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  1. 1. PRESENTATION: THYROID SWELLING(S) TYPICAL PRESENTING COMPLAINT 1. Cosmetic reason / noticed lump in the neck 4. Oesophageal compression → dysphagia 2. Discomfort 5. Worries about malignancy 3. Tracheal compression → SOB 6. Onset of hyperthyroidism CLINICAL APPROACH Once it is established that the neck swelling is indeed a thyroid swelling: T h y r o id s w e l lin g s D if f u s e N o d u la r e n la r g e m e n t e n la r g e m e n t T o x ic N o n -T o x ic S o lit a r y n o d u l e M u lt in o d u la r G o it r e U s u a lly G r a v e ' s D is e a s e O th e r S im p le c o l lo i d g o it r e C a r c in o m a / Adenom a p r o g r e s s io n t h y r o id i t e s ly m p h o m a o f s im p l e d i f f u s e e n la r g e m e n t U s u a lly T h y r o id it i s P r o m in e n t T o x ic N o n -to x ic te n d e r n o d u le in M N G H a s h im o t o ' s d e Q u e r v a in ' s C yst R ie d e l' s C o l lo i d H a e m o rrh a g e in t o n e c r o t ic n o d u le P a in f u l , s u d d e n HISTORY: Risk factors: female, age, past medical / surgical history, family history, diet /medication Onset of symptoms: Acute → more likely to be inflammatory / cystic Symptoms present: • Symptoms of hyperthyroidism (thyrotoxicosis → very severe hyperthyroidism) : o Metabolic: heat intolerance, excessive sweating, weight loss despite of excessive appetite o CVS: palpitations, shortness of breath, tiredness, o Neurological: nervousness/agitation/irritability (emotional lability), insomnia, depression and excitement (→ mania and melancholia noticed by relatives), tremors, headaches, vertigo, hyperaesthesia o GI: mild diarrhoea o GU: reduction in menses (oligomenorrhoea) or amenorrhoea o MS: muscle wasting and weakness (small muscles of hand, shoulder and face) → rarely: complete paralysis • Symptoms of hypothyroidism (myxoedema → very severe hypothyroidism) o Metabolic: tiredness, weakness, mental lethargy, cold intolerance, weight gain despite of poor/normal appetite, o CVS: breathlessness and ankle swelling (→ heart failure), o Neurological: difficulty to think and to speak clearly and quickly, hallucinations, dementia (‘myxoedema madness’) → ‘myxoedema coma’ o GI: progressive constipation o GU: menstrual disturbances (menorrhagia common when myxoedema occurs before menopause) o MS: carpal tunnel syndrome [pins and needles in the fingers, esp index and middle fingers; pain in the forearm, loss of function → drops small articles and cannot perform delicate movements due to loss of discriminatory sensation as median nerve is damaged, in severe nerve damage → loss of motor function → weakness and paralysis of muscles of the thenar eminence and 1st 2 lumbricals, i.e. median nerve palsy (wasting of thenar eminence, absent abduction of thumb, absent opposition of thumb); exacerbation of symptoms at night → often woken up at night, pathognomonic] • Associated symptoms: o Stridor/dyspnoea, dysphagia, and hoarseness → either due to mass effect/compression by goitre (i.e. tracheal deviation, oesophageal compression, and involvement of recurrent laryngeal nerve respectively) or might be due to infiltrating fibrosis
  2. 2. which may indicate either anaplastic carcinoma of the thyroid gland or de Quervain’s thyroiditis (fibrosing). Fever, drenching night sweats → lymphoma, tuberculous involvement of the thyroid gland, cancer of the thyroid gland o Fever, chills → infective causes o Pain → rare: in the neck, usually not localized, non-radiating dull pain; if the pain is sharp, severe and of sudden onset → consider rupture of thyroid cyst / bleeding into the cyst. o Other symptoms:  Bone pain  Chronic cough May indicate metastases  Haemoptysis PHYSICAL EXAMINATION: General & metabolic Hyperthyroidism: thin, face and hands wasted, hot and sweating in cold room Hypothyroidism: peaches and cream complexion (smooth, pale-yellow skin, pink-orange tinge on Eyes cheeks); overweight, excess CT in supraclavicular fossae, across back and neck and over the Look for signs of: shoulders, hair looks thin and ragged and falls out, tongue enlarges, voice becomes deep and Hyperthyroidism: lid hoarse retraction (upper eyelid → autonomic part of levator palpebrae superioris is hypertonic, N: ½ between Neck pupil and superior limbus of Look for swellings → midline, iris) (Dalrymple’s sign), lid moves with swallowing; scars, lag (von Graefe’s sign), ↓ nodular/diffuse; sgl/multiple. Chest [Note: size, tenderness, blinking (Stellwag’s sign), Retrosternal exophthalmos: oedema of mobility, consistency] extension LN. Trachea. Listen for thyroid retro-orbital tissues (rare) (appearance of sclera below bruit inferior limbus → popping out), proptosis, opthalmoplegia: often affects superior rectus and inferior Hands & other oblique → usu turn eye musculoskeletal signs upwards and outwards [diff in Hyperthyroidism: wasting and convergence → Mobius’ weakness of muscles of hands, sign] → diplopia, chemosis: shoulders and face → proximal oedema of conjunctiva (thick, myopathy (look for Plummer boggy and crinkled, eyes sign); enlarged finger tips water excessively), absence of (pseudoclubbing aka thyroid wrinkling of forehead when the acropachy – Grave’s); patient bends his head and increased sweating; palmar looks up (Joffroy’s sign) erythema; onycholysis Pallor in Grave’s disease (Plummer’s nails); areas of Hypothyroidism: Eyes are vitiligo (Grave’s), pulse. normal, but there is periorbital Hypothyroidism: puffy and puffiness (eyelids swollen and spade-like hands heavy → look sleepy and Patients with large retrosternal lethargic); outer third of the goitres: Pemberton’s sign eyebrows falls out suffusion of face/ giddiness/syncope Cardiovascular Hyperthyroidism: tachycardia at rest Neurological (90/min or more) → persists during Hyperthyroidism: worried, nervous, restless, moves Skin sleep; extrasystoles or AF; mild about in jerky movements, twist and twine handkerchief Grave’s disease: pretibial heart failure → rales at bases of between fingers, brisk reflexes; fine tremors when hands myxoedema (red, blotchy, lungs and oedema of ankles are stretched out hands with fingers spread and palm raised areas over the shin), Hypothyroidism: bradycardia (40-60/ facing downwards, similar tremor in protruded tongue increased sweating min), low BP; changes reversed if Hypothyroidism: mental alertness, ability to respond to Hypothyroidism: dry and heart failure develops; hands are questions and solve problems ↓; conversation also inelastic, does not sweat, may cold and finger tips blue hampered by enlargement of tongue; movements are look oedematous, does not pit In retrosternal goitre → SVC slow and deliberate (bradykinesia), reflexes are sluggish after prolonged pressure engorgement – look for prominent and relaxation period is delayed and prolonged (esp veins over chest ankle jerk)
  3. 3. Classification of severity of thyroid eye disease Werner’s mnemonic NO SPECS Class 0 N No signs or symptoms Class 1 O Only signs of upper eye lid retraction and stare, with or without lid lag and exophthalmos Class 2 S Soft-tissue involvement Class 3 P Proptosis Class 4 E Exophthalmos Class 5 C Corneal involvement Class 6 S Sight loss due to optic nerve involvement Difference between toxic MNG and Grave’s disease Toxic MNG Grave’s disease Older age group Younger age-group Nodular enlargement Diffuse enlargement Eye signs not present Eye signs present AF present in 40% of patients AF uncommon No associated autoimmune disease Autoimmune diseases commonly associated DIAGNOSIS / DIFFERENTIAL DIAGNOSIS GOITRES (visible when 3x normal size → weigh over 50g) 1. Benign pathological goitre a. Simple colloid goitre and multinodular goitre  Same underlying pathogenesis and multifactorial aetiology: Goitrogens (uncooked cabbage, Li & anti- thyroid drugs), Dyshormogenesis, Iodine deficiency (epidemic, endemic), Autoimmune b. Autoimmune thyroid disease (Hashimoto’s thyroiditis, Grave’s disease) c. Other thyroitides (de Quervain’s [acute] and Riedel’s [chronic fibrosing]) d. Benign neoplasm 2. Malignant pathological goitre WHO Grading for Goitres a. Primary (carcinoma) Grade 0 No palpable or visible goitre b. Secondary (lymphoma) Grade 1 Palpable goitre 3. Physiologic goitre Grade 1AGoitre detectable only by a. Puberty palpation b. Pregnancy Grade 1BGoitre palpable and visible with 4. Others extended neck a. Tuberculosis Grade 2 Goitre visible with neck in normal position b. Sarcoidosis Grade 3 Large goitre visible from distance SINGLE NODULE 1. Thyroid cyst (benign vs. malignant) 2. Thyroid tumour (CA/lymphoma) 3. Functioning adenoma 4. Thyroiditis INVESTIGATIONS: ESSENTIAL: 1. Blood tests  FBC & PBF – normocytic normochromic anaemia in Grave’s  Thyroid function test (TSH, T3 and T4)  Thyroid autoantibodies (e.g. TRAbs)  Calcium and albumin 2. Ultrasound  Dimension of goitre/nodules, look for cysts that can be aspirated: 3. CXR and thoracic inlet scan if tracheal deviation/ retrosternal extension 4. Isotope scan if discrete swelling and toxicity exist 5. FNAC (especially ‘cold’ nodules)  Cytology of all palpable discrete swellings
  4. 4. CLASSIFICATION OF THYROID SWELLINGS + MANAGEMENT Aetiology/ History Morphology type Age Sex Others SOLITARY THYROID NODULE  ♂/♀ = 1:4  40-50 years  10% in middle-aged → malignant, 50% malignant in young and elderly  FNAC is the most important investigation; surgery if malignant!  Technetium or iodine radioisotope scan differentiate ‘cold’ from ‘hot’ nodules  ‘Cold’ nodules that are solid or partly cystic → malignant until proven otherwise Cyst Completely smooth  Most are composite lesions with colloid wall → very rare degeneration, necrosis or haemorrhage in benign or malignant tumours Any age  ♂/♀ = ?? May be multiloculated  Only benign if completely aspirated  Cytology can be false-negative in 1/3 of malignant cysts Adenomas Most are follicular  >40 years  More common Family history, long-standing multinodular goitre Usually 2-4 cm & in ♀ than ♂ encapsulated Indistinguishable from CA as capsule cannot be demonstrated Surgical excision is diagnostic and curative
  5. 5. Neoplastic Malignant  Papillary:  Papillary:  75% of malignancies  Usually children and ♂/♀=1:3-4  Multicentric euthyroid young adults  Mixture of papillary and colloid-filled follicles  Well-  Histology: papillary projections, pale and differentiated empty nuclei (Orphan Annie-eyed nuclei); (pap / fol) → seldom encapsulated nodule  Lymphatic spread (esp in children)  CN may be  Slow growing, metastasize early to regional enlarged, bone LN (‘lateral aberrant thyroid’ → secondary pain, cough deposit of CA in LN)  Occult tumour – primary lesion of papillary CA with ø < 1.5 cm → excellent prognosis  TSH dependent  Mx: thyroid lobectomy / thyroidectomy  Follicular:  Follicular: ♀>♂  10% of malignancies 20-50 years  Macroscopically: encapsulated  Histology: invasion of capsule and of vascular spaces in capsular region  Histological variant: Hurthle cell tumours → oxyphil (hurthle /Askanazy) cells predominate  FNA cannot distinguish CA and adenoma (80% adenoma)  Haematogenous spread → usually to lung and bone  Mx: total thyroidectomy and lifelong thyroxine replacement +/- radioiodine  Anaplastic:  Anaplastic:  5% of malignancies 60-80 years ♀>♂  Debulking necessary  Hard, irregular mass → locally invasive with LN involvement; stridor, dysphagia, pain and hoarseness of voice  Mx: radiotherapy and doxorubicin  Medullary:  Medullary:  8% of malignancies 20-30 years OR ♂/♀=1:1  Medullary carcinoma is a neoplasm of the 50-70 years+ parafollicular (C) cells (derived from ultimobranchial bodies) → calcitonin (↓Ca2+)  90% Sporadic → 50-70 years  10 % Family history, 20-30 years → MEN syndrome 2a or 2b (mutation of RET proto- oncogene) • 2a (Sipple syndrome) → phaechromocytoma, parathyroid tumours, medullary thyroid CA • 2b→ phaeochromocytoma, neuromata of tongue, lips and conjuctiva, pale-brown birthmarks, megacolon, marfanoid habitus, medullary thyroid CA  Mx: radical surgery with f/u → sequential calcitonin assays  Lymphoma  2% of malignancies  Dx: trucut biopsy  Mx: radiotherapy and chemotherapy GOITRE
  6. 6. Simple goitre Diffuse hyperplasia to  In endemic  ♂/♀ = 1:5  Commonest form of thyroid abnormality meet physiologic areas:  Causes: demand for thyroxine childhood  Dyshormogenesis, usually in those with  Sporadic a family history of goitre, i.e. genetically Due to excess physiological predetermined defects in thyroid stimulation of TSH. goitres appear hormone metabolism (iodine trans-port Relative iodine at puberty, defects, abnormal secretion of deficiency most during iodoproteins, thyroid hormone common pathological pregnancy, and resistance syndromes) cause. during severe  Goitrogens: illness and Vegetables of the brassica family (e.g. Colloid goitre→ late emotional cabbage, sprouts and kale) → contain stage of diffuse disturbances: thiocyanate; lithium; para-aminosalicylic hyperplasia → acini Puberty / young acid (PAS); aminogluthetimide; distended w/ colloid adult sulfonamides, phenylbutazone; anti- not released because thyroid drugs (perchlorates, stimulation by TSH ↓ carbimazole and thiouracil); Iodides in large quantities  Common in places where drinking water has low iodine content  Mx: treat underlying cause / administer low dose thyroxine (0.1 – 0.3 mg/day) Multinodular goitre  In endemic  ♂/♀ = 1:6  Common in places where drinking water has areas: early low iodine content Either toxic or non- adult life (15-30  Overactivity in parts of an MNG may lead to toxic years) hyperthyroidism (Plummer’s syndrome)  Sporadic:  Progression of simple diffuse goitre to 25-40 years nodular enlargement  Positive family history. Malignant change in 5% of untreated MNG  No ophthalmic features seen  Mx: usually there is no need for intervention, but if the patient insists or the MNG is toxic:  Non-surgical • Remove goitrogens • Thyroxine • Thyrotoxic → treat like Grave’s • FNAC + aspiration of cysts (treat recurrent ones with tetracycline) • Radioiodine (elderly / unfit for surgery)  Surgical • Bilateral subtotal thyroidectomy + postop thyroxine replacement • Avoid total thyroidectomy  Indications for surgery: obstructive symptoms, suspicion of malignancy, cosmetic reasons, thyrotoxicosis, increasing in size despite thyroxin therapy, retrosternal extension
  7. 7. Toxic Diffuse  15-45 years  ♂/♀ = 1:10 Note: Graves’ disease  Thyrotoxicosis is caused by an excess of circulating thyroid hormone.  10 → arising from normal gland e.g. Grave’s disease (autoimmune)  Mx of Grave’s: • Medical: antithyroid drugs and beta-blockers • Radioiodine (absolute CI: pregnancy and lactation) → single oral dose; risks → early hyperthyroidism, late hypothyroidism and late hyperparathyroidism • Surgery: bilateral subtotal thyroidectomy (leaving 4-10 g behind)  The coexistence of a TSH dependent functioning nodule(s) and Grave's disease is referred to as Marine-Lenhart syndrome Multinodular  45-60 years if  More common  20 → arising from abnormal gland e.g. secondary in ♀ than ♂ Plummer’s disease (occurs in long standing multinodular goitre); note that in Plummer’s disease, no eye signs are observed.  Secondary thyrotoxicosis (Plummer’s disease) is more common in areas where simple hyperplastic goitre (and nodular goitre is endemic).  Note: Do not mistaken Plummer’s disease / Plummer’s syndrome with Plummer-Vinson syndrome (AKA Paterson-Brown-Kelly syndrome or Waldenstrom-Kjellberg syndrome) → iron deficiency anaemia a/w dysphagia and post-cricoid oesophageal webs in middle-aged women Toxic adenoma  >40 years  More common (solitary) in ♀ than ♂ Autonomous toxic nodule
  8. 8. Inflammatory Autoimmune  Hashimoto’s: middle age women (near Note: Chronic lymphocytic menopause) or men at any age  Hashimoto’s: Autoimmune → mitochondria thyroiditis  More common in ♀ than ♂ (♂/♀ = of thyroid cells and thyroglobulin produced (Hashimoto’s 1:15) → lymphocyte and plasma cell infiltration thyroiditis) → thyroid cell destruction → initially results in hyperplasia of intact cells causing thyrotoxicosis → eventually hypothyroidism Subacute  Chronic lymphocytic (focal) thyroiditis: lymphocytic varied histological picture, onset, thyroid thyroiditis status and type of goitre (diffuse → nodular, (postpartum bosselated). Infiltration of thyroid thyroiditis and parenchyma by lymphocytes and plasma sporadic painless cells resulting in formation of germinal thyroiditis) centres → common cause of sporadic goitrous hypothyroidism in non-iodine deficient areas, associated with the HLA- DR5 genotype  Subacute lymphocytic thyroiditis: antimicrosomal antibodies are present in 50 to 80 percent of patients, while antithyroid peroxidase antibodies are present in nearly all patients Granulomatous  Adults  De Quervain’s thyroiditis is a true subacute De Quervain’s  More common in ♀ than ♂ inflammation of the thyroid gland thyroiditis  Associated with mild hyperthyroidism  Viral aetiology / epidemics  Self-limiting (1-3 months)  Typical subacute presentation: pain in the neck, fever, malaise, myalgia, and a firm, tender, irregular enlargement of one or both thyroid lobes  Associated with giant cells and granulomata  ESR is raised  Aspirin and steroids give symptomatic relief  Acute symptoms: 10-14 days Fibrosing  Very rare (0.5% of goitres)  Woody hard goitre, fixed Riedel’s thyroiditis  Fibrous tissue may infiltrate beyond thyroid gland to adjacent structures (e.g. muscles, parathyroids, recurrent laryngeal nerves, carotid sheath)  Maybe unilateral/bilateral  Can be mistaken for signs of anaplastic CA → differentiation by means of histology (remove wedge from isthmus, this also frees the trachea)  Complication: hypothyroidism, etc  Surgery → confirm diagnosis and relieve pressure Infective  At any age, usually adults Acute (bacterial  More common in ♀ than ♂ thyroiditis, viral thyroiditis, subacute thyroiditis) Chronic (tuberculous, syphilitic) Other  At any age, usually adults Amyloid  More common in ♀ than ♂