回帖：Chapter 4 Inflammation
§1. Introduction
1. Definition: A defensive reaction in living tissue with vascular system to injurious stimuli
Reaction of blood vessel is the central link
2. Causes
·Biologic factors: Bacteria, Virus, Fungi, Parasites
·Chemical factors: exogenous, endogenous
·Physical agents: trauma, burn
·Tissue necrosis
·Allergic reaction
3. Basic pathologic changes
(1)Alteration
Degeneration, necrosis of local tissue cells
·Parenchymal cell: cellular swelling, fatty change, coagulative necrosis, liquefactive necrosis
·Mesenchymal cell: mucoid change, amyloid change, hyaline change, fibrinoid necrosis
(2)Exudation
In inflammatory foci, the escape of fluid, proteins (fibrin), blood cells from vascular wall into interstitial tissue, body cavities or surface of the body and mucosa
(3)Proliferation
4. Local manifestation and general reactions
(1)Local manifestation: Redness, Swelling, Heat, Pain, Loss of function
(2)General reactions
①Fever: Exogenous factors: toxin, virus, Ag-Ab complex
Endogenous factors: cytokines: IL-1, TNF → PGE
②Leukocytosis: Acute purulent inflammation: Neutrophils↑
Chronic or virus infection: Lymphocytes↑
Allergic disease or parasite: Eosinophils↑
③Others: Anorexia, somnolence, malaise
More synthesis of clotting factors
§2. Acute inflammation
1. Changes of hemodynamics
Alteration in vascular flow and caliber
(1)Transient vasoconstriction of arterioles
(2)Vasodilation and increased blood flow
(3)Slowing of blood flow
2. Increased vascular permeability
(1)Mechanism of increased permeability
·Endothelial cell retraction: Histamine, Bradykinin, Leukotriene, Substance P
Immediate transient response
·Cytoskeletal reorganization: IL-1, TNF, hypoxia
·Increased transcytosis: VEGF, Histamine, Bradykinin, Leukotriene, Substance P
·Direct endothelial injury: Immediate sustained response: Severe burn, purulent bacteria, result in endothelial cell necrosis and detachment, leakage starts immediately after injury, sustained at a high level for several hours until damaged blood vessel thrombosis and repaired
·Delayed prolonged leakage: Mild-to-moderate thermal injury, toxin, x-ray
Increased permeability after a delay of 2 to 12 hours, lasting for several hours or days, involves venules as well as capillary
·Leukocyte-mediated endothelial injury
·High permeability of new capillary
①New vessels sprouts remain leaky until endothelial cells differentiate and form intercellular junctions
②Certain factors (VEGF) that cause angiogenesis increase permeability
③Increased density of receptor for vasoactive mediators in the surface of endothelial cell
(2)Fluid exudation
①Main causes
·Increased vascular permeability → escape of a protein-rich fluid into the interstitium
·The loss of protein → reduces intravascular colloid osmotic pressure, increases the colloid osmotic pressure of the interstitial fluid
②Distinguish between exudate and transudate
Transudate Exudate
Vascular permeability Normal Increased
Protein concentration 0-1.5g/dl 1.5-6g/dl
Protein type Albumin Kinds of protein
Rivalta test Negative (-) Positive (+)
Fibrin No Have
Gravity < 1.018 > 1.018
Cell number < 0.1×109/L > 0.5×109/L
Appearance Clear Cloudy
3. Leukocyte extravasation and phagocytosis
(1)Leukocyte extravasation: leukocyte pass through vascular wall into the site of injury
①Margination and rolling
②Adhesion
·Adhesion molecules: Selectin
The immunoglobulin family: ICAM-1, VCAM-1
Integr