Renal Drugs Flashcards
(22 cards)
What is the MOA of Mannitol?
When do we px it?
Toxicity?
Osmotic diuretic: Increase tubular fluid osmolarity to increase urine flow and DECREASE intracranial/ocular pressure in PROXIMAL TUBULE
Use for Drug OD, or ICP
Toxicty: pulmonary edema, dehydration, don’t use if you are CHF
What is the MOA of Acetazolamide?
When do we use it?
Carbonic anhydrase inhibitor: thus self-limited NaHCO3 diuresis and DECREASE of total body HCO3- stores thus excrete bicarb in urine
Uses: glaucoma (HCO3- draws water out), to Alkalinize urine, metabolik alkaosis, altituide sickness, pseudotumor cerebri
Carbonic anhydrase inhibitor: thus self-limited NaHCO3 diuresis and DECREASE of total body HCO3- stores thus excrete bicarb in urine
What is the drug?
What are it’s side effects?
Acetazolamide (you are EXCREATING BICARB!)
Sides: Hyperchloremic metabolic acidosis (normal anion gap, a d_ecrease in plasmabicarbonate_ concentration, and an increase in plasma chloride concentration
Paretsthisas, NH3 toxicity and Sulfa allergy
ACIDasolmide caues ACIDosis
What is the MOA of Furosemide?
Inhibits co-trans sytem of Na/Cl/K in THICK ASCENDING loop, thus abolishes hypertonicity of medulla and you CANT conc urine.
Will also stimulate PGE relase (vasoDiation on AFFERENT) and inhibited by NSAIDS
will INCREASE Ca+ excreation becasue Loops Lose Calcium
What pts benefit from Loop diuretics?
What toxicicty are associated?
Edematous states (CHF, cirrhosis, nephritic syndrome, pulmonary edema, HTN, hypercalcemia)
Toxicity: OH DANG!
Ototoxicity, Hypokalemia, Dehydration, Allery (sulfa), Nephritis (interstitial) Gout
What is Ethacrynic acid?
What’s it’s MOA?
It’s a Loop diuretic that works same at Furosemide: blocks Na/K/Cl transort thus can’t concetrate urine
but DOESNT HAVE SULFA!
provides diuresis in pts with Sulfa allergies
Toxicty: Hyperuricemia so don’t use w/ gout pts
What is the MOA of Hydroclorthiazide (HCTZ)?
Where does it act in kidney?
When dwould we use this on a pt?
Thiazide that INHIBITS NaCl resporption in the Early distal tuble thsu decreases diluting capacity of nephron but don’t lose Ca+
(Thiazides save Ca+)
Uses: HTN, CHF safe, idiopathic hypercalcinuria (noram serum Ca+ with lots Ca+ in urine causing stones), nephrogenic DI, Osteoporosis (cuz saves Ca+
What are the side effects of Hydrochlorothiazide?
HYPOkalemic metabolic alkalosis adn HYPOnatremia then
hyperGLUC: hyperGlycemia hyperLipidimeia, hyperUricemia, hyperCalcemia
*sulfa allergy
What is the MOA of spirnolactone and Eplieronone?
Where do they act?
Who uses them?
Both are COMPETITIVE Aldosterone Receptor ANTAGONIST in cortical collecting tubule
thus block Na+ channels in the CCT but spare K+
Used for Hyperaldosteronism or K+ depleated states and safe in CHF
What are some (-) sides of Potassium sparing diuretics
(Sprionolactone, Eplieronone, Tramterene, Amiloride)
HYPERkalemia (leads to arrythmias), Endocrine effects (with spirnolactone like gynecomastia)
What effect do Diuretics have on Urine NaCl?
All will INCREASE urine NaCl (escept acetazolamde)
What changes are associated with Urine K+ and diuretics?
see INCREASE K+ in urine (you lose K) with loops adn Thiazides
What diuretics will cause metabolic Acidosis or lower the blood pH?
Carbonic anydrase inhibitor (Acetazolmide) will DECREASE HCO3- absorbtion (which is basic)
K+ sparing diuretics like Aldosterone block K+ and H+ secreation and the transient hyperkalemia leads to K+ entering all cells (useing the K/H+ exchanger) and pushes H+ into blood. (body wants to tight regulate K bc can cause arrythmia!)
What diuretics will cause metabolic Alkalosis?
Loops and Thiazides lead to Alkalosis
see volume contraction–> this increases AT II–> increase Na/H+ exchange in proximal tubules–> HCO3- gets reabsorbed (contraction alkalosis)
K+ loss can lead to K+ exiting cells to maintain that extracellar K+ balance (bc K+ key for heart regulation) and does so with K/H+ exchanger so H+ enters cells
In low K+ states, H+ (rather then K+) will be exchanged for Na+ in the cortical collecting tubule–> alkalosis and paradoxica aciduria
What happens to urine Ca+ levels with diruetics?
Loops?
Thiazides?
Loops: Increase urine Ca+ via DECREASING paracellular reabsorption
Thiazides: Decrease urine Ca+: they enhance paracecell Ca+ reabsorptionin distal tubule
What is the MOA of ACE inhibitors: Captopril, Lisonopril, Enalapril?
Inihibit ACe: thus No Ang II thus DECREASE GFR by prevetning the constriction of effferent arterioles.
will see renin levels increase as loss of feedback inhibition
Blocking ACE also STOP inactivation of bradykinin (key vasoDilator)
What pts benefit from ACE inhibitors
HTN, safe in CHF, pts with proteinuria, Diabetic nephropathy,
***prevents unfavorable heart remodeling from chronic HTN
What are my ARBS = Losartan MOA?
Who uses them?
Selectively block binding of angiotensin II to AT1 receptor. Effects similar to ACE inhibitors, but ARBs do not increase bradykinin.
Hypertension, HF, proteinuria, or diabetic nephropathy with intolerance to ACE inhibitors (e.g., cough, angioedema).
Direct renin inhibitor, blocks conversion of angiotensinogen to angiotensin I.
used to tx HTN
Aliskiren
Why do pts with diabetic nephropahty benefit from ACE inhibtors?
In diabetic nephropathy, DECREASES intraglomerular pressure, slowing GBM thickening
What toxicity is associated with ACE inhibitors
Cough, Angioedema (contraindicated in C1 esterase inhibitor deficiency), Teratogen (fetal renal malformations), Increase Creatinine (Decrease GFR), Hyperkalemia, and Hypotension.
Avoid in bilateral renal artery stenosis, because ACE inhibitors will further
decrease GFR ==> renal failure.
What diuretics are contraindicated in pts with bilateral renal arter stenosis?
ACE inhibitors: they will further decrease GFR and lead to renal failure
