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Y2 - CPT > Lecture 11 - Antiplatelets And Fibrinolytics > Flashcards

Lecture 11 - Antiplatelets And Fibrinolytics Flashcards

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1
Q

What are 2 examples of bleeding disorders?

A

Haemophilia (A and B)
Von Wille Brand disease

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2
Q

What is haemophilia A?

A

Dysfunction or absence of clotting factor VIII

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3
Q

What is haemophilia B?

A

Dysfunction or absence in clotting factor IX

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4
Q

What is Von Willebrand disease?

A

Dysfunction or absence of Von willebrand factor
Von willebrand factor allows platelets to adhere to blood vessel walls for clots to form

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5
Q

What is a thrombus?

A

A clot adhered to a vessel wall

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6
Q

What is an embolus?

A

An intravascular clot distal to the site of origin

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7
Q

What are some common thromboembolic disease?

A

DVT
PE
Can be caused by AF

Can lead to TIA, iscahmic stroke and MI

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8
Q

What part of the atria do thrombi most commonly form in atrial fibrillation?

A

Oracles

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9
Q

What usually causes venous thrombosis?

A

Stasis of blood
Damage to the veins

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10
Q

What usually causes arterial thrombosis?

A

Atherosclerotic plaque rupture

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11
Q

What are usually the contents of a venous thrombus?

A

High red cell count
High fibrin
Low platelet content EVENLY DISTRIBUTED

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12
Q

What are usually the contents of an arterial thrombus?

A

Lower fibrin content
Much higher platelet

Appearance has Lines Of Zahn

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13
Q

What is the triad that increases the risk of thrombosis?

A

Virchows triad

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14
Q

What is the triad for virchows traid?

A

Increased coagulability
Blood vessel injury
Reduced blood flow (Stasis)

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15
Q

What can causes blood stasis?

A

A fib
Long distance travel
Varicose veins
Immobility

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16
Q

What can cause increased blood coagulability?

A

Sepsis
Smoking
Coagulation disorders
Malignancy

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17
Q

What can cause blood vessel injury?

A

Trauma
Invasive procedures
Hypertension

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18
Q

What substance does healthy endothelium produce which inhibits platelet aggregation?

A

PGI2 (prostacyclin)

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19
Q

What is the action of PGI2 (prostacyclin) produced by healthy endothelium?

A

Inhibits platelet aggregation

PGI2 binds to platelet receptors causing increased cAMP in platelets
High cAMP in platelets leads to low Ca2+ in platelets
Low Ca2+ prevents platelet aggregation and keeps platelet aggregators agents low

This stabilises the GPIIb and GPIIIa receptors on the platetlet surface

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20
Q

Where are GPIIb/IIIa receptors located?

A

On surface of platelets

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21
Q

What is the lifespan of a platelet?

A

8-10 days

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22
Q

How can atherosclerosis lead to thrombus formation?

A

Fibrous cap thin, plaque ruptures and clotting factors released

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23
Q

How do platelets become activated?

A

Bind to exposed collagen fibres and release platelet granules contains ADP, Thromboxane A2, platelet activation factor and thrombin

This leads to increased calcium and decreased cAMP in platelet

The inc calcium activates GPIIb/IIIa receptors and fibrinogen

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24
Q

How does omega 3 fish oils help prevent thrombus formation?

A

Contains substance that acts like PGI2 so prevents platelets adhering to endothelium

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25
What colour are platelet rich arterial thrombi?
White
26
What type of drugs are given for arterial thrombi?
Anitplatelet Fibrinolytics
27
What type are drugs are given for lower platelet content Red VENOUS thrombi?
Parenteral anticoagulants like heparins and oral anticoagulants like warfarin
28
What type of drug is aspirin?
COX inhibitor (Cyclo-oxygenase inhibitor) Antiplatelelt
29
How does Aspirin work as an antiplatelet?
Inhibits COX1 production of Thromboxane A2 so leads to irreversible platelet aggregation
30
Why does aspirin not completely inhibit all platelet aggregation?
Only prevents Thromboxane A2 production from COX Their are other aggregating factors
31
What is a low non-analgesic dose of aspirin?
75mg
32
What is a loading dose of aspirin used in acute coronary syndromes?
300mg
33
What dose aspirin do at its low 75mg dose?
Anti-platelet aggregation No analgesic effect
34
How can higher doses of aspirin affect PGI2?
Can inhibit it (bad?)
35
How is aspirin normally absorbed?
Passive diffusion
36
1.) What type of drug is aspirin? 2.) what is it used for? 3.) MoA? 4.) Adverse effects? 5.) Contra-indications? 6.) Drug-drug interaction?
1.) COX inhibitor 1.) antiplatelet aggregation 3.) prevents COX producing Thromboxane A2 which normally helps elevate platelet Ca2+ contetn leading to aggregation 4.) GI irritation, GI bleeding (peptic ulcer), haemorrhagic stroke, aspirin hypersensitivity 5.) Reye’s syndrome Aspirin hypersensitivity 3rd. Trimester of pregnancy leads to closure of ductus Arterioles 6.) other antiplatelets and anticoagulants
37
What is given to help close ductus arteriosus?
Ibruprofen
38
What is given to help keep ductus arteriosus open?
Prostaglandins
39
Why does the antiplatelet effect of aspirin last the life span of a platelet so 7-10 days?
The dont have nuclei so cant make more Thromboxane A2
40
When is aspirin given?
AF patients post stroke Secondary prevention of stroke and TIA 2ndary prevention of Acute Coronary syndromes Post primary percuatneous coronary intervention and stent
41
What type of drug is given alongside long term use aspirin?
Proton pump inhibitors like omeprazole for gastric protection
42
What doses of aspirin are given for NSTEMI and STEMI? Acute ischamic stroke?/
NSTEMI/STEMI = 1 300mg loading dose Acute ischameic stroke = initial 300mg daily for 2 weeks
43
What are some examples of ADP receptor antagonists?
Clopidogrel Prasugrel Ticagrelor
44
What is the general mechanism of action of clopidogrel, prasugrel and ticagrelor?
ADP receptor antagonists Prevent ADP binding to P2Y12 which prevents the activation of GPIIb/IIIa receptors
45
What is the difference in the mechanism of action for Clopidogrel and prasugrel compared to ticagrelor?
Clopidogrel and prasugrel are irreversible inhibitors of P2Y12 They are also booth prodrugs also need hepatic metabolism Ticagrelor acts reversibly at a different site
46
How are the ADP receptor antagonists typically taken?
Orally
47
1.) What type of drug is clopidogrel, prasugrel and ticagrelor? 2.) what is it used for? 3.) MoA? 4.) Adverse effects? 5.) Contra-indications? 6.) Drug-drug interaction?
1.) ADP receptor antagonists 2.) Antiplatelet therapy 3.) Clopidogrel adn prasugrel bind irreversibly to. P2Y12 preventing ADP binding and inhibiting activation of GPIIb/IIIa receptors Ticagrelor accts reversibly elsewhere 4.) BLEEDING, GI upset, dyspepsia, diarrhoea, rarely thrombocytopenia 5.)high bleedrisk patients with renal or heptaic impairment. 6.) CYP inhibitors (CYP2C19 needed to activate clopidogrel), Omeprazole, ciprofloxacin, erythromycin some SSRIs Other antiplatelets, anticoagulants or NSAIDs
48
What area the indications for using ADP receptor antagonists?
Ischamic stroke (and TIA) Clopidogrel long term mono therapy where aspirin is contraindicated NSTEMI take with aspirin Percutaneous coronary intervention (prasugrel)
49
What is an example of a phosphodiesterase inhibitor?
Dipyridamole
50
What is the mechanism of action of dipyridamole (phosphodiesterase inhibitor)?
Inhibits cellular reuptake of adenosine leading to increased concentration of adenosine, this inhibits platetlet aggregation via adenosine (A2) receptors Also prevents cAMP degradation which prevents expression of GPIIb/IIIa
51
1.) What type of drug is dipyridamole? 2.) what is it used for? 3.) MoA? 4.) Adverse effects? 5.) Contra-indications? 6.) Drug-drug interaction?
1.) phosphodiesterase inhibotr 2.) secondary prevention of ischameic stroke and TIAs, prophylaxis for thromboembolism following valve replacement Stroke 3.)inhibits cellular reuptake of adenosine, leads to increased conc of adenosine inhibiting platelet aggregation via adenosine A2 receptors 4.)Vomitng, diarrhoea and dizziness 5.) ??? 6.) antiplatelets, anticoagulants and adenosine
52
What is an example of Glycoprotein IIb/IIIa inhibitor?
Abciximab
53
What is the mechanism of action of GPIIb/IIIa inhibitors like abciximab?
Antibodies block GPIIb/IIIa receptors preventing the binding of fibrinogen and Von Willebrand factor to the GPIIb/IIIa receptors preventing aggregation
54
How is abciximab administered?
IV
55
1.) What type of drug is abciximab? 2.) what is it used for? 3.) MoA? 4.) Adverse effects? 5.) Contra-indications? 6.) Drug-drug interaction?
1.) GPIIb/IIIa inhibitors 2.) high risk Percutaneous transluminal coronary angioplasty patients with other drugs 3.) antibodies block GPIIb/IIIa receptors preventing fibrinogen and Von Willebrand factor from binding reducing aggregation
56
What is the general mechanism that fibrinolytics work by?
Dissolve the fibrin meshwork of thrombus
57
What are 2 examples of fibrinolytic drugs that inhibit the conversion of plasminogen to plasmin?
Streptokinase Alteplase
58
Why can streptokinase only be used once?
Antibodies will develop to it other wise since it’s extracted from haemolytic streptococci
59
What type of drug is alteplase?
Recombinant tissue plasminogen activator
60
When is aletplase typically I used?
Acute ischamic stroke must be given less than 4.5hrs from symptoms In some following STEMI PE
61
What is tranexamic acid?
Drug which inhibits plasminogen Given for epistaxis or Haemorrhagia so stops bleeding
62
What are some adverse effects and drug interactions of alteplase and streptokinase?
Adverse = bleeding Drug = antiplatelets and anticoagulants
63
When is Percutaneous coronary intervention used over thrombolytics follwing an STEMI?
When presentation is within 12hrs of onset of symptoms and primary PCI can be done within 120mmins of the time where fibrinolytics could have been given
64
What is a negative consequence of PCI following a STEMI?
Reperfusion injury
65
What is reperfusion injury?
When a tissue becomes re perfused with blood, further damage occurs due to increased production of ROS, inflammatory mediators and plasma membrane disruption
66
What drugs can be given as a secondary prevention of acute coronary syndrome once haemodynamically stable?
ACEi (ARBs if ACEi contraindicated) B blocker Dual antiplatelet therapy so 75mg aspirin + ADP receptor antagonist (clopidogrel or ticagrelor) Statin (80mg Atorvastatin starting point)
67
Why do GPIIb/IIIa inhibitors afford more complete anti-platelet aggregation than other agents?
Targets the final common pathway
68
What is the overall function of phosphodiesterase
Controls the production of secondary messengers like cAMP and cGMP
69
Why are antiplatelet drugs used in secondary prevention of ACS and TIA?
Reduce risk of cardiovascular events be preventing platelet aggregation

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