Thyroid Disorders Flashcards
Hypothyroidism - Causes
Hypothyroidism: causes
Hypothyroidism affects around 1-2% of women in the UK and is around 5-10 times more common in females than males.
Primary hypothyroidism:
1) Hashimoto’s thyroiditis
- most common cause
- autoimmune disease, associated with IDDM, Addison’s or pernicious anaemia
- may cause transient thyrotoxicosis in the acute phase
- 5-10 times more common in women
2) Subacute thyroiditis (de Quervain’s)
3) Riedel thyroiditis
4) After thyroidectomy or radioiodine treatment
5) Drug therapy (e.g. lithium, amiodarone or anti-thyroid drugs such as carbimazole)
6) Dietary iodine deficiency
Secondary hypothyroidism (rare):
1) From pituitary failure
2) Other associated conditions
Down’s syndrome
Turner’s syndrome
coeliac disease
Thyroid Eye Disease
Thyroid eye disease
Thyroid eye disease affects between 25-50% of patients with Graves’ disease.
Pathophysiology
it is thought to be caused by an autoimmune response against an autoantigen, possibly the TSH receptor → retro-orbital inflammation
the inflammation results in glycosaminoglycan and collagen deposition in the muscles
Prevention
smoking is the most important modifiable risk factor for the development of thyroid eye disease
radioiodine treatment may increase the inflammatory symptoms seen in thyroid eye disease. In a recent study of patients with Graves’ disease around 15% developed, or had worsening of, eye disease. Prednisolone may help reduce the risk
Features
the patient may be eu-, hypo- or hyperthyroid at the time of presentation
exophthalmos
conjunctival oedema
optic disc swelling
ophthalmoplegia
inability to close the eye lids may lead to sore, dry eyes. If severe and untreated patients can be at risk of exposure keratopathy
Management topical lubricants may be needed to help prevent corneal inflammation caused by exposure steroids radiotherapy surgery
IV methylprednisolone is the treatment of choice for moderately severe active Graves’ ophthalmopathy. IV steroids have fewer side effects than oral steroids. If symptoms or vision do not improve then urgent surgical decompression should be considered.
Artificial tear drops are useful for symptomatic relief.
Total thyroidectomy has shown no benefit in the treatment of thyroid eye disease.
Outcomes have been shown to be worse in those patients who smoke, therefore smoking cessation advice should be given.
Monitoring patients with established thyroid eye disease
For patients with established thyroid eye disease the following symptoms/signs should indicate the need for urgent review by an ophthalmologist (see EUGOGO guidelines):
unexplained deterioration in vision
awareness of change in intensity or quality of colour vision in one or both eyes
history of eye suddenly ‘popping out’ (globe subluxation)
obvious corneal opacity
cornea still visible when the eyelids are closed
disc swelling
Thyroid Eye Disease - Example Question
A 24-year-old female presents with one week of progressive and persistent double vision. She reports increasing tiredness at all times of day over the past 2 months and occasional chest tightness associated with palpitations. She has no past medical history. She was also adopted and unaware of any family history. On examination, you find a loss of left eye abduction, right eye upwards gaze, right eye adduction. Systemic examination also reveals bilateral clammy hands and a heart rate of 120 per minute, irregular. Which test is most likely to be diagnostic?
Autoimmune screen > Thyroid function tests CT thorax Anti-acetylcholine receptor antibodies 12 lead ECG
This patient presents with systemic symptoms and a complex ophthalmoplegia, the diagnosis of thyroid eye disease, secondary to Graves disease, is most likely. The important test would be thyroid function tests and also MRI of her orbits, which would almost certainly demonstrate retro-orbital and extraocular muscle inflammation. The severity of the patient’s eye disease needs to be assessed: the most frequently used criteria was developed by the American thyroid association, which spells out helpfully NO SPECS
Class 0 No symptoms or signs
Class I Only signs, no symptoms (lid retraction, stare, lid lag)
Class II Soft tissue involvement
Class III Proptosis
Class IV Extraocular muscle involvement
Class V Corneal involvement
Class VI Sight loss (optic nerve involvement)
Any patient presenting with eye movement weaknesses that cannot be explained by isolated or multiple cranial nerve palsies is called complex ophthalmoplegia. The differentials include myasthenia gravis, mononeuritis multiplex, thyroid eye disease, Kearns-Sayre syndrome, complex progressive external ophthalmoplegia, Miller-Fisher syndrome and botulinum poisoning.
Hypothyroidism - Mx : Key Points
Key points
initial starting dose of levothyroxine should be lower in elderly patients and those with ischaemic heart disease. The BNF recommends that for patients with cardiac disease, severe hypothyroidism or patients over 50 years the initial starting dose should be 25mcg od with dose slowly titrated. Other patients should be started on a dose of 50-100mcg od
following a change in thyroxine dose thyroid function tests should be checked after 8-12 weeks
the therapeutic goal is ‘normalisation’ of the thyroid stimulating hormone (TSH) level. As the majority of unaffected people have a TSH value 0.5-2.5 mU/l it is now thought preferable to aim for a TSH in this range
women with established hypothyroidism who become pregnant should have their dose increased ‘by at least 25-50 micrograms levothyroxine’* due to the increased demands of pregnancy. The TSH should be monitored carefully, aiming for a low-normal value
there is no evidence to support combination therapy with levothyroxine and liothyronine
SE of Thyroxine Therapy
Side-effects of thyroxine therapy hyperthyroidism: due to over treatment reduced bone mineral density worsening of angina atrial fibrillation
Thyroxine - Interactions
Interactions
iron: absorption of levothyroxine reduced, give at least 2 hours apart
Hypothyroidism Mx - Example Question
A 29-year-old woman presentsis referred to the Endocrinology clinic as she has just found out she is pregnant. She was diagnosed with hypothyroidism three years ago and is currently stable on a dose of levothyroxine 75mcg od. She has also been taking folic acid 400mcg od for the past 6 months. Her last bloods taken 6 months ago show the following:
TSH 1.4 mU/l
You request a repeat TSH and free T4 measurement. What is the most appropriate next step?
Decrease levothyroxine to 50mcg od Keep levothyroxine at 75mcg od > Increase levothyroxine to 100mcg od Keep levothyroxine at 75mcg od + increase folic acid to 5mg od Stop levothyroxine until TSH known Female with hypothyroidism → immediately increase levothyroxine and monitor TSH closely
Thyrotoxicosis
Thyrotoxicosis
Graves’ disease accounts for around 50-60% of cases of thyrotoxicosis.
Causes
Graves’ disease
toxic nodular goitre
acute phase of subacute (de Quervain’s) thyroiditis
acute phase of post-partum thyroiditis
acute phase of Hashimoto’s thyroiditis (later results in hypothyroidism)
amiodarone therapy
Investigation
TSH down, T4 and T3 up
thyroid autoantibodies
other investigations are not routinely done but includes isotope scanning
Thyrotoxicosis - Example Question
A 42 year-old man presents to his GP with a 3 month history of increasing anxiety. On further questioning, he has lost 6 kg of weight over the past 2 months and has been experiencing increased bowel movements and diarrhoea.
Blood tests are performed and reveal:
Hb 14.2 g/dL
Platelets 210 * 109/l
WBC 6.9 * 109/l
Thyroid stimulating hormone (TSH) 0.08 mu/l
Free thyroxine (T4) 17.4 pmol/l
Total triiodothyronine (T3) 13.4 nmol/l Normal range (4.0-8.3 nmol/l)
What is the most appropriate treatment?
Reassurance > Carbimazole Radio-iodine Surgery Propranolol
The diagnosis in this scenario is triiodothyronine thyrotoxicosis. A small subset of those patients experiencing thyrotoxicosis (roughly 5%) have isolated triiodothyronine thyrotoxicosis. As with other types of thyrotoxicosis, carbimazole is the main initial treatment for the condition.
Sick Euthyroid Syndrome
Sick euthyroid syndrome
In sick euthyroid syndrome (now referred to as non-thyroidal illness) it is often said that everything (TSH, thyroxine and T3) is low. In the majority of cases however the TSH level is within the normal range (inappropriately normal given the low thyroxine and T3).
Changes are reversible upon recovery from the systemic illness.
Sick Euthyroid Syndrome - Example Question
A 76 year old woman was admitted to hospital after presenting to the Emergency Department with shortness of breath, productive cough and palpitations. A chest x-ray demonstrated a left lower lobe pneumonia and ECG showed atrial fibrillation with a fast ventricular response. Initial management included intravenous antibiotics, intravenous fluids and oral digoxin loading.
Two days after admission, the patient’s condition had significantly improved and she was able to start mobilising on the ward. The palpitations that she had been experiencing at presentation had also ceased. Following review by the Senior House Officer on the ward round, a repeat ECG was requested when demonstrated that the patient had cardioverted back to sinus rhythm. Digoxin therapy was subsequently held.
To investigate for an underlying cause of atrial fibrillation, thyroid function tests were added to blood tests from admission, with results as listed below.
Haemoglobin 125 g / dL White cell count 13.7* 109/l Neutrophils 11.9* 109/l Platelets 351 * 109/l Urea 4.6 mmol / L Creatinine 130 micromol / L Sodium 139 mmol / L Potassium 3.6 mmol / L C-reactive protein 105 mg / L Thyroid stimulating hormone 0.25 microU / L T4 free serum 14.1 pmol / L T3 free serum 7.4 pmol / L
What is the most appropriate next investigation to assess deranged thyroid function tests?
Thyroid ultrasound Thyroid peroxidase antibody levels > Repeat TFT in 6 weeks Thyroid scintiscanning Thyroglobulin antibody levels
Any acute and severe illness may alter thyroid hormone deiodination through the effects of cytokines and result in various changes in levels of TSH, fT3 and fT4. Low TSH levels in hospitalised patients are three times more likely to be due to this effect than to hyperthyroidism.
It is therefore best to avoid thyroid function testing around the time of an acute illness unless there is good clinical evidence of a primary thyroid illness. If TFT remain deranged following recovery from acute illness then further investigation to assess for thyroid disease can be considered.
Amiodarone and The Thyroid Gland
Amiodarone and the thyroid gland
Around 1 in 6 patients taking amiodarone develop thyroid dysfunction
Amiodarone-induced hypothyroidism
The pathophysiology of amiodarone-induced hypothyroidism (AIH) is thought to be due to the high iodine content of amiodarone causing a Wolff-Chaikoff effect*
Amiodarone may be continued if this is desirable
Amiodarone-induced thyrotoxicosis
Amiodarone-induced thyrotoxicosis (AIT) may be divided into two types:
AIT type 1
Pathophysiology = Excess iodine-induced thyroid hormone synthesis
Goitre = Present
Management = Carbimazole or potassium perchlorate
AIT Type 2
Pathophysiology = Amiodarone-related destructive thyroiditis
Goitre = Absent
Management = Corticosteroids
Unlike in AIH, amiodarone should be stopped if possible in patients who develop AIT
*an autoregulatory phenomenon where thyroxine formation is inhibited due to high levels of circulating iodide
Amiodarone and the Thyroid Gland - Example Question
A 64-year-old woman comes to the Emergency department complaining of palpitations at rest, and worsening angina over the past month. She has been treated with amiodarone for the past 3 years for recurrent ventricular tachycardia. She has a blood pressure of 110/70 mmHg, pulse of 95 beats per minute, and a fine tremor. There is no goitre. TSH is suppressed at less than 0.05 U/ml.
You suspect she has amiodarone induced thyrotoxicosis. How best can you determine the underlying pathophysiology?
IL6 level Thyroglobulin level TSH level Duration of amiodarone therapy > Colour flow doppler ultrasonography
Type 1 amiodarone induced thyrotoxicosis is caused by increased production of thyroid hormone, most likely as a result of the excess iodine load administered to the patient as a result of amiodarone treatment. Type 2 amiodarone induced thyrotoxicosis is caused by a destructive thyroiditis. Colour flow doppler ultrasonography needs to be performed by an experienced operator, but is thought to distinguish between the two causes of amiodarone induced thyrotoxicosis around 80% of the time. In patients where the diagnosis is uncertain, radioiodine uptake, (which is low in type 2 disease) my further help differentiating between the two.
Type 2 disease is generally seen later in the time course of amiodarone therapy, although this isn’t an invariable differentiating factor, and data on the usefulness of IL6 and thyroglobulin is conflicting.
TFTs - Thyrotoxicosis (eg Graves)
Thyrotoxicosis (e.g. Graves’ disease)
TSH = Low
Free T4 = High
In T3 thyrotoxicosis the free T4 will be normal
TFTs - Primary Hypothyroidism
Primary hypothyroidism (primary atrophic hypothyroidism) TSH = High Free T4 = Low
TFTs - Secondary Hypothyroidism
Secondary hypothyroidism
TSH = Low
Free T4 = Low
Replacement steroid therapy is required prior to thyroxine
Secondary hypothyroidism is very rare and results in a low TSH and low T4. In these cases, pituitary insufficiency is most likely and therefore an MRI of the gland should be performed.
TFTs - Sick Euthyroid Syndrome
Sick euthyroid syndrome* TSH = Low** T4 = Low Common in hospital inpatients T3 is particularly low in these patients
- now referred to as non-thyroidal illness
- *TSH may be normal in some cases
TFTs - Subclinical Hypothyroidism
Subclinical hypothyroidism
TSH = High
Free T4 = Normal
TFTs - Poor Compliance with Thyroxine
Poor compliance with thyroxine
TSH = High
Free T4 = Normal
TFTs - Steroid Therapy
Steroid therapy
TSH = Low
Free T4 = Normal
Toxic Goitre - Example Question
A 55-year-old female has noticed an enlarging neck lump and comes for review with you. Her TSH is low. Apart from the large goitre, there were no other significant findings on physical examination. What is the best next test to performed?
Anti-TSH antibodies Thyroid US > Thyroid Technetium scan Thyroid nodule biopsy Thyroidectomy
The underlying diagnosis is that of a toxic-goitre (low TSH) due to a toxic adenoma. The concern is always that the goitre may be carcinogenic. To rule carcinogenesis out a thyroid technetium scan can be done. If the technetium scan shows a ‘hot’ nodule, then cancer can be ruled out because it is exceedingly rare that a hot nodule is cancer. Thus an over functioning thyroid nodule is diagnosed.
A toxic adenoma occurs due to somatic mutations of the TSH receptor gene that confers autonomous hyperactivity to that thyroid tissue. It responds will to radioiodine ablation or surgical removal
Thyroid Storm
Thyroid storm
Thyroid storm is a rare but life-threatening complication of thyrotoxicosis. It is typically seen in patients with established thyrotoxicosis and is rarely seen as the presenting feature. Iatrogenic thyroxine excess does not usually result in thyroid storm
Clinical features include: fever > 38.5ºC tachycardia confusion and agitation nausea and vomiting hypertension heart failure abnormal liver function test
Thyroid Storm - Mx
Management
symptomatic treatment e.g. paracetamol
treatment of underlying precipitating event
propranolol
anti-thyroid drugs: e.g. carbimazole/ methimazole or propylthiouracil
Lugol’s iodine
dexamethasone - e.g. 4mg IV qds - blocks the conversion of T4 to T3
Thyroid Storm - First Line Treatment
First line treatment for this medical emergency is carbimazole, corticosteroids and propranolol, although chlorpromazine can be added for severe anxiety.
Thyroid Storm - Example Question
A 52 year-old woman presents with a two day history of nausea and fever. On admission she is confused and her husband states that she was recovering from a recent upper respiratory tract infection and sore throat. He also mentions she has previously been experiencing episodes of diarrhoea and palpitations over the last three months.
Examination reveals a temperature of 40.6ºC, pulse rate of 160 beats per minute and blood pressure of 110/70 mmHg. Her pulse is irregularly irregular. Heart sounds 1 and 2 are present with no added sounds, lung fields are clear and her abdomen is soft and none tender, with bowel sounds being present.
Blood tests are taken and reveal:
Hb 13.2 g/dL Platelets 180 * 109/l WBC 10.2 * 109/l Na+ 135 mmol/l K+ 4.2 mmol/l Urea 7.2 mmol/l Creatinine 132 µmol/l Thyroid stimulating hormone (TSH) 0.03 mu/l Free thyroxine (T4) 31 pmol/l Total thyroxine (T4) 220 nmol/l
What is the most appropriate immediate treatment?
> Carbimazole, corticosteroids and propranolol Carbimazole and propranolol Radio-iodine, corticosteroids and propranolol Carbimazole and corticosteroids Propylthiouracil, propranolol and carbimazole
This patient is having a thyrotoxic storm (hyperthyroid crisis) a rare medical emergency that is caused by an exacerbation of hyperthyroidism and characterised by decompensation of one or more organ systems in people with untreated or poorly treated hyperthyroidism. The precipitating cause is most commonly infection, as with this case, although it is important to check for other causes. The patient above is in atrial fibrillation and shows signs of renal impairment due to dehydration. First line treatment for this medical emergency is carbimazole, corticosteroids and propranolol, although chlorpromazine can be added for severe anxiety.
Post Partum Thyroiditis
Post-partum thyroiditis
Three stages
•1. Thyrotoxicosis
•2. Hypothyroidism
•3. Normal thyroid function (but high recurrence rate in future pregnancies)
Thyroid peroxidase antibodies are found in 90% of patients
Management
•the thyrotoxic phase is not usually treated with anti-thyroid drugs as the thyroid is not overactive. Propranolol is typically used for symptom control
•the hypothyroid phase is usually treated with thyroxine
Post-partum Thyroiditis - Example Question
A 34-year-old woman is referred to endocrinology clinic for assessment after reporting symptoms of heat intolerance, tremors and diarrhoea to her General Practitioner. Blood tests in primary care showed evidence of thyrotoxicosis. Further assessment at clinic revealed the symptoms had been present for approximately 4 weeks. The patient had initially attributed the symptoms to the stress of caring for her new baby, who had been born 6 weeks previously. She denied any symptoms of pain on eye movements, diplopia or skin rashes.
Past medical history included only her recent pregnancy with delivery by vaginal delivery. The patient took no regular medications. There was no family history of thyroid disorders. Prior to taking maternity leave, the patient worked as a lawyer. She did not drink or smoke.
Examination revealed a small, diffuse and mildly tender goitre with no evidence of thyroid bruit. There was fine tremor of outstretched hands but no exophthalmos or proptosis. Investigations requested following clinic review are listed below.
Thyroid stimulating hormone 0.1 microU / L (reference 0.4-5.0)
T4 free serum 19.5 pmol / L (reference 8.5-15.2)
T3 free serum 8.1 pmol / L (reference 3.5-6.5)
Thyroid peroxidase antibodies 250 mU / L (reference < 150)
Erythrocyte sedimentation rate 21 ml / h
Thyroid scintiscanning (Technitium-99): no significant thyroid uptake
What is the most likely diagnosis?
Graves' disease Toxic thyroid nodule Viral thyroiditis Toxic multinodular goitre > Post-partum thyroiditis
Post-partum thyroiditis is associated with elevated thyroid peroxidase antibodies but no significant uptake on thyroid scintiscanning and is, therefore, the correct answer in this case given that symptoms began approximately two weeks postpartum.
Viral thyroiditis is usually associated with an elevated ESR and negative anti-thyroid antibodies. Graves’ disease, toxic multinodular goitre and a toxic thyroid nodule would be associated with different patterns of uptake on thyroid scintiscanning.
Weetman A. Investigating low thyroid stimulating hormone (TSH) level. BMJ 2013;347:f6842.
Thyroid Storm Initial Mx: Example Question
You are asked to review a 43-year-old man in theatre recovery who has developed a fever and tachycardia post-operatively. He is previously fit and well, does not smoke and drinks alcohol only occasionally. He had fallen the previous night and suffered a distal radius fracture and has just undergone a open reduction and internal fixation under general anaesthetic. During anaesthesia he received 4mg ondansetron and 8mg dexamethasone for post-operative nausea and 10mg morphine for pain. He denies feeling unwell and has no symptoms suggestive of intercurrent infection.
On examination his heart rate is 130 beats/min and irregular, his blood pressure is 135/74 mmHg and his temperature is 39.4ºC. His chest is clear to auscultation, his abdomen soft and non-tender and there is no rash or meningism. His right forearm is in plaster, but is not particularly painful and his fingers are warm and have normal sensation.
Hb 130 g/l Platelets 460 * 109/l WBC 10.5 * 109/l Na+ 138 mmol/l K+ 4.1 mmol/l Urea 5.1 mmol/l Creatinine 95 µmol/l C-reactive protein 1 mg/L Thyroid stimulating hormone <0.02 mIU/L Cortisol 45 µg/dL
What is the most appropriate initial treatment?
Carbimazole Hydrocortisone > Propranolol Broad spectrum antibiotics Crystalloid infusion
The diagnosis here is thyrotoxicosis as a presenting feature of hyperthyroidism. Infection is unlikely given the normal clinical examination and normal CRP. During initial treatment of thyrotoxicosis it is important to treat hypoadrenalism first - if present - in order to not precipitate a addisonian crisis. However, this patient has no features in the history to suggest pre-existing Addisons disease, he has normal electrolytes and the suppressed cortisol can be explained by the peri-operative use of dexamethasone. Initial treatment of thyrotoxicosis should focus on sympathetic storm suppression using beta blockade. Anti-thyroid medications - i.e. carbimazole - take up to six weeks to take full effect and are not useful in the acute scenario.
Subclinical Hyperthyroidism
Subclinical hyperthyroidism
Subclinical hyperthyroidism is an entity which is gaining increasing recognition. It is defined as:
normal serum free thyroxine and triiodothyronine levels
with a thyroid stimulating hormone (TSH) below normal range (usually < 0.1 mu/l)
NB majority of unaffected people have a TSH value 0.5-2.5 mU/l
Causes
multinodular goitre, particularly in elderly females
excessive thyroxine may give a similar biochemical picture
Subclinical hyperthyroidism = persistently suppressed TSH levels but normal serum thyroid hormone levels and with no clinical evidence of thyrotoxicosis. This usually occurs in the setting of thyroid overactivity due to Graves’ disease or autonomously functioning thyroid nodules sufficient to suppress pituitary TSH secretion but insufficient to cause an elevation of circulating hormones. Progression to overt hyperthyroidism occurs in 1-3 % of elderly patients per year.
The importance in recognising subclinical hyperthyroidism lies in the potential effect on the cardiovascular system (atrial fibrillation) and bone metabolism (osteoporosis). It may also impact on quality of life and increase the likelihood of dementia.
The American Association of Clinical Endocrinologists recommends that treatment is considered in patients with a persistently low TSH level if they are older than 65 years or are at risk of osteoporosis or heart disease.
DEXA scan can be performed to quantify osteoporosis risk and guide treatment
Management
TSH levels often revert to normal - therefore levels must be persistently low to warrant intervention
a reasonable treatment option is a therapeutic trial of low-dose antithyroid agents for approximately 6 months in an effort to induce a remission
Subclinical Hyperthyroidism - Example Question
A 60 year old woman had a thyroid function test requested by her General Practitioner after reporting some symptoms of mild lethargy. This had unexpectedly demonstrated a suppressed Thyroid Stimulating Hormone level (0.25 microU / L) but normal free T4 level (14.1 pmol / L). During further consultation, the patient denied any heat intolerance, weight loss, diarrhoea, hair or skin changes, palpitations or eye symptoms.
The patient had had a hysterectomy without oophorectomy at age 45 as treatment for menorrhagia secondary to fibroids. She remember reaching menarche at around the age of 13 or 14 years. There was no significant family history of coronary artery disease. The patient reported her mother had suffered a fractured neck of femur at the age of 75 years following a fall. The patient was a retired school teacher with an active lifestyle. She had never smoked and drank very little alcohol.
Examination showed no evidence of a goitre, no fine tremor and no lid lag. External examination of the eyes was unremarkable. Cardiovascular and respiratory examination was unremarkable.
The GP requested some further basic investigations and then repeated blood tests 2 months after the original test. At this time, the patient reported her previous symptoms of lethargy had improved; with hindsight she attributed this to grief due to the recent death of a close friend.
Ambulatory blood pressure monitoring: average blood pressure 125 / 75 mmHg
ECG: sinus rhythm at 75 bpm; normal axis; no abnormality of QRS, ST interval or T waves.
Haemoglobin 12.8 g / dL White cell count 6.5 x 109/l Platelets 206 x 109/l Urea 6.2 mmol / L Creatinine 95 micromol / L Sodium 137 mmol / L Potassium 4.0 mmol / L C-reactive protein < 1 Parathyroid hormone 3.7 pmol / L (reference 1.2-5.8) Thyroid-stimulating hormone 0.21 microU / L (reference 0.4-5.0) T4 free serum 13.8 pmol / L (reference 8.5-15.2) T3 free serum 5.6 pmol / L (reference 3.5-6.5) HbA1C 5.6 % (reference 4-6) Total cholesterol 4.0 mmol / L LDL cholesterol 1.8 mmol / L HDL cholesterol 1.9 mmol / L
What is the most appropriate management of the deranged thyroid function tests?
> DEXA scan Thyroid ultrasound Start treatment with simvastatin Radioiodine therapy Treat with propylthiouracil
The patient has subclinical hyperthyroidism with persistently suppressed TSH levels but normal serum thyroid hormone levels and with no clinical evidence of thyrotoxicosis. This usual occurs in the setting of thyroid overactivity due to Graves’ disease or autonomously functioning thyroid nodules sufficient to suppress pituitary TSH secretion but insufficient to cause an elevation of circulating hormones. Progression to overt hyperthyroidism occurs in 1-3 % of elderly patients per year.
The main risk of subclinical hyperthyroidism is its affects on heart and bone health with increased risk of atrial fibrillation and hip fractures. The American Association of Clinical Endocrinologists recommends that treatment is considered in patients with a persistently low TSH level if they are older than 65 years or are at risk of osteoporosis or heart disease.
This patient has a low level of cardiac risk factors with a low risk lipid profile. Assessment of her osteoporosis risk is complicated by her hysterectomy preventing knowledge of her age at menopause. Therefore, a DEXA scan is appropriate next line management to quantify her osteoporosis risk and inform the decision as to whether or not to treat the sub-clinical hyperthyroidism.
Thyroid ultrasound would not influence decision to treat at this stage and so is not required.
Weetman A. Investigating low thyroid stimulating hormone (TSH) level. BMJ 2013;347:f6842
Thyroid Problems in Pregnancy
Pregnancy: thyroid problems
In pregnancy there is an increase in the levels of thyroxine-binding globulin (TBG). This causes an increase in the levels of total thyroxine but does not affect the free thyroxine level
Thyrotoxicosis in Pregnancy
Thyrotoxicosis in Pregnancy
Untreated thyrotoxicosis increases the risk of fetal loss, maternal heart failure and premature labour
Graves’ disease is the most common cause of thyrotoxicosis in pregnancy. It is also recognised that activation of the TSH receptor by HCG may also occur - often termed transient gestational hyperthyroidism. HCG levels will fall in second and third trimester
Management
propylthiouracil has traditionally been the antithyroid drug of choice. This approach was supported by the 2007 Endocrine Society consensus guidelines
maternal free thyroxine levels should be kept in the upper third of the normal reference range to avoid fetal hypothyroidism
thyrotrophin receptor stimulating antibodies should be checked at 30-36 weeks gestation - helps to determine risk of neonatal thyroid problems
block-and-replace regimes should not be used in pregnancy
radioiodine therapy is contraindicated
Carbimazole, whilst normally first line, has been associated with neonatal aplasia cutis before 12 weeks gestation and is therefore usually avoided. This leaves propylthiouracil as the current safest option. During the second trimester, propylthiouracil should be changed to carbimazole due to potential risk of hepatotoxicity with propylthiouracil. The lowest dose that controls the hyperthyroid state should be used as both medications can cross the placenta.
Hypothyroidism in Pregnancy
Hypothyroidism
Key points
thyroxine is safe during pregnancy
serum thyroid stimulating hormone measured in each trimester and 6-8 weeks post-partum
some women require an increased dose of thyroxine during pregnancy
breast feeding is safe whilst on thyroxine
