Adaptation of cellular growth & differentiation

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Adaptation of cellular growth & differentiation

  1. 1. ADAPTATION OFCELLULAR GROWTH & DIFFERENTIATION PRESENTED BY: Dr. Hrudi Sundar Sahoo
  2. 2. CONTENTS: Introduction Adaptation of cells Mechanisms Adaptive disorders Atrophy Hypertrophy Hyperplasia Metaplasia Dysplasia
  3. 3. INTRODUCTION: On exposure to stress, the cells make adjustments with the changes in their environment to: * Physiologic needs *Pathologic injury
  4. 4. ADAPTATION: PHYSIOLOGIC: Represents cells to normal stimulation by hormones/ endogenous chemical substances. PATHOLOGIC: The cells have the ability to modulate their environment.
  5. 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. 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. 7. ADAPTIVE DISORDERS OFGROWTH: SIZE & NUMBER: Atrophy Hypertrophy Hyperplasia DIFFERENTIATION OF CELLS: Metaplasia Dysplasia
  8. 8. ATROPHY: Shrinkage in the size of the cell by loss of cell substance. It represents a form of adaptive response.
  9. 9. CAUSES: PHYSIOLOGIC: Normal process of aging in some tissues, which could be due to endocrine stimulation & arteriosclerosis. Eg: Atrophy of lymphoid tissue.
  10. 10. 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
  11. 11. 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.
  12. 12. CAUSES: PHYSIOLOGIC: Enlargement of uterus in pregnancy. PATHOLOGIC: Hypertrophy of: * cardiac muscle *smooth muscle * skeletal muscle *compensatory hypertrophy
  13. 13. HYPERPLASIA: An increase in number of parenchymal cells, which results in enlargement of organ/tissue.
  14. 14. CAUSES: PHYSIOLOGIC: HORMONAL: Eg: Hyperplasia of pregnant uterus COMPENSATORY: Eg: Regeneratio of liver.
  15. 15. CAUSES: PATHOLOGIC: Occurs due to excessive stimulation of hormones & growth factors. Eg: Endometrial hyperplasia-following oestrogen excess.
  16. 16. 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.
  17. 17. CLASSIFICATION: EPITHELIAL METAPLASIA: *Sqamous metaplasia *Columnar metaplasia MESENCHYMAL METAPLASIA: *Osseous metaplasia *Cartilaginous metaplasia
  18. 18. 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.
  19. 19. 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.
  20. 20. MESENCHYMALMETAPLASIA: 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.
  21. 21. 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.
  22. 22. 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.
  23. 23. 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.
  24. 24. THANK YOU

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