352
Chapter 11
SECTION E KEY TERMS
SECTION E CLINICAL TERMS
bone age
346
catch-up growth
347
chondrocyte
346
epiphyseal closure
346
epiphyseal growth plate
346
epiphysis
346
growth factor
347
growth-inhibiting factor
347
insulin-like growth factor 1
(IGF-1)
348
insulin-like growth factor 2
(IGF-2)
349
mitogen
347
osteoblast
346
shaft
346
acromegaly
350
anabolic steroid
349
dwarfi sm
348
gigantism
350
growth hormone insensitivity
syndrome
348
Laron Dwarfi sm
348
prognathism
350
SECTION E REVIEW QUESTIONS
1. Describe the process by which bone lengthens.
2. What are the effects of malnutrition on growth?
3. List the major hormones that control growth.
4. Describe the relationship between growth hormone and IGF-1
and the roles of each in growth.
5. What are the effects of growth hormone on protein synthesis?
6. What is the status of growth hormone secretion at different
stages of life?
7. State the effects of the thyroid hormones on growth.
8. Describe the effects of testosterone on growth, cessation of
growth, and protein synthesis. Which of these effects does
estrogen also exert?
9. What is the effect of cortisol on growth?
10. Give two ways in which dwarfi sm can occur.
11. What are the typical signs and symptoms of acromegaly?
SECTION F
Endocrine Control of Ca
2+
Homeostasis
Many of the hormones of the body control functions that,
while important, are not necessarily vital for survival, such as
growth. By contrast, some hormones control functions so vital
that the absence of the hormone would be catastrophic, even
life-threatening. One such function is Ca
2+
homeostasis.
Extracellular calcium concentration normally remains
within a narrow range. Large deviations in either direction can
cause problems. For example, a low plasma calcium concen-
tration increases the excitability of nerve and muscle plasma
membranes. A high plasma calcium concentration causes car-
diac arrhythmias as well as depressed neuromuscular excitabil-
ity via its effects on membrane potential.
Effector Sites for Calcium
Homeostasis
Calcium homeostasis depends on an interplay among bone,
the kidneys, and the gastrointestinal tract. The activities of
the gastrointestinal tract and kidneys determine the net intake
and output of calcium for the entire body and, thereby, the
overall state of calcium balance. In contrast, interchanges
of calcium between extracellular fl uid and bone do not alter
total-body balance, but instead change the
distribution
of cal-
cium within the body. We begin, therefore, with a discussion
of the cellular and mineral composition of bone.
Bone
Approximately 99 percent of total-body calcium is contained
in bone. Therefore, the fl ux of calcium into and out of bone is
paramount in controlling plasma calcium concentration.
Bone is a special connective tissue made up of several
cell types surrounded by a collagen matrix, called
osteoid,
upon which are deposited minerals, particularly the crystals
of calcium and phosphate known as
hydroxyapatite.
In some
instances, bones have central marrow cavities where blood
cells form. Approximately one-third of a bone, by weight, is
osteoid, and two-thirds is mineral (the bone cells contribute
negligible weight).
The three types of bone cells involved in bone formation
and breakdown are osteoblasts, osteocytes, and osteoclasts
(
Figure 11–30
). As described in Section E, osteoblasts are
Figure 11–30
Cross section through a small portion of bone. The light tan area is
mineralized osteoid. The osteocytes have long processes that extend
through small canals and connect with each other and to osteoblasts
via tight junctions.
Adapted from Goodman.
Osteoclast
Osteoblasts
Osteocyte
Calcified matrix
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