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lipid disorders drug

drug treatments of lipid disorder

QuestionAnswer
Niacin uses: familial disease with elevated VLDL, Chylomicrons, or Lp(a) or want to decrease VLDL, LDL, and Lp(a) levels and increase HDL proven to prevent heart disease and decrease rates of nonfatal and fatal KI's
niacin MOA incorporates into NAD as nicotinamide, decreaes mobilization of peripheral FFA, decreases VLDL secretion, increases VLDL clearance via activation of LPL. decresaes HDL catabolism
niacin dosage: in most indications: immediate release- 1.5-3.5 g/d; divided with meals extended release: 1.2 g major actions: lowers LDL-C 5-25%; lowers TG 20-50%; raises HDL-c 15-35%
niacin toxicity: warm flushes: cutaneous vasodialation, initially after each dose, can be prevented by aspirin, tachyphylaxis in a few days heart: Sv arrhythmias skin: prutisus, rashes, dry skin-CI GI: CI in peptic ulcer disease liver: CI in chronic liver disease, gou
The fibrates fenofibrate Gemfibrozil
gemfibrozil and fenofibrate receptor action ligand for nuclear transcription receptor, peroxsome activated receptor- alpha. transcriptional up regulate LPL, apoA-I and II and down regulates apoCIII (inhibitor of lipolysis)
gemfibrozil MOA LPL activity is increased; intracellular lipolysis is decreased in adipocytes, vldl secretion decreases major actions: lower LDL-C 5-20%, may raise LDL-C, lower TG 20-50%, raise HDL 10-20%
gemfibrozil pharmacokinetics: absorbed quantitatively, crosses placenta, binds to plasma proteins, enterohepatic circulation, t1/2= 1.5 hr, mostly eliminated unchanged in urine, uses similar to niacin, but better tolerated.
gemfibrozil toxicity: skin rash, GI tract; stomach upset, abdominal pain, GU tract: erectile dysfunction, muscle: myositis with impaired renal function. drug-drug interaction: displaces warfarin. liver: inc. seer amitotransferase. don't use in kidney, liver, billary disease
bile binding resins colestipol, cholestyramine, colesevalam, work by forming insoluble complex with bile acids and salts preventing reabsorption
Bile binding resins MOA: anion-exchange resins large, cationic (quat amine) polymers, bind bile acids, release chloride, water insoluble, not absorbed, prevent reabsorption of bile acid from intestine. decreases CE content in liver, upreg of LDL receptors. attracts LDL to liver
resins therapeutic use: major actions: reduce LDL-C, raise HDL-C, may increases TG in combined hyperlipidemia, increase in VLDL may require a 2nd agent can be used in cholestasis, or digitalis toxicity in the gut.
resins- admin and dosage bulk or packets of 5g granular sugar. colestipol also comes in 1g tablets. daily dose is 10-30 g. use with meals
resins- toxicity: GI: bloating, heart burn, diarrhea; liver: aminotransferse increases metabolic system: increase serum TG, don't use in dysbetalipoproteinemia or TG>400; electrolytes: acidosis in children and pts. with renal failure.
resins drug interactions binds many anionic drugs in the intestine, impaired absorption of fat soluble vit. and folic acid, drugs ike digitalis, thiazides, warfarin, statins, aspirin, ascorbic acid, iron, and others. less with colesvelam
Ezetimibe effets, pharmocokinetics and MOA effect: inhibits intestinal absorption of phytosterol and cholesterol, reduces LDL levels P-kinetics: T1/2- 22 hrs, 80% excreted in feces MOA: inhibits NPC1L1 transport protein:
ezetmibe use and toxicity use: reduce LDL cholesterol, synergistic with satins toxicity: reversible impaired hepatic function (in combo with statin) myositis has been reported rarely
hydroxymethylglutaryl-coenzyme A reductase inhibitors (statins) lovastatin, pravastatin, simvastatin, atorvastatin, fluvastatin, cerivastatin, rosuvastatin
Created by: 925love
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