Thyroid nodules: They are a common finding on neck ultrasounds. They present with an anterior neck nodule, some may have compressive symptoms like difficulty swallowing, choking sensation and sometimes tenderness. Nodules presenting in children and adolescents or in adults > 70 years of age, previous history of neck irradiation, family history and MEN type 2A or 2B are at increased risk of malignancy. Physical examination findings indicative of malignancy are 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 with risk factors of malignancy, extracapsular invasion or cervical lymphadenopathy should be biopsied by ultrasound guided fine needle aspiration biopsy or FNAC. Radioactive thyroid scan showing “cold or non-functioning” nodule is more suspicious for malignancy and should be biopsied. Hyperfunctioning or “hot” nodules need not be biopsied.
2. Thyroiditis: It is inflammation of the thyroid gland. It is of the following types:
i)Acute thyroiditis: It 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 overlying skin, tenderness, fever and dysphagia. ESR and WBC count are elevated.
ii) Subacute granulomatous thyroiditis: It 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, tender thyroid, diffuse goitre in some cases. Damage of the thyroid follicles by cytotoxic T cells leads to the release T3 and T4 into the bloodstream which may cause hyperthyroidism. It is a transient condition lasting 3-6 weeks characterized by initial hyperthyroidism, followed by transient hypothyroidism which then slowly reverts back to normal. ESR, CRP, WBC count and mild anemia may be present. Iodine scan will show 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 hyperthyroidism signs.
iii) Chronic lymphocytic thyroiditis or Hashimoto’s thyroiditis: It 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 heralded by a short history of hyperthyroidism in some patients. Antithyroid peroxidase (TPO) and antithyroglobulin antibodies are positive. TSH receptor blocking antibodies are also seen which may cause transient hypothyroidism in babies born to mothers with Hashimoto’s thyroiditis. There is increased risk of thyroid lymphoma. It is associated with other autoimmune disorders such as Addison’s disease, premature ovarian failure, diabetes, vitiligo, pernicious anemia etc. Treatment is with thyroid hormone replacement , if needed, preferably when TSH > 10 mcU/ml or lower TSH with symptoms.
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: It is similar to Hashimoto’s thyroiditis but lacks fibrosis and Hurthle cells on biopsy
vi) Riedel’s or fibrous thyroiditis: It is characterized by extensive fibrosis involving the thyroid gland and adjoining structures like trachea and parathyroid glands. It is more common in 30-60 year old women. It presents with rock-hard, fixed, painless goitre with dysphagia, dyspnea, stridor, hoarseness and sensation of a lump in the throat. Clinically, it mimics thyroid cancer. Hypothyroidism and anti-TPO antibodies may be seen. Serum IgG4 is elevated. There is low uptake of radioactive iodine. FNAC often fails to get a good sample in Riedel’s thyroiditis , so open biopsy is needed. Treatment is with surgical resection, steroids, methotrexate, rituximab and tamoxifen. Tamoxifen acts by inhibition of fibroblast proliferation.
vii) Drug induced thyroiditis: It is caused by drugs like amiodarone, alpha interferon, interleukin 2, lithium which damage the thyroid gland. They may cause hyper and/or hypothyroidism with low uptake of radioactive iodine on thyroid scan.
viii) Radiation induced thyroiditis: Follows radioactive iodine therapy or radiotherapy to head and neck. Painful, tender thyroiditis with transient hyperthyroidism. Treatment is with NSAIDS, steroids and beta blockers.
Goitre: It is an enlarged thyroid gland, which may be diffuse or nodular. Goitres may be accompanied by normal thyroid function called non-toxic goitre, hyperfunctioning goitres are called toxic goitres while hypofunctioning goitres are called hypothyroid goitres. 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 is with TSH and free T4, ultrasound of the thyroid, biopsy if indicated, MRI, CT and calcitonin levels on a case-by-case basis. Small, benign goitres do not need to be treated. Levothyroxine helps to shrink larger, euthyroid goitres. Iodine supplementation is done in endemic goiter in iodine-deficient areas. Surgery is indicated in large goitres causing compressive symptoms and in malignancy. Specific management is guided by the probable cause of goitre.
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