Inflammation Flashcards
What at some stimulants of acute inflammation
Microorganism Trauma Ischeamic necrosis radiation Chemicals
What does acute inflammatory exudate contain
Blood components Fluid Neutrophils Fibrin Maybe macrophages and lymphocytes
What is the role of fluid in exudate
Dilutes toxins
Carries nutrients/mediators/antibodies
What is the role of fibrin in exudate
Induces migration- chemo taxis
What is the told of neutrophils in exudate
Phagocytise living tissue ( bacteria) and necrotic debris
What is the first step in exudate formation
Blood vessels near damage become dilated
Increased blood flow then slows
Turbulent flow-redness
Cellular contents in centre and plans and fluid at edges
What is the second step in exudate formation
Vessels become more permeable and endothelial cells swell and retract
Water/salts/protein leak into damaged area
What is the third step in exudate formation
Neutrophils marginate and emigrate,
Adhere to endothelial cells and migrate to damaged area under influence of chemotaxins
What types of exudate exist
Serous (pericardial sac)
Purulent (pus eg meninges)
Fibrinous (coagulates)
Fibrino-purulent
What is elevated ESR
Erythrocytes segmentation time, means increased viscosity
What are the possible outcomes from acute inflammation
Resolution
Abscess formation
Organisation and repair
Chronic inflammation
What processes lead to resolution
Damage neutralised/eliminated
Macrophages remove dead cells and exudate
Local cells re-grow
Tissue structure and function returns to normal
Give examples of resolution
Pneumonia
Tubular necrosis kidney
Sunburn
What are the processes that lead to abscess formation
Large accumulation of liquid purple my exudate in area of extensive necrosis due to tissue damage
especially caused by bacteria (necrotoxins)
Attempt to walk off and limit spread
What are stages of healing by repair
Vascular- macrophages and enzymes remove debris and new vessels grow and support cells (
Fibrovascular- fibroblasts proliferate and lay down collagen
Collagenous- mature collagen, granulation tissues mature to scar
Finally new capillaries regress
What does organisation always lead to
Scarring
When does chronic inflammation occur. What does it always result in
Damaging stimulus persists. scarring
What cell is the main effector of chronic inflammation
Macrophage activated by gamma interferon
What are the roles of a macrophage
Phagocytise
Secretory- mediators on inflammation, oxygen metabolites, professes and hydrolases
Cytokines (il-1 and tnf-a)
Growth factors
Why might a damaging stimuli persist
Gastric acid is repeatedly produced
Bacteria distance from neutrophils/antibiotics ( endocarditis)
Resistance to neutrophil phagocytosis
What are the two outcomes from stalemate between gastric mucosa damage and repair
Better- gastric acid neutralised or removed and damages stops - scar
Worse- increased gastric acid or repair impaired- ulcer perforation
What causes chronic inflammation
When damaging stimulus not eradicated
Stalemate between continuing damage and attempts to repairs by fibrous scar formation
What is granulomatous inflammation.
Chronic inflammation in which neutrophils are ineffective so macrophages invoked as part of early immune response
Aggregates of macrophages around damaging agent, associated with surrounding lymphocytes and fibroblasts= granuloma
What causes granulomatous inflammation
Low pathogenicity organisms which excite a type iv immune response Organic or inorganic foreign material Fungi Sarcoidosis Parasites
Give and example of granulomatous inflammation
Tuberculosis
Tuberuloculosis mycobacterium resistant to neutrophils
Type IV response- macrophages attracted by cytokines that T cells secrete
How can TB get worse
Necrosis expands and cannot be contained in granuloma, may spread via lymphatic system/ veins/ bronchi
What is first intention healing
Surgery, wound trauma minimised, edges closely appeared-minimal exudate
Collagenous scar by exudate and organisation
What is second intention healing
Extensive damage, infection
Healing characterised by increased necrotic debris/ granulation tissue
Wound contraction
What are the problems with acute inflammatory exudate
Causes symptoms- meningitis
Croup/diphtheria, pericarditis, pleurisy, peritonitis
What is the problem with scar formation
Skin- unslightly,
not elastic not contractile not secretory not absorptive
Name five factors that lead to inadequate healing
Continuing infection Foreign/uncleared necrotic material Ischaemia Diabetes Steroid therapy Denervation of area Irradiation previous
How does the brain parenchyma heal
Doesn’t contain fibroblasts so cannot make collagen
Necrosis= liquifactive
A strictures proliferate and lay down glial fibres to walk off area- cystic
Explain healing of a bone fracture
Defect filled with heamatoma Phagocytosis of debris Heamatoma undergoes organisation Vascular then fibrovascular granulation tissue Osteoprogenitor cells develop convert to osteoblasts Synthesis of osteiod collagen Calcified Woven bone links with old bone Active remodelling= strong lamellar bone
What at the aims of acute inflammation
Destroy/neutralise
Liquefy/remove dead tissue
Prepare for healing
