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..3 > Hypothalamic Pituitary Relationships And Biofeedback Pt. 1 > Flashcards

Hypothalamic Pituitary Relationships And Biofeedback Pt. 1 Flashcards

1
Q

What will a tumor of the pituitary gland cause?

A

Will put pressure on optic nerves

Can present w/ visual problems, dizziness

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2
Q

How is the posterior pituitary gland connected to the Hypothalamus?

A

Via hypophyseal stalk

And via neural signal hypothalamic-hypophyseal tract

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3
Q

What makes up the

Hypothalamic-hypophyseal tract?

A

Axons from SON and VPN carrying ADH and Oxytocin

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4
Q

What is the anterior pituitary gland?

A

Collection of endocrine cells derived from primitive foregut

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5
Q

What does the anterior pituitary secrete?

A 
GH
FSH
LH
ACTH
TSH
MSH
Prolactin
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6
Q

How is the ANterior pituitary connected to the hypothalamus?

A

Via hypothalamic-hypophyseal portal blood vessels

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7
Q

What is in the ACTH family?

When is it released?

A

corticotrophs (ACTH)

When when CRF comes from hypothalamus

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8
Q

What is CRF?

A

Corticotropin releasing factor

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9
Q

What is in the TSH, FSH, LH family?

A

Thyrotrophs -TSH

Gonadotrophs- FSH and LH

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10
Q

What is TSH released from Thyrotroph cells?

A

When TRH come from hypothalamus

Thyrotrophin releasing hormone

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11
Q

When are FSH and LH released from Gonadotroph cells?

A

When GnRH comes from hypothalamus

Gonadotrophin releasing hormone

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12
Q

What is in the GH, Prolactin family?

A

Somatotropin - GH

Lactotrophs - Prolactin

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13
Q

What releases GH from Somatotropic cells?

A

When GHRH comes from hypothalamus

Growth hormone releasing hormone

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14
Q

What will inhibit the release of GH from somatotropic cells?

A

Inhibited when Somatostatin comes from hypothalAmus

Somatostatin = growth hormone inhibiting hormone

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15
Q

What is Prolactin released from lactotrophic cells?

A

When TRH is elevated
(Thyrotrophin releasing hormone)

Otherwise it is ALWAYS INHIBITED

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16
Q

What inhibits the release of Prolactin from Lactotrophic cells?

A

When Prolactin-inhibiting factor (PIF) comes from the hypothalamus

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17
Q

What is a primary endocrine disorder?

A

◦ Low or high levels of hormone due to defect @ PERIPHERAL ENDOCRINE GLAND

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18
Q

What is a secondary endocrine disorder?

A

◦ Low or high levels of hormone due to Defect @ PITUITARY GLAND

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19
Q

What is a tertiary endocrine disorder?

A

◦ Low or high levels of hormone due to Defect @ hypothalamus

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20
Q

What are the different HP axes?

A

HP-gonad

HP-liver

HP-prolactin

HP-thyroid

HP-adrenal

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21
Q

In the HP-Gonad axis what is the hypothalamic hormone?

A

GnHR

Gonadotrophin releasing hormone

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22
Q

In the HP-Gonad axis, what are the pituitary hormones released?

A

LH (lutenizing hormone)

FSH (Follicle stimulating hormone)

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23
Q

What can inhibit the release of GnHR?

A

◦ Extreme energy deficits
(anorexia nervosa or starvation)

◦ Extreme exercise

◦ Depression

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24
Q

What characterizes the release of GnRH?

A

Pulsatile release

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25
Q

What is the function of FSH and LH?

A

‣ Promotes Estrogen and progesterone secretion in Females

‣ promotes Testosterone production in Males

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26
Q

A normal men’s rural cycle is dependent upon what?

A

LH

FSH

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27
Q

What is the target of LH?

In males?

Females?

A

Males:
LH—> Leydig cell —> testosterone

Females:
LH —> Theca cell —> Androgens

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28
Q

What is the target of FSH?

In males?

Females?

A

Males:
FSH —> Sertoli cells —> Androgen binding protein & inhibin

Females:
FSH —> Granulosa cells —> Progestins, estrogens, inhibin

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29
Q

What will androgen binding protein do?

A

Bind testosterone and do spermatogenesis

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30
Q

How is the HP-gonad axis regulated in males?

A

‣ Testosterone from Leydig cell will feedback = Inhibit Pituitary LH and Hypothalamus GnRH

‣ Inhibin from Sertoli cell will feed back and inhibit pituitary FSH

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31
Q

How is the HP-gonad axis regulated in women?

A
  • Progesterins & Estogens inhibit pituitary LH and FSH and Hypothalmaus GnRH
  • Inhibin from Granulosa Cell inhibits pituitary FSH
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32
Q

What produces GH?

A

Somatotropes

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33
Q

What are the direct targets of GH?

A

Liver and bone

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34
Q

What is the pathway for Growth Homrone?

A

GH —> GH R. —> jak stat signaling

35
Q

What inhibits GH?

A

Somatostin (GHIH)

IGF-1

36
Q

What will stimulate the release of GH?

A 
‣ Fasting/hunger/starvation
		‣ Hypoglycemia
		‣ Hormones of puberty
		‣ Exercise
		‣ Sleep 
		‣ Stress
37
Q

What are the 3 functions of GH?

A

Growth (Hypertrophy of cells)

Cell reproduction (Hyperplasia)

Metabolism

38
Q

What are the hypothalamic hormones secreted in the Growth Hormone pathway?

A

Growth hormone releasing hormone (GHRH)

GHIH (will inhibit release of GH from anteiror pit.)

39
Q

What will act as negative feedback to the Growth Hormone Releasing HORmone in the Hypothalamus?

A

Growth hormone

40
Q

In the Growth hormone pathway, what does the Liver secrete?

A

Insulin-like growth factor (IGF-1)

41
Q

What is the function of IGF-1?

What is another name for it?

A

Stimulates hypertorphy and hyperplasia

Somatomedins C

42
Q

What are the feedback mechanisms of IGF-1?

A

+ to GHIH

  • to GH
43
Q

If the release of GHRH is defective, what is the tx?

What kind endocrine disorder is this?

A

Soma relain

Tertiary endocrine disorder (defect @ hypothalamus)

44
Q

If GH is too low, what is the treatment?

What kind endocrine disorder is this?

A

Somatotropin
Somatrem

Secondary endocrine disorder (pituitary defective)

45
Q

If the liver fails to release IGF-1 when stimulated by GH, what is the treatment?

A

Mecasermin

46
Q

What could cause the liver to not release IGF-1?

What kind endocrine disorder is this?

A

GH deficiency

GH abs

Primary endocrine disorder

47
Q

If you are in a Fed state, what happens to IGF-1 and GH?

What are the results?

A

Increased carbs and proteins —> GH

GH —> liver —> IGF-1

Mitogenesis, lypolysis, differentiation

48
Q

What will a fed state, cause in bone?

A

‣ Osteoblasts production
‣ Collagen production
‣ Bone matrix production

49
Q

What will happen to IGF-1 and GH, if you are in FED state but with NO Protein?

Results?

A

Increased carbs —> insulin available

But no AAs available

GH = INHIBITED
Liver —X—> IGF-1

Lipogenesis, carb storage (weight gain)

50
Q

What happens to IGF-1 and GH, if you are in FASTING STATE?

Causes?

Results?

A

Decrease carbs —> inadequate insulin

Increased use of Proteins —> AAs available

Causes peripheral metabolism to use LIPIDS as ENERGY source now

Lyolysis, ketogenic metabolism, diabetogenic (insulin insensitivity)

51
Q

How does GH promote lipolysis but also promote insulin insensitivity?

A

Raises blood glucose by DECREASING peripheral glucose uptake

Stimulates hepatic gluconeogenesis

52
Q

How does GH have a Diabetogenic effect?

A

Decreased glucose uptake and utilization by target tissues

Increases lipolysis in adipose tissue

Increases blood insulin levels = raises blood glucose levels

—> insulin resistance

53
Q

How does GH increase protein synthesis and organ grwoth?

A

Increase uptake of AAs

Stimulates synthesis of DNA, RNA, and proteins

(Mediated by IGF-1)

54
Q

How does GH increase linear growth?

A

Increases metabolism in cartilage forming cells and chondrocyte proliferation

Thru stimulating DNA, RNA, and Protein synthesis (mediated by IGF-1)

55
Q

When is GH primarily released?

What can mess w/ GH secretioN?

A

During sleep

Sleep disturbances

56
Q

When will GH peak during the day?

A

W/ exercise

57
Q

When will GH have its peak in life?

A

During puberty

58
Q

What can cause a GH deficiency?

A
  • decreased secretion of GHRH due to hypothalamic dysfunction
  • Decreased GH secretion
  • Failure to generate somatomedins
  • GH or somatomedin resistance (deficiency of receptors)
59
Q

What can cause a GH excess?

A

• Grwoth hormone secreting pituitary adenoma

60
Q

What are the consequences of GH excess

BEFORE puberty?

AFTER puberty?

A

Before = gigantism

After = acromegaly

61
Q

What is acromegaly?

A

◦ Rare disease
◦ Characterized by xs growth of soft tissue, cartilage, & bone in face, hands and feet
◦ Develop gradually

62
Q

What is acromegaly caused by?

A

◦ Caused by prolonged and excessive secretion of Growth Hormone (GH) in adult life AFTER closure of bone epiphyses

63
Q

What is the test for Acromegaly?

What will be elevated?

A

‣ Evaluated serum GH and IGF-1 levels

‣ Failure to suppress GH production in response to an oral load of glucose

‣ Pituitary enlargement on MRI

64
Q

When is secretion of prolactin increased?

A

5th week of pregnancy

65
Q

What is the unique characteristic about Prolactin secretion?

A

◦ PRL is under tonic inhibition by hypothalamic dopamine

66
Q

What is the function of Prolactin?

A

Stimulate and maintain lactation

Suppresses GnRH
• Thus inhibiting LH and FSH
◦ Decreases reproductive function
◦ Suppresses sexual drive

67
Q

What are the stimulatory factors for PRL secretion?

A 
‣ Pregnancy (estrogen) 
		‣ Breast-feeding (Suckling)
		‣ Sleep
		‣ Stress
		‣ TRH
68
Q

What are the inhibitory factors for PRL secretion?

A

‣ Dopamine
‣ Dopamine agonists
‣ Somatostatin (GHIH)
‣ Prolactin via negative feedback

69
Q

What is prolactinoma caused by?

Sxs?

A

pituitary adenomas (mostly causes Prolactinoma (60%))

Sxs related to hormones action on body (suppression of GnRH - no periods?)

70
Q

What hyperpituitarism cause?

GH, PRL, LH & FSH, ACTH, TSH

A
  • Xs of GH = acromegaly/gigantism
  • Xs of PRL = prolactinoma
  • XS of LH and FSH = non functioning adenoma
  • XS of ACTH (cortisol) = Cushing’s Disease
  • XS of TSH = Secreting adenoma
71
Q

What can hypopituitarism cause?

GH, FSH/LH, TSH, ACTH, ADH

A

‣ GH = kids short, adults no effect

‣ FSH/LH = infertility, hypogonadism in males and females (reduced sperm count, menstrual irregularity)

‣ TSH = hypothyroidism

‣ACTH = loss of pigementation, hypoadrenalism

‣ ADH = Diabetes insipidis

72
Q

What can cause hypopituitarism?

A

Brain damage

Pituitary tumors

Non pituitary tumors (Craniopharyngioma)

Infections

Sheehan syndrome

Aids

Pitutiary hyplasia/aphasia

Genetic disordes

73
Q

What is Sheehan syndrome?

Results in?

A

In pregnancy

Pitutiary enlarged, vulnerable to infarction

Results: HYPO-pituitarism

74
Q

What makes oxytocin?

A

Paraventricular Nucleus of the HYpothalamus

Dennis was wroooooong

75
Q

Where are the cell bodies of ADH neurons?

A

In the SON nuclei of the hypothalamus

76
Q

Where are the cell bodies of Oxytocin neurons?

A

In Paraventricular nucleus of hypothalamus

77
Q

How is oxytocin secreted?

Where is it secreted to?

A

In hypothalmaus, pro-oxyphysin is cleaved and packed into vesicles

Travels via hypothalamic-hypophyseal tract to posterior pituitary

To breast and uterus

78
Q

What are the 2 functions of oxytocin?

A
  1. Milk ejection

2. Uterine contraction

79
Q

What produces breast milk? What ejects breast milk?

A
  1. Prolactin

2. Oxytocin

80
Q

What is Milk letdown?

Stimulated by?

A

Oxytocin stimulates contraction of myoepithelial cells lining milk ducts to eject milk

81
Q

What is the stimulus for milk ejection?

A

Suckling

Sight/sound/smell of infant

82
Q

What is the stimulus for uterine contraction by oxytocin?

A

Dilation of cervix or organism

83
Q

What is pitocin?

A

Synthesized Oxytocin that can be administered to induce labor

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