Inflammatory Response Part 1 Acute Inflammation PDF

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SplendidNephrite8490

Uploaded by SplendidNephrite8490

LSBU

Sarah Balian

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inflammation biomedical science medical education inflammatory responses

Summary

This document presents an overview of inflammatory responses, focusing on acute inflammation. It covers key aspects like the classical signs, the roles of cellular and fluid exudates, phagocytosis, and chemical mediators. The document likely forms part of a learning module for biomedical science students.

Full Transcript

Inflammatory Responses Part 1 Sarah Balian Biomedical Science Intended Learning Outcomes By the end of this session students should be able to: Describe the classical signs of acute inflammation and their relevance. Explain significance of the formation of a cellular and a fluid exudate and...

Inflammatory Responses Part 1 Sarah Balian Biomedical Science Intended Learning Outcomes By the end of this session students should be able to: Describe the classical signs of acute inflammation and their relevance. Explain significance of the formation of a cellular and a fluid exudate and how they are formed. Discuss the assorted ways by which acute inflammation can be generated. Explain the processes of phagocytosis and bacterial killing. Recognise the effects and action of chemical mediators involved with acute inflammation on tissues. Inflammation What does inflammation mean to you? Purpose? Armed with your writing utensils Friend or Foe? Jot down bullet points to the following questions What does it ‘look’ like? Relevance of inflammation in dentistry? Define Inflammation What key words would you use? Local response of tissue to injury Stimulus can be variable: 1. Microbial 2. Immunological 3. Physical 4. Chemical agents Will inflammation & its chemicals really stay local? Types of Inflammation Inflammation Acute Chronic Inflammation Inflammation Features comparing Acute & Chronic Inflammation Feature Acute Chronic Onset Fast Slow Cellular infiltrate Mainly neutrophils Monocytes/macrophages & lymphocytes Tissue injury / fibrosis Usually mild and self-limited Local & systemic factors Prominent Presence of cardinal signs Likely to be present No cardinal signs Presence of stimulus Long term exposure Response Fibrosis & angiogenesis Infections Tissue necrosis Bacteria, viruses, fungi, Physical / chemical injuries parasites Heart attack Collection of dead tissue in confined space Trauma Foreign bodies Blunt & penetrating trauma Splinters, sutures, bones, Burns, frostbite, chemicals finger nails Popcorn kernels Immune (hypersensitivity reactions) Triggered by environmental factors Or autoimmune diseases Cardinal Signs of Acute Inflammation Five Cardinal Signs of Inflammation Rubor (redness) Calor (heat) Tumor (swelling) Dolor (pain) Loss of function Event in Acute Inflammation Linked with Immunology Lectures Events Vascular Events 1. Persistent vasodilation 2. Elevation of hydrostatic pressure 3. Increase in vascular permeability 4. Transudation of fluid into extracellular space 5. Slowing of or statis of micro circulation Causes of increased vascular permeability Endothelial cell contraction Endothelial injury 1. Direct 2. Leucocyte induced Increased transcytosis fluid Leakage from new blood vessels Image from Researchgate Feb 2021 Leucocyte recruitment to site – Cellular Events chemotaxsis Phagocytosis of particles – engulfment of particles Phagocytosis 2 types of phagocytic cells 1. PMN’s part of early inflammatory response 2. Monocytes & macrophages Opsonisation – ‘marker’ Neutrophils and macrophages Phagocytosis when at inflamed tissue site release proteolytic enzymes: Protease Collagenase Elastase Lipase So the ‘host’ is calling upon the immune cells to ‘come and fight’ against an ‘insult’. The immune response arrives however as well as impacting the ‘insult’, who else is it impacting? Patterns of Inflammation Suppurative Serous Fibrinous Ulcerative (purulent) Chemical Mediators Image from Nature Feb 2021 18 Chemical Mediators – a chemical messenger that acts upon a blood vessel, inflammatory cells or other cells to cause a inflammatory response Exogenous Endogenous Endotoxins Plasma Coming from where? Leucocytes Endothelial cells Fibroblasts Image from pinterest website Feb 2021 Chemical Mediators - CYTOKINES Chemical proteins produced by many cells E.g. Produced by PMN’s 1. Macrophages 2. B Lymphocytes 3. Epithelial cells 4. Gingival Fibroblasts 5. Osteoblasts Mediate & regulate immune & inflammatory reactions Cytokines – be pro-inflammatory & anti- inflammatory Interleukin (IL-1, IL-6 & IL-8) Tumor Necrosis Factor (TNF) Produced by leucocytes & many Immune cell recruitment, other cells, role in activation & produced by macrophages, TNF differentiation, neutrophil is able to induce fever recruitment Cytokines – Vasoactive amine - Histamine Histamine comes from mast cells Acts on blood vessels Histamine causes dilation of arterioles & increase permeability Image from Wikipedia website Feb 2021 Prostaglandins Produced by mast cells, macrophages & endothelial cells Lipid compound Involved in vascular & systemic reactions of inflammation Causes vasodilation Fever Pain Leukotrienes Produced by leucocytes and mast cells by the action of lipoxygenase Act as chemotactic for neutrophils Usually accompanied by histamine & prostaglandins Releases lysosomal enzymes Vasoconstriction Chemokines Family of small proteins that act as primarily chemo-attractants for specific types of leukocytes. Enhancing chemotaxis Image from Wikipedia website Feb 2021 Summary Causes of inflammation Chemical mediators Difference between in inflammation acute & chronic Patterns of acute Sign of inflammation Inflammation Events occurring in acute inflammation Where does this become relevant? Pathogenesis of Periodontal Disease Note down key words from today Inflammation friend or foe? Reading recommendations Ross & Wilson Anatomy and Physiology in Health and Illness, 13e Paperback – 6 Jun. 2018 Acute Inflammation - TeachMePhysiology

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