Diuretics Flashcards
CA inhibitors
Acetazolamide
Dorzolamide (topical)
Brinzolamide (topical)
Where do CA inhibitors work
proximal tubule
Use of CAI
Bicarb diuresis
Alkalinization of urine (increase weak acid excretion) alkalosis (metabolic or respiratory)
Moutain sickness (resp alkalosis)
GLAUCOMA (topicals) – dec CSF and aqueous humor
Kinetics of CAI
renal excretion: dose adjust in renal insufficiency oral absorption (30 min) not used as long term diureti - H accumulation
Why is CAI not used as long term diuretics
metabolic process eventually cause H+ to build up in cell and eventually NHE will begin to work again
SE of CAI
Hyperchloremic metabolic acidosis (excreted as NaHCO3)
Hypokalemia (Na/K ATPase)
Renal stones (inc. calcium in urine)
Hyperuricemia (compete)
Contraindications for CAI
hepatic cirrhosis (alkalinization of urine decreases ammonia excretion) sulfonamide hypersensitivity
Loop diuretics
Furosemide
Bumetanide
Torsemide
Ethacrynic acid
Which loop diuretic is not a sulfa?
Ethacrynic acid
What works best at low GFR?
loop diuretics
Use of loop diuretics
HF
Pulmonary edema (vasodilator effect)
Edema due to impaired renal function
HYPERCALCEMIA
MOA of loops
Inhibit NKCC2, thereby also inhibit Mg and Ca absorption
Induce kidney PGs (vasodilation, decreases salt transport)
SE of loop diuretics
High potentcy- abnormal fluid and electrolytes
HYPOKALEMIC METABOLIC ALKALOSIS (Na/K and Na/H in distal tubule exchange)
Hypocalcemia and hypomagneseia
Hyperuricemia
GI
IRREVERSIBLE OTOTOXCITY
Worse ototoxicity
ethacrynic acid
Ototoxicity is worse when given with
amingolycosides
Contraindictions of loops
sulfa allergy (except ethacrynic acid) Drug interactions
Overzealous use of loops is dangerous in
Hepatic cirrhosis
borderline renal failure
HF
Drug interactions of loop
COX inhibitors (PG synthesis required- vasodilation)
aminoglycoside (ototoxic)
litium (loss of Na increases Li retention and toxicity)
Digoxin (loss of K increases toxicity)
Most widely used diuretic
thiazides
Dependent on PG synthesis
CAI
Thiazides
Thiazide drugs
Hydrochlorothiazide Chlorothiazide Chlorthalidone Metolazone Indapamide Quinethazone
MOA of thiazide
inhibit NCC in early distal tubule (Na-Cl symporter)
Inc. ATP-dep K+ channel opening- vasodilation (dec. insulin secretion)
effect dependent on PG synthsis
Use of thiazides
HTN!
HF - not as effective as loops
nephrolithiasis - dec Calcium excretion due to increaed activity of PTH-dep calcium channels (Na pushes Ca through)
nephrogenic DI
Thiazide with longest duration
Chlorthalidone (preffered because of this)
Indapamide
Excreted 50/50 liver and kidney (renal insufficiency)
No increase in lipid levels
Vasodilation (CCB)
Good thiazide for renal insufficiency
indapamide
SE of thiazides
Hypokalemic metabolis alkalosis Hyperuricemia Magnesium loss Iodide/bromide loss HYPERGLYCEMIA Elevated lipid levels (except indapamide)
Contra to thiazides
sulfa inhibited by NSAIDs (depend on PG) Digitalis (hypkalemia) Diabetics (hyperglycemia) Lithium (low Na)
Metolazone
produces diuresis in patients w/ reduced GFR (exception to the thiazides)
Used in low GFR
loop diuretics
Metolazone (thiazide)
Classes of potassium sparing diuretics
aldosterone antagonist
direct inhibitor of Na flux
Where do potassium sparing diuretics work
distal tuble/CD
DOC for lithium induced DI
Amiloride
Do not cause hyperuricemia
Amiloriide
Triameterene
MOA of Amiloride, triamterene
inhibit eNaC channel in distal tubule/CD -
SE of amiloride and triamterene
Hyperkalemia (chronic or in combo w/ other K sparing)
N/V/leg cramps dizziness
Contra of amiloride/triamterone
Hyperkalemia (burns)
Not dependent on sodum
mannitol, isosorbide, glycerin, urea (osmotic diuretics)
DOC for central DI
Desmopressin
SE of desmopressin
hyponaremia
GI, H/a, dizziness, allergic reaction
SIADH DOC
Conivaptan or tolvaptan (outpatient)
Conivaptan administration
IV only
Tolvaptan administration
oral, send home on medication
Contraindication of vaptans
Hypovolemic hyponatremia
