Theombosis Embolism Ischamia Infarction Flashcards by Jade Fellows

Define thrombosis

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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Mechanism of thrombosis

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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What is a predisposing factor of thrombosis

Virchows triad

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What is virchows triad

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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Composition and appearance of a thrombus

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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Thrombus sites of occurrence

Heart
Arteries
Veins

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Where are cardiac thrombosis occur

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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Causes of arterial thrombosis

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

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Appearance of arterial thrombosis

Mural thrombosis - large vessels

Occlusive thrombosis - medium sized/small vessels

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Predisposing factors to venous thrombosis

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

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Pathological features of venous thrombosis

Usually occlusive

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

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Sequelae of thrombosis

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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Features/ how does a thrombus go through resolution

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

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Features/ how does a thrombus go through organisation

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

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Features/ how does a thrombus go through recanalisation

There is a reconstituted lumen within the thrombus

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What are the main complications of an arterial thrombus

Ischaemia and infarction.

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What are the main complications of the veins /heart

Embolism

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Define embolism

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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Composition of an embolus

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

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Sites of emboli impaction

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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Define ischaemia

Reduced blood supply to tissue or organ

Harmful effects due to hypoxia

Causes of ischaemia

Intrinsic disease of vessels
Occlusion by thrombus/ embolus
External compression

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

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

Define infarction

Death of tissue due to ischaemia

Usually arterial occlusion, occasionally venous

How are infractions classified

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

Histological changes in infarction - what are the four stages

Necrosis Acute inflam Organisation Scar formation

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

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

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

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

What are the applications of the histological changes classficiation

Used to determine the age of infarcts | Understanding complications of infections - MI

Sources of pulmonary embolism

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

Consequences of PE

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

Things to consider in a PE

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

What happens when there is a PE and pulmonary venous congestion

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

Features of a PE and why

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

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

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

Systemic emboli sources

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

What are the 2 main patterns of MI

Regional - transmural >90% - sharply localised - thrombosis of main coronary artery branch Subendocardial <10% - poorly localised - sever triple vessel atheroma - no thrombosis

Posterior MI is due to thrombosis of which coronary artery

Right

What is a haemopericardium and what can cause it

Rupture of the left ventricular wall following an MI | Each time the heart pumps it goes into the pericardium and causes cardiac tamponade

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

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

What is a cardiac aneurysm

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

What is a saddle embolism

Thrombus travelled down aorta and straddles the bifurcation

Define gangrene

Necrosis - tissue death with superadded bacterial infection

Rare types of embolus

``` Fat Air/gas Tumour Amniotic fluid Infective material - septic ```

What causes a fat embolus

Bone fractures and other soft tissue trauma

What is the mortality of a fat embolus

10-15%

What happens if a fat embolus is in the pulmonary circulation

Dyspnoea | Haemoptysis

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

widespread microemboli esp brain

Causes of an air/ gas emboli

Venous rupture - neck wound Accidental infusion Decompression sickness

Effects of an air/gas embolus

Nothing in small amounts Sudden death is above 200ml Microemboli

What is an amniotic fluid embolism

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