1. Endocrine System Hormones

2. 14th edition
13th edition
12th edition
Same figure or table reference in all three editions
Much of the text material is from, “Principles of Anatomy and Physiology” by Gerald J. Tortora and Bryan Derrickson (2009, 2011, and 2014). I don’t claim authorship. Other sources are noted when they are used.
The lecture slides are mapped to the three editions of the textbook based on the color-coded key below.
Note

3. Outline Hypothalamus and pituitary gland Anterior pituitary
Posterior pituitary
Endocrine glands and their actions
Other endocrine organs and tissues
Long-term stress response
Aging

4. Hypothalamus and Pituitary Gland

5. Hypothalamus and Pituitary Gland
The pituitary gland is sometimes called the master gland because it releases hormones that control some, but not all, endocrine glands of the body.
The pituitary is regulated by the hypothalamus, which is a major link between the nervous system and endocrine system.
Cells in the hypothalamus and pituitary gland synthesize and secrete hormones.
Pituitary hormones are involved in growth and development, metab-olism, homeostatis, and sexual reproduction.
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6. Pituitary Structure
The pituitary gland is a pea-shaped structure located inferior to the hypothalamus, and measures about 13 mm in diameter.
The pituitary is almost completely enclosed in the sphenoid bone at the base of the brain cavity.
It is attached to the hypothalamus by the pituitary stalk, or infundib-ulum.
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Figure 18.5

7. Location
Magnetic resonance image (MRI)

8. Pituitary Structure (continued)
The pituitary consists of two major tissues of different embryonic origin: 1) anterior lobe or adenohypophysis, and 2) posterior lobe or neurohyphophysis.
The anterior lobe is about 3/4 of the total mass of the pituitary gland.
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Figure 18.5 8 8

9. Anterior Pituitary

10. Anterior Pituitary
The anterior pituitary secretes hormones that regulate many body functions.
Secretion of pituitary hormones is controlled by releasing hormones and inhibiting hormones secreted by the hypothalamus.
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Figure 18.5

11. Hypophyseal Portal System
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Figure 18.5
Releasing hormones and inhibiting hormones secreted by the hypo-thalamus reach the anterior pituitary through the hypophyseal portal system.
Blood in the portal system flows:
Through a capillary network in the hypothalamus,
Into a portal vein through the pituitary stalk, and
Then through a second capillary network in the anterior pituitary.
This portal system enables the chemical control of the anterior pituitary by the hypothalamus.

12. Anterior Pituitary Control
Hypothalamus
Anterior
pituitary
Hypophyseal
portal system
Releasing hormones and inhibiting hormones
Hormones that affect target tissues in the body
General
blood circulation
Target tissues

13. Entry into Blood Circulation
In response to releasing hormones, hormones secreted by specialized cells of the anterior pituitary are secreted into the anterior hypophyseal veins.
Pituitary hormones enter general blood circulation to exert their effects on target tissues.
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Figure 18.5

14. Anterior Pituitary Hormones
General
blood circulation
Human growth hormone—hGH
Thyroid stimulating hormone—TSH
Follicle stimulating hormone—FSH
Luteinizing hormone—LH
Prolactin—PRL
Adrenocorticotropic hormone—ACTH

15. Neurosecretory Cells
The anterior pituitary has groups of specialized cells that produce six hormones (each group ends in -troph).
Somatatrophs synthesize and secrete human growth hormone (hGH) to stimulate many body tissues to release insulin-like growth factors (IGFs).
Growth factors promote body growth and regulate certain aspects of metabolism.
Thyrotrophs synthesize and secrete thyroid stimulating hormone (TSH) to control hormonal secretions and other activity of the thyroid gland.
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Figure 18.5
Table 18.3

16. Neurosecretory Cells (continued)
Gonadotrophs synthesize and secrete follicle stimulating hormone (FSH) and luteinizing hormone (LH) to act on the ovaries and testes.
FSH and LH stimulate the secretion of estrogens and proges-terone, and promote the maturation of the oocytes (eggs) in the ovaries.
FSH and LH also stimulate testosterone secretion and sperm production (spermatogenesis) in the testes.
Lactotrophs synthesize and secrete prolactin (PRL) to stimulate milk production in the mammary glands of the breasts.
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Table 18.3

17. Neurosecretory Cells (continued)
Corticotrophs secrete adrenocorticotropic hormone (ACTH), also known as corticotropin.
ACTH stimulates the adrenal cortex, the outer tissue layers of the adrenal gland, to secrete glucocorticoids including cortisol.
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Table 18.3

18. Control of Hormonal Secretions
Two mechanisms control the secretion of hormones from the anterior pituitary:
Neurosecretory cells in the hypothalamus secrete releasing hormones to stimulate hormonal secretions from the anterior pituitary.
Other neurosecretory cells in the hypothalamus secrete inhibit- ing hormones to suppress hormonal secretions from the anterior pituitary.
Not every releasing hormone has a corresponding inhibiting hormone.
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19. Control of Hormonal Secretions (continued)
The hormones from the anterior pituitary bind to cell receptors in target tissues of the body.
Hormone secretions from target tissues generally provide negative feedback to the anterior pituitary or hypothalamus to decrease their hormonal activity.
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20. Human Growth Hormone
Human growth hormone (hGH) is the most abundant hormone of the anterior pituitary.
hGH promotes the synthesis and release of small protein molecules known as insulin-like growth factors (IGFs).
IGFs are released by cells in the liver, skeletal muscles, bones, carti-lage, and other tissues in response to hGH.
IGFs act locally in the body’s tissues either as paracrines or autocrines.
Paracrine = a hormone or other chemical produced by a cell that acts on nearby cells.
Autocrine = a hormone or other chemical that acts on the cell that produced it.
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21. Human Growth Hormone (continued)
hGH and IGFs stimulate cells to multiply (by mitosis), and grow by in-creasing the uptake of amino acids and accelerating protein synthesis in the translation process.
Due to these physiological effects, hGH increases the growth rate of the skeleton and skeletal muscles during childhood and the teenage years.
In adults, hGH and IGFs help maintain skeletal muscle and bone mass and promote tissue repair.
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22. Human Growth Hormone (continued)
IGFs enhance lipolysis in adipose tissue to increase fatty acids available for ATP production.
hGH stimulates the breakdown of glycogen, a polysaccharide, in the liver to release glucose molecules—this process is known as glycogenolysis.
hGH and IGFs also decrease glucose uptake in many tissues, making glucose available to neurons when blood glucose level is low.
Lipolysis = the metabolic breakdown of fat stored in fat cells; the reverse of lipogenesis.
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23. Human Growth Hormone (continued)
The anterior pituitary secretes bursts of hGH every few hours, especi-ally during slow wave sleep.
Secretion of hGH is controlled by two hormones by the hypothalamus:
Growth hormone-releasing hormone (GHRH)
Growth hormone-inhibiting hormone (GHIH)
GHRH and GHIH are regulated via negative feedback of blood glucose level.
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Figure 18.7

24. - GHRH, GHIH, and hGH—Control and Feedback Hypothalamus GHRH and GHIH
Anterior
pituitary
Hypophyseal
portal system
GHRH and
GHIH
hGH
General
blood circulation
Liver
(glycogen
breakdown)
Decreased blood glucose level (inhibits release of GHIH)
Increased blood glucose level (inhibits release of GHRH) -

25. Hyposecretion = under-secretion.
Pituitary Dwarfism
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Hyposecretion of hGH during childhood slows the growth of the long bones and other organs.
The epiphyseal plates close before the child reaches expected height.
The condition, known as pituitary dwarfism, results in short stature and normal body proportions.
Medical treatment involves the administration of growth hormone dur-ing childhood before the epiphyseal plates close at puberty.
Hyposecretion = under-secretion.
Epiphyseal plate = hyaline cartilage plate in the metaphysis at the end of each long bone. 25 25

26. Pituitary Gigantism
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Figure 18.22
Hypersecretion of hGH results in an abnormal increase in the length of the long bones before the epiphyseal plates close in late childhood.
The condition, known as pituitary gigantism, results in very tall stature and normal body proportions.
Treatment may require surgical removal of an anterior pituitary tumor.
Hypersecretion = over-secretion.

27. Acromegaly
Hypersecretion of hGH after puberty does not increase the length of the long bones because the epiphyseal plates are closed.
The condition, known as acromegaly, leads to thickening of the bones of the hands, feet, cheeks, and jaws, among other tissues.
The eyelids, lips, tongue, and nose enlarge, and the skin—especially of the forehead and soles—thickens and develops furrows.
Treatment may require surgical removal of an anterior pituitary tumor.
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Figure 18.22 27 27

28. Thyroid Stimulating Hormone
Thyrotropin releasing hormone (TRH) from the hypothalamus controls the secretion of thyroid stimulating hormone (TSH) from the anterior pituitary.
TSH stimulates the synthesis and secretion of triiodothyronine (T3) and thyroxine (T4) from the thyroid gland.
T3 and T4 regulate aspects of the body’s metabolism, to be discussed later.
High blood levels of T3 and T4 inhibit further secretion of TRH from the hypothalamus via a negative feedback pathway.
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Figure 18.12 28 28

29. TRH and TSH—Control and Feedback
Hypothalamus
Anterior
pituitary
Hypophyseal
portal system
TRH
TSH
General
blood circulation
Thyroid gland
T3 and T4 -

30. Follicle Stimulating Hormone
FSH stimulates development of an ovarian follicle each month that surrounds a developing oocyte (egg).
It also stimulates follicular cells to secrete the female sex hormone, estrogen.
The hormone stimulates spermatogenesis (sperm production) in the testes.
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31. Follicle Stimulating Hormone (continued)
Gonadotropin-releasing hormone (GnRH) from the hypothalamus controls the secretion of FSH from the anterior pituitary.
The release of FSH from the pituitary is suppressed in a negative feedback pathway of inhibin released by the ovaries and Sertoli cells in the testes.
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32. GnRH and FSH—Control and Feedback
Hypothalamus
Anterior
pituitary
Hypophyseal
portal system
GnRH
FSH
General
blood circulation
Gonads
(ovaries and testes)
Inhibin -

33. Luteinizing Hormone
LH triggers ovulation, the expulsion of one or more oocytes from the ovaries.
It also stimulates the formation of the corpus luteum in the ovary after ovulation and the secretion of progesterone.
LH and FSH together stimulate the secretion of estrogens by ovarian cells.
Estrogens and progesterone prepare the uterus for the implantation of a fertilized ovum, and help prepare the mammary glands for milk secre-tion.
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34. Luteinizing Hormone (continued)
LH stimulates the Leydig cells in the testes to secrete the androgen, testosterone.
The secretion of LH, like FSH, is controlled by GnRH in both females and males.
Estrogen, at moderate levels, and testosterone inhibit the release of GnRH from the hypothalamus and LH from the anterior pituitary via negative feedback pathways.
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35. - GnRH and LH—Control and Feedback Hypothalamus GnRH Anterior
About hours before ovulation, the estrogen feedback effect becomes positive to initiate the surge of LH that triggers egg release.
Hypothalamus
Anterior
pituitary
Hypophyseal
portal system
GnRH LH
General
blood circulation
Gonads
(ovaries and testes)
Estrogen (moderate level)
Testosterone -

36. Prolactin
Prolactin, along with other hormones, initiates and maintains milk secre-tion by the mammary glands.
Prolactin stimulates milk secretion after the mammary glands have been primed by other hormones (a permissive effect).
The hormones include estrogens, progesterone, glucocorticoids, human growth hormone, thyroxine (T4), and insulin.
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37. Lactation
Ejection of milk from the mammary glands is triggered by oxytocin from the posterior pituitary in response to the touch and suckling of an infant on a mother’s breast.
Milk synthesis and ejection together are called lactation.
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38. Prolactin (continued)
The hypothalamus secretes releasing and inhibiting hormones to regulate prolactin secretion from the anterior pituitary.
In females, prolactin-inhibiting hormone (PIH) inhibits the release of prolactin from the anterior pituitary during most of the monthly cycle.
Prior to menstruation, the secretion of PIH diminishes, and the blood level of prolactin increases.
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39. Prolactin (continued)
During pregnancy, in preparation for lactation, prolactin level rises due to stimulation by prolactin-releasing hormone (PRH) from the hypothal-amus.
Small amounts of dopamine released by the anterior pituitary can exert a negative feedback effect on the further release of prolactin releasing hormone.
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40. Adrenocorticotropic Hormone
Adrenocorticotropic hormone (ACTH) regulates the synthesis and secretion of cortisol and other glucocorticoids from the adrenal cor-tex.
Glucocorticoids have a wide range of physiological effects, which we will discuss later.
Corticotropin-releasing hormone (CRH) secreted by the hypothal-amus stimulates the secretion of ACTH from the anterior pituitary.
High blood levels of glucocorticoids inhibit CRH and ACTH secre-tion from the hypothalamus and anterior pituitary via negative feed-back pathways.
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41. CRH and ACTH—Control and Feedback
Hypothalamus
Anterior
pituitary
Hypophyseal
portal system
CRH
ACTH
General
blood circulation
Adrenal cortex
(zona fasciculata)
Glucocorticoids -

42. Adrenocorticotropic Hormone (continued)
Stress-related stimuli—such as low blood glucose level, physical trauma, and interleukin-1 (from immune responses)—can trigger the secretion of ACTH.
ACTH is also involved in the resistance reaction, as will be covered in this lecture.
Interleukin = a type of messenger molecule among different cells of the immune system.
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43. Cushing’s Syndrome
Hypersecretion of ACTH from the anterior pituitary or cortisol from the adrenal cortex results in signs and symptoms known as Cush-ing’s syndrome.
Muscle proteins breakdown, and body fat is redistributed resulting is spindly arms and legs, “moon” (round) face,“buffalo” back hump, and hanging (pendulous) abdomen.
Other signs include hyperglycemia, osteoporosis, muscle weak-ness, hypertension, susceptibility to infection, and poor response to stressors.
Treatment may require surgical removal of an anterior pituitary or adrenal tumor.
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Figure 18.22 43 43

44. Posterior Pituitary

45. Posterior Pituitary
The posterior pituitary contains axon terminals for more than 10,000 neurosecretory cell bodies (specialized neurons) located in the hypo-thalamus.
The axons of the cell bodies form the hypothalamohypophyseal tract in the pituitary stalk.
Cell bodies in the hypothalamus synthesize oxytocin and antidiuretic hormone (ADH).
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Figure 18.8

46. Posterior Pituitary Hormones
General
blood circulation
Oxytocin
Antidiuretic hormone—ADH (also called vasopressin)

47. Synthesis, Transport, and Secretion
Oxytocin and ADH are:
Synthesized in neurosecretory cell bodies in the hypothalamus,
Packaged in vesicles,
Moved via fast axonal transport along the hypothalamohypohy-seal tract to the axon terminals in the posterior pituitary, and
Released into general blood circulation through exocytosis when triggered by action potentials from the hypothalamus.
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48. Posterior Pituitary Control
Hypothalamus
Posterior
pituitary
Hypothalamo-
hypophyseal tract
Hormones synthesized in the hypothalamus are moved via fast axonal transport (an active process requiring chemical energy).
Hormones are released by the posterior pituitary to act upon target tissues in the body.
General
blood circulation
Target tissues

49. Oxytocin
During labor and delivery, oxytocin enhances the contractions of smooth muscle in the uterine wall.
After delivery, oxytocin stimulates milk ejection from the mammary glands in response to mechanical stimuli of suckling by an infant.
Oxytocin may be involved in mediating feelings of emotional pleasure during and after sexual intercourse in females and males.
Uterine = pertaining to the uterus.
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50. Antidiuretic Hormone
ADH stimulates the kidneys to return water to the blood, decreasing urine production.
Without ADH, urine output would increase from normally 1 to 2 liters to about 20 liters per day.
This condition is known as diabetes insipidis, or weak urine.
Drinking alcohol inhibits the production and secretion of ADH, which can lead to frequent and copious urination.
Copious = substantial amounts.
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Figure 18.9

51. Antidiuretic Hormone (continued)
In addition to its action on the kidneys, ADH decreases water loss from sweating and constricts the arterioles to raise blood pressure.
ADH is also known as vasopressin because it constricts arterioles in systemic circulation.
Arterioles = arteries divide into smaller and smaller branches, called arterioles, which have muscles in their walls and can actively contract and relax. (
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Figure 18.9

52. Endocrine Glands and Their Actions

53. Vascularized = blood vessels and capillaries in tissue.
Thyroid Gland
The butterfly-shaped thyroid gland, consisting of left and right lateral lobes, is located inferior to the larynx.
Thyroid tissue is highly-vascularized and receives substantial blood supply.
Microscopic spherical sacs, known as thyroid follicles, form most of the thyroid gland.
Vascularized = blood vessels and capillaries in tissue.
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Figure 18.10

54. Thyroid Gland (continued)

55. T3 and T4
The walls of a follicle have follicular cells that synthesize and secrete triiodothyronine (T3) and thyroxine (T4) in response to TSH from the anterior pituitary.
T3 has three atoms and T4 has four atoms of the trace element iodine covalently bonded to the amino acid, tyrosine.
Iodine is necessary in our diets—deficiencies can lead to problems such as slowed physical growth and mental deficits in children, and goiter in adults.
As prevention, table salt (NaCl) is fortified with iodine as mandated by federal law.
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Figure 18.11

56. Physiological Responses
T3 and T4 have widespread effects since most cells have receptors.
The two hormones:
Increase basal metabolic rate (BMR) by stimulating aerobic respiration (Krebs cycle) to produce ATP for metabolism of carbohydrates, lipids, and proteins.
Exert a calorigenic effect to maintain body temperature by the cellular use of ATP to produce heat.
Calorigenic = production of heat from the digestion of food and the action of certain hormones.
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57. Physiological Responses (continued)
T3 and T4 also:
Stimulate the synthesis of proteins for the sodium-potassium transport pump to maintain the extracellular and intracellular concentrations of Na+ and K+.
Enhance some actions of norepinephrine and epinephrine though the up-regulation of -adrenergic synaptic receptors.
Accelerate body growth in conjunction with human growth hormone and insulin by exerting a permissive effect.
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58. Physiological Responses (continued)
T3 and T4 secretion increases in conditions that increase the body’s demands for ATP.
The conditions include:
Cold environments
High altitude
Hypoglycemia
Pregnancy
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59. Hypothyroidism—Children
Disorders of the thyroid gland, which are the most common types of endocrine disorders, affect all major organ systems.
Hyposecretion of thyroid hormones at birth, known as congenital hypothyroidism, results in severe mental impairments and slowed bone growth and short stature.
Prior to birth, the fetus is protected by the mother’s thyroid hormones (T3 and T4), which are lipid-soluble and cross the placenta.
State-mandated testing at birth assures that lifelong thyroid hormone treatment can promptly begin.
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60. Hypothyroidism—Adults
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Hypothyroidism in adults results in myxedema, which is about five times more common in females than males.
Signs and symptoms include edema causing the face to swell and look puffy, slowed heart rate, low body temperature, sensitivity to cold, and dry hair and skin.
Other signs and symptoms include muscle weakness, lethargy, and weight gain.
Edema = accumulation of interstitial fluid in a tissue. 60 60

61. Hypothyroidism—Adults (continued)
Although mental impairment does not occur because the brain has already reached maturity, the person may show diminished mental alertness.
Treatment for myxedema involves the oral administration of thyroid hormones (T3 and T4).
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62. Hyperthyroidism
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Figure 18.22
The most common form of hyperthyroidism is Graves disease, which is seven to ten times more common in females than males.
Graves disease is an autoimmune disease in which antibodies mimic the effects of thyroid stimulating hormone (TSH).
A telling sign is goiter, in which the thyroid gland is about two to three times its normal mass.
Edema behind the eyes causes the eyeballs to protrude, a condition known as exophthalmos.
Autoimmune disease = a disease in which the body’s immune system attacks healthy cells. 62 62

63. Goiter
Goiter can result from hyperthyroidism, hypothyroidism, or euthyroidism (insufficient intake of iodine). Goiter can be much more severe than this example.

64. Hyperthyroidism (continued)
Treatment for hyperthyroidism includes surgical removal of all or part of the thyroid gland, known as thyroidectomy.
Other treatments include use of a radioactive isotope of iodine (131I) and the use of antithyroid drugs to inhibit the synthesis of T3 and T4.
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65. Calcitonin
Calcitonin is produced and secreted by parafollicular cells of the thy-roid gland.
The hormone decreases the level of calcium (Ca2+) in the blood by inhibiting the action of osteoclasts, the cells that breakdown the extra-cellular matrix of bone.
Secretion is controlled via a local negative feedback pathway, which does not involve the hypothalamus or pituitary.
Miacalcin, calcitonin extracted from salmon, is ten times more potent than human calcitonin, and is used to treat osteoporosis.
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Figure 18.14

66. Osteoporosis Comparison of the extracellular matrix of the long bones
(normal to the left and osteoporosis to the right).
Osteoporosis

67. Osteoporosis
Osteoporosis is a condition in which bone resorption (breakdown) is greater than bone deposition (formation).
Bone mass may become so depleted and porous that bone fractures can occur in everyday living.
The condition mostly affects the middle-aged and seniors, and about 80 percent are women.
Risk factors include decreased estrogen levels in postmenopausal women, inactive lifestyles, eating disorders, low-calcium diets, smok-ing, excessive drinking, and certain medications.
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Figure 6.11 67 67

68. Osteoporosis (continued)
Osteoporosis can be diagnosed with a bone mineral density (BMD) test.
A wide range of treatment options are available depending on the circumstances.
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Figure 6.11 68 68

69. Hormone Storage in the Thyroid Gland
The thyroid is the only endocrine gland that can store hormones (T3, T4, and calcitonin) to maintain its normal physiological func-tioning.
It stores about a 100-day supply.
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70. Parathyroid Glands
The pararathyroid glands are four small masses of tissue embedded in the posterior surface of the thyroid gland.
Chief or principal cells synthesize and secrete parathyroid hormone (PTH), also known as parathormone.
The functions of oxyphil cells in the parathyroid glands are not known.
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Figure 18.13

71. Physiological Responses
PTH regulates the levels of calcium (Ca2+), magnesium (Mg2+), and phosphate (HPO42-) ions in the blood.
The hormone stimulates the osteoclasts in bone to elevate bone resorption of calcium and phosphate, and increase their levels in the blood.
PTH stimulates the kidneys to slow the rates at which calcium and magnesium are lost from the blood.
It also increases the rate at which phosphate is excreted from the kidneys.
Resorption = the process of losing certain substances.
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Figure 18.14

72. Physiological Responses (continued)
PTH stimulates the kidneys to synthesize the hormone, calcitrol, the active form of vitamin D.
Blood calcium level directly controls the secretion of PTH and calci-tonin via negative feedback—this process does not involve the pitu-itary gland.
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Figure 18.14

73. Adrenal Glands
The adrenal glands are located superior to each kidney in the retro-peritoneal space.
During embryonic development the adrenal glands differentiate into two structurally- and functionally-distinct regions:
Adrenal cortex—the outer tissue layers called zones or zonas.
Adrenal medulla—the inner tissue layer.
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74. Adrenal Glands (continued)
The adrenal cortex, about 80 to 90 percent of the mass of the adrenal gland, synthesizes and secretes several steroid hormones.
The adrenal medulla synthesizes and secretes three catecholamine hormones—epinephrine, norepinephrine, and small amounts of dopa-mine.
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Figure 18.15 74 74

75. Adrenal Glands (continued)
Adrenal medulla
Adrenal cortex

76. Adrenal Cortex
The adrenal cortex has three zones—each zone secretes different steroids.
The zona glomerulosa secretes mineralcorticoids that help control mineral homeostatis.
The zona fasciculata secretes glucocorticoids that help control glu-cose homeostatis.
The zona reticularis secretes small amounts of androgens that have masculinizing effects (the androgens can also be converted to estro-gens).
Homeostatis = the condition in which the body’s internal environment remains relatively constant within physiological limits.
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Figure 18.15

77. Mineralcorticoids
The mineralcorticoid, aldosterone, by acting on the kidneys, regulates homeostatis of sodium (Na+) and potassium (K+) ions to control blood pressure and blood volume.
The hormone also promotes the excretion of hydrogen ions in the urine—the removal of acids from the body helps prevent acidosis (blood pH < 7.35).
The renin-angiotensin-aldosterone pathway controls the secretion of aldosterone from the adrenal cortex.
This complex physiological pathway is described in detail in the text-book.
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Figure 18.16

78. Glucocorticoids
Glucocorticoids include cortisol (hydrocortisone), corticosterone, and cortisone.
Cortisol is the most abundant, accounting for about 95 percent of glucocorticoids.
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79. Physiological Responses
Glucocorticoids increase the catabolism of proteins, especially in skeletal muscle fibers, to provide amino acids for the synthesis of new proteins.
These hormones also stimulate the conversion of amino acids and lactic acid in the liver for use by neurons and other cells for ATP pro-duction.
Glucocorticoids also stimulate lipolysis, the breakdown of trigylcer-ides in adipose cells, and release of fatty acids into blood circulation.
Catabolism - the metabolic breakdown of complex molecules into simpler ones, often resulting in a release of energy. (
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80. Physiological Responses (continued)
Glucocorticoids supply cells with additional glucose for generating ATP in response to a wide range of stressors.
Stressors can include physical exercise, dietary fasting, temperature extremes, high altitude, bleeding, infection, surgery, trauma, disease, and fear and other emotional states.
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81. Physiological Responses (continued)
Glucocorticoids inhibit the actions of white blood cells (WBCs) in inflammatory responses.
Tissue repair and wound healing is slowed, which can be useful in the treatment of chronic inflammatory conditions such as rheuma-tism.
Glucocorticoids depress immune system responses, which can help to slow tissue rejection in organ transplant patients by administering glucocorticoids.
Rheumatism = inflammation, stiffness, and pain of the joints, skeletal muscles, or their connective tissues.
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82. Adrenal Androgens
The adrenal cortex secretes small amounts of weak-acting androgens including DHEA in males and females.
Adrenal androgens stimulate the growth of axillary (armpit) and pubic hair in boys and girls, and contribute to the pre-pubertal growth spurt in both sexes.
After puberty, the effects of adrenal androgens is very modest in males since a more potent androgen, testosterone, is secreted in much larger amounts by the testes.
DHEA = dehydroepiandrosterone, a steroid hormone produced by the adrenal glands and converted to other hormones including estrogen and testosterone. (
Puberty = a stage in female and male development when the reproductive organs mature.
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83. Adrenal Androgens (continued)
Adrenal androgens promote the sex drive (libido) in females and are converted into feminizing sex steroids, estrogens, by other tissues in the body.
After menopause, all estrogens are synthesized from adrenal andro-gens.
ACTH can stimulate the secretion of adrenal androgens, but the mech-anism is not well-understood.
Menopause = the point marking the end of menstruation and childbearing; defined by the World Health Organization (WHO) as one year after the last menstrual period. (
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84. Adrenal Medulla
The adrenal medulla is a ganglion of the sympathetic division of the autonomic nervous system.
The chromaffin cells of the gland are innervated by sympathetic pre-ganglionic neurons.
The cells release hormones, specifically catecholamines, into blood circulation.
The response is rapid since the preganglionic neurons act directly on the chromaffin cells.
Catecholamines include epinephrine (adrenalin), norepinephrine (noradrenalin), and dopamine.
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Figure 18.15

85. Adrenal Catecholamines
The chromaffin cells synthesize and secrete epinephrine and nor-epinephrine in an approximate ratio of 4:1.
Minute amounts of dopamine are also synthesized and secreted.
The hormones, unlike those of the adrenal cortex, are not essential for life.
However, they intensify sympathetic responses in many parts of the body.
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86. Adrenal Catecholamines (continued)
The hypothalamus activates the sympathetic preganglionic neurons in response to stress or physical exercise.
The chromaffin cells respond by secreting epinephrine and norepineph-rine.
The hormones contribute to the fight or flight response as discussed in the lecture module on the autonomic nervous system.
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87. Physiological Responses
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Epinephrine and norepinephrine increase heart rate and the force of cardiac contraction, which together increase cardiac output and blood pressure.
Blood flow increases to the heart, liver, and skeletal muscle due to the dilation of the arterioles that supply these tissues.
Other responses to these hormones include dilation of bronchioles in the airways of the lungs to increase pulmonary ventilation (airflow into and out of the lungs), and increased blood levels of glucose and fatty acids.
Cardiac output = volume of blood pumped from the heart’s ventricles.

88. Pancreas
The pancreas has a dual role as an exocrine gland and an endocrine gland.
It is located in the curve of the duodenum, the first section of the small intestine.
About 99 percent of its cells are arranged in clusters known as acini.
These cells produce digestive enzymes that flow into the gastrointes-tinal tract through a network of ducts (an exocrine function).
Among the acini are 1 to 2 million clusters of pancreatic islet cells that have endocrine functions.
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Figure 18.18

89. Pancreatic Islet Cells
Alpha cells, about 17 percent of the islet cells, secrete glucagon.
Beta cells, about 70 percent of islet cells, secrete insulin.
Delta cells, about 7 percent of islet cells, secrete somatostatin, which is identical to growth hormone-inhibiting hormone (GHIH) secreted by the hypothalamus.
F cells the remaining 6 percent of islet cells, secrete pancreatic poly-peptide.
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Table 18.9
Figure 18.18

90. Glucagon and Insulin
Glucagon increases blood glucose when blood glucose falls below normal levels, while insulin helps lower blood glucose when its level is too high.
Blood glucose level controls the secretion of glucagon and insulin via negative feedback pathways as shown in the textbook illustration (see the figure reference below).
Although blood glucose level is the most important regulator of insulin and glucagon, several other hormones and neurotransmitters are also involved.
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Figure 18.19

91. Diabetes Mellitus
Diabetes mellitus (sweet urine) results from an inability to produce or use insulin
Diabetes can damage the heart, blood vessels, kidneys, and retina (retinopathy).
Blood glucose level is high because insulin, a hormone, is lacking for transporting glucose into cells for energy production and metab-olism.
The disease is characterized by signs of polyuria (excessive urine production), polydipsia (excessive thirst), and polyphagia (excessive eating).
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92. Diabetes Mellitus (continued)
Diabetes mellitus is the fourth leading cause of death by disease in the United States.
The condition may contribute to premature death from other causes including cardiovascular disease.
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93. Type 1 Diabetes
In Type 1 diabetes, the immune system damages or destroys the pan-creatic beta cells in an autoimmune reaction, and therefore little or no insulin is produced.
The disease usually develops in young people (less than 20 years old) and it persists for a lifetime.
By the time Type 1 diabetes has typically been diagnosed, about 80 to 90 percent of the beta cells often have been destroyed.
Because of the lack of insulin, glucose cannot be transported into cells to meet their metabolic needs for energy production.
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94. Type 1 Diabetes (continued)
Thus, triglycerides in adipose cells are catabolized to glycerol and fatty acids, and the fatty acids are used by cells for energy produc-tion.
The byproducts of fatty acids are ketones that cause a decrease in blood pH.
The result is ketoacidosis, which can result in death if not treated im-mediately.
Ketone = a type of acid—one feature is an oxygen atom that has a double bond with a carbon atom.
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95. Type 2 Diabetes
Type 2 diabetes is the more frequently-occurring form, representing about 90 percent of all cases of diabetes mellitus.
It is most common in overweight people over the age of 35, although type 2 diabetes is increasingly seen in overweight children and teen-agers.
The effects can sometimes be controlled with proper diet, exercise, and weight loss.
Medications exist that can stimulate insulin secretion from beta cells.
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96. Type 2 Diabetes (continued)
Some people with Type 2 diabetes have a normal level of blood insulin, but the body cells have become less sensitive to the hormone.
Decreased sensitivity is due to the down-regulation of insulin receptors on the plasma membranes of cells.
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97. Complications
Uncontrolled high blood sugar can damage blood vessels through-out the body.
Complications of diabetes related to blood vessel damage include:
Blindness
Kidney failure
Cardiovascular disease
Poor wound healing
Tissue death in the extremities 97 97

98. Prevention
As previously noted, primary prevention of type 2 diabetes includes diet, weight control, and physical exercise.
About one of every four people who have diabetes are unaware they have the disease.
Secondary prevention requires early diagnosis so that treatment can begin at an early stage when it is most treatable.
Lack of available, routine medical care for many people contributes to the seriousness of the problem. 98 98

99. Bovine and Porcine Insulin
Beginning in the 1920s, diabetes mellitus was treated using insulin from the pancreases of cows and pigs (bovine and porcine insulin).
Allergic reactions sometimes resulted because the protein structures are not exactly the same as in human insulin.
By the 1970s, the supply of bovine and porcine insulin could not keep up with demand.
Human insulin (to the left) and porcine insulin—the difference in the protein structure is one amino acid: alanine versus threonine.
Ala
Thr 99 99

100. Synthetic Insulin
Recombinant DNA technology enables the mass production of synthetic insulin.
Since the amino acid sequence for human insulin was already known, researchers could identify the DNA nucleotide sequence that codes for the protein.
Individual segments of DNA were synthesized and linked to form human insulin genes.
The artificially-produced human genes were inserted into the DNA of E. coli bacteria that can rapidly multiply through replication to produce large quantities of insulin.
Recombinant DNA = DNA that has been artificially formed by combining constituents from different organisms.
100
100

101. Synthetic Insulin (continued)
Today, more than four million people in the United States rely on synthetic insulin.
101
101

102. Ovaries
The gonads (ovaries and testes) produce gametes—oocytes (eggs) in females and spermatogonia (sperm) in males.
The ovaries also secrete hormones including estrogens (estradiol and estrone) and progesterone.
These hormones, along with FSH and LH from the anterior pituitary, regulate the menstrual cycle, maintain a pregnancy, and prepare the mammary glands for lactation.
The hormones also promote enlargement of the breasts and widening of the hips at puberty, and help maintain other female secondary sexual characteristics.
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Table 18.10

103. Ovaries (continued)
The ovaries also secrete the hormone inhibin, a hormone that inhibits secretion of FSH from the anterior pituitary via a negative feedback pathway.
During the late stage of pregnancy, the ovaries and placenta secrete the hormone relaxin, to help ease the baby’s passage by enlarging the birth canal.
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Table 18.10

104. Testes
The testes secrete a strong-acting androgen known as testosterone.
Testosterone from the fetal testes stimulates the their descent usually before birth.
The hormone regulates spermatogenesis (sperm production) starting at puberty.
It also stimulates the development and maintenance of male secondary sex characteristics including beard growth and deepening of the voice at puberty.
Sertoli cells produce the hormone inhibin to inhibit release of FSH from the anterior pituitary via a negative feedback pathway.
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Table 18.10

105. Other Endocrine Organs and Tissues

106. Pineal Gland
The pineal gland is located near the posterior portion of the third ven-tricle roof.
It has neurosecretory cells (specialized neurons) that secrete melatonin, a hormone derived from serotonin.
Melatonin contributes to the control of circadian rhythms including the sleep cycle.
The pineal gland is regulated by nuclei in the hypothalamus, with input from the visual system, including ambient (environmental) light levels.
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Figure 18.1

107. Thymus
The thymus is located posterior to the sternum between the lungs.
The hormone thymosin secreted by the thymus promotes the matu-ration of T cells, a type of white blood cell that destroys microbes and foreign substances.
The thymus is described further in the lecture module on the immune system.
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108. Other Organs and Tissues
Cells in other organs and tissues have endocrine functions since they secrete hormones.
They include the digestive tract, placenta, kidneys, heart, and adipose tissue.
We will discuss their hormones and physiological actions when we cover other organ systems during the rest of the semester.
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Table 18.11

109. Eicosanoids
Two families of eicosanoid molecules—leuokotrienes and prosta-glandins—are found in most body cells, except for red blood cells.
They function as local hormones in response to mechanical and chemical stimuli.
Leukotrienes stimulate the chemotaxic responses of white blood cells to combat inflammation.
Chemotaxis = movement of a cell or organism in response to a chemical stimulus.
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110. Prostaglandins
Prostaglandins have widespread effects on the body—they affect:
Smooth muscle function
Glandular secretions
Blood flow
Reproductive processes
Platelet function
Respiration
Nerve impulses
Lipid metabolism
Immune responses
Prostaglandins also promote inflammation and fever, and can intensify pain by stimulating nocireceptors (pain receptors).
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111. Growth Factors
Insulin-like growth factor, thymosin (from the thymus), thyroid hormones, human growth hormone, and prolactin stimulate mitotic cell division and growth.
Hormones known as growth factors promote tissue development, growth, and repair.
Growth factors are mitogenic since they promote tissue growth through stimulation of mitotic cell division.
Many growth factors can act locally either as paracrines or autocrines.
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Table 18.12

112. Long-Term Stress Response

113. Stressors
A stimulus that produces a physiological stress response is known as a stressor.
A stressor can be almost any physical disturbance of the human body.
Stressors can also include emotional disturbances.
Stressors can be pleasant or unpleasant, and may vary among people and even within the same person at different times.
An individual’s reaction to the stressor is key in whether or not a stress response occurs.
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114. Fight or Flight Response
The fight or flight response is initiated and controlled by the sympa-thetic division of the autonomic nervous system.
The overall response is to mobilize the body’s resources to respond to a stressor.
We previously discussed a number of the physiological changes in the lecture module on the autonomic nervous system.
The changes greatly enhance the body’s ability to fight or take flight.
The fight or flight response is relatively short in duration.
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115. The Body’s Response to a Stressor
The body’s various homeostatic (physiological) mechanisms function to counteract a stressor.
The internal environment remains within normal limits when a response is successful.
Homeostatic mechanisms may not be sufficient if a stressor is extreme, unusual, or long-lasting.
Prolonged stress can elicit a series of physiological changes known as the resistance reaction or general adaptation syndrome.
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116. Resistance Reaction
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Figure 18.20
The second stage of the stress response is the resistance reaction to severe, prolonged stress.
While a fight or flight response is short-lived, the resistance reaction is initiated and maintained by releasing hormones from the hypothalamus that are longer-lasting.
The releasing hormones from the hypothalamus that are involved in the resistance reaction are CRH, GHRH, and TRH.
CRH = corticotropin releasing hormone
GHRH = growth hormone releasing hormone
TRH = thyrotropin releasing hormone

117. Resistance Reaction (continued)
Corticotropin releasing hormone (CRH) stimulates the anterior pituitary to secrete ACTH.
ACTH stimulates the adrenal cortex to release the glucocorticoid, cor-tisol.
Cortisol stimulates gluconeogenesis, lipolysis, and catabolism—tissues use the glucose, fatty acids, and amino acids to produce ATP for energy and repairing damaged cells.
Cortisol also reduces inflammation.
Gluconeogenesis = glucose synthesis
Lipolysis = metabolic break-down of triglycerides
Catabolism = metabolic breakdown of proteins into amino acids
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Figure 18.20

118. Resistance Reaction (continued)
Growth hormone releasing hormone (GHRH) stimulates the anterior pituitary to secrete human growth hormone (hGH).
hGH stimulates glycogenolysis and lipolysis by acting through insu-lin-like factors.
Thyrotropin releasing hormone (TRH) stimulates the anterior pituitary to secrete thyroid stimulating hormone (TSH).
TSH stimulates secretion of thyroid hormones (T3 and T4) to increase the use of glucose for ATP production.
Glycogenolysis = metabolic breakdown of glycogen to glucose.
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Figure 18.20

119. Outcomes
The resistance reaction helps the body to continue combating a stressor after the shorter-lived, fight or flight response has ended.
If the resistance reaction is successful in responding to a stressor, the body returns to normal.
If the resistance reaction fails to combat the stressor, the body can enter a state of exhaustion.
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120. Prolonged Exposure
Prolonged exposure to cortisol and the other hormones involved in the resistance reaction can result in:
Wasting-away of skeletal muscle
Suppression of the immune system
Ulcerations of the digestive tract
Failure of pancreatic beta cells that secrete insulin
These pathological changes can persist after the stressor has been removed.
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121. Resistance Reaction and Disease
A prolonged or severe resistance reaction can increase the likely-hood of some diseases by suppressing the immune system.
Stress-related disorders include gastritis, ulcerative colitis, irritable bowel syndrome, rheumatoid arthritis, migraine headaches, anxiety, and depression.
Stress has also been implicated in a number of other diseases and disorders.
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122. Aging

123. Aging Effects
Endocrine glands decrease in tissue mass as a person ages, although their performance may or may not diminish.
The production of hGH by the anterior pituitary decreases, which is one cause of age-related atrophy of skeletal muscle.
The thyroid gland secretes less T3 and T4, reducing metabolic rate and increasing body fat.
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124. Aging Effects (continued)
The blood level of parathyroid hormone (PTH) rises, possibly due to an inadequate dietary intake of calcium.
Calcitriol and calcitonin levels are lower in older persons, and in com-bination with increased PTH, promote an age-related decrease in bone density and mass.
The loss of bone mass can result in osteoporosis and increased risk of bone fractures in seniors.
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125. Aging Effects (continued)
The adrenal glands develop increasingly more fibrous tissue, and the cortex produces less cortisol and aldosterone.
Production of epinephrine and norepinephrine by the medulla remains at near-normal levels.
The pancreas releases insulin more slowly, and the cell receptors are less sensitive to glucose.
Blood glucose levels increase faster and return to normal less slowly than in younger persons.
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126. Aging Effects (continued)
The thymus begins to decease in size after puberty, and its tissue is increasingly replaced with adipose and areolar connective tissues.
The ovaries decrease in size with age, and no longer respond as well to FSH and LH (eventually menopause occurs).
Decreasedestrogen levels with menopause can lead to osteoporosis, high blood cholesterol, and atherosclerosis.
Although testosterone production in the testes decreases with age, many older males still produce healthy sperm, although the sperm count may diminish.
Atherosclerosis = build-up of fatty deposits, or atheromas, inside the arterial walls, thus narrowing the arteries (this is one aspect of cardiovascular disease know as arteriosclerosis).
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