Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Haematology > Arterial Thrombus and Antiplatelet Drugs > Flashcards

Arterial Thrombus and Antiplatelet Drugs Flashcards

1
Q

What are the 2 main types of thrombotic event?

A
  1. Arterial: conorary, cerebral, peripheral

2. Venous: DVT, PE

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

What type of drug is used to treat an arterial thrombus?

A

Antiplatelet

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

What type of drug is used to treat a venous thrombus?

A

Anticoagulant

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

Arterial thrombus are found in a ____ pressure system

A

HIGH

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

How do arterial thrombus form?

A
  • Atherosclerosis narrows the blood vessel
  • This damages the vessel wall
  • vWF recruits platelets
  • Platelets come and aggregate
  • PLATELET RICH THROMBUS is formed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How is an arterial thrombus treated?

A
  • Aspirin and other anti-platelet drugs (e.g. clopidogrel).

* Modify risk factors for atherosclerosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is atherosclerosis not the same as?

A

Arterial thrombus

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

Describe how atherosclerosis forms.

A
  • Damage to endothelium.
  • Recruitment of ‘foamy’ macrophages rich in cholesterol.
  • Forms plaques rich in cholesterol.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Describe stable atherosclerotic plaques.

A

Hyalinised and calcified

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

What are the 2 clinical conditions that people get from having a stable atherosclerotic plaque?

A
  • Stable angina (coronary artery).

* Intermittent claudication (leg artery).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How does an unstable atherosclerotic plaque cause an acute thrombus?

A

Plaques rupture, damage to endothelium, platelets are recruited and cause acute thrombosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What symptoms arise from an acute thrombus?

A

Sudden onset sx:

  • Unstable angina or myocardial infarction (coronary arteries).
  • Stroke (cerebral arteries).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What can an acute thrombus ultimately lead to?

A

** LEADS TO ACUTE ORGAN ISCHAEMIA AND INFARCTION **

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

In what type of environment is the rupture of a plaque more likely to happen?

A

In the high pressure environment of arteries.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Outline how an arterial thrombus develops after the rupture of a plaque?

A
  • Platelets adhere to the ruptured plaque – exposed endothelium and release of Von Willebrand factor.
  • Platelets become activated – release granules that activate coagulation and recruit other platelets to developing platelet plug.
  • Platelet aggregation via membrane glycoproteins.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What do all the risk factors for an arterial thrombus ultimately do?

A

Cause damage to the endothelium, increase in foamy macrophages and platelet activation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

List risk factors for arterial thrombus (and state what they effect).

A
  • Hypertension – damage to endothelium, platelet activation.
  • Smoking – endothelium, platelets.
  • High cholesterol (accumulated in plaque).
  • Diabetes mellitus (endothelium, platelets, cholesterol).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How can an arterial thrombus be prevented?

A
  • Stop smoking.
  • Treat hypertension.
  • Treat diabetes.
  • Lower cholesterol.
  • Anti-platelet drugs.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

The venous system is a ____ pressure system

A

LOW

20
Q

What triad is important in understanding the aetiology of a venous thrombus?

A

Virchow’s triad:

  • Stasis.
  • Vessel wall (valves not atheroma).
  • Hypercoagulability (high clotting factors).
21
Q

The clot in a venous thrombus is ______ rich

A

FIBRIN

22
Q

How is a venous thrombus treated?

A
  • Heparin
  • Warfarin
  • NOAC’s
23
Q

Where are platelets formed? How?

A

In the bone marrow, by ‘budding’ from megakaryocytes.

24
Q

Describe the appearance of platelets.

A

Small anucleate discs

25
Q

What is the lifespan of a platelet?

A

7-10 days

26
Q

Explain the steps which lead to PLATELET ADHESION at the site of injury.

A

Endothelial (vessel wall) damage exposes collagen, Von Willebrand Factor, and other proteins to which platelets have receptors.

27
Q

After platelet aggregation has occurred at a site of injury what happens?

A

There is then secretion of various chemicals from the platelets (eg ADP, thromboxane A2), which leads to aggregation of platelets at the site of injury.

28
Q

What are the 3 main stages (3 A’s) in the formation of a platelet plug?

A
  1. Adhersion
  2. Aggregation
  3. Activation
29
Q

Describe what happens in adhesion.

A

Platelets bind to subendothelial collagen via glycoprotein 1b and vWF.

30
Q

Describe what happens in aggregation.

A

Platelets attach to each other via GPIIbIIIa and fibrinogen

31
Q

Describe what happens in activation.

A

Platelets alter their shape to expose more phospholipid on the surface-provides a greater surface area for coagulation activation and fibrin production to stabilise the clot.

Granules release TXA2, thrombin and ADP to further recruit platelets

32
Q

What is the activation stage augmented by?

A

Release of granules that further stimulate platelet activation – e.g. thrombin, thromboxane A2 and ADP – in order to recruit more platelets to the process.

33
Q

What does the activation stage occur via?

A

Receptors to ADP etc. on the platelet surface

34
Q

How does Aspirin work?

A

By inhibiting cyclo-oxygenase. (can no longer convert arachidonic acid to prostaglandins which are then converted to TXA2 which is then blocked from activated platelet aggregation)

35
Q

Why does aspirin lead to an anti-platelet function?

A

COX is necessary to produce Thromboxane A2.

36
Q

What is thromboxane A2?

A

A platelet agonist released from granules on activation.

37
Q

What are the main side effects of aspirin?

A
  1. Bleeding.
  2. Block of prostaglandin production leads to:
  • GI ulceration.
  • Bronchospasm, especially in pts with asthma.
38
Q

How do CLOPIDOGREL and PRASUGREL work?

A

They are ADP receptor antagonists.

39
Q

How does dipyridamole work?

A

It is a phosphodiesterase inhibitor – reduced production of cAMP which is ‘second messenger’ in platelet activation.

40
Q

Give an example of a new anti platelet drug.

A

Abciximab

41
Q

How do new anti platelet drugs work?

A

GPIIb/IIIa inhibitors - inhibit aggregation

Platelets attach to each other via GPIIbIIIa and fibrinogen

42
Q

When are new anticoagulants given?

A

These are very potent, so are given IV in heart surgery/angioplasty.

43
Q

How long do anti-platelet drugs tend to affect platelet function for?

A

7-10 days - this makes sense as the lifespan of platelets is 7-10 days

44
Q

Prior to elective operations, when should anti-platelet agents be stopped?

A

7 days prior

45
Q

If serious (life-threatening) bleeding, how can the action of anti-platelets be reversed?

A

Give a platelet transfusion

Haematology (26 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions