Cell adaptation

PRE BY: ZAHID REHMAN(BSST,CHPE,MSPH,MSST)

IPMS(KMU)
Lecture objective

 At the end of this lecture the students will be able to

know

 Cellular adaptation
 Types of cellular adaptation with example
Cell
Cell has three components.
Cell membrane , nucleus and cytoplasm.
In cytoplasm there are some organelles which have some various
function these are
Mitochondria
Power house of the cell, extract energy from nutrients in the form of
ATP.
Ribosomes
Synthesize protein in the cell
Lysosome
Intracellular digestion .and removed unwanted subst.
Endoplasmic reticulum
Detoxifies the damaging subs to the cell.
Nucleus.
Control center of the cell and composed of DNA.
Cell adaptation

 Adaptations are reversible changes in the

number, size, metabolic activity, or functions
of cells in response to changes in their
environment. cell are active participants in
their environments, constantly adjusting their
structer and function to accommodate
changing demands and extracellular stresses.
 cell are normally in homeostasis state.
cell encounter physiological stress or
pathologic stimuli, they can undergo
adaptation, achieving new steady state
and preserving viability and function.
The changes made by a cell in response to adverse
environmental changes. The adaptation may be
physiological (normal) or pathological (abnormal). Some
major types of adaptation are
Atrophy
Hypertrophy
Hyperplasia
Metaplasia
dysplasia
 Atrophy
Atrophy is a decrease in cell size or shrinkage in
the size of the cell by the loss of cell substances
is known as atrophy. atrophic cells may have
diminished function, but they are not dead.
Causes of atrophy
 Decreased workload(e.g immobilization of a limb
to permit healing of a fracture)
 Loss of innervations
 Diminished blood supply
 Decrease work load(e.g immobilization ,
limb fracture)
 Inadequate nutrition
 loss of endocrine stimulation
 Aging(loss of teeth, hair, thinning of skin
that creates wrinkles, weakening of
muscles, loss of weight in organs and
sluggish mental activity)
Atrophy
Some stimulus are physiologic (e.g. loss of hormone
stimulation in menopause due to decrease level of
estrogen hormones and then shut down the
reproductive system)
Atrophy of the breasts can occur with
prolonged estrogen reduction, as
with menopause. Testicular atrophy with prolonged
use of enough exogenous sex steroid
(either androgen or estrogen) to
reduce gonadotropin secretion.
Pathological atrophy example

 Starvation atrophy
 Ischemic atrophy
 Disuse atrophy
 Denervation
 Neuropathic atrophy
Pathological atrophy
Mechanism of atrophy
Atrophy mechanism consist of a combination of
decrease protein synthesis and increased protein
degradation in cell.
Protein synthesis decrease b/c of reduced metabolic
activity.
In many situations , atrophy is also accompanied by
increase autophagy,.
Autophagy (self eating) is the process in which the
starved cell eats its own components in an attempt to
survive.
Hypertrophy(excessive
nourishment)
Hypertrophy is an increase in cell size or organ or tissue
due to increase in the size of the cell.
In hypertrophy there is no new cell , just bigger cells
containing increased amounts of structural proteins
and organelles.
 Hypertrophy can be physiologic or pathologic and is
caused either by increased functional demand or by
growth factor or hormonal stimulation.
 An example of physiologic hypertrophy is
in skeletal muscle with sustained weight
bearing exercise.
 Massive physiological enlargement of the
uterus during pregnancy occur as a
consequence of estrogen stimulated smooth
muscles hypertrophy and smooth muscle
hyperplasia.
 An example of pathologic hypertrophy is in
cardiac muscle as a result of hypertension or
aortic valve disease.
 increased workload the striated muscle cells
in both the skeletal muscle and the heart
undergo only hypertrophy because adult
muscle cells have a limited capacity to divide.
 Myocardium subjected to a persistently
increased workload, as in hypertension
or with a narrowed (stenotic) valve,
 the myocardium is subjected to reduced
blood flow (ischemia) due to an occluded
coronary artery, the muscle cells may
undergo injury.
Mechanism

 Increased production of cellular protein.

 The stimuli turn on signal transduction pathways that
lead to the induction of a number of genes, which in
turn stimulate synthesis of many cellular proteins,
including growth factors and structural proteins.
 The result is the synthesis of more proteins and
myofilaments per cell, which increases the force
generated with each contraction, enabling the cell to
meet increased work demands.
Hyperplasia(over formation)

 Hyperplasia is an increase in the number

of cells which result increase the size of
an organ. It is the result of increased
cell mitosis, or division .
 Hyperplasia can be physiological or
pathological.
 in both situations, cellular proliferation is
stimulated by growth factors that are
produced by a variety of cell types.
Physiological hyperplasia are
Hormonal hyperplasia , the proliferation of the glandular
epithelium of the female breast at puberty and during
pregnancy.
Compensatory hyperplasia, in which residual tissue
grows after removal or loss of part of an organ. (e.g.
when part of a liver is respected , mitotic activity in
the remaining cells begins as early as 12 hrs later ,
eventually restoring the liver to its normal weight).
 The stimuli for hyperplasia in this setting are
polypeptide growth factors produced by uninjured
hepatocytes as well as nonparenchymal cells in the
liver
 Most forms of pathologic hyperplasia are caused by
excessive hormonal or growth factor stimulation.
 For example, after a normal menstrual period there is
a burst of uterine epithelial proliferation that is
normally tightly regulated by the stimulatory effects
of pituitary hormones and ovarian estrogen and the
inhibitory effects of progesterone. A disturbance in
this balance leading to increased estrogenic
stimulation causes endometrial hyperplasia, which is
a common cause of abnormal menstrual bleeding.
 Benign prostatic hyperplasia is another common
example of pathologic hyperplasia induced in
responses to hormonal stimulation by androgens.
Stimulation by growth factors also is involved in the
hyperplasia that is associated with certain viral
infections; for
 example, papillomaviruses cause skin warts and
mucosal lesions that are composed of masses of
hyperplastic epithelium.
Intiman hyperplasia The thickening of the Tunica
intimae of a blood vessel as a complication of a
reconstruction procedure . Intiman hyperplasia is the
universal response of a vessel to injury and is an
important reason of late bypass graft failure,
particularly in vein and synthetic vascular grafts.
 Hyperplasia is also important role in connective
tissue cell in wound healing, in which
proliferating fibroblast and blood vessel aid in
repair. Or uterine enlargement during
pregnancy.
 The hyperplastic process remains
controlled; if the signals that
initiate it reduce, the hyperplasia
disappears. It is this responsiveness to
normal regulatory control mechanisms
that distinguishes pathologic
hyperplasias from cancer, in which the
growth control mechanisms become
permanently dysregulated or ineffective
Metaplasia (Greek: "change in
form")
Is the reversible replacement of
one differentiated cell type with another
mature differentiated cell type. In simplistic
terms, it is as if the original cells are not
robust enough to withstand the new
environment, and so they change into another
type more suited to the new environment. If
the stimulus that caused metaplasia is
removed or ceases, tissues return to their
normal pattern of differentiation.
prominent example of metaplasia involves the changes
associated with the respiratory tract in response to
inhalation of irritants, such as smog or smoke.
The bronchial cells convert from mucus-secreting,
ciliated, columnar epithelium to non-
ciliated, squamus epithelium incapable of secreting
mucus. These transformed cells may become
dysplastic or cancerous if the stimulus (e.g., cigarette
smoking) is not removed.
 The most common example of metaplasia is
Barrett's esophagus, when the non-keratinizing
squamuss epithelium of the esophagus undergoes
metaplasia to become mutinous columnar cells,
ultimately protecting the esophagus from acid reflux
originating in the stomach. If stress persists,
metaplasia can progress to dysplasia and eventually
carcinoma; Barrett's esophagus, for example, can
eventually progress to adenocarcinoma of the
esophagus if not treated.
Dysplasia

 Dysplasia also involves cell transformation.

 Metaplasia is brought on by external
environmental stressors, whereas dysplasia
involves abnormal cell development caused by
internal issues. Dysplasia occurs during a
breakdown of existing cell tissue that loses its
uniformity and structure.
 Transforms a cell into an abnormal version of
itself; caused by internal stimulus; is not
reversible; more likely to lead to cancer
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