Hypothalamic- Pituitary Relationships And Biofeedback 1

Question 1

Adenohypophysis

Neurohypophysis

Answer 1

AP (epithelial)

PP (neural)

Question 2

How if the hypothalamus and pituitary connected

Answer 2

Hypophyseal stalk

Lesion in this= no hormones can travel to the AP

Question 3

Tumors of the pituitary

Answer 3

Pressure on the optic nerves
Visual problems
Dizziness

Question 4

How the hypothalamus and PP are connected

Answer 4

The nerve cell bodies are in the hypothalamus (SON and PVN) and send vesicles of oxytocin and ADH down the axon traveling through the hypophyseal stalk and into the PP,
The PP has capillaries inside that the ADH and O are released around and absorbed into the blood

Question 5

How is the hypothalamus and AP connected

Answer 5

1. The nerve cell bodies and axons are all in the hypothalamus and make the H.1 and release it to the Hypothalamc-Hypophyseal portal system right on the edge of the hypothalamus
2. The H-H portal system is blood vessels that then travel from the Hypothalamus to the AP and release the H1. there
3. The cells of the AP react to H1 and release H2 which is absorbed by the blood

Question 6

Target for AP Hormones

Answer 6

Thyroid gland

Question 7

Target tissues for PP

Answer 7

Kidney

Question 8

3 Hormone Families of AP

Answer 8

1. ACTH : Corticotrophs——-> ACTH
2. TSH, FSH, LH : Thyrotrophs——-> TSH and Gonadotrophs—-> FSH and LH
3. GH, PROLACTIN : Somatotrophs ——-> GH and Lactotrophs—-> PRO

Question 9

Hypothalamus releases what that goes to what cell in the AP

Answer 9

1. TRH —-> Thyrotrophs
2. CRF —-> Corticotrophs
3. GnRH—-> Gonadotrophs
4. GHRH—-> Somatotrophs
5. Somatostatin (GHIH) —-> inhibits Somatotrophs
6. PIF (dopamine)—-> inhibits Lactotrophs
7. TRH (elevated)—-> Lactotrophs

Question 10

Tropic H

Releasing H

Answer 10

Pituitary

Hypothalamus

Question 11

Primary Endocrine Disorder

Answer 11

Altered levels of hormones due to a defect in the Peripheral gland
(EX: Thyroid gland)

Question 12

Secondary Endocrine Disorder

Answer 12

Altered level of Hormone due to disruption of the Pituitary gland

Question 13

Tertiary Endocrine Disorder

Answer 13

Altered levels of Hormones due to defect in the hypothalamus

Question 14

Long loop regulation

Answer 14

The hormone X released from the peripheral gland inhibits the pituitary gland (from releasing XTH) or the hypothalamus (from releasing XRH)

Question 15

Short loop inhibition

Answer 15

The hormone released from the Pituitary gland (XTH) inhibits the hypothalamus (from releasing the XRH)

Question 16

The HPG axis:

Negative Feedback Pathway in OVARY

Answer 16

1. GnRH released from the hypothalamus to AP
2. LH and FSH released from AP
3. LH goes to Theca cells—-> Androgens
4. FSH goes to Granulosa cells —-> Estrogen and Progestins
5. Androgens increase Estrogen and Progestins
6. Estrogen and Progestins inhibit Hypothalamus GnRH and AP FSH +LH

Question 17

The HPG axis:

Negative feedback loop of TESTES

Answer 17

1. GnRH released from the hypothalamus to AP
2. LH and FSH released from AP
3. LH goes to Leydig cells—-> Testosterone
4. FSH goes to Sertoli cells —-> Androgen binding protein and Spermatogenesis and inhibin
5. Testosterone increase stimulation of Sertoli cells
6. Testosterone inhibit Hypothalamus GnRH and AP LH
7. Inhibin inhibits the AP FSH

Question 18

GnRH I released how

Answer 18

In a pulsatile manner, to stimulate the AP

Effected by low energy and low body fat and depression

Question 19

The HPG axis:
The positive feedback in the OVARY
(At LH surge and ovulation, as FSH increases and estrogen increased a lot)

Answer 19

1. GnRH released from the hypothalamus to AP
2. LH and FSH released from AP
3. LH goes to Theca cells—-> Androgens
4. FSH goes to Granulosa cells —-> a lot of Estrogen
5. Androgens increase Estrogen
6. HIGH Estrogen stimulates Hypothalamus GnRH and AP FSH +LH

Question 20

Acromegaly

Answer 20

Excess growth of soft tissue, cartilage, bones in hands and feet and face
EXCESSIVE GH AFTER CLOSURE OF BONE EPIPHYSES
causes insulin desensitization causing hyperinsulemia

HTN, Cardiomegaly….

Question 21

Growth Hormone axis

Answer 21

GH = somatotropin
Hypothalamus makes GHRH and GHIH(somatostatin)
AP releases (somatotropin)
Goes to liver and bone, binds to JAKSTAK receptors and cause release of IGF(insulin-like GF) and IGF-1(somatomedin C)

Question 22

Somatomedin C

Answer 22

Inhibits Hypothalamus and AP form releasing GHRH and GH
Also helps growth of adipose, bone, and tissues and repair

Is IGF-1

Question 23

Highest level of GH release and some peaks

Answer 23

HIGHEST: during sleep after midnight

Exercise, early morning

Stress and sleep disturbances can effect this

Question 24

How if GH released throughout life

Answer 24

Increase thought birth and childhood
Huge peak in puberty
Decrease a lot in adulthood and stays steady
And decrease more when you hit senescence

Question 25

Acute stimulation of GH release

Answer 25

1. Fasting and Hunger 2. Hypoglycemia 3. Puberty Hormones 4. Exercise 5. Sleep 6. Stress

Question 26

GH Direct actions

Answer 26

Fix muscle tear or hypertrophy Cause increase in fat breakdown to increase energy for protein synthesis Liver and bone

Question 27

GH Indirect effects

Answer 27

Acts on liver—-> IGF-1—-> proliferation and increase growth all over the body and increase metabolic function

Question 28

Gigantism

Answer 28

EXCESS GH BEFORE CLOSURE OF BONE EPIPHYSES, due to IGF-1 stimulating Long bone growth

Question 29

Negative feedback of GH axis

Answer 29

1. GH ——I GHRH | 2. IGF-1——I GH and ——> GHIH(which inhibits the AP release of GH)

Question 30

GH Insensitivity

Answer 30

``` The Liver is not responsive to GH = the IGF-1 would not be released, so 1. No growth and increased hypertrophy 2. No inhibition of GH and stimulation of GHIH 3. Excess GH production ``` PRIMARY GH DISORDER

Question 31

Secondary deficiency of GH

Answer 31

GH is not released from AP 1. No IGF-1 produced 2. No growth and increased hypertrophy

Question 32

Tertiary GH Deficiency

Answer 32

The Hypothalamus can’t produce GHRH The GH is not release and the IGF-1 not released No growth and atrophy produced

Question 33

GH in the FED state

Answer 33

Increase carbs and increase Blood sugar and high insulin Increase proteins and high AA —-> LIVER MAKES IGF-1 ———> Mitogenesis, Lypolysis, Differentiation In bone makes matrix, collagen, osteoblasts

Question 34

GH in Unfavorable or LOW PROTIEN

Answer 34

``` High carbs, BS, and insulin and low AA ——I GH NO IGF-1 produced 1. Lipogenesis (fat storage) 2. Carbohydrate Storage ``` =weight gain

Question 35

GH in FASTING state or LOW CARBS

Answer 35

``` Hypoglycemic and low insulin and high AA ——>GH increases IGF-1 is produced 1. Lypolysis 2. Ketogenic metabolism 3. Diabetogenic ``` GH causes Lypolysis and also insulin insensitivity

Question 36

Increase prolactin when and how is it secreted

Answer 36

5th week of pregnancy Pulsatile Tonically Inhibited by Dopamine

Question 37

PROLACTIN function and main regulator

Answer 37

Stimulate Growth of breasts, increase milk production ——I GnRH causing no menstrual cycle Dopamine and negative inhibitor of AP release of PLA

Question 38

Oxytocin secretion and pathway

Answer 38

Prepro-oxytocin made in hypothalamus and cleaved in vesicle ——> PRO-OXYTOCIN ——> (by axon of hypothalamic nerve) to PP where it is cleaved again to OXYTOCIN ——> released from vesicle to circulation to uterus and breasts

Question 39

Function of OXYTOCIN in breasts

Answer 39

MILK EJECTION (MILK LETDOWN) = stimulates contraction of myoepithelial cells in the ducts INITIAL STIMULUS to cause oxytocin release= sucking, sight, sound or smell of infant Oxytocin then contracts the myoepithelial cells to ecreate milk PROLACTIN= MILK PRODCTION

Question 40

PROLACTIN

Answer 40

PROLACTIN= MILK PRODCTION

Question 41

Function of OXYTOCIN in uterus

Answer 41

UTERINE CONTRACTION Stimulated initially by dilation or cervix or orgasm Causes oxytocin release—> uterine contraction —> causes more oxytocin release POSITIVE FEEDBACK LOOP