病理学-炎症学习课件
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Chemokines
Sources
Actions
Mast cells, basophils, Vasodilation, increased vascular permeability,
platelets
endothelial activation
Platelets
Vasodilation, increased vascular permeability
Local endothelial activation (expression of adhesion molecules), fever/pain/anorexia/hypotension, decreased vascular resistance (shock) Chemotaxis, leukocyte activation
non-inflammation clear <1.018 < 30g/L <100/mm3 -
Local manifestations of Inflammation
rubor (redness) tumor (swelling) calor (heat) dolor (pain)
Systemic manifestations of inflammation
Chemotaxis and activation
The multiple process of leukocyte migration through blood vessels.
Robbins and Cotran Pathologic Basis of Disease 7th edition
2) Recognition of microbes Leukocyte receptors and responses
3) Removal of the offending agents
Phagocytosis Engulfment Killing and degradation
A. Phagocytosis: Attachment Engulfment Fusion with lysosomes
Chronic inflammation: e.g., arthritis; asthma; chronic lung disease
Inflammatory Mediator
Function of chemical mediators: directing the vascular and cellular events in inflammation Cell-derived or Plasma-derived mediators Act as a complicated network
Chronic inflammation
Part 1 General Considerations
Definition
Inflammation is a protective response intended to eliminate the initial cause of cell injury as well as the necrotic cells and tissues resulting from the original insult.
Endothelium, macrophages
Macrophages, endothelial cells, mast cells
Leukocytes, activated macrophages
Vascular smooth muscle relaxation, killing of microbes
Exudation of plasma proteins
Exudate and transudate
Cause inflammation
Gross
cloudy
Gravity >1.018
Protein
>30g/L
Cell no.
>100/mm3
Coagulation +
Mucoprotein +
B. oxygendependent bactericidal mechanism
Robbins Basic Pathology
4) Release of leukocyte products and leukocyte-mediated tissue injury
Acute inflammation: e.g., acute respiratory distress syndrome; acute transplant rejection; reperfusion injury
Mast cells, leukocytes
Vasodilation, pain, fever
Mast cells, leukocytes
Increased vascular permeability, chemotaxis, leukocyte adhesion and activation
Leukocytes, mast cells
Increased vascular permeability, smooth
Components of acute and chronic inflammation
Inflammatory agents
Infections (bacterial, viral, parasitic) and microbial toxins
Physical agents (e.g., irradiation, burns) and Trauma (blunt and penetrating)
Generation of arachidonic acid metabolites and their roles in inflammation
Major effects of IL-1 and TNF
plasma protein-derived mediators
Mediators
Sources
➢ Vasodilation of precapillary arterioles then increases blood flow to the tissue
Increased vascular permeability
The major local manifestations of acute inflammation: (1) vascular dilation; (2) extravasation of plasma fluid and protein; (3) leukocyte emigration and accumulation in the site of injury
Cell-derived mediators
Mediators
Histamine
Serotonin Prostaglandins
Leukotrienes
Platelet-activating factor
Reactive oxygen species Nitric oxide
Cytokines (TNF, IL-1)
Vasodilation, increased vascular permeability, leukocyte adhesion, chemotaxis, degranulation, oxidative burst
Leukocytes
Killing of microbes, tissue damage
The process of acute inflammation
Vascular events Cellular events Molecular events
Vascular Events
Changes in vascular caliber Байду номын сангаасnd flow
➢ Transient vasoconstriction of arterioles at the site of injury
mediated tissue injury
1) Recruitment of leukocytes to sites of infection and injury
Margination, rolling and adhesion to endothelium
Leukocyte migration through endothelium
Chemical agents (some environmental chemicals) Ischemic and necrotic tissues Foreign particle (dirt, sutures) Allergic reactions
The basic pathological changes
Acute inflammation
➢ The process of vascular and cellular events in inflammation, Inflammatory mediators
➢ The classification and outcomes of acute inflammation
Chemotaxis
After extravasating from the blood, leukocytes migrate toward sites of injury along a chemical gradient in a process called Chemotaxis.
Chemotactic Factors including bacterial products, chemokines, C5a, leukotriene B4
Fever Increased acute-phase proteins Leukocytosis Others: increased pulse and blood
pressure; decreased sweating; rigors; anorexia
Part 2 Acute inflammation
General Considerations
➢ Definition; Inflammatory agents; Basic pathological changes of inflammation; Local and systemic manifestations of Inflammation
Actions
Complement
Plasma
Leukocyte chemotaxis and activation,
products (C5a, C3a, (produced in liver) vasodilation (mast cell stimulation)
C4a)
Kinins
Plasma
Inflammation
Skin blister result from burning
Serous effusion accumulated within and underneath the epidermis of skin
Carbuncle（痈) Furuncle（疖）
Outlines of inflammation
Cellular Events
1) Recruitment of leukocytes to sites of infection and injury
2) Recognition of microbes and dead tissues 3) Removal of the offending agents 4) Release of leukocyte products and leukocyte-
Alteration (degeneration, necrosis) Exudation (hallmark, vascular change,
leukocyte reaction, inflammatory mediators ) Proliferation (parenchymal and strmal cells)
Sources
Actions
Mast cells, basophils, Vasodilation, increased vascular permeability,
platelets
endothelial activation
Platelets
Vasodilation, increased vascular permeability
Local endothelial activation (expression of adhesion molecules), fever/pain/anorexia/hypotension, decreased vascular resistance (shock) Chemotaxis, leukocyte activation
non-inflammation clear <1.018 < 30g/L <100/mm3 -
Local manifestations of Inflammation
rubor (redness) tumor (swelling) calor (heat) dolor (pain)
Systemic manifestations of inflammation
Chemotaxis and activation
The multiple process of leukocyte migration through blood vessels.
Robbins and Cotran Pathologic Basis of Disease 7th edition
2) Recognition of microbes Leukocyte receptors and responses
3) Removal of the offending agents
Phagocytosis Engulfment Killing and degradation
A. Phagocytosis: Attachment Engulfment Fusion with lysosomes
Chronic inflammation: e.g., arthritis; asthma; chronic lung disease
Inflammatory Mediator
Function of chemical mediators: directing the vascular and cellular events in inflammation Cell-derived or Plasma-derived mediators Act as a complicated network
Chronic inflammation
Part 1 General Considerations
Definition
Inflammation is a protective response intended to eliminate the initial cause of cell injury as well as the necrotic cells and tissues resulting from the original insult.
Endothelium, macrophages
Macrophages, endothelial cells, mast cells
Leukocytes, activated macrophages
Vascular smooth muscle relaxation, killing of microbes
Exudation of plasma proteins
Exudate and transudate
Cause inflammation
Gross
cloudy
Gravity >1.018
Protein
>30g/L
Cell no.
>100/mm3
Coagulation +
Mucoprotein +
B. oxygendependent bactericidal mechanism
Robbins Basic Pathology
4) Release of leukocyte products and leukocyte-mediated tissue injury
Acute inflammation: e.g., acute respiratory distress syndrome; acute transplant rejection; reperfusion injury
Mast cells, leukocytes
Vasodilation, pain, fever
Mast cells, leukocytes
Increased vascular permeability, chemotaxis, leukocyte adhesion and activation
Leukocytes, mast cells
Increased vascular permeability, smooth
Components of acute and chronic inflammation
Inflammatory agents
Infections (bacterial, viral, parasitic) and microbial toxins
Physical agents (e.g., irradiation, burns) and Trauma (blunt and penetrating)
Generation of arachidonic acid metabolites and their roles in inflammation
Major effects of IL-1 and TNF
plasma protein-derived mediators
Mediators
Sources
➢ Vasodilation of precapillary arterioles then increases blood flow to the tissue
Increased vascular permeability
The major local manifestations of acute inflammation: (1) vascular dilation; (2) extravasation of plasma fluid and protein; (3) leukocyte emigration and accumulation in the site of injury
Cell-derived mediators
Mediators
Histamine
Serotonin Prostaglandins
Leukotrienes
Platelet-activating factor
Reactive oxygen species Nitric oxide
Cytokines (TNF, IL-1)
Vasodilation, increased vascular permeability, leukocyte adhesion, chemotaxis, degranulation, oxidative burst
Leukocytes
Killing of microbes, tissue damage
The process of acute inflammation
Vascular events Cellular events Molecular events
Vascular Events
Changes in vascular caliber Байду номын сангаасnd flow
➢ Transient vasoconstriction of arterioles at the site of injury
mediated tissue injury
1) Recruitment of leukocytes to sites of infection and injury
Margination, rolling and adhesion to endothelium
Leukocyte migration through endothelium
Chemical agents (some environmental chemicals) Ischemic and necrotic tissues Foreign particle (dirt, sutures) Allergic reactions
The basic pathological changes
Acute inflammation
➢ The process of vascular and cellular events in inflammation, Inflammatory mediators
➢ The classification and outcomes of acute inflammation
Chemotaxis
After extravasating from the blood, leukocytes migrate toward sites of injury along a chemical gradient in a process called Chemotaxis.
Chemotactic Factors including bacterial products, chemokines, C5a, leukotriene B4
Fever Increased acute-phase proteins Leukocytosis Others: increased pulse and blood
pressure; decreased sweating; rigors; anorexia
Part 2 Acute inflammation
General Considerations
➢ Definition; Inflammatory agents; Basic pathological changes of inflammation; Local and systemic manifestations of Inflammation
Actions
Complement
Plasma
Leukocyte chemotaxis and activation,
products (C5a, C3a, (produced in liver) vasodilation (mast cell stimulation)
C4a)
Kinins
Plasma
Inflammation
Skin blister result from burning
Serous effusion accumulated within and underneath the epidermis of skin
Carbuncle（痈) Furuncle（疖）
Outlines of inflammation
Cellular Events
1) Recruitment of leukocytes to sites of infection and injury
2) Recognition of microbes and dead tissues 3) Removal of the offending agents 4) Release of leukocyte products and leukocyte-
Alteration (degeneration, necrosis) Exudation (hallmark, vascular change,
leukocyte reaction, inflammatory mediators ) Proliferation (parenchymal and strmal cells)