Pathology : Robbins & Cotran : Adaptations of cellular growth & differentiation

Pathology : Robbins & Cotran : Adaptations of cellular growth & differentiation Hypertrophy| Hyperplasia| Atrophy | Metaplasia Hypertrophy
Hypertrophy is an increase in the size of cells resulting
in an increase in the size of the organ. In contrast, hyper-
plasia (discussed next) is an increase in cell number. Stated
another way, in pure hypertrophy there are no new cells,
just bigger cells containing increased amounts of structural
proteins and organelles. Hyperplasia is an adaptive
response in cells capable of replication, whereas hypertro-
phy occurs when cells have a limited capacity to divide.
Hypertrophy and hyperplasia also can occur together,
and obviously both result in an enlarged organ.
Hypertrophy can be physiologic or pathologic and is
caused either by increased functional demand or by
growth factor or hormonal stimulation. Hyperplasia
Hyperplasia is an increase in the number of cells in an
organ that stems from increased proliferation, either of
differentiated cells or, in some instances, less differenti-
ated progenitor cells. As discussed earlier, hyperplasia
takes place if the tissue contains cell populations capable
of replication; it may occur concurrently with hypertrophy
and often in response to the same stimuli.
Hyperplasia can be physiologic or pathologic; in both
situations, cellular proliferation is stimulated by growth
factors that are produced by a variety of cell types.Metaplasia
Metaplasia is a change in which one adult cell type (epi-
thelial or mesenchymal) is replaced by another adult cell
type. In this type of cellular adaptation, a cell type sensitive
to a particular stress is replaced by another cell type better
able to withstand the adverse environment. Metaplasia
is thought to arise by the reprogramming of stem cells.Atrophy
Atrophy is shrinkage in the size of cells by the loss of
cell substance. When a sufficient number of cells are involved, the entire tissue or organ is reduced in size, or
atrophic Although atrophic cells may have
diminished function, they are not dead.
Causes of atrophy include a decreased workload (e.g.,
immobilization of a limb to permit healing of a fracture),
loss of innervation, diminished blood supply, inadequate
nutrition, loss of endocrine stimulation, and aging (senile
atrophy). Although some of these stimuli are physiologic
(e.g., the loss of hormone stimulation in menopause) and
others are pathologic (e.g., denervation), the fundamental
cellular changes are similar. They represent a retreat by the
cell to a smaller size at which survival is still possible; a
new equilibrium is achieved between cell size and dimin-
ished blood supply, nutrition, or trophic stimulation.
Cellular atrophy results from a combination of
decreased protein synthesis and increased protein
degradation.
• Protein synthesis decreases because of reduced meta-
bolic activity.
• The degradation of cellular proteins occurs mainly by
the ubiquitin-proteasome pathway. Nutrient deficiency
and disuse may activate ubiquitin ligases, which attach
multiple copies of the small peptide ubiquitin to cellular
proteins and target them for degradation in protea-
somes. This pathway is also thought to be responsible
for the accelerated proteolysis seen in a variety of cata-
bolic conditions, including the cachexia associated with
cancer.
• In many situations, atrophy also is associated with
autophagy, with resulting increases in the number of
autophagic vacuoles. As discussed previously, autoph-
agy is the process in which the starved cell eats its own
organelles in an attempt to survive.