Thyroid Gland Lec1 PDF

The Thyroid gland Intended Learning Outcomes: By the end of this lecture the student will be able to:  To understand the development and anatomy of the thyroid gland.  To know the physiology and investigation of thyroid function.  To understand the etiology and types of...

The Thyroid gland Intended Learning Outcomes: By the end of this lecture the student will be able to:  To understand the development and anatomy of the thyroid gland.  To know the physiology and investigation of thyroid function.  To understand the etiology and types of thyroid swellings. References: Bailey and Love 28th ed. EMBRYOLOGY: The Thyroglossal duct develops from the median bud of the pharynx. It passes from foramen caecum at junction of anterior 2/3 and posterior 1/3 of the tongue and descend toward the root of the neck forming two lobes linked by isthmus. The parathyroid glands develop from the third and fourth pharyngeal pouches. The thymus also develops from the third pouch. As it descends, the thymus takes the associated parathyroid gland with it. The fourth pharyngeal pouch give rise to Para follicular cells (C cell) which integrate with the lobes of the gland. Anterior view of primitive pharynx SURGICAL ANATOMY The normal thyroid gland weighs 20–25 g. The functioning unit is the lobule supplied by a single arteriole and consists of 24–40 follicles lined with cuboidal epithelium. The follicle contains colloid in which thyroglobulin is stored. The thyroid gland lies over the 2nd, 3rd and 4th tracheal rings. Blood supply by superior thyroid artery from ext. carotid artery, inferior thyroid artery from thyrocervical trunk and thyroidea ima artery from the aorta. Venous drainage by superior, middle (drain to internal jugular vein) and inferior thyroid veins (drain to innominate V). Lymphatic drainage by subcapsuler plexus to the pre and para tracheal LN as well to the deep cervical and mediastinal LN. The relationship between the recurrent laryngeal nerve (RLN) and the thyroid is of supreme importance to the operating surgeon. The nerve runs posterior to the thyroid and enters the larynx at the cricothyroid joint. This entry point is at the level of Berry’s ligament, a condensation of pretracheal fascia that binds the thyroid to the trachea. This is the point at which the nerve is at most risk of injury during surgery. PHYSIOLOGY The function of the thyroid gland is to secrete thyroid hormones (T3 and T4) and calcitonin. The functions of thyroid hormones are: 1. facilitate growth and development. 2. increase tissue metabolism. 3. increase O2 consumption and heat production by the tissue. 4. increase O2 release from HB. 5. augmentation of adrenalin and noradrenalin. Thyroxine: The hormones tri-iodothyronine (T3) and l-thyroxine (T4) are bound to thyroglobulin within the colloid. Synthesis within the thyroglobulin complex is controlled by several enzymes, in distinct steps: 1. trapping of inorganic iodide from the blood. 2. oxidation of iodide to iodine. 3. binding of iodine with tyrosine to form iodotyrosine. 4. coupling of monoiodotyrosines and di-iodotyrosines to form T3 and T4. 5. Storage of the hormone in the thyroglobuline with in the colloid. 6. Release of the hormone in response to stimulation by TSH to the blood. The key enzyme in these steps is thyroid peroxidase enzyme which influenced and controlled by TSH. The thyroid gland produces about 80% T4 and 20% T3, most of the released hormone will bind to protein (albumin, TBG), eventually all T4 will change to T3 at the cellular level. T3 is four times more powerful than T4 and less adherent to binding protein. T3 is quick acting (within a few hours), whereas T4 acts more slowly (4–14 days. The hypothalamic-pituitary–thyroid axis: Synthesis and release of thyroid hormones from the thyroid is controlled by thyroid-stimulating hormone (TSH) from the anterior pituitary. Secretion of TSH depends upon the level of circulating thyroid hormones and is modified in a negative feedback manner. In hyperthyroidism TSH production is suppressed, whereas in hypothyroidism it is stimulated. Regulation of TSH secretion also results from the action of thyrotropin releasing hormone (TRH) produced in the hypothalamus. Thyroid autoantibodies Serum levels of antibodies against thyroid peroxidase (TPO) and thyroglobulin are useful in determining the cause of thyroid dysfunction and swellings. TSH receptor antibodies (TRAB) are often present in Graves’ disease. Thyroid investigations 1) Thyroid hormones: Serum TSH (T3 and T4 if abnormal TSH). 2) Thyroid autoantibodies: TPO, antithyroglobulin, TRAB. 3) Imaging: chest radiograph and thoracic inlet view: in case of tracheal deviation/retrosternal goiter. ultrasonography: it will describe the characteristics of the gland substance, regional lymphatics, presence and features of thyroid nodules, number, size, shape, margins, vascularity and specific features such as the presence of microcalcifcations can be used to predict the risk of malignancy within a specific nodule. CT scan and MRI scan: for known cancer, recurrent goiters and retrosternal goiters (superior to CXR). Isotope scanning: if discrete swelling and toxicity coexist. The uptake by the thyroid of a low dose of either radiolabeled iodine (I123) or the technetium (Tc99) will demonstrate the distribution of activity in the whole gland. Its principal value is in the toxic patient with a nodule or nodularity of the thyroid. Localization of over activity in the gland will differentiate between a toxic nodule with suppression of the remainder of the gland and toxic multinodular goiter with several areas of increased uptake with important implications for therapy. 4) Fine-needle aspiration cytology: FNAC is the investigation of choice in discrete thyroid swellings. Ultrasound guidance allows more accurate sampling and reduces the rate of unsatisfactory aspirates. FNAC is reliable in identifying papillary thyroid carcinoma but cannot distinguish between a benign follicular adenoma and follicular carcinoma, as this distinction is dependent not on cytology but on histological criteria, which include capsular and vascular invasion. THYROID ENLARGEMENT Simple goiter: Simple goiter may develop as a result of stimulation of the thyroid gland by TSH in response to a chronically low level of circulating thyroid hormones. Causes: 1- Iodine deficiency: due to low intake (endemic goiter). 2- Dyshormogeneses: deficiency in enzyme responsible for hormone production (sporadic goiter). 3- Goiterogenic food: vegetables of the brassica family (cabbage, kale and rape). 4- Drug: antithyroid, PAS, high dose of iodine. 5- Increase demand to hormone: in pregnancy, lactation and teenage (physiological goiter) Stages in goiter formation are: 1- Persistent growth stimulation causes diffuse hyperplasia; all lobules are composed of active follicles and iodine uptake is uniform. This is a diffuse hyperplastic goiter, which may persist but is reversible if stimulation ceases. 2- Later, as a result of fluctuating stimulation, a mixed pattern develops with areas of active lobules and areas of inactive lobules. 3- Active lobules become more vascular and hyperplastic until hemorrhage occurs, causing central necrosis and leaving only a surrounding rim of active follicles. 4- Necrotic lobules coalesce to form nodules filled either with iodine-free colloid or a mass of new but inactive follicles. 5- Continual repetition of this process results in a nodular goiter. Most nodules are inactive, and active follicles are present only in the internodular tissue. 1) simple diffuse hyperplastic goiter: Diffuse hyperplasia corresponds to the first stages of the natural history. If TSH stimulation ceases the goiter may regress, but tends to recur later at times of stress such as pregnancy. The goiter is soft, diffuse and may become large enough to cause discomfort. A colloid goiter is a late stage of diffuse hyperplasia, when TSH stimulation has fallen of and when many follicles are inactive and full of colloid In endemic areas the incidence of goiter has been strikingly reduced by the introduction of iodized salt. In the early stages, a hyperplastic goiter may regress if thyroxine is given in a dose of 0.15–0.2 mg daily for a few months. 2) Simple multinodular goiter: It is the final stage of simple goiter. Occasionally, only one macroscopic nodule is found, but microscopic changes will be present throughout the gland; this is one form of a clinically solitary nodule. Nodules may be colloid or cellular, and cystic degeneration and hemorrhage are common, as is subsequent calcification. Most patients with multinodular goiter are asymptomatic and do not require operation. Surgery is indicated for nodular goiters with features of underlying malignancy, for pressure symptoms if other causes have been excluded, for cosmetic reasons and in case of retrosternal extension. Complications of simple goiter: 1)Tracheal obstruction may be due to gross lateral displacement or compression in a lateral or anteroposterior plane by retrosternal extension of the goiter. Acute respiratory obstruction may follow hemorrhage into a nodule impacted in the thoracic inlet. 2) Secondary thyrotoxicosis: toxic diffuse goiter (Grave’s disease) or toxic multinodular goiter. 3) Carcinoma: An increased incidence of cancer (usually follicular) has been reported from endemic areas. Dominant or rapidly growing nodules in longstanding goiters should always be subjected to aspiration cytology. Solitary thyroid nodule: A discrete swelling in an otherwise impalpable gland is termed isolated or solitary, whereas the preferred term is dominant for a similar swelling in a gland with clinical evidence of generalized mild nodularity. About 70% of discrete thyroid swellings are clinically isolated and about 30% are dominant. It could be simple (euthyroid) or toxic. The importance of discrete swellings lies in the risk of neoplasia compared with other thyroid swellings. Some 15% of isolated swellings prove to be malignant and an additional 30–40% are follicular adenomas. The remainder are non-neoplastic, largely consisting of areas of colloid degeneration, thyroiditis or cysts. The problem is to differentiate benign from malignant mass and this can be achieved by: 1- History and Physical examination: The criteria that suggest malignancy in solitary thyroid nodule are:  age less than 20 or age greater than 70  male gender  resent onset of swallowing difficulties or SOB  resent onset of hoarseness (RLN palsy which confirmed by laryngoscopy)  history of external neck irradiation during childhood  rapid growing, hard, irregular and fixed nodule  presence of cervical lymphadenopathy 2-Ultrasound which differentiate cystic from solid or mixed lesions (solid and mixed has increased risk and should undergo FNA). 4-FNAC which can differentiate various types of thyroid diseases apart from follicular carcinoma. Indications for operation in solitary thyroid swellings: 1) Neoplasia: FNAC positive (Thy3–5), Clinical suspicion: (Age, male sex, hard texture, fixity, RLN palsy, lymphadenopathy, recurrent cyst. 2) Toxic adenoma. 3) Pressure symptoms. 5) Cosmetic.