Chapter 16
The Endocrine System
627
16
Endocrine System; Topic: The Actions of Hormones
on Target Cells, p. 3.
Control of Hormone Release
(pp. 596–597)
8.
Humoral, neural, or hormonal stimuli activate endocrine organs
to release their hormones. Negative feedback is important in
regulating hormone levels in the blood.
9.
Te nervous system, acting through hypothalamic controls, can
in certain cases override or modulate hormonal effects.
Half-Life, Onset, and Duration of Hormone Activity
(p. 598)
10.
Blood levels of hormones reflect a balance between secretion
and degradation/excretion. Te liver and kidneys are the major
organs that degrade hormones; breakdown products are excreted
in urine and feces.
11.
Hormone half-life and duration of activity are limited and vary
from hormone to hormone.
Interaction of Hormones at Target Cells
(p. 598)
12.
Permissiveness is the situation in which one hormone must be
present in order for another hormone to exert its full effects.
13.
Synergism occurs when two or more hormones produce the same
effects in a target cell and their results together are amplified.
14.
Antagonism occurs when a hormone opposes or reverses the
effect of another hormone.
Endocrine System; Topic: The Hypothalamic–Pituitary Axis,
pp. 4 and 5.
The Pituitary Gland and Hypothalamus
(pp. 598–606)
Pituitary-Hypothalamic Relationships
(p. 599)
1.
Te pituitary gland hangs from the base of the brain and is
enclosed by bone. It consists of a hormone-producing glandular
portion (anterior pituitary or adenohypophysis) and a neural
portion (posterior pituitary or neurohypophysis), which is an
extension of the hypothalamus. Te neurohypophysis includes
the infundibulum (stalk) and the posterior pituitary.
2.
Te hypothalamus (a) synthesizes two hormones that it exports
to the posterior pituitary for storage and later release and (b)
regulates the hormonal output of the anterior pituitary via
releasing and inhibiting hormones.
The Posterior Pituitary and Hypothalamic Hormones
(pp. 599–601)
3.
Te posterior pituitary stores and releases two hypothalamic
hormones, oxytocin and antidiuretic hormone (ADH).
4.
Oxytocin stimulates powerful uterine contractions, which trigger
labor and delivery of an infant, and milk ejection in nursing
women. Its release is mediated reflexively by the hypothalamus
and represents a positive feedback mechanism.
5.
Antidiuretic hormone stimulates the kidney tubules to reabsorb
and conserve water, resulting in small volumes of highly
concentrated urine and decreased plasma solute concentration.
ADH is released in response to high solute concentrations in the
blood and inhibited by low solute concentrations in the blood.
Hyposecretion results in diabetes insipidus.
Anterior Pituitary Hormones
(pp. 601–606)
6.
Four of the six anterior pituitary hormones are tropic hormones
that regulate the function of other endocrine organs. Most
anterior pituitary hormones exhibit a diurnal rhythm of release,
which is subject to modification by stimuli influencing the
hypothalamus.
7.
Growth hormone (GH) is an anabolic hormone that stimulates
growth of all body tissues but especially skeletal muscle
and bone. It may act directly, or indirectly, via insulin-like
growth factors (IGFs). GH mobilizes fats, stimulates protein
synthesis, and inhibits glucose uptake and metabolism. Its
secretion is regulated by growth hormone–releasing hormone
(GHRH) and growth hormone–inhibiting hormone (GHIH),
or somatostatin. Hypersecretion causes gigantism in children
and acromegaly in adults; hyposecretion in children causes
pituitary dwarfism.
8.
Tyroid-stimulating hormone (±SH) promotes normal
development and activity of the thyroid gland. Tyrotropin-
releasing hormone (±RH) stimulates release of ±SH; negative
feedback of thyroid hormone inhibits it.
9.
Adrenocorticotropic hormone (AC±H) stimulates the adrenal
cortex to release corticosteroids. Corticotropin-releasing
hormone (CRH) triggers AC±H release; rising glucocorticoid
levels inhibit it.
10.
Te gonadotropins—follicle-stimulating hormone (FSH) and
luteinizing hormone (LH)—regulate the functions of the gonads
in both sexes. FSH stimulates sex cell production; LH stimulates
gonadal hormone production. Gonadotropin levels rise in
response to gonadotropin-releasing hormone (GnRH). Negative
feedback of gonadal hormones inhibits gonadotropin release.
11.
Prolactin (PRL) promotes milk production in humans. Its
secretion is inhibited by prolactin-inhibiting hormone (PIH).
The Thyroid Gland
(pp. 606–610)
1.
Te thyroid gland is located in the anterior neck. Tyroid follicles
store colloid containing thyroglobulin, a glycoprotein from which
thyroid hormone is derived.
2.
Tyroid hormone (±H) includes thyroxine (±
4
) and
triiodothyronine (±
3
), which increase the rate of cellular
metabolism. Consequently, oxygen use and heat production rise.
3.
Secretion of thyroid hormone, prompted by ±SH, requires the
follicular cells to take up the stored colloid and split the hormones
from the colloid for release. Rising levels of thyroid hormone feed
back to inhibit the anterior pituitary and hypothalamus.
4.
Most ±
4
is converted to ±
3
(the more active form) in the target
tissues. Tese hormones act by turning on gene transcription and
protein synthesis.
5.
Graves’ disease is the most common cause of hyperthyroidism.
Hyposecretion causes cretinism in infants and myxedema in
adults.
6.
Te parafollicular (C) cells of the thyroid gland produce
calcitonin. It is not normally important in calcium homeostasis.
At pharmacological levels, it inhibits bone matrix resorption and
enhances calcium deposit in bone.
Endocrine System; Topic: The Hypothalamic–Pituitary Axis, p. 6.
The Parathyroid Glands
(pp. 610–611)
1.
Te parathyroid glands, located on the dorsal aspect of the
thyroid gland, secrete parathyroid hormone (P±H), which
increases blood calcium levels. It targets bone, the kidneys, and
the small intestine (indirectly via vitamin D activation). P±H is
the key hormone for calcium homeostasis.
2.
Falling blood calcium levels trigger P±H release; rising blood
calcium levels inhibit its release.
3.
Hyperparathyroidism results in hypercalcemia and extreme bone
wasting. Hypoparathyroidism leads to hypocalcemia, evidenced
by tetany and respiratory paralysis.
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