Body Response to Inflammation Flashcards
Function of Acute Inflammatory Response
AIR = Most common response of body tissues to nearby damage - Destroy or neutralise damaging agent - Liquefy and remove dead tissue - Prepare damaged area for healing
Situations causing AIR
- Microorganisms - Physical trauma - Ischaemic Necrosis - Radiation damage - Chemical damage
Main steps in AIR
Production of AI Exudate:
- Vessels dilate due to substances released from damaged tissue e.g. histamine; loss of axial flow pattern
- Endothelial cells swell and retracts, vessels leak; increases permeability; allows water, salts, protein(fibrinogen and Ig) to leak into damaged area; tissue becomes oedamatous
- Neutrophils marginate and emigrate; Stick to endothelial cells, marginatino. Emigrate through capillary to area of damage
Mediators of AIR
Chemokines
Cytokines
Eicosanoids
Adhesion molecules (selectins, integrins)
Composition of AIE
Fluid of blood serum
Fibrinogen
Neutrophils
Macrophages(in chronic inflammtion)
Types of AIE
Serous:
Fluid rich, Cell poor
e.g. congestive cardiac failure
Purulent
High concentration of leukocytes
e.g. meningitis
Fibrinous
Fibrin cross-links
Specific role of fluid in AIE
Dilutes toxins
Carries substances preformed in blood
Function of Neutrophils in AIE
Actively phagocytotic of
living tissue; bacteria
necrotic debris; breaks down damaged tissue
Clinical effects/symptoms of AIR
Calor = heat
Dolor = pain
Rubor = redness
Tumor = swelling
Malaise, fever, Pain, tachycardia
incr neutrophil count, acute phase proteins and ESR
Possible outcomes of acute inflammation
- Resolution
- Abscess formation
- Organisation and repair
- Chronic inflammation
Resolution of acute inflammation
AIE eliminates damaging agents completely
Macrophages remove dead cells and exudate
Local cells re-grow; function returns to normal
e.g. Pneumonia
Abcsess formation as result of Acute inflammation
= A large accumulation of liquid purulent in an area where tissue damage has led to extensive necrosis
Becomes walled off in attempt to limit spread
Especially caused by bacteria
Healing by repair in response to Acute inflammation
- Tackling debris by macrophages, area becomes semi liquid.
vascular: Capillaries grow into area
fibrovascular: Fibroblasts lay down collagen fibres but also capillaries
collagenous: Reduced vascularity. large amount of collagen fibre
Definition of chronic inflammation
Inflammation that may have rapid or slow onset, but characterised primarily by its persistence and lack of clear resolution; occurs when the tissues are unable to overcome the injuring agent
Damaging stimulus cant be removed
Or Complete healing cant occur
Pathological features of chronical inflammation
- Continued inflammation
- Damage occuring together with organisatino and repair
- Macrophage is main effector cell
Role of macrophages in chronic inflammation
Activated by interferon-y
- Phagocytotic role
- Secretory role:
proteases
hydrolases
Growth factors -> healing response
Inflammatory mediators->immune response
IL-1, TNFa
3 outcomes of chronic inflammation
- Improvement
- Stimulus removed or neutralised
- Healing gains upper hand, scarring completes e.g. peptic ulcer
- Stalemate
- Continuing damage and reapir
- Cant complete scarring
- Worsening
- Stimulus increases or impaired healing
- Damage too extensive for repair
Definition granulomatous inflammation
Form of inflammation where neutrophils are ineffective so macrophages are involved early on
If organism low pathogenicity, or resistant to neutrophils = type IV
Granuloma = fusion of macrophages
Interaction with T cells
Main stages of wound healing
Inflammatory: 2-5 days
Haemostasis, inflammation
Proliferation: 3d-3weeks
Granulation tissue bridges defect, contraction, epithelialisation
Remodelling: 3w-2y
New collagen->incre tensile strenght
Healing by primary intention
- clean incision
- edges cloesely apposed
- minimal exudate
- no wound infection
Results in granulation itssue, matures to clean collagenous scar
Healing by second intention
- Extensive damage/tissue destruction
- Wound edges cant be approximated
- +/-infection
Result
- Greater amount of necrotic debris
- Greater amount of tissue remodelling
- Larger area of necrosis, worse scars
Disadvantages of AIE
AIE can have secondary effects
- e.g. meningitis, increased intracranial pressure
- Pericarditis
- Pleurisy, fibrous AIE in lungs, rubbing
- Peritionitis etc
Factors leading to inadequate healing
ISchaemia
Continuing infection
Diabetes
Denervation
Steroid therapy
Repair process in brain
Cant make collagen, instead:
Macrophages cause liquefication, phagocytose debris and tissue dies
Astrocytes proliferate and lay down glial fibres, wall off area, limit damage
Repair in bone
Collagen itself not strong enough, needs to lay down new bone
- Defect filled with haematoma
- Phagocytosis of debris; haematoma undergoes organisation; defect filled with granulation tissue, first vascular, then fibrovascular; osteoprogenitor cells develop
- Become osteoblasts and synthesise osteoid collagen; calcifies to woven bone
- Woven bone links up with old bone
- Remodelling continues
