Cell adaptation complete discussion

1. Cell adaptation

2. Cell

3. Components of cell
cell has three components.
Cell membrane , nucleolus 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.

4. Endoplasmic reticulum
Detoxifies the damaging subs to the cell.
Nucleus.
Control center of the cell and composed of DNA.

5. Cell adaptation
Cell are active participants in their environments, constantly adjusting their
structure 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

6. 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.
Causes of atrophy
 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
Aging(loss of teeth, hair, thinning of skin that creates wrinkles,
weakening of muscles, loss of weight in organs and sluggish mental
activity)

7. 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) and other pathologic(e.g. denervation)
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.

8. 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.

9. 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.
The heart and kidneys have increased susceptibility to hypertrophy. 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.

11. 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.
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
resected , mitotic activity in the remaining cells begins as early as
12 hrs later , eventually restoring the liver to its normal weight).

12. Benign prostatic hyperplasia, also known as prostate
enlargement.
 Hemi hyperplasia when only half (or one side) of the body is
affected, sometimes generating limbs of different lengths.
Intimal hyperplasia The thickening of the Tunica intima of a
blood vessel as a complication of a reconstruction procedure
. Intimal 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.

13.  Sebaceous hyperplasia
In this condition, small yellowish growths develop on the skin,
usually on the face. This condition is neither contagious nor
dangerous.
For example, the estrogen-dependent uterine cells undergo
hyperplasia and hypertrophy following pregnancy. Pathologic
hyperplasia is an abnormal increase in cell division. A
common pathologic hyperplasia in women occurs in
the endometrium and is called endometriosis. Or uterine
enlargement during pregnancy.

15. 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 healthy enough to with stand 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.

16. 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, squamous 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 squamous epithelium of the esophagus
undergoes metaplasia to become mucinous 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.

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