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Physiology Block 3- Endocrine Physiology > L3 - Anterior Pituitary > Flashcards

L3 - Anterior Pituitary Flashcards

1
Q

What kind of hormones are released from the anterior pituitary?

A

FLAT PIG

FSH, LSH ACTH, TSH, PROLACTIN, GH

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2
Q

What directly regulates the release of anterior pituitary hormones?

A

Hypophysiotropic neuropeptides

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3
Q

How are hypophysiotropic hormones transported to the anterior pituitary?

A

They are released in the median eminence and travel down the long hypophysial portal veins

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4
Q

What produces the overall rhythmic patterns of pituitary hormone release?

A

The interaction of sleep and circadian effects

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5
Q

What are the three categories of anterior pituitary hormones?

A

Glycoproteins,
Proopiomelanocortin-derivatives,
GH and prolactin family

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6
Q

What are the anterior pituitary glycoprotein hormones?

A

Thyroid-stimulating hormone (TSH), follicle-stimulating hormone (FSH), and luteinizing hormone (LH)

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7
Q

What is the general structure of the glycoprotein anterior pituitary hormones?
What part confers the biological specificity of each hormone?

A

Alpha subunit shared by all of the glycoprotein hormones and unique beta subunit that confers the physiologic effect

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8
Q

What cells produce proopiomelanocortin?

A

Corticotrophs of the anterior pituitary

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9
Q

What hormones are derived from proopiomelanocortin?

A

Adrenocorticotropic hormone, beta-endorphin, and melanocyte stimulating hormone

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10
Q

Approximately what percentage of the anterior pituitary produces growth hormone?

A

At least 50%

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11
Q

What hormone stimulates production of thyroid-stimulating hormone?
What cells produce that hormone?

A

Thyrotropin-releasing hormone;

predominantly parvicellular neurons in the paraventricular nucleus

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12
Q

On what cells does thyrotropin-releasing hormone act? To what type of receptor does it bind?

A

Anterior pituitary thyrotrophs;

GPCRq (inc. PLC)

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13
Q

What hormone stimulates production of follicle-stimulating and luteinizing hormones?
On what cells does that hormone act?
To what type of receptor does it bind?

A

Gonadotropin-releasing hormone;
anterior pituitary gonadotrophs;
GPCRq (inc. PLC)

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14
Q

What hormone stimulates production of adrenocorticotropic hormone?
On what cells does that hormone act?
To what type of receptor does it bind?

A

Corticotropin-releasing hormone;
anterior pituitary corticotrophs;
GPCRs (inc. AC)

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15
Q

On what cells does somatostatin act?
To what receptor?
What is the effect?

A

Somatotrophs;
GPCRi (dec. AC)
inhibition of growth hormone release

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16
Q

On what cells does Growth-hormone-releasing hormone act? To what receptor? What is the effect?

A

Somatotrophs;
GPCRs (inc. AC);
release of growth hormone

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17
Q

How does dopamine regulate prolactin release?

A

Dopamine binds to dopaminergic GPCRi receptors, decreasing adenylyl cyclase activity, increasing potassium channel activation and inhibiting calcium channels to overall inhibit prolactin release

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18
Q

Which isoform of growth hormone is most important in terms of physiologic function

A

22 kDa isoform

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19
Q

What is the half-life of growth hormone?

A

20-30 minutes

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20
Q

When is growth hormone released?

A

During slow-wave sleep, post-prandially, and during exercise

21
Q

At what point of development is growth hormone released in its highest levels?

A

Peak during adolescence

22
Q

How does blood glucose level affect growth hormone release?

A

-low blood glucose stimulates growth hormone

(ultimate goal is to increase blood glucose: GH inhibits insulin receptor => increasing blood glucose)

GH release is stimulated by severe hypoglycemia and suppressed by high spikes in hyperglycemia

23
Q

What compounds can stimulate GH release? What can suppress it?

A

(+) GHRH, Ghrelin, ACh, alpha-adrenergic agonists, dopamine, serotonin;

(-) Somatostatin and IGF-1

24
Q

What is the receptor for growth hormone?

Where is it expressed?

A

Receptor associated kinase;

liver, bone, muscle, adipose, kidney, brain, heart, and immune cells

25
Q

How does GH affect the liver?

A

Stimulates production and release of Insulin-like growth factor 1

26
Q

How does GH affect the muscle?

A

Stimulates protein synthesis; stimulation of IGF1 synthesis

27
Q

How does GH affect the bone?

A

Increases collagen synthesis, increases cell size, and number and increases longitudinal growth ; stimulation of IGF1 synthesis

28
Q

How does GH affect adipose tissue?

How does it affect glucose utilization?

A

Stimulation of lipolysis (inhibits lipoprotein lipase, stimulates hormone sensitive lipase);
Muscles will take up the hydrolyzed fatty acids and so there will be more glucose available in the blood

29
Q

Where is IGF1 produced? How does it circulate?

A

Liver, muscle, bone; circulates bound to a protein

30
Q

What are the effects of IGF1?

A

Increased DNA, RNA, protein synthesis–> growth

31
Q

To what kind of receptor does IGF-1 bind?

What subunits make up the structure and what is the function of each subunit?

A

Binds to a ligand-activated receptor kinase;

Consists of the alpha subunit (binds to hormone) and the beta subunit (tyrosine kinase activity)

32
Q

What is Laron syndrome?
How does it present?
How does it affect IGF-1?

A

An autosomal recessive disorder characterized by insensitivity to GH due to a variant of GH receptor; Presents with short stature and resistance to diabetes and cancer;
Impairs IGF-1 release

33
Q

How does a GH deficiency present in childhood?

How is the diagnosis made?

A

Decreased linear growth– short stature;

Height below 2 SD below average

34
Q

How does GH-deficiency affect infants?

GH-resistance?

A

Deficiency- low birth weight;

resistance- low birth length and weight

35
Q

How does a GH deficiency manifest in adulthood?

A

Decreased GH release and pulsatility is associated with aging, cancer and HIV and is associated with increased cardiovascular risk and loss of muscle mass

36
Q

How does a growth hormone excess present in children and in adults?
What is the most frequent cause?

A

Children- gigantism; adult- acromegaly; Piuitary adenoma

37
Q

How can a GH deficiency be evaluated through GH stimulation tests?

A

Challenging with either insulin and GHRH to measure the increase in growth hormone elicited

38
Q

What is the main mechanism by which prolactin is increased in pregnancy?

A

Increased estrogen stimulates the growth and replication of lactotrophs

39
Q

What are the physiologic effects of prolactin? What physical stimulus results in prolactin release?

A

Breast differentiation, duct proliferation and branching, glandular tissue development, milk production and lactogenic enzyme synthesis; Suckling

40
Q

How is the release of prolactin regulated? What other compounds are required for prolactin to have full effect?

A

Prolactin release is predominantly under tonic inhibition by hypothalamic dopamine release and is additionally inhibited by somatostatin and GABA and can be stimulated by several factors; requires insulin and cortisol to be normal in circulation

41
Q

How does prolactin affect its own production?

A

Prolactin increases dopaminergic inhibition of prolactin release (negative feedback loop)

42
Q

What is the only hormone solely under hypothalamic inhibitory control by dopamine?

A

Prolactin

43
Q

How can a prolactinoma cause infertility and gonadal dysfunction?

A

High levels of prolactin can inhibit GnRH release, which lowers LH and FSH and so gonadal steroidogenesis will decrease leading to amenorrhea, impotence, and decreased libido

44
Q

During pregnancy, what keeps the action of prolactin in check?

A

High progesterone levels in the breasts

45
Q

(L3 - Anterior Pituitary) On a hot, sunny day:

A) ADH release would be lowest at noon
B) aquaporin 1 expression would be stimulated at noon
C) AVP signaling would involve PKA activation
D) Urine osmolality would be unaffected by ADH release

A

C) AVP signaling would involve PKA activation

  • ADH released from bloodstream
  • binds to V2R (alpha Gs)
  • increase AC, cAMP, PKA
  • PKA phosphorylates aquaporin 2
  • aquaporin 2 releases on apical side
  • allowing water inside collection duct to pass via aquaporin 3, 4 on basolateral side to enter the bloodstream
46
Q

(L3 - Anterior Pituitary) Laceration of the median eminence would result in:

A) increased release of all pituitary hormones
B) decreased release of hypothalamic peptides
C) increased release of prolactin
D) decreased release of all pituitary hormones

A

C) increased release of prolactin

Prolactin is under negative control via dopamine via hypo-physio-tropic control

*laceration of median eminence would not decrease RELEASE of hypothalamic peptides, but would DECREASE DELIVERY

47
Q

What is the relationship between GH and glucose storage?

A

As you increase GH, decrease glucose storage => releasing glucose into bloodstream to be used for energy

48
Q

(L3 - Anterior Pituitary) TRUE/FALSE? Laron Syndrome is associated with low levels of IGF-1.

A

TRUE

Laron’s disease - GH activity deficiency

  • GH receptor insensitivity (mutated receptor)
  • GH stimulates IGF-1 production in liver
  • GH is not binding to its receptor, IGF-1 not being produced => lower levels of IGF-1

Physiology Block 3- Endocrine Physiology (10 decks)

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