Shared Flashcard Set


Complete List (Exam 6)
Complete List (Exam 6)

Additional Pharmacology Flashcards




-usually used in an inpatient setting
-heterogeneous mixture
MOA: binds to endothelial cell surfaces, activates antithrombin III; inhibits factor X (LMW) and thrombin (HMW)-overall greater effect on thrombin; inhibits in vivo and in vitro blood clotting
PK: admin IV, excreted by kidney (zero-order kinetics)
CI: one-stage tests of coagulation (?), deep vein thrombosis and pulmonary embolism, major abdominal or pelvic surgery, arterial embolism, MI and CAD, reduces incidence of coronary occlusion and reinfarction, DIC, large increase in coagulation (depletion of protein factors)
AE: bleeding, thrombocytopenia
Contra: hypersensitivity to heparin, pt actively bleeding, hemophilia, GI ulcerative lesions, active TB, severe hypertension, advanced renal or hepatic disease
DI: drugs that inhibit platelet aggregation, synergistic effects with oral anticoagulants
-excessive anticoagulant heparin -> discontinue, if bleeding occurs -> IV protamine sulfate
Warfarin sodium
-used in inpatient and outpatient setting
MOA: blocks gamma-carboxylation of gluatmate residues in prothrombin and factors VII, IX, X, anticoagulant proteins C and S (inhibit synthesis); blocks epoxide reductase -> inhibit hepatic synthesis of clotting factors; only inhibit in vivo clotting
PK: oral admin, 8-12 hr delayed onset of action, rapidly absorbed, >90% bound to plasma albumin, relatively long half-life, does not cross BBB, hydoxylated in liver
CI: prevention of arterial emboil from heart valve disease/valve replacement, conditions of high thromboembolic risk (prophylaxis), coronary artery bypass graft and angioplasty -> combo with antiplately drugs reduce incidence of thrombus formation and reocclusion after surgery
SE: hemorrhage, cutaneous necrosis, minor hemorrhage -> discontinue drug and give vit K, serious bleeding -> admin plasma and plasma concentrates containing K-dependent factors
Contra: chronic alcoholism -> decreases drug metabolism rate, pregnancy -> hemorrhagic disorder of fetus, serious birth defects
DI: enzyme induction (barbituates/ rifampin) -> decrease anticoagulant effect; enzyme inhibition (pyrazolones phenylbutazone and sulfinpyrazone) -> inhibit warfarin metabolism; reduced plasma protein binding (pyrazolones) -> displace albumin-bound warfarin; synergism with certain drugs; competitive antagonism (vit K); altered physiologic control loop for vit K (hereditary resistance to oral anticoagulants); aspirin, hepatic disease, hyperthyroidism -> augment warfarin PDs; heparain -> directly prolongs prothrombin time
-narrow window of safety
-pts with variant of vkorc1 (associated with body’s processing of vit K) need lower drug doses
Protamine sulfate
heparin neutralizer
MOA: treat bleeding due to excessive anticoagulant heparin
-human protease enzyme synthesized by kidney, directly converts plasminogen -> plasmin
MOA: lyse already formed thrombi, catalzye formation of plasmin from precursor plasminogen
-unmodified recombinant human t-PA
MOA: lyse already formed thrombi, catalzye formation of plasmin from precursor plasminogen
CI: treatment of coronary artery thrombosis associated with MI
Aminocaproic acid
fibrinolytic inhibitor
MOA: competitively inhibits plasminogen activation, reverse effects of thrombolytic agents
PK: dosage and route of admin adjusted to specific situation
AE: intravascular thrombosis, hypotension
Contra: DIC or GU bleeding of uppe r tract b/c potential for excessive clotting
Vitamin K1 (phytonadione)
MOA: increases synthesis of clotting factors, confers biological activity upon prothrombin, factors VII, IX, X by participating in their post-ribosomal modification
PK: oral admin
CI: treat decreased prothrombin activity due to excess warfarin or vit K1 deficiency, admin to all newborns as prophylaxis for hemorrhagic disease of vit K deficiency
MOA: inhibit thromboxane A2 synthesis by irreversible acetylation, inhibit plately content release and aggregation -> prolong bleeding time
CI: small doses for primary prophylaxis of myocardial mortality (prevention of 1st heart attack)
AE: increase risk of occurrence of stroke, peptic ulcer, GI bleeding
ADP receptor blocker/antiplatelet
-useful in pts non-tolerating aspirin
MOA: prodrug, reduce platelet aggregation by irreversibly inhibiting BINDING of ADP to its platelet receptors
PK: effectiveness depends on activation to an active metabolie by CYP2C19
-some pts are CYP2C19 poor metabolizers, if these pts with acute coronary syndrome or undergoing coronary intervention with recommended doses -> exhibit higher CV event rates
CI: prevention of vascular events in pts with TIAs, complex strokes, unstable angina; prevent thrombosis in pts undergoing placement of coronary stent
SE: nausea and diarrhea, leukopenia, hemorrhage
DI: heart attack pts that take an acid-reduction PPI (prilosec, nexium, prevacid, aciphex) in combo with this drug -> more likely to have 2nd heart attack or need revascularization procedures
GP IIB/IIIA receptor blocker/antiplatelet
MOA: Fab (fragment antigen binding), platelet-inhibiting drug that blocks platelet receptors for integrin and other aggregating substances
PK: admin IV
CI: adjunct in percutaneous angioplasty for coronary thromboses; in combo with aspirin and heparain -> effective in preventing restenosis, recurrent MI, death
Cholestyramine, Colestipol
bile acid binding resins
MOA: bind cholesterol-containing bile acids and prevent reabsorption, increase clearance, increased hepatic metabolism of cholesterol to bile acids (regulated by neg feedback), decreased hepatic cholesterol content, upregulation of hepatic LDL receptors
PK: negligible systemic bioavailaility, must be taken with meals to be effective
CI: familial hypercholesterolemia, combo therapy for familial combined hyperlipoproteinemia
AE: GI disturbances (constipation and abdominal discomfort)
DI: may reduce absorption of vitamins and drugs taken at the same time -> patients should take other drugs at least 1 hour before or at least 2 hours after resin
cholesterol absorption inhibitor
MOA: localizes and acts at the brush border of small intestine -> inhibit absorption of cholesterol (decrease delivery of intestinal cholesterol to liver, decrease hepatic cholesterol stores, increase clearance of cholesterol from blood
CI: monotherapy-cholesterol lowering is limited (reduced uptake of dietary cholesterol but upregulates hepatic cholesterol synthesis), combo with HMG CoA reductase inhibitors -> 20% additional decrease (allow reduction of statin dose while achieving cholesterol-lowering goal)
Fenofibrate, Gemfibrozil
fibrates/cholesterol absorption inhibitor
-ligand for PPAR-alpha
MOA: decrease apoB synthesis, decrease VLDL synthesis, decrease apoC-III synthesis, increase apoA-I and A-II synthesis, increase LPL synthesis, increase catabolism of TRLs -> decrease TG (major effect) and increase HDL
PK (fenofibrate): more potent than gemfibrozil, longer ½ life, renal and fecal excretion
PK (gemfibrozil): well absorbed when taken with meal, shorter ½ life than fenofibrate, most excreted unchanged in urine
CI: dysbetalipoproteinemia, hypertriglyceridemia
AE: GI disturbances, skin rashes, MYOPATHY, arrythmias, fatigue
Contra: renal or hepatic dysfunction
Preexisting gallbladder disease, hypersensitivity
DI: potentiate effects of coumarin and indanedione anticoagulants(reduce anticoagulant doses and monitor prothrombin levels), myalgias and rhabdmyolysis for combo of gemfibrozil and HMG CoA reductase inhibitors
Atorvastatin, Lovastatin, Simvastatin, Rosuvastatin
HMG CoA reductase inhibitors
MOA: forms analog of intermediate in conversion of HMG CoA to mevalonic acid, competitively inhibit HMG CoA reductase (rate-limiting and committed step of cholesterol synthesis), hepatic LDL receptors are upregulated -> LDL and IDL clearance increased; inhibition of apoB-100 synthesis, inhibition of TRL synthesis and secretion, improve endothelial function and stabilize atherschlerotic plaque
-atovastatin and simvastatin reduce LDL in homozygous familial hypercholesterolemia
PK: oral bioavail differs between statins; lovastatin and simvastatin admin lactone form (prodrugs); extensive 1st pass metabolism, bound to protein; lovastatin, simvuastatin, atorvastatin -> CYP3A4 (affected by grapefruit juice)
CI: most commonly used drugs for hypercholesterolemia (monotherapy or combo therapy), preservation of bone mineral density, increase osteoblast differentiation and activity
AE: generally well tolerated, hepatotoxicity, myopathy -> rhabdomyolysis and renal failure (risk is increased in combo therapy with fibric acid derivatives and other drugs that inhibit CYP3A4)
Contra: pregnancy, liver disease, major illness or trauma
DI: lovastatin and simvastatin potentiate action of coumarin anticoagulants
Niacin (Nicotinic Acid)
-vit B3, used in synthesis of NAD and NADP, inhibits adipocyte adenyl cyclase
MOA: decrease TG synthesis, decrease VLDL secretion, decrease apoA-1 clearance, increases LDL, increases VLDL clearance -> decreased TG, decreased LDL, decreased Lp(a), increased HDL (major effect)
PK: rapidly absorbed, sustained-release tablets, distributes throughout body, excreted by kidneys, high doses required for lipid lowering
CI: hypertriglyceridemia w/ elevated LDL-C and low HDL-C; combo therapy w/ resins for familial hypercholesterolemia, any pt whose LDL-C is controlled but HDL-C is low; combo therapy with resin and statin -> reduce LDL-C by 70% or more
AE: CUTANEOUS VASODILATION -> flushing and pruitis (take aspirin prior to reduce rxn), nausea and diarrhea; may precipitate abnormal liver function, hepatoxicity, glucose intolerance, peptic ulcers, gout
Contra: peptic ulcers, glucose intolerance, gout, hepatic function should be monitored
DI: induce hypotension in combo with anti-HTN drugs
Omega-3 Fatty Acid Ethyl Ester
MOA: adjunct to lipid-lowering diet to reduce TGs in adults with severe hypertriglyceridemia, reduced hepatic TG synthesis and increased plasma lipoprotein lipase activity
CI: hypersensitivity, fish allergies
Nonselective: Propanolol, Carvedilol, Nadolol, Pindolol, Labetolol / Beta 1-cardioselective: Acebutolol, Metoprolol, Atenolol, Esmolol
beta-blockers MOA: block beta-1 receptors in heart PD: decrease myocardial oxygen consumption CI: post MI; anti-angina-combine with nitrates for exertional angina, combine with dihydropyridines to inhibit reflex tachycardia) AE: abrupt discontinuation can cause rebound symptoms, myocardial depression, bradycardia, bronchospams, exacerbates hypoglycemia in diabetics
Captopril, Lisinopril, Enalapril and Benazepril (prodrugs)
ACE inhibitors
Losartan, Valsartan
Nifedipine (primarily arteriolar); Verapamil and Diltiazem (primarily cardiac)
Ca2+ channel blockers
MOA: primarily SA/AV nodes-blocks Ca2+ channels, inhibits phase 0 in nodal tissue, inhibits phase 2 in muscle tissue, slows conduction through nodal tissue
CI: acute or chronic SVTs (helps with rate control)
AE: myocardial depression, severe sinus bradycardia, heart block, postural hypotension, reflex tachycardia
ECG: slowing of cardiac rate
Verapamil, Diltiazem
Ca2+ channel blockers (primarily cardiac)
MOA: blocks Ca2+ channels, slows Ca2+ channel recovery time
CI: suppresses SA/AV nodal re-entrant activity
AE: myocardial depression, severe sinus bradycardia, heart block, postural hypotension, reflex tachycardia, GI disturbances-constipation
-diltiazem has less severe AEs than verapamil
Ca2+ channel blocker (primarily arteriolar)
MOA: inhibition of Ca2+ channels
PD: vascular smooth muscle (arteriolar vasodilation); cardiac cells (inhibit phase 2 in cardiac muscle and inhibits phase 0 in pacemaker cells)
PK: oral admin, liver metabolism, highly protein bound
CI: vasospastic angina (with a nitrate), exercise induced angina, AV nodal reentrant arrhythmia, hypertension
AE: worsening angina due to reflex tachycardia, negative inotrope, heart block, sinus bradycardia, hypotension/dizziness/heachache, edema due to venous pooling, constipation, coughing/wheezing
Hydralazine, Sodium Nitroprusside
MOA: denitrated which released NO -> smooth muscle relaxation/vasodilation
PD: decrease in preload and afterload, improved distribution of coronary blood flow, reduce work of heart
PK: absorption can be sublingual, buccal, transdermal, ointment, spray, IV; rapid 1st pass metabolism; rapid development of tolerance
CI: stable angina, variant angina, pulmonary congestion of CHF
AE: headache, dizziness, nitrate syncope, decreased coronary perfusion with excessive hypotension
Isosorbide Dinitrate
PK: oral admin, liver metabolism, onset of action in 30min
Overdose: methemoglobinemia
Quinidine (Class IA)
MOA: moderate recovery (3 sec), Na+ channel blocker, K+ channel blocker, alpha receptor blocker, cholinergic receptor blocker (vagolytic)
CI: 2nd line treatment for chronic SVTs
AE: torsades de pointe tachycardia, paradoxical tachycardia, hepatic granulomas, GI upset and diarrhea, quinidine syncope, cinchonism (headache, dizziness, tinnitus)
PD: decreases automaticity-blocks Na+ channels, decreases conduction velocity through heart muscle, increases conduction velocity through nodes, lengthens duration of AP
PK: given IV or oral, 80% protein bound, metabolized by liver, inhibited by P450 system
ECG: prolonged QT, widened QRS
Procainamide (Class IA)
MOA: moderate recovery (1.8sec), Na+ channel blocker, K+ channel blocker, active metabolite (NAPA) only has K+ channel blocking effects
CI: 2nd line treatment for sustained V-tach; acute or chronic SVTs
AE: lupus-like syndrome, torsades do pointe tachycardia, hypotension due to ganglionic blockade, bone marrow aplasia-agranulcytosis, GI upset
PD: decreases automaticity, decreases conduction velocity through heart muscles, lengthens duration of AP; esp. NAPA
PK: metabolized by liver, NAPA excreted by kidney
Lidocaine (Class IB)
MOA: rapid recovery (0.1sec), Na+ channel blocker, increases K+ conductance during phases 3&4
CI: 2nd line treatment for sustained V-tach or V-fib (try amiodarone first)
AE: CNS disturbances (nystagmus, tremor), seizures that are often refractory to treatment
PD: decreases automaticity, decreases conduction velocity through heart muscles, SHORTENS DURATION OF AP
PK: IV admin only, rapid 1st pass metabolism, redistibution to fat tissue increases ½ life
VAP: decreased slope and amplitude, shortened duration of AP
ECG: widened QRS, shortened QT
Mexiletine (Class IB)
-same as lidocaine, but in oral form
Flecainade (Class 1C)
MOA: slow recovery (11sec), Na+ channel blocker, K+ channel blocker, Ca2+ channel blocker
CI: atrial arrhythmias when no other structural heart disease is present (CAST)
AE: proarrhythmic agent, depress left ventricular function, heart block
PD: decreases conduction velocity through heart muscle, decreases conduction velocity through nodes, lengthens AP duration
PK: oral admin, metabolized by liver with renal excretion
ECG: widened QRS, prolonged QT
Propafenone (Class IC)
MOA: Slow recovery (11sec), Na+ channel blocker, K+ channel blocker, beta-blocker
CI: chronic treatment of atrial tachyarrthymias
AE: proarrthymic agent (torsades de pointe), myocardial depression, sinus bradycardia, bronchospasm
PD: decreases conduction velocity through heart muscle, decreases conduction velocity through nodes, lengthens AP duration
PK: oral admin, metabolized by liver with renal excretion
Propanolol (Class II)
MOA: non-selective beta-blocker, mild Na+ channel blocker at higher conc.
CI: acute and chronic management of atrial flutter and fib, prvent post-MI ventricular arrhythmias
AE: myocardial depression, bronchospasm (exacerbates asthma)< augments hypoglycemia in diabetics, rebound sympathetic effects following abrupt withdrawal
PD: decreases automaticity, decreases conduction velocity through nodes
PK: oral admin, metabolized by liver
AP: see more effect in nodes thanin muscle
ECG: bradycardia
Amiodarone (Class III)
MOA: K+ channel blocker, Na+ channel blocker, beta-blocker, Ca2+ channel blocker (weak)
CI: acute and chronic treatment for atrial and ventricular arrhythmias; may be combined with ICD to help with stabilization
AE: corneal deposits; liver, lungs, thyroid dysfunction, postural hypotension, photosensitivity, blue-gray skin discoloration
PD: decreases automaticity, decreases conduction velocity through heart muscle, decreases conduction velocity through nodes, lengthens AP duration
PK: oral or IV admin, highly lipophilic, LONG ½ LIFE (55 days)
ECG: very similar to quinidine (prolonged QT, widened QRS)
Sotalol (Class III)
MOA: K+ channel blocker, non-selective beta-blocker
CI: chronic management of atrial arrhythmias
AE: torsades do pointe tachycardia, myocardial depression, bronchospasm, augments hypoglylcemia in diabetics, rebound sympathetic effects following abrupt withdrawal
PD: decreases automaticity, decreases conduction velocity through nodes, lengthens AP duration
Ibutilide, Dofetilide (Class III)
MOA: K+ channel blocker
CI (ibutilide): acute managemet of atrial arrhythmias
CI (dofetilide): chronic management of atrial arrhythmias
AE: torsades de pointe arrhytmia
PD: lengthens duration of AP
PK: dofetilide-oral; ibutilide-IV
-patients must be hospitalized to initiate therapy with dofetilide
AP: prolonged AP
ECG: long QT
MOA: binds to adenosine receptors (G-protein coupled), opens ACh sensitive K+ channels
CI: acute termination of atrial flutter and fibrillation
AE: transient asystole, dyspnea, a-fib
PD: decreases automaticity, shortens AP duration in atrial muscle, lengthens AP duration in nodes, slows nodal conduction velocity (Ca2+ inhibition)
PK: IV admin, eliminated by cellular uptake (1/2 <10sec)
AP: shortened duration
ECG: slowing of HR
Digoxin/Digitoxin (Digitalis)
-digoxin shorter effects than digitoxin (except digitoxin has greater volume of distribution than digoxin)
MOA: reversible inhibition of Na+/K+ ATPase, binding affinity greater to phosphorylated E2 conformation
PD: mechanical effects (increase tension development, improvement in cardiac function); direct electrical effects (increased automaticity, decreased conduction velocity, shorter duration of AP); indirect electrical effects (increase in vagal tone -> bradycardia and heart block)
PK: narrow therapeutic window, oral admin
CI: CHF, AV nodal reentrant arrhythmias, a-fib
AE: altered serum electrolytes, acidosis inhibits Na/K pump, altered thyroid status, renal disease impairs elimination, increased sympathetic tone, respiratory disease/hypoxia
AE (neurological and GI signs): malaise, dizziness, confusion, delirium; anorexia, nausea, vomiting, abdominal pain; disturbed color vision -> adjust dose
AE (early cardiac signs): sinus bradycardia, 1st degree AV block, AV pacemaker or ectopic impulses orginiating from AV node -> adjust dose
AE (serious cardiac signs): marked sinus bradycardia, SA node arrest, 2nd or 3rd degree AV block -> give atropine and K+
AE (most serious cardiac signs): any of above signs + premature ventricular arrhythmias (PVCs), worsening ventricular arrhythmias -> DIGIBIND (Fab immunoglobulin against digoxin)
DI: decreases absorption (cholestyramine, bran); increase plasma levels (antiarrhythmics), increase absorption (antibiotics); increase automaticity due to electrolyte alteration (furosemide, chlorothiazide); exacerbate AV node inhibition (verapamil, diltiazem)
ECG: bradycardia and prolonged PR, shortened QT interval
B1 agonist/cardiotonic
MOA: stimulated beta-1 adrenergic and dopamine receptors
PD: positive inotropic effect, at low doses causes dilation of renal vessels via D1 receptors
AE: tachycardia, proarrhythmogenic
b1 agonist//cardiotonic
MOA: stimulates beta-1 and -2 adrenergic receptors
PD: positive inotropic effect (beta-1); vasodilation of vasculature (beta-2)
AE: tachycardia and proarrhythmogenic (but less than dopamine), tolerance after several days
phosphodiesterase inhibitor/cardiotonic
MOA: phosphodiesterase inhibitor
PD: positive inotropic effect, vasodilation
AE: proarrhythmogenic with prolonged used (few days), thrombocytopenia and liver damage
Ca2+ channel blockers, beta-blockers, nitrates
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