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21 Cards in this Set
- Front
- Back
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2 situations for glucocorticoids with dose and duration
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1) replacement therapy: low dose for long duration. 2) anti-inf. / immunosuppressive therapy: high dose for short duration
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Major distinctions between glucocorticoid/mineracorticoids (3)
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potency, duration of action, and ratio of glucocorticoid/mineralcorticoid activity
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1) Storage of cortisol? 2) Rate limiting step?
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1) little storage in gland. 2) cholesterol side-chain cleavage to generate pregnenolone
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Cycle of GC in plasma? What's it related to? What induces a massive secretion of ACTH?
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Diurnal with rise at 3-4am that peaks at 8am. 2) Related to waking activity -> NOT light/dark cycle. 3) Stress
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Active form of cortisol? Halflife?
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Free cortisol active (94% bound to plasma proteins). 2) 90 min
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affinity/capacity for 2 proteins involved with cortisol?
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1) Corticosteroid-binding globulin (CBG, transcortin): high affinity, low capacity. 2) Albumin: low affinity, high capacity
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Metabolism of cortisol (3). Excretion?
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1) Ring A reduction leads to inactivation. 2) C20 reduction leads to inactivation. 3) glucuronic acid conjugation occurs mainly in liver, some in kidney. 4) Urinary excretion
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What group is important for Cortisol to function? Talk about activity in each form.
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1) 11-OH required for activity (11B-HSD type 1 in liver activates it). 11-ketone (in kidney 11B-HSD type 2 inactivates cortisol)
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What increases cortisol clearance? 2) How are plasma levels maintained?
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1) liver enzyme induction. 2) plasma levels maintained via feedback mechanism: e.g. diphenylhydantoin
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GCs increase glycogen synthesis how? 2) Affect electrolyte balance? 3) CV system?
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Indirect activation of glycogen synthase. 2) Increase resorption of sodium which increases Cl and Water while potassium is excreted
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GCs affect CNS how (3)? 2) GI (3)?
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1) GCs needed for normal alpha; lower threshold -> convulsions; and high dose can cause personality changes. 2) Facilitate absorption of fats; increase secretion of gastric HCL, pepsinogen, and pancreatic trypsinogen; decrease resistance of gastric mucosa to irritants -> ulcers
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What do GCs do to arachadonic acid? 2) What do GCs induce?
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1) Inhibit release of arachadonic acid. 2) induce transcription of annexin I -> Phospholipase A2 and inhibits COX2
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What do GCs bind to and inactivate? Result?
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NFkB and AP-1 which are transcription factors. 2) decrease inflammatory cytokines
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What 'stuff' is associated with Stimulus? 2) Increased vascular permeability? 3) PMN migration?
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1) PGs, HETES. 2) PG/TX. 3) PGs, HETEs
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What levels of GCs are required to inhibit inflammation?
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Supra-physiologic (high)
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Synthetic GCs have d ecreased number of hydroxyl groups which results in what?
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Decreased or absent protein binding -> increased bioactivity and excretion rate
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How can solubility be affected? 2) Water soluble is good for? 3) less-soluble good for?
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Different salts at position 21. 2) injection; rapid onset. 3) topical, slow release
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Synthetic GCs and receptor? Na retention?
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synthetic GCs have higher binding affinity than natural GCs to receptor. 2) synthetic GCs have low Na retention
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How do GCs affect vitamin D/PTH? 2) Osteoblasts. 3) Ca in kidney?
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1) Antagonistic on Ca absorption effects which causes inc. PTH. 2) GCs inhibit osteoblastic activity. 3) GCs increase Ca excretion by kidney
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Consider reviewing pathology material covered in pharm starting on page 100
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Consider reviewing pathology material covered in pharm starting on page 100
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Review general effects/dosing on page 101 and 102
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Review general effects/dosing on page 101 and 102
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