Acute Inflammation Flashcards
Define acute inflammation
Acute inflammation is the stereotyped immediate transient response of vascularised living tissue to injury
State the major causes of acute inflammation
Microbial infections - particular bacteria eg. Pyogenic organism (pus-forming) Hypersensitivity reactions Physical agents - heat, light, radiation Chemicals - drugs, toxins Tissue necrosis
Discuss the clinical signs of acute inflammation
Main clinical signs are rubor, tumour, calor, dolor and loss of function
Loss of function enforces rest and reduces the chance of further damage
State the 3 main steps of acute inflammation
Changes in blood flow
Exudation of fluid into tissue
Infiltration of inflammatory cells
Outline the changes in blood flow that occur in acute inflammation
Transient vasoconstriction of arterioles
Vasodilation of arterioles and then capillaries to increase blood flow (heat and redness)
Increase permeability of blood vessels leads to exudation of protein-rich fluid into tissues causes slowing of circulation (swelling)
Red blood cells concentrated in small vessels and increase viscosity of blood - stasis
Major mediator is histamine - causes vascular dilation, transient increase in vascular permeability and pain
Outline the processes of exudation of fluid into tissue
Starling’s law - fluid flow across vessel walls is determined by the balance of hydrostatic and colloid osmotic pressure comparing plasma and interstitial fluid
Increased hydrostatic pressure leads to increased fluid flow out of vessel
Increased colloid osmotic pressure of interstitium increase fluid flow out of vessel
Arteriolar dilation leads to increase in hydrostatic pressure (more flow to capillaries)
Increased permeability of vessel walls leads to loss of protein into interstitium
Vascular leaks leads to oedema - increases lymphatic drainage to tissue spaces
Oedema = excess of fluid in interstitium
Mechanisms of vascular leakage
Endothelial contraction - gaps due to histamine, leukotriennes
Cytoskeletal reorganisation - gaps
Direct injury - toxic burns, chemicals
Leukocyte dependent injury
Increased transcytosis - channels across endothelial cytoplasm
Transcytosis - fluid travels across non-leaky membrane
Fibrin - causes mesh work to localise inflammation
Important in aerosol surface, pleural and peritoneum cavity to prevent loss of BV
State the difference between transudate and exudate
Transudate - fluid loss due to hydrostatic pressure imbalance - fluid lower protein content
Eg. Cardiac failure, or venous outflow obstruction
Exudate - fluid loss due to inflammation - fluid higher protein content
Whats the primary inflammatory cell in acute inflammation
Neutrophils
Explain the process that neutrophils enter tissue
Margination - stasis causes neutrophils to line up at the edge of blood vessels along the endothelium
Rolling - neutrophils then roll along endothelium, sticking to it intermittently
Adhesion - then stick more avidly
Surface receptors of epithelial cells change to mediate adhesion
Relaxation of inter-endothelial cell junctions
Digestion of vascular basement membrane
Emigration - neutrophils emigrate through blood vessel wall
Usually laminar flow, in inflammation, they flow at the edge
Neutrophils move through diapedesis and emigration through chemotaxis
Chemotaxis - movement along concentration gradient of chemoattractants
Attract to inflammation locations - go to where chemicals are highest
Diapedesis - passage of blood cells through the intact walls of the capillaries
What do neutrophils do at tissue sites
Neutrophils undertake phagocytosis
Contact, recognition, internalisation
Opsonins - coated with immunoglobulin components to allow them to be recognised
Cytoskeletal changes
Phagosomes fuse with lysosomes to produce secondary lysosomes
Killing mechanisms - activated neutrophils may release toxin metabolites and enzymes causing damage to host tissue
Oxygen dependent systems very effective in killing bacteria
Produces superoxide and hydrogen peroxide
Oxygen independent uses lysosomes and hydrolases
Discuss how acute inflammation clinical signs relate to the tissue changes
Vasodilation of arterioles and then capillaries to increase blood flow (heat and redness)
Increase permeability of blood vessels leads to exudation of protein-rich fluid into tissues causes slowing of circulation (swelling)
Red blood cells concentrated in small vessels and increase viscosity of blood - stasis
Major mediator is histamine - causes vascular dilation, transient increase in vascular permeability and pain
Discuss why tissue changes constitute an effective response to injury in acute inflammation
Exudation of fluid
Delivers plasma proteins to area of injury- immunoglobulins, inflammatory mediators, fibrinogen
Dilutes toxins
Increases lymphatic drainage - delivers microorganisms to phagocytes and antigens to immune system
Infiltration of cells - removes pathogenic organisms, necrotic debris
Vasodilation - increases delivery, increases temperature
Pain and loss of function - enforces rest, reduces change of further traumatic damage
Discuss some important chemical mediators in acute inflammation
Increased blood flow - histamine, prostaglandins
Increase vascular permeability - histamine, leukotrienes, bradykinin
Neutrophil chemotaxis - C3a, C5a, bacterial peptides
Phagocytosis (opsonization) - C3b
Discuss local complications of acute inflammation
Swelling - blockage of tubes eg. Bile duct, intestine
Exudate - compression, serositis (inflammation of serous membrane)
Loss of fluid - burns
Pain and loss of function - especially if prolonged
Discuss some systemic complication of acute inflammation
Fever - endogenous pyrogens produced
Prostaglandins - aspirin inhibits it and reduces fever
Leukocytosis
IL-1 and TNFα produce an accelerated release form marrow
Macrophages, T lymphocytes produce colony stimulating factors
Bacterial infections - neutrophils, viral - lymphocytes
Acutely phase response - decrease appetite, raised pulse rate, altered sleep patterns and change sin plasma concentrations of acute phase proteins
Acute phase proteins
C reactive protein marker for inflammation
α1 - antitrypsin
Haptoglobin
Fibrinogen
Serum amyloid A protein
Shock - clinical syndrome of circulatory failure
Abscess - localisation of permanent inflammation
