Cell pathology 4- Inflammation Flashcards
What is inflammation
Reactions of living vascularised tissue to sub-lethal cellular injury
Evolutionary development to protect against infection and trauma
Describe acute inflammation (5)
Transient and early response to injury Hours/few days Involves release of chemical mediators Typical vascular and leucocyte response NOT the same as infection
Describe chronic inflammation (3)
Inflammation of prolonged duration
Weeks/months/years
Usually due to persistent injury causing agent
What five cells are involved in inflammatory response
Neutrophils-
Produced in bone marrow, circulate in blood, contain cytoplasmic granules
Involved in phagocytosis
Degranulation
Macrophages
Phagocytosis
Control other inflammatory cells
Release cytokines
Lymphocytes
Eosinophils-
Seen with allergic and parasitic causes of inflammation
Mast cells
Also seen in allergic diseases
What three parts of ECM are involved in inflammatory response
Collagen
Proteoglycan
Fibroblasts
What soluable factors are involved in inflammatory response
Antibodies
Cytokines
Complement system
Coagulation system
5 cardial signs of inflammation
Rubor- Redness
Blood flow isn’t as fast so you get redness
Calor- Heat
Caused by histamine mediated vasodilation
Tumor- Swelling
Oedema - increased fluid in interstitial fluid
Caused by histamine mediated increase in permeability
of vessels
Dolor- Pain
Functio laesa- loss of function
Due to swelling and pain
What is histamine
Where is it produced
What is it packaged into
What does its secretion lead too
Vasoactive amine
Produced by mass cells
Packaged into granules inside mast cells - when antigen binds to IgE on the surface of mast cells - causes cross-linking and degranulation
Leads to: Vasodilation and Increased Vascular Permeability
Dysregulation - allergy (Type 1 Hypersensitivity)
3 targeting inflammatory medications
Histamine = Anti-histamines
Prostaglandins = Aspirin
IL-1 and TNF = Anti-TNF antibodies
Types of exudates
Purlent= pus filled
Serous= Fluid filled
Fibrinous= High fibrin content
Hemorrhagic
Describe the action of Neutrophils in inflammatory response
Enter tissue
Migrate to site of cell injury - chemotaxis
Become activated
Carry out their designated role - e.g. phagocytosis
Interact with other cell types - release of soluble mediators
How do cells get to site of injury
Margination, Rolling, Adhesion, Transmigration, Chemotaxis, Phagocytosis
Describe the process of margination
Cells pushed to edges of vessel
Process of rolling and adhesion
Selectins on endothelial cells and leucocytes bind white blood cells to endothelial cells
Process of Transmigration
Neutrophil dissolves basement, enter interstitium
Process of chemotaxis
Follow chemical gradient followed to site of inflammation
What are the soluble factors in exudates (5)
Factors made by local cells Vasoactive amines Cytokines Antibodies proteins
Process of phagocytosis
Opsonisation
Opsonins (various protein/chemical mediators) attach to bacteria
Enhances neutrophil recognition and attachment
Ingestion
Phagocytosis (engulfment) and entrapment in vacuoles
Killing
Destruction in vacuole by free radicals, lysozyme, lactoferrin, major basic protein
Describe the control of Inflammatory Reaction
Mediators and neutrophils have short half life
Stimulus (e.g. bacteria) removed
Mast cells and lymphocytes release anti-inflammatory products (lipoxins)
Macrophages release anti-inflammatory products
How can the acute inflammation return to normal
If resolution or repair occur
Histological Features of Acute Inflammation
There are lots of Neutrophils
There will also be mast cells and eosinophils
Histological Features of Chronic Inflammation
Macrophages, lymphocytes and plasma cells will be abundant
What hinders repair
Not having enough:
Protein
Vit C- fibroblasts
Vit A- required for epithelial regeneration
Poor blood supply
Persistent foreign body
Movement
What are the Complications of repair
Keloid Formation
Excess collagen deposition
You can get scar tissue formation other than at the site of original injury
Contractures
Fibrous scar tissue contracts as part of its maturing process
If this happens across a joint, you can get reduced joint mobility
Impaired Organ Function
Fibrous scars forming in organs will cause loss of functional tissue
This affects organ function
What are the causes of chronic inflammation
Persistent damage Persistent infection Prolonged exposure to toxic agent Autoimmunity Foreign body
What is Granulomatous inflammation and name 4 causes
Particular form of chronic inflammation showing granuloma formation
Cluster of macrophages
Involves specific immune reaction T cells
Causes Infection – TB, fungi Foreign material Reaction to tumours Immune diseases (sarcoid, Crohn’s)
What is the ‘good’ outcome of inflammation
Removal of causative agent
Cessation of the inflammatory reaction
Healing of tissue damage to preserve integrity and function (resolution)
What is the ‘bad’ outcome
LOCAL
Can cause excess local tissue damage and scarring
Secondary effects on nearby tissue
E.g. Bronchoconstriction in asthma
SYSTEMIC
Can evolve into systemic inflammatory reaction and secondary multi-organ failure
E.g. Septic shock
Amyloid
Difference between repair and resolution
RESOLUTION = regeneration of normal functional parenchymal cells
REPAIR = connective tissue and SCAR TISSUE formation
When can resolution occur?
Tissue contains cells able to regenerate to replace lost cells E.g. Liver
Little structural damage done
When does repair occur
Tissue loss too great, and cells unable to regenerate
Replace normal tissue with fibrous scar tissue
Fibroblasts – produce collagen
Collagen – strong “scar” type collagen
Remodelling – reorientation of collagen fibres for maximal tensile strength
