cellular adaptations

     Cellular Adaptation

Definition- Cellular adaptation are reversible functional and structural responses.

       ↬     It is the adjustment of the cells which may be physiological need and pathological injury responses to stress.

      ↬      Cellular Adaptations based on mainly physiological and pathological adaptation and this adaptation occurs by same process.

Process of Adaptation- 

Atrophy- Decreasing the size of cell

Hypertrophy- Increasing the size of cell

Hyperplasia- Increase the number of cell

Metaplasia- Changing the one type of cell charge in to another type of cell, means cell transformation.

Dysplasia- derangement or bad development of cell

Atrophy- Atrophy is the decrease the number and size of parenchymal cells of the organ but  it's not a part of cell death.  

↬ Atrophy means decrease protein synthesis and increased protein degradation.

↬If we are seeing cell atrophy in light microscope then we can see small shrunken cell with lip of uncin granules

↬Shrunken of the cell is due to decrease in cells organelles for example- Mitochondria, myofilaments, endoplasmic reticulum.

↬ If we are seeing in electron microscope then we can see decreased intracular components.

Cause of atrophy based on- Physiology atrophy and pathology atrophy  

Physiology atrophy- 

A. Physiologic atrophy is a normal process of ageing in some tissues, in which due to loss of endocrine stimulation or from senile arteriosclerosis. 

For example:

i) Atrophy of lymphoid tissue with ageing.

ii) Atrophy of thymus in adult life.

ii) Atrophy of gonads after menopause.

iv) Atrophy of brain with ageing

v) Osteoporosis with reduction in size of bony trabeculae due to ageing

B. Pathologic atrophy 

Pathologic atrophy causes are as under:

1. Starvation atrophy In starvation, there is first depletion of carbohydrate and fat stores followed by protein catabolism.

↬There  is general weakness, emaciation and anaemia referred to as cachexia seen in cancer and severely ill patients.

2. Ischaemic atrophy Gradual decrease of blood supply due to atherosclerosis may result in shrinkage of the affected organ for example- 

i) Small atrophic kidney in atherosclerosis of renal artery.

ii) Atrophy of the brain in cerebral atherosclerosis.

3.  Disuse atrophy Prolonged diminished functional activity is associated with disuse atrophy of the organ for example

i) Wasting of muscles of limb immobilised in a plaster cast.

ii) Atrophy of the pancreas in obstruction of pancreatic duct.

.4. Neuropathic atrophy Interruption in nerve supply leads to wasting of muscles for example- 

i) Poliomyelitis

ii) Motor neuron disease

ii) Nerve section.

5. Endocrine atrophy Loss of endocrine regulatory mechanism results in reduced metabolic activity of tissues and hence atrophy for example- 

i) Hypopituitarism may lead to atrophy of thyroid, adrenal and gonads.

ii) Hypothyroidism may cause atrophy of the skin and its adnexal structures.

6. Pressure atrophy Prolonged pressure from benign tumours or cyst or aneurysm may cause compression and atrophy of the tissues for example-

i) Erosion of the spine by tumour in nerve root.

ii) Erosion of the skull by meningioma arising from pia-arachnoid.

ii) Erosion of the sternum by aneurysm of arch of aorta.

7. Developmental disorders e.g. cryptorchid testis due to incomplete descent of testis into normal scrotal position causing testicular atrophy.

8. ldiopathic atrophy There are certain examples of atrophy where no obvious cause is present e.g. myopathies.

HYPERTROPHY-

Hypertrophy is an increase the size of parenchymal cells that resulting in enlargement of the organ or tissue, without any change in the number of cells.

Mechanism- increase the functional demand or stimulation by hormones and growth factors

   Increase the production of the cellular protein due to the increased activation of genes responsible for the production of these protein.  

CAUSES-  Hypertrophy may be physiologic or pathologic. 

A. Physiologic hypertrophy-

Increase the endocrine stimulation is an example of physiologic hypertrophy as well as hyperplasia. by- Breast development at puberty

                             Uterus development in pregnancy

                              Breast development in lactation

                Increase mechanical demand physiologic (striated muscle of weight lifters)

B. Pathologic hypertrophy associated with hypertrophy are as under:

1. Hypertrophy of cardiac muscle may occur in a number of cardiovascular diseases. A few conditions producing left ventricular hypertrophy are as under:

a) Systemic hypertension

b) Aortic valve disease (stenosis and insufficiency)

c) Mitral insufficiency

2. Hypertrophy of smooth muscle e.g.

       a)  Cardiac achalasia (in oesophagus)

       b) Pyloric stenosis (in stomach)

       c) Intestinal strictures

       d) Muscular arteries in hypertension.

3. Hypertrophy of skeletal muscle 

e.g. hypertrophied muscles in athletes and manual labourers.

4. Compensatory hypertrophy may occur in an organ when the contralateral organ is removed e.g.

i) Following nephrectomy on one side in a young patient, there is compensatory hypertrophy as well as hyperplasia of the nephrons of the other kidney.

i) Adrenal hyperplasia following removal of one adrenal gland.

HYPERPLASIA

Hyperplasia is an increase the number of parenchymal cells resulting in enlargement of the organ or tissue. 

Both hyperplasia and hypertrophy occur together.

Hyperplasia occurs when the cell population is capable of dividing.

 Hyperplasia occurs due to increased recruitment of cells from GO (resting) phase of the cell cycle to undergo mitosis, when stimulated.

All body cells do not possess hyperplastic growth potential

 Labile cells (e.g. epithelial cells of the skin and mucous membranes, cells of the bone marrow and lymph nodes).

 Stable cells (e.g. parenchymal cells of the liver, pancreas, kidney, adrenal, and thyroid) can undergo hyperplasia, 

 Permanent cells (e.g. neurons, cardiac and skeletal muscle) have little or no capacity for regenerative hyperplastic growth. 

 Neoplasia differs from hyperplasia in having hyperplastic growth 

CAUSES As with other adaptive disorders of growth, hyperplasia may also be physiologic and pathologic.

A. Physiologic hyperplasia The two most common types are Hormonal hyperplasia i.e. hyperplasia occurring under the influence of hormonal stimulation e.g.

i Hyperplasia of female breast at puberty, during pregnancy and lactation.

ii) Hyperplasia of pregnant uterus.

iii) Proliferative activity of normal endometrium after a normal menstrual cycle.

iv) Prostatic hyperplasia in old age.

2. Compensatory hyperplasia i.e. hyperplasia occurring following removal of part of an organ or in the contralateral organ in paired organ e.g.

i) Regeneration of the liver following partial hepatectomy.

ii) Regeneration of epidermis after skin abrasion.

ii) Following nephrectomy on one side, there is hyperplasia of

nephrons of the other kidney.

B. Pathologic hyperplasia Most examples of pathologic hyperplasia are due to excessive stimulation of hormones or growth factors e.g.

i) Endometrial hyperplasia following oestrogen excess.

ii) In wound healing, there is formation of granulation tissue due to proliferation of fibroblasts and endothelial cells.

iii) Formation of skin warts from hyperplasia of epidermis due to human papilloma virus.

iv) Pseudocarcinomatous hyperplasia of the skin occurring at the margin of a non-healing ulcer.

v) Intraductal epithelial hyperplasia in fibrocystic change in the breast.

METAPLASIA

Metaplasia is defined as a reversible change of one type of epithelial or mesenchymal adult cells to another type of adult epithelial or mesenchymal cells,

Usually in response to abnormal stimuli, and often reverts back to normal on removal of stimulus. 

 If the stimulus persists for a long time, epithelial metaplasia may progress to dysplasia and further into cancer.

Metaplasia is broadly divided into 2 types: epithelial and

mesenchymal.

A. EPITHELIAL METAPLASIA This is the more common type. The metaplastic change may be patchy or diffuse and usually results in replacement by stronger but less well-

specialised epithelium. However, 

Metaplastic epithelium being less well-specialised such as squamous type, results in

deprivation of protective mucus secretion and hence more prone to infection. 

Depending upon the type of epithelium transformed, two types of epithelial metaplasia are seen: squamous and columnar.

1. Squamous metaplasia

types of specialised epithelium are capable of undergoing squamous metaplastic change due to chronic irritation that may be mechanical, chemical or infective in origin. Some common

examples of squamous metaplasia are seen at following sites:

i) This is more common. Various In bronchus (normally lined by pseudostratified columnar

ciliated epithelium) in chronic smokers.

ii) In uterine endocervix (normally lined by simple columnar epithelium) in prolapse of the uterus and in old age

ii) In gallbladder (normally lined by simple columnar epithelium) in chronic cholecystitis with cholelithiasis.

iv) In prostate (ducts normally lined by simple columnaar epithelium) in chronic prostatitis and oestrogen therapy.

v) In renal pelvis and urinary bladder (normally lined by transitional epithelium) in chronic infection and stones.

vi) In vitamin A deficiency, apart from xerophthalmia, there is squamous metaplasia in the nose, bronchi, urinary tract, lacrimal and salivary glands.

There are some conditions in

Columnar metaplasia

which there is transformation to columnar epithelium. For example:

i) Intestinal metaplasia in healed chronic gastric ulcer.

ii) Columnar metaplasia in Barrett's oesophagus, in which there is change of normal squamous epithelium to columnar epithelium.

ii) Conversion of pseudostratified ciliated columnar epithelium in chronic bronchitis and bronchiectasis to columnar type.

iv) In cervical erosion (congenital and adult type), there is variable area of endocervical glandular mucosa everted into the vagina.

B. MESENCHYMAL METAPLASIA Less often, there is transformation of one adult type of mesenchymal tissue to another. The examples are as under:

1. Osseous metaplasia Osseous metaplasia is formation of bone in fibrous tissue, cartilage and myxoid tissue. Examples of

osseous metaplasia are as under:

i) In arterial wall in old age (Mönckeberg's medial calcific sclerosis)

ii) In soft tissues in myositis ossificans

ii) In cartilage of larynx and bronchi in elderly people

iv) In scar of chronic inflammation of prolonged duration

v In the fibrous stroma of tumour e.g. in leiomyoma.

2. Cartilaginous metaplasia In healing of fractures, cartilaginous metaplasia may occur where there is undue mobility.

DYSPLASIA

Dysplasia means 'disordered cellular development, often preceded or accompanied with metaplasia and hyperplasia; 

it is therefore also referred to as atypical hyperplasia.

 Dysplasia occurs most often in epithelial cells. 

Epithelial dysplasia is characterised by cellular proliferation and cytologic changes as

under:

1. Increased number of layers of epithelial cells

2. Disorderly arrangement of cells from basal layer to the

surface layer

3. Loss of basal polarity i.e. nuclei lying away from basement

membrane

4. Cellular and nuclear pleomorphism

5. Increased nucleocytoplasmic ratio

6. Nuclear hyperchromatism

7. Increased mitotic activity.

The two most common examples of dysplastic changes are the uterine cervix and respiratory tract.

Dysplastic changes often occur due to chronic irritation or prolonged inflammation. 

On removal of the inciting stimulus, the changes may disappear. 

In a proportion of cases, however, dysplasia may progress into carcinoma in situ

(cancer confined to layers superficial to basement membrane) or invasive cancer.