corticosteroids

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ahalvors
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80720
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corticosteroids
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2011-04-19 19:35:57
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corticosteroids
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Pharm exam 4-corticosteroids
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  1. Which two adrenal glucocorticoids (GC) are produced in response to signals from the pituitary (ACTH) and hypothalamus (CRH)?
    cortisol and corticosterone
  2. Adrenal produces 2 other major hormone types
    • 1)androgens (mainly DHEA) which are also produced in response to ACTH and
    • 2)MC (aldosterone and deoxycorticosterone) which are regulated mainly by Ang II and K+
  3. 1)GC are used to:
    2)MC are used to:
    • 1)suppress immune function and inflammation
    • 2)treat adrenal insufficiency
  4. All adrenal steroids are derived from
    cholesterol
  5. HYPOTHALAMO-PITUITARY-ADRENAL AXIS
    Stress stimulates release of CRH (hypothal) which stimulates release of ACTH (pituitary) which stimlulates release of GC (adrenal). What provides negative feedback to CRH and ACTH?
    GC
  6. GC ACTIONS
    1)metabolic pathways
    2)immune system
    3)ca++
    4)BP
    • 1)intermediary metabolism
    • 2)decrease capillary permeability, decrease WBC migration, decrease WBC activation
    • 3)decrease absorption of ca++ in GI tract, increase absorption of Ca++ from bone
    • 4)increase (via increase adrenergic recept.?)
  7. Glucocorticoid regulated pathways (catabolic)
    • 1)a.a's get broken down into pyruvate and then glc
    • 2)protein gets broken down into a.a's
    • 3)triglycerides get broken down into fatty acid's (enhanced catecholamine induced lipolysis)
  8. Aldosterone: Production and Actions
    • 1)aldosterone's release is stimulated by Ang II and III and K+
    • 2)aldosterone secreted by adrenal gland causes increased Na+ reabsorption, increased water reabsorption and decreased K+ and H+ reabsorption (in kidney)
    • 3) #2 leads to low BP, bld volume and bld Na+
    • 4) #3 stimulates secretion of renin from the kidney to convert angiotensinogen to Ang I (Ang I to Ang II conversion done by ACE)
  9. Aldosterone uses
    • 1)suppression of inflammation and allergic responses
    • 2)chronic hypoglycemia
    • 3)replacement therapy for adrenal insufficiency
  10. Adrenal Insufficiency
    1)causes
    2)symptoms
    3)outcome
    4)treatment
    • 1)acute: adrenal damage, GC withdrawal; chronic: disease (Addison's)
    • 2)hypoglycemia (upon fasting) and hypotension
    • 3)decrease BP and bld flow leads to decrease CV/renal function
    • 4)GC and/or MC
  11. GC
    1)cortisol(aka hydrocortisone): relative potency (GC and MC) and duration
    2)cortisone
    3)prednisolone
    4)prednisone
    5)methylprednisolone
    6)triamcinolone
    7)betamethasone
    8)dexamethasone
    • 1)GC=1, MC=1; Short
    • 2)GC=.8, MC=.8; short
    • 3)GC=4, MC=.8; intermediate
    • 4)GC=4, MC=.8; intermediate
    • 5)GC=5, MC=.3; intermediate
    • 6)GC=5, MC=0; intermediate
    • 7)GC=30, MC=0; long
    • 8)GC=30, MC=0; long

    • *1-2=topical use, used for hypoglycemia and produces minimal side effects
    • *3-8=systemic anti inflammatory activity
    • *3-6=first choice drug; has more side effects than 1-2 and 7-8=second choice drug; has a lot more adverse effects than drugs 3-6
  12. MC
    1)aldosterone: relative potency (GC and MC); duration
    2)deoxycorticosterone
    3)fludrocortisone
    • 1)GC=.2, MC=3000; very short (1-2 hours)
    • 2)GC=0, MC=20; short (6-12 hours)
    • 3)GC=10, MC=250; intermediate (12-24 hours)
  13. Routes of administration
    • 1)oral
    • 2)parenteral (im, iv, sc)
    • 3)topical(prodrugs not effective as topical)
  14. Adverse Effects of GC
    1)metabolic
    2)immune system
    3)other
    4)H-P-A suppression
    • 1)plasma glc leads to diabetes; a.a's lead to decrease muscle mass; ca++ leads to osteoporosis; increase AR?, Na+, H2O lead to hypertension (HTN)
    • 2)decrease inflammation, immunosuppression, increased infections
    • 3)glaucoma, cataracts, peptic ulcers, psychosis, growth suppresion in children
  15. GC--H-P-A suppression
    • potential for adrenal insufficiency
    • duration vs dose
    • route of administration
    • length of suppression variable (1wk-1yr)
    • measures to minimize suppression=taper drug after therapy and alternate day of dosing
  16. GC Cautions
    symptomatic tx usually doesn't correct underlying problem

    diet: high protein, high K+, low Na+, antacids

    prolonged administration leads to HPA suppression which requires GC supplements

    exacerbate pre existing conditions
  17. Congenital adrenal hyperplasia
    1)cause
    2)effects
    3)treatment
    • 1)defect in corticoid synthesis: decrease corticoids (no negative feedback), increase ACTH, increase androgen
    • 2)adrenal insufficiency, hyperandrogenism (virilization/precocious puberty)
    • 3)GC/MC, anti androgen ?, aminoglutethimide ?
  18. Congenital adrenal hyperplasia is a result of 2 enzymes
    • 1)21 beta OHase-deficiency of both MC and GC
    • 2)11 beta OHase-deficiency of this enzyme can't make GC or aldosterone but CAN MAKE deoxycorticosterone
  19. Cushing's Syndrome (excess GC)
    1)cause
    2)effects
    3)treatment
    • 1)pituitary tumor (cushing disease)-75%; adrenal tumor-20%; other tumor-5%
    • 2)increase GC; metabolic, immune or other
    • 3)surgery and antagonists ?
  20. Corticoid Antagonists
    1)aminoglutethimide (blocks all steroid production)
    2)metyrapone (used for cushing's syndrome)
    3)ketoconazole
    4)spironolactone (eplerenone)
    5)RU486 (mifepristone)
    • 1)decrease SCC enzyme activity
    • 2)decrease 11 beta OHase activity
    • 3)decrease several OHase enzymes
    • 4)MC receptor antagonists
    • 5)GC receptor antagonists

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