anticoagulants Flashcards
anticoagulants (103 cards)
1
Q
Aspirin mechanism
A
inhibits platelet aggregation by inhibiting COX irreversibly via acetylation COX inhibition means that membrane arachidonic acid can’t be broken down to TXA2 which means that platelet aggregation is stopped
2
Q
Aspirin peak platelet effect (time to)
A
1 hr or 3-4 for enteric coated
3
Q
Aspirin oral bioavailability
A
40-50%
4
Q
aspirin half life
A
15-20 minutes, but irreversible effect and 10-15% of circulating platelets are replaced every 24 hours
5
Q
Aspirin adverse effects (3)
A
GI upset, ulcer, bleeding
6
Q
aspirin indications
A
primary and secondary prevention of arterial thrombosis, disorders of placental insufficiency (ie preeclampsia) , sometimes used for VTE prevention
7
Q
what is better for stroke prevention in afib and mechanical heart valves: aspirin or anticoagulants?
A
anticoagulants
8
Q
NSAID mechanism
A
reversible inhibition of COX
9
Q
Ibuprofen peak effect
A
1-2 hours
10
Q
Ibuprofen half life
A
2 hours
11
Q
Naproxen half life
A
12-17 hours
12
Q
discontinue aspirin, ibuprofen, and naproxen how many days before surgery?
A
10 days, 1-2 days, and several days
13
Q
clopidogrel metabolized by which enzyme
A
CYP3A4
14
Q
clopidogrel metabolism inhibited by which drugs
A
atorvastatin
15
Q
clopidogrel peak effect
A
4-6 hours after dose
16
Q
clopidogrel half life
A
8 hours
17
Q
clopidogrel use (2)
A
2nd prevention of arterial thrombosis and prevention of coronary stent thrombosis
18
Q
clopidgorel adverse effects (3)
A
thrombotic thromyocytopenic purpura (TTP), rash, diarrhea
19
Q
clopidgorel mechanism
A
irreversibly inhibits PY12 a ADP receptor
20
Q
t/f prasugel has to be metabolized before it is activated
A
true
21
Q
prasugrel peak effect
A
1-2 horus after oral dose
22
Q
prasugrel half life
A
7 hours
23
Q
prasugrel use (2)
A
management of ACS w/ PCI
prevention of coronary stent thromboisis
24
Q
prasugrel adverse effects (2)
A
increased risk of stroke (stroke history= contraindication), TTP
25
prasugrel mechanism
irreversible inhibition of ADP receptor, PY12
26
ticagrelor mechanism
reversible inhibition of ADP recpetor, PY12
27
ticargrelor-- is parent drug or metabolite active
both
28
ticagrelor peak effect
2 hours after oral dose
29
ticagrelor half life
7-9 hours
30
ticagrelor uses
prevention of CV events in patients w/ ACS
31
ticagrelor adverse effects (3)
dyspnea, bradycardia, gynecomastia
32
Heparin is produced by which cells
mast cells
33
heparin mechanism
inhibits coagulation via antithrombin which blocks factor 10a and thrombin
34
heparin bioavailability
100% when given IV , but because of plasma binding= 30-35%
35
heparin time until anticoagulant effect if IV
immediate
36
what decreases heparin efficacy
binding to plasma proteins
37
heparin route (2)
IV subQ
38
time until effect if heparin is given subQ
1-3 hours
39
unfractionated heparin clearance
initial rapid phase where it's internalized by endothelial cells and macrophages where it's metabolized to smaller forms and binds to plasma proteins second slow phase = renal
40
2 types of heparin dosing and uses of each
mini: subQ for thromboprophylaxis therapeutic: IV, treatment of acute thrombosis : dose adjusted by aPTT (goal is 80-114 sec at DH)
41
heparin greatest risk of osteoporosis is at what time
over 3 months of treatment
42
Heparin induced Thombocytopenia mechanism
immune mediated ( IgG) directed against heparin/ PF4 antigen on platelet surface which leads to clearance and thromboisis from activation
43
Heparin Induced Thrombocytopenia usually occurs when
5-15 days of initiation of therapy
44
is HIT a bleeding or thrombotic state
thrombotic
45
unfractionated Heparin size
5000-30,000
46
LMWH size
around 5000
47
name of 4 LMWHs
enoxaparin, dalteparin, tinzaparin, fondaparinux
48
heparin side effects
osteoporosis, skin lesions (urticaria, papules and plaques, necosis), hyperaldosteronism
49
what is difference in bioavailability b/w unfractionated and LMWH
LMWH doesn't bind as much to plasma proteins, so alsmost 100% bioavailable and there's less interpatient variability
50
unfractionated hep vs LMWH monitioring
UH= aPTT LMWH= anti-Xa
51
risk of HIT wish UH vs LMWH
1-5% for UH less than 1% for LMWH
52
LMWH peak effect
4-6 hrs after dose
53
LMWH advantage (5)
fixed, weight based dosed
subQ admin
no routine lab monitoring needed
more predictable response
less HIT
54
LMWH disadvantage (2)
long half life may be problem in bleeding patients b/c no antidote.
renal excretion makes use in renal insufficiency difficult
55
Heparin use/ indication
primary prevention of venous and arterial thrombosis
stops thrombus propagation and new clot formation in case of acute venous and arterial thrombosis
56
what do you give to reverse heparin if bleeding is severe and how does it work?
protamine sulfate
protamine is positively charged and heparin is negatively charged
57
What is anticoagulant of choice in pregnancy
heparin
58
Warfarin mechanism of action
vitamin K antagonist which is required as a cofactor in pathways that effects gamma carboxylation on vit-K dependent factors (2,7, 9, 10, Protein C, Protein S, and PZ)
Gamma carboxylation is necessary for coagulation factor binding to phospholipid surfaces ie long story short, inhiibts synthesis of active coagulation factors
59
big mechanistic difference b/w warfarin and heparin
warfarin inhibits synthesis of active coagulation factors and heparin inhibits activity of preformed factors
60
Warfarin time to peak activity
90 minutes
61
warfarin route
oral
62
does warfarin get bound to plasma proteins
yes
63
does clearance of warfarin decrease in patients w/ renal dysfunction
no, but it does increase in peeps undergoing dialysis
64
warfarin half life
33 hours
65
warfarin steady state anticoagulation is reached in how long?
7-10 days
66
how is warfarindose adjuged?
according to PT/INR
67
what is INR range for warfarin?
3-Feb
68
what is special issue w/ starting warfarin
slow onset of action so need to be used concurrently w/ fast acting anticoagulant and it's important to overlap heparin and warfarin by 2 days once therapeutic INR has been reached
69
PT/INR effect of warfarin depends on
Anticoagulant effect depends on (which factors)
VII which has shortest half life
IIa and Xa
70
caveat w/ warfarin
can induce transient hypercoagulable state b/c VitK dependent Anticoag factors (Protein c and S) have shorter half life than coagulant factors
71
indications for warfarin use
primary and secondary prevention of venous thromboembolism
primary and secondary prevention of arterial thromboisis in some circumstances (stroke prevention in Afib/ mechanical heart valves, failure of antiplatelet therapy, added to anti platelet in high risk patients)
72
Warfarin side effects (2)
skin necrosis and teratogenic
73
skin necrosis induced by warfarin use occurs when?
between days 3-8 of therapy
74
what 3 things can reverse warfarin effect
vit K
fresh frozen plasma (for immediate)
prothrombin complex concentrates (for immediate)
75
DTIs are used when
heparins are contraindicatedie HIT
76
2 DTIs used in states
argatroban, bivalirudin
77
DTI route
IV
78
DTI half life
0.5-2 hours
79
DTI effect is monitored how
PTT
goal is 1.5-3x midpoint of normal range ie 45-90 sec at DH
80
in addition to being an anticoagulantargatroban is also approved for
treatment and prevention of thrombosis in HIT
81
bivalirudin and argatroban are also approved for what scenario
anticoaguation during PCI in patients w/ HIT
82
Dabigatran ie Pradaxa target
Thrombin
83
Dabigatran ie pradaxa time to peak
2-3 hrs
84
Dabigatran ie Pradaxa route
oral
85
dabigatran is parent drug active
no rapidly covnerted to active by the liver
86
dabigatran oral availability
7%
87
dabigatran cleared how?
renal excretion
88
dabigatran drug itneractions
verapamil, quinidine
89
dabigatran monitored how?
thrombin time
90
dabigatran side effects
bleeding and GI
91
dabigatran use/ approved for
stroke prevention in A fib and acute VTE treatment
92
does dabigatran have a antidote
yes
93
Rivaroxaban ie Xarelto target
Xa
94
Rivaroxaban ie Xarelto time to peak
3 hrs
95
Rivaroxaban ie Xarelto bioavailability
80-100%
96
Rivaroxaban ie Xarelto cleared how
renal excretion
97
does Rivaroxaban ie Xarelto gave an antidote
no
98
Rivaroxaban ie Xarelto use/ approved for
prevention, treatmentof acute VTE and stroke prevention in A fib
99
Rivaroxaban t/f has a lot of food/drug interactions
false, has few
100
Mechanism of tpA and urokinase plasminogen activator
convert plasminogen to plasmin which degrades fibrin
101
Mechanism of streptokinase
bind to plasminogen and complex degrades fibrin
102
fibrinolytic agent uses
ischemic stroke , arterial occlusion, PE, DVT, occluded central venous catheters
103
major adverse event of fibrinolytic agents
bleeding
