pathology of ischaemia and infarction Flashcards

1
Q

what is ischaemia?

A

Relative lack of blood supply to tissue/organ leading to inadequate O2 supply to meet needs of tissue/organ: hypoxia

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2
Q

what is hypoxic?

A

Low inspired O2 level

(b) Normal inspired O2 but low PaO2

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3
Q

what is anaemic?

A

Normal inspired O2 but blood abnormal

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4
Q

what is stagnant?

A

Normal inspired O2 but abnormal delivery
Local e.g. occlusion of vessel
Systemic e.g. shock

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5
Q

what is cytoxic?

A

Normal inspired O2 but abnormal at tissue level

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6
Q

factors affecting oxygen supply?

A

Inspired O2

  1. Pulmonary function
  2. Blood constituents
  3. Blood flow
  4. Integrity of vasculature
  5. Tissue mechanisms
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7
Q

factors affecting oxygen demand?

A

Tissue itself - different tissues have different requirements

  1. Activity of tissue above baseline value
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8
Q

what are the supply issues for ischaemic heart disease?

A

coronary artery atheroma, cardiac failure (flow), pulmonary function – other disease or pulmonary oedema (LVF), anaemia, previous MI

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9
Q

what are the demand issues for ischaemic heart disease?

A

heart has high intrinsic demand, exertion/stress

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10
Q

what is atheroma/atherosclerosis?

A

Localised accumulation of lipid and fibrous tissue in intima of arteries

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11
Q

whats the correlation between atheroma and stable angina?

A

established atheroma in coronary artery

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12
Q

whats the correlation between atheroma and unstable angina?

A

Complicated atheroma in coronary artery

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13
Q

what would an atheroma in aorta be?

A

aneurysm

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14
Q

what would ulcerated/fissured plaques be?

A

thrombosis which could lead to ischaemia/infarction

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15
Q

what are the effects of ischaemia functionally ?

A

Blood/O2 supply fails to meet demand due to supply; demand; or both
Related to rate of onset

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16
Q

what are the effects of ischaemia biochemically?

A

Normal aerobic metabolism
glucose+36ADP+36Pi+36H++6O2 6CO2+36ATP+42H2O
Anaerobic metabolism
glucose+2Pi+2ADP 2lactate+2ATP+2H2O
L-lactatepyruvate
Pyruvate+NAD++CoAacetylCoA+CO2+NADH
decreased O2 anaerobic metabolism leads to cell death

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17
Q

what is infarction?

A

Ischaemic necrosis within a tissue/organ in living body produced by occlusion of either the arterial supply or venous drainage

18
Q

whats the aetiology of infraction?

A
cessation of blood flow
For example:
1. Thrombosis
2. Embolism
3. Strangulation e.g. gut
4. Trauma - cut/ruptured vessel
19
Q

what is the scale of infarction dependent on?

A

Time period
Tissue/organ
Pattern of blood supply
Previous disease

20
Q

what happens with an infarction?

A

Anaerobic metabolism goes to cell death goes to liberation of enzymes goes to breakdown of tissue

Coagulative necrosis e.g. heart, lung

21
Q

how long does anaerobic metabolism, onset of ATP depletion take

A

seconds

22
Q

how long does loss of myocardial contractility leading to heart failure

A

over 2 minutes

23
Q

how long does myocyte necrosis take?

A

20-40 minutes

24
Q

how long does injury to the microvasculature take?

A

over 1 hour

25
Q

what visual changes can you see in less than 24 hours?

A

No change on visual inspection

A few hours to 12 hours post insult, see swollen mitochondria on Electron Microscopy

26
Q

what visual changes can you see in less than 24 - 48 hours?

A

Pale infarct: e.g. myocardium, spleen, kidney Solid tissues
Red infarct: e.g. in lung, liver Loose tissues, previously congested tissue; second/continuing blood supply, venous occlusion

Microscopically: acute inflammation initially at edge of infarct; loss of specialised cell features

27
Q

what visual changes can you see in less than 72 hours ?

A

Macroscopically:
Pale infarct - yellow/white and red periphery
Red infarct - little change

Microscopically: chronic inflammation; macrophages remove debris; granulation tissue; fibrosis

28
Q

whats the end result of infarcts?

A

Scar replaces area of tissue damage
Shape depends on territory of occluded vessel

Reperfusion Injury

29
Q

what is the repartive process of MI

A
Cell death
Acute inflammation
Macrophage phagocytosis of dead cells
Granulation tissue
Collagen deposition (fibrosis)
Scar formation
30
Q

what would you see in 4-12 hours in myocardial infarction?

A

Early coagulation necrosis, oedema, haemorrhage

31
Q

what would you see in 12-24 hours in myocardial infarction?

A

Ongoing coagulation necrosis, myocyte changes, early neutrophilic infiltrate

32
Q

what would you see in 1-3 days in myocardial infarction?

A

Coagulation necrosis, loss of nuclei and striations, brisk neutrophilic infiltrate

33
Q

what would you see in 3-7 days in myocardial infarction?

A

Disintegration of dead myofibres, dying neutrophils, early phagocytosis

34
Q

what would you see in 7-10 days

in myocardial infarction?

A

Well developed phagocytosis, granulation tissue at margins

35
Q

what would you see in 10-14 days

in myocardial infarction?

A

Well established granulation tissue with new blood vessels and collagen deposition

36
Q

what would you see in 2-8 weeks in myocardial infarction?

A

Increased collagen deposition, decreased cellularity

37
Q

what would you see in >2 months

in myocardial infarction?

A

Dense collagenous scar

38
Q

what is Transmural infarction

A

: ischaemic necrosis affects full thickness of the myocardium

39
Q

what is Subendocardial infarction

A

ischaemic necrosis mostly limited to a zone of myocardium under the endocardial lining of the heart

40
Q

what are acute infarcts classified as?

A

whether there is elevation of the ST segment on the ECG

41
Q

what would a ‘If no ST segment elevation but a significantly elevated serum troponin level’ mean?

A

non-STEMI

42
Q

what are the complications of myocardial infarction?

A

Immediate; early; late

Sudden death; arrhythmias; angina; cardiac failure; cardiac rupture - ventricular wall, septum, papillary muscle; reinfarction; pericarditis; pulmonary embolism secondary to DVT; papillary muscle dysfunction - necrosis/rupture mitral incompetence; mural thrombosis; ventricular aneurysm; Dressler’s syndrome