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IBI Test 4 > B3.087 - Anticoagulant Therapies COPY > Flashcards

B3.087 - Anticoagulant Therapies COPY Flashcards

1
Q

why do clots form

A
  1. turbulence in blood flow
  2. abnormalities of surface in contact with blood
  3. abnormalities in clotting factors
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2
Q

what are conditions with abnormal clotting factors

A

Protein C deficiency
Protein S deficiency
Antithrombin III deficiency
antiphospholipid antibody syndrome

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3
Q

what are the general classes of drugs that treat hemostasis disorders

A

platelet inhibitors
anticoagulants
thrombolytic drugs
Drugs for bleeding disorders

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4
Q

what do TxA2 and ADP do in primary hemostasis

A

platelet granule release reaction

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5
Q

what are the antiplatelet drugs

A 
Abciximab
Tirofiban
Aspririn 
Ticlopidine
Clopidogrel
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6
Q

what is acetylsalicylic acid

A

aspirin

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7
Q

what does aspirin do

A

inhibits synthesis of thromboxane A2 by irreversible acetylation of cyclooxygenase COX 1 in platelets

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8
Q

what does thromboxane A2 do

A

potent mediator of platelet aggregation and degranulation and promotes vasoconstriction

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9
Q

what is aspirin used for

A

prevents and reduces risk of MI and recurring transient ischemic attacks

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10
Q

how does aspirin work

A

irreversibly inactivates COX-1; TXA2 end product causes platelet activation and vasoconstriction which is prevented here

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11
Q

what does COX2 do

A

is in endothelial cells and is inhibited by aspirin and by COX 2 inhibitors; PGI2 causes platelet inhibition and vasodilation

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12
Q

when do you see effects of aspirin

A

1-2 days after administration and lasts the duration of the platelet life span (7-10 days)

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13
Q

why does wiping out the COX1 affect platelets more than other cell types

A

they have no nucleus so they cant make new proteins in response, so the effects are seen until the platelets die and are replaced

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14
Q

what type of drug is ticlopidine and how does it work

A

ADP antagonist, inhibits ADP receptors on platelets which prevents activation of GPIIb-IIIa

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15
Q

what is ticlopidine indicated for

A

alternative to aspirin to prevent an initial or recurrent thromboembolic stroke and MI thromboembolic stroke

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16
Q

how is ticlopidine administered

A

orally, bioavailability 80%

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17
Q

adverse effects of ticlopidine

A

nausea, dyspepsia, diarrhea in 20% of patients, hemorrhage in 5%

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18
Q

what is ticlopidine associated with (AEs that are more severe)

A

TTP (thrombotic thrombocytopenia purpura)

Severe bone marrow toxicity

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19
Q

what does clopidogrel do

A

similar mechanism to ticlopidine (ADP antagonist) but lower incidence of adverse effects

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20
Q

what is clopidogrel used for

A

patients with a history of recent stroke, MI or established peripheral vascular disease, pts with stents

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21
Q

what is an important AE of clopidogrel

A

many drug drug interactions because requires activation by CYP2C9

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22
Q

what are other drugs metabolized by 2C9 and what drug can cause interactions with these

A 
Clopidogrel causes interactions
Fluvastatin
NSAIDs
Phenytoin
tamoxifen
tolbutmide
warfarin
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23
Q

when would ticlodipine be preferred over clopidogrel

A

if drug drug interactions are difficult to manage

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24
Q

where is clopidogrel metabolized

A

liver

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25
Q

how does abciximab work

A

inhibits platelet aggregation by preventing binding of fibrinogen to glycoprotein receptor IIb/IIIa on activated platelets

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26
Q

how is abciximab administered

A

IV to high risk pts undergoing coronary angioplasty and pts undergoing angioplasty, atherectomy and stent placement often with clopidogrel

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27
Q

downsides to Abciximab including AEs

A

Expensive

Bleeding most common AE

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28
Q

what does Tirofiban do

A

small molecule that with short half life that works similar to Abciximab, has to be continually infused bc of short half life

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29
Q

How does dipyridamole work

A

inhibits phosphodiesterase which leads to increased cAMP levels, inhibiting platelet activation

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30
Q

what does phosphodiesterase do normally

A

breaks down cAMP

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31
Q

what effects does dipyridamole do

A

coronary vasodilator that also inhibits platelet aggregation

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32
Q

what is dipyridamole used for

A

in combo with warfarin, inhibits embolism from prosthetic heart valves (main use)`

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33
Q

what is dipyridamole combined with aspirin to treat

A

patients with thrombotic disease, reduces thrombosis

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34
Q

what do calcium chelators do

A

inhibit blood coagulation in vitro

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35
Q

what do heparins do

A

accelerate the action of antithrombin III to neutralize thrombin and other coagulation factors

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36
Q

what do rudins do

A

direct thrombin inhibitors

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37
Q

what do coumarin derivatives do

A

interfere with the hepatic synthesis of functional vitamin K dependent clotting factors

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38
Q

what are calcium chelators used for and why cant you use them in the body

A

for lab draws to prevent coagulation

cant use them in the body because calcium is used on so many function

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39
Q

structure of standard heparin

A

sulfated mucopolysaccharide (acidic molecule)

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40
Q

route of admin for standard heparin

A

NOT ORAL OR IM

infusion pump or intermittent Subcutaneous

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41
Q

onset of action of standard heparin

A

immediate

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42
Q

mechanism of action of standard heparin

A

heparin binds to antithrombin III and stimulates complex formation with antithrombin III
Main mech is heparin-antithrombin III complex inactivates factor IIa (thrombin) and Xa

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43
Q

heparin AEs

A

endothelial cell/protein binding

Clearance is dose dependent

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44
Q

therapeutic goal of standard heparin

A

prolong PTT to 1.5-2.5x normal

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45
Q

contraindications of standard heparin

A

bleeding disorders, hemorrhage

liver, kidney disease, HT, certain infections

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46
Q

indications of standard heparin

A

preferable to other anticoagulants during pregnancy due to lack of placental transfer

47
Q

how does the indication of heparin differ from warfarin

A

preferable during pregnancy due to lack of placental transfer

48
Q

AEs of standard heparin

A

bleeding/hemorrhage
allergic reaction
osteoperosis
HIT (heparin induced thrombocytopenia)

49
Q

what is type I HIT

A

transient and rapidly reversible heparin induced thrombocytopenia
Abs generated against platelets –> decrease in platelet count

50
Q

what is type II HIT

A

severe heparin induced thrombocytopenia
Ab decrease platelet count
Ab also activate platelets–>thormboembolism which may be life threatening

51
Q

standard heparin antidote

A

protamine sulfate

52
Q

what does protamine sulfate do

A

antidote to heparin, binds to heparin (anion/cation interaction)

53
Q

why must excessive protamine sulfate be avoided when used as a heparin antidote

A

its an anticoagulant

54
Q

what is a disadvantage of LMWH (low molecular weight heparin)

A

protamine sulfate is less capable of reversing its effects

55
Q

what are the LMWHs

A

Enoxaparin
Dalteparin
Tinzaparin

56
Q

what are LMWHs used for

A 
less sticky than bigger molecules so not as dose dependent
more convenient (sub q, dont have to check PTT as much)
57
Q

how do you monitor LMWH

A

an anti-Xa activity assay

58
Q

how does fondaparinux work

A

it exerts antithrombotic activity as a result of ATIII-mediated selective inhibition of factor Xa

59
Q

what is the half life of fondaparinux

A

18 hours, allows once daily dosing, given subc

60
Q

warfarin is a derivative of what

A

coumarin

61
Q

what does the nature of warfarin plasma protein binding mean for its distribution

A

it has extensive binding which accounts for low volume of distribution, long half life

62
Q

describe metabolism of warfarin

A

metabolized by liver by CYP2C9, site of numerous drug interactions

63
Q

which has activity in vitro heparin or warfarin?

A

heparin

64
Q

describe the route of heparin and warfarin

A

heparin - parenteral

warfarin - oral

65
Q

onset of heparin v warfarin

A

heparin - immediate

warfarin - 1-3 days

66
Q

how do you monitor heparin

A

PTT

67
Q

how do you monitor warfarin

A

PT (INR)

68
Q

where are the rudins derived from

A

leeches

69
Q

who is lepirudin approved for

A

its a recombinant yeast driven form of hirudin patients with HIT

70
Q

what can argatroban be used for

A

its a rudin that is approved for HIT patients and cleared by liver so can be used in pts with end stage renal disease

71
Q

how do rudins work

A

direct thrombin inhibitors

72
Q

what is the main rudin

A

hirudin (thrombin inhibitor)

73
Q

what are the oral direct thrombin inhibitors

A

Dabigatran etexilate

Rivaroxaban

74
Q

what is a problem with the oran direct thrombin inhibitors

A

theres not a way to reverse their effects

75
Q

what is apixaban

A

FXa inhibitor

76
Q

what is praxbind

A

the first reversal agent for the oral anticoagulants

77
Q

how does praxbind work

A

binds and sequesters dabigatran and dabigatran glucuronides

78
Q

what do thrombolytics do

A

activate plasminogen to be converted to plasmin which degrades fibrin and lyses thrombi

79
Q

why cant you use plasmin for thrombolytic therapy?

A

circulating antiplasmins

80
Q

how is urokinase used as a thrombolytic

A

its made in the kidney and plasma doesnt have inhibitors to it but it can break down clots

81
Q

how does streptokinase work

A

facilitates thrombolysis through formation of activator complex with plasminogen results in formation of plasmin

82
Q

what is a major AE of streptokinase

A

hypersensitivity

83
Q

what are the recombinant thrombolytics

A

Alteplase
Reteplase
Tenecteplase, TNK-t-PA

84
Q

what is Alteplase

A

Biosynthetic recombinant form of human tissue plasminogen activator

85
Q

what is Reteplase

A

recombinant plasminogen activator

86
Q

what is tenecteplase

A

modified human t-PA, prolonged half life compared to alteplase

87
Q

when do you use thrombolytic agenst

A

when you already have a clot

88
Q

how do you rule out intracranial bleeding and why is it important

A

CT scan, because you need to be sure its a clot not a bleeding episode

89
Q

thrombolytic therapy should be followed with what

A

anticoagulant therapy with heparin and then warfarin

90
Q

contraindication of thrombolytics

A

surger, GI bleeidng, hx of hypertension

91
Q

what is vitamin K used for

A

gamma carboxylation of glutamate residues in PT factors VII, 9, 10

92
Q

how fast does vitamin K restore clotting function

A

days

93
Q

if you need clotting function faster than vitamin K can provide what can you do

A

plasma fractions/clotting factors

recombinant factors

94
Q

what discourages the use of plasma fractions in treatments of patients with hemophilia

A

AIDS and viral hepatitis

95
Q

what is aminocaproic acid

A

fibrinolytic inhibitor

96
Q

what isomoer is the most active of warfarin

A

S isomer

97
Q

describe distribution of warfarin

A

extensive plasma protein binding accounts for low volume of distribution and a long half life

98
Q

how is warfarin metabolized

A

CTP2C9, site of numerous drug interactions

99
Q

target of warfarin

A

vitamin K epoxide reductase

100
Q

speed of onset of warfarin

A

slow, t1/2 is 1.5 days

101
Q

antidote to warfarin

A

large doses of vitamin K and fresh frozen plasma

102
Q

drugs that diminish warfarin absorption

A

cholestyramine (also affects Vit K absorption)

103
Q

what drugs can interfere with hepatic microsomal enzymes needed for warfarin metabolism

A 
antoconvulsants
Barbiturates
carbamazepine
phenytoin
primidone
rifampin
St. Johns Wort
104
Q

what hormone can interfere with warfarin from stimulation of clotting factor synthesis

A

estrogens

105
Q

which drugs inhibit anticoagulant mechanism (warfarin) and are selective for S warfarin

A

Metronidazole

fluconazole

106
Q

therapeutic goal of warfarin

A

prolonged PT time

107
Q

what is an important factor to consider when prescribing warfarin in women

A

its a teratogen

contraindicated in pregnancy (category X)

108
Q

compare and contrast heparin and warfarins mechanism

A

heparin - accelerates action of ATIII to neutralize thrombin

Warfarin - decreases vit K dependent clotting factors

109
Q

compare and contrast heparin and warfarin route of admin

A

heparin - PE

warfarin - oral

110
Q

compare and contrast heparin and warfarin onset

A

heparin - immediate

warfarin - gradual (1-3 days)

111
Q

compare and contrast heparin and warfarin duration

A

heparin - 4 hours

warfarin - 2-5 days

112
Q

compare and contrast heparin and warfarin monitoring tests

A

heparin - PTT

warfarin - PT (INR)

113
Q

compare and contrast heparin and warfarin treatment of overdose

A

heparin - protamine sulfate

warfarin - vit k; fresh frozen plasma

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