When tissues are damaged, cell injury will occur. This
injury can be reversible up to a point but if the harmful stimulus is too
severe, the cell will die. Sometimes, the cell doesn’t die, but adapts to the
stimulus in order to survive. In order to do this, the tissue uses Adaptive
Tissue Responses, such as atrophy, hyperplasia, hypertrophy and metaplasia
(we’ll be covering these in this post).
Adaptive changes are reversible changes (however, some
pathological conditions can prevent this from happening) in mature cells and
tissues after growth has occurred. The ability of a tissue to adapt is
dependent on several factors including: vulnerability to certain agents, state
of differentiation, blood supply, nutrition, and previous state of the cell (i.e.
is it trying to adapt to another harmful stimulus?).
Atrophy is defined as a reduction in the size or amount of
an organ, tissue or cell. This is due to a decrease in the size and/or number
of its specialised cells or organelles. Atrophy may be physiological (for
example: when the thymus decreases in size with age) or pathological (e.g.
Disuse atrophy).
Several causes of atrophy exist, these include:
o
Decreased blood supply
o
Loss of innervation: normal function of skeletal
muscle depends on intact innervation. Damage to a nerve leads to rapid muscle
atrophy of those muscle fibres supplied by the nerve.
o
Decreased workload: e.g. skeletal muscle atrophy
occurs soon after a broken limb is immobilised in a cast.
o
Prolonged pressure: chronic tissue compression
will result in atrophy of the surrounding tissues that have been compressed.
This is likely due to the ischaemic change caused by the compressed blood
vessels and lower blood supply to the area. E.g. A tumour that slowly enlarges
will cause atrophy of the surrounding compressed tissues.
o
Loss of hormonal/endocrine stimulation: many
endocrine glands depend on hormonal stimulation for normal metabolism and
function. Interruption of these signals results in atrophy. This is seen in the
testes of males who take anabolic steroids.
o
Physiological: This is a common occurrence in
early development as well as later in life.
o
Lack of nutrition: Significant protein and
energy malnutrition will result in catabolism of the skeletal muscle after
other stores of energy in the body have been exhausted. This results in muscle
wasting.
o
Senile atrophy: The aging process is associated
with tissue and organ atrophy due to the loss of cells. This is mainly seen in
cells made up of predominantly permanent cell populations.
A loss of cells in atrophy is due to an increase in
apoptosis while a decrease in the size of cells is due to an increase in
catabolic processes relative to anabolic processes.
Hypertrophy is the opposite of atrophy and results in an
increase in the size of an organ or tissue due to an increase in size of its
specialised cells. Hypertrophy doesn’t result in more cells, just larger ones.
The increase in size is due to an increase in the number of organelles within
the cells. It is often seen in cells that have an increased workload but aren’t
able to divide.
Hypertrophy may be physiological or pathological and is
either compensatory or hormonal. An example of compensatory hypertrophy is seen
when a kidney is removed from an animal or when there is increased workload in
cardiac or skeletal muscle. This type of atrophy tries to achieve homeostasis.
An example of hormonal atrophy is during pregnancy which causes hypertrophy of
the uterus.
Hypertrophy can be triggered by mechanical or trophic
stimuli, such as growth factors, hormones and cytokines. The mechanism of
hypertrophy involves signal transduction pathways which lead to the induction
of many genes which in turn stimulate the synthesis of many cellular proteins which
results in an increase in organelles and size.
Hyperplasia is the increase in the size of an organ due to
an increase in the number of its specialised cells. It too, may be due to
physiological or pathological causes and it can only occur in stable or labile
cell types. Physiological and pathological hyperplasia can be further
categorised as follows:
o
Compensatory: E.g. haematopoietic system after
blood loss, lymph nodes after infection.
o
Reparatory: to restore tissue architecture or function
o
Hormonal: e.g. normal cyclical changes in the
mammary gland or endometrium.
This condition is usually caused by increased local production
of growth factors, increased levels of growth factor receptors on the
responding cells, or activation of specific intracellular signalling pathways.
These changes result in the production of transcription factors which switch on
various genes which ultimately results in cellular proliferation.
Metaplasia results in a change from one type of specialised,
fully differentiated adult cell to another type of stem cell (that is usually
less specialised). This is a protective mechanism as the cell is replaced with
another type of cell that is more suitable to withstand the stressor. In this
process, some functions are lost. It involves the reprogramming of stem cells
by cytokines, growth factors and extracellular matrix components. The cells
themselves don’t magically change into different cells. Instead, the stem cells
are told to differentiate into a type of cell that they normally wouldn’t. An
example of metaplasia is connective tissue metaplasia. This is when cartilage,
bone or adipose tissue form in organs that do not normally contain these cells.
That’s all for this post, see you next time :)
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