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IHO Week 6 (EH) > Anticoag Drugs > Flashcards

Anticoag Drugs Flashcards

1
Q

Phase 1 hemostasis

A

Vascular constriction limits the flow of blood to the area of injury

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2
Q

Phase 2 hemostasis

A

Platelets become activated and aggregate at the site of injury, forming a temporary, loose platelet plug (Primary Hemostasis)

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3
Q

Phase 3 hemostasis

A

A fibrin mesh (also called the clot) forms and entraps the plug (Secondary Hemostasis)

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4
Q

Phase 4 hemostasis

A

The clot is dissolved in order for normal blood flow to resume following tissue repair.

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5
Q

3 classes of drugs to reduce clotting

A

antiplatelet
anticoagulants
fibrinolytic

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6
Q

antiplatelet drug types

A

COX inhibitor
ADP Receptor Antagonists
GPIIb/IIIa Receptor Inhibitors
Adenosine Reuptake Inhibitor

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7
Q

anticoagulants types

A

indirect thrombin inhibitors
direct thrombin inhibitors
Vitamin K analogue
Factor Xa Inhibitors (oral)

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8
Q

Fibrinolytic drugs types

A

Tissue Plasminogen Activators

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9
Q

When do we interfere with hemostasis

A

Treat bleeding disorders due to deficiencies and disease, etc
Prevention and treatment of thrombosis

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10
Q

Acetylsalicylate

A

aspirin

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11
Q

aspirin mechanism

A

irreversible inhibitor of COX

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12
Q

Do platelets have COX2?

A

No

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13
Q

Can platelets make more COX

A

No

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14
Q

Why don’t other NSAIDs work well as anti-platelet agents?

A

They are reversible inhibitors

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15
Q

3 As of aspirin

A

Antipyretic, analgesic and anti-inflammatory

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16
Q

Adverse effects of Aspirin

A

Bleeding
GI disturbances
Tinnitus

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17
Q

Low dose vs high dose aspirin

A

Low dose, effect on the platelet

High dose, effect on inflammation

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18
Q

ADP Receptor Antagonists

A

Clopidogrel, Prasugrel, Ticlopidine

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19
Q

Clopidogrel, Prasugrel, Ticlopidine

A

ADP Receptor Antagonists

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20
Q

ADP receptor antagonist mechanism

A

Irreversible ADP receptor antagonists that prevent activation of ADP receptor

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21
Q

ADP receptor antagonist route

A

oral

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22
Q

ADP receptor antagonists use

A

Used during stenting and recommended for patients that don’t tolerate aspirin

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23
Q

Adverse Effects ADP Rec Antagonists

A

BLEEDING, nausea, diarrhea, rash (10-50% of patients)
severe leukopenia (1% of patients)
thrombotic thrombocytopenic purpura (TTP) – very rare (ticlopidine)

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24
Q

_____ and ______ have fewer side effects than ______ (ADP rec ant)

A

Clopidogrel and Prasugrel have fewer side effects than Ticlopidine

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25
Q

Clopidogrel may require activation via ________ so drugs that impair this isoform should be used with caution

A

CYP2C19 (ie. omeprazole)

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26
Q

ADP Receptor antagonists reversible?

A

NO, but new drugs are coming out that are reversible (Ticagrelor, Cangrelor)

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27
Q

GPIIb/IIIa receptor inhibitors mechanism

A

Prevent binding of adhesive glycoproteins such as fibrinogen and vWF to activated platelets
Inhibits the final common pathway for platelet aggregation

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28
Q

GPIIb/IIIa receptor inhibitors

A

Abciximab
Eptifibatide
Tirofiban
(fib binds where fibrinogen binds, + abciximab)

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29
Q

Abciximab

A

humanized MAB against GPIIb/IIIa

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30
Q

Eptifibatide

A

fibrinogen analogue

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31
Q

Tirofiban

A

non-peptide competitive inhibitor

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32
Q

GPIIb/IIIa receptor inh route, uses

A

IV with aspirin and heparin during angioplasty, for acute coronary syndromes

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33
Q

AE GPIIb/IIIa rec inh

A

Bleeding

Thrombocytopenia (chronic use)

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34
Q

Dipyridamole mechanism

A

Inc. cAMP and inhibit platelet activation
(PDE3 inhibitor - block breakdown into 5’AMP)
(Inhibit platelet uptake of adenosine –> more adenosine at Adenosine A2 receptor –> Inc. cAMP)
Also a vasodilator

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35
Q

Dipyridamole AE

A

headache

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36
Q

Dipyridamole USe

A

Little or no beneficial effect by itself
Used in combination with aspirin or warfarin
Unclear that the combination of dipyridamole and aspirin is more beneficial than aspirin alone

37
Q

thrombin two big jobs

A

activate platelets

cleave fibrinogen to fibrin

38
Q

thrombin inhibitors - 2 major kinds

A

indirect

direct

39
Q

thrombin inhibitors route

A

parenteral

40
Q

indirect thrombin inhibitors

A

Unfractionated heparin
Low molecular weight heparin
Fondaparinux

41
Q

direct thrombin inhibitors

A

Lepirudin
Bivalirudin
Argatroban
Dabigatran etexylate (oral, new)

42
Q

UFH =

A

Unfractionated heparin (UFH) is the same thing as high molecular weight (HMW) heparin, often just called heparin

43
Q

mechanism indirect thrombin inhibitors

A

Bind to antithrombin to have their effect
Antithrombin normally inactivates both thrombin and Factor Xa
When the indirect thrombin inhibitors bind to antithrombin, antithrombin does a better job

44
Q

Heparin’s activity against thrombin is ____ dependent

A

size

45
Q

what limits heparin’s bioavailability

A

Binding to plasma proteins, platelet (platelet factor 4), macrophages, and endothelial cells
account for highly variable anticoagulant response

46
Q

UFH can inhibit

A

both Xa and thrombin

47
Q

LMWH can inhibit

A

Xa > thrombin

48
Q

Fondaparinux can inhibit

A

Xa only (too short to bridge antithrombin)

49
Q

sources of indirect thrombin inhibitors

A

heparin, LMWH = biological (porcine)

fondaparinux = synthetic

50
Q

which indirect thrombin inhib has longest half life

A

fondaparinux > LMWH > heparin

51
Q

antidote effects vs indirect thrombin inhibitors

A

heparin - complete
LMWH - partial
Fondaparinux - none

52
Q

Thrombocytopenia most common with ____ (AE)

A

Heparin (still possible with others)

53
Q

Protamine

A

Highly basic positively charged peptide that combines with negatively charged heparin to form a stable complex that lacks anticoagulant activity
Only binds long heparin molecules

54
Q

How to monitor Heparin (lab)

A

Requires close monitoring of activated partial thromboplastin time (aPTT or PTT) (Intrinsic pathway)

55
Q

LMWH vs. Heparin

A

LMWH - more predictable pharmacokinetics, no monitoring required in most patients, fewer non-hemorrhagic side effects

56
Q

aPTT measures

A

intrinsic pathway

57
Q

If a PTT is long, and PT normal,

A

then the person is considered to have a defect in the intrinsic pathway

58
Q

Normal PTT times require presence of the following coagulation factors

A

I, II, V, VIII, IX, X, XI, & XII

59
Q

PT and INR measure

A

extrinsic pathway

60
Q

If PT is prolonged and aPTT is normal, then person has a defect in

A

extrinsic pathway

61
Q

PT measures factors

A

I (fibrinogen), II (prothrombin), V, VII, X

62
Q

What is best for monitoring warfarin

A

PT/INR Best for monitoring warfarin because it assess Factor VII status right away

63
Q

AE heparin, LMWH, fondaparinux

A

Bleeding

Heparin-induced thrombocytopenia

64
Q

Heparin induced thrombocytopenia

A

Thrombotic complications may precede the drop in platelets
Twice as likely in women than men
Probably due to development of IgG antibodies against complexes of heparin with platelet factor 4

65
Q

Direct thrombin inhibitors

A

Lepirudin, Bivalirudin, Argatroban

Dabigatran etexylate

66
Q

Lepirudin, Bivalirudin, Argatroban mechanism

A

Bind directly to thrombin and inhibits the enzyme

67
Q

derivative of leech salivary gland hirudin

A

Lepirudin

68
Q

Dabigatran etexylate mechanism

A

Binds directly to thrombin

69
Q

WArfarin mechanism

A

Blocks synthesis of Vitamin K dependent clotting factors

70
Q

Why is warfarin tricky

A

requires monitoring (PT/INR) and has tons of drug interactions

71
Q

Direct Factor Xa inhibitors

A

Rivaroxaban
Apixaban
Edoxaban

72
Q

direct factor Xa inhibitors have NO (2)

A

antidote

monitoring

73
Q

Direct factor Xa inhibitors have ____ onset and ____ half life

A 
rapid
shorter (than warfarin)
74
Q

Route warfarin, direct Xa inhibitors

A

Oral

75
Q

warfarin mechanism

A

inhibits conversion of oxidized vitamin K epoxide into its reduced form, vitamin K hydroquinone (Vitamin K dependent epoxide reductase (VKORC1)) –> inhibits vitamin K-dependent gamma-carboxylation of factors II, VII, IX, and X and Protein C

76
Q

Warfarin inhibits (summary)

A

inhibits vitamin K-dependent gamma-carboxylation of factors II, VII, IX, and X and Protein C

77
Q

AE warfarin

A 
BLEEDING
DRUG INTERACTIONS
flatulence and diarrhea
cutaneous necrosis
chondrodysplasia punctata = A birth defect from first trimester exposure
78
Q

Warfarin racemic mixture

A

S is the more active enantiomer

R- and S- Warfarin are metabolized differently in the liver by different cytochromes

79
Q

warfarin dosing

A

polymorphisms in VKORC1 can affect susceptibility to warfarin, influencing dosing (Pharmacodynamics)
Genetic polymorphisms in CYP2C9 influence metabolism (pharmacokinetics)

80
Q

For oral anticoagulants pharmacokinetic drug interactions are primarily due to

A

enzyme induction
enzyme inhibition
reduced plasma protein binding

81
Q

For oral anticoagulants pharmacodynamic drug interactions are primarily due to:

A

reduced clotting factor synthesis
competitive antagonism with Vitamin K
hereditary resistance to oral anticoagulants

82
Q

AE Bleeding with Warfarin

A 
Stop the drug
Add Vitamin K
Phytonadione (vitamin K1)
Or Prothromin complex concentrates
Or Recombinant factor VIIa
83
Q

Tissue plasminogen activators

A

tPAs = tissue plasminogen activators
Alteplase
Reteplase
Tenecteplase

84
Q

mechanism tPA

A

Preferentially activate plasminogen that is bound to fibrin which confines it to the thrombus rather than systemic activation. (both plasmin and tPA bind fibrin)

85
Q

common features of tPA

A

Dissolve EXISTING life-threatening thrombi
Activate plasminogen
Narrow spectrum of use

86
Q

route tPAs

A

Given IV

87
Q

AE tPAs

A

Bleeding

88
Q

Alteplase, Reteplase, Tenecteplase mechanism

A

“selective” activation of fibrin-bound plasminogen

89
Q

Aminocaproic acid

A

tPA inhibitor
Potent inhibitor of fibrinolysis
Blocks the interaction of plasmin with fibrin
Very minor uses

IHO Week 6 (EH) (9 decks)

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