Chapter 1
adaptation and injury
of tissue and cell
adaptation and injury of
tissue and cell
1.what is adaptation?
define,atrophy,hypertrophy,
hyperplasia,metaplasia.
department of pathology
2,describe the mechanisms
of damage of tissue and cell
3,describe the main
morphological change of
degeneration
department of pathology
4.tissue necrosis:
? define; morphological change;
? describe the mechanisms of cell death and histological
types of necrosis;
? the key difference between necrosis and apoptosis;
? outcome of tissue necrosis
department of pathology
adaptation and injury of
tissue and cell
inside and/or
outside stimulate
the factor
tissue and cell
adaptation injury
metabolism+ function +morphology
department of pathology
Section 1,adaptation
1.Atrophy---
Atrophy is the decrease in size of an
organ or cell by reduction in cell size
and/or reduction in cell number,often
by a mechanism involving apoptosis.
cell size and/or number
department of pathology
Atrophy occurs
physiological conditions
pathologic conditions
department of pathology
normal
Endocrine atrophy
department of pathology
Atrophy of brain
department of pathology
cardiac atrophy
Normal
department of pathology
atrophy of myocardial cells
department of pathology
Muscular atrophy
department of pathology
department of pathology
Hypertrophy:
cell size (physical volume )
physiological hypertrophy
pathological hypertrophy
compensatory hypertrophy
endocrine hypertrophy
department of pathology
Physiological
hypertrophy
1
department of pathology
hypertrophy
normal
atrophy
department of pathology
cardiac hypertrophy (compensatory)
endocrine hypertrophy
hyperplasia:
increase in cell number by mitosis
increase tissue or organ size
the stimuli for hypertrophy and
hyperplasia are very similar
department of pathology
hyperplasia
hypertrophy
combined
hypertrophy and
hyperplasia
department of pathology
department of pathology
Increasing its size without cell
replication ( hypertrophy )
Increasing its numbers by cell
division ( hyperplasia )
department of pathology
metaplasia:
is the transformation of one
mature differentiated cell type
into another
usually in response to an
irritating stimulus
e.g,smoking
bronchial epithelium metaplasia
department of pathology
Squamous metaplasia of
the bronchus
department of pathology
important types of metaplasia,
Squamous metaplasia:
bronchial epithelium
cervical epithelium
intestinal metaplasia:
gastric mucosal epithelium
transformatio
n to neoplasia
may be…
department of pathology
Squamous
metaplasia
of the cervix
department of pathology
intestinal
metaplasia
department of pathology
Section 2:
tissue and cell injury
1.causative agents of cell injury
physical,chemical,…
The hypoxia is the most basic
2.mechanisms of cell injury
department of pathology
DNA damage or loss
Membrane damage
Membrane pumps
? Na/K ATPase
Deficiency of metabolism
?Oxygen
?Glucose
?hormones
Intracellular
swelling
Membrane pumps
?Ca/Mg ATPase
O2,-
Failure of
membrane function
?Complement-mediated
cytolysis
?Alteration of
membrane lipids
?Cross-linking of
membrane proteins
lysosome
necrosis
Cell injury
reversible cell injury
irreversible cell injury
reversible --- degeneration
irreversible --- necrosis
department of pathology
Cell injury
reversible cell injury
irreversible cell injury
reversible --- degeneration
irreversible --- necrosis
department of pathology
3.morphologic lesions of
cell damage
… cause a variety of
histological abnormalities
hydropic change and fatty change
are two patterns commonly
department of pathology
Morphology---Reversible cell injury
Ultrastructural change:
plasma membrane alteration
mitochondrial change
dilation of the endoplasmic reticulum
Light microscope:
cellular swelling
(the first manifestation of almost all forms of
injury to cell)
fatty change
department of pathology
3-1,degeneration:
are a variety of changes
occurrence at
intracellular or
intercellular tissue
normal or abnormal
department of pathology
3-1-1 cellular swelling (hydropic degeneration)
is the most familiar type
is applied to cells when the
cytoplasm becomes pale and swollen due to the accumulation
of fluid
are called cloudy swelling
department of pathology
Cellular
swelling
department of pathology
Cellular
swelling
department of pathology
3-1-2 fatty change
accumulation of lipid droplets
( neutral fat )to intracellular
many small vacuoles to form
one large vacuole
filling the cell and displacing the
nucleus
department of pathology
Gross appearance:
becomes increasingly yellow
transform into a bright yellow,
soft,greasy organ
fatty liver( heart )
department of pathology
Light microscopy:
clear vacuoles within
parenchymal cells
fat solvents fat fusion
fatty change is the most often seen
the liver and heart
department of pathology
fatty metamorphosis (fatty change) of the liver
fatty change of liver
fatty heart
3-1-3.hyaline change
Hyaline refers to any alteration
within cells or in extracellular
space,which gives a homogeneous,
glassy,pink,any architecture
appearance in routine histological
sections stained with HE.
department of pathology
three subtypes:
1.vessels,important
2.Extracellular,scar tissue
3.Intracellular:
kidney,plasma cells,
viral infection,liver cells
department of pathology
three subtypes:
1.vessels,important
2.Extracellular,scar tissue
3.Intracellular:
kidney,plasma cells,
viral infection,liver cells
department of pathology
arteriolosclerosis
arteriolosclerosis
department of pathology
hyaline change arteriolosclerosis
three subtypes:
1.vessels,important
2.Extracellular,scar tissue
3.Intracellular:
kidney,plasma cells,
viral infection,liver cells
department of pathology
department of pathology
3-1-4,Amyloidosis:
With light microscope,amyloid appears
as an amorphous,eosinophilic,hyaline,
extracellular substance accumulation
Iodine solution dilute sulfuric acid
Amyloid yellow-red blue
Congo red
Amyloid pink or red
amyloidosis
department of pathology
3-1-5,Mucoid degeneration
mucus polysaccharide
accumulation in extracellular
department of pathology
Mucoid
degeneration
department of pathology
3-1-6,Pathologic pigmentation
Pigments accumulated normally
at intracellular or extracellular.
hemosiderin
lipofuscin
melanin
department of pathology
3-1-6,Pathologic pigmentation
Pigments accumulated normally
at intracellular or extracellular.
hemosiderin
lipofuscin
melanin
department of pathology
HE staining
Hemosiderin
staining
department of pathology
iron stain of
the liver
demonstrate of
hemosiderin
3-1-6,Pathologic pigmentation
Pigments accumulated normally
at intracellular or extracellular.
hemosiderin
lipofuscin
melanin
department of pathology
Lipofuscin in
myocardial cell
Electro
microscopy
department of pathology
lipochrome in the hepatocytes
3-1-6,Pathologic pigmentation
Pigments accumulated normally
at intracellular or extracellular.
hemosiderin
lipofuscin
melanin
department of pathology
anthracotic pigment in macrophages in a lymph node
department of pathology
Melanin body
3-1-7,Pathologic calcification
Calcium salts are normally found only in bone
and teeth.
In disease states,however,tissue can become
hardened by deposits of calcium salts,this
process is called calcification.
Calcification may be:
dystrophic,abnormal tissue
metastatic,normal tissue
Calcium
salts
Dystrophic
calcification
?Atheromatous plaque
?Old tuberculous lesions
?Fat necrosis
?Breast lesions
department of pathology
Dystrophic
calcification
department of pathology
dystrophic calcification of stomach
Metastatic
calcification
?Hyperparathyriodism
?Hypercalcaemia of
malignancy
metastatic calcification
Cell injury
reversible cell injury
irreversible cell injury
reversible --- degeneration
irreversible --- necrosis
department of pathology
3-2,necrosis
Cell death,
Cells can be recognized as dead with
metabolism stopped,morphologic
pattern changed,function disappeared.
Cell death may be two types:
necrosis and apoptosis
department of pathology
3-2-1,What is, necrosis”?
Necrosis is the death of
cells or tissues which are
still part of the living
organism.
department of pathology
? living organism?
differ from ?autolysis after death?
difference between
necrosis and autolysis?
? part of ?
differ from? whole or systemic?
difference between
necrosis and death?
department of pathology
3-2-2,Base lesion
normal
pyknosis karyorrhexis karyolysis
important histological marking of necrosis
department of pathology
karyolysis
department of pathology
Pyknosis and karorrhexis and karyolysis
Nuclear change
( pyknosis,karyolysis,karyorrhexis)
cell membrane broken
swelling and lysis of cells
eosinophilic,thin granular,
lacks any structure
3-2-3,histological types
? coagulative necrosis
caseous necrosis
gangrene (dry,moist,gas)
? liquefactive necrosis
( colliquative necrosis )
fat necrosis
? fibrinoid necrosis
? gangrene
Ⅰ,coagulative necrosis:
That is the most common form of
necrosis and occurs in almost all
organ.
occurring in the heart,kidney and
spleen,but occurring in most tissues
department of pathology
gross appearance,depend upon its size
swollen and firm
later become soft as a result…?
microscopic examination:
occurring loss of nucleus but preservation
of the basic cellular shape,permitting
recognition of the cell outlines and tissues
architecture
department of pathology
Coagulative
necrosis
department of pathology
department of pathology
Coagulative necrosis
Coagulative necrosis
coagulative necrosis
coagulative necrosis of adrenal cortex
Caseous necrosis:
commonly seen in TB
gross section:,caseous”
histologically:
The complete loss of normal tissue
architecture is replaced by amorphous,
granular and eosinophilic tissue.
department of pathology
Caseous necrosis of the tuberculosis
Ⅱ,Liquefactive necrosis:
commonly seen in brain
because of its lack of any substantial
supporting stroma,its lack of protein and
full of phospholipids.
hydrolytic enzyme
autolysis or heterolysis
liquefaction
department of pathology
Liquefactive
necrosis of
the brain
tissue
Brain
malacia
department of pathology
Liquefactive necrosis of the brain tissue
department of pathology
Fat necrosis:
? direct trauma:
release of triglycerides following trauma elicits a rapid inflammatory response.
? enzymatic lipolysis,
lipase liberated from damaged acini act on fat cells in the peritoneal cavity thus:
lipases Ca+
triglycerides fatty acids insoluble soaps
department of pathology
fat necrosis of the pancreas
fat necrosis of the pancreas
Ⅲ,Fibrinoid necrosis:
This occurs in malignant hypertension,where increased
arterial pressure results in necrosis of the smooth muscle wall.
This allows seepage of plasma into the media with consequent deposition
of fibrin.
The appearance is termed fibrinoid necrosis,
department of pathology
department of pathology
Ⅳ, Gangrene:
necrosis + secondary infection
as a result of action of certain
bacteria,notably clostridia.
The affected tissue appear
black,because of the deposition of iron
sulphide from degraded haemoglobin.
three subtypes,dry,wet,gas.
department of pathology
Dry gangrene
department of pathology
"dry" gangrene department of pathology
Dry gangrene
department of pathology
"dry" gangrene department of pathology
Wet (moist) gangrene department of pathology
3-2-4,Outcome of necrosis
ⅰ, Autolysis or heterolysis
acute inflammation
ⅱ, are removed by phagocytes
or blood vessel and lymph vessel
ⅲ, abruption and exclusion
ⅳ, organization
ⅴ, encapsulation and calcification
department of pathology
Outcome of necrosis
ⅴ
ⅳ
ⅲ
ⅱ
ⅰ
department of pathology
3-3,apoptosis
Apoptosis is energy
dependent mechanism of
cell death for the deletion of
unwanted individual cell,it
is also known as
?programmed cell death?.
department of pathology
Inhibition of apoptosis
cell accumulation
e.g,neoplasia (tumour)
Increase of apoptosis
cell loss
e.g,atrophy (brain)
department of pathology
A 14-years-old
boy shows the
signs of
accelerated aging
Abnormal
apoptosis
aging
department of pathology
Apoptosis can be either physiological or pathological
Physiological:
? maintenance of organ size in adults
? organ development
? remodelling in embryo
Pathological:
? response to irreparable DNA damage
? preventing the perpetuation of a
genetically abnormal cell
department of pathology
Stages of apoptosis:
The process of apoptosis occurs
the following four stages.
1.priming
2.enzyme activation
3.fragmentation of the cell
4.phagocytosis
department of pathology
1.Priming:
Synthesis of enzymes
e.g,proteases and nucleases
No structural cellular changes
department of pathology
2.Enzyme activation:
endonucleases
chromatin DNA fragmentation
proteases
cytoskeleton shrinkage
plasma membrane organelles
remain intact
department of pathology
3.fragmentation of the cell:
fragmentation into
apoptotic bodies
apoptotic bodies contains
intact plasma membranes
absence of any inflammation
department of pathology
department of pathology
department of pathology
department of pathology
Apoptotic bodies
department of pathology
4.phagocytosis
Apoptotic fragments are
phagocytosed and destroyed
by adjacent cells.
Surrounding cells then move
together to fill vacant space.
department of pathology
department of pathology
Apoptotic
bodies
phagocyte
phagocytosis
department of pathology
necrosis
apoptosisnormal
inflammation
phagocytosis
department of pathology
injury
recovery
normal cell normal cell
death
necrosis apoptosis
department of pathology
Apoptosis
department of pathology
necrosis
department of pathology
the key difference between necrosis and apoptosis
Feature Necrosis Apoptosis
occurrence Pathological conditions Physiological or pathological conditions
Number of cells
involved
More than one cell in
the group Single cells
Cellular status Cell membrane broken Cell membrane remains whole
appearances Swelling and lysis of cell Shrinkage and fragmentation of cell
Surrounding
response
Inflammatory cell
present None
Destiny of dead
cells
Phagocytosed by
inflammatory cells
Phagocytosed by
adjacent cells in the
same tissue
department of pathology
2002年度诺贝尔生理学或医学奖
授予三位在 凋亡研究领域 作出重大贡
献的科学家。
Sydney Brenner,(1927~)
英国科学家,Salk生物
研究所
John Sulston,(1942~),
英国科学家,剑桥大学
Sanger中心
Robert Horvitz,
(1947~),美国科学家，
麻省理工学院
3-2,necrosis
Cell death,
Cells can be recognized as dead with
metabolism stopped,morphologic
pattern changed,function disappeared.
Cell death may be two types:
necrosis and apoptosis
department of pathology
3-2-1,What is, necrosis”?
Necrosis is the death of
cells or tissues which are
still part of the living
organism.
department of pathology
3-2-2,Base lesion
normal
pyknosis karyorrhexis karyolysis
3-2-3.histological types
? coagulative necrosis
caseous necrosis
gangrene (dry,moist,gas)
? liquefactive necrosis
( colliquative necrosis )
fat necrosis
? fibrinoid necrosis
? gangrene department of pathology
3-2-4,Outcome of necrosis
ⅰ, Autolysis or heterolysis
acute inflammation
ⅱ, are removed by phagocytes
or blood vessel and lymph vessel
ⅲ, abruption and exclusion
ⅳ, organization
ⅴ, encapsulation and calcification
department of pathology
3-3,apoptosis
Apoptosis is energy
dependent mechanism of
cell death for the deletion of
unwanted individual cell,it
is also known as
?programmed cell death?.
department of pathology
tissue necrosis:
√ define
√ morphological change
√ histological types
√ outcome
√ necrosis and apoptosis
department of pathology
department of pathology
adaptation and injury
of tissue and cell
adaptation and injury of
tissue and cell
1.what is adaptation?
define,atrophy,hypertrophy,
hyperplasia,metaplasia.
department of pathology
2,describe the mechanisms
of damage of tissue and cell
3,describe the main
morphological change of
degeneration
department of pathology
4.tissue necrosis:
? define; morphological change;
? describe the mechanisms of cell death and histological
types of necrosis;
? the key difference between necrosis and apoptosis;
? outcome of tissue necrosis
department of pathology
adaptation and injury of
tissue and cell
inside and/or
outside stimulate
the factor
tissue and cell
adaptation injury
metabolism+ function +morphology
department of pathology
Section 1,adaptation
1.Atrophy---
Atrophy is the decrease in size of an
organ or cell by reduction in cell size
and/or reduction in cell number,often
by a mechanism involving apoptosis.
cell size and/or number
department of pathology
Atrophy occurs
physiological conditions
pathologic conditions
department of pathology
normal
Endocrine atrophy
department of pathology
Atrophy of brain
department of pathology
cardiac atrophy
Normal
department of pathology
atrophy of myocardial cells
department of pathology
Muscular atrophy
department of pathology
department of pathology
Hypertrophy:
cell size (physical volume )
physiological hypertrophy
pathological hypertrophy
compensatory hypertrophy
endocrine hypertrophy
department of pathology
Physiological
hypertrophy
1
department of pathology
hypertrophy
normal
atrophy
department of pathology
cardiac hypertrophy (compensatory)
endocrine hypertrophy
hyperplasia:
increase in cell number by mitosis
increase tissue or organ size
the stimuli for hypertrophy and
hyperplasia are very similar
department of pathology
hyperplasia
hypertrophy
combined
hypertrophy and
hyperplasia
department of pathology
department of pathology
Increasing its size without cell
replication ( hypertrophy )
Increasing its numbers by cell
division ( hyperplasia )
department of pathology
metaplasia:
is the transformation of one
mature differentiated cell type
into another
usually in response to an
irritating stimulus
e.g,smoking
bronchial epithelium metaplasia
department of pathology
Squamous metaplasia of
the bronchus
department of pathology
important types of metaplasia,
Squamous metaplasia:
bronchial epithelium
cervical epithelium
intestinal metaplasia:
gastric mucosal epithelium
transformatio
n to neoplasia
may be…
department of pathology
Squamous
metaplasia
of the cervix
department of pathology
intestinal
metaplasia
department of pathology
Section 2:
tissue and cell injury
1.causative agents of cell injury
physical,chemical,…
The hypoxia is the most basic
2.mechanisms of cell injury
department of pathology
DNA damage or loss
Membrane damage
Membrane pumps
? Na/K ATPase
Deficiency of metabolism
?Oxygen
?Glucose
?hormones
Intracellular
swelling
Membrane pumps
?Ca/Mg ATPase
O2,-
Failure of
membrane function
?Complement-mediated
cytolysis
?Alteration of
membrane lipids
?Cross-linking of
membrane proteins
lysosome
necrosis
Cell injury
reversible cell injury
irreversible cell injury
reversible --- degeneration
irreversible --- necrosis
department of pathology
Cell injury
reversible cell injury
irreversible cell injury
reversible --- degeneration
irreversible --- necrosis
department of pathology
3.morphologic lesions of
cell damage
… cause a variety of
histological abnormalities
hydropic change and fatty change
are two patterns commonly
department of pathology
Morphology---Reversible cell injury
Ultrastructural change:
plasma membrane alteration
mitochondrial change
dilation of the endoplasmic reticulum
Light microscope:
cellular swelling
(the first manifestation of almost all forms of
injury to cell)
fatty change
department of pathology
3-1,degeneration:
are a variety of changes
occurrence at
intracellular or
intercellular tissue
normal or abnormal
department of pathology
3-1-1 cellular swelling (hydropic degeneration)
is the most familiar type
is applied to cells when the
cytoplasm becomes pale and swollen due to the accumulation
of fluid
are called cloudy swelling
department of pathology
Cellular
swelling
department of pathology
Cellular
swelling
department of pathology
3-1-2 fatty change
accumulation of lipid droplets
( neutral fat )to intracellular
many small vacuoles to form
one large vacuole
filling the cell and displacing the
nucleus
department of pathology
Gross appearance:
becomes increasingly yellow
transform into a bright yellow,
soft,greasy organ
fatty liver( heart )
department of pathology
Light microscopy:
clear vacuoles within
parenchymal cells
fat solvents fat fusion
fatty change is the most often seen
the liver and heart
department of pathology
fatty metamorphosis (fatty change) of the liver
fatty change of liver
fatty heart
3-1-3.hyaline change
Hyaline refers to any alteration
within cells or in extracellular
space,which gives a homogeneous,
glassy,pink,any architecture
appearance in routine histological
sections stained with HE.
department of pathology
three subtypes:
1.vessels,important
2.Extracellular,scar tissue
3.Intracellular:
kidney,plasma cells,
viral infection,liver cells
department of pathology
three subtypes:
1.vessels,important
2.Extracellular,scar tissue
3.Intracellular:
kidney,plasma cells,
viral infection,liver cells
department of pathology
arteriolosclerosis
arteriolosclerosis
department of pathology
hyaline change arteriolosclerosis
three subtypes:
1.vessels,important
2.Extracellular,scar tissue
3.Intracellular:
kidney,plasma cells,
viral infection,liver cells
department of pathology
department of pathology
3-1-4,Amyloidosis:
With light microscope,amyloid appears
as an amorphous,eosinophilic,hyaline,
extracellular substance accumulation
Iodine solution dilute sulfuric acid
Amyloid yellow-red blue
Congo red
Amyloid pink or red
amyloidosis
department of pathology
3-1-5,Mucoid degeneration
mucus polysaccharide
accumulation in extracellular
department of pathology
Mucoid
degeneration
department of pathology
3-1-6,Pathologic pigmentation
Pigments accumulated normally
at intracellular or extracellular.
hemosiderin
lipofuscin
melanin
department of pathology
3-1-6,Pathologic pigmentation
Pigments accumulated normally
at intracellular or extracellular.
hemosiderin
lipofuscin
melanin
department of pathology
HE staining
Hemosiderin
staining
department of pathology
iron stain of
the liver
demonstrate of
hemosiderin
3-1-6,Pathologic pigmentation
Pigments accumulated normally
at intracellular or extracellular.
hemosiderin
lipofuscin
melanin
department of pathology
Lipofuscin in
myocardial cell
Electro
microscopy
department of pathology
lipochrome in the hepatocytes
3-1-6,Pathologic pigmentation
Pigments accumulated normally
at intracellular or extracellular.
hemosiderin
lipofuscin
melanin
department of pathology
anthracotic pigment in macrophages in a lymph node
department of pathology
Melanin body
3-1-7,Pathologic calcification
Calcium salts are normally found only in bone
and teeth.
In disease states,however,tissue can become
hardened by deposits of calcium salts,this
process is called calcification.
Calcification may be:
dystrophic,abnormal tissue
metastatic,normal tissue
Calcium
salts
Dystrophic
calcification
?Atheromatous plaque
?Old tuberculous lesions
?Fat necrosis
?Breast lesions
department of pathology
Dystrophic
calcification
department of pathology
dystrophic calcification of stomach
Metastatic
calcification
?Hyperparathyriodism
?Hypercalcaemia of
malignancy
metastatic calcification
Cell injury
reversible cell injury
irreversible cell injury
reversible --- degeneration
irreversible --- necrosis
department of pathology
3-2,necrosis
Cell death,
Cells can be recognized as dead with
metabolism stopped,morphologic
pattern changed,function disappeared.
Cell death may be two types:
necrosis and apoptosis
department of pathology
3-2-1,What is, necrosis”?
Necrosis is the death of
cells or tissues which are
still part of the living
organism.
department of pathology
? living organism?
differ from ?autolysis after death?
difference between
necrosis and autolysis?
? part of ?
differ from? whole or systemic?
difference between
necrosis and death?
department of pathology
3-2-2,Base lesion
normal
pyknosis karyorrhexis karyolysis
important histological marking of necrosis
department of pathology
karyolysis
department of pathology
Pyknosis and karorrhexis and karyolysis
Nuclear change
( pyknosis,karyolysis,karyorrhexis)
cell membrane broken
swelling and lysis of cells
eosinophilic,thin granular,
lacks any structure
3-2-3,histological types
? coagulative necrosis
caseous necrosis
gangrene (dry,moist,gas)
? liquefactive necrosis
( colliquative necrosis )
fat necrosis
? fibrinoid necrosis
? gangrene
Ⅰ,coagulative necrosis:
That is the most common form of
necrosis and occurs in almost all
organ.
occurring in the heart,kidney and
spleen,but occurring in most tissues
department of pathology
gross appearance,depend upon its size
swollen and firm
later become soft as a result…?
microscopic examination:
occurring loss of nucleus but preservation
of the basic cellular shape,permitting
recognition of the cell outlines and tissues
architecture
department of pathology
Coagulative
necrosis
department of pathology
department of pathology
Coagulative necrosis
Coagulative necrosis
coagulative necrosis
coagulative necrosis of adrenal cortex
Caseous necrosis:
commonly seen in TB
gross section:,caseous”
histologically:
The complete loss of normal tissue
architecture is replaced by amorphous,
granular and eosinophilic tissue.
department of pathology
Caseous necrosis of the tuberculosis
Ⅱ,Liquefactive necrosis:
commonly seen in brain
because of its lack of any substantial
supporting stroma,its lack of protein and
full of phospholipids.
hydrolytic enzyme
autolysis or heterolysis
liquefaction
department of pathology
Liquefactive
necrosis of
the brain
tissue
Brain
malacia
department of pathology
Liquefactive necrosis of the brain tissue
department of pathology
Fat necrosis:
? direct trauma:
release of triglycerides following trauma elicits a rapid inflammatory response.
? enzymatic lipolysis,
lipase liberated from damaged acini act on fat cells in the peritoneal cavity thus:
lipases Ca+
triglycerides fatty acids insoluble soaps
department of pathology
fat necrosis of the pancreas
fat necrosis of the pancreas
Ⅲ,Fibrinoid necrosis:
This occurs in malignant hypertension,where increased
arterial pressure results in necrosis of the smooth muscle wall.
This allows seepage of plasma into the media with consequent deposition
of fibrin.
The appearance is termed fibrinoid necrosis,
department of pathology
department of pathology
Ⅳ, Gangrene:
necrosis + secondary infection
as a result of action of certain
bacteria,notably clostridia.
The affected tissue appear
black,because of the deposition of iron
sulphide from degraded haemoglobin.
three subtypes,dry,wet,gas.
department of pathology
Dry gangrene
department of pathology
"dry" gangrene department of pathology
Dry gangrene
department of pathology
"dry" gangrene department of pathology
Wet (moist) gangrene department of pathology
3-2-4,Outcome of necrosis
ⅰ, Autolysis or heterolysis
acute inflammation
ⅱ, are removed by phagocytes
or blood vessel and lymph vessel
ⅲ, abruption and exclusion
ⅳ, organization
ⅴ, encapsulation and calcification
department of pathology
Outcome of necrosis
ⅴ
ⅳ
ⅲ
ⅱ
ⅰ
department of pathology
3-3,apoptosis
Apoptosis is energy
dependent mechanism of
cell death for the deletion of
unwanted individual cell,it
is also known as
?programmed cell death?.
department of pathology
Inhibition of apoptosis
cell accumulation
e.g,neoplasia (tumour)
Increase of apoptosis
cell loss
e.g,atrophy (brain)
department of pathology
A 14-years-old
boy shows the
signs of
accelerated aging
Abnormal
apoptosis
aging
department of pathology
Apoptosis can be either physiological or pathological
Physiological:
? maintenance of organ size in adults
? organ development
? remodelling in embryo
Pathological:
? response to irreparable DNA damage
? preventing the perpetuation of a
genetically abnormal cell
department of pathology
Stages of apoptosis:
The process of apoptosis occurs
the following four stages.
1.priming
2.enzyme activation
3.fragmentation of the cell
4.phagocytosis
department of pathology
1.Priming:
Synthesis of enzymes
e.g,proteases and nucleases
No structural cellular changes
department of pathology
2.Enzyme activation:
endonucleases
chromatin DNA fragmentation
proteases
cytoskeleton shrinkage
plasma membrane organelles
remain intact
department of pathology
3.fragmentation of the cell:
fragmentation into
apoptotic bodies
apoptotic bodies contains
intact plasma membranes
absence of any inflammation
department of pathology
department of pathology
department of pathology
department of pathology
Apoptotic bodies
department of pathology
4.phagocytosis
Apoptotic fragments are
phagocytosed and destroyed
by adjacent cells.
Surrounding cells then move
together to fill vacant space.
department of pathology
department of pathology
Apoptotic
bodies
phagocyte
phagocytosis
department of pathology
necrosis
apoptosisnormal
inflammation
phagocytosis
department of pathology
injury
recovery
normal cell normal cell
death
necrosis apoptosis
department of pathology
Apoptosis
department of pathology
necrosis
department of pathology
the key difference between necrosis and apoptosis
Feature Necrosis Apoptosis
occurrence Pathological conditions Physiological or pathological conditions
Number of cells
involved
More than one cell in
the group Single cells
Cellular status Cell membrane broken Cell membrane remains whole
appearances Swelling and lysis of cell Shrinkage and fragmentation of cell
Surrounding
response
Inflammatory cell
present None
Destiny of dead
cells
Phagocytosed by
inflammatory cells
Phagocytosed by
adjacent cells in the
same tissue
department of pathology
2002年度诺贝尔生理学或医学奖
授予三位在 凋亡研究领域 作出重大贡
献的科学家。
Sydney Brenner,(1927~)
英国科学家,Salk生物
研究所
John Sulston,(1942~),
英国科学家,剑桥大学
Sanger中心
Robert Horvitz,
(1947~),美国科学家，
麻省理工学院
3-2,necrosis
Cell death,
Cells can be recognized as dead with
metabolism stopped,morphologic
pattern changed,function disappeared.
Cell death may be two types:
necrosis and apoptosis
department of pathology
3-2-1,What is, necrosis”?
Necrosis is the death of
cells or tissues which are
still part of the living
organism.
department of pathology
3-2-2,Base lesion
normal
pyknosis karyorrhexis karyolysis
3-2-3.histological types
? coagulative necrosis
caseous necrosis
gangrene (dry,moist,gas)
? liquefactive necrosis
( colliquative necrosis )
fat necrosis
? fibrinoid necrosis
? gangrene department of pathology
3-2-4,Outcome of necrosis
ⅰ, Autolysis or heterolysis
acute inflammation
ⅱ, are removed by phagocytes
or blood vessel and lymph vessel
ⅲ, abruption and exclusion
ⅳ, organization
ⅴ, encapsulation and calcification
department of pathology
3-3,apoptosis
Apoptosis is energy
dependent mechanism of
cell death for the deletion of
unwanted individual cell,it
is also known as
?programmed cell death?.
department of pathology
tissue necrosis:
√ define
√ morphological change
√ histological types
√ outcome
√ necrosis and apoptosis
department of pathology
department of pathology
