1. Inflammation

2. Learning Objectives: 1.Describe the definition and classification of Inflammation. 2.Know the causes of inflammation 3.Understand the process of inflammations 4.Comprehend the etiopathogeneses of granulomatous inflammations 5.Contrast the differences between acute and chronic inflammations

3. Inflammation Inflammation: Local defense and protective response against cell injury or irritation or Local vascular and cellular reaction, against an irritant. Irritating or injurious agents (Irritant) Living: Bacteria, Fungi, Virus, Parasite or their toxins Non-Living: Chemical Physical Mechanical Inflammation is designated by adding the suffix (itis) to the end of the name of the inflamed organ or tissue.

4. 1. Acute inflammation Microscopic signs:  Inflammatory response Macroscopic signs: classical 5 cardinal symptoms 1. heat 2. redness 3. swelling 4. pain & Tenderness 5. loss (or impairment) of function 1. Local vascular change 2. Formation of inflammatory exudate

5. Inflammatory response: (microscopic signs) Normal Inflammation First: Local vascular changes: 1. Initial temporary vasoconstriction for few seconds. 2. Active vasodilatation of arterioles and capillaries (by chemical mediators: Histamine) and passive dilatation of venules. Increase in capillary permeability (fluid exudate to the extravascular tissue) thus concentration of blood cells, slowing of blood flow (stasis) 3. Pavmentation: the margination of leukocytes.

7. Second: Formation of inflammatory exudates: Immigration or infiltration of the various leukocytes, fluid and plasma proteins outside the blood vessels into the surrounding tissue without injury of the blood vessels. Leukocytes seem to leave the smallest blood vessels due to the increased capillary permeability caused by the high osmotic pressure of the surroundings. The early stages are marked by the predominance of polymorphs especially neutrophils migration, particularly when the inflammation is caused by pyogenic cocci, later on monocytes infiltration occurs.

9. Function of inflammatory exudates 1- Dilute the invading microorganism and its toxins. 2-Bring antibodies through the plasma to the inflamed area. 3-Bring leukocytes that engulf the invading microorganisms. 4-Bring fibrinogen through the plasma, which is converted, to fibrin mesh, helping in trapping the microorganism and localize the infection.

10. Blood stem cell

12. Cells of inflammatory response 1)Polymorphonuclear leukocytes: are basophils, neutrophils and eosinophils; Microphages (small eaters) 2)Monocytes or histocytes: macrophages. (big eaters) 3)Lymphocytes: leukocyte of fundamental importance; they determine the specificity of the immune response. 4)Plasma cells: A type of immune cell that makes large amounts of a specific antibody, developed from activated B cells.

13. Phagocytosis Process by which Phagocytic cell (microphages and macrophages) engulf and kill foreign particles (bacteria) Two main types of phagocytes: 1- Motile phagocytes found in the blood stream and migrate to the inflamed area (microphages) 2- Histocytes (macrophages) of the reticuloendothelial system (RES) which remove bacteria that escapes from the inflamed area.

14. Phagocytosis

15. Steps of Phagocytosis 1. Recognition 2. Ingestion- pseudopods engulf microbe through endocytosis 3. Vacuole Formation- vacuole contains microbe 4. Digestion- merges with enzymes to destroy microbes 5. Exocytosis- microbial debris is released

16. Types of acute inflammation (based on type of exudates) 1-Catarrhal inflammation: 2-Serous inflammation: 3-Fibrinous inflammation: 4-Membranous inflammation: 5-Hemorrhagic inflammation: 6-Gangrenous inflammation: 7-Allergic inflammation: 8-Suppurative or purulent inflammation:

17. NameOccur inCharacterized by Catarrhal Mild inflammation in mucous membrane of respiratory or alimentary tracts e.g. common cold and catarrhal appendicitis Exudates rich in mucous Serous Mild inflammation in serous surface such as pleural cavity, joint cavity where no damage in endothelium ex. Tuberculosis pleurisy and Common blisters Extensive watery low protein exudates Fibrinous Outpouring of exudates with high protein and less volume ex. in lobar pneumonia due to Streptococcus pneumonia & pericardium inflammation Exudates rich in fibrinogen Membranous Fibrinous inflammation in which network of fibrin entangling inflammatory cells and bacteria forms pseudo-membrane. Example: Diphtheria, Bacillary dysentery. Yellowish grey pseudo membrane rich in fibrin, polymorphs & necrotic tissues Hemorrhagic In blood vessels e.g. in plagueExudates rich RBCs Gangrenous Acute appendicitis Necrotic tissues resulting from thrombi or emboli Allergic Result to Ag – Ab reaction Hypersensitivity Presence of edema & increase in vascularity. Suppurative Caused by pyogenic bacteria and is characterized by pus formation Example: Abscess. Large amount of Pus & Purulent exudates produced

18. Suppurative or purulent inflammation Pus: thick fluid containing viable and necrotic polymorph and necrotic tissue 1.Localized: ex. Abscess: Abscess is the localized collection of pus, commonly seen solid block of tissue - Example: dermis, liver, kidney, brain etc. Pus consists of partly or completely liquefied dead tissue mixed with dead or dying neutrophils and living or dead bacteria, formed of 3 zones 1. Small abscess is called boil or furuncle 2. Large one carbuncle 3. Fistula 2. Diffused: Spreading of pus to adjacent areas e.g. cellulites occurring in subcutaneous tissue. Usually caused by streptococci.

19. Abscess:

20. Fate of acute inflammation 1- Resolution: exudates are reabsorbed and tissue becomes normal again. 2- Healing: by repair and regeneration. 3- Spread: through lymphatics or blood stream. 4- Chronicity

21. Chronic inflammation: (granulomatous) Results from increased resistance of the causative agent to phagocytosis or the body defense mechanism is depressed. Shows lower vascular and exudative response The inflammatory cells are mainly macrophages, plasma cells, giant cells, lymphocytes, fibroblasts. Occurs in the form of granuloma. Chronic inflammation usually occur with granulomatous infections; e.g. leprosy, tuberculosis and fungal infections.