Regional SpR Teaching
Woo-Young Yang
ST5

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Simple Non-Toxic
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Toxic
Inflammatory
Neoplastic
Rare

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Simple Non-Toxic
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Iodine Difficiency
Multinodular Goitre
Solitary Nodule
Physiological
Toxic
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Grave’s Disease
Plummer’s Disease
Inflammatory
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Hashimoto’s Thyroiditis
De Quervain’s
Thyroiditis
Riedel’s Thyroiditis
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Neoplastic
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Follicular
Papillary
Medullary
Anaplastic
Lymphoma
Metastatic
Rare
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Infective
Iatrogenic

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Epidemiology
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Commonest cause of goitre and hypothyroidism world wide
Not common in the western world
Pathophysiology
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Insufficient iodination of thyroglobulin
Decrease in Thyroid Hormone
Increase in TSH
Diffuse hyperplasia(+/- multinodular appearance)
Pregnancy
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Increased demand on maternal iodine
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Worsening features with subsequent pregnancies
Treatment
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Iodine Replacement

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Epidemiology
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Incidence by Palpation – 10%
Incidence by Imaging – up to 50%
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Aetiology
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Benign
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Colloid cyst
Simple cyst
Adenoma
Infection
Malignant

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Serological
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TFT
Serum Calcitonin?
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FNAC
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USS
((useful in looking for malignant features such as microcalcification and capsular invasion/increased vascularity))
CT/MRI – for retrosternal component
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Tc99/I123 Scintigraphy – NOT useful in MNG/SN
((BTA and ATA, incidence of cancer 10% in cold nodules))

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Surgery
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Cosmetic
Compressive symptom
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Suspicion for cancer
Radioiodine
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Indicated if unfit for surgery
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Regression of the goitre size

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Mx is broadly similar to MNG
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Cystic nodules
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Many resolve spontaneously
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Larger cysts tend to recur
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Treatment
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Simple aspiration and expectant approach with small cysts(<3ml)
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Surgery for the larger ones(10% cancer risk)




Simple Non-Toxic




Iodine Difficiency
Multinodular Goitre
Solitary Nodule
Physiological
Toxic


Grave’s Disease
Plummer’s Disease
Inflammatory



Hashimoto’s Thyroiditis
De Quervain’s
Thyroiditis
Riedel’s Thyroiditis
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
Neoplastic
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



Follicular
Papillary
Medullary
Anaplastic
Lymphoma
Rare
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
Infective
Iatrogenic

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Cardiac
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Tachycardia, AF
High output congestive heart failure
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Thermoregulatory
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Heat intolerance
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Metabolic
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Weight loss
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Increased appetite
GI
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Diarrhoea
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Neuopsychiatric
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Irritability
Anxiety
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Dermatological
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Hair loss and brittle nails
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Hormonal
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Irregular menstruation
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Misc
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Fine tremor
Thyroid bruit

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Cardiac
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Bradycardia
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Thermoregulatory
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Cold intolerance
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Metabolic
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Weight gain
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Decreased appetite
Glucose intolerance
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GI
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Constipation
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Neuopsychiatric
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Depression
Mental impairment
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Dermatological
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Dry skin
Myxoedema
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Hormonal
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Irregular menstruation
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Misc
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Hoarseness

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Epidemiology
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Commonest cause of hyperthyroidism(60%)
UK incidence 80/100,000
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Pathophysiology
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Autoantibodies against TSH receptor
Stimulation of thyroid gland hyperplasia
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Autonomous production of T3 and T4
Association with other organ-specific autoimmune diseases
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Pernicious anaemia, DM, Addison Disease, Myesthenia
Gravis
HLA-DR3, B8

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Thyroid
Manifestations
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Diffuse symmetrical goitre +/- bruits
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Hyperthyroidism
Extrathyroid
Manifestations
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Acropachy
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Myxoedema
Grave’s ophthalmopathy

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Pathophysiology
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Lymphocytic infiltration and glycosaminoglycan deposition
Extraocular muscle swelling
Periorbital fat proliferation

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Clinical Features
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Proptosis greater than 22 mm
Lid retraction and lid lag
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Conjunctival oedema and corneal ulceration
Oculomotor problem
Decreasing visual acuity
Rx options
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High dose steroids
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Radiotherapy
Surgical – alignment/decompression

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Epidemiology
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Commonly found in the elderly
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Pathophysiology
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Jod-Baselow Phenomenon
((exact mechanism is obscure. Background iodine deficiency, followed by iodine Xs, leading to unmasking hyperthyroidism. Normal follicular architecture becomes disrupted, leading to inefficient iodine trapping))
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‘T3 toxicosis’ – subclinical hyperthyroidism
((importance of
T3 measurement))

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Plummer’s Disease
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Epidemiology
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Rare – 2 % of hyperthyroidism
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Younger than Toxic MNG
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Pathophysiology
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Somatic, non-inherited TSH receptor mutation
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Autonomous TSHR activation and

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TFT
Thyroid Autoantibodies
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TPO
((actually the most senstive marker of grave’s disease – 45% for
TSH R))
Thyroglobulin
TSH receptor
Scintigraphy
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Distinction between toxic nodule and Grave’s disease

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Difference between Grave’s disease and Toxic
MNG/Adenoma
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Grave’s disease may go into remission(30%)
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Toxic MNG/Adenoma does not go into remission
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Treatment Options
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Antithyroid Drugs
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Radioiodine
Surgery

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Thionamides
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Carbimazole, Methimazole, Popylthiouracile(PTU)
Pharmacophysiology
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Inhibition of the organification and oxidation of iodine
T4/T3 synthesis inhibition
? Immunomodulation effect for Grave’s disease?
Side effects
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Deranged LFT - rarely drug-induced hepatitis
Agranulocytosis(1/1,000)

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Beta-blocker
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Propranolol
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Anticoagulants
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AF management

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First treatment of choice for Grave’s Disease and
MNG
PO administration
Pharmacophysiology
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Beta radiation – DNA damage and apoptosis
(different from I 123, which emits gamma rays)
Dose
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? Titration
400 – 600 MBq sufficient for both Grave’s and Toxic MNG

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Side effect
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Hypothyroidism
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Thyroiditis
Safety?
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Outpatient treatment
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Avoid contact with children
((sleep alone/no sharing utensils))
Contraindication
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Pregnancy
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Breast feeding

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Indications
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Refractory to radioiodine
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Patient’s rejection of radioiodine
Severe ophthalmopathy
Pregnancy with uncontrolled disease
Cosmetic
Pre-op Preparation
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Antithyroid treatment
Potassium Iodide if antithyroid drug not tolerated
((saturates the thyroid with iodine, then the gland turns off the absorption mechanism))

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Grave’s Disease
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Total thyroidectomy
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Toxic Adenoma
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Thyroid Lobectomy
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Toxic SMG
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? Subtotal thyroidectomy

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Grave’s Disease
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Thionamides are safe in pregnancy
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PTU is preferred as less drug is delivered to foetus
Intra-partum – Transient Hyperthyroidism of hyperemesis gravidarum
((betaHCG and TSH share the same subunit))
Post-partum Thyroiditis
((distinction by autoAb, clinical signs, iodine uptake(postpartum)))

INFLAMMATORY GOITRES -
HASHIMOTO’S THYROIDITIS
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Anti-TPO/Thyroglobulin/TSHR autoAb
Initial transient hyperthyroidism due to cellular destruction and release of the preformed thyroid hormones
Subsequent hypothyroidism
Rubbery diffuse thyroid enlargement
Treatment
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Thyroid replacement
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Surgery if necessary

INFAMMATORY GOITRES – DE
QUERVAIN’S SUBACUTE THYROIDITIS
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Granulomatous inflammation of the thyroid gland ? 2y to viral infection
Subacute course over weeks/months
Tender symmetrical diffusely enlarged goitre
Phases
 hyperthyroid – hypothyroid – euthyroid(recovery)
Treatment
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Thyroid status control
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NSAIDs

INFLAMMATORY GOITRES – RIEDEL’S
FIBROSING THYROIDITIS
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Chronic Inflammation and Fibrosis of Thyroid
Gland
Very rare – 1.6/100,000
Uncertain Pathophysiology
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? Autoimmune
? Part of systemic fibrosis
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Spread of the fibrosis outside the thyroid gland – can cause RLN dysfunction/tracheal compression/hypoparathyroidism

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Clinical features
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Extent of hypothyroidism depends on extent of fibrosis of the gland
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Hard wooden goitre WITHOUT cervical lymphadenopathy
May have extra-cervical involvements – retroperitoneal fibrosis/mediastinal fibrosis
Investigation
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Neither FNAC nor Imaging can reliably distinguish Riedel’s
Fibrosing Thyroiditis from malignancy
? PET-CT?
Open surgical biopsy is required by wedge resection

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Medical Treatment
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Steroid
Tamoxifen
((not by oe inhibition but by grow factor level decrease therefore fibroblasts down))
Thyroid hormone replacement
Surgical Treatment
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Wedge Resection
Further surgical Rx not recommended due to the extensive fibrosis
Prognosis
 self-limiting, good prognosis