INFLAMMATION
Chapter 3
Xu ruobing
OUTLINE
1 Definition
2 Causes
3 Basic pathological changes
4 Local signs and general reaction
5 Histological types
6 Inflammatory mediator and
chemotaxis
7 Sequels
Definition
Inflammation is a dynamic
processes by which living
tissue reacts to injury,They
concern vascular and
connective tissue particularly.
INFLAMMATION
Local signs and general
reaction
Local signs:
Redness (rubor)
Heat (calor)------hyperemia
Swelling (tumor)-------hyperemia
and edema
Pain (dolor)-----nerve ending
irritated by exudates and
inflammatory mediators,
Dysfunction
General reaction:
(1) Fever
(2) Increased leukocyte count
(2) ------releasing leukocytes from
bone marrow by IL-1 and TNF,
immature neutrophils (rod nucleus)
increased in peripheral blood (left
divert).
Depending on the duration,
inflammation is divided into acute
and chronic inflammation.
2 Causes
Physical agents,mechanical
trauma; over heat or cold;
ultra-violet or ionising
radiation.
Chemical substances,simple
chemicals eg,acids,alkaline
and organic poisons,
toxins from various bacteria
Infective agents,bacteria,
virus,and parasites,
Immunological and
hypersensitive reactions
necrotic tissue
3 Basic pathological changes
1 Alteration,degeneration,
necrosis
2 Exudation,escape of
fluid and cells from vessels
into injured tissue due to
permeability increasing.
3 Proliferation
1) Serum,differs from
transudate which occurs in
conditions where intravascular
pressure increases,
intravascular osmotic pressure
decreases,vascular
permeability does not increase.
Exudate Transudate
Appearance opaque clear
Sp,gravity >1.020 <1.020
Protein rich >2.5g% poor<2.5g%
Cells more few
>500/mm,Neu.+ <500/mm Neu,–
Coagulability + _
Rivata test + _
2) Fibrin Transformed from
fibrinogen in blood
3) Cells,neutrophils,monocytes,
lymphocytes,eosinophils,Red cells
may also leave vessels,but this
process is passive due to
endothelium injured and
intravascular hydrostatic pressure
increased.
The process of exudation is as
follows:
1 changes of vascular caliber and
flow
a) Transient arteriolar contraction,
b) Arteriolar dilatation within 30 min.
c) Blood flow slowing and stasis,
leukocytic margination and adhesion.
2 Increased vascular
permeability due to
a) Contraction of endothelial cells
and / or transcytosis increased
The injury is usually mild,The
response begins immediately,5-
10 min,at peak and disappears in
15-30 min,Venules involved,
Called immediate
transient response.(速发
短暂反应 )
cdjs:cdjs:
b) Damage of endothelial cells by
serious injury eg,Burn,infection,
The response begins
immediately and lasts hours-days,
Endothelial necrosis of
venules,capillaries and arteioles
involved.,Called immediate-
sustained response.
（速发持续反应）
Damage of endothelial cells may
also be injured by moderate
injury eg,X-ray,ultra-
violet,bacterial toxins,It begins 2-
12 hrs after injury,lasts hrs-days,
Venules and capillaries involved,
Called delayed-
prolonged response.
（迟发延续反应）
The damage of endothelium
may also be injured by
leukocyte adhesion.
c) High permeability of
new born capillary walls.
Beneficial effect of the
fluid exudate:
?Dilution of toxins
?Entry of antibodies
?Delivery of nutrients and oxygen
?Fibrin formation
?Stimulation of immune response
3).Leukocyte emigration
and functions-----an
important feature of
inflammatory reaction.
a) Margination and Rolling
b) Adhesion and Transmigration
c) Chemotaxis and Activation
d) Phagocytosis and Degranulation
(3)Proliferation,mainly fibroblasts,
endothelial cells and
macrophages (granulation tissue)
in chronic inflammation,epithelial
cells in viral infection.
Local signs and general
reaction
Local signs:
Redness (rubor)
Heat (calor)------hyperemia
Swelling (tumor)-------hyperemia
and edema
Pain (dolor)-----nerve ending
irritated by exudates and
inflammatory mediators,
Dysfunction
General reaction:
(1) Fever----- cytokines eg,IL-1,
TNF and mediators eg,PGE
irritate
sympathetic nerve and result in
vascular contraction in skin,
reduce heat dissipation.
(2) Increased leukocyte count 1.5-
2.0x109/L------releasing leukocytes
from bone marrow by IL-1 and TNF,
immature neutrophils (rod nucleus)
increased in peripheral blood (left
divert).
Depending on the duration,
inflammation is divided into acute
and chronic inflammation.
4 Sequels
(1)Heal
Complete heal repaired by
original tissue,recover original
structure and function,
Incomplete heal repaired by
granulation tissue,left scar after
organisation,can not recover original
structure and function.
(2)Spreading through
1) locally along interstitial tissue
space or natural canal of organ,eg,
renal TB → ureter →bladder
2) Lymphatics produce
lymphangitis and lymphadenitis The
agent may enter blood stream via
lymphatics.
3) Blood stream
Bacteremia Bacteria enter but not
multiply in blood,no toxic symptoms
systemically,bacteria may be found by
blood culture.
Toxemia toxins or derivatives of
bacteria enter blood and produce toxic
symptoms eg,high temperature,rigor,
degeneration or necrosis of heart,liver,
kidney,Toxic shock may happen in
serious case.
Septicemia Bacteria enter and multiply
in blood,produce toxic symptoms with
hemorrhagic spots or patches on skin or
mucous membrane.
Pyemia develop from septicemia
caused by pyogenic bacteria,multiple
abscess occur in many organs with
bacteria thrombi in small vessels (embolic
or metastatic abscess)
5 Classification according to
time course:
?Acute inflammation
?chronic inflammation
Histological types of inflammation
(1)Alterative inf,Often happens in
solid organs eg,Liver,kidney,heart
and brain,Caused by serious
infection or toxin,Eg,Mass necrosis
in acute hepatitis,Degeneration and
necrosis in encephalitis.
(2) Exudative inf,Depending
on predominant component of exudate,
it may be subdivided into,
1)Serous inflammation often
occurs in loosen connective tissue,
mucous or serous membrane,
produce inflammatory edema in
interstitial tissue,fluid
accumulation in serous cavity,flow
down on mucous membrane
(Catarrhal).
2)Fibrinous inflammation often
occurs on serous or mucous
membrane,
Pseudomembraneous inflammaton fibrin
is mixed with necrotic epithelium,
neutrophils to form false membrane on
mucous surface of pharynx,larynx,
trachea,bronchi and intestine,eg
diphtheria,dysentery.
假
膜
性
炎
结肠
喉
绒
毛
心
可
见
大
量
纤
维
素
渗
出
（
箭
头
所
指
）
，
造
成
心
包
腔
的
粘
连
。
3)Suppurative
(purulent)
inflammation
Always caused by
infection,pyogenic
bacteria,characterised by
a great number of
neutrophil exudation,
various degree tissue
necrosis and formation of
pus.
a) Surface suppuration occurs
on mucous membrane (suppurative
catarrhal) or in serous cavity (empyema).
b) Phlegmonous inflammation
occurs in loosen tissue in skin,muscle,
appendix,caused by haemolytic strepto-
cocci which can produce hyaluronidase as
spreading factor,break down hyaluronic
acid of connective tissue,The infitration of
neutrophils is diffuse and without limitation.
c) Abscess, a localized suppuration,
characterised by collection of pus,Great
number of neutrophils concentrated in an
injured area and liberate large amounts of
trypsin,which digests the tissue and convert it
into semiliquid material known as pus
(composed of neutrophils,necrotic tissue and
bacteria),Abscess is often caused by the
infection of staphylococci,The surrounding
inflamed tissue (necrotic tissue in acute
abscess,granulation tissue in chronic abscess)
is known as abscess wall.
心
包
腔
内
脓
性
渗
出
箭
头
所
指
为
积
脓
Pus may be drained by
Sinus,Pus is discharged through a
pathological canal with one opening
from abscess to body surface
Fistura Pus is discharged through a
pathological canal with two or more
openings from abscess to both body
surface and natural cavity (canal),or
between natural cavities (canals).
SINUS FISTURA
深部脓肿的结局：窦道与瘘管形成
(4)Hemorrhagic inflammation
lots of red cells in exudates due
to the damage of blood vessels,
(3) Proliferative inflammation
Most proliferative inflammation
are chronic
1),Non-specific proliferative inf,
Essential changes
(a)chronic inflammatory cells,
macrophages,lymphocytes,plasma
cells.
(b)proliferation of granulation tissue
(c)proliferation of parenchyma cells
2 ) granulomatous inflammation
(1)Composition
Epithelioid cells derived from macrophages
with abundant,pale-pink cytoplasm,resembling
epithelial cells.
Langhans’ giant cells or foreign body-type
giant cells,derived from coalescence of
macrophages,Huge cells with as many as 50
nuclei arranged in partial ring (Langhans’ type)
or scattered form (foreign body-type)
Caseous necrosis occur in tuberculosis
Lymphocytes
Fibroblasts
(2)Common causes,
infection eg,TB,leprosy,fungus,
parasites
immune disease eg,rheumatism,
Crohn’s disease,Wegener
granuloma.
Foreign materials eg,suture,
asbestos,talcum.
Tumor and tumor-like lesion eg,
xanthoma,histiocytosis X
Unknown,eg,sarcoidosis
(3)Conditions
1),Presence of indigestable
organism eg,tubercle bacilli or
particles eg,mineral oil.
2),Cell-mediated immunity to the
inciting agent,Lymphokines enhance
the transformation of macrophages
to multinucleated giant cells in
culture.
Chapter 3
Xu ruobing
OUTLINE
1 Definition
2 Causes
3 Basic pathological changes
4 Local signs and general reaction
5 Histological types
6 Inflammatory mediator and
chemotaxis
7 Sequels
Definition
Inflammation is a dynamic
processes by which living
tissue reacts to injury,They
concern vascular and
connective tissue particularly.
INFLAMMATION
Local signs and general
reaction
Local signs:
Redness (rubor)
Heat (calor)------hyperemia
Swelling (tumor)-------hyperemia
and edema
Pain (dolor)-----nerve ending
irritated by exudates and
inflammatory mediators,
Dysfunction
General reaction:
(1) Fever
(2) Increased leukocyte count
(2) ------releasing leukocytes from
bone marrow by IL-1 and TNF,
immature neutrophils (rod nucleus)
increased in peripheral blood (left
divert).
Depending on the duration,
inflammation is divided into acute
and chronic inflammation.
2 Causes
Physical agents,mechanical
trauma; over heat or cold;
ultra-violet or ionising
radiation.
Chemical substances,simple
chemicals eg,acids,alkaline
and organic poisons,
toxins from various bacteria
Infective agents,bacteria,
virus,and parasites,
Immunological and
hypersensitive reactions
necrotic tissue
3 Basic pathological changes
1 Alteration,degeneration,
necrosis
2 Exudation,escape of
fluid and cells from vessels
into injured tissue due to
permeability increasing.
3 Proliferation
1) Serum,differs from
transudate which occurs in
conditions where intravascular
pressure increases,
intravascular osmotic pressure
decreases,vascular
permeability does not increase.
Exudate Transudate
Appearance opaque clear
Sp,gravity >1.020 <1.020
Protein rich >2.5g% poor<2.5g%
Cells more few
>500/mm,Neu.+ <500/mm Neu,–
Coagulability + _
Rivata test + _
2) Fibrin Transformed from
fibrinogen in blood
3) Cells,neutrophils,monocytes,
lymphocytes,eosinophils,Red cells
may also leave vessels,but this
process is passive due to
endothelium injured and
intravascular hydrostatic pressure
increased.
The process of exudation is as
follows:
1 changes of vascular caliber and
flow
a) Transient arteriolar contraction,
b) Arteriolar dilatation within 30 min.
c) Blood flow slowing and stasis,
leukocytic margination and adhesion.
2 Increased vascular
permeability due to
a) Contraction of endothelial cells
and / or transcytosis increased
The injury is usually mild,The
response begins immediately,5-
10 min,at peak and disappears in
15-30 min,Venules involved,
Called immediate
transient response.(速发
短暂反应 )
cdjs:cdjs:
b) Damage of endothelial cells by
serious injury eg,Burn,infection,
The response begins
immediately and lasts hours-days,
Endothelial necrosis of
venules,capillaries and arteioles
involved.,Called immediate-
sustained response.
（速发持续反应）
Damage of endothelial cells may
also be injured by moderate
injury eg,X-ray,ultra-
violet,bacterial toxins,It begins 2-
12 hrs after injury,lasts hrs-days,
Venules and capillaries involved,
Called delayed-
prolonged response.
（迟发延续反应）
The damage of endothelium
may also be injured by
leukocyte adhesion.
c) High permeability of
new born capillary walls.
Beneficial effect of the
fluid exudate:
?Dilution of toxins
?Entry of antibodies
?Delivery of nutrients and oxygen
?Fibrin formation
?Stimulation of immune response
3).Leukocyte emigration
and functions-----an
important feature of
inflammatory reaction.
a) Margination and Rolling
b) Adhesion and Transmigration
c) Chemotaxis and Activation
d) Phagocytosis and Degranulation
(3)Proliferation,mainly fibroblasts,
endothelial cells and
macrophages (granulation tissue)
in chronic inflammation,epithelial
cells in viral infection.
Local signs and general
reaction
Local signs:
Redness (rubor)
Heat (calor)------hyperemia
Swelling (tumor)-------hyperemia
and edema
Pain (dolor)-----nerve ending
irritated by exudates and
inflammatory mediators,
Dysfunction
General reaction:
(1) Fever----- cytokines eg,IL-1,
TNF and mediators eg,PGE
irritate
sympathetic nerve and result in
vascular contraction in skin,
reduce heat dissipation.
(2) Increased leukocyte count 1.5-
2.0x109/L------releasing leukocytes
from bone marrow by IL-1 and TNF,
immature neutrophils (rod nucleus)
increased in peripheral blood (left
divert).
Depending on the duration,
inflammation is divided into acute
and chronic inflammation.
4 Sequels
(1)Heal
Complete heal repaired by
original tissue,recover original
structure and function,
Incomplete heal repaired by
granulation tissue,left scar after
organisation,can not recover original
structure and function.
(2)Spreading through
1) locally along interstitial tissue
space or natural canal of organ,eg,
renal TB → ureter →bladder
2) Lymphatics produce
lymphangitis and lymphadenitis The
agent may enter blood stream via
lymphatics.
3) Blood stream
Bacteremia Bacteria enter but not
multiply in blood,no toxic symptoms
systemically,bacteria may be found by
blood culture.
Toxemia toxins or derivatives of
bacteria enter blood and produce toxic
symptoms eg,high temperature,rigor,
degeneration or necrosis of heart,liver,
kidney,Toxic shock may happen in
serious case.
Septicemia Bacteria enter and multiply
in blood,produce toxic symptoms with
hemorrhagic spots or patches on skin or
mucous membrane.
Pyemia develop from septicemia
caused by pyogenic bacteria,multiple
abscess occur in many organs with
bacteria thrombi in small vessels (embolic
or metastatic abscess)
5 Classification according to
time course:
?Acute inflammation
?chronic inflammation
Histological types of inflammation
(1)Alterative inf,Often happens in
solid organs eg,Liver,kidney,heart
and brain,Caused by serious
infection or toxin,Eg,Mass necrosis
in acute hepatitis,Degeneration and
necrosis in encephalitis.
(2) Exudative inf,Depending
on predominant component of exudate,
it may be subdivided into,
1)Serous inflammation often
occurs in loosen connective tissue,
mucous or serous membrane,
produce inflammatory edema in
interstitial tissue,fluid
accumulation in serous cavity,flow
down on mucous membrane
(Catarrhal).
2)Fibrinous inflammation often
occurs on serous or mucous
membrane,
Pseudomembraneous inflammaton fibrin
is mixed with necrotic epithelium,
neutrophils to form false membrane on
mucous surface of pharynx,larynx,
trachea,bronchi and intestine,eg
diphtheria,dysentery.
假
膜
性
炎
结肠
喉
绒
毛
心
可
见
大
量
纤
维
素
渗
出
（
箭
头
所
指
）
，
造
成
心
包
腔
的
粘
连
。
3)Suppurative
(purulent)
inflammation
Always caused by
infection,pyogenic
bacteria,characterised by
a great number of
neutrophil exudation,
various degree tissue
necrosis and formation of
pus.
a) Surface suppuration occurs
on mucous membrane (suppurative
catarrhal) or in serous cavity (empyema).
b) Phlegmonous inflammation
occurs in loosen tissue in skin,muscle,
appendix,caused by haemolytic strepto-
cocci which can produce hyaluronidase as
spreading factor,break down hyaluronic
acid of connective tissue,The infitration of
neutrophils is diffuse and without limitation.
c) Abscess, a localized suppuration,
characterised by collection of pus,Great
number of neutrophils concentrated in an
injured area and liberate large amounts of
trypsin,which digests the tissue and convert it
into semiliquid material known as pus
(composed of neutrophils,necrotic tissue and
bacteria),Abscess is often caused by the
infection of staphylococci,The surrounding
inflamed tissue (necrotic tissue in acute
abscess,granulation tissue in chronic abscess)
is known as abscess wall.
心
包
腔
内
脓
性
渗
出
箭
头
所
指
为
积
脓
Pus may be drained by
Sinus,Pus is discharged through a
pathological canal with one opening
from abscess to body surface
Fistura Pus is discharged through a
pathological canal with two or more
openings from abscess to both body
surface and natural cavity (canal),or
between natural cavities (canals).
SINUS FISTURA
深部脓肿的结局：窦道与瘘管形成
(4)Hemorrhagic inflammation
lots of red cells in exudates due
to the damage of blood vessels,
(3) Proliferative inflammation
Most proliferative inflammation
are chronic
1),Non-specific proliferative inf,
Essential changes
(a)chronic inflammatory cells,
macrophages,lymphocytes,plasma
cells.
(b)proliferation of granulation tissue
(c)proliferation of parenchyma cells
2 ) granulomatous inflammation
(1)Composition
Epithelioid cells derived from macrophages
with abundant,pale-pink cytoplasm,resembling
epithelial cells.
Langhans’ giant cells or foreign body-type
giant cells,derived from coalescence of
macrophages,Huge cells with as many as 50
nuclei arranged in partial ring (Langhans’ type)
or scattered form (foreign body-type)
Caseous necrosis occur in tuberculosis
Lymphocytes
Fibroblasts
(2)Common causes,
infection eg,TB,leprosy,fungus,
parasites
immune disease eg,rheumatism,
Crohn’s disease,Wegener
granuloma.
Foreign materials eg,suture,
asbestos,talcum.
Tumor and tumor-like lesion eg,
xanthoma,histiocytosis X
Unknown,eg,sarcoidosis
(3)Conditions
1),Presence of indigestable
organism eg,tubercle bacilli or
particles eg,mineral oil.
2),Cell-mediated immunity to the
inciting agent,Lymphokines enhance
the transformation of macrophages
to multinucleated giant cells in
culture.
