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.
Defnition: Increase in the size of the tissue or organ due to increase in the size of cells
Increased functional demand/workload
Hypertrophy of skeletal muscle
Hypertrophy of smooth muscle
Hypertrophy of cardiac muscle
Hypertrophy of smooth muscle
Defnition: Increase in the number of cells in an organ or tissue, resulting in increased size/mass of the organ or tissue.
— 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.
Defnition: Atrophy is the reduced size of an organ or tissue resulting from a decrease in cell size and number.
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
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.
Starvation (inadequate nutrition) atrophy: For example, protein-calorie malnutrition
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
Original epithelium is replaced by squamous epithelium
Respiratory tract: For example, chronic irritation due to tobacco smoke
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
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.
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)