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Endocrine MBCHB > Thyroid Conditions > Flashcards

Thyroid Conditions Flashcards

1
Q

What are differentiated thyroid cancer?

A

Differentiated thyroid cancer (DTC) refers to papillary and follicular variants

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2
Q

Who is affected by DCTs?

A

Can affect any age group - childhood to elderly.
In females, rates increase from 15-40 then plateaus
In males, rates steadily increase with age

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3
Q

Are DCTs associated with any diet or lifestyle risk factors?

A
  • Not associated with diet, other proven malignancies, family history, smoking or other lifestyle factors
  • Other than clusters associated with nuclear incidence, the overall incidence is constant at present
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4
Q

What is papillary carcinoma?

A
  • Derived from follicular epithelium
  • Associated with Hashimoto’s
  • Associated with ionising radiation
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5
Q

What are the genetic associations with papillary carcinoma?

A
  • Activation of MAP kinase pathway
  • Rearrangements of RET or NTKR1
  • Activating point mutation in BRAF
  • Mutation of ras
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6
Q

What is follicular carcinoma?

A
  • Derived from follicular epithelium
  • Higher incidence in females
  • Higher incidence at 40-50 years
  • Incidence slightly higher in regions of iodine deficiency
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7
Q

What are the genetic associations with follicular carcinoma?

A
  • Mutations in PI3K/AKT pathway
  • Mutations in ras family
  • Translocation involving Pax8 and PPAR𝛾1
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8
Q

Describe the histology of papillary carcinoma.

A
  • Can be multifocal
  • Often cystic
  • May be calcified - psammoma bodies
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9
Q

Describe the histology of follicular carcinoma.

A
  • Diagnosis depends on invasion of the capsule or vascular invasion
  • Classed as minimally invasive or widely invasive
    • Widely invasive: more solid architecture, less follicular architecture, more mitotic activity
    • Minimally invasive: (most common) follicular architecture (well differentiated), may have part surrounding capsule, difficult to distinguish from adenoma
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10
Q

What does this histology slide indicate?

A

Papillary Carcinoma

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11
Q

What does this histology slide indicate?

A

Follicular Carcinoma

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12
Q

Describe the spread of papillary carcinoma

A
  • Papillary carcinomas tend to spread via lymphatics e.g. cervical lymph node metastases
  • Haematogenous spread is uncommon but if occurs spread is usually to the lung, bone, liver and brain
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13
Q

Describe the spread of follicular carcinoma.

A
  • Rarely lymphatic spread, propensity for haematogenous spread (bones, lungs, liver)
  • Uncommon to have multicentric disease
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14
Q

What is the typical presentation of DTCs?

A
  • Majority present with palpable nodules
  • Small percentage are chance findings on histological section of thyroidectomy tissue
  • Approx. 5% present with local or disseminated metastases
    • Local effects e.g. hoarseness, dysphagia, cough suggest advanced disease
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15
Q

What are the investigations for DTCs?

A
  • TSH, US
  • Confirmation: usually US-FNA, can involve excisional biopsy of lymph node
  • No role for isotope thyroid scan (in diagnosis), CT or MRI
  • Pre-operative laryngoscopy if vocal cord palsy suspected clinically
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16
Q

Who are in the low risk group for surgical management of DTCs?

A

Age <50 years, tumour <4 cm

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17
Q

What is the surgical management for the low risk DTCs?

A

Thyroid lobectomy + biopsy, thyroidectomy following biopsy results if needed

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18
Q

Who is in the high risk group for DTCs?

A

Stage Thy3 or higher on FNA (atypical)

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19
Q

What is the surgical management for someone in the high risk group of DTCs?

A
  • Subtotal/total thyroidectomy
  • Consider radioactive iodine
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20
Q

Who gets a whole body iodine scan? and why?

A
  • Used in patients who have undergone sub-total or total thyroidectomy
  • Usually performed 3-6 months post-op
  • Used to determine incomplete incision or present of occult metastases, and therefore inform need for further investigation/treatment
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21
Q

Why is RAI ablation used?

A
  • Ablate residual thyroid tissue in order to destroy occult microfoci
  • Remove residual thyroid tissue which may be a source of Tg and therefore confound the levels during follow-up
  • Permit predictively useful scanning in whole body scans and subsequent high dose therapy if required
  • Small but significant incidence of acute myeloid leukaemia, no convincing evidence of increase in incidence of other solid tumours
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22
Q

What follow up should be done for someone with DTCs?

A
  • In both the low and high-risk groups, measure TSH and Tg every 6 months for first 5 years, then annually for next 5 years
    • Consider discharge after 5 years if low risk
  • To minimise risk of recurrence patients are treated with suppressive doses of levothyroxine (sufficient to suppress TSH below the normal range)
  • For low-risk group, TSH should be kept in lower range of normal (0.4-4 mU/L), whereas in the high-risk group TSH should be kept <0.1 mU/L and fT4 below 25
  • Thyroglobulin (Tg) is the protein precursor of T4/T3, made by thyroid follicular epithelial cell - can be used as ‘tumour marker’
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23
Q

What is the management of recurrent DTCs?

A
  • Can be detected clinically, by rising Tg, or by imaging
  • Recurrence in cervical lymph nodes is more common in papillary cancer
  • Haematogenous spread to lungs, bone or brain more common in follicular lesions
  • Usually, patients undergo whole body scan to determine ability to take up iodine with a view to RAI
  • Difficult group are those with rising Tg but negative whole body iodine scan - management options include PET scan to allow targeted treatment, and systemic anti-cancer therapy e.g., sorafenib and Lenvatinib
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24
Q

What is thyrotoxicosis?

A

the clinical, physiological, and biochemical state arising when the tissues are exposed to excess thyroid hormone

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25
Q

What is hyperthyroidism?

A

refers specifically to conditions in which overactivity of the thyroid gland leads to thyrotoxicosis

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26
Q

What is the aetiology of hyperthyroidism?

A

Graves’ disease

  • Accounts for 85% of cases
  • Higher incidence in females - 10:1
  • Usually presents between 20-40 years
  • Interacting susceptibility genes plus environmental factors

Other causes of thyrotoxicosis associated with hyperthyroidism

Excessive thyroid stimulation

  • Hashitoxicosis - transient hyperthyroidism caused by inflammation associated with Hashimoto’s thyroiditis, patient will then develop hypothyroidism
  • Thyrotropinoma - TSH secreting pituitary adenoma (very rare)
  • Thyroid cancer - only very rarely cause thyrotoxicosis
  • Choriocarcinoma - trophoblast tumour secreting hCG

Thyroid nodules

  • Toxic solitary nodule
  • Toxic multinodular goitre
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27
Q

What are the causes of thyrotoxicosis that are not associated with hyperthyroidism?

A

Thyroid inflammation (thyroiditis)

  • Subacute (de Quervain’s) thyroiditis
  • Post-partum thyroiditis
  • Drug-induced thyroiditis (e.g., amiodarone)

Exogenous thyroid hormones

  • Over-treatment with levothyroxine
  • Thyrotoxicosis factitia

Ectopic thyroid tissue

  • Metastatic thyroid carcinoma
  • Struma ovarii (teratoma containing thyroid tissue)
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28
Q

What is the pathophysiology of Graves’ Disease?

A
  • Involves auto-antibodies to TSH receptor, thyroid peroxisomes and thyroglobulin
  • The anti-TSH receptor antibodies stimulate the thyroid resulting in increased function
  • Some antibodies can inhibit function - may explain paradoxical episodes of hypofunction which can occur
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29
Q

What is the presentation of thyrotoxicosis?

A
  • Weight loss despite increased appetite
  • Frequent, loose bowel movements
  • Sweating and heat intolerance
  • Goitre - diffuse in Graves, goitre with firm nodules if toxic multinodular goitre
  • Thyroid bruit - associated only with large goitres
    • Reflective of hypervascularity of thyroid
    • Auscultate over the thyroid
  • Double vision
  • Graves ophthalmopathy (see below)
  • Increased pulse rate
  • Palpitations, AF
  • Rarely cardiac failure
  • Fine tremor of the outstretched fingers
  • Muscle weakness, especially in thighs and upper arms
  • Increased nervousness and excessively emotional
  • Sleep disturbance
  • Depression
  • Insomnia
  • Hair change (thin, brittle hair)
  • Rapid fingernail growth
  • Menstrual cycle changes, including lighter bleeding and less frequent periods
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30
Q

What is the specific Graves’ presentation?

A
  • Pretibial myxoedema (also occasionally seen in Hashimoto’s thyroiditis)
  • Thyroid acropachy - thickening of the extremities manifested by digital clubbing, soft tissue swelling of the hands and feet, and periosteal new bone formation
  • Graves eye disease
    • Autoimmune inflammatory disorder of the orbit and periorbital tissues, characterized by upper eyelid retraction, lid lag, swelling, erythema, conjunctivitis, and bulging eyes (exophthalmos)
    • Occurs in ~20% of Graves’ patients
    • Results from autoimmune inflammation of the extra-ocular muscles as orbital fat and connective tissue TSH receptors
    • Association with smoking (smoking cessation very important)
    • Presentation can precede diagnosis of Graves’
    • Can be unilateral
    • Most disease is mild but can be severe and sight-threatening
  • Diffuse goitre
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31
Q

What are the investigations of thyrotoxicosis?

A

Thyroid hormones

Primary hyperthyroidism

  • TSH low
  • Free T3/T4 high

Secondary hyperthyroidism

  • TSH high
  • Free T4 and T3 high (or ‘normal’)

Thyroid autoantibodies in Graves’ disease

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

Scintiscan

  • Used in patients who are antibody negative to look for toxic nodular disease
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32
Q

What is the management of Grave’s disease?

A
  • Antithyroid drugs - carbimazole (first line), PTU (1st trimester of pregnancy)
  • Gradual dose regimen lasts 12-18 months, block and replace regimen takes 6 months
  • ~50% relapse rate

Management of Graves’ eye disease

  • Mild disease treated topically e.g., lubricants
  • More severe disease: steroids, radiotherapy, surgery
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33
Q

What is the management of thyrotoxicosis?

A

Antithyroid drugs such as carbimazole

β-blockers

  • Useful for immediate symptomatic relief of thyrotoxic symptoms
  • CCBs can be used where β-blockers are contraindicated e.g., asthma

Radioiodine

  • 1st choice treatment for relapsed Graves’ disease and nodular thyroid disease
  • High risk of hypothyroidism when used in Graves’ disease (1:2)

Thyroidectomy

  • Useful when radioiodine is contraindicated e.g., pregnancy
  • Will leave a scar
  • Surgical/anaesthetic risks:
    • Recurrent laryngeal nerve palsy
    • Hypothyroidism
    • Hypoparathyroidism
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34
Q

What is thyroid storm?

A
  • Rapid deterioration of hyperthyroidism with hyperpyrexia, severe tachycardia, extreme restlessness, cardiac failure and liver dysfunction
  • Typically seen in hyperthyroid patient with an acute infection/illness or recent thyroid surgery
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35
Q

What is the management of thyroid storm?

A
  • High dose carbimazole
  • β-blockers (propranolol)
  • Potassium iodide
  • Hydrocortisone
  • IV fluids +/- inotropes
  • Treat precipitating cause e.g. MI, infection, PE
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36
Q

What is subacute thyroiditis?

A

Refers to a transient patchy inflammation of the thyroid

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37
Q

What is De Quervain’s Thyroiditis?

A

Describes the presentation of a viral infection with fever, neck pain and tenderness, dysphagia and features of hyperthyroidism

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38
Q

What is the aetiology of subacute thyroiditis?

A
  • Ages 20-50
  • May be triggered by viral infection
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39
Q

What is the presentation of subacute thyroiditis?

A
  • Painful, diffuse, firm goitre
  • Fever and/or malaise may be present
  • There is a hyperthyroid phase followed by a hypothyroid phase as the TSH level falls due to negative feedback
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40
Q

What are the investigations for subacute thyroiditis?

A
  • Thyroid function tests
  • May perform scintigraphy scan to rule out other causes of hyperthyroidism, will be low uptake throughout
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41
Q

What is the management of De Quervain’s thyroiditis?

A
  • Self-limiting condition - supportive treatment with NSAIDs for pain and inflammation and beta-blockers for symptomatic relief of hyperthyroidism is usually all that is necessary
  • Short course of steroids may be needed
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42
Q

What is the aetiology of drug-induced thyroiditis?

A
  • Drugs which can induce thyroiditis include amiodarone and lithium
  • Amiodarone inhibits DIO1 - increased free T4, decreased free T3, normal TSH
    • Hypothyroidism occurs in 13% - tends to occur in iodine rich areas
    • Hyperthyroidism occurs in 2% - tends to occur in iodine deficient areas, split into type 1 (similar to Graves’, type 2 (destructive thyroiditis) or mixed
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43
Q

What is the management of drug-induced thyroiditis?

A
  • Resolves without treatment in many cases
  • Steroid therapy may be necessary with some drugs
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44
Q

What is hypothyroidism?

A

Results from any disorder that results in insufficient secretion of thyroid hormones from the thyroid gland

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45
Q

What is the aetiology of congenital hypothyroidism?

A
  • Absent or under-developed thyroid gland
  • Dyshormogenesis - genetic defects in the synthesis of thyroid hormones, resulting in hypothyroidism with goitre
  • Iodine deficiency during pregnancy
  • Maternal transmission of antithyroid drugs
46
Q

What is the aetiology of acquired hypothyroidism?

A

Primary hypothyroidism:

Insufficient thyroid hormone production:

  • Hashimoto’s thyroiditis (chronic lymphocytic thyroiditis)
    • Most common cause of hypothyroidism in iodine-sufficient regions
    • Affects middle aged women (45-60 years)
    • Associated with family history of autoimmune thyroiditis or other autoimmune diseases
    • Associated with HLA - DR3 and DR5
  • Iodine deficiency - most common cause worldwide, particularly in iodine-deficient regions
  • Iatrogenic e.g., post-ablative therapy (e.g., radioiodine, surgery)
  • Others: atrophic thyroiditis (autoimmune), de Quervain’s thyroiditis and post-partum thyroiditis

Secondary hypothyroidism

  • Pituitary disorders (e.g., pituitary adenoma) resulting in TSHdeficiency

Tertiary hypothyroidism

  • Hypothalamic disorders resulting in TRH deficiency
47
Q

What is the pathophysiology of Hashimoto’s thyroiditis?

A
  • Gradual failure of thyroid function due to autoimmune destruction of thyroid tissue
  • Characterised by anti-thyroglobulin and anti-peroxidase antibodies which, when bound, cause antibody dependent cell mediated cytotoxicity
  • CD 8+ cells may mediate destruction of thyroid epithelium
  • Cytokine mediated cell death
    • 𝛾 interferon from T cell activation recruits’ macrophages that may damage thyroid follicles
  • May be preceded by transient hyperthyroidism (Hashitoxicosis)
48
Q

Describe the histology of Hashimoto’s thyroiditis?

A
  • Thyroid may be diffusely enlarged.
  • Prominent lymphoid infiltrate - lymphocytes, plasma cells and reactive follicles with germinal centres
  • Thyroid follicles atrophy
  • Follicular cells have abundant eosinophilic cytoplasm (Hurthle cells)
  • May see progressive fibrosis within the gland
49
Q

What is the presentation of hypothyroidism?

A
  • Tiredness/malaise
  • Weight gain, despite decreased appetite
  • Cold intolerance
  • Decreased sweating
  • Coarse, sparse hair, brittle nails and cold, dry skin
  • Constipation
  • Bradycardia - slow pulse
  • Hypothyroid myopathy - myalgia, stiffness, cramps
  • Delayed relaxation of deep tendon reflexes
  • Hyperlipidaemia - xanthelasma
  • Hypercarotenaemia
    Deep hoarse voice
  • Goitre (in Hashimoto thyroiditis) or atrophic thyroid (in atrophic thyroiditis)
  • Impaired cognition, depression
  • Vitiligo may be present
  • Obstructive sleep apnoea - macroglossia or the presence of a goitre can inhibit breathing during sleep
50
Q

What are the investigations of primary hypothyroidism?

A

Thyroid hormones

  • TSH high
  • Free T4 and T3 low

Other abnormalities

  • Macrocytosis (↑ MCV)
  • ↑ creatinine kinase
  • ↑ LDL cholesterol
  • Hyponatraemia
    • ↓ renal tubular water loss
  • Hyperprolactinaemia

Thyroid antibodies in autoimmune hypothyroidism

  • Anti-TPO antibody - 95%
  • Anti-thyroglobulin - 60%
  • TSH receptor antibody (blocking) - 10-20%
51
Q

What are the investigations for secondary hypothyroidism?

A
  • TSH low (or ‘normal’)
  • Free T4 and T3 low
52
Q

What is the management of primary hypothyroidism?

A
  • Younger patients: start levothyroxine at 50-100 µg daily and gradually increase
  • In the elderly with a history of IHD: start levothyroxine at 25-50 µg daily, adjusted every 4 weeks according to response
  • Check TSH 2 months after any dose change
  • Once stabilised within the normal range, TSH should be checked every 12-18 months
53
Q

What is the management of secondary hypothyroidism?

A

Titrate dose of levothyroxine to the tT4 level - should be higher end of normal (TSH unreliable due to low TSH production)

54
Q

What are the complications of hypothyroidism?

A

Myxoedema coma

  • Typically affects elderly women with long standing but frequently unrecognised or untreated hypothyroidism
  • Mortality up to 60% despite early diagnosis and treatment
    Long-term complications of autoimmune hypothyroidism
  • Increases risk of developing other auto-immune diseases
  • Increased risk of developing B-cell NHL in the affected gland
55
Q

What are the investigations for myxoedema coma?

A
  • ECG: bradycardia, low voltage complexes, varying degrees of heart block, T wave inversion, prolongation of the QT interval
  • ABGs: type 2 respiratory failure (hypoxia, hypercarbia, respiratory acidosis)
  • Co-existing adrenal failure present in 10% of patients
56
Q

What is the management of myxoedema coma?

A
  • Passively rewarm - aim for slow rise in body temperature
  • Cardiac monitoring for arrhythmias
  • Close monitoring of urine output, fluid balance, central venous pressure, blood sugars, oxygenation
  • Broad spectrum antibiotics
  • Thyroxine cautiously, hydrocortisone if adrenal failure
57
Q

What is subclinical hypothyroidism?

A
  • ↑TSH, normal fT4/3
  • Risk of progression to overt hypothyroidism
  • Higher risk if strongly TPO antibody positive
  • Treatment generally advised if TSH > 10
  • Always treat in pregnancy to maintain normal TSH
58
Q

What is subclinical hyperthyroidism?

A
  • ↓TSH, normal fT4/3
  • Risk of progression to overt hyperthyroidism
  • Often seen in multinodular goitre
  • Association with osteoporosis and atrial fibrillation
  • Treatment generally advised if TSH <0.1% (or if co-existing osteoporosis/fracture or AF)
59
Q

What is the aetiology of solitary thyroid nodules?

A
  • Very common; affect 5% of women
  • Vast majority (95%) are benign
  • Malignant thyroid nodules can affect any age group; there is a higher incidence in females after childhood and before older age
60
Q

What are the classifications of benign solitary thyroid nodules?

A
  • Cyst
  • Colloid nodule
  • Benign follicular adenoma
  • Hyperplastic nodule
61
Q

What are the features of benign solitary thyroid nodules?

A
  • Family history autoimmune disorders
  • Family history benign nodules/goitre
  • Associated hormonal disturbance
  • Pain/tenderness
  • Soft, smooth, mobile
62
Q

What are the types of malignant solitary thyroid nodules?

A
  • Papillary thyroid carcinoma (80%)
  • Medullary thyroid carcinoma (3%)
  • Lymphoma - primary (5%) or secondary
  • Anaplastic - poorly differentiated, aggressive and associated with worse outcomes
63
Q

What are the features of malignant solitary thyroid nodules?

A
  • <20 and >50 years old
  • Male
  • FHx of thyroid cancer
  • Dysphagia/dysphonia
  • Previous neck irradiation
  • Firm, hard, immobile
  • Cervical lymphadenopathy
  • Nodule increasing in size
  • Lesion >4cm
64
Q

What is the presentation of a solitary thyroid nodule?

A
  • If lump moves on swallowing, it is in the thyroid - invested in pretracheal fascia
  • Majority are painless
    • Pain is usually caused by intra-thyroidal bleed into a cyst
  • Signs of malignancy include enlarged neck lymph nodes and hoarseness
  • Can be toxic or non-toxic - if toxic may be signs of hypothyroidism
65
Q

What are the investigations for solitary thyroid nodules?

A
  • Thyroid function tests
  • US scan
  • USS-FNA (ultrasound fine needle aspiration)
  • Thyroid scan (scintigraphy) - can be useful in distinguishing between functioning (hot) or non-functioning (cold) nodules
    • Hot nodule is only rarely malignant
    • FNA has largely replaced isotope scans in the diagnosis of thyroid nodules
66
Q

How are solitary thyroid nodules classified?

A

FNA Bethesda classification - Thy1-5

  • Thy1 - inadequate
  • Thy2 - benign
  • Thy3 - atypical
  • Thy4 - probably malignant
  • Thy5 - malignant
67
Q

What is follicular adenoma?

A

A benign encapsulated tumour of the thyroid gland that is surrounded by a thin fibrous capsule

68
Q

What is the aetiology of follicular adenoma?

A
  • More commonly found in women
  • Increases in incidence with increasing age
  • Increased incidence in regions of iodine deficiency
69
Q

What are the genetic factors associated with follicular adenoma?

A
  • <20% have a mutant ras or PIK3CA
  • Functional adenomas have an activating mutation in the TSHR signalling pathway → increased cAMP
  • N-ras and K-ras mutations have been implicated in the evolution of follicular adenoma to follicular carcinoma
70
Q

What is the pathophysiology of follicular adenoma?

A
  • Usually, non-functional
  • Around 1% develop into a toxic adenoma - produces thyroid hormone autonomously
  • FA histology shows neoplastic thyroid follicles encapsulated by a surrounding collagen cuff
71
Q

What is the presentation of follicular adenoma?

A
  • Discrete solitary mass in an otherwise normal thyroid gland
  • May be incidental finding
  • Patients with larger tumours may present with local symptoms e.g., dysphagia
72
Q

What are the investigations of follicular adenoma?

A
  • US scan
  • FNA - cannot distinguish between follicular adenoma and follicular carcinoma
  • Serum TSH
73
Q

What is the management of follicular adenoma?

A

Lobectomy with biopsy is required for treatment and definitive diagnosis as FNA cannot distinguish between follicular adenoma and follicular carcinoma

74
Q

What is anaplastic carcinoma?

A

Undifferentiated and aggressive tumours derived from follicular epithelium

75
Q

What is the aetiology of anaplastic carcinoma?

A
  • Can arise de novo or be due to dedifferentiation of another carcinoma
  • Usually, older patients
  • Similar genetic features to papillary carcinomas and follicular carcinomas as well as p53 and β-catenin mutations
76
Q

What is the pathophysiology of anaplastic carcinoma?

A
  • May occur in people with a history of differentiated thyroid cancer
  • Rapid growth and involvement of neck structures and death
77
Q

What is the presentation of anaplastic carcinoma?

A
  • Thyroid nodule
  • Features of local infiltration/compression
  • Cervical lymphadenopathy
  • Signs of distant metastases
78
Q

What are the investigations for anaplastic carcinoma?

A
  • TSH, US
  • Confirmation: US-FNA or biopsy
79
Q

What is the management of anaplastic carcinoma?

A
  • Total thyroidectomy if resectable +/- adjuvant radio chemotherapy as needed
  • Do not respond to RAI
80
Q

What are medullary carcinoma?

A

Tumour of the parafollicular cells which secrete calcitonin (C-cells)

81
Q

What is the aetiology of medullary carcinoma?

A
  • Can be:
    • Sporadic (70%) - seen in adults (40s-50s)
    • Medullary carcinoma associated with Multiple Endocrine Neoplasia Type 2a (MEN2a) can arise in very young patients
      • MTC associated with phaeochromocytoma and hyperparathyroidism in these patients
      • Consider prophylactic thyroidectomy as child
    • Familial non-MEN seen in adults (40s-50s)

Genetic features

  • Germline RET mutations
82
Q

What is the morphology of medullary carcinoma?

A
  • Sporadic cases - solitary nodule
  • Familial cases - bilateral/multicentric
    • C cell hyperplasia
  • Composed of spindle or polygonal cells arranged in nests, trabeculae or follicles
  • Associated amyloid deposition (abnormally folded calcitonin)
83
Q

What are the prognostic factors of medullary carcinoma?

A

Good prognostic factors

  • Young age, female
  • Smaller tumour rise, confined to thyroid, no metastases

Negative prognostic factors

  • Necrosis
  • Many mitosis
  • Squamous metaplasia
  • Small cell morphology
  • <50% cells calcitonin positive
  • Type of RET mutation
  • Some familial forms have more aggressive potential (MEN2B)
84
Q

What is the presentation of medullary carcinoma?

A
  • Neck mass with local effects - dysphagia, hoarseness, airway compromise
  • Paraneoplastic syndrome
    • Diarrhoea - VIP production
    • Cushing’s - ACTH production
85
Q

What are the investigations of medullary carcinoma?

A
  • Neck USS and FNA
  • Measure serum base calcitonin
  • 24 hour urinary metanephrines
  • Further imaging to detect localised/advanced disease
  • Check genetics for MEN
86
Q

What is the management of medullary carcinoma?

A

Localised disease

  • Total thyroidectomy - curative
  • Local recurrence in 35% of patients

Advanced disease

  • May involve tyrosine kinase inhibitors
87
Q

What is thyroid lymphoma?

A

Lymphoma that arises from the thyroid gland

88
Q

What is the aetiology of thyroid lymphoma?

A
  • Background of auto-immune hypothyroidism
  • Females aged 70-80 years
89
Q

What is the presentation of thyroid lymphoma?

A

Rapid onset mass in thyroid

90
Q

What is the investigation for thyroid lymphoma?

A

Core biopsy

91
Q

What is the management of thyroid lymphoma?

A
  • Chemotherapy (R-CHOP), radiotherapy or steroids
  • Does not respond to RAI
92
Q

What is a goitre?

A

Enlarged palpable thyroid gland, which moves on swallowing

93
Q

What is the aetiology of a goitre?

A

May be a benign disorder but is also associated with several thyroid diseases, including iodine deficiency, Hashimoto’s thyroiditis, and some of the causes of hyperthyroidism

94
Q

What is the pathophysiology of a goitre?

A
  • Reduced T3/T3 production causes a rise in TSH, stimulating gland enlargement
  • This may maintain euthyroid state or if compensation fails there will be goitrous hypothyroidism
95
Q

What is the aetiology of a diffuse goitre?

A
  • Physiological goitre - puberty, pregnancy
  • Autoimmune thyroid disease - Hashimoto’s thyroiditis, Grave’s disease thyrotoxicosis
  • Endemic - iodine deficiency +/- ingestion of goitrogens (chemicals which exaggerate the effects of iodine deficiency)
  • Inflammation - acute (de Quervain’s) thyroiditis
  • Sporadic
    • 4:1 female, usually during puberty/YA
    • Most cases have no clear cause
    • Some associated with ingestion of substances limiting T3/T4 production or inborn errors of metabolism (dyshormonogenesis)
96
Q

What is the presentation of a diffuse goitre?

A
  • Entire thyroid gland swells and is smooth to the touch
  • Usually euthyroid, if not may be symptoms of hyper/hypothyroidism
  • Present with mass effects
    • Cosmetic
    • Compression of the trachea→ exertional dyspnoeaand, in severe cases, stridoror wheezing
    • Compression of theoesophagus → dysphagia
  • In children dyshormonogenesis may cause cretinism
97
Q

What are the investigations for a goitre?

A

Thyroid function tests - T3/T4 normal, TSH high or upper limit of normal

98
Q

What is the management of a diffuse goitre?

A
  • Treat underlying cause if appropriate (iodine deficiency, autoimmune thyroid disease)
  • Usually no further treatment needed (unless causing obstructive symptoms - surgery)
99
Q

What is the aetiology of a multi-nodular goitre?

A

Develops from a long-standing simple sporadic goitre

100
Q

What is the pathophysiology of a multi-nodular goitre?

A
  • Variation of response of follicular cells to external stimuli - recurrent hyperplasia and involution
  • Mutations of TSH signalling pathway
  • There will be a varying degree of fibrosis, haemorrhage and calcification
101
Q

What is the presentation of a multi-nodular goitre?

A
  • Irregular enlarged thyroid due to nodule formation - thyroid feels bumpy on palpation
  • Enlargement can be impressive
  • Presents with mass effects
  • Can be inactive or toxic
    • Toxic multinodular goitres are responsible for ~35% of cases of hyperthyroidism
    • Toxic nodules have an increased risk of malignant transformation
102
Q

What are the investigations of a multi-nodular goitre?

A
  • Thyroid function tests - TSH usually normal or slightly suppressed, fT3/T4 normal if inactive or increased if toxic
  • US scan - sensitive method for delineating nodules and can demonstrate whether they are cystic or solid
  • FNA - to assess cancer risk for prominent palpable and suspicious nodules
  • CT scan - may detect retrosternal extension and tracheal compression in patients with a very large goitre or clinical symptoms
  • Thyroid isotope scan - toxic or non-toxic
  • Flow volume loops if considering other potential causes of breathlessness
103
Q

What is the management of a multi-nodular goitre?

A
  • Most can leave alone
  • Antithyroid drugs if toxic
  • Radioactive iodine if significant hyperthyroid
  • Surgery if structural problem or significant retrosternal extension
104
Q

What is the management of pre-existing hypothyroidism in pregnancy?

A
  • Unable to compensate for increased demand
  • Increase thyroxine dose by 25mcg as soon as pregnancy suspected
  • Check TFTs monthly for first 20 weeks then 2 monthly until term
  • The average dose increase is by 50% by 20 weeks
  • Aim for TSH <3 mU/l
105
Q

What are the complications of pre-existing hypothyroidism in pregnancy?

A
  • Increased abortion, preeclampsia, abruption, postpartum haemorrhage, preterm labour
  • Impacts on foetal neurophysical development - average of 7 IQ points less in children of untreated hypothyroid mother’s vs normal mothers
106
Q

What are the causes of hyperthyroidism in pregnancy?

A
  • Most common cause in this age group (fertile women) is Graves’ disease
  • Other causes include TMNG, toxic adenoma and thyroiditis
107
Q

What are the complications of hyperthyroidism in pregnancy?

A
  • Infertility/amenorrhoea
  • Spontaneous miscarriage
  • Stillbirth
  • Thyroid crisis in labour
  • Transient neonatal thyrotoxicosis
108
Q

What is the management of hyperthyroidism in pregnancy?

A
  • Wait and see (supportive management)
    • If hyperemesis, will settle
    • Graves may settle as pregnancy suppresses autoimmunity
    • Check TRAb antibodies - if present alert neonatologist as TRAb antibodies can cross the placenta and cause neonatal transient hyperthyroidism
  • β-blockers if needed
  • LOW DOSE antithyroid drugs - wait as late as possible due to side effects on foetus
    • Propylthiouracil 1st trimester
    • Carbimazole 2/3rd trimester
109
Q

What is the aetiology of post-partum thyroiditis?

A
  • Affects 5% postpartum women (25% in T1DM)
  • Occurs within 6 months of giving birth
    • In the postpartum phase there is exacerbation of all autoimmune diseases
110
Q

What is the presentation of post-partum thyroiditis?

A
  • After delivery, the mother develops transient over-active thyroid, classically at around 6 weeks, and then at around 3 months has an underactive thyroid
  • Will develop small, diffuse, nontender goitre
  • Hypothyroid phase associated with neonatal depression
  • Can persist up to 1-year post-partum
  • 25-50% will have persistent hypothyroidism beyond 1 year
111
Q

What are the investigations for post-partum thyroiditis?

A
  • Thyroid function tests
  • Thyroid antibody tests
  • Scintigraphy scan
112
Q

What is the management of post-partum thyroiditis?

A
  • No treatment for hyperthyroid phase, if symptomatic hypothyroid treat with thyroxine
  • Should eventually be able to stop thyroxine but if patient is still on thyroxine after a year it is likely they will need it long term

Endocrine MBCHB (13 decks)

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