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Block 7 Week 4 > Anticoagulants, Antiplatelets, and Thrombolytics- leblanc > Flashcards

Anticoagulants, Antiplatelets, and Thrombolytics- leblanc Flashcards

1
Q

What are some anticoagulants?

A
  • Unfractionated or high molecular weight heparin
  • low molecular weight heparins
  • factor IIa and Xa inhibitors
  • Warfarin (coumadin)
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2
Q

What is a procoagulant?

A

desmopressin acetate

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3
Q

What are some antiplatelet drugs?

A 
Acetylsalicylic acid (aspirin)
Clopidogrel bisulfate (Plavix)
Abciximab (ReoPro)
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4
Q

What are some thrombolytic agents?

A

Tissue plasminogen activator (t-PA)

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5
Q

What are some antagonists?

A

Protamine sulfate

Aminocaproic acid

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6
Q

T or F

under normal physiological conditions, little or no intravascular coagulation occurs

A

T

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7
Q

Why don’t you have intravascular coagulation under normal physiological conditions?

A
  • Dilution
  • Presence of plasma inhibitors
  • activated clotting factors are rapidly removed by the liver
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8
Q

When vascular damage occurs, several physiologic reactions participate to contrl blood loss?

A 
Platelet adhesion reaction
Platelet activation
Platelet aggregation
Formation of a clot (coagulatio)
Fibrinolysis
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9
Q

What are the three major risk factors for thromboembolism?

A
  • abnormalities of blood flow
  • abnormalities of surfaces in contact with blood
  • abnormalities of clotting components
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10
Q

How do you get vasoconstriction or vasospasm in hemostasis?

A

thomboxane A2 (TA2) and serotonin (5-HT) released by platelets which triggers powerful constrictions stimulating the contraction of smooth muscle cells within the walls of blood vessels

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11
Q

What is this:
coagulation occurs due to trauma originating from the extra-vascular space (formation of a macromolecular complex involving thromboplastin or tissue factor, and factor VII); the most important in vivo.

A

Extrinsic Pathway

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12
Q

What is this:

coagulation is triggered by trauma to the blood itself (from large glycoprotein complexes released by platelets)

A

Intrinisic pathway

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13
Q

What does t-PA and urokinase do?

A

upregulated plasmin to degrade blood clots (degrades fibrin, fibrinogen)

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14
Q

So tell me what happens if you have a damaged vessel wall?

A

platelet adhesion and initiation of coagulation

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15
Q

If you get platelet adhesion and thrombin what happens next?

A

you get release of mediators which will cause platelet aggregtes and fibrin

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16
Q

What will platelet aggregates and fibrin cause?

A

a thrombus

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17
Q

What will a thrombus induce?

A

fibrinolysis which will degrade products

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18
Q

What three major categories of anticoagulant drugs?

A

Direct acting anticoagulants
Indirect acting anticoagulants
Antiplatelet agents

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19
Q

What are some examples of direct acting anticoagulants?

A

Calcium Chelators (useful for in vitro testing; sodium citrate, EDTA)
Heparin (unfractionated and low molecular weight fractions)
Factor IIa and Xa inhibitors

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20
Q

What is an example of an indirect acting anticoagulants?

A

warfarin (coumadin)

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21
Q

What is an example of an antiplatelet agent?

A

aspirin, plavix

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22
Q

What are the clinical tests for assessing antiplatelet, anticoagulant and thrombolytic therapies?

A

Bleeding time
platelet count (normal: 150,000-400,000)
Pro-thrombin time (PT)

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23
Q

What does pro-thrombin time tell you?

A

reflects alterations in the extrinsic pathway

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24
Q

What is a normal pro-thrombin time?

A

12 seconds

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25
Q

What does INR stand for and what does it tell you?

A

International normalized ratio

-> used to normalize PT

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26
Q

What is the desired therapeutic INR?

A

2 and 3 (human thromboplastin)

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27
Q

(blank) is an enzyme released from damaged cells, especially platelets, that converts prothrombin to thrombin during the early stages of blood coagulation

A

thromboplastin

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28
Q

What test will reflect the intrinsic pathway?

A

aPTT (activated partial thromboplastin time)

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29
Q

What is the normal aPTT?

A

24 to 34 seconds

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30
Q

How do you test for abnormalities in fibrinogen?

A

immunological tests

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31
Q

What test will detect simple deficiencies of a factor or the presence of a clotting inhibitor?

A

Mixing studies

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32
Q

(blank) is an anionic mixture of linear mucopolysaccharide molecules with molecular weights in the range of 3,000 to 30,000

A

Heparin

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33
Q

(blank) is prepared from bovine lung and porcine intestinal mucosa

A

Commercial heparin

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34
Q

What does heparin do?

A

inhibits blood coagulation by forming complexes with an a2 globin and each of the activated proteases of the coagulation cascade.

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35
Q

After formation of the heparin-antithrombin III-coagulation factor, what happens to heparin?

A

it is released and becomes available again to bind to gree ATIII

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36
Q

What does heparin bind to and upregulate and why?

A

antithrombin III to form a complex that will inhibit Kallikrein, XIIa, XIa, IXa, Xa, thrombin)

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37
Q

Heparin blocks conversion of (blank) to (blank) and thus inhibits the synthesis of fibrin from fibrinogen

A

prothrombin to thrombin

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38
Q

What factors does heparin inhibit?

A

factors Xa and thrombin (IIa) and factors IXa and XIa

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39
Q

At low doses heparin primarily neutralizes factor (blank). At high doses, it prevents the thrombin-induced activation of platelets, and activation factors (bank) and (blank)

A

XA

V and VIII

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40
Q

What inhibits platelet function and increases vascular permeability?

A

Heparin

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41
Q

What factors are vit K dependent?

A

2,7,9,10 and proteins C and S

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42
Q

What is super scary about heparin?

A

some people have a fucked up reaction to it called HIT which induces a hypercoagulable state! (heparin induced thrombocytopenia)

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43
Q

What is HIT?

A

You get IgG antibodies to heparin when it is bound to platelet factor 4 inducing a hypercoagauable state

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44
Q

T or F

Heparin is not effective after oral administration

A

T

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45
Q

How should you give heparin?

A

intravenous infusion or deep sub-cutaneous injections (may take 2-4 hours to reach therapeutic plasma levels)

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46
Q

Why shouldnt you give heparin via intramuscular injections?

A

due to the formation of hematomas

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47
Q

What happens if you give heparin to a pregnant mother or one who is breastfeeding?

A

nothing cuz heparin does not cross the placenta and does not pass into maternal milk

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48
Q

Heparin is (blank) dependent

A

dose-> half life depends on the dose administered

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49
Q

What is the half life of heparin at 100?
400?
800?

A

1 hour
2.5 hours
5 hours

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50
Q

When should you not give heparin?

A

any situation where active bleeding must be avoided (ulcerative lesions, intracranial hemorrhage, brain or spinal cord surgery)

  • Patients with thrombocytopenia, or prior history of HIT
  • patients susceptible to severe allergies; heparin is extracted from animal sources
  • severe hypertension
  • older patients (especially women)
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51
Q

What do you give a patient if they are overdosing on heparin?

A
  • simple withdrawal

- protamine sulfate (PS): highly basic peptide that binds heparin and thus neutralizes its effect

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52
Q

What is the dosage of protamine sulfate (PS)?

A

1 mg of PS for every 100 units of heparin (not to exceed 50 mg for any 10 min period)

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53
Q

What testing should you give following heparin treatment

A 
-aPTTT 1.5 to 2.5 times normal 
(normal ~24-34 seconds)
-antifactor Xa heparin activity assay (0.3-0.7 units/ml)
-hematocrit (Hct)
-platelet count
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54
Q

How often should you give antifactor Xa heparin activity assay?

A

6 hour intervals after initiation of heparin infusion until stabilization, then once daily

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55
Q

What are the four low molecular weight forms of heparin (LMWH)?

A

Dalteparin sodium (fragmin)
Tinzaparin Sodium (innohep)
Enoxaparin (lovenox)
Fondaparinux (arixtra)

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56
Q

LMWH selectively accelerates interactions of antithrombin with (blank)

A

factor Xa

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57
Q

Unfractionated heparin accelerates interaction of antithrombin with (blank) and (blank)

A

thrombin

Factor Xa

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58
Q

Both LMWH and UFH have equal efficacy.

T or F

A

T

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59
Q

Which has a more predictable outcome and a longer half-life than the other (2x the half-life); UFH or LMWH?

60
Q

Which is better LMWH or UFH?

A

LMWH because it has less frequent bleeding and you can dose it less frequently AND has increased bioavailability from site of injection.
(LMWH 90%, UFH 20%)

61
Q

What are the clinical indications for UFH or LMWH therapy?

A
  • blood transfusions
  • atrial fibrillation
  • disseminated intravascular coagulation (DIC)
  • open heart surgery
  • pulmonary embolism
  • venous thromboembolism
  • venous catheter occlusion
62
Q

What factor is thrombin?

63
Q

What is this:
a recombinant 65-AA polypeptide derivative of hirudin, the natural anticoagulant isolated from the salivary gland of medicinal leech.

A

Lepirudin (refludan)-> a thrombin inhibitor

64
Q

How do thrombin inhibitors work?

A

block the enzyme by binding to the catalytic site

65
Q

What is this:

a synthetic 20 amino acid polypeptide inhibitor with similar activity to lepirudin

A

Bivalirudin (angiomax)-> a thrombin inhibitor

66
Q

What is this: synthetic compound based on the structure of L-arginine

A

Argatroban-> a thrombin inhibitor

67
Q

How do you give the thrombin inhibitors (argatroban, bivalirudin, lepirudin)?

A

IV infusion

68
Q

What are the clinical indications for thrombin inhibitors?

A

Patients susceptible to developing HIT

Coronary angioplasty or coronary bypass surgery

69
Q

What is the first orally active factor IIa inhibitor approved by the FDA?

A

Dabigatran Etexilate (pradaxa/ pradax)

70
Q

What is the drug company name for lepirudin?

71
Q

What is the drug company name for bivalirudin?

72
Q

What are the clinical indications for Pradaxa/pradax?

A
  • thromboembolic disorders

- prophylactic anticoagulant used to minimize the risk of stroke in pnts with non-valvular a fib.

73
Q

What are the Factor Xa inhibitors?

A

Rivaroxaban (Xarelto)

Apixaban (Eliquis)

74
Q

What is Rivaroxaban (Xarelto)?

A

an oral anticoagulant that is a factor Xa inhibitor.

75
Q

What are the clinical indications for Rivaroxaban (xarelto)?

A 
DVT: treatment and secondary prophylaxis
Hip or knee surgery as prophylactic agent
Non-vascular A Fib
cerebrovascular accident
PE
76
Q

What are the clinical indications for Apixaban (eliquis)?

A

Non-valvular A fib.

CV accidents

77
Q

What is the most common oral anticoagulant?

A

Warfarin (coumadin)

78
Q

When does coumadin (warfarin) start to work?

A

only works in vivo after a latent period of 12 to 24 hours

79
Q

How does coumadin (warfarin) work?

A

it is a structural analogue of vit K and depletes vit K so that the vit K dependent clotting factors cant work

80
Q

Warfarin is a racemic mixture of two (blank)

A

enantiomers (R and S forms)

81
Q

What are the vit k dependent clotting factors that warfarin inhibits?

A

VII, IX, X and prothrombin (II)

82
Q

What does Vit K do for certain clotting factors?

A

Post-ribosomal carboxylation of specific glutamic acid residues. These AA residues chelates Ca2+

83
Q

Warfarin down-regulates (blank)

84
Q

What does protein c do?

A

when bound to thrombomodulin in endothelial cells, alters the specificity of thrombin and favors the degredation of factors Va and VIIIa into inactive proteases.

85
Q

What is this:

These proteins are naturally occuring anticoagulants

A

Protein C and Protein S

86
Q

What explains the procoagulant activity of warfarin observed in the early stage of therapy?

A

well warfarin down regulates protein C which is an natural anticoagulant therefore you get some coagulation :(

87
Q

What is the half-life of factor VII?

88
Q

What is the half life of Factor IX?

89
Q

What is the half life of factor X?

90
Q

What is the half life of prothrombin?

91
Q

Warfarin is largely bound to (blank) and is metablized by the (Blank) into inactive metabolites which are then excreted into the urine

A

albumin (>98%)

liver by cytochrome p450

92
Q

How do you monitor warfarin?

A

with PT (prothrombin time) and INR

93
Q

How do you treat warfarin overdose?

A
  • withdrawal of drug
  • give vit K (24 hour delay) supplementation
  • transfusion of whole blood or plasma (major bleeding)
94
Q

What are the contraindications for warfarin?

A

Conditions where active bleeding must be avoided, Vitamin K deficiency and severe hepatic or renal disease, where intensive salicylate therapy is required, and in pregnant women

95
Q

Why can you not give warfarin to pregnant women or breast feeding women?

A

Coumadin anticoagulants pass the placental barrier and may lead to abortion and birth defects
AND
Newborn infants are have low vit K so they are more susceptible to oral anticoags and have lower rates of metabolisms

96
Q

What will diminish the response to warfarin?

A
  • inhibition of drug absorption
  • induction of hepatic microsomal enzymes
  • stimulation of the synthesis of clotting factors
97
Q

What will increase the response to warfarin?

A
  • displacement of anticoagulant from plasma proteins
  • inhibition of hepatic microsomal enzymes
  • reduction in availability of vit K
  • inhibition of synthesis of clotting factors
  • decreased platelet aggregation (e.g. aspirin)
98
Q

What is a drug that inhibits drug absorption?

A

cholestyramine

99
Q

(blank) is a synthetic analogue of the pituitary antiduiretic hormone (ADH)

A

desmopressin acetate

100
Q

What does desmopressin acetate do?

A

stimulates the activity of coag factor VIII (8)

101
Q

What do you use desmopressin for?

A

hemophilia A with factor 8 levels equal or greater than 5% OR in clients who have factor 8 antibodies.
In treatment of classic von willebrands disease (type I) and when abnormal molecular form of factor 8 antigen is present

102
Q

What does acetylsalicicylic acid do?

A

inhibits release of ADP by platelets and their aggregation

103
Q

What is the MOA of acetylsalicycic acid (aspirin)?

A

acetylates the COX enzyme of platelets so that it can no longer create thromboxane which induces platelet aggregation and vasoconstriction

104
Q

A (blank) dose (160-320 mg) may be more effective at inhibiting thromboxane A2 than PGI2

105
Q

THe effect of aspirin is (blank)

A

irreversibe

106
Q

Why is aspirin used in CV stuff?

A

not known to prevent primary MI but known to be beneficial in patients with history of vascular events (secondary)

107
Q

(blank) represents an alternative antiplatelet drug for treatment of recurrent stroke in patients intolerant to aspirin

A

Ticlopidine (Ticlid)

108
Q

What is the MOA of ticlopidine (ticlid)?

A

Inhibits response of ADP on its platelet receptor and thus prevents aggregation of platelets - > impairs GPIIb/IIIa receptor

109
Q

How does clopidogrel bisulfate (plavix) work?

A

same was as triclopidine, impairs GPIIb/IIIa receptor thus inhibits platelet aggregation

110
Q

Why is clipidogrel bisulfate (plavex) better than ticlid?

A

has less side effects

111
Q

What is this:

chimeric monoclonal antibody inhibitor of platelet glycoprotein IIb/IIIaa

A

Abciximab (reopro)

112
Q

What does abciximab prevent?

A

prevents binding of fibrinogen and von willebrand factor and prevents platelet aggregation.

113
Q

What is the primary use of abciximab (reopro)?

A

acute coronary syndromes and percutaneous coronary intervention

114
Q

The fibrinoytic system dissolves intravascular clots as a result of the action of (blank)

115
Q

What does plasmin do?

A

digests fibrin

116
Q

How do you get plasminogen to become plasmin?

A

via cleavage of peptide bond

117
Q

(blank) is a relatively non-specific protease, which digests fibrin clots and other plasma proteins, including several coagulation factors.

118
Q

Therapy with (blank) drugs tend to dissolve pathological thrombi and also fibrin deposits at sites of vascular injury.

A

Thrombolytic drugs

119
Q

What is a worry about using thrombolytic agents?

A

hemorrhage as a major side effect

120
Q

Thrombolytic therapy is indicated in patients with extensive (blank), (blank) and (blank)

A

pulmonary emboli

severe iliofemoral thrombophlebitis and acute coronary occlusion

121
Q

(blank) is released from endothelial cells in response to various signals, including stasis produced by vascular occlusion.

A

tissue plasminogen activator (t-PA)

122
Q

(blank) binds to fibrin and converts plasminogen to plasmin

A

t-PA (tissue plasminogen activator)

123
Q

Free plasmin is rapidly inhibited in the plasma by an a2-antiplasmin. (blank-bound) plasmin is protected from inhibition

124
Q

t-PA (activase) is a (blank) protease

125
Q

T-PA (activase) is a (good/poor) plasminogen activator in the absence of fibrin

126
Q

t-PA binds to (blank) and activates bound plasminogen several hundred-fold more rapidly than it activates Plasminogen in the circulation.

127
Q

(blank) is a protein produced by beta-hemolytic streptococci

A

streptokinase

128
Q

How does streptokinase (streptase) work?

A

forms non-covalent complex with plasminogen -> induces conformational change that exposes active site on plasminogen that cleaves a peptide bond on free plasminogen molecules to form free plasmin

129
Q

Does streptokinase (streptase) have intrinisc enzymatic activity?

130
Q

What are the 2 thrombolytic agents?

A

Tissue plasminogen activator (t-PA, Activase)

Streptokinase (streptase)

131
Q

You should NOT give thrombolytic therapy to someone who has had surgery within the last (blank) days. What kinds of surgeries does this include?

A

10

organ biopsy, puncture of non-compressible vessles, serious trauma, cardiopulmonary resuscitation

132
Q

You should NOT give thrombolytic therapy to someone who has serious (Blank) bleeding within the last 3 months

133
Q

You should NOT give thrombolytic agents to anyone with a history of (blank)

A

hypertension-> diastolic pressure greater than 110 mm Hg

134
Q

You should not give thrombolytic agents to anyone with active bleeding or hemorrhagic disorders and patients with previous (blnak) or (blank)

A

cerebrovascular accident

active intracranial bleeding

135
Q

(blank) prevents the binding of plasminogen and plasmin to fibrin. So what does it do?

A

Aminocaproic acid

inhibits fibrinolysis

136
Q

When do you use aminocaproic acid?

A

can reverse states that are associated with excessive fibrinolysis

137
Q

What signs and symptoms demonstrated by D.P. are consistent with DVT?

A
  • unilateral leg swelling accompanied by local tenderness and pain
  • discoloration of the affected limb
  • arterial spasm, cyanosis from obstruction or reddish color from perivascuar inflammation
138
Q

How do you test for DVT?

A
  • l-fibrinogen scanning
  • D-dimer test (detects fibrin breakdown product D-dimer)
  • Impedance plethysmography (pneumatic cuffs for detection of blood volume changes)
  • doppler ultrasonography
139
Q

What is the standardized dosing regimen for heparin?

A

5,000 U IV to be followed by a continuous infusion of 1,000 U/hr

140
Q

What is the loading dose for heparin?

A

70-100 U/kg

141
Q

What is the maintenance dose for heparin?

A

15-25 U/kg/hr

142
Q

When can you give a aPTT?

A

6 hours after loading dose

143
Q

What is the correct dose for therapeutic heparin level?

A

1.5-2.5 times that of normal range (24 to 34 sec is normal)

144
Q

How do you monitor heparin

A

check aPTT every 6 hours after loading dose, and 6 hours after any change in infusion rate
-> if dosing is stable, aPTT should be evauated once daily, along with Hct and platelet count (1 to 2 days)

145
Q

How long should heparin therapy be maintained?

A

traditionally 7-10 days

Warfarin initiated around day 5 (3 to 6 months)

146
Q

Which drug has the latent period, heparin or warfarin?

A

warfarin!!!

Block 7 Week 4 (7 decks)

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