moa angina Flashcards

(67 cards)

1
Q

asa moa

A

MOA: irreversibly inhibits COX1 causing dec PG and thromboxane A2 so platelets don’t stick

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2
Q

Ranolazine moa

A

MOA: blocks Na from coming into the cell so Ca overload does not occur and coronary blood flow is improved

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3
Q

P2Y12 inhibitor prodrugs/irreversible

A

clopidogrel, prasugrel, ticlopidine

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4
Q

P2Y12 inhibitor not prodrugs/reversible

A

cangrelor, ticagrelor

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5
Q

Inhibits platelet aggregation faster than clopidogrel

A

prasugrel

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6
Q

Acts faster but not as long as clopidogrel or prasugrel

A

ticagrelor

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7
Q

Significant drug interactions with CYP3A4 inhibitors and inducers

A

tigagrelor

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8
Q

GPIIb/IIIa inhibitors moa

A

MOA: prevent fibrinogen from binding to glycoprotein IIb/IIIa receptors on platelets

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9
Q

what does fibrinogen do?

A

forms bridge between 2 platelets by binding to each glycoprotein IIb/IIIa sites

causes platelets to aggregate

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10
Q

cilostazol moa

A

MOA: selective inhibitors of PDE3; this causes cAMP to inc which then causes protein kinase A to inc (PKA) which inhibits platelet aggregation

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11
Q

Dipyridamole moa

A

MOA: inhibits reuptake of adenosine by RBC causing blood vessels to vasodilate; inhibits PDE 3 and PDE 5 which inc cAMP

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12
Q

Intrinsic pathway AKA _____ pathway

A

contact activation

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13
Q

Extrinsic pathway AKA______pathway

A

tissue factor

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14
Q

intricsic pathway deals with factor

A

12

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15
Q

extrinsic pathway deals with factor

A

7

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16
Q

PT- ______(8 letters +PT=10) (dont use PT anymore… use INR)

A

warfarin

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17
Q

aPTT- ______ (7 letters + PTT=10)

A

heparin

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18
Q

heparin moa

A

MOA: catalyzes antithrombin and inactivates thrombin which prevents conversion of fibrinogen to fibrin; inhibits factors 2a, 9a, 10a, 11a, and 12a

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19
Q

common pathway : factor ___

A

X

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20
Q

LMWH: Exoxaparin and dalteparin

moa

A

MOA: inhibits clotting factor 10a

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21
Q

LMWH: Exoxaparin and dalteparin

pregnancy

A

B

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22
Q

do we monitor LMWH: Exoxaparin and dalteparin

A

no

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23
Q

do we monitor heparin?

A

yes by PTT

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24
Q

warfarin moa

A

MOA: liver uses vitamin K to make clotting proteins. Warfarin is a vit K antagonist and depletes factors 2a, 7a, 9a, 10a (intrinsic and extrinsic pathway) and protein C and S which slows fibrin formation

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25
warfarin preganncy
X
26
warfarin dosing
Start with maintenance dose of 5mg/day Bridge therapy- giving heparin or LMWH before warfarin kicks in. warfarin takes 3-5 days to kick in so sometimes ppl need anticoag immediately and cant wait 3-5 days
27
low INR?
coag
28
high INR
anticoag/bleeding
29
check a pts INR_____ if on warfarin
once a month
30
warfarin interacts with_____
acetominophen (APAP), but still DOC for pain
31
Initial inc in PT is from diminished_____ and does not show an anticoag state; full anticoag effect does not occur for 3-5 days
factor 7
32
Factor Xa inhibitors | moa
MOA: selectively blocks factor Xa
33
direct thrombin inhibitors MOA
MOA: prevent thrombus through direct, competitive inhibition of thrombin (FIIa)
34
Thrombolysis?
breakdown of thrombus
35
Fibrinogenolysis?
inhibits clotting cascade; stops the final step
36
Plasminogen?
uses tissue plasminogen activator to form plasmin such as urokinase
37
active component in the fibrinolytic cascade
Plasmin-
38
plasmin ____ clots
breaks down
39
fibrin _____ clots
forms
40
Thrombolytic/fibrinolytic agents | moa
MOA: converts plasminogen to plasmin to break down the clot
41
Vit K- ____ antidote
warfarin
42
Protamine- _____antidote
heparin
43
Aminocaproic acid | moa
MOA: inhibits plasminogen from converting to plasmin so fibrinolysis cant occur
44
Tranexamic acid | moa
MOA: competitively inhibits activation of plasminogen so plasminogen cant be converted to plasmin
45
hemoglobin F does this
prevents RBC from sickling
46
Hemoglobin F is replaced by _____
sickle hemoglobin
47
Pain is MC complication and why most ppl go to the ER
SSD
48
moa hydroxyurea
MOA: makes RBC bigger and helps them stay rounder so they are less likely to turn into a sickle shape by reactivating hemoglobin F
49
Pentoxifylline moa
MOA: dec blood viscosity which dec platelet aggregation
50
l glutamine moa
MOA: Increases glutathione which reduces oxidative stress
51
hydroxyurea se
SE: myelosuppression, secondary infections
52
SE- neutropenia, agranulocytosis, thrombotic thrombocytopenic purpura, aplastic anemia
ticlopidine
53
BBW: may cause life threatening heme events described in the SE
ticlopidine
54
SE inc bleeding
antiplatelets, factor Xa inhibitors, direct thrombin inhibitors
55
Chimeric monoclonal Ab (not bolded)
Abciximab
56
antiplatelet with vasodilating properties
Cilostazol
57
Used for intermittent claudication
Cilostazol
58
BBW: (not bolded) dec survival of pts with class III or IV CHF
Cilostazol
59
SE: anything bleeding like ecchymosis, bleeding, hemorrhage, hematoma, anaphylaxis, HIT
Heparin | LMWH (not HIT)
60
mild reduction of platelets after taking heparin
HAT-
61
more serious; significant dec in platelets 5-10 days after taking heparin
HIT
62
Trmt for overdose heparin
STOP all heparin Mild-moderate bleeding? Give protamine sulfate, a heparin antidote Severe bleeding? Give FFP bc it has all the anticoag factors
63
SE: bleeding, birth defects and fetal hemorrhage, bruising
warfarin
64
blopod monitoring required for xa inhibitors?
no
65
Dibigatran antidote
Praxbind
66
Synthetic analog: leech saliva
hirudens
67
Only used if PCI is not available | Door to needle time under 30 min
Thrombolytic/fibrinolytic agents