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Physiology II Exam 2 (Lauren) > L14 Hypothalamus And Pituitary > Flashcards

L14 Hypothalamus And Pituitary Flashcards

1
Q

What hormones are released from the anterior pituitary?

A

Adrenocorticotropic hormone ACTH

Growth Hormone GH

Thyroid stimulating hormone TSH

Prolactin PRL

Luteinizing hormone LH

Follicle stimulating hormone FSH

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2
Q

What hormones are released from the posterior pituitary?

A

Oxytocin OT

Arginine vasopressin AVP aka Antidiuretic hormone ADH

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3
Q

What is another name for antidiruetic hormone ADH?

A

Arginine vasopressin AVP

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4
Q

What are magnocellular neurons?

A

Large neurons that originate in the hypothalamus that project into the posterior pituitary, where they release their hormones into a capillary bed

(The hormones that are produced by the magnocellular neurons are the final product that get released into the blood!)

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5
Q

Where exactly in the hypothalamus do the magnocellular neurons originate?

A

Paraventricular nuclei

Supraoptic nuclei

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6
Q

What hormones are released from the magnocellular neurons?

A

Oxytocin

AVP aka ADH

NP (Neurophysin)

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7
Q

What are the parvicellular neurons?

A

Neurons that originate in the hypothalamus and extend to a capillary bed in the Median Eminence and release Hypothalamic hormones (releasing or inhibitory)

These hormones then travel down blood vessels into the anterior pituitary where they cause the anterior pituitary to release trophic hormones

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8
Q

What hormones are released into the anterior pituitary by parvicellular neurons?

A

CRH

TRH

GnRH

GHRH

SS (Somatostatin)

DA (dopamine)

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9
Q

What hormones are released by the anterior pituitary into the systemic circulation?

A

ACTH

TSH

LH/FSH

GH

PRL

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10
Q

GHRH causes the release of what hormone from the anterior pituitary?

A

GH

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11
Q

TRH causes the release of what hormones from the anterior pituitary?

A

TSH

Prolactin

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12
Q

What effect does somatostatin have on the anterior pituitary?

A

It INHIBITS the synthesis of GH and TSH

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13
Q

GnRH causes the release of what hormones from the anterior pituitary?

A

LH

FSH

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14
Q

CRH causes the release of what hormone from the anterior pituitary?

A

ACTH

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15
Q

PRF (prolactin releasing Factor) causes the release of what hormone from the anterior pituitary?

A

Prolactin lol

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16
Q

What effect does Dopamine have on the anterior pituitary?

A

It INHIBITS prolactin synthesis

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17
Q

Where are ADH and Oxytocin synthesized?

A

In the cell bodies of the magnocellular neurons

Which are located in the supraoptic and paraventricular nuclei

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18
Q

What is the half life of ADH and Oxytocin?

A

Short, about 8 min

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19
Q

ADH and Oxytocin are (steroid/peptide/amine) hormones

A

Peptides

Which means that when they are synthesized, they start as preprohormones that then get cleaved into prohormones (in the ER) and then get converted to hormones (in the Golgi)

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20
Q

What do neurophysins (NP) do?

A

Bind to ADH or Oxytocin and prevent them from leaving the axon of the neuron before it’s ready to be released

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21
Q

Where do neurophysins (NP) come from?

A

They are released when the precursor hormone is cleaved into ADH or oxytocin

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22
Q

There are two kinds of neurophysins: NP-I and NP-II. Which one binds to ADH and which one binds to Oxytocin?

A

NP-I binds to oxytocin

NP-II binds to ADH

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23
Q

As the precursor hormone travels down the hypothalamic-hypophyseal tract (axon of the magnocellular neuron) it gets cleaved into these three things:

A
  1. ADH or Oxytocin
  2. Nurophysin (NP)
  3. A terminal glycoprotein
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24
Q

Central diabetes insipidus happens when there’s not enough ADH reaching the kidney. Why doesn’t the ADH reach the kidney?

A 
The neurophysin (NP-II) that binds to ADH and keeps it from diffusing out of the axon prematurely is defective.
ADH never reaches the circulation
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25
Q

What does oxytocin do to the uterus and the lactating breast?

A

Uterus: opens cervix and contracts uterus

Lactating breast: milk ejection

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26
Q

Suckling on a lactating breast (or hearing a baby cry or smelling a baby) will cause the release of what hormone?

A

Oxytocin

Which will then cause milk ejection from the nipple

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27
Q

Stretching of the cervix causes the release of what hormone ?

A

Oxytocin

Which then causes more uterus contraction

A POSITIVE FEEDBACK LOOP WHOAAAAAA 🙇‍♀️

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28
Q

What the F does oxytocin do in the heart?

A

The heart synthesizes and has receptors for OT.

When OT is released, it causes ANP/BNP to be released from the cardiomyocytes, and the ANP stimulates the release of nitric oxide from vascular endothelium.

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29
Q

Is there more oxytocin in the heart’s atria or ventricles?

A

3-4x more abundant in atria

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30
Q

What causes the release of OT from the heart?

A

Stretch (increased blood volume)

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31
Q

In what ways can Oxytocin regulate blood pressure?

A
  1. In peripheral arterioles, it induces nitric oxide release, causing vasodilation
  2. In cardiac muscle, it causes the synthesis and release of ANP and NO, causing negative inotropic and chronotropic effects. ANP induces vasodilation of peripheral arterioles.
  3. In the kidney, OT stimulates diuresis and natriuresis
  4. Decreases CRF which leads to decreased cortisol production= less stress hormone
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32
Q

What receptors does ANP bind to?

A

natriuretic peptide A Receptor (NPR-A)

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33
Q

What are the 2 sources of OT that the heart can respond to?

A

Pituitary

Cardiac

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34
Q

What effect does OT have on the heart?

A

Causes nitric oxide synthesis=dilation of coronary vessels

Slows heart rate

Decreases strength of contraction

Increase in glucose uptake

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35
Q

Why would we be interested in giving oxytocin to people with prediabetes?

A

Because OT increases glucose uptake by a GLUT4 mechanism, independent of the insulin pathway

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36
Q

What does this professor prefer to call ADH?

A

AVP

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37
Q

What is this professors name

A

I don’t know

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38
Q

Is this professor a serial killer

A

Probably

39
Q

What causes the release of ADH?

A

Increase in plasma osmolarity

Decrease in blood volume

Angiotensin II

40
Q

What effect will dehydration have on AVP/ADH release?

A

Increase

Dehydration causes hypovolemia and increase in osmolarity

41
Q

Where are the osmoreceptors that detect changes in plasma osmolality?

A

In the anterior hypothalamus and outside the BBB

42
Q

Which happens first: release of AVP/ADH or stimulation of thirst?

A

Release of AVP

43
Q

What effect does AVP/ADH have on the kidney?

A

Causes water reabsorption from the distal tubule and collecting duct

Results in increased plasma volume and decrease in osmolarity

Low urine output

44
Q

Does it take a small or large change in plasma osmolarity to stimulate release of AVP/ADH?

A

VERY SMALL CHANGE

This is a VERY sensitive system

45
Q

A (large/small) change in blood volume will cause the release of ADH/AVP

A

VERY large blood volume decrease is required

8-10% of blood volume must be lost

46
Q

What happens to GH levels as you age?

A

Decrease

47
Q

When do GH levels peak?

A

Puberty

48
Q

With the increase of GH release, the release of _________ also increases

A

IGF-1

49
Q

What time of day does GH secretion peak?

A

During sleep

50
Q

Is GH released in a steady stream?>

A

No, it is released in pulsatile bursts, so hormone levels fluctuate throughout the day, and plasma measurements are not a good reflection of the function of the anterior pituitary

51
Q

Which hormones amplify the secretion of GH in men vs women

A

Men: testosterone

Women: estradiol (premenopausal women have more GH)

52
Q

The pattern and frequency of pulse release is (the same/different) for males and females

A

The same

53
Q

The principal regulators of GH release are:
1.

2.

A
  1. GH-releasing hormone

2. Somatostatin

54
Q

Which cells release GH?

A

Somatotrophs

55
Q

What are the target cells of GH-RH?

A

Somatotrophs

56
Q

What kind of a receptor does GH-RH bind to on a somatotrophs?

A

Gα-s

Causes increase in cAMP

57
Q

What kind of receptor does somatostatin bind to on somatotrophs?

A

Gα-i

Decrease in cAMP

58
Q

What happens when GH-RH binds to a somatotroph

A
  1. Increased Adenylate cyclase activity
  2. Increased cAMP
  3. PKA is activated
  4. PKA phosphroylates CREB
  5. CREB causes the transcription of Pit-1
  6. Pit-1 activates the transcription of the GH gene, causing increased GH levels
  7. Pit-1 also upregulates the GH-RH receptor on the somatotroph
59
Q

What happens when somatostatin binds to a somatotroph?

A

Adenylate Cyclase is inhibited

=no PKA to phosphorylation CREB, no Pit-1 transcription and no GH transcription

60
Q

What things will stimulate GH release?

A

Hypoglycemia

Decreased FFAs

Arginine

Fasting/starvation/exercise

Stress

Sleep

Thyroid hormone

Androgens

Ghrelin

61
Q

What things will inhibit GH release?

A

Hyperglycemia

Increased FFAs

Obesity

Aging

GH

IGF-1

62
Q

How does arginine increase GH release?

A

It suppresses somatostatin release, allowing GH to be secreted unopposed

63
Q

What are the 2 clinical methods of measuring GH status?

A
  1. Arginine

2. Insulin challenges to induce hypoglycemia

64
Q

True or False:

GH has direct and indirect effects

A

True

65
Q

The direct effects of GH are mostly __________

A

Metabolic

66
Q

The indirect effects of GH are mostly ___________

A

Growth related

67
Q

What 3 ways does GH affect metabolism?

A
  1. Protein anabolism (muscle)
  2. Lipolysis in adipose tissue to mobilize lipids for energy during fasting
  3. Stimulates hepatic gluconeogenesis (to provide fuel for the brain during fasting)
68
Q

How could over secretion of GH lead to a form of diabetes?

A

Because it causes lipolysis in adipose tissue,and an increase of FFAs, muscle and adipocytes don’t uptake glucose

In addition, it stimulates gluconeogenesis by the liver.

Net effect is an increase in glucose and plasma insulin.

Because GH antagonizes the action of insulin, this can lead to a diabetogenic effect

**MUST KNOW THIS**

69
Q

Why are GH’s effects on growth called “indirect”

A

Because GH causes the release of IGF-1 and IGFBP from the liver and IGF-1 is a peptide that actually acts on muscles, tissues, organs and chondrocytes to increase growth

70
Q

IGF-1 is a peptide that should dissolve nicely in the plasma, yet 80% of it is bound to IGFBP! WHY

A

Becasue it increases the half-life of IGF1, which is important during times of growth

71
Q

What are the effects of GH on growth?

A

These are actually indirect effects of GH since these are being done by IGF-1:

  1. Muscle- increase lean body mass via increased amino acid uptake and protein synthesis
  2. Tissues/organs- increased protein synthesis, DNA synthesis, cell size/number
  3. Chondrocytes- increase linear growth via increased amino acid uptake, protein synthesis, DNA synthesis, collagen, chondroitin sulfate, and cell size/number
72
Q

Can GH-RH suppress its own release?

A

Yes

This is an ultrashort feedback loop!

73
Q

How does GH have an ~autocrine~ inhibitory effect on the somatotroph?

A

GH feeds back to the hypothalamus to suppress GH-RH release

74
Q

What effects does IGF-1 have on GH release

A

Suppresses GH release directly from the somatotrophs

Stimulates somatostatin production to inhibit the synthesis of GH

75
Q

GH levels increase when:

Food is abundant and anabolic/growth states are favored

Or

Food is scarce and catabolic states are favored

A

BOTH!

However, the effects of GH are different

76
Q

When protein and energy intake are ample, what happens to:

GH

IGF

Insulin

A

GH increases

IGF increases due to GH and insulin

Insulin increases due to the protein

77
Q

When protein and energy intake are both ample, what happens to:

Protein synthesis

Growth

Caloric storage

A

Protein synthesis increases

Growth increases

No change in caloric storage

78
Q

When carbohydrates alone are ingested, what happens to:

GH

IGF

Insulin

Protein synthesis

Growth

Caloric storage

A

GH decreases

IGF no change

Insulin increases

Protein synthesis no change

Growth no change

Caloric storage increased (due to insulin)

79
Q

If you drink 2 L of sugary Cola what happens to your IGF levels

A

No change

80
Q

In the fasted state, what happens to:

GH

IGF

Insulin

Protein synthesis

Growth

Caloric mobilization

A

GH increases

IGF DECREASES

Insulin decreases

Protein synthesis/growth DECREASE due to no IGF

Caloric mobilization increased (gluconeogenesis, lipolysis)

81
Q

Why does IGF1 decrease in the fasted state even though the hypoglycemia increases GH release?

A

Fasting increases cortisol levels as well, so the GH and Cortisol promote the production of IGF-BPs.

The increase of IGF-BP in the plasma limits the bioavailability of IGF1 to the tissues, and growth is diverted

82
Q

What is the difference between hypopituitarism and panhypopituitarism

A

Hypopituitarism: only GH is deficient

Panhypopituitarism: more than one anterior pituitary hormone is deficient

83
Q

What is the most frequent cause of hypopituitarism?

A

Traumatic injury such as surgery, car accident, or ischemic damage

84
Q

What is it called when there is ischemic damage to the mother’s anterior pituitary during the postpartum period?

A

Sheehan Syndrome

85
Q

Can GH deficiency result from impairment at any site of the hypothalamus-pituitary-GH-IGF-axis?

A

Yes

86
Q

What causes dwarfism?

A

GH deficiency before puberty

87
Q

Why do some people affected by dwarfism appear pudgy?

A

Loss of GH-induced lipolysis

88
Q

What causes Laron dwarfism?

A

Genetic defect in the GH receptor.

They have high GH levels but do not produce IGFs or IGF-BPs in response to GH.

Their hypothalamus-pituitary axis is totally fine, the defect is in the liver

89
Q

What causes African pigmy-ism?

A

Partial resistance of GH-receptors in the liver leads to low levels of IGF during puberty

90
Q

What causes acromegaly?

A

GH hypersecretion AFTER the epiphysis close in adults.

Usually caused by a tumor of the somatotrophs. IGF levels become very high.

91
Q

What happens to patients who have acromegaly?

A

They have appositional bone growth and soft tissue deformities

Enlarged hands and feet, decreased fat content

Slow onset diabetes

Prognathism

Gynecomastia

Lactation

(Last two when prolactin and mammosomatotrophs are involved)

92
Q

How is acromegaly treated?

A

Surgery to remove pituitary tumor

Octreotide (somatostatin analogues)

Dopamine analogues

GH-receptor antagonists if PRL is co-secreted

(He didn’t talk about the last two)

93
Q

What causes gigantism?

A

GH oversecretion before puberty

94
Q

What happens to people with gigantism

A

Excessive growth in long bones

Hyperinsulinemia/diabetes

Cardiac enlargement

Physiology II Exam 2 (Lauren) (4 decks)

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