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

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
what visual changes can you see in less than 24 hours?
No change on visual inspection | A few hours to 12 hours post insult, see swollen mitochondria on Electron Microscopy
26
what visual changes can you see in less than 24 - 48 hours?
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
what visual changes can you see in less than 72 hours ?
Macroscopically: Pale infarct - yellow/white and red periphery Red infarct - little change Microscopically: chronic inflammation; macrophages remove debris; granulation tissue; fibrosis
28
whats the end result of infarcts?
Scar replaces area of tissue damage Shape depends on territory of occluded vessel Reperfusion Injury
29
what is the repartive process of MI
``` Cell death Acute inflammation Macrophage phagocytosis of dead cells Granulation tissue Collagen deposition (fibrosis) Scar formation ```
30
what would you see in 4-12 hours in myocardial infarction?
Early coagulation necrosis, oedema, haemorrhage
31
what would you see in 12-24 hours in myocardial infarction?
Ongoing coagulation necrosis, myocyte changes, early neutrophilic infiltrate
32
what would you see in 1-3 days in myocardial infarction?
Coagulation necrosis, loss of nuclei and striations, brisk neutrophilic infiltrate
33
what would you see in 3-7 days in myocardial infarction?
Disintegration of dead myofibres, dying neutrophils, early phagocytosis
34
what would you see in 7-10 days | in myocardial infarction?
Well developed phagocytosis, granulation tissue at margins
35
what would you see in 10-14 days | in myocardial infarction?
Well established granulation tissue with new blood vessels and collagen deposition
36
what would you see in 2-8 weeks in myocardial infarction?
Increased collagen deposition, decreased cellularity
37
what would you see in >2 months | in myocardial infarction?
Dense collagenous scar
38
what is Transmural infarction
: ischaemic necrosis affects full thickness of the myocardium
39
what is Subendocardial infarction
ischaemic necrosis mostly limited to a zone of myocardium under the endocardial lining of the heart
40
what are acute infarcts classified as?
whether there is elevation of the ST segment on the ECG
41
what would a 'If no ST segment elevation but a significantly elevated serum troponin level' mean?
non-STEMI
42
what are the complications of myocardial infarction?
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