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STEP 1 > Hematology Drugs > Flashcards

Hematology Drugs Flashcards

1
Q

Mechanism of heparin

A

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

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2
Q

Use of heparin

A

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

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3
Q

Can heparin be used during pregnancy?

A

YES

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4
Q

Which will change with heparin use, PT or PTT?

A

PTT needs to be monitored

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5
Q

Toxicity of heparin

A

bleeding
thrombocytopenia (HIT)
osteoporosis
drug-drug interactions

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6
Q

What is the heparin antidote?

A

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

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7
Q

What are the low molecular weight heparins?

A

enoxaparin, dalteparin, and fondaparinux

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8
Q

Benefit of LMWH?

A 
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
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9
Q

What is HIT?

A

heparin induced thrombocytopenia

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10
Q

What is the mechanism of HIT?

A

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

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11
Q

Mechanism of argatroban, bivalirudin and dabigatran?

A

inhibit thrombin directly

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12
Q

Use of argatroban, bivalirudin and dabigatran?

A

alternative to heparin for anticoagulating patients with HIT

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13
Q

Mechanism of warfarin

A

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

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14
Q

What are the vitamin K dependent clotting factors?

A

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

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15
Q

Can have polymorphism to warfarin response?

A

YES via the VKORC1 gene which is K epoxide reductase complex

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16
Q

Labs to monitor warfarin use?

A

extrinsic pathway so monitor PT (sooner) and INR

also affects intrinsic and PTT

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17
Q

Use of warfarin

A

chronic anticoagulation

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18
Q

Can you use warfarin in pregnant women?

A

NO - crosses the placenta

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19
Q

Toxicity of warfarin

A

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

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20
Q

Warfarin and protein C and S

A

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

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21
Q

Antidote to warfarin overdose? rapid reversal?

A

vitamin K; fresh frozen plasma

22
Q

what is Heparin “bridging”?

A

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
Q

Name the direct factor Xa inhibitors

A

apixaban and rivaroxaban

24
Q

Mech of the direct Xa inhibitors

A

bind to and directly inhibit factor Xa

25
Q

Use of direct Xa inhibitors

A

tx and prophylaxis for DVT and PE (rivaroxiban)

stroke prophylaxis in patients with atrial fibrillation

26
Q

Do you need to monitor labs with direct Xa inhibitors?

A

not usually because oral agents don’t require coagulation monitoring

27
Q

Toxicity of direct Xa inhibitors

A

bleeding (no reversal agent available)

28
Q

Name the thrombolytics

A

alteplase, reteplase, streptokinase, tenecteplase

29
Q

Mechanism of thrombolytics

A

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

30
Q

Lab changes with thrombolytics

A

increased PT and PTT, no change in platelet count

31
Q

Use of thrombolytics

A

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

32
Q

Toxicity of thrombolytics

A

bleeding

33
Q

Contraindication of thrombolytics

A

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

34
Q

Antidote to thrombolytics

A

aminocaproic acid, an inhibitor of fibrinolysis

fresh frozen plasma and cryoprecipitate can also be used to correct factor deficiencies

35
Q

Mechanism of aspirin

A

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

36
Q

Lab changes with aspirin

A

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

37
Q

Use of aspirin

A

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

38
Q

Toxicity of aspirin

A

gastric ulceration, tinnitus (CN VIII)

chronic: acute renal failure, intersitial nephritis, upper GI bleeding

39
Q

What is Reye syndrome?

A

precipitated by aspirin use in children with viral infection

40
Q

Overdose of aspirin presentation?

A

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

41
Q

Name the ADP receptor inhibitors

A

clopidogrel, prasugrel, ticagrelor (reversible), ticlodipine

42
Q

Mechanism of ADP receptor inhibitors

A

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

43
Q

Use of ADP receptor inhibitors

A

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

44
Q

Toxicity of ADP receptor inhibitors

Specifically ticlodipine? Presentation?

A

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

45
Q

Name the 2 phosphodiesterase III inhibitors

A

cilostazol, dipyridamole

46
Q

Mech of PDE 3 inhibitors

A

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

VASODILATION as well

47
Q

Use of PDE 3 inhibitors

A

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

48
Q

Toxicity of PDE 3 inhibitors

A

nasuea, headache, facial flushing, hypotension, abdominal pain

49
Q

Name the GP IIb/IIIa inhibitors

A

abciximab, eptifibatide, tirofiban

50
Q

Mechanism of GP IIb/IIIa inhibitors

A

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

51
Q

Use of GP IIb/IIIa inhibitors

A

unstable angina

percutaneous transluminal coronary angioplasty (PCI)

52
Q

Toxicity of GP IIb/IIIa inhibitors

A

bleeding

thrombocytopenia

STEP 1 (26 decks)

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