bbs ii slide cellular adaptations of growth diffrentiation
Definitions
• Pathology is a dicipline bridging clinical
practice & basic sience
• To render diagnosis & guide therapy
• Identity changes in :
– Gross
– Morphology (microscopy) appearance of cell
tissues
The scientific focus of pathology is :
Etiology
• On the cause of disease
Pathogenesis
• Mechanisme of its development & the
pathways by which morphologic changes
occur
Normal Homeostasis
If cell adjusting structure & function
to accommodate changing demands &
extracellular stresses
Stages in the cellular response to stress & injurious
stimuli
Stresses/pathologic stimuli the cell:
Adaptation
• Atrophy
• Hypertrophy
• Hyperplasia
• Metaplasia
Irreversible injury & ultimately dies
Perubahan sel & jaringan :
Agenesis
Hyperplasia
Aplasia
Metaplasia
Hypoplasia
Dysplasia
Atrophy
Anaplasia
Hypertrophy
Granuloma
Agenesis
Aplasia
• Complete absent of an
organ
• E.g. :
• Anlarge is present but
never develops
• E.g. :
– Renal agenesis
– Ovarial agenesis
– Tubal agenesis, etc.
– Lung aplasia with tissue
containing rudimentary
duct & connective tissue
Hypoplasia
• Anlarge develoved incompletly but the tissue
histhologicaly normal
• Ex. : microcephaly
Atrophy
• Decrease in the:
– Size
– Function of a cell
• But not dead
!
Causes of atrophy :
1.
2.
3.
4.
5.
6.
functional demand (immobilitation in fracture, prolonged
bed rest)
Inadequate supply O2 (ischemia)
Insufficient nutrients (starvation, inadequate nutrition,
chronic disease)
Interrruption of trophic signals transmitted by chemical
mediators (endocrine system/Neuromusculator transmission)
e.g. : thyroid, adrenal cortex, ovarium, testis.
Persistent cell injury by chronic inflamation
e.g. : chronic gastritis, prolonged pressure
Aging : brain, heart (Senile Atrophy)
#
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The mechanism of atrophy :
• synthesis
• catabolism
• Influenced by a number of hormones
e.g. :
• Insulin
• Tyroid stimulating hormon
• Glucocorticoids
Hypertrophy
•
in the size of cell accompanied by augmented
functional capacity
• Hypertrophy is a response to trophic signals
• Commonly a normal procesess
4
… hypertrophy
Physiological (hormonal) hypertrophy
• in puberty
• production of sex hormon
• Hypertrophy breast tissue
• Abnormal hormon production in cancer
Functional demands
• Exercise
• Pathological conditions (myocardial cell)
• Kidney hypertrophy on surgical removed
')
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Hyperplasia
the number of cells in an organ / tissue
Hyperplasia can be :
1. Physiologic hyperplasia
– Hormonal hyperplasia
– Compensatory hyperplasia
2. Pathologic hyperplasia
– Excessive hormonal / growth factor stimulation
e.g. : Endometrial hyperplasia
:
/
(
)&
•
•
/
/
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%
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)& % ((
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+
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• Squamous metaplasia of the bronchial epithelium to tobacco
• Lower oesophagus by reflux acidic gastric
• Endocervical metaplasia
Metaplasia is usually reversible if the stimulus is
removed
;
Metaplasia of normal columnar (left) to squamous epithelium
(right) in a bronchus, shown (A) schematically and (B)
histologically
Dysplasia
++ +
+&
&' ' &# )'9 3 )# 0
% ++ + % (0
& *
'9 &'
* &#
&'))
1. Variation in the size & shape of cells
2. Enlargment, irregularity & hyperchromatism of the
nuclei
3. Disorderly arrangement of the cells within the
epithelium
# ( )& % ((
' &# % 8'@
1
%# )
Dysplasia is a preneoplastic lession in the sense
that it is a necessary stage in the multistep cellular
evolution to cancer.
Dysplasia included in the morphological classification of the
stage if intraepithelial neoplasia
Anaplasia
• Normal cell
primitive cell
• E.g. : Malignant cell
– Carcinoma
– Sarcoma
– Adenocarcinoma
– Lymphoma
– Etc.
2 principal pattern of cell death :
NECROSIS
APOPTOSIS
•
•
•
•
•
Commonly : coagulative necrosis
Cellular swelling
Protein denaturation
Organellar breakdown
Cell rupture
• Regulated event
• Programmed death
Term
Definition
Necrosis
Antemortem pathologic cell death
Apoptosis
Antemortem programmed cell death
Autolysis
Postmortem cell death
CAUSES OF CELL INJURY
Hypoxia
Physical Agent
Chemical and drugs
Microbiology Agents
Immunologic Reaction
Genetic Defects
Nutritional Inbalance
Aging
… CAUSES OF CELL INJURY
Hypoxia
•
•
•
•
Anemia
Ischemia
Intoxication CO2
Aerobic oxidative
respiration
Physical Agent
• Mechanical trauma
• Extreme temprature :
heat, cold
• Radiation: X-ray, sun light
• Electric shock
• Athmosphere pressure
… CAUSES OF CELL INJURY
Chemical agent & drugs
• Sufficiently concentrated :
– Glucose
– Salt
– O2
•
•
•
•
•
Air pollutants
Insecticides
Asbestosis
Ethanol
Cellular metabolism (i.e.
waste products)
Microbiology Agents
•
•
•
•
•
Tape worms
Rickettsia
Virus
Bacteria
Fungi
!
… CAUSES OF CELL INJURY
Immunologic Reaction
• Anaphylactic reaction
• Autoimmune diseases
Genetic Defects
• Congenital malformation
• Sickle cell anemia
• G-6-PD
Nutritional Imbalance
• Protein calori insufficiency
• Vitamins defficiency
• Diabetes
Aging
"
Mechanism of Cell Injury
Cellular
response to
injurious
stimuli
depends on :
• Injury type
• Duration
• Severity
Current
Status :
• Nutritional
• Hormonal
• Adaptibility
of the cell
Intercellular
systems :
• Cell membrane
integrity
• Aerobic
respiration
• Protein synthesis
• Integrity genetic
apparatus
O2 & oxygen
derived free
radicals :
• Ischemic
• Hypoxic
injury
Normal cell & changes in reversible & irreversible cell injury
(necrosis)
The ultrastructural features of these stages of cell injury.
4
Reversible injury
• Reduced of :
– Oxidative
phosphorylation in
mitochondria
– Activity Na Pump
• Cellular swelling
• Loss of microvilli
Irreversible injury
• Severe vacuolization of
the mitochondria
• Damage of :
– Mitochondrial matrix
– Plasma membrane
• Swelling of lysosomes
Glycogen depleted
• Accumulation of
↓ protein synthesis
amorphous calcium
Formation of cell surface
• Rich dentities in
blebs
mitochondrial matrix
5
:
Figure 1-6.
Cellular features of
necrosis (left) &
apoptosis (right)
Forms & Morphology of Cell Injury
1. Reversible acute cell injury
2. Necrosis (cell death after irreversible injury)
3. Apoptosis (cell death by suicide)
4. Subcellular alteration as a respond to chronic
or persistent injury stimuli
5. Intracellular accumulations of a number of
substance
;
Sublethal Damage
1. Recoverable (but
necrosis is not)
2. Ultrastructural damage mitochondria
3. Swelling of cellular organelles ( hydrophic deg.)
4. Fatty change is impairment of metabolism
Necrosis
Morphologic changes that follow cell death in living tissue
1. Intense eosinophilia of the dead cell is due to
loss of RNA & coagulation of protein
2. Nuclei undergo:
1. Pyknosis
2. Karyorhexis
3. Karyolysis
Leaving a shrunken cell devoid of nucleus
1. Protein may be liberated from the dead cell
# ( 0# +
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/
/
))
9-( &'% '
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)&'
* &# % ++
*0 & '
Autolysis : is a cell death by hydrolitic
enzymes.
Heterolysis : cell death by the lysosomes of
invading inflammatory cells.
Nuclear Changes: This nucleus is faded -- karyolysis.
Karyolytic nuclei suggest that cells have died (undergone necrosis).
)0 %'*'%3 %+
%#
)
)( ++
2 ' '% & )
)
)& &# & % ++) # 8 '
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7 )& *& ' * %& * & 1 % + ) ' * %&' 2'&#
% & + % )')
!
• Gumatous Necrosis
• Dead tissue, it is firm & rubbery like caseous necrosis in the
spirochetal infection syphilis.
• Hemorrhagic Necrosis
• Dead tissue suffused with extravasated red cell, when cell
death is due to blockage
• Fat Necrosis
• Not really necrosis.
• Focal areas of fat destruction tipically occuring following
pancreatic injury /after trauma to fat for (ex. in the breast)
• Describes foci of hard yellow material seen in dead adipose
tissue
• Fibrinoid Necrosis
• Fibrin deposited in damage necrotic vessel
walls in hypertension and vasculitis
• Gangrene
• Extensive tissue necrosis ; is complicated to
a variable degree by secondary bacterial
infection
"
APOPTOSIS
• Responsible for the programmed cell death in several
important physiology processes
• Including :
– During embryogenesis (in implantation, organogenesis, &
developmental involution)
– Hormon dependent physiologic involution (endometrium,
lactating, prostate after castration)
– Cell deletion in proliferating population (intestinal crypt
epithelium / cell dead in tumor)
– Deletion of autoreactive T cell in the thymus,
cell death of cytokine starved lymphocytes
CLINICAL EFFECTS OF NECROSIS
• Abnormal function
– Kidney
–
–
–
–
: renal failure
Cortex in brain : muscle paralysis
Heart
: heart failure
Lung
: hemoptysis
Bacterial infection : gangrene
4
• Realease of contens of necrotic cells
– Liver
: elevation SGOT
– Heart : creatine kinase
• Systemic effects
– Fever
– Inflamatoar Reaction
• Local effects
– Hemorrhage
– Ulceration
Apoptosis of epidermal cells in an immunemediated reaction
A. Apoptotic cells are visible in the
epidermis with eosinophilic cytoplasm
and small, dense nuclei.
B. High power of apoptotic cell in liver in
immune-mediated hepatic cell injury.
(Courtesy of Dr. Scott Granter, Brigham and Women's Hospital, Boston, AM.) (Courtesy of Dr. Dhanpat Jain, Yale University, New Haven, CT.)
5
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Granuloma
• Special type of chronic inflamation in tissue
reaction.
• Cause :
infection :
TBC
fungal
noninfection :
sarcoidosis
Crohn’s
disease
syphilis,
etc
:
NECROBIOSIS
•
•
•
•
•
Gradual cell damage
Progressive
Singly or small group cells.
Reversible (+/-)
Example : hepar cell deg.
cell death healing
fibrosis.
Alterations in structure and function that may
lead to cell death, or at least diminished capacity
of the cell to respond an injury
• Reduced cell in :
– Pleomorphic vacuolated mitochondria
– Repair of chromosomal damage
;
Morphologic alteration in :
• Pleomorphic vacuolated mitochondria
• endoplasmic reticulum
• Disorted Golgi Apparatus
• Accumutaion of lipofuscin pigment
Cellular senescence is multifactorial :
1. The cumulative effects of extrinsic influences:
free radical damage
2. Intrinsic molecular program of cellular aging
cell have a finite life span
DEGENERATION
Cloudy
swelling
Fatty
change
Hydropic
Hyaline
Mucoid
Amyloid
D ++
'
&'
Atropy
Calcification
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)& %& )
• Pathology is a dicipline bridging clinical
practice & basic sience
• To render diagnosis & guide therapy
• Identity changes in :
– Gross
– Morphology (microscopy) appearance of cell
tissues
The scientific focus of pathology is :
Etiology
• On the cause of disease
Pathogenesis
• Mechanisme of its development & the
pathways by which morphologic changes
occur
Normal Homeostasis
If cell adjusting structure & function
to accommodate changing demands &
extracellular stresses
Stages in the cellular response to stress & injurious
stimuli
Stresses/pathologic stimuli the cell:
Adaptation
• Atrophy
• Hypertrophy
• Hyperplasia
• Metaplasia
Irreversible injury & ultimately dies
Perubahan sel & jaringan :
Agenesis
Hyperplasia
Aplasia
Metaplasia
Hypoplasia
Dysplasia
Atrophy
Anaplasia
Hypertrophy
Granuloma
Agenesis
Aplasia
• Complete absent of an
organ
• E.g. :
• Anlarge is present but
never develops
• E.g. :
– Renal agenesis
– Ovarial agenesis
– Tubal agenesis, etc.
– Lung aplasia with tissue
containing rudimentary
duct & connective tissue
Hypoplasia
• Anlarge develoved incompletly but the tissue
histhologicaly normal
• Ex. : microcephaly
Atrophy
• Decrease in the:
– Size
– Function of a cell
• But not dead
!
Causes of atrophy :
1.
2.
3.
4.
5.
6.
functional demand (immobilitation in fracture, prolonged
bed rest)
Inadequate supply O2 (ischemia)
Insufficient nutrients (starvation, inadequate nutrition,
chronic disease)
Interrruption of trophic signals transmitted by chemical
mediators (endocrine system/Neuromusculator transmission)
e.g. : thyroid, adrenal cortex, ovarium, testis.
Persistent cell injury by chronic inflamation
e.g. : chronic gastritis, prolonged pressure
Aging : brain, heart (Senile Atrophy)
#
$ %
&0 ) &'
&# (3 *' ' )
& '(
') ) %&'
* # & ( )%+ ,(- %
( + (- % ' (/ # ( )%+ *'1 )
&#'
)&'
& 0#-/
' (./ # )0 % ) 1 &2
( )%+ *'1 )
&#
( + % &' )0 % ) 1 &2
"
The mechanism of atrophy :
• synthesis
• catabolism
• Influenced by a number of hormones
e.g. :
• Insulin
• Tyroid stimulating hormon
• Glucocorticoids
Hypertrophy
•
in the size of cell accompanied by augmented
functional capacity
• Hypertrophy is a response to trophic signals
• Commonly a normal procesess
4
… hypertrophy
Physiological (hormonal) hypertrophy
• in puberty
• production of sex hormon
• Hypertrophy breast tissue
• Abnormal hormon production in cancer
Functional demands
• Exercise
• Pathological conditions (myocardial cell)
• Kidney hypertrophy on surgical removed
')
&# ) %&'
* (- % ' ( '
$ % &&
# + (- % ' + ' * %& ,6# &
&& %76./ ' % % ' % ( )%+ %
&
& 3 *'1 ) %
%&'8 &'))
*'++) ' &#
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1- 8' 1+
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% (0 ) & * % ++) &# & ' /
&#')
) %&'
+
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& #' #
(
'*'% &' 3 &#
+
* % ' % ( )%+ % ++)
%+ ' ') 00
&/ ' %
( )%+ % ++) %
& '8'
0& 1- ' % )' &# '
,#-0 & 0-./
(
&
% ' %
3 &# )'9
5
Hyperplasia
the number of cells in an organ / tissue
Hyperplasia can be :
1. Physiologic hyperplasia
– Hormonal hyperplasia
– Compensatory hyperplasia
2. Pathologic hyperplasia
– Excessive hormonal / growth factor stimulation
e.g. : Endometrial hyperplasia
:
/
(
)&
•
•
/
/
+ )&'( + &'
%
( & ' ( ,#-0 0+ )' .
% ( )&'
) * %&'
+ (
)& % ((
') &#
0+ %( & *
+
1- )? ( ) % ++/
+
0'&# +' (
• Squamous metaplasia of the bronchial epithelium to tobacco
• Lower oesophagus by reflux acidic gastric
• Endocervical metaplasia
Metaplasia is usually reversible if the stimulus is
removed
;
Metaplasia of normal columnar (left) to squamous epithelium
(right) in a bronchus, shown (A) schematically and (B)
histologically
Dysplasia
++ +
+&
&' ' &# )'9 3 )# 0
% ++ + % (0
& *
'9 &'
* &#
&'))
1. Variation in the size & shape of cells
2. Enlargment, irregularity & hyperchromatism of the
nuclei
3. Disorderly arrangement of the cells within the
epithelium
# ( )& % ((
' &# % 8'@
1
%# )
Dysplasia is a preneoplastic lession in the sense
that it is a necessary stage in the multistep cellular
evolution to cancer.
Dysplasia included in the morphological classification of the
stage if intraepithelial neoplasia
Anaplasia
• Normal cell
primitive cell
• E.g. : Malignant cell
– Carcinoma
– Sarcoma
– Adenocarcinoma
– Lymphoma
– Etc.
2 principal pattern of cell death :
NECROSIS
APOPTOSIS
•
•
•
•
•
Commonly : coagulative necrosis
Cellular swelling
Protein denaturation
Organellar breakdown
Cell rupture
• Regulated event
• Programmed death
Term
Definition
Necrosis
Antemortem pathologic cell death
Apoptosis
Antemortem programmed cell death
Autolysis
Postmortem cell death
CAUSES OF CELL INJURY
Hypoxia
Physical Agent
Chemical and drugs
Microbiology Agents
Immunologic Reaction
Genetic Defects
Nutritional Inbalance
Aging
… CAUSES OF CELL INJURY
Hypoxia
•
•
•
•
Anemia
Ischemia
Intoxication CO2
Aerobic oxidative
respiration
Physical Agent
• Mechanical trauma
• Extreme temprature :
heat, cold
• Radiation: X-ray, sun light
• Electric shock
• Athmosphere pressure
… CAUSES OF CELL INJURY
Chemical agent & drugs
• Sufficiently concentrated :
– Glucose
– Salt
– O2
•
•
•
•
•
Air pollutants
Insecticides
Asbestosis
Ethanol
Cellular metabolism (i.e.
waste products)
Microbiology Agents
•
•
•
•
•
Tape worms
Rickettsia
Virus
Bacteria
Fungi
!
… CAUSES OF CELL INJURY
Immunologic Reaction
• Anaphylactic reaction
• Autoimmune diseases
Genetic Defects
• Congenital malformation
• Sickle cell anemia
• G-6-PD
Nutritional Imbalance
• Protein calori insufficiency
• Vitamins defficiency
• Diabetes
Aging
"
Mechanism of Cell Injury
Cellular
response to
injurious
stimuli
depends on :
• Injury type
• Duration
• Severity
Current
Status :
• Nutritional
• Hormonal
• Adaptibility
of the cell
Intercellular
systems :
• Cell membrane
integrity
• Aerobic
respiration
• Protein synthesis
• Integrity genetic
apparatus
O2 & oxygen
derived free
radicals :
• Ischemic
• Hypoxic
injury
Normal cell & changes in reversible & irreversible cell injury
(necrosis)
The ultrastructural features of these stages of cell injury.
4
Reversible injury
• Reduced of :
– Oxidative
phosphorylation in
mitochondria
– Activity Na Pump
• Cellular swelling
• Loss of microvilli
Irreversible injury
• Severe vacuolization of
the mitochondria
• Damage of :
– Mitochondrial matrix
– Plasma membrane
• Swelling of lysosomes
Glycogen depleted
• Accumulation of
↓ protein synthesis
amorphous calcium
Formation of cell surface
• Rich dentities in
blebs
mitochondrial matrix
5
:
Figure 1-6.
Cellular features of
necrosis (left) &
apoptosis (right)
Forms & Morphology of Cell Injury
1. Reversible acute cell injury
2. Necrosis (cell death after irreversible injury)
3. Apoptosis (cell death by suicide)
4. Subcellular alteration as a respond to chronic
or persistent injury stimuli
5. Intracellular accumulations of a number of
substance
;
Sublethal Damage
1. Recoverable (but
necrosis is not)
2. Ultrastructural damage mitochondria
3. Swelling of cellular organelles ( hydrophic deg.)
4. Fatty change is impairment of metabolism
Necrosis
Morphologic changes that follow cell death in living tissue
1. Intense eosinophilia of the dead cell is due to
loss of RNA & coagulation of protein
2. Nuclei undergo:
1. Pyknosis
2. Karyorhexis
3. Karyolysis
Leaving a shrunken cell devoid of nucleus
1. Protein may be liberated from the dead cell
# ( 0# +
&#
'% 00
) +& * &2
/
/
))
9-( &'% '
& &'
%
*
% )') ')
&' ++- 0 % )) ) A
)&'
* &# % ++
*0 & '
Autolysis : is a cell death by hydrolitic
enzymes.
Heterolysis : cell death by the lysosomes of
invading inflammatory cells.
Nuclear Changes: This nucleus is faded -- karyolysis.
Karyolytic nuclei suggest that cells have died (undergone necrosis).
)0 %'*'%3 %+
%#
)
)( ++
2 ' '% & )
)
)& &# & % ++) # 8 '
#'+ %-& 0+ )('% %#
) )) %' & 2'&# % ++
&#
&
/ # +
2 ' '% & )
( +< 00 '
%+ ) 2#'+ &#
%+ ) &# & ') )( ++
7 )& *& ' * %& * & 1 % + ) ' * %&' 2'&#
% & + % )')
!
• Gumatous Necrosis
• Dead tissue, it is firm & rubbery like caseous necrosis in the
spirochetal infection syphilis.
• Hemorrhagic Necrosis
• Dead tissue suffused with extravasated red cell, when cell
death is due to blockage
• Fat Necrosis
• Not really necrosis.
• Focal areas of fat destruction tipically occuring following
pancreatic injury /after trauma to fat for (ex. in the breast)
• Describes foci of hard yellow material seen in dead adipose
tissue
• Fibrinoid Necrosis
• Fibrin deposited in damage necrotic vessel
walls in hypertension and vasculitis
• Gangrene
• Extensive tissue necrosis ; is complicated to
a variable degree by secondary bacterial
infection
"
APOPTOSIS
• Responsible for the programmed cell death in several
important physiology processes
• Including :
– During embryogenesis (in implantation, organogenesis, &
developmental involution)
– Hormon dependent physiologic involution (endometrium,
lactating, prostate after castration)
– Cell deletion in proliferating population (intestinal crypt
epithelium / cell dead in tumor)
– Deletion of autoreactive T cell in the thymus,
cell death of cytokine starved lymphocytes
CLINICAL EFFECTS OF NECROSIS
• Abnormal function
– Kidney
–
–
–
–
: renal failure
Cortex in brain : muscle paralysis
Heart
: heart failure
Lung
: hemoptysis
Bacterial infection : gangrene
4
• Realease of contens of necrotic cells
– Liver
: elevation SGOT
– Heart : creatine kinase
• Systemic effects
– Fever
– Inflamatoar Reaction
• Local effects
– Hemorrhage
– Ulceration
Apoptosis of epidermal cells in an immunemediated reaction
A. Apoptotic cells are visible in the
epidermis with eosinophilic cytoplasm
and small, dense nuclei.
B. High power of apoptotic cell in liver in
immune-mediated hepatic cell injury.
(Courtesy of Dr. Scott Granter, Brigham and Women's Hospital, Boston, AM.) (Courtesy of Dr. Dhanpat Jain, Yale University, New Haven, CT.)
5
!"" " #
% ! $% $%&
$ $%&
&
'#&($
8'
( &
0& &'
* &# % ++
/ #-)' + '%
0& &'
<
(
)
<
) %# ('% + ( ' & )
/ &# + '%
0& &'
<
%&'
* 2 0 & ' )- &# )') 1- &
% ++
++ $ - A
&# * % ++) , 0 (
&
' $ -.
1+ &# + ' $ - ,
0& &' .
&
Granuloma
• Special type of chronic inflamation in tissue
reaction.
• Cause :
infection :
TBC
fungal
noninfection :
sarcoidosis
Crohn’s
disease
syphilis,
etc
:
NECROBIOSIS
•
•
•
•
•
Gradual cell damage
Progressive
Singly or small group cells.
Reversible (+/-)
Example : hepar cell deg.
cell death healing
fibrosis.
Alterations in structure and function that may
lead to cell death, or at least diminished capacity
of the cell to respond an injury
• Reduced cell in :
– Pleomorphic vacuolated mitochondria
– Repair of chromosomal damage
;
Morphologic alteration in :
• Pleomorphic vacuolated mitochondria
• endoplasmic reticulum
• Disorted Golgi Apparatus
• Accumutaion of lipofuscin pigment
Cellular senescence is multifactorial :
1. The cumulative effects of extrinsic influences:
free radical damage
2. Intrinsic molecular program of cellular aging
cell have a finite life span
DEGENERATION
Cloudy
swelling
Fatty
change
Hydropic
Hyaline
Mucoid
Amyloid
D ++
'
&'
Atropy
Calcification
- 0'% %#
* )& &'
+
( +
& #' #
(
'*'% &' &#
' & %-& 0+ )('% * &
0+ &)
%+ +8'
&/
%-E& 0+ )( * )'%7 % ++)/ # )
)& %& )