1. Cell injury, adaptation and cell death

2. Normal cell (Homeostasis) Cell injury Adaptation cell death
Stress injurious stimulus
Increased demand
Cell injury
Adaptation cell death
Inability to adapt

3. HYPERPLASIA
Increase in tissue or organ size due to increase in the number of component cells
It takes place if the cellular population is capable of synthesizing DNA, thus permitting mitotic division
Occurs in tissues with labile and stable cells

4. Two types of hyperplasia
1. Physiological hyperplasia
Hormonal – eg: proliferation of glandular epithelium of breast at puberty and pregnancy
Compensatory hyperplasia – eg: following resection of part of liver, hyperplasia of connective tissue cells in wound healing

5. 2. Pathological hyperplasia
Hormonal – endometrial hyperplasia, adrenal hyperplasia, thyroid hyperplasia, bone marrow hyperplasia, lymph node hyperplasia, benign prostatic hyperplasia
Growth factors – skin wart – papilloma virus and transcription factors

6. Mechanisms of physiological hyperplasia
Increased local production of growth factors
Increased levels of growth factor receptors on the responding cells
Activation of intracellular signaling pathways

7. Hypertrophy
Increase in tissue or organ size due to increase in the size of the cell
Cell size increased due to increased synthesis of structural proteins and organels
Usually occurs in tissues with permanent cells.

8. Hypertrophy may be physiological or pathological and caused either by
Increased functional demand or
Specific hormonal stimulation
Eg.
1. Uterus in pregnancy – oestrogenic stimulation causing hyperplasia of endometrium, smooth muscle hypertrophy
2. Body builders – hypertrophy of skeletal muscle
3. Cardiomegaly – hypertension/aortic valve disease
4. Post myocardial infarct enlargement of residual viable cardiac myocytes hypertrophy

9. Mechanisms of hypertrophy
Signal transduction pathways -- induction of genes -- synthesis of numerous cellular protiens
Trigger factors
Mechanical triggers eg. Strech
Trophic triggers eg. Polypeptide growth factor

10. Hyperplasia and hypertrophy often occur together

11. How does hyperplasia differ from neoplasia ?
Hyperplasia is induced by known stimuli
It stops when the stimulus which provoked it,
is removed

12. ATROPHY Decrease in tissue size due to decrease in
size of a sufficient number of cells,
secondary to protein degradation
Cell metabolism and function are reduced
to a level at which survival is possible

13. Two types of atrophy
1. Physiologic atrophy – During early development some embryonic structures undergo atrophy, Uterus after parturition
2. Pathologic atrophy – Local or generalized

14. Causes of atrophy
1. Decreased work load –immobilisation of a limb after fracture 2. Loss of innervation 3. Decreased blood supply 4. Loss of endocrine stimulation – in menopause 5. Lack of nutrients 6. Ageing

15. Mechanisms of atrophy
Proteolytic pathways of protein degradation are activated
Lysosomes containing proteases are activated

16. METAPLASIA
Replacement of one type of mature (specialised) tissue by another type of mature (specialised) tissue, not normally found at that site.
Can occur in epithelium and connective tissue.

17. Occurs as an adaptive response to a stimulus
Although new mature cell type is better able to withstand the adverse conditions (adaptive advantage) , protective mechanisms, like mucus secretion and ciliary clearance can be lost eg resp tract of smokers
Structurally normal
is potentially reversible

18. Epithelial metaplasia
Squamous metaplasia – Excretory ducts of
salivary glands, pancreas, bile ducts, cervix
-Ciliated epithelium of resp tract of smokers
-Respiratory tract in Vitamin A deficiency
Glandular metaplasia –
Intestinal or gastric metaplasia of oesophagus in
chronic gastric reflux

19. Mesenchymal metaplasia
Osseous metaplasia of fibrous scars
Usually no adverse effects but rarely
some functional defects

20. Mechanisms of metaplasia
No change in phenotype of a differentiated cell type.
Result of reprogramming of stem cells which exist in normal tissue, or of undifferentiated mesenchymal cells in connective tissue