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Section 1: Cellular Adaptations

This document discusses various types of cellular adaptations. It describes hyperplasia as an increase in cell number that can be physiological, compensatory, due to excessive stimulation, a failure of regulation, or neoplastic. Hypertrophy is defined as an increase in cell size, leading to organ enlargement. It can be physiological or pathological due to increased workload or hormonal/growth factor stimulation. Atrophy is the acquired loss of cell size or number, and can be physiological, due to reduced blood supply, nerve stimulus, endocrine stimulation, nutrition, or pressure. Metaplasia is a reversible change where one adult cell type replaces another, often due to environmental changes, irritation/inflammation, or nutrition.

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Virli Ana
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26 views

Section 1: Cellular Adaptations

This document discusses various types of cellular adaptations. It describes hyperplasia as an increase in cell number that can be physiological, compensatory, due to excessive stimulation, a failure of regulation, or neoplastic. Hypertrophy is defined as an increase in cell size, leading to organ enlargement. It can be physiological or pathological due to increased workload or hormonal/growth factor stimulation. Atrophy is the acquired loss of cell size or number, and can be physiological, due to reduced blood supply, nerve stimulus, endocrine stimulation, nutrition, or pressure. Metaplasia is a reversible change where one adult cell type replaces another, often due to environmental changes, irritation/inflammation, or nutrition.

Uploaded by

Virli Ana
Copyright
© © All Rights Reserved
Available Formats
Download as PPT, PDF, TXT or read online on Scribd
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Section 1

Cellular
Adaptations

Cells must constantly adapt, even


under normal conditions, to changes
in their environment.
These physiological adaptations
usually represent responses of cells
to normal stimulation by hormones or
endogenous chemical substances. For
example, as in the enlargement of
the breast and induction of lactation
by pregnancy.

Pathologic adaptations may share


the same underlying mechanisms,
but they provide the cells with the
ability to survive in their environment
and perhaps escape injury.
Then cellular adaptation is a state that
lies
intermediate
between
the
normal, unstressed cell and the
injured, overstressed cell.

There are numerous types of cellular


adaptations:
some involve up or down regulation of
specific cellular receptors involved in
metabolism of certain components.
Others are associated with the induction of
new protein synthesis by the target cell.
Other adaptations involve a switch by cells
from producing one type of a family of
proteins to another or markedly
overproducing one protein.

These adaptations then involve all


steps of cellular metabolism of
proteinsreceptor binding, signal
transduction, transcription, translation, or
regulation of protein packaging and
release.

In this section we consider some


common adaptive changes in cell
growth, size, and differentiation that
underlie many pathologic processes.

1. Hyperplasia
(1) Definition: An increase in the number
of cells in an organ or tissue, which may
then have increased volume.
(2) Types:

Physiologic: Response to need, e. g.


hyperplasia of the female breast
epithelium at puberty or in pregnancy.

Left Normal breast

Right Hyperplasia

From ROBBINS BASIC PATHOLOGY 2003

Compensatory: Response to deficiency, e.


g. Hyperplasia following surgical removal
of part of liver or of one kidney;
hyperplasia of the bone marrow in
anemia.

Excessive stimulation: Pathologic: as in


ovarian tumor producing estrogen and
stimulating endometrial hyperplasia;
pancreatic islet hyperplasia in infants of a
diabetic mother (stimulated by high
glucose level).

Failure of regulation: Pathologic, as in


hyperthyroidism
or
as
in
hyperparathyroidism resulting from renal
failure or vitamin D deficiency.

Neoplastic: Total loss of normal control


mechanism.
hyperplasia.

Should

not

be

termed

Hyperplasia is also an important


response of connective tissue cells in
wound healing, in which proliferating
fibroblasts and blood vessels aid in repair.

(3) Mechanisms:
Most forms of pathologic
hyperplasia are instances of
excessive hormonal stimulation or
are the effects of growth factors on
target cells.

2. Hypertrophy:
(1) Definition: An increase in the
size of cells, and with such change,
an increase in the size of the
organ.

Left Normal heart


center Hypertrophied heart
Right Hypertrophied and dilated heart

Hypertrophied heart
From ROBBINS BASIC PATHOLOGY 2003

Normal uterus

gravid uterus

Physiologic hypertrophy of the uterus during


pregnancy.A, gross appearance of a normal uterus
(right) and a gravid uterus (left) that was removed
for postpartum bleeding,
From ROBBINS BASIC PATHOLOGY 2003

(2) Types:
Physiologic:

i. e. the physiologic
growth of the uterus during
pregnancy involves both
hypertrophy and hyperplasia. The
cellular hypertrophy is stimulated
by estrogenic hormones through
smooth muscle estrogen receptors.

Pathologic:

causes:

increased workload, hormonal stimulation


and growth factors stimulation.
i.e. hypertrophy of heart the most common
stimulus is chronic hemodynamic overload,
due either to hypertension or to faulty
valves. It eventually reaches a limit beyond
which enlargement of muscle mass is no
longer able to compensate for the
increased burden, and cardiac failure
ensues.

The relationship between


hyperplasia and
hypertrophy:
Although hypertrophy and
hyperplasia are two distinct
processes, frequently both occur
together, and they well be
triggered by the same mechanism.

3. Atrophy
(1) Definition: Acquired loss of size
due to reduction of cell size or
number of parenchyma cells in an
organ.
(2) Types:
Physiologic:

i. e. Aging; shrinking
mammary gland after lactation; the
uterus after delivery or in old age.

Diminished blood supply:

Loss of nerve stimulus:

Loss of endocrine stimulation:

Inadequate nutrition:

pressure:

The fundamental cellular change


is identical in all, representing a
retreat by the cell to a smaller
size at which survival is still
possible.
Although atrophic cells may have
diminished function, they are not
dead.

Atrophy represents a reduction


in the structural components of
the cell. The cell contains
fewer mitochondria,
myofilaments, a lesser amount
of endoplasmic reticulum, and
increasing in the number of
autophagy vacuoles.

Some of the cell debris within the


autophage vacuole may resist
digestion and persist as membrane
bound residual bodies that may
remain as a sarcophagus in the
cytoplasm. When present in sufficient
amounts, they impart a brown
discoloration to the tissue (brown
atrophy).

Left Normal

Right Atrophy

Atrophy of the brain


(offered by Prof.
Orr )

4. Metaplasia
(1) Definition: Metaplasia is a reversible
change in which one adult cell type is
replaced by another adult cell type.
(2) Causes:

Changes in environment: i. e. stones


in excretory ducts of salivary gland,
pancreas, or bile duct lead to change
from columnar epithelium to stratified
squamous epithelium.

Squamous metaplasia in bronchitis


offered by Prof.Orr

Schematic diagram of columnar to squamous metaplasia


From ROBBINS BASIC PATHOLOGY 2003

Irritation or inflammation: i. e. In
the habitual cigarettes smoker, the
normal columnar ciliated epithelial
cells of the trachea and bronchi are
often replaced focally or widely by
stratified squamous epithelial cells.

Nutritional: vitamin A deficiency


causing squamous metaplasia.

Epithelial metaplasia is a two-edged


sword and, in most circumstances,
represents an undesirable change.
Moreover,
the
influences
that
predispose to such metaplasia, if
persistent, may induce cancer
transformation
in
metaplastic
epithelium. Thus, the common form
of cancer in the respiratory tract is
composed of squamous cells.

Metaplasia may also occur in


mesenchymal cells but less clearly
as an adaptive response. i. e.
fibrous connective tissue cells may
be come transformed to osteoblast
chondroblasts to produce bone or
cartilage where it is normally not
encountered.

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