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S&F IV: Exam Two- European Gigalo > Hypothalamus and Pituitary Gland > Flashcards

Hypothalamus and Pituitary Gland Flashcards

1
Q

Neurohypophysis origin

A

Downward evagination of the floor of the primitive brain; composed of neurons

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2
Q

Posterior Pituitary Neurons

A

Magnocellular neurons that originate from the supraoptic and PVN nuclei that terminate near the capillary beds of the pituitary

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3
Q

Synthesis of posterior pituitary hormones

A

Synthesized in the cell bodies of neurons and transported to the posterior pituitary in a secretory granule w/ neurophysin (chaperone)

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4
Q

Secondary Capillary Plexus

A

Receives tropic hormones from the hypothalamus that were secreted into the hypothalamophyseal portal system

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5
Q

Somatotrope

A

Releases GH

Activated by GHRH

Inhibited by SS

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6
Q

Thyrotrope

A

Releases TSH

Activated by TRH

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7
Q

Lactotrope

A

Releases PRL

*Inhibited by dopamine; otherwise would secrete constantly

Slightly stimulated by TRH

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8
Q

Gonadotrope

A

Secretes FSH and LH

Activated by GnRH

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9
Q

Corticotrope

A

Releases ACTH, y-LPH, and B-endorphin

Activated by CRH and AVP

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10
Q

Gs activating Releasing Hormones

A

GHRH and CRH

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11
Q

Gi-mediated Releasing Hormones

A

SS and Dopamine

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12
Q

Gq-mediated Releasing hormones

A

TRH, GnRH, AVP

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13
Q

Glycoprotein family

A

Consists of FSH, LH, TSH, and hCG

a-subunits all the same; b-subunits are what makes them different

*All act by increasing cytosolic cAMP

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14
Q

Somatommamotropin family

A

Consists of GH and PRL (acidophiles) and single chain proteins connected by interacting S-S bonds

*Also includes placental hGH, hPRL, and hSS

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15
Q

POMC family

A

Cleavage of product from POMC gene can form ACTH, y-lipotropin, and B-endorphin

*Alternate cleavage produces a-MSH instead

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16
Q

GH binding protein

A

Formed from the cleavage of GH receptor on the external surface of target cells, therefore, it easily reacts w/ the receptor

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17
Q

Direct actions of GH

A

*Actions are diabetogenic

Stimulates IGF-1 production in the liver

Stimulates lipolysis in adipose => Increased FFAs

Inhibits glucose uptake in adipose and skeletal muscle

Decreases insulin sensitivity of tissues

Increase lean body mass (increased protein synthesis; decreased urea nitrogen)

18
Q

GH Receptor Action

A

GH binding induces dimerization of the JAK receptors and autophosphorylation of their intracellular tyrosine residues

=> STATs bind via SH2 domains, form dimers, and migrate to the nucleus to promote genetic transcription

19
Q

IGF-1 source

A

Mostly the liver, however, prechondrocytes also express GH receptors and will increase production of IGF in response to stimulation

20
Q

Circulating IGF-1

A

Bound to a complex including IGFBP-3 and an acid-labile unit

*Fnxns to provide a circulating reservoir and increase the T 1/2 of IGF-1

21
Q

IGF-1 Mechanism of Action

A

Binds to a receptor TK causing the autophosphorylation of 3 receptors leading to activation

=> IRS binds via SH2 domains and activates signaling cascade

  • Also activates the MAP/Kinase pathway to induce gene transcription
  • IGF-1 is similar to proinsulin and activates a similar receptor => high concentrations of IGF-1 will mimic insulin actions
22
Q

Target cells of IGFs

A

Fibroblasts, Chondrocytes, Adipocytes, Muscle Cells

Stimulates: cell proliferation, protein synthesis, insulin-like effects

23
Q

Ghrelin

A

Enhances the activity of GHRH on the anterior pituitary

=> Opening of Ca2+ channels causing depolarization and release of secretory vesicles

24
Q

SS Action on Somatotrope

A

By using the Gi pathway, opens K+ channels causing hyperpolarization of cell

25
Q

Negative Inhibition of GH

A

Exhibited primarily by IGF-1 on the hypothalamus; GH also inhibits its own release at the hypothalamus

26
Q

Stimulators of GH Secretion

A

Normally occurs 1-2 hours after onset of deep sleep but also with:

Stress

Exercise

Post-prandial hypoglycemia

Sex Androgens

Ghrelin

27
Q

Fasting effects on GH

A

48 hours => Increased GH, unchanged IGF-1

Prolonged fasting => Increased GH, decreased IGF-1

*IGF-1 production in the liver requires adequate nutrition causing this decrease, however, IGFBP-3 will still be made

28
Q

Prenatal Growth factors

A
  1. Genetics
  2. Placenta (weight directly weighted to birth weight)
  3. Maternal environment (Smoking and Alcohol cause MR and birth defects)
  4. Hormones (IGF and IGFBP levels are directly correlated to birthweight; insulin also important in tissue uptake of nutrients)
29
Q

Postnatal Growth

A

Stabilizes by age 2; spikes again at the onset of puberty as well as GH levels

30
Q

Principal extrinsic regulator of post-natal growth

A

Adequate nutrition

31
Q

Principal hormone regulating growth

A

GH; duh

  • Actions are mediated by IGF-1
  • T3 acts synergistically w/ GH by promoting GH secretion and IGF-1 production; w/o it, growth will be stunted
32
Q

Treatment of hypothyroid children w/ thyroxine

A

Effects on growth will show increased GH secretion w/ a rapid catch-up phase

*Hyperthyroidism causes child to grow fast; but not larger

33
Q

Growth spurt @ puberty

A

Primarily mediated by sex steroids; promote linear growth and maturation of epiphyseal plate

34
Q

Estradiol

A

Principal hormone that binds to the epiphyseal plate in BOTH boys and girls; binds to receptors on epiphyseal growth plate stimulating growth and closure

35
Q

Aromatase

A

Enzyme responsible for converting testosterone into estradiol in males

*Boys defective in aromatase will continue to grow after the normal age for growth spurt since estrogen will not close the epiphyseal plates

36
Q

Testosterone on developing males

A

Increases periosteal bone expansion and muscle growth

37
Q

Insulin effects on growth

A

Promotes protein anabolism; hyperinsulinemic children grow excessively

38
Q

Glucocorticoid effects on growth

A

When present in excess, will limit growth

*After removal, catch-up growth occurs but is not complete

39
Q

Laron Dwarfism

A

GH receptor defects; pts. will have increased GH but no IGF-1 production

40
Q

GH deficiencies

A

Produce dwarfism, delayed puberty, tendency towards hypoglycemia, mild obesity

41
Q

Adenohypophysis Origin

A

Upgrowth of ectodermal cells from the primitive pharnyx; composed of epithelial tissues

42
Q

Fetal IGF-1

A

U correlated w/ GH secretion; directly correlated to birthweight

S&F IV: Exam Two- European Gigalo (14 decks)

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