CELLULAR ADAPTATION
Adaptations are reversible changes in the size, number, phenotype,
metabolic activity, or functions of cells in response to changes in
their environment.
HYPERTROPHY
HYPERPLASIA
ATROPHY
METAPLASIA
HYPERTROPHY
• DEFINATION – Hypertrophy is an increase in the size of cells that results in
an increase in the size of the affected organ.
• TISSUE INVOLVED – Does not have the capacity to divide ( eg Myocardial
Fibres) due to the synthesis and assembly of additional intracellular
structural components.
• High DNA content than normal, because of cell cycle arrest.
• TYPES –Physiological/ Pathological
HYPERTROPHY
• CAUSE - Specific demand or specific hormone stimulation
• PHYSIOLOGICAL HYPERTROPHY- Exercise induced hypertrophy of
muscles- excess load shared by increasd size of the muscle
• PATHOLOGICAL HYPERTROPHY-Left ventricular hyperttrophy in
hypertension, aortic stenosis
• HYPERTOPHY AND HYPERPLASIA OCCURS SIMULTANEOUSLY IN
PREGNANT UTERUS
HYPERTROPHY
• CHANGES IN MORPHOLOGY-INCREASE IN MYOFILAMENT
• INCREASE IN SIZE OF INDIVIDUAL CELLS AND ORGAN
• INCREASE IN PROTEIN CONTENT
HYPERTROPHY
MECHANISM INVOVED
1) SIGNAL TRANSDUCTION PATHWAYS-
INITIATION OF GENES INVOLVED IN
PROTEIN SYNTHESIS LIKE GF (TGF, IGF),
TRANSCRIPTION GENES (C-FOS, C-JUN)
2) SWITCH OF CONTRACTILE PROTEIN
FROM ADULT TO FOETAL TYPE, ALFA -
MYOSIN REPLACED BY BETA- MYOSIN
TO REDUCE REQUIREMENT OF ATP
3) SOME GENES REEXPRESSED IN
HYPERTROPHY LIKE ANF
Other Factors Involved In Hypertrophy
 MECHANICAL STRETCH
 TROPIC TRIGGERS LIKE ANGIOTENSIN -
2,ALFA- ADRENERGIC AGONISTS
 NUTRIENTS , ENVIRONMENTAL FACTORS
 FAILURE OF HYPERTROPHY
HYPERPLASIA
• DEFINATION – Hyperplasia is an increase in the number of cells in an
organ or tissue in response to a stimulus.
• SITE- Any tissue that contains divisible cells
• TYPES - PHYSIOLOGICAL/ PATHOLOGICAL
• PHYSIOLOGICAL HYPERPLASIA – HORMONAL/ COMPENSATORY
PHYSIOLOGICAL HYPERPLASIA
• HOMONAL HYPERPLASIA – Happens when functional capacity of
tissue needs to be increasd. Eg- Glandular Epithelial Hyperplasia
in female breast during Puberty and Pregnancy, Muscle Layer
of Pregnant Uterus
• COMPENSATORY HYPERPLASIA -- Partial Resection of Liver Or
Kidney. Bone Marrow cell Hyperplasia in case of acute bleeding
or hemolysis.
MECHANISM OH HYPERPLASIA
PHYSIOLOGICAL-- Transcription Of Genes Encoding Growth
Factors, Receptors of GF, Cell Cycle Regulators
Increased Production of Growth Factors And Growth Factor
Receptor, Activation of Certain Intracellular Pathways
Role of Stem Cells Present in Tissue
PATHOLOGICAL HYPERPLASIA
MECHANISM – Excess Hormone Secretion or Growth Factors
Hormone/GF act only on TARGET CELLS
Eg:
 Endometrial Hyperplasia due to Hormone imbalance
 BHP due to Hormone ANF GF
 Gynaecomasta in Male Breast
 Bone Marrow Hyperplasia in Anaemia
 Epidermal/Ectocervical Hyperplasia (Viral Wart) due to HPV--
Precancerous
ATROPHY
DEFINATION –Atrophy is a reduction in the size of an
organ or tissue due to a decrease in cell size and
number.
Following injury , cell size de cell size decreases,
organ size decreased but survives
Types – Physiological & Pathological
PHYSIOLOGICAL ATROPHY
• In Foetus- T.G Duct, Notocord
• In Childhood- PDA
• In Adults- Tonsil, Thymus, Few Lymph Nodes
PATHOLOGICAL ATROPHY
• Disuse Atrophy , Eg Muscles
• Denervation Atrophy
• Ischaemic Atrophy-Atheroslerosis, Changes In Brain In Old Age
• Inadequate Nutrition – Protein Energy Malnutrition
• Loss Of Endocrine Function –Endometrium, Breast
• Pressure Atrophy-hydronephrosis
• Aging
ATROPHY
MORPHOLOGY
 Decrease in Cell Size
 Decrease in Structural Component
 Atrophic Musce-decreasd
Myofilament,mitochondion, ER
In Summary- Atrophic Cells Are
Reduced In Size But Not Dead.
ATROPHY
MECHANISM :-- Imbalance between Protein Synthesis And Degradation
Breakdown of Protein by :-
1) Lysosome- Destroy endocytose protein, some cell components
2)Ubiquitine-Proteosome Pathway-degrade Cytosol And Nuclear
Protein. Protein Ubiquitine Complex Degrade in Proteosome.
Important in Cancer Cachexia, Muscle Atrophy
METAPLASIA
DEFINATION: Metaplasia is a reversible change in which one
differentiated cell type (epithelial or mesenchymal) is replaced
by another cell type.
OBJECTIVE: Bodies response to external stimuli.
CONSIDERED TO BE AN EARLY PHAGE OF CARCINOGENESIS
DOUBLE AGED SWORD
METAPLASIA
Change due to Stress , like Physical or Chemical Irritation
Cells of Origin Still Debatable, may be Stem Cells or Resident
Embryonic Cells.
Other Factors- GF, Cytokines and ECM
Most Common Change -Squamous Metaplasia
METAPLASIA
Epithelial Change
Bronchous- Cilliated Columner to
Squamous
Gall Bladder Stone- Columner to
Squamous
Barrets Oesophagus – Squamous to
Columner
Mesenchymal Change – Myositis
Ossificans
DYSPLASIA
 DYSPLASIA MEANS DISORDER OF GROWTH
 IT IS A PRECANCEROUS CONDITION
 IT MAY FOLLOW METAPLASIA BUT CAN ALSO OCCURS INDEPENDENTLY. NOT ALL METAPLASIA DYSPLASTIC
 MAINLY FOUND IN EPITHELIUM
 CHARACTERISED BY LOSS OF ARCHIETECTURE AND UNIFORMITY OF CELLS.
 MITOSIS INCRESED AND MAY PRESENT IN ABNORMAL LOCATION
 CIN-1,CIN-2,CIN-3,CIS
 UNTREATED PROGRESS TO CARCINOMA

CELLULR ADAPTATIONS Pathology MBBS 2nd Prof

  • 1.
    CELLULAR ADAPTATION Adaptations arereversible changes in the size, number, phenotype, metabolic activity, or functions of cells in response to changes in their environment. HYPERTROPHY HYPERPLASIA ATROPHY METAPLASIA
  • 2.
    HYPERTROPHY • DEFINATION –Hypertrophy is an increase in the size of cells that results in an increase in the size of the affected organ. • TISSUE INVOLVED – Does not have the capacity to divide ( eg Myocardial Fibres) due to the synthesis and assembly of additional intracellular structural components. • High DNA content than normal, because of cell cycle arrest. • TYPES –Physiological/ Pathological
  • 3.
    HYPERTROPHY • CAUSE -Specific demand or specific hormone stimulation • PHYSIOLOGICAL HYPERTROPHY- Exercise induced hypertrophy of muscles- excess load shared by increasd size of the muscle • PATHOLOGICAL HYPERTROPHY-Left ventricular hyperttrophy in hypertension, aortic stenosis • HYPERTOPHY AND HYPERPLASIA OCCURS SIMULTANEOUSLY IN PREGNANT UTERUS
  • 4.
    HYPERTROPHY • CHANGES INMORPHOLOGY-INCREASE IN MYOFILAMENT • INCREASE IN SIZE OF INDIVIDUAL CELLS AND ORGAN • INCREASE IN PROTEIN CONTENT
  • 5.
    HYPERTROPHY MECHANISM INVOVED 1) SIGNALTRANSDUCTION PATHWAYS- INITIATION OF GENES INVOLVED IN PROTEIN SYNTHESIS LIKE GF (TGF, IGF), TRANSCRIPTION GENES (C-FOS, C-JUN) 2) SWITCH OF CONTRACTILE PROTEIN FROM ADULT TO FOETAL TYPE, ALFA - MYOSIN REPLACED BY BETA- MYOSIN TO REDUCE REQUIREMENT OF ATP 3) SOME GENES REEXPRESSED IN HYPERTROPHY LIKE ANF Other Factors Involved In Hypertrophy  MECHANICAL STRETCH  TROPIC TRIGGERS LIKE ANGIOTENSIN - 2,ALFA- ADRENERGIC AGONISTS  NUTRIENTS , ENVIRONMENTAL FACTORS  FAILURE OF HYPERTROPHY
  • 6.
    HYPERPLASIA • DEFINATION –Hyperplasia is an increase in the number of cells in an organ or tissue in response to a stimulus. • SITE- Any tissue that contains divisible cells • TYPES - PHYSIOLOGICAL/ PATHOLOGICAL • PHYSIOLOGICAL HYPERPLASIA – HORMONAL/ COMPENSATORY
  • 7.
    PHYSIOLOGICAL HYPERPLASIA • HOMONALHYPERPLASIA – Happens when functional capacity of tissue needs to be increasd. Eg- Glandular Epithelial Hyperplasia in female breast during Puberty and Pregnancy, Muscle Layer of Pregnant Uterus • COMPENSATORY HYPERPLASIA -- Partial Resection of Liver Or Kidney. Bone Marrow cell Hyperplasia in case of acute bleeding or hemolysis.
  • 8.
    MECHANISM OH HYPERPLASIA PHYSIOLOGICAL--Transcription Of Genes Encoding Growth Factors, Receptors of GF, Cell Cycle Regulators Increased Production of Growth Factors And Growth Factor Receptor, Activation of Certain Intracellular Pathways Role of Stem Cells Present in Tissue
  • 9.
    PATHOLOGICAL HYPERPLASIA MECHANISM –Excess Hormone Secretion or Growth Factors Hormone/GF act only on TARGET CELLS Eg:  Endometrial Hyperplasia due to Hormone imbalance  BHP due to Hormone ANF GF  Gynaecomasta in Male Breast  Bone Marrow Hyperplasia in Anaemia  Epidermal/Ectocervical Hyperplasia (Viral Wart) due to HPV-- Precancerous
  • 10.
    ATROPHY DEFINATION –Atrophy isa reduction in the size of an organ or tissue due to a decrease in cell size and number. Following injury , cell size de cell size decreases, organ size decreased but survives Types – Physiological & Pathological
  • 11.
    PHYSIOLOGICAL ATROPHY • InFoetus- T.G Duct, Notocord • In Childhood- PDA • In Adults- Tonsil, Thymus, Few Lymph Nodes
  • 12.
    PATHOLOGICAL ATROPHY • DisuseAtrophy , Eg Muscles • Denervation Atrophy • Ischaemic Atrophy-Atheroslerosis, Changes In Brain In Old Age • Inadequate Nutrition – Protein Energy Malnutrition • Loss Of Endocrine Function –Endometrium, Breast • Pressure Atrophy-hydronephrosis • Aging
  • 13.
    ATROPHY MORPHOLOGY  Decrease inCell Size  Decrease in Structural Component  Atrophic Musce-decreasd Myofilament,mitochondion, ER In Summary- Atrophic Cells Are Reduced In Size But Not Dead.
  • 14.
    ATROPHY MECHANISM :-- Imbalancebetween Protein Synthesis And Degradation Breakdown of Protein by :- 1) Lysosome- Destroy endocytose protein, some cell components 2)Ubiquitine-Proteosome Pathway-degrade Cytosol And Nuclear Protein. Protein Ubiquitine Complex Degrade in Proteosome. Important in Cancer Cachexia, Muscle Atrophy
  • 15.
    METAPLASIA DEFINATION: Metaplasia isa reversible change in which one differentiated cell type (epithelial or mesenchymal) is replaced by another cell type. OBJECTIVE: Bodies response to external stimuli. CONSIDERED TO BE AN EARLY PHAGE OF CARCINOGENESIS DOUBLE AGED SWORD
  • 16.
    METAPLASIA Change due toStress , like Physical or Chemical Irritation Cells of Origin Still Debatable, may be Stem Cells or Resident Embryonic Cells. Other Factors- GF, Cytokines and ECM Most Common Change -Squamous Metaplasia
  • 17.
    METAPLASIA Epithelial Change Bronchous- CilliatedColumner to Squamous Gall Bladder Stone- Columner to Squamous Barrets Oesophagus – Squamous to Columner Mesenchymal Change – Myositis Ossificans
  • 18.
    DYSPLASIA  DYSPLASIA MEANSDISORDER OF GROWTH  IT IS A PRECANCEROUS CONDITION  IT MAY FOLLOW METAPLASIA BUT CAN ALSO OCCURS INDEPENDENTLY. NOT ALL METAPLASIA DYSPLASTIC  MAINLY FOUND IN EPITHELIUM  CHARACTERISED BY LOSS OF ARCHIETECTURE AND UNIFORMITY OF CELLS.  MITOSIS INCRESED AND MAY PRESENT IN ABNORMAL LOCATION  CIN-1,CIN-2,CIN-3,CIS  UNTREATED PROGRESS TO CARCINOMA