Acute Inflammation Flashcards
Main cell type involved in acute inflammation
Neutrophils
Main Cell types involved in chronic inflammation
Macrophages
Signs of acute inflammation
Heat, redness, swelling, pain, loss of function
Definition of acute inflammation
A redunant, complex, adaptive adn protective response of vessels, resident cells and leucocytes to noxious stimuli.
It brings cells and molecules of host defense from the circulation to the sites where they are needed, in order to eliminate the offending agents and repair the tissues.
How long does acute inflammation last
Hours to days
Possible causes of acute inflammation (4)
infections and microbial toxins
Tissue necrosis; ischemia, trauma, physical and chemical injury, irradiation
Foreign bodies (splinters, dirt, dutures); endogenous substances, urate crystals, cholesterol crystals (in atherosclerosis) and lipids
Immune reactions (hypersensitivity)
Morphological hallmarks of acute inflammation (3)
Dilation of Blood vessels
Activation and recruitment of leukocytes
Active exudation of fluid in the extravascular tissues
Steps of acute inflammation (6 Rs)
Recognition of the injurious agent
Reaction of blood vessels
recruitment of leukocytes
Removal/clearance of the agent
Regulation (control) of the response
Repair (resolution)
Mediators in Acute Inflammation
Vasoactive Amines
Inflammatory Lipids
Complement
Cytokines
Others- chemokines, nitric oxide, coagulation cascade…..
Examples of vasoactive amines and where are they produced/released
Histamine, serotonin
Released/produced by mast cells, basophils, platelets
Examples of inflammatory lipids and where are they produced/released
Prostaglandins, leukotrienes
Produced by mast cells, leukocytes
Examples of complement and where are they produced
C5a, C3a
Produced in liver, present in plasma
Examples of cytokines and where are they produced
IL-1, TNF, IL-6
Produced by macrophages, endothelial cells, mast cells
Which mediators cause vasodilation
Inflammatory lipids (prostaglandins, leukotrienes)
Which mediators cause increased vascular permeability
Vasoactive amines
Complement (C5a, C3a)
Inflammatory lipids
Cytokines (IL-1, TNF)
Which mediators cause Leukocytes recruitment and activation
Inflammatory lipids
Complement
Cytokines
Which mediators cause pain
Inflammatory lipids
Which mediators cause tissue damage
Neutrophil granule content
Reactive oxygen species (ROS)
3 possible outcomes of acute inflammation
1- Complete resolution
Clearance of the offending agent and regeneration
2- Scarring, or fibrosis
Connective tissue growth into the area of damage or exudate, this occurs after substantial tissue destruction
3- Progression to chronic inflammation
Unresolved inflammatory process due to either the persistence of the injurious agent or some interference with the normal process of healing
What is the acute phase response
characterised by different systemic effects of acute inflammation (and other conditions) including pyrexia, leucocytosis and metabolic changes
It also includes changes to the concentrations of plasma proteins, called acute phase proteins (APPs)
Example of an exogenous pyrogen (trigger of pyrexia)
Bacteria
Examples of endogenous triggers of pyrexia
Phagocytosis, tissue damage, immune complexes
Endogenous pyrogens (3)
IL-1
TNF
IL-6
How is PGE2 produced and what does it do
Produced in response to endogenous pyrogens
Increases the hypothalamic set point for body temperature