Hyperthyroidism: Clinical
Presentation and Investigation
Hyperthyroidism, also known as thyrotoxicosis, is a common
condition. It most commonly affects young women but can also develop in men and
occur at any age.
Causes
Graves’ disease (autoimmune thyroid disease)
Graves’ disease is the most common cause of
hyperthyroidism, and results from the production of TSH receptor stimulating
antibodies (Figure 10.1a). It typically affects young women and usually follows
a relapsing–remitting course.
Nodular thyroid disease
The second most common cause of hyperthyroidism, which
typically presents at an older age than Graves’ disease, nodular
hyperthyroidism is caused by autonomous secretion of T3 and/ or T4, either from
a solitary toxic nodule or, more commonly, numerous nodules situated within a
multinodular goitre (toxic multinodular goitre; Chapter 14).
Thyroiditis
This is less common, and refers to inflammation of the
thyroid gland causing a destructive release of thyroxine. Thyroiditis is caused
by viral infection, medication (commonly amiodarone) or follows childbirth
(post-partum thyroiditis). A hypothyroid phase may follow the initial
hyperthyroidism.
Clinical presentation
Symptoms
Hyperthyroidism manifests with a range of symptoms caused
by increased activation of the sympathetic nervous system (Figure 10.1b).
Classic features include weight loss (often with increased appetite), insomnia
and irritability, anxiety, heat intolerance, palpitations and resting tremor.
Other common symptoms of hyperthyroidism include pruritus, increased bowel
frequency and loose motions, menstrual disturbance and reduced fertility.
Elderly patients can present atypically with reduced energy
levels (termed apathetic thyrotoxicosis). Hyperthyroidism is less common in
children than adults. Patients can present with classic symptoms, or with
accelerated growth and behavioural disturbance.
Signs
General signs of hyperthyroidism include a resting
tachycardia (sinus rhythm or atrial fibrillation), warm peripheries, resting
tremor, hyper-reflexia and lid lag. Lid lag can be seen in any cause of
hyperthyroidism, because of increased sympathetic tone of the upper eyelid. Lid
retraction and proptosis are only seen in Graves’ disease. Patients may have a
hyperdynamic circulation, causing hypertension and a flow murmur. Patients with
hyperthyroidism often appear agitated and hyperkinetic (‘thyroid affect’).
Graves’ disease
Specific clinical signs of Graves’ disease include thyroid
eye disease (Chapter 11), and rarer extra-thyroidal manifestations, including
skin changes (dermopathy) characterised by pre-tibial myxoedema as well as nail
changes similar to clubbing (thyroid acropachy). These are a result of
cross-reactivity with TSH receptors in the back of the orbit and skin.
Goitre
Goitre refers to enlargement of the thyroid gland (Chapter
14). Goitres in Graves’ disease are typically smooth, symmetrical and vascular,
often withathrill andbruit onpalpation andauscultation. Nodular goitres are
less vascular, and dominant nodules may be clinically palpable. Nodules can be
single or multiple.
Thyroid disease and the heart
Hyperthyroidism can present as an acute cardiovascular
emergency (Figure 10.1c). The most common acute presentation is
supraventricular tachycardia (SVT) or fast atrial fibrillation (AF). Patients
more rarely present with a thyrotoxic cardiomyopathy, which is more common in
Graves’ disease. Thyroid storm is a rare medical emergency that presents with
high output cardiac failure and extreme agitation. It has a high mortality and
requires high dependency care (Chapter 38).
Investigation
T3, T4 and TSH
The hallmark of hyperthyroidism is an elevated free T4
(fT4) and free T3 (fT3) with undetectable TSH (Figure 10.1d). Elevated fT3
alone with suppressed TSH is termed T3 toxicosis. Patients with a normal
fT4/fT3 and suppressed TSH have subclinical hyperthyroidism, suggesting
autonomous thyroid activity. The presence of elevated fT4 and fT3 with
non-suppressed TSH is unusual and requires further investigation.
Thyroid antibodies
Graves’ disease may be clinically obvious on examination,
but can be confirmed by measuring thyroid antibodies. Thyroid peroxidase
antibodies (TPO) are non-specific markers of autoimmune thyroid disease. TSH
receptor stimulating antibodies are more specific and can be helpful in
particular clinical situations such as pregnancy, in addition to supporting a
clinical diagnosis of Graves’ disease.
Imaging
Thyroid ultrasound (US) can help to confirm nodular thyroid
disease but does not assess gland activity. Nuclear imaging (technetium or
iodine uptake isotope scan) helps determine functionality and therefore the
cause of hyperthyroidism. In Graves’ disease there is uniform increase uptake,
whereas in nodular disease there is increased uptake only in the autonomous
nodule(s). In t sent uptake on isotope scan (Figure 10.1e).
