Laboratory: CELLULAR ADAPTATION AND ACCUMULATION

CELLULAR ADAPTATION
• Adaptation are reversible changes in the size, HYPERTROPHY OF UTERUS: GROSS
number, phenotype, metabolic activity, or functions
of cell in response to changes in their environment. Physiologic
hypertrophy of
• It is a state that lies intermediate between the the uterus during
normal, unstressed cell and the injured, pregnancy (left)
overstressed cell.

• Cells constantly adapt, even under normal Gross

conditions, to changes in their environment. appearance of
normal uterus
PHYSIOLOGIC PATHOLOGIC (right)
Usually represent May share the same
responses of cells to underlying mechanisms,
normal stimulation by but they provide the cells
hormones or endogenous with the ability to survive
chemical substances. in their environment and
perhaps escape injury.

Cells can adapt themselves by undergoing the following

different conditions:
MYOMETRIAL HYPERTROPHY. UTERUS:
1. Hypertrophy MICROSCOPIC
2. Hyperplasia
3. Atrophy
4. Metaplasia

HYPERTROPHY
An increase in the size of cells that results in an
increase in the size of the affected organ

TYPES
PHYSIOLOGIC PATHOLOGIC
Physiologic growth of the Increase workload,
uterus during pregnancy hormonal stimulation and
involves both hypertrophy growth factors stimulation
and hyperplasia HYPERPLASIA
Ex: Hypertrophy of the
heart of which the most • Increase in number of cells in organ or tissue in
common stimulus is response to a stimulus.
chronic hemodynamic load • Takes place only if the tissue is capable of dividing.

PHYSIOLOGIC PATHOLOGIC
• Due to action of Caused by excessive or
hormones or growth inappropriate actions of
factors hormones of growth
factors on target cells
• Occurs in several
circumstance:

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Laboratory: CELLULAR ADAPTATION AND ACCUMULATION
1. When there is a Ex: Benign prostatic
need to increase hyperplasia (BPH) in
functional capacity response to hormonal
of hormone- stimulation of androgens ATROPHY
sensitive organ • A reduction in the size of an organ or tissue due to a
2. When there is a decrease in cell size and number.
need for
compensatory PHYSIOLOGIC PATHOLOGIC
increase after Normal process of aging in Has several causes which
damage or some tissues which could could be local or generalized
resection be due to loss of endocrine
Ex: hyperplasia of stimulation or Common causes:
female breast arteriosclerosis
epithelium at puberty
• Decreased workload
or pregnancy Ex: decrease in the size of (atrophy of disuse)
the uterus occurring shortly • Loss of innervation
after parturition (denervation atrophy)
BENIGN PROSTATIC HYPERPLASIA: GROSS • Diminished blood supply
Cross section shows • Inadequate nutrtion
well defined • Loss of endocrine
nodules of benign stimulation
prostatic tissues • Pressure
compressing the
urethra into slit-like
lumen
CEREBRAL ATROPHY: GROSS

BENIGN PROSTATIC HYPEPRPLASIA: MICROSCOPIC

METAPLASIA
• A reversible change in which one differentiated cell
type (epithelial or mesenchymal) is replaced by
another cell type

• Represent an adaptive response in which one cell

type that is sensitive to a particular stress is
replaced by another cell type that is better able to
withstand the adverse environment.
Causes:
o Changes in environment
o Irritation metaplasia (cervix)
o Nutritional

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Laboratory: CELLULAR ADAPTATION AND ACCUMULATION

Types:
1. Epithelial metaplasia
o Squamous metaplasia (cervix) CELLULAR ACCUMULATION
o Columnar metaplasia (Barrett’s esophagus) • A manifestation of metabolic derangements in the
2. Mesenchymal metaplasia (Osseous/cartilaginous cells with accumulation amounts of various
metaplasia) substances (harmless or associated with varying
degrees of injury)
o Intracytoplasmic
BARRETT’S ESOPHAGUS: GROSS o Within organelles (lysozomes)
o Intranuclear

4 main pathways of abnormal cellular accumulations

1. Inadequate removal substances due to mechanical
defects in packaging and transport
Ex: fatty change-liver
2. Abnormal accumulation of endogenous substance
due to genetic or acquired defects in its folding,
packaging, transport, or secretion
3. Abnormal accumulation/deposition of exogenous
substances where cell has defective enzymatic
machinery to degrade substance nor ability to
transport to other sites.
4. Failure to degrade a metabolite due to inherited
enzyme deficiencies (storage diseases)

CHOLESTEROL AND CHOLESTEROL ESTERS

A. Normal gastroesophageal junction
B. Barrett’s esophagus grossly showing small
islands of residual pale squamous mucosa
interfacing with light brown columnar (gastric)
mucosa distally
• Cellular metabolism of cholesterol is tightly
regulated such that most cells cholesterol for the
synthesis of cells membranes without intracellular
accumulation of cholesterol or cholesterol ester.
• CHOLESTEROLOSIS refers to the focal
accumulations of cholesterol-laden macrophages in
the lamina propria of the gall bladder

CHOLESTEROLOSIS: GALL BLADDER

BARRETT’S ESOPHAGUS: MICROSCOPIC

GROSS
An opened gall bladder showing mucosal wall with
adherent yellowish particles (cholesterolosis)

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Laboratory: CELLULAR ADAPTATION AND ACCUMULATION

MICROSCOPIC

MICROSCOPIC

MALIGNANT MELANOMA, SKIN

• Most deadly of all skin cancers and is strongly linked
to acquired mutations caused by exposure to UV REFERENCES:
radiation in sunlight. CELLUALR ADAPTATION AND ACCUMULATION PPT

• Great preponderance of melanoma arises in the

skin.
o Other sites include oral and anogenital mucosal
surfaces, esophagus, meninges, and uvea of the
eye.

MALIGNANT MELANOMA

GROSS
• Grossly show variation in color appearing in
shades of black, red, dark-blue and gray.

• Borders show irregular contour and are often

notched