diuretics

Card Set Information

Author:
thedewhub
ID:
298907
Filename:
diuretics
Updated:
2015-03-22 13:52:43
Tags:
diuretics
Folders:
diuretics
Description:
diuretics
Show Answers:

Home > Flashcards > Print Preview

The flashcards below were created by user thedewhub on FreezingBlue Flashcards. What would you like to do?


  1. Carbonic Anhydrase Inhibitors
    Acts in the proximal tubule through inhibition of carbonic anhydrase that is present in both the luminal border and cytoplasm of the epithelial cell. - increases excretion of Na+, K+, HCO3 , and water; decreases excretion of H+
  2. Disadvantages CarbonicAI:
    mild, production of metabolic acidosis. Infrequent toxic effects: sulfonamide related adverse reactions - bone marrow depression, skin toxicity, allergic reactions. Kinetics: oral (or i.v.) administration, t 1/2 6-9 hrs., renal excretion. Dorzolamide topical Therapeutic uses: - short term diuretic therapy, alternative/adjunct to other diuretics - correction of diuretic-induced alkalosis - epilepsy - glaucoma
  3. (Dorzolamide (Trusopt)) weird use
    - acute mountain sickness
  4. Loop Diuretics agents
    • Furosemide
    • Bumetanide
    • Ethacrynic acid
    • Torsemide
  5. Loop diuretic MOA
    Inhibit na/kcl active co cotransporter in the thick ascending limb causing decreased absorption of NA/k/Cl, countercurrent conc collapses increases urine loss of ions, also pulmonary vasodilation, increased venous compliance
  6. Loop diuretics advatages/ disadvantages/ kinetics
    • High efficacy and prompt action
    • Hypo K M, alkalosis, hyper uric glycemic, ototox- watch out if impaired renal fn or coadmin of aminoglycosides
    • PO rapid on/ off, plasma protein bound, organic acid secretion
  7. Loop therapeutic uses
    • Acute pulmonary edema
    • Nephrotic syndrome edema
    • CHF
    • Hypercalcemia
    • Asthma
  8. Thiazides agents
    Chlorothiazide, hydrochlorathiazide, indpramide, metalozone
  9. Thiazide MOA
    • Inhibit NaCl cotransporrter causing decreased Na reabsorption in the early distal tubule
    • Some CAI
    • Vasodilation in HTN pts with extended treatment
    • Increased K excretion
    • Ca sparing
  10. Thiazide advantage. Dis/ kinetics
    • PO active, minimal tolerance to diuretic effect
    • Hypokal, dehydration, hypercalcemia, hyperureicemia, hyperglycemia, and hyperlipidemia
    • Range of half life, plasma protein bound, secreted into lumen in proximal tubule
  11. Thiazide therapeutic uses
    • HTN
    • CHF edema
    • Hepatorenal edema
    • Nephrogenic diabetes insipidus
    • Ca dynamics- ca wasting and stones
  12. Osmotic diuretics agents
    Mannitol, glycerin, isosorbide
  13. Osmotic agents
    • Free filtered at glomerulus, limited reabsorption, and are relatively inert
    • Increased renal tubular osmolarity
    • Interfere with na and h2o reabsorption in the nephron due to the osmotic effect of increased conc of solute in urone
    • Can sustain flow even with low GFR
    • Increased electrolyte excretion
  14. Osmotic agent disadvantage
    • EC volume expansion
    • CHF and pulmonary edema precipitation
    • Hyponatremic
    • Headache N/V
  15. Osmotic kinetics
    Glycerin and isosornbide PO, mannitol IV, renal and metabolic elimination
  16. Osmotic therapeutics
    • Acute renal failure
    • Prophylactic or acute elimination of toxins
    • Decrease cell volume from cerebral edema
    • Decrease aq humor in glaucoma
  17. K sparing diuretic agents
    • Spironolactone
    • Eplerrenone
    • Triamterene
    • Amiloride
  18. K sparing moa
    • Spironolactone competively antagonizes aldosterone binding to mineraloCC receptor decreasing transport proteins
    • Triamterene and amilioride directly inhibit na channel in the late distal tubule through an aldost independent mech- excretion pattern is similar to spironolactone
    • These agents increase NaCl excretion and decrease K excretion hence k sparing
  19. Amount of k reabsorbed and location
    90% in prox tubule, small amount is handled by distal nephron- this segment determines net gain or loss
  20. Factors that promote K secretion
    • Increase Na to the collecting duct
    • Elevated aldosterone
    • Enhanced Na reabsorption
  21. Why do most diuretics cause K loss?
    • Many have direct effects on nephron segments
    • Presentation of elevated Na, nd subsequent h2o to the collecting duct
    • Stimulation of aldo release
  22. Compared to other diuretics K sparing
    • mild diuretic due to indiviual effcts of Na reabsorption
    • do nto lose K
    • spirano blocks aldo
    • amilioride blocks diuretic enchanced activity of na reabsorb and k excretion
  23. K sparing Disadvantages:
    • - hyperkalemia
    • - CNS, GI, musculoskeletal, dermatological, and hematological effects
    • - Gynecomastia, menstrual irregularities, androgen-like side effects with
    • spironolactone
    • - Spironolactone efficacy related to levels of circulating aldosterone
  24. K sparing Kinetics:
    • orally available, variable half times, excreted through kidneys and
    • metabolism
  25. K sparing Therapeutic uses:
    • - rarely used alone
    • - very useful in combination with thiazides to provide additive increase in Na
    • excretion with moderation of K+ loss
    • - hypertension, edema
    • - spironolactone: primary and secondary aldosteronism
    • - spironolactone: diuretic of choice in patients with hepatic cirrhosis
  26. Spiranolactone and cardiac
    • Contractility
    • Angiotensin II
    • Fibrosis
    • Free radicals
  27. Causes of diuretic resistance
    • noncompliance
    • bioavailability impaired
    • secretion impaired
    • protein binding in tubule lumen
    • reduced gfr
    • enhanced nacl reabsorp
  28. In patients with CHF, cirrhosis with ascites, hypovolemia NSAIDS
    reduce RBF and GFR; promote Na+ and water retention

What would you like to do?

Home > Flashcards > Print Preview