Thrombosis Flashcards

1
Q

normal haemostasis

A

Well-regulated process that maintains blood in a fluid, clot free state in normal vessels and induces the rapid formation of a localised haemostatic plug at the site of vascular injury

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2
Q

Haemostasis and thrombosis are dependent on what three components

A
  • Vessel wall
  • Platelets
  • Coagulation cascade
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3
Q

thrombosis

A

the inappropriate activation of blood clotting in an uninjured vessel/minimally injured vessel leading to the formation of a blood clot (thrombus) within the vascular system, which can obstruct the flow of blood

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4
Q

thrombus

A

an aggregate of coagulated blood containing platelets, fibrin and entrapped cellular elements.

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5
Q

virchows triad

A

change in surface - endothelial injury
change in flow - stasis and turbulence
change its constituents - hypercoagulability

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6
Q

where in the endothelial surface does thrombosis commonly occur and why

A

atheromatous plaques
Injury occurs due to HTN(Hypertension), turbulent
flow, radiation
results from -exposure of stroma, increased platelet adhesion

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7
Q

how does turbulent blood flow cause or influence thrombosis

A

Disrupted flow brings platelets into contact with
the endothelium
Prevent dilution of activated clotting factors by flowing blood

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8
Q

hypercoagulability

A

alteration of the coagulation pathways

-> predisposes to thrombosis

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9
Q

heritable hypercoagulability

A

Factor V leiden, protein c/protein s deficiencies,

prothrombin mutations

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10
Q

examples of Acquired Hypercoagulability

A

Oral contraceptives, pregnancy, malignancy,

nephrotic syndrome

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11
Q

sites of venous thrombus formation

A

– most commonly due to stasis in capillaries and heart

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12
Q

sites of arterial thrombus formation

A

most commonly superimposed on atheroma

capillaries and heart

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13
Q

causes of arterial thrombosis

A

Atheromatous plaque
Smokers
High cholesterol

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14
Q

causes of venous thrombosis

A

Blood pressure lower – atheroma does not occur
Most begin at valves – turbulence, stasis, occlusion
Venous return from the legs relies on calf muscle
contraction and relaxation
Any fall in blood pressure (e.g. during surgery) can
precipitate development

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15
Q

risk factors for venous thrombosis

A
Immobility
Smoking
Cancer
Pregnancy
Oestrogen therapy
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16
Q

Clinical effects of a arterial thrombus

A

Loss of pulse
Pale, cold
Painful
Death & gangrene of the affected limb/site

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17
Q

Clinical effects of a venous thrombus

A
  • 95% occur in leg veins
  • Tender
  • Swollen
  • Reddened
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18
Q

fate of a thrombus

A
Lysis and resolution 
Organisation - scar tissue
Recanalization
Propagation
Embolization
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19
Q

Recanalization

A

– ingrowth of new vessel which eventually

join up to restore blood flow, at least partially

20
Q

Propagation

A

enlarges leading to vessel obstruction

21
Q

Embolization

A

dislodges, travelling to a different site

22
Q

embolism

A

 An embolus is a detached intravascular physical mass,
which is carried in the circulation until it reaches a vessel
too small to permit its further passage when occlusion
occurs

23
Q

embolism that arise from a thrombus

A

thromboembolism

24
Q

types of embolism

A
Fat
Air or gas
Thrombus
Bacteria emboli
Amniotic fluid
Tumour fragments
25
pulmonary embolism
Venous thrombi in the leg veins can travel to the lungs | Small emboli may cause no effects
26
larger emboli in pulmonary embolisms can cause
``` • Chest pain • Shortness of breath • Infarction • Sudden death o Saddle embolus ```
27
systemic embolism
Arise in the arterial system Arise in the heart or from atheromatous plaques May travel to various sites and cause
28
examples of systemic embolism
* Brain – TIA, stroke * Renal – infarction * Bowel – ischaemic bowel * Limbs – ischaemia and gangrene
29
low blood supply
• Imbalance between perfusion and demand of | oxygenated blood to a tissue
30
ischaemia
Deficient supply of blood
31
how is ischaemia characterised
insufficiency of O2 lack of nutrient substrates and inadequate removal of metabolites (perfusion)
32
Susceptibility of tissues to ischaemia
 Blood supply and collateral circulation – may compensate | for reduced perfusion
33
tissues with what kind of metabolism rate are highly susceptible ischaemia
Organs with high metabolic rate and aerobic metabolism – | susceptible (heart)
34
tissues of what kind are lowly susceptible to ischaemia
Supporting tissues (fibrous, bone) – less susceptible
35
infarction
Area of ischaemic necrosis caused by occlusion of either the arterial supply or the venous drainage in a particular tissue
36
what embolic events cause infarction
 Torsion: testicular/bowel  Extrinsic compression  Traumatic rupture
37
clinical examples of infarction
```  Myocardial infarction  Cerebrovascular accident (infarct)  Pulmonary infarction  Bowel infarction  Ischaemic necrosis of the extremities ```
38
causes of iscaemia
THROMBOSIS EMBOLUS Local vasospasm Extrinsic compression of vessel
39
macrscopic appearances of infarct
Wedge shaped (occluded vessel at apex
40
early macrscopic appearances of infarct
• Poorly defined, irregular • Narrow rim of hyperaemia at edge due to inflammation
41
late signs of macroscopic appearances of infarct on solid organ
few RBC lysed  some haemosiderin pigment. Pale and sharply defined
42
late signs of macroscopic appearances of infarct on spongy organ
Firm and brown | Haemosiderin pigment
43
Microscopic features of infarcts
first 12 - 18hrs →Necrotic tissue stimulates inflammatory response at edge (1-2days) →Phagocytosis of cellular debris and dead tissue →Reparative phase with scar formation
44
exception to microscopic features of infarcts
Brain exception – liquefactive necrosis
45
examples of vulnerable tissue
‘Watershed’ areas (especially during shock/hypotension) o Splenic flexure of the colon o Brain o Deep myocardium
46
low flow infarction
Impaired blood flow rather than absolute cessation
47
susceptibility of infarcts
low flow | vulnerable tissue