Hypothalamus and Pituitary DSA

Question 1

Hormones of the anterior pituitary

Answer 1

TSH, FSH, LH, growth hormone, prolactin, ACTH, Melanocyte-stimulating hormone

Question 2

Hormones of the posterior pituitary

Answer 2

Oxytocin, Vasopressin or ADH

Question 3

Embryologic origin of of the anterior pituitary

Answer 3

primitive foregut

Question 4

Embryologic origin of the posterior pituitary

Answer 4

neural tissue

Question 5

Connections between the hypothalamus and the posterior lobe of the pituitary

Answer 5

= neural.
Posterior pituitary is a collection of nerve axons whose cell bodies are located in the hypothalamus. Thus, hormones secreted by the posterior lobe (ADH and oxytocin) = neuropeptides: peptides released from neurons.

Question 6

The relationship between the hypothalamus and the posterior pituitary

Answer 6

a hormone-secreting neuron has its cell body in the hypothalamus and its axons in the posterior lobe of the pituitary.

Question 7

What is the anterior pituitary composed of?

Answer 7

primarily endocrine cells.

Question 8

The nature of the relationship between the hypothalamus and the anterior pituitary

Answer 8

is both neural and endocrine (in contrast to the posterior lobe, which is only neural).

Question 9

blood supply between the hypothalamus and the anterior pituitary

Answer 9

linked directly by the hypothalamic-hypophysial portal blood vessels, which provide most of the blood supply to the anterior lobe.

The blood supply of the anterior pituitary differs from that of other organs: Most of its blood supply is venous blood from the hypothalamus, supplied by the long and short hypophysial portal vessels.

Question 10

two important implications of the portal blood supply to the anterior lobe of the pituitary:

Answer 10

(1) The hypothalamic hormones can be delivered to the anterior pituitary directly and in high concentration, and (2) the hypothalamic hormones do not appear in the systemic circulation in high concentrations. The cells of the anterior pituitary, therefore, are the only cells in the body to receive high concentrations of the hypothalamic hormones.

Question 11

TRH–TSH–thyroid hormone system.

Answer 11

TRH is synthesized in hypothalamic neurons
–> secreted in the median eminence of the hypothalamus, –> capillaries and then hypophysial portal vessels –> anterior lobe of the pituitary, where it stimulates TSH secretion.
TSH –> systemic circulation –> thyroid gland, where it stimulates secretion of thyroid hormones.

Question 12

Regulation of GH release

Answer 12

Growth hormone is secreted in a pulsatile pattern, with bursts of secretion occurring approximately every 2 hours. The largest secretory burst occurs within 1 hour of falling asleep (during sleep stages III and IV). The bursting pattern, in terms of both frequency and magnitude, is affected by several agents that alter the overall level of growth hormone secretion.

Question 13

Stimulatory factors for GH release

Answer 13

Decreased glucose concentration
Decreased free fatty acid concentration
Arginine
Fasting or starvation
Hormones of puberty (estrogen, testosterone)
Exercise
Stress
Stage III and IV sleep
α-Adrenergic agonists

Question 14

factors inhibiting GH release

Answer 14

Increased glucose concentration
Increased free fatty acid concentration
Obesity
Senescence
Somatostatin
Somatomedins
Growth hormone
β-Adrenergic agonists
Pregnancy

Question 15

GH levels- how they change over the span of a normal lifetime

Answer 15

The rate of secretion increases steadily from birth into early childhood. During childhood, secretion remains relatively stable. At puberty, there is an enormous secretory burst, induced in females by estrogen and in males by testosterone. The high pubertal levels of growth hormone are associated with both increased frequency and increased magnitude of the secretory pulses and are responsible for the growth spurt of puberty. After puberty, the rate of growth hormone secretion declines to a stable level. Finally, in senescence, growth hormone secretory rates and pulsatility decline to their lowest levels.

Question 16

Two pathways of growth hormone regulation from the hypothalamus

Answer 16

GHRH and Somatostatin (SRIF)

Question 17

GHRH

Answer 17

GHRH acts directly on somatotrophs of the anterior pituitary to induce transcription of the growth hor­mone gene and, thereby, to stimulate both synthesis and secretion of growth hormone. In initiating its action on the somatotroph, GHRH binds to a membrane receptor, which is coupled through a G s protein to both adenylyl cyclase and phospholipase C. Thus, GHRH stimulates growth hormone secretion by utilizing both cAMP and IP 3 /Ca 2+ as second messengers.

Question 18

Somatostatin ( somatotropin release–inhibiting hormone, SRIF

Answer 18

) is also secreted by the hypothalamus and acts on the somatotrophs to inhibit growth hormone secretion. Somatostatin inhibits growth hormone secretion by blocking the action of GHRH on the somatotroph. Somatostatin binds to its own membrane receptor, which is coupled to adenylyl cyclase by a G i protein, inhibiting the generation of cAMP and decreasing growth hormone secretion.

Question 19

actions of growth hormone

Answer 19

♦ Diabetogenic effect. Growth hormone causes in­sulin resistance and decreases glucose uptake and utilization by target tissues such as muscle and adipose tissue. These effects are called “diabetogenic” because they produce an increase in blood glucose concentration, as occurs when insulin is lacking or when tissues are resistant to insulin (e.g., diabetes mellitus). Growth hormone also increases lipolysis in adipose tissue. As a consequence of these metabolic effects, growth hormone causes an increase in blood insulin levels.
♦ Increased protein synthesis and organ growth. In virtually all organs, growth hormone increases the uptake of amino acids and stimulates the synthesis of DNA, RNA, and protein. These effects account for the hormone’s growth-promoting actions: increased lean body mass and increased organ size. As noted, many of the growth effects of growth hormone are mediated by somatomedins.
♦ Increased linear growth. The most striking effect of growth hormone is its ability to increase linear growth. Mediated by the somatomedins, growth hormone alters every aspect of cartilage metabolism: stimulation of DNA synthesis, RNA synthesis, and protein synthesis. In growing bones, the epiphyseal plates widen and more bone is laid down at the ends of long bones. There also is increased metabolism in cartilage-forming cells and proliferation of chondrocytes.

Question 20

Prolactin

Answer 20

Prolactin is the major hormone responsible for milk production and also participates in the development of the breasts. In nonpregnant, nonlactating females and in males, blood levels of prolactin are low. However, during pregnancy and lactation, blood levels of prolactin increase, consistent with the hormone’s role in breast development and lactogenesis (milk production).

Question 21

regulation of prolactin secretion

Answer 21

There are two regulatory paths from the hypothalamus, one inhibitory (via dopamine, which acts by decreasing cAMP levels) and the other stimulatory (via TRH).

Question 22

ADH

Answer 22

ADH (or vasopressin) is the major hormone concerned with regulation of body fluid osmolarity. ADH is secreted by the posterior pituitary in response to an increase in serum osmolarity. ADH then acts on the principal cells of the late distal tubule and collecting duct to increase water reabsorption, thus decreasing body fluid osmolarity back toward normal.

Question 23

factors that stimulate ADH

Answer 23

Increased serum osmolarity
Decreased ECF volume
Angiotensin II
Pain
Nausea
Hypoglycemia
Nicotine
Opiates
Antineoplastic drugs

Question 24

factors that suppress ADH

Answer 24

Decreased serum osmolarity
Ethanol
α-Adrenergic agonists
Atrial natriuretic peptide (ANP)

Question 25

actions of ADH

Answer 25

Increase in water permeability. The major action of ADH is to increase the water permeability of principal cells in the late distal tubule and collecting duct. The receptor for ADH on the principal cells is a V 2 receptor, which is coupled to adenylyl cyclase via a G s protein. The second messenger is cAMP, which, via phosphorylation steps, directs the insertion of water channels, aquaporin 2 ( AQP2 ) , in the luminal membranes. The increased water permeability of the principal cells allows water to be reabsorbed by the collecting ducts and makes the urine concentrated, or hyperosmotic (see Chapter 6 ). ♦ Contraction of vascular smooth muscle. The second action of ADH is to cause contraction of vascular smooth muscle (as implied by its other name, vasopressin). The receptor for ADH on vascular smooth muscle is a V 1 receptor, which is coupled to phospholipase C via a G q protein. The second messenger for this action is IP 3 /Ca 2+ , which produces contraction of vascular smooth muscle, constriction of arterioles, and increased total peripheral resistance.

Question 26

Central diabetes insipidus

Answer 26

is caused by failure of the posterior pituitary to secrete ADH. In this disorder, circulating levels of ADH are low, the collecting ducts are impermeable to water, and the urine cannot be concentrated. Thus, persons with central diabetes insipidus produce large volumes of dilute urine, and their body fluids become concentrated (e.g., increased serum osmolarity, increased serum Na + concentration). Central diabetes insipidus is treated with an ADH analogue, dDAVP.

Question 27

nephrogenic diabetes insipidus,

Answer 27

the posterior pituitary is normal but the principal cells of the collecting duct are unresponsive to ADH due to a defect in the V 2 receptor, G s protein, or adenylyl cyclase. As in central diabetes insipidus, water is not reabsorbed in the collecting ducts and the urine cannot be concentrated, resulting in excretion of large volumes of dilute urine. As a result, the body fluids become concentrated and the serum osmolarity increases. In contrast to central diabetes insipidus, however, ADH levels are elevated in nephrogenic diabetes insipidus due to stimulation of secretion by the increased serum osmolarity. Nephrogenic diabetes insipidus is treated with thiazide diuretics. The usefulness of thiazide diuretics in treating nephrogenic diabetes insipidus is explained as follows: (1) Thiazide diuretics inhibit Na + reabsorption in the early distal tubule. By preventing dilution of the urine at that site, the final, excreted urine is less dilute (than it would be without treatment). (2) Thiazide diuretics decrease glomerular filtration rate; because less water is filtered, less water is excreted. (3) Thiazide diuretics, by increasing Na + excretion, can cause a secondary ECF volume contraction. In response to volume contraction, proximal reabsorption of solutes and water is increased; because more water is reabsorbed, less water is excreted.

Question 28

SIADH

Answer 28

excess ADH is secreted from an autonomous site (e.g., oat cell carcinoma of the lung ). High levels of ADH cause excess water reabsorption by the collecting ducts, which dilutes the body fluids (e.g., decreases plasma osmolarity and Na + concentration). The urine is inappropriately concentrated (i.e., too concentrated for the serum osmolarity). SIADH is treated with an ADH antagonist such as demeclocycline or water restriction.

Question 29

Oxytocin

Answer 29

Oxytocin produces milk “letdown” or milk ejection from the lactating breast by stimulating contraction of myoepithelial cells lining the milk ducts.

Question 30

oxytocin stimulatory factors

Answer 30

Suckling Sight, sound, or smell of the infant Dilation of the cervix Orgasm

Question 31

oxytocin inhibitory factors

Answer 31

Opioids (endorphins)

Question 32

actions of oxytocin

Answer 32

♦ Milk ejection. Prolactin stimulates lactogenesis. The milk is stored in mammary alveoli and small milk ducts. The major action of oxytocin is to cause milk letdown. When oxytocin is secreted in response to suckling or to conditioned responses, it causes contraction of myoepithelial cells lining these small ducts, forcing the milk into large ducts. The milk collects in cisterns and then flows out through the nipple. ♦ Uterine contraction. At a very low concentration, oxytocin also causes powerful rhythmic contractions of uterine smooth muscle. Although it is tempting to speculate that oxytocin is the critical hormone involved in parturition, it is unclear whether oxytocin plays a physiologic role in either the initiation of or the normal course of labor. However, this action of oxytocin is the basis for its use in inducing labor and in reducing postpartum bleeding.