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CELLULAR ADAPTATION & CELLULAR AGING

CELLULAR ADAPTATIONS

These are reversible changes in the size, number, phenotype, metabolic activity or functions of cells constitute cellular adaptations.

Types of adaptations: Hypertrophy, hyperplasia, atrophy and metaplasia.

Hypertrophy

Defnition: Increase in the size of the tissue or organ due to increase in the size of cells

Causes
Increased functional demand/workload

Physiological

• Hypertrophy of skeletal muscle

• Hypertrophy of smooth muscle

Pathological

• Hypertrophy of cardiac muscle

• Hypertrophy of smooth muscle

Hyperplasia

Defnition: Increase in the number of cells in an organ or tissue, resulting in increased size/mass of the organ or tissue.

Causes

Physiological hyperplasia: Hormonal stimulation or as compensatory process.

Compensatory hyperplasia: For example, in liver following partial hepatectomy.

Hyperplasia due to hormones: For example, hyperplasia of glandular epithelium of the female breast at puberty, pregnancy and lactation

Pathological hyperplasia: Due to excess endocrine stimulation or chronic injury/irritation.

Atrophy

Defnition: Atrophy is the reduced size of an organ or tissue resulting from a decrease in cell size and number.

Causes

Physiological atrophy: Common during normal fetal development and in adult life.

During fetal development: For example, atrophy of embryonic structures such as thyroglossal duct.

During adult life: For example, involution of thymus, atrophy of brain, gonads and heart due to aging (senile atrophy).

Pathological atrophy: Local or generalized

Local

 1.Disuse atrophy (decreased workload): For example, atrophy of limb muscles immobilized in a plaster cast (as treatment for fracture) or after prolonged bed rest

2. Denervation (loss of innervation) atrophy: For example, atrophy of muscle due to damage to the nerves (e.g. poliomyelitis).

3. Ischemic (diminished blood supply) atrophy: For example, brain atrophy produced by ischemia due to atherosclerosis of the carotid artery.

4.Pressure atrophy: For example, atrophy of renal parenchyma in hydronephrosis due to increased pressure.

 Generalized
Starvation (inadequate nutrition) atrophy: For example, protein-calorie malnutrition

 Metaplasia

Defnition: Metaplasia is a reversible change in which one adult cell type is replaced by another adult cell type.

Metaplasia is mainly seen in association with tissue damage, repair and regeneration.
The replacing cell type is usually more suited to a change in environment.

 Types of Metaplasia

1.Epithelial Metaplasia:

Original epithelium is replaced by squamous epithelium

Respiratory tract: For example, chronic irritation due to tobacco smoke

2.Squamous metaplasia

Cervix: Squamous metaplasia in cervix is associated with chronic infection

Squamous to columnar: In Barrett esophagus, the squamous epithelium of the esophagus replaced by columnar cells

3. Intestinal metaplasia: Te gastric glands are replaced by cells resembling those of the small intestine

4.Connective Tissue Metaplasia

5.Osseous metaplasia: Formation of new bone at sites of tissue injury is known as osseous metaplasia.

Differences between atrophy, hypertrophy and hyperplasia cellular adaptation

CELLULAR AGING

Definition of aging: It is the gradual, insidious and progressive declines in structure and function (involving molecules, cells, tissues, organs and organisms) that begin to unfold after the achievement of sexual maturity.

 Causes

Aging is multifactorial and is affected by genetic factors and environmental factors.

Genetic abnormalities: It causes progressive decline in cellular function and viability.

Environmental factors: These include diet, social conditions and development of age-related diseases (e.g. atherosclerosis, diabetes and osteoarthritis).

Mechanism of Cellular Aging

Decreased Cellular Replication

Most normal cells have a limited capacity for replication. After about 60–70 cell divisions, all cells become arrested in a terminally nondividing state, known as senescence. Werner syndrome is a rare disease characterized by premature aging, damaged DNA and a markedly reduced capacity of cells to divide (shortening of telomere). Te following mechanisms may be responsible for progressive senescence of cells and decreased cellular replication in aging.

Accumulation of Metabolic and Genetic

DamageMetabolic DamageReactive oxygen species: One of the toxic products that cause damage to the cells is free radical mainly reactive oxygen species (ROS). ROS may be either produced in excess, or there is reduction of antioxidant defense mechanisms

Excessive production of ROS may be due to environmental influences (ionizing radiation) and mitochondrial dysfunction.

Reduction of antioxidant defense mechanisms may occur with age (e.g. vitamin E, glutathione peroxidase)

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