The Endocrine System
345
organs. Thus, bone strength diminishes and can even lead to
osteoporosis
(loss of bone mass); muscles weaken, and the skin
becomes thinned and easily bruised. The increased catabolism
may produce such a large quantity of precursors for hepatic
gluconeogenesis that blood sugar increases to levels observed
in diabetes. Thus, a person with Cushing’s Syndrome may
show some of the same symptoms as a person with diabetes.
Equally troubling is the possibility of
immunosuppression,
brought about by the anti-immune actions of cortisol.
Cushing’s Syndrome is often associated with loss of fat mass
from the extremities, and with redistribution of the fat in
the trunk, face, and the back of the neck. Combined with
an increased appetite, often triggered by high concentrations
of cortisol, this results in obesity and a characteristic facial
appearance in many patients (
Figure 11–25
). A further
problem associated with Cushing’s Syndrome is the possibility
of developing hypertension (high blood pressure). This is due
not to increased aldosterone production, but instead to the
pharmacological effects of cortisol, including cortisol’s ability
to potentiate the effects of epinephrine and norepinephrine on
the heart and blood vessels. At high enough concentrations,
cortisol exerts aldosterone-like actions on the kidney,
resulting in salt and water retention, which contributes to
hypertension.
Treatment of Cushing’s Syndrome depends on the
cause. In Cushing’s disease, for example, surgical removal
of the pituitary tumor, if possible, is the best alternative.
Unfortunately, these tumors may regrow over a number
of years, necessitating a second pituitary surgery or even
adrenalectomy. Unilateral adrenalectomy is the appropriate
treatment for an adrenal tumor making too much cortisol.
Of importance is the fact that glucocorticoids are often
used therapeutically to treat infl ammation, lung disease,
and other disorders. If glucocorticoids are administered at a
high enough dosage for long periods, the side effect of such
treatment can be Cushing’s Syndrome.
Figure 11–25
A young patient from the original series of Harvey Cushing. Left:
before onset of disease. Right: after development of Cushing’s
Syndrome.
II. In response to stress, the usual physiological functions of cortisol
are enhanced as cortisol levels in the plasma increase. Thus,
gluconeogenesis, lipolysis, and inhibition of insulin actions
increase. This results in increased blood levels of fuel sources
(glucose, fatty acids) needed to cope with stressful situations.
III. Cortisol levels at high concentrations also inhibit
“nonessential” processes, such as reproduction, during stressful
situations, and inhibit immune function.
Other Hormones Released During Stress
I. In addition to CRH, ACTH, and cortisol, several other
hormones are released during stress. Beta-endorphin is
coreleased with ACTH and may act to reduce pain. Vasopressin
stimulates ACTH secretion and also acts on the kidney to
increase water retention. Other hormones that are increased
in the blood by stress are aldosterone, growth hormone, and
glucagon. Insulin secretion, by contrast, decreases during
stress.
SECTION D SUMMARY
Physiological Functions of Cortisol
I. Cortisol is released from the adrenal cortex upon stimulation
with ACTH. ACTH, in turn, is stimulated by the release
of corticotropin-releasing hormone (CRH) from the
hypothalamus.
II. The physiological functions of cortisol are to maintain
the responsiveness of target cells to epinephrine and
norepinephrine, to provide a “check” on the immune system,
to participate in energy homeostasis, and to promote normal
differentiation of tissues during fetal life.
Functions of Cortisol in Stress
I. The stimulus that activates the CRH/ACTH/cortisol
endocrine pathway is stress, which encompasses a wide array of
sensory and physical inputs that disrupt, or potentially disrupt,
homeostasis.
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