pharmacology final exam review

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  1. what is the primary use of diuretics

    A primary use is to treat edematous states, i.e. mobilize edema fluid by enhancing the excretion of Na+; Natriureis (increase the excretion of Na+); Diuresis (increase in urine volume); the overall effect of diuretics is to reduce the extracellular fluid volume

    ion transport in PCT and conservation of base (from steve's notes?)

    diuretics can have adverse effects: hypokalemia (dec. amount of potassium in the blood), hypovolemia (reduced blood volume)- esp. in pts. recently Rx'd a diuretic; will have dizziness w/ standing, decreased AP (arterial pressure)
  2. Mannitol

    an osmotic diuretic; works near bowman's capsule; effective in PCT/ areas that are permeable to water. inhibits retention of water and Na+
  3. carbonic anhydrase inhibitors

    a diuretic that works on the PCT and DCT; suppresses the activity of carbonic anhydrase

    increase excretion of Na+ (small change) and HCO3. mild diretic. duretic effect is short lived; not good for chronic use.
  4. What are the overall functions of drugs on the kidney?
    • (diuretics)
    • waste excretion, ECF (extracellular fluid) homeostasis, arterial pressure (AP) regulation, endocrine function (renin/angiotensin system), drug disposition

    we reabsorb 99% of water; alterations can change weight and plasma volume
  5. fucosamide
    • (diuretics)
    • a loop diuretic; works in the thick ascending loop of henleinhibits symporter (cotransporter) Na+/K/2Cl- which inhibits reabsorption of Na+ and Cl-

    moa: Na+ and Cl- cnc are disrupted and affect the reabsorption of other ions... leads to hypertonic renal medulla and inc.

    urine output very important for maintaining Na+ infiltrate (infiltrate comes from glomerulus to bowman's to PCT, etc.)

    * Loop diuretics are the MOST POTENT DIURETICS(most potent diuretics work at 1. thick ascending loop of henle (fucosamide) and 2. DCT, sice most of Na+ reabsorption occurs here)
  6. Thiazides

    work in the DCT and inhibit the cotransporter for Na and Cl (inhibit their reabsorption)

    important side effect for both thiazides and loop diuretics: hypokalemia (lots of K+ in serum)interact with loop diuretics- can increase arrhythmias
  7. Aldosterone

    a diuretic antagonist; steroid hormoneacts on the DCT and collecting ducts of the nephron; conservation of sodium, secretion of potassium, increased water retention, and increased blood pressure.
  8. potassium sparing diuretics

    a diuretic that doesn't cause secretion of potassium in the urine; often used w/ other diuretics (prevent hypokalemia)moa: inhibit sodium channels; spironolactone and eplernone are potassium sparing diuretics and competetive antagonist of aldosterone (block MR/ mineralcorticoid receptor)
  9. Diuretics effect on RAAS (renin angiotention aldosterone system)
    • (diuretics)
    • increase activity of RAAS!
    • RAAS: hormone system- regulates BP and water balance.
    • low BP/ Blood volume (diuretics would cause dec blood volume)
    • renin released, become angiotension I, then Angiotension II (acts on Na+/ H+ pump in proximal tubule to inc reabsorption of Na+) 
    • vessels constrict inc blood pressure; aldosterone (acts on distal tubules) released acts as diuretic antagonist- inc water retention

    this causes a inc in K+ excretion: delivery of more Na+ to the collecting tubule/ duct results in Na/K exchange and therefore loss of K+inc in RAAS ultimately leads to inc K+ excretion
  10. indications for diuretic use

    edema, HTN, CHF, kidney stones, drug toxicity
  11. Natriuretic peptides
    • (diuretics)
    • hormone like biological substance produced by heart, ex. BN (?) and ANP (atrial natriuretic peptide)
    • produced by the heart in response to inc. blood pressure: causes vasodialiation

    • regulates fluids: induces natriuresis (the discharge of sodium through urine) and
    • urine outputopposite effect of aldosterone
  12. prostaglandin (PG) I and E
    • (diuretics)
    • lipids, hormones that regulate:vascular homeostasis (contraction and vasodialation)natriuretic, diuretic;PGE antagonizes ADH (vasopressin)

    vasopressin is a hormone that constricts blood vessels and inc. water resorption (made in hypothalamus and released from P. Pituitary)

    synthesis of PG's inhibited by: NSAIDs (ex. ibuprofen, celecoxib)
  13. vasopressin

    hormone permissive for water reabsorption; vasopressin is a hormone that constricts blood vessels and inc. waterresorption (made in hypothalamus and released from P. Pituitary)
  14. aldosterone

    steroid hormone; inc Na+ reabsorption (water retention, inc. blood volume/ pressure etc.)synthesis and secretion from adrenal gland is promoted by Ang II (part of RAAS)
  15. dopamine

    hormone in the body that acts as a natriuretic (diuretic; inc in Na+ discharge in urine)
  16. adenosine

    hormone or hormone like biological productdecreases GFR; dec. urine output
  17. A) Alcohol and urine output

    B) coffee and urine output

    C) diuretics abuse
    A) inhibits ADH/ Vasopressin; diuresis

    B) blocks receptors for adeosine (decreases GFR/ decreases urine) which acts on extracellular receptors

    C) some ppl use for weightloss- not a Good way to lose weight! Breastfeed instead!!!
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pharmacology final exam review
2013-04-30 04:41:48

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