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Z OLD ESA 1- Metabolism > Structure and Function of Thyroid Gland > Flashcards

Structure and Function of Thyroid Gland Flashcards

1
Q

Where is the thyroid gland located?

A

In the neck, in front of the lower larynx and upper trachea

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2
Q

When is the thyroid gland visible and palpable?

A

When enlarged

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3
Q

What is the thyroid gland called when its enlarged?

A

A goitre

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4
Q

What lies in close proximity to the thyroid gland?

A

Two nerves

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5
Q

What nerves lie in close proximity to the thyroid gland?

A

The recurrent laryngeal and the external branch of the superior laryngeal

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6
Q

What is the problem with thyroid surgery?

A

During surgery, the close nerves are at risk, and must be avoided

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7
Q

What is the consequence of damage to the nerves close to the thyroid?

A

They supply the larynx, and are involved in speech

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8
Q

Describe the vascular supply to the thyroid

A

Very good, with three arteries supplying it and three veins draining it

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9
Q

What are the three arteries and veins supplying the thyroid gland called?

A

Superior, muddle and inferior thyroid arteries/veins

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10
Q

What shape is the thyroid gland?

A

Butterfly, with two lateral lobes joined by a central isthmus

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11
Q

How big is the thyroid gland?

A

Varies in size, but usually 2-3cm across, and weighs 15-20g

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12
Q

What are the the major cell types found in the thyroid gland?

A
  • Follicular

- Parafollicular (C-cells)

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13
Q

How are the follicular cells of the thyroid gland arranged?

A

In numerous functional units called follicles, separated by connective tissue

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14
Q

Where are the parafollicular cells found?

A

ln the connective tissue

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15
Q

What shape are follicles?

A

Spherical

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16
Q

Describe the structure of follicles

A

Lined with epithelial (follicular) cells, surrounding a central lumen

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17
Q

What do the follicle lumens contain?

A

Colloid

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18
Q

What is colloid rich in?

A

The protein thyroglobulin

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19
Q

What does the thyroid gland produce?

A

3 hormones

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20
Q

What hormones are produced in the follicular cells?

A

NAME?

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21
Q

What hormone is produced in the parafollicular cells?

A

Calcitonin

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22
Q

What are T3 and T4?

A

Small molecules derived from the amino acid tyrosine

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23
Q

How are T3 and T4 derived from tyrosine?

A

With the addition of atoms of iodine

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24
Q

What is calcitonin?

A

A polypeptide hormone

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25
Q

What is calcitonin involved in?

A

Calcium metabolism

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26
Q

What are the basic steps of synthesis of T3 and T4 in the thyroid follicles?

A
  • Transport of iodide into the epithelial cells against a concentration gradient
  • Synthesis of a tyrosine rich protein (thyroglobulin) in epithelial cells
  • Secretion (exocytosis) of thyroglobulin into the lumen of follicle
  • Oxidation of iodide to produce an iodinating species
  • Iodination of side chains of tyrosine residues in thyroglobulin to form MIT (mono-iodotyrosine) and DIT (di-iodotyrosine)
  • Coupling of DIT with MIT or DIT to form T3 and T4 respectively within the thyroglobulin.
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27
Q

What ratios are T3 and T4 produced in?

A

~1:10

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28
Q

How are T3 and T4 stored?

A

Extracellularly in the lumen of the follicles as part of the thyroglobulin molecules

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29
Q

How much T3 and T4 is stored?

A

Normally considerable- enough so would last for several months at normal rates of secretion

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30
Q

How is T3 and T4 secreted?

A

Thyroglobulin is taken into the epithelial cells from the lumen of the follicles by the process of endocytosis. Here, proteolytic cleavage of the thyroglobulin occurs to release T3 and T4, and these diffuse from the epithelial cells into the circulation

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31
Q

What is the synthesis and secretion of T3 and T4 under the control of?

A

The hypothalamus and the anterior pituitary gland

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32
Q

What is the hypothalamic factor for T3 and T4 secretion control?

A

Thyrotropin-releasing hormone (TRH)

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33
Q

What kind of molecule is TRH?

A

Tri-peptide

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34
Q

Where is TRH released from?

A

Cells in the dorsomedial nucleus of the hypothalamus

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35
Q

What is TRH release under the influence of?

A

NAME?

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36
Q

What do increased stress levels cause regarding TRH?

A

Increases release

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37
Q

What do increased temperatures cause regarding TRH?

A

Decreases releases

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38
Q

What does TRH do once released?

A

Travels in the hypothalamic/pituitary portal system to stimulate the secretion of Thyroid Stimulating Hormone (TSH)

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39
Q

Where is TSH secreted from?

A

The thyrotropes in the anterior pituitary

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40
Q

What does TSH do once secreted?

A

Travels in the blood to affect the follicular cells of the thyroid gland

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41
Q

What kind of molecule is TSH?

A

Glycoprotein hormone

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42
Q

What does TSH consist of?

A

Two covalently linked subunit s (α and ß subunit s)

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43
Q

In what manner is TSH released?

A

In low-amplitude pulses following a diurnal rhythm

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44
Q

When are higher levels of TSH released?

A

At night

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45
Q

What does TSH interact with?

A

Receptors on the surface of the follicle cells

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46
Q

What does TSH do when it has interacted with the receptors on the follicle cells?

A

Stimulates all aspects of the synthesis and secretion of T3 and T4

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47
Q

What effects does TSH have?

A

Trophic effects on the thyroid gland

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48
Q

What are the trophic effects of TSH on the thyroid gland?

A
  • Increased vascularity
  • Increase in size
  • Number of follicle cells
49
Q

How can the trophic effects of TSH have negative consequences?

A

May result in an enlarged thyroid (goitre) that may or may not be overactive

50
Q

Are T3 and T4 hydrophilic or hydrophobic?

A

Hydrophobic

51
Q

How are T3 and T4 transported in the blood?

A

Bound to the proteins thyronine binding globulin, pre-albumin and albumin

52
Q

How much T3 and T4 is free in solution?

A
53
Q

What is important about the free T3 and T4?

A

It is biologically active

54
Q

How do T3 and T4 differ in affinity?

A

T3 has a slightly lower affinity for transport proteins than T4

55
Q

What is the result of T3 having a lower affinity to the receptor than T4?

A

A greater percentage is free, and it’s half-life in the circulation is shorter

56
Q

What increases the synthesis of thyronine binding globulin (TBG)?

A

Oestrogen during pregnancy

57
Q

What is the result in the increased TBG during pregnancy?

A

Fall in the amount of T3 and T4 in the blood, as more in bound

58
Q

What is the result in the fall of free T3 and T4 in pregnancy?

A

Removes the inhibitory feedback on the pituitary and hypothalamus, and so more TRH and TSH are produced, so thyroid gland secretes more T3 and T4

59
Q

What is the result in the increased T3 and T4 synthesis in pregnancy?

A

Amount of free T3 and T4 returns to normal, but total amount in the blood increases

60
Q

Where do T3 and T4 exert their influences?

A

They have general effects on the metabolic activity of most tissues, and more specific effects on particular tissues

61
Q

How long does the response of target tissues to T3 and T4 generally take?

A

Generally occurs slowly, taking day’s/weeks to manifest themselves

62
Q

What are the effects of T3 and T4?

A

NAME?

63
Q

Of what nature are the metabolic effects of T3 and T4?

A

Generally catabolic

64
Q

What do the metabolic effects of T3 and T4 lead to?

A
  • Increase in BMR
  • Heat production
  • Increased oxygen consumption
65
Q

What is T3 and T4 important for?

A

Normal growth and development

66
Q

What are their effects on physical growth related to?

A

In part, their metabolic effects on tissues

67
Q

What specific effects do T3 and T4 have that affects growth?

A
  • Affect bone mineralisation

- Increase synthesis of heart muscle protein

68
Q

What is particularly sensitive to T3 and T4?

A

The nervous system

69
Q

When is the nervous system particularly sensitive to T3 and T4?

A

During development

70
Q

Why is the nervous system especially sensitive to T3 and T4 during development?

A

Because T3 and T4 are required for the development of the cellular processes of nerve cells, hyperplasia of cortical neurones and myelination of nerve fibres

71
Q

What happens in the absence of thyroid hormones from birth to puberty?

A

The child remains mentally retarded (cretinism)

72
Q

What happens if a thyroid hormone deficiency is not corrected within a few weeks of birth?

A

Irreversible damage occurs

73
Q

What happens to newborns soon after birth?

A

They have their thyroid function assessed

74
Q

What is lack of thyroid hormones characterised by in adults?

A
  • Poor concentration
  • Poor memory
  • Lack of initiative
75
Q

What is true of some of the actions of T3 and T4?

A

They are indirect

76
Q

What are the indirect actions of T3 and T4 related to?

A

Important interactions with other hormones and neurotransmitters

77
Q

What effects do T3 and T4 have on hormones and neurotransmitters?

A

They stimulate them

78
Q

Where do T3 and T4 stimulate hormones and neurotransmitters?

A

In a variety of tissues, e.g. heart muscle, GI tract

79
Q

What may the stimulation of hormones and neurotransmitters produce?

A

Increased responsiveness of these tissues to regulatory factors

80
Q

What does T3 and T4 stimulation lead to in the heart muscle?

A

Tachycardia

81
Q

What does T3 and T4 stimulation lead to in the GI tract?

A

Increased motility

82
Q

What role does T3 and T4 have in the actions of hormones such as FSH and LH?

A

Permissive

83
Q

What happens in the absence of thyroid hormones due to their permissive roles?

A

Ovulation fails to occur

84
Q

How do T3 and T4 exert their actions?

A

The cross the plasma membrane of target cells, and interact with specific high affinity receptors

85
Q

Where are the T3 and T4 receptors found?

A

In the nucleus and possibly the mitochondria

86
Q

What are the receptors made up of?

A

Protein

87
Q

How does receptor affinity for T3 differ from that of T4?

A

The affinity for T3 is 10-fold that of T4

88
Q

What do the receptors have?

A

A number of domains

89
Q

What happens when T3 binds to the hormone-binding domain of it’s receptor?

A

It is thought it produces a conformational change in the receptor that unmasks the DNA binding domina

90
Q

What happens on interaction of the hormone-receptor complex with DNA?

A

It increases the rate of transcription of specific genes, that are then translated into proteins

91
Q

What DNA does the T3 hormone-receptor complex interact with?

A

Nuclear or mitochondrial

92
Q

What does the increased rate of protein synthesis due to the action of T3 stimulate?

A

Oxidative energy metabolism in the target cells

93
Q

What is the purpose of T3 stimulation of oxidative energy metabolism in the cells?

A

Provides the extra energy required for protein synthesis

94
Q

What does increased protein synthesis by T3 produce?

A

Increased amounts of specific functional proteins

95
Q

What does increased amounts of functional proteins result in?

A
  • Increased cell activity

- Increased demand for energy

96
Q

How can T4 be converted to T3 in tissues?

A

By removal of the 5’-iodine

97
Q

Where is T4 to T3 an important mechanism?

A

In regulating the amount of active hormone in cells

98
Q

Why is T4 to T3 conversion an important regulatory mechanism?

A

T3 has 10 times the activity of T4

99
Q

What does the removal of the 3’-iodide produce?

A

Inactive reverse T3 (rT3)

100
Q

What can rT2 do?

A

Bind to thyroid hormone receptors without stimulating them, but blocks the effect of T3

101
Q

What is hyperthyroidism?

A

When there is too much physiological active thyroid hormones

102
Q

What is hypothyroidism?

A

When there is too little physiologically active thyroid hormone

103
Q

What is the most common form of hypothyroidism?

A

Hashimotos’ disease

104
Q

How much of the population does Hasimotos’ disease affect?

A

1%, mostly women

105
Q

What is Hashimotos’ disease?

A

An autoimmune disease, that results either in the destruction of thyroid follicles, or production of an antibody that blocks the TSH receptor on follicle cells, preventing them from responding to TSH

106
Q

How are patients with Hashimotos’ disease generally treated?

A

With oral thyroxine

107
Q

What does the dosage of thyroxine in treatment of Hashimotos disease depend on?

A

Patient’s signs and symptoms, and TSH levels

108
Q

What is the most common form of hyperthyroidism?

A

Graves disease

109
Q

How many people does Graves disease affect?

A

~1% of population, mostly women

110
Q

What is Grave’s disease?

A

An autoimmune disease in which antibodies (thyroid stimulating immunoglobulin (TSI)) are produced that stimulate the TSH receptors on follicle cells, resulting in increased production and release of T3 and T4

111
Q

Why do TSH levels fall in Grave’s disease?

A

Due to the negative feedback exerted by T3 and T4 on the anterior pituitary gland

112
Q

Does the fall in TSH affect thyroid hormone secretion?

A

No

113
Q

Why does the fall in TSH secretion not affect thyroid hormone secretion?

A

The stimulus for thyroid hormone release is TSI, rather than TSH

114
Q

How are patients with Graves disease treated?

A

With carbimazole

115
Q

What is carbimazole?

A

A drug that inhibits the incorporation of iodine into thyroglobulin

116
Q

How does carbimazole work?

A

It inhibits the enzyme thyroid peroxidase, and therefore prevents coupling and iodination of tyrosine residues on thyroglobulin

117
Q

What are the signs and symptoms of hypothyroidism in adults?

A
  • Cold intolerance and reduced BMR
  • Weight gain tiredness and lethargy
  • Bradycardia
  • Neuromuscular system signs
  • Weakness
  • Muscle cramps
  • Cerebellar ataxia
  • Dry and flaky skin
  • Alopecia
  • Deep, husky voice
118
Q

What are the signs and symptoms of hyperthyroidism?

A
  • Heat intolerance, increased oxygen consumption and increased BMR
  • Weight loss
  • Physical and mental hyperactivity
  • Tachycardia
  • Intestinal hyper-mobility
  • Skeletal and cardiac myopathy giving rise to tiredness, weakness and breathlessness
  • Osteoporosis due to increased bone turnover and preferential resorption

Z OLD ESA 1- Metabolism (17 decks)

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