Artlabeling Activity Location and Anatomy of the Thyroid Gland 2 of 2

Introduction

The thyroid gland is a vital butterfly-shaped endocrine gland situated in the lower function of the neck. It is present in the front and sides of the trachea, junior to the larynx. It plays an essential office in regulating the basal metabolic charge per unit (BMR) and stimulates somatic and psychic growth, too having a vital function in calcium metabolism.

Information technology is a gland consisting of two lobes, the right, and the left lobes, joined together by an intermediate structure, the isthmus. Sometimes a 3rd lobe called the pyramidal lobe projects from the isthmus. Information technology has a gristly/fibromuscular ring, i.east., levator glandulae thyroideae running from the body of the hyoid to the isthmus.[ane] The lobes are v ten two.5 10 2.five cm in dimension and weigh around 25 gm. It extends from the 5th cervical to the first thoracic vertebrae. The lobes extend from the center of the thyroid cartilage to the fifth tracheal ring. The isthmus is one.2 x 1.ii cm in dimensions and extends from 2d to third tracheal rings. It grows larger in females during the flow of menstruation and pregnancy.

The lobes are conical in shape and have an apex, a base of operations, iii surfaces – lateral, medial, and posterolateral, and two borders – the anterior and posterior. The isthmus, yet, has two surfaces – anterior and posterior and two borders – superior and inferior.

The lobes are related anteriorly to the skin, superficial and deep fascia, and platysma.  Posteriorly, the lobes are associated with the laminae of the thyroid cartilage and tracheal rings and laterally to the external carotid artery and internal jugular vein.

The thyroid gland is a richly vascular organ supplied by the superior and inferior thyroid arteries and sometimes by an additional avenue known as the thyroidea ima artery.[2] The venous drainage is by superior, middle, and inferior thyroid veins. Sometimes a 4th thyroid vein might exist nowadays, chosen the vein of Kocher. The nerve supply is mainly from center cervical ganglion only also partly from superior and inferior cervical ganglions.

Two capsules completely cover the thyroid gland. The truthful capsule is made up of fibro-elastic connective tissue. The simulated sheathing comprises the pre-tracheal layer of the deep cervical fascia. It consists of deep capillary plexus deep to the true capsule. Hence, it is crucial to remove the plexus with sheathing during thyroidectomy.

Problems of Business organisation

Fretfulness Related to the Thyroid Gland

The thyroid gland is shut to two crucial fretfulness: the external branch of the superior laryngeal nerve and the recurrent laryngeal nervus. Both are branches of the vagus nervus. During thyroidectomy, impairment to these nerves leads to inability in vox and/or difficulty in breathing. Injury to one of the branches of the superior laryngeal nerve leads to great difficulty in singing. Injury to the recurrent laryngeal nerve unilaterally may pb to hoarseness of the voice and difficulty in breathing. Bilateral recurrent laryngeal nerve injury is serious and ofttimes necessitates a tracheostomy.[3]

The thyroid gland is entirely covered by two capsules- truthful and imitation. The thyroid gland consists of deep capillary plexus deeper to the true capsule. This concrete arrangement makes it crucial to remove the plexus with capsule during thyroidectomy.[4]

Structure

The thyroid gland is divided into lobules by the septae dipping from the capsule. The thyroid lobules consist of many typical units chosen thyroid follicles.[v] The thyroid follicles are the structural and functional units of a thyroid gland. These are spherical, and the wall is made up of a large number of cuboidal cells, the follicular cells. These follicular cells are the derivates of the endoderm and secrete thyroid hormone. The circulating form of this hormone is thyroxine, which is tetraiodothyronine (T4) along with a small quantity of triiodothyronine (T3). Even though most of T4 afterward converts to the more agile form T3, both impact the target cells with varying degrees of stimulation. These hormones assistance in regulating the BMR of the body. In betwixt these thyroid follicles or inside the wall of the thyroid follicles, we find the modest C cells, likewise known asParafollicular cells. These are derived from neural crest cells and secrete polypeptide hormone known as calcitonin. The calcitonin helps deposit calcium and phosphate in skeletal and other tissues leading to hypocalcemia. This function is the opposite of the parathormone.

These thyroid follicles act as storage compartments filled with a substance called thecolloid. This colloid is thyroglobulin, which is nothing merely acidophilic secretory glycoprotein that is PAS-positive. These follicles are held together tightly inside a delicate network of reticular fibers with an extensive capillary bed.

Function

Some of the essential functions of the thyroid hormones are as follows:

1. They assistance in the overall growth, evolution, and differentiation of all the body cells.[6][seven]

2. They regulate the basal metabolic rate (BMR).

3. They play an essential role in calcium metabolism

4. They help in the overall evolution and function of CNS in children.[eight]

5. They stimulate somatic and psychic growth.

6. They stimulate center rate and wrinkle.[9]

7. They help in the deposition of calcium and phosphate in os and brand the bones strong.

8. They decrease the level of calcium in the blood.

9. They regulate carbohydrate, fat, and protein metabolism.

10. They as well assistance in the metabolism of vitamins.

11. They control the body temperature.

12. They assist dethrone cholesterol and triglycerides.

13. They maintain the electrolyte balance.

14. They support the process of RBC formation.

15. They heighten mitochondrial metabolism.

16. They increase the oxygen consumptions past the cells and tissues.

17. They influence the mood and beliefs of a person.[10]

18. They stimulate gut motion.[11]

19. They besides raise the sensitivity of the beta-adrenergic receptors to catecholamines.

Thus the thyroid hormones act on almost all the cells of the body. They also take upwardly a vital role in the development, growth, and role of most of the tissues and organs of the body. 1 can also say that the thyroid hormones are mandatory for the normal metabolic activity of all the cells of the body.

Tissue Preparation

Tissue preparation for immunohistochemistry requires surgically resecting the thyroid lesions. The preparation of thyroid samples includes fixation using 10% zinc formalin, subsequently which the tissue requires embedding in paraffin. The embedding protocols vary co-ordinate to the substrate, whether the protocol uses a chromogenic or fluorescent substrate. Paraffin embedding provides an option for the long-term preservation of tissues. The tissues must not be left to ready for more than 24 hours because over fixation could cause mask the antigen. If necessary, tissues can get transferred to alcohol following fixation before the embedding procedure. Contrarily, the tissues can be frozen instead of fixing. Snap freezing is usually done to discover mail-translational modifications such as phosphorylation, nitration, etc. Tissue freezing can be done by immersing tissues in liquid nitrogen or isopentane or by snap freezing in dry ice. Frozen tissue sections crave alcohol fixing. This process avoids the need to call up epitopes that get masked past the formaldehyde/ formalin fixing method.

Side by side, the embedded sections get cut using a microtome.  Usually, 4mm thick sections provide accurate staining with hematoxylin and eosin for routine histological examination. For immunohistochemical staining, separate areas are used and stained with selected markers. Immunostaining requires precise experimental conditions to generate a strong and specific immunohistochemical staining for each antigen of interest.

For Immunocytochemical staining, the thyroid cells from the lesion or fine-needle aspiration specimens are transferred and attached to a solid support, usually a microscope slide or coverslip. The use of pre-coated coverslip with poly-L-lysine and/or an extracellular matrix poly peptide such equally laminin, fibronectin, or collagen enhances the attachment of thyroid tissue cells. Air-dried smear grooming is with a Romanovsky stain. Wetfixed smears are usually prepared with a modified Papanicolaou stain and used to find nuclear detail. MayGrünwald-Giemsa is a staining procedure also used in thyroid cytologic preparations.[12]

Histochemistry and Cytochemistry

Cytochemical techniques are essential for diagnosing thyroid lesions of the thyroid gland pathologies. Directly and indirect immunofluorescence techniques are helpful to localize the thyroid hormones tri-iodothyronine (T3) and thyroxine (T4). The techniques manipulate the specificity of antibodies for T3 or T4, which gives enhanced fluorescence for the apical cytoplasm of follicular cells and the colloid pools, indicating thyroglobulin. The technique is specific for the thyroid gland and does not stain the adjacent gland.[13] Histochemical analyses of the patterns of activeness and localization of 5-nucleotidase (CD73) through the apply of anti-five' nucleotidase ecto antibody in the thyroid gland provide valuable insight into several pathologies associated with the thyroid gland. The activity of the enzyme is increased in papillary thyroid cancer (PTC). Monitoring the expression patterns is used to observe tumor size and lymph node metastasis in PTC. Additionally, the sites of localization of this enzyme also indicate cell ship mechanisms.[14]

Other enzyme-based histochemical reactions utilized to monitor thyroid functions are adenosine triphosphatase, alkaline and acid phosphatases, galectin-3, and alpha-naphthyl acetate esterase. Papillary and follicular carcinomas, besides as Graves disease, evidence positive staining for adenosine triphosphatase. The reaction distinguishes between benign and malignant neoplasms of the thyroid epithelium in humans. The benign neoplasms are positive for 5'-nucleotidase, alpha-naphthyl acetate esterase, and acrid phosphatase and negative for alkaline phosphatase and adenosine triphosphatase. Histochemical cess of FoxA1 expression in C cells and its absenteeism in follicular cells is a method to notice medullary thyroid carcinomas. FoxA1 expression has as well been suggested as a potential oncogene testing in anaplastic thyroid carcinomas.[xv] Similarly, GAL-iii expression shows a focal expression blueprint in benign lesions and diffused expression in malignant lesions.[xvi] Immunohistochemistry staining pattern for intrathyroidal cancer-to-cancer metastasis within a not-neoplastic thyroid gland, a sporadic characteristic, is also precisely discernable with histochemical techniques. Immunohistochemical staining with CD10, renal cell carcinoma (RCC) marker, mammaglobin, estrogen receptor (ER), thyroid transcription factor-1 (TTF-one), and thyroglobulin could provide an insight into the origin (renal or breast) of the metastatic carcinoma.[17]

Normal follicular epithelium of the thyroid gland shows no detectable CK19 expression, while in PTC, it gets overexpressed. Hence, cytokeratin 19 could be a expert immunomarkers for diagnosing PTC. Monitoring the upregulation or downregulation of specific jail cell adhesion molecules (E-cadherin, fibronectin), cell cycle regulatory proteins (CD44, p27Kip1), and oncogenes (BRAF) through cytochemical staining are helpful techniques to examination thyroid cancers.[xviii]

Many classical cytochemical techniques yet hold significance in the analyses of thyroid pathologies. Localization of endogenous thyroperoxidase in thyroid follicles acts equally an indicator of iodination during the synthesis of the thyroid hormones. Cytochemical staining of C and oxyphil cells serve as diagnostic markers for tumor, teratoma, and cyst formation in the thyroid gland.[19]

Microscopy Light

Capsules of Thyroid

2 capsules entirely cover the thyroid gland.

1. True – peripheral condensation of the glandular tissue

2. Faux – the pre-tracheal layer of deep cervical fascia

The gland is surrounded past a thin fibro-elastic (truthful) capsule. This capsule, in turn, is covered by a pre-tracheal fascia from the outside and acts as a false sheathing. The truthful capsule gives rise to septa deep into the parenchyma dividing the gland into lobules. The septa requite passage for the blood vessels, nerves, and lymphatics into the gland.

Each lobule is made of aggregation of follicles, which are the structural and functional units of the thyroid gland. The follicles are lined past follicular cells (simple) that rest on the basement membrane and take a cavity filled with a homogenous gelatinous material called thecolloid. The collide is composed of thyroglobulin, an iodinated glycoprotein, which is an inactive storage form of thyroid hormone.[20] The space between the follicles is filled with connective tissue stroma, numerous capillaries, and lymphatics. It is the just endocrine gland whose secretory products are stored in such nifty quantity and that too extracellularly. Inbetween the follicles are the parafollicular cells, also known every bit C-cells.

Follicular Cells

The follicular cells are the lining cells of a thyroid follicle. They vary in size, depending on the activity. When the follicles are in the resting (inactive) stage, the follicular cells are flat uncomplicated squamous, with abundant collide within the cavity.[21] When the follicles are highly agile, the follicular cells are uncomplicated columnar with scanty collide. In a normal state of follicles during moderate activity, the cells are uncomplicated cuboidal, and the cavity is filled with a reasonable amount of colloid. Simply it is likewise possible for dissimilar cells to evidence different levels of activity within the same thyroid tissue.[22]

They secrete two hormones that influence the rate of metabolism[23]:

1. T3 (tri-iodothyronine) and

2. T4 (tetra-iodothyronine or thyroxine)

T3 is more active than T4, even though both affect the target cells.

EM features: Electron microscopy of follicular cells shows apical microvilli, abundant granular endoplasmic reticulum, supranuclear Golgi complex, lysosomes, microtubules, and microfilaments. The action of these cells is influenced by thyroid-stimulating hormone (TSH) secreted by hypophysis cerebri.[24][25]

Parafollicular Cells (C–cells)

These are also known as clear cells or light cells. The C stands for calcitonin or clear.[26] These are large, polyhedral, pale-staining cells with oval and eccentric nuclei. They are widely distributed between follicular cells and their basement membrane. They as well lie betwixt adjoining follicular cells but practise not accomplish the lumen. Merely in some species, they are also seen between the follicles in connective tissue in groups. They secrete a hormone known as calcitonin.[27][28] The secretion of this hormone is independent of hypophysis cerebri and mainly depends on the level of serum calcium.[29]

EM features: When seen under the electron microscope, the C-cells are visibly filled with electron-dense secretory granules (100 to 200 nm in diameter) of hormone calcitonin. The activity of calcitonin is antagonistic to that of the parathyroid hormone. Information technology lowers serum calcium by suppressing bone resorption by inhibiting osteoclastic activity and stimulating osteoblastic activity.[30]

Pathophysiology

The follicular cells take up the iodinated thyroglobulins from the colloid present inside the lumen of the thyroid follicle. This process is under the influence of follicle-stimulating hormone (FSH). Afterwards, lysosomal digestion and intracellular proteolysis release the thyroid hormone in the course of T3 and T4. These amino acid derivates are and so small that they tin hands escape the follicular cells and enter the bloodstream through fenestrations present in the capillaries.

The thyroid-stimulating hormone (TSH) secreted by the anterior pituitary gland affects not only the changes in the follicular cells simply also the thyroid follicles and the activity of the gland itself. TSH stimulation occurs when there is a low iodine level in the nutrition past a negative feedback mechanism on pituitary thyrotrophs. TSH increases the size of the follicular cells (hypertrophy) and increases the number of follicular cells (hyperplasia). Thus under the influence of the TSH, the follicular cells become tall and columnar, demonstrating the heavy activity of the follicular cells and the follicles. The TSH as well enhances the exocytosis, synthesis, and iodination of thyroglobulin. It too enhances endocytosis and intracellular breakdown of colloid. Thus the intraluminal colloid is greatly reduced, which manifests externally past the enlargement of the thyroid gland. Usually, enlargement of the thyroid gland is calledgoiter, which is a diseased state. But in this status, the enlargement of the thyroid gland is considering of the hypertrophy and hyperplasia of the parenchyma. Hence it is calledparenchymatous goiter.[31] This condition differentiates from another type of goiter where the enlargement is not because of the hypertrophy and hyperplasia of the parenchyma merely due to an increase in the production of colloid within the thyroid follicle. This condition is known as colloid goiter.[32][33]If this status becomes longstanding with recurrent stages of hyperplasia and involution, it leads to a more irregular enlargement as a multinodular goiter [34]. They later too show fibrosis, calcification, cystic changes, and hemorrhagic spots.

If there is no stimulation of TSH, it leads to a decrease in the size of follicular cells to the cuboidal and later squamous cells.

In Graves'south disease, the follicular cells are tall, columnar, and overcrowded, resulting in small papillae formation. These papillae will project into the follicular lumen. The colloid is stake and shows scalloped margins. The interstitium becomes infiltrated with T lymphocytes.

In the example of adenoma, the follicular cells are compatible and contain colloid in the lumen. They show atypia and prominent nucleoli and focal nuclear pleomorphism. They are well encapsulated in an intact capsule, which distinguishes them from follicular carcinoma. The papillary carcinoma shows typical "Orphan Annie eye" nuclei, which are due to finely dispersed chromatin.[35][34] Information technology also shows a papillary architecture with the papillae andpsammoma bodies (calcified concentric structures).[36][37] The cytoplasm of follicular cells also shows invaginations, which give an intranuclear inclusions-similar appearance. Anaplastic carcinomas present themselves with large, pleomorphic giant cell lesions, spindle cells, etc.

The parafollicular cells secrete calcitonin whenever the plasma calcium level exceeds its normal limit. The target site for calcitonin in the bone is the osteoclast cells, thus reducing their number and action. Calcitonin also promotes the excretion of phosphate and calcium through urine. No significant clinical manifestations have been observed due to an increment or subtract of calcitonin, and hence, its role in humans is debatable. In parathyroid adenomas, the predominant cells will be master cells, with few nests of oxyphil cells.[27] The chief cells are larger and show variability in nuclear size compared to the normal. Some cells too evidence bizarre and pleomorphic nuclei. Parathyroid carcinomas are difficult to distinguish from adenomas based on microscopic features, and hence only local and metastatic features are conclusive in making a diagnosis.

Clinical Significance

Goiter:It is a condition where the thyroid gland shows an abnormal enlargement. Goiters are broadly classified into uni-nodular, multinodular, and diffuse types. Each further includes many different types of goiters. Some of the commonest with some of their of import features are described below.[38][39]

Colloid nodular goiter: This is the commonest of the non-neoplastic lesions of the thyroid.[38] In these types of goiter, the thyroid follicles are filled with an arable corporeality of colloid in their lumens and lined past squamous follicular cells.

Hyperthyroidism (Thyrotoxicosis): It is a condition of hypermetabolic state and hyperfunctioning of the thyroid gland resulting in increased T3 and T4 levels. Some symptoms included palpitations, tachycardia, nervousness, etc.

Graves disease: This illness is a combination of thyrotoxicosis, exophthalmos, and dermopathy (myxedema). Information technology is especially seen in women in the age grouping of 20 to 40 years, manifesting in the form of prolonged and violent palpitations.

Hypothyroidism: This condition develops due to any functional and structural derangement that leads to decreased thyroid hormone production. This condition clinically manifests as cretinism in infants and myxoedema in adults. Cretinism patients present themselves every bit short-statured, with coarse facial features, mental retardation, protruding natural language, etc.

Thyroid cancer: Thyroid carcinomas arise either from the follicular epithelium or parafollicular C-cells. They are painless nodules and compression, displacing the side by side structures. The carcinomas of the thyroid can manifest in the form of papillary carcinoma, follicular carcinoma, anaplastic carcinoma, and medullary carcinoma.

Review Questions

Figure

The Ductless Glands, Section of thyroid gland of sheep, Colloid material, Colloid in lymphatic vessel, Cubical epithelium. Contribute by Gray's Beefcake Plates

Figure

Hashimoto thyroiditis. Image courtesy South Bhimji Dr.

Figure

Papillary thyroid cancer psammoma torso. Paradigm courtesy South Bhimji Doc

Figure

Thyroid avenue. Image courtesy S Bhimji MD

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