The Thyroid gland ppt and throidectomy.pptx

husnazaheer 63 views 28 slides May 23, 2024
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About This Presentation

thyroid gland


Slide Content

The Thyroid Gland

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 Histology of the normal thyroid

The arterial supply is rich, and extensive anastomoses occur between the main thyroid arteries and branches of the tracheal and esophageal arteries The thyroid gland from behind

There is an extensive lymphatic network within and around the gland some lymph channels pass directly to the deep cervical nodes, the subcapsular plexus drains principally to the central compartment juxtathyroid – ‘Delphian’ and paratracheal nodes and nodes on the superior and inferior thyroid veins (level VI), and from there to the deep cervical (levels II, III, IV and V) and mediastinal groups of nodes (level VII) Cervical lymph node levels . Cervical Drainage

The relationship between the recurrent laryngeal nerve (RLN) and the thyroid is of supreme importance to the operating surgeon. A branch of the vagus , the nerve recurs round the arch of the aorta on the left and the subclavian artery on the right. The clinical significance of this is that on the left the nerve has more distance in which to reach the tracheoesophageal groove and therefore runs in a medial plane. On the right, there is less distance and the nerve runs more obliquely to reach the tracheoesophageal groove. Approximately 2% of nerves on the right are non-recurrent and will enter the larynx from above. Nerve supply

The nerve runs posterior to the thyroid and enters the larynx at the cricothyroid joint. This entery point is fascia that binds the thyroid to the trachea. This is the point at which the nerve is at most risk of injury during surgery. In terms of surgical anatomy, the nerve can be located in the tracheoesophageal groove where it forms one side of Beahrs ’ triangle (the other two sides are the carotid artery and the inferior thyroid artery) or at the cricothyroid joint. The nerve will normally be found as the thyroid lobe is mobilized laterally, lying under the most posterolateral portion of the gland called the tubercle of Zuckerkandl .

Physiology of Thyroid Gland The hormones T3 & T4 are bound to thyroglobulin within the colloid. When hormones are required, the complex is resorbed into the cell and thyroglobulin is broken down. T3 and T4 are liberated and enter blood, where they are bound to serum proteins: albumin, TBG and TBPA The small amount of hormone that remains free in the serum is biologically active Formation of T3 and T4 Oxidation of iodide to iodine Binding of iodine with tyrosine to form iodotyrosine Synthesis within the thyroglobulin complex is controlled by several enzymes, in distinct steps Trapping of inorganic iodide from the blood

Calcitonin The parafollicular C cells of the thyroid are of neuroendocrine origin and arrive in the thyroid via the ultimobranchial Body. They produce calcitonin. Role of calcitonin physiology of thyroid gland

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. Regulation o f TSH secretion also results from the action of thyrotrophin-releasing hormone (TRH) produced in the hypothalamus. The Pituitary–thyroid axis In hyperthyroidism, TSH production is suppressed In hypothyroidism, TSH production is stimulated

Thyroid-stimulating antibodies A family of IgG immunoglobulins bind with TSH receptor sites ( TRAbs ) and activate TSH receptors on the follicular cell membrane. They are responsible for virtually all cases of thyrotoxicosis not due to autonomous toxic nodules. Serum concentrations are very low but their measurement is not essential to make the diagnosis. IgG immunoglobulins have a more protracted action than TSH (16–24 versus 1.5–3 hours)

Thyroid autoantibodies Serum levels of antibodies against thyroid peroxidase (TPO) and thyroglobulin are useful in determining the cause of thyroid dysfunction and swellings. Autoimmunethyroiditis may be associated with thyroid toxicity, failure or euthyroid goitre . Levels above 25 units/mL for TPO antibody and titres of greater than 1:100 for antithyroglobulin are considered significant, although a proportion of patients with histological evidence of lymphocytic (autoimmune) thyroiditis are seronegative. The presence of antithyroglobulin antibody interferes with assays of serum thyroglobulin, with implications for follow-up of thyroid cancers. TSH r eceptor antibodies (TSH-Rab or TRAB) are often present in Graves’ disease. They are largely produced within the thyroid itself.

Simple goiter Aetiology Simple goitre may develop as a result of stimulation of the thyroid gland by TSH, either as a result of inappropriate secretion from a microadenoma in the anterior pituitary (which is rare), or in response to a chronically low level of circulating thyroid hormones. Endemic goitre is a dietary deficiency of iodine TSH is not the only stimulus to thyroid follicular cell proliferation and other growth factors, including immunoglobulins, exert an influence. The heterogeneous structural and functional response in the thyroid resulting in characteristic nodularity may be due to the presence of clones of cells particularly sensitive to growth stimulation.

DIFFUSE HYPERPLASTIC GOITRE Diffuse hyperplasia is the first stages of the natural history. The goitre appears in childhood in endemic areas but, in sporadic cases, it usually occurs at puberty when metabolic demands are high. If TSH stimulation ceases the goitre may regress, but tends to recur later at times of stress such as pregnancy. The goitre is soft, diffuse and may become large enough to cause discomfort. A colloid goitre is a late stage of diffuse hyperplasia when TSH stimulation has fallen off and when many follicles are inactive and full of colloid

NODULAR GOITRE Nodules are usually multiple, forming a multinodular goitre . 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 haemorrhage are common, as is subsequent calcification. Nodules appear early in endemic goitre and later (between 20 and 30 years) in sporadic goitre , although the patient may be unaware of the goitre until his or her late 40s or 50s. All types of simple goitre are more common in the female than in the male owing to the presence of oestrogen receptors in thyroid tissue.

Diffuse Toxic goiter Graves’ disease, a diffuse vascular goitre appearing at the same time as hyperthyroidism usually occurs in younger women and is frequently associated with eye signs . Type of Primary thyrotoxicosis : 50% of patients have a family history of autoimmune endocrine diseases. The whole functioning thyroid tissue is involved, and the hypertrophy and hyperplasia are due to abnormal TSH- RAb that bind to TSH receptor sites and produce a disproportionate and prolonged effect.

Toxic Nodular Goiter present for a long time before hyperthyroidism, usually in the middle-aged or elderly very infrequently is associated with eye signs . The syndrome is that of secondary thyrotoxicosis . In many cases of toxic nodular goitre , the nodules are inactive , and it is the internodular thyroid tissue that is overactive . OR In other forms, one or more nodules are overactive and here the hyperthyroidism is due to autonomous thyroid tissue as in a toxic adenoma.

Toxic nodule A toxic nodule is a solitary overactive nodule, which may be part of a generalized nodularity or a true toxic adenoma . It is autonomous and its hypertrophy and hyperplasia are not due to TSH- RAb . TSH secretion is suppressed by the high level of circulating thyroid hormones and the normal thyroid tissue surrounding the nodule is itself suppressed and inactive

HYPERTHYROIDISM Thyrotoxicosis Clinical types of Hyperthyroidism (Thyrotoxicosis )are: diffuse toxic goiter (Graves’ disease) toxic nodular goiter toxic nodule hyperthyroidism due to rarer causes

Investigations THYROID FUNCTION Serum TSH and T3, T4 If hyperthyroidism associated with a discrete swelling is confirmed biochemically, it indicates either a ‘toxic adenoma’ or a manifestation of toxic multinodular goiter. The combination of toxicity and nodularity is important and is an indication for isotope scanning to localize the area(s) of hyperfunction

AUTOANTIBODY TITRES The autoantibody status may determine whether a swelling is a manifestation of chronic lymphocytic thyroiditis. The presence of circulating antibodies increases the risk of thyroid failure after lobectomy. ISOTOPE SCAN Isotope scanning used to be the mainstay of investigation of discrete thyroid swellings but has been abandoned except when toxicity is associated with nodularity

FINE-NEEDLE ASPIRATION CYTOLOGY FNAC should be used, ideally under ultrasound guidance, on all nodules that do not fulfill a fully benign (U2) classification on ultrasound. FNAC is reliable in identifying papillary thyroid cancer 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. Thy3 aspiration cytology. Follicular neoplasm showing increased cellularity with a follicular pattern.

Five-needle aspiration cytology Indication for operation in thyroid swelling

Plain films have previously been used to assess tracheal compression and deviation, but the modality of choice now is CT scanning. CT scanning is also useful if ultrasound has identified metastatic disease in the neck as it can assist in surgical planning and assessing the superior mediastinum and lungs vascularity of the thyroid gland and the risk of post procedure hemorrhage. It can be useful in the rapid diagnosis of widely invasive malignant disease, for example anaplastic carcinoma, or in the diagnosis of lymphadenopathy Flexible laryngoscopy has rendered indirect laryngoscopy obsolete and is widely used preoperatively to determine the mobility of the vocal cords. The presence of a unilateral cord palsy coexisting with an ipsilateral thyroid nodule of concern is usually diagnostic of malignant disease. RADIOLOGY LARYNGOSCOPY CORE BIOPSY

Choice of therapy Most patients have an initial course of antithyroid drugs with radioiodine for relapse. Exceptions are those who refuse radi ation , have large goitres , progressive eye signs or are pregnant Toxic nodular goitre is often large and uncomfortable and enlarges still further with antithyroid drugs. large goitre should be treated surgically because it does not respond as well or as rapidly to radioiodine or antithyroid drugs as does a diffuse toxic goitre . Surgery or radioiodine treatment is appropriate. Radioiodine is a good alternative for patients over the age of 45 years because the suppressed thyroid tissue does not take up iodine and thus there is minimal risk of delayed thyroid insufficiency DIFFUSE TOXIC GOITRE Toxic nodule Toxic Nodular Goiter

THYROIDECTOMY INDICATIONS malignancies Multinodular goiter Graves’ disease

Thyroidectomy- operative surgery Semi-fowler’s position with neck hyperextension Kocher’s low collar incision Subdermal platysma muscle incision Skin with platysma flaps mobilized cranially up to thyroid cartilage- upper flap Lower flap mobilized caudally up to suprasternal notch Ligation of anterior jugular veins Division of strap muscles & pretracheal fascia Dissect laterally in between the pretracheal fascia(false capsule) and true capsule of thyroid gland Mobilisation of  lateral lobe and ligation of middle thyroid vein

Exposure of superior pedicle - Clamp, divide, and transfix the superior pedicle as close to the gland as possible Retract the lateral part of the lobe medially Division of  inferior thyroid pedicle - clamped, divided, and transfixed Division of Berry’s ligament allows the thyroid to be mobilized medially Preserve parathyroids and recurrent laryngeal nerves Resection is completed and hemostasis is ensured, closure is performed by first reapproximating the strap muscles at the midline using interrupted 3-0 Vicryl sutures Closure of Incision The platysma muscle is likewise reapproximated using interrupted 3-0 Vicryl sutures Finally, the skin is reapproximated with a subcuticular stitch of 4-0 Monocryl suture Keeping a suction drain is surgeon’s option

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