Thrombosis, embolism, ischaemia and infarction Flashcards

1
Q

What is the definition of thrombosis?

A

formation of a solid mass
form the constituents of blood
within the vascular system during life (different to a simple blood clot)

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2
Q

What is the mechanism behind thrombosis?

A

exaggeration of normal haemostatic mechanisms:

1) coagulation system - formation of blood clot
2) platelets - adhesion, aggregation, secretion
3) vascular endothelium - promotion/inhibition of 1 & 2, protection of circulating blood from highly thrombogenic subendothelium

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3
Q

What is virchow’s triad?

A

1) changes in vessel wall - endothelial damage
2) changes in blood flow - stasis, turbulence
3) changes in blood composition - many poorly defined (polycythaemia, nephrotic synrome, malignancy, oral contraceptive pill)

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4
Q

What is the composition and appearance of thrombi?

A

blood clots + platelets
= variable proportions depending on speed of blood flow

characteristic laminations - lines of zahn

1) arterial/cardiac (rapid flow)
- mainly platelets (pale)
- mural or occlusive (depending on size of vessel)

2) venous (slow flow)
- mainly blood clot (red)
- usually occlusive

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5
Q

What are the sites where thrombosis usually occurs?

A

heart
arteries
veins

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6
Q

What are examples of cardiac thrombosis?

A

1) atria
- most common in appendages
- associated with HF and AF

2) valves (vegetations)
- rheumatic fever (Sterile), infective endocarditis (infective), non-bacterial thombotic endocarditis (sterile - malignancy, SLE)

3) ventricles
- mural thrombosis
- associated MI and cardiomyopathy

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7
Q

What are the causes and appearance of arterial thrombosis ?

A

causes:
- atherosclerosis, aneurysms, inflammation (vasculitis)

appearance: mural thrombosis (large vessels), occlusive thrombosis (medium/small vessels)

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8
Q

What are the predisposing factors to venous thrombosis?

A
immobility 
post op
severe trauma
MI
congestive HF
pelvic mass (inc pregnancy)
thrombophlebitis
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9
Q

What are the pathological features of venous thrombosis?

A

usually occlusive

propagation

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10
Q

What is the sequelae of thrombosis?

A

1) resolution = dissolution of clot by fibrinolysis (venous thrombi)
2) organisation = ingrowth of fibroblasts, capillaries, phagocytes (granulation tissue)
3) recanalisation = restoration of original lumen, fibrosis = formation of webs, cords

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11
Q

What are the main complications of thrombosis?

A

arteries - ischaemia/infarction

veins/heart = embolism

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12
Q

What is the definition of embolism?

A

passage of insoluble mass (embolus)

within the blood stream and impaction at a site distant from its point of origin

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13
Q

What is the composition of emboli?

A

1) thrombus (>95%)

2) other (rare) - fat, gas/air, tumour, amniotic fluid, infective material

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14
Q

What are the sites of impaction of emboli?

A

1) pulmonary arteries = thrombi from veins, to right side of heart
2) systemic arteries = thrombi from left side of heart and aorta

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15
Q

What is the definition of ischaemia?

A

reduced blood supply to tissue or organ

harmful effects due to hypoxia

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16
Q

What are the causes of ischaemia?

A

1) intrinsic disease of vessels
2) occlusion by thrombus/embolus
3) external compression

17
Q

What factors determine the severity of ischaemia?

A

1) speed of onset
2) extent of obstruction
3) anatomy of local blood supply = end arteries, parallel arteries, inter-arterial branches
4) pathology of collateral circulation
5) general factors - cardiac state, oxygenation of blood
6) vulnerability of tissue supplied to anoxia

18
Q

What is the definition of infarction?

A

death of tissue due to ischaemia

usually arterial occlusion, occasionally venous

19
Q

How are infarctions classified?

A

shape - wedge shaped or other
colour - white or red
infection - bland or septic

20
Q

What are the 4 stages of infarction?

A

1) necrosis = usually coagulative - 6-12 hours
2) acute inflammation = congestion, oedema, migration of polymorphs - 24 hours - 7 days
3) organisation = ingrowth of capillaries, macrophages, fibroblasts - 3 days - 2 weeks
4) scar formation = deposition of collagen polymerisation - 2 weeks - 3 months

21
Q

Why are the stages of infarction important?

A

determining the age of infarcts

understanding complications of infarction

22
Q

What are the sources of PE?

A

1) dvt - >95%
2) other veins - pelvic, iliac, vena cava
3) right side of heart

23
Q

What are the consequences of PE?

A

1) Sudden death - massive embolism
2) pulmonary infarction - pulmonary venous congestion, haemorrhagic, peripheral, wedge-shaped
3) pulmonary hypertension - recurrent PE
4) asymptomatic - complete resolution (up to 60-80%)

24
Q

What are the common and rare sources of systemic emboli?

A

common

  • left atrium - AF
  • valves - infective endocarditis
  • left ventricle - MI
  • aorta - atherosclerosis

rare

  • paradoxical embolus - atrial septal defect
  • atrial myxoma
25
Q

What is the clinical relevance of knowing the source of a systemic emboli?

A

patient presenting with complications of embolism e.g. cerebral infarction
consider predisposing factors and treat to prevent further episodes

26
Q

What are the 2 main patterns of MI?

A

regional (transmural) >90%
- sharply localised, thrombosis of main coronary artery branch

subendocardial <10%
- poorly localised, severe triple vessel atheroma

27
Q

What is the definition of gangrene?

A

necrosis (tissue death) with superadded bacterial infection

28
Q

When do fat embolisms occur?

A

bone fractures and other soft tissue trauma

pulmonary circulation => dyspnoea, haemoptysis

systemic circulation => widespread microemboli (esp brain)
mortality = 10-15%

29
Q

What are the causes and effects of air/gas embolism?

A

causes = venous rupture, accidental infusion, decompression sickness

Effects = nil (small amounts), sudden death (>200ml), microemboli

30
Q

What happens and what is the prognosis of amniotic fluid embolism?

A

rare - 1 in 50,000 deliveries
high mortality >80%
rupture of uterine veins during labour
impaction of amniotic contents in pulmonary vessels