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Inflammation 1

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Designed for UG pathology teaching.

Designed for UG pathology teaching.


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  • Background shows flame. I have chosen this because of its similarities to inflammation in the tissues. Flame is red (Rubor), Hot (Calor), Burns (Pain)=Dolor and it’s a life giver (light) and it can destroy life too.
  • Look at the clinical examples and settings where you will come across inflammation in your practice.
  • Photo: A coastal town, devastated by super Typhoon Haiyan, in Samar province in central Philippines on November 11, 2013. (Reuters: Erik De Castro )
    Arial food drop as this area was inaccessible because of destroyed road system.
    I give this example to stress the need of connectivity to reach and deliver the goods (in inflammation vessels are equated with roads, without vessels it is impossible to connect the tissue in a Multicellular organism like humans)
  • Connectivity is needed to maintain integrity and health of the country.
    Here the railway network is equated with vessels in our body.
  • This is fundamentally a protective response, designed to rid the organism of both the initial cause of cell injury (e.g., microbes, toxins) and the consequences of such injury (e.g., necrotic cells and tissues). Without inflammation infections would go unchecked, wounds would never heal, and injured tissues might remain permanent festering sores.
  • This is fundamentally a protective response, designed to rid the organism of both the initial cause of cell injury (e.g., microbes, toxins) and the consequences of such injury (e.g., necrotic cells and tissues). Without inflammation infections would go unchecked, wounds would never heal, and injured tissues might remain permanent festering sores.
  • Inflammation is a complex reaction in tissues that consists mainly of responses of blood vessels and leukocytes.
  • Inflammation is a complex reaction in tissues that consists mainly of responses of blood vessels and leukocytes.
  • The vascular and cellular reactions of inflammation are triggered by soluble factors that are produced by various cells or derived from plasma proteins and are generated or activated in response to the inflammatory stimulus. Microbes, necrotic cells (whatever the cause of cell death) and even hypoxia can trigger the elaboration of inflammatory mediators, and thus elicit inflammation. Such mediators initiate and amplify the inflammatory response and determine its pattern, severity, and clinical and pathologic manifestations.
  • Cellulits = acute skin infection commonly caused by Streptococcus pyogenes or Staphylococcus aureus.
  • Exposure to too much sunlight with the eyes covered.
  • Eosinophils
    However, in some circumstances eosinophils rather than neutrophils predominate in acute inflammation. This tends to occur with parasitic worms, against which neutrophils have little success, or with a response involving the antibody IgE. Eosinophils release several proteins, such as major basic protein, which are often effective against parasites. Eosinophils also release several regulatory molecules that increase endothelial permeability. Note that eosinophils are also linked to certain types of allergies.
  • Transcript

    • 1. Inflammation and Repair -1 Dr.CSBR.Prasad, M.D. V4-Nov,2013
    • 2. What is this about? Clinical Examples V4-Nov,2013
    • 3. V4-Nov,2013
    • 4. V4-Nov,2013
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    • 6. V4-Nov,2013
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    • 11. V4-Nov,2013
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    • 15. V4-Nov,2013
    • 16. V4-Nov,2013
    • 17. In Gist: Inflammed areas are: Red Swollen & Malfunction V4-Nov,2013
    • 18. V4-Nov,2013
    • 19. V4-Nov,2013
    • 20. Essential to the survival of organisms is their ability to get rid of damaged or necrotic tissues and foreign invaders, such as microbes V4-Nov,2013
    • 21. Unicellular organisms Simple mechanisms • Diffusion • Phagocytosis Mammals Complex systems • Respiratory / CVS • Hemopoietic sys • GIT • Immune system V4-Nov,2013
    • 22. Essential to the survival of organisms is 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 V4-Nov,2013
    • 23. Inflammation This is fundamentally a protective response Without inflammation • Infections would go unchecked • Wounds would never heal V4-Nov,2013
    • 24. Inflammation In clinical practice: we see sometimes….. Inappropriately triggered or Poorly controlled inflammation Causing tissue injury !!!!!! Eg: Autoimmune diseases, type-2 DM, AS V4-Nov,2013
    • 25. Inflammation Inflammation is a complex reaction involving 1. Blood vessels 2. Plasma components & 3. Leukocytes V4-Nov,2013
    • 26. V4-Nov,2013
    • 27. Inflammation Inflammation is a complex reaction involving 1. Blood vessels 2. Plasma proteins & 3. Leukocytes Changes in these structures / factors are brought about by inflammatory stimulus V4-Nov,2013
    • 28. Inflammation Inflammatory stimuli: Microbes Necrotic cells Hypoxia Physical injury V4-Nov,2013
    • 29. Acute inflammatory reactions are triggered by a variety of stimuli: • Infections (bacterial, viral, parasitic) and microbial toxins • Trauma (blunt and penetrating) • Physical and chemical agents (thermal injury, e.g., burns or frostbite; irradiation; some environmental chemicals) • Tissue necrosis (from any cause) • Foreign bodies (splinters, dirt, sutures) • Immune reactions (hypersensitivity reactions) V4-Nov,2013
    • 30. Inflammation Can be: Acute (a few hours to days) Chronic (days to months / years) V4-Nov,2013
    • 31. Inflammation Acute inflammation • Rapid in onset • Short duration • Exudation of fluid and plasma proteins (edema) • Infiltrated by neutrophils • When acute inflammation is successful in eliminating the offenders the reaction subsides, but if the response fails to clear the invaders it can progress to a chronic phase Chronic inflammation • Follow acute inflammation • Insidious in onset • Longer duration • Infiltrated by lymphocytes and macrophages • Proliferation of blood vessels, fibrosis, and • Tissue destruction V4-Nov,2013
    • 32. Inflammation Inflammation is terminated when the offending agent is eliminated V4-Nov,2013
    • 33. The NOMENCLATURE used to describe inflammation in different tissues employs: 1-the tissue name & 2-the suffix “-itis” Tissue suffix Inflammed tissue Pancreas itis Pancreatitis Meninges Pericardium Joint itis itis itis Meningitis Pericarditis Arthritis V4-Nov,2013
    • 34. “4+1” Cardinal signs of (acute) inflammation • • • • Rubor = Redness Tumor = Swelling Calor = Heat Dolor = Pain (described by Celsus 1st. Century AD) • Functio laesa = Loss of function (added by R. Virchow) V4-Nov,2013
    • 35. Rubor Tumor V4-Nov,2013
    • 36. Rubor Tumor Functio laesa V4-Nov,2013
    • 37. Rubor Tumor Functio laesa V4-Nov,2013
    • 38. V4-Nov,2013 Tumor Functio laesa
    • 39. Vessels make inflammation a reality without vascularity there is no inflammation V4-Nov,2013
    • 40. Vascular events in acute inflammation Changes in: Caliber of the vessel Porosity / permeability of vessels V4-Nov,2013
    • 41. Acute inflammation involves: Alteration of vascular caliber following very brief vasoconstriction (seconds), vasodilation leads to increased blood flow and blood pooling creating redness and warmth (rubor and calor) Changes of microvasculature increased permeability for plasma proteins and cells creating swelling (tumor). Fluid loss leads to concentration of red blood cells and slowed blood flow (stasis) Emigration of leukocytes from microcirculation due to stasis and activation leads migration towards offending agent V4-Nov,2013
    • 42. EXUDATION: Vascular changes and fluid leakage during acute inflammation lead to Edema in a process called Exudation Transudate •Result of hydrostatic or osmotic imbalance •Ultrafiltrate of plasma •Low protein content •Specific gravity < 1.015 Exudate •Result of inflammation •Vascular permeability •High protein content •Rich in cells •Specific gravity >1.020 V4-Nov,2013
    • 43. Increased vascular permeability and edema: a hallmark of acute inflammation • Leakage is restricted to venules of 20-60µm in diameter • caused by endothelial gaps • usually an immediate and transient response (30 min.) • Gaps occur due to contraction of e.g myosin and shortening of the individual endothelial cell • loss of protein from plasma leads to edema • due to reduced osmotic pressure in the vasculature • and increased osmotic pressure in the interstitium V4-Nov,2013
    • 44. • Direct endothelial injury causing necrotic cell death will result in leakage from all levels of microcirculation (venules, capillaries and arterioles) • This reaction is immediate and sustained • Delayed prolonged leakage begins after 2-12 hours and can last several days due to thermal, x-ray or ultraviolet radiation (sunburn) and involves venules and capillaries • Leakage from new blood vessels during tissue repair (angiogenesis) due to immature endothelial layer All these described mechanisms may occur in one wound (e.g burns) and can be life threatening V4-Nov,2013
    • 45. Inflammation – Components in the DEFINITION • Response to tissue injury • • • • chemical agents cold, heat trauma invasion of microbes • by the vascularized tissue • Serves to destroy, dilute or wall off the injurious agent • Protective response • Induces repair • Can be potentially harmful V4-Nov,2013
    • 46. Inflammation – DEFINITION Can be defined as Response to tissue injury by the vascularized tissue, which Serves to destroy, dilute or wall off the injurious agent. It is a Protective response and Can be potentially harmful. V4-Nov,2013
    • 47. Guess, what is the problem with this person? V4-Nov,2013
    • 48. Important points V4-Nov,2013
    • 49. What are the cardinal signs of inflammation? • • • • Rubor Tumor Calor Dolor = redness = swelling = heat = pain • (described by Celsus 1st. Century AD) • Functio laesa = loss of function – (added by R. Virchow) V4-Nov,2013
    • 50. Which sign was introduced by Virchow? • Functio laesa = loss of function V4-Nov,2013
    • 51. Which is the fifth sign of inflammation? • Functio laesa = loss of function V4-Nov,2013
    • 52. Factors that control the fluid balance between the intravascular and extravascular compartments • OP and HP V4-Nov,2013
    • 53. What happens to total white count in acute inflammation? • Usually elevated V4-Nov,2013
    • 54. Name THREE elements which make the inflammation possible? 1. Vessels 2. Plasma components a) Immunoglobulins b) Complement components 3. Leucocytes V4-Nov,2013
    • 55. Name THREE differences between Necrosis and Apoptosis? In Apoptosis: • Structures are membrane bound • Changes occur before death [Until the last moment the cell is alive] • Absence of inflammation • ATP dependent process V4-Nov,2013
    • 56. What makes inflammation a reality? Blood vessels V4-Nov,2013
    • 57. Why we need inflammation? • To remove infectious / injurious agents • To remove dead tissue form the body • It’s protective. V4-Nov,2013
    • 58. Name some instances where inflammation is damaging? • Laryngitis • Inflammation of the 4th ventricular area • Encephalitis / Meningitis V4-Nov,2013
    • 59. Name the acute inflammatory cells? • Pyogenic infections – Neutrophil • Allergic inflammation – Eosinophil • Viral infections – Lymphocyte V4-Nov,2013
    • 60. Name the chronic inflammatory cells? • Lymphocytes • Macrophages • Plasma cells V4-Nov,2013
    • 61. How do you differentiate acute from chronic inflammation? • Onset / duration • Type of inflammatory cells V4-Nov,2013
    • 62. END V4-Nov,2013
    • 63. www.slideshare.net Search for csbrprasad V4-Nov,2013
    • 64. V4-Nov,2013