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22 Cards in this Set
- Front
- Back
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Carbonic Anhydrase Inhibitors
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Systemic: Acetazolamide (Diamox)
Topical: dorzolamide (Trusopt), Brinzolamide (Azopt) Carbonic anhydrase catalyzes H2O + CO2 ↔ H2CO3 H2CO3 ↔ H+ & HCO3- (uncatalyzed) Inhibitors prevent prodxn of H2O + CO2 in lumen, also prodxn of H2CO3 in epithelium, ultimately decreasing H+ avilable for Na+/H+ antiporter Effects: --diuresis w/in 1h --HCO3- wasting → renal stones, urinary alkalinization, metabolic acidification -- ↑ Na+ flowing through distal tubule → K+ wasting -- ↓ aqueous humor & CSF prodxn PhK: oral renal Uses: glaucoma, urinary alkalinization, metabolic acidification, epilepsy (?) Contras: Cirrhosis (alkaline urine = NH3 escape), Sulfa allergy (all sulfas) |
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Acetazolamide (Diamox)
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Systemic Carbonic Anhydrase Inhibitors
Carbonic anhydrase catalyzes H2O + CO2 ↔ H2CO3 H2CO3 ↔ H+ & HCO3- (uncatalyzed) Inhibitors prevent prodxn of H2O + CO2 in lumen, also prodxn of H2CO3 in epithelium, ultimately decreasing H+ avilable for Na+/H+ antiporter Effects: --diuresis w/in 1h --HCO3- wasting → renal stones, urinary alkalinization, metabolic acidification -- ↑ Na+ flowing through distal tubule → K+ wasting -- ↓ aqueous humor & CSF prodxn PhK: oral renal Uses: glaucoma, urinary alkalinization, metabolic acidification, epilepsy (?) Contras: Cirrhosis (alkaline urine = NH3 escape), Sulfa allergy (all sulfas) |
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Brinzolamide (Azopt)
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topical carbonic anhydrase inhibitor like dorzolamide (Trusopt)
while systemic carbonic anhydrase inhibitors (Acetazolamid ie Diamox) produce diruesis, topicals are limited to ↓ Aqueous humor prodxn used for glaucoma |
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dorzolamide (Trusopt)
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topical carbonic anhydrase inhibitor like Brinzolamide (Azopt)
while systemic carbonic anhydrase inhibitors (Acetazolamid ie Diamox) produce diruesis, topicals are limited to ↓ Aqueous humor prodxn used for glaucoma |
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Loop Diuretics
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Furosimde (Lasix): sulfa
Ethacrynic Acid (Edercrine) non-sulfa, higher ototoxicity block the 1Na1K2Cl co-transporter in the ascending limb of the loop of henle actions mediated by PG's, do not co-tx c COX inhibitors simultaneously interferes with Na+ retention and gradient maintenance (concentrating & diluting capacities) PhK: oral-renal, onset w/in an hour Mg2+, Ca2+, K+, Cl-, H+ loss, Urate retention metabolic alkalosis enhance toxicity of aminoglycosides, lithium, & digoxin Uses: most potent diuretic, hypercalceemia, hyperkalemia: furosimide + Normal Saline |
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Furosimde (Lasix)
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Sulfa Loop Diuretic
block the 1Na1K2Cl co-transporter in the ascending limb of the loop of henle actions mediated by PG's, do not co-tx c COX inhibitors simultaneously interferes with Na+ retention and gradient maintenance (concentrating & diluting capacities) PhK: oral-renal, onset w/in an hour Mg2+, Ca2+, K+, Cl-, H+ loss, Urate retention metabolic alkalosis enhance toxicity of aminoglycosides, lithium, & digoxin Uses: most potent diuretic, hypercalceemia, hyperkalemia: furosimide + Normal Saline |
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Ethacrynic Acid (Edecrine)
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Non-Sulfa Loop Diuretic
block the 1Na1K2Cl co-transporter in the ascending limb of the loop of henle actions mediated by PG's, do not co-tx c COX inhibitors simultaneously interferes with Na+ retention and gradient maintenance (concentrating & diluting capacities) PhK: oral-renal, onset w/in an hour Mg2+, Ca2+, K+, Cl-, H+ loss, Urate retention metabolic alkalosis enhance toxicity of aminoglycosides, lithium, & digoxin Uses: most potent diuretic, hypercalceemia, hyperkalemia: furosimide + Normal Saline |
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Thiazides
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Hydrochlorithiazide (Esidrix) -Sulfa
Inhibit Sodium Resorption in the Cortical Diluting site (Distal convoluted tubule) PhK: oral-renal --Chlorthalidone: more slowly absorbed, longer action --Indapamide (Lozol) biliary excretion: good for renal insufficiency, no ↑lipids More Na+ Delivered to Collecting Duct → K+ wasting Competes c Uric Acid for Organic Anion Pump → Hyperuricemia Calcium Resorption → not enough v osteoporosis, good v calcium stones I-, Br- Mg2+, loss ↓Insuline Release → Hyperglycemia, Glucose intolerance (contra: T2DM) Toxicity: GLUCKAS: hyper: glycemia, lipidemia, uricemia, calcemia; hypokalemia, acidosis, sulfa rxns (incl blood dyscrasia & infantile jaundice) |
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Metoazone (Mykrox)
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similar to thiazides, able to produce diruesis in pts w/ GFR <20
[Thiazides: Inhibit Sodium Resorption in the Cortical Diluting site (Distal convoluted tubule) PhK: oral-renal More Na+ Delivered to Collecting Duct → K+ wasting Competes c Uric Acid for Organic Anion Pump → Hyperuricemia Calcium Resorption → not enough v osteoporosis, good v calcium stones I-, Br- Mg2+, loss ↓Insuline Release → Hyperglycemia, Glucose intolerance (contra: T2DM) Toxicity: GLUCKAS: hyper: glycemia, lipidemia, uricemia, calcemia; hypokalemia, acidosis, sulfa rxns (incl blood dyscrasia & infantile jaundice) |
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Spirolactone
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Competitive Aldosterone Antagonist, binds glucocortocoid & sex hormone receptors at high doese
inhibits Na/K ATPase in collecting tubule Low toxicity: gynecomastia most effective in hyperaldosteroneism or as K+ sparing ajunct to K+ wasting dirutics |
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Eplerenone (Inspra)
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Selective Aldosterone Receptor Antagonist
inhibits Na/K ATPase in collecting tubule Lower endocrine related side effects (No gynecomastia like spirolactone) CYP3A4 metzm |
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Amiloride (Midamor)
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like Triamterene (Dyrenium)
Potassium sparing diuretic: Non-hormonal inhibition of Na+/K+ ATPase Weak diuresis, used in combo w/ K+ wasting diuretics Toxicity: hyperkalemia Amiloride is the DOC for lithium induced diabetes insipidus |
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Triamterene (Dyrenium)
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like Amiloride (Midamor)
Potassium sparing diuretic: Non-hormonal inhibition of Na+/K+ ATPase Weak diuresis, used in combo w/ K+ wasting diuretics Toxicity: hyperkalemia Amiloride is the DOC for lithium induced diabetes insipidus |
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Mannitol
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Osmotic Diuretic
IV admin, renal excretion used for acute oliguria/renal failure prophylaxis ↓ Intracranial/Intraocular Pressures To protect Kidney from substances which may be toxic in concentrated doses |
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Order of Expected Maximum Diuretic Effect by Category
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Loop >> Thiazides >> CA inhibitors > K+ sparing
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Vasopressin
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ADH
used for central diabetes inspidius IV in ACLS for cardiac arrest |
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Desmopressin
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Synthetic ADH, more potent, longer acting
strong V2 agonst w/ no effect on V1 receptors (renal >> blood) |
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Lithium
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Uncouples V2 receptors from Adenylyl cyclase
Nephrogenic Diabetes Insipidus potential treatment for SIADH |
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Conivaptan
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-vaptan's
non-peptide Vasopressin receptor antagonist useful for SIADH |
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Democlocycline
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a tetracycline antibiotic which uncouples V2 from adenylyl cyclase
preferred to lithium for lower toxicity |
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Drugs which induce SIADH
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TCA's
Carbamazepine Seulfonureas Chlorpropamide Anti-psychotics SSRI's SNRI's Venlafaxine Opiods Vinblastine Vincristine |
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Non-hormonal inhibition of Na+/K+ ATPase
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Amiloride (Midamor) & Triamterene (Dyrenium)
Potassium sparing diuretic: Non-hormonal inhibition of Na+/K+ ATPase Weak diuresis, used in combo w/ K+ wasting diuretics Toxicity: hyperkalemia Amiloride is the DOC for lithium induced diabetes insipidus |
