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Neuroendocrine Exam 3 > Hypothalamic- Pituitary Relationships And Biofeedback 1 > Flashcards

Hypothalamic- Pituitary Relationships And Biofeedback 1 Flashcards

1
Q

Adenohypophysis

Neurohypophysis

A

AP (epithelial)

PP (neural)

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2
Q

How if the hypothalamus and pituitary connected

A

Hypophyseal stalk

Lesion in this= no hormones can travel to the AP

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3
Q

Tumors of the pituitary

A

Pressure on the optic nerves
Visual problems
Dizziness

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4
Q

How the hypothalamus and PP are connected

A

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

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5
Q

How is the hypothalamus and AP connected

A
  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
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6
Q

Target for AP Hormones

A

Thyroid gland

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7
Q

Target tissues for PP

A

Kidney

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8
Q

3 Hormone Families of AP

A
  1. ACTH : Corticotrophs——-> ACTH
  2. TSH, FSH, LH : Thyrotrophs——-> TSH and Gonadotrophs—-> FSH and LH
  3. GH, PROLACTIN : Somatotrophs ——-> GH and Lactotrophs—-> PRO
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9
Q

Hypothalamus releases what that goes to what cell in the AP

A
  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
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10
Q

Tropic H

Releasing H

A

Pituitary

Hypothalamus

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11
Q

Primary Endocrine Disorder

A

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

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12
Q

Secondary Endocrine Disorder

A

Altered level of Hormone due to disruption of the Pituitary gland

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13
Q

Tertiary Endocrine Disorder

A

Altered levels of Hormones due to defect in the hypothalamus

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14
Q

Long loop regulation

A

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

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15
Q

Short loop inhibition

A

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

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16
Q

The HPG axis:

Negative Feedback Pathway in OVARY

A
  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
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17
Q

The HPG axis:

Negative feedback loop of TESTES

A
  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
18
Q

GnRH I released how

A

In a pulsatile manner, to stimulate the AP

Effected by low energy and low body fat and depression

19
Q

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

A
  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
20
Q

Acromegaly

A

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….

21
Q

Growth Hormone axis

A

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)

22
Q

Somatomedin C

A

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

Is IGF-1

23
Q

Highest level of GH release and some peaks

A

HIGHEST: during sleep after midnight

Exercise, early morning

Stress and sleep disturbances can effect this

24
Q

How if GH released throughout life

A

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

25
Q

Acute stimulation of GH release

A
  1. Fasting and Hunger
  2. Hypoglycemia
  3. Puberty Hormones
  4. Exercise
  5. Sleep
  6. Stress
26
Q

GH Direct actions

A

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

27
Q

GH Indirect effects

A

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

28
Q

Gigantism

A

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

29
Q

Negative feedback of GH axis

A
  1. GH ——I GHRH

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

30
Q

GH Insensitivity

A 
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

31
Q

Secondary deficiency of GH

A

GH is not released from AP

  1. No IGF-1 produced
  2. No growth and increased hypertrophy
32
Q

Tertiary GH Deficiency

A

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

33
Q

GH in the FED state

A

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

34
Q

GH in Unfavorable or LOW PROTIEN

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

=weight gain

35
Q

GH in FASTING state or LOW CARBS

A 
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

36
Q

Increase prolactin when and how is it secreted

A

5th week of pregnancy
Pulsatile
Tonically Inhibited by Dopamine

37
Q

PROLACTIN function and main regulator

A

Stimulate Growth of breasts, increase milk production

——I GnRH causing no menstrual cycle

Dopamine and negative inhibitor of AP release of PLA

38
Q

Oxytocin secretion and pathway

A

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

39
Q

Function of OXYTOCIN in breasts

A

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

40
Q

PROLACTIN

A

PROLACTIN= MILK PRODCTION

41
Q

Function of OXYTOCIN in uterus

A

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

Neuroendocrine Exam 3 (18 decks)

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