Inflammation Flashcards
What is inflammation?
The local physiological response to tissue injury/infection
Beneficial effects of inflammation
Destruction of invading microorganisms
Walling off an abscess cavity -> preventing spread of infection
Acute inflammation
Neutrophil mediated inflammation
Chronic inflammation
Macrophage/lymphocyte-mediated inflammation
Disadvantageous effects of inflammation
Abscess - brain - space-occupying lesion -> compression of vital structures
Fibrosis due to chronic inflammation - distort tissues -> permanently alter tissue function
What cells are involved in inflammation?
Neutrophil polymorphs
Macrophages
Lymphocytes
Endothelial cells
Fibroblasts
Neutrophil polymorphs
2-3 day lifespan
Polylobed nucleus
Perform phagocytosis
Cytoplasmic granules containing lysosomes that digest phagocytosed bacteria
Stick to endothelial cells, squeeze through gaps & migrate to tissues
How are neutrophil polymorphs involved in inflammation?
-first on scene of acute inflammation
-phagocytosis
-release chemicals which attract inflammatory cells, eg. macrophages
-usually die on scene of inflammation - phagocytosed by macrophages
Macrophages
Weeks-months/years
Phagocytic - bacteria, debris
Carry debris to lymph nodes
May present antigen to lymphocytes -> induce 2. immune reaction
Lymphocytes
Years
Minimal cytoplasm - do not produce many proteins therefore minimal ER
Produce chemicals which attract other inflammatory cells and antibodies (from B lymphocyte plasma cells)
Immunological memory for past infections & antigens
Plasma cells
B-cell antibody producing - produce antibodies
Lots of ER
How are endothelial cells involved in inflammation?
-line capillary blood vessels in areas of inflammation
-normal conditions - produce NO to prevent adherence - however become sticky in areas of inflammation so inflammatory cells adhere to them (pull apart inflammatory cells)
-become porous to allow inflammatory cells to pass into tissues
-grow in areas of damage to form new capillary vessels
Fibroblasts
Long lived cells
Spindle shaped
Lots of ER - to produce collagen, fibrin
How are fibroblasts involved in inflammation?
-late in inflammation
-form collagenous connective tissue in areas of chronic inflammation & repair
Features of acute inflammation
-sudden onset
-short duration
-usually resolves
-fluid leaks into tissues - oedema
Stages of acute inflammation:
VASCULAR PHASE
-vasodilation - BF to area increases
-endothelial cells swell then contract -> increasing vascular barrier permeability
-exudation of fluid - leakage of protein-rich fluid from vascular space -> interstitial space -> oedema
CELLULAR PHASE
-neutrophil polymorph - arrive, phagocytose, release lysosomes, release chemicals which attract other inflammatory cells, eg. macrophages
-macrophages - arrive, phagocytose, release lysosomes
OUTCOMES
-resolution/suppuration/organisation/progression to chronic inflammation
What are the potential outcomes of acute inflammation?
Resolution
Supparation
Organisation
Progression to chronic inflammation
What is resolution?
The complete restoration of the tissues to normal after an episode of acute inflammation
What is suppuration?
The formation of a pus:
-living, dying & dead neutrophils & bacteria
-cellular debris
-globules of lipid
(an abscess)
What is organisation as an outcome of acute inflammation?
Tissue replacement by granulation tissue as part of the process of repair
What 3 processes are involved in the acute inflammation response?
1)changes in vessel calibre & flow
2) increased vascular permeability & formation of the fluid exudate
3)formation of the cellular exudate - emigration of the neutrophil polymorphs into the extravascular space
What are the characteristic features of inflammation?
Redness - 2. to vasodilation & increased BF
Heat - localised increase in temp., also due to increased BF
Swelling - due to increased vessel permeability - fluid loss from vascular space -> interstitial space
Pain - causes by stimulation of local nerve endings from mechanical & chemical mediators
Causes of acute inflammation
Microbial infections, eg. viruses
Hypersensitivity reactions, eg. parasites
Physical agents, eg. trauma/radiation
Chemicals, eg. corrosives/acids
Bacterial toxins
Tissue necrosis, eg. ischaemic infarction
Acute appendicitis as an example of acute inflammation
-unknown precipitating factor
-neutrophils appear
-vasodilation
-inflammation of serosal surface (outer lining of organs)
-pain
-appendix surgically removed or inflammation resolves
or
-appendix bursts with generalised peritonitis & possible death
