ischaemia, infarction and the results Flashcards

lecture 34

1
Q

define ischaemia

A

an inadequate rate of blood flow to an organ. inadequate quantity not quality.

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2
Q

define infarction

A

necrosis due to ischaemia. a localised area = infarct

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3
Q

5 causes of ischaemia

A

1 - external occlusion (tumours, compression (bed sores))
2 - internal stenosis or occlusion, athero, thrombosis, embolism
3 - spasm of vessel ie cold in frost bite
4 - capillary blockage eg sickle cell, cerebral malaria
5 - shock

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4
Q

define shock

A

circulatory failure with low ABP, causing impaired perfusion of tissues.

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5
Q

4 causes of shock

A

1- cardiogenic - MI, arrythmia, outflow obstruction (pulmonary embolism), external compression.
2 - hypovolaemic - haemorrhage, severe burns
3 - septic - gram positive and negative bacteria
4 - anaphylactic - generalised type 1 hypersensitivity.

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6
Q

3 generic metabolic consequences of ischaemia

A

1 - hypoxia
2 - poor nutrient supply
3 - failure to remove waste products so may alter pH and electrolyt balance.

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7
Q

5 cells types in decreasing order of sensitivity to ischaemia

A

1 - neurons - very sensitive, irreversibly damaged by only 3 minutes of anoxia
2 - renal proximal tubular epithelium - sensitive, rapid impairment of ion reabsorption.
3 - myocardium - irreversible damage after 20 mins anoxia, but functional impairment (risk of dysrhythmia) in 1 minute.
4 - skeletal muscle - capable of anoxic work
5 - fibroblasts and macrophages - insensitive.

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8
Q

what affects an organ’s susceptability to ischaemia

A

largley the anatomy of the blood supply to it.
1 - collateral circulation may reduce susceptability. - venous circulation, some arterial systems (gut), can develop collateral if slow and progressive stenosis (coronary)

2 - organs with dual blood supply - 2nd may suffice. lungs = pulmonary and bronchial arteries and alveolar air. liver = hepatic portal vein and hepatic artery. brain = circle of willis

3 - single vessel = functional end arteries. very susceptible eg kidney, spleen.

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9
Q

8 factors affecting outcome from ischaemia

A

1 - anatomy of blood supply
2 - size of block (vessel size)
3 - degree of block (stenosis or occlusion)
4 - speed of onset (develop collateral)
5 -persistence of block - some thrombi are unstable
6 - vulnerability of the tissue
7 - demand of the tissue - inadequate on exertion (heart angina, leg in intermittent claudication)
8 - general inadequacy of the circulatory system ie coexisting anaemia, heart failure, shock etc

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10
Q

5 effects of ischaemia

A

1 - nothing
2 - functional defects (dysrhythmia, renal insufficiency)
3 - reversible cell damage (cell swelling, fatty change in myocardium (subendocardial zone) and hepatocytes (centrilobular region).
4 - infarction
5 - ischaemic reperfusion injury

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11
Q

microscopic appearances in infarction

A

1 - ischaemic coagulative necrosis
2 - acute inflammation at the viable margins
3 - some regeneration or organisation.

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12
Q

describe the changes in ischaemic coagulative necrosis

A

1 - visable 4-12 hours afterwards. earlier biochemical damage (eg enzyme leak)
2 - cytoplasm increase eosinophilia due to protein denaturation and loss of RNA.
3 - nuclei can undergo - karyolysis (pale), pyknosis (shrunken), karyorhexis (fragmentation)
4 - tissue architecture preserved for several days.

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13
Q

describe acute inflammation in infarction

A

developes at the viable margins within 24hrs.

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14
Q

describe tissue regen or organisation in infarction

A

liver may attempt regeneration but usually the infarct is organised. 3-5 days macrophages appear, granulation tissue develops. 6-8 weeks replaced by nonfunctional scar.

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15
Q

7 changes in the macroscopic appearance in infarction

A
1 - acute anoxia may - capillary dilation or haemorrhage hence poorly defined and red early on.
2 - pale infarcts
3 - red infarcts
4 - cone shaped/wedge shaped
5 - fibrinous exudate , red margins
6 - septic infarct and abscess
7 - liquefactive necrosis
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16
Q

describe pale infarcts

A

in soft tissue where infarct goes pale and rapidly demarcates in 24hrs. heart, kidney, spleen.

17
Q

describe red infarcts

A

due to haemorrhage
arterial occlusion - in spongy tissue such as lung, tissue with collateral blood supply (gut), congested tissues.

venous occlusion

18
Q

infarct shapes?

A

determines by blood supply. usually cone shaped with apex at point of occlusion and base at organ surface. = wedge shaped in 2 dimensions.

19
Q

margins and exudate of infarcts

A

in early stages the margins of pale infarct can be red due to acute inflam and granulation tissue. may be a fibrinous exudate on the organ surface. eventually replaced by grey scar tissue.

20
Q

secondary infection after necrosis

A

in some tissue ie lung. leads to a septic infarct and possibly and abscess.

21
Q

brain infarct

A

undergoes liquefactive necrosis. necrotic cells are digested quickly, form a liquid containing cyst, surrounded by reactive glial cells.

22
Q

define ischaemic reperfusion injury

A

when blood flow is restored to ischaemic cells that havent died and reversible injury becomes irreversible.

23
Q

mechanisms of reperfusion injury

A

1 - generation fo fresh mdiators of cell injury - free radicals, calcium overload.

2 - initiation of acute inflammation by delivery of neutrophils and complement.

24
Q

4 examples of infarction

A

1 - myocardial infarction
2 - cerebral infarction
3 - pulmonary infarction
4 - renal infarction

25
Q

8 effects of myocardial infarction

A
1 - dysrhythmia
2 - sudden death
3 - cardiogenic shock
4 - rupture of the infarct
5 - mural thrombosis on the endocardium
6 - scarring 
7 - adaptation to reduced CO - hypertrophy
8 - cardiac failure
26
Q

common cause of cerebral infarction

A

common carotid thrombus or plaque that forms an embolus.

shock - common in the elderly

27
Q

cause of pulmonary infarct

A

pelvic or leg vein thromboembolism

28
Q

effect of pulmonary infarct

A

1 - silent
2 - impaired lung function
3 - pressure overload on right heart and right sided heart failure
4 - infection - septic infarct, abscess, pneumonia
5 - shock

29
Q

cause of renal infarction

A

thromboemboli from the heart or elsewhere. kidneys recieve 25% of CO through one vessel so are at risk.

30
Q

effects of renal infarct

A

small infarcts are often silent

- large - haematuria, renal failure.