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pharmacology > moa angina > Flashcards

moa angina Flashcards

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
Q

warfarin preganncy

A

X

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26
Q

warfarin dosing

A

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

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27
Q

low INR?

28
Q

high INR

A

anticoag/bleeding

29
Q

check a pts INR_____ if on warfarin

A

once a month

30
Q

warfarin interacts with_____

A

acetominophen (APAP), but still DOC for pain

31
Q

Initial inc in PT is from diminished_____ and does not show an anticoag state; full anticoag effect does not occur for 3-5 days

32
Q

Factor Xa inhibitors

moa

A

MOA: selectively blocks factor Xa

33
Q

direct thrombin inhibitors MOA

A

MOA: prevent thrombus through direct, competitive inhibition of thrombin (FIIa)

34
Q

Thrombolysis?

A

breakdown of thrombus

35
Q

Fibrinogenolysis?

A

inhibits clotting cascade; stops the final step

36
Q

Plasminogen?

A

uses tissue plasminogen activator to form plasmin such as urokinase

37
Q

active component in the fibrinolytic cascade

38
Q

plasmin ____ clots

A

breaks down

39
Q

fibrin _____ clots

40
Q

Thrombolytic/fibrinolytic agents

moa

A

MOA: converts plasminogen to plasmin to break down the clot

41
Q

Vit K- ____ antidote

42
Q

Protamine- _____antidote

43
Q

Aminocaproic acid

moa

A

MOA: inhibits plasminogen from converting to plasmin so fibrinolysis cant occur

44
Q

Tranexamic acid

moa

A

MOA: competitively inhibits activation of plasminogen so plasminogen cant be converted to plasmin

45
Q

hemoglobin F does this

A

prevents RBC from sickling

46
Q

Hemoglobin F is replaced by _____

A

sickle hemoglobin

47
Q

Pain is MC complication and why most ppl go to the ER

48
Q

moa hydroxyurea

A

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
Q

Pentoxifylline moa

A

MOA: dec blood viscosity which dec platelet aggregation

50
Q

l glutamine moa

A

MOA: Increases glutathione which reduces oxidative stress

51
Q

hydroxyurea se

A

SE: myelosuppression, secondary infections

52
Q

SE- neutropenia, agranulocytosis, thrombotic thrombocytopenic purpura, aplastic anemia

A

ticlopidine

53
Q

BBW: may cause life threatening heme events described in the SE

A

ticlopidine

54
Q

SE inc bleeding

A

antiplatelets, factor Xa inhibitors, direct thrombin inhibitors

55
Q

Chimeric monoclonal Ab (not bolded)

56
Q

antiplatelet with vasodilating properties

A

Cilostazol

57
Q

Used for intermittent claudication

A

Cilostazol

58
Q

BBW: (not bolded) dec survival of pts with class III or IV CHF

A

Cilostazol

59
Q

SE: anything bleeding like ecchymosis, bleeding, hemorrhage, hematoma, anaphylaxis, HIT

A

Heparin

LMWH (not HIT)

60
Q

mild reduction of platelets after taking heparin

61
Q

more serious; significant dec in platelets 5-10 days after taking heparin

62
Q

Trmt for overdose heparin

A

STOP all heparin
Mild-moderate bleeding? Give protamine sulfate, a heparin antidote
Severe bleeding? Give FFP bc it has all the anticoag factors

63
Q

SE: bleeding, birth defects and fetal hemorrhage, bruising

64
Q

blopod monitoring required for xa inhibitors?

65
Q

Dibigatran antidote

66
Q

Synthetic analog: leech saliva

67
Q

Only used if PCI is not available

Door to needle time under 30 min

A

Thrombolytic/fibrinolytic agents

pharmacology (16 decks)

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