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tissue growth disorders


  • increase in individual cell size due to a stimulus (eg. functional stress);
  • physiologic:
    • hormonal stimulation eg. uterus in pregnancy
    • increased workload eg. skeletal & cardiac muscle
    • mechanical triggers eg. stretch
    • trophic triggers eg. growth factors, AGII, alpha-agonists;
  • pathologic


  • increase size of organ or tissue due to increased no. of specialised constituent cells;
    • ⇒ increased function esp. endocrine glands;
      • once stimulus removed → regression;
  • physiologic:
    • hormonal stimulation eg. uterus/breast in pregnancy
    • compensatory eg. liver post-partial resection
      • priming factors
        • oxidative stress, cytokines,
        • metabolic overload, etc.
        • ⇒ activate early growth response genes
          • eg. c-fos, c-jun & c-myc
  • proliferation:
    • growth factors eg.TGF-a, HGF
    • adjuvants eg. NA, glucagon, insulin
    • growth inhibition:
      • growth inhibitors eg. TGF-b, etc
      • decreased growth factors & adjuvants
    • wound healing eg. proliferating fibroblasts & blood vessels.
  • pathologic:
    • XS hormonal stimulation eg. endometrial hyperplasia
    • effects of growth factors eg. viral warts


  • complete failure to develop → absent


  • failure of development to full, mature size;


  • acquired dimunition in size either by decr. cell size or decr. cell numbers
  • apoptosis
    • “dropping off” of cells - programmed cell death;
    • contributes to atrophy due to either:
      • endocrine withdrawal
      • duct obstruction → secretory gland shrinkage
  • cellular changes of atrophied cells:
    • loss of size
    • fewer mitochondria, myofilaments & less endoplasmic reticulum
    • often marked increase in number of autophagic vacuoles which contain
    • fragments of cell components destined for destruction by lysosomes.
    • these can occur within 5-10min of occlusion of blood supply!
    • residual bodies eg. lipofuscin granules → 'brown' atrophy
  • may be caused by:
    • aging physiologic senile atrophy;
    • malnutrition - local/general;
    • decreased workload - disuse atrophy - usually reversible;
    • neuropathic atrophy - accelerated muscle catabolism;
    • impaired blood supply
    • decreased endocrine stimulation - eg. menopausal
    • fever/severe trauma/surgery → incr. protein catabolism;
    • pressure atrophy - decreased blood supply, decreased function;


  • disorder of function/structure of tissue due to perverted nutrition & not fitting in other categories better.
  • eg. B12 defic. cells;


  • only used now for bone marrow: inadequate regeneration of cells;


  • anomalous primary diff. of tissue (eg. gastric muc. in Meckel's);


  • reversible change of one type of differentiat. tissue to another similar diff. tissue;
  • Usually occurs because substituted cell type better able to withstand adverse environment but may sacrifice functionality eg. secretory ability.
  • The transformation of one type of differentiated tissue into another is an interesting cellular response to injury & is presumably due to a change in gene repression & activation. Retinoids, TGF-b-1 family factors & cytostatic drugs can cause metaplastic transformation.
  • Many stimuli that produce metaplasia are able to produce neoplasia & thus metaplasia may represent an intermediate cellular injury.
examples of metaplasia:
  • respiratory tract:
    • tracheal/bronchial columnar epithelium replaced by stratified squamous
      • eg. chronic smoking, vitamin A deficiency;
  • chronic irritation elsewhere → squamous metaplasia;
    • eg. columnar duct epithelium → stratified squamous if calculi
  • vitamin A deficiency → metaplasia of epithelia of nose, bronchi, urine tract:
    • transitional/columnar epithelia → stratified squamous;
  • vitamin A excess → suppression of keratinisation
  • autoimmune ch. gastritis → specialised epith → intest. epith;
  • Barret's oesophagus:
    • squamous epithelium replaced by columnar gastric epithelium;
  • foci of injury:
    • osteoblasts/chondroblasts transform.


  • abnormal development of tissues - but some use it as 'dystrophy';
  • often used for a form of hyperplasia with atypical cells (eg. cervical) hence:
    • “A loss of uniformity of the individual cells as well as a loss in their architectural orientation”.
  • characteristics:
    • pleomorphism - cells vary in size & shape
    • nuclei - hyperchromatic & abnormally large
    • mitoses - more abundant & at abnormal locations (eg. not only basally)
    • anarchy of architecture - usual cell maturation process disrupted


  • dysplastic changes involving the entire thickness of epithelium;
  • pre-invasive neoplasm but does not necessarily progress to cancer;
  • may be reversible on removal of stimulus;


  • “bad mixing” - used for blood disorders of uncertain aetiology;


  • abnormal type of new growth in response to non-physiological stimulus & which proceeds despite removal of stimulus thus autonomous;
  • classed by:
    • naked-eye appearance
    • histogenetic - epithelial; connective tissue; etc.
    • histological if too undifferentiated for histogenetic;
    • behaviour - benign,in-situ, intermediate, malignant
    • aetiological - not useful;
    • functional - sometimes useful;


  • tumour-like malformation where tissues are arranged haphazardly & has no tendency of XS growth or neoplasia, although neoplasias may arise.
  • eg. cart. lung; haemangioma; naevi; neurofibroma; tuberous sclerosis; exostoses;


  • pathological fluid-filled sac bounded by a wall;
  • due to:
    • developmental:
      • persistent normal vestigious remnants - branchial
      • ectopia - dermoid
      • failed connexion tubules - polycystic kidneys;
      • hamartomatous - cystic hygroma
    • inflammatory - pancreatic 'pseudocysts'
    • degenerative - cystic change goitres, etc
    • retention (obstructed duct) - ranula
    • implantation - epidermoid
    • parasitic - hydatid
    • hyperplastic - mammary dysplasia → blue-domed cyst
    • neoplastic - cystadenoma, cystic teratoma;
onc_growth_disorders.txt · Last modified: 2009/10/22 17:45 (external edit)