16. Anti thromb/plat drugs Flashcards

1
Q

The pharmacologic treatment of NSTEMI, UA, and STEMI is similar, and is consists of

A

antithrombotic/antiplatelet agents, statins, beta adrenergic
blockers and nitrates.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q
These are all examples of:
Cyclooxygenase inhibitors
• Aspirin
– ADP receptor inhibitors
• Clopidogrel
• Prasugrel
• Ticagrelor
– Glycoprotein IIb/IIIa inhibitors
Abciximab
• Eptifibatide
A

Anti-Plats Drugs

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

Coag Cascade: series of transformations of proenzymes to activated enzymes resulting in the formation of _______which converts soluble fibrinogen to insoluble
fibrin

A

thrombin (IIa)

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

Key actions in CoAg cascade:

A

– activation of Factor X to Xa
– conversion of prothrombin(II) to thrombin (IIa)
– thrombin-mediated transformation of fibrinogen to fibrin (the GLUE)

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

Factors II, IX, X, VII depend on synthesis of:

A

Vit K

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

What is the point of convergence between

extrinsic pathway and intrinsic pathway

A

Factor Xa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Why do we want to accelerate lysis of occlusive intracoronary thrombosis in STEMI with Fibrinolytics?

A

– Restore coronary blood flow
– Limit myocardial damage
– Translate to increased survival rate and fewer complications

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

What patients benefit from fibrinolytic therapy?

A

Pts with STEMI:
Patients with UA or NSTEMI do not benefit from
fibrinolytic therapy

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

Alteplase (tPA) is what type of drug therapy?

A

Recombinant tissue-type plasminogen activators

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

Mech of action of tPA

A

Transforms the inactive precursor plasminogen

into active protease plasmin, which lyses fibrin clots

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

• No matter which thrombolytic is used, the

key point is that need to be

A

administered ASAP, ideally within 30 min of patient’s presentation at hospital

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

Complication of tPA?

A

Bleeding

lytic state for older fibrinolytics (streptokinase)

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

What patients should we NOT put on fibrinolytics (tPA)?

A

therapy could impair necessary fibrin clots w/i circulation
– Active peptic ulcer
– Recent stroke
– Recovering from recent surgery

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

In patients with STEMI,
the earlier the patient presents, and the earlier the artery can be recanalised, the better:
• degree of reversibility and extent of myocardial necrosis are both:
Which is better: an open artery or closed artery?

A

both time dependent

an open artery is better than a closed artery.

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

Goals of Anti-Coags

A

inhibit activation of thrombin by Xa
Directly inhibit thrombin
Decrease production of functional prothrombin

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

Interfere with coagulation cascade and impair secondary

hemostasis

A

Anti-Coags

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

enoxaparin, dalteparin are examples of

A

Low molecular weight heparins

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

What additional side effect besides bleeding in unfractionated Heparin is:

A

heparin-induced thrombocytopenia (HIT)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Side effect of all ‘heparins’

A

bleeding

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

LMWH (enoxaparin and dalteparin) as well as fondaparinux advantage over UFH is

A

longer half-life and more predictable bioavailablity

less bleeding, less risk of HIT

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

Direct Thrombin Inhibitor

A

Bivalirudin

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

INhibits independent of antithrombin and acts on circulating and clot-bound thrombin

A

Bivalirudin (direct thrombin inhibitor)

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

Unstable angina patients undergoing percutaneous coronary intervention should use

A

Bivalirudin

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

Bivalirudin should be used for patients:

A

Unstable angina patients undergoing percutaneous coronary intervention

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Does Bivalirudin cause thrombocytopenia?

A

NOPE

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

Whats the issue with thrombin bound to fibrin?

A

thrombin bound to fibrin within a thrombus remains enzymatically active and protected from inactivation by antithrombin— can locally activate plateletes causing thrombus growth

27
Q

Whats the difference in how Heparin and Direct Thrombin inhibitors (Bivalirudin) act on throbmin?

A
  • Heparin only inactivates circulating thrombin

* Direct thrombin inhibitors inactive free and fibrin-bound

28
Q

Clopidogrel, Ticlopidine, Prasugrel and Ticagrelor are all examples of

A

Thienopyriadines: Anti-Plat drugs

29
Q

Abciximab and Eptifbatide are examples of?

A

GP 11b/IIIa receptor antagonists

30
Q

Plat activation is associated with increase in:

A

Ca++ in numerous different mechanisms

31
Q

Aspirin irreversibly acetylates:

A

cyclooxygenase-1 in platelet

32
Q

What effect does aspirin have on thromboxane?

A
  • Blocks production of thromboxane

* Platelets lack nuclei so permanant effect of aspirin

33
Q

What is the role of prostacyclin in platelets?

A

Inhibits platelet aggregation: EC’s make this and can regenerate and make more of this to keep platelets from being activated vs aspirin which is irreversible

34
Q

Aspirin use in patients with

A

CVD for Secondary Prevention

35
Q

What benefit does aspirin used in patients with unstable angina, acute myocardial infarction (MI), history of MI provide?

A

– Reduces incidence of future fatal and nonfatal coronary events

36
Q

What benefit does aspirin provide in patients with chronic stable angina without a history of MI?

A

Decreases occurrence of subsequent MI and mortality

37
Q

What benefit does aspirin provide in patients who have had a minor stroke or transient cerebral ischemic attack

A

Reduces rate of future stroke and CV events

38
Q

What benefit does aspirin have in patients who have undergone coronary artery bypass surgery?

A

Decreases chance of graft occlusion

39
Q

What pts should use asprin?

Shouldn’t use it?

A

Low dose for those with clinical manifestations of coronary artery disease
DONT use in health individuals

40
Q

Mech of action of Thienopyridines; clopidogrel, ticlopidine, prasugrel and ticagrelor:

A

Inhibit ADP-mediated activation of platelets
• ADP simultaneously activates two purinergic
receptors, P2Y1 and P2Y12
– P2Y1 –> increase PLC –> increase calcium
– P2Y12 –> decrease cAMP–>increase calcium

41
Q

Inhibit ADP-mediated activation of platelets
• ADP simultaneously activates two purinergic
receptors, P2Y1 and P2Y12

A

Thienopyridines

42
Q

Which thienopryidines are irreversible?

A

clopidegrel, prasurgrel

43
Q

Which thienopryadines are reversible?

A

ticagrelor

44
Q

Drugs inhibit P2Y12 receptor

A

Thienopryidines

45
Q

What is the advantage of reversible platelet

inhibitors?

A

If patient requires surgery (like coronary bypass surgery) and is taking drug like
clopidogrel (or aspirin), waiting period is
necessary to prevent platelet function to
return to normal.
– Life span of the platelet?
– 7-10 days

46
Q

Clopidogrel, ticlopidine and
prasugrel are____
(which is more readily metabolized?)

A

pro-drugs

– Prasugrel more readily metabolized and increased potency

47
Q

Side effects of Thienopryidines

A

Side effects include bleeding and GI related symptoms

48
Q

Thienopryidine associated with life threating adverse effects such as severe neutropenia and thrombitic purpura

A

Ticlopidine

49
Q

Clopidogrel is metabolized by

A

CYP2C19
– Variability of response in patients
with CYP2C19 polymorphisms

50
Q

What drug do we need to be careful of administering with Clopidogrel?

A

Co-administration with protein pump inhibitor (omeprazole) a concern since PPI inhibit CYP2C19

51
Q

As monotherapy, drugs are modestly superior to aspirin
in reducing risk of myocardial infarction
– Increased risk of side effects
– Increased cost

A

Thienopryidine

52
Q

Combination of______ with aspirin has increased
benefit compared to aspirin alone
– Increased bleeding risk

A

clopidogrel

53
Q

Mech of Abciximab

A

blocks access of fibrinogen, vWF and other adhesive

molecules to the GP IIb-IIIa receptor

54
Q

blocks access of fibrinogen, vWF and other adhesive

molecules to the GP IIb-IIIa receptor

A

Abciximab

55
Q

Mech of Eptifibatide

A

Contains a sequence motif that binds specifically to GP

IIb-IIIa receptors

56
Q

Both Abciximab and Eptifibatibe are Glycoprotein IIb/IIIa Receptor Antagonists:
Which one is competitive?

A

Eptifibatibe is competitive

Abciximabe is non-competitive

57
Q

Indications of Abciximab or Eptifibatibe?

A

Patients undergoing PCI, including angioplasty or

stent placement

58
Q

Patients undergoing PCI, including angioplasty or stent

placement OR Patients with unstable angina and myocardial infarction, often with LMWH

A

Eptifibatibe

59
Q

What other drugs do we use or can we use when giving Abciximab?

A

In combination with aspirin and heparin (or LMWH)

• Also used with alteplase for thrombolysis

60
Q

All you need to know about Dipryidamole

A

Occasionally prescribed to patients that
cannot tolerate aspirin; relatively ineffective
• Mechanism of action-unclear, may increase in platelet cAMP
• Blocking phosphodiesterase
• Blocking cellular uptake and destruction of adenosine
• Given alone, the drug has no proven cardiac
benefits

61
Q

Dabigitran
Rivaroxaban
are what kinds of drugs?

A

New oral anticoags

62
Q

Whats the benefit of Dabigitran and rivaroxaban?

A

reduce the risk of stroke and systemic embolism in

patients with nonvalvular atrial fibrillation

63
Q

Rivaroxaban inhibits:

Dabigitraban inhibits

A

Xa

Thrombin