Inflammation-2 Lecture Notes PDF

INFLAMMATION-2 Dr.Gehan Abdelmenam 0  Intended Learning Objectives Recall definition, mechanism of formation of Inflammatory cellular exudate. Define phagocytosis and its steps. List Systemic effects and Local signs of acute inflammation. Describe Fate,type...

INFLAMMATION-2 Dr.Gehan Abdelmenam 0  Intended Learning Objectives Recall definition, mechanism of formation of Inflammatory cellular exudate. Define phagocytosis and its steps. List Systemic effects and Local signs of acute inflammation. Describe Fate,types of acute inflammation. Recall definition,sites,complication of an abscess.  II. Inflammatory cellular exudate * Definition: passage of leucocytes to the interstitium of the inflamed area. * Steps: 1.Margination 2.Rolling 3.Adhesion 4.Transmigration (also called diapedesis) 5.Chemotaxis = locomotion toward the irritant.  Margination Accumulation of leukocytes along the endothelial surface. Rolling, adhesion and transmigration Mediated by binding of complementary adhesion molecules on leukocytes and endothelial surfaces  Chemotaxis * Definition: locomotion of neutrophils & macrophages toward the irritant under the effect of chemotactic factors that is released in the area of inflammation. * Chemotactic factors are: 1. Bacterial products. 2. Leukotriene B4 (LT-B4). 3. Complement system products C5a.  Phagocytosis Engulfment of particulate material (e.g. tissue debris, living and dead bacteria, other foreign particles) by phagocytic cells. Neutrophils and macrophages are the most important phagocytic cells. Three steps: 1. Recognition and attachment 2. Engulfment 3. Killing and degradation of the ingested material.  Opsonins Phagolysosome Engulfment Formation and degranulation Attachment Bacterium Opsonin receptors  1. Recognition and attachment Receptors on leukocytes recognize the particle to be ingested and attach to it by Opsonization which means coating of particulate matter by substances referred to as OPSONINS e.g. IgG and C3b.  2. Engulfment Phagocytic cell sends out cytoplasmic processes (pseudopods) that surround the bacteria. The bacteria are internalized within a phagosome. The phagosome fuses with lysosome to form phagolysosome. Release of lysosomal contents (degranulation). 3. Killing and degradation of the ingested material The final step in Phagocytosis of microbes is killing and degradation. Mediated within phagocytic cells by: 1. Oxygen dependent mechanisms. 2. Oxygen independent mechanisms.  Oxygen dependent killing Killing of bacteria by reactive oxygen species (ROS) Oxygen independent killing Mediated by hydrolytic substances in leukocyte granules:  Opsonins Phagolysosome Engulfment Formation and degranulation Attachment Bacterium Opsonin receptors Local signs of acute inflammation 1. Hotness: - due to vasodilatation and hyperemia. 2. Redness: - due to vasodilatation and hyperemia. 3. Swelling: - due to fluid exudate. 4. Pain: - Caused by irritation of the nerve endings by toxins and Pressure of the inflammatory exudate on the sensory nerves and release of prostaglandin E2 and bradykinin. 5. Loss of function: - due to destruction of tissues or to avoid Pain. 0  Bee Sting Systemic effects of acute Inflammation 1. Fever (Pyrexia),anorexia,headache and maliase. 2. Leucocytosis. 0  Fate of acute inflammation 0  1. Resolution: Resolution is the usual course of acute inflammation caused by mild chemical , physical irritant, viral infections and lobar pneumonia. No tissue loss but only morphologic changes in the cells which can undergo resolution ( complete restoration of the inflamed area to normal as products of inflammation are rapidly removed and cells return to normal again) 0  2. Regression and Healing: The body defense overcomes the irritant. Part of the necrotic tissue, dead cells and fibrin are removed by the macrophages. Healing occur by replacement of damaged cells by new healthy cells of the same type(regeneration) in case of labile and stable cells injury. Healing occurs by fibrosis in case of permanent cells injury. 0  3. Progression and Spread: The bacteria overcome the defense mechanism and inflammation spreads directly, by lymphatics and by blood causing toxaemia, bacteraemia, septicaemia. 4. Chronicity: The causative agent is partially overcomed, but the body is unable to get rid of it completely. It remains as a weak irritant acting on the tissue for a long time. 0  * Acute inflammatory reaction: Consists of: 1. Dilated blood vessels. 2. Acute inflammatory cells (macrophages and neutrophils). 3. Exudate. 0  1 3 2 0  Types of acute inflammation Suppurative Non-suppurative – Localized: – Catarrhal Boil (furuncle) – Psudomembranous Abscess carbuncle – Serous – Fibrinous – Diffuse: – Sero-fibrinous – Hemorrhagic Cellulitis Acute suppurative – Allergic appendicitis – Necrotizing meningitis 0  I. ACUTE SUPPURATIVE INFLAMMATION (Pyogenic or Septic) * Definition: Severe acute inflammation characterized by pus formation Causes: Pyogenic microorganisms as: -staphylococcus aureus(Most common cause of abscess,carbuncle) - pneumococcus, - gonococcus - bacillus coli. 0  Abscess * Definition: Localized suppurative inflammation resulting in the formation of an irregular cavity filled with pus. * Etiology: Caused mainly by staphylococcus aureus which produce coagulase enzyme that helps fibrin formation and localize the infection. * Sites: Commonly the abscess occurs in in the subcutaneous tissue and in any organ as the lung, brain, liver, breast. 0 Subcutaneous abscess  * Complications: – Blood spread: Septicemia, and toxemia. – Chronicity. – Lymphangitis and lymphadenitis. lymphangitis 0  REFERENCES Robbins and Cotran Pathologic Basis of Disease, 9th edition, 2014 ( Kumar, Abbas, Aster) Robbins Basic Pathology 10th edition, 2017 ( Kumar, Abbas, Aster)