Stage 2 - Inflammation

• Definition of Inflammation

  prep for repair phase = approx 3-5 days

  the response of living tissues to cellular injury

  involves innate + adaptive immune mechanisms

  process takes approx 6 weeks to recover

  the inflammatory respone to injury is the same regardless of the nature of injury, agent or the location of the injury itself
• Factors Leading to Acute Inflammation

  healing

  infection by pathogens

  excessive cooling + heating (thermal damage)

  irritant + corrosive damage (chem damage)

  immune reactions

  tissue necrosis
• Chronic Inflammation

  mechanisms originally designed to protect us can do considerable damage

  inflammatory response lasting more than a ear as a result of overuse

  sometimes really severe attacks of acute - those occuring in gall bladder, large intestine/kidney

  some inflammatory responses r not so obv w no reddening, pain + heat - chronic bronchitis

  a perm increase in secretion of viscid mucus w more + larger mucus glands

  prolonged over stimulation causes clogging of airways, lung function eventually irretrievably damaged
• Factors Leading to Chronic Inflammation

  micro-organisms resistant to phagocytosis - TB

  autoimmune disease - hypersensitivity reactions

  granulomatous diseases - Crohn's disease = inflammatory disease of GI tract

  foreign bodies - endogenous (bone, adipose tissue, uric acid crystals)

  exogenous (silica, suture material, implanted prosthesis)
• Infection

  the body has a symbiotic relatonship w many of it microbial flora

  infection is caused by a change in this pop, a deficiency in mechanisms that control their presence of a new pathogen/foreign particles
• Agents of Infection

  viruses - v small, cause many diseases from smallpox to the common cols, multiply w in cells of the host, can also live for long periods outside cells in a resting form

  bacteria - highly organised organisms, increase outside of cells by binary fission, survive in varying in enviro conditions
• Pathological Processes of Infection

  unknown pathogen is carried by intestitial fluid into the lymph vessels + then nodes or arrive via natural opening

  immune system is triggered to make antibodies to kill antigens on the surface of the virus, fungi + bacteria

  pathogen is immobilised

  macrophages + antibodies engulf + digest it
• Spread of Infection

  virulence - breakdown of norm flora pop control can allow a more virulent strain to spread

  droplet infection - coughing + sneezing

  shedding skin

  enviro - soil, contact w diseased humans/animals

  lack of initial physical defence - skin (wounds + surgery)
• Hospital Acquired Infections

  staphylococcus aureus can spread from the nose to a surgical wound

  MRSA - Methicillin Resistant Staphylococcus Aureus can be fatal in ppl w a lowered resistance to infection, those w long-term ill-health, following surgery, injuries, catheters..

  problems of cross infections
• Clinical Features of Infection

  local - pain, temp, redness, pus, swelling, boils

  systemic - flu-like symptoms = weakness + aching joints
• Treatment Principles for Infection

  immunity will deal w minor infections

  severe infections will need antiviral + antibacterial treatment

  surgical drainage of localised infection
• Pathological Processes of Inflammation

  mobilisation of body's defences

  contain + destroy pathogens

  tissue clean up + repair
• Mobilisation of Body Defences

  rapid delivery of cells + chems needed to combat pathogens, repair damaged tissue + to wash away toxins + metabolic waste

  = helped by elevated blood flow (hyperaemia)
• Containing & Destroying Pathogens - Role of Fibrinogen

  fibrinogen = plasma protein that filters into the tissue fluid + clots in areas adjacent to the injury, forming a sticky mesh that walls off bacteria + other microbes
• Containing & Destroying Pathogens - Role of Heparin

  prevents clotting in the area of injury

  this causes pathogens to be trapeed in a fluid pocket surrounded by a gelatinous capsule of clotted fluid

  they r attacked by antibodies, phagocytes ..., whilst the surrounding areas of clotted tissue prevent them from escaping
• Containing & Destroying Pathogens - Neutorphils

  rapidly increases in inflamed tissue w in 1hr of injury

  they emigrate from the blood stream

  chemotaxis (movement of a cell along a chem conc grad) enables the neutrophils to become attracted to chms rleased by pathogens of inflamed tissues

  as they encounter bacteria, neutrophils phagocytise, digest + destroy
• Tissue Clean-up & Repair

  monocytes arrive w in 8-12 hrs of an injury + turn into macrophages which engulf + destroy bacteria, damaged host cells + dying neutorphils

  they also act ass antigen-presenting cells (APCs) which activate immune responses
• Immune Response - Pus Formation

  neutrophils + macrophages die

  pus forms from dead cells, other tissue debris + tissue fluid

  pus = yellowish fluid + accumulates in a tissue cavity = abscess

  sometimes pus is absorbed but sometimes forms a blister between the epidermis + dermis + is release when ruptured
• Immune Response - Platelet-Derived Growth Factor

  cytokines r secreted by blood platelets + endothelial cells

  it stimulates fibroblasts to multiply + synthesise collagen
• Immune Response - Hyperaemia

  hyperaemia = elevated blood flow

  delivers more oxygen, ions (clotting factors) + immune blood cells
• Benefits of Inflammation

  prevents spread of damaging cells

  removes cell debris + pathogens

  helps w tissue repair