Cellular Adaptations

Hyperplasia

Increase in no. of specialized cells in an organ

Only in cells capable of dividing

Hypertrophy

Increase in size of cells leading to increase in size of organ

Non dividing cells can only hypertrophy

Myocardial Cells

Triggers

Increased Functional Demand

Muscular Hypertrophy of Bodybuilders

Myocardial hypertrophy in chronic hemodynamic overload

Regeneration of injured liver

Hormonal Triggers

Proliferation of Endometrium during menstrual cycle

Increase in size of thyroid gland due to excess TSH

Mechanical Factors

Mechanical load in long bones causes hypertrophy of bone

Pathologic

Excess Growth Factor stimulation

Common

Endometrial hyperplasia

Keloids

Benign prostatic hyperplasia

Predisposes to carcinogenesis

Chronic Overload

Cariomegaly in chronic hypertension

Glomerular hyperplasia in renal failure

Overtime hypertrophy exhausts organ's ability to compensate

Organ failure

State of between normal unstressed cell and overstressed injured cell

Ohysiologic or pathologic

Reversible process

Epithelial

Reversible change in which one cell type is replaced by another

Adaptive substitution of cells sensitive to stress by cell types better able to survive adverse environment

Often predisposes cell to neoplastic change

Connective Tissue

Formation of mesenchymal tissues in tissues that do not contain these elements

Less clearly seen as adaptive change

E.g. Myositis ossificans

Bone formation in muscle, usually after fracture

Mechanisms

Reprogrammin of undifferentiated cells in tissue

Precursor differentiate along a new pathway

Signals generated by cytokines, GFs and ECM components

Examples

Columnar to Stratified Squamous

Most common epithelial metaplasia

Chronic irritation caused by cigarettes

Stones in excretory ducts of exocrine glands

Improved survival

Protective mechanism of mucus secretion lost

May predispose to neo-plastic change if persistant

SCCarcinoma

Strat Squamous to Columnar

Barrett's Esophagus

Due to chronic GERD

Squamous Epithelium replaced by intestinal-like columnar cells

Predisposition to adenocarcinoma of esophagus

Shrinkage of cell size by loss of cell substance

Diminished function

Retreat by cell to a smaller size where survival is possible

New equilibrium achieved by decreasing cell volume in relation to reduced nutrient supply

Mechanisms

Shift in balance of protein synthesis and degradation

Increased degradation via

Lysosomes

Ubiquitin-proteosome pathway

Cell death may occur when atrophy progress to cellular injury

Physiologic

Occurs during normal development

Loss of embryonic structures

Thyroglossal duct

Notochord

Uterus after parturition

Pathologic

Decreased workload

Loss of neurological/hormonal stimulation

Pressure

Reduced nutrient/O2 supply

Cell aging