Hypothalamic Pituitary Relationships and Biofeedback Pt. 1 Flashcards

1
Q

Describe the parts and structure of the pituitary gland

A

Anterior (epithelial/adenohypophysis)
Posterior (neural/neurohypophysis)
Hypophyseal stalk connects it to hypothalamus

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2
Q

What is the first structure affected by a pituitary tumor? Why?

A

Vision as it puts pressure on the optic nerves

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3
Q

What are the features of the posterior pituitary?

A

Neural. Axons extending into the gland and releases hormones (ADH and oxytocin)

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4
Q

What nuclei control the posterior pituitary?

A

SON (supraoptic) and PVN (paraventricular)

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5
Q

What are the features of the anterior pituitary?

A
  • Neural and hormonal connections (connected to hypothalamus via the hypothalamic-hypophyseal blood vessels)
  • release FLAT PG
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6
Q

Describe how the anterior pituitary communicate via hypothalamic-hypophyseal portal system

A

Hormones are released in high concentrations to tropic cells in AP > AP releases hormones in circulation
-Rapid response = prevents buildup of hormones in the circulation

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7
Q

3 families of hormones of the AP
Corticotrophs
Gonadotrophs
Somatotrophs/lactotrophs

A
  • ACTH (stimulated by CRH)
  • TSH/FSH/LH (stimulated by GnRH)
  • GH/Pro (stimulated by GHRH, TRH)
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8
Q

Which hormones have inhibitory mechanisms of action?

A

GHIH (somatostatin) - prevents GH release by somatotrophs

PIF (dopamine) - prevents prolactin release by lactotrophs

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9
Q

What does primary, secondary and tertiary disorder mean?

A

Primary - problem level of the peripheral gland
Secondary - problem level of the pituitary gland
Tertiary - problem level of the hypothalamus

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10
Q

Draw the HPG (hypothalamus-pituitary-gonad axis)

A

Ok

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11
Q

Regulation and action of the FSH and LH hormones

A

Regulated by the pulsatile release of GnRH (fueled by enough body energy). They promote spermatogenesis and estrogen/progesterone/testosterone release

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12
Q

Acromegaly
Cause
Clinical

A
  • Increased exposure to growth hormone due to pituitary adenoma after puberty after the epiphyseal plates have closed
  • growth of extra bone/soft tissue/cartilage growth
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13
Q

Draw the growth hormone axis

A

Ok

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14
Q

What type of signaling does the GH receptor use?

A

JAK-STAT

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15
Q

At what physiological state is the growth hormone usually secreted?

A

Times of hunger/hypoglycemia

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16
Q

What are the actions of GH as it binds directly to MSK?

A

Hypertrophy of cells
Hyperplasia (make more cells)
Increase metabolism

17
Q

How does GH indirectly cause growth?

A

Stimulates the liver to produce IGF-1 which encourages growth of everythingmajority of its effects are done indirectly

18
Q

What happens if there is insensitivity of receptors to growth hormone (primary)?

A

-High GH in circulation and low IGF-1 production in liver

19
Q

What happens when there is secondary (pituitary level deficiency?)
How would you treat this?

A
Pituitary isn't making the GH and liver isn't making IGF-1. High GHRH
GH replacement (Somatropin, Somatrem, Mecasermin)
20
Q

What happens in tertiary (hypothalamic level) deficiency?

How would you treat this?

A

No release of GHRH from the hypothalamus. Low everything.

Semorelin

21
Q

Gigantism
Cause
Clinical

A

Exposure to excess GH due to pituitary adenoma before epiphyseal plates close (before puberty)
-giant

22
Q

How is the HPG axis working during the fed state (favrable)

A

Adequate insulin and amino acid availability. Liver produces IGF-1 > trigger growth processes

23
Q

How is the HPG axis altered in unbalanced fed state (high carbs low protein)

A

High insulin but low AA availability. Can’t make GH, can’t make IGF-1

24
Q

How is HPG axis altered in unbalanced fed state (low carbs high protein)?

A

IGF-1 produced and triggers growth. Inadequate sugar = use fat as energy and result in lipolysis.
Since sugar is low - stimulate gluconeogenesis and increase blood sugar levels

25
Q

How do you diagnoses someone with excess GH (gigantism/acromegaly?

A

Serum has elevated GH and IGF-1 and fail the oral glucose test (no decrease of GH after oral glucose)
Also pituitary enlargement (adenoma)

26
Q

Describe the fluctuation of GH secretion throughout the day

A

Spike during sleep. During waking hours highest while exercising.

27
Q

What causes stimulation of prolactin secretion?

A
Pregnancy (via estrogen)
Breast feeding (suckling)
Sleep 
Stress
TRH
28
Q

What are pituitary adenomas?

A

Adenomas release extra hormone and release into bloodstream

Result in hyperpituitarism (prolactinoma)

29
Q

What does the posterior pituitary release?

A

Oxytocin and ADH (neuropeptides)

30
Q

In the posterior pituitary, what nuclei controls ADH and Oxytocin?

A
ADH = supraoptic nuclei
Oxytocin = paraventricular nuclei
31
Q

Draw the oxytocin axis

A

Ok

32
Q

How does Oxytocin stimulate milk ejection?

A

Contracts the myoepithelial cells lining milk ducts (stimulated by suckling mostly)

33
Q

How does oxytocin stimulate uterine contraction?

A

Dilation stimulates oxytocin release which stimulates contractions and further dilations. Pitocin induces labor.