Anticoagulant, Antiplatelet, Thrombolytic Drugs Flashcards Preview

Pharmacology > Anticoagulant, Antiplatelet, Thrombolytic Drugs > Flashcards

Flashcards in Anticoagulant, Antiplatelet, Thrombolytic Drugs Deck (23):
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Clotting process

-Blood vessel injury causes vessel spasm (constriction)
-Platelets are attracted to and adhere to injured area
-Aggregation of platelets forms plug
-Formation of insoluble fibrin strand and coagulation (coagulation cascade)
Normal clotting occurs in six minutes

1

Coagulation cascade

Intrinsic or extrinsic pathways lead to formation of fibrin clot;
-Injured cells release prothrombin activator, prothrombin activator changes prothrombin to thrombin, thrombin changes fibrinogen to fibrin, fibrin forms insoluble web over injured area to stop blood flow

2

Fibrinolysis

Clot removal; initiated by release of tissue plasminogen activator (tPA) > tPA converts plasminogen to plasmin, plasmin digests fibrin strands-thus, circulation is restored.
Regulated so unwanted clots are removed and fibrin is left in wounds

3

Anticoagulants

Prevent formation of clots
-Most serious side effect to assess is bleeding; to assess internal bleeding: monitor CBC, lumbar pain, abdominal bulging, guaiac tests on stool
-Essential for patient safety to assess coagulation studies

4

Thrombolytics

Dissolve life-threatening clots; assess for exclusion to therapy, monitor baseline coagulation studies, monitor level of consciousness for symptoms of cerebral hemorrhage, observe for reperfusion arrhythmias, teach client about the risk of bleeding

5

Hemostatics

Prevent formation of clots; monitor for clotting, administer intrevenously, monitor site closely
-Assess for myopathy and myoglobinuria (reddish-brown urine), teach client to report symptoms of clotting or bleeding, DO NOT take aspirin!
-Prototype drug: aminocaproic acid (Amincar), mechanism of action: prevent fibrin from dissolving

6

Heparin

Mechanism of action: Anitcoagulant effect of heparin is mediated through its interaction with antithrombin III

7

Heparin monitoring

Activated partial thromboplastin time (aPTT):
-normal aPTT range = 26-33 seconds; heparin causes prolongation of aPTT

8

Heparin/pharmacokinetics

Not absorbed through GI tract, must be administered parentally (IV, SQ); onset of action: IV immediate/SQ 1-2 hours, half life: 1-2 hours (dose-dependent), clearance: reticuloendothelial system (RES), safe in pregnancy, not secreted in breast milk

9

Heparin/adverse effects

Hemorrhage/bleeding; hypersensitivity reaction
Management: mild: adjust infusion rate or stop infusion; severe: administer protamine sulfate 1 mg IV for every 100 units of heparin administered during the past 4 hours; administer protamine sulfate 50 mg IV over 10 min

10

Warfarin

Oral anticoagulant; antagonist vitamin K
-Blocks the biosynthesis of factors VII, IX, X and prothrombin; therapeutic uses: long-term prophylaxis of thrombosis

11

Aspirin (ASA)

Antiplatelet drug; inhibition of cyclooxygenase
-adverse effect: increased risk of GI bleeding

12

Ticlopidine (Ticlid)

Inhibits ADP-mediated aggregation; adverse effects: hematologic effects

13

Clopidogrel (Plavix)

ADP receptor antagonist

14

Management of STEMI

Adjuncts to reperfusion therapy; heparin, antiplatelet drugs

15

Drug management of STEMI

Thrombolytic drugs: alteplase (a tissue plasminogen activator), reteplase, streptokinase, tenecteplase, urokinase
-Percutaneous coronary intervention (PCI)

16

Primary percutaneous coronary intervention

Primary: refers to the use of angioplasty rather than fibrinolytic therapy; stents may be placed
-Goal: primary PCI within 90 minutes of patient contact; success rate w/ PCI somewhat higher than with thrombolytics

17

Fibrinolytic (Thrombolytic) therapy

Dissolves clots; converts plasminogen to plasmin (proteolytic enzyme)
1. Alteplase, a tissue plasminogen activator
2. Reteplase
3. Streptokinase
4. Tenecteplase
5. Urokinase

18

Fibrinolytic (thrombolytic) therapy

Most effective when patient presents early; not given if pain has been present longer than 12 hours (best if given during first 4-6 hours)
Goal: to improve ventricular function, limit size of infarct, and reduce mortality; timely administration: opening of occluded artery in 80% of patients
-Guidelines suggest 30 minute target time, best for patients younger than 75 years

19

Adjuncts to reperfusion therapy: management of STEMI

-Unfractionated heparin used for treatment lasting less than 48 hours; low molecular weight (LMW) heparin used for treatment lasting longer than 48 hours

20

Complications of STEMI

Ventricular dysrhythmias, cardiogenic shock, heart failure, cardiac rupture

21

Adjuncts to reperfusion therapy: management of STEMI (drug therapy)

-Antiplatelet drugs: clopidogrel (plavix), glycoprotein (GP) IIb/IIIa inhibitors
-Low dose aspirin: may use concurrently with clopidogrel, should take indefinitely, higher dose for PCI patients
-Angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs)
-Calcium channel blockers: antianginal, vasodilation, and antihypertensive actions

22

Secondary Prevention of STEMI

Discharge 6-10 days after event; 5% of patients have another infarct in first year. Outcome improved with risk factor reduction; All post-MI patients should take: beta blocker, ACE inhibitor, antiplatelet drug or anticoagulant