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Vascular Surgery > Anticoagulants antiplatelets fibrinolytics > Flashcards

Anticoagulants antiplatelets fibrinolytics Flashcards

1
Q

Steps of normal hemostasis

A

Vasospasm (reduce blood flow and enhance platelet aggregation+coagulation). Formation of platelet plug. Thombin catalyzes fibrinogen to fibrin. Fibrin clot formation. Fibrinolysis by plasmin.

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2
Q

When are the different coagulation pathways activated?

A

Intrinsic pathway: surface contact with a foreign body or extravascular tissue.
Extrinsic pathway: Thromboplastin

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3
Q

Coagulation factors that are dependent on vitamin K

A

II - prothrombin.
VII - proconvertin (no longer considered a coagulation factor).
IX - plasma thromboplastin component.
X - Stuart factor.

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4
Q

Major rate limiting step in coagulation cascade

A

Activation of factor X

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5
Q

Thrombin - effects

A

Catalyzes fibrinogen to fibrin, and is a powerful stimulus for platelet aggregation.

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6
Q

Stimulus for platelet aggregation and coagulation

A

Atherosclerosis, venous pooling, thrombophlebitis

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7
Q

White vs red thrombi - location and mechanism

A

White thrombi: arterial circulation - often caused bu platelet aggregation.
Red thrombi: venous ciculation - often caused bu coagulation.

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8
Q

Main types of anticoagulants

A

Vitamin K antagonists.
Drugs that potentiate antithrombin III.
Drug that directly inhibit thrombin or active factor X.

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9
Q

Which coagulation factors are inhibited by warfarin, and in which pathway are these factors found?

A 
IX - intrinsic
VII - extrinsic
X - both pathways
Prothrombin - both pathways
(all are inactive factors)
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10
Q

Which coagulation factors are inhibited by heparin?

A

All active coagulation factors

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11
Q

Intrinsic coagulation pathway - cascade

A

1) Surface contact
2) XII (Hageman factor) activation
3) XI activation
4) IX activation
5) X (Stuart factor) activation
6) II (prothrombin) activation.
7) activation of fibrin, and formation of stabilized fibrin by factor XIII

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12
Q

Extrinsic coagulation pathway - cascade

A

1) Tissue factor.
2) VII (proconvertin) activation
3) Activation of X (Stuart factor)
4) II (prothrombin) activation.
5) activation of fibrin, and formation of stabilized fibrin by factor XIII

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13
Q

Drugs that may increase prothrombin time (15 drugs)

mnemonic, letter for each drug) ADD CAMP CHARTS FA(st

A 
Amiodarone
Cimetidine
Disulfiram
Fluconazole
Metronidazole
Phenylbutazone
Sulfinpyrazone
Trimethoprim-sulfamethoxazole
Aspirin (high doses)
Cephalosporins, third-generation
Heparin, argatroban, dabigatran, rivaroxaban, apixaban
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14
Q

Body factors that may increase prothrombin time

A

Hyperthyroidism, hepatic disease

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15
Q

Drugs that may decrease prothrombin time

A 
Barbiturates
Cholestyramine
Rifampin
Diuretics
Vit K
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16
Q

Body factors that may decrease prothrombin time

A

Hereditary resistance, hypothyroidism

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17
Q

Anticoagulants - 3 groups

A

Vitamin K antagonists.
Drugs that potentiate antithrombin III (AT-III).
Direct thrombin inhibitors

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18
Q

Vitamin K antagonists - 1 drug

A

Warfarin

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19
Q

Warfarin - classification

A

Vitamin K antagonist, coumarin compound.

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20
Q

Warfarin - MOA

A

Inhibit the reduction of oxidized vit K, which blocks posttranslational carboxylation of factors II (prothrombin), VII, IX and X, and these factors cannot be synthesized.
Also inhibits proteins C and S (may cause transient procoagulant effect).

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21
Q

Protein C and S - function

A

Endogenous anticoagulants that inactivate factors V and VIII and promote fibrinolysis.

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22
Q

Warfarin - contraindications

A

Pregnancy (crosses placenta and may cause fetal warfarin syndrome - fetal hemorrhage and birth defects).
Starting/discontinuing other drugs: must be evaluated by physician because of interactions.

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23
Q

Warfarin - onset of action

A

Delayed 3-5 days because of the time it takes to deplete the pool of circulating clotting factors.

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24
Q

How should chronic treatment for thromboembolic disorders be started?

A

Low-molecular-weight heparin and warfarin. When warfarin has started working, heparin is discontinued.

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25
Q

Adverse effets of warfarin

A

Bleeding (pts should report hematuria and ecchymoses)

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26
Q

Fetal warfarin syndrome - symptoms

A

Chondrodysplasia puncta, malformation of ears & eyes, mental retardation, nasal hypoplasia, optic atrophy, skeletal deformities, hemorrhage)

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27
Q

Why does warfarin cause fetal deformities?

A

Antagonizes vit K-dependent maturation of bone proteins.

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28
Q

Interactions of warfarin (direct increasers of prothrombin time, inducing CYP enzymes, and inhibit absorption)

A

Direct reduction of prothrombin levels: High dose of salicylates. Some 3rd generation cephalosporins.
Induce CYP enzymes: rifampin and barbiturates.
Inhibit absorption: Cholestyramine

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29
Q

Interactions of warfarin (drugs that inhibit CYP enzymes)

A

Amiodarone, cimetidine, erythromycin, fluconazole, gemfibrozil, isoniazid, metronidazole, sulfinpyrazone.

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30
Q

Treatment of warfarin-associated hemorrhage

A

Withdraw/reduce dose of warfarin. Phytonadione (vitamin K1) - direct antagonism of warfarin.
Severe: (INR>20) fresh plasma or factor IX concentrate

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31
Q

Warfarin - indications

A

Long-term treatments. DVT, AF, artificial heart valve. MI with heparin.

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32
Q

How to measure the effect of warfarin?

A

PT (1.3-1.5 times control PT)

INR (observedPT/controlPT): 2-3 (3-4.5 mechanical prosthetic valves and recurrent embolization)

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33
Q

Heparins - 2 drugs + 1 group

A

Unfractionated hepatin
Low-molecular-weight heparins (LMWHs)
Fondaparinux

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34
Q

LMWHs (3 drugs)

A

Enoxaparin
Dalteparin
Tinzaparin

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35
Q

Heparins - MOA

A

Inactivates clotting factors by potentiating antithrombin III

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36
Q

AT-III - functions

A

Most potent endogenous inhibitor of active factor X (Stuart factor) and II (thrombin).

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37
Q

LMWHs - MOA

A

Primarily inactivation of factor X (LMWH-AT-III complex has less affinity for thrombin than heparin-AT-III complex)

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38
Q

Heparin - adm

A

Parenterally, usually continuous IV infusion

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39
Q

How is the effect of heparin determined?

A

aPPT (activated partial thromboplastin time) - 1.5-2 times normal is adequate dosing. Not needed for LMWHs

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40
Q

LMWHs - adm

A

Subcutaneously

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41
Q

Heparins - adverse effects

A

Bleeding.
Heparin-induced thrombocytopenia (HIT) type I & type 2
Hyperkalemia (because of suppression of aldosterone secretion)

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42
Q

Type 1 HIT - mechanism and what should be done

A

Direct interaction between heparin and platelets that lead to a usually mild platelet aggregation. Reversible within 4 days despite continued heparin treatment.
25 % of pts.

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43
Q

Type 2 HIT - mechanism and what should be done

A

Immunoglobulin-mediated platelet inactivation with high risk of thrombotic complications. The drug must be discontinued.

44
Q

Heparin - indications

A

Acute thromboembolic disorders: peripheral and pulmonary embolisms, venous thrombosis, coagulopathies (e.g. DIC)
Prophylaxis: Arterial and heart surgeries, blood transfusions, renal dialysis, blood sample collection, acute atrial fibrillation.
Low doses for prevention of DVT/pulmonary embolism in high-risk pts.

45
Q

LMWHs - indications

A

Prevent venous thromboembolism after abdominal surgery and hip/knee replacements.
Unstable angina & non-ST-segment elevation MI, acute coronary syndrome, angioplasty

46
Q

Enoxaparin - indications

A

Prevent DVT in severely immobilized pts.

47
Q

Fondaparinux - adm and indications

A

Subcutaneous adm for DVT prophylaxis after hip fracture or hip/knee-replacements

48
Q

Hemorrhage by heparin - treatment and adm

A

Protamine sulfate - combines with heparin and inactivates it. Adm IV.
Severe bleeding: fresh plasma or clotting factors

49
Q

Direct thrombin inhibitors - groups/drugs and adm

A

Hirudin derivatives - parenterally (IV)

Dabigatran - orally

50
Q

Hirudin derivatives

A

Hirudin
Lepirudin
Bivalirudin
Argatroban

51
Q

Hirdurin derivatives - adverse effects

A

Bleeding

Do not cause thrombocytopenia

52
Q

Lepirudin - indications

A

Replace heparin after HIT.

53
Q

Hirudin derivatives - indiactions

A

Prevent thrombosis in unstable angina, acute MI, stent insertions and coronary angioplasty.

54
Q

Argatroban - indications

A

Prophylaxis and treatment of thrombosis in pts with HIT.

Pts undergoing percutaneous coronary interventions for MI.

55
Q

Dabigatran - interactions

A 
Few interactions with drugs and food.
Renal impairment decreases elimination (reduce dose).
The drug (bot not the active metabolite) is a substrate for P-glycoprotein (Pgp) transporter --> contraindicated with rifampin (inducer of Pgp transporter.
56
Q

Dabigatran - MOA

A

Potent, competitive and reversible inhibition of thrombin.

57
Q

How can the effect of dabigatran be monitored?

A

Thrombin clotting time (TT). However, monitoring is not usually necessary.

58
Q

Dabigatran - indications

A

Nonvalvular atrial fibrillation (reduce risk of stroke and embolism).
Hip/knee replacements - prevent thromotic complications.

59
Q

Dabigatran - adverse effects

A

Bleeding.

Dyspepsia, gastritis-like symptoms (reduced with food or H2 blocker).

60
Q

Hemorrhage associated with dabigatran - treatment

A

There is no antidote. Give plasma or RBCs.

61
Q

Active factor X inhibitors - 2 drugs

A

Apixaban

Rivaroxaban

62
Q

Rivaroxaban - indications

A

Hip/knee replacement: prevent DVT, blood clots, pulmonary embolism

63
Q

Rivaroxaban - interactions

A

Metabolized by P450 isoenzymes (esp 3A4).

Increased levels bu Pgp transporter inhibitor.

64
Q

Rivaroxaban - adverse effects

A

Bleeding

Careful in pregnancy.

65
Q

Apixaban - indications

A

Atrial fibrillation when warfarin cannot be used.

Prevent venous thromboembolism and cardiovascular events in MI.

66
Q

Rivaroxaban, Apixaban, Endoxaban - antidote

A

Andexanet alfa (AndexXa). Dosing for the initial bolus and subsequent infusion depend on the dose level of the factor Xa inhibitor and the interval since it was last taken.

-OR-

4-factor PCC (Kcentra, Beriplex P/N, Octaplex). Dosing can be done with a fixed dose of 2000 units OR a weight-based dose of 25 to 50 units per kg.

Active factor VII

67
Q

Dabigatran(Pradaxa) reversal agent

A

Idarucizumab (Praxbind). Dose: 5 grams*

68
Q

Aspirin - MOA of antiplatelet effect

A

In low doses aspirin selectively inhibits thromboxane A2 (TXA2) synthesis (promotes aggregation). Prostacyclin (platelet aggregation inhibiting) inhibition: higher doses.
Irreversible inhibition of COX.

69
Q

Aspirin - indications

A

Ischemic heart disease & stroke: Secondary prevention.
Angina: prevent MI
Primary prevention: men>45, women>55 with risk factors for heart disease/stroke (diabetes).
Acute MI, TIA (prevent stroke), artificial heart valves, percutaneous coronary angioplasty.
Peripheral occlusive disease, chronic limb ischemia.

70
Q

Aspirin - adverse effects

A

Bleeding (esp GI, inhibition of prostaglandins = inhibition of bicarbonate & mucus secretion).
High doses: hypoprothrombinemia

71
Q

Antiplatelet drugs - 3 drugs, 2 groups

A 
Aspirin
Dipyridamole
Cilostazol
ADP inhibitors
Glycoprotein IIb/IIIa antagonists
72
Q

Dipyridamole - MOA

A

Coronary vasodilator and weak antiplatelet.
Inhibits platelet adhesion to the vessel wall, and platelet aggregation (latter by increasing cAMP and decreasing Ca in platelets)

73
Q

Dipyridamole - indications

A

Vasodilation: myocardial perfusion imaging (thallium imaging).
Antiplatelet: with aspirin for prevention of ischemic (thrombotic) stroke in pts who had this or have TIA.

74
Q

Cilostazol - MOA

A

Inhibits phosphodiesterase III and increase cAMP in platelets & blood vessels. This causes vasodilation and inhibition of platelet aggregation

75
Q

Cilostazol - Indications

A

Intermittent claudication (limb weakness & pain)

76
Q

Cilostazol - interactions

A

Metabolized by CYP3A4 (e.g. erythromycin may increase antiplatelet effect)

77
Q

ADP inhibitors - 4 drugs

A

Clopidogrel
Prasugrel
Ticlopidine
Ticagrelor

78
Q

ADP inhibitors - interactions

A

Ticlopidine, clopidogrel, prasugrel: metabolized into active metabolite by CYPs.
Clopidogrel: activation is potentially inhibited by PPI (but they can be given together).
Ticagrelor does not need activation.

79
Q

Which ADP inhibitor has greater potency?

A

Prasugrel

80
Q

ADP inhibitors - MOA

A

Clopidogrel requires in vivo biotransformation to an active thiol metabolite. The active metabolite irreversibly blocks the P2Y12 component of ADP receptors on the platelet surface, which prevents activation of the GPIIb/IIIa receptor complex, thereby reducing platelet aggregation. Platelets blocked by clopidogrel are affected for the remainder of their lifespan (~7 to 10 day)

Clopidogrel, ticlopidine, prasugrel: irreversible antagonists

Ticagrelor - reversible antagonists.

81
Q

When is ticagrelor better to use than other ADP-inhibitors

A

E.g. surgery - when irreversible inhibition is not needed.

82
Q

Clopidogrel & prasugrel - indications

A

Pts who cannot take aspirin: Prevent thrombotic stroke.
With aspirin: ACS.
Clopidogrel also in: Intermittent claudication of blood vessels, chronic arterial occlusion, atrioventricular shunts/fistulas, open heart surgery, sickle cell anemia.

83
Q

Ticagrelor - indications

A

Prevention of thrombotic events in MI or STEMI (with aspirin unless contraindicated).

84
Q

Ticagrelor - adverse effects

A

Dyspnea

85
Q

Ticlopidine - adverse effects

A

Severe neutropenia (complete blood count evr 2 weeks).

86
Q

Glycoprotein IIb/IIIa antagonists - 3 drugs

A

Abciximab
Tirofiban
Eptifibatide

87
Q

GP IIb/IIIa antagonists - MOA

A

Binds to platelet GP IIb/IIIa reveptors and prevents fibrinogen to bind and crosslinking of platelets.
Tirofiban and eptifibatide: competitive, reversible inhibitors.

88
Q

Abciximab - indications

A

Combo with aspirin and heparin/LMWHs: Percutaneous coronary interventions (coronary angioplasty, stent placement).
Adjunct to thrombolysis

89
Q

Abciximab - adverse effects

A

Bleeding, thrombocytopenia, hypotension, bradycardia.

90
Q

Tirofiban and eptifibatide - indications

A

Unstable angina and MI (often combo with LMWHs).

Eptifibatide - STEMI, coronary angioplasty/stent placement

91
Q

Aspirin - interactions

A

Sulfonylureas: increased hypoglycemic effect.
Methotrexate, valproate: increased GI bleeding+ ulceration.
Probenecid: inhibits uricosuric effect.

92
Q

Fibrinolytic drugs 1 group and 3 drugs

A

Recombinant tissue plasminogen activators (t-PA)
Urokinase
Streptokinase
Anistreplase

93
Q

Fibrinolytic drugs - indications

A

Degrade thrombus in MI, thrombotic stroke, pulmonary embolism.

94
Q

t-PAs - 3 drugs

A

Alteplase
Reteplase
Tenecteplase

95
Q

Fibrinolytic drugs - MOA

A

Convert plasminogen to plasmin.

96
Q

Fibrinolytic drugs - adverse effects

A

Bleeding, but less with t-PAs.
Arrhythmias (tachy and brady) –> from free radicals after reperfusion of coronary arteries after thrombolysis.
Streptokinase - hypersensitivity (anaphylactic shock), should not be used repeatedly in same pt.

97
Q

Treatment of fibrinolytic drug-associated hemorrhage

A

Aminocaproic acid - inhibits fibrinolysis.

98
Q

Aminocaproic acid - indications

A

Hemorrhage by fibrinolytic drugs.
After GI or prostate surgery.
Cancer pts during radiation/chemo.

99
Q

Aminocaproic acid - amd

A

Orally or intravenously

100
Q

Aminocaproic acid - adverse effects

A

Thrombosis, hypotension, arrhythmias.

101
Q

Tranexamic acid - what is it, and MOA.

A

Antifibrinolytic drug. Occupies the lysine binding sites of plasmin for fibrin.

102
Q

Tranexamic acid - indications

A

Heavy menstrual bleedings.

103
Q

Tansexamic acid - adverse effects

A

Thrombotic events (esp if pts are on hormonal contraceptives, are obese or smoking).

104
Q

Fibrinolytic drugs that may be given by infusion

A

Streptokinase, alteplase

105
Q

Fibrinolytic drugs that may be given in bolus

A

Reteplase

Tenecteplase

106
Q

Systemic fibrinogen depletion of fibrinolytic drugs

A

Streptokinase: marked
Reteplase: moderate
Alteplase: mild
Tenecteplase: minimal.

107
Q

Contraindications to thrombolysis

A

Contraindications to fibrinolytic therapy for deep venous thrombosis or acute pulmonary embolism

Absolute contraindications
Prior intracranial hemorrhage
Known structural cerebral vascular lesion
Known malignant intracranial neoplasm
Ischemic stroke within three months (excluding stroke within three hours*)
Suspected aortic dissection
Active bleeding or bleeding diathesis (excluding menses)
Significant closed-head trauma or facial trauma within three months

Relative contraindications
History of chronic, severe, poorly controlled hypertension
Severe uncontrolled hypertension on presentation (SBP >180 mmHg or DBP >110 mmHg)
History of ischemic stroke more than three months prior
Traumatic or prolonged (>10 minute) CPR or major surgery less than three weeks
Recent (within two to four weeks) internal bleeding
Noncompressible vascular punctures
Recent invasive procedure
For streptokinase/anistreplase - Prior exposure (more than five days ago) or prior allergic reaction to these agents
Pregnancy
Active peptic ulcer
Pericarditis or pericardial fluid
Current use of anticoagulant (eg, warfarin sodium) that has produced an elevated international normalized ratio (INR) >1.7 or prothrombin time (PT) >15 seconds
Age >75 years
Diabetic retinopathy

Vascular Surgery (37 decks)

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