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Flashcards in Hematology Drugs Deck (52)
1

Mechanism of heparin

activator of antithrombin
decreases thrombin and factor Xa
short half-life

2

Use of heparin

immediate anticogaulation for PE
acute coronary syndrome
MI
deep venous thrombosis (DVT)

3

Can heparin be used during pregnancy?

YES

4

Which will change with heparin use, PT or PTT?

PTT needs to be monitored

5

Toxicity of heparin

bleeding
thrombocytopenia (HIT)
osteoporosis
drug-drug interactions

6

What is the heparin antidote?

protamine sulfate that has + charge that will bind - charged heparin

7

What are the low molecular weight heparins?

enoxaparin, dalteparin, and fondaparinux

8

Benefit of LMWH?

act more on factor Xa
have better bioavailability
2-4 times longer half-life
can be administered subQ
need less laboratory monitoring
NOT easily reversible

9

What is HIT?

heparin induced thrombocytopenia

10

What is the mechanism of HIT?

development of IgG antibodies against heparin-bound platelet factor 4 (PF4)
antibody-heparin-PF4 complex activates platelets --> thrombosis and thrombocytopenia

11

Mechanism of argatroban, bivalirudin and dabigatran?

inhibit thrombin directly

12

Use of argatroban, bivalirudin and dabigatran?

alternative to heparin for anticoagulating patients with HIT

13

Mechanism of warfarin

interferes with gamma-carboxylation of vitamin K-dependent clotting factors and protein C and S by blocking vitamin K epoxide reductase

14

What are the vitamin K dependent clotting factors?

II, VII, IX, X (plus protein C and S inhibited)

15

Can have polymorphism to warfarin response?

YES via the VKORC1 gene which is K epoxide reductase complex

16

Labs to monitor warfarin use?

extrinsic pathway so monitor PT (sooner) and INR
also affects intrinsic and PTT

17

Use of warfarin

chronic anticoagulation

18

Can you use warfarin in pregnant women?

NO - crosses the placenta

19

Toxicity of warfarin

bleeding, teratogenic, skin/tissue necrosis (believed to be due to small vessel microthromboses), drug-drug interactions

20

Warfarin and protein C and S

protein C and S have shorter half-lives than clotting factors II, VII, IX, X resulting in early transient hypercoagulability with warfarin use

21

Antidote to warfarin overdose? rapid reversal?

vitamin K; fresh frozen plasma

22

what is Heparin "bridging"?

heparin frequently used when starting warfarin because it only inhibits the new production of clotting factors not those that already exist

initial heparin with warfarin decreases risk of recurrent venous thromboembolism and skin/tissue necrosis

23

Name the direct factor Xa inhibitors

apixaban and rivaroxaban

24

Mech of the direct Xa inhibitors

bind to and directly inhibit factor Xa

25

Use of direct Xa inhibitors

tx and prophylaxis for DVT and PE (rivaroxiban)
stroke prophylaxis in patients with atrial fibrillation

26

Do you need to monitor labs with direct Xa inhibitors?

not usually because oral agents don't require coagulation monitoring

27

Toxicity of direct Xa inhibitors

bleeding (no reversal agent available)

28

Name the thrombolytics

alteplase, reteplase, streptokinase, tenecteplase

29

Mechanism of thrombolytics

directly or indirectly aid in conversion of plasminogen to plasmin which cleaves thrombin and fibrin clots

30

Lab changes with thrombolytics

increased PT and PTT, no change in platelet count

31

Use of thrombolytics

early MI (within first 6 hrs)
early sichemic stroke
direct thrombolysis of severe PE

32

Toxicity of thrombolytics

bleeding

33

Contraindication of thrombolytics

in patients with active bleeding, history of intracranial bleeding, recent surgery, known bleeding diatheses, or severe hypertension

34

Antidote to thrombolytics

aminocaproic acid, an inhibitor of fibrinolysis
fresh frozen plasma and cryoprecipitate can also be used to correct factor deficiencies

35

Mechanism of aspirin

irreversibly inhibits COX1 and COX2 enzyme by covalent acetylation
platelets cannot synthesize new enzyme, so effect lasts until new platelets are produced

36

Lab changes with aspirin

increased bleeding time
decreased TXA2 and prostaglandins
no effect on PT or PTT

37

Use of aspirin

antipyrectic, analgesic, anti-inflammatory, antiplatelet (decrease aggregation)

38

Toxicity of aspirin

gastric ulceration, tinnitus (CN VIII)
chronic: acute renal failure, intersitial nephritis, upper GI bleeding

39

What is Reye syndrome?

precipitated by aspirin use in children with viral infection

40

Overdose of aspirin presentation?

early presents with hyperventilation and respiratory alkalosis but transitions to mixed metabolic acidosis-respiratory alkalosis

41

Name the ADP receptor inhibitors

clopidogrel, prasugrel, ticagrelor (reversible), ticlodipine

42

Mechanism of ADP receptor inhibitors

inhibit platelet aggregation by irreversibly blocking ADP receptors
prevent expression of glycoproteins IIb/IIIa on platelet surface and prevents platelet-platelet interactions

43

Use of ADP receptor inhibitors

acute coronary syndrome
coronary stenting
decreased incidence or recurrence of thrombotic stroke

44

Toxicity of ADP receptor inhibitors
Specifically ticlodipine? Presentation?

neutropenia (ticlodipine) - presents with fever and mouth ulcers
TTP may be seen

45

Name the 2 phosphodiesterase III inhibitors

cilostazol, dipyridamole

46

Mech of PDE 3 inhibitors

inhibit enzyme leading to increase cAMP in platelets resulting in inhibition of platelet aggregation

VASODILATION as well

47

Use of PDE 3 inhibitors

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

48

Toxicity of PDE 3 inhibitors

nasuea, headache, facial flushing, hypotension, abdominal pain

49

Name the GP IIb/IIIa inhibitors

abciximab, eptifibatide, tirofiban

50

Mechanism of GP IIb/IIIa inhibitors

bind to glycoprotein receptor IIb/IIIa on activated platelets and prevent aggregation

51

Use of GP IIb/IIIa inhibitors

unstable angina
percutaneous transluminal coronary angioplasty (PCI)

52

Toxicity of GP IIb/IIIa inhibitors

bleeding
thrombocytopenia