Infarction and Embolism Flashcards

1
Q

What is an infarct?

A

An area of ischaemic necrosis within a tissue or organ, produced by occlusion of either its arterial supply or its venous drainage

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2
Q

What do infarcts usually results from?

A

Acute arterial occlusion

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3
Q

Where do the different types of acute arterial occlusion occur?

A

1) Thrombosis e.g. coronary arteries → MI
2) Embolism e.g. lung, kidney, spleen
3) Either thrombosis or embolism e.g. brain (but also hypotension)

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4
Q

Why is venous infarction less common?

A

Because arrest of blood flow due to venous obstruction is unusual as most tissues have numerous anastomoses

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5
Q

When can venous infarction occur?

A

1) Thrombosis of the mesenteric veins → intestinal infarction (usually red)
2) In the brain following thrombosis in the superior sagittal (longitudinal) sinus
3) In the testis or ovary following torsion

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6
Q

What happens in an intestinal infarction?

A
  • Bright, red dilation due to blood in the bowel

- Can be reperfused but mostly has to be removed otherwise it will rupture

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7
Q

How are infarcts divided?

A

1) Colour → red/haemorrhagic vs white/pale/anaemic)

2) Presence (septic) or absence (bland) of bacterial contamination

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8
Q

When do white infarcts occur?

A
  • With arterial occlusion (bc no blood)

- In solid tissues e.g. heart, spleen, kidneys

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9
Q

What is the most important form of ischaemic heart disease and a leading cause of death?

A

AMI

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10
Q

What are the two types of myocardial infarction?

A

1) Transmural

2) Subendocardial

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11
Q

Describe a transmural infarct

A
  • Commonest
  • The ischaemic necrosis involves the full or nearly full thickness of the ventricular wall in the distribution of a single coronary artery
  • Usually associated with coronary atherosclerosis, plaque rupture and super-imposed thrombosis
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12
Q

Describe a subendocardial infarct

A
  • This constitutes an area of ischaemic necrosis limited to the inner ⅓ or at most inner ½, of the ventricular wall
  • There is diffuse stenosing coronary atherosclerosis and global reduction of coronary flow e.g. due to shock but no plaque rupture and no thrombosis
  • RV collapsed
  • Inner ⅓ of heart (endocardium) supplied by blood in lumen so if blood supply stops, this blood supply will also stop
  • Can occur in road traffic accident → not enough blood in heart or in blood supply to heart
  • Pallor in area of myocardium with infarct
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13
Q

What can a recent MI cause?

A

Severe arrhythmia

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14
Q

What happens initially to cells in an AMI?

A
  • Cell shape starts to change and infiltration by other cells
  • Lose nuclear definition
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15
Q

What happens after a while to cells in an AMI?

A
  • Nuclei start to fragment → dead cells so can’t bring them back
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16
Q

What happens to the myocardium after infarct?

A

Fibrous tissue (scar) is laid down bc can’t regenerate myocyte

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17
Q

What can happen if the infarct is transmural?

A

Can get fibrin deposition

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18
Q

What are complications of an MI from early to late?

A

Arrhythmias, HF → pericarditis, papillary muscle dysfunction, mural thrombus → ventricular/papillary muscle rupture → aneurysm, post MI syndrome, ischaemia and re-infarction

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19
Q

What are the main morphological complications following MI?

A

1) Cardiac rupture
2) Pericarditis
3) Mural thrombosis
4) Ventricular aneurysm

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20
Q

How does cardiac rupture as a complication of MI result from?

A

Results from the mechanical weakening that occurs in necrotic and inflamed myocardium

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21
Q

When does cardiac rupture most commonly occur?

A

4-7 days post infarct

22
Q

Which part of the heart does cardiac rupture usually involve and what does this lead to?

A

Ventricular free wall → haemopericardium and cardiac tamponade

23
Q

When does pericarditis usually develop?

A

2-3 days post infarct

24
Q

Describe the pericarditis resulting as a complication of MI

A
  • Fibrinous or fibrinohaemorrhagic

- Usually localised to the region overlying the necrotic area

25
Q

What causes mural thrombosis and thromboembolism?

A

The combination of a local myocardial abnormality in contractility (causing stasis) and endocardial damage (causing a thrombogenic surface)

26
Q

What is the result of mural thrombosis?

A

Endothelium gets sticky, clot forms inside ventricle → coronary or cerebral arteries

27
Q

What is a ventricular aneurysm and how does it form?

A

A late complication that most commonly results from a large anteroseptal, transmural infarct that heals into a large area of thin scar tissue that paradoxically bulges during systole

28
Q

What are the consequences of cardiac rupture?

A
  • Rupture of inter-ventricular septum → left-to-right shunt

- Rupture of papillary muscle → severe acute mitral incompetence

29
Q

What is embolism?

A

The transfer of abnormal material by the bloodstream and its impaction in a vessel

30
Q

In what % of cases does cardiac rupture occur?

A

1-5%

31
Q

In what % of cases does mural thrombosis occur?

A

15-40%

32
Q

What is an embolus?

A

The impacted material

33
Q

What are 7 different types of emboli?

A

1) Fragments of thrombus (commonest)
2) Material from ulcerating atheromatous plaques (common in distal leg arteries)
3) Septic emboli
4) Fragment of tumour growing into a vein
5) Fat globules from bone marrow
6) Air emboli (due to external trauma of vessels)
7) Parenchymal cells

34
Q

Embolus in what blood vessel would be catastrophic?

A

Inferior vena cava

35
Q

What type of emboli might lead to a lung infarct?

A

Tumour emboli (hepatocellular carcinoma) in pulmonary circulation

36
Q

What colour is a lung infarct?

A

Red

37
Q

What is an example of something that could cause a fat embolism?

A

A fracture of a long bone

38
Q

What does PE result from?

A

Detachment of a thrombus in a systemic vein, usually in the deep venous plexus in the leg (DVT)

39
Q

When is PE the most common?

A

Post-operative day 10

40
Q

What are the consequences of PE?

A
  • Sudden death or death after a short period of respiratory distress
  • Large thrombi may be detached en masse → RH
  • Can cause sudden blockage of the pulmonary trunk or at a major division
41
Q

Where are fatal pulmonary emboli usually derived from?

A

Femoral and iliac veins

42
Q

What is the morphology of a PE?

A
  • Form a cylinder about 1cm diameter and up to 30cm long

- At autopsy are found coiled like a snake in pulmonary artery and RV

43
Q

Where do less gross fragments impact in?

A

Major or minor pulmonary arteries

44
Q

What may be present if a patient lives after PE?

A

Varying amounts of haemorrhagic infarction in the territory of the blocked vessels

45
Q

Why is infarction never co-extensive with the area of distribution?

A

Because of collateral vessels and the bronchial circulation

46
Q

What else can PE cause?

A

Breathlessness and crepitations

47
Q

How else can PEs occur?

A

As multiple small emboli, impacting over time

48
Q

What do multiple small emboli rarely cause?

A

Chronic pulmonary hypertension

49
Q

What are some causes of chronic pulmonary hypertension?

A

Congenital cardiac shunts
Chronic hypoxia
Pulmonary fibrosis

50
Q

What is in the structure of a thrombus?

A

RBCs, platelets