Tissue infarction, tissue repair

===Lecture Details===
John Pedersen; Week 10 MED1022; Pathology
===Lecture Content===
Ischaemia is interruption of blood supply resulting in tissue damage, necrosis is irreversible cell damage resulting in cell death, can be coagulative, liquefactive, caseous, fibrinoid, apoptosis. Infarction is tissue death from lack of blood supply, due to metabolic failure, loss of O2, buildup of metabolites. There are two tissue patterns, pale and red. Pale is in solid organs and tissues and red is in soft tissues such as lung. Resolution is return of normal structure and function following injury. Organisation is replacement with fibrous tissue, which has a low metabolic requirement. Fibrous tissue is mature granulation tissue. 
Cellular and cytoplasmic swelling along with nuclear changes cause loss of membrane integrity. Cell changes include cellular respiration changes (O2 loss, glucose loss, free radical generation), protein synthesis, DNA damage. Cardiac muscle cells cannot divide so death results in organisation. Coronary arteries arise above aortic valve, fill in diastole. Arteries are external to myocardium, in hypertrophy vessels are stretched. Arteries are small caliber, any narrowing results in poor flow. There is only some degree of collateral supply. 
Ischaemia is clinically angina, due to insufficient blood supply resulting in swelling. Commonest cause is atheroma (atherosclerosis) or spasm. Other causes are hypotension from sepsis, cerebral, CVS explosion, aortic valve problems, illicit drugs, coronary artery aneurysms, electrical failure. Acute MI is usually in the left ventricle as it is the thicker muscle. Replaced by fibrous tissue. Serum enzymes released from dying muscle (troponin) as well as ECG conduction changes can diagnose. Consequences of infarction are death, cardiac failure, pericarditis, thrombus, muscle rupture, electrical dysrhythmias, left ventricular aneurysm, further infarction and pulmonary embolus.
Coagulative necrosis is the most common, cells die losing nuclei but they retain cell outlines. Tissues are initially firm due to swelling. Tissue softens as cell integrity fails and macrophages phagocytose, Swelling causes membrane breakdown which releases chemotactic factors, granulation tissue starts here and there is finally fibrosis. Mural thrombus can form in ventricular lumen outside area of infarction
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