Thyroid nodules: These are a common finding on neck ultrasound. They usually present as an anterior neck nodule. Some patients may have compressive symptoms such as difficulty swallowing, a choking sensation, and sometimes tenderness.
Nodules are at increased risk of malignancy in:
Physical examination findings that suggest malignancy include a firm, fixed nodule, associated lymphadenopathy, or vocal cord immobility.
Evaluation of a thyroid nodule begins with TSH and thyroid ultrasound. Any nodule > 1 cm in size, or any nodule with risk factors for malignancy, extracapsular invasion, or cervical lymphadenopathy should be biopsied with ultrasound-guided fine needle aspiration biopsy (FNAC).
A radioactive thyroid scan showing a “cold” (non-functioning) nodule is more suspicious for malignancy and should be biopsied. Hyperfunctioning (“hot”) nodules generally do not need biopsy.
Thyroiditis: This is inflammation of the thyroid gland. It includes the following types:
i) Acute thyroiditis: This is caused by infection of the thyroid gland with Streptococcus pyogenes, Staphylococcus aureus, mycobacteria, fungi, or parasites. Clinical features include acute neck pain, erythema of the overlying skin, tenderness, fever, and dysphagia. ESR and WBC count are elevated.
ii) Subacute granulomatous thyroiditis: This is also called giant cell thyroiditis or de Quervain’s thyroiditis. It is the most common cause of thyroid pain. It is seen in middle-aged females following a viral infection. It presents with fever, myalgia, flu-like symptoms, a tender thyroid, and (in some cases) a diffuse goitre.
Cytotoxic T-cell-mediated damage to thyroid follicles causes release of T3 and T4 into the bloodstream, which may lead to hyperthyroidism. This is a transient condition lasting 3-6 weeks, characterized by:
ESR, CRP, WBC count, and mild anemia may be present. An iodine scan shows low uptake. Anti-thyroid peroxidase and anti-thyroglobulin antibodies are negative.
Treatment is symptomatic with NSAIDs, steroids in resistant cases, and propranolol or atenolol for signs of hyperthyroidism.
iii) Chronic lymphocytic thyroiditis or Hashimoto’s thyroiditis: This is an autoimmune thyroiditis seen more commonly in 40-60-year-old women. It is associated with HLA DRB, DR4, and DR5.
Biopsy shows extensive lymphocytic infiltrate, germinal center formation, fibrosis, T cells and plasma cells, Hurthle cells, and giant cells. Hurthle cells are follicular epithelial cells with eosinophilic cytoplasm (rich in mitochondria) and large hyperchromatic nuclei with prominent nucleoli.
It presents with a symmetrically enlarged, non-tender thyroid gland. It leads to primary hypothyroidism, sometimes preceded by a short period of hyperthyroidism.
Antithyroid peroxidase (TPO) and antithyroglobulin antibodies are positive. TSH receptor blocking antibodies may also be present; these can cause transient hypothyroidism in babies born to mothers with Hashimoto’s thyroiditis.
There is an increased risk of thyroid lymphoma. Hashimoto’s thyroiditis is associated with other autoimmune disorders such as Addison’s disease, premature ovarian failure, diabetes, vitiligo, and pernicious anemia.
Treatment is thyroid hormone replacement if needed, preferably when TSH > 10 mcU/ml, or at lower TSH levels if symptoms are present.
iv) Postpartum thyroiditis: Patients present within 2-6 months after delivery with painless goitre and hypothyroidism. Some cases may have short periods of hyperthyroidism. It is autoimmune in nature and is associated with HLA DRB, DR4, and DR5. Elevated levels of antithyroid peroxidase antibodies are seen.
v) Subacute lymphocytic or silent thyroiditis: This is similar to Hashimoto’s thyroiditis but lacks fibrosis and Hurthle cells on biopsy.
vi) Riedel’s or fibrous thyroiditis: This is characterized by extensive fibrosis involving the thyroid gland and adjoining structures such as the trachea and parathyroid glands. It is more common in 30-60-year-old women.
It presents with a rock-hard, fixed, painless goitre and may cause dysphagia, dyspnea, stridor, hoarseness, and a sensation of a lump in the throat. Clinically, it can mimic thyroid cancer.
Hypothyroidism and anti-TPO antibodies may be present. Serum IgG4 is elevated. There is low uptake of radioactive iodine.
FNAC often fails to obtain an adequate sample in Riedel’s thyroiditis, so open biopsy is needed.
Treatment includes surgical resection, steroids, methotrexate, rituximab, and tamoxifen. Tamoxifen acts by inhibiting fibroblast proliferation.
vii) Drug induced thyroiditis: This is caused by drugs such as amiodarone, alpha interferon, interleukin 2, and lithium, which damage the thyroid gland. These drugs may cause hyperthyroidism and/or hypothyroidism, with low uptake of radioactive iodine on thyroid scan.
viii) Radiation induced thyroiditis: This follows radioactive iodine therapy or radiotherapy to the head and neck. It causes painful, tender thyroiditis with transient hyperthyroidism. Treatment is with NSAIDs, steroids, and beta blockers.
Goitre: This is an enlarged thyroid gland, which may be diffuse or nodular.
Causes of goitre include Grave’s disease, toxic adenoma (Plummer disease), toxic multinodular goitre, Hashimoto’s disease, endemic goitre, puberty, congenital goitre, excess iodine, lithium, goitrogens, secondary hyperthyroidism, thyroiditis, and malignancies.
Initial evaluation includes TSH and free T4, ultrasound of the thyroid, and biopsy if indicated. MRI, CT, and calcitonin levels are used on a case-by-case basis.
Small, benign goitres do not need treatment. Levothyroxine can help shrink larger, euthyroid goitres. Iodine supplementation is used for endemic goiter in iodine-deficient areas. Surgery is indicated for large goitres causing compressive symptoms and for malignancy. Specific management is guided by the probable cause of the goitre.
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