Anti-Platelet Drugs, Anti-Coagulants, Thrombolytics - Regal Flashcards

(70 cards)

1
Q

What is Phase I of Hemostasis?

A

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

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

What is Phase II of Hemostasis?

A

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

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

What is Phase III of Hemostasis?

A

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

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

What is Phase IV of Hemostasis?

A

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

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

How is venous thrombosis acquired and what are the risk factors for venous thrombosis?

A

Inherited disorders characterized by tendency to form thrombi with increased risk due to prolonged bed rest, surgery, cancer, atrial fibrillation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the therapeutic uses for anti-platelet drugs?

A
Venous Thromboembolism
Unstable Angina
Acute MI
Stroke
Prevent thrombosis during angioplasty and cardiopulmonary bypass
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the MOA of Aspirin (Acetylsalicylate Acid)?

A

Irreversible inhibitor of COX1

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

Do platelets have COX2?

A

No

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

Can platelets make more COX?

A

No - no nucleus

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

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

A

Reversible

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

What are the therapeutic properties of Aspirin?

A

Anti-Pyretic
Analgesic
Anti-Inflammatory

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the adverse effects of Aspirin?

A

Bleeding
GI disturbances
Tinnitus

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

What are the benefits of low-dose aspirin?

A

Anti-Platelet aggregation

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

What are the benefits of high-dose aspirin?

A

Anti-Platelet aggregation and Anti-Inflammatory

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

What are the 3 ADP Receptor Antagonist Drugs?

A

Clopidogrel
Prasugrel
Ticlopidine

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

How do ADP Receptor Antagonists work?

A

Irreversibly prevent activation of ADP receptor

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

How are ADP Receptor Antagonists administered and what is their duration of action?

A

Oral Administration

Duration of Days

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

What are the adverse effects of ADP Receptor Antagonists?

A
BLEEDING
Nausea
Diarrhea
Rash
Severe Leukopenia
TTP (Thrombotic Thrombocytopenic Purpura)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What ADP Receptor Antagonist has the most side effects?

A

Ticlopidine

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

How is Clopidogrel activated?

A

CYP2C19 – don’t take omeprazole with this!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Are the effects of ADP Receptor Antagonists reversible?

A

NO! Lasts the life of the platelet

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

What is the MOA of GPIIb-IIIa Receptor Inhibitors?

A

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

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

What are the 3 GPIIb-IIIa Receptor Inhibitor Drugs?

A

Abciximab
Eptifibatide
Tirofiban

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

What is the MOA of Abciximab?

A

Humanized MAB against GPIIb-IIIa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What is the MOA of Eptifibatide?
Fibrinogen Analogue
26
What is the MOA of Tirofiban?
Non-peptide competitive inhibitor
27
How are GPIIb-IIIa Receptor Inhibitors administered?
IV with aspirin and heparin during angioplasty or for acute coronary syndromes
28
What are the adverse effects for GPIIb-IIIa Receptor Inhibitors?
Bleeding | Thrombocytopenia
29
What is the MOA of Dipyridamole?
Increases cAMP and inhibits platelet activation (Phosphodiesterase 3 Inhibitor and inhibits platelet uptake of adenosine and increases adenosine interaction with Adenosine A2 receptor)
30
What is Dipyridamole used in combination with?
Aspirin or Warfarin
31
What is the adverse effect of Dipyridamole?
Headache (Vasodilator)
32
What are the different names of Heparin?
``` Unfractionated Heparin (UFH) High Molecular Weight Heparin (HMW) Fondaparinux (pentasacharide) ```
33
What is the MOA of Indirect Thrombin Inhibitors?
Bind to Anti-Thrombin to have their effect
34
What is the normal activity of Anti-thrombin?
Inactivates both Thrombin and Factor Xa
35
What is heparin's activity against thrombin dependent on?
Size of Heparin Molecule
36
With HMW Heparin, what is inactivated?
Thrombin and Xa
37
With LMW Heparin, what is inactivated?
Mostly Xa, some thrombin
38
With Fondaparinux, what is inactivated?
Only Xa
39
What test monitors Heparin?
PTT
40
What are the adverse effects of Heparin, LMW Heparin, and Fondaparinux?
Bleeding | Thrombocytopenia
41
What is Protamine?
Highly basic positively charged peptide that combines with negatively charged heparin to form a stable complex that lacks anticoagulant activity - will only inhibit HMW Heparin, and some LMW Heparin
42
What are the 3 Direct Thrombin Inhibitor drugs?
Bivalirudin Argatroban Dabigatran etexylate
43
What is the MOA of Direct Thrombin Inhibitors?
Bind directly to Thrombin and inhibits the enzyme
44
Which of the Direct Thrombin Inhibitors is orally administered?
Dabigtran etexylate
45
What is the MOA of Warfarin?
Blocks synthesis of Vitamin K dependent clotting factors
46
What are the 3 Direct Factor Xa Inhibitor drugs?
Rivaroxaban Apixaban Edoxaban
47
Do Direct Factor Xa Inhibitors need monitoring?
NO
48
Do Direct Factor Xa Inhibitors have an antidote?
NO
49
What are the benefits of Direct Factor Xa Inhibitors?
Rapid Onset of Action | Shorter half life than warfarin
50
What is the MOA of warfarin?
Inhibits conversion of oxidized vitamin K epoxide into its reduced form, vitamin K hydroquinone via vitamin K dependent epoxide reductase
51
What vitamin K-dependent gamma-carboxylation factors does warfarin inhibit?
Factors II, VII, IX, and X and Protein C
52
What are the adverse effects of Warfarin?
Bleeding Flatulence and diarrhea Cutaneous necrosis Chondrodysplasia puctata
53
What is the antidote to warfarin?
High doses of Vitamin K
54
When does warfarin start working?
Delayed hypothrombic effect with initial hyperthrombic effect
55
What test monitors Warfarin?
INR
56
What enantiomer is the more active form of warfarin?
S-Warfarin
57
What affects the susceptibility of the enzyme to warfarin-induced inhibition?
Polymorphisms in the C1 subunit of Vitamin K Reductase (VKORC1) --> affects warfarin pharmacodynamics
58
What common genetic polymorphisms can influence warfarin metabolism?
CYP2C9 --> affects warfarin pharmacokinetics (30% of patients are slow metabolizers)
59
What are some pharmacokinetics of Warfarin?
Absorption (oral administration --> plasma concentration), Distribution, (Plasma Protein Binding), Metabolism, Elimination (CYP450)
60
What are the pharmacodynamics of Warfarin?
Decrease in Vitamin K-Dependent Clotting Factor Concentrations --Biochemical and physiological effects of drugs and their MOA
61
What are the pharmacokinetic drug interactions for oral anticoagulants?
Enzyme Induction Enzyme Inhibition Reduced Plasma Protein Binding
62
What are the pharmcodynamic drug interactions for oral anticoagulants?
Reduced clotting factor synthesis Competitive antagonism with Vitamin K Hereditary Resistance to oral anticoagulation
63
What do we do when too much warfarin causes bleeding?
``` STOP THE DRUG! Add Vitamin K - Phytonadione (Vitamin K1) - Prothrombin Complex Concentrates - Recombinant Factor VIIa ```
64
What are the Fibrinolytic Drugs?
Streptokinase and Urokinase
65
What is the MOA of Streptokinase?
Complexes with plasminogen wherever it is and facilitates formation of plasmin
66
What is the MOA of Urokinase?
Kidney enzyme that directly converts plasminogen to plasmin, promoting extravascular fibrinolysis in response to inflammatory stimuli
67
What are the tPA (tissue Plasminogen Activator) Fibrinolytic drugs?
Alteplase Reteplase Tenecteplase
68
What is the MOA of tPAs?
Activate plasminogen that is bound to fibrin, which confines it to the thrombus rather than systemically
69
How are tPAs administered?
IV with narrow spectrum of use
70
What are thrombolytics approved for?
Stroke