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Endocrinology > Lec7 Thyroid hormone Physiology > Flashcards

Lec7 Thyroid hormone Physiology Flashcards

Anatomy of the thyroid Synthesis and actions of the thyroid hormones Drugs affecting thyroid gland function

1
Q

Are the thyroid gland and its secretions essential for life?

A

No but they are essential for normal development and for physical and mental wellbeing of the individual

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2
Q

What is the thyroid gland composed of?

A

Follicles each consisting of a monolayer of epithelial cells enclosing a large core of viscous, homogeneous colloid

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3
Q

What is the function of the colloid?

A

It acts as a reservoir of thyroid hormone

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4
Q

What are the primary hormones secreted by the thyroid gland

A

T3 - triiodothyronine
T4 - thyroxine
Calcitonin –> concerned with calcium homeostasis and is secreted independently of the thyroid hormones

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5
Q

What makes T3 and T4 and where do they come from?

A

Tyrosine - from avocado & nuts

Iodine comes from meat

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6
Q

How are T3 and T4 made?

A

Tyrosine combines with iodine to form mono-iodotyrosince (MIT) or di-iodotyrosine (DIT)

MIT can combine with another MIT or a DIT to form
tri-iodothyronine (T3) or tetra-iodothyronine (T4)

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7
Q

What formations are biologically active?

A

3-monoiodotyrosine (MIT)
3,5-diiodotyrosine (DIT)
3,5,3’-triiodothyronine (T3)
3,5,3’,5’-tetraiodothyronine (T4)

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8
Q

Is reverse triiodothyronine biologically active?

A

No

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9
Q

Women who have iron deficiency can lead to what?

A

Dysfunction of the thyroid gland

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10
Q

How could indices of the thyroid hormone be improved?

A

By improving the iron status

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11
Q

Nuclear incidents can result in:

A

an increase of thyroid cancers and thyroid damage due to radioactive iodine

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12
Q

Thyroid function can be adversely effected by:

A

industrial contamination, pollution and nuclear incidents

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13
Q

How are MIT and DIT degraded?

A

By halogenases

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14
Q

Why are MIT and DIT degraded by halogenases?

A

To free the iodide which is reutilised by combination with THYROGLOBULIN

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15
Q

If industrial contamination gets into the food chain it can:

A

influence peoples thyroid function

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16
Q

What happens to the T3 and T4 once they are synthesised?

A

They leave the follicular cells and enter the blood stream for distribution to target cells

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17
Q

What percentage of thyroid hormone leaving the thyroid gland is in the form of T4?

A

95%

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18
Q

Where does the majority of conversion from T4 to T3 happen?

A

In the target tissues

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19
Q

What is required to convert T4 into T3?

A

Deiodinase enzymes

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20
Q

What percentage of T4 is converted into T3?

A

80%

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21
Q

What percentage of T4 is converted into reverse-T3?

A

20%

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22
Q

What is T3’s biological activity in comparison to T4?

A

T3 has biological activity 40 times greater than that of T4

Reverse T3 is biologically inactive

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23
Q

What percentage of biologically active thyroid hormone within the cell is in the form of T3?

A

90%

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24
Q

What is the plasma half life of T4?

A

6-8 days

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25
Q

What is the plasma half life of T3?

A

1 day

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26
Q

T3 is expensive to buy/prescribe because of pharma companies - what can you do instead?

A

Prescribe T4 - cheaper - the target tissues will convert it to T3 anyway

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27
Q

What is the control of thyroid hormone secretion?

A

The hypothalamus secretes thyrotrophin releasing hormone (TRH)

TRH - stimulates secretion of TSH from the anterior pituitary gland

This stimulates secretion of T3 of T4 by thyroid gland

T3 and T4 causes negative feedback on TRH and TSH secretion

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28
Q

What percentage of T3 and T4 is protein bound?

A

99%

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29
Q

If you lose the negative feedback of T3 and T4 what happens?

A

Increased TSH secretion

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30
Q

What could be a consequence of iodine deficiency?

A

Increased TSH secretion and therefore the thyroid gland enlarges

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31
Q

What is the Derbyshire neck?

A

Goitre due to increased TSH

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32
Q

Are thyroid hormones soluble in water?

A

No

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33
Q

How do thyroid hormones travel in blood?

A

Bound to plasma proteins - over 99% of circulating thyroid hormones are bound to plasma proteins

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34
Q

What are the plasma proteins that T4 is bound to?

A

Thyronine binding globulin (TBG) - 75%
Thyroxine-binding pre albumin (TBPA) - 15-20%
Albumin - 5-10%

35
Q

Where are the receptors for thyroid hormones?

A

Intracellular - specifically nuclear

36
Q

What is the effect of the interaction of thyroid hormones with their receptors?

A

They influence gene transcription and thus protein synthesis

37
Q

What is the main biological effect of thyroid hormones?

A

To increase basal metabolic rate

38
Q

How do thyroid hormones increase basal metabolic rate?

A

By increasing carbohydrate metabolism
Increased synthesis, mobilisation and degradation of lipids
Increased protein synthesis

39
Q

How are aspects of carbohydrate metabolism increased to increase basal metabolic rate?

A

Potentiating the effects of insulin
Potentiating effects of catecholamines
Increasing glucose absorption in the GI tract
Glycogenolysis and glucose uptake by muscle cells and adipose cells

40
Q

What effects does increased carb metabolism have?

A

Lose weight even when appetite is increased

41
Q

Why does the appetite become increased?

A

Due to fat metabolism

42
Q

Why is it not a good idea to take thyroid hormone to lose weight?

A

Excess T3 and T4 suppress TSH secretion
Atrophy of thyroid gland
So when you come off them - there is no thyroid hormone and become thyroid hormone deficient - feel the cold and gain weight
Interferes with entire endocrine balance

43
Q

Increased basal metabolic rate means that there is increased oxygen consumption in nearly every organ except:

A 
Brain
Uterus 
Testes 
Spleen 
Thyroid gland 
Anterior pituitary gland
44
Q

Thyroid hormones are not essential for life but they are:

A

necessary for the normal development of the CNS - especially myelination of nerve fibres

45
Q

What is the primary mechanism of increased basal metabolic rate?

A

An increase in the number and size of mitochondria and an increased activity of metabolically important enzymes

46
Q

Thyroid hormones are essential for:

A

Normal growth and development

47
Q

What does a lack of iodine translate to in puberty?

A

There is a great deal of change in puberty and pre-pubertal girls and boys will not undergo the change in puberty if they are iodine deficient and therefore thyroid hormone deficient

48
Q

What happens to growth hormone deficient individuals?

A

They stay short by undergo normal raging

49
Q

Thyroid hormone deficient individuals

A

stay short and looking like a child

50
Q

What happens to iodine deficient tadpoles?

A

They grow into big tadpoles but don’t change into frogs

51
Q

What is levothyroxine used for?

A

To treat thyroid hormone deficiency

Suppress TSH secretion in the treatment of some thyroid tumours

52
Q

How can levothyroxine be administered?

A

Orally or by injection

53
Q

What is the oral bioavailability of levothyroxine?

A

100%

54
Q

What percentage of levothyroxine is protein bound?

A

> 99%

55
Q

How is levothyroxine metabolised?

A

By the liver - glucuronidation

56
Q

What is the half life of levothyroxine

A

Approximately 7 days

57
Q

How is levothyroxine excreted?

A

20-40% excreted in urine

58
Q

What is the standard maintenance dose of levothyroxine?

A

50-100micrograms/day

59
Q

What are the adverse effects of levothyroxine?

A

Over active metabolism leading to:

palpitations, arrhythmias, diarrhoea, insomnia, tremor, weight loss

60
Q

Name the drugs affecting thyroid function:

A

Levothyroxine - treats thyroid deficiency
Carbimazole and methimazole - inhibit synthesis of thyroid hormones
Propylthiouracil - prevents peripheral conversion of T4 to T3
Potassium perchlorate - acts by competing with iodide for the active iodide uptake pump

61
Q

What is way of treating hyperthyroidism?

A

Carbimazole - inhibits synthesis of thyroid hormones

62
Q

What is an alternative to thyroidectomy to treat hyperthyroidism?

A

Use radioactive (I131) iodine - selectively concentrated in the thyroid gland where it causes tissue damage and therefore reduces thyroid hormone secretions

63
Q

What is carbimazole?

A

It is used to treat hyperthyroidism

64
Q

Carbimazole is a pro drug, what is the name of the active form and when/ how is it converted to the active form?

A

Carbimazole is converted to the active form methimazole after absorption
Methimazole prevents peroxidase iodinating the tyrosine residues on thyroglobulin - hence reducing production of thyroid hormones T3 and T4

65
Q

What is the oral bioavailability of carbimazole?

A

> 90%

66
Q

How much of carbimazole is protein bound?

A

85%

67
Q

What is the standard dose of carbimazole?

A

5-15mg/ day

68
Q

How is carbimazole metabolised?

A

Rapidly metabolised to methimazole

69
Q

What is the half-life of carbimazole?

A

6.4 hours as methimazole

70
Q

How is carbimazole excreted?

A

90% excreted in urine as metabolites

71
Q

What are the adverse effects of carbimazole?

A

Rashes and pruritus are common - treatable with antihistamines
Neutropenia and agranulocytosis (most serious rare side effect) –> teratogenic
Neutropenia can be fatal - can’t respond to minor infections which leads to sepsis

72
Q

What is propylthiouracil (PTU)?

A

It is used to treat hyperthyroidism including Grave’s disease

73
Q

How does propylthiouracil work?

A

By inhibiting THYROPEROXIDASE which normally acts in thyroid hormone synthesis
PTU also works by inhibiting tetra-iodothyronine deiodinase which converts T4 to T3

74
Q

What is the drug of choice to treat hyperthyroidism in the first trimester of pregnancy?

A

Propylthiouracil

75
Q

What is the oral bioavailability of propylthiouracil?

A

80-95%

76
Q

What is the percentage of protein binding in propylthiouracil?

A

70%

77
Q

How is propylthiouracil metabolised?

A

By hepatic glucoronidation

78
Q

Half life of propylthiouracil?

A

2 hours

79
Q

Excretion of propylthiouracil?

A

Renal

80
Q

Standard dose of propylthiouracil?

A

50-100 mg/day

81
Q

Adverse effects of propylthiouracil:

A

Rashes and pruritus - common and treatable with antihistamines
Notable side effects = risk of agranulocytosis and risk of serious liver injury, including liver failure and death

82
Q

Name the ways in which incidence of endemic goitre has been reduced worldwide

A

Prophylactic administration of iodine
Either by injection OR
Incorporation into table salt or flour

83
Q

What is the risk of iodine administration?

A

Jod-Basedow phenomenon - precipitates hyperthyroidism

84
Q

Name drugs that can induce goitre:

A

Lithium - used to treat bipolar depression - inhibits TH
Iodides contained in some vitamin preparations and cough remedies - interfere with iodide incorporation and hormone release

Endocrinology (11 decks)

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