Anticoagulant, Antiplatelet, Thrombolytic Drugs

Question 0

Coagulation cascade

Answer 0

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

Question 1

Clotting process

Answer 1

-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

Question 2

Fibrinolysis

Answer 2

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

Question 3

Anticoagulants

Answer 3

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

Question 4

Thrombolytics

Answer 4

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

Question 5

Hemostatics

Answer 5

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

Question 6

Heparin

Answer 6

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

Question 7

Heparin monitoring

Answer 7

Activated partial thromboplastin time (aPTT):

-normal aPTT range = 26-33 seconds; heparin causes prolongation of aPTT

Question 8

Heparin/pharmacokinetics

Answer 8

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

Question 9

Heparin/adverse effects

Answer 9

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

Question 10

Warfarin

Answer 10

Oral anticoagulant; antagonist vitamin K

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

Question 11

Aspirin (ASA)

Answer 11

Antiplatelet drug; inhibition of cyclooxygenase

-adverse effect: increased risk of GI bleeding

Question 12

Ticlopidine (Ticlid)

Answer 12

Inhibits ADP-mediated aggregation; adverse effects: hematologic effects

Question 13

Clopidogrel (Plavix)

Answer 13

ADP receptor antagonist

Question 14

Management of STEMI

Answer 14

Adjuncts to reperfusion therapy; heparin, antiplatelet drugs

Question 15

Drug management of STEMI

Answer 15

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

Question 16

Primary percutaneous coronary intervention

Answer 16

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

Question 17

Fibrinolytic (Thrombolytic) therapy

Answer 17

Dissolves clots; converts plasminogen to plasmin (proteolytic enzyme)

1. Alteplase, a tissue plasminogen activator
2. Reteplase
3. Streptokinase
4. Tenecteplase
5. Urokinase

Question 18

Fibrinolytic (thrombolytic) therapy

Answer 18

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

Question 19

Adjuncts to reperfusion therapy: management of STEMI

Answer 19

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

Question 20

Complications of STEMI

Answer 20

Ventricular dysrhythmias, cardiogenic shock, heart failure, cardiac rupture

Question 21

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

Answer 21

• 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

Question 22

Secondary Prevention of STEMI

Answer 22

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