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Path + CR - Ischaemia + Infarction (i) (causes of cell damage (infarct,…
Path + CR - Ischaemia + Infarction (i)
Response to necrosis (cell death in a living tissue = acute inflamm
ischaemia
hypoxia (O2 insufficiency) + nutrient insufficiency + inadequate removal of metabolites
due to reduced perfusion (occlusion of art supply/venous drainage) and/or increased tissue requirements
causes infarct (necrosis due to ischaemia, v common cellular injury)
susceptible tissues
poor blood supply (e.g. due to atheroma)
no collat circulation that could compensate for reduced perfusion
art anastomoses present in liver, lung, bowel, brain
absent in kidney (end organ of renal art), spleen, heart (end organ of coronary arts)
high requirements
high aerobic metabolic rate (e.g. heart)
low requirements in supporting tissues (e.g. bone, fibrous)
hypertrophy
watershed areas
regions of body that receive dual blood supply from most distal beaches of 2 large arts
splenic flexure of colon, brain, deep myocardium (lumen of ventricle)
= most common cause of hypoxia
reperfusion injury
restoration of blood supply following its loss
restored o2, free radicals form
Ca-ATPase pumps fail to control Ca cytosol + mt levels
causes loss of cell integrity + necrosis
give Ca channel blockers to slow Ca influx
hence why there's only a narrow window to treat cerebral/myocardial infarcts with anticoags
too late - will cause a haemorrhage (conversion of ischaemic infarct to haemorrhage infarct) + worsen the situation
Common clinical illnesses due to infarcts
MI (can lead to haemopericardium)
cerebrovasc accident
pul infarction (blood in alveoli - poor oxygenation - dyspnoea)
bowel infarct
ischaemic necrosis of extremities (smaller arts in peripheries) - esp in DM (macro + micro angiopathies)
Causes of Ischaemia + Infarcts
obstruction in lumen
atherosclerosis
thrombus
embolus
in wall
vasculitis (reduced lumen diameter)
vasospasm (e.g. due to cocaine)
external
shock
hypotensive
septic
cardiogenic
multi-organ failure
compression of vessel
hypertrophy of surrounding structures
oedema
hernias
tumours
torsion of vessel (e.g. testicular)
traumatic rupture
thrombosis
solid mass in FLOWING blood
causes = virchow's triad (endothelial damage, abnormal flow, hypercoaguability)
causes differ in arts (atheroma) + veins (stasis)
embolus
solid/liquid/gaseous mass that moves from one part of circulation to another
many types: thrombotic, tumour, septic, fat, air, chol, foreign body, nitrogen, amniotic fluid
types of infarcts
red
made up of RBCs + haemosiderin pigment (Fe storage complex)
occur in loose tissues / spongy organs (e.g. lung), venous occlusion (e.g. in ovary), dual circulation (e.g. in intestine) + reperfusion
firm, brown
white
occur in solid organs (heart, spleen, kidney)
limited haemorrhaging (few RBCs lysed), only some haemosiderin
yellow/white sharply-defined wedge-shapes, with widest part of wedge furthest from blood supply
causes of cell damage
infarct
ischaemia
inflamm
infection
immune (auto)
irritant
idiopathic