Renal Flashcards
Mannitol:
MOA?
Therapeutic Uses?
ADR/CI’s?
Osmotic diuretic (^ urine flow, DECREASE intraocular + intracranial pressure)
Tx: Drug OD, ^ IOP/ICP,
ADRs: Pulmonary Edema, Dehydration
CI: Anuria, HF
Acetazolamde: MOA? Therapeutic Use (5)? ADRs? CI?
Carbonic Anhydrase Inhibitor–> Dump HCO3- @ PT
Tx:
- Glaucoma
- ALTITUDE SICKNESS
- PSEUDOTUMOR CEREBRI
- Uriniary alkalization; metabolic alkalosis
ADRs: PT acidosis, paresthesia, NH3 Toxicity
CI: SULFA ALLERGY
List Three Loop Diuretics that are SULFA DRUGS:
MOA?
Tx?
Mnemonic for ADRs?
Furosemide, Bumetanide, Torsimide (Furry Bum Tortoise)
MOA:
- Inhib Na/Cl/K cotransport in TAL –> No Hypertonic Medulla–> No concentration of urine…
- ^ PGE release
- Waste CALCIUM
Tx: Edema, HTN, HYPERcalcemia
ADRs: “OH DANG”
- Ototoxicity
- HYPOkalemia
- Dehydration
- Allergy to sulfa
- Alkalosis
- Nephritis (interstitial)
- Gout
What is the one loop diuretic that is NOT a sulfa drug?
How does it work?
What is it used to treat?
What are its ADRs?
Ethacrynic Acid
- MOA same as sofa drug loops
- Treats edema, HTN, hypercalcemia in patients w sulfa allergy
- ADRs are same as sulfa but with WORSE OTOTOXICITY
Which diuretics can be used to treat nephrogenic DI?!
How does this work?
Thiazide diuretics:
Slight dehydration–> DECREASE plasma volume + GFR–> ^ resorption Na, H2O in PT
What are our three thiazide diuretics? What is the MOA? What are 5 therapeutic uses? What is a mnemonic for 6 ADRs? When are these drugs CI?
Hydrochloriothiazide, Chorthaladone, Metolazone
MOA:
Inhibit NaCl reabsorption in DT–> Dilute urine, DECREASE Ca Excretion
Tx: HTN, HF, Hypercalcinuria, nephrogenic DI, osteoporosis
ADRs: “HyperGLUC”
- HYPOkalemic metabolic alkalosis
- HYPOnatremia
- HyperGLYCEMIA
- HYyperLIPIDEMIA
- HyperURICEMIA
- HyperCALCEMIA
CI: Sulfa allergy
What are the 4 K sparing diuretics?
“Take a SEAt, Potassium”
- Spironolactone
- Eplerenone
- Amiloride
- Triemterine
What is the shared MOA between spironolactone and Epleronone?
These are aldosterone receptor antagonists in the collecting duct
What is the shared MOA between triamterine and amiloride?
Block Na channels in the collecting duct to prevent K wasting…
What are the therapeutic uses for K sparing diuretics?
5–2 are for specific drugs
- Coadmin w other diuretics: px K depletion
- Hyperaldosteronism
- HF
- Neprhogenic DI (amiloride)
- Hepatic ascites (spironolactone)
What is the one common salient ADR with all K sparing diuretics? Which one has some other weird ADRs?
ALL can cause HYPERkalemia; remember spironolactone causes the gynecomastia, etc.
How does urine NaCl change with ALL diuretics?
INCREASES
How does urine K+ change with ALL diuretics?
INCREASES (unless coadmin w K sparing)
Thiazides and Loops deplete K the most
Which diuretics can induce academia and which can induce alkalemia? Describe the mechanisms by which this can occur.
Acidemia:
- Acetazolamide (CA inhibitors);
- Aldo-R antagonists (via preventing K and H secretion)
Alkamemia: Loops and thiazides
- Contraction alkalosis (^ ATII)
- K depletion–> pump K out of cels in XGE for H
- Low K–> H replaces K in Na/KATPase of collecting duct
How does urine Ca change depending upon the diuretic used?
Thiazides: DECREASE urine Ca
Loops: INCREASE urine Ca
CaptoPRIL, EnalaPRIL, LisinoPRIL, RamiPRIL are all examples of what type of drug?
Describe the MOA.
ACE Inhibitors!!!
ACEi–> STOP AT II–> STOP constrxn efferent arteriole–> DECREASE GFR
- Will also ^ renin due to DECREASE in (-) feedback
- Potent Vasodilatory effects (inhib deactivation bradykinin)
List some therapeutic uses for ACEi’s. In which diseases do they decrease mortality?
- HTN
- DECERASE mortality in HF (inhib remodeling)
- Proteinuria, DM Nephropathy (DECREASE intraglomerular pressure and SLOW GBM thickening)
List the ADRs for ACEi’s–what is the helpful mnemonic?
What are three CI circumstances?
CATCHH
- Cough
- Angioedema (due to ^ bradykinin)
- TERATOGEN
- ^ Cr, DECERASE GFR
- HYPERkalemia
- HypoTN
CI: C1 ESTERASE DEFICIENCY (angioedema), Preggos, bilateral renal stenosis
LoSARTAN, CandeSARTAN, ValSARTAN
What is the common MOA? How are they different from ACEi’s?
These are Angiotensin II Receptor Blockers (ARBs)!!
Block AT II-R –> Effects similar yo ACEi’s WITHOUT ^ Bradykinin–> NO COUGH
What are the clinical uses for ARBs?
How about the ADRs?
All things ACEi for patients intolerant to ACEi’s (i.e w cough or angioedema)
ADRs are the same with exception of COUGH/ C1 Esterase deficiency!!!
Aliskiren:
MOA?
Clinical use?
ADRs?
Direct inhibition of renin (Stops AT I –> AT II)
Used ONLY to treat HTN
ADR/ CI:
- Do NOT coadmin w ACEi/ARBs
- Hyperkamenia
- HypoTN
- Low GFR
