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J Endocrine > Thyroid gland > Flashcards

Thyroid gland Flashcards

1
Q

what is the large cell surrounded by lots of small cells in a follicle

A

colloid

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2
Q

what is the small cells that surround the colloid cell in a follicle

A

follicular cells

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3
Q

what cells surround follicles

A

parafollicular C cells

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4
Q

what do follicular cells secrete

A

calcitonin

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5
Q

where are the follicular cells in between

what is their function

A

colloid cells
blood vessels

allow T3 and T4 into blood stream (from colloid cells)

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6
Q

is T3 or T4 secreted more

A

T4

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7
Q

what is T4

A

thyroxine

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8
Q

what is T3

A

tri-iodothyronine

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9
Q

what is T4 made from

A

2 DIT (di-iodo tyrosine) molecules

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10
Q

what is T3 made from

A

1 DIT (di-iodo tyrosine) and 1 MIT (mono-iodo tyrosine) molecule

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11
Q

% of T4 thats free

A

1%

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12
Q

what do the 99% of bound thyroxine (T4) bind to

A

thyroxine binding globulin (70%)
albumin
transthyretin (TTR)

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13
Q

why are most of T4 (thyroxine) bound in the blood

A

need to be bound to be transported

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14
Q

which type of T4 (thyroxine) is active (bound or free)

A

free

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15
Q

which type of thyroxine (T4) is measured when we measure T4 levels

A

free T4

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16
Q

what hormone does the hypothalamus produce in the hypothalamic pituitary thyroid axis

A

thyrotropin releasing hormone (TRH)

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17
Q

what hormone does the anterior pituitary release in response to thyrotropin releasing hormone (TRH)

A

thyroid stimulating hormone (TSH)

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18
Q

which cell does TSH (thyroid stimulating hormone) act on in the follicle

what does this cause

A

follicular cells

release of T4 and T3 from colloid cells

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19
Q

even though there is more T4 secreted, what happens to it when it reaches cells

A

turns in to T3

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20
Q

what converts T4 to T3

A

iodothyronine deiodinase (ID) types I, II and III

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21
Q

significance of IDI in T4 to T3 conversion

A

determines T3 in blood

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22
Q

significance of IDII in T4 to T3 conversion

what % of the overall T4 to T3 conversion is this

A

determines T3 in peripheral tissues

80%

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23
Q

significance of IDIII in T4 to T4 conversion

A

occurs in brain, fetal tissue, placenta

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24
Q

what are the 2 things taken up by the colloid cells for T3 and T4 synthesis

A 
iodine
thyroid peroxidase (TPO) enzyme
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25
Q

when are T3 and T4 released from colloid cells

what needs to happen to them before they are released

A

TSH stimulation

lysosomes break down thyroglobulin

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26
Q

what are the 2 types of thyroid receptors

A

beta and alpha

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27
Q

where are alpha thyroid receptors

A

peripheral tissues (basically everywhere = vast symptoms)

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28
Q

where are beta thyroid receptors

A

brain/thyroid feedback loop

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29
Q

generally what does the presence of thyroid hormones cause

A

increased metabolic rate

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30
Q

first line investigation for any ?thyroid problem

A

thyroid function tests - TSH, free T4, free T3

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31
Q

imaging options for ?thyroid problem (2)

A

ultrasound (with FNA if ?malignancy)

thyroid uptake scan (darker = more uptake = hyperthyroid (increased metabolism))

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32
Q

most common cause of hypothyroidism

A

hashimotos thyroiditis (chronic thyroiditis)

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33
Q

aetiology of hashimotos thyroiditis

A

autoimmune

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34
Q

which group of people (age and gender) are most likely to get hashimotos thyroiditis

A

middle aged females

same as all autoimmune conditions

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35
Q

autoimmune attack of thyroid peroxidase (TPO) = destruction of thyroid gland = reduced thyroid hormone production

A

hashimotos thyroiditis

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36
Q

goitre in hashimotos thyroiditis?

A

yes

bc its a chronic condition

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37
Q

which autoantibody is positive in hashimotos thyroiditis

A

anti-TPO

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38
Q

although hashimotos is a hypothyroid problem, what may happen in the initial stages of the disease

A

hyperthyroidism THEN hypothyroidism

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39
Q

apart from hashimotos thyroiditis what are the other aetiologies of primary hypothyroidism (6)

A

iodine deficiency
congenital
postpartum thyroiditis (in mums after birth , self limiting)
atrophic thyroiditis (acute thyroiditis)
drugs
post surgery

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40
Q

investigation results for primary hypothyroidism

A 
low free T3/T4 
high TSH (negative feedback)
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41
Q

where is the problem in primary hypothyroidism

A

thyroid gland itself

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42
Q

where is the problem in secondary hypothyroidism

A

above the thyroid gland (hypothalamus or pituitary)

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43
Q

in primary hypothyroidism bc TSH is high (negative feedback of low T3/T4), what else is high

A

prolactin

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44
Q

aetiology of secondary hypothyroidism (3)

A

vague things;
malignancy
drugs
infection (sick euthyroid syndrome)

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45
Q

why dont you check thyroid function tests in people with infection

A

sick euthyroid syndrome

completely normal, but T3/T4 are low - will fix itself so dont worry

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46
Q

overt hypothyroidism definition

A

clinical presentation

low T3/T4

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47
Q

subclinical hypothyroidism definition (investigation results)

A

high TSH, normal T3/T4 = probs dont have symptoms

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48
Q

BMI in hypothyroidism

A

high

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49
Q

face in hypothyroidism

A

‘toad like’

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50
Q

eyes in hypothyroidism (3)

A

exophthalmos
closed
puffy

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51
Q

heart in hypothyroidism

A

bradycardia (slow) - be careful of arrhythmias when treating if you treat it too fast

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52
Q

temp in hypothyroidism

A

cold

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53
Q

bowel movements in hypothyroidism

A

constipation

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54
Q

reflexes in hypothyroidism

A

slow

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55
Q

periods in hypothyroidism

A

menorrhagia - heavy periods (think hypo = slows things down = makes them worse = makes periods worse too)

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56
Q

hypothyroidism treatment

A

levothyroxine (T4)

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57
Q

levothyroxine dose in young for hypothyroidism

A

50-100ug

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58
Q

levothyroxine dose in old/CVD risk for hypothyroidism

A

25ug

59
Q

medication advice for levothyroxine (when to take, what not to take with) for hypothyroidism

A

before breakfast

not at same time as Ca supplement, PPI, iron tablets

60
Q

causes of levothyroxine malabsorption in hypothyroidism (2)

A

other drugs at same time - PPI, Ca supplement, iron tablets

coeliac disease

61
Q

in pregnancy what do you do to levothyroxine dose in hypothyroidism

A

increase dose by 25ug

62
Q

complication of untreated hypothyroidism

treatment

A

myxoedema coma - puffy face, hands

medical emergency - warm up, thyroxine slowly, ABCDE

63
Q

aetiology of acute thyrotoxicosis (hyperthyroidism) (2)

A

thyroiditis - de quervains (viral infection), post partum, drug induced, hashimotos (before it turns hypothyroid)
thyroxine tablet overdose

64
Q

aetiology of chronic thyrotoxicosis (hyperthyroidism) (3)

A

graves disease
thyroid nodules
thyroid cancer

65
Q

for hyper and hypothyroid disease, when do goitres occur

A

if the condition is chronic (not acute)

66
Q

aetiology of graves disease

A

autoimmune

67
Q

most common cause of hyperthyroidism

A

graves disease

68
Q

which group (age and gender) usually presents with graves

A

middle aged females

like all other autoimmune conditions

69
Q

graves disease is an autoimmune condition, what thing is produced that causes the hyperthyroidism

what does it act like
what does this cause

A

thyroid stimulating immunoglobulin (TSI)

thyroid stimulating hormone (TSH)

increased T3 and T4 release

70
Q

histology of graves disease

A

lymphoid follicles scattered through thyroid

71
Q

presentation of graves disease (6)

A 
hyperthyroid presentation (long list lol)
symmetrical smooth goitre (sometimes)
pretibial myxoedema  
thyroid bruit (on auscultation) 
graves eye disease 
clubbing of fingers (thyroid acropachy)
72
Q

leg presentation of graves disease and description

A

pretibial myxoedema - bilateral plaques, red bumpy rash on legs

73
Q

presentation of graves eye disease (4)

A

double vision (diplopia)
lid lag/lid retraction
protruding eyes
exophthalmos

74
Q

treatment of severe graves eye disease

A

decompression surgery to bring down swelling

75
Q

positive investigations in graves disease (4)

A

high T3/T4
low TSH (negative feedback)
anti-TPO positive (non specific, also positive in hashimotos)
TSH receptor antibody positive (TRAbs) - specific, not positive in hashimotos
thyroid uptake scan

76
Q

treatment of graves (3)

A

carbimazole
surgery if severe
smoking cessation

77
Q

investigation findings of primary hyperthyroid disease (2)

A 
high free T3/T4 
low TSH (from negative feedback)
78
Q

investigation findings of secondary hyperthyroid disease (2)

A 
high free T3/T4
high TSH (this is the cause)
79
Q

investigation results for secondary hypothyroid disease (2)

A 
low free T3/T4 
low TSH (this is the cause)
80
Q

in chronic hyperthyroid disease, what is the most likely aetiology for an elderly patient

A

thyroid nodules

81
Q

asymmetrical rough goitre in hyperthyroidism

A

thyroid nodules

82
Q

symmetrical smooth goitre in hyperthyroidism

A

graves disease

83
Q

treatment of thyroid nodules causing hyperthyroidism

A

radioiodine
surgery
carbimazole long term

84
Q

where is the problem in primary hyperthyroidism

A

thyroid gland itself

85
Q

where is the problem in secondary hyperthyroidism

A

above the thyroid gland (hypothalamus or pituitary)

86
Q

overt hyperthyroidism definition

A

has clinical evidence

high T4/T3

87
Q

subclinical hyperthyroidism definition

A

low TSH but normal T4/3 = probs no symptoms

88
Q

when do you treat subclinical hyperthyroidism

A

TSH <0.1

89
Q

when do you treat subclinical hypothyroidism

A

TSH >10

90
Q

BMI in hyperthyroidism

A

low

91
Q

temp in hyperthyroidism

A

high

92
Q

CNS response to hyperthyroidism (3)

A

tremor, anxiety, nervous

93
Q

heart in hyperthyroidism (2)

A

tachycardia, palpitations

94
Q

bowel habits in hyperthyroidism

A

diarrhoea

95
Q

periods in hyperthyroidism

A

lighter

think hyper = speeds things up = makes them better

96
Q

reflexes in hyperthyroidism

A

fast

97
Q

skin in hyperthyroidism

A

thin skin

98
Q

how does hyperthyroidism present in pregnancy

A

like hyperemesis - vomiting, nausea, tachycardia, warm

need to check TSH, will last >20 weeks (hyperemesis only lasts <20 weeks)

99
Q

imaging for hyperthyroid disease (after TFTs)

A

thyroid isotope uptake scan to differentiate between graves, nodules etc

100
Q

treatment physiology of hyperthyroid disease (antithyroid drugs)

A

block TPO (thyroid peroxidase enzyme ) = decrease T3 and T4 production

101
Q

treatment options for hyperthyroid disease (4)

A

antithyroid drugs; carbimazole, propylthiouracil (PTU)
radioiodine
surgery

102
Q

1st line treatment for hyperthyroidism

A

carbimazole

103
Q

1st line treatment for hyperthyroidism in 1st trimester of pregnancy

A

propylthiouracil (PTU)

104
Q

why is prophylthiouracil (PTU) preferred over carbimazole in 1st trimester of pregnancy

A

less potent

105
Q

side effect of propylthiouracil (PTU)

why its not used all the time (just in 1st trimester of pregnancy

A

liver toxicity

106
Q

side effect of all anti thyroid drugs (carbimazole, propylthiouracil (PTU))

A

agranulocytosis

NEED TO WARN PATIENTS need to stop drug immediately

107
Q

patient with hyperthyroidism on carcbimazole develops mouth/throat infection

what do they have
what do you do

A

agranulocytosis (side effect of antithyroid drugs)

stop drug immediately, FBC looking for increased WCC (infection)

108
Q

immediate symptomatic treatment for hyperthyroidism (bc the antithyroid drugs take a couple weeks to work)

A

beta blockers (propranolol)

109
Q

2nd line treatment for graves after antithyroid drugs (carbimazole, propylthiouracil)

what do you give alongside this

A

radioiodine

need thyroxine replacement bc you destroy the entire thyroid gland (otherwise will cause hypothyroidism)

110
Q

1st line treatment of nodules causing hyperthyroidism

A

radioiodine

111
Q

treatment of hyperthyroidism if radioiodine contraindicated

what do you give alongside this

A

surgery

thyroxine bc you are destroying the thyroid gland = hypothyroidism

112
Q

what do you need to watch out for in hyperthyroid patient with infection

management of this

A

sever hyperthyroidism (thyroid storm)

emergency treatment - ABCDE, ventilation, high dose steroids (inhibit conversion of T4 to T3), beta blockers, fluid etc etc

113
Q

are solitary or multinodular thyroid goitres more common

A

solitary

114
Q

types of benign thyroid nodule (3)

A

benign follicular adenoma
cyst
colloid nodule

115
Q

are most thyroid nodules benign or malignant (%)

A

95% benign

116
Q

most common malignant thyroid cancer (80%)

A

papillary thyroid cancer

117
Q

what clinical condition can benign thyroid nodules cause

A

hyperthyroidism (thyrotoxicosis)

118
Q

types of malignant thyroid cancer (5)

A 
papillary thyroid carcinoma
follicular thyroid carcinoma 
medullary thyroid carcinoma 
thyroid lymphoma
anaplastic thyroid carcinoma
119
Q

risk factors for thyroid cancer (3)

A

nuclear incidents/neck exposure
genetics (ask about family history)
iodine deficiency

120
Q

which thyroid cancer is associated with hashimotos thyroiditis

A

papillary thyroid carcinoma

121
Q

histology of papillary thyroid carcinoma (2)

A 
'orphan annie' nucleus (looks like her big white eyes) 
psammoma bodies (collection of calcium)
122
Q

are males or females more likely to get thyroid cancer

A

females

123
Q

investigations for ?thyroid cancer

A

TFTs (thyroid function tests)

US (ultrasound) guided FNA (fine needle aspiration)

124
Q

treatment of malignant thyroid cancer

A

surgery - lobectomy if AMES low risk, total thyroidectomy if AMES high risk

125
Q

what does AMES stand for in determining the risk of thyroid cancer

A

Age
Metastasis
Extent of tumour
Size of tumour

eg high risk = >50, extrathyroidal if papillary OR capsular invasion if follicular, >5cm

126
Q

after thyroid surgery for thyroid cancer, what do you need to give patient

A

levothyroxine

127
Q

if prognosis generally good or bad for papillary and follicular thyroid cancer

A

good
5% mortality for papillary thyroid carcinoma
10% mortality for follicular thyroid carcinoma

128
Q

how does papillary thyroid cancer spread

A

lymph nodes

129
Q

how does follicular thyroid cancer spread

A

blood = bone, brain, lungs

130
Q

what 2 groups of patients are associated with medullary thyroid carcinomas

A

40s/50s

young patients with MEN2 (familial phaeochromocytoma and medullary thyroid carcinoma)

131
Q

where are medullary thyroid carcinomas

hence what do they secrete

A

parafollicular C cells

calcitonin

132
Q

which thyroid cancer has worst prognosis bc it is v aggressive

A

anaplastic thyroid cancer

133
Q

presentation of thyroid cancer

A

rough asymmetrical goitre
moves on swallowing
not painful

134
Q

rough asymmetrical goitre with lymphadenopathy

A

papillary thyroid carcinoma

135
Q

rough asymmetrical goitre with hoarseness

A

anaplastic thyroid carcinoma (v aggressive = vocal cord palsy)

136
Q

aetiology of a multinodular goitre

pathophysiology

A

iodine deficiency

decrease in T3/T4 secretion = increase in TSH - increased thyroid gland size

137
Q

what complication may a multinodular goitre have (bc its so big)

A

compression of trachea

138
Q

when would you treat a multinodular goitre (you normally dont do anything)

A

if compression of trachea or ?cancer

139
Q

viral infection
high T4/T3
low TSH

(few weeks later, more normal TFTs)

A

acute thyroiditis (cause by viral infection = dequervains thyroiditis)

140
Q

aetiology of a goitre (5)

A 
chronic hyperthyroidism 
chronic hypothyroidism 
benign thyroid cancer 
malignant thyroid cancer 
multinodular goitre (iodine deficiency)
141
Q

how does congenital thyroid disease present in babies

A

poor appetite but normal weight (= weight gain)

delayed jaundice

142
Q

aetiology of congenital thyroid disease (3)

A

missing thyroid
abnormally located thyroid
congenital pituitary disease

143
Q

complication of baby with congenital thyroid disease that isnt treated within 3 months

A

cretinism (permanent developmental delay)

144
Q

is acquired thyroid disease common in kids

A

no

J Endocrine (12 decks)

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