Hypothalamus and Pituitary Gland Flashcards

(42 cards)

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
Negative Inhibition of GH
Exhibited primarily by IGF-1 on the hypothalamus; GH also inhibits its own release at the hypothalamus
26
Stimulators of GH Secretion
Normally occurs 1-2 hours after onset of deep sleep but also with: Stress Exercise Post-prandial hypoglycemia Sex Androgens Ghrelin
27
Fasting effects on GH
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
Prenatal Growth factors
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
Postnatal Growth
Stabilizes by age 2; spikes again at the onset of puberty as well as GH levels
30
Principal extrinsic regulator of post-natal growth
Adequate nutrition
31
Principal hormone regulating growth
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
Treatment of hypothyroid children w/ thyroxine
Effects on growth will show increased GH secretion w/ a rapid catch-up phase *Hyperthyroidism causes child to grow fast; but not larger
33
Growth spurt @ puberty
Primarily mediated by sex steroids; promote linear growth and maturation of epiphyseal plate
34
Estradiol
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
Aromatase
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
Testosterone on developing males
Increases periosteal bone expansion and muscle growth
37
Insulin effects on growth
Promotes protein anabolism; hyperinsulinemic children grow excessively
38
Glucocorticoid effects on growth
When present in excess, will limit growth *After removal, catch-up growth occurs but is not complete
39
Laron Dwarfism
GH receptor defects; pts. will have increased GH but no IGF-1 production
40
GH deficiencies
Produce dwarfism, delayed puberty, tendency towards hypoglycemia, mild obesity
41
Adenohypophysis Origin
Upgrowth of ectodermal cells from the primitive pharnyx; composed of epithelial tissues
42
Fetal IGF-1
U correlated w/ GH secretion; directly correlated to birthweight