Thrombosis, Embolism, Ischaemia & Infaction

Question 1

The two most common cause of vascular disease is Ischaemic Heart Disease and stroke.

Define thrombosis

Thrombosis mechanism is

Answer 1

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

1. Coagulation system – formation of blood clot
2. Platelets: • Adhesion • Aggregation • Secretion
3. Vascular endothelium: • promotion/inhibition of 1 & 2 above. • protection of circulating blood from highly thrombogenic subendothelium

Question 2

Thrombosis – Predisposing Factors

What is virchow’s triad

Answer 2

1. Changes in vessel wall – endothelial damage
2. Changes in blood flow – stasis, turbulence
3. Changes in blood composition – many poorly defined (e.g. polycythaemia/myeloproliferative disease, nephrotic syndrome, malignancy, oral contraceptive pill, post-operative)

Question 3

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?

Answer 3

BLOOD CLOT + PLATELETS – variable proportions depending on speed of blood flow

• CHARACTERISTIC LAMINATIONS – lines of Zahn(streaks caused by the clots)

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

Question 4

What is the difference between mural and occlusive thrombi?

Answer 4

Mural(wall) means it adheres to the wall - blood can still pass through

Occlusive - stops blood going through

Question 5

Main causes of cardiac thrombosis

Answer 5

1. ATRIA • most common in appendages(slower flow) • associated with a) heart failure b) atrial fibrillation.
2. 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

Question 6

This person had rheumatic fever which lead to what in the heart?

Answer 6

Mitral stenosis and it can also cause atrial fibrillation

Mitral Stenosis (post-rheumatic) Thrombus in Left Atrial Appendage

Question 7

What does this person have?

Answer 7

Infective Endocarditis Vegetation (infected thrombus) on mitral valve

Question 8

What are causes of arterial thrombosis?

Where are mural thrombosis more common in?

Where are occlusive thrombosis more common in?

Answer 8

Causes: 1. Atherosclerosis

2. Aneurysms
3. Inflammation, vasculitis - e.g. polyarteritis nodosa.

Appearances:

• MURAL THROMBOSIS – large vessels.
• OCCLUSIVE THROMBOSIS – medium sized/small vessels.

Question 9

What does this person have?

Answer 9

Mural thrombus overlying atheromatous plaque

Question 10

What doest this person have

Answer 10

aneurysm in the lower abdominal aorta due to stasis and turbulence

Question 11

VENOUS THROMBOSIS

What are predisposing factors?

What are pathological features?

What does the image show?

Answer 11

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

Question 12

What is the thrombosis sequelae?

Answer 12

1. RESOLUTION – dissolution of clot by fibrinolysis (venous thrombi)
2. ORGANISATION – Ingrowth of fibroblasts, capillaries, phagocytes (granulation tissue).
3. A) RECANALISATION – restoration of original lumen.

B) FIBROSIS – formation of webs, cords.

Question 13

What are the main complication in arteries and what are the main complications in vein and heart?

Answer 13

1. ARTERIES – Ischaemia/Infarction.
2. VEINS/HEART – Embolism.

Question 14

EMBOLI - COMPOSITION

What is it commonly?

Where does it commonly impact?

Answer 14

1. 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

2. Systemic arteries • Thrombi from left side of heart and aorta -> impacts the smaller branches

Question 15

Define embolism

Answer 15

• passage of insoluble mass (embolus)
• within the blood stream and
• impaction at a site distant from its point of origin.

Question 16

Define ischaemia

What are 3 causes of ischaemia?

Answer 16

Reduced blood supply to tissue or organ Harmful effects due to hypoxia

1. Intrinsic disease of vessels
2. Occlusion by thrombus/embolus
3. External compression

Question 17

What determines the severity of ischaemia for vascular occlusions?

Answer 17

1. Speed of onset
2. Extent of obstruction
3. 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)

4. Pathology of collateral circulation
5. General factors – cardiac state, oxygenation of blood
6. Vulnerability of tissue supplied to anoxia

Question 18

Define infarction

How is infarction classified?

Answer 18

Death of tissue due to ISCHAEMIA

Usually arterial occlusion, occasionally venous

Classified as the following:

SHAPE Wedge-shaped or other

COLOUR White or red

INFECTION Bland or septic

Question 19

What are the histological changes that occur during infarction?

6-12 hours, 24 hours - 7 days, 3 days - 2 weeks, 2 weeks - 3 months

Answer 19

Question 20

What are the changes seen here and when does it occur?

Answer 20

Question 21

What are common places for pulmonary embolism to originate from?

Answer 21

1. DEEP VENOUS THROMBOSIS - > 95% #
2. OTHER VEINS – pelvic, iliac, vena cava
3. RIGHT SIDE OF HEART

Question 22

PULMONARY EMBOLISM - Consequences

Answer 22

N.B. Dual blood supply to lungs SIZE and NUMBER of emboli also important

1. SUDDEN DEATH – massive embolism
2. PULMONARY INFARCTION - pulmonary venous congestion - haemorrhagic, peripheral, wedge-shaped
3. PULMONARY HYPERTENSION – recurrent pulmonary emboli
4. ASYMPTOMATIC – complete resolution (up to 60-80% of cases)

Question 23

Name two clinical manifestations of pulmonary infarction that can be explained by the characteristic pathological changes illustrated above

Answer 23

haemorrhagic tissue leads to haemoptysis.

Acute inflammation on pleura(pl - pleuritic chest pain

Question 24

What are sources of systemic emboli?
What is the clinical relevance

Answer 24

Common

1. LEFT ATRIUM – atrial fibrillation
2. VALVES (mitral, aortic) – infective endocarditis
3. LEFT VENTRICLE – mural thrombosis overlying myocardial infarction
4. AORTA – atherosclerosis

Rare

1. PARADOXICAL EMBOLUS – atrial septal defect
2. ATRIAL MYXOMA

Clinical relevance

Patient presenting with complications of embolism (e.g. cerebral infarction)

• Consider predisposing factors + treat to prevent further episodes

Question 25

MYOCARDIAL INFARCTION 2 main patterns

Answer 25

1. REGIONAL (TRANSMURAL) \> 90% - sharply localised - thrombosis of main coronary artery branch 2. SUBENDOCARDIAL \< 10% - poorly localised (diffuse) - severe triple vessel atheroma (no thrombosis)

Question 26

QUESTION Posterior myocardial infarction is due to thrombosis of which coronary artery? 1. Left anterior descending 2. Left circumflex 3. Right

Answer 26

Right

Question 27

The peak time at which left ventricular wall rupture occurs following myocardial infarction is: 1. 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

Answer 27

4-10 days

Question 28

What does this show

Answer 28

Rupture of left ventricular wall following myocardial infarction

Question 29

What does the top picture show What does the bottom picture show

Answer 29

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

Question 30

What is this?

Answer 30

Gangrene - Necrosis (Tissue Death) with Superadded Bacterial Infection

Question 31

EMBOLISM RARE TYPES are 1. FAT (image showing it in the brain) 2. AIR/GAS 3. TUMOUR 4. AMNIOTIC FLUID 5. INFECTIVE MATERIAL (SEPTIC) What are the causes and presentation of each?

Answer 31

**_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