Hyperthyroidism Clinical Presentation and Investigation - pediagenosis
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Thursday, June 11, 2020

Hyperthyroidism Clinical Presentation and Investigation

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.

Hyperthyroidism Clinical Presentation and Investigation

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).
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
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.
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 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).

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.
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).

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