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TAS Endocrinology > Thyroid Gland ✅ > Flashcards

Thyroid Gland ✅ Flashcards

1
Q

When does thyroid development start?

A

About 4 weeks gestation

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2
Q

What does the thyroid develop from?

A

An outpouching of the floor of the pharynx and bilateral protrusions of the fourth pharyngeal pouches

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3
Q

What is the outpouching of the floor of the pharynx the precursor of?

A

T4-producing follicular cells

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4
Q

What are the bilateral protrusions of the fourth pharyngeal pouches the precursor of?

A

The calcitonin secreting cells

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5
Q

What happens to the thyroid during development?

A

It descends along the thyroglossal tract, which then regresses

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6
Q

What can happen if there are remnants of the thyroglossal tract?

A

They may form thyroglossal cysts

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7
Q

What does failure of descent of the thyroid result in?

A

Ectopic thyroid gland (which is a common form of congenital hypothyroidism)

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8
Q

What is the process of thyroid development regulated by?

A

A number of transcription factors, including PAX-8, FOXE-1, and NKX2

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9
Q

Describe the gross anatomy of the thyroid gland?

A

It is butterfly shaped with two lobes connected by an isthmus

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10
Q

Where is the thyroid gland located?

A

Below the larynx, anterior to the second and fourth tracheal rings

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11
Q

What does the thyroid gland consist of?

A

Spherical iodine-absorbing follicles

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12
Q

What does the lumen of the thyroid follicles contain?

A

Colloid

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13
Q

What is present of the colloid of the thyroid follicles?

A

Substrates necessary for thyroid synthesis, particularly thyroglobulin

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14
Q

What are the thyroid follicles surrounded by?

A

A single layer of epithelial cells

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15
Q

What do the epithelial cells of the thyroid secrete?

A

T3 and T4

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16
Q

What are found between the follicles of the thyroid?

A

Parafollicular cells

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17
Q

What do the parafollicular cells secrete?

A

Calcitonin

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18
Q

What is TSH release regulated by?

A

Thyrotropin-releasing hormone (TRH)

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19
Q

Where is TRH released from?

A

Hypothalamus

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20
Q

What is thyroid hormone synthesis stimulated by?

A

Binding of pituitary-derived TSH to TSH receptor

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21
Q

What kind of receptor is the TSH receptor?

A

GPCR

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22
Q

What does binding of TSH to the TSH receptor lead to?

A

Iodine uptake by a sodium-iodine transporter

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23
Q

What happens once iodine has been taken up by the thyroid?

A

It is transported to the colloid

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24
Q

How is iodine transported to the colloid?

A

By a protein (pendrin) within the thyrocyte

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25
Q

What happens to iodine in the colloid?

A

It is oxidised to iodide by hydrogen peroxide

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26
Q

What is responsible for regulating hydrogen peroxide in the colloid?

A

Thyroid peroxidase (TPO)

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27
Q

What happens once iodine has been oxidised to iodide?

A

Tyrosyl residues on thyroglobulin are iodinated

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28
Q

What is formed when tyrosyl residues on thyroglobulin are iodinated?

A

Monoiodotyrosine (MIT) and diiodotyrosine (DIT)

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29
Q

What happens to MIT and DIT after formation?

A

They are coupled under TPO control to form iodothyronines

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30
Q

What happens following cleavage of thyroglobulin?

A

Molecules of MIT, DIT, T3, and T4 are released

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31
Q

What is T3 formed by?

A

Deiodination of T4

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32
Q

Where is T4 produced?

A

Solely in thyroid

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33
Q

Where is T3 produced?

A

Majority is produced by deiodination of T4 in peripheral tissues

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34
Q

Compare the potency of T3 to T4?

A

T3 is 3-4x more potent in it’s physiological actions than T4

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35
Q

What is the inactive form of T4?

A

rT3

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36
Q

What converts T4 into rT3?

A

Type III deiodinase

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37
Q

On what systems does thyroxine have an effect?

A
  • Neurological
  • Metabolic
  • Cardiovascular
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38
Q

What receptors does thyroxine bind to in the heart?

A

Alpha

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39
Q

What receptors does thyroxine bind to in the brain?

A

Alpha and beta1

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40
Q

What receptors does thyroxine bind to in the liver?

A

Beta1 and beta2

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41
Q

What receptors does thyroxine bind to in the pituitary?

A

Beta2

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42
Q

What receptors does thyroxine bind to in the hypothalamus?

A

Beta2

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43
Q

What is the fetus largely dependent on during fetal life regarding thyroxine?

A

Transplacental passage of T3 and T4

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44
Q

What changes are there to the source of thyroxine during fetal life?

A

There is an increasing contribution from the second trimester onwards of fetally derived thyroxine

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45
Q

Is it maternal or fetally derived thyroxine that protects the fetus from congenital hypothyroidism?

A

Largely fetally-derived

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46
Q

Describe the thyroxine levels in a premature infant?

A

Low T3 and 4, but high rT3 levels (as in the fetus)

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47
Q

Is there benefit to thyroxine replacement in premature infants?

A

Unknown, currently undergoing clinical trials

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48
Q

What happens to thyroid hormone levels postnatally?

A

There is an acute surge in TSH, T3 and T4 concentrations in the first day or two of life, and then falling to childhood levels by 2 weeks of age

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49
Q

What should the history include in suspected cases of thyroid disease?

A
  • Growth and pubertal development
  • Weight
  • Bowel habit
  • Neurodevelopment
  • Sleep patterns
  • Behavioural functioning
  • Environmental temperature tolerance
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50
Q

What happens to growth in thyroid disorders?

A
  • Delayed in hypothyroidism

- Advanced in hyperthyroidism

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51
Q

What happens to weight in thyroid disorders?

A

Loss in hyperthyroidism

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52
Q

What happens to bowel habit in thyroid disorders?

A
  • Constipation in hypothyroidism

- Diarrhoea in hyperthyroidism

53
Q

What happens to neurodevelopment in thyroid disorders?

A

Delayed in hypothyroidism

54
Q

What happens to sleep pattern in thyroid disorders?

A
  • Excess fatigue in hypothyroidism

- Reduced sleep requirements in hyperthyroidism

55
Q

What happens to behavioural functioning in thyroid disorders?

A
  • Deteriorating school progress in hypothyroidism

- Poor attention span in hyperthyroidism

56
Q

What happens to environmental temperature tolerance in thyroid disorders?

A
  • Cold intolerance in hypothyroidism

- Heat intolerance in hyperthyroidism

57
Q

What general clinical observations might suggest hypothyroidism?

A
  • Short stature
  • Overweight
  • Delayed puberty
  • Dry skin
  • Increased hair
  • Vitiligo
58
Q

Why does precocious puberty sometimes (but rarely) happen in hypothyroidism?

A

Due to cross-stimulation of FSH receptors by TSH

59
Q

What general clinical observations might suggest hyperthyroidism?

A
  • Tall statue
  • Underweight
  • Facial flushing
  • Tremor
  • Sweatiness
60
Q

Why are hyperthyroid children underweight?

A

Because of increased metabolic rate

61
Q

What should be looked for in the neck in thyroid disease?

A

Goitre

62
Q

Describe the goitre in Hashimoto’s disease?

A

Nodular

63
Q

Describe the goitre in Grave’s disease?

A

Smooth, homogenous, occasionally associated with a bruit

64
Q

What happens to the pulse in thyroid disease?

A
  • Slow in hypothyroidism

- Fast, and associated with flow murmurs, in hyperthyroidism

65
Q

What might be found on MSK examination in thyroid disease?

A
  • Proximal muscle weakness in hypothyroidism

- Tremor and choreiform movements in hyperthyroidism

66
Q

What might be found on neuro examination in thyroid disease?

A

Relaxation of the ankle jerk is prolonged in hypothyroidism, but reduced in hyperthyroidism

67
Q

What might be found on ophthalmological examination in thyroid disease?

A

Exophthalmos and occasionally ophthalmoplegia

68
Q

What is the importance of exophthalmos and ophthalmoplegia in thyroid disease?

A

These findings are pathognomonic for Grave’s disease

69
Q

What might the presence of deafness suggest in congenital hypothyroidism?

A

Pendred syndrome

70
Q

What might the presence of a lump at the back of the throat suggest in congenital hypothyroidism?

A

Ectopic thyroid

71
Q

What % of circulating T3 and T4 are bound to TBG?

A

50% of T3

70% of T4

72
Q

What is most of the remainder of T3 and T4 circulating bound to?

A

Other proteins, such as albumin

73
Q

What % of T3 and T4 circulates unbound?

A
  1. 3% of T3

0. 03% of T4

74
Q

What is the result of the majority of T3 and T4 circulating bound?

A

The measurement of free hormones (T3, T4, and TSH) provides a more relevant assessment of thyroid function than total thyroxine

75
Q

What is total thyroxine a better measurement of?

A

TBG levels

76
Q

What antibodies are usually positive in Graves’ and Hashimoto’s?

A

TPO (thyroid peroxidase)

77
Q

What investigation finding indicates Graves’ disease?

A

Excess titres of TSH receptor antibodies (TRAb)

78
Q

How is congenital hypothyroidism usually detected?

A

Screening with capillary blood spot TSH

79
Q

What investigations are performed in congenital hypothyroidism (in addition to formal thyroid function testing)?

A

Ultrasound or isotope scanning

80
Q

What is the purpose of ultrasound or isotope scanning in congenital hypothyroidism?

A

To clarify if gland is absent, hypoplastic, or ectopic

81
Q

What suggests dyshormonogenesis in isotope scanning for congenital hypothyroidism?

A

Abnormalities of iodine uptake and trapping

82
Q

What is essential when a thyroid nodule or cancer is suspected?

A

Imaging

83
Q

What investigation should be done in suspected thyroid cancer?

A

Calcitonin

84
Q

What does a raised plasma calcitonin indicate in suspected thyroid cancer?

A

Medullary thyroid cancer

85
Q

How common is congenital hypothyroidism?

A

Common, affects 1:3,500 births

86
Q

What is the importance of congenital hypothyroidism?

A

It is the most common treatable cause of learning disability worldwide

87
Q

What is congenital hypothyroidism most commonly caused by?

A

Maternal iodine deficiency

88
Q

What are the most common form of congenital hypothyroidism in developed countries?

A

Ectopic gland most common, followed by aplasia and hypoplasia

89
Q

How important are transcription factor mutations as a cause of congenital hypothyroidism?

A

They are responsible for less than 2% of dysgenesis cases

90
Q

What causes dyshormonogenesis?

A

Defects in a range of genes encoding proteins involved in thyroid hormone biosynthesis

91
Q

How does dyshormonogenic thyroid appear on ultrasound?

A

Normal

92
Q

What % of cases of congenital hypothyroidism are caused by dyshormonogenesis in the UK?

A

10-15%

93
Q

What is the purpose of the newborn screening programme for hypothyroidism?

A

To identify cases to be started on thyroxine treatment before 2 weeks of age

94
Q

What is the aim of starting thyroxine early in congenital hypothyroidism?

A

Aims to normalise thyroid function within 2 weeks, to optimise neurodevelopment outcomes

95
Q

What are changes in the dose of thyroxine guided by in congenital hypothyroidism?

A

Recurrent elevations in TSH

96
Q

What should be done if a dose increase has not been done by the 3rd birthday in congenital hypothyroidism?

A

Consideration should be given to temporary withdrawal of therapy, to establish if lifelong thyroxine treatment is actually required

97
Q

What does long-term follow up for congenital hypothyroidism require?

A

Monitoring of growth and neurodevelopment

98
Q

What might acquired hypothyroidism be due to?

A
  • Iodine deficiency
  • Autoimmunity
  • Irradiation
  • Antithyroid drugs
  • Goitrogens
  • Diseases affecting pituitary or hypothalamus
99
Q

Give an example of an autoimmune cause of hypothyroidism?

A

Hashimoto’s disease

100
Q

Give 3 examples of goitrogens?

A
  • Iodide
  • Cabbage
  • Soya
101
Q

What does management of acquired hypothyroidism involve?

A

Thyroxine replacement

102
Q

What is the prognosis of treated acquired hypothyroidism?

A

Good

103
Q

What might cause transient hyperthyroidism in children of affected mothers?

A

Graves’ disease, due to TRAb (thyroid-stimulating hormone receptor antibody) crossing the placenta and causing transient hyperthyroidism in the offspring of affected mothers

104
Q

What might the early stages of Hashimoto’s disease be associated with?

A

Transient hyperthyroidism

105
Q

What are the rare causes of hyperthyroidism in children?

A
  • Autonomous nodules
  • TSH hypersecretion
  • Activating mutation of the TSH receptor
106
Q

What is the initial treatment for Graves’ disease?

A

Carbimazole or methimazole

107
Q

What can be used for initial Graves’ treatment if adverse reactions are experienced with carbimazole or methimazole?

A

Propylthiouracil

108
Q

How do carbimazole, methimazole, and propylthiouracil act?

A

By blocking synthesis of thyroxine

109
Q

How can emergency control of symptoms be achieved in severely thyrotoxic patients?

A

Propanolol and Lugol’s iodine solution

110
Q

What should be done if relapse occurs after withdrawal of anti-thyroid medication after 2 or 3 years?

A

More definitive treatment in the form of radio iodine or surgery may be considered

111
Q

How serious is neonatal thyrotoxicosis due to maternal Graves’ disease?

A

Self-limiting

112
Q

When does neonatal thyrotoxicosis caused by maternal Graves’ disease resolve?

A

Once maternally derived TRAbs have disappeared, within 3 months of birth

113
Q

What might be required in neonatal thyrotoxicosis caused by maternal Graves’ disease?

A

Anti-thyroid treatment may be required in early weeks after birth

114
Q

What is the thyroid hormone resistance?

A

An unusual inherited disorder due to a mutation in the beta-thyroid hormone receptor gene

115
Q

What does the mutation in the beta-thyroid hormone receptor gene in thyroid hormone resistance result in?

A

Reduced feedback inhibition, leading to elevated T4 and T3 concentrations but inappropriately normal or raised TSH levels

116
Q

How is thyroid hormone resistance treated?

A

It doesn’t require therapy in most cases

117
Q

Does thyroid hormone resistance cause symptoms?

A

Sometimes

118
Q

Why are the symptoms of thyroid hormone resistance variable?

A

Because of variable tissue sensitivity to thyroid hormones, which can lead to some irritating symptoms of hyperthyroidism in certain individuals

119
Q

What are most thyroid nodules in childhood?

A

Cysts or benign adenomas

120
Q

Of what type are most malignant nodules in childhood?

A

Papillary or follicular carcinomas

121
Q

How might thyroid cancers in childhood present?

A

Painless, rapidly enlarging mass, sometimes with lymphadenopathy

122
Q

How should suspected thyroid cancer in children be investigated?

A

Ultrasound and fine needle aspiration

123
Q

What does treatment require in thyroid cancer?

A

Surgery and aggressive thyroxine replacement

124
Q

What is the purpose of aggressive thyroxine replacement after surgery for thyroid cancer?

A

To suppress TSH levels, which may be a risk factor for recurrence

125
Q

Why are high TSH levels a risk factor for recurrence of thyroid cancer?

A

Due to trophic effects on thyroid tissue growth

126
Q

How is metastatic thyroid cancer treated?

A

Radioiodine therapy is given post-op

127
Q

How is the recurrence of functioning thyroid tissue monitored in treated thyroid cancer?

A

Thyroglobulin measurements

128
Q

What is the prognosis of thyroid cancer in children?

A

Generally good

TAS Endocrinology (6 decks)

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