8977 Lecture Notes - Lecture 1: Edema, Vasospasm, Macrophage
3 Jul 2018
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Tissue Injury and Repair
Initiated by:
- Tissue damage
- Heat
- Irritating chemicals
- Infection
- Actual physical damage
- Cell death
- Loss of communication between adjacent cells, or cells and their support
Stages of Repair
1. Inflammation Stage
2. Proliferation Phase
3. Remodelling Phase
Inflammation
- Stop bleeding
- Remove debris and dead tissue
- Destroy infection
Vaso-regulation and blood clotting
- Primary Vessel Constriction:
oRelease of noradrenaline
oOpposing cell walls contact and form adhesion
- Secondary Vessel Constriction
oCaused by serotonin, adenosine diphosphate, calcium and thrombin
oLymphatic and blood vessels are plugged to limit fluid loss
oPlatelet adhesion and aggregation is stimulated
- Blood Clotting
oBlood loss to tissues initiates platelet activity and blood coagulation
oChemical factors are produced to initiate + control the healing process
oBlood clots provide a provisional matrix – migrates cells to wound
oBlood involvement promotes a greater healing capacity, than if not
Inflammatory Cascade:
- Signals appropriate cells
- Drugs are able to modify inflammatory reaction by acting on cascade
oHistamine: vasodilation
oComplement: increased capillary permability
oKinins: attract neutrophils
oProstagladins: ^^ vascular permeability, sensitise pain receptiors, attract
leucocytes and some anti-inflammatory
oLeucocytosis inducing factor: attracts leucocytes
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Document Summary
Loss of communication between adjacent cells, or cells and their support. Primary vessel constriction: release of noradrenaline, opposing cell walls contact and form adhesion. Secondary vessel constriction: caused by serotonin, adenosine diphosphate, calcium and thrombin, lymphatic and blood vessels are plugged to limit fluid loss, platelet adhesion and aggregation is stimulated. Drugs are able to modify inflammatory reaction by acting on cascade: histamine: vasodilation, complement: increased capillary permability, kinins: attract neutrophils, prostagladins: ^^ vascular permeability, sensitise pain receptiors, attract leucocytes and some anti-inflammatory, leucocytosis inducing factor: attracts leucocytes. Platelets contain actin and myosin that contacts just like muscle, squeezing serum and contracting the clot bringing the sides of the wound together. Trauma attracts monocytes (differentiate into macrophages) + neutrophils out of dilated capillaries into interstitial tissue. Macrophages role is phagocytosis, cleaning up tissue debris, fragments of dead and dying cells and bacteria. Once neutrophils enter the extravascular tissue, marks end of early inflammatory phase. Cleaning clot (fibrinolysis) 2 7 days.
