Inflamation Flashcards
Causes of acute inflammation
Micro-organisms
Trauma including if sterile e.g surgery
Chemical changes e.g upset pH
Extreme physical conditions e.g heat,cold, radiation
Necrosis of tissues irritates adjacent tissues
Hypersensitivity
Steps in acute inflamation
Changes in vessel radius
-triple response (constriction, dilation, relaxation)
- increased radius increases blood flow e.g redness and heat
Changes in vessel permeability
-results in oedema causing swelling and loss of function
-fluid loss results in increased blood viscosity so rate of flow slows (stasis)
Movement of neutrophils from vessel to extra vascular space
-migration, pavementing, emigration
Benefits of AI
Rapid response to injury
Cardinal signs and loss of function protects the damaged area
Neutrophils destroy organisms and denature antigens for the macrophages
Plasma proteins wall off the area
Results in resolution
Types of mediators
On the endothelial cell surface these are sticky
Released from cells eg histamine, cytokines and chemotaxis
Inside cells (signalling) NF-KB, MAPK pathways
In plasma - 4 enzyme cascades have an effect on each other
Mediators
Favour or inhibit acute inflammation
Outcomes of AI
Suppuration -pus Organisation - granulation tissue Resolution Chronic inflammation Dissemination ; spread to the blood stream -sepsis -septicaemia -toxaemia -bacteremia
Systemic effects AI
Pyrexia, malaise, neutrophilia, septic shock
Granulation tissue
Universal repair kit
New capillaries grow into the inflammatory mass. Giving access to plasma proteins, macrophages, and fibroblasts which lay down collagen to relain damage (angiogenesis)
Cells in CI
Lymphocytes -bcells tcells and nk macrophages -antigen presenting, removes debris plasma cells (anti production) fibroblast are also present later they make collagen
Clinical presentation CI
Malaise, weight loss, loss of organ function,
Angiogenesis
Formation of new vessels stimulated by VEGF released from hypoxic cells
Can be used therapeutically for some cancers
Causes of CI
from acute inflammation because -large volume of damage -Inability to remove debris -couldn’t resolve From a primary lesion because -Autosomal disorder -Material resistant to digestion -Endogenous substances e.g sutures, glass -Exogenous e.g keratin,hair
Effects of CI
scarring and fibrosis
Granuloma formation
Factors good for healing
Keep wound clean
Edges together to prevent microorganisms settling there
Patient is well nourished
Stable and normal metabolism
Normal inflammatory and coagulation mechanisms
Mediators work together in a balanced way
Factors bad for healing
Dirty open wound with large blood clot (haematoma)
Poorly nourished patient lacks Vit c&a
Abnormal carb metabolism e.g diabetes
Inhibition of angiogenesis
