Survey
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
THYROID GLAND The thyroid gland releases thyroid hormones. It is under the influence of thyroidstimulating hormone (TSH or thyrotropin) from the pituitary gland, which is itself regulated by thyrotropin-releasing hormone (TRH) from the hypothalamus. Thyroid hormones, stored as iodide-rich 'thyroid colloid', are: o thyroxine (T4; tetraiodothyronine) mainly, which has a half life of one week, and is converted to o triiodothyronine (T3) a small amount only - the active form, which has a half life of one day. Thyroid hormones feed back to the hypothalamus and pituitary to regulate TSH release. Thyroid hormones act on: 1. metabolism by regulating protein synthesis via effects on gene transcription and mRNA stabilization. 2. They have profound effects on the sensitivity of tissues to catecholamines. 3. mitochondrial oxidative activity. 4. synthesis and degradation of proteins. 5. differentiation of muscle fibres. 6. capillary growth. 7. levels of antioxidant compounds. Thyroid function tests include the following: Levels of free T4 and free T3 in serum provide a better assessment of the thyroid status than do total T4 and T3. About 95% of thyroid hormones are bound to plasma proteins, especially thyroid-binding globulin (TBG) and thyroid-binding prealbumin (TBPA). Thyroid-stimulating hormone (TSH) levels can be assayed. Thyroid antibody tests. ultrasound and radio-iodine uptake using 131I or 123I are the other common LINGUAL THYROID The thyroid normally develops as a downgrowth from the foramen caecum at the junction of the posterior third with the anterior two-thirds of the tongue. Rarely, ectopic thyroid tissue remains in this tract and may be seen as a lump anywhere in the midline between the foramen caecum and epiglottis, but has also been recorded in the oropharynx, infra-hyoid region, larynx, oesophagus, heart and mediastinum. A lingual thyroid is seen mainly in females, and is often asymptomatic but may cause dysphagia, airway obstruction or ewn haemorrhage. Hypothyroidism may be associated in about one-third of cases and, occasionally, the lingual thyroid becomes malignant. There is a raised incidence of thyroid disease in relatives. I A lingual thyroid may not be suspected until the lump in the tongue has been biopsied or excised and examined histologically. The diagnosis can be confirmed by iodine-123 or -131, or technetium-99 uptake in the tongue or by biopsy or by CT scanning without contrast or by MRI. Treatment depends on the size of the lingual thyroid but thyroxine may be needed and if the lump does not regress sufficiently, the lingual thyroid can be ablated, best by surgery, or if the patient is unfit, by iodine-131, if normal functioning thyroid tissue is identified in the neck. GOITRE A goitre is an enlarged thyroid gland, usually a consequence of hyperplasia secondary to excessive TSH levels caused by low circulating thyroid hormone. Most goitres are acquired and seen in Graves' disease, or thyroiditis, but a few are congenital and seen in cretinism. Thyroid cancer is another possible cause. H The cause of the goitre should be sought. Thyroid function is assessed to determine whether it is: normal (euthyroid) hyperactive (hyperthyroid) hypoactive (hypothyroid). Most goitres do not require surgery but this is indicated if there is a danger of airways obstruction (cough, voice changes, dyspnoea, tracheal deviation or dysphagia), or for cosmetic reasons. Dental management in goitre may be influenced by abnormal thyroid function, by the underlying cause of the goitre, or by complications such as respiratory obstruction. A rare cause of goitre is a medullary carcinoma of the thyroid, which can be part of a multiple endocrine adenomatosis syndrome (MEA II and MEA III). In the latter, numerous small plexiform neuromas form in the oral mucosa, lips, eyelids and skin. The patient may also have a Marfanoid habitus and diarrhoea. THYROID NODULES A nodule in the thyroid gland may represent a benign or malignant neoplasm. Patients are examined with radio-iodine thyroid scans and thyroid function tests. A nodule that takes up radio-iodine is termed a hot nodule and unlikely to be malignant, and more usually is an adenoma. A nodule that fails to take up the radio-iodine is termed a cold nodule, and may be malignant, usually a papillary, follicular or medullary cell carcinoma. Needle biopsy is indicated. II HYPERTHYROIDISM General aspects Hyperthyroidism is associated: usually, with a diffuse goitre due to autoimmune disease (Graves' disease, primary hyperthyroidism) when there are thyroidstimulating autoantibodies against thyroid TSH receptor (TRAbs) and thyroid microsomal antibodies (TMAbs) sometimes, with a hyperfunctioning (toxic) multinodular goitre or nodule due to one or more thyroid adenomas producing excess thyroxine. 90% of the swellings are benign rarely, with thyroiditis, thyroid hormone overdosage, or ectopic thyroid tissue. Clinical features Hyperthyroidism mimics the effects of cpinephrine, and can cause: anorexia, vomiting or diarrhea, weight loss, anxiety and tremor, sweating and heat intolerance, cardiac disturbances, particularly in older patients: These include tachycardia, dysrhythmias (especially atrial fibrillation) or cardiac failure, exophthalmos, eyelid lag and eyelid retraction. Thyrotoxic periodic paralysis comprises attacks of mild to severe weakness, during which serum potassium levels are generally low. Myasthenia gravis may occasionally be associated. III General management The diagnosis of hyperthyroidism should be confirmed by: 1) raised serum levels of T3 and T4 IV 2) circulating TMAbs and TRAbs in 55% of patients with Graves' disease. 3) a radioactive iodine uptake test or thyroid scan. Radioactive iodine (RAI) uptake can differentiate causes of hyperthyroidism: subacute thyroiditis (low uptake) versus Graves' disease (high uptake). Hyperthyroidism can be treated with: beta blockers. These achieve rapid control of many of the signs and symptoms by moderating sympathetic overactivity. However, suddenly stopping beta-blocker treatment can precipitate a thyroid crisis within 4 h. Carbimazole - the usual antithyroid drug but it can suppress the bone marrow and rarely cause rashes. Nearly 50% of patients have a relapse. Propylthiouracil is an alternative. 131 Iodine effective, but can result in hypothyroidism. There appears to be no risk of neoplastic change surgery. This is effective, but leads to hypothyroidism in about 30%. Hypoparathyroidism or recurrent laryngeal nerve palsy are rare complications. In untreated patients with hyperthyroidism, pain, anxiety, trauma, general anaesthesia, or premature cessation of antithyroid treatment may precipitate a thyroid (thyrotoxic) crisis. Thyroid crisis, characterized by anxiety, tremor and dyspnoea, is dangerous and can go on to ventricular fibrillation. Medical assistance is essential as treatment requires the use of potassium iodide and propylthiouracil, and propranolol or chlorpromazine. Dental aspects Patients with untreated hyperthyroidism can be difficult to deal with as a result of heightened anxiety and irritability. The sympathetic overactivity may lead to fainting. Local anaesthesia is the main means of pain control. The risk from epinephrine exacerbating symphathetic overactivity is only theoretical: prilocaine with felypressin is not known to be safer than lidocaine. Conscious sedation is frequently desirable to control excessive anxiety. Benzodiazepines may potentiate antithyroid drugs, and therefore nitrous oxide, which is more rapidly controllable, is probably safer. Povidone-iodine and similar compounds are best avoided. Carbimazole occasionally causes agranulocytqsis, which may cause oral or oropharyngeal ulceration. Otherwise the treated thyrotoxic patient presents no special problems in dental treatment. However, after treatment of hyperthyroidism the patient is at risk from hypothyroidism, which may pass unrecognized. This point must especially be borne in mind if a general anaesthetic is required. V Hyperthyroidism Hypothyroidism Heat intolerance Cold intolerance Excess sweating Warm moist skin No Decreased sweating Dry cold skin hair loss Hair loss Increased appetite Weight loss Decreased appetite Weight gain Tachycardia (atrial fibrillation) Heart Bradycardia Angina Hoarseness Slow failure No voice change Tremor reactions Diarrhoea Irritability Psychosis Atrial Constipation Slow cerebration, poor fibrillation memory Psychosis Ischaemic heart disease Exophthalmos in some Amenorrhoea Periorbital oedema Menorrhagia Gynaecomastia Serous effusions HYPOTHYROIDISM General aspects hypothyroidism may be: primary (due to thyroid disease) secondary (to hypothalamic or pituitary dysfunction). The common causes of hypothyroidism are: thyroid loss from surgical removal of too much thyroid tissue in a previously hyperthyroid patient destruction by irradiation of the neck or thyroid gland autoimmune disease (Hashimoto's thyroiditis), associated with autoantibodies to thyroglobulin and thyroid microsomes drugs such as amiodarone, carbimazole, lithium or radio-iodine. Rare cases in the developed world are caused by iodine deficiency. Clinical features Subclinical hypothyroidism, with raised TSH but normal T4 levels, may be found in up to 10% of postmenopausal females. Hypothyroidism is often unrecognized but can cause: weight gain lassitude dry skin, myxoedema, loss of hair cardiac failure or ischaemic heart disease, bradycardia, anaemia neurological or psychiatric changes, hypotonia, cerebellar signs of ataxia, tremor, and dysmetria, polyneuropathy, cranial nerve deficits, entrapment VI neuropathy (e.g. carpal tunnel syndrome), myopathic weakness, dementia, apathy, mental dullness, irritability, sleepiness hoarseness hypothermia and may be complicated by coma. Sjogren's syndrome may be associated Congenital hypothyroidism (cretinism) has similar features, together with an enlarged tongue and learning impairment. General management -The diagnosis of hypothyroidism is confirmed by demonstrating. -Serum T4 and T3 levels (low in hypothyroidism). TSH levels. The TSH-immunometric assay can discriminate directly between normal TSH and low levels without requiring the use of the thyrotropin-releasing hormone (TRH) infusion test, serum TSH is raised in primary hypothyroidism depressed in secondary hypothyroidism, serum antibodies in patients with Hashimoto's thyroiditis, thyroid microsomal antibodies (TMAb) in 95% thyroglobulin antibodies (TGAbs) in 60%. -Symptomatic patients are managed with daily oral thyroxine sodium. Treatment is started slowly but, especially if there is evidence of ischaemic heart disease, angina, MI or sudden death may be precipitated. Dental aspects The main danger is of precipitating myxoedema coma by the use of sedatives (including diazepam or midazolam), opioidanalgesics (including codeine), or tranquillizers. These should, therefore, be either avoided or given in low dose. Local anaesthesia is satisfactory for pain control. Conscious sedation can be carried out with nitrous oxide and oxygen. Diazepam or midazolam may precipitate coma. General anaesthesia may be complicated because of possible ischaemic heart disease and the danger of coma, and the respiratory centre is also hypersensitive to drugs such as opioids or sedatives. General anaesthesia, if unavoidable, should be delayed if possible until thyroxine has been started. Associated problems may include hypoadrenocorticism, anaemia, hypotension, diminished cardiac output and bradycardia. Occasional associations include hypopituitarism and other autoimmune disorders such as Sjogren's syndrome. Povidone-iodine and similar compounds are best avoided. VII