Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Hematology And Oncology > Hematology Drugs > Flashcards

Hematology Drugs Flashcards

1
Q

Heparin - mechanism of action

A

Activator of antithrombin (decrease thrombin and 10a)

Short half life

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Heparin clinical use

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Heparin - pregnancy

A

Used during pregnancy - do not cross placenta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Follow heparin by

A

PTT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Heparin toxicity

A
  1. Bleeding
  2. Thrombocytopenia HIT
  3. Osteoporosis
  4. Drug-drug interactions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Heparin antidote (for rapid reversal) and mechanism of action

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Heparin - induced thrombocytopenia (HIT)

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

HIT symptoms

A
  1. Thrombosis

2. Thrombocytopenia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Low molecular weight heparin (examples)

A

-PARIN
Enoxaparin
Dalteparin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Low molecular weight heparina and fondaparunix (vs heparin)

A
  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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Direct thrombin inhibitors

A
  1. Argatroban
  2. Bivalirudin
  3. Dabigatran
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Bivalirudin is related to

A

Hirudin: the anticoagulant used by leeches

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Direct thrombin inhibitors are alternatives to heparin in

A

HIT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Warfarin duration of life

A

Long half life

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Warfarin mechanism of action

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

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

A

Extrinsic

Increased PT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Follow warfarin by

A

PT/INR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Warfarin clinical use

A

Chronic anticoagulation:

  1. Venous thromboembolism prophylaxis
  2. Prevention of stroke in atrial fibrillation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Warfarin in pregnancy

A

No - it crosses placenta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Warfarin toxicity

A
  1. Bleeding
  2. Teratogenic
  3. Skin-tissue necrosis (small vessel microthromboses)
  4. Drug-drug interactions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Cause of transient hypercoagulability with warfarin use

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

For reversal and rapid reversal of warfarin

A

Reversal: vit K

Rapid reversal: fresh frozen plasma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Heparin bridging?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Warfarin action and dose is affected by

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Heparin vs warfarin

Pregnancy

A

Heparin +

Warfarin - (teratogenic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Heparin vs warfarin

Monitoring

A

Heparin PTT

warfarin PT/INR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Heparin vs warfarin reversal

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Heparin vs warfarin

Inhibits coagulation in vitro

A

Heparin +

Warfarin -

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Heparin vs warfarin

Duration of action

A

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

30
Q

Heparin vs warfarin

Onset of action

A

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

31
Q

Heparin vs warfarin

Site of action

A

Heparin: blood
Warfarin: liver

32
Q

Heparin vs warfarin

Route of administration

A

Warfarin: oral
Heparin: parenteral (IV, subcutaneous)

33
Q

Heparin vs warfarin

Structure

A

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

34
Q

Heparin mechanism of action

A

Activator of antithrombin (decrease thrombin and 10a)

35
Q

Direct factor Xa inhibitors

A
  1. Apixaban

2. Rivaroxaban

36
Q

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

A

Bleeding

No reversal agent

37
Q

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

A

Bind to and directly inhibit factor Xa

38
Q

Direct factor Xa inhibitors (apixaban, rivaroxaban) monitoring

A

Oral agents do not need monitoring

39
Q

Direct factor Xa inhibitors (apixaban, rivaroxaban) clinical use

A

Treatment and prophylaxis of 1. DVT 2. PE (rivaroxaban)

Stroke prophylaxis in atrial fibrillation

40
Q

Eculizumab mechanism of action and clinical use

A

Terminal complement inhibitor

Paroxismal noctural hemoglobinuria

41
Q

Iron poisoning treatment

A
  1. Chelation (iv deferoxamine, oral deferasirox)

2. Dialysis

42
Q

Thrombolytics

A

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

43
Q

Thrombolytics - mechanism of action

A

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

44
Q

Thrombolytics

PT, PTT, PC

A

PT increased
PTT increased
PC normal

45
Q

Thrombolytics: clinical use

A
  1. Early MI
  2. Early ischemic stroke
  3. Direct thrombolysis of severe PE
46
Q

Thrombolytics toxicity

47
Q

Thrombolytics antidote

A
  1. Aminocaproic acid (inhibits fibrinolysis)

2. Fresh plasma and cryoprecipitate (to correct factor deficiencies)

48
Q

Thrombolytics is contraindicated

A
  1. Active bleeding
  2. History of intracranial bleeding
  3. Recent surgery
  4. Known bleeding diathesis
  5. Severe hypertension
49
Q

Aspirin mechanism of action

A

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

50
Q

Aspirin decreased the production of

A
  1. Prostaglandins

2. TXA2

51
Q

Aspirin - BT PT PTT

A

No effect on PT PTT

Increased BT

52
Q

Aspirin clinical use

A
  1. Antipyretic
  2. Analgesic
  3. Anti-inflammatory
  4. Antiplatelet (anti-aggregation)
53
Q

Aspirin toxicity

A
  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
Q

ADP inhibitors

A
  1. Clopidogrel
  2. Ticlopidine
  3. Prasurgel
  4. Ticagrelor (reversible)
55
Q

ADP inhibitors mechanism of action

A

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

56
Q

Reversible ADP inhibitor

A

Ticagrelor

57
Q

ADP inhibitors side effects

A
  1. Neutropenia (ticlopidine)

2. TTP may be seen

58
Q

ADP inhibitors clinical use

A
  1. Acute coronary syndrome
  2. Coronary stent (decreases incidence or recurrence of thrombotic stroke)
  3. decrease incidence or reccurence of thrombotic stroke
59
Q

GPII/IIIa inhibitors

A
  1. Abciximab
  2. Eptifibatide
  3. Tirofiban
60
Q

GPII/IIIa inhibitors toxicity

A
  1. Bleeding

2. Thrombocytopenia

61
Q

GPII/IIIa inhibitors clinical use

A
  1. Unstable angina

2. Percutaenous transluminal angioplasty

62
Q

Aciximab is made from

A

Monoclonal antibody Fab fragments

63
Q

Alternative of heparin in HIT

A

Direct thrombin inhibitor

64
Q

Phosphodiesterase III inhibitors

A
  1. Cilostazol

2. Dipyridamole

65
Q

Cilostazole, dipyridamol, mechanism of action

A

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

66
Q

Cilostazol, dipyridamol toxicity

A
  1. Nausea
  2. Headache
  3. Facial flashing
  4. Hypotension
  5. Abdominal pain
67
Q

Cilostazol dipyridamole clinical use

A
  1. Intermittent claudication
  2. Coronary vasodilation
  3. Angina prophylaxis
  4. Prevention of stroke or Transient ischemic attacks (combined with aspirin)
68
Q

Bivalirudin - mechanism of action

A

directly inhibits activity of free and clot-associated thrombin

69
Q

Bivalirudin - clinical use

A
  1. Venous thrombooembolism
  2. atrial fibrilation
    (can used in HIT)
70
Q

Bivalirudin - lab monitoring

A

does not require

71
Q

Bivalirudin - side effects

72
Q

Bivalirudin - antidote

A
  • no specific reversal agent

- can attempt to use activated prothrombin complex concentrates (PCC) and/or fibrinolytics (tranxamic acid)

Hematology And Oncology (21 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions