Hyperthyroidism, Hypothyroidism and Thyroiditis Flashcards

1
Q

what causes secondary thyroid disease

A

hypothalamic or pituitary disease

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2
Q

what is thyrotropin

A

thyroid stimulating hormone

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3
Q

what makes up 80% of TSH

A

T4- biologically inactive

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4
Q

what plasma proteins does TSH bind to

A

TBG, albumin, pre albumin

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5
Q

what is TSH released in response to

A

TRH

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6
Q

what happens to TSH when you are hypothyroid

A

is increased in attempt to get euthyriod

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7
Q

what is diodination

A

removal of iodine - T4 into T3

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8
Q

what are hormone levels like in primary hypothyroidism

A

free T3/4 low

TSH high

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9
Q

what are hormone levels like in primary hyperthyroidism

A
free T3/4 high
TSH low (often 0)
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10
Q

what are hormone levels like in secondary hypothyroidism

A

free T3/4 low

TSH low/ normal

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11
Q

what are hormone levels like in secondary hyperthyroidism

A

free T3/4 high

TSH high/ normal

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12
Q

what is myxoedema

A

either
coma-severe hypothyroidism, a medical emergency

or
swelling of the skin and underlying tissues giving a waxy consistency, typical of patients with underactive thyroid glands.

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13
Q

what is pretibial myxoedema

A

sign of graves disease (hyperthyroidism) - infiltrative dermopathy resulting in localised lesions of the skin

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14
Q

what ethnicity is hypothyroidism most common in

A

white populations

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15
Q

what are the causes of primary goitrous hypothyroidism

A

chronic thyroiditis (hashimotos), iodine deficiency, drug induced (amiodarone, lithium), maternally transmitted (antithyroid drugs e.g. for graves), hereditary biosynthetic defects

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16
Q

what are the causes of primary non- goitrous hypothyroidism

A

atrophic thyroiditis (untreated hashimotos), post ablative therapy (radioiodine, surgery), post-radiotherapy (lymphoma treatment), congenital developmental defect

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17
Q

what are the causes of primary self limiting hypothyroidism

A

withdrawal of antithyroid drugs, subacute thyroiditis with transient hypothyroidism, post partum thyroiditis

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18
Q

what is hashimotos disease

A

autoimmune hypothyroidism - autoimmune destruction of thyroid gland and reduced thyroid hormone production

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19
Q

what characterised hashimotos (antibodies and histologically)

A

antibodies against thyroid peroxidase (TPO)

T cell infiltrate and inflammation microscopically

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20
Q

what are the clinical features of hypothyroidism in the hair and skin

A

coarse sparse hair,
dull expressionless face,
periorbital puffiness,
pale cool skin that feels doughy to touch,
vitiligo may be present (another autoimmune disease),
hypercarotenaemia (yellowing of the skin)

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21
Q

what are the clinical features of hypothyroidism in thermogenesis

A

cold intolerance

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22
Q

what are the clinical features of hypothyroidism in fluid balance

A

fluid retention- pitting oedema

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23
Q

what are the cardiac clinical features of hypothyroidism

A

reduced heart rate, cardiac dilatation, pericardial effusion, worsening of heart failure

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24
Q

what are the metabolic clinical features of hypothyroidism

A

hyperlipidaemia, decreased appetite, weight gain

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25
Q

what are the GI clinical features of hypothyroidism

A

constipation, (megacolon, intestinal obstruction, ascites)

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26
Q

what are the respiratory clinical features of hypothyroidism

A

deep hoarse voice, macoglossia, obstructive sleep apnoea

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27
Q

what are the neurological clinical features of hypothyroidism

A
decreased intellectual and motor activities,
depression, psychosis, neuro-psychiatric,
muscle stiffness, cramps,
peripheral neuropathy, 
prolongation of tendon jerks,
carpal tunnel,
cerebellar ataxia, encephalopathy,
decreased visual acuity
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28
Q

what are the gynae/ reproductive clinical features of hypothyroidism

A

menorrhagia, later oligo- or amenorrhoea, hyperprolactinaemia (increased TRH causes increased PRL)

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29
Q

what other lab abnormalities are seen in primary hypothyroidism

A

increased MCV
increased CK
increased LDL cholesterol
hyponatraemia (decreased tubular water loss)
hyperprolactinaemia (increased TRH and increased PRL)

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30
Q

what antibodies for graves

A

anti TPO (70-80%)
anti-thyroglobulin (30-50%)
TSH receptor antibody (70-100%) (stimulating

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31
Q

what antibodies for autoimmune hypothyroidism

A

anti TPO (95%)
anti-thyroglobulin (60%)
TSH receptor antibody (10-20%) (blocking)

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32
Q

what might rapid restoration of metabolic rate from hypothyroidism precipitate

A

cardiac arrhythmias

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33
Q

what is the management for hypothryoidism

A

slowly restore metabolic rate
Younger patients: start levothyroxine at 50-100 μg daily

In the elderly with a history of IHD: start levothyroxine at 25-50 μg daily, adjusted every 4 weeks according to response

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34
Q

when should you check TSH when managing hypothyroidism

A

2 months after changing dose

if stable every 12-18 months

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35
Q

how do you manage secondary hypothyroidism

A

titrate dose of levothyroxine to the fT4 level

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36
Q

what is levothyroxine

A

T4

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37
Q

when should levothyroxine be taken

A

preferable before breakfast

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38
Q

what can require the levothyroxine dose to be increased

A

pregnancy

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39
Q

who usually gets myxoedema coma

A

elderly women with longstanding hypothyroidism that is frequently unrecognised or untreated

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40
Q

what is seen on ECG in myxoedema coma

A

bradycardia, low voltage complexes, varying degree heart block, T wave inversion, prolongation of the QT interval

41
Q

what are the resp signs of myxoedema coma

A

Type 2 respiratory failure: hypoxia, hypercarbia, respiratory acidosis

42
Q

how do you treat myxoedema coma

A
ABC
passively warm to raise body temp 
cardiac monitoring for arrhythmias 
monitor: urine output, fluid balance, central venous system pressure, blood sugars, oxygenation 
broad spectrum antibiotics 
thyroxine cautiosly
43
Q

what precipitates myxoedema coma

A

when the body compensatory mechanism to hypothyroidism are overwhelmed by e.g an infection

44
Q

what is thyrotoxicosis

A

when tissues are exposed to excess thyroid hormone

45
Q

what is hyperthyroidism

A

conditions in which overactivity of the thyroid gland leads to thyroidtoxicosis

46
Q

what are the cardiac symptoms of thyrotoxicosis

A

palpation, AF, cardiac failure (rare)

47
Q

what are the sympathetic symptoms of thyrotoxicosis

A

tremor, sweating

48
Q

what are the CNS symptoms of thyrotoxicosis

A

anxiety, nervousness, irritability, sleep disturbance

49
Q

what are the GI symptoms of thyrotoxicosis

A

frequent loos bowel movements

50
Q

what are the vision symptoms of thyrotoxicosis

A

lid retraction, double vision (diplopia), proptosis (graves)

51
Q

what are the hair and skin symptoms of thyrotoxicosis

A

hair change (brittle, thin hair), rapid fingernail growth

52
Q

what are the reproductive symptoms of thyrotoxicosis

A

menstrual cycle changes, lighter bleeding and less frequent periods

53
Q

what are the muscular symptoms of thyrotoxicosis

A

muscle weakness- esp in upper arms and thighs

54
Q

what are the metabolic symptoms of thyrotoxicosis

A

weight loss despite increased appetite

55
Q

what are the thermogenesis symptoms of thyrotoxicosis

A

intolerance to heat

56
Q

what can cause excessive thryoid stimulation

A

graves disease, hashitoxicosis, thyrotropinoma (TSHoma rare), thyroid cancer (rarely causes thyrotoxicosis), choriocarcinoma (trophoblast tumour secreting hCG (similar to TSH))

57
Q

what are the types of thyroid nodules with autonomous function

A

toxic solitary nodule, toxic multinodular goitre

58
Q

what are the cases of thyrotoxicosis associated with hyperthyroidism

A

excessive thyroid stimulation and thyroid nodules with autonomous function

59
Q

what are the cases of thyrotoxicosis not associated with hyperthyroidism

A

thyroiditis, exogenous thyroid hormones, ectopic thyroid tissue

60
Q

what can cause thyroid inflammation (thyroiditis)

A

subacute (de Quervain’s) thyroiditis (self limiting viral condition),
post partum thyroiditis (self limiting),
drug induced (amiodarone (contains iodine))

61
Q

what can cause exogenous thryoid hormones to cause thyrotoxicosis

A

over treatment with levothyroxine,

thyrotoxicosis factitia

62
Q

what can lead to the production of ectopic thyroid tissue causing thyrotoxicosis

A
metastatic thyroid carcinoma,
struma ovarii (teratoma containing thyroid tissue)
63
Q

who gets graves

A

slightly more common in women,

20-50 years

64
Q

what are the risk factors for graves

A

genes (70%) + environment
sister and children of women with graves
smoking important

65
Q

what other lab abnormalities are seen in graves

A

hypercalcaemia and increased alkaline phosphate (increased bone turnover- graves associated with osteoporosis),
leucopenia,
TSH receptor antibody

66
Q

what clinical signs are specific to graves

A

pretibial myxoedema, thyroid acropachy, thyroid bruit, graves eye disease (unilateral or bilateral)

67
Q

what causes a thyroid bruit

A

only large goitre in graves- reflects the hypervascularity of the thyoid
not heard in other goitrous conditiond

68
Q

what is graves eye disease associated with

A

smoking- really important to stop

69
Q

how is graves eye disease treated

A

mild- topically (e.g. lubricants)

more severe- steroids, radiotherapy, surgery

70
Q

is graves eye disease bad

A

can be sight threatening

71
Q

how many people with graves get graves eye disease

A

20%

72
Q

what is the onset for nodular thyroid disease

A

insidious onset

73
Q

who gets nodular thyroid disease

A

older patients

74
Q

what does nodular thyroid disease feel like

A

thyroid feels nodular, asymmetrical goitre (smooth in graves)

75
Q

what test results are seen in nodular thyroid disease

A

increased fT3/4, decreased TSH
antibody negative (TRAb),
scintigraphy high uptake,
thyoid ultrasound

76
Q

what is a thyroid storm

A
medical emergency (ABC)
severe hyperthyroidism causing:
-respiratory and cardiac collapse 
-hyperthermia 
-exaggerated reflexes 
-(may require mechanical ventilation)
77
Q

who gets a thyroid storm

A

hyperthyroid patients with an acute illness/ infection or recent thyroid surgery

78
Q

what is the treatment for a thyroid storm

A

lugols iodine, glucocorticoids, PTU, beta blockers, fluids, monitoring

79
Q

what are the antithryoid drugs used to treat hyperthyroidism

A

carbimazole (1st line)

propylthiouracil (PTU) (first line in 1st trimester pregnancy)

80
Q

how to antithyroid drugs work

A

inhibits TPO (enzyme helps produce thyroid hormones)

81
Q

what are the side effects of anti thyroid drugs

A

well tolerated
1-5% rash, urticaria, arthralgia
cholestatic jaundice, increased liver enzymes, fulminant hepatic failure,
agranulocytosis (rare but warm patients for fever, oral ulcer or oropharyngeal infection)

82
Q

what is used for immediate symptomatic treatment for hyperthyroidism

A

beta blockers- propanalol (reduce activity of sympathetic nervous system)
CCB in those with asthma

83
Q

when is radioiodine used to treat hyperthyroidism

A

in relapsed graves disease and nodular thyroid disease

never in pregnancy

84
Q

when is a thyroiectomy used for hyperthyroidism

A

when radioiodine is CI

85
Q

what are the risks of a thyroidectomy

A

recurrent laryngeal nerve palsy, hypothyroidism, hypoparathyroidism

86
Q

what can cause thyroiditis

A
Hashimoto’s
De Quervain’s/subacute (viral)
Post-partum
Drug-induced (amiodarone, lithium)
Radiation
Acute suppurative thyroiditis (bacterial)
87
Q

who gets subacute thyroiditis

A

females more than males, 20-50, can be triggered by viral infection

88
Q

what are the symptoms or subacute thyroiditis

A

neck tenderness, fever, viral symptoms, self limiting over a few months

89
Q

where in UK does hypothyroidism occur

A

in iodine rish areas

90
Q

where in UK does hyperthyroidism occur

A

in iodine deficient areas

91
Q

describe subclinical hypothyroidism

A
increased TSH, normal fT3/4, risk of developing into overt hypothyroidism 
treatment advised (always in pregnancy)
92
Q

describe subclinical hyperthyroidism

A

decreased TSH, normal fT3/4, risk of developing into overt hyperthyroidism
treatment advised, associated with osteoporosis and AF, seen in multinodular goitres

93
Q

what is non thyroidal illness

A

when illness impacts the HPT axis- TSH typically suppressed initially then rises during recovery

94
Q
68 yr old lady 
Tiredness
Weight gain
Slowness
Goitre 

TSH 42 mU/L
Free T4 4 pmol/L

Normal Results:
TSH 0.4-4.0 mU/L
Free T4 9.8-18.8 pmol/L

A

Primary hypothyroidism

95
Q

68 yr old lady
Family history of thyroid disease
Tiredness
Goitre

TSH 12 mU/L
Free T4 11 pmol/L
TPO Antibodies 200 (elevated)

Normal Results:
TSH 0.4-4.0 mU/L
Free T4 9.8-18.8 pmol/L

A

Subclinical hypothyroidism

96
Q
52 yr old male
Headache
Visual field defect
Dizziness/weakness
Poor libido/loss of erections
TSH 0.20 mU/L
Free T4 6 pmol/L

Normal Results:
TSH 0.4-4.0 mU/L
Free T4 9.8-18.8 pmol/L

A

Pituitary tumour causing secondary hypothyroidism

97
Q
32 yr old lady 
Weight loss and tremor
Feels tired
Sleep disturbance
TSH <0.01 mU/L
Free T4 54 pmol/L

Normal Results:
TSH 0.4-4.0 mU/L
Free T4 9.8-18.8 pmol/L

A

Graves’ disease

98
Q
70 yr old lady 
Diagnosed with atrial fibrillation
No symptoms
TSH <0.01 mU/L
Free T4  26 pmol/L

Normal Results:
TSH 0.4-4.0 mU/L
Free T4 9.8-18.8 pmol/L

A

Toxic multinodular goitre

99
Q
32 yr old
Sore throat and febrile illness
Tired, weight loss, poor sleep
GP blood tests:
TSH<0.01, T4 36 pmol/L
Seen in clinic 6 weeks later
TSH 12 mU/L, Free T4 9 pmol/L

Normal Results:
TSH 0.4-4.0 mU/L
Free T4 9.8-18.8 pmol/L

A

Subacute thyroiditis