HMG-CoA Reductase InhibitorsPravastatinSimvastatinAtorvastatin (Lipitor)Rosuvastatin (crestor)
MOA: inhibits early step in cholesterol synthesis. cells increase thier LDL receptors primarily in liver due to high first pass bioavailability. ADE: SAMS, diabetes, hepatotoxicity, cognitive issuesUse: LDL lowering 15%, double dose w/ 5-8%, anti-inflammatory effects and decreased oxidative stress causing stable atherosclerotic lesions***drug interactions: CyP34A inhibitors: Azoles, Macrolides, Dilitiazem, Amiodarone, Verapamil, grapefruit juice
Ezetemibe (Zetia)
MOA: inhibits NPC1L1 transport and absorption of cholesterol in the small intestine Use: Added to statin therapy for additional 15% LDL reductionADE: abdominal pain, diarrhea
PCSK9 inhibitorsAlirocumabEvolocumab
MOA: blocks PCSK9 which normally breaks down LDL receptors from removing cholesterol from blood. Causes more LDL receptors on liver surface. Use: ADE: A- diarrhea, myalgias, injection site, LFT elevated E- nasopharyngitis, HTN, flu, injection site, UTICleared: proteolysisAdministered subQ every 2 weeks or 1 month
Bile Sequestering Resins CholestyramineColestipolColesevelam (Welchol)
MOA: resin is not absorbed, and binds to bile removing more cholesterol from feces. LDL receptors upregulated.USE: add to statin or statin/ezetimibe, low LDL 15-30%, can't be used with homoz familial hypercholesterolemiaADE: Constipation, diverticulitis, LFT, increase in TG 10%*** take w/ foodCONTRAINDICATED: TG >400
Fibric Acid Derivatives Gemfibrozil Fenorfibrate
MOA: binds to PPAR-alpha to up regulate lipoprotein lipase, decrease ApoC-III which inreases lipolysis of lipoprotein TG via LPLUSE: severe hypertriclyceridemia >500ADE: dispepsia, cholelithiasis, A-fib Drug interactions: HMG CoA Reductase inhibitors, increased risk of rhabdomyolysis, Fenofibrate is preferred. increased warfarin effect, cyclosporin increased nephrotoxicity
Polyunsaturated fatty acids (PUFA)Omega 3 fatty acids (Lovaza)Icosapent ehtyl (Vascepa)
USE: elevated TG >500
Carbonic Anhydrase InhibitorsAcetazolamideDorzolamideBrinzolamide
MOA: inhibits formation of H+ and HCO3 from H2O and CO2. increases excretion of bicarb, Na, and K. Alkaline urine. block ciliary body from releasing HCO3 into aqueous humor. Use: Glaucoma, Altitude sickness, loses efficacy after a few days when treating edema due to reduced bicarbADE: Hypokalemia, hyperglycemia/glucosuria, hyperchloremic metabolic acidosis, drowsiness with high dose, paresthesias, hypersensitivity, hematologic
Loop DiureticsFurosemide (Lasix)Bumetanide (Bumex)Torsemide (Demadex)
MOA: inhibit NaCl resorption in thick ascending loop at Na/K/2Cl transport. increasews prostaglandin synthesis which increases renal blood flow and relieves pulmonary congestion. Use: edema due to CHF, acute pulmonary edema, nephrotic syndrome, hepatic cirrhosis, HF, HTNADE: electrolyte/ hypokalemia, orthostatic htn, Gout, ototoxicity, hyperglycemia/glycosuriaDrug interactions: Digoxin. amphotericin, corticosteroids, aminoglycodises, erythromycin, NSAID
Thiazide diureticsChlorthalidoneHydrochlorothiazide (HCTZ)Indapamide -doesn't efect cholesterol levelsMetolazone -least effected by Clcr
MOA: Inhibit NaCl reabsorption in DCT. increase Ca++ reabsorption, increase renal prostaglandin production.USE: HTN (first line). early HF for for symptom relief (can lose efficacy with Clcr= 30 ml/min, Diabetes InsipidusADE: Hypokalemia, hyponatremia, hyperuricemia, Hypercalcemia, increase in TC and LDL***drug interaction with lithium
Potassium sparing (Mineralocorticoid antagonist)Spironolactone
MOA: