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Pharmacology Exam 4 > Procoagulants & Anticoagulants > Flashcards

Procoagulants & Anticoagulants Flashcards

1
Q

How is major bleeding defined and examples?

A

by how it affects patient: intracranial, intraspinal, intraocular, mediastinal.

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2
Q

What are the risk factors for bleeding while on anticoagulation?

A

anti-coagulation effect, increased age, female, Hx GI bleed, use of ASA along with other anticoagulation

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3
Q

What are the triple As?

A

Primary hemostasis: platelet adhesion, activation, and aggregation

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4
Q

What is Adhesion dependent on?

A

von Willebrand’s factor (vWF) aka Factor VIII:v

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5
Q

What does vWF do?

A

acts as a bridge, one end attaches to platelet and the other to the damaged tissue

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6
Q

Where is vWF made?

A

synthesized and released from endothelial cells (not made in liver)

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7
Q

What connects the platelet to the endothelium via vWF?

A

Gp1B

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8
Q

What is the MOA of Desmopressin (DDAVP)?

A

stimulates a large release of vWF from the endothelium, will shorten bleeding time in patients with mild forms of hemophilia A or VWD.

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9
Q

When can you use Desmopressin?

A

in Type 1 & 3, qualitative disease. DDAVP doesn’t work in type 2

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10
Q

What’s the IV dose of DDAVP?

A

0.3mg/kg over 15-30 min to avoid hypotension. slow infusion. (can release local vasoactive mediators causing hypotension)

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11
Q

What can increase MI postop in CV patients two-fold?

A

desmopressin

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12
Q

What’s the MOA of activation?

A

thrombin combines with a thrombin receptor on the platelet surface and platelet changes shape and releases mediators that promote aggregation.

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13
Q

What are the important mediators in activation?

A

ADP and thromboxane A2

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14
Q

What acts on ADP?

A

plavix

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15
Q

What acts on thromboxane A2?

A

aspirin

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16
Q

When should you stop plavix preop?

A

7-10 days preop. Noncompetitive drug that has to live out life of platelets

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17
Q

What’s the MOA of thienopyridine derivatives?

A

antiplatelet effect from inhibition of adenosine diphosphate-induced platelet aggregation. inhibits P2y12 receptor on the platelet

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18
Q

Where does plavix affect hemostasis?

A

at binding

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19
Q

What are examples of thienopyridine derivatives?

A

ticagrelor, clopidogrel, prasugral

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20
Q

What is different about ticagrelor from the other thienopyridine derivatives?

A

ticagrelor is reversible and not a prodrug. clopidogrel and prasugral are prodrugs and irreversibly bind so require metabolism to work

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21
Q

How is thromboxaine A2 formed?

A

phospholipids–>phospholipase A2–>Arachidonic acid–>cyclo-oxygenase–>prostaglandin A2–>Prostaglandin H2–>Thromboxane A2. (Arachidonic acid breaks off from phospholipids and converts with cox to prostaglandin)

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22
Q

What is the MOA of cyclooxygenase inhibitors?

A

inhibit platelet cycooxygenase and prevent synthesis of thromboxane A2 (at activation)

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23
Q

What inhibits platelet cyclooxygenase?

A

low-dose aspiring (60-325 mg/d)

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24
Q

What are some examples of cyclooxygenase inhibitors?

A

ASA, NSAIDs, Celebrex

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25
Q

When should you stop ASA preop?

A

7-10 days stop, restart 24h post surgery

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26
Q

T/F, a clot is still water-soluble after the triple As.

A

True

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27
Q

What do ADP and Thromboxane A2 uncover?

A

fibrin receptors GPIIb/IIIa

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28
Q

What does fibrin do?

A

links platelets together

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29
Q

What is the MOA of GPIIb/IIIa inhibitors?

A

inhibit platelet aggregation by interfering with platelet-fibrin receptors

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30
Q

What are examples of GPIIb/IIIa inhibitors?

A

abciximab, eptifibatide, tirofiban

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31
Q

When do you stop GPIIb/IIIa inhibitors prior to surgery?

A

eptifibatide(integrilin)/tirofiban(aggrastat) DC 8 hours preop, abciximab (reopro) DC 24-48hours preop

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32
Q

Where does aspirin act in the clotting cascade?

A

between vWF and TxA2

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33
Q

Where does plavix act in the clotting cascade?

A

between ADP and GPIIb/IIIa activation

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34
Q

Where do GPIIb/IIIa inhibitors act?

A

between GPIIb/IIIa activation and platelet aggregation

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35
Q

What is the key player in secondary hemostatsis?

A

fibrin

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36
Q

What is involved in fibrin production?

A

extrinsic, intrinsic, and final common pathway. incorporating all 13 clotting factors

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37
Q

When do clots become stable.

A

secondary hemostasis, after platelet aggregation fibrin is woven into platelets and they are cross-linked making them insoluble in water/stable

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38
Q

Which clotting factors are made in the liver?

A

(10 of them)I fibrinogen, II prothrombin, V proaccelerin, VII proconvertin, VIII antihemophilia, IX christmas factor, X stuart prower factor, XI plasma thromboplatin antecedent, XII Hageman factor, XIII fibrin-stabilizing factor

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39
Q

Which clotting factors are NOT made in the liver?

A

(3 of them) III thromboplastin–vascular wall/extravascular cell membranes, IV Calcium–diet, VIII vWF–vascular endothelial cells

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40
Q

What clotting factors are dependent on Vit K?

A

(4 of them) II prothrombin, VII proconvertin, IX Christmas Factor, X Stuart Prower Factor

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41
Q

What factor is missing in the clotting factors?

A

VI, there isn’t one

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42
Q

What initiates the extrinsic pathway?

A

initiated in response to injury occuring outside the blood vessel

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43
Q

What factors are involved in the extrinsic pathway?

A

Factor III and VII

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44
Q

What leads to the release of Factor III?

A

damage to the vessel

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45
Q

What is the primary physiologic initiator of coagulation?

A

thromboplastin

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46
Q

What activates Factor VII?

A

Factor III

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47
Q

What is the beginning of the final pathway?

A

Factor VII and Factor III and calcium on the surface of platelet activate Factor X

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48
Q

How does coumadin work?

A

binding the vitamin K receptors in the liver and competitively inhibiting Vitamin K

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49
Q

What does coumadin do?

A

depress production of Vit K dependent clotting factors II, VII, IX, X, blocks classic extrinsic pathway and final common factors

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50
Q

What does coumadin do to PT?

A

prolong it

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51
Q

What assesses extrinsic pathway?

A

PT and INR

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52
Q

When do you DC coumadin preop?

A

very surgery/surgeon dependent but generally 5 days preop. still assess INR, possible bridging or reversal needed

53
Q

Where does heparin work?

A

intrinsic pathway

54
Q

What initiates the intrinsic pathway?

A

injury to INSIDE of blood vessel

55
Q

What factors are part of the intrinsic pathway?

A

XII, XI, IX, VIII

56
Q

Describe intrinsic pathway

A

trauma to vessel activates XII, XIIa activates XI, XIa activates IX, IXa combines on platelet surface with activated VIII:C and calcium which activates X (beginning of final common pathway)

57
Q

What triggers the final common pathway?

A

activated factor X occurring from either extrinsic or intrinsic pathway complexes on platelet surface with factor V and calcium to convert factor II to thrombin IIa.

58
Q

What does thrombin IIa do?

A

converts fibrinogen (factor I) to fibrin

59
Q

What are the factors in the final common pathway?

A

X, V, II, I, XIII

60
Q

What forms a stable clot in the final common pathway?

A

Factor XIII and fibrin Ia cross-linking occurs and forms stable clot

61
Q

What is the main player in anticoagulation?

A

antithrombin III

62
Q

Where is AT3 made and what does it do?

A

made in liver and neutralizes final common pathway factors II and X and intrinsic factors IX, XI, and XII by forming complexes with them.

63
Q

What does heparin do to AT3?

A

increases it

64
Q

What types of patients have AT3 deficiencies?

A

cirrhosis and nephrotic syndrome.

65
Q

How does heparin work?

A

increasing effectiveness of AT3 >1000 fold

interferes with intrinsic pathway

66
Q

What’s the #1 reason a patient is unresponsive to heparin?

A

AT3 deficiency

67
Q

How do you treat someone deficient in AT3?

A

FFP

68
Q

What assesses the intrinsic pathway?

A

aPTT and ACT

69
Q

What ACT level is adequate heparinization for cardiac pump cases?

A

> 450

70
Q

What does larger MW unfractionated heparin do?

A

catalyze inhibition of factor IIa and Xa

71
Q

When do you DC unfractionated heparin preop?

A

4-6 hours preop

72
Q

What’s the differences with LMWH?

A

smaller MW catalyzes inhibition of only factor Xa, less protein bound, irreversibility with protamine, prolonged 1/2 life, lack of monitoring by anticoagulant response

73
Q

What are examples of LMWH?

A

Lovenox, dalteparin

74
Q

When do you stop LMWH preop?

A

12 hours preop

75
Q

What is the MOA of direct thrombin inhibitors?

A

bind to thrombin in varying degrees

76
Q

What are examples of direct thrombin inhibitors?

A

bivalrudin, argatroban, lepirudin, desirudin, ximelagatran, dabigatran

77
Q

When do you DC direct thrombin inhibitors?

A

bivalrudin/argatroban 4-6h
Lepirudin, Desirudin 24h
Ximelagatran, Dabigatran 48h

78
Q

What coagulation factors make up Prothrombin Complex Concentrates (PCC)?

A

II, VII, IX, X

79
Q

What are PCCs used for in other countries?

A

coumadin reversal

80
Q

What are examples of PCCs?

A

KCENTRA, octaplex, FEIBA, profilnine, Bebulin

81
Q

What is bebulin for?

A

indicated for the prevention and control of bleeding episodes in adult patients with hemophilia B (factor IX deficiency or Christmas disease)

82
Q

What does bebulin contain?

A

factor IX, II, X, and low amounts of factor VII

83
Q

What are the Vit K dependent clotting factors?

A

factor IX, II, X

84
Q

Where does Apixaban (eliquis) work?

A

final common pathway, anti Xa

85
Q

What is the main FDA use for Eliquis?

A

VTE prophylaxis, also afib

86
Q

What is the reversal in trial for eliquis?

A

FEIBA (factor eight inhibitor bypass activity)

87
Q

When do you stop eliquis preop?

A

1-4 days preop

88
Q

Is there any lab screening for eliquis?

A

No

89
Q

What is the dose of eliquis?

A

8mg bid, 2.5mg if old or little, VTE prophylaxis 2.5mg bid

90
Q

Where does Xarelto (rivaroxaban) work?

A

final common pathway, anti Xa

91
Q

What is Xarleto used for/dosing?

A

VTE prophylaxis 10mg qd, AF 20mg qd unless old or decreased CrCl then 15mg qd, VTE treatment 15mg bid x21 days then 20mg qd

92
Q

What lab can be screened for Xarelto?

A

PT

93
Q

What is the reversal in trial for Xarelto?

A

PCCs, ?FEIBA

94
Q

When do you stop Xarelto?

A

1-4 days preop

95
Q

Where does Edoxaban (savaysa) work?

A

anti Xa

96
Q

What is Edoxaban for/dosing?

A

AF 60 mg qd, VTE treatment 60mg qd, 30 mg qd if old or decreased Cr Cl

97
Q

What labs do you screen with Edoxaban?

A

PT/INR

98
Q

What reversal is in trial for Edoxaban?

A

PCCs, FEIBA

99
Q

When do you stop Edoxaban?

A

1-4 days preop

100
Q

Where does Dabigatran (pradaxa) work?

A

anti-IIa

101
Q

What are the indications/doses for pradaxa?

A

AF 150 mg bid, VTE prophylaxis 220mg qd

102
Q

What lab do you screen with pradaxa?

A

aPTT

103
Q

What is the reversal for pradaxa?

A

dialysis, now can add PCCs/FEIBA

104
Q

When do you stop pradaxa preop?

A

3-5 days

105
Q

Which NOAC can cause increased GI bleed?

A

Pradaxa

106
Q

In general when should NOACs be stopped preop?

A

3-5 half lives, 2-5 days depending on drug and CrCl

107
Q

What is the main player in fibrinolysis?

A

Plasmin

108
Q

What is the inactive form of plasmin formed in the liver and circulating in the blood?

A

plasminogen

109
Q

T/F. Plasminogen is incorporated into all clots when they form.

A

True, but its not active

110
Q

What converts plasminogen to plasmin?

A

tissue type plasminogen activator (tPA) and urokinase type plasminogen activator (uPA)

111
Q

What does plasmin do?

A

breaks down fibrin in the clot and splits products. clot buster

112
Q

What are anti-fibrinolytic agents?

A

lysine analogs, competitively inhibit the activation of plasminogen to plasmin

113
Q

What types of patients were anti-fibrinolytics studied in?

A

cardiac and orthopedic

114
Q

What were the results of studying anti-fibrinolytics?

A

all seemed to decrease blood loss but not proven to decrease transfusion rate or mortality. major outcome in CV was CT output postop day 1

115
Q

What are 2 types of anti-fibrinolytics?

A

Tranexamic Acid, Amicaproic acid

116
Q

Which is proven to decrease transfusions? TXa or Amicar?

A

Txa.

117
Q

What are some effects of Txa?

A

decreases transfusions, can inhibit plasmin at high levels, causes seizures, can give orally for heavy menstrual bleeding

118
Q

What does Aprotinin do?

A

inhibit plasmin so fibrin breakdown is slow and bleeding is decreased.

119
Q

When is Aprotinin used?

A

primarily cardiac bypass cases especially reops to decrease postop bleeding

120
Q

What are the risks of aprotinin?

A

primary allergic reaction after first dose or severe anaphylaxis after 2nd. can also worsen renal function

121
Q

What is protamine made of?

A

salmon semen

122
Q

What is the MOA of protamine?

A

inhibits platelets and serine proteases involved with coagulation

123
Q

What is protamine used for?

A

reverse unfractionated heparin through neutralization reaction (acid-base)

124
Q

What is the dose of protamine?

A

1mg per 100u of heparin, or give based on circulating heparin level

125
Q

What are the adverse reactions of protamine?

A

anaphylaxis, acute pulm vasoconstriction, RV failure, hypotension. GIVE SLOW

126
Q

What are common herbal medications that affect coagulation?

A

3 g’s: garlic, ginkgo, ginseng

127
Q

What does garlic do?

A

inhibit platelet aggregation possibly irreversibly, increased fibrinolysis, antihypertensive activity. DC 7days

128
Q

What does ginkgo do?

A

inhibit platelet-activating factor. DC 36h

129
Q

What does ginseng do?

A

lowers blood glucose, increase prothrombin and activated partial PTs in animals. DC 24h

Pharmacology Exam 4 (7 decks)

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