Renal Pharm from FA Flashcards
Mannitol
Mechanism?
Osmotic diuretic
Incr tubular fluid osmolarity producing increased urine flow
decreases intracranial/ontraocular pressure
Mannitol
Clinical Use?
Drug OD
increased intracranial or intraocular pressure
Mannitol
Tox?
Pulmonary edema
Dehydration
Contraindicated in anuria, CHF
Acetazolamide
Mechanism?
Carbonic anhydrase inhibitor
Cuases self-limited NaHCO3 diuresis and decreased total-body HCO3- stores
Acetazolamide
Clinical Use?
- Glaucoma
- Urinary alkalization
- Metabolic alkalosis
- Altitude sickness
- Pseudotumor cerebri (hydrocephalus, occurs w young obese women, decreased CSF outflow at arachnoid villi)
Acetazolamide
Tox?
Hypercloremic metabolic acidosis
Paresthesias
NH3 toxicity
Sulfa allergies
Acetazolamide
site of action?
Prox convoluted tubule
Mannitol
site of action?
Descending tubule
Loop Diuretics: name 2
- Furosemide
- Ethacrynic acid
Furosemide
site of action?
Loop - thick ascending limb
Ethacrynic acid
site of action?
Loop - thick ascending limb
Furosemide
Mech?
effect on Ca excretion?
Sulfonamide loop diuretic
Inhibits cotransport system (Na/K/2Cl) of thick ascending limb of LOH
abolishes hypertonicity of medulla, preventing concentration of urine.
Stimulates PGE release (vasodilatory effect on afferent arteriole)
Increases Ca excretion
“Loops Lose calcium”
Furosemide
what inhibits it?
NSAIDs
Furosemide
Use?
- Edematous states (CHF, cirrhosis, nephrotic syndrome, pulm edema)
- Hypertension
- Hypercalcemia
Furosemide
Tox?
Ototoxicity
Hypokalemia
Dehydration
Allergy (sulfa)
Nephritis (interstitial)
Gout
“OH DANG”
Ethacrynic Acid
Mech?
effect on Ca excretion?
Phenoxyacetic acid derivative (NOT a sulfanamide!)
Same action as Furosemide (inhibits cotransport (Na/K/2Cl).
-> Prevents urine concentration.
Increases Ca excretion
“Loops Lose Ca”
Ethacrynic Acid
Use?
Diuresis in patients allergic to sulfa drugs
Ethacrynic Acid
Tox?
similar to Furosemide (OH DANG)
Can cause hyperuricemia
Never use to treat gout
Thiazides
site of action?
Distal convoluted tubule
Hydrochlorothiazide
Mech?
Effect on Ca excretion?
Thiazide diuretic
Inhibts NaCl reabsorption in early distal tubule, decreasing the diluting capacity of the nephron.
Decreases Ca excretion (Ca-sparing)
Hydrochlorothiazide
Use?
HTN
CHF
Idiopathic hypercalciuria
nephrogenic diabetes insipidus
osteoporosis
Hydrochlorothiazide
Tox?
Hypokalemic metabolic alkalosis
Hyponatremia
HyperGlycemia
HyperLipidemia
HyperUricemia
HyperCalcemia
Sulfa drug -> allergies
“HyperGLUC”
K+ sparing diuretics
Name 4
Spironolactone (& Eplerenone)
Triamterene
Amiloride
“The K+ STAyEs”
K+ sparing diuretics/Spironolactone and Eplerenone
Mech?
Site of action?
Competitive aldosterone receptor antagonists
Cortical collecting tubule
K+ sparing diuretics/Trimterene, Amiloride
Mech?
Site of action?
Cortical collecting tubule
Block Na+ channels
K+ sparing diuretics
Use?
Hyperaldosteronism
K+ depletion
CHF
K+ sparing diuretics
Tox?
Hyperkalemia (can lead to arrhythmias)
Spironolactone: Endocrine effects (gynecomastia, andiandrogen)
Diuretics in general
Effect on Urine NaCl?
All increase Urine NaCl except Acetazolamide
Serum NaCl may decrease as a result.
Diuretics in general
Effect on Urine K?
Loop and Thiazide diuretics: Urine K increases
Serum K may decrease
Loop diuretics: effect on Urine Ca2+?
Urine Ca2+ increases with Loop Diuretics
Mech: decreased paracellular Ca2+ absorption -> hypocalcemia
Thiazide diuretics: effect on Urine Ca2+?
Urine Ca2+ decreases with Thiazides
Mech: enhanced paracellular Ca2+ reabsorbtion in the distal tubule
Which diuretics cause acidemia? mech?
Carbonic anhydrase inhibitors (acetazolamide)
Mech: **decreases HCO3- absorption. **
- > K+ sparing aldosterone blockade prevents K+ secretion and H+ secretion.
- > Hyperkalemia leads to K+ entering all cells (via H/K exchanger) in exchange for H+ exiting cells
What diuretics cause alkalemia?
mech?
Loop diuretics and thiazides.
Mech 1: Volume contraction -> incr AT II -> incr Na/H exchange in prox tubule -> incr HCO3- reabsorption (contraction alkalosis)
Mech 2: K+ loss leads to K+ exiting all cells in exchange for H+ entering cells
Mech 3: in low K+ state, H+ is exchanged for Na+ (rather than K+) in cortical collecting tubule -> alkalosis and “paradoxical aciduria”
ACE inhibitors
name 3
Captopril
Enalapril
Lisinopril
ACE inhibitors
mech?
inhibit ACE -> decr At II -> decr GFR by preventing constriction of efferent arterioles.
Renin increases due to loss of feedback inhibition.
ACE inhibition also prevents inactivation of bradykinin (vasodilator)
AT II blockers (-sartans)
effect?
similar to ACE inhibitors
do not increase bradykinin so there is decr risk of cough or angioedema
ACE inhibitors
use?
HTN
CHF
proteinuria
diabetic nephropathy
Prevent heart remodeling as a result of chronic HTN
ACE inhibitors
Tox?
Cough
Angioedema
Teratogen
incr Creatinine (decr GFR)
HyperKalemia
Hypotension
“Captoprils CATCHH”
ACE inhibitors
teratogenic effect?
fetal renal malformations
ACE inhibitors
contraindications?
- C1 esterase inhbitor deficiency
- Bilateral renal artery stenosis (because ACE inh will further decr GFR -> renal failure)
