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Lec: 2 Dr. Mohammed Alhamdany(continue) Thyrotoxicosis InvestigationsThe first-line investigations are serum T3, T4 and TSH. If abnormal values are found, the tests should be repeated and the abnormality confirmed in view of the likely need for prolonged medical treatment or destructive therapy.In most patients, serum T3 and T4 are both elevated, but T4 is in the upper part of the reference range and T3 raised (T3 toxicosis) in about 5%.Serum TSH is undetectable in primary thyrotoxicosis, but values can be raised in the secondary thyrotoxicosis.An ECG may demonstrate sinus tachycardia or atrial fibrillation.Further investigations should be undertaken to determine the underlying cause, including measurement of TSH receptor antibodies (TRAb, elevated in Graves’ disease), isotope scanning (99mtechnetium scintigraphy) as shown below: (approach to the patient with thyrotoxicosis) to differentiate between thyroiditis and factious thyrotoxicosis (extrathyroidal T4), we have to do:1- T4:T3 ratio (normally 30/1 while in factious hyperthyroidism is up to 70/1.2- thyroglobuline level (undetectable in factious hyperthyroidism and high in thyroiditis).Other lab. Abnormality in thyrotoxicosis include:(should not misdiagnosed as liver disease or DM)1- Serum enzymes: raised alanine aminotransferase, γ-glutamyl transferase (GGT), and alkaline phosphatase from liver and bone.2- Raised bilirubin.3- Mild hypercalcaemia.4- Glycosuria: associated diabetes mellitus, ‘lag storage’ glycosuria. Atrial fibrillation in thyrotoxicosis:Atrial fibrillation occurs in about 10% of patients with thyrotoxicosis. The incidence increases with age, so that almost half of all males with thyrotoxicosis over the age of 60 are affected. Moreover, subclinical thyrotoxicosis is a risk factor for atrial fibrillation. Characteristically, the ventricular rate is little influenced by digoxin, but responds to the addition of a β-blocker.Once thyroid hormone and TSH concentrations have been returned to normal, atrial fibrillation will spontaneously revert to sinus rhythm in about 50% of patients, but cardioversion may be required in the remainder.Thyrotoxic crisis (‘thyroid storm’)This is a rare but life-threatening complication of thyrotoxicosis. Clinical feature:1- Fever.2- Agitation,3- Confusion.3- Tachycardia or atrial fibrillation.4- In the older patient, cardiac failure. It is a medical emergency, which has a mortality of 10% despite early recognition and treatment. Causes:1- Thyrotoxic crisis is most commonly precipitated by infection in a patient with previously unrecognized or inadequately treated thyrotoxicosis. 2- It may also develop shortly after subtotal thyroidectomy in an ill-prepared patient.3- within a few days following 131I therapy, when acute irradiation damage may lead to a transient rise in serum thyroid hormone levels.Treatment:Patients should be rehydrated and given propranolol, either orally or intravenously. Sodium ipodate (500 mg per day orally) will restore serum T3 levels to normal in 48–72 hours. This is a radiographic contrast medium which not only inhibits the release of thyroid hormones, but also reduces the conversion of T4 to T3.Dexamethasone (2 mg 4 times daily) and amiodarone have similar effects. Oral carbimazole 40–60 mg daily should be given to inhibit the synthesis of new thyroid hormone. If the patient is unconscious or uncooperative, carbimazole can be administered rectally with good effect, but no preparation is available for parenteral use. After 10–14 days the patient can usually be maintained on carbimazole alone.Hypothyroidism:Women are affected approximately six times more frequently than men.Causes:1- Autoimmune: as Hashimoto’s thyroiditis (most common cause).2- Iatrogenic including radioactive iodine ablation, thyroidectomy, and drugs such as Carbimazole, methimazole,Propylthiouraciland Amiodarone.3- Transient thyroiditis such as Subacute (de Quervain’s) thyroiditis and Post-partum thyroiditis.4- Iodine deficiency, e.g. in mountainous regions.Clinical assessmentThe clinical presentation depends on the duration and severity of the hypothyroidism. Those in whom complete thyroid failure has developed insidiously over months or years A consequence of prolonged hypothyroidism is the infiltration of many body tissues by the mucopolysaccharides, hyaluronic acid and chondroitin sulphate, resulting in a low-pitched voice, poor hearing, slurred speech due to a large tongue, and compression of the median nerve at the wrist (carpal tunnel syndrome). Infiltration of the dermis gives rise to nonpitting oedema (myxoedema), which is most marked in the skin of the hands, feet and eyelids. The resultant periorbital puffiness is often striking and may be combined with facial pallor due to vasoconstriction and anaemia, or a lemon-yellow tint to the skin caused by carotenaemia, along with purplish lips and malar flush.Most cases of hypothyroidism are not clinically obvious, however, and a high index of suspicion needs to be maintained so that the diagnosis is not overlooked in individuals complaining of non-specific symptoms such as tiredness, weight gain, depression or carpal tunnel syndrome.Other symptom includes Cold intolerance, somnolence, dry skin, dry hair, menorrhagia, constipation and alopecia.The other signs include Loss of lateral eyebrows, anaemia, carotenaemia, erythema ab igne, bradycardia, hypertension, and delayed relaxation of reflexesIn the vast majority of cases, hypothyroidism results from an intrinsic disorder of the thyroid gland (primary hypothyroidism). In this situation, serum T4 is low and TSH is elevated, usually in excess of 20 mU/L. Measurements of serum T3 are unhelpful since they do not discriminate reliably between euthyroidism and hypothyroidism. Secondary hypothyroidism is rare and is caused by failure of TSH secretion in an individual with hypothalamic or anterior pituitary disease.The electrocardiogram (ECG) classically demonstrates sinus bradycardia with low-voltage complexes and ST segment and T-wave abnormalities. Measurement of thyroid peroxidase antibodies is helpful.Other nonspecific lab result includes:1- Serum enzymes: raised creatine kinase, aspartate aminotransferase, lactate dehydrogenase (LDH).2- Hypercholesterolaemia.3- Anaemia: normochromic normocytic or macrocytic.4- Hyponatraemia.The approach to the patient with hypothyroidism is;ManagementTreatment is with levothyroxine replacement. It is customary to start with a low dose of 50 μg per day for 3 weeks, increasing thereafter to 100 μg per day for a further 3 weeks and finally to a maintenance dose of 100–150 μg per day.Levothyroxine has a half-life of 7 days so it should always be taken as a single daily dose and at least 6 weeks should pass before repeating thyroid function tests and adjusting the dose usually by 25 μg per day.The adjustment of dose depend level of TSH (normalize) and T4 (in the upper limit).It is important to measure thyroid function every 1–2 years once the dose of levothyroxine is stabilized.Levothyroxine replacement in ischaemic heart disease:In patients with known ischaemic heart disease, thyroid hormone replacement should be introduced at low dose (25 mg) and increased very slowly under specialist supervision.Hypothyroidism in pregnancyMost pregnant women with primary hypothyroidism require an increase in the dose of levothyroxine of approximately 25–50 μg daily to maintain normal TSH levels. This may reflect increased metabolism of thyroxine by the placenta and increased serum thyroxinebinding globulin during pregnancy. Inadequate maternal T4 therapy may be associated with impaired cognitive development in an unborn child and so women are usually advised to increase their daily levothyroxine dose by 25 μg when pregnancy is confirmed. Serum TSH and free T4 should be measured during each trimester and the dose of levothyroxine adjusted to maintain a normal TSH.Myxoedema com:This is a very rare presentation of hypothyroidism in which there is a depressed level of consciousness, usually in an elderly patient who appears myxoedematous. Body temperature may be as low as 25°C, convulsions are not uncommon and cerebrospinal fluid (CSF) pressure and protein content are raised. The mortality rate is 50%.Myxoedema coma is a medical emergency and treatment must begin before biochemical confirmation of the diagnosis. Suspected cases should be treated with an intravenous injection of 20 μg triiodothyronine, followed by further injections of 20 μg 3 times daily until there is sustained clinical improvement. In survivors, there is a rise in body temperature within 24 hours and, after 48–72 hours, it is usually possible to switch patients to oral levothyroxine in a dose of 50 μg daily. Unless it is apparent that the patient has primary hypothyroidism, the thyroid failure should also be assumed to be secondary to hypothalamic or pituitary disease and treatment given with hydrocortisone 100 mg IM 3 times daily, pending the results of T4, TSH and cortisol measurement (p. 787). Other measures include slow rewarming, cautious use of intravenous fluids, broad-spectrum antibiotics and high-flow oxygen. Occasionally, assisted ventilation may be necessary.Asymptomatic abnormal thyroid function tests:One of the most common problems in medical practice is how to manage patients with abnormal thyroid function tests who have no obvious signs or symptoms of thyroid disease. These can be divided into three categories.Subclinical thyrotoxicosis:Serum TSH is undetectable, and serum T3 and T4 are at the upper end of the reference range. This combination is most often found in older patients with multinodular goitre. These patients are at increased risk of atrial fibrillation and osteoporosis, and hence the consensus view is that they have mild thyrotoxicosis and require therapy, usually with 131I.Subclinical hypothyroidismSerum TSH is raised, and serum T3 and T4 concentrations are at the lower end of the reference range. This may persist for many years, although there is a risk of progression to overt thyroid failure, particularly if antibodies to thyroid peroxidase are present or if the TSH rises above 10 mU/L. In patients with non-specific symptoms, a trial of levothyroxine therapy may be appropriate. In those with positive autoantibodies or TSH greater than 10 mU/L. Levothyroxine should be given in a dose sufficient to restore the serum TSH concentration to normal.Non-thyroidal illness (‘sick euthyroidism’)This typically presents with a low serum TSH, raised T4 and normal or low T3, in a patient with systemic illness who does not have clinical evidence of thyroid disease. These abnormalities are caused by decreased peripheral conversion of T4 to T3, altered levels of binding proteins and their affinity for thyroid hormones, and often reduced secretion of TSH. As thyroid function tests are difficult to interpret in patients with non-thyroidal illness, it is wise to avoid performing thyroid function tests unless there is clinical evidence of concomitant thyroid disease.With best wishes ................
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