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Y3 > Theombosis Embolism Ischamia Infarction > Flashcards

Theombosis Embolism Ischamia Infarction Flashcards

1
Q

Define thrombosis

A

Formation of a solid mass from the constituents of blood

Within the vascular system during life - different to a simple blood clot a

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2
Q

Mechanism of thrombosis

A

Exaggeration of normal haemostatic mechanisms

1) coagulation system - formation of a blood clot
2) platelets: adhesion, aggregation, secretion
3) vascular endothelium : promotion /inhibition of 1/2 , protection of circulating blood form highly thrombogenic sunendlthelium

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3
Q

What is a predisposing factor of thrombosis

A

Virchows triad

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4
Q

What is virchows 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/myeloproliferative disease, nephrotic syndrome, malignancy, oral contraceptive pill, post-op)

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5
Q

Composition and appearance of a thrombus

A

Blood clot + platelets
- variable composition depending on speed of blood flow
Characteristic laminations - lines of zahn
1) arterial /cardiac (rapid flow)
- mainly platelets (pale)
Mural or occlusive (depending on the vessel SIZE)
2) venous (slow flow)
Mainly blood clot - red
Usually occlusive

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6
Q

Thrombus sites of occurrence

A

Heart
Arteries
Veins

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7
Q

Where are cardiac thrombosis occur

A 
Atria 
- most common in the appendages 
- associated with heart failure and AF
Valves ( vegetations) 
- rheumatic fever (sterile) 
- infective endocarditis (infective) 
- non bacterial thrombotic endocarditis (sterile) e.g. Malignancy or SLE 
Ventricles 
- mural thrombosis 
Associated with MI and cardiomyopathy
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8
Q

Causes of arterial thrombosis

A

Atherosclerosis
Aneurysms
Inflammation , vasculitis - e.g. Polyarteritis nodosa

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9
Q

Appearance of arterial thrombosis

A

Mural thrombosis - large vessels

Occlusive thrombosis - medium sized/small vessels

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10
Q

Predisposing factors to venous thrombosis

A 
Immobility 
Post op esp abdo surgery
Severe trauma
MI
congestive heart failure 
Pelvic mass - inc pregnancy 
Thrombophlebitis
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11
Q

Pathological features of venous thrombosis

A

Usually occlusive

Propagation - progressive spread of the thrombus to a site more proximal

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12
Q

Sequelae of thrombosis

A

Resolution:dissolution of clot by fibrinolysis - venous thrombi
Organisation : ingrowth of fibroblasts, capillaries, phagocytes - granulation tissue
Recanalisation- restoration of original lumen or fibrosis - formation of webs and cords

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13
Q

Features/ how does a thrombus go through resolution

A

There is central liquification of the thrombus
Retraction of thrombus
Slip like clefts

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14
Q

Features/ how does a thrombus go through organisation

A

Ingrowth of vascular smooth muscle cells
Ingrowth of capillaries
Endothelised channels through the thrombus

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15
Q

Features/ how does a thrombus go through recanalisation

A

There is a reconstituted lumen within the thrombus

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16
Q

What are the main complications of an arterial thrombus

A

Ischaemia and infarction.

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17
Q

What are the main complications of the veins /heart

A

Embolism

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18
Q

Define embolism

A

Passage of insoluble mass (embolus)

Within the blood stream and has an impaction site that is distant from its point of origin

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19
Q

Composition of an embolus

A

Thrombus 95% of the time
Others which are rare
- fat, air/gas, tumour, amniotic fluid, infective material septic

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20
Q

Sites of emboli impaction

A

1) pulmonary arteries
- thrombosis from veins - femoral, Iliac, vena cava
- right side of the heart
2) systemic arteries
- thrombus from the left side of the heart and aorta

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21
Q

Define ischaemia

A

Reduced blood supply to tissue or organ

Harmful effects due to hypoxia

22
Q

Causes of ischaemia

A

Intrinsic disease of vessels
Occlusion by thrombus/ embolus
External compression

23
Q

What are the effects of vascular occlusion - factors determining the severity of ischaemia

A 
Speed of onset 
Extent of obstruction
Anatomy of local blood supply 
- end arteries - kidney
- parallel arteries - brain
- intrarterial branches - intestine 
Pathology of collateral circulation
General factors - cardiac state, oxygenation of blood 
Vulnerability of tissue supplied to anoxia
24
Q

Define infarction

A

Death of tissue due to ischaemia

Usually arterial occlusion, occasionally venous

25
Q

How are infractions classified

A

Shape - wedge shaped or other
Colour - white or red
Infection - bland or septic

26
Q

Histological changes in infarction - what are the four stages

A

Necrosis
Acute inflam
Organisation
Scar formation

27
Q

Histological changes in infarction - what are the four stages and the time in which they occur

A

Necrosis 6-12 hours
Acute inflam 24hrs - 7days
Organisation - 3days - 2 weeks
Scar formation - 2 weeks - 3 months

28
Q

Histological changes in infarction - what are the four stages and what occurs during those stages

A

Necrosis - usually coagulative
Acute inflam - congestion, oedema migration of polymorphs
Organisation - ingrowth of capillaries, macrophages, fibroblasts
Scar formation - deposition of collagen, polymerisation

29
Q

What are the applications of the histological changes classficiation

A

Used to determine the age of infarcts

Understanding complications of infections - MI

30
Q

Sources of pulmonary embolism

A

DVT - 95%
Other veins, pelvic, Iliac, vena cava
Right Side of the heart

31
Q

Consequences of PE

A

Sudden death if a massive embolism
Pulmonary infarction - pulmonary venous congestion
- haemorrhagic, peripheral, wedge shaped
Pulmonary hypertension - recurrent PE
Asymptomatic - compete resolution - 60-80% of cases

32
Q

Things to consider in a PE

A

The lungs have a dual blood supply so if the pulmonary artery in infarcted with an e,bolts the bronchial artery can still supply the area
The size and the munger of emboli are important considerations as to the outcome

33
Q

What happens when there is a PE and pulmonary venous congestion

A

There is venous back pressure this impedes the bronchial supply as the venous pressure is higher than the arterial supply as the pulmonary artery is blocked and there isn’t enough pressure in the bronchial artery so leads to not enough capacity to perfused the lung

34
Q

Features of a PE and why

A

Wedge shaped due to the supply of the end arteries
Peripheral due to where the blockage occurs - as the artery narrows
Haemorrhagic due to the venous back pressure

35
Q

Name 2 clinical manifestations of pulmonary infractions that can be explained by understanding the characteristic pathological changes -

A

Haemoptysis - haemorrhagic dead tissue breaks down and the bronchi is where is can be extended into
Subpleural location infarction - pleuritic chest pain the overlying pleura can become irritated

36
Q

Systemic emboli sources

A

Left atrium - AF
Valves mitral aortic - infective endocarditis
Left ventricle -MI
Aorta - atherosclerosis

Rarer
Paradoxical embolus - atrial septal defect - DVT passes across as
Atrial myxoma

Clinical relevance - patient present with complications of embolism - cerebral infarction
Consider predisposing factors + treat to prevent further episodes

37
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 - sever triple vessel atheroma - no thrombosis

38
Q

Posterior MI is due to thrombosis of which coronary artery

A

Right

39
Q

What is a haemopericardium and what can cause it

A

Rupture of the left ventricular wall following an MI

Each time the heart pumps it goes into the pericardium and causes cardiac tamponade

40
Q

What is the peak time at which left ventricular wall rupture occurs following MI

A

4-10 days
Due to acute inflammation causing congestion, oedema, migration of polymorphs
Heart is at it’s weakness doe to inflammatory infiltrate

41
Q

What is a cardiac aneurysm

A

It is a late complication of MI

Usually >3 months
Dead myocardium replaced by fibrosis tissue so cannot contract
If very thin the sac can balloon out so this can be a cuss of late myocardiac failure requires surgical intervention

42
Q

What is a saddle embolism

A

Thrombus travelled down aorta and straddles the bifurcation

43
Q

Define gangrene

A

Necrosis - tissue death with superadded bacterial infection

44
Q

Rare types of embolus

A 
Fat 
Air/gas
Tumour
Amniotic fluid
Infective material - septic
45
Q

What causes a fat embolus

A

Bone fractures and other soft tissue trauma

46
Q

What is the mortality of a fat embolus

A

10-15%

47
Q

What happens if a fat embolus is in the pulmonary circulation

A

Dyspnoea

Haemoptysis

48
Q

What happens if the fat embolus gets into the systemic circulation -

A

widespread microemboli esp brain

49
Q

Causes of an air/ gas emboli

A

Venous rupture - neck wound
Accidental infusion
Decompression sickness

50
Q

Effects of an air/gas embolus

A

Nothing in small amounts
Sudden death is above 200ml
Microemboli

51
Q

What is an amniotic fluid embolism

A

Rupture of the uterine veins during labour
Impaction of amniotic contents in pulmonary vessels
Rare and has a high mortality

Y3 (22 decks)

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