Diuretics Flashcards
Furosemide (Lasik)
Loop Diuretic
K+ losing
Sulfa Drug
- Na+-K+-2Cl- co-transporter blocker
- Indirectly blocks Ca++ and Mg++ paracellular reabsorption
- Due to blockage of K+, less K+ will leak back out into tubular lumen = Less Positive lumen charge = blocks Ca++ and Mg++ paracellular reabsorption
**- Effect: causes Increased excretion of: H2O, Na+, K+, Cl-, Ca++, Mg++
**- Causes PROFOUND DIURESIS of ISOTONIC urine!! (does not matter if it was dilute or concentrated before)
**- Uses: For Rapid/Massive fluid removal!!
**- Still works when GFR is LOW!!
- Some HCO3 - loss (not as much as thiazides)
Adverse effects:
- Loses more solute than water so (hyponatremia, kypokalemia, hypochloremia, hypocalcemia, hypomagnesemia)
Still have hypovolemia and hypotension tho
****- Hypochloremic Metabolic Acidosis (Low K+ results in cells exchanging K+ to the outside for H+!!!)
** - Increases risk of Kidney Stones (causes hypocalcemia which makes body react and absorb more Ca++ and retain it!!!) (counterintuitive)
** sulfur drug
Torsemide
Loop diuretic Sulfa Drug same as Furosemide BUT: **- Longer 1/2 life!! **- Better oral absorption!! *** Works better for heart failure pts
Bumetanide
Loop Diruretic
Sulfa Drug
Same as Furosemide BUT:
**- More predictable Oral absorption
Ethacrynic Acid
Loop Diuretic
same as Furosemide BUT:
** a NON-SULFUR diuretic = CAN BE USED IN PTS WITH SULFUR ALLERGY (Wolffs mother!)
Hydrochlorothiazide (HCTZ)
Thiazide Diuretic
K+ Losing
- Na+ Cl- Co-transporter Blocker in the Distal Convoluted Tubule
- Increases Excretion of: Na+, H2O, K+ and TONS of Mg++
- Increases Ca++ Reabsorption!!
- Less diuresis than Loop diuretics, more than K+ sparring diuretics
***- DOES NOT WORK well if GFR/RBF is low
** Paradoxically treats Nephrogenic Diabetes Insipidus
** Lowers the risk of Kidney Stones (Decreases Ca++ excretion (opposite of loop diuretics)
- More loss of HCO3- than Loop diuretics (helps slightly offset the Hypochloremic Metabolic Alkalosis)
- Adverse Effects:
- Hypovolemia
- K+ losing
- Hypochlormeic Metabolic Alkalosis
- *- Hypomagnesemia (may be SEVERE)
Chlorothiazide
Thiazide Diuretic
- Similar to HCTZ BUT:
- ***POOR ORAL ABSORPTION
Chlorthalidone
Thiazide Diuretic
- Similar to HCTZ BUT:
- ** LONG 1/2 life (40-60 hours!!!!)
- prolonged/stable response and benefits - **- Often preferred by HTN specialists!!
Metolazone
Thiazide Diuretic
- Similar to HCTZ BUT:
- ** LONG ACTING
- Favorite of Cardiologists for use as adjunct diuretic of CHF!!
Amiloride
K+ sparring Diuretic
- Na+ channel Blocker (ENaC) in Collecting Ducts
- Causes small increase in Na+ excretion (late in the nephron so most has been absorbed)
- K+ is retained!!
- Indirect decrease in excretion of H+, Ca2+, Mg2+
Used to COUNTERACT K+ LOSS induced by other Diuretics
Used to treat HTN and edema, usually with combo of other diuretic
** Rapid effects (compared to spironolactone!!!)
Adverse Effects:
- *- Hyperkalemia
- Hyponatremia, hypovolemia,
- **- Hypercholremic Metabolic Acidosis
Triameterene
K+ Sparring Diuretic
Same as Amiloride = Na+ channel blocker (ENaC)!!!
*** Rapidly absorbed
Spironolactone
K+ Sparring Diuretic
- Aldosterone Antagonist (Competitive Antagonist) = Blocks Aldosterone Receptors in Collecting Ducts
- Blunts the ability of Aldosterone to promote Na+-K+ exchange in the Collecting Tubulues
- Because decreased passage of Na+ so less K+ is excreted
- Decreases Basolateral Na+/K+ ATPase
- Blunts the ability of Aldosterone to promote Na+-K+ exchange in the Collecting Tubulues
- So small Na+ excretion increase, spares K+
Used to COUNTERACT K+ LOSS due to other diuretics
- *Used to treat PRIMARY HYPERALDOSTERONISM
- ** Greatly reduces mortality rate in CHF patients!
- Reduces FIBROSIS POST-MI HEART FAILURE
- *** “Slow on effect, slow off effect” (CAN TAKE 48 HOURS TO WORK!!!!)
- Adverse Effects:
- *- Hyperkalemia
- ** A PARTIAL ANDROGEN AGONIST- Amennorhea, hirsutism, gynomastia, impotence, deepening of voice
- Partial agonist: so in men = less androgen activity, and gives women androgen activity!
- Is a sulfa drug but because it is a steroid it is rarely hypersensitive
Eplerenone
More selective Aldosterone Antagonist
Also LACK SULFUR
Conivaptan
Aquaretic (Vaptan)
**- Non peptide, Arginine Vasopressin Receptor (AVPR) Antagonist
= Blocks Antidiuretic Hormone (ADH) from binding the AVPR, thus blocking Aquaporins from being inserted!!!
= More H2O excretion WITHOUT Serum Electrolytes!!
- So corrects plasma Na+ concentration by decreasing H2O and keeping Na+ the same!!!!
- Given to pts who are Hypervolemic (Euvolemic) and Hyponatremic
**Too rapid Na+ plasma correction = Seizures, coma, death, osmotic demyelination
- *Administered IV!
- Nonselective = Affinity for AVP V1A and V2 Receptors
Tolvaptan
Aquaretic (Vaptan)
Same as Conivaptan BUT:
- ** Selective for AVP V2 receptor!!
- Given Orally!
- use under 30 days, can cause fatal hepatotoxicity!!
Acetazolamide
Carbonic Anhydrase Inhibitor in the Proximal Tubule
K+ losing
- Blocks Carbonic Anhydrase so Bicarbonate is not absorbed and H+ cycling is inhibited
= - Na+ Bicarbonate Diuresis
= - Hyperchoremic Metabolic Acidosis
Uses: Urinary Alkalinization, Metabolic Alkalosis, Glaucoma, Acute Motion sickness
Adverse Effects: Too much Hyperchloremic Metabolic Acidosis, Kidney stones, K+ wasting
