CAM102 Lecture Notes - Lecture 7: Mast Cell, Endothelial Activation, Lectin

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8 Jun 2018
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Learning Objectives
Definition of acute inflammation
Aetiology of acute inflammation
Pathogenesis of acute inflammation
Vascular changes associated with acute inflammation
The mobilisation and role of leukocytes (in acute inflammation mainly, neutrophils
Chemical mediators involve in acute inflammation
Morphology (macroscopic/microscopic) of acute inflammation
Terminology and clinical features (local and systemic) of acute inflammation
Outcomes following acute inflammation
Inflammation
Definition
The response of the vascular microcirculation to injury resulting in the local:
Accumulation of fluid and plasma proteins
Migration and activation of leukocytes
± a systemic response (eg. Fever)
Key Features
Vasodilation that leads to an increase in but slowing of blood flow
Increased vascular permeability due to structural changes in the microvasculature
Permits plasma proteins and leukocytes to leave the circulation
Emigration of the leukocytes from the microcirculation
Accumulation in the focus of injury
Activation to eliminate the offending agent
Signs of Inflammation
Pain
Fever
Loss of function of tissue or organ that has been inflamed
Acute vs Chronic
Acute
Initial rapid response occurring in minutes to hours
Short duration lasting only days
Exudation of fluid and plasma proteins (oedema)
Emigration of leukocytes (neutrophils)
Chronic
If acute inflammation fails the chronic inflammation ensues
Days to months to years
Associated with more tissue destruction
Lymphocytes and macrophages predominate
Attempts at healing and repair coincide
Tissues is replaced through regeneration of surviving cells and filling of residual defects with
connective tissue scarring
Aetiology and Outcomes of Injury
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Pathogenesis of Acute Inflammation
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Document Summary

The response of the vascular microcirculation to injury resulting in the local: accumulation of fluid and plasma proteins, migration and activation of leukocytes, a systemic response (eg. fever) Key features: vasodilation that leads to an increase in but slowing of blood flow. Increased vascular permeability due to structural changes in the microvasculature: permits plasma proteins and leukocytes to leave the circulation, emigration of the leukocytes from the microcirculation, accumulation in the focus of injury, activation to eliminate the offending agent. Loss of function of tissue or organ that has been inflamed. Initial rapid response occurring in minutes to hours. Short duration lasting only days: exudation of fluid and plasma proteins (oedema, emigration of leukocytes (neutrophils) If acute inflammation fails the chronic inflammation ensues: days to months to years, associated with more tissue destruction, attempts at healing and repair coincide, tissues is replaced through regeneration of surviving cells and filling of residual defects with.

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