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Clinical Pharmacology > 6.2.1 Aspirin > Flashcards

6.2.1 Aspirin Flashcards

1
Q

What is a thrombus?

A

A clot adhered to a vessel wall

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2
Q

What is an embolus?

A

Intravascular clot distal to site of origin

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3
Q

What is a venous thrombosis associated with?

A

Stasis of blood or damage to veins

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4
Q

Describe the characteristics of a venous thrombosis

A

High red blood cell and fibrin content

Low platelet content evenly distributed

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5
Q

What is an arterial thrombosis caused by?

A

Forms at site of atherosclerosis following a plaque rupture

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6
Q

Describe the characteristics of an arterial thrombosis

A

Lower fibrin content

Higher platelet content

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7
Q

What causes thrombosis?

A

Virchow’s Triad

Way to remember
Triad=3

Skip 3 letters

Vessel wall damage
i
r
c
Hypercoaguability
o
w
‘
Stasis

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8
Q

What happens in healthy endothelium?

A

Prostacyclin (PGI2) produced and released by endothelial cells

Inhibits platelet aggregation

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9
Q

How does prostacyclin inhibit platelet aggregation?

A

PGI2 binds to platelet receptors

Increased concentration of cAMP in platelets, this leads to a decrease in calcium

Reduced calcium prevents platelet aggregation

Decrease in platelet aggregatory agents

Stabilises inactive GPIIb/ IIIa receptors

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10
Q

What is the lifespan of a platelet?

A

8-10 days

10% replaced each day

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11
Q

What is the process of a thrombus formation?

A

Adhesion
Platelets adhere to exposed collagen fibres on damaged vessel endothelium

Activation
Chemical mediators released by platelets attract more platelets

Aggregation
Platelets are recruited by mediators forming the plateleg plug

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12
Q

What happens in atherosclerosis which causes the formation of a thrombus?

A

Fibrous cap formation
Plaque ruptures
Thrombus forms over ruptured plaque

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13
Q

What platelet granules are released in platelet activation?

A

ADP
Thromboxane A2
Serotonin
Platelet activation factor
Thrombin

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14
Q

What happens in platelets after chemical mediators are released?

A

Increased calcium and decreased cAMP in platelets

This leads to cascade and amplification from platelet to platelet

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15
Q

What drugs are used to treat arterial thrombi?

A

Antiplatelet and fibrinolytic drugs

Arterial thrombi are platelet rich

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16
Q

What drugs are used for venous thrombi?

A

Parenteral and oral anticoagulants

17
Q

What is an example of a parenteral anticoagulant drug?

A

Heparin

18
Q

Give an example of an oral anticoagulant

A

Warfarin

19
Q

When are both antiplatelet and anticoagulants used?

A

Secondary prevention

Targeting multiple sites and mechanisms

20
Q

What does thromboxane A2 form from?

A

Arachidonic acid by COX-1 (cyclooxygenase)

21
Q

Give an example of a Cyclo-oxygenase inhibitor

A

Aspirin

22
Q

How does aspirin work?

A

Inhibits cyclooxygenase-1 mediated production of thromboxane A2

Reduces platelet aggregation

Irreversible

23
Q

Why does aspirin not completely inhibit platelet aggregation?

A

Other chemical mediators

COX1 not inhibited on all platelets

24
Q

What are the different dosing regiments of aspirin?

A

75 mg
Baby aspirin, used long-term to inhibit platelets

Just inhibits COX1

300 mg
Used in acute coronary syndromes

25
Q

What does aspirin do at higher doses?

A

Inhibits endothelial prostacyclin PGI2

Causing a decrease in cAMP, increased in Ca2, increase in platelet mediators released and aggregation by activating GPIIb/IIIa

26
Q

How is aspirin absorbed?

A

Passive diffusion

Hepatic hydrloysis converts aspirin to salicylic acid

27
Q

What are the adverse effects of aspirin?

A

GI irritation
GI bleeding (peptic ulcer)
Haemorrhage (stroke)
Hypersensitivity

28
Q

When should you not use aspirin?

A

Reye’s syndrome, avoid in under 16s
Hypersensitivity
3rd trimester of pregnancy - can cause premature closure of ductus arteriosus

29
Q

What are some important drug to drug interactions with aspirin?

A

Other anti-platelet and anti-coagulant drugs

(additive/synergistic action)

30
Q

Why does aspirin not work that well in some people?

A

COX-1 polymorphisms result in lack of efficacy

31
Q

Why does anti-platelet effect last lifespan of platelet?

A

Platelets have no nuclei
Cannot make more COX-1
Inhibition lasts lifespan of the platelet

32
Q

When do we use aspirin?

A
  • AF patients post stroke
  • Secondary prevention of stroke/ TIA and ACS
  • Post PCI and stent to reduce ischaemic complications
  • Co-prescribed with other anti-platelet agents
  • NSTEMI/STEMI- inital once 300mg loading dose, chewable is best
  • Acute ischamic stroke 300mg daily 2 weeks
33
Q

What is required with long-term use of aspirin?

A

Proton pump inhibitors

Clinical Pharmacology (45 decks)

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