaglandins
  12. What is the effect of one dose of glucocorticoids?
    • 1. Increase circulating neutrophils
    • 2. Decrease circulating lymph (T&B)
    • -Max effect 6 hrs
  13. Decrease cortisol in the CNS causes what?
    • -Slowed alpha rhythm on EEG
    • -Associated w/ depression
  14. What are the effects of high doses of cortisol in the CNS?
    • 1. Insomnia, euphoria--> depression
    • 2. Increased ICP
    • 3. Chronic exposure: pituitary suppression (decrease ACTH, GH, TSH, LH)
  15. What are the effects of excess cortisol on GI, fat, Vit D, Heme?
    • GI: PUD (H. pylori overgrowth)
    • Fat: redistribution (buffalo hump)
    • Vit D: Antagonism (impaired CA absorption)
    • Heme: Increase platelets and RBCs
    • ** important for fetal lung maturity
  16. T or F. Synthetic corticosteroids are rapidly & completely absorbed.
    True
  17. Where does synthetic corticoids bind?
    Intracellular receptor proteins
  18. How is synthetic cortisol used in diagnostics?
    • -Suppress ACTH to identify a hormone & if production is due to ACTH
    • --> Dex suppression test (Cushing's diag vs depression
    • -R/o tumor or ectopic ACTH syndrome
  19. With Dex test, what level is normal and what is considered Cushings?
    • Normal < 3mcg/dl
    • Cushings >5mcg/dl
  20. List 4 common therapeutic uses of synthetic cortisol?
    • 1. Adrenocortical insufficiency (addison's)
    • 2. Adrenocortical hypo/hyper function (CAH, Cushings, Aldosteronism)
    • 3. Fetal lung maturity
    • 4. Nonadrenal disorders (transplant rejection)
    • 5. Immuno problems
    • 6. Lots others
  21. What are some toxic effects of cortisol?
    • -metabolic (glucose)
    • -Myopathy
    • -Depression (long term)
    • -Eye (cataracts, glaucoma)
    • -ICP
    • -growth retardation in children
    • -Mineralcorticoid effects (Na/fluid retention, K+ loss)--> HF
  22. When can adrenal suppression occur when taking cortisol?
    • -> 2weeks
    • -wean 2-12mo for normal HPA axis
    • -Takes 6-9mo for cortisol levels to normalize
  23. List 6 contraindications of cortisol?
    • 1. PUD, CVD, HTN
    • 2. Infections (varicella & TB)
    • 3. Psych
    • 4. DM
    • 5. Osteoporisis
    • 6. glaucoma
  24. If you want to increase androgen levels, where should you start?
    ACTH (start at tip--> pituitary)
  25. What is Fludrocortison?
    Synthetic aldosterone--> most commonly prescribed salt-retaining hormone
  26. What is the precursor to aldosterone?
    Deoxycorticosterone, primarily controlled by ACTH, 1/2life-->70min
  27. T or F.  Fludrocortisone has very little anti-inflammatory or anti-growth impact.
    True (potent salt retaining)
  28. What drug is a mineralocorticoid antagonist and when is it used?
    • -Spironolactone
    • 1. Primary aldosteronism (reverses manifestations, establishes diagnosis,relieves pre-operative symptoms
    • 2. Diuretic
    • 3. Androgen antagonist (for Hirsutism)
  29. What are some S/E of Spironolactone?
    • -HyperK
    • -arrhythmia
    • -menstrual abnormality, gynecomastia
    • -sedation, H/A
    • -GI upset
    • -Skin rash
  30. Discuss eplerenone.
    • -Mineralocorticoid antagonist
    • -more selective than spironolactone
    • -NO impact on androgen receptors
  31. T or F.  Adrenal androgen stimulate puberty.
    FALSE--> contributes but doesn't stimulate
  32. What is the effect of adrenal androgens on lupus and adrenal insufficiency?
    • Lupus--> improves disease
    • Adrenal insufficiency--> enhanced well-being
  33. Name 3 Androgen SYNTHESIS inhibitors?
    • 1. Ketoconazole
    • 2. Mefepristone (RU-486)
    • 3. Aminoglutethimide
  34. Discuss Ketoconazole.
    -High vs low dose
    -Metabolism
    -Clinical use
    -Adverse rxn
    • -Antifungal in low doses
    • -Non-selective inhibition of adrenal/gonadal steroid synthesis (high doses)
    • -P450 pathway
    • -Cushings syndrome
    • -Hepatotoxity
  35. T or F.  Mifepristone is an ENZYME inhibitor.
    FALSE, androgen SYNTHESIS inhibitor
  36. T or F.  Mifepristone binds to CBG not albumin.
    FALSE (RU-486 binds to albumin NOT CBG)
  37. What are the 2 current recommendations for RU-486?
    • 1. Non-operable disease (ectopic ACTH prod)
    • 2. Adrenal CA non-responsive to other therapy
  38. MOA: Aminoglutethimide
    -Blocks conversion of cholesterol to pregnolone (decrease steroid production)
  39. What are 2 uses for Aminoglutethimide?
    • 1. Hormone + Br Ca (but replaced by Tamoxifen)
    • 2. Cushing syndrom
  40. What are 4 S/E or cautions for Aminoglutethimide?
    • 1. Lethargy
    • 2. skin rash
    • 3. Decrease stress tolerance (accelerates steroid clearance)
    • 4. Enhances metabolism of Dex

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