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Yr 1 - Blood > Thrombosis > Flashcards

Thrombosis Flashcards

1
Q

What is thrombosis?

A

Formation of blood clot inside a vessel that blocks the blood circulation

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2
Q

What can result of thrombosis be?

A

Causes ischaemia (tissue death), malfunction, pain or swelling in the organ/tissue

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3
Q

Is thrombosis in arteries and vein different or similar?

A

Different

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4
Q

What does arterial thrombosis lead to?

A

Physical damage in arterial wall

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5
Q

What disorders can arterial thrombosis lead to?

A
  • Myocardial infarction
  • Atrial fibrillation
  • Peripheral vascular disease (leg)
  • Stroke
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6
Q

What does venous thrombosis lead to?

A

Pooling and ineffective movement of blood

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7
Q

What disorders can venous thrombosis lead to?

A
  • DVT

- Pulmonary embolism

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8
Q

What is Virchow’s Triad?

A

Describes the three broad categories of factors that are thought to contribute to thrombosis

  1. Hypercoagulability
  2. Hemodynamic changes (stasis, turbulence)
  3. Endothelial injury/dysfunction
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9
Q

What is arterial thrombosis caused by?

A

Atherosclerosis

Rupture of plaque drives formation of thombus

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10
Q

What is atherosclerosis?

A

Deposition of lipids in form of lipoproteins forming atherosclerotic plaque inside ARTERIES

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11
Q

How does an atherosclerotic plaque affect vessel wall?

A

Inflammation of vessel wall with infiltration of macrophages and fat deposition

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12
Q

What does the rupture of an atherosclerotic plaque lead to?

A

Drives formation of thrombus due to exposure of collagen etc

Leads to overactive element of platelet element and uncontrolled platelet activation (thrombus is platelet rich)

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13
Q

Describe the phases of thrombotic response to plaque rupture

A
  1. Plaque fissure or rupture
  2. Adhesion and activation of platelets
  3. Activation of coagulation cascade

This is normal clotting response but gone wrong as happening in wrong place at wrong time.

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14
Q

What are the risk factors for arterial thrombosis?

A
  • Advanced age
  • Smoking
  • Diabetes
  • Hypertension
  • Cholesterol
  • Poor diet
  • Lack of exercise
  • Ethnicity
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15
Q

What are the 2 types of arterial thrombi?

A

Mural thrombi and occlusive thrombi

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16
Q

What is the key driver of both mural and occlusive thrombi?

A

Uncontrolled platelet activation

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17
Q

What is mural thorombi?

A

Little thrombus formed on top of atherosclerotic plaque. Doesn’t obstruct vessel

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18
Q

What does mural thrombi lead to?

A

Unstable angina and transient ischaemic attacks. Chest pain but not fatal

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19
Q

What is occlusive thrombi?

A

Thrombus forms and completely blocks vessel

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20
Q

What does occlusive thrombi lead to?

A

MI and cerebral infarction

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21
Q

What are the prothrombotic factors?

A 
ADP
Adrenaline
Collagen
Fibrinogen
Thrombin
Thromboxane A2
Von Willebrand Factor
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22
Q

What are the antithrombotic factors?

A

Adenosine
Nitric oxide
Prostacyclin (PGI2)

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23
Q

What is required to maintain effective haemostasis?

A

A balance between prothrombotic and antithrombotic factors

Thrombosis is due to a hyper-thrombotic response (i.e. prothrombotic factors override antithrombotic factors)

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24
Q

Where is ADP released from?

A

Platelet dense granules

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25
Q

Where is thromboxane A2 released from?

A

Synthesised and release by platelet from arachidonic acid

26
Q

Where is thrombin generated?

A

Generated on the platelet surface as the endpoint of the coagulation cascade

27
Q

How do plaque contents affect antithrombotic factors?

A

Reduce the actions of the inhibitors

28
Q

What antiplatelets are used to treat atherothrombosis?

A
  • Aspirin
  • Anti GP2b/3a
  • Anti P2Y
29
Q

How does aspirin treat atherothrombosis?

A

Inhibition of COX-1 and thromboxane A2 production –> stop production of factor that drives platelet activation

30
Q

How does anti GP2b/3a treat atherothrombosis?

A

Inhibits receptor for fibrinogen and vWf

31
Q

How does anti P2Y treat atherothrombosis?

A

Inhibits receptor for ADP induced platelet aggregation

32
Q

How do fibrinolytics work?

A

Agents that block fibrinogen binding to platelet

33
Q

What is the normal 1ary haemostatic response?

A
  • Platelets bind to collagen
  • Adhesion & activation
  • Release of pro-aggregatory substances: ADP, thromboxane A2
  • Autocatalytic expansion of thrombus
34
Q

What is the normal 1ary haemostatic response controlled by?

A

Controlled by endothelial NO and prostacyclin

35
Q

What is the thrombotic response?

A
  • Platelets bind to collagen and exposed to oxidised lipids from plaques
  • Activation
  • Release of pro-aggregatory substances ADP & thromboxane A2
  • Autocatalytic expansion of thrombus
  • Reduced bioavailability of endothelial NO and production of prostacyclin
  • Occlusive thrombi: gets bigger and starts to protrude in blood vessel
36
Q

What is a DVT?

A

A blood clot that forms in a vein deep in the body (often deep veins of legs)

37
Q

Where do DVTs most often occur?

A

In areas of low blood flow that leads to accumulation of cells

38
Q

Describe a venous thrombus

A

Fibrin and erythrocyte rich

39
Q

How is a venous thrombus thought to form?

A

Inflammation effect caused by accumulation is thought to expose tissue factor due to platelet activation, leading to fibrin generation.

40
Q

What is a venous thrombus driven by? Why does it occur around valves?

A

Involves platelets but driven by excess thrombin in areas around valves

41
Q

How can a DVT lead to a pulmonary embolism?

A

Blood clot, or part of it, can break free (embolism) and become lodged in the blood vessels of the lung –> pulmonary embolism (PE)

42
Q

What are the symptoms of a DVT?

A

Calf swelling, pain, lack of venous return

43
Q

What is the swelling in a DVT caused by? What quick test can be done?

A

Oedema –> clot starts to put pressure on endothelial cells, fluid starts to escape and accumulate outside vessels (do the press test)

44
Q

What are the risk factors for a DVT?

A
  • Immobilisation
  • Surgery
  • Cancer
  • Pregnancy
  • Oral contraceptives
  • Genetic risk factors
45
Q

What are the genetic risk factors for a DVT?

A

o Deficiencies in coagulation inhibitors (antithrombin, protein C, protein S)
o Factor V Leiden mutation

46
Q

What is antithrombin?

A

Protein in blood which controls any thrombin generation that escapes from site of injury

47
Q

How can circulatory stasis lead to DVT?

A

Loss of laminar flow and pooling especially around valves, gaps between endothelial cells and minor platelet activation

48
Q

How can endothelial dysfunction lead to DVT?

A

Inflammation leads to activation and exposure of tissue factor which drives coagulation cascade

49
Q

How can hypercoaguability lead to DVT?

A
  • Localised inflammation
  • Loss of inhibitor function – activity of thrombomodulin (TM) and protein C/S system leading to thrombin accumulation (can be genetic)
  • Lupus anticoagulants (anti-phospholipid antibodies)
  • Impaired fibrinolysis
50
Q

What is a pulmonary embolism?

A

A DVT, or part of it, breaks off from vein and ravels through bloodstream to the heart and towards the lung causing poor blood flow. Clot blocks a vessel in the lung, interrupting blood supply.

51
Q

What are the symptoms of a pulmonary embolism?

A

Chest pain, sweating, acute shortness of breath

52
Q

How can d-dimer test be used to diagnose venous thrombosis?

A

D-dimer not normally produced in blood so is indicator of ongoing thrombotic events

53
Q

How is d-dimer produced?

A

Produced as result of breakdown of plasminogen to plasmin

54
Q

What is the treatment for a venous thrombus?

A

Immediate onset of anticoagulant effect –> Unfractionated Heparin (UH)

Low Molecular Weight Heparin (LMWH; subcutaneous)

Vitamin K Antagonists (reduce clotting by reducing action of vitamin K)

55
Q

How does UH work?

A

Immediate onset

Helps antithrombin work more effectively and helps it to inhibit thrombin and Factor Xa

56
Q

Why is it essential to get heparin dose right?

A

Bleeding

57
Q

What is 1ary treatment for arterial thrombi?

A

Anti-platelets

58
Q

How can an arterial thrombosis lead to a heart attack?

A

Arterial thrombus in coronary artery supplying the heart

59
Q

How can an arterial thrombosis lead to a stroke?

A

Arterial thrombus in vessel in brain

60
Q

Difference between arterial and venous thrombus?

A
  • Arterial thrombosis occurs under high shear flow
  • Venous thrombosis occurs under low shear flow
  • Arterial thrombus involves platelet rich thrombi forming around ruptured atherosclerotic plaques and damaged endothelium.
  • Venous thrombus occurs mostly around intact endothelial wall.
  • Venous thrombi are fibrin rich, encapsulating a large amount of RBCs in addition to activated platelets.
  • Arterial thrombi are platelet rich
61
Q

Explain the production of NO and prostacyclin

A

In healthy vessels, the endothelium expresses constitutive forms of nitric oxide synthase (NOSIII) and cyclo-oxygenase (COX-1)

  • NOSIII produces NO
  • COX-1 produces prostacyclin (prostaglandin member)
62
Q

What are the effects of NO and prostacyclin?

A

Both NO and prostacyclin and vasoactive and relax blood vessels and inhibit platelet activation.

Yr 1 - Blood (18 decks)

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