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Endo: Sem 2 > The Thyroid Gland > Flashcards

The Thyroid Gland Flashcards

1
Q

what are the two classes of thyroid function?

A

developmental and metabolic

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2
Q

what is developmental thyroid function?

A

essential for normal development, especially in CNS and bone during early life

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3
Q

what is metabolic thyroid function?

A

essential for normal metabolism of many body tissues and in cardiovascular function

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4
Q

what is congenital hypothyroidism?

A

condition of thyroid hormone deficiency present at birth

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5
Q

what is congenital hypothyroidism associated with?

A

retarded growth and learning impairment, linked to iodine deficiency so avoiding by monitoring idoine levels during pregnancy

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6
Q

what is thyroid hormone controlled by?

A

hypothalamic-pituitary axis

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7
Q

how is thyroid hormone released?

A

thyroid gland is stimulated by its stimulating hormone released from anterior pituitary gland (TSH)

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8
Q

euthyroid

A

thyroid function in normal range

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9
Q

hypothyroid

A

thyroid function below normal

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10
Q

hyperthyroid

A

thyroid function above normal

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11
Q

what are the two types of hypo/hyper thyroidism?

A

primary and secondary

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12
Q

what is primary hypo/hyper thyroidism?

A

the problem is with the thyroid gland itself

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13
Q

what is secondary hypo/hyper thyroidism?

A

the problem is with the pituitary regulation of the thyroid gland

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14
Q

what is the anatomy of the thyroid gland?

A

there are two lobes and sometimes a third pyramidal lobe. rich blood supply (more blood per unit weight than kidneys).

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15
Q

what vessels supply the thyroid gland?

A

supplied by inferior thryoid artry from thyroicervical trunk of subclavian artery and superior thyoid artery as branch of external carotid artery

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16
Q

what is the functional unit of thyroid tissue?

A

the follicle

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17
Q

what does a follicle consist of?

A

a mass of colloid (protein rich storage material containing hormones available for release). the colloid is surrounded by a single layer of follicular cells

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18
Q

what do the follicular cells do?

A

they synthesise thyroid hormones and release into colloid and also take them back up from colloid when there is need for release

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19
Q

what is there between the follicles?

A

capillaries, with the basal membrane of follicular cells facing the capillary and apical membrane facing the colloid

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20
Q

what are C-cells?

A

they secrete calcitonin involved in calcium regulation

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21
Q

what are thryoid hormones derived from?

A

joining of two iodinated tyrosine molecules

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22
Q

what are the two thyroid hormones?

A

T4 and T3

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23
Q

what is T4?

A

thyroxine (4 iodines)

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24
Q

what is T3?

A

triiodothyronine (3 iodines)

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25
Q

what is reverse T3?

A

iodines in the opposite arrangement, this is inactive

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26
Q

which thyroid hormone is more active?

A

T3 is more active at the thyroid receptor but T4 is the major form released into the blood

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27
Q

what does the basolateral membrane face?

A

the blood

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28
Q

what does the apical membrane face?

A

the colloid

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29
Q

what is the process of TH release?

A

uptake of iodine occurs against conc gradient. (high in follicular cell and low in plasma) so actively transported (secondary active transport mechanism)

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30
Q

how is the iodine actively transported?

A

sodium gradient generated by Na+/K+ ATPase used to transport iodide into follicular cell via Na+/I- symporter

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31
Q

what happens to the iodide once it is inside the cell?

A

diffuses out via apical membrane and iodide is oxidised to iodine

32
Q

what enzyme oxidises iodide into iodine?

A

thyroid peroxidase (TPO)

33
Q

what is thyroglobulin?

A

large protein synthesised in follicular cell containing lots of tyrosine residues, used in oxidation of iodide to iodine

34
Q

what does thyroid peroxidase do?

A

oxidises iodide to iodine then iodinates tyrosine residues (covalently bonds iodine to them). if it iodinates them in one place you get mono-iodotyrosine (MIT), two places gives di-iodotyrosine (DIT)

35
Q

what is MIT?

A

mono-iodotyrosine

36
Q

what is DIT?

A

di-iodotyrosine (DIT)

37
Q

how is thyroid hormone released?

A

endocytosis/pinocytosis occurs into the follicular cell, then there is combining of colloid droplet with lysosomes and via lysosomal enzymes, the T3/T4 units are frees from protein stores as well as hydrolysis of thyroglobulin

38
Q

what happens if you combine MIT and DIT?

A

you get T3

39
Q

what happen if you combine DIT and DIT?

A

you get T4

40
Q

how is some of the iodine recycled in the cell?

A

by diodinising enzymes (DEHAL-1)

41
Q

how are T3 and T4 released into the circulation?

A

via transporters

42
Q

why do T3/T4 exist in plasma bound to thyroid-binding globulin?

A

they are lipophilic

43
Q

which thyroid hormone is more present in circulation?

A

T4

44
Q

which thyroid hormone is more important?

A

T3 as its the free thyroid hormone to stimulate receptors

45
Q

what are relative levels of T3 and T4 controlled by?

A

three iodothyronine selenodeiodinases D1-3 so selenium is important in diet

46
Q

what do the D1-3 enzymes do?

A

de-iodinate the thyroid hormones converting T4 to T3 or convert T3 to an inactive form

47
Q

How can levels of T3 be increased?

A

Convert T4 to T3

48
Q

How can levels of T3 be decreased?

A

Convert T3 to an inactive form

49
Q

What type of receptor is the thyroid hormone receptor?

A

nuclear (in the nucleas of the cell)

50
Q

what are the implications of thyroid hormones receptors being nuclear?

A

the thyroid hormones need to enter the cell via specific thyroid hormone transporters

51
Q

how can T3 be upregulated?

A

convert T4 into T3 by D2 as T3 is more active

52
Q

How does D1 de-iodinate?

A

removed an iodine from the 5 and 5’ position

53
Q

how does D2 de-iodinate?

A

removes only from the 5’ position

54
Q

how does D3 de-iodinate?

A

removes from the position 5

55
Q

what type of feedback control regulates thyroid synthesis and secretion?

A

negative feedback via the hypothalamo-pituitary axis

56
Q

how is the thyroid gland stimulated?

A

hypothalamus releases TRH which causes anterioir pituitiary to secrete TSH which then releases T3/T4 from the thyroid gland. Via negative feeback, increasing levels of T3/T4 causes TRH/TSH to shut off

57
Q

what type of molecule is TSH?

A

glycoprotein with its receptor being a surface transmembrane receptor

58
Q

what type of receptor is the TSH receptor?

A

GPCR (G protein couples receptor)

59
Q

What are the actions of TSH?

A
  • increase iodide uptake by increasing sodium-iodide symporter
  • stimulates uptake of colloid
  • induces growth of thyroid gland
60
Q

what leads to a goitre?

A

lack of T3/T4 synthesis so no more -ve feedback so there is increased release of TSH and TRH

61
Q

what are nuclear receptors?

A

ligand-activated transcription factors with higher affinity for T3

62
Q

what genes code for TH receptors?

A

TR alpha and TR beta

63
Q

how are TH receptors activated?

A

must be dimerised with another T3 receptor or retinoic acid receptor . there are certain domains on the receptor which bind to the hormone and bind to the DNA

64
Q

what happens when the ligand binds T3?

A

combination of the receptor and cofactors present results in an activating effect

65
Q

what must TH do to access the nuclear receptor?

A

cross the cell membrane via transporters as they are NOT lipophilic

66
Q

what is MCT8?

A

transporter. mutations in gene discovered to underlie an X-linked condition, Allan-herndon-Dudley Syndrome

67
Q

how can you regulate TH?

A

increase via selective activation of the D1-D3 diodinases to up/down regulate TH in a tissue specific manner

68
Q

what are the functions of TH?

A
  • increase metabolic rate
  • positive inotropic and chronotropic effect on heart
  • role in growth and development
69
Q

what is primary hyperthyroidism?

A

thyroid gland is overproducing TH, would negatively feedback onto the hypothalamus and pituitary gland leading to decrease in TRH/TSH

70
Q

what is wrong with thyroid gland in primary hypothyroidism?

A

thyroid gland isnt producing enough TH so there is absence of negative feeback. TSH/TRH increased

71
Q

what is secondary hyperthyroidism caused by?

A

tumour effecting the thyrotrophs. there would be increased synthesis and secretion of TSH so levels increase. T3/T4 will increase and negative feeback still there but working at a higher level. So high TSH and T3/T4 indicate secondary.

72
Q

what is Grave’s disease?

A

auto-immune disease as it is primary hyperthyroidism so high levels of TH and low TSH

73
Q

symptoms of Graves disease

A

weight loss, tachycardia, fatigue. Diffuse goitre and opthalmopathy

74
Q

pathology of Graves disease

A

Its due to stimulating auto-antibodies. Normally the TSH receptor binds TSH and TH synthesis/secretion is stimulated in the normal way. There is then also negative feedback on levels of TSH. Auto-antibodies get generated by the body and bind to TSH receptors as agonists. So the receptor is permanently activated

75
Q

what is Hashimoto’s?

A

autoimmune disease characterised by low circulating TH but high TSH

76
Q

symptoms of Hashimoto’s?

A

lack of TH activity therefore lethargy and intolerance to the cold. Lack of growth and development and diffuse goitre.

Endo: Sem 2 (11 decks)

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