The basic pathologic changes of inflammation in the site of injury are alteration, exudation, and...

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.

Section 2 Basic Pathologic ChangesSection 2 Basic Pathologic Changes

(2) Causes and mechanism:Be damaged by inflammatory factors directly.Local blood circulation disturbanceBe 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 ① Changes in caliberChanges in caliber

Transient arteriolar constriction

Persistent vasodilatation

② ② Changes in flowChanges 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 ③ Changes in the endotheliumChanges 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 tissuesb. Scaffold for repair processesc. Barrier to the spread of organismsd. Surface against which phagocytosis of adherent

organisms is enhanced

④ Therapeutic agents-antibiotics, anti-inflammatory 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 transmigrationWhite cell transmigration

It is include following handings:

WBC margination

WBC adhesion with endothelial

surface adhesion molecule

WBC transmigration 2-12 minute

EM: White cell transmigrationEM: 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:Exogenous chemo attractants: bacterial products, etc.

Endogenous chemo attractants: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 Langhan’s giant cell

foamy cell

Macrophages could epithelioid cell

Formation 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:Proliferate constitution:

Endothelium, macrophages, and fibroblasts commonly seen in later stage of inflammation