Renal Pharm

  1. Diuretic drug: Osmotic Diuretic
    • Drug: mannitol
    • Location: Proximal tubule
    • Mechanism: inhibits water reabsorption thru tubules, increases urinary vol
    • Use: decrease IOP in glaucoma, decreases intracerebral pressure, oliguric states (ie rhabdomyolysis), shock, drug OD
    • Side effects: acute hypovolemia pulmonary edema, contraindicated in anuria and CHF
  2. Diuretic Drug: Carbonic Anhydrase Inhibitors
    • Drug: acetazolamide, dorzolamide
    • Location: Proximal tubule
    • Mechanism: CA inhibition results in:
    • decreased H formation in PCT
    • decreased Na/H antiport
    • Increased Na and HCO3- in lumen
    • increased diuresis and reduction in total body bicarb
    • Use: glaucoma, acute mountain sickness (>1000 ft, you likely hyperventilate, so give CAI to cause a metabolic acidosis prior), metabolic alkalosis,
    • Side effects: biocarbonaturia & acidosis, hypokalemia, hyperchloremia, paresthesia, renal stones (due to hi pH), sulfonamide hypersensitivity

    ACIDazolamide causes ACIDosis
  3. Diuretic Drug: Loop Diuretic
    • Drug: furosamide
    • Location: Thick ascending loop
    • Mechanism: Na/K/2Cl- transporter inhibition causes:
    • decreased intracellular K, decreased back diffusion, decreased reabsorption of Ca and Mg, inreased diuresis
    • Use: DOC for acute pulmonary edema, CHF that causes pulmonary edema, htn, refractory edemas, acute renal failure, anion OD, hypercalcemic states
    • Side effects: sulfonamide hypersensitivity, hypokalemia and alkalosis, hypocalcemia, hypomagnesemia, hyperuricemia, OTOXOCITY (MC tested question)
    • Drug interactions: aminoglycosides, lithium clearance decreased, increased toxicity of digoxin due to elyte disturbances

    • Loops Loose Ca
    • OH DANG toxicity = Ototoxicity, Hypokalemia, Dehydration, Allergery (sulfa), Nephritis (interstitial), Gout
  4. Diuretics: Loop Diuretic
    • Drug: ethacrynic acid
    • Location: Thick ascending loop
    • Mechanism: same as furosamide (inhibition of Na/K/2Cl-)
    • Derivative: phenoxyacetic acid
    • Clinical Use: diuresis in pts allergic to sulfa drugs
    • Toxicity: similar to furosamide (OH DANG) can be used in hyperuricemia and acute gout (not used to treat gout!)
  5. Sulfonamide containing drugs:
    • Carbonic anhydrase inhibitors
    • All loop diuretics (except ethacrynic acid)
    • Thiazides
    • Sulfa abx
    • Celecoxib
  6. Drugs that cause ototoxicity:
    • Loop diuretcis (mostly ehtacrynic acid)
    • Aminoglycoside abx
    • Quinidine (cinchonism)
  7. Diuretics: Thiazides
    • Drugs: Hydrochlorothiazide, indapamide, metolozone
    • Location: early distal tubule
    • Mechanism: Na/Cl transporter inhibition, results in: more Na, Cl in DCT, diuresis
    • Use: htn, CHF, nephrolithiasis, nephrogenic diabetes insipidis
    • Side effects: sulfa hypersensitivity, hypokalemia, alkalosis, hypercalemia, hyperuricemia, hyperglycemia (lessK = inhibits insulin release = increased BG), hyperlipidemia (except indapmide), sulfa allergy
    • Drug interactions/cautions: digoxin has increased toxicity bc of elyte disturbances), avoid in pts w/ DM
    • Ineffective w/ GFR < 30 (should use a loop)
  8. Diuretics & Nephrogenic Diabetes Insipidis
    • Pathology of NDI: uncoupled V2 receptors in the kidney = can't respond to ADH
    • tx: is hydrochlorothiazide
    • Mechanism: initially the thiazide causes loss of Na and water, then starts to absorbe more Na and lose less water
  9. How to distinguish between loops and thiazides?
    1. Loops: Oxotoxicity and hypocalcemia 2. Thiazides: Hypercalcemia, hyperglycemia, hyperlipidemia, sexual dysfunction
  10. Diuretics: K Sparing Agents: Spironolactone
    • Mechanism: aldosterone receptor antagonist
    • Use: hyperaldosteronic state, adjuct to K wasting diurectics, antiandrogenic use (female hirsuitism bc it blocks androgen receptors), CHF (inhibits remodeling)
    • Side Effects: Hyperkalemia, acidosis, antiandrogen (gynecomastia = spironolactating :) ) Example: pt starts on a new drug for CHF and starts developing breasts what is the drug?

    the K STAys: Spironolactone, Triamterene, Amiloride, eplerenone
  11. Diuretics: K Sparing Agents: Eplerenone
    • Mechanism: aldosterone receptor antagonist
    • Similar to spironolactone but does not have the antiandrogenic effect

    the K STAys: Spironolactone, Triamterene, Amiloride, eplerenone
  12. Diuretics: K Sparing Agents: Amiloride & Triamterene: Na channel Blockers
    • Mechanism: Na channel blockers
    • Use: adjunct to K wasting diuretics, Li induced nephrogenic diabetes isipidis (amiloride)
    • Side Effects: hyperkalemia, acidosis

    the K STAys: Spironolactone, Triamterene, Amiloride, eplerenone
  13. What is the most common cause of hypokalemia and metabolic alkalosis?
    Loops and thiazides
  14. What is the most common cause of hyperkalemia?
    renal failure
  15. Does acetazolamide cause alkalosis or acidosis?
  16. Does ethacrynic acid, furosemide, torsemide cause alkalosis or acidosis?
  17. Does HCTZ, indapamide, metolazone cause alkalosis or acidosis?
  18. Does amiloride, triamterene, spironolactone, eplerenone cause alkalosis or acidosis?
  19. ACEI and the kidney
    • Drugs: Captopril, enlalpril, lisinopril
    • Mechanism: inhibits angio-converting enzyme, preventing inactivation of bradykinin ( produces VD, angioedema, cough), increases renin release due to loss of FB inhibition
    • clinical use: CHF, diabetic renal dz (nephroprotective)
    • Toxicity: CAPTOPRIL
    • Cough
    • Angioedema
    • Proteinuria
    • Taste changes
    • hypOtension
    • Pregnancy problems (fetal renal damage)
    • Rash
    • Increased renin
    • Lowers angioII
    • Also....hyperkalemia
    • avoid use w/ renal stenosis :)
  20. "But I can do all things through Christ who strengths me" Phillipians 4:13
    A little encouragement :)
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Renal Pharm