26. Ischaemia and infarction Flashcards
Define ischaemia and infarction
Ischaemia: inadequate local blood supply to a tissue- inadequate transfer of metabolic substances in and out of tissues.
Infarction: necrosis of a tissue due to ischaemia.
What are the possible causes of ischaemia
external occlusion, tumours, internal occlusion: artherosclerosis Spasm of vessel: frost bite Capillary blockage, Shock : circulatory failure with low map Increased demand and venous obstruction.
Describe the effects of ischaemia at the levels of individual cells
Ischaemia which is not sufficiently severe to kill can change the biology of the cell, reduces the ATP - less oxd phosph, activate signalling cascades, less protein/dna synthesis and repair, cell swelling,
Describe the effects of ischaemia at the level of tissue - relative to damage level
- There is some functional defects due to sub optimal tissue perfusion- renal , heart dysrhythmia 2. insufficiency, adaption, atrophy or shutdown,
- apoptosis of isolated cells, then 4. infarction : necrosis
What are the two different types of infarctions
Red (haemorrhagic) in tissues with dual blood supply- or tissues where blood flow is re-established
White (anaemic) in solid tissues supplied by a single artery
What is the timing of a typical infarction- after survival starts with inflammation.
Within 24hrs acute inflammation starts with neutrophils, including. 1-3 days, macrophages and lymphocytes join.
Fibroblasts and endothelial cells are then recruited to form granulation tissue. Then the damage is organised replaced to make a fibrous scar (or regeneration)
What are the treatments for myocardial infarction
Thrombolitic agents: eg, streptokinase/ plasminogen activator
- Mechanical re-expansion of oclulded vessel: angioplasty and stenting
What is re-perfusion injury? (additional damage to cells due to restoration of blood flow after a LONG period of ischaemia/cell injury not short).
When blood flow is reintroduced damaging Reactive oxygen species are produced in cells and cause oxidative stress.
-they damage unsat fat, aa side chains for enzymes and thymine chains for DNA.
What is the complication of myocardial infarction
Heart failure: dead cells reduce contractility
Mural thrombus : injury increases coagulant factors, more turbulence due to uncoordinated, injured endothelial cells leading to embolism via aorta to brain, gut, spleen
Dysrhythmia: uncoordinated contraction