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HOPC: Mr. Brix has noted over the last 6 months that he lacks energy and he has lost about
10 kg despite quite normal appetite. He admits to have occasional palpitations which he
thought was due to drinking coffee at work. He also has sometimes a bit of shaking of his
summer weather anymore.
FHx.: Both parents died in their early 50ies in a car crash. He knows that his mother had a
problem with her thyroid gland but he cant remember what it was.
PHx.: unremarkable
SHx.: married structural engineer, two children age 15 and 12, smokes 12 cig. per day, drinks
alchol socially, NKA, no medication, no recreational drugs.
EXAMINATION: thin looking man (BMI 19) with exophthalmus (staring gaze with lid
retraction and proptosis / protrusion of the eyes).
BP 148/76, P 125, irregular, afebrile, RR 18/min., SaO2 98% on RA.
There is a smooth, enlarged, non tender, symmetrical thyroid gland visible and palpable with
a bruit present. His skin is warm and he has moist palms.
DIAGNOSIS: HYPERTHYROIDISM SECONDARY TO GRAVES DISEASE!
The thyroid gland produces the iodine-containing hormones thyroxine (tetraiodothyronine,
T4) and thriiodothyronine (T3). They are incorporatee in the protein thyroglobulin which is
stored in the thyroid follicles and are released into the circulation after proteolysis.
Production of the hormones depends on the utilisation of adequate amounts of iodine.
Thyroid hormones influence growth and metabolism! Therefore, thyroid disorders are usually
characterised by over- or underporduction of these hormones, are more common in women
and may be classified as:
1. Hypothyroidism
2. Hyperthyroidism (toxic diffuse goiter, Graves disease, Basedows disease, toxic nodular
goiter, Plummers disease)
3. Non-toxic goiter
4. Thyroiditis
5. Thyroid neoplasm
Adequate amounts of thyroid hormone are maintained in the blood by a negative feedback
mechanism which operates through the hypothalamus and the anterior pituitary
(adenohypophysis) in accordance with the metabolic needs fo the body. Secretion of hormone
form the thyroid depends on the amount of circulating thyroid stimulating hormone (TSH),
also known as thyrotropin, released from the adenohypophysis. The level of TSH depends on
the amount of thyrotropin releasing hormone (TRH), also called thyrotropin-releasing factor
(TFR), and on the level of thyroid hormone found in the hypophyseoprtal circulation. Since
increased amounts of thyroid hormone suppress TSH release, a negative feedback mechanism
is thus established, maintaining a steady state of thyroid secretory activity.
GRAVES DISEASE: an autoimmune condition chracterised by diffuse hyperplasia of the
thyroid parenchyma, excessive secretion of its hormones and increased metabolic rate. The
cause is unknown, but the condition is often familial. The disease may follow emotional or
physical stress. It may also occur because of increased iodides (Jod-Basedow phenomenon). I
may be due to production of long-acting thyroid stimulator hormone (LATS) IgG.
Graves disease is marked by goiter, exophthalmus, tachycardia and pretibial myxoedema!
MANAGEMENT:
1. Antithyroid drugs (propylthiouracil, carbimazole and methimazole)
2. Beta-blockers to block some of the peripheral effects of the excessive thyroxine
3. RADIO ACTIVE IODINE which destroys the thyroid gland (cave! Hypothyroidism!),
although not in pregnant or breastfeeding women and children!
4. Surgical removal of the thyroid gland, usually only for large goiters or airway
compromise