Hypothalamic-Pituitary Relationships Flashcards

1
Q

What are the connections between the hypothalamus and posterior pituitary?

LO1

A

hypophysial stalk: physical connection between the hypothalamus and pituitary gland

communication: neural signal. collection of axons in posterior pituitary - cell bodies in hypothalamus

  • Supraoptic nucleus (SON)
  • Paraventricular nucleus (PVN)
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2
Q

What does the posterior pituitary secrete? (From which part of hypothalamus?)

A

ADH (SON)

oxytocin (PVN)

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3
Q

What are the connections between the hypothalamus and anterior pituitary?

LO2

A

neural and hormonal

-connected by hypophysial portal system

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4
Q

How are hormones delivered to the anterior pituitary?

LO2/LO3

A

-directly delivered to the anterior pituitary in high concentrations through the hypothalamic-hypophysial portal system

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5
Q

What is a primary endocrine disorder?

LO4

A

low or high levels of hormone due to defect in the peripheral endocrine gland

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6
Q

What is a secondary endocrine disorder?

LO4

A

low or high levels of hormone due to defect in the pituitary gland

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7
Q

What is a tertiary endocrine disorder?

LO4

A

low or high levels of hormone due to defect in the hypothalamus

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8
Q

What is in the ACTH family?

A

corticotrophs - secrete ACTH

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9
Q

What is in the TSH, FSH, LH family?

A

thyrotrophs - secrete TSH

gonadotrophs - secrete FSH and LH

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10
Q

What is in the prolactin family?

A

somatotrophs - secrete GH

lactotrophs - secrete Pro

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11
Q

Describe the HPA axis

LO5 overview

A
  • corticotrophs in anterior pituitary produce ACTH
  • ACTH is under the stimulatory control of hypothalamus - CRH
  • ACTH targets adrenal gland
  • stress is a regulator of the HPA axis: neurogenic (fear) or systemic (infection, surgery)
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12
Q

HPA axis
major hypothalamic and pituitary hormones

LO5a

A

hypothalamic: CRH

anterior pituitary: ACTH

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13
Q

HPA axis
peripheral target organ

LO5b

A

adrenal gland

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14
Q

HPA axis
peripheral hormone

LO5c

A

cortisol

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15
Q

HPA axis
regulation of the axis

LO5d

A

stress

  • neurogenic (fear)
  • systemic (infection, surgery)
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16
Q

HPT axis
overview

LO6

A

TSH is released by thyrotrophs in the anterior pituitary
-TSH is a glycoprotein hormone

TSH is under the stimulatory control of the hypothalamus: TRH

TSH stimulates thyroid gland

Stress inhibits TRH secretion

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17
Q

HPT axis
major hypothalamic and pituitary hormones

LO6a

A

hypothalamic: TRH

anterior pituitary: TSH

18
Q

HPT axis
peripheral target organ

LO6b

A

thyroid gland

19
Q

HPT axis
peripheral hormones

LO6c

A

T4, T3

20
Q

HPT axis
regulation of the axis

LO6d

A

stress (physical stress, starvation, infection) inhibits TRH secretion

21
Q

HPG axis
overview

LO7

A
  • FSH and LH released by gonadotrophs in anterior pituitary
  • secreted into different secretory granules allowing independent secretion by gonadotrophs
  • FSH and LH are under the stimulatory control of the hypothalamus: GnRH
  • FSH and LH regulate the function of the gonads
22
Q

HPG axis
major hypothalamic and pituitary hormones

LO7a

A

hypothalamic: GnRH

anterior pituitary (gonadotrophs): FSH and LH

23
Q

HPG axis
peripheral target organs

LO7b

A

gonads

24
Q

HPG axis
peripheral hormones

LO7c

A

FSH

males: sperm maturation in Sertoli cells
females: follicular development and estrogen synthesis in ovaries

LH

males: testosterone
females: estradiol, progesterone

25
Q

HPG axis
regulation of the axis

LO7d

A

negative feedback

Prolactin inhibits GnRH

26
Q

Describe the relationship between growth hormone and insulin-like growth factor-1 in regulation of growth

LO8a

A

IGF-1 is a somatomedin that has a positive feedback loop to the hypothalamus to promote somatostatin and a negative feedback loop to the anterior pituitary to inhibit GH.

27
Q

What is the role of GHRH on regulation of GH secretion?

LO8b

A

stimulates

28
Q

What is the role of somatostatin (SRIF) on GH secretion?

LO8b

A

inhibits

29
Q

What is the role of glucose on the regulation of GH secretion?

LO8b

A

inhibits

30
Q

What is the role of insulin-like growth factor 1 (IGF-1) on the regulation of GH secretion?

LO8b

A
  • stimulates somatostatin which inhibits growth hormone.

- therefore, IGF-1 (somatomedin) inhibits the secretion of GH

31
Q

What are the changes of IGF-1 and GH in the fasting state?

LO8c

A

GH is stimulated in the fasting state
-produces an increase in blood glucose = diabetogenic

-more GH = more IGF-1 –> mediates effects of GH

32
Q

What are the metabolic and growth promoting actions of GH?

LO8d

A
  • diabetogenic or anti-insulin effect (insulin resistance and decreased glucose uptake and utilization by target tissues; increases lipolysis in adipose tissue) –> increases blood insulin level
  • increased protein synthesis and organ growth (increases amino acid uptake and stimulates DNA, RNA, and protein synthesis)–> increased lean body mass and increased organ size
  • increased linear growth (mediated by somatomedins, GH stimulates DNA, RNA, and protein syntheis, promotes epiphyseal plate widening, chondrocyte proliferation, and bone formation)
33
Q

Explain how the regulation of prolactin secretion differs from the secretion of most anterior pituitary hormones

LO9

A

hypothalamus secretes dopamine, a catecholamine, (the main regulator of prolactin) which INHIBITS prolactin secretion from the anterior pituitary.
-prolactin stimulates dopamine secretion so that prolactin is inhibited (feedback loop)

-TRH is a minor regulator that stimulates prolactin secretion

34
Q

Describe the production and release of oxytocin from the posterior pituitary

LO10

A

Hypothalamus is made in the paraventricular nucleus of the hypothalamus (cell body of neurons) as prepro-oxyphysin –> cleavage of signal peptide and packaging in vesicles –> pro-oxyphysin –> cleavage of neurophysins and axoplasmic flow in hypothalamic hypophyseal tract (axons) –> posterior lobe of pituitary where stored as oxytocin with NP1 in granules –> oxytocin released into systemic circulation for breast and uterus

35
Q

Describe the synthesis and release of ADH

LO11

A

supraoptic nuclei of hypothalamus (cell body of neurons) prepropressophysin – cleavage of signal peptide and packaging in vesicles –> propressophysin – hypothalamic hypophyseal tract (axon of neurons) cleavage of neurophysins and axoplasmic flow –> posterior lobe of pituitary ADH and NPII in granules –> ADH to systemic circulation for kidney and arterioles

36
Q

What triggers ADH release?

LO12

A
  • low blood pressure sensed by cardiac and aortic baroreceptors (sensory neuron to hypothalamus)
  • low arterial stretch due to low blood volume sensed by atrial stretch receptors (sensory neuron to hypothalamus)
  • increased osmolarity > 280 mOsm sensed by hypothalamic osmoreceptors (interneuron to hypothalamus)
37
Q

Mechanisms of action of ADH on kidney and vasculature

LO13

A

vasculature: V1 receptors –> vasoconstriction
kidney: V2 receptors –> increased reabsorption of water

net result: increased BP and blood volume

38
Q

Pathological changes in ADH secretion in diabetes insipidus
-overview

LO14

A
  • lack of an effect of ADH on the renal collecting duct
  • causes frequent urination
  • large volume of urine is diluted
39
Q

Central DI vs Nephrogenic DI

LO14a

A

central

  • lack of ADH resulting from damage to pituitary or destruction of hypothalamus
  • treatment: desmopressin (drug that prevents water excretion)

nephrogenic

  • kidneys unable to respond to ADH (increased plasma ADH)
  • caused by drugs like lithium or chronic disorders (polycystic kidney disease or sickle cell anemia)
  • desmopressin treatment does not work
40
Q

Impact of water restriction on urine osmolality in central and nephrogenic DI

LO14b

A
  1. allow fluids overnight before test and give breakfast w/out fluids
  2. weigh pt
  3. allow no fluid for 8 hrs. weigh pt every 1-2 hrs. pt empties bladder: measure urine volume and osmolarity. measure plasma osmolarity.
  4. If results suggest DI, allow pt to drink (no more than twice urine volume of perior of fluid deprivation) and administer desmopresin
  5. measure plasma urine osmolarity and urine volume

urine osmolarity will be much closer to normal for central DI with desmopressin

41
Q

Pathophysiological changes in ADH secretion associated wtih SIADH

LO15

A
  • excessive secretion of ADH
  • excessive water retention
  • hypoosmolarity fails to inhibit ADH release
  • low plasma osmolality
  • increase urinary osmolality

SIADH treatment

  • fluid restriction
  • IV hypertonic saline
  • V2 receptor antagonist
  • demeclocycline