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Pharm II Final > Anticoagulants & Thrombolytics > Flashcards

Anticoagulants & Thrombolytics Flashcards

1
Q

What type of substances promote coagulation?

A

Procoagulants

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2
Q

What type of substances inhibit coagulation?

A

Anticoagulants

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3
Q

What term is used to describe the prevention of blood loss?

A

Hemostasis

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4
Q

What are the four phases of hemostasis?

A

Vascular constriction
Formation of platelet plug
Formation of blood clot
Clot dissolution

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5
Q

What two process of hemostasis are immediate?

A

Vascular constriction and Formation of platelet plug

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6
Q

How long does it take the body to form a blood clot when injury occurs?

A

15-20 seconds to 1-2 minutes

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7
Q

What components are required for clot formation?

A

Vascular endothelium
Platelets
Plasma mediated hemostasis

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8
Q

What roles do the platelets play in clot formation?

A

Anchoring sites for coagulation factor activation complexes
Delivery vehicles releasing hemostatically active proteins
Major structural components of the clot

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9
Q

What factors induce prothrombotic endothelial changes?

A

Thrombin
Hypoxia
High fluid sheer stress

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10
Q

What products in the extracellular matrix promote clot formation?

A 
Collagen
Von Willebrand factor
Hormones
Cytokines
Procoagulants
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11
Q

Where do platelets form and what is their normal lifetime?

A

Formed in the bone marrow and the life of a platelet is 8-12 days

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12
Q

What is the normal concentration of platelets?

A

150,000-300,000 per microliter

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13
Q

At what platelet count would a person more than likely being to spontaneously bleed?

A

Less than 50,000 (below 10,000 is considered lethal)

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14
Q

What occurs when platelets are exposed to the extracellular matrix in damaged endothelium?

A

Adhesion
Activation
Aggregation

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15
Q

What component of the extracellular matrix plays an important role in platelet adhesion to the vascular wall?

A

Von Willebrand factor

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16
Q

What is the primary role of vWF?

A

It is a bridging molecule between the sub endothelial matrix and platelets

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17
Q

What occurs during the activation phase of the hemostasis?

A

Platelets release granular contents (ADP, Ca, serotonin, histamine, TXA2 etc.) resulting in recruitment and activation of additional platelets

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18
Q

What receptors on the surface of platelets bind fibrinogen to provide for cross-linking with adjacent platelets?

A

Glycoprotein IIb/IIIa

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19
Q

What is the inactivated precursor to thrombin?

A

Prothrombin

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20
Q

What is the goal of clot formation?

A

To convert a soluble to insoluble clot

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21
Q

What stimulates activation of new platelets as well as increases platelet aggregation?

A

Thromboxane A2 (TXA2)

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22
Q

What type of receptor is the TXA2 receptor?

A

It is a G protein coupled receptor

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23
Q

Why is TXA2 important during tissue injury and inflammation?

A

It is a known vasoconstrictor

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24
Q

How does TXA2 contribute to activation of new platelets?

A

It mediates expression of the glycoprotein complex IIb/IIIa in the cell membrane of platelets

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25
Q

Where are most coagulation factors synthesized?

A

In the liver

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26
Q

How are coagulation factors present in the body when no injury is present?

A

Inactive proteins

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27
Q

How are coagulation factors labeled?

A

With Roman Numerals in the others in which they were discovered

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28
Q

What coagulation factor is not a true factor and comes from a person’s diet?

A

Calcium

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29
Q

Where is Von Willebrand synthesized?

A

In endothelial cells

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30
Q

What factors are vitamin K dependent for utilization?

A

II, VII, IX, and X

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31
Q

What is factor I?

A

Fibrinogen –> fibrin

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32
Q

What is factor II?

A

Prothrombin –> thrombin

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33
Q

How does the intrinsic pathway begin?

A

With damage to the blood vessels themselves

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34
Q

What is the common pathway?

A

It is common to both the intrinsic and extrinsic pathway, it depicts thrombin generation and subsequent fibrin formation

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35
Q

What is factor III?

A

Tissue thromboplastin

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36
Q

What is the initial step in the extrinsic pathway?

A

Plasma-mediated hemostasis, begins with exposure of blood plasma to tissue factor

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37
Q

What is the significance of fibrin activation?

A

Activates platelets and factor XIII
Converts inactive cofactors V and VIII to active forms
Activates factor XI
Up-regulates tissue factor
Stimulates vascular endothelium to express down regulation of fibrinolytic activity

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38
Q

What is factor IV?

A

Calcium

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39
Q

How does prothrombin contribute to the clotting cascade?

A

Attaches to receptors on the surface of a platelet

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40
Q

What is factor V?

A

Proaccelerin, labile factor

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41
Q

What two things would cause a deficiency of prothrombin in the blood?

A

Lack of vitamin K or liver disease

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42
Q

What causes the formation of fibrin?

A

Thrombin acts on fibrinogen to form fibrin

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43
Q

What is factor VII?

A

Serum prothrombin conversion accelerator, proconvertin

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44
Q

How is a meshwork in all directions of blood cells created?

A

Covalent bonds between fibrin molecules and cross-linking of fibers

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45
Q

What is a clot composed of?

A

Plasminogen
Plasmin
Fibrin and
Fibrin degradation products

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46
Q

How is plasminogen activated to plasmin?

A

By tissue plasminogen activator (t-PA) released from the tissue and vascular endothelium

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47
Q

What is factor VIII?

A

Antihemophilic A Factor

Antihemophilic globulin

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48
Q

What does plasmin do?

A

It digests fibrin fibers, fibrinogen, Factor V, Factor VIII, prothrombin and Factor XII

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49
Q

What is the function of anticoagulants?

A

Prevent clot formation or extension of existing clot

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50
Q

What is factor IX?

A

Plasmin thromboplastin Component (PTC)
Christmas factor
Antihemophilic B Factor

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51
Q

What is the function of anti platelet drugs?

A

Reduces platelet aggregation and prevents Stroke, MI and TIA

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52
Q

What three drugs do we commonly use that are anticoagulants?

A

Heparin
Lovenox LMWH
Warfarin

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53
Q

What is Factor X?

A

Stuart-Prower Factor

Autoprothrombin III

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54
Q

What herbal products have an effect on coagulation?

A

Garlic, giner, ginko, fish oil, flax seed, cranberry, black cohosh

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55
Q

How does citrate prevent blood clotting in donor blood?

A

Deionizes the Calcium (negatively charges citrate combines with calcium in the blood to cause an un-ionized calcium compound)

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56
Q

How is citrate metabolized when done blood is given?

A

Metabolized in the liver and is polymerized into glucose or metabolized

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57
Q

What is Factor XI?

A

Plasma Thromboplastin antecedent (PTA)

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58
Q

How does Heparin work?

A

Binds to antithrombin (antithrombin III) and accelerates the normally occurring antithrombin induced neutralization of activated clotting factors (Xa, XII, XI & IX)

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59
Q

What is the purpose of neutralizing thrombin?

A

It prevents the conversion of fibrinogen to fibrin

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60
Q

Where is heparin produced endogenously?

A

Basophils, mast cells and the liver

61
Q

What are the three forms of heparin?

A

Bovine
Porcine
Endogenous

62
Q

How does heparin effect the clotting cascade?

A

It blocks the classic intrinsic and final common pathways

63
Q

What is the definition of a unit?

A

One unit of activity as the amount of heparin that maintains the fluidity of 1mL of citrated sheep plasma for 1h after re-calcification

64
Q

How many units must heparin contain?

A

At least 120 USP units/mL

65
Q

Why do we prescribe heparin in units instead of mg?

A

Commercial preparations varying in the number of USP units per mL

66
Q

How does temperature affect heparin?

A

Decrease in body temperature prolongs its elimination half time

67
Q

How is heparin monitored?

A

Biologic Activity:
PTT: 1.5-2.5 times pre drug value
ACT:

68
Q

What is unique about heparin’s dose response?

A

It is not linear

69
Q

What is the typical dose of heparin and how much does it increase clotting time?

A

100u/kg (o.5-1mg/kg) causes blood clotting time to increase from 6 to 30 or more minutes

70
Q

What enzyme breaks down injected heparin?

A

Heparinase

71
Q

How often should ACTs be drawn on a patient receiving heparin therapy?

A

Baseline
3-5m post administration
30m-1h interval post administration

72
Q

What lab value is the most widely used and reliable for high heparin concentrations?

A

Activated Coagulation Time (ACT)

73
Q

What physiological processes can influence ACT results?

A

Hypothermia
Thrombocytopenia
Aprotinin
Coagulation deficiencies

74
Q

How long is a typical control ACT?

A

80-120s

75
Q

If a patient is on CPB what is a desirable ACT?

A

> 400-450s

76
Q

What is a desirable ACT in patients that are not on CPB but had a vascular procedure done?

A

> 200-300s

77
Q

How is an ACT preformed?

A

Mixing whole blood with an activated substance to initiate activation of the clotting cascade

78
Q

What is significant about the size of lovenox?

A

1/3 size of heparin and can cross placenta

79
Q

Why is it that low molecular weight heparin only has to be given once a day?

A

There is less binding to the endothelial cells and therefore a longer half life

80
Q

What are some advantage of using lovenox over heparin?

A

Lack in need of monitoring
More predictable
Fewer effects on platelet function
Reduced risk of HIT

81
Q

What is the mechanism of action of lovenox?

A

It binds to and accelerates antithrombin III, inhibits factor Xa and IIa

82
Q

What is factor XII?

A

Hageman factor, glass factor, contact factor

83
Q

How much lovenox should be administered for DVT prophylaxis?

A

30mg SQ Q12H

84
Q

What is one of the most important risk factors of an epidural hematoma?

A

Anticoagulant therapy/length of use

85
Q

How does heparin induce thrombocytopenia occur (HIT)?

A

Heparin-dependent antibodies that agglutinate platelets and produce thrombocytopenia

86
Q

What is considered mild HIT syndrome?

A

Platelet count of less than 100,000 cells/mm

30-40% of heparin treated patients

87
Q

What is considered severe HIT syndrome?

A

Platelet count of less than 50,000 cells/mm

0.5% -6% of patients treated with heaprin

88
Q

When would it be okay to administer Heparin to a patient with a history of HIT?

A

If remote history and no loner can demonstrate antibodies

89
Q

What medication is not effective if a patient has an antithrombin deficiency?

A

Heparin, no antithrombin nothing for heparin to bind to

90
Q

What is the treatment for antithrombin deficiency?

A

2-4 units FFP in adults OR

Antithrombin concentrate 1,000 units in adults

91
Q

What drug can be given for heparin reversal?

A

Protamine

can also give FFP & prothrombin complex concentrate

92
Q

What is the mechanism of action of protamine?

A

The positively charged alkaline protamine combines with the negatively charged acidic heparin to form a stable complex void of anticoagulant activity

93
Q

How is the Heparin-Protamine complex removed from the body?

A

Removed by Reticuloendothelial system (phagocytosis)

94
Q

What is the dose of protamine?

A

1mg for every 100 units of Heparin

It can be guided by last ACT and estimated amount of heparin within the last two hours

95
Q

If protamine is given too rapidly what can occur?

A

Histamine release causing HoTN, facial flushing and tachycardia

96
Q

What effect can the Heparin-protamine complex have on the pulmonary vasculature?

A

Can cause vasoconstriction –> Pulmonary HTN

97
Q

What population is at risk for protamine allergy?

A

Diabetics, insulin contains protamine and chronic exposure to low dose protamine may produce antibodies against protamine

98
Q

What is another indication for having a protamine allergy?

A

Fish allergy (protamine derived from salmon sperm)

99
Q

What is population has the highest actual risk of having a protamine allergy?

A

Patients that have previously had a reaction to protamine (could be from bypass surgery)

100
Q

What is the mechanism of action of Coumadin?

A

Competitively inhibits vitamin K dependent coagulation proteins (Factors II, VII, IX, X)
Inhibits protein C and S which prevent extensive clot formation

101
Q

How are Coumadin levels measured?

A

PT/INR

102
Q

What is the goal of the INR in patients on Coumadin therapy?

A

2-3

103
Q

What is the typical dose of Coumadin?

A

5-10mg orally

104
Q

Why is Coumadin contraindicated in pregnancy?

A

It crosses the BBB and is severely teratogenic

105
Q

How long does it take to see an effect in the patients INR with Coumadin use?

A

8-12h due to depletion of factor VII, however full clinical effects are not appreciated for several days

106
Q

What is factor XIII?

A

Fibrin stabilizing factor, fibrinase

107
Q

How is the INR calculated?

A

INR = Platelets PT

Control PT

108
Q

What is the normal INR range?

A

0.9-1.2

109
Q

How often is the INR repeated while on Coumadin therapy?

A

4-6 weeks

110
Q

What are INR goals with Coumadin therapy?

A

2-3 (may be higher with mechanical valve and recurrent MI)

111
Q

When should Coumadin be discontinued for minor surgery?

A

D/c 1-5 days prep for PT 20% within baseline

112
Q

What can be given to offset the effects of Coumadin if emergency surgery is required?

A

IV Vitamin K

FFP or PCC

113
Q

What is the mechanism of action of antiplatelet drugs?

A

Suppress platelet function (inhibit platelet aggregation)

114
Q

What are three well known antiplatelet drugs given?

A

ASA
Plavix
NSAIDs

115
Q

What is the mechanism of action of Aspirin?

A

Inhibits platelet aggregation by irreversibly inhibiting COX-1, via acetylation, the effects last the life of the platelet (8-12days)

116
Q

What is the typical dose of Aspirin?

A

81-325mg

117
Q

What is the importance of COX-1 in the conversion of arachidonic acid to thromboxane A-2?

A

COX-1 is the rate limiting enzyme for the conversion

118
Q

What is ASA utilized for in primary prophylaxis?

A

Used for prevention in the absence of an established diagnosis of CV disease

119
Q

What is ASA utilized for in secondary prophylaxis?

A

Treatment with ASA in the presence of overt CV disease or conditions conferring particular risk.

120
Q

What are the general guidelines for taking ASA prior to surgery?

A

It should be continues in both primary and secondary prophylaxis prior to and day of surgery unless surgical procedure has a high EBV

121
Q

What is the mechanism of action of Plavix?

A

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

122
Q

What is significant about patients with liver disease taking plavix?

A

Plavix must be metabolize by CYP enzymes to produce the active metabolite that inhibits platelet aggregation (prodrug)
Liver failure may not get full effects

123
Q

What laboratory value should be drawn when a patient is taking plavix?

A

P2Y12 point of care assay, can measure actual level of drug

124
Q

Which type of stent requires longer use of plavix?

A

Medicine releasing, delayed healing

125
Q

How do ASA and plavix act when used in combination?

A

Synergistically

126
Q

What is the mechanism of action of NSAIDs in relation to antiplatelet therapy?

A

Reversibly depress thromboxane A2 production by platelets –> more temporary (24-48h)

127
Q

What are the two mechanisms in which thrombolytics work?

A

Process inherent fibrinolytic effects OR

Enhance the body’s fibrinolytic system

128
Q

What is the main use of thrombolytics?

A

To restore circulation through a previously occluded vessel

129
Q

What are contraindication to thrombolytic therapy?

A

Trauma
Severe HTN
Active bleeding
Pregnancy

130
Q

What is the most common risk of thrombolytic use?

A

Hemorrhage or bleeding

131
Q

What is the mechanism of action of tPa?

A

It converts plasminogen to the active form, plasmin and plasmin breaks down fibrin

132
Q

What reaction allows plasminogen to become plasmin?

A

t-Pa cleaves the plasminogen peptide bond into the serine protease plasmin

133
Q

Why do we typically seen t-PA given as a bolus and followed by a gtt?

A

It has a short half life of only about 5 minutes

134
Q

What agent could you coadminister with t-PA to prevent re-thrombosis?

A

Heparin

135
Q

What is significant about the age of the clot?

A

Older clots have more cross linking and are more compacted = more difficult to dissolve

136
Q

What are direct thrombin inhibitors?

A

Class of medications that act as anticoagulants by directly inhibiting the enzyme thrombin (factor II)

137
Q

What is a benefit to using DTI?

A

Does not require a cofactor and may be used if patient has a positive history for HIT

138
Q

What is a major disadvantage to using DTIs?

A

There is no reversal

139
Q

What is a major disadvantage to using DTIs?

A

There is no reversal

140
Q

What is the mechanism of action of bivalent DTIs?

A

Block simultaneously the active site and secondary binding site (exosist 1) and act as competitive inhibitors of fibrin

141
Q

What is the mechanism of action of univalent DTIs?

A

Block only the active site and can therefore both inhibit unbound and fibrin-bound thrombin

142
Q

What is the normal bleeding time?

A

3-10m

143
Q

What is the normal prothrombin time?

A

12-14s

144
Q

What is the normal INR?

A

0.9-1.2

145
Q

What is the normal aPTT?

A

25-35s

146
Q

What is the normal thrombin time?

A

less than 30 seconds

147
Q

What is the normal ACT?

A

80-150s

148
Q

What is the normal amount of fibrinogen?

A

greater than 150mg/dL

149
Q

Why is TXA2 important during tissue injury and inflammation?

A

It causes vessel wall vasoconstriction initially after injury

Pharm II Final (12 decks)

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