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Cell Adaptations
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Cell Adaptations

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LECTURE BY DR EJAZ WARIS

LECTURE BY DR EJAZ WARIS

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Cell Adaptations Cell Adaptations Presentation Transcript

    • Small minds discuss people…
    • Average minds discuss events..
    • Great minds discuss ideas..
    • Genius silently acts.
  • Intracellular Acuumulations
    • The stockpiled substances fall into three
    • categories:
    • (1) a normal cellular constituent accumulated in
    • excess, such as water, lipids, proteins, and carbohydrates
    • 2) an abnormal substance , either exogenous, such as a mineral
    • or products of infectious agents, or endogenous, such as a
    • product of abnormal synthesis or metabolism; and
    • (3) a pigment .
  • Most accumulations are attributable to three types of abnormalities
    • 1) A normal endogenous substance is produced at a normaL or increased rate, but the rate of metabolism is inadequate to remove it .
    • 2) A normal or abnormal endogenous substance accumulates because of genetic or acquired defects in the metabolism,packaging,transport, or secretion of these substances .
    • 3) An abnormal exogenous substance is deposited and accumulates
    View slide
  • LIPIDS
    • Steatosis:The terms steatosis and fatty change describe abnormal accumulations of triglycerides within parenchymal cells
    • the most common cause of significant fatty change in the liver (fatty liver) is alcohol abuse
    • Mechanisms
    • Morphology: a)Liver b) Heart
    View slide
  • Fatty Change,Liver
    • Cholesterol and Cholesterol Esters
    • a)Atherosclerosis
    • b)Xanthomas
    • c)Inflammation & necrosis
    • d)Cholesterolosis
    • e)Niemann Pick disease
  • Cholesterolosis,gall bladder
  • PROTEINS
    • Reabsorption droplets in proximal renal tubules are seen in renal diseases associated with protein loss in the urine (proteinuria).
    • A second cause is synthesis of excessive amounts of normal secretory protein, as occurs in certain plasma cells engaged in active synthesis of immunoglobulins.
    • Defects in protein folding may underlie some of these depositions in a variety of unrelated diseases
  • Other Accumulations
    • Hyaline Change
    • Glycogen:
    • Pigments:
    • Exogenous : Carbon
    • Endogenous: melanin,hemosiderin,lipfuscin
  • Lipofuscin
  • Hemosiderin
  • Melanin
  • Hemosiderosis
  • Billirubin Liver
  • Carbon,Lungs
  • Pathologic Calcification
    • Pathologic calcification is the abnormal tissue deposition of calcium salts, together with smaller amounts of iron, magnesium,and other mineral salts. It is a common process occurring in a variety of pathologic conditions.
    • Two types: Dystrophic & Metastatic
  • DYSTROPHIC CALCIFICATION
    • Dystrophic calcification is encountered in areas of necrosis,whether they are of coagulative, caseous, or liquefactive type,and in foci of enzymatic necrosis of fat.
    • Calcification is almost inevitable in the atheromas of advanced atherosclerosis.
    • Psamomma bodies
    • Pathogenesis
  • METASTATIC CALCIFICATION
    • Metastatic calcification may occur in normal tissues whenever there is hypercalcemia. Hypercalcemia also accentuates dystrophic calcification.
    • 4 causes of hypercalcemia:
    • i) increased secretion of parathyroid hormone (PTH) with subsequent bone resorption,
  • Continued…
    • ii) destruction of bone tissue , occurring with primary tumors of bone marrow,
    • Iii) vitamin D–related disorders ,
    • Iv) renal failure
  • Dystrophic Calcification
  • Metastatic Calcification
  • Cellular adaptations
  • Objectives:
    • Understand Growth disorders.
    • Difference between Neoplastic & Non neoplastic growths.
    • Classification of growth disorders.
  •  
  • Non-Neoplastic Proliferation:
    • *Controlled & Reversible
    • Hypertrophy – Size
    • Hyperplasia – Number
    • Metaplasia – Change
    • Dysplasia – Disordered
    • Atrophy - size
  • Neoplastic Proliferation:Tumors
    • Uncontrolled & Irreversible*
    • Benign
      • Localized, non-invasive.
    • Malignant ( Cancer )
      • Spreading, Invasive.
  • Metaplasia
    • Reversible change in which one adult cell type (epithelial/mesenchymal) is replaced by another cell type
    • Adaptive substitution of cells that are sensitive to stress
  • Examples
    • Squamous metaplasia
    • Intestinal metaplasia
    • Connective tissue metaplasia
    • Why is it two edged sword????
  • Mechanisms of metaplasia
    • Reprogramming of stem cells known to exist in normal tissues or of undifferentiated stem mesenchymal cells present in connective tissue
    • The precursor cells differentiate along a new pathway,signalled by cytokines,growth factors,and ECM components in the cell’s environment
  • Influences that predispose to metaplasia ,if persistent,may induce malignant transformation in metaplastic epithelium
  •  
  •  
  •  
  • Atrophy
    • Shrinkage in the size of the cell by loss of cell substance
    • Physiologic or pathologic
    • Common causes are :
    • i)decreased work load
    • ii)loss of innervation
    • Iii)diminished blood supply
  • Atrophy
    • iv)inadequate nutrition
    • v)loss of endocrine stimulation
    • vi)ageing
    • vii)pressure
    • ALTHOUGH ATROPHIC CELLS MAY HAVE DIMINISHED FUNCTION,THEY R NOT DEAD
    • Mechansims
  •  
  •  
  • Hyperplasia
    • Increase in the number of cells in an organ or tissue ,usually resulting in increased volume of the organ or tissue
    • Physiologic hyperplasia:
    • i)hormonal ii)compensatory
    • Mechanisms
    • Pathologic hyperplasia
  • Pathologic hyperplasia constitutes a fertile soil in which cancerous proliferation may eventually arise
  •  
  •  
  • Goitre – Iodine Deficiency
  • Hypertrophy
    • Increase in the size of the cells resulting in an increase in the size of the organ
    • No new cells,just larger cells
    • Physiologic
    • Pathologic
    • Mechanisms
  • LVH in Chronic Hypertension: Left Ventricular Hypertrophy
  • Dysplasia
    • Disordered growth
    • Loss in the uniformity of the individual cells as well as loss in their architectural orientation
    • Cellular and nuclear changes
    • Is it reversible or irreversible ?
    • Carcinoma in situ
    • Does not necessarily progress to cancer
  •  
  •  
  • Pathogenesis – Smoke - Lung Dis.
  • Normal Adaptation Benign Malignant Polyclonal Monoclonal Mechanism of Growth Disorders
  • Take home messages
    • Understanding of Growth disorders.
    • Difference between Neoplastic & Non neoplastic growths.
    • Classification of growth disorders
  • Watch your thoughts; they become words. Watch your words; they become actions. Watch your actions; they become habits. Watch your habits; they become character. Watch your character; it becomes your destiny
  • Thank you