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Y2 Endocrine > Thyroid: Science and Diseases > Flashcards

Thyroid: Science and Diseases Flashcards

1
Q

Where do the thyroid lobes attach?

A

thyroid and cricoid cartilages

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2
Q

Which cartilages does the thyroid attach? Which is superior and which is inferior?

A

Thyroid (superior), Cricoid (inferior)

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3
Q

Where does the isthmus of the thyroid gland lie?

A

2-3rd tracheal cartilages – C5-T1 vertebrae

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4
Q

Where does the thyroid gland originally develop?

A

between the anterior and posterior parts of the tongue, where the foramen caecum is found in adults

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5
Q

How does the thyroid migrate to its adult location?

A

via the thyroglossal duct - around week 7

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6
Q

Working anteriorly to posteriorly, what is the first level of fascia found at the neck?

A

Superficial fascia

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7
Q

What does the superficial fascia of the neck contain?

A

platysmus

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8
Q

Working anteriorly to posteriorly, what is found after the superficial fascia in the neck?

A

anterior investing fascia

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9
Q

What does the anterior investing fascia contain?

A

the sternocleidomastoid muscles

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10
Q

Working anteriorly to posteriorly, what is found after the anterior investing fascia in the neck?

A

pretracheal fascia

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11
Q

What is found within the pretracheal fascia? (5)

A

strap muscles, trachea, oesophagus, recurrent laryngeal nerves, thyroid gland

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12
Q

What is found bilaterally to the pretracheal fascia in the neck?

A

carotid sheath

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13
Q

What is found within the carotid sheath? (4)

A

internal jugular vein, deep cervical lymph nodes, vagus nerves, carotid arteries

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14
Q

Which fascia is found beyond the pre-tracheal fascia?

A

pre-vertebral fascia

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15
Q

What is found within the pre-vertebral fascia?

A

c-vertebrae, postural neck muscles

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16
Q

What muscle is found within the posterior investing fascia?

A

the trapezius muscles (bilaterally)

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17
Q

Which arteries supply the thyroid gland? (2)

A

superior and inferior thyroid arteries

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18
Q

What are the origins of the superior and inferior thyroid arteries?

A

superior - external carotid; inferior - branch of subclavian

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19
Q

Which veins does the thyroid gland drain? (3)

A

the superior (2), middle (2) and inferior thyroid (1) veins

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20
Q

Where do the veins from the thyroid gland drain?

A

superior and middle –> internal jugular –> brachiocephalic; inferior –> brachiocephalic

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21
Q

Which lymph nodes does the thyroid gland drain into? (4)

A

the inferior pretracheal node; paratrachial nodes; superior deep cervical nodes and deep cervical nodes

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22
Q

Which aortic arch is the subclavian artery formed from?

A

4th

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23
Q

Which aortic arch is the arch of the aorta formed from?

A

4th

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24
Q

Name the 4 strap muscles

A

Omohyoid, sternohyoid, sternothyroid, thyrohyoid

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25
Q

What 3 things does the thyroid gland secrete?

A

T4 (thyroxine), T3 (triiodothyronine), calcitonin

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26
Q

What naturally causes an increase in the size of the thyroid gland?

A

menstruation and pregnancy

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27
Q

Innervation of the thyroid gland (2)

A

ANS including Vagus nerve (Parasympathetic) and the sympathetic trunk

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28
Q

Describe the structure of the thyroid gland

A

follicles surround by follicular cells; parafollicular C cells found dotted about

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29
Q

What is found within the follicle of the thyroid gland?

A

colloid - tyrosine containing thyroglobulin

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30
Q

How are T3/T4 secreted into the blood stream?

A

via pinocytosis

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31
Q

How is T3 made?

A

Iodine taken into the follicle is attached to tyrosine residues in the form of mono-iodotyrosine (MIT) or di-iodotyrosine (DIT). T3 is made up of MIT+DIT

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32
Q

How is T4 made?

A

Iodine taken into the follicle is attached to tyrosine residues in the form of mono-iodotyrosine (MIT) or di-iodotyrosine (DIT). T4 is made up of DIT + DIT

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33
Q

Which thyroid hormone is more potent?

A

T3

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34
Q

Which thyroid hormone is more biologically active?

A

T3

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35
Q

Which thyroid hormone is most commonly secreted?

A

T4

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36
Q

Where is T4 converted to T3?

A

the liver and kidney

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37
Q

What stimulates the release of T3 and T4 from the follicular cell?

A

TSH

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38
Q

How are T3/T4 carried within the blood stream and why?

A

T3/T4 are hydrophobic so are carried in the plasma bound to plasma proteins - when they are in the free form they are biologically active

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39
Q

Name the 3 proteins which T3/T4 are most commonly bound to

A

Thyroxine binding globulin (TBG) ~70%; Transthyretin thyroxine binding pre-albumin (TTR); Albumin (5%)

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40
Q

Which form of T3/T4 is more closely correlated to the metabolic state?

A

free T3 and free T4

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41
Q

What is the result of increasing TBG?

A

increased total T4, not free T4

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42
Q

States where there may be increased TBG (4/7)

A

pregnancy, newborn, hepatitis, biliary cirrohosis, oral contraceptive pill (or other sources of oestrogen), acute intermittent porphyrias, heroin

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43
Q

What is the result of decreasing TBG?

A

decreased total T4, not free T4

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44
Q

States where there may be a decrease in TBG (4/7)

A

androgens, large doses of glucocorticoids, active acromegaly, severe systemic illness, chronic liver disease, phenytoin, carbemazepine

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45
Q

Physiological effect of increasing thyroid hormones (5/8)

A

increased BMR; increased thermogenesis; increased carbohydrate/lipid metabolism; increased protein synthesis; growth; development of foetal/neonatal brain; normal CNS activity

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46
Q

How does thyroid hormone affect the response to adrenaline?

A

increases responsiveness to adrenaline and NA by increasing the number of receptors –> increase in HR and force

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47
Q

Why is propanolol an initial treatment of hyperthyroidism?

A

It antagonises the adrenoreceptors to reduce HR and force which can be found in hyperthyroidism

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48
Q

How does thyroid hormone increase BMR?

A

increases the number and size of mitochondria, increases oxygen use and ATP hyrdolysis and increases the synthesis of respiratory chain enzymes

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49
Q

How much of temperature regulation is affected by thyroid hormone?

A

30%

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50
Q

How does thyroid hormone affect carbohydrate metabolism?

A

increased blood glucose through glycogenolysis and gluconeogenesis while increasing insulin dependent uptake into cells

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51
Q

How does thyroid hormone affect growth?

A

GHRH production and secretion requires TH

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52
Q

How does thyroid hormone affec the development of the neonatal brain?

A

increases myelinogenesis and axonal growth

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53
Q

How is thyroid hormone release regulated?

A

Thyrotropin RH is released from the hypothalamus and stimulates TSH release from the anterior pituitary

54
Q

How do T3/T4 impact the release of TRH?

A

negative feedback system: T3/T4 inhibit the release of TRH and TSH

55
Q

What kind of receptor is the TSH receptor?

A

A GPCR which stimulates cAMP in the follicular cell

56
Q

When is TH highest in the day?

A

Late at night; lowest in the morning

57
Q

How many types of de-iodinase enzymes are there?

A

3

58
Q

Which de-iodinase enzyme is most important for converting T4 to T3 ?

A

type 2

59
Q

Where is type 2 de-iodinase enzyme mostly found?

A

within the heart, skeletal muscle, CNS, fat, thyroid and pituitary

60
Q

Where is type 3 de-iodinase enzyme mostly found?

A

foetal tissue, the placenta and brain (-pituitary)

61
Q

Where is type 1 de-iodinase enzyme mostly found?

A

liver and kidneys

62
Q

How does T3 activate the TH receptor?

A

TH receptor is activated and travels to the nucleus of the cell where it binds with the RXR and a transcription factor

63
Q

What are the 4 thyroid hormone receptor isoforms?

A

TRa1, TRa2, TRb1, TRb2

64
Q

Which is the predominant form of thyroid hormone receptor in most tissues?

A

TRa

65
Q

Which tissues is TRb the predominant form of thyroid hormone receptor?

A

liver and negative feedback loop

66
Q

Test results show: high TSH, low fT4…diagnosis is…

A

primary hypothyroidism

67
Q

Test results show: high TSH, normal fT4…diagnosis is…

A

subclinical hypothyroidism

68
Q

Test results show: high TSH, high fT4…diagnosis is…

A

TSH secreting tumour or TH resistance

69
Q

Test results show: high TSH, high fT4/ low fT3..diagnosis is…

A

deiodinase deficiency, TH antibody

70
Q

Test results show: low TSH, high fT4/T3…diagnosis is…

A

primary hyperthyroidism

71
Q

Test results show: low TSH, normal fT4…diagnosis is…

A

subclinical hyperthyroidism

72
Q

Test results show: low TSH, low fT4…diagnosis is…

A

secondary hypothyroidism

73
Q

Test results show: low TSH, lowfT4/T3…diagnosis is…

A

sick euthyroid or pituitary disease

74
Q

Test results show: normal TSH, abnormal fT4…diagnosis is…

A

consider TBG, amiodarone, pituitary TSH tumour

75
Q

Chief cause of hypothyroidism worldwide

A

iodine deficiency

76
Q

Chief cause of hypothyroidism in the UK

A

Hashimotos disease

77
Q

Clinical features of hypothyroidism that might be seen in the hair and skin (4+)

A

coarse, sparse hair; dull expressionless face; periorbital puffiness; pale cool skin that feels doughy

78
Q

Clinical features involving thermogenesis of hypothyroidism

A

cold intolerance

79
Q

Cardiac features of hypothyroidism

A

bradycardia, worsening heart failure

80
Q

Metabolic features of hypothyroidism

A

hyperlipidaemia, weight gain, decreased appetite

81
Q

Common GI feature of hypothyroidism

A

constipation

82
Q

Common neurological features of hypothyroidism

A

depression, psychosis, carpal tunnel syndrome and decreased visual acuity

83
Q

Common gynae features of hypothyroidism

A

menorrhagia follows by amenorrhoea

84
Q

Goitrous causes of primary hypothyroidism (4)

A

chronic thyroiditis (Hashimotos), iodine deficiency, drug induced (lithium, amiodarone), maternally transmitted

85
Q

Non-goitrous causes of primary hypothyroidism (3)

A

atrophic thyroiditis (autoimmune), post-ablative, congenital developmental defect

86
Q

Subclinical hypothyroidism may present with what blood test features?

A

high TSH, normal T4

87
Q

Common clinical investigations other than thyroid function tests which may be ordered when considering hypothyroidism

A

MCV - macrocytosis, increased CK, increased LDL and cholesterol, hyponatraemia, hyperprolactinaemia

88
Q

Main drug treatment of hypothyroidism

A

levothyroxine (T4) - taken before breakfast

89
Q

Why might levothyroxine dose need to be increased in pregnancy?

A

due to increased TBG produced by the liver

90
Q

Why is it important to slowly restore normal thyroid function in hypothyroidism?

A

it may cause cardiac arrhythmias

91
Q

Dose of levothyroxine in young person?

A

50-100µg/day

92
Q

Dose of levothyroxine in elderly

A

25-50µg/day

93
Q

Antibodies associated with Hashimoto’s thyroiditis

A

anti-TPO - thyroid peroxidase

94
Q

group most commonly affected by myxoedema coma

A

elderly women with longstanding or undiagnosed hypothyroidism

95
Q

Signs of myxoedema coma

A

bradycardia, type 2 resp failure, hypoxia, hypercarbia, co-existing adrenal failure

96
Q

cardiac features of hyperthyroidism

A

palpitations, AF, rarely cardiac failure

97
Q

General feelings when suffering from hyperthyroidism

A

anxiety, irritibility, sleep disturbance

98
Q

How might hyperthyroidism affect the sympathetic nervous system?

A

sweating and tremors

99
Q

Visual features of hyperthyroidism

A

lid retraction (non-specific), diplopia, proptosis - Graves

100
Q

Gynae features of hyperthyroidism

A

lighter and less frequent periods

101
Q

Where might a patient experience weakness in hyperthyroidism?

A

thighs and upper arms

102
Q

Thermogenesis in hyperthryoidism

A

heat intolerance

103
Q

Weight in hyperthyroidism

A

decreased despite increased appetite

104
Q

Causes of thyrotoxicosis associated with hyperthyroidism (7)

A

Graves, Hashitoxicosis, thyrotropinoma, thryoid cancer, toxic solitary nodule, toxic multinodular goitre

105
Q

Causes of thyrotoxicosis associated with hyperthyroidism (3)

A

thyroid inflammation (post-partum, sub-acute, drug induced), exogenous TH, ectopic thyroid tissue

106
Q

Age associated with Grave’s disease

A

younger patients (20-50years)

107
Q

Is there a genetic component to Graves?

A

Yes - 70% have susceptibility factors and sisters and children of women with Graves have a 5-8% chance of developing an autoimmune thyroid disease of any kind

108
Q

Key exacerbating factor in Grave’s disease

A

smoking - more severe and difficult to treat in smokers

109
Q

Investigations in Graves disease

A 
TFT 
LFTs
Calcium
WCC
TSH receptor antibody
110
Q

Thyroid function test results expected in Graves disease

A

Decreased TSH and increased fT3/T4

111
Q

Expected LFTs and calcium results in Graves disease

A

hypercalcaemia and raised ALP due to increased bone turnover –> association with osteoporosis

112
Q

Expected WCC in Graves disease

A

leucopaenia - often milk

113
Q

TSH receptor antibody is confirmation of diagnosis of Graves - True/False

A

True - If this is present then there is no need to image the thyroid gland

114
Q

Clinical signs of Graves disease (4)

A

Pretibial myxoedema, thyroid acropachy, thyroid bruit, graves eye disease

115
Q

Graves eye disease occurs in what percentage of patients…what group are particularly high risk?

A

20%, particularly smokers

116
Q

confirmation of graves eye disease on MRI

A

inflammation behind the eye

117
Q

Which group of patients is most likely to experience nodular thyroid disease?

A

older patients - occurs with insidious onset

118
Q

What features suggest a thyroid storm?

A

resp and cardiac collapse, severe hyperthermia, exaggerated reflexes

119
Q

Patients at risk of thyroid storm?

A

those with acute infection or recent surgery

120
Q

treatment of a thyroid storm?

A

Lugol’s iodine, glucocorticoids, PTU, b-blockers, fluids and monitoring

121
Q

Brief overview of deQuervains thyroiditis

A

subacture granulomatous thyroiditis, inflammation of thyroid which may be painful and oftern preceeded by a viral illness

122
Q

3 phases of deQuervains thyroiditis

A

thyrotoxicosis, hypothyroid, euthryroid

123
Q

investigation results confirming deQuervains thyroiditis

A

raised ESR, CRP and TH levels

124
Q

First line treatment of hyperthyroidism

A

carbimazole

125
Q

mechanism of action of treatment of hyperthyroidism

A

inhibition of thyroid peroxidase –> blocks TH synthesis

126
Q

situation where carbimazole is not first line treatment

A

early pregnancy - may cause aplasia cutis

127
Q

1st line treatment in early pregnancy for hyperthyroidism

A

polythiouracil (PTU) - 10x less potent than carbimazole

128
Q

mechanism of action of PTU

A

inhibits DIO1

129
Q

main risk of PTU

A

1:10000 liver failure

130
Q

in the first 6 weeks of hyperthyroid treatment, what is the biggest side effect risk

A

agranulocytosis - warn verbally, get urgent FBC if fever, oral ulcer or oropharyngeal infection

131
Q

common side effects of hyperthyroidism treatments

A

cholestatic jaundic, increased liver enzymes, fulminant liver failure

Y2 Endocrine (4 decks)

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