Synopsis
Distinguish the major thyroid cancer phenotypes, recognise airway-threatening disease and route investigation, surgery, surveillance and genomic treatment through the correct specialist pathway.
- Papillary and follicular cancers arise from follicular cells and are grouped as differentiated thyroid cancer; papillary disease commonly spreads to cervical nodes, whereas follicular carcinoma more characteristically spreads haematogenously.
- Medullary thyroid cancer arises from parafollicular C cells, may secrete calcitonin and CEA, and can be sporadic or associated with germline RET variants and MEN2; family implications begin at diagnosis.
- Anaplastic thyroid cancer is an aggressive, rapidly progressive malignancy in which airway, swallowing, voice and performance status must be assessed immediately rather than after a routine diagnostic sequence.
- A euthyroid result does not make a thyroid nodule benign. Ultrasound risk assessment and ultrasound-guided cytology, reported within the local thyroid cytology system, determine the diagnostic route.
- NICE NG230 covers differentiated thyroid cancer but explicitly does not provide the treatment pathway for medullary cancer; use a thyroid cancer MDT and appropriate specialist guidance rather than extrapolating radioiodine practice.
- Radioiodine targets iodine-avid follicular-cell tissue and has no useful role in medullary or anaplastic thyroid cancer. Its use after differentiated cancer surgery depends on recurrence risk and MDT assessment.
- Serum thyroglobulin is a differentiated-cancer tumour marker only after the relevant thyroid tissue has been treated; antibodies can invalidate interpretation. Calcitonin and CEA serve a different biological pathway in medullary disease.
- RET testing can affect both inherited-risk counselling and systemic treatment selection. Consent, germline-versus-somatic distinction and referral of relatives belong in clinical genetics, not an informal family blood-test plan.
Key red flags
A hard or fixed nodule, rapid enlargement, cervical lymphadenopathy, persistent hoarseness, dysphagia, stridor, childhood neck irradiation or relevant familial syndrome increases concern. Normal thyroid function does not lower the structural risk enough to avoid imaging.
A thyroid nodule with raised calcitonin, diarrhoea or flushing, a family history of medullary cancer, phaeochromocytoma or hyperparathyroidism should prompt a medullary/MEN2 pathway. Exclude phaeochromocytoma before elective thyroid surgery if MEN2 is plausible.
Weeks of explosive neck growth, pain, dysphonia, dysphagia, dyspnoea, stridor or skin fixation in an older adult is a time-critical pattern. Airway compromise, bleeding and inability to handle secretions require emergency escalation.
Investigation priorities
Characterise the thyroid lesion and cervical lymph-node compartments before biopsy or operation.
Management branches
A palpable or incidentally detected thyroid lesion without current airway compromise.
- Take focused history and examination, check TSH, and arrange high-quality ultrasound that includes the central and lateral cervical nodes.
- Biopsy lesions meeting the local ultrasound threshold and any suspicious node; obtain an expedited thyroid MDT opinion for malignant, suspicious or discordant results.
- Stage confirmed cancer according to histology and risk. Avoid ordering untargeted scans that delay surgery, and communicate uncertainty when cytology cannot distinguish adenoma from follicular carcinoma.