BENIGN THYROID DISORDERSRegional SpR Teaching

Woo-Young Yang

ST5

CLASSIFICATION

Simple Non-Toxic Toxic Inflammatory Neoplastic Rare

CLASSIFICATION 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

Neoplastic Follicular Papillary Medullary Anaplastic Lymphoma Metastatic

Rare Infective Iatrogenic

IODINE DIFFICIENCY

Epidemiology Commonest cause of goitre and hypothyroidism world wide

Not common in the western world Pathophysiology

Insufficient iodination of thyroglobulin Decrease in Thyroid Hormone Increase in TSH Diffuse hyperplasia(+/- multinodular appearance)

Pregnancy Increased demand on maternal iodine Worsening features with subsequent pregnancies

Treatment Iodine Replacement

EUTHYROID MNG

Epidemiology Incidence by Palpation – 10% Incidence by Imaging – up to 50%

Aetiology Benign

Colloid cyst Simple cyst Adenoma Infection

Malignant

INVESTIGATIONS

Serological TFT Serum Calcitonin?

FNAC USS ((useful in looking for malignant features such as

microcalcification and capsular invasion/increased vascularity))

CT/MRI – for retrosternal component

Tc99/I123 Scintigraphy – NOT useful in MNG/SN ((BTA and ATA, incidence of cancer 10% in cold nodules))

TREATMENT

Surgery Cosmetic Compressive symptom Suspicion for cancer

Radioiodine Indicated if unfit for surgery Regression of the goitre size

SOLITARY NODULES

Mx is broadly similar to MNG Cystic nodules

Many resolve spontaneously Larger cysts tend to recur

Treatment Simple aspiration and expectant approach with small cysts(<3ml)

Surgery for the larger ones(10% cancer risk)

CLASSIFICATION 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

Neoplastic Follicular Papillary Medullary Anaplastic Lymphoma

Rare Infective Iatrogenic

HYPERTHYROIDISM – CLINICAL FEATURES

Cardiac Tachycardia, AF High output congestive heart failure

Thermoregulatory Heat intolerance

Metabolic Weight loss Increased appetite

GI Diarrhoea

Neuopsychiatric Irritability Anxiety

Dermatological Hair loss and brittle nails

Hormonal Irregular menstruation

Misc Fine tremor Thyroid bruit

HYPOTHYROIDISM – CLINICAL FEATURES

Cardiac Bradycardia

Thermoregulatory Cold intolerance

Metabolic Weight gain Decreased appetite

Glucose intolerance

GI Constipation

Neuopsychiatric Depression Mental impairment

Dermatological Dry skin Myxoedema

Hormonal Irregular menstruation

Misc Hoarseness

GRAVE’S DISEASE

Epidemiology Commonest cause of hyperthyroidism(60%) UK incidence 80/100,000

Pathophysiology Autoantibodies against TSH receptor Stimulation of thyroid gland hyperplasia Autonomous production of T3 and T4 Association with other organ-specific autoimmune diseases Pernicious anaemia, DM, Addison Disease, Myesthenia Gravis

HLA-DR3, B8

GRAVE’S DISEASE – CLINICAL PRESENTATION

Thyroid Manifestations Diffuse symmetrical goitre +/- bruits

Hyperthyroidism Extrathyroid Manifestations Acropachy Myxoedema Grave’s ophthalmopathy

GRAVE’S OPHTHALMOPATHY

Pathophysiology Lymphocytic infiltration and glycosaminoglycan deposition

Extraocular muscle swelling

Periorbital fat proliferation

GRAVE’S OPHTHALMOPATHY

Clinical Features Proptosis greater than 22 mm Lid retraction and lid lag Conjunctival oedema and corneal ulceration

Oculomotor problem Decreasing visual acuity

Rx options High dose steroids Radiotherapy Surgical – alignment/decompression

TOXIC MULTINODULAR GOITRE

Epidemiology Commonly found in the elderly

Pathophysiology 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))

‘T3 toxicosis’ – subclinical hyperthyroidism ((importance of T3 measurement))

TOXIC ADENOMA

Plummer’s Disease Epidemiology

Rare – 2 % of hyperthyroidism Younger than Toxic MNG

Pathophysiology Somatic, non-inherited TSH receptor mutation

Autonomous TSHR activation and

TOXIC GOITRE - INVESTIGATIONS

TFT Thyroid Autoantibodies TPO ((actually the most

senstive marker of grave’s disease – 45% for TSH R))

Thyroglobulin TSH receptor

Scintigraphy Distinction between toxic nodule and Grave’s disease

TOXIC GOITRE - TREATMENT

Difference between Grave’s disease and Toxic MNG/Adenoma Grave’s disease may go into remission(30%)

Toxic MNG/Adenoma does not go into remission

Treatment Options Antithyroid Drugs Radioiodine Surgery

ANTITHYROID DRUGS

Thionamides Carbimazole, Methimazole, Popylthiouracile(PTU)

Pharmacophysiology Inhibition of the organification and oxidation of iodine

T4/T3 synthesis inhibition ? Immunomodulation effect for Grave’s disease?

Side effects Deranged LFT - rarely drug-induced hepatitis Agranulocytosis(1/1,000)

OTHER DRUGS

Beta-blocker Propranolol

Anticoagulants AF management

RADIOIODINE 131 First treatment of choice for Grave’s Disease and MNG

PO administration Pharmacophysiology

Beta radiation – DNA damage and apoptosis (different from I 123, which emits gamma rays)

Dose ? Titration 400 – 600 MBq sufficient for both Grave’s and Toxic MNG

RADIOIODINE 131 Side effect

Hypothyroidism Thyroiditis

Safety? Outpatient treatment Avoid contact with children ((sleep alone/no

sharing utensils))

Contraindication Pregnancy Breast feeding

TOXIC GOITRE - SURGERY Indications

Refractory to radioiodine Patient’s rejection of radioiodine Severe ophthalmopathy Pregnancy with uncontrolled disease Cosmetic

Pre-op Preparation Antithyroid treatment Potassium Iodide if antithyroid drug not tolerated ((saturates the thyroid with iodine, then the gland turns off the absorption mechanism))

TOXIC GOITRE - SURGERY

Grave’s Disease Total thyroidectomy

Toxic Adenoma Thyroid Lobectomy

Toxic SMG ? Subtotal thyroidectomy

HYPERTHYROIDISM IN PREGNANCY

Grave’s Disease Thionamides are safe in pregnancy 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

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

Thyroid replacement Surgery if necessary

INFAMMATORY GOITRES – DE QUERVAIN’S SUBACUTE THYROIDITIS

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 Thyroid status control NSAIDs

INFLAMMATORY GOITRES – RIEDEL’S FIBROSING THYROIDITIS

Chronic Inflammation and Fibrosis of Thyroid Gland

Very rare – 1.6/100,000 Uncertain Pathophysiology

? Autoimmune ? Part of systemic fibrosis Spread of the fibrosis outside the thyroid gland – can cause RLN dysfunction/tracheal compression/hypoparathyroidism

RIEDEL’S FIBROSING THYROIDITIS Clinical features

Extent of hypothyroidism depends on extent of fibrosis of the gland

Hard wooden goitre WITHOUT cervical lymphadenopathy

May have extra-cervical involvements – retroperitoneal fibrosis/mediastinal fibrosis

Investigation Neither FNAC nor Imaging can reliably distinguish Riedel’s Fibrosing Thyroiditis from malignancy

? PET-CT? Open surgical biopsy is required by wedge resection

RIEDEL’S THYROIDITIS Medical Treatment

Steroid Tamoxifen ((not by oe inhibition but by grow factor level decrease

therefore fibroblasts down))

Thyroid hormone replacement Surgical Treatment

Wedge Resection Further surgical Rx not recommended due to the extensive fibrosis

Prognosis self-limiting, good prognosis

THANK YOU