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Flashcards in chapter 26 pharm 343 Deck (56):
1

*alteplase (activase)

t-PA made by recombinant DNA techniques. it is fibrin specific and does not lyse. does not induce an antigen-antibody reaction. can be administered in the event of reinfarction. has a short half-life of 5 mins. it is believed to open clogged artery rapidly but it is short lived. it is given with heparin to prevent reocclusion. only in parenteral form.

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*aspirin

is used for its analgesic, inflammatory, and antipyretic properties. it also has antiplatelet properties. it inhibits cyclooxygenase in the platelet irreversibily si that the platelet cant regenerate this enzyme. last a lifespan of platelet which is 7 days. causes blood vessels to constrict and platelet to aggregate. aspririn prevents TXA2 formation which results in dilation of the vessels and preventions of platelets from forming a clot.
flulike symptoms in children and teens. occrance of reyes syndrome, a rare acute fatal condition involving hepatic and CNS damage. aspirin allergy must not get NSAIDS. both oral and rectal forms. aspirin withdopyridamole is used antiplatelet purposes.

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*clopidogrel (plavix)

ADP inhibitor. only oral form. neutorpenia and agranulocytosis adverse effects.

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*dabigatran (pradaxa)

first oral thombin inhibitor for prevention of strokes and thrombosis in pts with nonvalvular atrial fribrillation. becomes activated in the liver. binds to both free and clot bound thrombin. dose is dependent on renal function. 150mg twice daily. and 75 for renal difficulties. no antidote side effect is bleeding. no monitoring is required. interactions include phenytoin and amiodarone.

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*enoxaparin (lovenox)

low molecular weight heparin is from synthetic. activate factors X (Xa) than for activated factor II.
making large molecules of heaparin smaller fragments. have higher degree of bioavailability and a longer elimination half-life than unfractionated heparin. no monitoring required. only in injectable forms. deadly is to mix heparin with lovenox.

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*epitifibatide (integrilin)

is a GP inhibitor. administered in ICU or cardiac catheterization labs. only IV use.

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*fondaparinux (arixtra)

inhibits thrombosis by its specific action against factor Xa alone.
indicated for prophylaxis or treatment of DVT or PE. pts with creatinine clearance less than 30 or body weight less than 50kg. bleeding side effect. thrombocytopenia has been reported and therapy should be topped if platelet count falls and used with caution with warfarin and other anticoags. only subcu injections. pro is 2.5mg and dvt and pe is 5-10mg daily.

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*heparin

heparin is unfractioned heparin which is a large molecule from animal sources. heparin works by binding to a substance called antithrombin III which turns off factors II X and IX. heparin turns off the coagulation pathway and prevents clots from forming but cant lyse it. aPTT test done for this. when it is used for flushing, no monitoring.
heparin use for DVT prophylaxis in 5000units 2 or 3 times a day subcu and no monitoring. most hospitals have a wight based protocols for heparin.

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*warfarin (coumadin)

works by inhibiting vitamin K synthesis by bacteria in the GI tract. clotting factors II VII IX and X. these are vitamin K dependent clotting factors.
available in oral or IV. monitor PT/INR. normal INR is 1.0 with warfarin is 2-3.5. 1/3 pts deal with warfarin differently bcuz of genes such as CYP2CP and VKORC1. combining warfarin withamidarone will lead to 50% high in INR it is recommended to cut warfarin in half.

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antifibrinolytic drugs

drugs that prevent the lysis of fibrin in doing so promote clot formation.
also called hemostatic drugs. aminocaproic, tranexamic acids, and desmopressin. used topically.

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anticoagulants aka antithrobotic drugs

substances that prevent or delay coagulation of the blood. no direct effect on a blood clot that has already formed. they prevent intravascular thhrombosis by decreasing coagulability. their uses from preventing clot formation to preventing the extension of an established clot. orally and parenterally administered.

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antiplatelet drugs

substances that prevent platelet plugs from forming.
prevent platelet adhesion to the site of blood vessel injury which actually occurs before clot cascade.injury cause collagen and fibronectin to be exposed. collagen is stimulant of platelet adhesion and membranes called glycoprotein . cause platelet to accumulate in site of injury. change shape and release their contents, ADP, serotonin, and platelet factor IV. it is twofold. acts as recruiters attracting platelets to the site, and they are potent vasocontrictors. platelet plug can be dislodged.clotting cascade is then stimulated to form a more permanent fibrin plug.

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antithrombin III

a substance that inactivates three major activating factors of the clotting cascade; activated factor II (thrombin), activated factor X, and activated factor IX.

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coagulation cascade

the series of steps beginning with the intrinsic or extrinsic pathways of coagulation and proceeding through the formation of a fibrin clot.

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coagulation

the process of blood clotting. the process by which multiple coagulation factors of the blood interact in the coagulation cascade, forming an insoluble fibrin clot.

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fibrin

a stringy, insoluble, protein produced by the action of thrombin on fibrinogen during the clotting process; a major component of blood clots.

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clot

insoluble solid elements of blood that have chemically separated from the liquid (plasma) component of the blood.

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fibrin specificity

the property of some thrombolytic drugs of activating the conversion of plasminogen to plasmin only in the presence of established clots having fibrin threads rather than inducing systemic plasminogen activation thruout body.

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enzyme

a protein molecule that catalyzes chemical reactions of other substances without being altered or destroyed in the process.

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fibrinogen

a plasma protein that is converted into fibrin by thrombin in the presence of calcium ions.

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fibrinolysis

the continual process of fibrin decomposition produced by the actions of enzymatic protein fibrinolysin. it is the normal mechanism for removing small fibrin clots and is timulated by anoxia, inflammatory reactions and other kinds of stress.

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DVT

the formation of a thrombus in one of the deep veins in the body. the deep veins most commonly affected are the iliac and femoral veins.

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fibrinolytic system

an area of the circulatory system undergoing fibrinolysis.

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embolus

a blood clot that has been dislodged from the wall of a blood vessel and is traveling thruout the bloodstream. emboli that lodge in a critical blood vessel can result in disability or death. causes an MI, stroke, and PE.

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hemophilia

a rare, inherited blood disorder in which the blood does not clot normally.

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hemorheologic drugs

drugs that alter the function of platelets without compromising their blood-clotting properties.

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hemostasis

the arrest of bleeding, either by the physiologic properties of vasocontriction and coagulation or by mechanical, surgical, or pharmacologic means.

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plasmin

the enzymatic protein that breaks down fibrin into fibrin degradation products, it is derived from plasminogen.

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plasminogen

a plasma protein that is converted to plasmin

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pulmonary embolism

the blockage of a pulmonary artery by foreign ,matter such as fat, air, a tumor, or a clot.

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thrombolytic drugs (fibrinolytic)

drugs that dissolve thrombi by functioning similarly to tissue plasminogen activator.
lyse thrombi in vessels that supply heart with blood. substance that broke down fibrin clots was isolated from pts. this substance determined to be produced by the bacteria growing in body.
it is used by activating plasminogen and converting it to plasmin, which is capable of digesting fibrin, a major componenet of clots.

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tissue plasminogen activator

a naturally occuring plasminogen activator secreted by vascular endothelial cells in the walls of blood vessels. thrombolytic drugs based on this blood componenet.

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extrinsic

damaged by pentrations from the outside, thromboplastin is released. which initiates extrinsic pathways.

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thromboembolic events

events in which a blood vessel is blocked by an embolus carried in the blooodstream from the site of its formation. the tissue supplied by an obstructed artery may tingle and become cold, numb, cyonotic, and eventually necrotic.

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intrinsic

present in the blood in their active forms. factor XII come sin contact with exposed collagen on the inside of the damaged vessles.

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hemostatic

referring to any procedure, device, or substance that arrests the flow of blood.

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indicatiosn of anticoags

these include MI, unstable angina, atrial fibrilation, use of indwelling devices such as mechanical heart valves, and conditions in which blood flow may be slowed and pooled such as major surgeries or prolonged immobilization. consequence is stroke, heart attack, PE, or DVT. warfarin is preventions, heparin and LMWH are used for treatments and prevention.

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contraindications with coags

bleeding process occurances. warfarin with pregnancy whereas lower in other drugs. LMWH contraindicated with pts with indwelling epidural catheter they can be given 2 hrs after epi is removed.

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adverse effects of coags

bleeding may occur. heparin induced thrombocytopenia (HIT) is adverse effect of heparin. type 1 is more gradual reduction in platelets. type 2 is an acute fall in the number of platelets more than 50%. heparin must be discontinued in type 2. HIT can make paradoxical occurance of thrombosis, something heparin normally prevents. thrombosis from HIT can be fatal. ranges from 5-15% more higher in cow derived than pig derived heparins. warfarin can cause purple toes and skin necrosis.

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toxicity of anticoags

treatment is reversing the underlying cause. the toxic effect is hemorrhagic in nature, the management is different for each drug. symptoms are hematuria, melena, petechiae, ecchymoses, and gum or mucous bleeding. heparin and warfarin should be stopped. heaparin stop may be helpful alone bcuz of the short half life of drug (1-2 hrs). IV injection of protamine sulfate is indicated which is a heparin antidote and reverses its effects. 1mg can reverse 100 units of heparin. protamine can also reverse LMWHs 1mg dose for every miligram of LMWH given.
discontinue warfarin. synthesized in the liver 36-42 hrs before the liver can resynthesize enough clotting factors to reverse warfarin. giving vitamin K1 can hasten the return.10mg of vitamin K can reverse in 6hrs. warfarin resistance will occur and cant be given warfarin for anticoagulation. heparin or LMWH may need to be given.

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stroke

occlusion of the blood vessels of the brain by an embolus, clot, or cerebrovascular hemorrhage, resulting in ischemia of the brain tissue.

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interactions of anticoags

enzyme inhibition of metabolism. displacement of drugs from inactive protein-binding sites. decrease vitamin k by the bacteria flora in intestines. attention in the platelet count.

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bridge therapy

is when a drug takes too long to be activated that they use another drug in the mean time. refers to the fact that enoxaparin acts as a bridge to provide anticoagulation while the pt must be off his or her warfarin therapy.

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mechanism of antiplates

drugs affect the cyclooxygenase pathway which operates within platelets on the blood vessel walls.

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indications of antiplates

aspirin is prevention of strokes. clopidogrel is prevention for fatal and nonfatal thrombotic stroke and used for against ischmeic attacks and MI. dipyridamole used to prevent postop thrombolic complications and also decrease platelet aggregation. GP IIb/IIIa used to treat unstable angina and MI prevent throbi.

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thrombus

term for blood clot. an aggregation of platelets, fibrin, clotting factors, and the cellular elements of the blood that is attached to the interior wall of a vein or artery,sometimes occluding the vessel lumen.

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contraindications of plates

GI ulcer, thrombocytopenia, bleeding, leukemia, injury, vit K def, and recent stroke.

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interaction of plates

aspirin and NSAIDS produce additive antiplatelet activity and increased bleeding. combined steroids and non aspririn NSAIDS can increase the ulderogenic effects of aspirin. aspirin and heparin with Gp enhances antiplates acitivity and increases bleeding.

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indication of thrombolytic

`acute MI, arterial thrombosis, DVT, occlusions of shunts, PE, and acute ischemic stroke.

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adverse effect of thombolytic

internal, intracranial, and superficial bleeding. induce cardiac dysrythmias.

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toxicity of thrombolytic

extension of adverse effects. treatment is symptomatic and supportive bcuz of short half-life and no antidote.

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interactions of thrmobolytic

bleeding resulting from concurrent use of anticoags and antiplatelets or other drugs that affect platelet function.

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indications of antifibrinolytic

both the preventions and treatments of bleeding resulting from systemic hyperfibrinolysis and surgical complications.

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contraindications of antifibrin

disseminated intravascular coagulation.

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adverse effects antifibrin

uncommonly and are mild. causing thrombotic events cerebrovascular thrombosis and MI.

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interactions antifibrin

estrogen and contraceptives are used concurrently with aminocaproic acid or tranexamic acid.