S6 L2 Antiplatelets and Fibrinolytics Flashcards

You may prefer our related Brainscape-certified flashcards:
1
Q

A thrombus is a clot adhered to the vessel wall, what are the main differences between venous and arterial thrombi?

A

Venous: low platelet content but high red blood cell and fibrin content so would want to use a fibrinolytic to break down or anticoag. Often due to stasis

Arterial: high platelet count but low fibrin content. Often on top of atheromatous plaque. Would want to use an antiplatelet

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

What are some examples of thromboembolic disease?

A
  • DVT
  • PE
  • MI
  • TIA/Stroke
  • Consequence of AF
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How does healthy endothelium prevent platelet aggregation?

A
  • Endothelial cells produce and release prostacyclin (PGI2)
  • PGI2 binds to platelet receptors and increases the cAMP in the platelet
  • Increased cAMP decreases the calcium in the platelet preventing platelet aggregation by stabilising/inactivating GPIIB/IIIA receptors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How are platelets activated and aggregated?

A

- Endothelial damage e.g plaques fibrous cap ruptures, so platelets adhere to vWF at site of damage and release granules that signal

- Platelet granules contain ADP, thromboxane A2, serotonin, platelet activation factor and serotonin

  • Granules activate GPIIB/IIIA receptors and fibrinogen, increasing calcium and decreasing cAMP in the platelet
  • Cascade from platelet to platelet as newly activated platelet releases more granules
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Where in the clotting cascade are some of the targets of antiplatelets?

A
  • COX
  • GPIIB/IIIa receptors
  • ADP
  • Fibrinogen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the mechanism of action of aspirin and why does it not completely stop platelet aggregation?

A

- Irreversible cyclooxygenase inhibitor by acetylation so stops conversion of arachidonic acid into thromboxane A2

  • There are other platelet mediations not just thromboxane A2
  • At low doses, 75mg, it is an antiplatelet not analgesic. Baby aspirin. At high doses inhibits prostacyclin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the side effects and contraindications of aspirin use?

A

Side effects: prolong bleeding time so more likely to have haemorraghic stroke, peptic ulcers, increase risk of Reye’s syndome<16, hypersensitivity

Contraindications: 3rd trimester pregnancy as can prematurely close DA, be carefule with other antiplatelets and anticoags, stop 7-10 days before a surgery as irreversible COX inhibitor, some people have COX polymorpgism it doesn’t work on

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

How is aspirin metabolised?

A

Absorbed by passive diffusion and hepatically hydrolysed to salicyclic acid

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

When is the use of aspirin indicated?

A
  • Secondary prevention of stroke/TIA, ACS and MI in angina
  • Given after PCI and stents to stop ischaemic complications

- ACS (MI): 300mg loading dose chewable!!!!

- Acute ischaemic stroke: 300mg daily for 2 weeks

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

What drug do you need to give alongside long term aspirin?

A
  • Gastric protection e.g PPI inhibitors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the mechanism of ADP receptor antagonists as an antiplatelet and what are some examples of these drugs?

A
  • Inhibit ADP binding to P2Y12 receptors so GPIIB/IIIA receptors cannot be activated as no calcium release
  • Clopidogrel, Ticagrelor, Prasugrel (prodrugs - need hepatic function to be metabolised and activated)
  • Ticagrelor and Prasugrel have more rapid onset as shorter half life. All given orally. Clopidogrel needs loading dose
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are some side effects and contraindications of ADP receptor anatagonist use?

A

Side effects: bleeding, dyspepsia, diarrhoea, thrombocytopenia

Contraindications: cannot be used if renal or hepatic impairment, clopidogrel needs CYP2C19 so if drugs that inhibit these are used cannot be used, Ticagrelor can interact with CYP3A4 inhibitors and inducers, NSAIDs as increased risk of peptic ulcers, stop clopidogrel 7 days before surgery and ticagrelor 5 days before

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

What are some drugs that interact with CYP2C19 and mean that clopidogrel cannot be used?

A

Inhibitors:

  • Omeprazole
  • Ciprofloxacin
  • Erythromycine
  • SSRIs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

When should ADP receptor antagonists like clopidogrel be prescribed?

A
  • Monotherapy when aspirin is contraindicated for secondary prevention after TIA/Stroke
  • NSTEMI patients for up to 12 months and after STEMIs with stents. Stop before CABG
  • Have to weigh up bleeding risk with cardiovascular risk
  • Give prasugrel with aspirin in ACS patients undergoing PCI up to 12 months
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

When is prasugrel licensed for use?

A

In combination with aspirin for prevention of event in ACS up to 12 months

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

What is the mechanism of acton of Glycoprotein IIB/IIIA receptor inihibitors and what is an example of this class of drugs?

A

Abciximab - given IV.I bolus

  • Antibody that blocks the GIIB/IIIA receptors so they cannot bind fibrinogen and vWF so cannot aggregate and adhere
  • As they target final common pathway they stop aggregation the most but increased bleeding risk
17
Q

What are the side effects and contraindications for the use of GIIB/IIIA receptor antagonits like abciximab?

A

- Side effects: really high bleeding risk so dose needs to be adjusted for body weight, thrombocytopenia, hypotension and bradycardia

  • Be careful when using with antihypertensives and other antiplatelets
18
Q

What is the mechanism of acton of phosphodiesterase receptor inihibitors as an antiplatelet and what is an example of this class of drugs?

A

Dipyridamole

  • Inhibits cellular reuptake of adenosine so increased plasma adenosine which inhibits platelet aggregation by binding to A2 receptors and increasing cAMP
  • Also as a phosphodiesterase inhibitor it prevents cAMP degradation (like viagra) so prevents expression of GPIIB/IIIA receptors.
19
Q

When are phosphodiesterase inhibitors used as an antiplatelet, what are the side effects and the contraindications for their use?

A

Use: secondary prevention of ischaemic stroke and TIAs, prophylaxis of thromboembolism following valve replacement

Side effects: flushing, headaches, hypersensitivity

Contraindications: be careful when used with other antihypertensive, anticoagulants and antiplatelets

20
Q

What is the mechanism of acton of fibrinolytics and what is some examples of this class of drugs?

A

Streptokinase and Alteplase

  • Dissolve the fibrin meshwork of a thrombus
21
Q

When are fibrinolytics used and what are the side effects?

A
  • Alteplase in acute ischaemic stroke if less than 4.5 hours and after you’ve ruled out intracranial haemorraghe
  • Side effects of bleeding
  • Streptokinase can only be used once as we develop antibodies to it so need to know if used before
22
Q

For an acute STEMI when should you use thrombolysis and when should you use primary PCI?

A

- PCI used if presentation within 12 hours of onset of symptoms and if primary PCI can be delivered within 120 minutes of the time when fibrinolysis could have been given

  • ACEi should then be offered to all patients post MI once haemodynamically stable
  • PCI PREFERRED IF AVAILABLE
23
Q

What is tranexamic acid used for?

A

ANTIFIBRINOLYTIC

  • Used for menorraghia and epistaxis
24
Q

What are the five classes of antiarrythmics using the Vaughan Williams classification?

A
25
Q

How can adenosine convert an SVT?

A
  • Slows AV conduction by binding to A1 receptors and activating K+ channel hyperpolarising the cell
26
Q

Why can’t dipyridamole be used with adenosine or needs to be used in lower doses?

A
  • Dipyridamole can increase plasma adenosine so increased adenosine and therefore may get bradycardia and asytole!!
  • Facial flushing, headache and drug lasting longer than normal
27
Q

Why do patients who have had adenosine say they feel like they were about to die?

A

When given IV it causes transient asystole so feels like death! Short half life so doesn’t act for long

28
Q

Why should amiodarone be avoided in patients with active thyroid disease?

A

Amiodarone’s has a high iodine content and it has direct toxic effect on the thyroid

29
Q

What should you do before cardioverting a patient with AF?

A
  • If they have had the AF for more than 48 hours the patient may need to take warfin for at least a month before cardioversion to prevent blood clots in the heart
30
Q

What would happen if you prescribe a CCB and B blocker at the same time?

A

ASYSTOLE

31
Q

If a patient presents with symptomatic AF what needs to be prescribed?

A
  • Metoprolol instead of bisoprolol
  • Bisoprolol usually used as more cardioselective so will cause more bradycardia but metaprolol may act faster
32
Q

Why does digoxin have little effect on exertion?

A
  • Digoxin works by blocking Na/K ATPase but on exertion there is less ATP so channel inactive anyway
33
Q

Why is ivabradine considered for rate control in patients with heart failute and ACS?

A

DOESN’T HAVE A HYPOTENSIVE EFFECT WHEN IT DECREASES HEART RATE

34
Q

What channels can amiodarone act on?

A
  • Sodium
  • Potassium
  • Calcium
  • Non-competitive beta blocker
35
Q

Which ADP receptor antagonist binds reversibly to the P2Y12 receptor?

A

Ticagrelor - also binds at a different location to the other agents