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Antiplatelets + fibrinolytics Flashcards

(51 cards)

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1
Q

Give some examples of thromboembolic diseases

A
  • DVT, PE
  • AF consequence
  • TIA, ischaemic stroke
  • MI (NSTEMI/STEMI)
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2
Q

Give the definitions of thrombus and embolus

A

Thrombus:

Clot adhered to vessel wall, at local site

Embolus:

Intravascular clot distal to site of origin (eg PE)

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3
Q

Distinguish between venous and arterial thrombosis

A

VENOUS:

  • Associated with stasis of blood and/or damage to veins
  • Less likely to see endothelial damage (eg DVT in lower limbs)
  • High red blood cell + fibrin content, LOW PLATELET CONTENT

ARTERIAL:

  • Forms at site of atherosclerosis, following plaque rupture
  • Low fibrin content, much HIGHER PLATELET CONTENT

Varying platelet contents of arterial and venous thrombi dictate drugs initially offered

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4
Q

Describe how a healthy endothelium is maintained (with platelets in their resting state)

A
  • Prostacyclin (PGI2) produced and released by endothelial cells- INHIBITS PLATELET AGGREGATION
  • PGI2 binds to platelet receptors, increasing cAMP in platelets​
  • Increased cAMP = decreased Ca2+
  • Thus, preventing platelet aggregation
  • Reduction in platelet aggregatory agents
  • Stabilises GPIIb/IIIa receptors- maintains inactive resting state

Inactive GPIIb/IIIa receptor required for resting platelet (glycoprotein receptor)

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5
Q

Provide an outline of platelet activation and aggregation

A
  • Creation of a thrombus has a similar process to normal clot formation (pathological stimulus vs physical trauma- damaged endothelium)
  • Atherogenic pathway; fibrous cap, plaque rupture, thrombus formation
  • Platelet adhesion at damaged endothelium– cascade of signalling molecules
  • Chemical mediators released by activated platelets; thromboxane A2, ADP, serotonin, PAF (pt activating factor) - lead to plt aggregation
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6
Q

Describe the roles of Ca2+ and GPIIb/IIIa receptors in platelet activation and aggregation

A
  • Release of platelet granules- ADP, thromboxam A2, PAF, thrombin
  • Initiates activation and aggregation through GPIIb/IIIa receptors + fibrinogen – ACTIVATED GPIIb/IIIa RECEPTORS
  • Activated platelets bound to collagen of sub-endothelium cause increase in Ca2+ levels
  • Increased calcium + decreased cAMP in platelets
  • Plt aggregation via Vwf + thrombin (finrinogen to fibrin)
  • CASCADE + AMPLIFICATION IN PLTs

Elevated Ca2+ causes:

  • Release of plt granules
  • Activation of thromboxane A2 synthesis
  • Activation of GPIIb/IIIa receptors
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7
Q

What is the main target of antiplatelet drugs?

A

Reduction of pathological platelet aggregation

To reduce CV events + mortality

Disrupting various stages of signalling cascade

Effective in the arterial circulation, where anticoagulants have little effect

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8
Q

Distinguish between the drug classes used to prevent arterial and venous thrombi

A

ARTERIAL:

Platelet rich, arterial, white thrombi: ANTIPLATELET + FIBRINOLYTIC DRUGS

VENOUS:

Lower pletelet content, red, venous thrombi: PARENTERAL ANTICOAGULANTS (heparins), ORAL ANTICOAGULANTS (warfarin)

Combination can be used in some pt’s for secondary prevention

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9
Q

What do antiplatelet agents target?

A

Pt activation + aggregation

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10
Q

Describe the mechanism of action of cyclo-oxygenase inhibitors

A
  • Normally, potent platelet aggregating agent thromboxane A2 is formed from arachidonic acid by COX-1
  • Aspirin: inhibits (acetylates) COX-1 mediates production of TXA2 + reduced plt aggregation
  • IRREVERSIBLE INHIBITION OF ENZYMATIC CONVERSION (aspirin irreversibly inhibits COX-1)
  • Aspirin = a salicylate compound, thus has ability to acetylate COX-1
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11
Q

Give an example of a cyclo-oxygenase inhibitor

A

Aspirin

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12
Q

Why does aspirin not completely inhibit platelet aggregation?

A

As there are other mechanisms and mediators, independent of COX-1, by which platelets can aggregate

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13
Q

Distinguish between the doses of aspirin required for anti-platelet vs analgesic effects

A

Anti-platelet action: at low non-analgesic doses (75mg) - baby aspirin

Analgesia: loading, higher dose

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14
Q

Give some properties of aspirin

A

Higher doses inhibit endothelial prostacyclin (PGI2)- imp consideration in stable resting patients

Absorbed by passive diffusion, hepatic hydrolysis to salicylic acid

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15
Q

Give some warnings/contraindications of aspirin

A
  • Bleeding time prolonged- haemorrhagic stroke, GI bleeding (peptic ulcer); thus balance vs risk of bleeding
  • Reye’s syndrome - avoid aspirin in <16 yr/olds
  • Hypersensitivity to aspirin
  • 3rd trimester pregnancy - premature closure of ductus arteriosus into ligamentum arteriosum
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16
Q

What is Reye’s syndrome?

A

**Post viral infection + aspirin given on top

Hepatic + brain oedema

May be fatal

Reye’s (Reye) syndrome is a rare but serious condition that causes swelling in the liver and brain. Reye’s syndrome most often affects children and teenagers recovering from a viral infection, most commonly the flu or chickenpox.

Taking aspirin to treat such an infection greatly increases the risk of Reye’s

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17
Q

Give an important interaction/consideration of aspirin

A

Other antiplatelet + anticoagulants - additive/synergistic effect

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18
Q

Why does antiplatelet COX-1 inhibition last the lifespan of a platelet (7-10 days)?

A

As platelets lack nuclei; thus unable to produce more COX once inhibited

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19
Q

Describe the consequence of COX-1 polymorphisms on the effect of aspirin in some people

A

COX-1 polymorphisms result in lack of efficacy of aspirin in some pt’s

As there is a differing ability of aspirin to acetylate COX-1

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20
Q

Give some indications for the use of aspirin

A
  • Secondary prevention of stroke + TIA (post-ischaemic events)
  • Secondary prevention of acute coronary syndromes (ACS)- NSTEMI, STEMI, unstable angina
  • Post primary percutaneous coronary intervention (PCI) + stent to reduce ischaemic complications
  • Secondary prevention of MI in stable angina or peripheral vascular disease
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21
Q

How is aspirin often prescribed?

Study These Flashcards
A

Often co-prescribed with other agents; depending on pt’s age, presentation of ACS etc

22
Q

Describe the dose and frequency of aspirin generally used for secondary prevention of ACS

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A

Initial once only 300mg chewable loading dose of aspirin

To reduce incidence of re-occlusion

23
Q

Describe the dose and frequency of aspirin generally used for secondary prevention of acute ischaemic stroke

Study These Flashcards
A

Initial 300mg daily for 2 weeks

To reduce incidence of re-occlusion

24
Q

Which other type of medication should be considered in high risk patients on long term aspirin use?

Study These Flashcards
A

Gastric protection

PPIs

25
Describe the mechanism of action of ADP receptor antagonists
* **Inhibit binding of ADP to P2Y12 receptor (on platelet)** * **Thus, _inhibit activation of GPIIb/IIIa receptors_** * **INDEPENDENT OF COX PATHWAY** Decrease Ca2+ in platelet, thus inhibit plt aggregation *Inhibit ADP mediated platelet aggregation*
26
Give 3 examples of ADP receptor antagonists
**Clopidogrel** **Prasugrel** **Ticagrelor** **(All orally)**
27
Compare the properties and actions of clopidogrel, prasugrel and ticagrelor
_Clopidogrel + prasugrel = **irreversible inhibitors of P2Y12**_ **Pro-drugs - hepatic metobolites (need to be metabolised into active state)** Clopidogrel - **slow onset of action (5-6 hrs for full effect) without loading dose; inter-individual variability in antiplatelet action** Ticagrelor + prasugrel = **more rapid onset (1-2 hrs post oral dose)** **_Ticagrelor acts REVERSIBLY at DIFFERENT SITE to clopidogrel - has active metabolites_**
28
Give some warnings/contraindications of ADP receptor antagonists
* Bleeding * **GI upset; dyspepsia, diarrhoea** * **Thrombocytopaenia (low plt's)** * **Hepatic + renal impairment - caution; as metabolised from pro to active drug**
29
Give some important interactions/considerations of ADP receptor antagonists
* **Clopidogrel required CYPs for activation; drugs interfering- omeprazole (PPI), ciprofloxacin, erythromycin, SSRI's** * **CYP 2C19 invl** * Thus, need to consider use of other PPI's with clopidogrel * Ticagrelor can interact with CYP inhibitors and inducers - **CYP 3A4** * Caution when co-prescribed with other antiplatelet + anticoagulant agents or NSAIDS-- BLEEDING, peptic disease
30
Which drug needs stopping 7 days prior to surgery?
**Clopidogrel -** **Risk vs benefit - to allow time for drug to wear off** **(Ticagrelol 5 days before?)**
31
Give some indications for clopidogrel (ADP receptor antagonist)
* Monotherapy **where aspirin contraindicated** * NSTEMI pt's for **up to 12 mths (PPCI considerations)** * **STEMI with stent- for up to 12 mths - stop before CABG (high vs low risk pt's)** * **Ischaemic stroke + TIA - long term secondary prevention** RISK OF CARDIOVASCULAR EVENTS VS BLEEDING RISK
32
Give an indication for using prasugrel with aspirin
## Footnote **ACS patients undergoing PCI, up to 12 mths**
33
Provide an outline of the evidence (PLATO study) done to compare the use of ticagrelor or clopidogrel with aspirin
**TICAGRELOR significantly reduced rate of death from vascular causes** **Ticagrelor: currently licensed in combination with aspirin for p_revention of atherothrombotic events in ACS for UP TO 12 MTHS_**
34
Describe the mechanism of action of glycoprotein IIb/IIIa inhibitors
* **Monoclonal antibody** * Blocks binding of fibrinogen and von Willebrand factor (vWf) * **Antibody blocks GPIIb/IIIa receptors leading to 80% reduction in aggregation** **Abciximab binds irreversibly to the GPIIb/IIIa receptors and blocks the binding of fibrinogen**
35
Give an example of a glycoprotein IIb/IIIa inhibitor
## Footnote **Abciximab - IV injection with bolus** **Antibody blocks GPIIa/IIIb receptors** **Leads to 80% reduction in aggregation- bleeding risk greater than other agents**
36
Why do glycoprotein IIb/IIIa inhibitors have a greater associated bleeding risk compared to the other agents?
As they **target the final common pathway** where there is more complete plt aggregation Thus, there are not many other mechanisms by which platelets can aggregate (as with COX inhibitors) Hence, a substantial reduction in platelet aggregation (80%)-- increased bleeding risk
37
Give some warnings/contraindications and important interactions/considerations of glycoprotein IIb/IIIa inhibitors
* **BLEEDING (fuller antipletelet effects) - dose adjustment for body weight, thrombocytopaenia, hypotension, bradycardia** * Caution with other antipletelet + anticoagulant agents ***Specialist use in HIGH RISK PERCUTANEOUS TRANSLUMINAL CORONARY ANGIOPLASTY PATIENTS***
38
OVERVIEW
39
Give an example of a phosphodiesterase inhibitor
## Footnote **Dipyridamole**
40
Describe the mechanism of action of phosphodiesterase inhibitors (dipyridamole)
* Dipyridamole **inhibits cellular reuptake of adenosine- increased plasma adenosine- inhibits platelet aggregation via A2 receptors** * Normally, phosphodiesterases breakdown cyclic nucleotides, thus with a phosphodiesterase inhibitor, _cAMP degradation is prevented_ * Dipyridamole also acts as a **phosphodiesterase inhibitor which prevents cAMP degradation- inhibits expression of GPIIb/IIIa (increased cAMP, decreased Ca2+, reduced plt aggregation)** ***PHOSPHODIESTERASE 5 AND 3 INHIBITION***
41
Give some warnings/contraindications and any important interactions/considerations of phosphodiesterase inhibitors (dipyridamole)
* **Flushing, headache,** hypersensitivity * Caution with **antihypertensives (side effects), antiplatelets, anticoagulants**
42
Give some uses of phosphodiesterase inhibitors (dipyridamole)
## Footnote **Secondary prevention of ischaemic stroke + TIA** **Adjunct for prophylaxis of thromboembolism following _valve replacement_**
43
Briefly describe the mechanism of action of fibrinolytic agents (thrombolysis/clot busters)
**Fibrinolytics dissolve fibrin meshwork of thrombus** Fibrin clot into fibrin degradation products
44
Give 2 examples of fibrinolytics and explain how they work
**Streptokinase; promotes plasminogen production** **Alteplase; plasminogen activator- promotes conversion of plasminogen into plasmin**
45
What does plasmin do?
Breaks down fibrin clot into fibrin degradation products
46
What does tranexamic acid do? Give some of its uses
**Inhibits fibrinolysis - inhibits fibrin clot breakdown** Is used to treat **heavy bleeding during your menstrual period.** Tranexamic acid works by **slowing the breakdown of blood clots**, which helps to prevent prolonged bleeding. It belongs to a class of drugs known as **antifibrinolytics.** **Tranexamic acid has been found to be an excellent affordable nonhormonal treatment option for women with HMB and should be considered during major gynecological surgery.**
47
Which fibrinolytic is used in acute ischaemic stroke \<4.5 hours of presentation?
## Footnote **Alteplase**
48
Give another use of fibrinolytics
**Following acute MI diagnosis acutely vs primary PCI**
49
Give some warnings/contraindications of fibrinolytics eg streptokinase and alteplase
* **Bleeding** * **Streptokinase can only be used once- as antibodies develop to streptococci (hence not effective on 2nd use)** * **Intracranial haemorrhage needs ruling out**
50
When is coronary angiography with primary PCI indicated as the preferred coronary reperfusion strategy instead of thrombolysis for acute STEMI?
## Footnote **PRIMARY PCI IF:** **Presentation is within 12 hrs of onset of symtoms** **AND** **Primary PCI can be delivered _within 120 mins_ of the time when fibrinolysis could have been given**
51
What class of drug should be offered to all patients post MI once they are haemodynamically stable?
## Footnote **ACEi**

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