Inflammation and Wound Healing - L6-7

How do you describe an organ that is inflamed? [blank_start]Tissue affected + 'itis'[blank_end] = inflammation of that tissue

Acute Inflammation

Chronic Inflammation

What are the five classical signs associated with Inflammation? 1. [blank_start]Heat[blank_end] 2. [blank_start]Redness[blank_end] 3. [blank_start]Swelling[blank_end] 4. [blank_start]Pain[blank_end] 5. [blank_start]Loss of function[blank_end]

Changes occurring during the vascular phase of acute inflammation 1. [blank_start]Vasodilation of arterioles[blank_end] Capillary beds [blank_start]distend with blood[blank_end] Signs associated: [blank_start]Heat[blank_end] and [blank_start]Redness[blank_end] 2. [blank_start]Contraction of endothelial cells[blank_end] Chemical mediators are released [blank_start]causing contraction of endothelial cells[blank_end] Fluid flows through the [blank_start]gaps into the extracellular space[blank_end] Signs associated: [blank_start]Swelling[blank_end] 3. [blank_start]Leakage of Fluid[blank_end] Blood is more [blank_start]viscous[blank_end] - [blank_start]Slows[blank_end] the flow Increase in [blank_start]RBC[blank_end] and [blank_start]WBC[blank_end] in the area

Functions of the vascular phase 1. [blank_start]Dilution of toxic substances[blank_end] 2. [blank_start]Delivery of antibody[blank_end] 3. [blank_start]Provision on nutrients to WBC[blank_end] 4. [blank_start]Provides fibrinogen[blank_end]

Changes occurring during the cellular phase of inflammation 1. [blank_start]Margination[blank_end] Slowing of blood during the vascular phase - leukocytes contact endothelial cells 2. [blank_start]Emigration[blank_end] 2a. [blank_start]Tethering[blank_end] 2b. [blank_start]Rolling[blank_end] 2c. [blank_start]Activation[blank_end] and [blank_start]firm adhesion[blank_end] 2d. [blank_start]Transmigration[blank_end] 2e. [blank_start]Chemotaxis[blank_end]

Functions of the cellular phase 1. [blank_start]Prevent spread of bacteria[blank_end] 2. [blank_start]Destroy bacteria[blank_end] 3. [blank_start]Produce cytokines and chemokines[blank_end] to [blank_start]remove necrotic debris[blank_end] 4. [blank_start]liquefy clotted fibrin to aid in repair[blank_end]

What are the Leukocytes associated with inflammation? 1. [blank_start]Mast cells[blank_end] 2. [blank_start]Eosinophils[blank_end] 3. [blank_start]Lymphocytes[blank_end]

What are the four different inflammatory exudates? 1. [blank_start]Serous[blank_end] exudate [blank_start]Watery fluid[blank_end], low in [blank_start]protein[blank_end] 2. [blank_start]Fibrinous[blank_end] Inflammation Fibrinogen --> [blank_start]clots[blank_end] [blank_start]Neutrophils[blank_end] present 3. [blank_start]Catarrhal[blank_end] Inflammation Mucus Due to inflammation of [blank_start]mucous membranes[blank_end] 4. [blank_start]Suppurative[blank_end] or [blank_start]Purulent[blank_end] Inflammation [blank_start]Pus[blank_end] Lot of [blank_start]neutrophils[blank_end], [blank_start]necrotic debris[blank_end] and [blank_start]fluid[blank_end]

What is the purpose of inflammatory mediators? Be the [blank_start]messengers[blank_end] that [blank_start]stimulate[blank_end], [blank_start]amplify[blank_end] or [blank_start]inhibit[blank_end] inflammation

Demolition Phase What: The [blank_start]breakdown and removal of necrotic tissue[blank_end] after the fluid and cellular phases Processes occurring: [blank_start]Liquefaction[blank_end] and [blank_start]Phagocytosis[blank_end] Processes function: To [blank_start]prepare for repair and regeneration[blank_end]

What are the outcomes of acute inflammation? 1. [blank_start]Complete resolution[blank_end] If injury is [blank_start]short lived[blank_end] and there is [blank_start]little tissue destruction[blank_end] Damage is [blank_start]repaired[blank_end] or [blank_start]regenerates[blank_end] 2. [blank_start]Healing by connective tissue replacement[blank_end] [blank_start]Scarring[blank_end] OR [blank_start]Fibrosis[blank_end] occurs when there is lots of tissue destruction or they cant regenerate 3. [blank_start]Progression to chronic inflammation[blank_end] If the cause of [blank_start]acute inflammation is not resolved[blank_end] OR Something [blank_start]interferes with normal healing[blank_end]

Four phases of wound healing 1. [blank_start]Homeostasis[blank_end] AIM: [blank_start]To prevent further bleeding[blank_end] [blank_start]by blood clotting[blank_end] [blank_start]Vessel constriction[blank_end] --> [blank_start]Platelet plug[blank_end] --> [blank_start]Fibrin plug[blank_end] 2. [blank_start]Acute Inflammation[blank_end] [blank_start]Classical signs of inflammation[blank_end] present [blank_start]Neutrophils and Macrophages[blank_end] remove [blank_start]debris from injury[blank_end] 3. [blank_start]Granulation tissue formation[blank_end] & [blank_start]replacement of epithelial tissue cells[blank_end] AIM: [blank_start]Fill in gap of damaged tissue[blank_end] [blank_start]macrophages[blank_end] produce [blank_start]growth factors[blank_end] --> [blank_start]proliferation[blank_end] of epi. cells and fibroblasts Granulation tissue = [blank_start]fibrous connective tissue + capillaries[blank_end] 4. [blank_start]Wound maturation and Remodeling[blank_end] Once inflammation finished & new tissue forms - [blank_start]granulation tissue is replaced by mature[blank_end] [blank_start]connective tissue[blank_end]

Healing by First Intention [blank_start]Minimal tissue damage[blank_end] + [blank_start]closely apposed wound edges[blank_end] Occurs if: Minimal [blank_start]tissue injury and necrosis[blank_end] Minimal [blank_start]haemorrhage[blank_end] [blank_start]No bacterial infection[blank_end] [blank_start]Wound edges closely apposed[blank_end]

Healing by second intention [blank_start]Larger amounts of tissue[blank_end] - [blank_start]traumatic[blank_end], [blank_start]un-sutured[blank_end], [blank_start]infected[blank_end] Occurs when: Greater [blank_start]amount of necrosis[blank_end] [blank_start]Bacterial infection[blank_end] Wound edges [blank_start]NOT close together[blank_end] [blank_start]Large defect[blank_end] present

Process of wound contraction Feature of [blank_start]2nd Intention[blank_end] Wound margins [blank_start]grow towards each other[blank_end] - [blank_start]Myofibroblasts at edges contract[blank_end] [blank_start]bringing edges together[blank_end] - [blank_start]Makes smaller wound to fill with[blank_end] [blank_start]granulation tissue and epithelial cells[blank_end] - Continues [blank_start]after re-epithelialisation[blank_end]

Factors affecting wound healing 1. [blank_start]Age[blank_end] 2. [blank_start]Nutrition[blank_end] 3. [blank_start]Concurrent disease[blank_end] 4. [blank_start]Foreign materials[blank_end] 5. [blank_start]Infection[blank_end] 6. [blank_start]Blood Supply[blank_end]

What are the events involved in fracture repair? 1. [blank_start]Formation of a haematoma[blank_end] 2. [blank_start]Mesenchymal cell proliferation[blank_end] 3. [blank_start]Early callus[blank_end] 4. [blank_start]Advanced callus[blank_end]

What are the factors that affect fracture healing? 1. [blank_start]Inadequate blood supply[blank_end] 2. [blank_start]Infection[blank_end] 3. [blank_start]Instability[blank_end]

Antigen: substance that [blank_start]promotes production of antibodies[blank_end] or [blank_start]includes an immune response[blank_end] Antibody: [blank_start]Proteins manufactured[blank_end] in response to [blank_start]foreign material[blank_end] or [blank_start]antigenic stimulation[blank_end]

Hypersensitivity reactions P1 Type I = [blank_start]Immediate[blank_end] Hypersensitivity Due to [blank_start]IgE antibodies[blank_end] Occurs within [blank_start]minutes of repeat exposure[blank_end] Reactions directed against [blank_start]antigens from enviro & parasites[blank_end] activation of [blank_start]mast cells[blank_end], [blank_start]basophils[blank_end] & [blank_start]eosinophils[blank_end] Mediators that cause: [blank_start]smooth muscle spasm[blank_end], [blank_start]oedema[blank_end] --> [blank_start]swelling[blank_end], [blank_start]excessive mucus secretion[blank_end] E.g [blank_start]Allergic Rhinitis[blank_end] (Hay fever)

Hypersensitivity reactions P2 Type II = [blank_start]Antibody mediated[blank_end] hypersensitivity Formation of [blank_start]antibodies directed against antigens[blank_end] of the [blank_start]surface of a cell or tissue[blank_end] Leads to the [blank_start]cell being destroyed[blank_end] E.g. [blank_start]Immune mediated haemolytic anaemia[blank_end] Type III = [blank_start]Immune complex[blank_end] hypersensitiviity Occurs due to [blank_start]formation of antigen-antibody complexes[blank_end] [blank_start]in bloodstream[blank_end] These [blank_start]get stuck in capillaries[blank_end] Neutrophils release [blank_start]toxic free radicals and enzymes[blank_end] into tissue - damage tissue commonly occurs in the [blank_start]joints[blank_end], [blank_start]glomeruli[blank_end], [blank_start]eye[blank_end] and [blank_start]blood vessels[blank_end] E.g. [blank_start]Lupus[blank_end] (SLE)

Immunological Test Measures [blank_start]immunoglobulin[blank_end] - checks the [blank_start]passive transfer of antigens[blank_end] [blank_start]from colostrum[blank_end] E.g. [blank_start]ELISA - SNAP Test[blank_end] Serological Test Based on the ability to detect reactions [blank_start]between antibody and antigen[blank_end] from the [blank_start]animal in a serum[blank_end] E.g. S[blank_start]NAP tests - FIV/FeLV[blank_end]