Anticoag drugs 0504 Flashcards

1
Q

heparin moa

A

cofactor for activation of ANTITHROMBIN.
antithrombin inactivates thrombin and Xa, which converts prothrombin to thrombin

(decrease thrombin and Xa)

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2
Q

heparin use

A

short half life.
duration of action is only hours.
IMMEDIATE anticoag for PE, stroke, acute coronary syndrome, MI, DVT

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3
Q

can heparin be used in pregos?

A

yes - does not cross placenta

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4
Q

how should heparin tx be monitored?

A

follow PTT - intrinsic pathway
(three letters long, like “Hep”)

also causes increased thrombin time

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5
Q

heparin tox

A

bleeding
thrombocytopenia (HIT)
osteoporosis
drug-drug interaction

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6
Q

heparin antidote

A

protamine sulfate - positively charged molecule that binds negatively charged Hep

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7
Q

heparin-induced thrombocytopenia (HIT)

A

Hep binds factor IV, causing Ab production that binds to and activates plts - lead to plt clearance.

thrombocytopenic, hypercoagulable state.

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8
Q

LMWH (enoxaparin) moa

A

binds antithrombin III ONLY.

acts more to inhibit Xa.

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9
Q

enoxaparin pharmacodynamics

A
better bioavailability.
2-4 times longer half life.
admin SQ.
no lab monitoring.
not easily reversible.
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10
Q

fondaparinux

A

smallest heparin form.
synthetic pentasaccharide inhibitor of Xa.
no activity with antithrombin.

causes increased PT and aPTT.
no effect on thrombin time.

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11
Q

hirudin derivatives

A

lepirudin
bivalirudin
argatroban
dabigatran

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12
Q

hirudin derivatives moa

A

DIRECT thrombin inhibition. prevent new clot formation.
does not require ATIII.
prolongs thrombin time.

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13
Q

hirudin derivatives use

A

alternative to Hep in pts with HIT.

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14
Q

warfarin (Coumadin) moa

A

interferes with normal synthesis and gamma-carboxylation of vit K-dependent factors II, VII, IX, X, prot C and S.

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15
Q

warfarin metabolism

A

cyto P450

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16
Q

warfarin lab results

A

increase PT (affects extrinsic pathway)

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17
Q

warfarin use

A

long half life.
duration of action for days.
CHRONIC anticoag - post STEMI, prophylaxis for venous thromboembolism.

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18
Q

how is warfarin use monitored?

A

follow PT/INR values

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19
Q

can warfarin be used in pregos?

A

NO! can cross placenta

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20
Q

what other drug must be administered when warfarin is initiated?

A

Hep/enoxaparin - anticoag prot C and S are quickly depleted (shortest half lives); can result in paradoxical PROcoagulant state if Hep not given

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21
Q

warfarin tox

A

bleeding
teratogenic
skin/tissue necrosis**
drug-drug interactions

22
Q

warfarin antidote

A

reverse OD: IV vit K

rapidly reverse SEVERE OD: fresh frozen plasma

23
Q

why is the onset of therapeutic action for warfarin delayed for a few days?

A

vit K-dependent factors have long half lives

24
Q

route of admin for Hep

A

parenteral (IV, SC)

25
Q

site of action for Hep

A

blood

26
Q

Hep structure

A

large, anionic acidic polymer

27
Q

warfarin structure

A

small lipid soluble molecule

28
Q

route of admin for warfarin

A

oral

29
Q

site of action for warfarin

A

liver

30
Q

can Hep or warfarin inhibit coag in vitro?

A

Hep does, warfarin does not

31
Q

thrombolytics

A

streptokinase
urokinase
tPA (alteplase)
APSAC (anistreplase)

32
Q

thrombolytics moa

A

directly or indirectly aid conversion of PLASMINOGEN to PLASMIN, which cleaves thrombin and fibrin clots

33
Q

thrombolytics lab changes

A

increase PT
increase PTT
no change in plt count

34
Q

thrombolytics use

A

early MI

early ischemic stroke

35
Q

thrombolytics tox

A

bleeding

36
Q

thrombolytics contraindications

A
pts with: 
active bleeding 
history of intracranial bleeding
recent surg
known bleeding diatheses
severe HTN
37
Q

thrombolytics antidote

A

aminocaproic acid - inhibits fibrinolysis

38
Q

aspirin moa

A

acetylates and IRREVERSIBLY inhibits cyclooxygenase (COX1 and COX2) to prevent conversion of arachidonic acid to thromboxane A2

39
Q

aspirin lab changes

A

increase bleeding time

no effect on PT, PTT

40
Q

aspirin uses

A

antipyretic
analgesic
anti-inflamm
anti-platelet

41
Q

aspirin tox

A
gastric ulceration
bleeding
hyperventilation 
Reye's syndrome
tinnitus (CN VIII)
42
Q

clopidogrel, ticlodipine moa

A

inhibit plt aggregation by irreversibly blocking ADP receptors - block GpIIbIIIa expression, which is needed to bind fibrinogen

43
Q

clopidogrel, ticlodipine use

A

acute coronary syndrome.
coronary steal syndrome.
decrease incidence or recurrence of thrombotic stroke.

44
Q

ticlodipine tox

A

neutropenia

45
Q

cilastazol, dipyridamole moa

A

phosphodiesterase III inhibitor - increase cAMP in plts to inhibit plt aggregation.

also vasodilator.

46
Q

cilastazol, dipyridamole use

A

intermittent claudication.
coronary vasodilation.
prevention of stroke or TIAs (combined with aspirin).
angina prophylaxis.

47
Q

cilastazol, dipyridamole tox

A
nausea
headache
facial flushing
hypOtension
abd pain
48
Q

abciximab moa

A

monoclonal Ab that binds to GpIIbIIIa on activated plts, preventing aggregation

49
Q

abciximab use

A

acute coronary syndrome.

percutaneous transluminal coronary angioplasty

50
Q

abciximab tox

A

bleeding

thrombocytopenia