Cellular Adaptation and Pathology

Study Notes

Cellular adaptation involves reversible changes in cells responding to environmental changes (stress/stimulation) to maintain homeostasis (a new steady state) and preserve viability and function. This adaptation can be physiologic (response to normal stimulation) or pathologic (response to stressful stimulation).
Cellular adaptation includes changes in cell size (hypertrophy, atrophy), cell number (hyperplasia), and cell type (metaplasia).
Hypertrophy is an increase in cell size, resulting in an increase in organ size. This can be physiological—as seen in response to exercise or hormonal stimulation in some organs —or pathological.
Hyperplasia is an increase in cell number, which increases organ size. It can be physiological or pathological. Hyperplasia and hypertrophy can occur together. Examples include hormonal hyperplasia and compensatory hyperplasia.
Atrophy is a shrinkage in cell size due to loss of cell substance. This can be physiological, for example, the shrinkage of the uterus after pregnancy, or pathological, such as from decreased workload/demand, loss of innervation, reduced blood supply, or inadequate nutrition/energy.
Metaplasia is a change from one mature cell type to another mature cell type. This is an adaptive response to produce cells better equipped to withstand environmental changes. Examples include physiological squamous metaplasia in the cervix from hormonal changes and pathological squamous metaplasia in the lung from cigarette smoking.

Intracellular accumulations are the buildup of substances produced by the cell or elsewhere in cells. Possible locations include the cytoplasm, lysosomes, and nucleus.
Substances such as lipids, glycogen, proteins, and pigments can accumulate, potentially causing cellular dysfunction.
Lipids accumulate in cells due to increased intake, decreased catabolism, or abnormal metabolism. For example, excess lipid accumulation in parenchymal cells is called steatosis.
Protein accumulation can be from excessive synthesis, uptake, or from the misfolding of proteins. An accumulation of abnormal proteins in neurons is associated with Alzheimer's disease.
Glycogen accumulation can result from genetic disorders or issues with carbohydrate metabolism. Examples are in the cells of the renal tubules, cardiac myocytes, and islets of Langerhans in cases of diabetes.
Pigment accumulation is also possible. Examples include exogenous pigments from the outside, such as carbon and the endogenous pigments lipofuscin, melanin, and haemosiderin.

Pathological calcification is the abnormal deposition of calcium salts, smaller amounts of iron, or magnesium and other minerals. It can occur in either dystrophic or metastatic forms.
Dystrophic calcification happens in dead or degenerating tissues occurring at normal calcium levels. It can result in organ dysfunction, such as in the heart valves, and heterotopic bone formation.
Metastatic calcification involves an excess of calcium in the blood (hypercalcemia) causing calcium deposition in normal tissues. Common sites for deposition include the kidneys, lungs, and blood vessels and the synovium of joints. Common causes of this form of calcification include hyperparathyroidism, bony destructive lesions, and hypervitaminosis D and prolonged immobilisation.

Cellular aging is a progressive decline in the lifespan and functional activity of cells due to accumulation of DNA mutations, decreased replication, abnormal protein homeostasis, and persistent inflammation. Cellular adaptations, such as telomere shortening, are involved in aging.
Telomeres are critical protective structures at the ends of chromosomes and are progressively shortened with each cell division, ultimately leading to cellular arrest and aging.