Thrombosis, Embolism, Ischaemia & Infaction Flashcards

1
Q

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

Define thrombosis

Thrombosis mechanism is

A

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
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2
Q

Thrombosis – Predisposing Factors

What is virchow’s triad

A
  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)
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3
Q

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?

A

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
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4
Q

What is the difference between mural and occlusive thrombi?

A

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

Occlusive - stops blood going through

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5
Q

Main causes of cardiac thrombosis

A
  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

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6
Q

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

A

Mitral stenosis and it can also cause atrial fibrillation

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

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7
Q

What does this person have?

A

Infective Endocarditis Vegetation (infected thrombus) on mitral valve

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8
Q

What are causes of arterial thrombosis?

Where are mural thrombosis more common in?

Where are occlusive thrombosis more common in?

A

Causes: 1. Atherosclerosis

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

Appearances:

  • MURAL THROMBOSIS – large vessels.
  • OCCLUSIVE THROMBOSIS – medium sized/small vessels.
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9
Q

What does this person have?

A

Mural thrombus overlying atheromatous plaque

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10
Q

What doest this person have

A

aneurysm in the lower abdominal aorta due to stasis and turbulence

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11
Q

VENOUS THROMBOSIS

What are predisposing factors?

What are pathological features?

What does the image show?

A

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

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12
Q

What is the thrombosis sequelae?

A
  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.

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13
Q

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

A
  1. ARTERIES – Ischaemia/Infarction.
  2. VEINS/HEART – Embolism.
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14
Q

EMBOLI - COMPOSITION

What is it commonly?

Where does it commonly impact?

A
  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

  1. Systemic arteries • Thrombi from left side of heart and aorta -> impacts the smaller branches
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15
Q

Define embolism

A
  • passage of insoluble mass (embolus)
  • within the blood stream and
  • impaction at a site distant from its point of origin.
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16
Q

Define ischaemia

What are 3 causes of ischaemia?

A

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
17
Q

What determines the severity of ischaemia for vascular occlusions?

A
  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)
  1. Pathology of collateral circulation
  2. General factors – cardiac state, oxygenation of blood
  3. Vulnerability of tissue supplied to anoxia
18
Q

Define infarction

How is infarction classified?

A

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

19
Q

What are the histological changes that occur during infarction?

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

A
20
Q

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

A
21
Q

What are common places for pulmonary embolism to originate from?

A
  1. DEEP VENOUS THROMBOSIS - > 95% #
  2. OTHER VEINS – pelvic, iliac, vena cava
  3. RIGHT SIDE OF HEART
22
Q

PULMONARY EMBOLISM - Consequences

A

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)
23
Q

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

A

haemorrhagic tissue leads to haemoptysis.

Acute inflammation on pleura(pl - pleuritic chest pain

24
Q

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

A

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

25
Q

MYOCARDIAL INFARCTION

2 main patterns

A
  1. REGIONAL (TRANSMURAL) > 90% - sharply localised - thrombosis of main coronary artery branch
  2. SUBENDOCARDIAL < 10% - poorly localised (diffuse) - severe triple vessel atheroma (no thrombosis)
26
Q

QUESTION Posterior myocardial infarction is due to thrombosis of which coronary artery?

  1. Left anterior descending 2. Left circumflex 3. Right
A

Right

27
Q

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

A

4-10 days

28
Q

What does this show

A

Rupture of left ventricular wall following myocardial infarction

29
Q

What does the top picture show

What does the bottom picture show

A

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

30
Q

What is this?

A

Gangrene - Necrosis (Tissue Death) with Superadded Bacterial Infection

31
Q

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?

A

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