37: Hypothalamic/Pituitary Relations Flashcards

1
Q

Neurohypophysis vs adenohypophysis

A

Neuro: posterior pituitary
Adeno: anterior pituitary

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2
Q

How is the posterior pituitary connected to the hypothalamus?

A

Post pit is a collection of axons whose cell bodies are in the hypothalamus

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3
Q

Two nuclei of the posterior pituitary

A

SON (supraoptic nulcei) and PVN (paraventricular nuclei)

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4
Q

Two neuropeptides secreted by the posterior pituitary

A

ADH, oxytocin

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5
Q

How does ant pit communicate with hypothalamus

A

Neurally and hormonally

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6
Q

Connection between hypothalamus and pituitary gland and what’s inside it

A

Hypophyseal stalk, holds the hypothalamic-hypophyseal portal blood vessels

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7
Q

What can pituitary tumors cause?

A

Pressure on optic nerves -> visual issues and dizziness

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8
Q

Primary, secondary, and tertiary endocrine disorders regarding the HPA axis

A

Primary: targets peripheral gland
Secondary: targets pituitary
Tertiary: targets hypothalamus

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9
Q

GH fluctuation during the day

A

Peaks with exercise and sleep

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10
Q

GH fluctuation throughout lifetime

A

Peak at puberty, moderate amount as an adult, almost none in senescence

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11
Q

Things that stimulate GH production

A
  1. Fasting/hunger/starvation
  2. Hypoglycemia
  3. Puberty hormones
  4. Exercise
  5. Sleep
  6. Stress
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12
Q

Fed state influence on GH

A

Carbs and proteins -> GH produced -> liver produces IGF-1

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13
Q

What is stimulated by GH in fed state?

A

Lipolysis, mitogenesis, differentiation of cells, synthesis of DNA/RNA/proteins

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14
Q

GH action in low protein state

A

GH is inhibited -> no IGF-1 from liver

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15
Q

What happens in low protein state?

A

Lipogenesis, carb storage, weight gain

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16
Q

What happens with GH in a low carb state?

A

GH levels increase -> IGF-1 is produced

17
Q

What is stimulated by a low carb state?

A

Lipolysis, ketogenic metabolism, diabetogenic state

18
Q

Diabetogenic state

A

Insulin sensitivity - increased blood glucose causes insulin resistance, so there is decreased glucose uptake and utilization by target tissues -> increased blood insulin levels

19
Q

Causes of gigantism vs acromegaly

A

Gigantism: excess GH before closure of bone epiphyses
Acromegaly: excess GH after closure of bone epiphyses

20
Q

What occurs in acromegaly?

A

Promotion of growth of deep organs, bones, and cartilage

21
Q

Hormonal cause of gigantism

A

IGF-1 stimulates long bone growth

22
Q

GH insensitivity

A

GH receptors on liver are non-functional -> less IGF-1 -> less negative feedback on GH -> lots of GH produced

23
Q

Secondary deficiency of the HPGH axis: levels of GH and IGF-1

A

Low GH and low IGF-1

24
Q

Tertiary deficiency of the HPGH axis: GHRH, GH, and IGF-1 amounts

A

All three are low

25
Q

What hormone is inhibited by prolactin?

A

GnRH

26
Q

Two major actions of oxytocin

A

Milk ejection, uterine contraction

27
Q

Major stimulus of milk ejection besides oxytocin

A

Suckling, signs/sounds/smells of an infant