Thrombosis, Embolism, Ischaemia & Infaction Flashcards
The two most common cause of vascular disease is Ischaemic Heart Disease and stroke.
Define thrombosis
Thrombosis mechanism is
Formation of a solid mass – From the constituents of blood – Within the vascular system during life (different to a simple blood clot)
Exaggeration of normal haemostatic mechanisms
- Coagulation system – formation of blood clot
- Platelets: • Adhesion • Aggregation • Secretion
- Vascular endothelium: • promotion/inhibition of 1 & 2 above. • protection of circulating blood from highly thrombogenic subendothelium
Thrombosis – Predisposing Factors
What is virchow’s triad
- Changes in vessel wall – endothelial damage
- Changes in blood flow – stasis, turbulence
- Changes in blood composition – many poorly defined (e.g. polycythaemia/myeloproliferative disease, nephrotic syndrome, malignancy, oral contraceptive pill, post-operative)
What is the composition of thrombi?
What is the characterestic lamination of thrombi called? See the picture.
What is the composition of arterial blood compared to venous?
BLOOD CLOT + PLATELETS – variable proportions depending on speed of blood flow
• CHARACTERISTIC LAMINATIONS – lines of Zahn(streaks caused by the clots)
- ARTERIAL/CARDIAC (rapid flow) - Mainly platelets (pale) - Mural or occlusive (depending on SIZE of vessel)
- VENOUS (slow flow) - Mainly blood clot (red) - Usually occlusive
What is the difference between mural and occlusive thrombi?
Mural(wall) means it adheres to the wall - blood can still pass through
Occlusive - stops blood going through
Main causes of cardiac thrombosis
- ATRIA • most common in appendages(slower flow) • associated with a) heart failure b) atrial fibrillation.
- VALVES (VEGETATIONS) • rheumatic fever (sterile) • infective endocarditis (infective). • non-bacterial thrombotic endocarditis (sterile) e.g. malignancy, SLE 3.
VENTRICLES • mural thrombosis • associated with (a) myocardial infarction (b) cardiomyopathy
This person had rheumatic fever which lead to what in the heart?
Mitral stenosis and it can also cause atrial fibrillation
Mitral Stenosis (post-rheumatic) Thrombus in Left Atrial Appendage
What does this person have?
Infective Endocarditis Vegetation (infected thrombus) on mitral valve
What are causes of arterial thrombosis?
Where are mural thrombosis more common in?
Where are occlusive thrombosis more common in?
Causes: 1. Atherosclerosis
- Aneurysms
- Inflammation, vasculitis - e.g. polyarteritis nodosa.
Appearances:
- MURAL THROMBOSIS – large vessels.
- OCCLUSIVE THROMBOSIS – medium sized/small vessels.
What does this person have?
Mural thrombus overlying atheromatous plaque
What doest this person have
aneurysm in the lower abdominal aorta due to stasis and turbulence
VENOUS THROMBOSIS
What are predisposing factors?
What are pathological features?
What does the image show?
PREDISPOSING FACTORS: • Immobility • Post-operative (especially abdominal surgery - e.g anaesthetic - muscle relaxant, respiratory problem) • Severe trauma • Myocardial infarction • Congestive heart failure • Pelvic mass (including pregnancy) • Thrombophlebitis (rare)
PATHOLOGICAL FEATURES: • Usually occlusive • Propagation(goes distal to where it occured
Image shows Deep a Vein Thrombus with Propagation Red colour – few platelets
What is the thrombosis sequelae?
- RESOLUTION – dissolution of clot by fibrinolysis (venous thrombi)
- ORGANISATION – Ingrowth of fibroblasts, capillaries, phagocytes (granulation tissue).
- A) RECANALISATION – restoration of original lumen.
B) FIBROSIS – formation of webs, cords.
What are the main complication in arteries and what are the main complications in vein and heart?
- ARTERIES – Ischaemia/Infarction.
- VEINS/HEART – Embolism.
EMBOLI - COMPOSITION
What is it commonly?
Where does it commonly impact?
- THROMBUS (> 95%) 2. OTHER (RARE): - Fat - Air/gas - Tumour - Amniotic fluid - Infective material (septic)
Pulmonary arteries • Thrombi from veins (e.g. femoral, iliac, vena cava), right side of heart
- Systemic arteries • Thrombi from left side of heart and aorta -> impacts the smaller branches
Define embolism
- passage of insoluble mass (embolus)
- within the blood stream and
- impaction at a site distant from its point of origin.
What determines the severity of ischaemia for vascular occlusions?
- Speed of onset
- Extent of obstruction
- Anatomy of local blood supply
- end arteries e.g. kidney (if these are blocked this causes ischaemia)
- parallel arteries e.g. brain
- Interarterial branches e.g.intestine (if these are blocked there are collateral available)
- Pathology of collateral circulation
- General factors – cardiac state, oxygenation of blood
- Vulnerability of tissue supplied to anoxia
What are the histological changes that occur during infarction?
6-12 hours, 24 hours - 7 days, 3 days - 2 weeks, 2 weeks - 3 months
What are the changes seen here and when does it occur?
PULMONARY EMBOLISM - Consequences
N.B. Dual blood supply to lungs SIZE and NUMBER of emboli also important
- SUDDEN DEATH – massive embolism
- PULMONARY INFARCTION - pulmonary venous congestion - haemorrhagic, peripheral, wedge-shaped
- PULMONARY HYPERTENSION – recurrent pulmonary emboli
- ASYMPTOMATIC – complete resolution (up to 60-80% of cases)
Name two clinical manifestations of pulmonary infarction that can be explained by the characteristic pathological changes illustrated above
haemorrhagic tissue leads to haemoptysis.
Acute inflammation on pleura(pl - pleuritic chest pain
QUESTION Posterior myocardial infarction is due to thrombosis of which coronary artery?
- Left anterior descending 2. Left circumflex 3. Right
Right
The peak time at which left ventricular wall rupture occurs following myocardial infarction is:
- 1 st 24 hours 2. 4-10 days 3. 2-4 weeks 4. >3 months
Picture shows cardiac tamponade(fluid in pericardial sac) - Haemopericardium Rupture of left ventricular wall following myocardial infarction
4-10 days
What does this show
Rupture of left ventricular wall following myocardial infarction
What does the top picture show
What does the bottom picture show
Cardiac Aneurysm A later complication of MI – usually > 3 months (thinned due to scarring and fibrosis) - why there is a cardiac heart failure after a few months
Saddle emboli - Atrial fibrillation - goning down into the aorta and seperatred into the bifurcation
What is this?
Gangrene - Necrosis (Tissue Death) with Superadded Bacterial Infection
EMBOLISM RARE TYPES are
- FAT (image showing it in the brain)
- AIR/GAS
- TUMOUR
- AMNIOTIC FLUID
- INFECTIVE MATERIAL (SEPTIC)
What are the causes and presentation of each?
FAT EMBOLISM
Causes: Bone fractures & other soft tissue trauma
PULMONARY CIRCULATION: dyspnoea, haemoptysis
SYSTEMIC CIRCULATION: widespread microemboli (esp brain)
Mortality - 10 - 15%
AIR / GAS EMBOLISM
CAUSE: Venous rupture (e.g. neck wound), accidental infusion, decompression sickness
EFFECTS: nil (small amounts), sudden death (> 200ml), microemboli
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
