The post Euthyroid Sick Syndrome appeared first on almostadoctor.

Epidemiology

• Affects 2-5% of females and 0.2-03% of men.
• The female : male ratio is 5:1.
• Onset usually occurs between the ages of 20 and 40 in cases of Graves disease, but later in life where the cause is nodular thyroid disease.
• 99% of cases are caused by intrinsic thyroid disease, and less than 1% caused by a primary pituitary problem.
• Grave’s disease accounts for 60-80% of cases of thyrotoxicosis.
• Nodular thyroid disease accounts for most of the rest (20-40%).
• Rarer causes include:
  • Thyroiditis
  • Exogenous thyroid hormone
  • Iodine excess
  • Thyroid carcinoma
  • Mutation of TSH receptor
• Secondary causes:
  • TSH secreting pituitary tumour
  • Thyroid hormone resistance
  • Gonadotrophin-secreting tumours

Grave’s disease

• Grave’s disease is and autoimmune disorder caused by the production of TSH receptor stimulating antibodies.
• These antibodies stimulate the thyroid gland to produce more T3 and T4

Epidemiology

• Can occur at any age
• Peak onset age 40-60
• F:M 5-10 : 1

Aetiology

• Environment triggers include:
  • High iodine intake
  • Stress
  • Smoking
  • Smoking is also a major risk factor in thyroid associated Grave’s opthalmopathy.
• Genetic factors – In monozygotic twins, concordance is 20-50% – so there is some genetic factor involved. In dizygotic twins concordance is 5%. The antibodies are detectable in the blood. The exact cause is unknown, however it is interesting to note that E. Coli and other Gram-negative bacteria contain TSH binding sites. Thus, Grave’s disease may result from some sort of initiating event caused by one of these pathogens in a genetically susceptible individual
  • No specific genes have been identified as being involved
  • Grave’s disease is also closely related to other auto-immune diseases such as myasthaenia gravis, coeliac disease and pernicious anaemia. The disease follows a relapse and remission pattern. Up to 40% of patients may have only a single episode. Many patients eventually become hypothyroid.

Pathology

• There is thyroid hypertrophy and hyperplasia.
• The follicles have a very small colloid, and the follicular cells are columnar.
• There are focal and generalised lymphocytic infiltrates
• Lymph node hyperplasia can occur in the spleen, lymph nodes and thymus.
• The above changes are all reversed by antithyroid drugs.

Clinical features of thyrotoxicosis

These vary depending on the age of the patient and severity of the disease. Occasionally, the symptoms may seem paradoxical, for example:

• 10% of patients may have weight gain
• This is due to the increased appetite caused by the condition, and in 10% of cases the increase in appetite exceeds the effects of increased metabolism.

General features of thyrotoxicosis

• Hyperactivity, irritability, altered mood
• Heat intolerance, sweating
• Palpitations
• Fatigue, weakness
• Weight loss with increased appetite
• Hyper-reflexia
• Diarrhoea, steatorrhea
• Polyuria
• Loss of libido
• Oligomenorrhoea (infrequent periods)
• Menorrhagia (very heavy periods)
• Sinus tachycardia
• Atrial fibrillation (particularly in elderly)
  • Up to 20% of patients
• Fine tremor
• Warm, moist skin
• Goitre
• Diffuse pigmentation
• Palmar erythema
• Muscle weakness and wasting
• Eyelid retraction
• Gynecomastia
• Rarely there may be psychosis
• Periodic paralysis (common in Asian males)
• Impaired consciousness

Thyrotoxic Storm

• Thyrotoxic storm is severe acute presentation of thyrotoxicosis (thyrotoxic crisis). In a similar way to myxedema coma, this often presents as a result of acute illness, and there may not be any previous history of thyrotoxicosis. It has a 20-30% mortality rate. With this there is:
  • A marked fever (>38.5’)
  • Seizures
  • Vomiting
  • Diarrhoea
  • Jaundice
  • Death – can  be caused by arrhythmias, heart failure or hyperthermia.
• Treatment should be started as soon as possible – and patients should be given propanolol, antithyroid drugs, potassium iodide (to reduce vascular flow to the gland) and corticosteroids.

Types of presentation

The “classical” presentation is that of a woman aged 40-60 with a diffuse goitre and thyrotoxicosis. 50% of patients with have thyroid eye disease.

Goitre

• Occurs in almost all presentations of Grave’s disease – in which case it is usually diffuse and symmetrical

The eye signs – Ophthalmopathy

• Occur in 50% of cases of Grave’s disease
• The eye signs only occur in Grave’s disease, and not in other causes of thyrotoxicosis
• Signs include:
  • Eye-lid retraction
  • Periorbital oedema
  • Proptosis

Other signs

• Pretibial myxoedema is a sign appearing on the leg which usually occurs in conjunction with the eye signs.
  • It is a big lumpy fatty looking growth. It can actually occur anywhere on the body.
  • 5% of Grave’s patients will have this.
  • Patients with this sign will always have ophthalmic symptoms and 10-20% will have clubbing. A small to moderate diffuse firm goitre is also present in many Grave’s patients.
  • Other autoimmune conditions may be present in the family. Hyperplasia of lymphoid tissue (such as splenomegaly) is sometimes found accompanying Grave’s disease.

The elderly

Elderly patients typically present with atrial fibrillation and tachycardia with or without other heart signs. Other general signs are often not present. Thyroid function tests are mandatory in any patient with atrial fibrillation.

Children

May frequently present with excessive growth rate and height, along with behavioural problems such as hyperactivity. They are likely to show eight gain rather than weight loss.

Apathetic thyrotoxicosis

This is a condition found in the elderly. There may be very few signs, and what signs there are may mimic that of hypothyroidism, when in actual fact the underlying cause is thyrotoxicosis.

Differential diagnosis

Investigations

Serum TSH will be low, typically <0.05mU/L. Normal levels are 0.4-5 U/L. To confirm diagnosis, you will also need increased levels of T4 / T3.

– T3 in this instance is more sensitive than T4.

TPO and thyroglobulin antibodies are likely to also be present in Grave’s disease. TSH receptor antibodies are not commonly tested but are usually present (in Grave’s disease these will be detectable in 60-90% of cases).

Treatments

• Surgery is rarely used – it is normally only used when there is mechanical obstruction of the trachea from an enlarged thyroid.

Symptomatic Agents

• Tachycardia
• Dysrhythmias
• Tremor
• Agitation

Antithyroid drugs

Radioiodine

• ¹³¹I has a half-life of 8 days; so after 2 months the radiation has disappeared.

Patients with thyroid eye disease are likely to show worse eye symptoms after treatment with radioiodine, and thus they are more likely to be treated with carbimazole.

Surgery – subtotal thyroidectomy

This should only be performed in patients who are already euthyroid. Normal practice prior to surgery, is to stop the treatment 10-14 days before surgery, and give potassium iodide which reduce vascular flow to the gland. Indications for surgery are:

• Patient choice
• Persistent side-effects of drugs
• Poor compliance with drug therapy
• Recurrent hyperthyroidism after drug treatments
• A large goitre which may be causing trouble swallowing

Long-term risks of hyperthyroidism

There is a slightly increased risk of mortality in hyperthyroidism, although death normally occurs within one year of diagnosis, so in the long-term, the increase in mortality is not noticeable. The only major long term risk is increased risk of osteoporosis.

Hyperthyroidism and pregnancy

Carbimazole – easily crosses the placenta, but T4 does not. As a result, and block and replace regimen cannot be used, and so to treat this condition during pregnancy, the smallest possible use of carbimazole should be used, and the foetus should be monitored.

It has also been associated with birth defects, especially when given in the first trimester.

As a result, propylthiouracil is preferred in the first trimester, and patient care often switched to carbimazole in the second trimester. Up to 30% of women can cease treatment by the third trimester.

The baby should be checked straight after birth, as treatment in this way can cause a goitre.
Assessing the child during pregnancy – if the mother suffers from Grave’s disease, then even if she is made euthyroid by treatment, her foetus may still be hyperthyroid. An easy may to monitor if this is the case is to check the child’s heartbeat – a heart rate of above 160 strongly suggests hyperthyroidism. To compensate for this, the dose of carbimazole given to the mother may be increased, and she may be given T4 (as this does not easily cross the placenta).
Breast feeding whilst on carbimazole or propylthiouracil at normal levels appears to be safe.
Radioactive iodine should definitely not be used.
Surgery may be necessary if it is expected that large doses of carbimazole will be needed to get the patient under control. This is best carried out in the second trimester.
Untreated neonatal hyperthyroidism is associated with hyperactivity in later age.
Thyroid function tests are difficult to interpret fro a neonate as the levels vary greatly. It is best to assess whether the child in hyperthyroid by checking for sings and symptoms.

Other causes of hyperthyroidism

Toxic Multinodular Goitre

Responsible for about 35% of cases of hyperthyroidism. This commonly occurs in older women. It is associated with an increase in iodine intake. This can be a result of dietary increase, but it has been specifically linked with iodine containing agents, such as amiodarone and some types of contrast media. The nodules in this type of goitre are adenomatous. It develops from a simple sporadic goitre. More than 50% of these are due to a genetic mutation involving the TSH receptor, or the protein it produces. Remission can rarely be achieved, and life-long treatment may be required.

• Caused by one or more thyroid nodules
• F > M
• Onset typically at >50 years of age

Pathology

• There is a mixture of relatively normal tissue, and areas of hyperplasia with nodules filled with colloid.
• There will be a varying degree of fibrosis, haemorrhage and calcification.

Toxic solitary adenoma / nodule

Responsible for about 5% of cases of hyperthyroidism It will not usually remit after a course of treatment, but symptoms can be controlled with continual antithyroid drugs.

• F > M
• Onset usually age 30 – 50

Thyroiditis

• An autoimmune disorder whereby the thyroid tissues are destroyed, and the thyroxine contained within the tissue is released
• This causes a brief thyrotoxicosis – often lasting only 1-2 months, and then a hypothyroid period lasting 4-6 months
• In 20% of patients, the hypothyroidism is permanent
• Thyroperoxidase and thyroglobulin antibodies are often present in chronic autoimmune thyroiditis
  • These are present in 90%+ of cases
  • They are also present in about 80% of Grave’s Disease patients
  • TSH receptor stimulating antibodies are usually negative

Flashcard

References

• Murtagh’s General Practice. 6th Ed. (2015) John Murtagh, Jill Rosenblatt
• Evaluating and managing patients with thyrotoxicosis

The post Hyperthyroidism (Thyrotoxicosis) appeared first on almostadoctor.

• Primary disease of the thyroid – In the developed world, this can often be autoimmune thyroid disease (several types of this exist, the most common type is Hashimoto’s thyroiditis).
  • It can can also be due to damage caused by radioiodine that has been used to treat hyperthyroidism.
• In the developing world iodine deficiency is the major cause
• Very occasionally, the disease may be secondary to pituitary or hypothalamic disorders.

• TSH levels are typically used as a screening test for hypothyroidism. If an abnormality is detected, then T4 levels can be used to confirm the diagnosis
• The point where TSH levels are above normal, but T4 remains normal is known as sub-clinical hypothyroidism.
• As the damage continues, TSH levels will rise higher, and free T4 levels will fall.
• Once levels of TSH are greater than 10u/L then symptoms will usually be apparent, and T4 levels will be low. At this stage, we say the patient has overt or clinical hypothyroidism
• There is some debate as to the benefit of treating those with “sub-clinical hypothyroidism” – in symptomatic patients with a high TSH, but normal T4 – a trial of treatment may be suitable

Hypothyroidism is typically treated with a daily dose of thyroxine – 1.6 μg/kg lean body weight daily. This is usually a dose of 100 – 150mcg daily.

• Doses should be titrated up or down by 12.5 – 25mcg per day, every 6-8 weeks according to effect
• TSH is the main marker used to monitor the effectiveness of treatment. T4 levels are only a secondary marker

• If hypothyroidism is diagnosed in pregnancy then specialist management should be sought

Epidemiology

• Prevalence in the UK is about 1% in women, but only 0.1% in men.
• Lifetime risk is actually higher – about 9% for women and 1% for men.
• The mean age of diagnosis is about 60.
• Prevalence of subclinical hypothyroidism is about 7% of women and 3% of men. About 4% of these people will progress to clinical hyperthyroidism annually.
• Congenital hypothyroidism is present in about 1 in 4000 babies, and this has lead to screening programs of neonates.

Normal Thyroid Physiology

The functioning of the thyroid gland is dependent on the hypothalamic-pituitary-thyroid axis. 

• The hypothalamus first releases thyrotropin releasing hormone
• The pituitary produces thyroid stimulating hormone (TSH) in response to this, and in response to feedback loops from T4 and T3
• TSH acts upon the thyroid gland to stimulate it to produce thyroid hormones
  • T4
  • T3 – only about 25% of the circulating T3 is produced by the thyroid gland. The rest is produced in the tissues by converting T4 to T3
  • This is why when we replace thyroid hormone we only need to give T4 – as T3 is subsequently produced by the metabolism of T4 to T3
• These thyroid hormones circulate in the blood, and act on the peripheral tissue to cause a wide variety of effects – mainly related to metabolism
• They also act as a feedback loop to the hypothalamus – which can then adjust the amount of TSH that is produced in response to this
  • Under normal control, the thyroid gland responds to the ‘signal’ of the TSH, to alter its production of T3 and T4 relative to the bodies needs
  • In thyroid disease, the production of T3 and T4 becomes “uncoupled” from the production of TSH
  • In primary hypothyroidism
    • The thyroid gland is unable to produce sufficient amounts of T4 and T3, despite a ‘strong signal” (high TSH) from the pituitary gland.
  • In secondary hypothyroidism
    • Either, insufficient TSH is produced, and thus the thyroid gland does not produce sufficient T3 and T4
    • Or, the thyroid gland has been removed or damaged surgically, or by radiotherapy or another process, and thus is unable to produce sufficient T3 and T4

It is crucial to understand this process to be able to interpret thyroid function test blood results.

Causes

There are several different pathologies that can lead to hypothyroidism, and several ways of classifying these. The simplest method is to separate the causes into autoimmune (Hashimoto’s and atrophic hypothyroidism) and non-autoimmune (everything else!).

• Primary
  • Autoimmune
    • These are by far the most common causes in the developed world
    • Autoimmune lymphocytic thyroiditis of which there are two man types:
    • Hashimoto thyroiditis
    • Atrophic thyroiditis
  • Congenital
  • Defects in hormone synthesis – usually be due to: Iodine deficiency, Antithyroid drugs (e.g. lithium, amiodarone, interferon)
  • Infective
• Secondary
  • Hypopituitarism (which produces isolated TSH deficiency)
  • Post Surgery – Post irradiation (e.g. radioactive iodine therapy, external neck irradiation)
• Other – peripheral resistance to thyroid hormone

Hashimoto’s Thyroiditis

• This is also an autoimmune disease. It was the first ever autoimmune disease to be recognised as such.
• Hashimoto’s disease may initially cause a transient hyperthyroidism which later becomes hypothyroid.
• In this disease, the thyroid is again attacked by T-cells. The main difference between this and atrophic hypothyroidism, is that atrophic hypothyroidism does not cause goitre, but that Hashimoto’s can do. 
• The condition causes an enlarged thyroid (goitre). The enlargement is due to infiltration of the thyroid with lymphocytes, and resultant fibrosis.
  • Goitre is often associated with hyperthyroidism, but in these circumstances, this is not the case.
• The thyroid usually becomes firm and rubbery but this is not always the case – it can be anywhere from soft to hard.
• It is approximately 15x more common in women, and onset occurs usually in middle age (about 50)
• You will find very high levels of TPO antibody in the blood. TPO (Thyroid peroxidase) is the enzyme that ionises iodine to I+, ready for release into the colloid. Without this enzyme, there will not be enough I+ released into the colloid to produce sufficient amounts of T3 and T4. Patients with this condition will often have TPO levels of > 1000 U/L.
• Patients with the condition may be hypothyroid or euthyroid (normal thyroid function). If they are euthyroid, you will only detect the condition with TPO tests and neck examination.
  • Treating patients with positive antibodies who have otherwise normal thyroid function has NOT been proven to be of benefit
• Initially, the disease may cause toxicity (Hashi-toxicity) – which can cause a transient hyperthyroidism – after this the patient may become hypothyroid or euthyroid.
• Pathology There will be massive lymphocytic infiltrate into the thyroid, and there will be varying destruction of tissue. Often there will be no colloid. The remaining cells will have an increased concentration of mitochondria. There will be varying degrees of fibrosis. With thyroxine replacement, the goitre will usually disappear
• Some people argue that Hashimoto’s disease progresses to atrophic hypothyroidism and as such – they may be the same disease. 

• Pernicious anaemia – in this disease, lymphocytes attack the parietal cells of the stomach and destroy them. This results in lack of intrinsic factor being produced, and thus vitamin B12 is not absorbed (in the terminal ileum). This produces a macrocytic anaemia. This skin and mucosa will become pale and the tongue becomes smooth. There may also often be peripheral neuropathy which causes parasthesaie, numbness, and possibly even ataxia. All that you need to keep the patient healthy is a monthly injection of vitamin B12. Before the discovery of B12, this condition was fatal.

Infiltrative

Post-partum thyroiditis

• This is a condition usually seen transiently after pregnancy, and it may involve hypothyroidism, hyperthyroidism or both.
• In pregnancy, hyperthyroidism may occurs because Beta-HCG can act on TSH receptors, producing more thyroid hormone.
• It is thought to arise from modifications to the immune system that occur during pregnancy, and histologically it can be seen as a lymphocytic thyroiditis.
• Often the disease is self-limiting, but in some instances, there may be conventional antibodies present – in which case the disease has a high chance of progressing to permanent hypothyroidism.

Iodine deficiency

• This is particularly common in mountainous areas such as the Alps, Himalayas, south America and Central Africa. In such regions, there may be endemic goitre where large proportions of the population suffer from goitre.
• Patients will either by euthyroid or hypothyroid depending on the severity of the deficiency.
• The goitre is caused by a continuing underlying iodine deficiency, that will ultimately stimulate TSH production, and thus result in thyroid enlargement to compensate for the low levels of iodine.

Congenital Hypothyroidism

• 60% of cases are due to thyroid aplasia or hypoplasia
• 30% of cases are due to ectopic tissue
• 10% of cases are due to dyshormonogenesis. In this condition, there are genetic defects that prevent the proper formation of thyroid hormones. The patients will develop lymphcytosis with goitre. One particular form of the disease is associated with sensori-neuro deafness – Pendred’s Syndrome – in this condition, there is a defect in the chloride / iodide transporter.

Myxoedema

Clinical features

• Autoimmune thyroid disease tends to present slowly over many years and symptoms are often much more vague

• Cold intolerance
• Fatigue
• Tiredness / malaise

• Headache
• Sluggish reflexes
• Parasethesia
• Cerebellar ataxia
• Carpal tunnel syndrome

• Poor appetite – especially when in combination with weight gain
• Constipation

• Poor libido
• Menorrhagia or oligomenorrhoea
• Infertility

Goitre

• This is most common with auto-immune hypothyroidism The goitre will often be firm and nodular raising the suspicion of thyroid malignancy. This should be investigated by biopsy to exclude this possibility. In hashimoto’s disease, goitre may be noticeable before other symptoms. Pain is a rare complication of auto-immune hypothyroidism (i.e. most patients don’t have pain!)

Myxoedema coma

• This is rare. It may present with hypothermia (sometimes as low as 23’C), coma and possibly seizures. Mortality for this presentation is about 50%. Patients are usually old, and there is often an additional condition on presentation such as heart failure, pneumonia, stroke, anaemia.
• Often patients will be undiagnosed (with hypothyroidism), but sometimes it occurs in diagnosed patients who have been un-compliant with treatment

• Children – hypothyroidism is generally rare. They may have retarded growth (both physical and mental) and have an infantile looking face. Puberty may be delayed, and there may also be muscle enlargement.
• Neonates – this is also very rare, and will probably present with failure to thrive, prolonged jaundice, feeding difficulties ad constipation. If left untreated for the first couple of weeks after birth it may cause permanent neurological damage.
• Young women – hypothyroidism should be excluded in all cases of oligomenorrhoea and amenhorroea
• The elderly – may show many signs that are difficult to distinguish from ‘signs of ageing’

Investigations

Thyroid stimulating hormone (TSH) is the main diagnostic test. A high TSH suggests hypothyroidism – the diagnosis is then usually confirmed with a T4 level. Together, TSH and T4 are often referred to as Thyroid function tests (TFTs). 

• TSH raised >10 on two separate occasions = overt hypothyroidism
• TSH >2.5 AND T4 low = overt hypothyroidism
• TSH 2.5 – 10 with normal T4 – subclinical hypothyroidism – see below

Interpreting TFTs is an important clinical skill and takes a little bit of practice.

•  If TSH is normal or low, and T4 is also low, then we can deduce that there is a TSH deficiency (i.e. a hypothalamic/pituitary cause). This is rare.
  • In normal physiology, a low T4, will feedback to the hypothalamus and result in a production of more TSH. So – high TSH alone will confirm a suspected diagnosis of primary hypothyroidism but if you suspect secondary hypothyroidism, then you should check T4 as well – if they are both low, then this will confirm a suspected diagnosis of hypothyroidism. You need a TSH of above 10U/L consistently to be able to diagnose hypothyroidism.
  • After surgery and radiotherapy, TSH and T4 levels may give the impression of hypothyroidism, but this is usually just compensatory, and levels will return to normal after a while.
• Measuring T3 is not very useful as in ¼ of patients T3 levels will be normal anyway due to the fact that T4 is converted to T3 in the bloodstream.
• In suspected cases of myxoedema then you need to start treatment straight away without waiting for confirmation of diagnosis

Additional Investigations

• TPO antibodies – confirm an autoimmune cause
• Cholesterol – patients often have hypercholesterolaemia
• FBC – for anaemia
  • Typically normocytic, although it may be macrocytic when pernicious anaemia is also present, and may even be microcytic in the presence of menorrhagia.
• U+Es – for hyponatraemia
• CK – may be raised – especially in cases which present with myopathy (muscle pain)
• AST levels may be increased due to muscle and liver problems (mainly myopathy

Congenital hypothyroidism

Congenital hypothyroidism is important as failure to treat can lead to permanent neurological deficit. Once the diagnosis is established, you should commence treatment on thyroxine immediately to reduce the risk of permanent neurological deficit. After 3-4 years, you can re-assess the situation to see if life-long thyroxine is necessary. By this age, there will be no permanent neurological consequences of stopping treatment.

Treatment

The only effective treatment is oral T4 – usually referred to as levothyroxine and occasionally thyroxine. 

• Treatment with triiodothyronine (T3) has been used in combination with levothyroxine previously but has not been shown to be of benefit
• It may be considered in specialist cases

Usually treatment is lifelong – except in cases where transient disease is caused by severe illness or drugs.

Principles of treatment

• The aim of treatment is to achieve a T4 level in the normal range AND a TSH level in the normal range
  • The doses is primarily titrated to the TSH level
• The typical dose is 1.6µg/Kg, but the dose should be started low and titrated up to this
  • Typically this means doses are in the 100-200µg per day range
• Initially give 25-50µg, and review after 6 weeks
  • Start at the lower end for frail and elderly patients
• Adjust the dose every 6 weeks so that TSH levels are in the normal range (not suppressed)
  • Low TSH suggests over-replacement of T4 (even if T4 is not elevated) – titrate the dose down until TSH returns to the normal range
  • High TSH suggests under-replacement – increase the dose of levothyroxine
• The half life of T4 is about 7 days, so any change in the dose will not be clinically noticeable for about 4 weeks. You should adjust the dose in 12.5-25µg/day increments. Once you have got the TSH to normal and relieved symptoms, then check every year.
• If levels fluctuate on follow-up it is probably a compliance issue. Because of the long half life of thyroxine, it is safe for patients to take missed tablets at a later time, and you should inform them of this.
• In secondary hypothyroidism the TSH is unreliable, and doses should be titrated to the T4 level
• Advise patients:
  • Treatment is usually lifelong
  • There is an association with other autoimmune diseases, particularly:
    • Pernicious anaemia
    • Addison’s disease
  • About the risk of side effects
    • Typically few, and usually dose related – due to too much thyroxine causing signs of hyperthyroidism:
      • Palpitations and atrial fibrillation
      • Diarrhoea
      • Increase appetite
      • Anxiety
      • Insomnia
      • Tremors

Subclinical hypothyroidism

• Historically, a contentious issue
• Defined as elevated TSH, with normal T4. It is seen in:
  • 4-8% of general population
  • 15% of women over 60
• About 10-15% of these patients will progress to overt hypothyroidism within 12 months
• A Cochrane review suggested no benefit in life-expectancy or other long-term measurable outcomes for cardiovascular health or other consequences of hypothyroidism, but did find an improvement in quality of life in patients treated with levothyroxine
• A practical approach would be to treat:
  • Those with positive TPO antibodies, who are symptomatic with a TSH >5
  • Those with a TSH >10
• Those who do not fit these criteria should be offered TSH testing every 3 years

Pregnancy – in pregnant patients you should increase the thyroxine dose by 25-50µg to ensure normal TSH levels and up until 20 weeks gestation, levees should be checked every 4 weeks. This is particularly important, because babies born in mothers with raised TSH have an increased risk of impaired cognitive function.

Depression – patients with hypothyroidism are at increased risk of depression, but in the elderly patient, sometimes a severe psychosis may develop – often shortly after commencing treatment. This will subside with prolonged treatment. Treatment is lifelong and patients have a normal life-expectancy. Occasionally patients may stop treatment and remain euthyroid.

Indications for specialist involvement

• Patients <18 yo
• Patients not responding to standard therapy
• Hypothyroidism in pregnancy
• Hypothyroidism in the presence of cardiac disease
• Hypothyroidism with goitre, thyroid nodules or other anatomical thyroid abnormalities

Flashcard

References

• NICE guideline: Thyroid disease assessment and management
• Hypothyroidism investigation and management – RACGP
• Murtagh’s General Practice. 6th Ed. (2015) John Murtagh, Jill Rosenblatt
• Oxford Handbook of General Practice. 3rd Ed. (2010) Simon, C., Everitt, H., van Drop, F.

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Goitre refers to an enlarged palpable thyroid gland, which moves on swallowing. It may be a benign disorder but is also associated with several thyroid diseases, including iodine deficiency (common in the developing world, and may or may not cause hypothyroidism), Hashimoto’s thyroiditis (a type of hypothyroidism), as well as some of the causes of hyperthyroidism.

• Best assessed via USS
  • If TSH low, also consider a radionuclide scan
• Not necessarily indicative of disease
• Simple Goitre – typically associated with normal thyroid hormone levels, no treatment necessary
• Multinodular Goitre – progresses with age, secrete autonomously, many nodules can cause hyperthyroidism
• Most common causes;
  • Problems with thyroid function (hypo or hyperthyroidism)
  • Endemic
  • Sporadic non-toxic

• Affects over 200 million people worldwide, caused by iodine deficiency or ‘goitrogens’ (chemicals found in food that exaggerate the effects of iodine deficiency eg. Cassava, selenium, cabbage).
• Usually diffuse goitre, becoming nodular with age, rarely compressing.
• Treated with iodine supplements, iodized salt/water

• 5% population, M:F – 1:4. Incidence declines with age.
• Usually changes from diffuse to multinodular. TSH levels are normal. Nodules from an entire follicle rather than a single cell. Mostly visible, with compression on the neck.
• Should be left alone unless causing pain or significant compression

References

Read more about our sources

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