Thyroid nodules and thyroid neoplasms

• A thyroid nodule is a discrete area within the thyroid that stands out from surrounding tissue on imaging or on palpation. Most are benign, but roughly 7 to 15% are malignant, so the whole clinical job is to separate the few cancers from the many benign nodules without over-treating people.
• A thyroid neoplasm is any new growth (benign or malignant) arising from thyroid cells; the important malignant types are papillary, follicular (including Hurthle), medullary, anaplastic and primary thyroid lymphoma.
• The first test in a person with a nodule is serum TSH. If TSH is low, a radionuclide scan tells you whether the nodule is "hot" (usually benign) and spares an unnecessary needle biopsy.
• If TSH is normal or high, ultrasound (and most clinicians now use the ACR TI-RADS score) decides whether and when to aspirate with fine needle aspiration. The result is reported in one of six Bethesda categories, which then guide next steps.
• Medullary thyroid cancer is a different disease from the others: it arises from calcitonin-secreting C cells, does not take up radioactive iodine, and is driven by RET mutations. Thyroglobulin is used to follow differentiated (papillary/follicular) thyroid cancer after surgery.

By the end of this page you should be able to:

1. Explain why most thyroid nodules are benign and which features make cancer more likely.
2. Plan the biochemical and imaging work-up of a newly discovered thyroid nodule, including when to scan rather than aspirate.
3. Describe the ACR TI-RADS ultrasound score and the size cut-offs at which fine needle aspiration is offered.
4. Interpret a Bethesda cytology report and outline the management that follows from each category.
5. Compare papillary, follicular, medullary, anaplastic and lymphoma neoplasms by origin, spread and prognosis.
6. Explain the roles of thyroidectomy, radioactive iodine, TSH suppression and targeted drugs.
7. Describe thyroglobulin follow-up and the common surgical complications.
8. Summarise the 2015 American Thyroid Association guideline position and its 2025 revision, with appropriate caution about low-resource settings.

A thyroid neoplasm is any abnormal proliferation of thyroid cells, benign or malignant. The spectrum runs from simple colloid and hyperplastic nodules, through benign follicular adenomas, to cancers of differing behaviour. Because most nodules (and a great many that are felt or scanned) are not cancer, modern practice aims for selective, risk-based investigation rather than operating on every lump.

This page focuses on the nodule as the clinical starting point and on the neoplasms that can be found within it. It does not cover thyroiditis, simple goitre or thyrotoxicosis in detail; those are handled on their own pages.

Palpable thyroid nodules are found in about 5% of women and 1% of men in iodine-sufficient parts of the world, while high-resolution ultrasound detects nodules in 19% to 68% of randomly selected people, more often in women and in older adults.^[1] At autopsy the figure is even higher, so nodular thyroid change is best regarded as a normal accompaniment of ageing rather than a rare disease.

Only a minority of nodules are malignant. Thyroid cancer is found in 7% to 15% of thyroid nodules, with the chance depending on age, sex, prior radiation exposure and family history, among other factors.^[1] Differentiated thyroid cancer (papillary and follicular together) makes up the vast majority, more than 90% in most series.^[1]

Some factors raise the likelihood that a thyroid nodule is malignant:

• Prior neck or chest radiation. External beam radiation in childhood and high-level childhood exposure to radioactive iodine (for example, after nuclear accidents) both increase thyroid cancer risk, with a long latency.
• Family history. A first-degree relative with thyroid cancer, or a hereditary syndrome such as multiple endocrine neoplasia type 2 (MEN2), Cowden syndrome or familial adenomatous polyposis, changes both the investigations and the treatment.
• Proposed risk factors of uncertain benefit. Iodine deficiency is linked to multinodular goitre and to the follicular cancer subtype in particular. Being female increases the chance of a nodule but not strongly of malignancy in any individual nodule.
• Age extremes and specific ultrasound patterns. Very young patients and older men with a solitary suspicious nodule carry a higher pre-test risk.

Benign nodules arise from many causes: colloid (hyperplastic) nodules, thyroid cysts, adenomas, and the nodular change of longstanding goitre or Hashimoto thyroiditis. They do not need treatment unless they cause compressive symptoms.

A nodule may be found by the patient, by a clinician who palpates the neck, or incidentally on imaging. Ask about:

• growth rate and duration;
• pressure symptoms: dysphagia, dyspnoea, dysphonia, discomfort on lying flat;
• symptoms of excess or deficient thyroid hormone;
• family history of thyroid disease, thyroid cancer or MEN syndromes;
• previous radiation to the head, neck or chest;
• endocrine clues in relatives: phaeochromocytoma or parathyroid disease.

A rapidly enlarging, hard, fixed mass, especially with vocal change, is a red flag rather than a routine nodule. Medullary thyroid cancer and thyroid lymphoma may present with rapid growth and local compression.

Palpate the thyroid and both sides of the neck. A benign nodule is often soft, smooth and moves with swallowing. Concerning features include a solitary, rock-hard, irregular mass; fixation to surrounding structures; and cervical lymphadenopathy. Metastatic cervical nodes (firm, non-tender, fixed) are a strong clue to malignancy.

Medullary thyroid cancer arises from calcitonin-producing parafollicular C cells. It can cause flushing and watery diarrhoea through hormone secretion. MEN2 carriers may show mucosal neuromas, a marfanoid body habitus (especially MEN2B) or a history of phaeochromocytoma in the family.

TSH is the single most useful first blood test because a suppressed TSH identifies functioning (hot) nodules, which are rarely malignant. If TSH is low, a radionuclide scan follows. If TSH is normal or raised, the next step is sonography. Measuring thyroglobulin in the blood does not diagnose or exclude cancer and is not recommended as a diagnostic test.

Calcitonin, secreted by parafollicular C cells, is the most useful marker for medullary thyroid cancer. Its routine use in every patient with a nodule is debated: it is more strongly recommended in European guidelines, whereas the American Thyroid Association is less supportive, citing cost-effectiveness, false positives from C-cell hyperplasia and non-thyroidal causes, and the risk of overdiagnosis of tiny indolent cancers.^[4] Measure calcitonin when the ultrasound appearance, family history or other clues raise the suspicion of medullary cancer. Calcitonin is also measured from the needle washout during aspiration of a suspicious nodule when medullary cancer is a concern. Before operating on a suspected familial case, exclude a phaeochromocytoma with plasma or urinary metanephrines.

Ultrasound is the imaging backbone of nodule evaluation. It views the solid or cystic nature of the nodule, vascularity, and the features that matter most for risk: composition, echogenicity, shape, margin and echogenic foci. The ACR TI-RADS system (2017) turns these features into points, which place the nodule in one of five categories, TR1 (benign) to TR5 (highly suspicious).^[2] Size is then used to decide whether and how often to aspirate or to follow with imaging. Commonly quoted size indications are aspiration for TI-RADS 3 nodules at 2.5 cm or larger, TI-RADS 4 nodules at 1.5 cm or larger, and TI-RADS 5 nodules at 1.0 cm or larger, and follow-up imaging at lower size thresholds.^[2] Ultrasound also examines the rest of the thyroid and both sides of the neck, because a suspicious nodule with abnormal cervical nodes raises the cancer probability dramatically.

Ultrasound-guided fine needle aspiration is the sampling method of choice. The sample is reported using the Bethesda system, which has six categories. Every report should open with one of these six, and an implied risk of malignancy is attached to each.^[3]

A benign (II) result means the patient can usually be reassured and discharged from sampling. Nondiagnostic (I) samples should be repeated, sometimes with core needle biopsy or rapid on-site adequacy testing. Indeterminate results (III and IV) are where management is hardest: repeat sampling, molecular testing, or diagnostic surgery may all be appropriate, and this is an area where national guidelines differ. Categories V and VI usually lead to surgery. It is worth remembering that the cytology categories do not always match final pathology, and that fine needle aspiration misses medullary cancer in a substantial proportion of cases, which is why calcitonin remains important when that diagnosis is suspected.^[4]

Within the Bethesda framework, molecular testing of the aspirate (for example BRAF V600E, RAS and other mutations and gene fusions) can refine the probability of cancer and guide the extent of surgery. National guidelines differ in how much weight they give to these tests, and in which patients they are recommended.

• Cross-sectional imaging. CT or MRI of the neck and mediastinum is used when advanced disease is suspected (gross extrathyroidal extension, large or invasive nodes, airway or oesophageal involvement). In many 2025 guideline systems, chest and abdominal imaging is done when the result would change the surgical plan.
• Cervical lymph node assessment. Suspicious nodes on ultrasound that are larger than 8 to 10 mm in the short axis can be aspirated, with or without thyroglobulin washout of the needle, to confirm metastasis.^[8]
• Voice assessment. Laryngoscopy documents vocal cord movement before operating on a large or suspicious cancer.
• Staging scans. A whole-body radioiodine scan belongs to the follow-up of differentiated cancer, not to the initial nodule work-up. Routine radioisotope scanning is not recommended for the initial diagnosis of thyroid cancer.

The table compares the main thyroid neoplasms. PTC (papillary thyroid cancer) is the commonest thyroid cancer. FTC (follicular thyroid cancer) includes the oncocytic or Hurthle cell variant. MTC (medullary thyroid cancer) is a neuroendocrine tumour of C cells. ATC (anaplastic thyroid cancer) is the most aggressive. PTL (primary thyroid lymphoma) is usually of B-cell type.

PTC is the dominant thyroid malignancy. It spreads first by lymphatics within the neck, which is why cystic lateral neck nodes in a young adult can be the first sign. Most tumours have the BRAF V600E mutation, and the 2025 revision of the ATA guidelines now follows papillary cancer as part of differentiated thyroid cancer alone. Long-term survival is excellent for localised disease.

FTC is diagnosed histologically by demonstrating capsular and/or vascular invasion; a follicular-patterned, encapsulated tumour without invasion is an adenoma. Hurthle (oncocytic) cell carcinoma is classified as a variant of FTC in the older systems used here. It metastasises to lung and bone. Prognosis relates to the degree of invasion, age and tumour size.

MTC is the neoplasm of C cells, described in its own right in several ways:

• It accounts for about 2 to 5% of thyroid cancers.^[4]
• About 70 to 75% are sporadic and 25 to 30% hereditary, occurring in MEN2A or MEN2B.^[4]
• In MEN2A, nearly all carriers develop MTC, phaeochromocytoma occurs in about half, and primary hyperparathyroidism in 25 to 30%. MEN2B is rarer and more aggressive, with MTC often presenting in infancy.^[4]
• Cervical node metastases are present in 30 to 60% of patients at diagnosis, and about 10% already have distant metastases.^[4]
• MTC cells secrete calcitonin as well as other peptides. Calcitonin is therefore both a marker and a source of the flushing and diarrhoea seen in some patients.
• MTC does not take up iodine and is not TSH-driven, so radioactive iodine and TSH suppression do not treat it.

The ATA divides RET mutations into three risk categories. Highest (ATA-HST: RET codon M918T) means surgery in the first year of life. High (ATA-H: C634, A883F) means by age 5 years, or earlier if calcitonin is raised. Moderate (ATA-MOD: many cysteine codons and others) means surgery when calcitonin rises, or around age 5 if follow-up is difficult, with annual neck ultrasound and basal calcitonin from about age 5.^[4] Before any operation in a MEN2 carrier, exclude a phaeochromocytoma and remove it first if present; the risk of a second (contralateral) phaeochromocytoma over ten years may be 60 to 80%.^[4]

Systemic symptoms of MTC include diarrhoea and flushing in about 10% of patients, and about 0.7% present with Cushing syndrome from ectopic ACTH. Histologically, three features determine the International Medullary Thyroid Carcinoma Grading System grade: a mitotic count of 5 or more per 2 mm squared, a Ki-67 index of 5% or more, or tumour necrosis. A tumour with any of these is high grade. Once disease is persistent, calcitonin and CEA levels checked 2 to 3 months after surgery guide prognosis. A doubling time of less than 2 years predicts structural progression. Undetectable postoperative calcitonin is associated with a recurrence risk of 0 to 5%, and levels above 400 to 500 pg per mL make distant metastases likely.^[4] Stage-based figures for MTC give five-year survival of about 80 to 97%, and ten-year survival of roughly 95% in stage I, 93% in stage II, 71% in stage III and 20 to 40% in stage IV.^{[4] [5]}

For advanced disease, two tyrosine kinase inhibitors are licensed: vandetanib improved progression-free survival from 19.3 to 30.5 months in its trial, with response rates of 45% versus 13%; cabozantinib improved progression-free survival from 4.0 to 11.2 months, with response rates of 28% versus 0%.^[4] Selective RET inhibitors (selpercatinib and pralsetinib) are highly effective in RET-altered disease. Selpercatinib, compared with vandetanib or cabozantinib in a trial, achieved progression-free survival of 86.8% at 12 months versus 65.7%, with response rates of 69.4% versus 38.8%.^[4] These drugs carry significant side-effects, seen in 30 to 60% of patients, and need monitoring for QT prolongation (vandetanib) and bleeding or fistula (cabozantinib). External radiotherapy palliates bone pain and pathological fracture risk; radioactive iodine and conventional chemotherapy do not work in MTC. Treatment of systemic disease is reserved for patients with progressive, symptomatic or high-volume metastatic disease, with those who are asymptomatic and slow-growing monitored every 6 months. ^[7]

ATC is rare and rapidly progressive, with 12-month overall survival historically around 21%.^[5] It usually presents as a rapidly enlarging, painful, fixed neck mass in an older person, with local invasion of trachea and great vessels, and metastases already present in up to half. Histology is heterogeneous; a high Ki-67 index, often 30% or more, and genetic alterations such as BRAF V600E (pooled estimate around 33%), RAS, TP53 (40 to 80%) and TERT promoter mutations (30 to 75%) are characteristic.^[5] Management is a medical emergency: secure the airway (but elective tracheostomy is not routinely recommended), achieve a rapid diagnosis with FNA and core biopsy, and stage with CT or MRI of the neck and 18F-FDG PET-CT where available, plus brain MRI. Surgery is offered only where a complete (R0/R1) resection is achievable; debulking alone helps nothing. After complete resection, postoperative external beam radiotherapy with a radiosensitising drug such as a taxane or doxorubicin is recommended. For unresectable BRAF V600E-positive disease, neoadjuvant dabrafenib plus trametinib can shrink the tumour and allow later surgery. External beam doses of 50 Gy or more, and higher when feasible, improve outcome in unresectable disease. Systemic therapy is otherwise cytotoxic chemotherapy or checkpoint inhibitors in selected patients. Radioactive iodine and TSH suppression are not used.

PTL is another rare cause of a rapidly enlarging neck mass, accounting for 2 to 5% of thyroid malignancies.^[6] It is usually diffuse large B-cell lymphoma (60 to 70%) or mucosa-associated lymphoid tissue (10 to 30%). It strongly associates with Hashimoto thyroiditis: the risk of thyroid lymphoma is 40 to 80 times higher in these patients than in the general population.^[6] Typical presentation is a painless, rapidly enlarging anterior neck mass with compressive symptoms. Core needle biopsy with immunohistochemistry is diagnostic more often than fine needle aspiration (about 90.9% versus 65% sensitivity).^[6] Treatment is chemotherapy, usually R-CHOP, with or without radiotherapy. Surgery is reserved for diagnosis or relief of airway obstruction and does not improve survival. Older literature describes Group B (fever, night sweats, weight loss) symptoms in about 10% of patients. ^[5]

The goal of nodule management is to find the cancers without subjecting benign nodules to surgery or to repeated, unnecessary procedures. The goal in confirmed cancer is to remove the thyroid safely, treat with radioactive iodine or other therapy when indicated, and follow with ultrasound and thyroglobulin.

Very small (T1a), node-negative papillary cancers may, in well-selected patients, be watched rather than operated on, with ultrasound monitoring and interval growth or new nodes prompting surgery. The 2025 ATA revision supports active surveillance and even percutaneous ablation (radiofrequency or laser) for selected cT1aN0M0 papillary cancers.^[8] Because even tiny cancers can be multifocal or accumulate further risk, this decision must be made by a team and with the patient.

Surgery is the cornerstone of treatment for differentiated cancer, and extent is chosen by tumour and patient factors.

From the 2025 ATA revision and standard practice:^[8] lobectomy is preferred as first treatment for intrathyroidal tumours smaller than 2 cm that are node negative, because it has a lower risk profile. For low-risk, unilateral tumours 2 to 4 cm that are node negative, lobectomy may also be preferred, although total thyroidectomy is chosen by the team to allow radioactive iodine and simplify follow-up. Total thyroidectomy with lymph node dissection is recommended for tumours larger than 4 cm, any tumour with gross extrathyroidal extension, and for those with clinically evident nodal or distant metastases. Completion thyroidectomy (removing the other lobe) is used when higher-risk features are found after an initial lobectomy, or when radioactive iodine or stricter follow-up is needed.

NICE (NG230) sets similar size boundaries: hemithyroidectomy or total thyroidectomy for differentiated tumours larger than 1 cm or for multifocal T1a to T2 disease; total thyroidectomy for T3/T4 tumours, nodal involvement, adverse pathology or distant metastases; hemithyroidectomy or active surveillance for a solitary T1a microcarcinoma without nodes.^[7] Prophylactic central neck dissection is not recommended for most small, node-negative cancers; therapeutic central dissection (levels VI and VII) and, where lateral nodes are involved, lateral dissection (levels IIa, III, IV, Vb) are performed for proven disease.^[8]

Before surgery, the surgeon should review the risks with the patient through informed consent, including possible nerve injury and parathyroid damage, and communicate significant findings to the anaesthetist and other colleagues.^[8]

RAI (radioactive iodine-131) is used after total thyroidectomy for differentiated cancer to ablate remnant tissue and treat or monitor disease. NICE recommends RAI based on the same risk criteria as total thyroidectomy: not for T1a or T1b tumours without adverse features, nodes or metastases; consider it for T2 disease in some patients; offer it where higher-risk features exist.^[7] Typical ablation activities of 1.1 GBq for low-risk cases and 3.7 GBq for higher-risk cases are used.^[7] Preparation is either thyroxine withdrawal or recombinant (thyrotropin alfa) stimulation; a low-iodine diet before ablation is usual in many centres. RAI does not work for medullary or anaplastic cancer. After therapy, a post-treatment scan localises iodine-avid tissue.

After total thyroidectomy and RAI for differentiated cancer, TSH is suppressed to keep stimulation of any cancer cells low:

• below 0.1 mIU per litre initially;^[7]
• after 9 to 12 months, dynamic risk stratification reduces the target to 0.3 to 2.0 mIU per litre for an excellent response (for life), or 0.1 to 0.5 mIU per litre for an intermediate response, while TSH stays below 0.1 mIU per litre in biochemical or structural persistent disease.^[7]

TSH suppression is not given where there is no indication for RAI or where significant comorbidity makes low TSH undesirable. Long-term suppression beyond 10 years is reviewed individually, because lowering TSH can reduce bone density and raise cardiac risk.^[7]

Thyroglobulin is the tumour marker for differentiated (papillary and follicular) thyroid cancer; it is produced only by thyroid follicular cells.

• After total thyroidectomy and RAI, measure Tg with anti-Tg antibodies at 3 to 6 month intervals in the first 2 years and then every 6 to 12 months. Tg should become undetectable; detectable Tg without antibodies suggests residual or recurrent disease.^[7]
• If Tg is undetectable, a stimulated Tg test or a highly sensitive assay further separates groups: well below 1 microgram per litre on stimulation suggests low risk; 1 to 10 micrograms per litre is indeterminate; 10 micrograms per litre or more with no resectable disease prompts further investigation or treatment. A highly sensitive assay can consider Tg below 0.2 microgram per litre as low risk.^[7]
• ULtrasound-only follow-up at 6 to 12 months and then clinically, rather than RAI, is usual when hemithyroidectomy or total thyroidectomy without RAI has been performed.
• Risk-stratified follow-up: low risk (no disease and Tg below 0.2 microgram per litre) for 2 to 5 years; medium risk (Tg 0.2 to 1.0) for 5 to 10 years; high risk (Tg above 1.0 or stimulated Tg above 10) for 10 years; lifelong follow-up with Tg and ultrasound for anyone with biochemical or structural evidence of disease.^[7]

Anti-Tg antibodies interfere with Tg assays and must be measured together with Tg. Rising antibody levels themselves can be a warning sign of recurrence.

External beam radiotherapy is considered for differentiated cancer with macroscopic residual disease after surgery, or local disease unlikely to be controlled with RAI, and for palliation.^[7] It also has its most established place in anaplastic cancer (above).

Systemic therapy for RAI-refractory metastatic differentiated cancer includes lenvatinib and sorafenib, and selpercatinib for RET-fusion-positive disease, all endorsed through NICE technology appraisals. Targeted therapy for medullary cancer is described above. In all cases these are cytostatic treatments with significant toxicity and are given to progressive, symptomatic or high-volume metastatic disease.

Thyroid surgery is safe in experienced hands, but two complications dominate counselling.

• Recurrent laryngeal nerve injury. The nerve runs close to the thyroid and parathyroid tissue. Injury causes hoarseness (unilateral) or stridor and airway compromise (bilateral). Evaluation of the voice is part of preoperative and postoperative assessment. Transient palsy is defined as recovery of vocal cord movement within 6 months; anything longer is permanent. In one recent series of 312 total thyroidectomies, recurrent laryngeal nerve palsy occurred in 1.3%, with permanent palsy in 0.3%.^[9]
• Hypoparathyroidism. Parathyroid glands or their blood supply can be bruised, devascularised or accidentally removed. Transient hypocalcaemia occurs in up to 25% after total thyroidectomy; permanent hypocalcaemia in roughly 2% (1.9% in the same series).^[9] Permanent hypocalcaemia means lifelong calcium and active vitamin D supplementation. Risk is highest with accidental parathyroid excision or more extensive surgery; multivariate studies show accidental parathyroid removal more than triples the risk of hypocalcaemia.
• Other complications. Postoperative haemorrhage or haematoma (about 3.5% in one series), wound infection, and hypothyroidism requiring lifelong thyroxine. ^[9] High-volume thyroid surgeons (more than 25 to 50 thyroidectomies per year) have lower complication rates, which is now an explicit recommendation in the 2025 ATA revision.^[8]

Prevention means identifying the nerve, preserving parathyroid blood supply, autotransplanting a bruised or removed gland, routine intraoperative nerve monitoring in many centres, and using early postoperative parathyroid hormone and calcium measurements to guide supplementation.

• Pregnancy. NICE suggests surgery be delayed until after pregnancy, balancing risk of delay, risk to pregnancy and rate of disease progression; if surgery cannot wait, it is ideally done in the second trimester. Pregnancy is also a time when fine needle aspiration is safe and radioactive iodine is contraindicated.
• Children and young people. Medullary cancer and hereditary disease present younger; prophylactic thyroidectomy timing is described above. Children are managed by paediatric endocrine and thyroid surgical teams.
• Older adults. Anaplastic cancer is a disease of older adults. Performance status and goals of care shape how aggressively to treat.
• Hereditary syndromes. Screening relatives of RET mutation carriers and PTEN, DICER1 and other syndromes as recommended by the 2025 ATA revision allows early detection and, in medullary disease, prophylactic surgery.

Thyroid cancer cure depends on two things that are unevenly distributed: a pathologist who can grade cytology and a surgeon who can remove the gland without injuring the nerve and parathyroids. In low-resource settings:

• A high-resolution ultrasound, even in an emergency department, is the one test that converts a clinical guess into a structured plan. Clinical examination and ultrasound together can identify which nodules need sampling, and core needle biopsy with immunohistochemistry reaches a diagnosis more often than aspiration alone in lymphoma and anaplastic cancer.
• Where nuclear medicine is unavailable, low TSH nodules are still scanned if possible, but many systems treat all cold nodules identified clinically with ultrasound biopsy.
• Pathology quality matters: core needle biopsy, rapid on-site evaluation where available and second opinion review reduce diagnostic errors. Bethesda and TI-RADS are intended to be usable without expensive equipment.
• Radioactive iodine requires nuclear medicine departments and radiation protection procedures; where these are unavailable, surgery with levothyroxine and ultrasound-based follow-up remains a reasonable backbone, and long-distance referral may be needed.
• Targeted drugs and PET-CT are often unavailable. Molecular testing for BRAF is cheap (immunohistochemistry) and can direct BRAF-directed therapy or referral.
• Surgical experience is essential: centralising cancer surgery to high-volume surgeons, or using telemedicine consultation, reduces permanent hypocalcaemia and nerve injury.
• Simultaneous screening for phaeochromocytoma before operating on suspected familial medullary cancer is non-negotiable, even where resources are tight.

• A thyroid nodule is common and usually benign; the clinical task is to find the 7 to 15% that are cancer, without over-treating.
• Serum TSH is the first test; a low TSH leads to a radioisotope scan, where a hot nodule is usually benign.
• Normal or raised TSH leads to ultrasound risk stratification (ACR TI-RADS), with aspiration at 2.5 cm for TR3, 1.5 cm for TR4 and 1.0 cm for TR5.
• Results are reported in six Bethesda categories, from nondiagnostic (I) to malignant (VI), and management follows from them.
• Papillary is the most common cancer, with excellent prognosis; follicular spreads haematogenously; medullary is a C-cell neuroendocrine tumour with calcitonin as its marker; anaplastic is rapidly fatal; lymphoma usually presents as a rapidly enlarging mass in a thyroid with Hashimoto disease.
• Medullary cancer is driven by RET and treated surgically; radioactive iodine and TSH suppression do not work. RET mutation category dictates the age of prophylactic thyroidectomy.
• Differentiated cancer is treated by thyroidectomy (lobectomy for smaller node-negative tumours, total for advanced), radioactive iodine when indicated, and TSH suppression adjusted by response.
• Thyroglobulin and neck ultrasound are the backbone of follow-up.
• Surgical complications to consent for include recurrent laryngeal nerve injury and hypoparathyroidism (transient up to about 25%, permanent about 2%).
• The 2015 ATA guideline covered nodules and differentiated cancer together; the 2025 revision splits them and focuses on differentiated cancer, with lobectomy now recommended to 2 cm.

Thyroid function tests, goitre and thyrotoxicosis are covered on their own pages; medullary cancer connects to multiple endocrine neoplasia type 2 and to phaeochromocytoma; thyroid surgery connects to hypocalcaemia and recurrent laryngeal nerve injury. Planning of radioactive iodine and TSH suppression cross-references the endocrine therapy pages.