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Inflammation and Cell Damage

Inflammation and Cell Damage. Peer Support 2014 Michael Iveson and Emily Hodgson. Give three advantages to inflammation?. dilution of toxins entry of antibodies fibrin formation nutrients and oxygen deliver neutrophils stimulation of the immune response entry of drugs.

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Inflammation and Cell Damage

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  1. Inflammation and Cell Damage Peer Support 2014 Michael Iveson and Emily Hodgson

  2. Give three advantages to inflammation? • dilution of toxins • entry of antibodies • fibrin formation • nutrients and oxygen • deliver neutrophils • stimulation of the immune response • entry of drugs

  3. Give two problems caused by inflammation? • destruction of normal tissue • swelling • blockage of tubes • loss of fluid • pain • inappropriate inflammation

  4. What are the FOUR cardinal signs of acute inflammation? • Rubor • Tumor • Calor • Dolor • (FunctioLaesa)

  5. What immune cell is key in acute inflammation? • Neutrophils

  6. What are the stages of neutrophil recruitment? (IN ORDER) • 1. Margination • 2. Adhesion • 3. Emigration • 4. Chemotaxis

  7. What are the vascular changes in acute inflammation? • Arteriole and capillaries dilate • Opening of new capillary beds • Increased blood flow • Red cell stasis • Endothelial cells swell and partially retract – more permeable

  8. What is exudate? • Inflammatory fluid which has high protein concentration

  9. Give the three types of exudate? • Fibrinous – large amounts of fibrinogen • Purulent – pyogenic bacterial infections • Transudate – lower protein content

  10. How do neutrophils move through the endothelial wall? • Inflammatory mediators increase expression of p-selectin on the endothelial walls • Neutrophil attaches to p-selectin • Pseudopodia push through the endothelial gaps and digest the basement membranes with proteolytic enzymes • Cells enter extravascular space

  11. Give three systemic signs and symptomsof acute inflammation. • Fever • Leukocytosis • Malaise • Nausea • Anorexia • Lymphoid hyperplasia • CRP, ESR raised

  12. Give three mediators of acute inflammation • Histamine • Prostaglandins • Leucotrienes • NO • PAF • Cytokines • Complement

  13. Give three outcomes of acute inflammation • Resolution • Suppuration • Organisation and repair • Calcification • Continued acute/ chronic inflammation • Septicemia • Death

  14. What are the three key features of chronic inflammation? • Ongoing inflammation • Ongoing tissue destruction • Ongoing attempts at tissue repair

  15. Give two cell types involved in chronic inflammation • Macrophages • Lymphocytes • Plasma cells • Eosinophils

  16. What do macrophages produce? • Proteases • Hydrolytic enzymes • Reactive O2 species • GF • Cytokines

  17. Give three possible outcomes of chronic inflammation • Continued chronic inflammation • Change in tissue function • Atrophy • Metaplasia (= change in cell type) • Resolution • Damaging stimulus removed, healing can occur • Scarring with dysfunction • Cirrhosis in viral hepatitis • Catastrophe • Damaging stimulus increases / tissue healing response weaken > tissue insult worsens • E.g. Perforated gastric ulcer

  18. What is granulomatous inflammation? • A subtype of chronic inflammation • Occurs when neutrophil phagocytosis is inadequate to control causative agent • Characterised by granulomas = collections of macrophages

  19. What cells are present in a granuloma?

  20. Make sure you know… • Phagocytosis • Types of necrosis • Differences between apoptosis and necrosis • Granulomatous inflammation/granuloma is different to granular tissue

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