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N929 Pharmacology II > Anticoagulants, antiplatelets, and thrombolytics > Flashcards

Anticoagulants, antiplatelets, and thrombolytics Flashcards

1
Q

Anticoagulants work by

A

prevent clot formation or extension of existing clot (DON’T BREAK DOWN CLOTS)

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2
Q

Antiplatelet agents work by

A

reducing PLT aggregation on the surface of the PLT

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3
Q

Thrombolytics work by

A

converting endogenous plasminogen to the fibrinolytic enzyme plasmin to dissolve newly formed blood clots

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4
Q

List the major counter-regulatory pathways for anticoagulants:

A

fibrinolysis, tissue factor plasminogen inhibitor, protein C system, serine protease inhibitors (SERPINs)

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5
Q

Prevention of blood coagulation outside of the body includes

A

siliconized containers (stored donated blood), heparin in CPB or artificial kidney machines, citrate ion

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6
Q

Random blood clotting is normally prevented by

A

the presence of endogenous anticoagulation factors- the capillary endothelium is the main source of anticoagulation factors

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7
Q

Tissue factor plasminogen inhibitor is a

A

polypeptide produced by endothelial cells. it acts as a natural inhibitor of the extrinsic pathway by inhibiting TF-VIIa complex

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8
Q

Coagulation propagation is inhibited by the

A

Protein C pathway that primarily consists of four key elements

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9
Q

The four key elements of the Protein C pathway includes

A

Protein C, thrombomodulin, endothelial protein C receptor, and protein S

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10
Q

Protein S is a

A

vitamin K-dependent glycoprotein

it functions as a cofactor to APC in the inactivation of FVa and FVIIIa

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11
Q

Endothelial protein C receptor is

A

another transmembrane receptors that helps in the activation of Protein C

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12
Q

Protein C is an

A

enzyme with potent anticoagulation, profibrinolytic, and anti-inflammatory properties. it is activated by thrombin to form activated protein C and acts by inhibiting activated factors V and VIII

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13
Q

Thrombomodulin is a

A

transmembrane receptor on the endothelial cells, it prevents the formation of the clot in the undamaged endothelium by binding to the thrombin

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14
Q

SERPIN or antithrombin is (alt. name and inhibitor of?)

A

known as AT III and is the main inhibitor of thrombin

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15
Q

Antithrombin binds and inactivates

A

thrombin, factor IIa, IXa, Xa, XIa, and XIIa

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16
Q

The enzymatic activity of AT is enhanced in

A

the presence of heparin

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17
Q

Patients can have an antithrombin deficiency as a result of

A

hereditary AT deficiency or acquired deficiency d/t prolonged heparin infusions

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18
Q

Antithrombin mainly inhibits

A

Xa and IIa but also inhibits VIIa, IXa, XIa, and XIIa

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19
Q

Citrate ion works by

A

negatively charged citrate ion combines with positively charged calcium in the blood to cause an un-ionized calcium compound

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20
Q

After injection, the citrate ion is

A

removed by liver and is polymerized into glucose or metabolized

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21
Q

Any substance that ____ ___ _____ _____ will prevent coagulation

A

deionizes the blood calcium

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22
Q

If there is liver damage or massive transfusion, the citrate ion

A

may not be removed quickly enough, and this can greatly depress the level of calcium ion in the blood

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23
Q

Anticoagulants include

A

vitamin K antagonists, unfractionated heparin, low molecular weight heparin and fondaparinux, direct thrombin inhibitors, and direct oral anticoagulants

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24
Q

Coumadin is considered a

A

vitamin K antagonist

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25
Q

Warfarin works by

A

inhibiting vitamin K which results in the hemostatically defective vitamin-K dependent coagulation proteins (II, VII, IX, and X)

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26
Q

Warfarin works on the following coagulation proteins:

A

II, VII, IX, and X

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27
Q

When warfarin is administered, platelet activity is

A

not altered

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28
Q

Coumadin is not suitable to use in

A

parturients because it crosses the placenta and is severely teratogenic

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29
Q

Coumadin has a (elimination half time)

A

long elimination half-time of 24-36 hours after PO administration

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30
Q

Coumadin is effective in preventing

A

thromboembolisms

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31
Q

The onset of action of coumadin and the duration of a single dose is

A

3-4 days

duration: 2-4 days

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32
Q

Coumadin levels are measured by

A

PT/INR

effects are see on INR in 8-12 hours d/t depletion of factor VIII

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33
Q

INR goals of 2-3 for coumadin are for

A

afib, tx of VTE, PE, prevention of VTE in high risk surgery, and tissue heart valves

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34
Q

INR goals of 2.5-3.5 for coumadin are for

A

mechanical heart valve, prevention of recurrent MI, history of VTE with INR 2-3

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35
Q

Coumadin management before surgery includes

A

checking the PT/INR

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36
Q

For minor surgery, coumadin is

A

discontinued 1-5 days preop for PT 20% within baseline and reinstituted the regimen 1-7 days postop

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37
Q

For immediate surgery (24-48 hours) or active bleeding,

A

vitamin K should be given to reverse coumadin

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38
Q

For emergency surgery in patients on coumadin,

A

FFP or 4 factor concentrate (Kcentra) can be used to reverse

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39
Q

Heparin is a naturally occurring

A

polysaccharide that inhibits coagulation

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40
Q

Heparin is released

A

endogenously by mast cells and basophils and used widely as an anticoagulation drug

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41
Q

Unfractionated heparin works by

A

enhancing the naturally occurring antithrombin

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42
Q

Unfractionated heparin binds to

A

antithrombin (III)
enhances 1,000 times the ability of antithrombin to inactivate a number of coagulation enzymes (thrombin IIa, factors Xa, XII, XI, and IX)

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43
Q

Neutralized thrombin prevents

A

the conversion of fibrinogen to fibrin

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44
Q

Unfractionated heparin must contain at least

A

120 UPS units/mL

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45
Q

The USP defines 1 unit of activity as the amount of heparin that

A

maintains the fluidity of 1 mL of citrated plasma for 1 hour after re-calcification

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46
Q

Unfractionated heparin does (placenta)

A

not cross the placenta and is safe in obstetrics)

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47
Q

The action of heparin lasts about

A

1.5-4 hours

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48
Q

Injected heparin is destroyed by

A

an enzyme in the blood (heparinase)

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49
Q

Unfractionated heparin cannot

A

cross lipid barriers in significant amounts

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50
Q

Monitoring heparin can be done through

A

monitoring aPTT, ACT (baseline, 3-5 minutes post admin, 30 min to 1 hour intervals post admin), Heptem

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51
Q

Clinical uses of heparin include

A

SQ VTE and PE prophylaxis- ERAS cases, orthopedic cases, post-MI, hemodialysis
Warfarin “bridge”
Vascular or non-CPB cases vary ACT >200-300 seconds
Interventional aneurysm clipping/coiling >250 seconds
CPB–ACT >400-480 seconds

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52
Q

The unfractionated heparin dosing in CPB includes

A

400 units/kg IV TBW

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53
Q

Heparin side effects include

A

hemorrhage/hematomas, thrombocytopenia (HIT), allergic reaction, hypotension with large doses, altered protein binding, chronic exposure can progress to reduction of antithrombin activity

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54
Q

Intraspinal hematoma is more likely to occur in

A

anticoagulated or thrombocytopenic patients, patients with neoplastic disease, liver disease, or alcoholism

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55
Q

IV heparin and neuraxial anesthesia

A

1 hour delay between needle placement and heparin administration
catheter should be removed 1 hour before heparin administration and 2-4 hours after last heparin dose
monitor PTT or ACT

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56
Q

Allergic reactions with heparin:

A

heparin is obtained from animal tissues & thus caution should be used in patients with a preexisting history of allergy
fever, urticaria, hemodynamic changes

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57
Q

Heparin induced thrombocytopenia is caused by

A

heparin dependent antibodies that aggregate platelets and leads to consumption which produces thrombocytopenia

58
Q

Mild or type 1 HIT is

A

non-immune mediated
platelet count <100,000 cells
typically presents 3-15 days after initiation of therapy

59
Q

Severe or type II HIT is

A

low incidence <6%
immune mediated
Platelet count <50,000
typically presents 6-10 days after initiation of therapy

60
Q

Heparin reversal is

A

protamine

1-1.5 mg for each 100 units of heparin administered

61
Q

When heparin resistance is secondary to an antithrombin deficiency, treatment is to restore normal values through

A

2-4 units FFP in adults

or antithrombin concentrate

62
Q

Patients with ______will have a resistance to heparin

A

antithrombin deficiency

63
Q

No antithrombin=

A

nothing for heparin to bind to

64
Q

The decrease in antithrombin may paradoxically

A

increase the thrombotic tendency

65
Q

Estrogen containing contraceptives also

A

decrease antithrombin’s ability to inhibit Xa

66
Q

Low molecular weight heparin is derived from

A

unfractionated heparin

67
Q

Comparison of LMWH to unfractionated heparin:

A

LMWH: inhibits factor X more than unfractionated, smaller molecular weight, less protein binding, 1x daily dosing

68
Q

Enoxaparin works by

A

binding to and accelerating antithrombin

inhibits factors Xa and IIa

69
Q

Factor Xa catalyzes the conversion of

A

prothrombin to thrombin so enoxaprin’s inhibition of this process results in decreased thrombin activity and prevention of fibrin clot formation

70
Q

Advantages to low molecular weight heparin include

A

reduced dosing frequency and the lack of need for monitoring, more predictable pharmacokinetic response, fever effects on platelet function, reduced risk for HIT

71
Q

Disadvantages to LMWH:

A

more expensive, surgery delayed for 12 hours after the last dose, protamine only neutralizes 65% of anti-factor X activity of LMWH- requires a more complete reversal of LMWH with FFP

72
Q

Direct oral anticoagulants are an alternative to warfarin

A

for tx of VTE, prevention of embolic stroke and prophylaxis in patients undergoing surgery

73
Q

Direct oral anticoagulants include

A

direct thrombin IIa inhibitor-dabigatran

direct factor Xa inhibitor- rivaroxaban, apixaban, and edoxaban

74
Q

Advantages to direct oral anticoagulants include

A

rapid onset with peak effect in 2-4 hours, predictable pharmacodynamics, minimal drug interactions, no required routine lab monitoring

75
Q

Dabigatran is a

A

direct thrombin IIa inhibitor

76
Q

Dabigatran is the only direct thrombin inhibitor that is

A

metabolized via renal elimination

77
Q

Reversal of direct thrombin inhibitor includes

A

idarucizumab (praxbind)- specific antidote for dabigatran

half-life is 45 minutes

78
Q

Monitoring for dabigatran includes

A

coagulation assay:
dilute thrombin time (more reliable and precise measurement)
aPTT
ROTEM (less specific than thrombin time)

79
Q

Direct factor Xa inhibitors include

A

rivaroxaban (Xarelto)
apixaban (eliquis)
edoxaban (savaysa)
all metabolized hepatic metabolism

80
Q

Monitoring of direct factor Xa inhibitors includes

A

coagulation assay- anti Xa
ROTEM is not sensitive
PT can be a helpful indicator for rivaroxaban only

81
Q

For patients requiring minimal bleeding risk procedures, they are likely safe to undergo with

A

no DOAC interruptions (cataracts, skin biopsies, minor dental procedures)

82
Q

Low bleeding risk procedures are recommended to (in regards to DOACs)

A

stop DOCAs for 24 hour hours prior to elective surgery (hernia repair)

83
Q

High bleeding risk procedures are recommended to

A

interrupt DOAC therapy 48 hours prior to elective surgery

cardiac, intracranial, etc.

84
Q

Longer interruption of DOACs is necessary for

A

dabigatran and impaired renal function

85
Q

_____ can be given to reverse dabigatran

A

Idarucizumab

86
Q

_____ can be given to reverse apixaban, betrixaban, edoxaban, rivaroxaban, and heparins

A

andexanet alfa

87
Q

______ can be given to reverse vitamin K antagonists

A

prothrombin complex concentrates

88
Q

Antiplatelet agents include

A

cyclooxygenase inhibitors: aspirin, NSAIDs
P2Y12 receptor antagonists
glycoprotein IIB/IIIA inhibitors

89
Q

Antiplatelets work by

A

suppressing platelet function (inhibit platelet aggregation) for the prevention of thrombosis

90
Q

Antiplatelet therapy is indicated for

A

patients at risk for CVAs, MI, or other vascular thrombosis complications

91
Q

Aspirin exerts an

A

antithrombotic effect by inhibiting platelet aggregation

92
Q

Aspirin inhibits

A

thromboxane A2 synthesis by interfering with the activity of cyclooxygenase 1 and 2 enzymes and the subsequent release of ADP by platelets and their aggregations

93
Q

Aspirins effects are

A

irreversible and last for the life of the platelet (8-12 days)

94
Q

_______ is the rate-limiting enzyme in the conversion of arachidonic acid to thromboxane A2

A

cyclooxygenase

95
Q

NSAIDs include

A

ketorolac, naprosyn, and ibuprofen

96
Q

NSAIDS mechanism of action

A

have the same MOA as aspirin (nonselective COX inhibitors) but they reversibly depress thromboxane A2 production by platelets

97
Q

NSAIDS (day of)

A

are more temporary (24-48 hours) and are often held prior to surgery

98
Q

Anticoagulants work by

A

delaying or preventing clotting and they have no affect after the clot is formed

99
Q

Thrombolytics possess inherent

A

fibrinolytic effects

100
Q

Antithrombotic drugs influence the

A

formation of clots by inhibiting platelet activity

101
Q

Adverse effects of thrombolytics include

A

bleeding
re-thrombosis- anticoagulants such as heparin are usually co-administered and continued after thrombolytic therapy
older clots are more difficult to dissolve

102
Q

Streptokinase is a

A

protein produced by beta-hemolytic streptococci

103
Q

Streptokinase works by

A

noncovalently binding to plasminogen and converting it to a plasminogen activator complex that acts on other plasminogen molecules to generate plasmin

104
Q

Streptokinase adverse effect

A

as a bacterial product it may stimulate antibody production and subsequent allergic reactions

105
Q

Alteplase is a

A

fibrin-specific thrombolytic drug synthesized by endothelial cells

106
Q

Alteplase is limited to use

A

in the first 3-6 hours of ischemic stroke

107
Q

Alteplase can be administered

A

systemically or directly into embolism (place of invasive lines before administration)

108
Q

Thrombolytics work by

A

converting plasminogen to the active form, plasmin

plasmin breaks down fibrin

109
Q

Thrombolytics are used to

A

restore circulation through a previously occluded vessel such as in STEMI, acute ischemic stroke, acute massive PE

110
Q

thrombolytics are contraindicated in

A

trauma, severe HTN, acute bleeding, and pregnancy

111
Q

Thrombolytics include

A

urokinase, streptokinase, alteplase

112
Q

The most common risk of thrombolytics is

A

hemorrhage or bleeding

113
Q

Thrombolytics are more capable of

A

dissolving newly formed clots (platelet rich and weaker fibrinogen bonds)

114
Q

Thrombolytics possess inherent

A

fibrinolytic effects or enhances the body’s fibrinolytic system by converting endogenous pro-enzyme plasminogen to the fibrinolytic enzyme plasmin

115
Q

Thrombolytic classes include:

A

fibrin-specific agents: alteplase, reteplase, tenecteplase

non-fibrin specific agents- streptokinase

116
Q

Plasminogen is a

A

serum protein that is absorbed into the clot at its formation

117
Q

Plasminogen is cleaved into

A

plasmin which breaks down fibrin and fibrinogen

TPA and urokinase type plasminogen activators are released from the capillary endothelium

118
Q

Garlic works by

A

inhibiting platelet aggregation and should be discontinued for 7 days

119
Q

Ginkgo works by

A

inhibiting platelet activating factor and should be discontinued for 36 hours

120
Q

Ginseng works by

A

inhibiting platelet aggregation and lowers blood glucose; check PT/PTT/glucose & d/c for 24 hours (preferably 7 days)

121
Q

Black cohosh

A

claims to be useful for menopausal symptoms and contains small amounts of anti-inflammatory compounds including salicylic acid

122
Q

Fish oil

A

claims to prevent/treat atherosclerotic CV disease; dose dependent bleeding risk increases with dose >3 g/day

123
Q

Feverfew:

A

claims to prevent migraines; increases the risk of bleeding because it individually inhibits platelet aggregation, has additive effects with other antiplatelet agents

124
Q

Primary prophylaxis of ASA:

A

hyperlipidemia in the absence of established CV disease- should be continued in the preop period up to and including the day of the procedure
may be held for a few days at the discretion of the surgeon or procedural physician

125
Q

Secondary prophylaxis of ASA (afib, previous MI, stent):

A

should be continued in the preoperative period up to and including the day of the procedure
stopping ASA in these patients needs an explicit discussion

126
Q

Holding ASA in specific circumstances:

A

intracranial, middle ear, posterior eye or intramedullarly spine surgery; possibly in prostate surgery

127
Q

Clopidogrel (Plavix) and ticagrelor (brilinta) are

A

inhibitors of platelet activation and aggregation through the irreversible binding of its active metabolite to the P2Y12 class of ADP receptors on platelets

128
Q

P2Y12 receptor antagonists must be (regarding day of surgery)

A

discontinued 7 days prior to elective surgery

129
Q

Clopidogrel is a

A

pro-drug and must be metabolized by CYP450 enzymes to produce the active metabolite that inhibits platelet aggregation for the life of the platelet

130
Q

Indications for P2Y12 receptor antagonists include

A

secondary prevention of MI, CVA; coronary artery stenting, acute coronary syndrome, peripheral artery disease

131
Q

As a general approach, elective surgical procedures should be delayed for at least

A

6 weeks and ideally 6 months after DES placement

132
Q

Withdrawal of ASA in patients with CAD is associated with

A

increase in death/MI

133
Q

ASA and P2Y12 receptor antagonists act

A

synergistically

134
Q

Platelet glycoprotein IIb/IIIa antagonists act at

A

the corresponding fibrinogen receptor that is important for platelet aggregation

135
Q

Platelet glycoprotein IIb/IIIa antagonists are utilized in

A

ACS, angioplasty failures, and stent thromboses

136
Q

Platelet glycoprotein IIb/IIIa antagonists include

A

abciximab, tirofiban, and eptifibatide (integrilin)

137
Q

Platelet glycoprotein IIb/IIIa blocks

A

fibrinogen which is the final common pathway of platelet aggregation

138
Q

The effects of platelet glycoprotein IIb/IIIa can be reversed with

A

platelet transfusions

139
Q

Platelet inhibitor glycoprotein IIb/IIIa antagonists monitoring can be done with

A

ACTs and reversible with the clearance of the drug

ACT is maintained between 200 and 400 seconds

140
Q

_____ should be monitoring with platelet inhibitor glycoprotein IIb/IIIa antagonists

A

platelet counts

therapy should be discontinued if thrombocytopenia develops

N929 Pharmacology II (16 decks)

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