CELLULAR ADAPTATIONS
I. CELLULAR ADAPTIVE CHANGES
II. OTHER RELATED OR CONTRASTING TERMS
III. ACCUMULATIONS
IV.. PIGMENTS
Adaptive Changes, Accumulations and Pigments
I. CELLULAR ADAPTIVE CHANGES
- Hypertrophy: Increased size of cells. Commonly seen in skeletal
and cardiac muscle, as a result of increased work demanded of the muscle.
In heart, it is usually a pathologic finding, indicative of disease, although
small degrees of hypertrophy are seen in trained athletes (marathon runners,
for example). Recognizable by the increased size of the cells, large squared-off
nuclei, and more variability in the diameter of the cells than usual.
- The term hypertrophy is also used to refer to the gross enlargement
of the uterus during pregnancy, or the prostate in elderly men (although
the term benign prostatic hypertrophy (BPH) is thought to represent mainly
hyperplasia).
Examples: Cardiac hypertrophy, unilateral hypertrophy of the body.
- Hyperplasia: Increased number of cells. This condition causes enlargement
of the organ or tissue, but the cells have the same appearance and size
as their normal counterparts. Often, the cause for hyperplasia is hormonal
stimulation.
Examples: Secretory endometrium during the menstrual cycle, hyperplasia
of the parathyroid glands, thyroid hyperplasia in Grave's disease, nodular
prostatic hyperplasia, nodular hyperplasia of the adrenals, bone marrow
hyperplasia due to anemia or increased erythropoietin, and lymphoid hyperplasia
in lymphadenopathy and tonsillitis.
The opposite of hyperplasia is involution, which results in fewer cells.
Example: thymic involution.
- Atrophy: Decreased size of cells. Can be due to decreased hormonal
trophic stimulation, decreased neural stimulation, or disuse, commonly
seen in endocrine organs, or in muscle due to either denervation or disuse.
Examples: Adrenal atrophy in Cushing's disease; breast, ovarian and
uterine atrophy following menopause; testicular atrophy (usually due to
disease or trauma, but also seen in panhypopituitarism); skeletal muscle
atrophy in disuse or denervation; cerebral atrophy in Alzheimer's disease;
thyroid atrophy.
- Metaplasia: Transformation of one type of cell into another. The
most common type is squamous metaplasia of a glandular epithelium, as in
the cervix or tracheal-bronchial tree. However, there are other types.
The cause is loosely thought to be stress or wear and tear on the tissue
involved, but that does not always explain its occurrence.
Examples:
- Glandular to squamous: squamous metaplasia of the cervix (important
in the genesis of squamous dysplasia and squamous carcinoma of the cervix);
squamous metaplasia of the bronchus (from which arise bronchogenic squamous
cell carcinomas).
- Squamous to glandular: Barrett's esophagus, in which glandular stomach
mucosa replaces the lining of the lower esophagus. Important as a site
for adenocarcinoma of the GE junction.
- Alveolar to glandular: bronchiolar (columnar) metaplasia of alveoli
(adenosis of the lung).
- Transitional to squamous: squamous metaplasia of the bladder.
Other Examples: Intestinal metaplasia of the stomach; osseous metaplasia
of calcified bronchial or tracheal cartilage, or of artery wall; myeloid
(marrow) metaplasia of the spleen or liver.
Back to Top
II. OTHER RELATED OR CONTRASTING TERMS
- Hypoplasia: Decreased growth of tissue.
- Aplasia: Absent growth of tissue.
- Atresia: Absent lumen (used with valves and arteries in congenital
heart disease, or in atresia of the bowel).
- Hyalin: any glassy, homogeneous, eosinophilic intra- or extracellular
substance deposited in the tissues, often associated with atrophy or fibrosis.
Not a particular or specific substance.
Examples: amyloid, Russell Bodies in plasma cells, Mallory's alcoholic
hyalin, diabetic hyalinosis of arterioles.
- Amyloid: A pathologic proteinaceous substance, deposited between
cells in a variety of tissues, in several different clinical settings.
Amyloid is a hyaline substance that progressively accumulates, encroaching
on cells and produces cellular atrophy. It accumulates in blood vessels,
causing them to become narrow, producing ischemia, or to become stiff so
that they cannot constrict when cut. As a result, biopsy of patients with
amyloid may cause hemorrhage.
- With Congo Red stain, amyloid stains salmon pink, and under polarized
light, exhibits green birefringence and dichroism.
- Physically: Non-branching fibers, 7.5 to 10 nm in width, variable
lengths, in a beta-pleated sheet conformation.
- Amyloid is chemically at least 15 different molecules. The most
common are:
- AL (amyloid light chain) produced by plasma cells, containing immunoglobulin
light chains;
- AA (amyloid-associated), a non-immunoglobulin synthesized by the
liver.
- Transthyretin (previously pre-albumin), a transport protein. An
abnormal form is deposited in the familial amyloid polyneuropathies; another
form is deposited in the heart and blood vessels of aged individuals;
- Beta2-amyloid protein, in cerebral plaques and blood vessels in
Alzheimer's disease;
- Classifications: Primary vs. Secondary.
- Primary: in plasma cell dyscrasias (monoclonal gammopathy, multiple
myeloma); light chain type (AL) called Bence-Jones protein, found in serum
and urine, and in tissues.
- Secondary: systemic deposits of AA protein, secondary to associated
inflammatory conditions (rheumatoid arthritis, ankylosing spondylitis,
inflammatory bowel disease, TB, broniectasis, chronic osteomyelitis).
- Endocrine amyloid: associated with medullary carcinoma of the thyroid,
islet cell tumor of pancreas, pheochromocytoma, pancreatic islets in Type
II diabetes. This type of amyloid is apparently formed from abnormal polypeptide
hormones (procalcitonin, e.g.).
- Other types: heredo-familial, hemodialysis associated, localized,
and amyloid of aging.
- Morphology: Grossly, if present in large amounts, makes organs larger,
stiffer and waxier. Microscopically, produces hyaline substance that stains
with Congo Red and is birefringent and dichroic under polarized light.
- Clinical: In kidney, causes proteinuria and renal failure. In heart,
causes restrictive cardiomyopathy and heart failure, and can mimic myocardial
infarction. In GI tract, causes stiffening and bleeding. In tongue, macroglossia.
Back to Top
IV. PIGMENTS
A variety of pigments are seen, both intra- and extracellularly. Most
are brown, yellow-brown, or black. Unpigmented tissue is normally clear
or white.
- Melanin- normal pigment of melanocytes, also seen in keratinocytes
in the skin, and in benign and malignant tumors of melanocytes.
- Bilirubin- Normal pigment produced in hepatocytes; seen only when
increased in concentration in liver; green-yellow; seen in cholestasis;
can be produced by tumors of liver.
- Iron- iron- containing pigments are produced by blood breakdown
or by increased uptake or decreased excretion. Commonly seen in areas of
old hemorrhage, also in chronically congested organs, hemochromatosis,
and various marrow abnormalities. Usually golden yellow-brown and chunky.
Can be stained blue with Perls iron stain.
- Lipochrome- aka lipofuscin- a wear and tear pigment produced by
the golgi apparatus, packaged in lysosomes, that accumulates in cells,
commonly in liver and heart. Usually not clinically significant.
- Anthracotic pigment- opaque black pigment of lung and mediastinal
lymph nodes. Clinically, usually innocuous.
Go Back to Cellular
Adaptations
Go Back to Course
Outline
Questions?
Comments? Send a message to the CATS guru: jkessler@salus.uvm.edu