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BMS 615 Cardiovascular > Test 1: Wk1: 5 Coagulation and Anticoagulants - Valentovic > Flashcards

Test 1: Wk1: 5 Coagulation and Anticoagulants - Valentovic Flashcards

1
Q

Anticoagulants (6)

A 
Heparin
LMW Heparin
Warfarin
Argatroban
Dabagatran
XaInhibitors
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2
Q

Anticoagulants work by

A

inhibiting fibrin formation

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3
Q

Antiplatelets (5)

A

Aspirin, Dipyridamole, Clopidogrel, Abciximab & Eptifibatide

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4
Q

Antiplatelets work by

A

inhibit platelet aggregation

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5
Q

Thrombolytics/ Fibrinolytics (4)

A

Streptokinase, Alteplase, Anistreplase& Tenecteplase

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6
Q

Thrombolytics/ Fibrinolytics work by

A

dissolve formed fibrin clots

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7
Q

Heparin Natural Product

A

Porcine MW 5-30 kDa

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8
Q

Heparin accelerates the reaction of — with —

A

AT-III (antithrombin 3) with coagulation factors

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9
Q

Heparin — binds AT-III and induces —

A

irreversibly

conformational change

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10
Q

Heparin binds AT-III — times faster with what coagulation factors

A

1000x

II, X, XI and XII

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11
Q

Heparin - active coagulation factors bind — to AT-III at the — site. This prevents — generation

A

irreversibly

Arg-Ser

Fibrin

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12
Q

AT-III is a — substrate

A

suicide; it binds and doesnt let go

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13
Q

Heparin is an anticoagulant in

A

vitro

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14
Q

Heparin use in vivo

A

Tx of Venous Thrombosis

Tx of Pulmonary thromboembolism

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15
Q

Is Heparin approved in pregnant women

A

yes - it does not cross placenta

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16
Q

Heparin Administration

What administration is contraindicated

A

SC or IV

IM contraindicated - induce hematoma

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17
Q

how is Heparin montored

A

aPTT

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18
Q

How much does heparin increase aPTT

A

1.5 - 2.5 x

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19
Q

Heparin has a lipid clearing effect that

A

increase lipoprotein lipase activity

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20
Q

What does aPTT asses

A

intrinsic pathway and factors I, II and X

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21
Q

Heparin Adverse Effects

A
  • bleeding

- Thrombocytopenia Type 1 and 2

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22
Q

Thrombocytopenia Type I

A

non-immune medicated platelet heparin interaction

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23
Q

Thrombocytopenia Type II

A

immune mediated; begins 4-10 days after tx

ab form to heparin-platelet factor 4 complex which binds to platelet surface causing aggregation

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24
Q

What should be monitored in long term use of unfractionated heparin

A

platelet count

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25
Q

Reverse Heparin with

A

Protamine

plasma or whole blood

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26
Q

Protamine MOA

A

binds heparin disabling anticoagulant activity

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27
Q

Protamine Allergy

A

diabetics

Fish allergy

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28
Q

Heparin Contrindications

A

Bleeding disorder

pre-existing bleeding site

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29
Q

low molecular weight Heparin (3)

A

Enoxaparin

Dalteparin

Tinzaparin

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30
Q

low molecular weight Heparin weight

A

4500 daltons

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31
Q

low molecular weight Heparin is too small to do what

A

simultaneously bind ATIII and thrombin

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32
Q

low molecular weight Heparin MOA

A

enhance ATIII inactivation of factor Xa

low affinity for thrombin

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33
Q

low molecular weight Heparin uses (4)

A

prophylaxis
acute venous thrombosis
DVT
Unstable angina or non Q-wave MI

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34
Q

low molecular weight Heparin administration

A

SC 1/day

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35
Q

low molecular weight Heparin monitoring

A

anti Xa activity

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36
Q

is low molecular weight Heparin approved in pregnant women

A

yes

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37
Q

LMW Enoxaparin vs Heparin

A

longer half life

outptx

lower thrombocytopenia

Predictable

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38
Q

Fondaparinux is a

A

Synthetic Pentasaccharide

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39
Q

Fondaparinux MOA

A

Specific for ATIII inactivation of Factor Xa

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40
Q

Fondaparinux adminstration

A

IV, SC

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41
Q

Fondaparinux uses

A

Prophylaxis and acute deep vein thrombosis

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42
Q

can Fondaparinux be used in pregnant women

A

yes

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43
Q

Fondaparinux contraindications

A

Contraindicated in bleeding or severe renal impairment

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44
Q

Warfarin is an anticoagulant where

A

only in vivo

Warfarin does not inhibit clotting when directly added to blood

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45
Q

Warfarin MOA

A

inhibits synthesis of biologically active VitK dependent clotting factors

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46
Q

Warfarin inhibits what enzyme

A

Vit K epoxide reductase

Vit K is stuck in epoxide form

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47
Q

Warfarin inhibits biologically active factors

A

II, VII, IX, X

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48
Q

how long for warfarin to work

A

actively after <24hrs but takes 5-7 days for generation of coagulation factors incapable of binding Calcium

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49
Q

Warfarin administration

A

oral anticoagulant of choice

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50
Q

Warfarin Uses (3)

A

Prophylaxis for DVT & pulmonary embolism

Prosthetic Heart valves

Arterial thromboembolism prophylaxis in atrial fibrillation

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51
Q

Warfarin monitoring

A

INR VALUES Standardization of Prothrombin time

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52
Q

Warfarin Adverse Effects

A

Bleeding

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53
Q

Warfarin adverse rxns occur with (4)

A

Change in absorption and/or metabolism of Warfarin

Change in synthesis and/or catabolism of Vitamin K or coagulation factors (decreased hepatic function)

Changes in platelet function

Alteration in fibrin degradation

54
Q

Warfarin genetic varients

A

CYP2C9 and VKORC genes

55
Q

reduce warfarin dose by 30% in

A

Hetero or homozygotes for CYP2C9*2

heterozygous for CYP2C9*3

56
Q

reduce warfarin dose by 90% in

A

Homozygote CYP2C9*3

57
Q

VKORC1 G allele

A

A allele synthesize less VKORC1

less protein for warfarin to bind

58
Q

Drugs that increase warfarin effects (6)

A 
Aspirin
Ketoconazole & erythromycin
Cimetidine
Ibuprofen
Cephalosporins
Sulfamethoxazole/trimethoprim
59
Q

Drugs that decrease warfarin effects (4)

A

Cholestyramine
Rifampin
Phenobarbital
Cigarette smoking

60
Q

Warfarin contraindications

A

Presence of bleeding disorder or active bleeding site

61
Q

can warfarin be given to pregnant women

62
Q

Warfarin 1st trimester

A

nasal hypoplasia

63
Q

Warfarin 2nd and 3rd trimester

A

CNS, increased fetal death

64
Q

Tx of excessive bleeding

A

Whole blood or plasma

VitK - takes 24 hrs

65
Q

Direct Thrombin Inhibitors (2)

A

ARGATROBAN (iv)

DABIGATRAN (ora)

66
Q

Argatroban MOA

A

directly block site on thrombin

67
Q

Argatroban adminstration

68
Q

Argatroban use (2)

A

pts at risk of heparin induce thrombocytopenia

coronary artery thrombosis

69
Q

Dabigatran Etexilate Mesylate (DEM) is a

A

Anticoagulant –direct thrombin inhibitor

70
Q

DEM MOA

A

affinity for free and fibrin bound thrombin

71
Q

DEM administration

72
Q

DEM is converted to — by plasma esterases

A

Dabigatran

73
Q

DEM uses (2)

A

prophylaxis DVT and thromboembolism

74
Q

DEM metabolites

A

4 Glucuronide metabolites (active)

75
Q

is DEM a p450 substrate

A

no - less drug interactions

76
Q

DEM is a substrate for

A

P-glycoprotein

77
Q

DEM is excreted in

A

urine - must have good kidney function

78
Q

Antidote for DEM associated excess bleeding

A

Idarucizumab

79
Q

Idarucizumab MOA

A

Humanized monoclonal antibody binds to dabigatrin

350x higher affinity dabigatrin> thrombin

80
Q

Direct factor Xa inhibitors (2)

A

Rivaroxaban and Apixaban

81
Q

Rivaroxaban and Apixaban MOA

A

bind directly to factor Xa

prevent Xa cleaving prothrombin to thrombin

82
Q

Rivaroxaban and Apixaban administration

83
Q

Rivaroxaban and Apixaban substrates for

A

CYP3A4

P-glycoprotein

84
Q

Rivaroxaban and Apixaban uses (3)

A

Tx DVT and embolism

Prevent DVT after hip/knee replacement

Decrease risk of stroke in nonvalvular atrial fibrillation

85
Q

Rivaroxaban and Apixaban side effects

A

BLACK BOX WARNING:
Bleeding can be life threatening

Bruising

86
Q

Rivaroxaban and Apixaban antidote

A

Andexanet

recombinant factor Xa

87
Q

Rivaroxaban and Apixabanc contraindications

A

active bleeding site

88
Q

antiplatelet drugs (7)

A

Aspirin

Dipyridamole

Clopidogrel

Abciximab

Eptifibatide

Cangrelor

Tirofiban

89
Q

Aspirin MOA

A

irreversible inhibitor of COX-1 and 2

Acetylates enzyme - thromboxane

90
Q

Aspirin goal

A

inhibit platelet prostaglandin formation

91
Q

Aspirin use

A

reduce risk of 2nd heart attack

92
Q

Aspirin adverse effects

A

bleeding, GI irritation, GI ulcers

93
Q

Dipyridamole MOA

A

inhibits phosphodiesterase increases platelet cAMP levels

94
Q

Dipyridamole use

A

combination with other agents, very little benefit when used alone

Combined with warfarin

95
Q

Clopidogrel is a platelet —

A

Platelet ADP Aggregation Inhibitors

irreversible inhibitor

96
Q

Clopidogrel is a prodrug that is metabolized to

A

thiol metabolite

97
Q

Clopidogrel MOA

A

Bind Irreversibly to ADP P2Y12 receptor on platelets

Inhibits ADP activation of IIb/IIIa complex needed for platelet aggregation

98
Q

Clopidogrel uses

A

prophylaxis for thrombosis

99
Q

reverse Clopidogrel

A

must generate new plataletes

100
Q

Clopidogrel side effects

A

bleeding

Thrombocytopenia purpura risk

101
Q

Clopidogrel monitoring

A

Monitor WBC and platelets

102
Q

Cangrelor MOA

A

reversible P2Y12 platelet receptor inhibitor

103
Q

Cangrelor administration

104
Q

Cangrelor half life

A

6 minutes - effect reverse within 1 hr

105
Q

Platelet glycoprotein IIb/IIIa receptor antagonists (2)

A

Abciximab

Eptifibatide

106
Q

Abciximab MOA

A

monoclonal antibody Fab fragment) construct of receptor

Ab binds to IIb/IIIa receptor

107
Q

Eptifibatide is a

A

peptide derivative

108
Q

what is more effective Abciximab or Eptifibatide

109
Q

Abciximab and Eptifibatide administration

110
Q

Abciximab and Eptifibatide uses

A

Prevent thrombotic occurrence in patients with unstable angina or undergoing angioplasty

111
Q

Tirofiban is a

A

PLATELET GLYCOPROTEIN IIb/IIIa RECEPTOR ANTAGONISTS

non peptide

112
Q

Tirofiban administered

113
Q

Platelet glycoprotein IIb/IIIa receptor antagonists MOA

A

Competitive reversible inhibitor of interaction of Von Willebrand factor and fibrinogen with glycoprotein IIb/IIIa receptor

prevent cross linking of fibrinogen with platalets

114
Q

Platelet glycoprotein IIb/IIIa receptor antagonists adverse effects

A

high incidence of bleeding
History of hemorrhagic stroke

Surgery, trauma past 6 weeks

Thrombocytopenia

Cannot use with warfarin

115
Q

Abciximab and Eptifibatide time of action

A

Abciximab (>24 h) action longer than Eptifibatide (4-6 h) and Tirofiban (8 h)

116
Q

Fibrinolytic system is responsible for degrading — during wound healing.

A

Fibrinolytic system is responsible for degrading fibrin during wound healing.

117
Q

what degrades fibrin, clotting factors, and fibrinogen

118
Q

Plasminogen is converted to PLASMIN by — which is released by — cells

A

Plasminogen is converted to PLASMIN by t-plasminogen activator (t-PA) which is released by endothelial cells

119
Q

Streptokinase MOA

A

streptokinase combines with 1 molecule of Plasminogen to form a complex

Complex then converts a second molecule of Plasminogen to plasmin

120
Q

Streptokinase use

A

reperfusion of occluded coronaries following an MI, works best if used within 4-6 hr of chest pain

Pulmonary embolism

Deep vein Thromboembolism

Arterial thrombosis

121
Q

Streptokinase adverse effects

A

33% of people develop fever

BLEEDING

LYTIC STATE excessive bleeding, circulating plasmin exceeds capacity of α2-antiplasmin

Highly antigenic

122
Q

Streptokinase contraindications

A

Surgery or trauma in past 10 days

Pre-existing bleeding disorder (GI ulcer, retinal bleeding)

Diastolic pressure >110 mm Hg

Intracranial trauma

123
Q

Anistreplase

A

Combination of streptokinase and plasminogen with catalytic site acylated

Acyl removed by plasma enzymes

Designed to provide more specific binding to fibrin

Less lytic state

124
Q

Anistreplase t-plasminogen activator (rt-PA)

A

high affinity for fibrin, more rapid binding to fibrin and activation of fibrin bound plasminogen

Low activity for circulating plasminogen

125
Q

t-PA directly activates — to —

A

t-PA directly activates plasminogen to plasmin

126
Q

Anistreplase t-plasminogen activator (rt-PA) uses

A 
•
Reperfusion of coronary arteries following an MI
•
Pulmonary embolism
•
Thrombotic stroke, use within 3 hrs
127
Q

Tenecteplase

A

Genetically engineered derivative of alteplase

128
Q

Tenecteplase Vs alteplase

A

More specific binding to fibrin

More resistant to PAI-1

Longer half-life

Higher incidence of reperfusion and functional outcome than alteplase for ischemic stroke treated

129
Q

Thrombolytics adverse rxns

A
  • inducing a hypocoagulable state
  • patients bruise very easily
  • any bleeding is difficult to stop
130
Q

Aminocaproic Acid

A

Inhibitor of fibrinolysis

Lysine analog competes for lysine binding sites on plasminogen and plasmin

Inhibits interaction of plasmin and fibrin

BMS 615 Cardiovascular (49 decks)

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