By; Dr.JEEJA.S, M.D.Hom (Repertory), M.D.Hom (HOMOEOPATHIC PHYLOSOPHY)
Tutor, Department of Organon of Medicine, Govt.Homoeopathic Medical College, Thiruvananthapuram, Kerala.
THE THYROID GLAND
The THYROID GLAND develops mainly from the Thyroglossalduct. The Thyroglossalduct develops from the median bud of the pharynx. The Foramen caecum at the base of the toung is the vestigial remnant of the duct. Para follicular cells are derived from the caudal Pharyngeal complex, derived from the fourth and fifth Pharyngeal pouches and ultimobrachial body.
The Thyroid gland is first identifiable in embyos of about twenty somites, as a median thickening of endoderm in the floor of the Pharynx between the first and second Pharyngeal pouches and immediately dorsal to the aortic sac. This area is later invaginated to form a median diverticulum, which appears in the later half of the fourth week in the Furrow immediately caudal to the Tuberculum- impar, the median thickening, separates the medial ends of two Mandibular arches. The invgination grows caudally as a tubular duct, which bifurcates and subsequently divides into a series of double cellular plates, from which the isthmus and the lateral lobes of the Thyroid gland are developed. The primary thyroid follicle differentiate by reorganization and proliferation of the cells of these plates. Secondary follicle subsequently arise by budding and subdivision
Initially the thyroid gland consists of small masses of endodermal cells. But small groups of epithelial cells are identified by 10 weeks d colloid synthesise is present by 13 weeks. Follicles appear around 14 weeks.
Each developing lobe amalgates with the ultimo branchial body, which is the endodermal diverticular part of the caudal Pharyngeal complex. This separates from the Ectoderm of the fourth branchial cleft and losses its connection with the Pharynx by attenuation and rupture of the common Pharyngo branchial duct. It becomes closely associated with the expanding lateral lobe of the thyroid gland, with the superior parathyroid component of the complex lying dorsally and outside the Thyroid gland. The remainder of the complex, which includes ultimo branchial body and possibly some vestiges of the Ventral recess of the fourth Pharyngeal pouch and of the transitory fifth Pharyngeal pouch, is enveloped by the Thyroid gland. The parafollicular cells(‘C’ cells) from the neural crest reach the Thyroid via the Ultimobranchial body.
The connection of the median diverticulum with the Pharyx is termed the Thyroglossal duct. The site of its connection with the Epithelial floor of the mouth is marked by the Foramen caecum. From here it extends cordally in the middle line and ventral to the primordium of the hyoid bone, behind which it may later form a recurrent loop. The distal part of the duct usually differentiates to a variable extend to form the pyramidal lobe of the Thyroid gland. The remainder fragments disappears but the lingual part is often identifiable until late in Foetal life and may branch and give rise to miniature salivary glands. Occasionally parts of the midline Thyro glossal duct persist, occurring in lingual, suprahyoid, retrohyoid or infrahyiod position. They may give rise to aberrant masses of thyroid tissue, cysts, fistula or sinuses usually in the midline. A lingual tyroid situated at the junction of the buccal and Pharyngeal parts of the tounge is not uncommon, but nodules of the glandular tissue may also be found other than in the midline. E.g. laterally placed posterior to sternomastoid, and even below the level of the thyroid isthmus.
Thyroglobulin can be detected at an early stage of histogenesis before colloid formation, a phenomenon apparently independent of TSH stimulation. Since this is not identifiable in the pitutory gland until about 12 weeks. Iodine trapping and synthesis of thyroid hormone appear to occur only in the presence of TSH. Thyroxine binding globulin may be detected by week 10 and increases to term.
ANOMALIES OF THE THYROGLOSSAL TRACT
Anomalies of shape: –
The pyramidal lobe: – Is present so often in fifty percentage of individuals that it is regarded as a normal structure. It may arise from the isthmus or from one of the lobes. It may have no connection with the rest of the Thyroid, and may be divided into two or more parts.
Absence of Isthmus: –
Absence of one of the lobes of the gland or may be very small lobe: –
Ectopic Thyroid – Anomalies of position: –
Some residual thyroid tissue along the course of the thyroglosal tract is common. Substantial rests of thyroid tissue may be lingual or cervical. Very rarely the whole gland is ectopic. Intrathorasic thyroid tissue is an acquired rather than a congenital phenomenon, which is usually associated with the development of a nodular Goitre.
Lingual Thyroid: – This forms a rounded swelling at the back of the tongue at the foramen caecum. It may cause dysphagia, impairment of speech, respiratory obstruction or haemorrhage.
Intralingual thyroid: – Thyroid may be embedded in the muscular substance of the tongue.
Median(thyroglossal) ectopic thyroid: – This forms a swelling in the upper part of the neck and is usually mistaken for a thyroglossal cyst.
Suprahyoid thyroid: – The gland may lie in the midline of the neck above the hyoid bone.
Infrahyoid thyroid: – The gland may lie below hyoid bone but above its normal position.
Intrathorasic thyroid: – The entire gland, or part of it may lie in the throat. When the thyroid tissue is present in the anomalous position, an additional thyroid may or may not present at the normal site.
Ectopic thyroid tissue: – Small masses of thyroid tissue may be presented abnormal sites. Thyroid tissue has been observed in the larynx, trachea, Oesophagus, Pons, pleura, pericardium and ovaries. When the thyroid tissue is present in the anomalous position, an additional thyroid may or may not present at the normal site.
Lateral aberrant thyroid: – “normal thyroid tissue” found laterally, separate from the thyroid gland must be considered and treated as a metastasis in a cervical lymphnode from a occult papillary thyroid carcinoma.
Struma ovary: – This is not ectopic thyroid tissue, but part of an ovarian teratoma. Very rarely, neoplastic change occurs or hyperthyroidism develops.
Remnants of thyroglossal duct: – Leads to the formation of
Thyroglossal cyst : This may be present in any part of the thyroglossal tract. The common situations, in order of frequency, are beneath the hyoid, in the region of the thyroid cartilage and above the hyoid bone. The cyst occupies the midline, except in the region of the thyroid cartilage, where the thyroglossal tract is pushed to one side. The swelling moves upwards on protrusion of the tongue as well as on swallowing, because of the attachment of the tract to the Foramen Caecum. The persistence of the cyst leads to infection. The wall contain nodules of lymphatic tissue and the initial presentation often follows an upper respiratory infection. The incision of the cyst may result tyroglossal fistula.
Thyroglossal fistula: – This is never congenital. It follows infection or inadequate removal of a thyroglossal cyst. Characteristically, the cutaneous opening of such a fistula is drawn upwards on protrusion of the tongue. A thyroglossal fistula is lined with columnar epithelium, it discharges mucus, and is the seat of recurrent attack of inflammation .
The Thyroid gland is a brownish red, highly vascular organ, situated anteriorly in the lower part of the neck, at the level of the fifth, sixth and seventh cervical and first thorasic vertebrae. It is ensheathed by the pretracheal layer of the deep cervical facia and consists of right and left lobes connected across the median plane by a narrow region termed ‘isthmus’. Its weight is somewhat variable. At birth 1-2 gram, at puberty 10-15 gram, in adult 15-35 gram. The mean weight is always higher in women and varies in size with menstrual cycle.
The lobes are approximately conical in shape, the apex of each ascending and diverging laterally to the level of the oblique line of the thyroid cartilage. The base is on a level with the fourth or fifth tracheal ring. Each lobe is about 5 cm long. Its greatest transverse and anteroposterior dimension being about 3cm and 2cm. The posteromedial aspect of each lobe is attached to the side of the cricoid cartilage by a ligamentous band called the lateral ligament of the Thyroid gland. The lateral or superficial surface is convex. External to the sheath of the pretracheal fascia, This aspect of the gland is closely covered with the sternothyroid and it is the insertion of this muscle into the oblique line on the lamina of the thyroid cartilage which prevents the upper part of the lobe from extending on to the thyrohyoid muscles. More anteriorly strnohyoid and superior belly of the omohyoid, overlaps below by the anterior border of the sternocleido mastoid. The medial surface is adapted to the larynx and trachea. At its superior pole, it is in contact with the inferior pharyngeal constrictor and posterior part of the cricothyroid, which intervenes between the gland, and the posterior part of the lamina of the thyroid gland and the side of the cricoid cartilage. The external laryngeal nerve is medial to this part of the gland. Below it is related to the trachea in front and to the recurrent laryngeal nerve and to the oesophagus posteriorly. The posterolateral surface is related to the carotid sheath and overlaps the common carotid artery. The anterior border closely related to the anterior branch of superior thyroid artery is thin and descends obliquely and medially. The posterior border blunt and rounded is between posterior and medial surfaces and is closely related below to the inferior thyroid artery and an anastomosing branch that connects it to the posterior branch of superior thyroid artery. The para thyroid glands are usually related to the posterior border. The lower end of the posterior border of the left lobe is closely related to the thorasic duct.
Connects the lower part of the two lobes measures about 1.25cms. transversely and vertically and usually extends anterior to the second and third ring of trachea. More superficially strenohyoid, anterior jugular vein, fascia and the skin cover it. An anastamotic branch of two superior thyroid arteries runs along its upper border. A fibrous or fibromascular band sometimes descends from the body of the hyoid bone to the isthmus. When muscular it is termed levator of the thyroid gland. Small detached masses of the thyroid tissue sometimes in the vicinity of the lobes or superior to the isthmus are called Acessorythyroid gland.
The thyroid gland is invested by a thin capsule of connective tissue and it is divided into masses of irregular form and size by extension of connective tissue. The thyroid parenchyma is mainly derived from the endoderm of the Thyro glossal duct. Branching, solid, epithelial cords and sheets grow out from the distal end of the duct, and the lumina filled with a yellow, viscid colloid appear within them. The endodermally derived epithelia are usually considered to develop into separate follicles, approximately spherical structures of about 0.02 to 0.9 mm in diameter. Each consisting of a central core of colloid surrounded by a single layer of epithelial cells and enclosed in a basal lamina. The 3 dimensional reconstruction of the thyroid gland have shown that the follicles are not usually separate units, but typically occur as aggregrates with a shared sheet of epithelial cells bordering on several masses of colloid, and thus linking the follicles together. The colloid constist of iodinated glycoprotien, thyroglobulin, a precursor of the thyroid hormones, tri-iodo thyronine(t3) and tetriodo thyronine or thyroxine(t4) and is a product of the follicular epithelial cells which surrounds it.
The aggregates of follicles in the delicate connective tissue stroma of the gland. Surrounded by close meshed plexuses of fenestrated blood capillaries. The stroma also contains an extensive network of lymphatic vessels. Sympathetic nerve fibres supply the arteriols and capillaries, and some end in aposition to the follicular epithelial cells. In addition to follicular cells the thyroid parenchyma also contains parafollicular cells or ‘C” cells which produce the peptitde hormone thyrocalcitone.
Circulating pituitary thyrotrophin controls the activity of the follicular cells. In the absence of thyrotrophin the follicular cells are squamous and are referred to as “Resting” , while the luminal colloid is copious and dense, reflecting increase storage of iodinated thyroglobin. The secretion TSH is followed by the uptake of colloidal droplets from the lumen by Endocytosis at the luminal aspect of the follicular cells, and cavities may be seen in the luminal colloid., adjoins the epithelium. The prolonged action of high levels of circulating TSH induces follicular cells hypertrophy and even hyperplasia, progressive resorption of luminal colloid and an increase in stromal vascularity. The active cells are columnar.
The follicular cells have a striking ultra structural and functional polarity. When activated by TSH or adnergic nerve terminals, in the apically directed process of thyroglobulin synthesis and exocytosis, and in the basally directed processes of thyroglobulin endocytosis, degradation and liberation of the thyroid hormones T3 and T4 into the blood capillaries. This dual polarity of function is reflected in the arrangement of the organelles concerned with these processes. Each follicular cell has a basally disposed nucleus, prominent granular endoplasmic reticulum, and a supranuclear golgi complex, which is particularly prominent in TSH activated cells. In the apical half of the cells, there are numerous golgi derived secretory vesicles which transport the glycoprotien manufactured by the rough endoplasmic reticulum and golgi complex to the apical plasma lemma, where it is released by exocytosis into the lumen of the follicle. The iodine required to complete the formation of thyroglobulin enters the basal aspect of the flicilar cells in the form of iodide by active transport across the basal plasma lemma from the blood capillaries. It is rapidly oxidized to iodine, mainly by the activity of thyroid peroxidase in the apical plasma lemma. The iodine combined with the thyrosyl group of glyocoprotien manufactured by the follicular cells, forming mono and di-iodothyrosyls. Endogenous peroxidase present in the perinuclear cisternae, granular endoplasmic reticulum, golgi complex, apical vesicles, and at the apical plasma lemma particularly over the micro villi project into the lumen of follicles, where only it is involved in iodide oxidation. The apical microvilli are numerous but short in resting follicular cells but becomes longer and often branched after stimulation by TSH. Such stimulation also results in the extension of long cytoplasmic processes into luminal colloid and it is taken up into the cell. Shortly after colloid endocytosis, lysosomes, which in the basal position while resting state migrate to the apex of the cell, fuse with the intracellular colloid droplets and form phagolysosome. These migrate back to the base of the cell. Degradation of iodinated thyroglobulin by acid protease and peptidase of lysosomes and release the thyroid hormones T3 and T4 to the blood capillaries via basal part. Deiodination of precursors mono and di iodo thyrosin by a dehalogenace and released apically to reiodination of thyroglobulin. Triiodo thyrosine.
The superior thyroidal arteries arise from the external carotid and enter at the upper pole. The inferior thyroidal artery arising from the subclavians enter at the lower pole. Sometimes an additional thyroeaidima artery, branch from bracheocephalic trunk or aortic arch that ascends upon the front of trachea. Remarkable anastamosis on the surface as well as within the substance.
Intralobular veins drains to plexus on the surface of the gland and on the front of the trachea. From this plexus superior, middle, inferior thyroid veins arise. Superior and middle thyroid veins drains to the external jugular vein. Inferior thyroid vein to the brachicephalic vein.
A wide spread lymphatic network drains to pre and paratracheal and to internal jugular lymph nodes. They contain colloid material. They ends in thorasic duct and right lymphatic duct. Nerves are derived from superior, middle and inferior cervical ganglia.
THE CONTROL OF THYROID FUNCTION
The control of thyroid hormone synthesis and secretion is mediated via thyroid stimulating hormone(TSH) secreted by the thyrotrophs of the anterior pituitary glands. This is a glycoprotien hormone consisting of a species -specific ‘Alpha’ subunit, which is also used in the syntesis of gonadotrophnis and a hormone specific ‘Beta’ subunit. It binds to a high affinity receptor on follicular cells and activates them via the cyclic adenosine monophosphate (cAMP) pathway. The secretion of TSH is stimulated by a hypothalamic tripeptide, thyrotrophin-releasing hormone (TRH), Thyroid hormones exerts negative feed back at pituitary level.
It is believed that regulatory peptides and amines released by intrathyroid nerves, and possibly from ‘C’cells interacts with TSH in the control of thyroid secretion. Also has a sympathetic control. Nor adrenaline can directly induce thyroid hormone secretion. Catecholamines and TSH interact with different receptors on the follicular cell surface and act independently but effect are similar both induce activation of adenyl cyclase, resulting increase formation of ‘cAMP’ which leads to increase release of thyroid hormone.
MODE OF ACTION OF THYROID HORMONE
The major proportion of thyroid hormones circulates bound to plasma protein. These include thyroxine binding globulin (TBG), thyroxine binding prealbumin (TBPA) and albumin. A small proportion circulates in unbound form. The hormones diffuse, or actively transported across the cell membrane. T4 is peripherally converted to T3, the active hormone, by tissue deiodinases 1 and 2, with varying distribution and affinity. Most of the action of the thyroid hormones are probably effected by T3, via binding to nuclear receptors encoded by two genes related to the viral onco gene ‘c-erb- A’. Binding alters the transcription of genes encoding proteins, with wide ranging effects on metabolic processes. Some of these contribute to the calorigenic effects of thyroid hormones, but additional direct action on mitochondrial function via a membrane receptor. Thyroid hormones also have complex interactions with sympathetic nervous system.
Parafolicular cells are a type of APUD cells. They are scattered among the follicular cells, particularly in the upper zones of the gland, are the C cells or calcitonin- producing cells, which account for less than 0.1%of total cell mass. They may lie in the stroma, or appear to interdigitate with follicular cells in the walls of the follicles. In most instances they are enclosed within the follicular basement membrane, either singly or in groups. Release of calcitonin is controlled by level of calcium. Hypercalcaemia stimulate while hypocalcaemia suppress. Difficult to detect thyrocalcitonin in normal human plasma
IMMUNO HISTO CHEMISTRY
Follicular cells are immunopositive for thyroglobulin and express low molecular weight cytokeratins. Vimentin may be coexpressed. Immunoreactive atrial natriuretic peptide(ANP) has also been reported in follicular cells. C cells show positivity for calcitonin and some stain for calcitonin gene related peptide (CGRP), somatostatin, katacalcin, gastrin releasing peptide and carcino embryonic antigen(CEA). C cells are also immunoreactive for such general ‘neuro endocrine’ markers as neuron specific enolase, chromogranin and synaptophysin. Vascular channels may be demonstrated by the binding of ulex europaeus to endothelial cells. Antibodies to factor VIII related antigen might identify vascular channels in normal gland.
TESTS OF THYROID FUNCTIONS
SERUM THYROID HORMONES
Serum Thyroid Stimulating Hormone (TSH)
TSH is a glycoprotien secreted by anterior pituitary in order to stimulate the secretion of thyroid hormone. The secretion of TSH is controlled by hypothalamus through TRH (a tripeptide), which in turn through a negative feed back. When the Serum TSH level is in the normal range, it is redundant to measure the T3 and T4 levels. In the euthyroid state T3, T4 and TSH levels will all be with in the normal range. Florid thyroid Failure results in depressed T3 and T4 levels with gross elevation of the TSH. Incipient or developing thyroid failure is characterized by low normal values of the T3 and T4 and elevation of TSH. In toxic state, the TSH level is suppressed and undetectable. In secondary hyper thyroidism with pituitary tumor TSH level is increased.
Thyroxine (T4) and Tri-iodothyronine (T3)
These are transported in plasma bound to specific proteins (Thyroxine-Binding Globulin, TBG). Only a small fraction of the total (0.03% of T4 and 0.3%of T3) is free and physiologically active. Assays of total hormone for both are now obsolete because of the confounding effect of circulating protein concentrations, influenced by the level of circulating oestrogren and nutritional state. Highly accurate radio immuno assays of free T3 and T4 are now routine. In T3 toxicity raised serum T3 but a normal T4 and suppressed TSH level. Biochemical assessment of thyroid function may be difficult in such patients as myocardial infarction or pneumonia.
The uptake of thyroid of a low dose of either radio labeled iodine (I 123) or technetium (Tc 99m) will demonstrate the distribution of activity in the whole gland. Routine isotopes scanning are unnecessary and inappropriate for distinguishing benign from malignant lesions because the majority (80%) of ‘cold ‘ swellings are benign and some (5%) functioning or ‘warm’ swellings will be malignant. Its principal value is in the toxic patient with a nodule or nodularity of the thyroid. Localization of overactivity 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.
Thyroid function Test Results in normal and Pathological State
|Thyroid functional state||TSH (0.3 to 3.3mU/l)||Free T4 (10- 30 nmol-l)||Free T3 (3.5 –7.5 Micro mol/l)|
|Suppressive T4 therapy||TSH undetectable||High||High|
Serum levels of antibodies against thyroid peroxidase (TPO), previously referred as thyroid microsomal antigen and Thyro globulin are useful in determining the cause of thyroid dysfunction and swellings. Autoimmune thyroiditis may be associated with thyroid toxicity, failure or euthyroid goiter. Levels above 25 units per ml for TPO antibody and titres of greater than 1:100 for anti Thyro globulin are considered significant, although a proportion of patients with autoimmune thyroiditis are sero negative.
Ultra sonography can demonstrate subclinical nodularity and cyst formation. It is an adjunct to aspiration cytology.
Fine-needle aspiration cytology
Thyroid conditions may be diagnosed by FNAC include colloid nodules, thyroiditis, papillary carcinoma, medullary carcinoma, anaplastic carcinoma and lymphoma. FNACV cannot distinguish benign follicular adenoma and follicular carcinoma. Distinction depends on histology include capsular and vascular invasion. There are very few false positive with respect to malignancy but there is a false negative rate with respect to both benign and malignant neoplasia.
Demonstrate tracheal deviation or compression, retrosternal extension.
Other scans: – CT and MRI give excellent anatomical details useful in retrosternal and recurrent swellings.
Indirect laryngoscopy: to determine mobility of vocal cord
Large Bore needle (Trucut) biopsy: Trucut biopsy has a high diagnostic accuracy. May be associated with complications such as pain, bleeding, tracheal and recurrent laryngeal nerve damage.
ABNORMAL THYROID FUNCTION
T4 and T3, which have important actions throughout the body. These hormones regulate many aspects of our metabolism. These hormones also have direct effects on most organs, including the heart, which beats faster and harder under the influence of thyroid hormones. Essentially all cells in the body will respond to increases in thyroid hormone with an increase in the rate at which they conduct their business. Hyperthyroidism is the medical term to describe the signs and symptoms associated with an over production of thyroid hormone
CAUSES OF HYPERTHYROIDISM
- Diffuse toxic goiter (Graves disease) 80%
- Toxic nodular goiter 10%.
- Toxic nodule 10%.
- Rare causes
A condition named for an Irish doctor who first described the condition. This condition can be summarized by noting that an enlarged thyroid (enlarged thyroids are called goiters) is producing way too much thyroid hormone. [Remember that only a small percentage of goiters produce too much thyroid hormone, the majority of thyroid goiters actually become large because they are not producing enough thyroid hormone]. Graves’ disease is classified as an autoimmune disease, a condition caused by the patient’s own immune system turning against the patient’s own thyroid gland. The hyperthyroidism of Graves’ disease, therefore, is caused by antibodies (TSH –Rab) that the patient’s immune system makes which attach to specific activating sites on thyroid gland which in turn cause the thyroid to make more hormone. There are actually three distinct parts of Graves’ disease:  over activity of the thyroid gland (hyperthyroidism),  inflammation of the tissues around the eyes causing swelling, and  thickening of the skin over the lower legs (pretibial myxedema). Most patients with Graves’ disease, however, have no obvious eye involvement. Their eyes may feel irritated or they may look like they are staring. About one out of 20 people with Graves’ disease will suffer more severe eye problems, which can include bulging of the eyes, severe inflammation, double vision, or blurred vision. If these serious problems are not recognized and treated, they can permanently damage the eyes and even cause blindness. Thyroid and eye involvement in Graves’ disease generally run a parallel course, with eye problems resolving slwly after hyperthyroidism is controlled.
- Graves Disease effects women much more often than men (about 8:1 ratio, thus 8 women get Graves Disease for every man that gets it.
- Graves Disease is often called diffuse toxic goiter because the entire thyroid gland is enlarged, usually moderately enlarged, sometimes quite big.
- Graves disease is uncommon over the age of 50 (more common in the 30’s and 40’s)
- Graves Disease tends to run in families.
- Hyperthyroidism can also be caused by a single nodule within the thyroid instead of the entire thyroid
- Inflammation of the thyroid gland, called thyroiditis, can lead to the release of excess amounts of thyroid hormones that are normally stored in the gland. In sub acute thyroiditis, the painful inflammation of the gland is believed to be caused by a virus, and the hyperthyroidism lasts a few weeks. A more common painless form of thyroiditis occurs in one out of 20 women, a few months after delivering a baby and is, therefore, known as postpartum thyroiditis.
- Hyperthyroidism can also occur in patients who take excessive doses of any of the available forms of thyroid hormone.
Hyperthyroidism associated with low iodine uptake
- Sub acute (de quervain’s) thyroiditis: Virus induced inflammation of thyroid gland (Coxackie, mumps or adenovirus) results colloid and its constituents into the circulation. Pain in the region of thyroid gland may radiate to the angle of jaw and the ears and is made worse by swallowing, coughing or any movement of neck. Thyroid enlarged and tender. Usually affects females 20 to 40 years. Thyroid hormone levels are raised for 4 to 6 weeks until the preformed colloid is depleted. The iodine uptake is low because the damaged follicular cells are unable to trap iodine and suppressed endogenous TSH secretion. Low titre thyroid autoantibodies and transiently raised ESR Followed by hypothyroidism and full recovery within 4 to 6 months.
- Postpartum thyroiditis. The maternal hormone response modified during pregnancy to allow survival of the foetal homograft is enhanced after delivery and may unmask previously unrecognized sub clinical autoimmune thyroid disease. Antithyroid peroxidace antibody may present in the serum. Biopsy shows lymphocytic thyroiditis.
- iodine induced hyperthyroidism: follows prophylatic iodinisation programme, radiographic contrast medium, iodine containing drugs. Usually in individuals having thyroid autonomy such as nodular goiter or graves disease.T4 is usually elevated with suppressed TSH. T3 lower part of normal range.
- Factitious hyperthyroidism: intake of excessive thyroid hormone preparation. The exogenous T4 supresses pituitary secretion of TSH and hence iodine uptake, Serum thyroglobulin and release of endogenous thyroid hormones. High T4, T3 ratio ranging from 30:1 to 70:1 low or undetectable thyroglobulin.
Other rare causes:
- Juvenile thyroiditis
- Granulomatous thyroiditis
- TSH secreting adenoma of the pituitary gland.
- Familiar syndromes of pituitary resistance to T3 orT4.
- Trophoblastic tumours is thought to reflect the interaction of high levels of human chorionic gonadotrophin(HCG) with TSH receptor, which shares an identical alpha subunit.
- Strumaovary – benign cystic ovarian teratoma.
Common symptoms and signs of hyperthyroidism
Enlarged thyroid gland with bruit especially in Graves disease.
- Rapid heart beat (sinus tachycardia) or heart palpitations, increase pulse rate.
- Smooth, velvety skin
- Tremor of the fingertips
- Exophthalmia, lidretraction, grittiness, excessive lacrimation, chemosis,corneal ulceration,opthalmoplegia, diplopia, papillodema, loss of visual acuity (in Graves disease)
Other symptoms are:
- Sweaty palms
- Weight loss
- Fine brittle hair
- Increased appetite
- Changes in sex drive
- Muscle weakness, especially in the upper arms and thighs
- Shortened attention span
- Heat intolerance
- Increased sweating
- Nervousness and irritability, emotional lability, psychosis.
- Restless sleep or insomnia
- Erratic behavior
- For women, irregular menstrual cycle and reduced menstrual flow
- Infertility, recurrent miscarriage
- Increased frequency of bowel movements.
- Pigmentation, vitiligo(Graves disease).
- Palmarerythema, spidernaevi, Onycholysis, Alopecia
- Hyper reflexia, ill sustained clonous, periodic paralysis
- Muscle weakness, proximal myopathy, bulbar myopathy.
- Digital clubbing.
- Pertibial myxoedama
- Amenorrhoea, infertility, spontaneous abortion, loss of libido, impotence.
- Atrial fibrallation.
- Angina, cardiomyopathy.
Hyperthyroid crisis: life threatening increase in the clinical features of hyper thyroidism. Fever, agitation, confusion, tachycardia, atrial fibrillation and in older patients, cardiac failure. Precipitating cause is stress such as infection or surgery in unrecognized or inadequately treated patients.
Hypothyroidism is a very common condition caused by deficiency or failure of thyroid function. In adult hypothyroidism causes myxoedema. It is estimated that 3 to 5% of the population has some form of hypothyroidism. The condition is more common in women than in men, and its incidence increases with age.
Causes of Hypothyroidism.
- Hashimoto’s Thyroiditis
- Lymphocytic Thyroiditis After Hyperthyroidism
- Thyroid Destruction (from radioactive iodine or surgery) post ablative
- Pituitary or Hypothalamic Disease
- Severe Iodine Deficiency
- Dyshormono genesis
- Spontaneous atrophic hypothyroidism (Non Goitorous)
Hashimoto’s Thyroiditis: The most common cause of hypothyroidism in the United States is an inherited condition called Hashimoto’s thyroiditis. This condition is named after Dr. Hakaru Hashimoto who first described it in 1912. In this condition, the thyroid gland is usually enlarged (goiter) and has a decreased ability to make thyroid hormones. Hashimoto’s is an autoimmune disease in which the body’s immune system inappropriately attacks the thyroid tissue. In part, this condition is believed to have a genetic basis. This means that the tendency toward developing Hashimoto’s thyroiditis can run in families. Hashimoto’s is 5 to 10 times more common in women than in men. Blood samples drawn from patients with this disease reveal an increased number of antibodies to the enzyme, thyroid peroxidase (anti-TPO antibodies). Since the basis for autoimmune diseases may have a common origin, it is not unusual to find that a patient with Hashimoto’s thyroiditis has one or more other autoimmune diseases such as diabetes or pernicious anemia ( B12 deficiency). Hashimoto’s can be identified by detecting anti-TPO antibodies in the blood and by performing a thyroid scan.
Lymphocytic Thyroiditis following hyperthyroidism: Thyroiditis refers to inflammation of the thyroid gland. When the inflammation is caused by a particular type of white blood cell known as a lymphocyte, the condition is referred to as lymphocytic thyroiditis. This condition is particularly common after pregnancy and can actually affect up to 8% of women after they deliver. In these cases, there is usually a hyperthyroid phase (in which excessive amounts of thyroid hormone leak out of the inflamed gland), which is followed by a hypothyroid phase that can last for up to 6 months. The majority of affected women eventually return to a state of normal thyroid function, although there is a possibility of remaining hypothyroid.
Thyroid destruction secondary to radioactive iodine or surgery: Patients who have been treated for a hyperthyroid condition (such as Graves’ disease) and received radioactive iodine may be left with little or no functioning thyroid tissue after treatment. The likelihood of this depends on a number of factors including the dose of iodine given, along with the size and the activity of the thyroid gland. If there is no significant activity of the thyroid gland six months after the radioactive iodine treatment, it is usually assumed that the thyroid will no longer function adequately. The result is hypothyroidism. Similarly, removal of the thyroid gland during surgery will be followed by hypothyroidism.
Pituitary or Hypothalamic disease: If for some reason the pituitary gland or the hypothalamus are unable to signal the thyroid and instruct it to produce thyroid hormones, a decreased level of circulating T4 and T3 may result, even if the thyroid gland itself is normal. If this defect is caused by pituitary disease, the condition is called “secondary hypothyroidism.” If the defect is due to hypothalamic disease, it is called “tertiary hypothyroidism.”
A pituitary injury may result after brain surgery or if there has been a decrease of blood supply to the area. In these cases of pituitary injury, the TSH that is produced by the pituitary gland is deficient and blood levels of TSH are low. Because the thyroid gland is no longer stimulated by the pituitary TSH, hypothyroidism results. This form of hypothyroidism can, therefore, be distinguished from hypothyroidism that is caused by thyroid gland disease, in which the TSH level becomes elevated as the pituitary gland attempts to encourage thyroid hormone production by stimulating the thyroid gland with more TSH. Usually, hypothyroidism from pituitary gland injury occurs in conjunction with other hormone deficiencies, since the pituitary regulates other processes such as growth, reproduction, and adrenal function.
Medications: Medications that are used to treat an over-active thyroid (hyperthyroidism) may actually cause hypothyroidism. These drugs include methimazole (Tapezole) and propylthiouracil (PTU). The psychiatric medication, lithium, is also known to alter thyroid function and cause hypothyroidism. Interestingly, drugs containing a large amount of iodine such as amiodarone (Cardorone), SSKI, and Lugol’s solution can cause a decrease in thyroid function, thereby resulting in low blood levels of thyroid hormone.
Severe Iodine Deficiency: In areas of the world where there is an iodine deficiency in the diet, severe hypothyroidism can be seen in 5 to 15% of the population. Examples of these areas include Zaire, Ecuador, India, and Chile. Severe iodine deficiency is also seen in remote mountain areas such as the Andes and the Himalayas. Since the addition of iodine to table salt and to bread, iodine deficiency is rarely seen in the United States.
Dyshormono genesis: Genetically determined enzyme deficiencies of varying severity may be responsible for defective thyroid hormone synthesis. It is an autosomal recessive inheritance. This condition causes cretinism or Hypothyroidism. Goiter may be present at birth were the defect is severe.
Pendred’s syndrome: Dyshormono genesis associated with sensory neural deafness.
Spontaneous atrophic hypothyroidism (Non Goitorous): An organ specific autoimmune disorder. Destructive lymphoid infiltration of thyroid leading to fibrosis and atrophy.
- cold intolerance
- weight gain (unintentional)
- joint or muscle pain
- thin, brittle fingernails
- thin and brittle hair
- slow speech
- dry flaky skin
- thickening of the skin
- puffy face, hands and feet
- decreased taste and smell
- thinning of eyebrows
- abnormal menstrual periods
Additional symptoms that may be associated with this disease:
- overall swelling
- muscle spasms (cramps)
- muscle pain
- muscle atrophy
- uncoordinated movement
- absent menstruation
- joint stiffness
- dry hair
- hair loss
- facial swelling
- appetite loss
- ankle, feet, and leg swelling
- short stature
- separated sutures
- delayed formation or absence of teeth
Signs and tests
A physical examination reveals delayed relaxation of muscles during tests of reflexes. Pale, yellow skin; loss of the outer edge of the eyebrows; thin and brittle hair; coarse facial features; brittle nails; firm swelling of the arms and legs; and mental slowing may be noted. Vital signs may reveal slow heart rate, low blood pressure, and low temperature.
A chest X-ray may reveal an enlarged heart.
Laboratory tests to determine thyroid function include:
- T4 test (low)
- serum TSH (high in primary hypothyroidism, low or low-normal in secondary hypothyroidism)
Additional laboratory abnormalities may include:
- increased cholesterol levels
- increased liver enzymes
- increased serum prolactin
- low serum sodium
- a complete blood count (CBC) that shows anemia
Myxedema coma, the most severe form of hypothyroidism, is rare. It may be caused by an infection, illness, exposure to cold, or certain medications in an individual with untreated hypothyroidism. Symptoms and signs of myxedema coma include unresponsiveness, decreased breathing, low blood pressure, low blood sugar, and below normal temperature.
Other complications are heart disease, increased risk of infection, infertility, and miscarriage.
Cretinism(fetal or infentile hypothyroidism):Severe hypothyroidism in infants results cretinism. Sphoradic cretinism due to complete or near complete failure of thyroid devolupment. Partial failure causes juvenile myxoedema. In endemic areas goitrous cretinism is common and is due to meternal iodine deficiency. Congenital hypothyroidism from thyroid agenesis, ectopic or hypoplastic glands or dishormono genesis. Immedite diagnosis and management is necessary as it is essential for physical and mental development. Hypothyroidism occurs one in 4000 live births and biochemical screening of neonates using TSH and T4 assays on a heel prick blood sample.
ENLARGEMENT OF THYROID GLAND- GOITRE
Normal gland is impalpable. The term goiter from the latin word ‘Guttur’ means ‘the throat’ is used to describe generalised enlargement of thyroid gland.
Classification of thyroid swellings
¨ Diffuse hyper plastic
¨ Multinodular goiter
- Graves’ disease
¨ Toxic adenoma
- Chronic Lymphocytic thyroiditis
- Hashimoto’s Disease
- De Quervain’s thyroiditis
- Riedel’s thyroiditis
- Acute(Bacterial thyroiditis), Viral thyroiditis, ‘subacute thyroiditis’
- Chronic(Tuberculous, Syphilitic)