thrombosis and embolism Flashcards

1
Q

thrombosis

A

the process leading to the formation of thrombus

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2
Q

thrombus

A

a solid mass composed of blood constituents which have aggregated together in flowing blood in the lumen of a blood vessel. the main constituents are platelets and fibrin

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3
Q

physiological thrombosis- primary haemostasis

A
  • vessel wall is breached
  • circulating platelets aggregate to plug gap
  • platelets release factors which trigger coagulation cascade
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4
Q

physiological thrombosis- secondary haemostasis

A
  • coagulation cascade converts fibrinogen to large molecules of insoluble fibrin
  • long fibrin molecules bind together platelets and entrapped red and white cells
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5
Q

fibrinolysis

A

fibrin holds the thrombus together. if fibrin is broken down, the thrombus dissolved = fibrinolysis. plasmin is the active enzyme which fragments fibrin. the fragmented fibrin are called ‘fibrin degradation products’ or FDPs

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6
Q

plasminogen in fibrinolysis

A

plasma contains the inactive proenzyme plasminogen.
plasminogen is converted to plasmin by plasminogen activators, particularly tissue plasminogen activator (t-PA) secreted by endothelial cells and Urokinase.
when fibrin is formed, plasminogen and t-PA secreted by endothelial cells and Urokinase.
when fibrin is formed, plasminogen and t-PA bind to it. the t-PA convert nearby plasminogen to plasmin, which binds to degrade the fibrin. this controls the size of the thrombus.

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7
Q

pathological thrombosis .

A

pathological thrombosis occurs when the thrombus enlarges beyond vessel healing requirements, and continues to grow. beyond a certain thrombus size and rate of development, the intrinsic fibrinolytic system is incapable of controlling the size to which the thrombus grows

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8
Q

D-dimer test

A

D-Dimers are FDBs. detected by monoclonal antibody test to D fragment. increased blood levels in thrombosis.
positive test in presence of active thrombosis:
- pulmonary embolus
- deep vein thrombosis
- aortic dissection.

best used as a test of exclusion rather than inclusion.

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9
Q

what factors predispose thrombus formation?

A

virchow’s triad:

1) damage to vessel wall, especially endothelium
2) stasis- slow or turbulent blood flow
3) hypercoagulability- change in character of blood especially increased platelets, increased red cell numbers, increased viscosity

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10
Q

pathological thrombosis- where does it occur?

A

arteries- main predisposing factors are vessel wall damage.
veins- stasis most important
heart- ventricles: chamber wall damage most important. Atrium- stasis most important. heart valves- valve surface damage most important

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11
Q

thrombo-embolism

A

thrombus fragments/ detaches completely and travel elsewhere in the circulation.

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12
Q

what happens when a thrombus occludes a vessel?

A

artery- thrombotic occlusion stops flow of blood, cuts off oxygen to tissues -> infarction.
vein- occlusion prevents venous drainage of tissues, blood pools, cannot escape –> congestion and infarction (that is often haemorrhagic)

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13
Q

organisation and recanalisation of pathological thrombus

A

new vessel grow into the thrombus. vascular granulation tissue develops. fibroblasts invade and deposit collagen. fibrovascular granulation tissue develops.

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14
Q

embolism

A

the transference of abnormal material by the blood stream with eventual impaction of the material in a vessel distal to its site of origin.
the most important materials to embolise are thrombus and cancer cells (metastasis)

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15
Q

embolism (non-thrombotic)

A
thrombus and malignant tumour are the most important materials to embolize.
others:
fat and marrow
air
nitrogen
amniotic fluid
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