THYROID NEOPLASMS

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Thyroid Neoplasms Benign 1. Adenoma Follicular – colloid, embryonal,foe Hurthle cell 2. Teratoma

Transcript of THYROID NEOPLASMS

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Thyroid Neoplasms

Benign1. Adenoma

•Follicular – colloid, embryonal,foetal

•Hurthle cell

2. Teratoma

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Thyroid NeoplasmsMalignant Tumours: 1. Well differentiated

Papillary Follicular Hurthle cell 2. Undifferentiated Anaplastic 3. Medullary carcinoma

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Thyroid neoplasms

Lymphomas Hodgkin`s lymphoma NonHodgkin`s lymphoma Others Squamous or Mucinous

carcinoma Secondaries

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Aetiology of Thyroid carcinoma

Molecular Biology RET – oncogene Papillary ca. & medullary carcinoma ras mutations in follicular ca. P53 mutations in anaplastic

ca.

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Aetiology of thyroid ca

Radiation

Iodine excess/ deficiency

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Pap Ca 60%

Foll Ca 17%

Anaplastic 13%

Medullary 6%

Lymphoma 4%

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Incidence 3.7/100000

Females more affected

3:1

Mortality 2-3%

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Papillary carcinoma Most common – 60 to 70%. Least aggressive cancer. Prolonged course. 3rd and 4th decades of life. More common in women. Predominant thyroid cancer in children.

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Pathology Grey white poorly defined nodule

varying in size from a few mm. To several cms.

In large lesions, haemorrhage, necrosis and cyst formation with visible papillae may be seen.

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Pathology - Microscopy Typical papillary structures Optically clear nuclei called Orphan

Annie nuclei Round laminated calcified bodies –

psammoma bodies. Nuclear grooves,lobulations and

atypia

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pathology Multiple foci in same lobe

Sometimes opposite lobe

Intrathyroidal lymphatic spread/

Multicentric growth

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Pathology They grow slowly and tend to

metastasize to lymph nodes Better prognosis than other forms

of thyroid cancer Tendency to more malignant

growth with advancing age Local spread to trachea,recurrent

laryngeal nerve and oesophagus

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Occult carcinoma Papillary CA less than 1.5 cm

Palpable LN

Jugular chain

Primary may be only few mms size

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Clinical Features Solitary Nodule (STN) Dysphagia,dyspnoea,hoarseness

indicate locally invasive disease Lymph node enlargement Occasionally lymph node

enlargement alone

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Investigations Thyroid function tests Ultrasound scan Isotope thyroid scan Fine needle aspiration

cytology

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Treatment Near total/total thyroidectomy Lobectomy/Hemithyroidectomy Modified neck dissection TSH suppression

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Total thyroidectomy

hemithyroidectomy

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Thyroid suppression 0.1-0.2 mg daily

Suppress endogenous TSH

Not very much useful in follicular Ca

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Thyroglobulin Tumour marker

Obviate the need of serial isotope scanning

Only adjunct to clinical examination

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Follicular carcinoma Occurs in the fifth decade More common in females 15% of thyroid malignancies Occurs more frequently in iodine

deficiency areas More aggressive and dangerous Blood stream spread

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Pathology Tumour is well encapsulated . Haematologic spread

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Microscopy

Follices are crowded with cells with hardly any colloid.

Capsular and vascular invasion are prominent features.

Tumour with large cells with abundant eosinophilic cytoplasm are called Hurthle cell carcinoma

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Clinical features Solitary nodule or multiple painless

nodules May arise in a long standing goiter Lymph node involvement rare Haematogenous spread to bones

lungs or liver Bony metastasis may be pulsatile

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Investigations FNAC not helpful Radiology - X –ray chest , neck,

bones, CT scan Raio isotope scan

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Treatment Total thyroidectomy/Near total

thyroidectomy Radioiodine External beam radiation Chemotherapy TSH suppression

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Prognosis of DTC Age

Histological variant

Extra thyroidal spread

size

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Low risk Men<40, women<50 Older patients - intrathyroid papillary Ca -foll with minor caps.

Invasion -<5cm -no distant mets

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High risk Distant mets

Older patients - extra thyroidal Pap - major caps.invasion - >5 cm

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2% mortality in 25 yr survival in low risk group

46% in high risk group

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Medullary carcinoma(MTC) Arises from the C – cells ,derived from the neural crest

– APUD system Sporadic or familial form

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Familial MTC Familial with MTC only

with MEN IIA – MTC hyperparathyroidism

& phaeochromocytoma

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MTC secretes calcitonin CEA, histamine,and serotonin

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Pathology Sporadic form – usually unilateral,

familial form – multinodular Sheets of infiltrating malignant

cells with areas amyloid Special staining can be performed

for calcitonin in the cells Lymphatic & haematogenous

spread

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Clinical features Age – sporadic form (80%) 40 – 60

yrs. Familial (20%) – younger age group

Single nodule (sporadic) , multinodular (familial)

Lymph node enlargement +(- ) Dysphagia ,dyspnoea hoarseness MEN IIA - symptoms of

hyperthyroidism or phaeochromocytoma

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Investigations FNAC OF Thyroid mass Urinary metabolites –

VMA,metanephrine,catecholamine Serum Calcium USG Abdomen Serum calcitonin

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Treatment Total thyroidectomy with central

neck dissection External – beam radiotherapy in

unresctable disease

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Anaplastic thyroid carcinoma Rapidly growing tumours with

invasion of surrounding structures Lymph node involvement is

frequent & early Foci of both undifferentiated and

differentiated cells are seen in follicular or papillary pattern

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Clinical features Presents with rapidly progressive

lump of short duration May be painful or ulcerated Compressive symptoms+ Mass hard and fixed to the

surrounding structures Stridor+ Metastasis lymph nodes,

liver ,lungs. bones

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Treatment FNAC – diagnostic Treatment – disappointing Debulking , tracheostomy

radiotherapy

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Secondaries Breast

Colon

Kidney

Melanoma

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hypothyroidism Commonest endocrine problem

5% of female population affected

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Types Primary

Secondary

tertiary

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Primary Auto immune

Surgery

Radioactive iodine

Ext.beam RT to neck

drugs

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Hashimoto’s thyroiditis Auto immune

Familial

Females 9:1

40-50 yrs

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features Compensated hypothyroidism

Hyperthyroidism

hypothyroidism

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TSH

ANTIBODIES antimicrosomal antiTG

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Treatment

Normalise the TSH

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Complications Other autoimmune disorders

lymphoma