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PRESENTATION: THYROID SWELLING(S)
PRESENTATION: THYROID SWELLING(S)
PRESENTATION: THYROID SWELLING(S)
PRESENTATION: THYROID SWELLING(S)
PRESENTATION: THYROID SWELLING(S)
PRESENTATION: THYROID SWELLING(S)
PRESENTATION: THYROID SWELLING(S)
PRESENTATION: THYROID SWELLING(S)
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PRESENTATION: THYROID SWELLING(S)

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  • 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. 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. 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. 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. 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. 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. 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. 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 ♂

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