Hormonal disturbance- Hypothyroid symptoms
Hypothyroidism is the clinical condition resulting from deficiency of thyroid hormones. Myxoedema is severe hypothyroidism with accumulation of mucopolysaccharides in the tissues. It leads to thickening of the facial features and gives a doughy appearance to the skin.
Hypothyroidism is much more common in women, with an incidence of approximately 350 per 100 000 per year, as compared to men who have an incidence of 60 per100 000 per year. The incidence of hypothyroidism increases with age.
Primary hypothyroidism accounts for the vast majority of cases and is diagnosed when the abnormality occurs in the thyroid gland . Destruction of thyroid tissue is often the result of autoimmune thyroiditis (Hashimoto's disease). Thyroid autoantibodies (anti-microsomal, anti-thyroglobulin and anti-peroxidase) are present in the serum, and there is a diffuse lymphocytic infiltrate affecting the thyroid gland. Although there may be a firm goitre initially, the autoimmune destruction subsequently leads to thyroid atrophy. Surgery or radiation to the neck can damage the thyroid gland and cause primary hypothyroidism. Drugs such as amiodarone, lithium and iodine can also interfere with thyroid function.
Transient inflammatory conditions such as subacute (de Quervain's) thyroiditis and lymphocytic thyroiditis can initially cause thyrotoxicosis, which then progresses to hypothyroidism. Subacute thyroiditis is thought to have a viral trigger, while lymphocytic thyroiditis is seen in post-partum women. The hypothyroidism is temporary in both instances, and resolves within 8 weeks.
Rarely, hypothyroidism can occur secondary to pituitary or hypothalamic tumours that disrupt the release of thyroid-stimulating hormone.
Scope of disease
The severity of hypothyroidism varies from subclinical (detected only by laboratory testing) to clinically overt. Patients with subclinical or compensated hypothyroidism have levels of thyroid-stimulating hormone above the reference range but normal thyroxine levels and no major signs or symptoms of thyroid disease. In contrast, patients with severe disease may present with myxoedema coma, psychosis, heart failure, hypothermia and hypoglycaemia. Untreated hypothyroidism in children leads to cretinism (mental retardation, deafness, short stature and facial deformities).
Hypothyroidism leads to a general slowing down of the body's physiological processes. Early symptoms are insidious and non-specific, which includes tiredness, weight gain , cold intolerance, constipation, angina, sinus bradycardia, ankle swelling,slowing of mental process, memory impairment,sleepiness, slow relaxing ankle reflex,skin thickening, hair loss, dry hair and skin, periorbital puffiness, hypercholesterolaemia,hyponatremia, macrocytic anaemia,raised creatine kinase. Patients with long-standing disease may have characteristic facies . It is occasionally difficult to diagnose hypothyroidism with confidence on clinical grounds alone.
The most important diagnostic test is the measurement of serum TSH. Elevated TSH levels are a simple and specific method of diagnosing primary hypothyroidism.
Patients with critical illness from non-thyroid causes may experience derangements in thyroid function, and the test results may be difficult to interpret. In such situations, thyroid testing should be delayed until patient recovery, unless there is substantial clinical suspicion of hypothyroidism.
Thyroid-stimulating hormone and free T4
Patients with suspected secondary hypothyroidism should have both the TSH and the serum thyroxine levels measured. Low thyroxine levels without marked TSH elevation are supportive of this diagnosis, and require further investigations including pituitary function tests and imaging.
Measurement of thyroid autoantibodies is not essential but can be used to confirm the aetiology of hypothyroidism if the diagnosis is not clear from the history and clinical examination.
Thyroid hormone deficiency can be treated by a number of synthetic preparations. The most commonly used are those of l-thyroxine (T4). The average maintenance dose ranges from 75 μg to 200 μg. Treatment should usually be started with 50 μg, except for elderly patients and those with heart disease whose dose should be slowly titrated upwards from an initial 25 μg.
TSH should be monitored at 6-8-weekly intervals to guide dosing, with a target TSH level of about 1.0 mU/L. Patients who are stable need monitoring only once a year. Thyroxine replacement therapy has a narrow therapeutic index and excessive doses can bring on symptoms of thyrotoxicosis such as angina and atrial arrhythmias.
Currently, there is no consensus on the management of patients with subclinical hypothyroidism as it is uncertain whether early therapy will improve the long-term outlook of asymptomatic patients.
Intravenous liothyronine and hydrocortisone
Myxoedema coma is treated with intravenous liothyronine (T3) 5-20 μg twice daily because liothyronine has a more rapid onset of action. In addition to this, hydrocortisone 100 mg is given intravenously prior to thyroxine therapy (to minimize the risk of acute adrenocortical deficiency induced by thyroxine under these specific circumstances) as it is not possible to rule out secondary hypothyroidism and pituitary failure as a cause of the coma. Supportive care has an important role in the management of myxoedema coma and the patient may need to be treated in the intensive care setting if he or she has respiratory or cardiac failure.
Subclinical hypothyroidism is associated with normal survival in elderly patients. The mortality of patients with myxoedema coma is up to 30%.
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