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Case 4 > The role of platelet activation and thrombosis in the pathophysiology of acute coronary syndrome- how does this influence treatment > Flashcards

The role of platelet activation and thrombosis in the pathophysiology of acute coronary syndrome- how does this influence treatment Flashcards

(61 cards)

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1
Q

What is the triad of conditions in acute coronary syndromes

A

Unstable angina (UNSA), non ST elevation myocardial infarction (NSTEMI) and ST elevation myocardial infarction (STEMI)

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2
Q

What can occur before an infarct is fully evolved

A

Sudden cardiac death

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3
Q

What happens in unstable angina

A

A quiescent plaque ruptures resulting in the underlying fatty material being exposed to blood

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4
Q

What happens when underlying fatty material is exposed to blood

A

Blood is intensely thrombogenic resulting in activation of the platelet cascade which can cause sub or complete occlusion

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5
Q

Describe occlusion

A

Occlusions can be micro or macro. Microvascular occlusions occur in the micro circulation

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6
Q

What can be used to study plaque rupture

A

OCT real time imaging

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7
Q

Describe OCT real time imaging

A

OCT is an angiogram which requires a catheter into the lumen of the artery from the brachial artery and are used to monitor erosion and plaque rupture

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8
Q

Describe the ‘vulnerable plaque’ and inflammation in ACS

A

Active plaques are vulnerable. An undiscovered virus may result in inflammation. In patients with ACS vulnerable plaques are numerous and inflammation is widespread

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9
Q

What would happen if a filling defect is seen on an angiogram catheter from the radial artery

A

It would be aspirated then stented

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10
Q

What keeps the stent in place

A

Platelet recruitment and adhesion at the site of injury forming a monolayer

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11
Q

Why does a clot arise

A

Due to activation of the clotting cascade resulting in tissue factor formation and activation of the coagulation cascade

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12
Q

What type of clots and clots in coronary arteries

A

Platelet clots

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13
Q

What treatment do platelet clots need

A

Antiplatelet medication

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14
Q

Describe the overlap between the coagulation and platelet cascade

A

Thrombin aggregates platelets

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15
Q

What do aspirin, clopidogrel, prasugrel and GPII/IIIa inhibitors target

A

Platelet cascade, are anti-platelets

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16
Q

What are the two types of drugs used as antithrombotics

A

Anti-coagulation and anti-platelet

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17
Q

What do fondaparinus. LMWH, heparin and bivalirudin target

A

Coagulation cascade so are anti-coagulation

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18
Q

What happens to platelets during activation

A

They change from the smooth, discoid shape they are at rest into spiny and spheric when activated

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19
Q

What can unstable angina result in

A

Either STEMI or NSTEMI

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20
Q

How do you treat a patient with a NSTEMI

A

NSTEMI= clopidogrel, prasugrel and ticagrelor

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21
Q

How do you treat a patient with STEMI

A

Immediate intervention is required meaning that you give IV drugs as well, the drugs given are Prasugrel, Ticagrelor and IV Gp2b3a inhibitors.

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22
Q

What is the first antiplatelet drug

A

Aspirin

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23
Q

Describe the antithrombotic trialists’ collaboration on efficacy of aspirin on vascular events in high risk patients

A

All studies show aspirin is better than the control by 22%. In unstable angina those with aspirin were 44% better

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24
Q

Describe the MOA of aspirin

A

Aspirin inhibits cyclo-oxygenase meaning that thromboxane is inhibited

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25
Describe the MOA of new drugs thienopyridine
They block the ADP receptors on the surface of platelets and therefore inhibit platelet aggregation by blocking the pro-aggregatory effects of ADP
26
Describe the MOA of GP IIb/ IIIa inhibitors
They inhibit the final common pathway
27
What are the three types of thienopyridines
Ticlopidine, Clopidogrel and Prasugrel
28
Describe the MOA of clopidogrel
Clopidogrel is an oral anti-platelet receptor that blocks ADP receptors and works synergistically with aspirin. Aspirin acts on thrombin and therefore the coagulation pathway as well
29
What did the CURE trial find in relation to Clopidogrel and aspirin
Clopidogrel has a further 20% improvement rate when with aspirin (instead of aspirin on its own) post ACS
30
How long do people continue to benefit for when treated with both aspirin and clopidogrel
Up to 12 months
31
How much does clopidogrel cost per month
£20
32
When does clopidogrel have to be stopped before surgery
7-10 days
33
What are the three categories of clopidogrel response variability
Clinical factors, genetic factors and cellular factors
34
What are the clinical factors that affect of response to Clopidogrel
Failure to prescribe/ poor compliance, under-dosing, poor absorption, drug-drug interactions involving CYP3A4, ACS, diabetes mellitus/ insulin resistance, elevated body mass index
35
What are the genetic factors that affect of response to Clopidogrel
Polymorphisms of CYP, polymorphisms of GPIa, polymorphisms of P2Y12, polymorphisms of GPIIIa
36
What are the cellular factors that affect of response to Clopidogrel
Accelerated platelet turnover, reduced CYP3A metabolic activity, increased ADP exposure, up-regulation of the P2Y12 pathway, up-reguation of the P2Y-independent pathways (collagen, epinephrine, TXA2, thrombin)
37
Describe repsonse to Prasugrel compared to Clopidogrel
With Prasugrel 80% of people responded. Even those who responsed to Clopidogrel to begin with only had a response of up to 80% inhibition of platelet aggregation. When give Prasugrel all non-responders to Clopidogrel were responders and all resposnder to Prasugrel increased in response
38
What does the fact that prasugrel is a pro-drug mean
It requires activation and takes a couple of days to kick in
39
What is one of the main reasons why Clopidogrel response is so variable
Because it is a PK problem effected by genotype polymorphism meaning there is a wide pharmacodynamic response
40
What do Prasugrel and Clopidogrel need to work
Conversion from an inactive to active metabolite
41
Describe Prasugrel in comparision to Clopidogrel
Clopidogrel is a prodrug and relatively weak anti-platelet. Prasugrel is a second-generation thienopyridine like Clopidogrel. Prasugrel is rapidly and more wholly metabolised to its active components
42
Describe Ticagrelor
Is a direct acting P2Y12 antagonist (adenosine (P2Y12) receptor inhibitor) which means that it isn;t a prodrug. Ticagrelor acts rapidly and has moer potent and consistent antiplatelet effects than Clopidogrel
43
What are oral antiplatelets used during ACS and what do they act on
Aspirin-COX, Clopidogrel-ADP, Prasugrel-ADP, Ticagrelor- ADP.
44
What are IV drugs used during ACS
GPIIb/IIIa inhibitors: Abciximab, Airofiban, Eptifibatide
45
Describe the 6 points of oral antiplatelet therapy
1. The first antiplatelet aspirin blocks the production of thromboxane A2. 2. The CURE trial established the benefits of addition of P2Y12 receptor blocker Clopidogrel. 3. Clopidogrel has a modest inhibition of platelet aggregation and a delayed onset and offset action. 4. Prasugrel is a second-generation thienopyridine and is rapidly and more wholly metabolised to its active components. 5. Ticagrelor is a direct-acting P2Y12 antagonist which acts rapidly and has more potent and consistent antiplatelet effects than Clopidogrel. 6. There is an increased risk of bleeding with Ticagrelor and they cost substantially higher
46
What does the fact that Clopidogrel is now off patent mean
It is considerably cheaper
47
Why is chosing the most effective treatment difficult
There is not a test to check if platelets are inhibited or not
48
What did the PLATO study show in terms of treatment
Aspirin improves outlook by 40% + Clopidogrel is another 20% + Ticagrelor is another 16%
49
Why are thrombin inhibitors also used
Tissue factor is released from atheroclerotic plaques, tissue factor activates thrombin
50
What is the number one thrombin inhibitor
IV heparin
51
What effect does inhibition of factor Xa have on thrombin
Inhibition of one molecule of factor Xa can inhibit the generation of 5 molecules of thrombin
52
Why do we need to produce factor Xa drugs instead of heparin
Blocking Xa which is higher up in the cascade blocks more thrombin
53
What is an IV drug administered during treatment of STEMI
Bivalirubin
54
What are thrombic and ischaemic events mediated by
Platelets
55
What is the main target in anti-platelet drugs
P2Y12 receptor blockage
56
What anti-coagulant can be given subcutaneously
Enoxaparin (lower molecular weight than heparin)
57
What are IV/ subcutaneous agents used for
Used acutely to block coagulation cascade and therefore the production of thrombin
58
What is one of the major risks of anti-coagulation drigs
Major bleeding, and those who suffer a major bleed have on average a 15% higher incidence of mortalilty
59
What anti-coalgulation treatment do you use for unstable angina
Antithrombins
60
What anti-coagulation treatment do you use for NSTEMI
SC controllable antithrombins, anoxaparin, fondaparinux
61
What anti-coagulation treatment do you use for STEMI
Needs quick treatment therefore you use IV heparin (at the right dose) or Bivalirudin

Case 4 (7 decks)

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