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Medsci 203 (my own) > L20 Thrombosis > Flashcards

L20 Thrombosis Flashcards

1
Q

What is haemostasis?

A

Physiological response of an injury to a blood vessel

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2
Q

What is the purpose of haemostasis?

A

Prevent blood loss by plugging leaks in injured vessels

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3
Q

Haemostasis is accomplished by co-operation between…

A

Endothelial cells, platelets, and clotting cascade
- Endothelial cells activate the process
- Platelets form a “plug”
- Clotting cascade produces the meshwork of fibrin which stabalises the platelet plug.

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4
Q

Which cells inhibit haemostasis in healthy vessels?

A

Endothelial cells

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5
Q

How is inhibition of haemostasis accomplished?

A
  • Physically insulating tissues from blood. Important because when underlying CT is exposed to blood, it activates coagulation system and platelets.
  • Endothelial cells produce enzymatic and chemical inhibitors of platelet activation
  • Produce antithrombin on endothelial cell surface which binds and inactivates coagulation enzyme thrombin
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6
Q

Which enzymatic and chemical inhibitors of platelet activation are produced by endothelial cells?

A

Nitric oxide (NO) and Prostacyclins

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7
Q

After a vessel injury, endothelial cells promote haemostasis by…

A
  • Producing endothelin, von Willebrand Factor, tissue factor (thromboplastin)
  • Activation of coagulation system through breech of endothelial cell barrier
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8
Q

What does endothelin do?

A

Causes vasoconstriction, preventing further loss of blood, rate of flow, and haemodynamic stress which could further damage the area.

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9
Q

What does von Willebrand factor do?

A

Promotes platelet adhesion to ECM proteins exposed by vessel injury in the vessel wall.

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10
Q

What does tissue factor (thromboplastin) do?

A

Activates coagulation cascade

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11
Q

What are platelets produced by?

A

Mytoplasmic fragmentation of megakaryocytes in the bone marrow.

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12
Q

What is the lifespan of platelets?

A

7 days

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13
Q

What is the structure of platelets?

A

Chocolate chip like structure, alpha and dense granules that contain chemical mediators of haemostasis

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14
Q

How are platelets activated?

A

Activated by ECM proteins (especially collagen) that are exposed when the endothelial cell layer is damaged

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15
Q

What do platelets secrete?

A
  • Thromboxane A2, vasoactive amines, ADP
  • Secretory granules for aggregation to form a platelet plug –> primary haemostasis
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16
Q

What do platelet signals do?

A

Vasoconstriction and platelet aggregation

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17
Q

What happens when there is reduced platelets?

A

Purpura (bleeding from skin capillaries), major spontaneous haemorrhage

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18
Q

The coagulation system is a cascade of _ reactions, whereby _ are activated

A

Proteolytic reactions, zymogens are activated

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19
Q

What does thrombin do?

A
  • Catalyses fibrinogen into fibrin monomers.
  • Induces further platelet aggregation and granule release - known as secondary haemostasis
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20
Q

What happens in primary and secondary haemostasis?

A

Platelets secrete granules for aggregation –> primary

Thrombin induces further platelet aggregation and granule release –> secondary.

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21
Q

What do fibrin monomers do (as part of the coagulation system)?

A

Polymerise into fibrin strands which form a meshwork with fused platelets to form a stable plug

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22
Q

How is the plug limited to the site of injury?

A

Counter regulatory mechanisms

23
Q

What is thrombosis?

A

The inappropriate activation of haemostasis, forming a ‘thrombi’ - a mass formed from constituents composed of fibrin and platelets, with entrapped RBCs and WBCs.

24
Q

Where may a thrombus form?

A

In a cardiac chamber or blood vessel, causing further damage to the lumen of vessels in which they form - or by breaking off and travelling as an embolus.

25
Q

What’s the difference between a blood clot and thrombi?

A

Blood clot is formed in static blood, primarily involving the coagulation system, without the interaction of platelets within vessel walls

26
Q

What is the Virchow’s triad?

A

3 factors that contribute to the etiology of thrombosis; changes to the endothelial cell wall, changes to the flow of blood (turbulence or stasis), and changes to the constituents of blood (hypercoagulability).

27
Q

What aspect of hemostasis does ‘changes to the endothelial cell wall (injury)’ activate?

A

Endothelial cells lose their ability to produce enzymatic and chemical inhibitors of platelet activation, and also lose their ability to produce antithrombin which inactivates coagulation enzyme - thrombin.

28
Q

What aspect of haemostasis does ‘changes to blood flow’ activate?

A

Endothelial cells, after injury produce endothelin which causes vasoconstriction. This causes change in flow of blood to the area.

29
Q

What aspect of haemostasis does ‘changes to constituents of blood’ activate?

A

von Willebrand factor promotes platelet adhesion to ECM proteins (after endothelial injury). Thus, changing contituents of blood. Tissue factor released by endothelial cells also changes the constituents of blood.

30
Q

What can cause endothelial cell injury?

A

Atherosclerosis, hypoxia, infection, physical (crushing veins, haemodynamic stress), and chemical insult

31
Q

How can artificial surfaces (vascular implants) induce thrombosis?

A

Activate intrinsic coagulation cascade, bind to pro-inflammatory compliment cascade proteins, proteins that may activate platelets

32
Q

Patients with vascular implants must take ___ drugs

A

Anticoagulant

33
Q

What causes turbulence in arteries or cardiac chambers?

A
  • Narrowing of vessels (caused by atherosclerotic plaque)
  • Aneurysms (widening of vessels)
  • Infected myocardium - altered vessel structure by pulling and pushing of tissues
  • Abnormal cardiac rhythm or valvular heart disease
34
Q

What can cause stasis in veins?

A

Failure of right side of heart to pump properly, immobilsation, compressed veins, altered blood viscosity (i.e. sickle cell anaemia, dehydration), varicose veins.

35
Q

What does changes to blood flow cause?

A
  • Platelets to be in contact with endothelium
  • impaired removal of pro-coagulant
  • delivery of anti-coagulant factors
  • injure endothelium
  • atherosclerotic plaques which are pro-coagulant.
36
Q

What are the genetic causes of hypercoagulability?

A

Deficiency of protein C and antithrombin III

37
Q

What are the acquired causes to hypercoagulability?

A

Tissue damage (i.e. trauma), Post-operative surgery, cancer, cigarette smoke, elevated blood lipids, oral contraceptives.

38
Q

How do acquired causes lead to activation of coagulation cascade?

A

The acquired causes can lead to an acute phase response from liver. This causes the release of pro-inflammatory and pro-coagulant factors to be released which increase the likelihood of coagulation cascade being turned on. It also leads to the secretion of cytokines, causing platelets to release from bone marrow. Thus, tissue damage can lead to activated of coagulation cascade and release of platelets from bone marrows.

39
Q

Cancers can cause a thrombosis by…

A

increasing the likelihood of coagulation

40
Q

facts to remember, flip too:

Cigarette smoke can increase platelet adhesion and degranulation (haemostatic mediators are released).

A

Elevated blood lipids and oral contraceptives can also alter the tendency for coagulation and platelet activation.

41
Q

What are the 3 types of natural anticoagulants

A

Antithrombins, proteins C and S (vit. K dependent), tissue factor pathway inhibitor.

42
Q

How does fibinolytic cascade limit size of final clot?

A

Plasmin breaks down fibrin

43
Q

What is arterial thrombosis?

A

When thrombosis forms on a region of an atherosclerotic plaque. Atherosclerosis is a silent diseases until an event occurs. Either there is a critical stenosis occlusion by thrombus.

44
Q

What is critical stenosis?

A

Plaque grows progressively, vessel becomes so narrow that not enough blood reaches downstream tissues when exercising.

45
Q

What is ‘occlusion by thrombus’?

A

Lots of haemodynamic stress on the vessel, tearing and ripping the endothelial cells, therefore damaging the vessel and exposing the C.T. proteins to the coagulation blood proteins in the plasma and to the platelets in the cellular components of blood.

46
Q

What is mural thrombosis?

A

Thrombus in the ventricles of heart

47
Q

What is embolisation?

A

Breaking off of a thrombus and flowing to a different place

48
Q

What’s an emboli?

A

Part of the thrombus - intravascular mass (solid, liquid, or gas) carried by blood flow from its point of origin to a distant site

49
Q

What are some types of emboli?

A

Thrombus, air, fat, bone marrow.

50
Q

What are the four effects of venous thrombosis?

A
  • Resolution (via fibrinolytic cascade)
  • Embolisation to lungs (propagation to heart just before lungs)
  • Organised and incorporated into wall
  • Organised and recanalised (new blood vessels).
51
Q

What is deep venous thrombosis?

A

Thrombosis in the deep veins of legs can break off and flow to the lungs (pulmonary thromboembolus).

52
Q

What are some effects of emboli?

A

Stenosis (narrowing of vessels) leading to occlusion

53
Q

Emboli from leg or pelvis will lodge in… which causes…

A

pulmonary artery, pulmonary embolus

54
Q

When there is an emboli on the left side of the heart or aorta…

A

The emboli enters the systemic arterial system and may pass to brain, spleen, kidney, etc.

Medsci 203 (my own) (18 decks)

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