ischaemia, infarction and the results Flashcards
lecture 34
define ischaemia
an inadequate rate of blood flow to an organ. inadequate quantity not quality.
define infarction
necrosis due to ischaemia. a localised area = infarct
5 causes of ischaemia
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
define shock
circulatory failure with low ABP, causing impaired perfusion of tissues.
4 causes of shock
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.
3 generic metabolic consequences of ischaemia
1 - hypoxia
2 - poor nutrient supply
3 - failure to remove waste products so may alter pH and electrolyt balance.
5 cells types in decreasing order of sensitivity to ischaemia
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.
what affects an organ’s susceptability to ischaemia
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.
8 factors affecting outcome from ischaemia
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
5 effects of ischaemia
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
microscopic appearances in infarction
1 - ischaemic coagulative necrosis
2 - acute inflammation at the viable margins
3 - some regeneration or organisation.
describe the changes in ischaemic coagulative necrosis
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.
describe acute inflammation in infarction
developes at the viable margins within 24hrs.
describe tissue regen or organisation in infarction
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.
7 changes in the macroscopic appearance in infarction
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