Lect.2
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Cellular response to injury can include adaptation, injury, or disease. Adaptation represents a new abnormal state where cells maintain viability and homeostasis in response to stress. Key types of cellular adaptation include hyperplasia (increased cell number), hypertrophy (increased cell size), atrophy (decreased cell size and number), and metaplasia (one cell type replaces another). While adaptation allows cell survival, the underlying stresses that cause adaptation could also promote cancer if persistent over time.
Lect.2
- 1. Cellular response to injury adaptation and injury
- 2. • Normal cell is in a steady state “Homeostasis” • Cells constantly adjust structure and function to accommodate changing demands and extracellular stress. • But within a relatively narrow range of physiologic parameters. • Change in Homeostasis due to prolonged stimuli Injury
- 3. FUNCTIONAL DEFINITION OF DISEASE ABNORMAL HOMEOSTASIS
- 4. CELLULAR ADAPTATION • A new altered state between normal, unstressed cell and the injured, overstressed cell due to excessive physiologic stresses & some pathologic stimuli. • A new abnormal state but remains functional i.e. preserving the viability of the cell.(i.e. able to maintain homeostasis. • Reversible
- 5. Types of adaptation Hyperplasia - ↑ organ size due to ↑ cell no. Hypertrophy - ↑ organ size due to ↑ cell mass or size. Atrophy - ↓ organ size due to ↓ cell mass & no. Metaplasia – change from one adult tissue to another
- 6. HYPERPLASIA • An organized increase in number of cells (versus: dysplasia, which is disorganized growth, and neoplasia, which is new growth). • It occurs in tissues with cells that are capable of mitotic division “i.e. Hyperplasia essentially does not occur in the brain , heart & skeletal muscle.
- 7. HYPER-PLASIA IN-CREASE IN NUMBER OF CELLS
- 8. HYPERTROPHY • Increase in the sizes of cells, and hence the size of the organ ultimately increase in the amount of functioning tissue mass
- 9. HYPER-TROPHY IN-CREASE IN SIZE OF CELLS
- 10. Cellular adaptation (con’t) **Hyperplasia and hypertrophy can be difficult to separate--not possible by gross exam; difficult by microscopic exam. In most cases, both hyperplasia and hypertrophy occur together (e.g., breast and uterus during pregnancy). Hyperplasia essentially does not occur in the brain , heart and skeletal muscles.
- 11. Hyperplasia Physiologic: ( Hormonal & compensatory) • Breast enlargement during pregnancy&puberty (and hypertrophy) • Uterine enlargement during pregnancy (and hypertrophy) • Liver re-growth after partial resection Pathologic: ( mostly hormonal ) • Benign prostatic hyperplasia ( due to androgens) • Endometrial hyperplasia (due to estrogen) • Viral infections (warts due to human papilloma virus). Effects of locally produced GFs on target cells. • Endocrine organs with increased stimulus (e.g., goiter)
- 12. Thyroid goiter (Diffuse thyroid hyperplasia) Insufficient available dietary iodine cannot make enough thyroid hormones. Extra demand by pituitary TSH cause thyroid enlargement
- 15. Hypertrophy Physiologic • Skeletal muscle hypertrophy associated with exercise • Compensatory hypertrophy of kidney after removal of other kidney Pathologic • Cardiac hypertrophy due to hypertension, valvular stenosis or insufficiency • Asthma--smooth muscle hypertrophy • Hypertrophy of bladder associated with prostatic gland hyperplasia
- 16. Hypertrophy of the muscles of a strength athlete
- 17. Heart Left Ventricle hypertrophy in hypertension:
- 19. Hypertrophy of the Uterus
- 20. ATROPHY • atrophy is defined as decrese in the size or function of an organ due to decrease in cell size 1st and number of cells 2nd. • Can be physiologic or pathologic
- 21. Atrophy Physiologic • Regression in size of breasts and uterus after pregnancy, thymus atrophy at adulthood. Pathologic • Disuse or ↓ workload (skeletal muscle atrophy in fracture) • Loss of endocrine stimulus (adrenal atrophy in patients on steroids) • Denervation ( polimyelitis ,paraplasia). • Inadequate nutrition • Decreased blood supply or Ischemia (atrophy of kidney due to renal artery stenosis). • Aging or Senile atrophy. • Compression atrophy.
- 22. Morphology of atrophy *Reduction in the number of cell’s organelles. *Increase in the number of autophagic vacuoles. *Lipofuscin granules (Brown atrophy)
- 23. Cerebral atrophy - Alzheimers:
- 25. Normal Atrophic
- 28. Hydronephrosis
- 29. Metaplasia "A reversible adaptive change in which one adult or fully differentiated cell type replaced by another adult cell type.“ "Conversion of a differentiated cell type into another" of same or less functional activity. genetic reprogramming of stem cells. Always pathologic
- 30. Epithelial metaplasia •Squamous metaplasia Bronchial epithelia Squamous epithelium Epithelia in bile duct Cervical epithelia •Glandular metaplasia Squamous Columnar epithelium epithelium Barrett’s esophagitis
- 33. significance of metaplasia o A two-edged sword o An undesirable change o Cells survive but some important protective mechanism is lost. o The influences that predispose to such squamous metaplasia, if persistent, may promote cancer transformation in metaplastic epithelium.
- 34. All Cellular adaptation types are reversible Both Hyperplasia & Metaplasia are preneoplastic: i.e. fertile soil for neoplastic transformation. while hypertrophy & atrophy are NOT preneoplastic .