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

B3.087 - Anticoagulant Therapies Flashcards

(113 cards)

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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
how does abciximab work
inhibits platelet aggregation by preventing binding of fibrinogen to glycoprotein receptor IIb/IIIa on activated platelets
26
how is abciximab administered
IV to high risk pts undergoing coronary angioplasty and pts undergoing angioplasty, atherectomy and stent placement often with clopidogrel
27
downsides to Abciximab including AEs
Expensive | Bleeding most common AE
28
what does Tirofiban do
small molecule that with short half life that works similar to Abciximab, has to be continually infused bc of short half life
29
How does dipyridamole work
inhibits phosphodiesterase which leads to increased cAMP levels, inhibiting platelet activation
30
what does phosphodiesterase do normally
breaks down cAMP
31
what effects does dipyridamole do
coronary vasodilator that also inhibits platelet aggregation
32
what is dipyridamole used for
in combo with warfarin, inhibits embolism from prosthetic heart valves (main use)`
33
what is dipyridamole combined with aspirin to treat
patients with thrombotic disease, reduces thrombosis
34
what do calcium chelators do
inhibit blood coagulation in vitro
35
what do heparins do
accelerate the action of antithrombin III to neutralize thrombin and other coagulation factors
36
what do rudins do
direct thrombin inhibitors
37
what do coumarin derivatives do
interfere with the hepatic synthesis of functional vitamin K dependent clotting factors
38
what are calcium chelators used for and why cant you use them in the body
for lab draws to prevent coagulation | cant use them in the body because calcium is used on so many function
39
structure of standard heparin
sulfated mucopolysaccharide (acidic molecule)
40
route of admin for standard heparin
NOT ORAL OR IM | infusion pump or intermittent Subcutaneous
41
onset of action of standard heparin
immediate
42
mechanism of action of standard heparin
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
43
heparin AEs
endothelial cell/protein binding | Clearance is dose dependent
44
therapeutic goal of standard heparin
prolong PTT to 1.5-2.5x normal
45
contraindications of standard heparin
bleeding disorders, hemorrhage | liver, kidney disease, HT, certain infections
46
indications of standard heparin
preferable to other anticoagulants during pregnancy due to lack of placental transfer
47
how does the indication of heparin differ from warfarin
preferable during pregnancy due to lack of placental transfer
48
AEs of standard heparin
bleeding/hemorrhage allergic reaction osteoperosis HIT (heparin induced thrombocytopenia)
49
what is type I HIT
transient and rapidly reversible heparin induced thrombocytopenia Abs generated against platelets --> decrease in platelet count
50
what is type II HIT
severe heparin induced thrombocytopenia Ab decrease platelet count Ab also activate platelets-->thormboembolism which may be life threatening
51
standard heparin antidote
protamine sulfate
52
what does protamine sulfate do
antidote to heparin, binds to heparin (anion/cation interaction)
53
why must excessive protamine sulfate be avoided when used as a heparin antidote
its an anticoagulant
54
what is a disadvantage of LMWH (low molecular weight heparin)
protamine sulfate is less capable of reversing its effects
55
what are the LMWHs
Enoxaparin Dalteparin Tinzaparin
56
what are LMWHs used for
``` less sticky than bigger molecules so not as dose dependent more convenient (sub q, dont have to check PTT as much) ```
57
how do you monitor LMWH
an anti-Xa activity assay
58
how does fondaparinux work
it exerts antithrombotic activity as a result of ATIII-mediated selective inhibition of factor Xa
59
what is the half life of fondaparinux
18 hours, allows once daily dosing, given subc
60
warfarin is a derivative of what
coumarin
61
what does the nature of warfarin plasma protein binding mean for its distribution
it has extensive binding which accounts for low volume of distribution, long half life
62
describe metabolism of warfarin
metabolized by liver by CYP2C9, site of numerous drug interactions
63
which has activity in vitro heparin or warfarin?
heparin
64
describe the route of heparin and warfarin
heparin - parenteral | warfarin - oral
65
onset of heparin v warfarin
heparin - immediate | warfarin - 1-3 days
66
how do you monitor heparin
PTT
67
how do you monitor warfarin
PT (INR)
68
where are the rudins derived from
leeches
69
who is lepirudin approved for
its a recombinant yeast driven form of hirudin patients with HIT
70
what can argatroban be used for
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
how do rudins work
direct thrombin inhibitors
72
what is the main rudin
hirudin (thrombin inhibitor)
73
what are the oral direct thrombin inhibitors
Dabigatran etexilate | Rivaroxaban
74
what is a problem with the oran direct thrombin inhibitors
theres not a way to reverse their effects
75
what is apixaban
FXa inhibitor
76
what is praxbind
the first reversal agent for the oral anticoagulants
77
how does praxbind work
binds and sequesters dabigatran and dabigatran glucuronides
78
what do thrombolytics do
activate plasminogen to be converted to plasmin which degrades fibrin and lyses thrombi
79
why cant you use plasmin for thrombolytic therapy?
circulating antiplasmins
80
how is urokinase used as a thrombolytic
its made in the kidney and plasma doesnt have inhibitors to it but it can break down clots
81
how does streptokinase work
facilitates thrombolysis through formation of activator complex with plasminogen results in formation of plasmin
82
what is a major AE of streptokinase
hypersensitivity
83
what are the recombinant thrombolytics
Alteplase Reteplase Tenecteplase, TNK-t-PA
84
what is Alteplase
Biosynthetic recombinant form of human tissue plasminogen activator
85
what is Reteplase
recombinant plasminogen activator
86
what is tenecteplase
modified human t-PA, prolonged half life compared to alteplase
87
when do you use thrombolytic agenst
when you already have a clot
88
how do you rule out intracranial bleeding and why is it important
CT scan, because you need to be sure its a clot not a bleeding episode
89
thrombolytic therapy should be followed with what
anticoagulant therapy with heparin and then warfarin
90
contraindication of thrombolytics
surger, GI bleeidng, hx of hypertension
91
what is vitamin K used for
gamma carboxylation of glutamate residues in PT factors VII, 9, 10
92
how fast does vitamin K restore clotting function
days
93
if you need clotting function faster than vitamin K can provide what can you do
plasma fractions/clotting factors | recombinant factors
94
what discourages the use of plasma fractions in treatments of patients with hemophilia
AIDS and viral hepatitis
95
what is aminocaproic acid
fibrinolytic inhibitor
96
what isomoer is the most active of warfarin
S isomer
97
describe distribution of warfarin
extensive plasma protein binding accounts for low volume of distribution and a long half life
98
how is warfarin metabolized
CTP2C9, site of numerous drug interactions
99
target of warfarin
vitamin K epoxide reductase
100
speed of onset of warfarin
slow, t1/2 is 1.5 days
101
antidote to warfarin
large doses of vitamin K and fresh frozen plasma
102
drugs that diminish warfarin absorption
cholestyramine (also affects Vit K absorption)
103
what drugs can interfere with hepatic microsomal enzymes needed for warfarin metabolism
``` antoconvulsants Barbiturates carbamazepine phenytoin primidone rifampin St. Johns Wort ```
104
what hormone can interfere with warfarin from stimulation of clotting factor synthesis
estrogens
105
which drugs inhibit anticoagulant mechanism (warfarin) and are selective for S warfarin
Metronidazole | fluconazole
106
therapeutic goal of warfarin
prolonged PT time
107
what is an important factor to consider when prescribing warfarin in women
its a teratogen | contraindicated in pregnancy (category X)
108
compare and contrast heparin and warfarins mechanism
heparin - accelerates action of ATIII to neutralize thrombin | Warfarin - decreases vit K dependent clotting factors
109
compare and contrast heparin and warfarin route of admin
heparin - PE | warfarin - oral
110
compare and contrast heparin and warfarin onset
heparin - immediate | warfarin - gradual (1-3 days)
111
compare and contrast heparin and warfarin duration
heparin - 4 hours | warfarin - 2-5 days
112
compare and contrast heparin and warfarin monitoring tests
heparin - PTT | warfarin - PT (INR)
113
compare and contrast heparin and warfarin treatment of overdose
heparin - protamine sulfate | warfarin - vit k; fresh frozen plasma

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