Anti-thrombotics Flashcards Preview

Cardiovascular System > Anti-thrombotics > Flashcards

Flashcards in Anti-thrombotics Deck (36):
1

What is the only anti-thrombotic treatment difference between STEMI and NSTEMI?

Thrombolytics (only for STEMI)

2

Which protease is responsible for converting fibrinogen to fibrin?

Thrombin

3

What cocagulation cascade protein is responsible for degradation of fibrin clots?

Plasmin

4

What is the length of platelet life span?

7-10 Days

5

What is hemostasis?

Process that prevents blood loss from damaged blood vesses

6

What is thrombosis?

Pathological formation of a hemostatic plug within the vasculature in the absence of bleeding

7

What causes thrombosis?

Injury to blood vessel wall
Altered blood flow
Abnormal coagulability of blood

8

What is the point of convergence for the intrinsic and extrinsic pathways?

Activation of Factor X to Factor Xa

9

What activates plasminogen to plasmin?

t-PA (tissue plasminogen activator)

10

What does GPIIb/GPIIIa do?

Glycoprotein receptor that binds fibrinogen on the platelets?

11

What does P2Y1/P2Y12 do?

Purinergic receptors for ADP, stimulates COX and GPIIb/IIIa

12

What does COX do (in respect to thrombogenesis)?

Production of TXA2/PGI2

13

What is the only drug that can actually lyse a clot?

t-PA: Alteplase

14

Why do we do fibrinolytic therapy in STEMIs?

Restore coronary blood flow, limit myocardial damage, better survival and fewer complications

15

What is the mechanism of t-PA?

Transforms plasminogen to plasmin

16

When should you try to administer thrombolytics by?

Within 30 minutes of patient's presentation at hospital

17

What are adverse effects of thromobolytics?

Bleeding is most common complication
Streptokinase can result in systemic lytic state - interfering with coagulation in general circulation

18

What are contraindications to thrombolytics?

Roughly 30% of patients may be unsuited
Situations where drug therapy could impair necessary clots within circulation (Peptic ulcer, recent stroke, surgery recovery)

19

Why do we not give heparin orally?

It is too large and too negative, needs parenteral delivery.

20

Which drug inhibits coagulation independently of antithrombin?

Bivalirudin

21

What is the only drug recommended for chronic angina?

Aspirin

22

What are the names of all the heparins/heparin-like drugs?

Unfractionated heparin
LMWH (Enoxaparin, Dalteparin)
Fondaparinux

23

What is the major unique side effect of UFH?

Heparin-induced thrombocytopenia (HIT)

24

Why are LMWH preferred?

Less risk of HIT
(Fondaparinux also confers this advantage)

25

What does bivalirudin act on?
What do heparins act on?

Bivalirudin: Acts on both circulating and clot-bound-thrombin
Heparins: Circulating thrombin

26

What indication for bivalirudin?

Unstable angina undergoing percutaneous coronary intervention.

27

What is the major adverse effect of bivalirudin?

Bleeding

28

What is the mechanism of aspirin?

Irreversibly acetylates COX1 in platelet, blocks thromboxane
Also encourages endothelial cells to produce prostacyclin (prevents platelet adhesion)

29

What are the thienopyridines?
What do the thienopyridines do?
Which thienopyridines are reversible?
Which are irreversible?
What is the advantage of reversible ones?

Clopidogrel (Irrev), ticlopidine (Irrev), prasugrel (Irrev), ticagrelor (Rev)
Block P2Y1 and P2Y12 to prevent ADP-mediated activation of platelets
Reversibles are advantageous for patients who need to go to surgery, platelets restore function earlier

30

Which thienopyridines need to be metabolized to be activated?
Which one needs CYP2C19 and what co-administration is a concern for it?

Clopidogrel, ticlopidine, and prasugrel
Clopidogrel requires CYP2C19 and care should be taken if co-administered with omeprazole (PPIs inhibit CYP2C19)

31

What side-effects are associated with thienopyridines?
What are the advantages and disadvantages of them versus aspirin?

In general bleeding and GI, ticlopidine associated with life threatening neutropenia and thrombotic thrombocytopenic purpura
Superior monotherapy to aspirin in reducing MI risk, but more expensive and higher risk of side effects. Can be paired with aspirin but still increases bleeding.

32

What are the GPIIb/IIIa receptor antagonists?
What is their mechanism?

Abciximab and Eptifibatide
Reversibly inhibit the final common pathway of platelet aggregation (GPIIb/IIIa receptor binding to fibrinogen and vWF)
Prevents formation of hemostatic plug

33

Differences between Abciximab and Eptifibatide:
Source
Binding
Kinetics
Indication
Co-administeration

Abciximab:
S - Chimeric human-mouse monoclonal Ab
B - Blocks Fibrinogen, vWF access to GP IIb/IIIa receptor
K - Non-competitive, IV
I - PCI: Angioplasty and stent
C - Aspirin and heparins; also with alteplase for thrombolysis

Eptifibatide
S - Synthetic peptide antagonist
B - Sequence motif specifically binds to GP IIb/IIIa receptor
K - Competitive. IV, Renal
I - PCI: Angioplasty and stent; Unstable angina and MI
C - LMWH often for unstable angina and MI

34

What is dipyridamole?
When is it given?
What is known about its action?
What is its efficacy?

Anti-platelet
Given to patients who cannot tolerate aspirin
Unclear: Increases platelet cAMP so blocks phosphodiesterase, blocks platelet uptake and destruction of adenosine
If given alone the drug has no proven cardiac benefits

35

What are some new oral anti-coagulants?
What are some potential indications for them?

Dabigatran and Rivaroxaban
Reduce risk of stroke, systemic embolism in patients with nonvalvular atrial fibrillation; Reduce the risk of recurrent ischemia after an ACS event

36

What are the aspirin recommendations for primary prevention?

Low dose (75 to 325 mg.day) to patients with clinical manifestation of CAD, assuming no contraindications in patient
Should not be prescribed routinely for primary prevention purposes to completely healthy individual
Possibly recommend to patients over 50 yo and have at least one major risk factor