Inflammation II Flashcards
Describe the aims of the vascular response in acute inflammation
- Protein passage
- Fluid movement
Decribe what causes increased permeability in the protein passage
- Direct endothelial injury
- Chemical mediators e.g histamines, leukotrienes
- Endothelial contraction - gap formation
What causes increased filtration pressure?
- Rise in capillary blood pressure - due to hyperaemia
- Reduced plasma osmotic pressure - Protein loss from capillaries
- Increase in interstitial tissue proteins causing greater tissue osmotic pressure
What does the increased filtration pressure cause?
OEDEMA
Compare and contrast transudate and exudate
SEE SLIDES
What cells are involved in inflammation?
- NEUTROPHILS - inflammatory mediators within the granules
- MACROPHAGES
- LYMPHOCYTES
- EOSINOPHILS
Outline macrophage development
- Stem cell to monoblast in bone marrow
- Forms monocyte in blood
- Forms macrophages in tissues which become activated
What do activated macrophages do during inflammation?
- Release cytokines e.g chemokines and coagulation factors
- Release growth and angiogenic factors in repair
Describe mast cells
- Bind to IgE molecules
- Primary mediators are cytokines, histamines and eosinophil chemotactic factors
Describe cellular phase in the acute inflammatory response.
- Movement of neutrophils from circulation to site of tissue damage to limit extent of injury
Outline some effects of cell recruitment in inflammation.
- NEUTROPHILS/MACROPHAGES/DENDRITIC CELLS - increase antigen presentation, antimicrobial activity and anti-inflammatory macrophage release
- CD4+ and CD8+ T cell - decrease in inflammatory cytokine release
Describe leucocyte motion during the cellular phase.
- MARGINATION - rolling of WBCs on endothelial surface
- ROLLING
- ADHESION to endothelium through expression of selectins on surface of endothelial cells
- PASS betwen adjacent cells and exit from circulation towards site of injury by chemotaxis (using concentration gradient of chemotaxins)
Describe phagocytosis. PART 1
- Microorganism opsonised with antibody or complement
- Opsonised particle attaches to neutrophil membrane receptors for opsonin
- Engulfment
- Opsonised microorganism internalised into phagocytic vacuole (phagosome)
Describe phagocytosis. PART 2
- Lysosome fusin with phagosome
- Discharge of lysosomal enzymes into phagolysosome
- Respiratory burst and degradation of microorganism
Outline timeline of cellular response to injury.
- Oedema rapidly develops
- Neutrophil count slowly begins to develop
- Macrophage count rises after an even longer amount of time