Inflammation Lecture Notes 2024 PDF

 Inflammation Inflammation: Local defense and protective response against cell injury or irritation or Local vascular ,cellular and lymphatic reaction, against an irritant. Irritating or injurious agents (Irritant) Living: Bacteria, No...

 Inflammation Inflammation: Local defense and protective response against cell injury or irritation or Local vascular ,cellular and lymphatic reaction, against an irritant. Irritating or injurious agents (Irritant) Living: Bacteria, Non-Living: Fungi, Chemical Virus, Physical Parasite Mechanical or their toxins Hypersensitivity reactions Inflammation is designated by adding the suffix (itis) to the end of the name of the inflamed organ or tissue.  Types of inflammation 1) Acute inflammation 3) Chronic 2) Sub acute inflammation inflammation: rarely occur.  Patterns of Inflammation Acute – Rapid response – Short duration (minutes-days) – Emigration of fluid, plasma proteins, and neutrophils into tissue. = polymarphs = PNL Chronic _ Slow response – Longer duration (days-months) – tissue accumulation of lymphocytes, plasma cells, macrophages plus variable proliferation of fibroblasts Epithilial cell. esinophils  Cells of inflammatory response 1) Polymorphonuclear leukocytes: are neutrophils. When death give pus cells 2) Monocytes or histocytes: macrophages. 3) Giant cells 4) Lymphocytes: B & T lymphocytes 5) Plasma cells: developed from activated B cells 6) Esinophils: in allargy and parasitic infl 7) Fibroblasts Acute inflammation Pathogenesis of acute inflammation 1) Local destruction of tissue 2) Local vascular changes 3) Reaction of tissue histiocytes  1) Local destruction of tissue In the area of tissue with maximum concentration of the irritant Local death of tissue (necrosis) Liberation of chemical mediators as histamine Local vascular changes around area of necrosis  2) 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. 3. Increase in capillary permeability (fluid exudate to the extravascular tissue) thus concentration of blood cells, slowing of blood flow (stasis) 4. Pavmentation and margination of leukocytes. 5. Emigration of the various leukocytes, fluid and plasma proteins outside the blood vessels into the surrounding tissue without injury of the blood vessels forming inflammatory fluid exudate. Leukocytes seem to leave the smallest blood vessels by inserting pseudopodia into the interendothelial junctions and sliding through the wall by amoeboid movement.  ****In some cases RBCs may also pass (Diapedesis) 6. Chemotaxis and phagocytosis 7. Dilatation of lymphatic vessels to accelerate lymph flow so drain fluid exudate Normal Inflammation  What do neutrophils do? Phagocytosis Contact, Recognition, Internalisation. Opsonins: e.g. Fc and C3b receptors Cytoskeletal changes (as with chemotaxis); ‘zipper’ effect.  Steps of Phagocytosis 1. Recognition 2. Ingestion- pseudopods engulf microbe through endocytosis 3. Vacuole Formation- vacuole contains microbe 4. Digestion- vacuole merges with enzymes to destroy microbes 5. Exocytosis- microbial debris is released  3) Reaction of tissue histiocytes Proliferation of tissue histocytes normally present in CT and body organs occur in inflammation to phagocyte: 1) Remaining bacteria 2) Cellular debris 3) Fibrin  Acute inflammation Macroscopic signs ( Cardinal signs): Symptoms 1) Redness: 2) Hotness: 3) Swelling: 4) Pain and tenderness: 5) Loss of function: General effects of acute inflammation 1. Fever: dt release of pyrogenic compounds and increased tissue metabolism. 2. Leucocytosis: increased number of leucocytes above 10000/cm dt liberation of leucocytosis promoting factor from injuried tissue. 3. Toxic effects as anorexia, headache……….  Fate of acute inflammation 1- Resolution: exudates are reabsorbed and tissue becomes normal again. 2- Healing: by repair and regeneration. 3- Progression and Spread: through lymphatics or blood stream. 4- Chronicity: when causative agent is partially overcome.  Types of acute inflammation (based on type of exudates) I) Suppurative or purulent inflammation 1. Localized as Abscess 2. Diffuse as cellulitis II) Non Suppurative inflammation: 1-Catarrhal inflammation: 2- Serous inflammation: 3- Fibrinous inflammation: 4- Membranous inflammation: 5- Hemorrhagic inflammation: Chronic inflammation Chronic inflammation (granulomatous) May follow acute inflammation or start chronic from beginning. 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.  Types of chronic inflammation 1) Chronic specific inflammation: Caused by specific organism produce characteristic histologic apperance (granuloma) as TB & B….. 2) Chronic non specific inflammation: Caused by different types of organisms which do not produce characteristic histologic apperance as chronic tonsilitis  Granuloma Def: A chronic swelling caused by chronic specific inflammation. Types: 1) Infective granuloma: bacterial, fungal, parasitic 2) Non Infective granuloma: silicosis, asbestosis, FG granulomas 3) Granuloma of unknown cause as chron’s, sarcodosis Histopathology: 1)Macrophages (essential present). 2)Chronic inflammatory cells ( lymphocytes, plasma cells and esinophils) 3)Fibrous tissue 4)Specific organism or Foreign body  Effects & clinical significance: 1) Infective granulomas ------ spread of infectious diseases 2) Scarring of organs ------- disturb of function 3) Obstructive effects in hollow or tubular organs. 4) Must be discriminated from other causes of chronic swelling especially malignant neoplasms.