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Flashcards in Hematology Drugs Deck (72):
1

Heparin - mechanism of action

Activator of antithrombin (decrease thrombin and 10a)
Short half life

2

Heparin clinical use

Immediate anticoagulation for: 1. PE 2. Acute coronary syndrome
3. MI 4. DVT

3

Heparin - pregnancy

Used during pregnancy - do not cross placenta

4

Follow heparin by

PTT

5

Heparin toxicity

1. Bleeding
2. Thrombocytopenia HIT
3. Osteoporosis
4. Drug-drug interactions

6

Heparin antidote (for rapid reversal) and mechanism of action

Protamine sulfate - + charged molecule that binds the - charged heparin

7

Heparin - induced thrombocytopenia (HIT)

Development of igG against heparin bounded to platelet factor (PF4). That complex activate platelets

8

HIT symptoms

1. Thrombosis
2. Thrombocytopenia

9

Low molecular weight heparin (examples)

-PARIN
Enoxaparin
Dalteparin

10

Low molecular weight heparina and fondaparunix (vs heparin)

1. Act more on X
2. Better bioavailability
3. 2-4 h longer half time
4. Can be administrated subcuntaneously
5. No lab monitoring
6. Not easily reversible

11

Direct thrombin inhibitors

1. Argatroban
2. Bivalirudin
3. Dabigatran

12

Bivalirudin is related to

Hirudin: the anticoagulant used by leeches

13

Direct thrombin inhibitors are alternatives to heparin in

HIT

14

Warfarin duration of life

Long half life

15

Warfarin mechanism of action

Interferes γ-carboxylation of vit K depended clotting factors 2,7, 9, 10, C, S

16

In lab assays, warfarin has effect on ..... pathway

Extrinsic
Increased PT

17

Follow warfarin by

PT/INR

18

Warfarin clinical use

Chronic anticoagulation:
1. Venous thromboembolism prophylaxis
2. Prevention of stroke in atrial fibrillation

19

Warfarin in pregnancy

No - it crosses placenta

20

Warfarin toxicity

1. Bleeding
2. Teratogenic
3. Skin-tissue necrosis (small vessel microthromboses)
4. Drug-drug interactions

21

Cause of transient hypercoagulability with warfarin use

Pr C and S have shorter half-lives than 2,7,9,10 --> skin tissue necrosis within 1st days of large doses

22

For reversal and rapid reversal of warfarin

Reversal: vit K
Rapid reversal: fresh frozen plasma

23

Heparin bridging?

Heparin frequently used when starting anticoagulation. Heparin enables anticoagulation during the initial transient hypercoagulable state by warfarin. Initial heparin reduces the risk of: 1. skin tissue necrosis. 2. Recurrent venous thrombosis

24

Warfarin action and dose is affected by

Polymorphism in the gene for vit K epoxide reductase complex (VKORC1)

25

Heparin vs warfarin
Pregnancy

Heparin +
Warfarin - (teratogenic)

26

Heparin vs warfarin
Monitoring

Heparin PTT
warfarin PT/INR

27

Heparin vs warfarin reversal

Heparin: protamine sulfate
Warfarin: vit K, fresh frozen plasma

28

Heparin vs warfarin
Inhibits coagulation in vitro

Heparin +
Warfarin -

29

Heparin vs warfarin
Duration of action

Heparin: acute (hours)
Warfarin: chronic (days)

30

Heparin vs warfarin
Onset of action

Heparin: rapid (sec)
Warfarin: slow (limited by half-lives of normal clotting factors)

31

Heparin vs warfarin
Site of action

Heparin: blood
Warfarin: liver

32

Heparin vs warfarin
Route of administration

Warfarin: oral
Heparin: parenteral (IV, subcutaneous)

33

Heparin vs warfarin
Structure

Heparin: large, anionic, acidic polymer
Warfarin: small amphipathic molecule

34

Heparin mechanism of action

Activator of antithrombin (decrease thrombin and 10a)

35

Direct factor Xa inhibitors

1. Apixaban
2. Rivaroxaban

36

Direct factor Xa inhibitors (apixaban, rivaroxaban) toxicity
Reversal agent

Bleeding
No reversal agent

37

Direct factor Xa inhibitors (apixaban, rivaroxaban) mechanism of action

Bind to and directly inhibit factor Xa

38

Direct factor Xa inhibitors (apixaban, rivaroxaban) monitoring

Oral agents do not need monitoring

39

Direct factor Xa inhibitors (apixaban, rivaroxaban) clinical use

Treatment and prophylaxis of 1. DVT 2. PE (rivaroxaban)
Stroke prophylaxis in atrial fibrillation

40

Eculizumab mechanism of action and clinical use

Terminal complement inhibitor
Paroxismal noctural hemoglobinuria

41

Iron poisoning treatment

1. Chelation (iv deferoxamine, oral deferasirox)
2. Dialysis

42

Thrombolytics

Alteplase (tPA) , reteplase (rPA), streptokinase, tenecteplase (TNK-tPA)

43

Thrombolytics - mechanism of action

Directly or indirectly aim conversion of plasminogen to plasmin which cleaves thrombin and fibrin clots

44

Thrombolytics
PT, PTT, PC

PT increased
PTT increased
PC normal

45

Thrombolytics: clinical use

1. Early MI
2. Early ischemic stroke
3. Direct thrombolysis of severe PE

46

Thrombolytics toxicity

Bleeding

47

Thrombolytics antidote

1. Aminocaproic acid (inhibits fibrinolysis)
2. Fresh plasma and cryoprecipitate (to correct factor deficiencies)

48

Thrombolytics is contraindicated

1. Active bleeding
2. History of intracranial bleeding
3. Recent surgery
4. Known bleeding diathesis
5. Severe hypertension

49

Aspirin mechanism of action

Irreversible inhibits cycloxygenase (both cox 1 and 2) BY COVALENT ACETYLATION. Platelets cannot synthesize new enzyme, so effect lasts until new platelets produced

50

Aspirin decreased the production of

1. Prostaglandins
2. TXA2

51

Aspirin - BT PT PTT

No effect on PT PTT
Increased BT

52

Aspirin clinical use

1. Antipyretic
2. Analgesic
3. Anti-inflammatory
4. Antiplatelet (anti-aggregation)

53

Aspirin toxicity

1. Gastric ulceration
2. Tinnitus (CN 8)
3. Chronic use --> a. Acute renal failure b. Interstitial nephritis c. Upper gi bleeding
4. Reye syndrome in children with viral infection
5. Overdose --> initially hyperventilation and respiratory alkalosis, but transition to mixed metabolic acidosis-resp alkalosis

54

ADP inhibitors

1. Clopidogrel
2. Ticlopidine
3. Prasurgel
4. Ticagrelor (reversible)

55

ADP inhibitors mechanism of action

Irreversible blocking ADP receptor (prevent expression of gpIIb/IIIa) (except ticagrelor --> reversible)

56

Reversible ADP inhibitor

Ticagrelor

57

ADP inhibitors side effects

1. Neutropenia (ticlopidine)
2. TTP may be seen

58

ADP inhibitors clinical use

1. Acute coronary syndrome
2. Coronary stent (decreases incidence or recurrence of thrombotic stroke)
3. decrease incidence or reccurence of thrombotic stroke

59

GPII/IIIa inhibitors

1. Abciximab
2. Eptifibatide
3. Tirofiban

60

GPII/IIIa inhibitors toxicity

1. Bleeding
2. Thrombocytopenia

61

GPII/IIIa inhibitors clinical use

1. Unstable angina
2. Percutaenous transluminal angioplasty

62

Aciximab is made from

Monoclonal antibody Fab fragments

63

Alternative of heparin in HIT

Direct thrombin inhibitor

64

Phosphodiesterase III inhibitors

1. Cilostazol
2. Dipyridamole

65

Cilostazole, dipyridamol, mechanism of action

Phosphodiesterase III inhibitor--> increased cAMP in platelets --> inhibitions of platelet aggregation.......and vasodilation

66

Cilostazol, dipyridamol toxicity

1. Nausea
2. Headache
3. Facial flashing
4. Hypotension
5. Abdominal pain

67

Cilostazol dipyridamole clinical use

1. Intermittent claudication
2. Coronary vasodilation
3. Angina prophylaxis
4. Prevention of stroke or Transient ischemic attacks (combined with aspirin)

68

Bivalirudin - mechanism of action

directly inhibits activity of free and clot-associated thrombin

69

Bivalirudin - clinical use

1. Venous thrombooembolism
2. atrial fibrilation
(can used in HIT)

70

Bivalirudin - lab monitoring

does not require

71

Bivalirudin - side effects

bleeding

72

Bivalirudin - antidote

- no specific reversal agent
- can attempt to use activated prothrombin complex concentrates (PCC) and/or fibrinolytics (tranxamic acid)