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Solitary thyroid nodules are more common in females yet more worrisome in males. Other associations with neoplastic nodules are family history of thyroid cancer and prior radiation to the head and neck. Solitary thyroid nodules are mostly benign colloid nodules. The second most common type is follicular adenoma. [25]
[1] [3] [4] [5] In the thyrotoxic phase, the follicular cells of the thyroid gland are damaged leading to release of pre-formed thyroid hormone and symptoms of thyrotoxicosis. The damage to the follicles impairs ability to produce and secrete thyroid hormones which then leads to a hypothyroid phase.
Colloid nodules may be initially identified as an unspecified kind of thyroid nodule. Follow-up examinations typically include an ultrasound if it is unclear whether or not there really is a nodule present. Once the presence of a nodule has been confirmed, the determination of the kind of thyroid nodule is done by fine needle aspiration biopsy. [7]
Treatment of a thyroid nodule depends on many things including size of the nodule, age of the patient, the type of thyroid cancer, and whether or not it has spread to other tissues in the body. If the nodule is benign, patients may receive thyroxine therapy to suppress thyroid-stimulating hormone and should be reevaluated in six months. [2]
Thyroid follicular cells form a simple cuboidal epithelium and are arranged in spherical thyroid follicles surrounding a fluid filled space known as the colloid. The interior space formed by the follicular cells is known as the follicular lumen .
Toxic multinodular goiter (TMNG), also known as multinodular toxic goiter (MNTG), is an active multinodular goiter associated with hyperthyroidism.. It is a common cause of hyperthyroidism [2] [3] in which there is excess production of thyroid hormones from functionally autonomous thyroid nodules, which do not require stimulation from thyroid stimulating hormone (TSH).
They are hypothesized to develop as a result of thyroid damage, where T-lymphocytes are sensitized to residual thyroid peroxidase and thyroglobulin, rather than as the initial cause of thyroid damage. [5] However, they may exacerbate further thyroid destruction by binding the complement system and triggering apoptosis of thyroid cells. [5]
Hashitoxicosis, which can be abbreviated "Htx", [1] is a transient hyperthyroidism caused by inflammation associated with Hashimoto's thyroiditis disturbing the thyroid follicles, resulting in excess release of thyroid hormone. [2
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