Pharmacology: Diuretic drugs flashcards


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Pharmacology: Diuretic drugs flashcards

  1. 1. CA Inhibitors Acetazolamide & Dorzolamide (topical eye drop)  MoA: Inhibits NaHCO3 reabsorption   Location: PROXIMAL TUBULE Sulfonamides = avoid in gout  Actions:   Causes metabolic acidosis (limits H+ excretion)  Decreases aqueous humor & CSF production
  2. 2. CA Inhibitors  Adverse  Nephrolithiasis since CaPO4 precipitates in alkaline urine  Hypokalemia (adverse effect of all diuretics except for K-sparring ones)  Contra-indicated in gout and COPD (because of effects of CA in lungs)  Therapeutic Uses  Open angle glaucoma  In combo with other diuretics to counter alkalosis effects  Edema from heart failure
  3. 3. Thiazides Hydrochlorothiazide & Indapamide  MoA: blocks the Na/Cl symport   Location: Acts in early DCT (diluting capacity is decreased) Also are sulfonamides (contra for gout)  Metabolic alkalosis (opposite of CA Inhibitors)  Calcium is retained  HYPERCALCEMIA  Only effective when GFR > 30 mL/min 
  4. 4. Thiazides  Adverse  Hypokalemia (more Na reaching collecting      tubule causes high K secretion) Hypercalcemia (lower intracellular Na limits Ca exchange; also limits Li excretion) Metabolic alkalosis Sexual dysfunction, postural hypotension Not for pregnancy Therapeutic Use  1st choice for hypertension  Used when there is any edema  Ca Nephrolithiasis
  5. 5. Loop Diuretics   Furosemide & Ethacrynic acid (not a sulfonamide) MoA: Blocks Na/K/Cl in the TAL of loop of henle  Decreased lumen positive potential = dilution ability is affected (Ca loss)  Decreased hypertonicity of medulla = decreased concentrating ability  Inhibition of macula densa sensitivity (work even with low GFR)   Osmolality is same as plasma due to loss of concentration and dilution ability!! Metabolic alkalosis; increased Ca and Mg excretion
  6. 6. Loop Diuretics   Only diuretics which work with low GFR!! (due to inhibition of macula densa sensitivity) ADVERSE      Hypocalcemia, hypokalemia, hypochloremia Tinnitus (due to alteration of endolymph) Hyperglycemia in DM pts Hypokalemia can increase digoxin and Li toxicity Therapeutic Use  Pulmonary edema, Heart failure  Hypertension – only if renal insufficiency (allows to work with low GFR)
  7. 7. K+ Sparring Diuretics   Triamterene; Amiloride; Spironolactone MoA:  Triamterene and Amiloride block Na channels directly  Spironolactone blocks aldosterone receptors (which prevents Na channels from even being produced)  Location: late DCT & Cortical Collecting Tube    ONLY diuretics which do not cause increased K excretion Spironolactone takes 1-3 days to take effect (blocks protein synthesis) and is metabolized to its active metabolite – canrenone Amiloride is excreted unchanged
  8. 8. K+ Sparring Diuretics  Adverse  Hyperkalemia (may cause asystole)  Sexual dysfunction (spironolactone)  Mixing with b-blockers, ACE inhibitors, NSAIDS (renin-angiotensin system blunters) may increase hyperkalemia  Therapeutic Uses  Prevention of hypokalemic states  Spironolactone for primary hyperaldosteronism (Conn syndrome), secondary hyperaldosteronism (Cushing’s), and hypertension with heart failure  Amiloride for Li-Induced nephrogenic DI
  9. 9. Osmotic Diuretics   Mannitol MoA: Increase the osmolarity of tubular fluid  Location: proximal tubule & thick descending limb of loop of Henle  Increases excretion of all ions  Urine becomes acidic (but body is normal)  Causes EXTRACELLULAR VOLUME EXPANSION initially but then diuresis causes EXTRACELLULAR VOLUME REDUCTION !!!!!!! ○ Can cause PULMONARY EDEMA  Therapeutic Use  Reduces cerebral edema (neurosurgery)  Reduces intraocular pressure in acute closed-angle glaucoma
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