Chapter 11
Quantitative and Thought Questions
11.1 Epinephrine decreases to very low concentrations during rest and fails to increase during stress.
The sympathetic preganglionics provide the only major control of the adrenal medulla.
11.2 The increased concentration of binding protein causes more T3 and T4 to be bound, thereby
lowering the plasma concentration of free T3 and T4. This causes less negative feedback inhibition of TSH
secretion by the anterior pituitary gland, and the increased TSH causes the thyroid to secrete more T3
and T4 until the free concentration has returned to normal. The end result is an increased total plasma T3
and T4 —most bound to the protein—but a normal free T3 and T4. There is no hyperthyroidism because
it is only the free concentration that exerts effects on T3 and T4 target cells.
11.3 Destruction of the anterior pituitary gland or hypothalamus. These symptoms reflect the absence
of, in order, growth hormone, the gonadotropins, and ACTH (the symptom is due to the resulting
decrease in cortisol secretion). The problem is either primary hyposecretion of anterior pituitary gland
hormones or secondary hyposecretion because the hypothalamus is not secreting hypophysiotropic
hormones normally.
11.4 Vasopressin and oxytocin (the posterior pituitary gland hormones) secretion would decrease. The
anterior pituitary gland hormones would not be affected because the influence of the hypothalamus on
these hormones is exerted not by connecting nerves but via the hypophysiotropic hormones in the
portal vascular system.
11.5 The secretion of GH increases. Somatostatin, coming from the hypothalamus, normally exerts an
inhibitory effect on the secretion of this hormone.
11.6 Norepinephrine and many other neurotransmitters are released by neurons that terminate on the
hypothalamic neurons that secrete the hypophysiotropic hormones. Therefore, manipulation of these
neurotransmitters will alter secretion of the hypophysiotropic hormones and thereby the anterior
pituitary gland hormones.
11.7 The high dose of the cortisol-like substance inhibits the secretion of ACTH by feedback inhibition of
(1) hypothalamic corticotropin releasing hormone and
(2) the response of the anterior pituitary gland to this hypophysiotropic hormone. The lack of ACTH
causes the adrenal to atrophy and decrease its secretion of cortisol.
11.8 The hypothalamus. The low basal TSH indicates either that the pituitary gland is defective or that it
is receiving inadequate stimulation (TRH) from the hypothalamus. If the thyroid itself were defective,
basal TSH would be elevated because of less negative feedback inhibition by T3 and T4. The TSH increase
in response to TRH shows that the pituitary gland is capable of responding to a stimulus and so is
unlikely to be defective. Therefore, the problem is that the hypothalamus is secreting too little TRH (in
reality, this is very rare).
11.9 In utero malnutrition. Neither growth hormone nor the thyroid hormones influence in utero
growth.
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11.10 Androgens stimulate growth but also cause the ultimate cessation of growth by closing the
epiphyseal plates. Therefore, there might be a rapid growth spurt in response to the androgens but a
subsequent premature cessation of growth. Estrogens exert similar effects.
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