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Hematology Drugs Flashcards

1
Q

Heparin - mechanism of action

A

Activator of antithrombin (decrease thrombin and 10a)

Short half life

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2
Q

Heparin clinical use

A

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

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3
Q

Heparin - pregnancy

A

Used during pregnancy - do not cross placenta

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4
Q

Follow heparin by

A

PTT

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5
Q

Heparin toxicity

A
  1. Bleeding
  2. Thrombocytopenia HIT
  3. Osteoporosis
  4. Drug-drug interactions
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6
Q

Heparin antidote (for rapid reversal) and mechanism of action

A

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

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7
Q

Heparin - induced thrombocytopenia (HIT)

A

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

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8
Q

HIT symptoms

A
  1. Thrombosis

2. Thrombocytopenia

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9
Q

Low molecular weight heparin (examples)

A

-PARIN
Enoxaparin
Dalteparin

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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
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11
Q

Direct thrombin inhibitors

A
  1. Argatroban
  2. Bivalirudin
  3. Dabigatran
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12
Q

Bivalirudin is related to

A

Hirudin: the anticoagulant used by leeches

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13
Q

Direct thrombin inhibitors are alternatives to heparin in

A

HIT

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14
Q

Warfarin duration of life

A

Long half life

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15
Q

Warfarin mechanism of action

A

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

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16
Q

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

A

Extrinsic

Increased PT

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17
Q

Follow warfarin by

A

PT/INR

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18
Q

Warfarin clinical use

A

Chronic anticoagulation:

  1. Venous thromboembolism prophylaxis
  2. Prevention of stroke in atrial fibrillation
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19
Q

Warfarin in pregnancy

A

No - it crosses placenta

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20
Q

Warfarin toxicity

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

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22
Q

For reversal and rapid reversal of warfarin

A

Reversal: vit K

Rapid reversal: fresh frozen plasma

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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

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24
Q

Warfarin action and dose is affected by

A

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

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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)

Hematology And Oncology (21 decks)

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