Lecture 6 - inflammation Flashcards
What is acute inflammation
Eliminating injured tissue & infectious agents and repairing tissue damage
What causes redness in acute inflammation
vasodilation - caused by histamine and prostaglandin
What causes swelling in acute inflammation
Increased vascular permeability - caused by histamine and leukotrienes
What causes heat in acute inflammation
Vasodilation - caused by histamine and prostaglandin
What causes pain in acute inflammation
Tissue damage - caused by prostaglandin and bradykinin
What causes loss of function in acute inflammation
Tissue damage - caused by ROS, NO, lysosomal enzymes
Describe purulent (suppurative) pattern of inflammation
Pus production (neutrophils)
Pyogenic organisms (tissue necrosis and liquefaction)
Abscess localised collection of pus
Describe serous pattern of inflammation
Fluid-rich, cell-poor exudate (peritoneum, pleura, pericardium)
Describe fibrinous pattern of inflammation
Fibrinogen-rich exudate and fibrin deposition (pericardium, peritoneum)
What are the steps in acute inflammation
Recognition (PRR, vascular changes)
Recruitment (leukocytes)
Removal (killing and degradation - ROS/NO, phagocytosis)
Resolution (‘turning off’)
Describe macrophages roles in recognition
In tissue - phagocytic and produce pro-inflammatory cytokines - damage/pathogen response (IL1-Beta and TNF-alpha)
Describe mast cells roles in recognition
tissue resident - numerous granules (chemical mediators - histamine, leukotrienes and prostaglandin) - mediates vascular changes, pain
Mast cells survive degranulation
Describe Pattern Recognition Receptors in recognition
DAMPs -> proinflammatory cytokines (TNF-alpha, IL-1-beta)
PAMPs -> chemical mediators
How is recognition measured
Increased temp
acute phase proteins
Increased neutrophils in blood
Describe neutrophils role in recruitment
Large granular cells - recruited into tissue in response to proinflammatory cytokines -> phagocytic (40-70% of WBC)
Describe monocytes role in recruitment
Produce pro-inflammatory cytokines (2-10% of peripheral blood)
What is involved in removal
Reactive oxygen species (ROS), Nitric Oxide (NO)
Complement pathways (Classical, lectin and alternate) - mediates opsonisation and agglutination
Lysis - MAC (release of contents)
Inflammation - increased adhesion to endothelium
What is opsonisation and agglutination
Opsonisation - complement binds to microbes
Agglutination - microbes stuck together by complement
Describe chemical mediators role in resolution
Short 1/2 life - destroyed by degradative enzymes
Describe neutrophils role in resolution
Short lifespan in blood - die and are phagocytosed
Describe activated macrophages role in resolution
Secretes IL-10 that down regulates macrophage response
What is osteomyelitis
Inflammation of the bone
What are the phases of osteomyelitis
Neutrophils attracted to site
Spread to periosteum
subperiosteal abscess - impaired blood supply -> necrosis
Dead bone -> released into sinus tract
What are the features of chronic inflammation
Inflammatory cell infiltrate
Tissue destruction
Connective tissue deposition
What WBC are involved in chronic inflammation
B cell -> antibody secretion - trigger inflammation
Mast cell accumulate - secrete vasoactive and pro-inflammatory mediators
eosinophils contribute to initiation and modulation of inflammation
What makes up a granulomatous inflammation
Necrotic centre (if pathogen)
Surrounded by macrophages and epithelioid cells
Surrounded by lymphocytes
Epithelioid cells fuse to form large giant cells (types of macrophages)
What are granulomatous inflammation
Attempt to contain offending agent
What conditions are associated with granulomatous inflammation
Infectious diseases (TB, leprosy, brucellosis, syphilis, mycotic infections)
Autoimmunity/inflammation (sarcoidosis, Crohn’s disease)
