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Inflammation overview


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Inflammation overview

  1. 1. ByDr Mohammad ManzoorMashwani
  2. 2.  What is inflammation? Causes Signs Types Components Functions of inflammation Overview of inflammation Specific host defences Summary 2
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  4. 4.  “Inflame” means to “set a fire” It is a dynamic response of vascularized tissue to injury. Fundamentally a protective response. To rid the organism of both the initial cause of cell injury like microbes and toxins and the consequences of such injury e.g necrotic cells and tissues. The survival of organisms depends on their ability to get rid of damaged or necrotic tissues and foreign invaders, such as microbes. The host response that accomplishes these goals is called inflammation. 4
  5. 5.  Inflammation to a specific tissue is denoted by the suffix " ITIS ", following the name of the tissue: Example: Appendicitis, cholecystitis, pulpitis and gingivitis. Pneumonia .
  6. 6.  If no inflammation Infections go unchecked Wounds would never heal Injured tissues might remain permanent sores. In the practice of medicine the importance of inflammation is that it can sometimes be inappropriately triggered or poorly controlled, and is thus the cause of tissue injury in many disorders. 6
  7. 7. a. Infections (viral,bacteral,parasitic)b. Trauma (blunt, penetrating)c. Physical & chemical agentsd. Tissue necrosise. Foreign bodies (dirt, sutures)f. Immune reactions (hypersensitivity reactions) 7
  8. 8. Four cardinal signs1. Callor (heat)2. Rubor (Redness)3. Tumor (Swelling)4. Dolor (Pain)May also obser ve:5. Loss of function 8
  9. 9. Cardinal Signs of Inflammation Calor Rubor Tumor Dolor Loss of Function first described by Celsus more than 2000 years ago.
  10. 10.  Chronological  Morphological pattern pattern1. Acute inflammation 1. Serous inflammation2. Chronic inflammation 2. Suppurative inflammation 3. Fibrinous inflammation 4. Ulcer 10
  11. 11. Time view 1. acute (days) 2. subacute (weeks) 3. chronic (months-years)
  12. 12. 1. Connective tissue cells2. Connective tissue matrix3. Vessels4. Soluble proteins 12
  13. 13. 1. Destroy and remove pathogens.2. If destruction is not possible, to limit effects by confining the pathogen and its products.3. Repair and replace tissue damaged by pathogen and its products. 13
  14. 14.  Inflammation is a complex reaction of responses of blood vessels and leukocytes. Principal defenders are:1. Plasma proteins2. Leukocytes &3. Tissue phagocytes derived from circulation. Being in blood they can home any site where they may be needed. As invaders such as microbes and necrotic cells are typically present in tissues, outside the circulation, it follows that the circulating cells and proteins have to be rapidly recruited to these extravascular sites. The inflammatory response coordinates to achieve this goal. 14
  15. 15.  Inflammator y response repair It destroys, dilutes, and walls of f the injurious agent, series of events that tr y to heal the damaged tissue. Repair begins during inflammation but reaches completion usually af ter the injurious influence has been neutralized. In the process of repair the injured tissue is replaced through regeneration of native parenchymal cells, by filling of the defect with fibrous tissue (scarring) or, most commonly, by a combination of 15
  16. 16.  Inflammation may be harmful in some situations. When inappropriately directed against self tissues or is not adequately controlled, it becomes the cause of injury and disease. Inflammatory reactions underlie common chronic diseases, such as rheumatoid arthritis, atherosclerosis, and lung fibrosis, as well as life-threatening hypersensitivity reactions to insect bites, drugs, and toxins. Anti-inflammatory drugs, control the harmful sequelae of inflammation yet not interfere with its beneficial effects. Inflammation may contribute to a variety of diseases that are not thought to be primarily due to abnormal host responses. 16
  17. 17. HostDefenses 17
  18. 18. IntroductionResistance: Ability to ward off (prevent) disease. 1. Nonspecific Resistance: Defenses that protect against all pathogens. 2. Specific Resistance: Protection against specific pathogens.Susceptibility: Vulnerability or lack of resistance. 18
  19. 19. 1. Mechanical Defenses2. Chemical Defenses3. Cellular elements of blood 19
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  21. 21. I.Mechanical DefensesSkin and Mucous MembranesA. Skin LayersEpidermis: Thin outer epithelial layer. Contains Langerhans cells, dead cells, and keratin.Dermis: Thick inner layer of connective tissue.Infections are rare in intact skin. Exceptions……. 21
  22. 22.  B. Mucous Membranes:Lining of gastrointestinal, genitourinary, andrespiratory tracts. Epithelial layer secretes mucus which maintains moist surfaces. Although they inhibit microbial entry, they offer less protection than skin. Several microorganisms are capable of penetrating mucous membranes:  Papilloma-virus  Treponema pallidum  Enteroinvasive E. coli  Entamoeba histolytica 22
  23. 23.  Lacrimal apparatus: Continual washing and blinking prevents microbes from settling on the eye surface. Saliva: Washes microbes from teeth and mouth mucous membranes. Mucus: Thick secretion that traps many microbes. Nose Hair: Coated with mucus, filter dust, pollen, and microbes. Ciliar y Escalator: Cilia on mucous membranes of lower respiratory tract move upwards towards throat at 1-3 cm/hour. Coughing and sneezing: Expel foreign objects. 23
  24. 24. II.Chemical Defenses:  Sebum: Oily substance produced by sebaceous glands that forms a protective layer over skin. Contains unsaturated fatty acids which inhibit growth of certain pathogenic bacteria and fungi.  pH: Low, skin pH usually between 3 and 5. Caused by lactic acid and fatty acids.  Perspiration: Produced by sweat glands. Contains lysozyme and acids.  Lysozyme: Enzyme that breaks down gram- positive cell walls. Found in nasal secretions, saliva, and tears. 24
  25. 25.  Gastric Juice: Mixture of hydrochloric acid, enzymes, and mucus. pH between 1.2 to 3 kills many microbes and destroys most toxins. Many enteric bacteria are protected by food particles.  Helicobacter pylori neutralizes stomach acid and can grow in the stomach, causing gastritis and ulcers. Transferrins: Iron-binding proteins in blood which inhibit bacterial growth by reducing available iron. 25
  26. 26. Cell Type # Cells/mm 3 FunctionErythrocytes (RBC) 4.8-5.4 million Transport O2 and CO2Leukocytes (WBC 5000-11000 Various A. Granulocytes: 1. Neutrophils Phagocytosis 2. Basophils Produce histamine 3. Eosinophils Toxins against parasites some phagocytosis B. Monocytes/Macrophages Phagocytosis C. Lymphocytes Antibody production (B cells) Cell mediated immunity (T cells)Platelets 300,000 Blood clotting 26
  27. 27. II. Second Line of Defense1. Phagocytosis: Derived from the Greek words “Eat - cell”. Phagocytosis is carried out by white blood cells: macrophages, neutrophils, and occasionally eosinophils. Neutrophils predominate early in infection. Wandering macrophages: Originate from monocytes that leave blood and enter infected tissue, and develop into phagocytic cells. Fixed Macrophages (Histiocytes): Located in liver, nervous system, lungs, lymph nodes, bone marrow, and several other tissues. 27
  28. 28. Stages of Phagocytosis1. Chemotaxis: Phagocytes are chemically attracted to site of infection.2. Adherence: Phagocyte plasma membrane attaches to surface of pathogen or foreign material.  Adherence can be inhibited by capsules (S. pneumoniae) or M protein (S. pyogenes).  Opsonization: Coating process with opsonins that facilitates attachment.  Opsonins include antibodies and complement proteins. 28
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  30. 30. Stages ofPhagocytosis3. Ingestion: Plasma membrane of phagocytes extends projections (pseudopods) which engulf the microbe. Microbe is enclosed in a sac called phagosome.4. Digestion: Inside the cell, phagosome fuses with lysosome to form a phagolysosome. Lysosomal enzymes kill most bacteria within minutes and include:  Lysozyme: Destroys cell wall peptidoglycan  Lipases and Proteases  RNAses and DNAses After digestion, residual body with undigestable 30
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