cellular adaptations and growth disturbances and their mechanisms. please refer the books given in reference section of this presentation for further understandings and examples of subtypes.

1. CELLULAR ADAPTATIONS AND
GROWTH DISTURBANCES
BY Dr ZAID WANI
MVSc

2. INTRODUCTION
• Cells constantly adapt to changes (acting as a stimuli or causing
injury) in their environment.
• Adaptations are reversible functional and structural responses to
more severe physiologic stresses and some pathologic stimuli, during
which new but altered steady states are achieved, allowing the cell to
survive and continue to function.
• Changes in the number, size, phenotype, metabolic activity, or
functions of cells in response to changes in their environment.
• Mostly has BENIFICIAL RESPONSES.

3. Adaptation Types:
• Physiologic adaptations: Usually represent responses of cells to
normal stimulation by hormones or endogenous chemicals or to the
demands of mechanical stress.
• Pathologic adaptations: Are responses to stress that allow cells to
modulate their structure and function and thus escape injury, but at
the expense of normal function.

5. 1. Hypertrophy
• Hypertrophy is an increase in the SIZE of cells and, as a result, an
increase in the size of the organ.
• No new cells, just bigger cells.
• Increase in size of cells is not due to cellular swelling, but because of
the increased synthesis of structural proteins and organelles.
• Hypertrophy occurs where cells have a limited or lost the capacity to
divide e.g. skeletal and cardiac muscle cells.
• Hypertrophy and hyperplasia can occur together - both result in an
enlarged organ.

6. Mechanism of Hypertrophy:

7. Types:
• Physiological hypertrophy e.g. Enlargement of the uterus during
pregnancy; Muscle development in race or draft horses due to
increased workload.
• Adaptive or Compensatory e.g. Cardiac enlargement that occurs
with hypertension or aortic valve disease ; one of a pair of
organs is destroyed, the other gradually enlarges and
compensates for the loss.
• Increased functional demand.
• Specific hormonal stimulation.
Causes:

8. Microscopically:
• Increase in the size of cells.
• Fewer cells in each microscopic
field.
Macroscopically:
• Organ or tissue is larger and
heavier than normal.
Normal Heart
Hypertrophied heart

10. Significance:
• Protective mechanism – Need for increased function.
• Occasionally harmful – Hypertrophy in heart distorts the valves.
• If stimuli is removed, hypertrophic process regresses although the
organ rarely regresses to normal size.

11. 2. HYPERPLASIA
• Absolute increase in the NUMBER of cells in an organ or tissue.
• Limited to cells capable of mitotic division.
• Does not increase functional units of an organ.
• Hyperplasia can be:
Physiological:
Hormonal hyperplasia e.g. Proliferation of the glandular epithelium of
the mammary gland at puberty and during pregnancy.
Compensatory hyperplasia e.g. Partial hepatectomy.

12. Pathological:
Repeated and prolonged irritation by mechanical, chemical, and thermal
agents.
Endocrine disturbances e.g. Hyperplasia of the prostate occurs in old
dogs and of epithelium and connective tissue of the mammary gland.
Nutritional disturbances e.g. Goitre and Vitamin A deficiency.
Infectious causes e.g. Pox viruses cause hyperplasia of epithelium.
Wound healing and repair.

13. Mechanism:
• Growth factor–driven proliferation of mature cells and, in some cases,
by increased output of new cells from tissue stem cells. For instance,
after partial hepatectomy growth factors are produced in the liver
that engage receptors on the surviving cells and activate signaling
pathways that stimulate cell proliferation. But if the proliferative
capacity of the liver cells is compromised, as in some forms of
hepatitis causing cell injury, hepatocytes can instead regenerate from
intrahepatic stem cells

14. Significance:
• Hyperplastic epithelial tissue usually disappears if the cause is
removed. However, connective tissue hyperplasia is a permanent
change and persists for the life of the individual. The great danger
associated with hyperplasia is that the cells have changed their
normal pattern and rate of growth. Pathological hyperplasia, thus,
constitutes a fertile soil in which cancerous proliferation may
eventually arise.

17. Skin Hyperplasia
Skin - Normal Skin - Hyperplasia

18. 3. ATROPHY
• Shrinking or wasting away of a cell due to loss of cell substance.
• Diminished function but not dead.
• Not to be confused with Hypoplasia.
• Occurs in cells that have reached their full development.
• TWO WAYS –
NUMERICAL ATROPY: Decrease in number of constituent cells.
QUANTATIVE ATROPHY: Decrease in size of each cell.

19. Mechanism:
• Ubiquitin-proteosome pathway:
Degradation of intermediate
filaments of the cytoskeleton.
• The cytoskeleton is a structure that
helps cells maintain their shape and
internal organization, and it also
provides mechanical support that
enables cells to carry out
essential functions like division and
movement.
• Autophagy of cellular components:
Generation of autophagic vacuoles
which fuse with lysosomes to
breakdown cellular components.

20. Causes:
• Physiological atrophy
• Aging (senile atrophy): Organs of
reproduction (testes and
ovaries) are among the first to
show senile changes.
• Inadequate nutrition (starvation
atrophy)
• Decreased workload (disuse
atrophy).
• Loss of innervation (denervation
or neurotropic atrophy).
• Diminished blood supply
(angiotrophic atrophy).
• Pressure (pressure atrophy).
• Loss of endocrine stimulation
(endocrine atrophy).

21. Macroscopically:
• Decrease in the size of the organ
or the tissue involved.
• Flabby, soft, and lacks its normal
tissue tone.
• Loses its normal tissue colour
and appears anaemic.
• WRINKLED CAPSULE in case of
capsulated organ.
Microscopically:
• Smaller than normal, and fewer
in number, or may have entirely
disappeared.
• Increase in the number of
'autophagic vacuoles'.
• Cells appear numerous n closer
in a microscopic field

25. 4. METAPLASIA
• Substitution of one variety of adult, fully differentiated cells (Epithelial as well as
mesenchymal) for another type of adult, fully differentiated cells.
• It is a substitution and not a transformation - cells sensitive to particular stress
replaced by other cell types better able to withstand the adverse environment.
• Alteration from a less specialized cell type to a more specialized cell type.
Causes:
Repeated and prolonged irritation e.g Squamous Metaplasia in Respiratory tract
due to Lungworm infection and Smoking.
Nutritional disturbances e.g. Vit-A deficiency
Endocrine disturbances e.g. Mammary gland tumors and sertoli cell tumors in
dogs.

26. Mechanism:

28. Metaplasia in mesenchymal cells less
clearly as an adaptive response. Fibroblasts
may get replaced by chondroblasts or
osteoblasts to produce cartilage or bone,
where it is normally not found.
Significance:
 Reversible change (Except cartilage or
bone formation)
 Squamous metaplasia may function as a
protective mechanism. However, the
influences that cause such metaplasia, if
persistent, may induce malignant
transformation in metaplastic epithelium.
 Early phase o carcinogenesis.

29. 5. APLASIA
• COMPLETE FAILURE of an organ or a tissue to develop DURING
EMBRYOGENESIS.
• The affected organ or tissue is missing.
• Involvement of a vital organ or tissue – foetal development may not proceed.
• Mostly goes undetected due to early abortion or resorption.
• CAUSES:
Inherited genetic diseases ( e.g. Tailessness in Manx cats)
Hereditary defects in germplasm.
Poisons e.g. Thalidomide poisoning causing Amelia.
Prenatal Infections
Death of a cell at some critical point in the development of the individual.
Macroscopically: Organ or tissue is absent.

30. Aplasia of Gall Bladder (Canine)

31. 6. HYPOPLASIA
• Failure of cells, tissue or an organ to develop to its normal mature size.
• Incomplete or underdevelopment with decreased number of cells.
• Differs from Atrophy.
• Occurs during period of growth, mostly before birth and sometimes
postnatal as well.
• CAUSES:
Congenital anomalies e.g. Hypoplasia of kidneys,eyes.
Inadequate blood supply
Inadequate innervation.
Malnutrition

32. Microscopically:
• Cells are not as large as normal
cells.
• Fewer in number.
• Excessive amount of connective
tissue and fat.
Macroscopically:
• Tissue or organ appears smaller
and never attains its normal
adult size.
• Variation in size determined by
weight, volume, or
measurement when compared
with normal tissue or organs.
Hypoplasia – Feline Kidney

33. 7. DYSPLASIA
• Abnormal development of cells and tissues.
• Loss in the uniformity architectural orientation of individual cells.
• Retrogressive change in a tissue after it has reached a stable adult
stage.
• Mainly seen in epithelial cells.
• Not an adaptive response, but is considered because it is closely
related to hyperplasia, and is sometimes called 'atypical hyperplasia'.
• Precursor of cancer – not necessarily.

34. Microscopically:
• Considerable variation in size
and shape of cells.
• Deeply stained (hyperchromatic)
nuclei.
• Mitotic figures are more
abundant than usual.
Macroscopically:
• Distorted shape.

36. 8. ANAPLASIA
• Reversion of cells to a more primitive and less differentiate type.
• Cells loose structural and functional characteristics.
• Increased mitotic activity.
• Irreversible
• Precursor of neoplasia.
• Feature of neoplastic tissue.

37. REFERENCES:
• JONES and HUNT. (1983). Veterinary Pathology. 5th
ed.Philadelphia;Lea and Febiger.
• Kumar,Abbas,Aster. (2018).Robbins Basic Pathology.10th ed.
Philadelphia;Elsevier.
• Vegad JL. (2007).A Text Book Of General Veterinary Pathology.2nd
ed.Delhi;International book distributing co.
• Ganti A Sastry.(2001).Veterinary Pathology.7th ed.New Delhi;CBS
Publishers.
• https://epomedicine.com/medical-students/understanding-cellular-
adaptations/

38. THANKYOU