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ADAPTATION OF
CELLULAR GROWTH &
  DIFFERENTIATION
               PRESENTED BY:
        Dr. Hrudi Sundar Sahoo
CONTENTS:
 Introduction
 Adaptation of cells
 Mechanisms
 Adaptive disorders
            Atrophy
            Hypertrophy
            Hyperplasia
            Metaplasia
            Dysplasia
INTRODUCTION:
   On exposure to stress, the cells make
    adjustments with the changes in their
    environment to:
      * Physiologic needs
      *Pathologic injury
ADAPTATION:
   PHYSIOLOGIC: Represents cells to
    normal stimulation by hormones/
    endogenous chemical substances.

   PATHOLOGIC: The cells have the
    ability to modulate their environment.
SURVIVAL OF THE FITTEST:
 Adaptive responses are reversible on
  withdrawal of stimulus.
 If the irritant / stimulus persists for a longer
  time cell may not be able to survive.
 Thus, the concept of evolution “ survival
  of fittest” holds true for adaptation as
  “survival of adaptable”.
MECHANISM:
   Altered cell surface receptor binding.

   Alterations in signal for protein synthesis.

   Synthesis of new proteins by the target
    cell such as heat-shock proteins.
ADAPTIVE DISORDERS OF
GROWTH:
 SIZE & NUMBER:
 Atrophy
 Hypertrophy
 Hyperplasia


 DIFFERENTIATION OF CELLS:
 Metaplasia
 Dysplasia
ATROPHY:
 Shrinkage in the size of the cell by loss of
  cell substance.
 It represents a form of adaptive response.
CAUSES:
 PHYSIOLOGIC:
 Normal process of aging in some tissues,
  which could be due to endocrine
  stimulation & arteriosclerosis.

      Eg: Atrophy of lymphoid tissue.
CAUSES:
 PATHOLOGIC:
 Starvation atrophy- carbohydrate/fat
 Ischemic atrophy- atrophic kidney
 Disuse atrophy- atrophy of pancrease
 Neuropathic atrophy- poliomyelitis
 Endocrine atrophy- hypopituitarism
 Pressure atrophy- erosion of spine
 Idiopathic atrophy- testicular atrophy
HYPERTROPHY:
 An increase in the size of the cells, which
  results in enlargement of organ without
  any changes in the number of cells.
 Occurs due to incresed functional demand
  & hormonal stimulation.
CAUSES:
   PHYSIOLOGIC: Enlargement of uterus
    in pregnancy.

   PATHOLOGIC: Hypertrophy of:
          * cardiac muscle
          *smooth muscle
          * skeletal muscle
          *compensatory hypertrophy
HYPERPLASIA:
   An increase in number of parenchymal
    cells, which results in enlargement of
    organ/tissue.
CAUSES:
   PHYSIOLOGIC:
 HORMONAL:
       Eg: Hyperplasia of pregnant uterus

   COMPENSATORY:
       Eg: Regeneratio of liver.
CAUSES:
 PATHOLOGIC:
 Occurs due to excessive stimulation of
  hormones & growth factors.

      Eg: Endometrial hyperplasia-following
    oestrogen excess.
METAPLASIA:
 META-Transformation
 PLASIA-Growth
 It is a reversible change of one type of
  epithelial or mesenchymal cells, usually in
  response to persistant abnormal stimulus
  which in turn may change into a
  malignant cell.
CLASSIFICATION:
   EPITHELIAL METAPLASIA:
        *Sqamous metaplasia
        *Columnar metaplasia

   MESENCHYMAL METAPLASIA:
       *Osseous metaplasia
       *Cartilaginous metaplasia
EPITHELIAL METAPLASIA:

 The most common type.
 Metaplastic change cane either patchy or
  diffuse.
 Leads to alterations in the epithelium.


   Deprivation of protective mucous secretion.

   More prone to infection.
TYPES:
 SQAMOUS METAPLASIA:
 Occurs due to chronic irritation
  (chemical/mechanical/infective)
      Eg: Bronchus in chronic smokers.

   COLUMNAR METAPLASIA:

        Eg: Intestinal metaplasia in healed
    chronic gastric ulcer.
MESENCHYMAL
METAPLASIA:
   Less often there is transformation of one
    type of mesenchymal tissue to another.

 OSSEOUS: Formation of bone in fibrous
  tissue, cartilage & myxoid tissue.
 Eg: In arterial wall in old people.


   CARTILAGENOUS: In healing of
    fractures, where there is undue mobility.
DYSPLASIA:
   Disordered cellular development often
    accompanied with metaplasia & hyperplasia
    (ATYPICAL HYPERPLASIA).

   Occurs most often in epithelial cells, which is
    characterised by cellular proliferation & cytologic
    changes.
CAUSES:
 Occurs due to chronic irritation or
  prolonged inflammation.
 On removal of simulus, the changes may
  disappear.
 In majority of cases dysplasia progresses
  into carcinoma insitu or invasive cancer.
CHANGES:
 Increased number of layers of epithelial
  cells.
 Disorderly arranged cells.
 Loss of basal polarity.
 Cellular & nuclear pleomorphism.
 Increased nucleocytoplasmic ratio.
 Nuclear hyperchromatism.
 Increased mitotic activity.
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Adaptation of cellular growth & differentiation

  • 1. ADAPTATION OF CELLULAR GROWTH & DIFFERENTIATION PRESENTED BY: Dr. Hrudi Sundar Sahoo
  • 2. CONTENTS:  Introduction  Adaptation of cells  Mechanisms  Adaptive disorders Atrophy Hypertrophy Hyperplasia Metaplasia Dysplasia
  • 3. INTRODUCTION:  On exposure to stress, the cells make adjustments with the changes in their environment to: * Physiologic needs *Pathologic injury
  • 4. ADAPTATION:  PHYSIOLOGIC: Represents cells to normal stimulation by hormones/ endogenous chemical substances.  PATHOLOGIC: The cells have the ability to modulate their environment.
  • 5. SURVIVAL OF THE FITTEST:  Adaptive responses are reversible on withdrawal of stimulus.  If the irritant / stimulus persists for a longer time cell may not be able to survive.  Thus, the concept of evolution “ survival of fittest” holds true for adaptation as “survival of adaptable”.
  • 6. MECHANISM:  Altered cell surface receptor binding.  Alterations in signal for protein synthesis.  Synthesis of new proteins by the target cell such as heat-shock proteins.
  • 7. ADAPTIVE DISORDERS OF GROWTH:  SIZE & NUMBER:  Atrophy  Hypertrophy  Hyperplasia  DIFFERENTIATION OF CELLS:  Metaplasia  Dysplasia
  • 8.
  • 9. ATROPHY:  Shrinkage in the size of the cell by loss of cell substance.  It represents a form of adaptive response.
  • 10. CAUSES:  PHYSIOLOGIC:  Normal process of aging in some tissues, which could be due to endocrine stimulation & arteriosclerosis. Eg: Atrophy of lymphoid tissue.
  • 11. CAUSES:  PATHOLOGIC:  Starvation atrophy- carbohydrate/fat  Ischemic atrophy- atrophic kidney  Disuse atrophy- atrophy of pancrease  Neuropathic atrophy- poliomyelitis  Endocrine atrophy- hypopituitarism  Pressure atrophy- erosion of spine  Idiopathic atrophy- testicular atrophy
  • 12. HYPERTROPHY:  An increase in the size of the cells, which results in enlargement of organ without any changes in the number of cells.  Occurs due to incresed functional demand & hormonal stimulation.
  • 13. CAUSES:  PHYSIOLOGIC: Enlargement of uterus in pregnancy.  PATHOLOGIC: Hypertrophy of: * cardiac muscle *smooth muscle * skeletal muscle *compensatory hypertrophy
  • 14. HYPERPLASIA:  An increase in number of parenchymal cells, which results in enlargement of organ/tissue.
  • 15. CAUSES:  PHYSIOLOGIC:  HORMONAL: Eg: Hyperplasia of pregnant uterus  COMPENSATORY: Eg: Regeneratio of liver.
  • 16. CAUSES:  PATHOLOGIC:  Occurs due to excessive stimulation of hormones & growth factors. Eg: Endometrial hyperplasia-following oestrogen excess.
  • 17. METAPLASIA:  META-Transformation  PLASIA-Growth  It is a reversible change of one type of epithelial or mesenchymal cells, usually in response to persistant abnormal stimulus which in turn may change into a malignant cell.
  • 18. CLASSIFICATION:  EPITHELIAL METAPLASIA: *Sqamous metaplasia *Columnar metaplasia  MESENCHYMAL METAPLASIA: *Osseous metaplasia *Cartilaginous metaplasia
  • 19. EPITHELIAL METAPLASIA:  The most common type.  Metaplastic change cane either patchy or diffuse.  Leads to alterations in the epithelium.  Deprivation of protective mucous secretion.  More prone to infection.
  • 20. TYPES:  SQAMOUS METAPLASIA:  Occurs due to chronic irritation (chemical/mechanical/infective) Eg: Bronchus in chronic smokers.  COLUMNAR METAPLASIA: Eg: Intestinal metaplasia in healed chronic gastric ulcer.
  • 21.
  • 22. MESENCHYMAL METAPLASIA:  Less often there is transformation of one type of mesenchymal tissue to another.  OSSEOUS: Formation of bone in fibrous tissue, cartilage & myxoid tissue.  Eg: In arterial wall in old people.  CARTILAGENOUS: In healing of fractures, where there is undue mobility.
  • 23. DYSPLASIA:  Disordered cellular development often accompanied with metaplasia & hyperplasia (ATYPICAL HYPERPLASIA).  Occurs most often in epithelial cells, which is characterised by cellular proliferation & cytologic changes.
  • 24.
  • 25.
  • 26. CAUSES:  Occurs due to chronic irritation or prolonged inflammation.  On removal of simulus, the changes may disappear.  In majority of cases dysplasia progresses into carcinoma insitu or invasive cancer.
  • 27. CHANGES:  Increased number of layers of epithelial cells.  Disorderly arranged cells.  Loss of basal polarity.  Cellular & nuclear pleomorphism.  Increased nucleocytoplasmic ratio.  Nuclear hyperchromatism.  Increased mitotic activity.