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Pharm Exam 2 > List: Anticoagulants and Thrombolytic Drugs > Flashcards

List: Anticoagulants and Thrombolytic Drugs Flashcards

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1
Q

Hemostasis:

A

Hemostasis: process that maintains the integrity of the circulatory systems after vascular damage

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2
Q

Primary hemostasis:

A

Primary hemostasis: platelet plug formation (platelets adhere to damaged endothelium to form plug)

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3
Q

Secondary hemostasis:

A

Secondary hemostasis: blood coagulation (clot forms upon the conversion of fibrinogen to fibrin, and its addition to the platelet plug) –> Formation of a thrombus

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4
Q

Thrombus Formation:

A

Thrombus Formation: extrinsic and intrinsic pathways merge into common pathway, leading to factor X activation

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5
Q

Factor X to fibrin:

A

Factor X cleaves prothrombin –> thrombin

Thrombin cleaves fibronigen –> fibrin

Fibrin incorporated into thrombus

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6
Q

Thrombolysis/Fibronolysis:

In response to injury, endothelial cells synthesize and release:

t-PA converts plasminogen:

Plasmin cleaves:

A

Thrombolysis/Fibronolysis: process of fibrin digestion by plasmin (protease)

  • In response to injury, endothelial cells synthesize and release tissue plasminogen activator (t-PA)
  • t-PA converts plasminogen  plasmin
  • Plasmin cleaves fibrin and dissolves the clot
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7
Q

Endogenous Inhibitors of this Process

PAI-1/PAI-2:
α2-antiplasmin:

A

PAI-1/PAI-2: inhibit t-PA

α2-antiplasmin: inhibitor of plasmin

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8
Q

3 Major Classes of Anticoagulant Drugs:

A

Indirect Thrombin Inhibitors

Parenteral Direct Thrombin Inhibitors

Oral Anticoagulants

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9
Q

Indirect Thrombin Inhibitors:
Parenteral Direct Thrombin Inhibitors:
Oral Anticoagulants:

A

Indirect Thrombin Inhibitors: Heparin, Fodaparinux

Parenteral Direct Thrombin Inhibitors: Hirudin, Bivalirudin, Argatroban

Oral Anticoagulants: Warfarin, next generation drugs (Apixaban, Pradaxa, Rivaroxaban)

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10
Q

Indirect Thrombin Activators

General MOA:

A

General MOA: antithrombotic effect due to interaction with antithrombin III (ATIII) and factor Xa

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11
Q

Indirect Thrombin Activators

Preparations: (3)

A

o Unfractionated heparin
o Low-molecular weight heparin
o Fondaparinux (synthetic polysaccharide)

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12
Q

Heparin

General:

A

General: heterogeneous mixture of sulfated mucopolysaccharides

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13
Q

Heparin Targets: (3)

A
  • Thrombin
  • Factor Xa
  • Factor IXa
    .
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14
Q

Heparin

MOA:

A

MOA: activated ATIII binds heparin and efficiently degrades thrombin and factor X

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15
Q

Heparin

Therapeutic Use: (6)

A
  • Venous thrombosis (initial treatment)
  • Pulmonary embolism (initial treatment)
  • Acute MI (initial treatment)
  • Surgery requiring cardiopulmonary bypass
  • Patients with DIC
  • Unstable angina
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16
Q

Heparin
Pharmacokinetics:
LMW can be given ____ and without ______

A

Pharmacokinetics: LMW heparin preparations have more predictable pharmacokinetics than HMW heparin
- LMW can be given subQ and without laboratory monitoring

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17
Q

Management of Heparin Treatment

Full-dose heparin therapy:
subQ heparin:

A

Full-dose heparin therapy by continuous IV infusion needs to be monitored by activated partial thromboplastin time (aPTT)

Can give subQ heparin for long-term anticoagulant therapy in patients with contraindications for warfarin use (ie. pregnancy)

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18
Q

Heparin
Toxicity

Bleeding:
Protamine Sulfate:
Heparin-induced thrombocytopenia:

A

Bleeding: incidence somewhat less in patients treated with LMW form
- Protamine Sulfate: can be given in cases of life-threatening hemorrhage to reverse the effects of heparin (binds tightly and neutralizes it)

Heparin-induced thrombocytopenia: decreased platelet count; lower incidence with LMW form

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19
Q

Fondaparinux

Use:

A

Use: approved for thromboprophylaxis of patients undergoing hip or knee surgery
- To prevent pulmonary embolism and deep vein thrombosis

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20
Q

Fondaparinux

Management:

A

Management: similar to LMW heparin

  • Can be used with daily subQ administration
  • Does not require monitoring
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21
Q

Parenteral Direct Thrombin Inhibitors

Drugs in this Class: (3)

A

Hirduin
Bivalirudin
Argatroban

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22
Q

Hirduin:
Bivalirudin:
Argatroban:

A

Hirduin: bivalent specific, irreversible thrombin inhibitor (leech saliva)
Bivalirudin: bivalent inhibitor of thrombin
Argatroban: small molecule thrombin inhibitor

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23
Q

Parenteral Direct Thrombin Inhibitors

Drug Targets:

A

Thrombin

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24
Q

Therapeutic Use/Management
Hirudin

Treatment of patients with:
Administered by:
Dose adjusted to maintain:

A
  • Treatment of patients with heparin-induced thrombocytopenia
  • Administered by IV
  • Dose adjusted to maintain aPTT at 1.5-2
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25
Therapeutic Use/Management Bivalirudin Alternative to: Administered by:
- Alternative to heparin in patients undergoing coronary angioplasty - Administered by IV
26
Therapeutic Use/Management Argatroban Alternative to:
Alternative to hirudin for prophylaxis treatment of patients with or at risk of developing heparin-induced thrombocytopenia
27
Parenteral Direct Thrombin Inhibitors Toxicity Use with caution in renal failure: Development of anti-hirudin Abs:
Use with caution in renal failure: can accumulate and cause bleeding Development of anti-hirudin Abs: can cause paradoxical increase in aPTT (daily monitoring of aPTT recommended)
28
Warfarin | General:
General: synthetic derivative of coumarin
29
Warfarin Administered as: bioavailability: T½: vs heparin:
- Administered as a sodium salt - Has 100% bioavailability - Long T½ in plasma (36 hours) - Slower acting than heparin (for long term management, NOT for an acute event)
30
Warfarin MOA: Blocks ______ of glutamate residues in coagulation factors
MOA: inhibits the vitamin-K dependent synthesis of biologically active forms of the Ca++-dependent clotting factors (prothrombin, VII, IX, X) and protein C (regulatory factor) - Blocks gamma-carboxylation of glutamate residues in coagulation factors
31
Warfarin Therapeutic Use Prevent progression or recurrence of: Prevention of ____________ in patients undergoing orthopedic or gynecological surgery
Prevent progression or recurrence of acute DVTs or pulmonary embolism (follows initial course of heparin) Prevention of venous thromboembolism in patients undergoing orthopedic or gynecological surgery
32
Warfarin | Preventing systemic emboli in patients with: (3)
Preventing systemic emboli in patients with: - Acute MI - Prosthetic heart valves - Chronic atrial fibrillation
33
Warfarin International Normalized Ration (INR) Therapeutic range for: Defined as: Prothrombin time determined from:
International Normalized Ration (INR): therapeutic range for oral anticoagulant therapy Defined as patient prothombin time/mean of normal prothrombin time for the lab Prothrombin time determined from a fasting blood sample obtained 8-14 hours after the last dose of an oral anticoagulant
34
Warfarin Use with caution in patients with: (3)
Patients with congenital coagulation deficiency Patients with thrombocytopenia Patients with hepatic or renal insufficiency
35
Warfarin | Never use:
Patients who are pregnant (readily crosses the placenta and causes hemorrhagic disorder in the fetus/serious birth defects)
36
Warfarin resistance: Difficult to manage because:
Warfarin resistance: can develop in some patients (most common in those with advanced cancer); progression/recurrence of the thrombotic event - Difficult to manage because raising INR in these patients also increases risk of bleeding
37
Warfarin DDIs Decrease anticoagulant effect:
Decrease anticoagulant effect: barbiturates and rifampin
38
Warfarin DDIs Increase anticoagulant effect:
Increased anticoagulant effect: aspirin and cephalosporins
39
Oral Direct Thrombin Inhibitors Main advantage to these new ones is: New Drugs: (3)
New Drugs: main advantage to these new ones is that they do not require drug monitoring o Pradaxa: targets thrombin only (already FDA approved) o Rivaroxiban: targets factor Xa o Apixaban: targets factor Xa
40
Oral Direct Thrombin Inhibitors (apart from warfarin) Pradaxa: Rivaroxiban: Apixaban:
Pradaxa: targets thrombin only (already FDA approved) Rivaroxiban: targets factor Xa Apixaban: targets factor Xa
41
Fibrinolytic Drugs | General MOA:
General MOA: cause rapid lysis of thrombi by catalyzing the activation of plasmin
42
Fibrinolytic Drugs Tissue Plasminogen Activator (tPA) General:
General: endogenous serine protease that is a poor plasminogen activator in the absence of fibrin
43
Fibrinolytic Drugs Tissue Plasminogen Activator (tPA) MOA: Presence of fibrin _____ the speed of activation Clearance: Half Life:
MOA: binds to fibrin via lysine binding sites at amino terminus and activates bound plasminogen - Presence of fibrin increases the speed of activation several hundredfold Clearance: occurs by hepatic metabolism - Half Life: 5-10 minutes
44
Fibrinolytic Drugs Tissue Plasminogen Activator (tPA) Use: (3)
Use: lyses thrombi during the treatment of - Acute MI - Pulmonary embolism - Severe DVT
45
Recombinant tPA: (2) Effect on half lives:
Recombinant tPA: Reteplase and Tenecteplase Increased half lives (allow for convenient bolus dosing)
46
Fibrinolytic Drugs Streptokinase General:
General: produced by beta-hemolytic streptococci
47
Fibrinolytic Drugs Streptokinase MOA:
MOA: no intrinsic enzymatic activity, but forms a stable complex with plasminogen, producing a conformational change that exposes the active site on plasminogen --> plasmin
48
Fibrinolytic Drugs Streptokinase Use:
Use: decreased due to advent of newer agents
49
Fibrinolytic Drugs | Recent Studies:
Recent Studies: suggest that angioplasty without stent placement is superior to thrombolytic therapy, when it is feasible
50
Fibrinolytic Drugs Hemorrhage: _____ at sites of vascular injury
Hemorrhage: major toxicity of all thrombolytic agents; results from 2 factors Lysis of fibrin in physiological thrombi at sites of vascular injury
51
Fibrinolytic Drugs Hemorrhage A systemic lytic state that results from systemic formation of plasmin, causing: (2)
- Fibrinogenolysis | - Destruction of other coagulation factors (V and VIII especially)
52
Fibrinolytic Drugs Toxicity Aminocaproic acid:
Aminocaproic acid: potent inhibitor of fibrinolysis (blocks interaction of fibrin and plasmi) and can reverse excessive fibrinolysis
53
Contraindications to Thrombolytic Therapy | Any of the following within 10 days: (4)
- Surgery (including organ biopsy) - Puncture of noncompressible vessels - Serious trauma - Cardiopulmonary resuscitation
54
Contraindications to Thrombolytic Therapy Within 3 months: History of : Active ____ or _____ disorder
o Within 3 months: serious GI bleeding o History of HTN (diastolic >110 mmHg) o Active bleeding or hemorrhagic disorder
55
Contraindications to Thrombolytic Therapy CV: Aorta; Pericardium:
o Previous cerebrovascular accident or active intracranial process o Aortic dissection o Acute pericarditis
56
Antiplatelet Drugs: (4)
- Aspirin - Dipyridamole - Clopidogrel (Plavix) - Ticlopidine
57
Aspirin MOA: Acetylates ______ near the active site of ______ Effects last for:
MOA: blocks platelet aggregation and vasoconstriction by inhibiting synthesis of thromboxane A2 Acetylates a serine residue near the active site of COX-1 (responsible for production of precursor of TXA2) Effects last for the life of the platelet (7-10 days)
58
Aspirin Low dose immediately after a heart attack to : Low dose long-term for prevention of: (3)
Low dose immediately after a heart attack to reduce the risk of another or to prevent the death of cardiac tissue Low dose long-term for prevention of: - Heart attacks - Strokes - Blood clot formation
59
Aspirin Toxicity At higher doses: Use in combination with _______ increases risk of upper GI bleeding
Increased at higher doses (especially bleeding) Use in combination with clopidogrel or warfarin increases risk of upper GI bleeding
60
Dipyridamole | MOA:
MOA: vasodilator
61
Dipyridamole | Use:
Use: only recommended for postoperative prophylaxis of thromboemboli in patients with prosthetic heart valves, in combination with warfarin
62
Dipyridamole Toxicity most common: most severe:
N/V/D most common | Leukopenia is most severe
63
Clopidogrel (Plavix) | MOA:
MOA: platelet ADP receptor antagonist (inhibits platelet activation)
64
Clopidogrel (Plavix) | Use: (4)
Used with aspiring after angioplasty (continued for at least 1 year) Reduce stroke and MI in patients with recent strokes and MIs Treatment of peripheral arterial disease Treatment of acute coronary syndrome
65
Clopidogrel (Plavix) Toxicity Vs dipyridamole and ticlopidine: Less frequent cases of:
Toxicity: more favorable side effect profile that dipyridamole and ticlopidine Less frequent cases of thrombocytopenia and leukopenia
66
Ticlopidine | MOA:
MOA: platelet ADP receptor antagonist (inhibits platelet activation)
67
Ticlopidine | Use:
Reduce the risk of thrombotic stroke in patients who have experience stroke precursors and/or in patients who have had a completed thrombotic stroke
68
Ticlopidine Toxicity most common: most severe:
N/V/D most common | Leukopenia is most severe
69
Glycoprotein IIb/IIIa Inhibitors Inhibit platelet aggregation by blocking: (2)
Glycoprotein IIb/IIIa Inhibitors: inhibit platelet aggregation by blocking the binding of these platelet-surface integrins to fibrinogen and von Willebrand factor (block cross-linking of platelets)
70
Glycoprotein IIb/IIIa Inhibitors: (3)
o Abciximab o Eptifibatide o Tirofiban
71
Abciximab | MOA:
MOA: Fab fragment of a humanized mAb against the AlphaIIbBeta3 receptor
72
Abciximab Use In conjunction with ______ for coronary thromboses Use along with aspirin and heparin effective in preventing: (3)
In conjunction with percutaneous angioplasty for coronary thromboses Use along with aspirin and heparin effective in preventing restenosis, recurrent MI and death
73
Abciximab Major side effect: If severe:
Toxicity: major side effect is bleeding If severe: platelet transfusions can reverse aggregation defect
74
Eptifibatide | MOA:
MOA: cyclic peptide inhibitor of the fibrongen binding site on AlphaIIbBeta3 integrin
75
Eptifibatide Use Treatment of: What have reduced MI and death by ~20%?
Treatment of acute coronary syndrome (IV) Angioplastic coronary interventions (IV)- have reduced MI and death by ~20%
76
Eptifibatide Major side effect: If severe:
Toxicity: major side effect is bleeding If severe: platelet transfusions can reverse aggregation defect
77
Tirofiban | MOA:
MOA: nonpeptide, small-molecule inhibitor of AlphaIIbBeta3 integrin
78
Tirofiban Use in conjunction with: For: (2)
Use: in conjunction with heparin - Non-Q wave MI - Unstable angina
79
Tirofiban Toxicity: What is possible? Transfusions required to:
Toxicity: bleeding on local sites of clinical intervention and systemically Major bleeding possible Transfusions required to terminate bleeding
80
Example of Treatment Regimen for Acute MI | Prehospital: (4)
o Aspirin o Oxygen (CPR if necessary) o Analgesia/ECG/Antiarryhtmics o Defibrillation
81
Example of Treatment Regimen for Acute MI | Hospital: (5)
o Antiarrhythmics an same supportive care as above o Fibrinolytic therapy (up to 12 hours after onset), OR o Coronary angioplasty, OR o Coronary artery bypass graft surgery o Anticoagulant (aspirin, heparin, start on warfarin)
82
Example of Treatment Regimen for Acute MI | Outpatient: (3)
o Antiarrhythmics as necessary o Anticoagulant (aspirin or warfarin) o Antiplatelet drug

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