Inflammation 2024 PDF

Prof Noha ElKady Professor pathology department Faculty of Medicine  1. Define inflammation, its causes and aims  2.Determine types and signs of inflammation  3.Comparebetween types of inflammation  4.Identify mechanism of exudate formation and extravasation of inflammatory ce...

Prof Noha ElKady Professor pathology department Faculty of Medicine  1. Define inflammation, its causes and aims  2.Determine types and signs of inflammation  3.Comparebetween types of inflammation  4.Identify mechanism of exudate formation and extravasation of inflammatory cells  5.Define chemotaxis and phagocytosis, steps and aims  6. Recognize types of acute inflammation and their causes  7. Compare between abscess and cellulitis  8. Identify non-suppurative inflammation  9.Recognize granuloma (definition, causes and types).  Definition and causes Acute and chronic inflammation Vascular and cellular response Types of acute inflammation Chronic inflammation A 30-year-old man presented with painful swelling in his finger. Examination revealed a red hot swelling in the index finger with central yellow area. Surgical incision was done and a yellow pus was discharging from the mass. What the diagnosis?  What are the possible complications? “In-flame” –to set fire. (red, hot, pain) Local vascular and cellular response of living tissue against an injurious agent  Aims of inflammation Fighting bacteria Localize infection Removal of damaged tissue 1- Acute 2- Chronic  Cells in acute and chronic inflammation  Neutrophils: Acute,  Lymphocytes: chronic  Plasma: chronic  Histiocytes: Chronic  Eosinophils: allergy, parasitic  Mast cells: allergy  Giant cells: granuloma  Acute & Chronic Inflammation Features Acute Chronic Onset Fast: minutes to hours Slow; days Cellular infiltrate Neutrophils mainly Lymphocytes, plasma macrophages Blood vessels Congestion Stenosis edema present absent fibrosis absent present Local & Systemic signs Prominent Less prominent Loss of function Events of inflammation 1) Vascular Response (1)Vasodilatation (histamine) (2) INCREASED PERMEABILITY Endothelial contraction “gaps”  Direct endothelial Injury  Transcytosis Transcytosis Inflammatory fluid exudate Function: 1. Dilute toxin, chemical, poison 2. Bring antibodies 3. Supply nutrition for cells remove toxins 4. Supply fibrinogen ( localization, movement of inflammatory cells and fibroblasts 2) Cellular exudate EXTRAVASATION of neutrophils  MARGINATION (PMN’s go toward wall)  ROLLING (tumbling and EAPING)  (selectine-glycoprotein)  ADHESION (integrine-Ig)  TRANSMIGRATION (DIAPEDESIS)(PCAM)  Chemotaxis Definition: Is the directed movement of neutrophilis and macrophages in the area of inflammation towards the irritant Depending on 1- exogenous mediators : bacteria product 2- endogenous mediators: chemokines. Definition: is the ingestion and destruction of bacteria, necrotic debris and foreign particles by the phagocytic inflammatory cells.  Phagocytosis Phagocytes Neutrophilis Macrophages 1- Recognition and attachment Opsonin (Ig, complement) 2- Engulfment 3- Killing and degradation (Oxidative and non-oxidative) CHEMICAL MEDIATORS  Cellular  Plasma  HISTAMINE  COMPLEMENT  SEROTONIN  KININS  EICOSANOIDS  CLOTTING FACTORS  NITRIC OXIDE  Fibrinolytic  PLATELET ACTIVATING FACTOR (PAF)  Resolution Outcome of acute Regression & Healing inflammation Progression & spread Progression & Chronicity Summary  VASODILATATION   INCREASED VASCULAR PERMEABILITY   Fluid exudate  Extravasation of cells: MARGINATION, ROLLING, ADHESION, TRANSMIGRATION (DIAPEDESIS)   CHEMOTAXIS   PHAGOCYTOSIS: Recognition,(Attachment), Engulfment, Killing (degradation or digestion)   TERMINATION 100% RESOLUTION, CHRONIC INFLAMMATION, progression Types of acute inflammation acute inflammation Suppurative Non-Suppurative Suppurative inflammation Pyogenic organism Pus  Non-coagulable creamy alkaline yellowish or yellow green fluid formed of: 1- fluid exudate without fibrin 2- pus cells, PNL, macropheges, RBCs 3- Liquified necrotic tissue 4- Bacteria and pigment Types of Acute Suppurative inflammation Suppurative inflammation Localised Diffuse Abscess Furuncle Carbuncle Cellulitis  Staph Strept Hyalouronidase Coagulase Fibrinolysin Localized Diffuse Abscess Definition Localized suppurative acute inflammation Cause Staph----Excess fibrin Microscopically: 1-Central zone of Pus. 2-Middle zone of infected granulation tissue 3-Peripheral zone of fibrous capsule. Fate: Chronicity Complications  PUS Clinical red, hot, swollen, Pus = PURULENT ABSCESS = POCKET OF PUS PURULENT, FIBRINOPURULENT Boil-Furuncle  Small abscess related to hair follicle or sebaceous gland Carbuncle multiple communicating abscess Risk: Diabetics Site: back of neck Diffuse suppurative Inflammation Causative organism:streptococcus haemolyticus producing Enzyme 1-fibrinolysin, hyalouronidase and 2-spreading factor Examples: Cellulitis Appendicitis Peritonitis  Abscess Cellulitis Localized suppurative Diffuse suppurative Def examination examination Staph Strept Causative organism Excess fibrin fibrinolysin, hyalouronidase Mechanism andspreading factor Any tissue Loose tissue Site Thick yellow Thin sangonous Pus Less More common Spread Types of Acute Non-Suppurative inflammation necrotizing Haemohrragic serous Non- Allergic Suppurative Fbrinous Membranous serofibrinous Catarrhal Types of Acute Non-Suppurative inflammation Inflammatio Type of example n fluid Catarrhal excess Rhinitis mucous Serous Excess Burn watery Fibrinous excess Fibrin Pleuritis Chronic inflammation  CAUSES of CHRONIC INFLAMMATION 1) PERSISTENCE of Infection 2) PROLONGED EXPOSURE to insult Types Non-specific: Specific: granuloma GRANULOMAS Def: Chronic specific inflammation with nodular collection of epithelioid cells , lymphocytes and giant cells GRANULOMAS Etiology Infective Non-infective Bacteria: TB, Selecosis, FB Leprosy, Syphilis Parasitic: Bilh, Leishmania Fungi: Madura foot Unknown Chron’s Sarcoidosis Components of Granuloma Components of Granuloma  4 COMPONENTS  HISTIOS, epitheliod cells (main component)  “GIANT” CELLS Langhan’s FB  LYMPHS  FIBROBLASTS  Classification (types)of GRANULOMAS Type of granuloma Example Granuloma with Tuberculosis TB caseation Granuloma without Sarcoidosis, Chron’s, caseation BILH, Selicosis Suppurative granuloma Cat scrach Foreign body thread, silicon implant granuloma  Langhans giant cell Foreign body giant cell