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Management of GI and Endocrine Conditions > Lecture 22 - Thyroid Disorders > Flashcards

Lecture 22 - Thyroid Disorders Flashcards

1
Q

What are the second most common endocrine disorder?

A

thyroid disorders

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2
Q

What has the use of iodine salt done?

A

eliminated iodine deficiencies in most countries

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3
Q

Levels of thyroid hormones in the body?

A

show little variation in plasma levels and are steady

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4
Q

Where does the thyroid gland sit?

A

within the neck, straddling the trachea

it is a butterfly shape with 2 lateral lobes connected by the isthmus

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5
Q

When does the thyroid gland become functional?

A

early in foetal life

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6
Q

What does the thyroid gland contain?

A

lots of follicles composed of epithelial cells and arranged in spheres

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7
Q

What are follicles filled with?

A

colloid

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8
Q

What do the follicles participate in?

A

all phases of thyroid hormone synthesis

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9
Q

What is a colloid?

A

proteinaceous depot of thyroid hormone precursors

stains pink

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10
Q

When does synthesis of thyroid hormones begin?

A

when circulatory iodide is actively cotransported with sodium ions across the basolateral membrane of the epithelial cells

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11
Q

What happens to the sodium once in the cell?

A

it is pumped out of the basolateral membrane by the sodium potassium pump

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12
Q

What happens to the iodide?

A

the negatively charged iodide diffuses across the epithelial to the apical membrane and is transported into the colloid

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13
Q

How is iodide transported into the colloid?

A

by a mechanism that is believed to require an integral membrane protein called pedrin

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14
Q

What does the colloid contain?

A

large amounts of a protein called thyroglobulin

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15
Q

What happens to the iodide once inside the colloid?

A

it is rapidly oxidised to iodine, which is then attached to the phenolic rings of tyrosine residues within the thyroglobulin molecule

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16
Q

Where is thyroglobulin synthesised?

A

within the thyroid epithelial cells and is secreted into the colloid by exocytosis

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17
Q

What is the enzyme which oxidises and attaches the iodide?

A

thyroid peroxidase, which is synthesised by thyroid epthelial cells and secreted into the colloid

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18
Q

What is a tyrosine with one iodine attached?

A

monoiodotyrosine

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19
Q

What is a tyrosine with two iodine attached?

A

diiodotyrosine

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20
Q

What then happens to the mono or diiodotyrosine?

A

the phenolic ring of it is removed from the remainder of the thyroglobulin molcule

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21
Q

If two diiodotyrosine molcules are coupled it becomes?

A

Thyroxine (T4)

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22
Q

If a mono and a diiodotyrosine are coupled it becomes?

A

Triiodothyronine (T3)

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23
Q

What happens for the hormones to be secreted into the blood?

A

there are extensions of the thyroid epithelial membrane which engulf portions of the colloid which contain the iodinated thyroglobulin by endoytosis

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24
Q

What happens to the thyroglobulin with its coupled mono or diiodotyrosine in the cell interior?

A

it is brought into contact with lysosomes, so there is proteolysis of the thyroglobulin which releases T3 and T4, which can diffuse into the blood

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25
Q

How much iodinated thyroglobulins are stored in the body?

A

enough to provide thyroid hormones for several weeks

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26
Q

What makes the thyroid gland unique?

A

its storage capacity - which is needed because of the unpredictable intake of iodine

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27
Q

What is the active thyroid hormone?

A

T3

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28
Q

What is most circulating T3 derived from?

A

~80% is derived from deiodination of T4

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29
Q

Where does the remaining T3 come from?

A

the thyroid gland itself

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30
Q

Solubility of thyroid hormones?

A

poorly soluble in water

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31
Q

Thyroid hormones in the plasma?

A

99.9% are extensively protein bound in the plasma

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32
Q

What are thyroid hormones bound to in the plasma?

A

thyroxine binding globulin (TBG) and transthyretin (TTR) thyroxine binding prealbumin

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33
Q

What are plasma proteins responsible for?

A

the maintenance of the large extra thyroidal pull of thyroid hormones present in our blood

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34
Q

What is thyroxine binding globulin (TBG)?

A

a glycoprotein that is synthesised in the liver

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35
Q

What synthesises and secretes thyrotropin releasing hormone (TRH)?

A

the hypothalamus

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36
Q

What does TRH do?

A

it is transported along the blood vessels to the anterior pituitary and acts on pituitary cells to stimulate secretion of thyrotropin (TSH)

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37
Q

What does TSH do?

A

is transported in the blood to the thyroid gland where is stimulates secretion of T3 and T4

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38
Q

What happens when levels of T4 in the blood increases?

A

the pituitary gland detects the increase and reduces amount of TSH is releases

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39
Q

What does this decreased amount of TSH cause?

A

less stimulation of the thyroid gland itself so a reduction in the secretion of thyroid hormones

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40
Q

What else does a high level of T4 inhibit?

A

the hypothalamus, but to a lesser extent

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41
Q

What is negative feedback due to?

A

T4 being taken up and converted to T3 by the deiodinase enzymes

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42
Q

Euthyroid state?

A

thyroid hormone secretion is normal

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43
Q

Hypothyroid state?

A

thyroid hormone secretion is subnormal (myxoedema)

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44
Q

Hyperthyroid state?

A

thyroid hormone secretion is excessive (thyrotoxicosis)

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45
Q

What does TSH do?

A

stimulate T3 and T4 production
ALSO

increases protein synthesis in follicular epithelial cells, increases DNA replication and cell division

increases rough endoplasmic reticulum and cell machinery required for protein synthesis

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46
Q

When exposed to greater TSH concentration what happens to the thyroid?

A

thyroid will undergo hypertrophy

this results in goitre

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47
Q

What is a goitre?

A

an enlarged thyroid gland

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48
Q

When can a goitre occur?

A

in hypothyroidism, hyperthyroidism and euthyroidism

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49
Q

Where can a goitre extend to?

A

into the retrosternal space with or without substantial interior enlargement

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50
Q

What can a goitre cause??

A

a variety of compressive syndromes

e.g. local compression causing dysphagia and strider

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51
Q

Non toxic goitre?

A

when thyroid stimulation is normal

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52
Q

Toxic goitre?

A

when thyroid is overactive

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53
Q

Hypothyroid goitre?

A

when thyroid is underactive

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54
Q

How do thyroid hormones get into cells?

A

they are lipophilic and can easily cross cell membranes

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55
Q

Where are receptors for T3 and T4?

A

present in the nuclei of most cells

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56
Q

How does T3 induce effects?

A

by inducing gene transcription and protein synthesis

57
Q

How long to thyroid hormones take to have an effect?

A

hours to days, but once effect is established it will last for days

58
Q

Tissue action of T3?

A

increase basal metabolic rate

increase heat production

responsiveness to sympathetic input

permits normal growth and development

59
Q

Nervous system effects of T3?

A

permits normal growth and development

permits maintenance of normal activity

60
Q

What are the primary actions of thyroid hormones?

A

to increase the bodies metabolic rate

61
Q

How do thyroid hormones increase heat production?

A

increased oxygen consumption and energy expenditure at rest

e.g. increase activity of Na+/K+ pump, as ATP is hydrolysed heat is generated

62
Q

How do thyroid hormones promote energy utilisation?

A

by promoting glycogenolysis and lipolysis

63
Q

What are the effects of the thyroid hormones described as?

A

permissive - they promote the synthesis of beta adrenoceptors this permitting the tissues to respond to sympathetic input and circulating adrenaline

64
Q

Why are developmental aspects of the nervous system important?

A

deficiency can lead to a form of irreversible brain damage called cretinism

65
Q

What is cretinism?

A

the most extreme manifestation of thyroid deficiency

66
Q

What does cretinism cause?

A

mental retardation, reduction in physical growth, deaf mutism

67
Q

What can cretinism be caused by?

A

inadequate dietary intake, maternal iodine deficiency during pregnancy

68
Q

What has been done to prevent cretinism?

A

salt is now fortified with iodine (iodide), 70mcg/g

69
Q

How many thyroid function tests are there in the UK per year?

A

10 million (~£30 million)

70
Q

What are thyroid function tests used for?

A

to establish if there is a thyroid disorder and also monitor the response to therapy

71
Q

What are the thyroid function tests?

A

TSH
free T4
free T3

72
Q

Normal TSH levels?

A

0.27-4.2mU/L

73
Q

Normal free T4?

A

12-22pmol/L

74
Q

Normal free T3?

A

3.1-6.8pmol/L

75
Q

What are free thyroid hormones?

A

the biologically active fraction of the total circulating thyroid hormone pool and are unaffected by changes in the concentration and affinity of the thyroid hormone binding proteins

76
Q

Signs of hypothyroidism?

A

cold intolerance

modest weight gain

bradycardia

tiredness for no reason

constipation

forgetfulness and personality changes (depression)

pale, dry, coarse skin

puffiness of face

77
Q

What can hypothyroidism be thought of?

A

by bringing about a reduction of particular systems within the body e.g. in intestine where it causes constipation by reducing GI motility

78
Q

What is primary hypothyroidism?

A

any condition characterised by plasma T3 or T4 below normal and increased TSH

79
Q

Cause of primary hypothyroidism?

A

95% due to damage or loss of thyroid tissue

can also be due to inadequate iodine consumption

80
Q

What does primary mean?

A

the thyroid gland itself is unable to produce sufficient amounts of the thyroid hormones

81
Q

Why does T3 usually remain normal in primary hypothyroidism?

A

due to the sustained TSH resulting in preferential synthesis and secretion of T3

82
Q

Most common cause of primary hypothyroidism?

A

Hashimoto’s thyroiditis

83
Q

What is Hashimoto’s thyroiditis?

A

an autoimmune disease where there is antibodies to thyroid peroxidase

thyroid is attacked by a variety of cell and antibody mediated immune processes

84
Q

What happens in Hashimoto’s thyroiditis?

A

Immune cells mistakenly attack healthy thyroid tissue causing inflammation of the thyroid and lead to its destruction

85
Q

Who is primary hypothyroidism more prevalent in?

A

women

86
Q

What may occur in primary hypothyroidism?

A

a goitre due to constant stimulatory effects of TSH

87
Q

Treatment for primary hypothyroidism?

A

levothyroxine

synthetic thyroid hormone that is identical to thyroxine (T4)

88
Q

How often should patients on levothyroxine be monitored?

A

annually

89
Q

How often should pregnant patients on levothyroxine be monitored?

A

monthly and should have a 50-100% dose increase

90
Q

How is the dose of levothyroxine adjusted?

A

until TSH levels are in mid range

91
Q

Why is early treatment of primary hypothyroidism important in neonates?

A

to prevent mental defect and serious complications

92
Q

When should primary hypothyroidism be treated?

A

if there is overt clinical hypothyroidism and the TSH is above reference range

93
Q

Adverse effects of levothyroxine?

A

hair loss during first few months

headaches

sleep problems (insomnia)

nervousness

fever, hot flashes, sweating

pounding heart beat or fluttering in chest

appetite changes, weight loss

94
Q

How long do side effects of levothyroxine last?

A

usually temporary as the body adjusts to medication and should resolve after first few months

95
Q

What is another treatment for primary hypothyroidism?

A

Liothyronine

synthetic form of T3

96
Q

What is different around liothyronine?

A

it is not supported in The Royal College of Physicians Consensus Statement on the diagnosis and management of primary hypothyroidism

97
Q

What are the risks of T3 therapy?

A

on bone (osteoporosis) and heart (arrhythmia)

98
Q

When can patients be given T3 therapy?

A

at discretion of endocrinologist - clinical evidence supports use of levothyroxine alone

99
Q

Levothyroxine effects?

A

single dose reaches maximum effect in ~10 days and passes off in 2-3 weeks

100
Q

Why is levothyroxine considered the ideal drug?

A

the conversion from T4 to T3 is constant and stable

101
Q

What is the half life of levothyroxine?

A

7 days in euthyroid and 14 days in hypothyroidism

102
Q

Liothyronine effects?

A

~5 times as biologically potent as T4

single dose reaches its maximum effect in ~24 hours and passes off within 1 week

103
Q

Half life of liothyronine?

A

2 days in euthyroid

104
Q

Binding of liothyronine to plasma proteins?

A

weak which is why it passes off so quickly

105
Q

How long can TSH levels take to return to normal?

A

3-6 months

106
Q

What effects dosage of these drugs?

A

age, pregnancy and weight

107
Q

Secondary hypothyroidism?

A

uncommon

pituitary doesn’t produce TSH

108
Q

Levels of T3, T4 and TSH in secondary hypothyroidism?

A

all below normal

109
Q

Tertiary hypothyroidism?

A

hypothalamus doesn’t produce sufficient TRH

110
Q

Symptoms and treatment of secondary hypothyroidism?

A

same as primary hypothyroidism

111
Q

What is myxoedema coma?

A

the end result of untreated hypothyroidism

progressive weakness leading to a loss of conciousness

112
Q

Symptoms of myxoedema coma?

A

extreme hypothermia (24-32 degrees)

areflexia, seizures, respiratory depression

113
Q

Precipitating factors of myxoedema coma?

A

Illness, infection, trauma, drugs that suppress the CNS, exposure to cold

114
Q

Who does myxoedema coma usually occur in?

A

patients who have a long history of hypothyroidism

115
Q

Why is rapid diagnosis of myxoedema coma important?

A

it is a medical emergency, the mortality rate is ~80% without rapid treatment

116
Q

How can corticosteroids affect thyroid function?

A

can decrease basal production of TRH and TSH, consequently decreasing thyroid hormone levels

high doses of these e.g. dexamethasone

117
Q

How does lithium affect thyroid function?

A

used for manic depression

inhibits the release of thyroid hormones and interfered with their peripheral deiodination

118
Q

How does amiodarone affect thyroid function?

A

an antiarrhythmic

contains iodine and can cause both hypothyroidism and hyperthyroidism

119
Q

How does cholestyramine affect thyroid function?

A

reduces blood cholesterol

reduces the absorption of thyroxine from the GI tract

120
Q

Symptoms of hyperthyroidism?

A

Heat intolerance

palpitations

weight loss (despite increased appetite)

restlessness and nervousness

fatigue

increased sweating

frequent bowel movements

goitre may be present

121
Q

What is hyperthyroidism?

A

thyroid produces an excess of T4, reduction in TSH due to negative feedback loop

122
Q

T3, T4 & TSH levels in hyperthyroidism?

A

T4 elevated
T3 usually elevated
TSH decreased

123
Q

What is the most common cause of hyperthyroidism?

A

Grave’s disease (85% of cases)

124
Q

Two characteristics of grave’s disease?

A

goitre

exopthalmos (protruding eyeballs)

125
Q

What is Grave’s disease?

A

an autoimmune disease caused by thyroid stimulation immunoglobulin (TSI)

126
Q

What does TSI do?

A

activates TSH receptor on thyroid follicular cells and causes increased secretion of thyroid hormones

127
Q

How does TSI function?

A

just like TSH, is stimulatory so produces a goitre

128
Q

When can Grave’s disease sometimes occur?

A

with other autoimmune disorders like diabetes, pernicious anaemia and connective tissue disorders

129
Q

What increases risk of grave’s disease?

A

hereditory

130
Q

Treatment for hyperthyroidism?

A

Surgery to remove the thyroid gland

radioactive iodine (131Iodine)

131
Q

How is radioactive iodine administered?

A

orally

132
Q

how does radioactive iodine work?

A

it is taken up by the thyroid gland and emmits gamma and beta radiation (T1/2 8.1 days), this leads to destruction of cells in the thyroid gland, causing it to shrink and reducing hormone production

133
Q

How long does radioactive iodine take to work?

A

usually has its maximum effect around 3 months but may be as long as 6 months

134
Q

Antithyroid drugs?

A

Thioamides e.g. carbimazole and propylthiouracil

135
Q

How do antithyroid drugs work?

A

accumulated by the thyroid and inhibit thyroid peroxidase, and prevent hormone synthesis

136
Q

What does propylthiouracil inhibit as well?

A

peripheral deiodination

137
Q

Onset of antithyroid drugs?

A

slow (4-6 weeks)

138
Q

Side effects of antithyroid drugs?

A

generally safe but may cause agranulocytosis, increasing the risk of infection (esp carbimazole)

Management of GI and Endocrine Conditions (24 decks)

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