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22 Cards in this Set

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Carbonic Anhydrase Inhibitors
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)
Acetazolamide (Diamox)
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)
Brinzolamide (Azopt)
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
dorzolamide (Trusopt)
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
Loop Diuretics
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
Furosimde (Lasix)
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
Ethacrynic Acid (Edecrine)
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
Thiazides
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)
Metoazone (Mykrox)
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)
Spirolactone
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
Eplerenone (Inspra)
Selective Aldosterone Receptor Antagonist

inhibits Na/K ATPase in collecting tubule

Lower endocrine related side effects (No gynecomastia like spirolactone)

CYP3A4 metzm
Amiloride (Midamor)
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
Triamterene (Dyrenium)
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
Mannitol
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
Order of Expected Maximum Diuretic Effect by Category
Loop >> Thiazides >> CA inhibitors > K+ sparing
Vasopressin
ADH

used for central diabetes inspidius
IV in ACLS for cardiac arrest
Desmopressin
Synthetic ADH, more potent, longer acting

strong V2 agonst w/ no effect on V1 receptors (renal >> blood)
Lithium
Uncouples V2 receptors from Adenylyl cyclase
Nephrogenic Diabetes Insipidus

potential treatment for SIADH
Conivaptan
-vaptan's

non-peptide Vasopressin receptor antagonist

useful for SIADH
Democlocycline
a tetracycline antibiotic which uncouples V2 from adenylyl cyclase

preferred to lithium for lower toxicity
Drugs which induce SIADH
TCA's
Carbamazepine
Seulfonureas
Chlorpropamide
Anti-psychotics
SSRI's
SNRI's
Venlafaxine
Opiods
Vinblastine
Vincristine
Non-hormonal inhibition of Na+/K+ ATPase
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