Acute Inflammation (4) Flashcards
Causes
Tissue death - Ischaemia, trauma, toxins, chemical insults, thermal injury, radiation
Infection - pus forming (pyogenic) bacterial
What is the purpose?
- Clear away dead tissues
- Locally protect from infection
- Allow access of immune system components
Cardinal signs
Calor - heat - vascular dilatation Rubor - redness - vascular dilatation Dolor - pain Tumor - swelling - inflammatory exudate into surrounding tissues Function laesa - disturbance of function
Serous inflammation
Abundant protein-rich fluid exudate, non-viscous serous fluid
Fibrinous inflammation
Exudate of coagulated fibrin
Purulent inflammation
Pus formation
Pseudomembranous inflammation
Response to a powerful necrotising toxin, formation on a mucosal surface of a false membrane composed of fibrin, necrotic epithelium and inflammatory leukocytes
Vascular reaction
Dilatation (rubor), changes in flow
Exudative reaction
Formation of inflammatory exudate (tumour)
Exudate
Mass of cells and fluid that has seeped out of a blood vessel/organ, especially in inflammation
Cellular reaction
Migration of inflammatory cells out of vessels
Pyrexia
(Systemic effect of inflammation) Increase body temperature and fever
Acute phase reaction
(Systemic effect of inflammation) Changes to the synthesis of certain protein within the serum during an inflammatory response, provides rapid protection for host against microorganisms through non-specific defence mechanisms
Markers of acute phase reaction
- C-reactive protein
- Erythrocyte sedimentation rate
Vascular reaction
- Microvascular dilatation
- Initially flow increases, then decreases
- Increased permeability
(Mediated - histamine, bradykinin, NO, leukotriene B4, complement components)
(Non-mediated - direct damage to endothelium e.g. toxins, physical agents)
Exudative reaction
- Protein rich (50g/l) - immunoglobulins and fibrinogen
- Constantly turning over - dilution of noxious agents, transport to lymph nodes, supply to nutrients O2, spread of inflammatory mediators, spread of antibodies, spread of drugs
Pericarditis
Inflammation of pericardium (fibrous from fibrin in inflammatory exudate)
Cellular reaction
- Accumulation of neutrophils in extracellular space
- If Severe > accumulation of neutrophils, cellular debris and bacteria > pus
Neutrophils
- Produced in bone marrow
- Commonest WBC
- Increase in acute inflammation
- Motile, amoeboid (crawling-like motion), can move into tissues
- Directional chemotaxis
- Short lifespan (hours in tissues)
- Phagocytotic and microbicidal (destructive to microorganisms)
O2 dependent phagocytosis
Myeloperoxidase, H2O2, Cl-, O2-, OH-
O2 independent phagocytosis
Lysozyme, lactoferrin, cationic proteins
Neutrophil process
1) Margination - align themselves on the wall e.g. selectin
2) Rolling - adhesion
3) Migration - out of vessel
4) Chemotaxis
Cell derived mediators of acute inflammation
- Histamine (stored)
- Prostaglandins (synthesised)
- Leukotrienes (synthesised)
- PAF (synthesised)
- Cytokines (synthesised)
- NO (synthesised)
- Chemokines (synthesised)
Plasma derived mediators of acute inflammation
- Kinin system
- Clotting pathway
- Thrombolytic pathway
- Complement pathway
Mediators of vascular dilatation
- Histamine
- PGE2/I2
- VIP
- NO
- PAF
Mediators of increased permeability
- Histamine
- Bradykinin
- NO
- C5a
- LTB4
- PAF
Mediators of neutrophil adhesion
Upregulation:
- IL-8
- C5a
- LTB4
- PAF
- IL-1
- TNF
Mediators of neutrophil chemotaxis
- LTB4
- IL-8
- Chemokines
Drugs that interfere
- Glucocorticoid steroids
- NSAIDs
- LT receptor antagonists
Minimal tissue damage
Resolution
Some tissue damage
Fibrosis
Marked neutrophil reaction with tissue damage
Suppuration - abscess
Damaging agent persists
Chronic inflammation
