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Endocrinology > Thyroid > Flashcards

Thyroid Flashcards

1
Q

Anti-TPO ab is associated with …

A

Hashimoto thyroiditis
Autoimmune thyroiditis

Highly sensitive and specific

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2
Q

When do we measure anti-TG?

A

Never

Limited clinical value

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3
Q

TSH receptor ab is associated with …

A

Grave’s

Highly sensitive and specific

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4
Q

Hypothalamus releases …. –> stimulates anterior pituitary to release …. –> stimulates thyroid gland to release …. –> gets converted to …. –> engages in negative feedback

A

TRH
TSH
T4
T3

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5
Q

Thyroid hormone in the circulation is 99% bound to…

A

Carrier protein - mainly thyroxine binding globulins, also transthyridin and albumin

We measure unbound free T4

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6
Q

Where does T4 get converted to T3?

A

Mostly liver (but also in kidneys, heart, skeletal muscle)

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7
Q

Alemtuzumab used in MS

What’s a major side effect?

A

Induces autoimmune disease
34% Graves!!
Can occur even years after stopping alemtuzumab (CD52 target monoclonal ab)

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8
Q

How does biotin affect thyroid levels?

A

Causes spurious thyroid test results

Stop biotin and recheck in 3-4/52

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9
Q

How does amiodarone affect thyroid levels?

A

Can cause both hypothyroidism and thyrotoxicosis
Most common is hypothyroidism
Very long t1/2 - can take 2 years for it to be eliminated

40% amiodarone by weight is iodine
Type 1: treated with anti-thyroid medication
Type 2: treated with glucocorticoids
May not be able to tell between the two and may have to treat both initially

Thyroid scintigraphy not useful due to high circulating iodine load

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10
Q

Which cancer therapies can affect thyroid?

A

CTLA4 inhibitor e.g. ipilimumab = hypophysitis (can cause adrenal insufficiency) + central hypothyroidism

PD1 inhibitor e.g. pembrolizumab, nivolumab = primary hypo or hyperthyroidism

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11
Q

How does lithium affect thyroid?

A

Hypothyroidism + goitre

Thyroid hormone can’t be released from the thyroid colloid –> goitre formation

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12
Q

How does hyperthyroidism increase basal metabolic rate?

A

Increase synthesis of Na+ K+ ATPase

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13
Q

How does hyperthyroidism increase sympathetic nervous system activity?

A

Increase expression of B1-adrenergic receptors

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14
Q

Clinical features of hyperthyroidism

A 
Weight loss
Palpitations, tachycardia, arrhythmia (AF), increased CO
Agitation, anxiety
Insomnia 
Tremor
Heat intolerance, sweating
Staring gaze with lid lag 
Diarrhoea
Oligomenorrhoea
Bone resorption with hypercalcaemia, osteoporosis
Decreased muscle mass with weakness
Hypercholesterolemia 
Hyperglycaemia
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15
Q

DDx hyperthyroidism

A 
Grave's
Toxic multinodular goitre 
Toxic adenoma 
Thyroiditis
Drugs (amiodarone, immune check point inhibitors, alemtuzumab)
Excess iodine
Excess thyroxine
Pregnancy related (hyperemesis gravidarum, hydatidiform mole)
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16
Q

Pathophysiology of Grave’s

A

IgG stimulates TSH receptor –> increased synthesis of thyroid hormone

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17
Q

4 Clinical features of Grave’s

A

Diffuse goitre (constant TSH stimulation leads to thyroid hyperplasia and hypertrophy)

Thyroid eye disease - bilateral proptosis, periorbital oedema, scleral injection, lid retraction, diplopia, extraocular dysfunction, exopthalmus (most specific for Grave’s)

Pretibial myxedema

Clubbing

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18
Q

Mechanism behind exopthalmus and pretibial myxedema

A

Not due to hyperthyroidism, but due to ab stimulating TSH receptor

Fibroblasts behind the orbit and overlying the shin express TSH receptor –> TSH activation results in glycosaminoglycan build up, inflammation, fibrosis and oedema

Dough like consistency when pushing on the skin

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19
Q

Labs in Grave’s

A

High T4, T3
Low TSH
Positive TSH receptor ab

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20
Q

Rx Grave’s

A

Antithyroid medication - slowly brings down TRAb

Radioactive iodine (iodine taken up by follicle cells then these cells are destroyed by radioactivity)

Thyroidectomy - if someone is very thyrotoxic, need antithyroid medication first to reduce anaesthetic risk

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21
Q

What therapy is contraindicated in thyroid eye disease?

A

Radioactive iodine - can flare up eye disease

- Transiently release TRAb when follicle cells die which can flare up eye disease

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22
Q

What’s a thyroid storm?

A

Storm of thyroid hormone and catecholamines
Occurs during times of stress e.g. childbirth, surgery

Presents as arrhythmia, hyperthermia, vomiting, hypovolemia shock

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23
Q

Rx thyroid storm

A

PTU
B blockers
Steroids

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24
Q

How does PTU work?

A

Inhibits peroxidase-mediated oxidation, organification and coupling steps of thyroid hormone synthesis, as well as stops conversion from T4 to T3

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25
Q

What 2 things increase the severity of thyroid eye disease i.e. Grave’s opthalmopathy?

A

Radioactive iodine

Smoking

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26
Q

Disadvantages of radioactive iodine

A 
Slower onset of effect 6-8 weeks
Permanent hypothyroidism
Can exacerbate ophthalmopathy
Don't use in suspected or confirmed thyroid malignancy 
Don't use in pregnancy
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27
Q

Adverse effects of anti-thyroid medications

A

Usually well tolerated

Common: GI effects, rash (exclude vasculitis), arthralgia, fever, transient mild neutropenia

Rare: agranulocytosis, cholestatic hepatitis, hepatocellular liver injury, ANCA positive vasculitis, polyarthritis

Need baseline FBC, LFTs

If fever, mouth ulcers, infection then must exclude agranulocytosis

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28
Q

What’s a multinodular goitre?

A

Enlarged thyroid gland with multiple nodules due to iodine deficiency
Usually non-toxic (euthyroid)
Rarely, can be toxic (produce T4 independent of TSH)

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29
Q

How do differentiate between Grave’s vs thyroid multinodular goitre vs toxic adenoma?

A

Thyroid antibodies and thyroid uptake scan

Grave’s: positive TSH receptor ab, mildly positive TPO ab, diffuse thyroid uptake/uniform uptake on scan

TMN: negative ab, normal or elevated multifocal uptake with suppression of surrounding thyroid

Toxic adenoma: negative ab, elevated focal uptake (>3cm) with suppression of surrounding thyroid

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30
Q

Clinical features of hypothyroidism

A

Myxedema (accumulation of glycosaminoglycans in the skin and soft tissue, can deposit in the larynx and cause a deep voice, large tongue)

Weight gain

Cold intolerance

Slowing of mental activity

Muscle weakness

Bradycardia + decreased CO (SOB, fatigue)

Oligomenorrhoea

Hypercholetserolaemia

Constipation

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31
Q

DDx primary hypothyroidism

A

Hashimoto’s thyroiditis (most common)
Iodine deficiency (common)
Post-radioiodine therapy
Post thyroidectomy
Subacute thyroiditis or any form of thyroiditis
Drugs - amiodarone, lithium, immune checkpoint inhibitors, anti-thyroid medication
Neck irradiation
Riedel’s thyroiditis (rare)
Thyroid infiltration (tumour, amyloid) (rare)
Congenital hypothyroidism (rare)

32
Q

Pathophysiology behind Hashimoto’s thyroiditis

A

Autoimmune destruction of the thyroid gland
Associated with HLA-DR5

Initial hyperthyroidism (due to follicle damage, and all the thyroid hormones leak out) –> euthyroid –> hypothyroidism with reduced T4 and increased TSH

33
Q

Labs in Hashimoto’s thyroiditis

A

Positive TPO ab (very sensitive and specific)

Low T4, high TSH

34
Q

Hashimoto’s thyroiditis is associated with what condition?

A

Marginal zone lymphoma

35
Q

How does subacute granulomatous (De Quervain) thyroiditis present?

A

After a viral infection
Tender thyroid with transient hyperthyroidism
Self limiting. Rarely progresses to hypothyroidism.

36
Q

How does Riedel fibrosing thyroiditis present?

A

Chronic inflammation with extensive fibrosis of the thyroid gland

Hypothyroidism
“hard as wood” non-tender thyroid
May extend to surrounding structures eg. airway

37
Q

When to order a thyroid US?

A

When they have palpable abnormalities of the thyroid

38
Q

What’s subclinical hyperthyroidism?

A

Low TSH
Normal T4, T3

Can occur when you first start antithyroid medication as TSH has a longer half life

39
Q

Should you treat subclinical hyperthyroidism?

A

Subclinical hyperthyroidism can be associated with CV disease (AF, CCF, CAD), bone loss, fractures, dementia, particularly in persons >65 with severe disease

Data lacking but should probably treat age >65, especially if TSH <0.1. Definitely treat if both.

40
Q

What’s subclinical hypothyroidism?

A

High TSH
Normal T4, T3

Transient - recovering from other illness, poor adherence to thyroxine, malabsorption of thyroxine, drugs (amiodarone, lithium)

Persistent - normal ageing, obesity, TSH or TRH resistance (rare), adrenal insufficiency (rare)

41
Q

Should you treat subclinical hypothyroidism?

A

TSH increases with age

TSH <10: no treatment unless convincing signs of hypothyroidism (not just fatigue, weight gain)

TSH >10: treat but careful in those age>70 due to risk of OP, CV disease, dementia if TSH becomes too low

42
Q

What’s secondary hypothyroidism?

A 
Low TSH (<10)
Low T3, T4

Central hypothyroidism - coming from the pituitary or hypothalamus
OR
Non-thyroid illness (sick euthyroidism)

43
Q

What’s non-thyroid illness (euthyroidism)?

A

In severe illness, get functional central hypothyroidism with fall in TSH and T4

44
Q

What’s secondary hyperthyroidism?

A

Normal/high TSH

High T4, T3

45
Q

DDx secondary hyperthyroidism

A

TSH secreting pituitary adenoma
Resistance to thyroid hormone (reduced responsiveness of target tissue to thyroid hormone)
Thyroxine replacement
Drugs e.g. amiodarone

46
Q

How to take a biopsy from a thyroid nodule?

A

FNA

47
Q

Name the 4 types of thyroid carcinoma

A

Papillary carcinoma
Follicular carcinoma
Anaplastic carcinoma
Medullary carcinoma

48
Q

Most common type of thyroid carcinoma?

A

Papillary carcinoma 80% of cases

49
Q

Prognosis of papillary carcinoma

A

Excellent prognosis
10 year survival is >95%
Often spreads to cervical lymph nodes

50
Q

Why can’t we do FNA for suspected follicular carcinoma?

A

Invasion through the capsule is what distinguishes follicular adenoma from follicular carcinoma
Entire capsule must be examined
FNA will only examine cells and not the capsule

51
Q

How does follicular carcinoma metastasise?

A

Spreads haematogenously (this is an exception as carcinomas tend to spread to lymph nodes)

52
Q

What is a follicular carcinoma?

A

Malignant proliferation of follicles surrounded by fibrous capsule with invasion through the capsule

53
Q

What’s a medullary carcinoma? What biochemical changes does it typically produce?

A

Malignant proliferation of parafollicular C cells (sits adjacent to the follicles)
C cells secrete calcitonin –> lowers serum calcium by increasing renal calcium excretion (inactive at normal physiological levels)

54
Q

What familial disorders is medullary carcinoma ssociated with?

A

MEN 2A and 2B

55
Q

What does it mean to have a RET mutation?

A

Associated with MEN2 syndrome

If you inherit the mutated RET gene from an affected parent, there is almost a 100% chance of developing medullary thyroid cancer and lower probabilities of developing other features of this syndrome during his or her lifetime.

Hence you would need a prophylactic thyroidectomy

56
Q

What conditions are associated with MEN2A and 2B?

A

MEN2 results in medullary carcinoma, pheochromocytoma, parathyroid adenoma (2A) or mucosa neuromas of the oral/GI mucosa (2B)

57
Q

Which type of thyroid carcinoma has the worst prognosis?

A

Anaplastic carcinoma

Seen in the elderly
Often invades local structures - oesophagus (dysphagia), lungs (respiratory compromise)

58
Q

Who does anaplastic carcinoma present?

A

Similar to Riedal thyroiditis

“hard as wood” non-tender thyroid

59
Q

What is gestational transient hyperthyroidism and how does it happen?

A

BHCG looks similar to TSH and binds to TSH receptor –> hyperthyroidism

Occurs when BHCG is the highest (peaks 10-12 weeks). Generally resolves after 15-20 weeks.

More likely if twin or molar pregnancy with high BHCG or when there is hyperemesis gravidarum

Generally less severe than Graves with no eye signs or large goiter, and self limiting.

60
Q

What is the most important reason to measure thyroid stimulating antibodies in the third trimester of pregnancy in a woman with Graves disease?

A

Maternal TSH receptor ab can go to the foetus and cause neonatal grave’s disease.

Neonatal hyperthyroidism is more likely when the maternal TSHR-ab activity is >500% ULN.

Warrants dose increase of anti-thyroid medication.

61
Q

What corrects mortality in Graves?

A

Definitive treatment - Radioactive iodine only

Not anti-thyroid medication

62
Q

What’s Pemberton’s sign?

A

Pemberton’s sign is used to evaluate venous obstruction in patients with goiters. The sign is positive when bilateral arm elevation causes facial plethora. It has been attributed to a “cork effect” resulting from the thyroid obstructing the thoracic inlet, thereby increasing pressure on the venous system.

63
Q

FT3>FT4 in Graves

True or false

A

True

64
Q

When to stop antithyroid medication in Graves?

A

Elevated TRAb 80-10% relapse

Low or undetectable TRAb 20-30% relapse

65
Q

Which eye sign is most specific for Grave’s orbitopathy?

A

Exopthalmus

66
Q

Which extraocular muscle is mostly commonly involved in Grave’s orbitopathy?

A

Inferior rectus

67
Q

Treatment Grave’s orbitopathy

A

Mild: selenium

Moderate-severe: IV methylprednisolone, orbital radiotherapy, consider steroid sparing treatments CSA, MMF, RTX, IgG, teprotumumab, orbital decompression

Vision threatening: IV methylprednisolone –> orbital decompression

Orbital decompression is only done in inactive disease

68
Q

Which thyroid condition can be cured?

A

Subclinical hyperthyroidism

If there is a nodule that’s releasing TSH –> wait for T3 to rise up so most of the thyroid won’t be releasing TSH –> do radioactive iodine to target nodule –> cure

69
Q

Treatment hypothyroidism in pregnancy

A

TSH ≥4

However TABLET trial showed no difference in miscarriage and delivery outcomes

70
Q

Treatment hyperthyroidism in pregnancy

A

Grave’s
HCG-mediated hyperthryoidism

Both PTU and Carbimazole cross placenta and may be associated with birth defect
PTU in 1st trimester then carbimazole in 2nd/3rd trimester

71
Q

Is serum TG/TGab usefulin evaluating thyroid nodules?

A

No

72
Q

Clinical and USS findings associated with an increased risk of thyroid cancer

A

Focal uptake of 18-FDG by the thyroid
Rapid growth of the nodule
New onset hoarseness of voice (invade into RLN and paralysis of VC)
Dysphagia (however big benign nodule can do this)
Serum calcitonin >50-100pg/ml

USS
Microcalcification 
Nodule hypoechogenicity compared with surrounding thyroid/muscle
Irregular margins
Taller than wide on a transverse view

Cystic = lower risk

73
Q

What’s a points system for USS findings to predict risk of malignancy in thyroid nodule?

A

2017 ACR TI-RADS

74
Q

Thyroid cancer therapy

A

For metastatic differentiated thyroid cancer that are radioiodine refractory

Targeted thyroid cancer treatment
Lenvatinib
Vandetanib
Sorafenic/pazopanib/sunitinib

75
Q

RET proto-oncogene

Why is it important?

A

Associated with more aggressive medullary thyroid cancer

Selpercatinib - at very low concentration, is 250x selective for RET proto-oncogene

This is groundbreaking treatment

Endocrinology (9 decks)

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