Disorders of Growth - PHTH1012 004 PDF

GENERAL PATHOLOGY DISORDERS OF GROWTH Gillian Hudson REFERENCES  Cawson, RA, McCracken, AW, & Marcus, PB: Pathologic Mechanisms & Human Disease. Chapter 9, pp. 145-173 (in library).  Goodman, CC, Fuller, KS, & Boissonnault, WG: Pathology: Implications for the Physical Therapist (2 nd ed.). Chapter...

GENERAL PATHOLOGY DISORDERS OF GROWTH Gillian Hudson REFERENCES  Cawson, RA, McCracken, AW, & Marcus, PB: Pathologic Mechanisms & Human Disease. Chapter 9, pp. 145-173 (in library).  Goodman, CC, Fuller, KS, & Boissonnault, WG: Pathology: Implications for the Physical Therapist (2 nd ed.). Chapter 8, pp. 236-263 (chapter available from me, copy in library). DISORDERS OF GROWTH  5 main types of disorders:  Hyperplasia  Hypoplasia  Metaplasia  Heterotopia  Dysplasia HYPERPLASIA  There is an absolute increase in the number of cells, results in increased tissue mass.  Usually there is no significant change in the structure, or disorder of function  Not to be confused with hypertrophy which is an increase in cell size. HYPERPLASIA  Hormonal  Inflammatory  Reactive and compensatory  Unknown cause HORMONAL HYPERPLASIA  Most common – enlargement of glands of the breast at puberty, during pregnancy and lactation.  Occasionally, will be out of control and will get males with increased size of breasts.  Thyroid – in response to pituitary hormones.  Prostate – relative oversecretion of oestrogen when testicular androgen production declines with age (BPH) INFLAMMATORY HYPERPLASIA  A proliferation of granulation cells – normal feature of healing and a characteristic of chronic inflammation.  This type of hyperplasia is common in the mouth – get inflammatory fibrous hyperplasia at the edge of dentures in response to local irritation. REACTIVE & COMPENSATORY HYPERPLASIA  Reactive – nodular cirrhosis of the liver – attempts to make new lobules. Cells are mostly nonfunctional.  Compensatory – loss of a kidney, remaining one increases to take up its function.  Polycythemia – increase red blood cells – if there is cardiac failure, deficient oxygenation; living at high altitudes.  Keloid skin formations – in response to surgical incisions, piercings, etc. HYPERPLASIA OF UNKNOWN CAUSE  In response to diphenylhydatoin (for epilepsy), persons get hyperplasia of the gingivae (gums)  Thought to be a stage in neoplastic change  Many times, no subsequent neoplastic change occurs HYPOPLASIA  This is a reduction in the number of cells in an organ.  May be developmental or acquired  Seen in kidney or lung where one of the pair is small and non-functional – the unaffected shows compensatory hyperplasia.  Aplasia – reduction to ZERO cells. An extreme of hypoplasia. E.g., in bone marrow, cessation of formation of red & white blood cells – aplastic anaemia. Can be a side effect of some drugs.  Agenesis – failure of development of an organ or a part of an organ, e.g., in liver, brain, teeth (anodontia) METAPLASIA  Change in cell type from highly specialized to less specialized. May be adaptive or protective. Causes a loss of function.  This is different from connective tissue replacement: cardiac cells die from ischaemia and are replaced by fibrous cells.  Respiratory tract – ciliated columnar epithelium replaced by stratified squamous cells in persons who smoke excessively. Causes decreased movement of mucous and foreign material by the cilia.  Anaplasia – most advanced form of metaplasia – loss of cellular differentiation, characteristic of malignant cells. HETEROTOPIA  Anomalous differentiation of tissue inappropriate to the site of origin: e.g., actively secreting gastric mucosal glands in the oesophagus.  Also call ECTOPIC, e.g., ectopic pregnancy is where fertilization of the ovum and development of the foetus occur outside of the uterus. DYSPLASIA  Disordered proliferation of a tissue.  Particularly affects epithelia which are normally well-defined tissues.  There is loss of normal uniformity: change in size, shape or organization.  Seen in the uterine cervix, respiratory tract (esp. in smokers), gall bladder and oral cavity. DYSPLASIA  Microscopic features:  Nuclear hyperchromatism – nuclei stain densely,       increased nucleic acid content Nuclear pleomorphism & increased nuclearcytoplasmic ratio: nuclei out of proportion with little cytoplasm. Mitosis – more frequently occurring Loss of polarity – basal cells esp. lie untidily at angles to one another Deep cell keratinization (dyskeratosis) – individual cells degenerate before reaching the tissue surface Differentiation – normal characteristics are lost Loss of intracellular adherence – boundaries may become separated DYSPLASIA  All features not always seen simultaneously, greatly     vary in intensity. If there is a precipitating cause, dysplasia may be reversed if cause removed. Not often possible: cells do not revert to normal. The usual tendency is to view dysplastic lesions as premalignant, but the change is not invariable. Carcinoma in situ – dysplastic change throughout the thickness of epithelium but there is no invasive activity. May be reversible, e.g., uterine cervix. Fibro-osseous dysplasia – shows no cellular abnormalities; there is no tendency for malignant change; certain bony lesions.