L15 Hypervolemia and Edematous States Flashcards
(32 cards)
Natriuresis vs. Diuresis
Natriuresis: Sodium Excretion
Diuresis: Water excretion
Loop Diuretics/MOA/Indications?
Furosemide (Lasix), Bumetanide, Ethacrynic acid, Torsemide
MOA: Na+/K+/2Cl-symporter inhibition in thick ascending loop
Main Indications
SEVERE Edematous states (Major Use of Loop Diuretics)
Hypercalcemia: Loop diuretics Increase calcium excretion
Other Indications
Hyperkalemia: Helps manage hyperkalemia in kidney failure
Hyponatremia
Pharmacodynamics of Loop Diuretics
Maximum antagonization is ~25% as that is the maximum amount of Na+ reabsorbed in Thick Ascending Loop
Loop Diuretic Drugs/Pharmacodynamics/Side Effects?
Bumetanide: More reliable oral absorption than Furosemide
Torsemide: Even more reliable in its absorption, occasionally used in heart failure pts
Ethacrynic Acid: RARELY Used due to ototoxicity, only used in cases of Sulphatoxicity towards other diuretics
Adverse Effects
○ Hypovolemia
○ Electrolyte depletion
○ Hyperuricemia (High Uric Acid in Blood, can worsen GOUT)
○ Metabolic Alkalosis
○ Sulfonamide Allergy: Ethacrynic Acid used in this case
○ Ototoxicity
Thiazide Diuretics/MOA/Indications?
Chlorothiazide, Indapamide, Metolazone
MOA
Blocks Na/Cl Cotransporter in distal convoluted tubule
Increases calcium retention (OPPOSITE of Loop)
Indications
Hypertension (Major use of Thiazides)
Minor Edematous states
Hypercalciuria (nephrolithiasis): Increases calcium back into the system, decreasing calcium in urine preventing stone formation
Nephrogenic Diabetes Insipidus: Increase in urine output due to problems with water absorption (Issue w/ ADH production/Action)
Thiazide Diuretic Drugs/Pharmacodynamics/Side Effects
Chlorothiazide: longer half-life, available IV and orally
Indapamide: Fewer metabolic Side effects
Metolazone: used in edematous patients in tandem w/ loop diuretics
Adverse Effects
○ Hypovolemia (WORSE than loop agents)
○ Electrolyte depletion (Hypokalemia, hypomagnesemia, hyponatremia (> loop agents))
○ Metabolic Effects (Glucose Intolerance, Hyperlipidemia)
○ Hyperuricemia
○ Hypercalcemia
○ Impotence
○ Sulfonamide Allergy
Diuretics Used in Sulfonamide Allergies?
Thiazide Diuretics (Chlorothiazide, Indapamide, Metolazone)
Ethacrynic Acid (No Other Loops)
Loop Diuretics vs. Thiazide Diurectics on calcium excretion?
Loop: Increases calcium excretion
Thiazide: Increases calcium retention=> Hypercalcemia
Potassium-Sparing Diuretics/MOA/Indications/Side Effects?
MOA:
Spironolactone/Eplenerone: Aldosterone antagonist
Amiloride: Principal cell Na+ channel blockade
Triamterene :Principal cell Na+ channel blockade
Indications:
Diuresis while preventing or Treatment of Hypokalemia: all
Treatment of edematous states (CHF, Cirrhosis): Spironolactone/Eplenerone (Aldosterone antagonists)
Side Effects of Potassium Sparing Diuretic?
Side Effects
Hyperkalemia: Interaction with ACE inhibitors, ARBs
Spironolactone: Gynecomastia, impotence, menstrual effects, Metabolic acidosis
Eplerenone: Newer aldosterone antagonist, fewer SEs, improves CHF survival
Triamterene: Renal stones
What should be blocked for the most profound diuresis?
FOR MOST PROFOUND DIURESIS BLOCK PROXIMAL TUBULE
(65% of Na Reabsorption)
Carbonic Anhydrase Inhibitors (Acetazolamide)
Osmotic Diuretics (Mannitol)
Sodium/Glucose (SGLT2) Inhibitors (Flozins)
Indications/Side effects of Mannitol?
Osmotic diuretic
Administered intravenously (EMERGENCY DRUG)
Indications
raised intracranial pressure
acute glaucoma
Flush away harmful substances due to Renal transplant, rhabdomyolysis
Adverse Effects
pulmonary edema
hyperosmolality
Volume/electrolyte depletion
AKI (“osmotic nephrosis”)
Indications for Acetazolamide?
Carbonic anhydrase inhibitor (FeNa <5%)
Indications
glaucoma
metabolic alkalosis with volume overload
Causes of Diuretic Resistance?
Kidney failure patients require HIGHER doses of diuretics to achieve the same effect
Nephrotic Syndrome (excessive protein excretion in urine): Low albumin in the blood =>Diuretics not effective as albumin in urine binds to diuretic limiting its effectiveness => Edema
ACEI/ARB => ↓proteinuria
Potency of Diuretics?
Loop diuretics MORE POTENT continue to increase with increased dose (Suitable for concerning Pulmonary edema)
Thiazides less potent, max out sooner
Consequence of Nephron Remodeling?
Remodeling degrades the effectiveness of loop diuretics => resistance
Loop PLUS Thiazides more effective (Diuretic Synergy)
Recommended delivery of Loop/Thiazide Diuretics?
Diuretic Synergy: Loop PLUS Thiazides more effective
Diuretics acting on the proximal tubule?
Carbonic Anhydrase Inhibitors (Acetazolamide)
Osmotic Diuretics (Mannitol)
Sodium/Glucose (SGLT2) Inhibitors (Flozins)
Diuretics acting on the thin descending/ascending limb?
Osmotic Diuretics (Mannitol)
Diuretics acting on the thick ascending limb?
Loop Diuretics (Furosemide (Lasix), Bumetanide, Ethacrynic acid, Torsemide)
Na+/K+/2Cl-symporter inhibition in thick ascending loop
Diuretics acting on the distal convoluted limb?
Thiazide Diuretics (Chlorothiazide, Indapamide, Metolazone): Block Na/Cl Cotransporter increasing calcium retention
Potassium-Sparing Diuretics (Amiloride/ Triamterene): Principal cell Na+ channel (ENaC) blockade
Diuretics acting on the Cortical Collecting Ducts?
K+ Sparing Diuretics
Spironolactone/Eplenerone: Aldosterone antagonist
Amiloride/Triamterene: Principal cell ENaC blockade
Diuretics acting on the medullary collecting tubule?
Vasopressin (ADH) Antagonists: Aquaretics (-Vaptins)
Diuretic indicated for Volume Overload?
Loop > Thiazides
