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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
What 2 things increase the severity of thyroid eye disease i.e. Grave's opthalmopathy?
Radioactive iodine | Smoking
26
Disadvantages of radioactive iodine
``` 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 ```
27
Adverse effects of anti-thyroid medications
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
28
What's a multinodular goitre?
Enlarged thyroid gland with multiple nodules due to iodine deficiency Usually non-toxic (euthyroid) Rarely, can be toxic (produce T4 independent of TSH)
29
How do differentiate between Grave's vs thyroid multinodular goitre vs toxic adenoma?
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
30
Clinical features of hypothyroidism
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
31
DDx primary hypothyroidism
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
Pathophysiology behind Hashimoto's thyroiditis
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
Labs in Hashimoto's thyroiditis
Positive TPO ab (very sensitive and specific) | Low T4, high TSH
34
Hashimoto's thyroiditis is associated with what condition?
Marginal zone lymphoma
35
How does subacute granulomatous (De Quervain) thyroiditis present?
After a viral infection Tender thyroid with transient hyperthyroidism Self limiting. Rarely progresses to hypothyroidism.
36
How does Riedel fibrosing thyroiditis present?
Chronic inflammation with extensive fibrosis of the thyroid gland Hypothyroidism "hard as wood" non-tender thyroid May extend to surrounding structures eg. airway
37
When to order a thyroid US?
When they have palpable abnormalities of the thyroid
38
What's subclinical hyperthyroidism?
Low TSH Normal T4, T3 Can occur when you first start antithyroid medication as TSH has a longer half life
39
Should you treat subclinical hyperthyroidism?
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
What's subclinical hypothyroidism?
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
Should you treat subclinical hypothyroidism?
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
What's secondary hypothyroidism?
``` Low TSH (<10) Low T3, T4 ``` Central hypothyroidism - coming from the pituitary or hypothalamus OR Non-thyroid illness (sick euthyroidism)
43
What's non-thyroid illness (euthyroidism)?
In severe illness, get functional central hypothyroidism with fall in TSH and T4
44
What's secondary hyperthyroidism?
Normal/high TSH | High T4, T3
45
DDx secondary hyperthyroidism
TSH secreting pituitary adenoma Resistance to thyroid hormone (reduced responsiveness of target tissue to thyroid hormone) Thyroxine replacement Drugs e.g. amiodarone
46
How to take a biopsy from a thyroid nodule?
FNA
47
Name the 4 types of thyroid carcinoma
Papillary carcinoma Follicular carcinoma Anaplastic carcinoma Medullary carcinoma
48
Most common type of thyroid carcinoma?
Papillary carcinoma 80% of cases
49
Prognosis of papillary carcinoma
Excellent prognosis 10 year survival is >95% Often spreads to cervical lymph nodes
50
Why can't we do FNA for suspected follicular carcinoma?
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
How does follicular carcinoma metastasise?
Spreads haematogenously (this is an exception as carcinomas tend to spread to lymph nodes)
52
What is a follicular carcinoma?
Malignant proliferation of follicles surrounded by fibrous capsule with invasion through the capsule
53
What's a medullary carcinoma? What biochemical changes does it typically produce?
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
What familial disorders is medullary carcinoma ssociated with?
MEN 2A and 2B
55
What does it mean to have a RET mutation?
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
What conditions are associated with MEN2A and 2B?
MEN2 results in medullary carcinoma, pheochromocytoma, parathyroid adenoma (2A) or mucosa neuromas of the oral/GI mucosa (2B)
57
Which type of thyroid carcinoma has the worst prognosis?
Anaplastic carcinoma Seen in the elderly Often invades local structures - oesophagus (dysphagia), lungs (respiratory compromise)
58
Who does anaplastic carcinoma present?
Similar to Riedal thyroiditis | "hard as wood" non-tender thyroid
59
What is gestational transient hyperthyroidism and how does it happen?
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
What is the most important reason to measure thyroid stimulating antibodies in the third trimester of pregnancy in a woman with Graves disease?
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
What corrects mortality in Graves?
Definitive treatment - Radioactive iodine only | Not anti-thyroid medication
62
What's Pemberton's sign?
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
FT3>FT4 in Graves | True or false
True
64
When to stop antithyroid medication in Graves?
Elevated TRAb 80-10% relapse | Low or undetectable TRAb 20-30% relapse
65
Which eye sign is most specific for Grave's orbitopathy?
Exopthalmus
66
Which extraocular muscle is mostly commonly involved in Grave's orbitopathy?
Inferior rectus
67
Treatment Grave's orbitopathy
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
Which thyroid condition can be cured?
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
Treatment hypothyroidism in pregnancy
TSH ≥4 However TABLET trial showed no difference in miscarriage and delivery outcomes
70
Treatment hyperthyroidism in pregnancy
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
Is serum TG/TGab usefulin evaluating thyroid nodules?
No
72
Clinical and USS findings associated with an increased risk of thyroid cancer
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
What's a points system for USS findings to predict risk of malignancy in thyroid nodule?
2017 ACR TI-RADS
74
Thyroid cancer therapy
For metastatic differentiated thyroid cancer that are radioiodine refractory Targeted thyroid cancer treatment Lenvatinib Vandetanib Sorafenic/pazopanib/sunitinib
75
RET proto-oncogene | Why is it important?
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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