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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
Clopidogrel may require activation via ________ so drugs that impair this isoform should be used with caution
CYP2C19 (ie. omeprazole)
26
ADP Receptor antagonists reversible?
NO, but new drugs are coming out that are reversible (Ticagrelor, Cangrelor)
27
GPIIb/IIIa receptor inhibitors mechanism
Prevent binding of adhesive glycoproteins such as fibrinogen and vWF to activated platelets Inhibits the final common pathway for platelet aggregation
28
GPIIb/IIIa receptor inhibitors
Abciximab Eptifibatide Tirofiban (fib binds where fibrinogen binds, + abciximab)
29
Abciximab
humanized MAB against GPIIb/IIIa
30
Eptifibatide
fibrinogen analogue
31
Tirofiban
non-peptide competitive inhibitor
32
GPIIb/IIIa receptor inh route, uses
IV with aspirin and heparin during angioplasty, for acute coronary syndromes
33
AE GPIIb/IIIa rec inh
Bleeding | Thrombocytopenia (chronic use)
34
Dipyridamole mechanism
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
35
Dipyridamole AE
headache
36
Dipyridamole USe
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
thrombin two big jobs
activate platelets | cleave fibrinogen to fibrin
38
thrombin inhibitors - 2 major kinds
indirect | direct
39
thrombin inhibitors route
parenteral
40
indirect thrombin inhibitors
Unfractionated heparin Low molecular weight heparin Fondaparinux
41
direct thrombin inhibitors
Lepirudin Bivalirudin Argatroban Dabigatran etexylate (oral, new)
42
UFH =
Unfractionated heparin (UFH) is the same thing as high molecular weight (HMW) heparin, often just called heparin
43
mechanism indirect thrombin inhibitors
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
Heparin's activity against thrombin is ____ dependent
size
45
what limits heparin's bioavailability
Binding to plasma proteins, platelet (platelet factor 4), macrophages, and endothelial cells account for highly variable anticoagulant response
46
UFH can inhibit
both Xa and thrombin
47
LMWH can inhibit
Xa > thrombin
48
Fondaparinux can inhibit
Xa only (too short to bridge antithrombin)
49
sources of indirect thrombin inhibitors
heparin, LMWH = biological (porcine) | fondaparinux = synthetic
50
which indirect thrombin inhib has longest half life
fondaparinux > LMWH > heparin
51
antidote effects vs indirect thrombin inhibitors
heparin - complete LMWH - partial Fondaparinux - none
52
Thrombocytopenia most common with ____ (AE)
Heparin (still possible with others)
53
Protamine
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
How to monitor Heparin (lab)
Requires close monitoring of activated partial thromboplastin time (aPTT or PTT) (Intrinsic pathway)
55
LMWH vs. Heparin
LMWH - more predictable pharmacokinetics, no monitoring required in most patients, fewer non-hemorrhagic side effects
56
aPTT measures
intrinsic pathway
57
If a PTT is long, and PT normal,
then the person is considered to have a defect in the intrinsic pathway
58
Normal PTT times require presence of the following coagulation factors
I, II, V, VIII, IX, X, XI, & XII
59
PT and INR measure
extrinsic pathway
60
If PT is prolonged and aPTT is normal, then person has a defect in
extrinsic pathway
61
PT measures factors
I (fibrinogen), II (prothrombin), V, VII, X
62
What is best for monitoring warfarin
PT/INR Best for monitoring warfarin because it assess Factor VII status right away
63
AE heparin, LMWH, fondaparinux
Bleeding | Heparin-induced thrombocytopenia
64
Heparin induced thrombocytopenia
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
Direct thrombin inhibitors
Lepirudin, Bivalirudin, Argatroban | Dabigatran etexylate
66
Lepirudin, Bivalirudin, Argatroban mechanism
Bind directly to thrombin and inhibits the enzyme
67
derivative of leech salivary gland hirudin
Lepirudin
68
Dabigatran etexylate mechanism
Binds directly to thrombin
69
WArfarin mechanism
Blocks synthesis of Vitamin K dependent clotting factors
70
Why is warfarin tricky
requires monitoring (PT/INR) and has tons of drug interactions
71
Direct Factor Xa inhibitors
Rivaroxaban Apixaban Edoxaban
72
direct factor Xa inhibitors have NO (2)
antidote | monitoring
73
Direct factor Xa inhibitors have ____ onset and ____ half life
``` rapid shorter (than warfarin) ```
74
Route warfarin, direct Xa inhibitors
Oral
75
warfarin mechanism
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
Warfarin inhibits (summary)
inhibits vitamin K-dependent gamma-carboxylation of factors II, VII, IX, and X and Protein C
77
AE warfarin
``` BLEEDING DRUG INTERACTIONS flatulence and diarrhea cutaneous necrosis chondrodysplasia punctata = A birth defect from first trimester exposure ```
78
Warfarin racemic mixture
S is the more active enantiomer | R- and S- Warfarin are metabolized differently in the liver by different cytochromes
79
warfarin dosing
polymorphisms in VKORC1 can affect susceptibility to warfarin, influencing dosing (Pharmacodynamics) Genetic polymorphisms in CYP2C9 influence metabolism (pharmacokinetics)
80
For oral anticoagulants pharmacokinetic drug interactions are primarily due to
enzyme induction enzyme inhibition reduced plasma protein binding
81
For oral anticoagulants pharmacodynamic drug interactions are primarily due to:
reduced clotting factor synthesis competitive antagonism with Vitamin K hereditary resistance to oral anticoagulants
82
AE Bleeding with Warfarin
``` Stop the drug Add Vitamin K Phytonadione (vitamin K1) Or Prothromin complex concentrates Or Recombinant factor VIIa ```
83
Tissue plasminogen activators
tPAs = tissue plasminogen activators Alteplase Reteplase Tenecteplase
84
mechanism tPA
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
common features of tPA
Dissolve EXISTING life-threatening thrombi Activate plasminogen Narrow spectrum of use
86
route tPAs
Given IV
87
AE tPAs
Bleeding
88
Alteplase, Reteplase, Tenecteplase mechanism
“selective” activation of fibrin-bound plasminogen
89
Aminocaproic acid
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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