Chapter
10
GROWTH
DISTURBANCES
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10.1
OVERVIEW
Growth disturbances include a broad category of
lesions that in general refer to deficient growth, abnormal patterns
of growth, and non-neoplastic excess growth. These conditions may
result from disturbances during embryonic development, prenatal
growth, or postnatal life.
Aplasia, agenesis, atresia, atrophy, dysplasia,
hyperplasia, hypoplasia, and metaplasia are growth disturbance
discussed in this section and neoplasia will be discussed in section
11.
Congenital anomalies are extremely numerous and
varied and this section of your syllabus only mentions a few
important examples.
10.2 TERMINAL
OBJECTIVES
Upon completion of this section, each student
should be able to perform the following tasks:
- 1. Discuss the similarities and differences
between agenesis, aplasia, atresia, dysplasia, and
hypoplasia.
- 2. Distinguish between atrophy,
hyperplasia, hypertrophy, and metaplasia on the basis of changes
observed at the subcellular, cellular, and/or organ
levels.
- 3. Distinguish aplasia, agenesis,
dysplasia, and hypoplasia from adaptive changes.
- 4. Outline the sequence of events for the
development of hypertrophy, hyperplasia, and atrophy following
stress or an injury.
- 5. Describe the circumstances under which
hypertrophy and hyperplasia are expected to occur together and/or
separately in organs and tissues.
- 6. Describe the differences and
similarities between metaplasia, anaplasia, and
dysplasia.
- 7. Discuss the differences and similarities
between hereditary anomalies and congenital anomalies.
- 8. List and describe the more common
general types of anomalies expected in animals.
- 9. Provide appropriate answers for the
post-instructional self examination questions located at the end
of this section.
10.3
KEYWORDS
Students should be able to define, describe,
spell correctly, and use the following terms as they relate to growth
disturbances.
- -- Atrophy -- Keloid
- -- Hypertrophy -- "Proud
Flesh"
- -- Hyperplasia -- Cystic
Hyperplasia
- -- Metaplasia -- Squamous
Metaplasia
- -- Hypoplasia -- Pressure
Atrophy
- -- Agenesis --
Involution
- -- Aplasia -- Disuse
Atrophy
- -- Dysplasia -- Denervation
Atrophy
- -- Adaptive Changes -- Iatrogenic
Lesions
- -- Anomalies -- Growth
Disturbances
- -- Malformations --
Neoplasia
- -- Congenital Anomalies -- Hereditary
Anomalies
- -- Serous Atrophy of Fat --
Mucus
- -- Mucin -- Malnutrition
- -- Emaciation --
Parakeratosis
- -- Acanthosis -- Myeloid
Hyperplasia
- -- Lymphoid Hyperplasia -- Nodular
Hyperplasia
- -- Aplastic Anemia --
Teratology
- -- Oncology --
Callus
10.4 ADAPTIVE
CHANGES
Atrophy, hypertrophy, hyperplasia, and
metaplasia are growth disturbances that occur in response to
alterations in the environment. Remember, when stress and/or noxious
influences impinge upon a cell, it will, to a limited extent, adapt
and achieve an "altered steady state", permitting it to
survive within its changed environment. As discussed earlier in the
section on the normal and adapted cell, atrophy, hypertrophy,
hyperplasia, and metaplasia are the most important adaptive changes
that occur in cells, tissues, and organs.
Atrophy is defined as a decrease in size or
wasting of a body part, organ, or tissue. It involves either a
decrease in the size of the cells or a decrease in the number of
cells or a combination of the two phenomenon. It is an adaptive
change that usually occurs in response to decreased workload, loss of
enervation, decreased blood supply, inadequate nutrition, and/or loss
of endocrine stimulation. It is distinguished from other similar
growth disturbances (hypoplasia, aplasia, and dysplasia) in
that atrophy occurs only in situations where the tissue was present,
typically in normal amounts, and has subsequently been reduced.
Serous atrophy of fat, also known as mucoid atrophy of fat, refers to
a reduction in the amount of fat in "fat depots" in the body.
In situations where inadequate nutrition occurs for several days, the
fat throughout the body is mobilized and utilized for nutrients. In
this situation, the adipose tissue throughout the body becomes
gelatinous in consistency. This lesions is indicative of emaciation
and it is usually most prominent on the heart, around the kidneys and
in the mesentery. The cause of the
emaciation may be something as simple as
malnutrition but it may involve a chronic infection, parasitism,
neoplasia, etc.
Hypertrophy
Refers
to an increase in the size of cells and subsequently, an increase
in size of involved organs. As applied to tissues and organs,
hypertrophy refers to an increase in size without an increase in
the number of cells.
Remember,
"pure" hypertrophy"
(without
hyperplasia) occurs only in
organs whose cells have generally lost the power to reproduce
themselves.
Hyperplasia
Refers
to an increase in the number of
cells in an organ or tissue and subsequently, an increase in size
of the involved organ or tissue. In should be noted that in most
organs, hypertrophy and hyperplasia occur together. Specific types
of hyperplasia include the following.
Acanthosis
Refers
to increased thickness of the
stratum spinosum of the skin.
Hyperkeratosis
Refers
to increased thickness of the cornified layer of the
skin.
Lymphoid hyperplasia
Refers
to an increase in the amount of lymphoid tissue of the body and is
usually a response to chronic infection.
Myeloid hyperplasia - refers to a change
from normal fatty bone marrow in the adult to normal red
marrow.
Nodular hyperplasia
Refers
to an increase in the number of cells in a localized area within
an organ. The lesion is common in the liver, pancreas, spleen,
adrenal cortex, prostate gland, and mammary glands of old
dogs.
Metaplasia
Refers
to a change in which one adult cell
type is replaced by another adult cell type. Only epithelial and
connective tissue have the capacity to undergo hyperplastic
changes.
10.5 AGENESIS AND
APLASIA
The term agenesis refers to a complete lack of
development of an organ or tissue, whereas aplasia is defined as
incomplete or faulty development of an organ or body part. The terms
agenesis and aplasia are often used synonymously, however, aplasia
implies that at least remnants of the organ or tissue exist (some
of the organ/tissue is present but markedly reduced in
size).
Agenesis is usually caused by an inherited
defect but aplasia has been associated with hereditary defects, death
of cells in embryonic development, infection of the dam during
gestation with certain viruses (modified hog cholera virus in
swine), as well as exposure of the dam to certain drugs
(thalidomide in man) and toxins (e.g. Veratrum californicum
in sheep) also during pregnancy.
NOTE:
The term "aplastic"
anemia is used to describe a decrease in the number of erythrocytes
in the vascular system due to a lack of production of these cells by
the bone marrow.
10.6 HYPOPLASIA AND
DYSPLASIA
The term hypoplasia refers to incomplete growth
of an organ or part resulting in a failure of the organ to mature or
reach normal size. Dysplasia refers to abnormal growth or development
of an organ or part. It usually involves variation in the somatotype
and results in disorganized development. A wide range of incomplete
and disorganized growths occur, and one of these terms will apply to
such disturbances ranging between normal development and agenesis or
aplasia. It is often difficult to impossible to distinguish between
hypoplasia and dysplasia grossly and therefore it is not uncommon to
find dysplastic organs being referred to as hypoplastic and vice
versa.
Hypoplasia and dysplasia differ from atrophy
which refers to a reduction in the size of an organ or part after it
has achieved normal growth. The causes of hypoplasia are similar to
or identical to those listed for aplasia. In addition, hypoplasia
after birth may be due to inadequate blood supply, inadequate
enervation, or malnutrition. Hypoplastic lesions are common, and the
best known are hypoplasia of the cerebellum, kidneys, and testes.
Cerebellar hypoplasia, for example is caused by the viruses
responsible for infectious feline enteritis in cats and bovine virus
diarrhea in cattle.
10.7 GROWTH DISTURBANCES
DURING EMBRYONAL OR FETAL LIFE
(Refer
to pages 97-l00 of your textbook)
The term teratology refers to the study of
disturbances of development during embryonal or fetal life. The
following terms are commonly encountered in the study of
teratology.
Anomaly:
Refers
to any deviation from the normal in development of an organ or part
(defects may be hereditary or non-hereditary). The terms malformation
and anomaly are used synonymously.
Hereditary Anomaly:
Refers
to abnormal development that has its
origin in the germ cells (transmitted from parent to
offspring).
Congenital Anomaly:
Refers
to an abnormal development existing at the time of birth. The anomaly
may be hereditary or due to some influence during gestation (up to
the time of birth).
Anomalies may occur during any stage of
development. They are usually expressed in the following
ways:
- Major defects are lethal during embryonic
life.
- Some defects permit survival in utero, but
not postnatally.
- Some defects permit survival postnatally,
but with impairment of normal existence.
- Some defects allow relatively normal
postnatal life.
- Some defects are recognized only at the
time of necropsy (referred
to as incidental findings).
The causes of most congenital anomalies are
basically unknown. The most important known causes are:
- (l) genetic factors,
- (2) prenatal infection with a virus,
- (3) intrauterine effects of poisons
ingested by the mother, and
- (4) vitamin deficiencies.
Numerous congenital anomalies occur in animals,
but most fall within the following general types:
- l. Arrested development in a certain part
of the embryo so that a certain structure is absent, or too small
(agenesis, aplasia, hypoplasia).
- 2. Failure of parts to coalesce or close
(patent foramen ovale, ventricular septal defects,
cranioschisis, etc.).
- 3. Persistence of vestigial structures
(ductus arteriosus, thyro-glossal duct, etc.).
- 4. Supernumerary or accessory parts
(polydactyly or excess digits, accessory lung,
etc.).
- 5. Ectopic or heterotopic parts
(pancreatic tissue in stomach wall, etc.).
- 6. Generalized anomalies of skeletal
development (chondrodys-plasia or dwarfism,
etc.).
10.3 POST-INSTRUCTIONAL
SELF EXAMINATION
Questions
After completing this section each
student should be in a position to provide appropriate
answers for the following questions.
- l. Discuss the circumstances in
which you would expect cells, organs, and/or tissues to
undergo atrophic, hypertrophic, hyperplastic, and
metaplastic changes.
- 2. How would you distinguish an
adapted cell from a normal cell?
-
- 3. What is numerical atrophy?
How would you distinguish numerical atrophy from
quantitative atrophy?
- 4. Describe the gross and
microscopic lesions expected in an atrophic
liver.
- 5. Distinguish starvation from
malnutrition. What organs and/or tissues would you expect
to undergo atrophic changes in a starved dog? What organs
and/or tissues would exhibit little or no atrophic
changes in a starved pig.
- 6. Why would you expect a
"decreased workload" to result in atrophic changes? What
is so-called disuse atrophy?
- 7. Why would you expect atrophy
to occur subsequent to "lack of proper enervation?"
Briefly, outline the sequence of events that leads to
atrophy in so-called "Sweeney" of the
horse.
- 8. Explain the manner in which
disturbed endocrine secretion leads to atrophic
changes.
- 9. Under what circumstances
would you expect so-called physiologic atrophy to occur?
Give appropriate examples.
- l0. Briefly, outline the
sequence of events that leads to serous atrophy of fat
around the heart.
- 11. Grossly, how would you
distinguish atrophic fat from normal fat?
- l2. Briefly, discuss the
circumstances in which you would expect to find "brown
fat cells" rather than "white fat cells" in fat depots of
an animal.
- l3. What is the fundamental
difference between atrophy and
hyperplasia?
- 14. How would you distinguish a
hypertrophic organ from a hyperplastic organ on gross
necropsy examination.
- l5. How would you distinguish a
hypertrophic organ from a hyperplastic organ on
microscopic examination.
- l6. What cellular organelle(s)
is usually enlarged in atrophic cells?
- l7. Under what circumstances
would you expect hypertrophy and hyperplasia to occur
together in an organ?
- l8. Under what circumstances
would you expect hypertrophy to occur in the absence of
hyperplasia?
- l9. Briefly, discuss the causes
and significance of hypertrophy and
hyperplasia.
- 20. What is "myeloid
hyperplasia?"
- 21. What is metaplasia? Under
what circumstances would you expect this condition to
occur?
- 22. In what primary tissue
types would you expect to find metaplastic changes? Give
appropriate examples of metaplastic changes. What is
squamous metaplasia and why would you expect this
alteration to occur?
- 23. MATCHING:
- ____ Hypoplasia A. Reversion
of cell to a more
- ____ Anaplasia primitive
type.
- ____ Metaplasia B. Increased
number of functional
- ____ Myeloid Hyperplasia
cells
- ____ Hyperkeratosis C.
Change from normal fatty
- ____ Acanthosis marrow to
normal red marrow.
- ____ Parakeratosis D.
Increased number of cornified
- ____ Atrophy epithelial
cells.
- ____ Hyperplasia E.
Increased number of cells in
- ____ Hypertrophy a localized
area of an organ.
- F. Increased number of cells
in
- the "prickle-cell" layer
of
- the skin.
- G. Increased size of
individual
- cells.
- H. Decreased size of
individual
- cells.
- I. Increased number of
keratinized epithelial cells.
- J. Change of one variety of
tissue into another.
- K. No correct choice
available.
- 24. What is aplasia? Give
likely causes of this condition. What is aplastic
anemia?
- 25. How would you distinguish a
congenital anomaly from a hereditary
anomaly?
- 26. How would you distinguish
atrophic from aplastic changes.
- 27. What viral agents may be
responsible for hypoplasia of the cerebellum in the
feline and bovine?
- 28 Distinguish hypoplasia from
aplasia on the basis of etiologic
mechanisms.
- 29. What is an
anomaly?
- 30. Distinguish teratology from
oncology.
- 3l. Briefly, discuss the causes
and significance of congenital anomalies.
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