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Lecture 4-disorders of thyroid function

Lecture 4-disorders of thyroid function

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02/01/2013

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DISORDERS OF THYROID FUNCTIONHYPERTHYROIDISM
Hyperthyroidism is a condition in which there are increased levels of thyroidhormones in the blood and one for which surgical correction is frequentlyappropriate.
Causes of thyrotoxicosis
Common causes:- diffuse toxic goiter (Grave’s disease)- toxic multinodular goiter (Plummer’s disease- toxic solitary nodule- nodular goiter with hyperthyroidism due to exogenous iodine.- exogenous thyroid hormone excess- thyroiditisRare causes:- metastatic thyroid carcinoma- pituitary tumour secreting TSH
Grave’s disease (Basedow’s disease)
It is the most common cause of hyperthyroidism, it is an immunologicaldisorder in which thyroid stimulating antibodies of the Ig G type bind to theTSH receptor and stimulate the thyroid cells to produce and secrete an excess of thyroid hormones.The thyroid gland hypertrophies producing diffuse enlargement.Most of the symptoms and signs of thyrotoxicosis result from excess thyroidhormones, stimulating metabolism, heat production and oxygen consumption.It is especially common in young women between 20 and 40 years of age.Ophthalmopathy has two major components:1- non infiltrating ophthalmopathy resulting from sympathetic activity leadingto upper lid retraction, a stare and infrequent blinking.2- infiltrating ophthalmopathy causing oedema of the orbital contents, lids and periorbital tissues, cellular infiltration and deposition of mucopolysaccharidematerial within the orbit.Diplopia results from weakening and paralysis of the external ocular muscles.The cornea is vulnerable to damage and ulceration may occur.Investigations:- measurement of free T4, T3, TSH will confirm the diagnosis.- a radioactive iodine or technetium scan is not essential in patients with
 
2Grave’s disease although it is necessary in the assessment of toxic solitary andmultinodular goiter to determine the site of nodular overactivity.- radioactive iodine uptake studies are particularly appropriate revealing anincreased uptake.- chest X ray- position of trachea- laryngoscopy- mobility of the vocal cords preoperatively- ecg- cardiac activity.
Treatment
In Graves’s disease three treatment modalities can be used either alone or incombination to restore the euthyroid state:- antithyroid drugs- radioactive iodine- surgery
Antithyroid drugs
These drugs interfere with the thyroid hormones synthesis.Medical treatment with antithyroid drugs has two principal roles:- treatment of newly diagnosed patients with Grave’s disease in the hopeof inducing a permanent remission- render the toxic patient euthyroid in preparation for surgery.
Beta-adrenergic blockers
Many of the manifestations of hyperthyroidism, particularly those relating to thecardiovascular system, can be ameliorated by the administration of beta- blockers such as metoprolol.Beta-blockers are usually used in combination with one of antithyroid drugs in patients who are severely toxic and in those patients being prepared for surgery.
Radioactive iodine
I
131
used to control thyrotoxicosis achieves its effect by destruction of overactive thyroid tissue.There would appear to be no adverse effects of I
131
treatment with respect toleukemia, thyroid carcinoma, fetal damage or genetic mutation.An ablative dose will render more than 60% of patients hypothyroid in one year.Regular long-term surveillance is required and thyroxine replacement given asnecessary.
Surgery
Thyroidectomy in patients with Graves’s disease is safe and rapidly renders the patient euthyroid. The principal indications for surgery are:- relapse after an adequate course of antithyroid drugs- severe thyrotoxicosis with a large goiter 
 
3- difficulty in controlling toxicity with antithyroid drugsThe surgical procedure: bilateral subtotal thyroidectomy leaving a posterior remnant of thyroid tissue on each side of the trachea or total thyroidectomy.
Toxic multinodular goitre
Antithyroid drugs are of no value as a long-term treatment because thyrotoxicityis due to autonomy and will recur once any medication is discontinued.I
131
can be used for small goitres but usually a subtotal thyroidectomy is mostappropriate after achievement of the euthyroid state or total thyroidectomy.
Toxic solitary nodule
This condition caused by a single autonomous thyroid can be treated by either aunilateral thyroid lobectomy or I
131
Follow-up
Because of the risk of developing postoperative hypothyroidism patients whohave undergone any form of treatment for hyperthyroidism must be followed ona long-term basis with regular clinical and biochemical assessment.
Preparation for surgery
Classically the patient comes to surgery in the euthyroid state, controlled by a period of antithyroid drug therapy. Because the antithyroid drugs block thesynthesis of thyroxine but do not inhibit the release of the hormone fromexisting colloid stores the time required for symptomatic improvement mayvary widely from two weeks to as long as three months.There has been a lot of interest in carrying out the operation of thyroidectomyfor thyrotoxicosis in patients prepared for operation by beta-adrenergic blockade with metoprolol. When the patient has become euthyroid, iodinegiven as Lugol’s solution is administered for ten days before surgery for thegood reason to induce a firmity of the gland and reduce the hemorrhagic risk atoperation.The operation is often made easier by avoidance of antithyroid drugs which areto a degree goitrogenic. Beta-blockers may be reduced after surgery anddiscontinued by 7 days after operation.
Postoperative complications
1. Postoperative bleedingThere is always a risk of postoperative bleeding after thyroid surgery.It is rare but sometimes dramatic and fatal. The bleeding may occur in one of two sites:

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