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16. Anti thromb/plat drugs Flashcards

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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.

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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

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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)

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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)

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5
Q

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

A

Vit K

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6
Q

What is the point of convergence between

extrinsic pathway and intrinsic pathway

A

Factor Xa

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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

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8
Q

What patients benefit from fibrinolytic therapy?

A

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

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9
Q

Alteplase (tPA) is what type of drug therapy?

A

Recombinant tissue-type plasminogen activators

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10
Q

Mech of action of tPA

A

Transforms the inactive precursor plasminogen

into active protease plasmin, which lyses fibrin clots

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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

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12
Q

Complication of tPA?

A

Bleeding

lytic state for older fibrinolytics (streptokinase)

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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

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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.

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15
Q

Goals of Anti-Coags

A

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

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16
Q

Interfere with coagulation cascade and impair secondary

hemostasis

A

Anti-Coags

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17
Q

enoxaparin, dalteparin are examples of

A

Low molecular weight heparins

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18
Q

What additional side effect besides bleeding in unfractionated Heparin is:

A

heparin-induced thrombocytopenia (HIT)

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19
Q

Side effect of all ‘heparins’

A

bleeding

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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

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21
Q

Direct Thrombin Inhibitor

A

Bivalirudin

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22
Q

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

A

Bivalirudin (direct thrombin inhibitor)

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23
Q

Unstable angina patients undergoing percutaneous coronary intervention should use

A

Bivalirudin

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24
Q

Bivalirudin should be used for patients:

A

Unstable angina patients undergoing percutaneous coronary intervention

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25
Does Bivalirudin cause thrombocytopenia?
NOPE
26
Whats the issue with thrombin bound to fibrin?
thrombin bound to fibrin within a thrombus remains enzymatically active and protected from inactivation by antithrombin--- can locally activate plateletes causing thrombus growth
27
Whats the difference in how Heparin and Direct Thrombin inhibitors (Bivalirudin) act on throbmin?
* Heparin only inactivates circulating thrombin | * Direct thrombin inhibitors inactive free and fibrin-bound
28
Clopidogrel, Ticlopidine, Prasugrel and Ticagrelor are all examples of
Thienopyriadines: Anti-Plat drugs
29
Abciximab and Eptifbatide are examples of?
GP 11b/IIIa receptor antagonists
30
Plat activation is associated with increase in:
Ca++ in numerous different mechanisms
31
Aspirin irreversibly acetylates:
cyclooxygenase-1 in platelet
32
What effect does aspirin have on thromboxane?
* Blocks production of thromboxane | * Platelets lack nuclei so permanant effect of aspirin
33
What is the role of prostacyclin in platelets?
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
Aspirin use in patients with
CVD for Secondary Prevention
35
What benefit does aspirin used in patients with unstable angina, acute myocardial infarction (MI), history of MI provide?
– Reduces incidence of future fatal and nonfatal coronary events
36
What benefit does aspirin provide in patients with chronic stable angina without a history of MI?
Decreases occurrence of subsequent MI and mortality
37
What benefit does aspirin provide in patients who have had a minor stroke or transient cerebral ischemic attack
Reduces rate of future stroke and CV events
38
What benefit does aspirin have in patients who have undergone coronary artery bypass surgery?
Decreases chance of graft occlusion
39
What pts should use asprin? | Shouldn't use it?
Low dose for those with clinical manifestations of coronary artery disease DONT use in health individuals
40
Mech of action of Thienopyridines; clopidogrel, ticlopidine, prasugrel and ticagrelor:
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
Inhibit ADP-mediated activation of platelets • ADP simultaneously activates two purinergic receptors, P2Y1 and P2Y12
Thienopyridines
42
Which thienopryidines are irreversible?
clopidegrel, prasurgrel
43
Which thienopryadines are reversible?
ticagrelor
44
Drugs inhibit P2Y12 receptor
Thienopryidines
45
What is the advantage of reversible platelet | inhibitors?
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
Clopidogrel, ticlopidine and prasugrel are____ (which is more readily metabolized?)
pro-drugs | – Prasugrel more readily metabolized and increased potency
47
Side effects of Thienopryidines
Side effects include bleeding and GI related symptoms
48
Thienopryidine associated with life threating adverse effects such as severe neutropenia and thrombitic purpura
Ticlopidine
49
Clopidogrel is metabolized by
CYP2C19 – Variability of response in patients with CYP2C19 polymorphisms
50
What drug do we need to be careful of administering with Clopidogrel?
Co-administration with protein pump inhibitor (omeprazole) a concern since PPI inhibit CYP2C19
51
As monotherapy, drugs are modestly superior to aspirin in reducing risk of myocardial infarction – Increased risk of side effects – Increased cost
Thienopryidine
52
Combination of______ with aspirin has increased benefit compared to aspirin alone – Increased bleeding risk
clopidogrel
53
Mech of Abciximab
blocks access of fibrinogen, vWF and other adhesive | molecules to the GP IIb-IIIa receptor
54
blocks access of fibrinogen, vWF and other adhesive | molecules to the GP IIb-IIIa receptor
Abciximab
55
Mech of Eptifibatide
Contains a sequence motif that binds specifically to GP | IIb-IIIa receptors
56
Both Abciximab and Eptifibatibe are Glycoprotein IIb/IIIa Receptor Antagonists: Which one is competitive?
Eptifibatibe is competitive | Abciximabe is non-competitive
57
Indications of Abciximab or Eptifibatibe?
Patients undergoing PCI, including angioplasty or | stent placement
58
Patients undergoing PCI, including angioplasty or stent | placement OR Patients with unstable angina and myocardial infarction, often with LMWH
Eptifibatibe
59
What other drugs do we use or can we use when giving Abciximab?
In combination with aspirin and heparin (or LMWH) | • Also used with alteplase for thrombolysis
60
All you need to know about Dipryidamole
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
Dabigitran Rivaroxaban are what kinds of drugs?
New oral anticoags
62
Whats the benefit of Dabigitran and rivaroxaban?
reduce the risk of stroke and systemic embolism in | patients with nonvalvular atrial fibrillation
63
Rivaroxaban inhibits: | Dabigitraban inhibits
Xa | Thrombin

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