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Cardio-Renal I Midterm > Pharmacology - VTE anticoagulants > Flashcards

Pharmacology - VTE anticoagulants Flashcards

1
Q

briefly explain the mechanism of clot formation

A

vasoconstriction

platelet plug formation – platelets aggregate and stick together

clot formation - FIBRIN proteins stick together to form a CLOT

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2
Q

briefly explain what is happening in deep vein thrombosis

A

clot forms in the legs

this can potentially form an embolus which travels to other areas of the body and can cause major issues

ie - pulmonary embolism

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3
Q

3 risk factors for venous thromboembolism

A

-stasis (not moving)
-endothelial injury (ie - surgery, trauma)
-hypercoagulability

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4
Q

____ use can potentially cause thromboembolism

A

estrogen

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5
Q

there are intrinsic and extrinsic coagulation pathways.

which factor is common to both???

A

Xa

therefore, Xa inhibitors are very common anticoagulants!

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6
Q

what causes coagulation factors to initiate coagulation?

A

when they come in contact with the endothelium — ie bc of injury

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7
Q

name 3 things that can be blocked to treat deep vein thrombosis

A

fibrinogen
Xa
prothrombin

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8
Q

unfractionated heparin is also called…

A

high MW heparin

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9
Q

name 4 LMWH’s

A

enoxaparin
dalteparin
tinzaparin
fondaparinux

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10
Q

name 4 oral Xa inhibitors

A

rivaroxaban
apixaban
edoxaban
betrixaban

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11
Q

name a thrombolytic

A

alteplase

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12
Q

low molecular weight heparins are ____ ____ antagonists

A

parenteral Xa

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13
Q

name 2 direct thrombin inhibitors

A

bivalirudin
argatroban

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14
Q

name a vitamin K antagonist

A

warfarin

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15
Q

explain the MOA of unfractionated heparin (high MW heparin)

A

it accelerates the formation of antithrombin III (our natural anticoagulant)-thrombin complex

this inactivates thrombin (IIa) (and inhibits its formation), as well as Xa, and prevents the conversion of fibrinogen to fibrin, and PREVENTS clot formation overall

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16
Q

true or false

unfractionated heparin cannot be given in pregnancy

A

FALSE

it does not cross the placenta

it’s ok in pregnancy

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17
Q

**major AE of high MW heparin (unfractionated)

A

THROMBOCYTOPENIA (low platelets)

called HIT (heparin-induced thrombocytopenia)

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18
Q

what does heparin do to aPTT time

A

increases it

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19
Q

name 2 monitoring parameters for heparin (unfractionated)

A

bleeding
APTT

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20
Q

heparin (unfractionated) contraindication

A

any bleeding issue

ie - another anticoagulant

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21
Q

name 4 types of drugs that antagonize anticoagulation and thus can cause a clot when administered with heparin

A

nicotine
cardiac glycosides
antihistamines
tetracyclines

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22
Q

thrombosis meaning

A

clot

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23
Q

3 major advantages of high MW heparin

A

continuous IV drip - accurate dosing

rapid onset and short duration

monitoring APTT can help to determine if it’s working as it should

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24
Q

low molecular weight heparins are said to have higher ___ activity than ____

A

higher inhibition of Xa than IIa (THROMBIN)

like a 4:1 ratio

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25
Q

true or false

low molecular weight heparins have a lower incidence of thrombocytopenia than unfractionated heparin

A

true

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26
Q

true or false

LMWH has focused action against IIa

A

FALSE - against Xa

not as much to thrombin

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27
Q

prototype for low MW heparins

A

enoxaparin

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28
Q

how is enoxaparin administered

A

subq injection

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29
Q

2 AE of enoxaparin

A

hemorrhage, thrombocytopenia

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30
Q

name some drugs that have a DDI concern with enoxaparin and have a bleeding concern

A

other anticoagulants, antiplatelets, NSAIDS

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31
Q

how often is enoxaparin administered**

A

Q12 for DVT treatment

and QD for prophylaxis

32
Q

***do labs need to be monitored for LMWH’s like enoxaparin

A

NO

33
Q

*****true or false

low molecular weight heparins have a lower incidence of HAT

A

true

this is the non-immune-mediated thrombocytopenia

34
Q

*****LMWH’s are administered subq

how is this an advantage?

A

dont need a hospital IV - reduced expenses

can administer at home to prevent DVT during the 9 months of pregnancy

35
Q

what is the QD dosing for LMWH’s

A

1mg/kg

36
Q

**what is the name of the heparin antagonist?

what is it used for?

A

protamine sulfate

to back titrate an over dose of heparin (high MW)

37
Q

what is a big caution when giving protamine sulfate

A

it releases histamine!

this can lower BP potentially too much and cause shock

therefore, infuse SLOWLY over 10 mins

38
Q

**big problem with high molecular weight IV heparin

A

HIT - heparin induced thrombocytopenia

39
Q

what are the findings when a patient gets HIT

is it immune mediated?

A

yes immune mediated

skin is bruised, red, itchy

platelets reduced to 50%

40
Q

HAT

A

heparin ASSOCIATED thrombocytopenia (type 1 )

41
Q

difference in platelet count between HIT and HAT

A

HIT - below 100,000

HAT - they rarely even go below 150,000

42
Q

***which drugs can be used in a patient that needs anticoagulation therapy but HAS HIT????

A

targeted Xa and IIa inhibitors:

fondaparinux (Xa)

hirudin, Bivalirudin, Argatroban, Melagatran (IIa)

43
Q

**name 1 subQ Xa inhibitor and 4 PO Xa inhibitors

A

subq - fondaparinux

PO - rivaraxoban, apixaban, edoxaban, betrixaban

44
Q

explain the MOA of fondaparinux

A

selectively inhibits factor Xa

does this indirectly through binding ATIII. this causes ATIII to change shape and this increased affinity for Xa to neutralize it more

this neutralization of Xa interrupts the blood coagulation cascade — inhibits thrombin formation and clot development

45
Q

common and severe SE of fondaparinux

A

bleeding, bruising

46
Q

can LMWHs be used in HIT patients

A

NO there is cross reactivity with the antibodies

47
Q

fondaparinux can be used as prophylaxis of DVT?

A

yes - after major orthopedic and abdominal sirgeries

48
Q

factor Xa is required in the clotting cascade to do what?

A

cleave prothrombin into THROMBIN

49
Q

Is there a DDI concern with eliquis and xarelto?

A

YES

3a4 and p-glycoprotein inhibitors and inducers

50
Q

*how to recognize the oral Xa inhibitors

A

“ban”

51
Q

what class is edoxaban

A

an oral Xa inhibitor – a NOAC

52
Q

what class is betrixaban

A

an oral XA inhibitor (BAN)

53
Q

how does betrixaban inhibit Xa

A

competitive and reversible

54
Q

***which drugs can be used for the treatment of venous thromboembolism?

A

any anticoagulant

55
Q

name 2 targeted IIa (thrombin) inhibitors

how are they each administered

A

bivalirudin - IV
dabigatran - PO

56
Q

**what are the 3 classes of thrombin inhibitors?

**name each drug in the class

A

indirect (univalent), bivalent (direct), univalent (direct)

bivalent means they bind at 2 sites

indirect - heparin

direct bivalent - bivalirudin, lepirudin, desirudin

univalent direct - argatroban, ximelagatran, dabigatran

57
Q

side effects bivalirudin

as a recap, what class is it?

A

hemorrhage, hypotension

a direct thrombin inhibitor (bivalent)

58
Q

true or false

dabigatran is an oral IIa inhibitor

A

TRUE

59
Q

what are the advantages of dabigatran over warfain

what’s a disadvantage of it

A

no dietary, DDI, and monitoring problems (INR)

bleeding

60
Q

true or false

dabigatran is a prodrug

A

TRUE

61
Q

dabigatran is a direct thrombin inhibitor

is it noncompetitive or competitive

A

competitive

62
Q

main AEs of dabigatran

A

bleeding - 17%!!!!

dyspepsia and GI complaints - take with food!! no antacids!

63
Q

a patient is having an issue with dyspepsia while on dabigatran

how do u counsel

A

they can try an H2 blocker BUT it may decrease bioavailability bc acidic environment is needed for absorption

64
Q

true or false

dabigatran has no CYP DDIs

A

true

BUT does have DDI with p-glycoprotein inducers/inhibitors

65
Q

name 2 ORAL anticoagulants that permit hospital discharge

A

warfarin (need monitoring)

dabigatran (do not need monitoring)

66
Q

MOA warfarin

A

inhibits vitamin K formation - vitamin K antagonist

does this by inhibiting vitamin K reductase and vitamin K epoxide reductase

this inhibits a lot of things – the functional form of a lot of factos, as well as proteins C,S, and Z

67
Q

true or false

warfarin does NOT dissolve a preexisting clot

A

TRU

68
Q

true or false

warfarin is not very protein bound

A

FALSE - it is 97-99%

69
Q

can warfarin be used in pregnancy

A

NO

crosses BBB

70
Q

polymorphisms in ___ and ____ affect the response to warfarin

explain how they affect it

A

CYP2C9 and CKOR (vitamin K epoxide reductase)

CYP2C9 will significantly inactive (s)-warfarin (the most potent form)

warfarin works by inhibiting VKOR

71
Q

endogenous role of vitamin K

A

causes clotting

72
Q

what is the coumadin antagonist and thus the antidote for warfarin overdose

A

VITAMIN K

73
Q

what is the antidote for dabigatran

A

idarucizumab (monoclonal antibody)

74
Q

what is the name of the factor Xa inhibitor (eliquis, xarelto) reversal agent

A

annexa-A

75
Q
A

Cardio-Renal I Midterm (14 decks)

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