1) Damage to local blood vessels (capillaries), bleeding and cell death (trigger inflammation)
2) Local initial vasoconstriction (to limit fluid loss - but results in more cell death due to increased lack of oxygenated blood available at injury site)
3) Release of chemical mediators (histamine/serotonin etc) from dying cells causing VASODILATION or surrounding undamaged vessels, increasing their permeability, which can be seens as REDNESS (erythema) and felt as HEAT (calor) - permeability allows leukocytes to emigrate into site of injury guided by chemotaxis.
4) Damaged nerve endings give rise to pain (dolor), chemical irritation from mediators and increasing pressure from excess fluid and inflammatory exudate in the area (more responsible for pain in the later stages)
5) 'Walling Off' - Local vasodilation is not enought to prevent fluid loss so we get platelets activated by cell death (necrosis) become very sticky and release chemicals to activate the enzyme thrombin which converts fibrinogen (element of blood plasma) into FIBRIN which creates a sticky matrix to trap cellular debris and platelets to form a blood clot (temporary solution to fluid loss)
6) Leukocytes (neutrophils 6-24 hrs / monocytes & lymphocytes 24-48hrs) or white blood cells clear debris that wasn't caught by the sticky matrix and fight off an infection present.
7) Histamine causes local vasodilation within hours to introduce new plasma* rich blood for next stage of repair (each phase is laying the ground work for the next)
*Plasma = liquid portion of blood (90% water)