OzEMedicine - Wiki for Australian Emergency Medicine Doctors

see also:

• oncology
• neoplasia / cancer / tumours
• pathology

• 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.

• 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;
• see neoplasia / cancer / tumours

• 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;