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)