01.Cellular Adaptations in human body.pdf

We are discuss from thus about cellular adaptation. Micro biologycal part.

1. CELLULAR ADAPTATIONS



Dr. A.M.D.S Karunaratna

2. Intended Learner Outcomes
•Outline the stages of cellular response in
stress and injurious stimuli.
•Define the term cellular adaptation.
•List and describe the types of cellular
adaptations.(Hypertrophy, Hyperplasia,
Atrophy, Dysplasia, Metaplasia)
•Give examples for cellular adaptations.

3. Introduction





Homeostasis
Cells maintaining their intracellular environment within a
very narrow range of physiological changes.
CELLULAR ADAPTATION
Due to stresses or pathologic stimuli cell may adapt

4. Cell injury
If the external stress exceed the adaptive capacity
cells get injured
REVERSIBLE CELL INJURY
Cells are able to returned back to normal
IRREVERSIBLE CELL INJURY- CELL DEATH
Necrosis

5. Stages in the cellular response in stress and
injurious stimuli

7. Cellular Adaptations










Adaptations are reversible changes in the
number, size, phenotype, metabolic activity,
or functions of cells in response to changes in
their environment.
Pathologic adaptationsPhysiologic adaptations

8. Physiological adaptations
•They represent the response of cells to normal
stimulation by hormones or endogenous
chemical substances
e.g.
enlargement of the breast and uterus during
pregnancy.
cyclic changes in endometrium.

9. Pathologic adaptations

•Cellular responses to pathological stimuli
•Allow the cell to modulate their structure and
function to escape the injury.
e.g.
Cardiac enlargement in response to hypertension.

state intermediate between normal unstressed cells
and injured overstressed ones.

10. Size and number of cellsDifferentiation of Cells
Hypertrophy
Hyperplasia
Atrophy

Metaplasia
Dysplasia

11. Hypertrophy



•Hypertrophic organ has no new cells.
•It may be physiological or pathological.
•Occurs in organs in which proliferation and
mitosis are restricted
e.g. skeletal muscle and heart muscles.

Hypertrophy is an increase in the size of cells
resulting in increase in the size of the organ.

12. Mechanism of hypertrophy
•Due to increased production of cellular
proteins and organelles.
•Induced by
–Mechanical sensors.eg: stretch
–Growth factors (TGF-beta, IGF-1, FGF)
–Vasoactive agents (alpha-adrenergic agonists,
endothelin-1, angiotensin II)
•Extreme levels of hypertrophy can lead to cell
death.

13. Physiological Hypertrophy
Pregnant uterus-Estrogen induced
smooth muscle hypertrophy.
Skeletal muscle hypertrophy in exercise

14. A. Gross appearance of a gravid uterus.
B. Smooth muscle cells from a normal uterus
C. Smooth muscle cells from a gravid uterus.

15. Skeletal muscle hypertrophy in response to
exercise

16. Skeletal muscle hypertrophy in response to exercise

17. Pathological Hypertrophy
•Cardiac muscle hypertrophy in chronic
hypertension and aortic valve disease

18. Hyperplasia
oDefinition: It is an increase in the size of an
organ or tissue due to increase in the number
of constituent parenchymal cells.

• It may be physiological or pathological.
•Hypertrophy and hyperplasia can occur
together resulting an enlarged organ.
e.g. Massive physiologic enlargement of the
uterus during pregnancy

19. Physiological hyperplasia
Hormonal Hyperplasia
Proliferation of the glandular epithelium of the
female breast at puberty and during pregnancy

20. Physiological Hyperplasia
Compensatory Hyperplasia
Hyperplasia following surgical removal of
part of liver.

21. Physiological Hyperplasia
Normal skin Hyperplasia after trauma
Wound healing
proliferation of fibroblasts and blood vessels aid in
wound healing-growth

22. Physiological Hyperplasia and Hypertrophy
Enlargement of the uterus during pregnancy
Hyperplasia and Hypertrophy of smooth muscles of
uterus

23. Pathological hyperplasia
•Caused by excessive hormonal or growth
factor stimulation.
Endometrial hyperplasia-Imbalances between
estrogen and progesterone levels
Skin warts caused by papilloma viruses
growth factors released by virus and infected
cells.
Benign prostatic hyperplasia- increase in the
level of androgens and estrogens.

24. Atrophy





•May be physiological or pathological.

Reduction of the size of an organ
after reaching its normal adult size as a
result of decrease in both the number and
size of the cells.

25. Mechanism of atrophy
•Decreased protein synthesis and increased
protein degradation in cells.
•Decreased protein synthesis is due to
decreased metabolic activity.
•degradation of cellular proteins-
ubiquitin-proteasome pathway
•Autophagy(self eating)- starved cells
eats their own components.

26. Types of Atrophy








Ischemic atrophy
due to decrease of blood supply e.g. Renal atrophy due
to obstruction of renal artery.

27. Types of Atrophy
Pressure atrophy
due to long continued pressure on a tissue.
e.g. Tumor
Due to Decreased work load
e.g. Atrophy of immobilized limb muscles.

Disuse Atrophy

28. Types of Atrophy
Denervation atrophy
when a motor nerve supplying a muscle is affected as in
poliomyelitis

29. Types of Atrophy
Atrophy due to Starvation
Leads to generalized atrophy
Atrophy due to loss of hormonal stimulation

Ovarian atrophy after menopause
Testicular atrophy

30. Metaplasia
•A process by which one type of mature cell
(epithelial or mesenchymal) is replaced by
another type of mature cell
•Due to abnormal differentiation of stem cells
in adverse conditions
•Cells are well adapted to the adverse
environment.
•Predispose to malignant transformation.

31. Causes for metapasia
•Changes in environment.
•Irritation or inflammation-Cigarette Smoking
•Nutritional deficiency-Vitamin A deficiency

32. Metaplasia
•Columnar to squamous.
•.
Barrett oesophagus – oesophageal squamous epithelium is
replaced by intestinal like columnar cells under the
influence of refluxed gastric acid. (increases the risk of
adeno carcinomas)

33. Epithelial Metaplasia
Columnar to squamous-Respiratory epithelium of smokers
and vitamin A deficiency

34. Epithelial metaplasia
Squamous to columnar
Barrett oesophagus
oesophageal squamous epithelium is replaced by
intestinal like columnar cells under the influence
of refluxed gastric acid. (increases the risk of
adeno carcinomas)

35. Normal oesophagus

37. Columnar metaplasia in lower
oesophagus

38. Dysplasia
•Growth of an abnormal group of cells due to a
growth stimulus. These changes are
reversible.
•Considered precancerous.
E.g. Cervical carcinoma

39. Dysplasia
Some abnormalities in cell maturation and
differentiation
•1. Cytological and architectural abnormalities

•2. Slight increase in cell number

•3. Partial loss of control and organization

•4. Partially reversible

40. Dysplasia
•The degree of dysplasia vary
•The risk of development of carcinoma vary
with
–degree of dysplasia, duration and site

41. QUIZ
•Give examples for adoptive responses in
reproduction system