Thrombosis, embolism, ischaemia and infarction Flashcards

(30 cards)

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
What is the clinical relevance of knowing the source of a systemic emboli?
patient presenting with complications of embolism e.g. cerebral infarction consider predisposing factors and treat to prevent further episodes
26
What are the 2 main patterns of MI?
regional (transmural) >90% - sharply localised, thrombosis of main coronary artery branch subendocardial <10% - poorly localised, severe triple vessel atheroma
27
What is the definition of gangrene?
necrosis (tissue death) with superadded bacterial infection
28
When do fat embolisms occur?
bone fractures and other soft tissue trauma pulmonary circulation => dyspnoea, haemoptysis systemic circulation => widespread microemboli (esp brain) mortality = 10-15%
29
What are the causes and effects of air/gas embolism?
causes = venous rupture, accidental infusion, decompression sickness Effects = nil (small amounts), sudden death (>200ml), microemboli
30
What happens and what is the prognosis of amniotic fluid embolism?
rare - 1 in 50,000 deliveries high mortality >80% rupture of uterine veins during labour impaction of amniotic contents in pulmonary vessels