The document discusses cellular adaptations, including hypertrophy, hyperplasia, atrophy, and metaplasia, describing their characteristics, mechanisms, and clinical significance. It emphasizes that adaptations can be physiological or pathological and may involve reversible changes in size, number, and function of cells. Additionally, it outlines the potential for hyperplastic processes to lead to cancer if dysregulation occurs.

1. Cellular adaptations and
growth disturbances

2. SLOs
• Characteristics of cellular adaptations
• Etiological types
• Morphological types
• Examples
• Clinical significance

3. Cellular adaptations
• Adaptations are reversible
• Response to changes in their environment
• Reversible change can affect
– Number
– Size
– Phenotype
– Metabolic activity
– Functions of cells

4. Etiopathogenesis of cellular
adaptations
• Physiologic adaptations
• Pathologic adaptations

5. Morphological types of cellular
adaptations
• Hypertrophy
• Hyperplasia
• Atrophy
• Metaplasia

6. Hypertrophy
• increase in the size of cells
• increase in the size of the organ
• bigger cells containing increased amounts
of structural proteins and organelles.
• cells have a limited capacity to divide

7. Physiologic Hypertrophy
• Smooth muscle fibres of uterus during
pregnancy - estrogen stimulation

8. Physiologic hyeprtrophy
• Skeletal muscle – increased work

9. Pathologic Hypertrophy
• Cardiac muscle - hypertension or
aortic valve disease

10. Mechanism of hypertrophy
• Triggers
– mechanical – stretch
– trophic triggers - growth factors & adrenergic
hormones
• Transduction pathways - Induction of
genes - Synthesis of many cellular
proteins

11. Hypertrophy is finite
• Beyond a critical point degenerative
changes start
• Eg : heart – initial hypertrophy – followed
by heart failure

12. Hyperplasia
• increase in the number of cells
• increase in the size of the organ
• cell populations capable of replication
• stimuli similar to those for hypertrophy

13. Physiologic Hyperplasia
• Hormonal hyperplasia
– glandular epithelium of the female breast at
puberty and during pregnancy

14. Physiologic Hyperplasia
• Compensatory hyperplasia
– residual tissue grows after removal or loss of
part of an organ

15. Pathologic Hyperplasia
• Cause –
–excessive hormonal stimulation
–excessive growth factor stimulation

16. Pathologic Hyperplasia
• Endometrial hyperplasia - disturbed
balance between estrogen and
progesterone

17. Pathologic Hyperplasia
• Proud flesh / Hyperplastic scar - growth
factors are produced by leukocytes

18. Pathologic Hyperplasia
• Hyperplastic epithelium (warts) - viral
infections

19. Hyperplasia – fertile soil for cancer
• Hyperplastic process remains controlled
• If signals abate - the hyperplasia disappears
• High chance of dysregulation creeping into
these cells – cancers can eventually arise

20. Atrophy
• Shrinkage in the size of the cell
• Loss of cell substance
• Tissue or organ diminishes in size
• Cells have diminished function – But are
not dead

21. Causes of atrophy
• Causes
– decreased workload
– loss of innervation
– diminished blood supply
– Inadequate nutrition
– loss of endocrine stimulation
– aging

22. Mechanisms of atrophy
• decreased protein synthesis - reduced
metabolic activity.
• increased protein degradation - ubiquitin-
proteasome pathway
• increased autophagy

23. Atrophy

24. Metaplasia
• reversible change
• one adult cell type (epithelial or
mesenchymal) is replaced by another adult
cell type
• The replaced cell type better able to
withstand the adverse environment
• Reprogramming of stem cells –
transdifferentiation
• Eg:
– Epithelial metaplasia in respiratory epithelium of
habitual smokers

25. Metaplasia

28. Metaplasia – Double edged sword
• Survival advantages
• Loss of important protective mechanisms
• Persistent stimuli - predispose to
malignant transformation

29. Summarise

30. Questions ?