Inflammation Flashcards
What is the cause of acute inflammation
Any form of tissue injury
Give the three phases of tissue injury
Fluidic, Cellular, Reparative
Give 4 signs of acute inflammation
Redness and heat (increased blood flow)
Swelling (fluid accumulation)
Pain (chemical release stimulates nerve endings)
Loss of function
Describe the process of cellular and vascular response through acute inflammation
- Momentary vasoconstriction - reflex process to reduce blood loss
- Dilation of Blood vessels - Caused by release of chemical mediators
- Exudation of fluid - Reduced blood flow, proteinaceous fluid released
- Leukocyte migration - Adherence of circulatory WBCs to altered endothelium
- Leukocyte emigration - Migrate into tissues via diapedesis
- Temperature increase
Define transudates and describe their appearance
Extracellular filtrate of plasma with a little protein and few/no nucleated cells
- Glossy, clear and watery appearance
Describe how transudate is produced
Produced by fluid leakage due to increased hydrostatic pressure or reduced osmotic potential in the blood vessels
Define exudates and describe its appearance
ECF that is protein rich and contains high numbers of cells
- Purulent, fibrinous, serous
Describe how exudates are formed
Formed during inflammation due to increased vascular permeability
Define effusion
Accumulation of fluid in a body space or cavity
Describe the process by which pyrexia is produced
= Raised body temperature/fever
- Exogenous factors cause release of endogenous factors which in turn activate the arachidonic pathway and PGE2 release
- PGE 2 acts on the preoptic are of the hypothalamus through the EP3 receptor leading to the stimulation of the sympathetic output system which evokes non-shivering and shivering thermogenesis to produce body heat and skin vasoconstriction to decrease heat loss from the body surface
Where do antipyretic drugs act on the pyrexia process?
Act at the hypothalamus, overriding the action of PGE2 in causing increased temperature
Give three inflammatory mediators that cause vasodilation
Nitric Oxide
Bradykinin
Prostaglandins PGE2
Give three inflammatory mediators that cause inceraced vascular permeabilities
Vasoconstrictive amines e.g. histamine
Complement factors e.g. C5a, C3a
Leukotrines
Give three inflammatory mediators that cause chemotaxis and leukocyte activation
Leukotrines
C5a
Chemokines e.g. IL-8, IL-5
Give two inflammatory mediators that cause tissue damage
Neutrophil granule content : matrix metalloproteinases
ROS
Give two inflammatory mediators that cause Pain
Bradykinin
PGE2
Give three inflammatory mediators that cause Fever
Cytokines e.g. IL-1 TNF, IL-6
Describe Plasma derived chemical mediators
e. g. complement proteins, kinins
- Present in the plasma as precursors that must be activated
Describe cell derived chemical mediators
e.g. histamine
Sequestered in intracellular granules that need to be secreted
Describe acute phase proteins
- Inflammatory biomarkers
- Plasma protein synthesised by liver
- Increase in serum concentration over 25% in response to cytokines
- Causes fever and leucocytosis (part of the innate immune system)
Describe the complement cascade
- Helps the innate immune system to clear pathogens from an organism
- Plasma complement C1-9 synthesized in the liver
- Are activated and induce inflammation and further activation of the immune system
- End result is cell killing membrane attack complex (MAC)
Describe arachidonic acid metabolites
- Damage of the cell leads to the cell membrane lipids rearranging to create biologically active lipid mediators (derived from arachidonic acids)
- Effects are short lived due to rapid decay and enzymatic destruction of lipid metabolites
Describe 4 causes of chronic infection
- Persistent infection
- Prolonged toxin exposure
- Indestructible foreign material
- Immune mediated disease
Describe the morphology of chronic inflammation
- Tissue destruction
- Healing attempts
- Infiltration with mononuclear cells (macrophages, lymphocytes)
Describe macrophage activity in chronic inflammation
Migration and Activation - extravasation controlled by ashesion molecules and chemical mediators with chemostatic activating properties.
Activated Macrophage
- Eliminate injurious agent
- Instigate the healing process (fibrosis and angiogenesis)
- Cause tissue injury (chronic)
- Release products that are toxic to microorganisms
Describe the involvement of lymphocytes in chronic inflammation
Interact bidirectionally by recruiting and being recruited by macrophages
Describe the involvement of Plasma cells in chronic inflammation
Activated by B lymphocytes and produce antibodies against persistent foreign antigens
Describe the involvement of eosinophils in chronic inflammation
Present in parasite and some fungal infections
Also hypersensitivity infection
Describe the involvement of mast cells in chronic inflammation
Found in the connective tissue both in acute and chronic inflammation
Describe the involvement of neutrophils in chronic inflammation
Characteristic in acute may be found in chronic e.g. abcesses
Give the three phases of healing
Blood clot
Proliferation and granulation
Remodelling and maturation
Describe an abcess
Collection of pus circumscribed by a fibrous capsule that is visible grossly (most commonly caused by bacteria)
Describe pus
Plasma proteins, leukocyte based yellow/green liquid
Describe a granuloma
Nodular aggregation of macrophages surrounded by a collar of mononuclear leucocytes
Aims to contain agent that is difficult to eradicate
against : parasite, fungi, bacteria, viruses, foreign body
Define regeneration
Proliferation of cells and tissues to replace lost structures
Define repair
Replacement of injured cells with connective tissue
Describe the blood clot stage of healing
- Activation and coagulation
- Blood clot formation
- Neutrophils arrive
Describe the Proliferation and granulation stage of healing
- Macrophages replace neutrophils (clean and promote proliferation)
- Granulation tissue formed from proliferation of fibroblasts and endothelial cells
- Fibroblasts and connective tissue grow parallel to the wound surface and perpendicular to proliferating capillaries
Describe the remodelling and maturation phase of healing
Leukocytes and increased vascularity disappear after the second week
Granulosa converted into a pale avascular scar (fibroblasts and dense collagen)
Wound contraction
