MPP Block 4 Drugs PDF

warfarin: vitamin K antagonist inhibition of factors 2, 7, 9 and 10 inhibition of VKOR1 reduces clotting factor due to lack of gamma-carboxylglutamyl side chains use for prosthetic heart valves hypercoaguable at start, need bridging drugs (heparin or enoxaparin) drug interactions oral...

warfarin: vitamin K antagonist inhibition of factors 2, 7, 9 and 10 inhibition of VKOR1 reduces clotting factor due to lack of gamma-carboxylglutamyl side chains use for prosthetic heart valves hypercoaguable at start, need bridging drugs (heparin or enoxaparin) drug interactions oral reversal: non-life threatening; vitamin K life threatening; vitamin K + 4F-PCC or FFP skin necrosis and contraindicated in pregnancy INR between 2 and 3 heparin highly acidic bind to antithrombin III via a pentasaccharide complex inactivates factors 2 and 10 subcutaneous injections (prophylaxis) and IV enoxaparin: LMWHs bind to antithrombin III via a pentasaccharide complex inactivates factor 10 subcutaneous injections adverse e ects of heparin and enoxaparin: bleeding HIT (greater with heparin) protamine sulfate: reversal agent to heparin and enoxaparin, fully to heparin, partially to enoxaparin, highly basic and forms stable salt fonaparinux pentasaccharide sequence found in heparin products inhibits factor 10 via antithrombin III injectable bleeding contraindicated in renal disease no reversal agent rivaroxaban and apixaban: direct factor 10 inhibitors oral tablets rivaroxaban: bleeding, taken with meal, contraindicated in renal disease andexant alfa: reversal agent, truncated inactive form of factor 10 (removal of gamma- carboxyglutamic acid), sequesters inhibitors dabigatran: direct thrombin inhibitor prodrug oral bleeding contraindicated in renal disease idarucizumab: reversal agent, humanized monoclonal antibody, sequesters in minutes bivalriduin and argatroban: direct thrombin inhibitors alternative to those with history of HIT IV bleeding no reversal alteplase: thrombolytics for acute ischemic stroke initiation of brinolysis by binding to brin and converting plasminogen to plasmin HIGHEST risk of bleeding renal disease contraindications: fonaparinux, rivaroxaban, dabigatran oral: warfarin, rivaroxaban, apixaban, dabigatran aspirin: COX inhibitor acetylation of a serine residue on COX reduces TxA GI bleeding and ulcer formation due to PgE2 asthma exacerbations oral tablet clopidogrel: P2Y12 ADP Receptor Inhibitor prodrug, irreversibly binds to and inactivates receptor at cysteine residue, creates disul de bond poor metabolizers oral ticagrelor: P2Y12 ADP Receptor Inhibitor reversibly binds to ADP receptor mimicking adenosine bleeding oral abciximab: GPIIb/IIIa inhibitor monoclonal antibody reversibly binds to and inactivates GPIIb/IIIa bleeding DURING PCI IV epti batides: GPIIb/IIIa inhibitor cyclic peptide that reversibly binds to and inactivates GPIIb/IIIa bleeding DURING PCI IV cilostazol: PDE3 inhibitor inhibition of PDE3 resulting in decreased catabolism of cAMP intermittent claudication bleeding and headache contraindication: heart failure oral statins: HMG-CoA reductase inhibitors  competitive inhibitors inhibiting de novo synthesis, deplete intracellular supply of cholesterol plaque stabilization, improvement of coronary endothelial function, inhibition of platelet thrombus formation. anti-in ammatory pharmacokinetics: absorption of the statins is variable following oral administration liver enzymes overall inhibitors of cholesterol absorption: reduce by SI reduce LDL cholesterol by inhibiting hepatic production of VLDL statins and bile acid sequestrants: reduce LDL cholesterol principally by increasing LDL clearance via the LDL receptor niacin: strongly inhibits lipolysis in adipose tissue, reducing production of FFA reduce VLDL, reduce LDL reduce LDL 10-20% most e ective for increasing HDL can be used with statins brates; feno brate and gem brozil derivates of bric acid that lower serum triglycerides and increase HDL levels activate PPARs decrease through increased expression of lipoprotein lipase and decreasing apoC-III HDL: increased by increasing expression of apo AI and AII resins: bile acid sequestrants bind negatively charged bile acids and bile salts in the small intestine complex is excreted in feces hepatocytes increase conversion of cholesterol to bile acids up-regulation of LDL receptors combination with niacin or diet ezetimibe selectively inhibits absorption of dietary and biliary cholesterol in the small intestine by block NPC1L1 lowers LDL by 17% adjuct to statins combination: statins and resins one pill: simvastatin and niacin elevated triglycerides: niacin and brates roszet: rosuvastatin and ezetimibe Diuretics: decreasing blood volume routine electrolyte monitoring thiazide B blockers: -olol reduce BP by decreasing CO by selectively blocking beta adrenergic receptor activity  decrease SNS and inhibit release of renin decrease formation of angiotensin II and secretion of aldosterone propranolol: acts both beta1 and beta2 metoprolol and atenolol: selective blockers of beta1 receptors are among the most commonly prescribed B blockers adverse e ects: bradycardia, hypotension and CNS side e ects, decrease libido and ED Renin inhibitors: aliskiren aliskiren: inhibits renin and thus acts earlier in the RAAS, rst approved prevents angiotensinogen to angiotensin I metabolized by CYP 3A4 drug interactions useful in slowing progression of heart failure lowers BP as e ectively as ARBs, ACE and thiazides ACE inhibitors: -pril rst line treatment of hypertension and heart failure lisinopril block enzyme that cleaves angiotensin I to angiotensin II vasodilation and decrease secretion of aldosterone due to increase angiotensin II adverse e ects: dry cough and angioedema due to increases levels of bradykinin ARBs: -sartan block the AT1 receptors, decreasing the activation of AT1 receptors by angiotensin II competitive antagonists valsartan and losartan advantage of more complete blockade of angiotensin II action substitute for ACE inhibitors calcium channel blockers: limit intracellular calcium binding to L-type calcium channels in the heart and in smooth muscle of the coronary and peripheral arteriolar vasculature verapamil: diphentylalkylamines ◦ least selective ◦ both cardiac and vascular smooth ◦ helps prevent migraines diltiazem: benzothiazepines ◦ a ects cardiac and vascular smooth muscles but less pronounced negative than verpamil nifedipine: dihydropyridines ◦ much greater a nity for vascular calcium channels than for calcium channels in the heart ◦ particulary bene cial for hypertension treatment adverse: verapamil and diltiazim avoided in heart failure peripheral edema