Transcript Inflammation

Section 2 Basic Pathologic Changes
The basic pathologic changes of inflammation
in the site of injury are alteration, exudation,
and proliferation.
1. Alteration
(1) Definition: The tissues or cells in the
inflammatory site become degeneration
and/or necrosis.
(2) Causes and mechanism:
 Be damaged by inflammatory factors directly.
 Local blood circulation disturbance
 Be affected by inflammatory mediators.
(3) Morphology
 Parenchyma cells: edema, fatty change,
necrosis etc.
 Interstitium: edema, mucoid degeneration,
fibrinoid degeneration, necrosis, etc.
2. Vascular changes
(hyperemia and exudation)
(1) Changes in vascular flow and caliber
① Changes in caliber


Transient arteriolar constriction
Persistent vasodilatation
② Changes in flow
a. Initially rapid as a result of
vasodilatation (active hyperemia)
b. Slowing and disturbance of axial flow as
a result of increased blood viscosity
secondary to loss of plasma into the tissue
(congestion and edema)
炎症是血液动力学变化模式图
(参照 武忠弼 病理学规划教材第一版 人民卫生出版社，修改)
③ Changes in the endothelium
Increased vascular permeability leading to the escape of
a protein-rich fluid (exudates) into the interstitium.
a. Endothelial cell contraction, or increased transcytosis
across the endothelial cytoplasm.
b. Direct endothelial injury, resulting in endothelial cell
necrosis and detachment
c. Leakage from regenerating capillaries
(2) Fluid exudate
Normally the walls of small blood vessels
are freely permeable to water and
crystalloids but relatively impermeable to
plasma proteins. The formation of
protein-rich fluid exudates is facilitated
by separation of the intercellular junction
of the endothelium.
The fluid exude carries into the inflamed
area the following important constituents:
① Serum bactericidal factors
a. Antibodies which act by opsonising
bacteria prior to phagocytosis and by
neutralizing exotoxins
b. Components of the complement system
② Interferon: a non-specific antiviral agent
③ Fibrinogen which is converted to fibrin.
Fibrin is important in providing:
a. Cement substance uniting severed tissues
b. Scaffold for repair processes
c. Barrier to the spread of organisms
d. Surface against which phagocytosis of adherent
organisms is enhanced
④ Therapeutic agents-antibiotics, antiinflammatory drugs, etc.
(3) Leukocyte exudates and phagocytosis
① Leukocytic margination,rolling
② Adhesion:by the binding of adhesion
molectures (selections, immunoglobulins,
intergrins, mucin-like glycoproteins)
③ Emigrating
It refers to the process by which motile white cells
migrate out of blood vessels.
Although all leukocytes are more or less motile, the
most active are the neutrophils and monocytes; the
most sluggish are the lymphocytes.
While cell emigration is an active, energy-dependent
process.
* Red blood cell out of blood vessels, called diapedesis,
is believed to be passive loss of red blood cells through
the points of rupture (blooding).
The molecular mechanism of Leukocyte emigration
（引自 Robbins Basic Pathology,2003）
White cell transmigration
It is include following
handings:
WBC margination

WBC adhesion with
endothelial surface adhesion
molecule

WBC transmigration
2-12 minute
EM: White cell transmigration
(参照武忠弼 病理学规划教材第一版,修改)
Leukocyte exudates
④ Chemotaxis
Following extravasations, leukocytes emigrate
in tissues toward the site of injury by a process
called chemotaxis.
Exogenous chemo attractants: bacterial products,
etc.
Endogenous chemo attractants: components of
the (LTB4), cytokines, etc.
⑤ Phagocytosis
Recognition and attachment of the
particle to the surface of the
phagocyte→ engulfment→ killing
and degradation
The mode of Phagocytosis
(引自 Robbins Basic Pathology,2003，稍改)
Types of leukocyte (inflammatory cells):
Leukocytes are out of blood vessels that are known as
inflammatory cells.
a. Neutrophils:
Small phagocytic cell
The two types of granules in the cytoplasm:
Azurophil granules and specific granules.
The first cells to appear in perivascular spaces are the
neutrophils.
Commonly seen in early stage of inflammation, and
acute inflammation, and purulent inflammation.
b. Macrophages:
Tissue macrophages are derived from blood
monocytes that emigrate from blood vessels under
influence of chemotactic factors.
Commonly seen in later stage of inflammation,
chronic inflammation, non-purulent inflammation,
and viral, or protozoal, or fungal infections. And
macrophages are also related to specific immune
response.
dusty cell
Macrophages could
Formation
Langhan’s giant cell
foamy cell
epithelioid cell
heart failure cell
Multinucleate giant-cells foreign-body giant cell
c. Eosinophilia
Commonly seen in hypersensitivity reaction
and human parasitological infections.
d. Lymphocytes and plasma cells
Commonly seen in virus infection and
chronic inflammation.
e. Basophilic and mast cell
MacrM
3. Proliferation
Proliferate constitution:
Endothelium, macrophages, and fibroblasts
commonly seen in later stage of inflammation