Theombosis Embolism Ischamia Infarction Flashcards
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
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
What is a predisposing factor of thrombosis
Virchows triad
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)
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
Thrombus sites of occurrence
Heart
Arteries
Veins
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
Causes of arterial thrombosis
Atherosclerosis
Aneurysms
Inflammation , vasculitis - e.g. Polyarteritis nodosa
Appearance of arterial thrombosis
Mural thrombosis - large vessels
Occlusive thrombosis - medium sized/small vessels
Predisposing factors to venous thrombosis
Immobility Post op esp abdo surgery Severe trauma MI congestive heart failure Pelvic mass - inc pregnancy Thrombophlebitis
Pathological features of venous thrombosis
Usually occlusive
Propagation - progressive spread of the thrombus to a site more proximal
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
Features/ how does a thrombus go through resolution
There is central liquification of the thrombus
Retraction of thrombus
Slip like clefts
Features/ how does a thrombus go through organisation
Ingrowth of vascular smooth muscle cells
Ingrowth of capillaries
Endothelised channels through the thrombus
Features/ how does a thrombus go through recanalisation
There is a reconstituted lumen within the thrombus
What are the main complications of an arterial thrombus
Ischaemia and infarction.
What are the main complications of the veins /heart
Embolism
Define embolism
Passage of insoluble mass (embolus)
Within the blood stream and has an impaction site that is distant from its point of origin
Composition of an embolus
Thrombus 95% of the time
Others which are rare
- fat, air/gas, tumour, amniotic fluid, infective material septic
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
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
