Acute inflammation Flashcards
Bad outcomes of acute inflammation
Allergy
Lupus
Rheumatoid arthritis
Analphyaxis
Positive effects of acute inflammation
Protective
Destroy, wall off or dilute injurious agent
Initiate repair
Inflammation is response of vascular living tissue to injury
Acute vs chronic
Onset immediate vs gradual
Short lived vs prolonged
Usually single episode vs frustrated healing
Neutrophils and other granulocytes vs macrophages and lymphocytes
Granulatomous inflammation
Specific types of chronic inflammation Collection of macrophages (granuloma) Lymphocytes Giant cells Wall off substances Chrohn's, Sarcoidosis, TB
Features of acute inflammation
Celsus (AD 35) -rubor (red) -calor (hot) -tumor (swollen) -dolor (pain) Virchow (added loss of function)
Examples in oral cavity
Abscess Acute pupitis Lacerations Acute herpetic gingivostomatis Parotitis Reactions to piercings
Causes: infection due to
Bacteria (exotoxins and endotoxins, enzymes)
Viruses (intraceluular replication causing cell damage)
Parasites
Causes
Infection due to bacteria, viruses, parasites
Trauma
Physical and chemical agents
Tissue necrosis (death of part of tissue) - would happen after heart attack
Foreign bodies e.g. splinters, dirt, sutures
Immune reactions
Causes: tissue necrosis
Death of part of tissue
Usually occurs due to lack of blood supply e.g. heart attack
Vascular events
Vasoconstriction of arterioles
-affected area becomes white (local axon reflex)
Arteriolar, capillary and venule dilation
-affected area red and warm
-histamine, serotonin, nitric oxide, prostaglandins
> Vascular permeability
-swelling due to oedema
-histamine, C3a and C5a, leukotrienes
Vascular stasis
-loss of fluid slows blood flow
Normal vs inflamed capillary bed
Normal: nearer heart plasma proteins forced into tissues, osmotic pressure further away from heart allows plasma proteins to reenter blood supply
Inflammation: > vascular permeability (so gaps between endothelial cells) causing oedema (no osmotic pressure as chemicals induce many plasma proteins to move into tissues as exudate)
Role of oedema
Contains complement Opsonization (may contain antibodies which act as an 'opsonin' and aid phagocytosis Contains clotting cascade Contains kininogens Dilutes bacterial and other toxins
Once complement for oedema activated –>
C3a, C3b and C5a produced
Dilation & > vascular permeability (C3a)
Stimulate histamine release (C3a and C5a)
Promote formation of leukotrienes (attracts neutrophils) and prostaglandins (vasodilation)
Attract phagocytes (C3a and C5a)
Opsonization
Aids phagocytosis
Antibody binds to pathogen allowing Fc receptor on phagocyte to bind Fc region on antibody
C3b can also bind to pathogens and phagocytes have a C3b receptor with which to bind to this
C5-9: membrane attack complex (MAC) destroys micro-organisms
MAC forms transmembrane channels
-these disrupt phosoplipid bilayer = cell lysis and death
Membrane Attack Complex function
C5-9: membrane attack complex (MAC) destroys micro-organisms
MAC forms transmembrane channels
-these disrupt phosoplipid bilayer = cell lysis and death
Complement
- innate immunity (not adaptable)
- C1-C9 (found inactivated in plasma)
- classical pathway (anitbodies bound to antigen)
- alternative pathway (direct binding to pathogen)
Clotting cascade
Fibrin forms barrier to spread of infection (fibrinogen converted to fibrin by thrombin)
Thrombin and Hageman factor promote the inflammatory response
Kininogens
Converted to kinins by proteases (e.g. thrombin)
Bradykinin - similar effect to histamine
Vascular reponse takes hour long
Minutes
Vascular response followed by
Cellular response
- hours
- neutrophils followed by macrophages
- 5 main stages described
Cellular response stages
Margination Pavementation Emigration Aggregation Phagocytosis
Margination
Due to vascular stasis
Pavementation
Neutrophils adhere using adhesion molecules on vessel wall known as selectins
Neutrophils then bind more strongly using integrins on their cell surface to ICAM on endothial cells (promoted by IL-1, TNF alpha)
Emigration
Movement of neutrophils between endothelial cells via chemotaxis via chemotactic gradient (e.g. IL-8, C5a)
