1. CELLULAR ADAPTATION
Lecture 4

2. Normal +Stress Adapted
cell Cell
- Stress
Stress = ?
Increased/decreased workload
* skeletal muscle and body building
* cardiac muscle and hypertension
* skeletal muscle disuse (limb immobilization)
Increased/decreased stimulation

3. Adapted
Cell
Cellular adaptations to stress
1. Hyperplasia (more cells)
2. Hypertrophy (bigger cells)
3. Atrophy (smaller cells)

4. 3. Atrophy
(smaller cells)
1. Physiologic
During development: i.e. notochord; thyroglossal duct
2. Pathologic (local or generalized) via
* disuse * Loss of endocrine stimulation
* denervation * Aging
* ischemia * Pressure

5. Atrophy
(Mechanism)
Reduction in structural components
Decreased number of mito, myofilaments, ER via
proteolysis (lysosomal proteases; ubiquitin-
proteosome system)
Increase in number of autophagic vacuoles
Residual bodies (i.e. lipofuscin  brown atrophy)

6. ATROPHY-THYMUS GLAND

7. ATROPHY-LIVER

9. CORTICAL ATROPHY

10. Normal Artophied
Brain atrophy

11. Muscle fiber atrophy. The number of cells is the same as before the
atrophy occurred, but the size of some fibers is reduced. This is a
response to injury by "downsizing" to conserve the cell. In this case,
innervation of the small fibers in the center was lost. This is a trichrome

12. DISUSE ATROPHY
(Poliomyelitis)

13. ATROPHY in OSTEOPOROSIS

14. HYPOPLASIA-GAS
INSUFFICIENCY

15. Hyperplasia
(more cells)
1. Physiologic
* Hormonal (breast/uterus in pregnancy)
* Compensatory (liver after partial hepatectomy)
2. Pathologic
Excessive hormone/GF stimulation of target
tissue
* Endometrial hyperplasia (x’s estrogen)

16. Hyperplasia
(Mechanism)
Cell proliferation
via increased production of TRANSCRIPTION FACTORS
due to
* Increased production of GF
* Increased levels of GF receptors
* Activation of intracellular signaling

17. HYPERPLASIA-PROSTATE GLAND

19. Thyroid hyperplasia

20. HYPERPLASIA-UTERUS

21. Adapted
Cell
2. Hypertrophy (larger cells)
* Not due to swelling
* Increased synthesis of structural
components
* Results in larger organ

22. HYPERTROPHY OF SMOOTH MUSCLE
IN ASTHMA

23. CARDIAC HYPERTROPHY
Myocardial
hypertrophy.
- Cross-section of the
heart of a patient with long-
standing hypertension
- Shows pronounced,
concentric left ventricular
hypertrophy

24. Hypertrophy (Heart)

26. Question
Which term is most likely to fit the
description of the uterus during
pregnancy?
A. hyperplasia
B. hypertrophy
C. aplasia
D. dysplasia
E. metaplasia

27. Metaplasia
(Mechanism)
Reprogramming
1. of stem cells present in normal tissues
2. of undifferentiated mesenchymal cells
in connective tissue
Mediated by signals from
cytokines, Growth Factor
Leading to induction of specific transcription
factors

28. METAPLASIA-ESOPHAGUS

29. 4. Metaplasia
**One adult cell type replaces another**
Reversible
Columnar to squamous epithelium (most common epithelial -type of
metaplasia)
Chronic irritation i.e. (in trachea and bronchi of smokers)
Vit A deficiency squamous metaplasia in respiratory epithelium

30. Photomicrograph of the junction of normal epithelium
(1) with hyperplastic transitional epithelium (2).

31. Photomicrograph of the trachea from a smoker. Note that the columnar
ciliated epithelium has been replaced by squamous epithelium.

32. METAPLASIA-LUNGS

33. DYSPLASIA-Left
• Cellular dysplasia refers to an alteration in the size, shape
and organization of the cellular components of a tissue.
• It is established that dysplasia is a preneoplastic lesion, in
the sence that, it is a necessary stage in the multi-step cellular
evolution to cancer.

34. DYSPLASIA

35. DYSPLASIA-CERVIX

36. Question
Which of the following best describes the
phenomenon of epithelial dysplasia?
A. an increase in thickness of the epithelium because of
increased number of cells
B. a decrease in thickness of the epithelium owing to
decrease in the number of dividing cells
C. an irregular proliferation and maturation of cells
throughout the layers of the epithelium
D. an increase in the thickness of the epithelium owing to
enlargement of the component cells
E. absence of epithelium because of lack of cell
proliferation

37. MUSCULAR DYSTROPHY

38. Muscular Dystrophy
• What Is Muscular Dystrophy?
Muscular dystrophy is a disease in which the
muscles of the body get weaker and weaker and
slowly stop working because of a lack of a
certain protein (see the relationship to
genetics?)
• Can be passed on by one or both parents,
depending on the form of MD (therefore is
autosomal dominant and recessive)

39. ANAPLASIA

40. • Next Meeting:
• Study Inflammation and Repair