Hyperthyroidism

Hyperthyroidism

The thyroid gland
Located in the lower front aspect of the neck, anterior to the trachea is the butterfly?shaped thyroid gland. The thyroid has two lobes, connected by the isthmus. When the thyroid is its normal size, it cannot be felt. The gland is brownish?red in colour, and highly vascularized. The laryngeal nerves pass through the thyroid. The thyroid gland and its hormones control the metabolic rate of tissues. It is stimulated and controlled by thyroid stimulating hormone (TSH) from the anterior pituitary. TSH is released by thyrotropin?releasing hormone (TRH) located in the hypothalamus. In response to TSH, the thyroid gland produces thyroxine (T4) and triiodothyronine (T3). There is more T4 produced than T3. T4 is inactive and for activation it needs to be converted to T3; this occurs peripherally (such as in the liver and
kidney). Most of the T3 and T4 in the circulation is bound to
protein (mostly thyroglobulin); it is only the free thyroid hormone
that is active. Free thyroid hormones that are in circulation
act negatively on the hypothalamus and pituitary gland and in so
doing reduce the release of TRH and TSH (see Figure 53.2).
Thyroid hormones act throughout the body, influencing metabolism,
growth and development, and body temperature. During
infancy and childhood, adequate thyroid hormone is essential for
brain development.


Hyperthyroidism
Hyperthyroidism is a set of disorders involving excess synthesis
and secretion of thyroid hormones by the thyroid gland, which
leads to the hypermetabolic condition of thyrotoxicosis. The most
common forms of hyperthyroidism include diffuse toxic goitre
(Graves’ disease), toxic multinodular goitre and toxic adenoma.
Hyperthyroidism can be classified as primary or secondary.
Primary hyperthyroidism occurs when the pathology is within the
thyroid gland. Secondary hyperthyroidism occurs when the thyroid
gland is stimulated by excessive thyroid?stimulating hormone
(TSH) in the circulation.


Pathophysiology
Risk factors include family history, high iodine intake, smoking,
trauma to the thyroid gland (including surgery), toxic multinodular
goitre (particularly related to an increased intake of iodine as a
result of a change in diet or an acute dose from iodine?containing
agents (amiodarone, contrast agents)), childbirth and highly active
antiretroviral therapy.
Graves’ disease (goitre) is genetic. There is a link with certain
genes, specific gene loci have been identified which are different in
different ethnic groups. An interaction between genetic predisposition
and certain trigger factors is then thought to initiate the disease
process.
An increase in the peripheral circulation of unbound thyroid
hormone (regardless of the process) can cause thyrotoxicosis.
Disturbances of the normal homeostatic mechanism can occur at
the level of the pituitary gland, the thyroid gland or in the periphery.
Regardless of cause, the result is an increase in transcription in
cellular proteins, causing an increase in the basal metabolic rate.
In Graves’ disease, circulating autoantibodies against the thyrotropin
receptor provide continuous stimulation of the thyroid
gland. These antibodies cause release of thyroid hormones and
thyroglobulin; they also stimulate iodine uptake, protein synthesis
as well as thyroid gland growth.


Signs and symptoms
How people present with thyrotoxicosis is variable. Thyrotoxicosis
causes an increase in sympathetic nervous system symptoms.
Those who are younger exhibit symptoms of sympathetic activation,
for example anxiety, hyperactivity and tremor; the older person
may have more cardiovascular symptoms, including dyspnoea
and atrial fibrillation. As the body’s metabolism is increased,
patients often feel hotter than those around them and can slowly
lose weight even though they may be eating more; this is confusing
as sometimes patients gain weight because of an increase in their
appetite. Those with hyperthyroidism usually experience fatigue at
the end of the day, yet they may have trouble sleeping. The person
may become irritable and easily upset. Usually the symptoms of
hyperthyroidism are so gradual in their onset that patients do
not realize the symptoms until they become more severe. The
آ?symptoms may continue for weeks or months before patients fully
grasp that they are sick. In older people, some or all of the typical
آ?symptoms of hyperthyroidism may be absent, and the patient may
just lose weight or become depressed. The clinical manifestations
associated with thyrotoxicosis do not always associate with the
degree of biochemical abnormality.



Investigations
A detailed medical history gleans information, including the extent
and duration of symptoms, past medical history and social and
family history: this, as well as the information gained from physical
examination, helps the clinician arrive at the appropriate diagnosis.
Graves’ disease, for example, is an autoimmune disease and patients
often have a family history or past medical history of autoimmune
disease (rheumatoid arthritis, vitiligo, pernicious anemia).
The family history should include careful documentation of
autoimmune disease, thyroid disease, emigration from iodinedeficient
parts of the world. The nurse should undertake a review
of medications and dietary supplements. A number of compounds,
including expectorants, amiodarone, iodinated contrast dyes and
health food supplements containing seaweed or thyroid gland
extracts contain large amounts of iodine that may induce thyrotoxicosis
in a person with thyroid autonomy.
Thyroid function tests serum TSH can exclude primary thyrotoxicosis;
diagnosis is confirmed with free T4 levels. Autoantibodies
are most commonly seen in Graves’ disease. Thyroid ultrasound
scan and thyroid uptake scans may be used to locate hot (over
activity) and cold (no activity) spots.


Management
Beta blockers can be used for rapid symptom control. Calciumchannel
blockers may be used if patients are intolerant of beta
blockers.
There are three kinds of definitive treatment:
•â•¢ Antithyroid drugs: carbimazole (methimazole) or propylthiouracil
•â•¢ Radio?iodine: increasingly the first?line treatment in teenagers
•â•¢ Surgical: subtotal or near total thyroidectomy
Both surgery and radioiodine require the person to be euthyroid