Brainscape's Knowledge GenomeTM

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


See full index

IHO Week 6 (Final) > Anti-Platelet Drugs, Anti-Coagulants, Thrombolytics - Regal > Flashcards

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

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
Q

What is the MOA of Eptifibatide?

A

Fibrinogen Analogue

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

What is the MOA of Tirofiban?

A

Non-peptide competitive inhibitor

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

How are GPIIb-IIIa Receptor Inhibitors administered?

A

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

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

What are the adverse effects for GPIIb-IIIa Receptor Inhibitors?

A

Bleeding

Thrombocytopenia

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

What is the MOA of Dipyridamole?

A

Increases cAMP and inhibits platelet activation (Phosphodiesterase 3 Inhibitor and inhibits platelet uptake of adenosine and increases adenosine interaction with Adenosine A2 receptor)

30
Q

What is Dipyridamole used in combination with?

A

Aspirin or Warfarin

31
Q

What is the adverse effect of Dipyridamole?

A

Headache (Vasodilator)

32
Q

What are the different names of Heparin?

A 
Unfractionated Heparin (UFH)
High Molecular Weight Heparin (HMW)
Fondaparinux (pentasacharide)
33
Q

What is the MOA of Indirect Thrombin Inhibitors?

A

Bind to Anti-Thrombin to have their effect

34
Q

What is the normal activity of Anti-thrombin?

A

Inactivates both Thrombin and Factor Xa

35
Q

What is heparin’s activity against thrombin dependent on?

A

Size of Heparin Molecule

36
Q

With HMW Heparin, what is inactivated?

A

Thrombin and Xa

37
Q

With LMW Heparin, what is inactivated?

A

Mostly Xa, some thrombin

38
Q

With Fondaparinux, what is inactivated?

A

Only Xa

39
Q

What test monitors Heparin?

A

PTT

40
Q

What are the adverse effects of Heparin, LMW Heparin, and Fondaparinux?

A

Bleeding

Thrombocytopenia

41
Q

What is Protamine?

A

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
Q

What are the 3 Direct Thrombin Inhibitor drugs?

A

Bivalirudin
Argatroban
Dabigatran etexylate

43
Q

What is the MOA of Direct Thrombin Inhibitors?

A

Bind directly to Thrombin and inhibits the enzyme

44
Q

Which of the Direct Thrombin Inhibitors is orally administered?

A

Dabigtran etexylate

45
Q

What is the MOA of Warfarin?

A

Blocks synthesis of Vitamin K dependent clotting factors

46
Q

What are the 3 Direct Factor Xa Inhibitor drugs?

A

Rivaroxaban
Apixaban
Edoxaban

47
Q

Do Direct Factor Xa Inhibitors need monitoring?

A

NO

48
Q

Do Direct Factor Xa Inhibitors have an antidote?

A

NO

49
Q

What are the benefits of Direct Factor Xa Inhibitors?

A

Rapid Onset of Action

Shorter half life than warfarin

50
Q

What is the MOA of warfarin?

A

Inhibits conversion of oxidized vitamin K epoxide into its reduced form, vitamin K hydroquinone via vitamin K dependent epoxide reductase

51
Q

What vitamin K-dependent gamma-carboxylation factors does warfarin inhibit?

A

Factors II, VII, IX, and X and Protein C

52
Q

What are the adverse effects of Warfarin?

A

Bleeding
Flatulence and diarrhea
Cutaneous necrosis
Chondrodysplasia puctata

53
Q

What is the antidote to warfarin?

A

High doses of Vitamin K

54
Q

When does warfarin start working?

A

Delayed hypothrombic effect with initial hyperthrombic effect

55
Q

What test monitors Warfarin?

A

INR

56
Q

What enantiomer is the more active form of warfarin?

A

S-Warfarin

57
Q

What affects the susceptibility of the enzyme to warfarin-induced inhibition?

A

Polymorphisms in the C1 subunit of Vitamin K Reductase (VKORC1) –> affects warfarin pharmacodynamics

58
Q

What common genetic polymorphisms can influence warfarin metabolism?

A

CYP2C9 –> affects warfarin pharmacokinetics (30% of patients are slow metabolizers)

59
Q

What are some pharmacokinetics of Warfarin?

A

Absorption (oral administration –> plasma concentration), Distribution, (Plasma Protein Binding), Metabolism, Elimination (CYP450)

60
Q

What are the pharmacodynamics of Warfarin?

A

Decrease in Vitamin K-Dependent Clotting Factor Concentrations
–Biochemical and physiological effects of drugs and their MOA

61
Q

What are the pharmacokinetic drug interactions for oral anticoagulants?

A

Enzyme Induction
Enzyme Inhibition
Reduced Plasma Protein Binding

62
Q

What are the pharmcodynamic drug interactions for oral anticoagulants?

A

Reduced clotting factor synthesis
Competitive antagonism with Vitamin K
Hereditary Resistance to oral anticoagulation

63
Q

What do we do when too much warfarin causes bleeding?

A 
STOP THE DRUG!
Add Vitamin K
  - Phytonadione (Vitamin K1)
  - Prothrombin Complex Concentrates
  - Recombinant Factor VIIa
64
Q

What are the Fibrinolytic Drugs?

A

Streptokinase and Urokinase

65
Q

What is the MOA of Streptokinase?

A

Complexes with plasminogen wherever it is and facilitates formation of plasmin

66
Q

What is the MOA of Urokinase?

A

Kidney enzyme that directly converts plasminogen to plasmin, promoting extravascular fibrinolysis in response to inflammatory stimuli

67
Q

What are the tPA (tissue Plasminogen Activator) Fibrinolytic drugs?

A

Alteplase
Reteplase
Tenecteplase

68
Q

What is the MOA of tPAs?

A

Activate plasminogen that is bound to fibrin, which confines it to the thrombus rather than systemically

69
Q

How are tPAs administered?

A

IV with narrow spectrum of use

70
Q

What are thrombolytics approved for?

A

Stroke

IHO Week 6 (Final) (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions