L4- Acute Inflammation Flashcards
Acute inflammation
Non-specific initial reaction to tissue damage
Acute inflammation - causes
Tissue death
- Ischaemia
- Trauma
- Toxins
- Chemical insults
- Thermal injury
- Radiation
Infection
-Especially bacterial (‘pyogenic’)
Purpose of acute inflammation
Clear away dead tissues
Locally protect from infection
Allow access of immune system components
Cardinal signs’ of inflammation
Calor= heat
Dolor= pain
Rubor= redness
Tumor= swelling
Components of the acute inflammatory response …reactions
Vascular reaction - dilatation (=rubor), changes in flow
Exudative reaction - formation of inflammatory exudate (=tumor)
Cellular reaction - migration of inflammatory cells out of vessels
Vascular reaction
Microvascular dilatation
Initially flow is increased and then decreased
There is an increased permeability (mediated and non mediated)
Mediated: Histamine, Bradykinin, NO, complement components
Non mediated: Direct damage to endothelium e.g toxins, physical agents
Exudative reaction
formation of inflammatory exudate (=tumor)
Protein rich:
-Immunoglobulins
-Fibrinogen
e.g The heart in a case of pericarditis
Cellular reaction
Migration of inflammatory cells out of vessels
Accumulation of neutrophils in extracellular space
In severe cases, accumulation of neutrophils, cellular debris and bacteria forms pus
-e.g acute meningitis caused by a pyogenic (=pus forming) bacterial infection
-bronchopneumonia - the airspaces are filled with a neutrophil rich exudate
Neutrophils
Produced in bone marrow Commonest white cell in blood Increase in acute inflammation Motile, amoeboid, can move into tissues Directional chemotaxis Short lifespan (hours in tissues)
Phagocytic, microbiocidal
Steps in a cellular reaction (Migration)
he movement or passage of blood cells, especially white blood cells, through intact capillary walls into surrounding body tissue. Also called migration
Margination –> Rolling- adhesion (pavementing) –> diapedesis
Cell derived Mediators of acute inflammation
Prostaglandins Leukotrienes PAF Cytokines (IL1,8; TNFa) NO Chemokines Histamine
Plasma derived Mediators of acute inflammation
Kinin system
Clotting pathway
Thrombolytic pathway
Complement pathway
Outcomes of acute inflammation
Minimal tissue damage = resolution
Some tissue damage =Fibrosis
Marked neutrophil reaction with tissue damage = Suppuration- abscess
Damaging agent persists = Chronic inflammation