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.

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:

18. Lt. Ventricular hypertrophy

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

26. Lipofuscin granules

27. Skeletal muscle atrophy:

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 .