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Pharmacology 514 > Anticoagulants, Thrombolytics, and Direct Thrombin Inhibitors > Flashcards

Anticoagulants, Thrombolytics, and Direct Thrombin Inhibitors Flashcards

1
Q

What are procoagulants?

A

Promote coagulation

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2
Q

What are anticoagulants?

A

Inhibit coagulation

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3
Q

Do procoagulants or anticoagulants normally predominate?

A

Anticoagulants

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4
Q

When are procoagulants activated in normal physiology?

A

When a vessel is ruptured

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5
Q

What is the process of normal hemostasis?

A
  • Damage occurs to a blood vessel
  • Vascular constriction (immediate)
  • Platelets immediately begin to adhere to the cut edges of the vessel and release chemicals to attract even more platelets (immediate)
  • Platelet plug forms
  • Clotting factors cause strands of fibrin to stick together and seal the inside of the wound (15-20 seconds up to 1-2 minutes)
  • Clot dissolution (few hours to 1-2 weeks)
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6
Q

How do platelets participate in clot formation? (3 ways)

A
  1. anchoring sites for coagulation factor activation complexes
  2. Delivery “vehicles” releasing hemostatically active proteins
  3. Major structural components of the clot
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7
Q

What participants are required for clot formation?

A

Vascular endothelium
Platelets
Plasma-mediated hemostasis

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8
Q

What is the vascular endothelial role in hemostasis?

A

Normal, intact vascular endothelium provides nonthrombogenic surface (antiplatelets, anticoagulants, profibrinolytics)

Damage to endothelium exposes the underlying extracellular matrix and releases collagen, von Willebrand factor, hormones, cytokines, and other procoagulants

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9
Q

What 3 things can induce prothrombotic endothelial changes?

A

Thrombin, hypoxia, and high fluid shear stress

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10
Q

Where are platelets formed?

A

bone marrow

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11
Q

What is the normal concentration of platelets?

A

150,000-300,000 per microliter

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12
Q

At what platelet level can spontaneous bleeding occur?

A

50,000

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13
Q

At what platelet level is it lethal and can definitely cause spontaneous hemorrhage?

A

20,000

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14
Q

How long is the life of a platelet?

A

8-12 days

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15
Q

How are platelets removed?

A

Macrophages in the spleen

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16
Q

What are the 3 major phases platelets undergo when they are exposed to the extracellular matrix in damaged endothelium?

A

Adhesion
Activation
Aggregation

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17
Q

What is platelet adhesion?

A

Exposure to subendothelial matrix proteins (collagen, vWF, fibronectin) allows platelets to adhere to vascular wall

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18
Q

Which of the molecules involved in platelet adhesion is particularly important?

A

vWF - bridging molecule between the subendothelial matrix and platelets (glycoprotein 1b, factor IX, factor V receptor complexes)

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19
Q

What is platelet activation?

A

Occurs after platelets adhere to endothelial damaged wall, series of physical and biochemical changes that occur
- platelets release granular contents (ADP, calcium, serotonin, histamine, epinephrine, TXA2, etc) resulting in recruitment and activation of additional platelets

  • platelets develop pseudopod-like membrane extensions to increase platelet surface area
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20
Q

What is platelet aggregation?

A
  • activators released during the activation phase recruit additional platelets to the site of injury
  • newly activated glycoprotein IIb/IIIa receptor on the platelet surface bind fibrinogen to provide for cross-linking with adjacent platelets
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21
Q

What is plasma mediated hemostasis?

A

Amplification of thrombin generated from an inactive precursor (prothrombin)

Trace plasma proteins, activated by exposure to tissue factor or foreign substances, initiate a cascading series of reactions culminating in conversion of soluble fibrinogen to insoluble fibrin clot

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22
Q

What is thromboxane A2 (TXA2) and how is it produced?

A

Produced by activated platelets and has prothrombotic properties, stimulates activation of new platelets as well as increases platelet aggregation (mediates expression of glycoprotein complex IIb/IIIa in cell membrane of platelets)

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23
Q

What is another property of thromboxane A2 that makes it especially important during tissue injury and inflammation?

A

Vasoconstrictor

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24
Q

Where are most coagulation factors synthesized?

A

liver

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25
Q

How are coagulation factors identified?

A

Roman numerals assigned in order of discovery

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26
Q

Where is vWF synthesized?

A

endothelial cells

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27
Q

Which factors are vitamin K dependent?

A

Factor II, VII, IX, and X

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28
Q

Are most factors enzymes?

A

Yes, with a few exception

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29
Q

Do coagulation factors circulate as active or inactive proteins?

A

Inactive

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30
Q

What is factor I?

A

Fibrinogen

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31
Q

What is factor II?

A

Prothrombin

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32
Q

How can you determine if a factor is an active or inactive enzyme?

A

a lower-case letter “a” indicates active enzyme

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33
Q

What is another name for the intrinsic pathway of coagulation?

A

“contact activation system”

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34
Q

What is the process of the intrinsic pathway of coagulation?

A
  • Begins with damage to blood vessels
  • Formation of the primary complex on collagen and thrombin generation by way of factor XII and ultimately merges to the common pathway and activates factor X
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35
Q

What is another name for the extrinsic pathway of coagulation?

A

“Tissue factor pathway”

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36
Q

What is the process of the extrinsic pathway of coagulation?

A
  • Initial step in plasma-mediated hemostasis
  • Begins with exposure of blood plasma to tissue factor
  • After injury factor VIIa circulating the plasma forms a complex with tissue factor, factor X and calcium to promote the conversion of X to Xa
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37
Q

What is the common pathway of coagulation?

A
  • Common to both intrinsic and extrinsic pathways
  • Formation of thrombin which causes subsequent fibrin formation
  • SIgnal amplification
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38
Q

Where is prothrombin (factor II) produced and what is required for the formation of prothrombin?

A

Produced in liver
Vitamin K required for its formation

  • Lack of vitamin K or liver disease will result in decreased prothrombin levels and bleeding tendencies
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39
Q

Where are the receptors for prothrombin?

A

attaches to receptors on the surface of platelets

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40
Q

Where is fibrinogen (factor I) formed?

A

liver

liver disease can decrease the concentration of circulating fibrinogen

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41
Q

What is a clot primarily composed of?

A

plasminogen, plasmin, fibrin, and fibrin degradation products

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42
Q

What is the process of forming a blood clot?

A
  • thrombin converts fibrinogen to fibrin
  • covalent bonds between fibrin molecules and cross-linking of fibers creates a meshwork in all directions of blood cells, platelets and plasma which adhere to the surface of the damaged blood vessel
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43
Q

How are blood clots lysed?

A
  • plasminogen activated to plasmin by tissue plasminogen activator (t-PA)
  • plasmin digests fibrin fibers, fibrinogen, factor V, factor VIII, prothrombin, and factor XII
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44
Q

What are anticoagulants?

A

prevent clot formation or extension of existing clot

Ex: Warfarin, heparin, LMWH, direct thrombin inhibitors

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45
Q

What are antiplatelet agents?

A

reduce platelet aggregation, prevent stroke, MI, TIA

Ex: ASA, plavix, ticlid, NSAIDS

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46
Q

What are GP IIB/IIIA inhibitors?

A

prevent platelet aggregation on the surface of the platelet

Ex: Abxicimab (reopro), eptifibatide (Integrillin)

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47
Q

Do anticoagulants have an effect on a clot after it is formed?

A

No

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48
Q

What anticoagulant is used to prevent blood coagulation outside of the body?

A

citrate ion - any substance that deionizes the blood calcium will prevent coagulation

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49
Q

How does citrate work?

A

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

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50
Q

How is citrate eliminated?

A

removed by liver and polymerized into glucose or metabolized

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51
Q

What happens with the citrate if there is liver damage or mass blood transfusion?

A

citrate ion may not be removed quickly enough and this can greatly depress the level of calcium ion in the blood –> citrate toxicity

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52
Q

What is the mechanism of action of heparin?

A
  • binds to antithrombin (antithrombin III) and enhances 1,000 times the ability of antithrombin to inactivate a number of coagulation enzymes (thrombin, factors Xa, XII, XI, and IX)
  • neutralized thrombin prevents the conversion of fibrinogen to fibrin
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53
Q

Where does heparin come from?

A

bovine (cattle), porcine (pig), and endogenous

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54
Q

What clotting pathways does heparin block?

A

classic intrinsic and final common pathway

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55
Q

How is heparin prescribed?

A

units

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56
Q

How does the United States Pharmacopoeia (USP) define 1 unit of heparin?

A

amount of heparin that maintains the fluidity of 1 mL of citrated sheep plasma for 1 hour after re-calcification

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57
Q

How many units/mL must heparin contain?

A

120 UPS units/mL

58
Q

Why is heparin prescribed in units?

A

Commerical preparations vary in the number of USP units/mL

59
Q

Is heparin lipophilic or hydrophilic?

A

Hydrophilic, poor lipid solubility and large molecule

60
Q

Can heparin be given PO?

A

No, due to poor lipid solubility

61
Q

Is the dose-response relationship of heparin linear?

A

No
100 units/kg IV elimination 1/2 time was 56 minutes
400 units/kg IV elimination 1/2 time was 152 minutes

62
Q

What can prolong elimination 1/2 time of heparin?

A

Hypothermia

63
Q

How long does the action of heparin work?

A

1.5-4 hours

64
Q

How much does 100 units/kg (or 0.5-1 mg/kg) affect blood clotting time?

A

Increases from a normal 6 minutes to 30 or more minutes which occurs almost instantly

65
Q

How is injected heparin destroyed?

A

heparinase, an enzyme in the blood

66
Q

What are the tests used to monitor heparin?

A

aPTT

ACT

67
Q

What is the aPTT test?

A

activated plasma thromboplastin time

1.5-2.5 times pre-drug value (30-35 seconds)

68
Q

When would you check an ACT after the administration of heparin?

A
  • baseline before heparin
  • 3-5 mins post administration
  • 30 mins to 1 hour intervals post administration
69
Q

When would you want to use an ACT over a aPTT?

A

most widely used and is reliable for high heparin concentrations

70
Q

What can influence the results of an ACT?

A

hypothermia
thrombocytopenia
aprotinin
coagulation deficiencies

71
Q

What is the value for a normal/control ACT?

A

80-120 seconds

72
Q

Where would you want an ACT for CPB?

A

> 400-450 seconds

73
Q

Where would you want an ACT for interventional aneurysm clipping/coiling?

A

> 250 seconds

74
Q

How does an ACT test work?

A

mixes whole blood with activation substance (celite or kaolin) which initiates activation of the clotting cascade and counts the seconds until a clot is formed

75
Q

What is the commonly used LMWH?

A

Enoxaparin (Lovenox)

76
Q

What are the differences between Lovenox and unfractionated heparin?

A
  • Lovenox more expensive
  • Approximately 1/3 the size of heparin
  • Less protein binding than heparin and more bioavailability
  • Longer elimination 1/2 time = once daily dosing
77
Q

What are some advantages of giving Lovenox?

A
  • reduced dosing frequency and lack of need for monitoring
  • more predictable pharmacokinetic response
  • fewer effects on platelet function
  • reduced risk for HIT
78
Q

What is the MOA of lovenox?

A

binds to and accelerates antithrombin III, inhibits factors Xa and IIa (Xa>IIa)

79
Q

What does the inhibition of factor Xa cause with the administration of lovenox?

A

inhibits the conversion of prothrombin to thrombin and results in decreased thrombin activity and prevention of fibrin clot formation

80
Q

Which factors does protamine neutralize?

A

Neutralizes anti-factor IIa activity and has limited activity on Xa, cannot completely reverse Lovenox

81
Q

What is the dose for heparin when using it for DVT prophylaxis?

A

5,000 units SUBQ every 8-12 hours

82
Q

What is the dose for lovenox when using it for DVT prophylaxis?

A

30 mg SUBQ every 12 hours

83
Q

What is the treatment for DVT using hepain?

A

Bolus of 5,000 units IV followed by infusion to maintain aPTT 1.5-2.5

84
Q

What is a heparin bridge?

A

stopping coumadin 5-7 days prior to surgery and administering heparin until day of surgery, coumadin restarted on the evening of surgery and heparin restarted day after surgery and continued until INR is therapeutic

85
Q

What are some side effects of heparin?

A
  • hemorrhage/hematomas
  • thrombocytopenia (HIT)
  • allergic reaction
  • hypotension with large doses
  • altered protein binding - displaces alkaline drugs from protein-binding sites
  • chronic exposure can progress to reduction of antithrombin activity
86
Q

How can heparin produce the side effect of hypotension?

A

Occurs during large IV bolus of heparin during CPB that can cause modest decreases in MAP and PA pressures, thought to occur from decreased SVR resulting from direct heparin-induced relaxant effect on vascular smooth muscle

87
Q

What is important to remember regarding anticoagulant therapy and epidurals/catheter placement?

A

anticoagulants need to be stopped before catheter placed, once catheter in place ok to restart anticoagulants until catheter is to be D/C’d

88
Q

What is important to remember when administering heparin?

A

can come in different concentrations so always verify dose before administering

89
Q

What is Heparin Induced Thrombocytopenia (HIT)?

A

Heparin-dependent antibodies that agglutinate platelets and produce thrombocytopenia

90
Q

What platelet count indicates severe HIT?

A

count

91
Q

What platelet count indicates mild HIT?

A

count

92
Q

Which is more common, mild or severe HIT?

A

Mild, occurs in 30-40% of patients (severe occurs in 0.5-6%)

93
Q

What is antithrombin deficiency?

A
  • Resistance to heparin
  • No antithrombin present for heparin to bind to
  • Common in cardiac cases
  • Ex: gave 20,000 units of heparin in cardiac case but no changes seen in ACT
94
Q

What is the treatment for antithrombin deficiency?

A
  • 2-4 units FFP in adults

- antithrombin concentrate 1,000 units

95
Q

What can be used to reverse heparin?

A
  • Protamine
  • FFP
  • Prothrombin complex concentrate (PCC)
96
Q

What are the different procoagulants?

A 
*Protamine
Desmopressin (DDAVP)
FFP
Factor 7A
Phytonadione (Vitamin K)
Prothrombin complex concentrate
Tranexamic acid
Fibrinogen
Prothrombin
Aminocaproic acid (Amicar)
Conjugated estrogen (IV)
97
Q

What is the MOA of protamine?

A

it is a positively charged alkaline molecule that combines with the negatively charged acidic heparin to form a stable complex void of anticoagulant activity

98
Q

How is the heparin-protamine complex eliminated?

A

reticuloendothelial system

99
Q

What is the dose of protamine?

A
  • 1 mg for every 100 units of heparin given

- also guided by last ACT and estimated amount of heparin IV administered within the last 2 hours

100
Q

How should protamine be administered?

A

Should be administered slowly in a peripheral IV, if given too fast in a central line can cause histamine release resulting in pulmonary HTN and systemic hypotension

  • don’t exceed 50 mg in any 10 minute period
101
Q

Besides systemic hypotension and pulmonary HTN from fast infusion of protamine, what is another common adverse effect?

A

Allergic reaction

102
Q

What things can trigger an allergic reaction to protamine?

A
  • protamine containing insulin (NPH) (approximately 0.5 mg protamine per 100 units of NPH)
  • fish allergy (controversial)
  • vasectomies or infertile males (presence of circulating antisperm antibodies)
103
Q

How is protamine obtained?

A

simple protein principles obtained from the sperm of salmon and other species of fish

104
Q

Which patients are at the highest risk for a reaction to protamine?

A

if they had a prior reaction to protamine (189 fold)
allergy to fish (24.5 fold)
exposure to NPH insulin (8.2 fold)

105
Q

What is the MOA of coumadin?

A

competitively inhibits vitamin-K dependent coagulation proteins (factors II, VII, IX, and X)

106
Q

How is coumadin monitored?

A

PT/INR

107
Q

What is a goal INR for someone on Coumadin?

A

2.0-3.0

108
Q

Is Coumadin safe to use in a parturient?

A

No, crosses placenta and severely teratogenic

109
Q

What is the onset of Coumadin?

A

3-4 days, effects are seen on 8-12 hours due to depletion of factor VII however full clinical effects are not appreciated for several days

110
Q

What is the duration of a single dose of Coumadin?

A

2-4 days

111
Q

What is the half-life of Coumadin?

A

40 hours

112
Q

What is the International Normalized Ratio (INR)?

A

Used to monitor Coumadin, compares ratio of patient’s PT to control PT with calculations done to determine a ratio to one decimal place, no units

113
Q

What conditions would require a slightly higher INR of 2.5-3.5?

A
  • Mechanical heart valve
  • Prevention of recurrent MI
  • History of VTE with INR 2-3
114
Q

For a patient having minor surgery, when should they stop Coumadin?

A

stop 1-5 days preop for PT 20% within baseline

115
Q

For immediate surgery within 24-48 hrs of someone taking Coumadin, what should be done to bring PT down to normal range?

A

IV vitamin K (10-20 mg PO or 1-5 mg IV at rate of 1 mg/min)

PT to normal range within 4-24 hours

116
Q

For emergency surgery on someone taking Coumadin, what should be given to normalize PT?

A

FFP or PCC

117
Q

How do antiplatelet drugs work?

A

suppresses platelet function (inhibits platelet aggregation)

Ex: ASA, plavix, NSAIDS

118
Q

What is the MOA of aspirin?

A

exerts antithrombotic effects by inhibiting platelet aggregation, biochemical mechanism accounting for this action is irreversible inhibition of COX-1 by the acetyl group of ASA that causes acetylation of cyclooxygenase

Inhibition of COX prevents conversion of arachidonic acid to thromboxane A2 (key factor in platelet activation and thrombus formations)

119
Q

How long do the effects of ASA last?

A

effects are irreversible and last the life of the platelet

120
Q

What is the primary prophylaxis dose of ASA?

A

81 mg

121
Q

What is ASA primary prophylaxis?

A

treatment with ASA in the absence of an established diagnosis of cardiovascular disease

122
Q

What is ASA secondary prophylaxis?

A

treatment with ASA in the presence of overt CV disease or conditions conferring particular risk
Ex: afib, angina, previous MI, stroke, CHF, CABG, PCI, vascular surgery, DM, noncardiac stents, renal insufficiency

123
Q

Should primary prophylaxis be continued until day of surgery?

A

Should be continued but can be held for a few days at the discretion of the surgeon or procedural physician due to a possible heightened risk for perioperative bleeding

124
Q

Should secondary ASA prophylaxis be continued until day of surgery?

A

Should be continued until day of surgery except for intracranial neurosurgical procedures, intramedullary spine surgery, surgery of the middle ear or posterior eye, and prostate

125
Q

What is the MOA of plavix?

A

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

126
Q

How is Plavix metabolized and why is this important?

A

metabolized by CYP450 and must be metabolized to produce active metabolite

127
Q

What are some indications for Plavix?

A
  • secondary prevention of MI, CVA
  • coronary artery stenting
  • acute coronary syndrome
  • peripheral artery disease
  • PCI
128
Q

How long should elective surgical procedures be delayed after DES placement?

A

at least 6 months but ideally 12 months

129
Q

What is the MOA of NSAIDS?

A

reversibly depress thromboxane A2 production by platelets

130
Q

How do thrombolytics work>?

A

Possess inherent fibrinolytic effects or enhances body’s fibrinolytic system

131
Q

What is the primary reason to use a thrombolytic?

A

restore circulation through a previously occluded vessel

  • STEMI
  • Acute ischemic stroke
  • Acute massive PE
132
Q

What are the contraindications to thrombolytics?

A

trauma
severe HTN
active bleeding
pregnancy

133
Q

What is the window of time you are able to administer thrombolytics?

A

6 hours within initial onset of clot symptoms

134
Q

What is the MOA of t-PA?

A

converts plasminogen to plasmin which breaks down fibrin

135
Q

How can t-PA be administered?

A

can be given systemically or directly into emboism

136
Q

What is the 1/2 life of t-PA?

A

about 5 mins, usually administered as bolus followed by infusion

137
Q

What are some adverse effects of thrombolytics?

A

bleeding

re-thrombosis (anticoagulants such as heparin are usually co-administered and continued after thrombolytic therapy)

138
Q

What does the efficacy of thrombolytics depend on?

A

the age of the clot, older clots have more cross-linking and are more compacted which makes them more difficult to dissolve

139
Q

What is the MOA of direct thrombin inhibitors?

A

act as anticoagulants by directly inhibiting the enzyme thrombin (factor II)

140
Q

What makes direct thrombin inhibitors different than anticoagulants such as heparin?

A

does not require cofactor such as antithrombin

141
Q

How do bivalent DTIs work?

A

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

142
Q

How do univalent DTIs work?

A

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

Pharmacology 514 (7 decks)

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