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ANAT322 > Neuroendocrine Regulation of Thyroid Function > Flashcards

Neuroendocrine Regulation of Thyroid Function Flashcards

1
Q

where is TRH synthesized? where is it secreted?

A

in parvocellular neurons of the PVN. secreted at the anterior pituitary.

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2
Q

where is TSH secreted from? what does it do?

A

secreted from anterior pituitary onto the thyroid gland to increase T4 and T3 thyroid hormones synthesis

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3
Q

what is T3 and T4’s effect on TRH?

A

inhibits TRH and TSH secretion (classic negative feedback)

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4
Q

what vessel does the hypothalamus receive blood from?

A

hypothalamic artery. sends direct arterial blood

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5
Q

what vessel does the anterior pituitary recieve blood from?

A

superior hypophyseal artery. sends venous blood)

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6
Q

examples of hormones released directly in the neurohypophysis?

A

oxytocin, arginine vasopressin

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7
Q

where in the PVN are TRH producing hormones located?

A

medially

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8
Q

what neurons project to the median eminence?

A

only the parvocellular neurons of the PVN

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9
Q

describe TRH structure

A

three-amino acid neuropeptide

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10
Q

what is the main driver of T4 synthesis?

A

TRH! not TSH

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11
Q

what is the main TRH negative regulator?

A

T3

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12
Q

how does T3 act as a negative regulator?

A

genomically and post-genomically: increases expression of TRH peptidase at the nerve ending (post-translational)

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13
Q

what is TSH necessary for?

A

normal glycosylation of TSH at post-translational level

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14
Q

why does hypothalamus injury cause low TSH?

A

without TRH action, anterior pituitary can’t produce as much TSH, and it lacks the post-translational glycosylation

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15
Q

what happened when they implanted T4 close to medial parvocellular PVN neurons?

A

decreased expression of TRH gene!

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16
Q

difference between T4 and T3?

A

T4 is the pro-hormone for T3

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17
Q

name the neurohypophysis (anterior pit) hormones

A

go look for that adenoma please Micheal
GH
LH
FSH
TSH
ACTH
prolactin
MSH

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18
Q

what is different between individuals relating to TSH/T4,T3 levels?

A

the set point varies between people

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19
Q

what do each glycoproteins have in common? name the glycoproteins

A

same alpha subunit, different beta subunit that determine interaction with receptor.
FSH, LH, CG, TSH

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20
Q

describe TSH structure

A

glycoprotein with 2 chains with CHO moiety, essential for biological activity

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21
Q

what does separation of the TSH chains cause?

A

inactivation of TSH

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22
Q

what receptor does TSH bind to?

A

G-protein coupled receptor

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23
Q

how is TSH secreted?

A

circadian rhythm; pulsatile secretions

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24
Q

what is different about the anterior pituitary’s TH receptor occupancy status? (THR in TSH producing cells)

A

over half are occupied by T3 that is derived from local intracellular T4

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25
Q

what “holds back” TSH secretion/linearly correlates with with TSH suppression?

A

nuclear T3

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26
Q

what level of TS receptors occupancy is needed to keep TSH levels normal?

A

high level of occupancy

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27
Q

how are thyroid cells organized?

A

in follicles: spherical hollow arrangements of epithelial cells

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28
Q

what are colloids?

A

it’s in the thyroid gland follicles, composed of thyroglobulin

29
Q

what is thyroglobulin?

A

protein in which TH are synthesized and stored until released.
serves as a template for TH synthesis

30
Q

what and where are C cells found?

A

between follicles in thyroid gland, they produce calcitonin and release in capillary network

31
Q

in what circumstances can you feel the thyroid gland?

A

when someone has a goiter (enlarged thyroid gland)

32
Q

what is the difference between T3 and T4?

A

T3 lacks the iodine at the 5” position of the outer ring

33
Q

where is thyroglobulin produced and stored?

A

produced in thyrocyte, stored in follicles

34
Q

what residues are sparsely spaced in thyroglobulin? they create what sites?

A

tyrosine residues create hormonogenic sites (TH production)

35
Q

do all tyrosine residues on thyroglobulin participate in TH formation?

A

no

36
Q

first step of TH biosynthesis

A

iodide uptake -> inorganic iodide anion gets oxidized to diatomic iodine -> gets covalently linked to tyrosyl residues -> tyrosine

37
Q

how many MIT/DIT are needed to produce T3 and T4?

A

1 MIT + 1 DIT = T3
2 DITs = T4

38
Q

how is iodide transported in the cell if the I conc inside > outside?

A

through the NIS: N & I symporter

39
Q

2nd step of TH biosynthesis?

A

coupling of iodinated tyrosines (MIT + DIT)

40
Q

how are TH released from the colloid (where they are stored in thyroglobulin)?

A

via endolysosomes. diffused into the blood

41
Q

what are TSH effects? what does it act on the fastest?

A
  • earliest effect = release of TH (Tg endocytosis, digestion & release of iodoaminoacids)
  • also stimulates synthesis (NIS, I oxidation & organification, iodotyrosines coupling, TG synthesis)
42
Q

where is most of T3 coming from?

A

liver, muscles, kidney where T4 is converted to T3.
only a small portion is from anterior pituitary.

43
Q

what can T4 be converted to with what enzymes?

A

D1, D2 -> converts to T3
D1, D3 -> converts to reverse T3 (inactivate T4)

44
Q

what dictates T4 conversion (activation or inactivation)?

A

T4 levels!
(too high = hyperthyroidism = converts to reverse T3 = inactivates /
too low = hypothyroidism = converts to T3 = activate)

45
Q

___ is about 10x more abundant than ___ at the nuclear receptor level

A

T3 is 10x more abundant than T4

46
Q

___ is 10x more potent than ___

A

T3 is 10x more potent than T4

47
Q

what happens to thyroxine, T3, and TSH levels as hypothyroidism gets worst?

A

thyroxine decreases,
T3 stays somewhat constant,
TSH increases

48
Q

how does T3 level stay constant even with a failing thyroid gland?

A

peripheral conversion of T4 to T3 is replaced by thyroidal secretion of T3.
-> because increased TSH stimulates D2 in the thyroid which increase T3

49
Q

what happens to T4 and TSH levels with hypothyroidism?

A

decrease in T4,
increase in TSH

50
Q

what happens to T4 in astrocytes?

A

converts to T3 via D2 and either binds to nuclear receptor OR exits cell and access neuron to bind to nuclear receptor there or gets inactivated by D3

51
Q

what can someone with intense hypothyroidism do to protect his brain?

A

increase D2, decrease D3, upregulated T4 and T3 transport proteins

52
Q

how is facultative adaptive thermogenesis linked to thyroid?

A

T3 increases UCP1 action (uncouples ATP production of smtg so all the energy is lost as heat -> increases thermogenesis

53
Q

do we need to be hyperthyroidism to use the adaptive thermogenesis? because T3 increases it?

A

no, because D2 converts T4 to T3 locally

54
Q

where does this thermogenesis happen?

A

in brown adipose tissue

55
Q

symptoms of hyperthyroidism

A
  • weight loss in spite of increased appetite
  • increased sweating from dissipating heat
  • anxiety and sleeplessness
56
Q

what causes increase in sweating during hyperthyroidism?

A

increase in energy expenditure and basal thermogenesis

57
Q

how does leptin affect hypothalamic pituitary thyroid axes?

A

it upregulates the axis (shown by T4 serum increase)

58
Q

what is leptin’s effect at hypothalamus?

A

inhibits AgRP/NPY secretion (inhibits orexigenic), stimulates hypothalamic-pituitary-thyroid axes to activate BAT thermogenesis

59
Q

what is somatostatin’s neurons effect on TSH production?

A

negative effect on TRH action

60
Q

what is dopaminergic neurons effect on TSH production?

A

inhibits TSH gene expression at nucleus, but stimulates TRH production

61
Q

what increase (?) the TSH:T4 ratio in individuals?

A
  • TRH
  • Increased leptin
  • adrenergic
  • CART
62
Q

what decreases (?) the TSH:T4 ratio in individuals?

A
  • Glucocorticoids
  • Reduced leptin
  • Dopamine
  • Somatostatin
  • Cytokines (TNF-a)
  • NFkB-induced D2 expression
63
Q

symptoms of hypothyroidism

A
  • Sensitivity to cold
  • Weight gain despite decreased appetite
64
Q

in what cases is TSH pulsatility lost?

A

in people with pituitary tumors

65
Q

what is acromegaly?

A

distal growth.
anabolic state -> everything is diverted to glucose metabolism

66
Q

what do elevated somatostation levels cause?

A

they decrease TSH secretion

67
Q

how does a heart attack affect thyroid hormones?

A

acute (right after) = normal TSH, normal T4, decreased T3 and increased rT3 because of decreased D1 and increased D3.
chronic (72h after)

68
Q

why does the acute phase happen?

A

high D3, low D1, low T3 to overcompensatw

69
Q

how is the affinity of T3 vs T4 with nuclear receptor?

A

T3 has 10x affinity than T4

ANAT322 (10 decks)

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