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
Hyperthyroidism in Pregnancy: Mx
A 29-year-old woman is referred by her GP to the outpatient department with increasing symptoms of heat intolerance, diarrhoea and anxiety over the past couple of weeks. The patient is 34 weeks pregnant with her first baby and has a past medical history of hyperthyroidism, currently being treated with 10mg carbimazole. She has no other past medical history of note and her mother also had hyperthyroidism. She does not smoke or drink alcohol and does not take any recreational drugs.
On examination, her pulse is 98 beats per minute, blood pressure is 124/82 mmHg and her respiratory rate is 14/min. Her oxygen saturation is 98% and temperature is 37.5ºC.
Blood tests are performed and reveal:
Thyroid stimulating hormone (TSH) 0.04 mu/l Free thyroxine (T4) 21 pmol/l Total thyroxine (T4) 152 nmol/l
What is the most appropriate management?
Refer patient for immediate caesarean section > Increase carbimazole dose to 20mg once daily Commence radioiodine treatment Switch carbimazole to propylthiouracil Refer for a thyroidectomy
The carbimazole can be increased to up to 20mg once daily during pregnancy. Propylthiouracil can be started instead of the carbimazole if the increased carbimazole dose does not adequately control the patients hyperthyroidism.
Addisonian Crisis and Thyroxine: Example Question
A 20-year-old female presented to the accident and emergency department with severe abdominal pain, vomiting and lethargy. On further questioning she stated that she had been generally unwell for the last four months during which time she lost 10 Kg in weight and had been tired all the time.
Last month she has been diagnosed with hypothyroidism and was prescribed levothyroxine 50 mcg daily.
Her mother and sister have hypothyroidism and take thyroxine. On examination, she looks unwell and dehydrated.
Her pulse is 105 beats per minute and blood pressure is 70/40 mmHg
Her temperature is 37.6ºC and BMI is 19 kg/m². Cardiovascular, respiratory and abdominal examination were normal. Investigations done last month showed:
Hb 9.5 g/dl
MCV 105 fl
Platelets 190 * 109/l
WBC 4.5 * 109/l
Serum free T4 8.5 pmol/l
Serum TSH 5.5 mU/l
While awaiting new investigations, what is the most appropriate immediate treatment for this patient?
Intravenous glucose 10% Intravenous normal saline Intravenous normal saline and antibiotics > Intravenous normal saline and hydrocortisone Intravenous thyroxine
This patient presented with Addisonian crisis (abdominal pain, vomiting, dehydration and hypotension). She has been complaining of tiredness and weight loss (which are features of Addisons disease) for four months but what precipitated the crisis is the thyroxine given for the presumed hypothyroidism.
Actually, a slightly raised TSH and a decreased T4 are features of primary hypoadrenalism and do not necessarily indicate frank hypothyroidism.
This is a medical emergency and should be treated immediately with intravenous normal saline and hydrocortisone. Thyroxine should not be given as it will exacerbate the condition.
Her low haemoglobin and high MCV may point towards pernicious anaemia which is an autoimmune disease seen sometimes in association with Addisons disease.
Hyperthyroidism in Early Pregnancy - Example Question
A 28-year-old woman has presented with a 5 month history of weight loss (despite an increase in appetite), tremor, loose bowels, and heat intolerance. She has otherwise been well and her only significant family history is that her brother has alopecia areata. She tells you that she had a positive pregnancy test last week and is awaiting her booking appointment. On examination, she appears anxious and her heart rate is 105 beats/minute. She has a tremor when her arms are outstretched and her eyes appear large. She also has a goitre. The rest of her examination is unremarkable. Her blood results find hyperthyroidism. Which of the following medications are most suited to treat her hyperthyroidism?
> Propylthiouracil Carbimazole Radioactive iodine Carbimazole and Levothyroxine Levothyroxine
During early pregnancy, propylthiouracil should be used. The block and replace strategy is not advised as it can lead to problems in the fetus and radioactive iodine is contraindicated. Please see the link below for more information:
https:www.evidence.nhs.uk/formulary/bnf/current/6-endocrine-system/62-thyroid-and-antithyroid-drugs/622-antithyroid-drugs
Hypothyroidism in Pregnancy: Example Question
A 34 year-old woman presents for the first time as being 12 weeks pregnant. She has a past medical history of Hashimotos thyroiditis and hypertension. Her current medication includes ramipril 2.5mg and levothyroxine 100 mcg and recent blood tests reveal a TSH level of 1.0 mU/l.
What is the most appropriate management with regards to her levothyroxine treatment, given her recent diagnosis of pregnancy?
Reduce her levothyroxine dose by an average of 25 mcg Increase her levothyroxine dose by an average of 100 mcg > Increase her levothyroxine dose by an average of 25-50 mcg Reduce her levothyroxine dose by an average of 50 mcg Keep her levothyroxine dose unchanged
In patients currently on levothyroxine who become pregnant, thyroid function tests should be assessed at 6-8 weeks gestation, 16-20 and at 28-32 weeks. During pregnancy, the average thyroxine requirements typically increase by 25-50 mcg. The patient normally returns to their original dose of levothyroxine straight after delivery.
Mx of Sx of Thyrotoxicosis: Example Question
A 42-year-old woman was seen in clinic with a history of palpitation, tremor and weight loss. There is no other past medical history and she takes no regular medication.
On examination, she had a palpable goitre, exophthalmos, and a tremor of the out-stretched hands.
Thyroid function tests showed:
Free thyroxine (T4) 36 pmol/L (10-25) Free triiodothyronine (T3) 15 pmol/L (5-10) Thyroid-stimulating hormone 0.1mU/L (0.4-5.0)
Which of the following treatments should be prescribed initially to improve symptoms?
Thyroidectomy > Propanolol Radioiodine ablation Carbimazole Propylthiouracil
There is a high suspicion of Grave’s disease in this patient, and further investigation with a thyroid autoantibody profile is warranted.
Beta blockers are used to treat the symptoms of increased beta-adrenergic tone that are seen in Grave’s disease. Other such symptoms include anxiety and heat intolerance.
Thioamides are used to treat Grave’s hyperthyroidism, but not specifically the symptoms of increased beta-adrenergic tone. While the anti-thyroid effect of these drugs has a rapid onset, their clinical effect is more delayed because the pre-formed store of hormone in the thyroid gland and bound to thyroid-binding globulin must first be exhausted.
Graves’ Disease Mx
Graves’ disease: management
Despite many trials there is no clear guidance on the optimal management of Graves’ disease. Treatment options include titration of anti-thyroid drugs (ATDs, for example carbimazole), block-and-replace regimes, radioiodine treatment and surgery. Propranolol is often given initially to block adrenergic effects
ATD titration
carbimazole is started at 40mg and reduced gradually to maintain euthyroidism
typically continued for 12-18 months
patients following an ATD titration regime have been shown to suffer fewer side-effects than those on a block-and-replace regime
Block-and-replace
carbimazole is started at 40mg
thyroxine is added when the patient is euthyroid
treatment typically lasts for 6-9 months
The major complication of carbimazole therapy is agranulocytosis
Radioiodine treatment
contraindications include pregnancy (should be avoided for 4-6 months following treatment) and age < 16 years. Thyroid eye disease is a relative contraindication, as it may worsen the condition
the proportion of patients who become hypothyroid depends on the dose given, but as a rule the majority of patient will require thyroxine supplementation after 5 years
Thyrotoxicosis Factitia - Example Question
A 19-year-old woman presents to her GP with a 7 month history of weight loss, diarrhoea and palpitations. The diarrhoea is normal colour and over the last three months she has had roughly 2-3 bowel motions per day. The heart palpitations occur randomly throughout the day and night. She has also noticed that she has recently been getting episodes of feeling very hot and sweaty. She has no other past medical history and her only family history is a mother who has Hashimotos thyroiditis.
On examination, the patient is sweaty and her blood pressure is 130/80 mmHg, pulse is 102 bpm and regular, respiratory rate is 16/min and her oxygen SATs are 98% on air.
Blood tests are performed and reveal:
Hb 135 g/l Platelets 220 * 109/l WBC 7.1 * 109/l Na+ 139 mmol/l K+ 3.9 mmol/l Urea 5.1 mmol/l Creatinine 60 µmol/l Free thyroxine (T4) 28 pmol/l Thyroid stimulating hormone (TSH) 0.08 mu/l
A thyroid radioisotope scan is performed and reveals a globally reduced uptake.
What is the most likely diagnosis?
Graves disease > Thyrotoxicosis factitia Hashimotos disease De Quervains thyroiditis Atrophic thyroiditis
The most like likely diagnosis in this case is thyrotoxicosis factitia. This is evidenced by the reduced thyroid uptake on radioisotope scanning, along with the fact she may have easy access to thyroxine he mother would be taking it for her Hashimotos thyroiditis. De Quervains thyroiditis can present with symptoms similar to factitious thyroiditis and a decreased uptake on radioisotope scan, however, the fact the symptom shave lasted for 7 months makes this diagnosis unlikely.
Hypothyroidism - Ix: Example Question
A 62-year-old woman attends her GP complaining of weight gain, lethargy and hair loss. She denies any intercurrent illness. Thyroid function tests are performed and the results are as follows:
Thyroid stimulating hormone (TSH) 0.3 mu/l
Free T4 8 pmol/l
Which investigation is most likely to be diagnostic?
Thyroid ultrasound Radio-iodine uptake scan Anti-thyroid peroxidase (TPO) antibodies Fine-needle aspiration of thyroid > MRI pituitary gland
This patient has hypothyroidism. The vast majority of cases are primary hypothyroidism with a high TSH and low T4. The common causes are:
Autoimmune (Hashimoto’s disease, atrophic)
Iodine deficiency
Thyroiditis (post-viral, post-partum)
Iatrogenic (thyroidectomy, radioiodine, drugs)
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.
Thyrotoxic Periodic Paralysis: Example Question
A 23-year-old Malaysian man presented to the emergency department with sudden onset right arm weakness that came on earlier in the morning after waking up. He denies any slurring of his speech. He has had one previous episode a month ago but that episode involved mild right leg weakness which resolved after 30 minutes, this time he is anxious as he was unable to move his arm and it has not resolved after 2 hours. His past medical history includes Grave’s disease, and he takes carbimazole 20mg twice daily, however, he admits he has not been taking his carbimazole for the past week as he just returned from a month long holiday and had run out of medication.
On examination his temperature was 37.5ºC, heart rate was 84 bpm, blood pressure was 114/68 mmHg, respiratory rate was 18 breaths per minute, and oxygen saturation was 98% on air. There was a fine tremor in both hands. Neurological examination revealed flaccid paralysis of the right arm, affecting the extensor muscles more than the flexor muscles (power 2/5 in the shoulder extensors). Reflexes and sensation to soft touch were normal. There was no disturbance of speech or facial asymmetry. There was a palpable smooth thyroid goitre in the midline of the neck.
C Reactive protein 6 mg/l
Haemoglobin 156 g/l
White cell count 6.6 x 10^9/L
Na+ 145 mmol/l
K+ 3.1 mmol/l
Urea 5.2 mmol/l
Creatinine 78 µmol/l
Corrected calcium 2.42 mmol/l
Thyroid stimulating hormone (TSH) <0.03 µU/ml (Reference range 0.3 - 4.0 µU/ml)
Free T4 3.14 ng/dL (Reference range 0.7 - 1.4ng/dL)
Free T3 1.44ng/dL (Reference range 0.2 - 0.5ng/dL)
What is the next most appropriate management step?
Computer Tomography scan (CT) of the head Hydrocortisone Fludrocortisone Carbimazole > Intravenous potassium chloride
This patient has thyrotoxic periodic paralysis, a rare condition associated with hyperthyroidism. It is more common in males of oriental descent and presents between the second to third decade of life. There is an association with the HLA-DRw8 genotype. It is characterised by recurrent episodes of proximal muscle weakness and can vary from mild weakness to quadriplegia. Bulbar, respiratory muscles and cranial nerves are rarely affected.
Patients are hypokalaemic during attacks as thyrotoxicosis leads to an intracellular potassium shift, which resolves when potassium returns to the extracellular space. Patients may also have hypophosphataemia and hypomagnesaemia.
Treatment for acute attacks is potassium replacement, but patients should be monitored closely for hyperkalaemia. Definitive management includes the management of thyrotoxicosis with pharmacological, surgical or radioactive iodine management.
TSH Secreting Pituitary Tumour - Example Question
A 55 year-old female presents to the outpatients department having been referred by her GP. She complains of fatigue, increased sweating and weight loss over the past four months. She also reports a loss of sex drive.
Examination reveals that she is pale and has a pulse rate of 121 per minute with a bounding pulse character. Her blood pressure is 118/79 mmHg and she has heart sounds 1 and 2 presents with no added sounds. On auscultation, her chest is clear and her abdomen is soft and non-tender with no organomegaly. She has a smooth goitre but has no signs of thyroid eye disease. Examination of her cranial nerves are normal.
The results of recent blood tests are as follows:
Hb 11.3 g/dl Platelets 190 * 109/l WBC 10.9 * 109/l Na+ 129 mmol/l K+ 4.3 mmol/l Urea 7.9 mmol/l Creatinine 94 µmol/l ALP 155 u/l Calcium 2.40 mmol/l Albumin 40 g/L TSH 11 mU/L Free T4 41 pmol/L Free T3 11 pmol/L
Which of the following is the most likely diagnosis?
Grave's disease Thyroid cancer Surreptitious thyroxine ingestion De Quervain's thyroiditis > TSH secreting pituitary tumour
Biochemistry reveals elevated thyroid-stimulating hormone (TSH) with concurrent elevated thyroxine (T4) and tri-iodothyronine (T3). An elevated alkaline phosphatase (ALP) is consistent with thyrotoxicosis. Hyponatraemia suggests hypoadrenalism.
Taken with the symptoms, this patient has a likely diagnosis of a thyrotropinoma, which is a rare type of pituitary tumour accounting for approximately less than 1% of cases of pituitary tumours. 90% are macroadenomas.
Presentation is typically with features of thyrotoxicosis and include weight loss, sweating, fatigue and tachycardia. There may also be signs of hypopituitarism.
Mx of Hyperthyroidism in Pregnancy - Example Question
A 28 year old pregnant lady presents to the Emergency Department with palpitations and sweating. She mentions that she has had these symptoms on and off for the past 4 months but that they have worsened over the past few weeks. Now she is feeling worried and wanted to be assessed medically due to her concern she was having a miscarriage. She looks particularly anxious to be in hospital. This is her first pregnancy. She is 7 weeks pregnant. She has had no vaginal bleeding or discharge during the course of her pregnancy. She is normally fit and well.
Initial observations reveal a blood pressure of 130/85 mmHg, a heart rate of 110 beats per minute, a respiratory rate of 19/min, oxygen saturations of 99% on air and a temperature of 37.5 degrees. Examination findings reveal a resting tachycardia and a subtle goitre is noted.
Blood test results are as follows:
Hb 110 g/l Wcc 12 x109/l Plt 245 x109/l CRP 12 mg/l Na+ 140 mmol/l K+ 5.0 mmol/l Ur 5.7 mmol/l Cr 110 µmol/l D-dimer 490 ng/ml T4 21 mU/l TSH <0.05 pmol/l
Given the most likely diagnosis, how should this lady be managed?
Watch and wait/symptomatic control with beta blockade Radioactive iodine therapy Subtotal thyroidectomy > Propylthiouracil Block and replace carbimazole + thyroxine
This lady has symptoms and biochemical evidence of hyperthyroidism. This lady’s symptoms predate her pregnancy, therefore it is not pregnancy induced thyrotoxicosis and will not self-limit - she will need treatment to prevent complications to her and the foetus. Radioactive iodine is contraindicated. Subtotal thyroidectomy is a little risky and extreme during pregnancy. 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.
Thyroid Eye Disease - Mx: Example Question
A 51-year-old lady librarian attends outpatient clinic with painful eyes. She reports that her vision has deteriorated over the past four weeks. On examination, she has proptosis, periorbital oedema and a painful complex ophthalmoplegia. She appears anxious and is worried about not coping at work. At present she smokes ten cigarettes daily.
What would be the most appropriate next step in managing this patient?
> IV methylprednisolone Surgical decompression Smoking cessation advice Total thyroidectomy Artificial tear drops
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.
Subacute (DeQuervain’s) Thyroiditis
Subacute (De Quervain’s) thyroiditis
Subacute thyroiditis (also known as De Quervain’s thyroiditis and subacute granulomatous thyroiditis) is thought to occur following viral infection and typically presents with hyperthyroidism.
There are typically 4 phases; phase 1 (lasts 3-6 weeks): hyperthyroidism, painful goitre, raised ESR phase 2 (1-3 weeks): euthyroid phase 3 (weeks - months): hypothyroidism phase 4: thyroid structure and function goes back to normal
Investigations
globally reduced uptake on iodine-131 scan (NB similar findings to Thyroxoticosis Facticia)
Management
usually self-limiting - most patients do not require treatment
thyroid pain may respond to aspirin or other NSAIDs
in more severe cases steroids are used, particularly if hypothyroidism develops
A short history of flu-like symptoms, coupled with pain over the thyroid gland is consistent with a diagnosis of subacute thyroiditis. The presentation with thyrotoxicosis is caused by a transient increase in thyroid hormone release (where thyroid inflammation drives increased release of stored thyroid hormone, rather than the clinical picture being due to overproduction of T3 and T4), hence anti-thyroid drugs are not indicated. Symptomatic relief with propranolol is indicated, as are non-steroidal anti-inflammatory agents for management of pain and inflammation. A period of hypothyroidism may follow, with later recovery to normal thyroid function.
Although a transient period of hypothyroidism may be seen after the thyrotoxicosis subsides, thyroxine replacement is usually not needed.
Subacute Thyroiditis - Example Question
A 62-year-old man presents to hospital with a three day history of tiredness, muscle aches, a fever and pain at the front of his neck. Two weeks ago he had an upper respiratory tract infection which he treated himself with paracetamol and oral decongestants. He did not receive any antibiotics. His only past medical history is mild arthritis of the right knee and he only takes occasional antihistamines during summer time.
On examination, he appears anxious with a fine resting tremor. He has a temperature 38.1°C, a pulse rate of 125 per minute which is regular and normal in character and a blood pressure of 131/78 mmHg. Heart sounds 1 and 2 were present with no added sounds and his chest was clear on auscultation. His abdomen was soft and non-tender with no organomegaly. Neurological examination was unremarkable apart from the resting tremor. Neck examination reveals a diffusely enlarged and tender thyroid gland.
Blood tests are requested and the results are as follows:
Hb 14.0 g/dl Platelets 378 * 109/l WBC 8.9 * 109/l ESR (Westergren) 94 mm/1st hour Normal range 0-30 Free T4 214 nmol/l Free T3 192 nmol/L Plasma TSH <0.05 mU/l
Which of the following investigations is likely to be most helpful in establishing the diagnosis?
Blood cultures Serum anti-thyroid antibodies Ultrasound scan of neck > Radioactive iodine uptake scan Fine needle aspiration
The patients presenting symptoms and signs are typical of a diagnosis of subacute thyroiditis, of which the most likely cause of this is De Quervains thyroiditis.
Radioactive iodine uptake scan is the most suitable investigation for confirming subacute thyroiditis which demonstrates reduced intake.
Hypothyroidism - Mx
Hypothyroidism: management
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
Side-effects of thyroxine therapy hyperthyroidism: due to over treatment reduced bone mineral density worsening of angina atrial fibrillation
Interactions
iron: absorption of levothyroxine reduced, give at least 2 hours apart
*source: NICE Clinical Knowledge Summaries
Myxoedema Coma - Example Question
An 85-year-old woman is brought into A+E with hypothermia, sinus bradycardia and unresponsive. A CT head reveals no acute intra-cranial pathology. Passive warming and intravenous fluids are commenced. Subsequent blood tests reveal the panel below. A collateral history from family members reveals symptoms of lethargy, cold intolerance and weight gain over the last few months.
TSH >30.0 mU/L
T3 <0.05 mU/L
What is the most appropriate initial treatment?
> Levothyroxine and Liothyronine Levothyroxine Lugol's iodine Liothyronine Carbimazole
This is myxedema coma, which is rare but has a high mortality rate.
Administration of both liothyronine (T3) and levothyroxine (T4) is the most appropriate treatment. Liothyronine (T3) has a greater biologic activity and faster onset than levothyroxine (T4) and should be continued until there is clinical improvement. The administration of hydrocortisone is also important as patients there may be coexisting adrenal insufficiency (primary or secondary).
Supportive measures are important such as re-warming, fluid resuscitation, electrolyte correction and vasopressors if required.
Carbimazole is used for hyperthyroidism.
Lugols iodine is used for rapid control of hyperthyroidism such as a thyroid storm or prior to a total thyroidectomy for poor medical compliance.
Hashimoto’s Thyroiditis - Example Question
A 60-year-old woman presents to her GP complaining of a swelling in her neck. She has a past medical history of rheumatoid arthritis and Sjogren’s syndrome.
On examination of the neck there was a mildly nodular, firm, rubbery goitre.
Thyroid function tests are shown below:
Total serum thyroxine 10 µg/dl (4.5-13.6)
Thyroid stimulating hormone 1.2 µU/ml (0.4-3.6)
Anti-thyroid peroxidase titre Increased
Which is the most likely diagnosis?
Sick euthyroid syndrome Graves disease > Hashimoto's thyroiditis Silent lymphocytic thyroiditis Subacute thyroiditis
Hashimoto’s thyroiditis is a chronic, destructive lymphocytic infiltration of the thyroid gland, which is mainly seen in patients with concurrent autoimmune diseases. Early on in the disease, T4 and TSH levels can be normal, as in this case. Later on the thyroid function tests adopt a hypothyroid picture. A goitre is classical for Hashimoto’s thyroiditis. Anti-thyroid peroxidase is almost always present in Hashimoto’s thyroiditis (note, can also be detected in Graves and silent lymphocytic thyroiditis)
Thyroid Storm - Example Question
A 72-year-old Japanese female presents to the emergency department with sudden onset shortness of breath associated with palpitations. She has previously experienced similar palpitations 6 months ago but did not seek medical attention. She was last completely well and described by her daughter to be at baseline 24 hours ago when they had dinner together. The patient denies any chest pain, nausea, vomiting or sweating. On examination, the patient is pyrexic at 38.2 degrees and tachycardic, with a regular pulse at 130-140 beats per minute. Heart sounds demonstrate a gallop rhythm; auscultation of her chest reveals bibasal inspiratory coarse crackles and no wheeze. She has bilateral mild lower limb pitting oedema to low ankles. Examination of the abdominal and neurological systems is unremarkable. A chest radiograph demonstrates bibasal alveolar shadowing with mild bilateral pleural effusions. An ECG demonstrates sinus tachycardia at 130 beats per minute. Blood tests are as follows:
Hb 123 g/l
Platelets 299 * 109/l
WBC 9.5 * 109/l
Na+ 139 mmol/l
K+ 4.2 mmol/l
Urea 7.2 mmol/l
Creatinine 98 µmol/l
TSH < 0.01 mU/l
Free T4 140 pmol/l
Free T3 40 pmol/l
Nursing staff have kindly taken blood cultures and taken measures to cool the patient. What is the next most appropriate immediate treatment?
> Intravenous propranolol Lugol's iodine Oral carbimazole Oral propylthiouracil Oral prednisolone
The patient has presented with sudden onset heart failure associated with sinus tachycardia, pyrexia and thyrotoxicosis: this represents a thyroid storm and is an endocrinological emergency. The treatment comprises of four aims: resuscitation, treat the sympathetic consequences of thyrotoxicosis, block underlying hyperthyroidism and treat any heart failure present. The first step involved intravenous followed by oral beta-blockade. Diltiazem is an appropriate alternative if the patient cannot tolerate beta blockers. In cases of simultaneous poor ventricular function and thyroid storm, intravenous infusions of short-acting beta blockers such as esmolol are also appropriate, which can be switched off immediately at the earliest sign of worsening cardiac function secondary to beta blockade. Thyroid blockers can be instituted after this immediate therapy. Oral corticosteroids are also important to reduce peripheral T4 to T3 conversion. However, both treatments can be instituted after achieving haemodynamic stability.
Type 2 Amiodarone-induced Thyroxoticosis: Example Question
A 48-year-old man is referred to the outpatient department by his GP, having experienced tremor, heat intolerance and 2 kg weight loss over the last 6 weeks. His past medical history includes having atrial fibrillation for which he takes warfarin and amiodarone. He is a non-smoker and drinks on average 10 units of alcohol per week.
Blood tests are performed and reveal:
Hb 142 g/l Platelets 220 * 109/l WBC 7.2 * 109/l Na+ 140 mmol/l K+ 4.2 mmol/l Urea 4.5 mmol/l Creatinine 45 µmol/l Thyroid stimulating hormone (TSH) 0.03 mu/l Free thyroxine (T4) 29 pmol/l Total T3 (TT3) 252 ng/dL Normal range 75 -200 ng/dL
A colour flow Doppler sonography of the thyroid is performed and shows absent vascularity and gland destruction.
What is the most likely diagnosis?
Type 1 amiodarone-induced thyrotoxicosis > Type 2 amiodarone-induced thyrotoxicosis Grave's disease Hashimotos thyroiditis De Quervains thyroiditis
Type 2 amiodarone-induced thyrotoxicosis typically occurs in patients without underlying thyroid disease and is the result of the toxic effect of amiodarone on the thyroid follicular cells, causing a destructive thyroiditis that results in excess release of preformed T4 and T3 into the circulation. The condition has two phases a thyrotoxic phase which can last weeks to months, which is often followed by a hypothyroid phase and an eventual recovery in most patients.
Type 1 amiodarone-induced thyrotoxicosis normally occurs in patients with underlying thyroid pathology like Graves disease. In these patients, there is accelerated thyroid hormone synthesis secondary to the iodide load from the amiodarone therapy.
Lithium and the Thyroid - Example Question
A 42-year-old woman is referred to the endocrine clinic. She is treated with lithium for bipolar disorder and presents with weight gain, lethargy, a dry cough and a hoarse voice over the past 3 months. Examination reveals patchy hair loss, a smooth goitre, and she is overweight with a body mass index of 32 kg/m². Her blood pressure is 122/82 mmHg, pulse is 60 beats per minute.
Investigations:
Na+ 130 mmol/l
TSH 14.2 mIU/l
Which of the following is the most appropriate way to manage her?
Iodine supplementation Start prednisolone Stop lithium Surgical thyroidectomy > Start thyroxine
Lithium increases intrathyroidal iodine content, inhibits the coupling of iodotyrosine residues to form iodothyronines (thyroxine and triiodothyronine), and it also inhibits release of T4 and T3 leading to hypothyroidism, the clinical picture seen here. The most appropriate intervention is thyroxine supplementation.
There is no need acutely to stop lithium therapy, although substitution may eventually be considered after discussion with the patient’s psychiatrist. Due to the fact that lithium prevents coupling of iodotyrosine, iodine supplementation is ineffective. Prednisolone is also not of value because thyroiditis isn’t the cause of the hypothyroidism seen here. Surgical thyroidectomy isn’t indicated because there are no symptoms of extrinsic airway obstruction.
Thyroid Eye Disease and Smoking - Example Question
A 38-year-old woman is referred by her GP for management of Graves’ disease, diagnosed by the presence of a goitre, suppressed thyroid stimulating hormone, and presence of thyroid antibodies on screening. She has no past medical history of note, drinks 10 units of alcohol per week and smokes 20 cigarettes per day. On examination her blood pressure is 112/88 mmHg, pulse is 89 beats per minute and regular, she has a fine tremor. There is a smooth goitre and marked proptosis.
Which of the following has the greatest negative impact on prognosis of her thyroid eye disease?
Alcohol consumption > Cigarette smoking DR4 HLA type LATS titre Use of block replace therapy
A systematic review published in 2006 has confirmed the strong link between cigarette smoking and thyroid eye disease. Across 15 studies a strong association between thyroid eye disease in patients with Graves’ disease and smoking was established, with an odds ratio of up to 20 for thyroid eye disease in current smokers vs non-smokers who have Graves’.
http://www.ncbi.nlm.nih.gov/pubmed/16980921
Block replace therapy establishes stable control of thyroid function, and is actually associated with reduced incidence of thyroid eye disease because thyroxine is consistently in the normal range. Alcohol consumption within the recommended safe limits may actually reduce the severity of thyroid eye disease in Graves’. Thyroid eye disease is primarily driven by pathogenic T cells, as such it isn’t closely related to LATS titre. HLA DR4 is more strongly associated with Type 1 diabetes, rheumatoid arthritis and autoimmune hepatitis than with thyroid disease.
T3 Toxicosis - Example Question
You receive a phone call from a general practitioner regarding a 50 year-old man who has had thyroid function tests performed for a history of weight loss. There is no history of illicitly taking levothyroxine. His results show : TSH 0.01 mIU/L, T4 8.5 ug/dL. You should advise which of the following:
Admit for urgent MRI head Repeat the bloods and include parathyroid hormone (PTH) > Add on T3 as this may represent T3 toxicosis Start radio-iodine treatment immediately Start thyroxine replacement
In approximately 5% of patients with clinical and biochemical hyperthyroidism T3 may be elevated prior to T4. This is known as T3 toxicosis.
When both free hormones are normal but TSH is low, the term subclinical thyrotoxicosis can be applied.
Radio-iodine treatment should never be started without discussion with the patient and is only used prior to carbimazole in certain circumstances. An MRI head would be part of the work up for secondary hyperthyroidism. PTH would not be useful in this circumstance and starting thyroxine would not be a good idea! T3 toxicosis is treated in the same manner as T4 hyperthyroidism.
Amiodarone-induced Thyrotoxicosis - Acute setting: Example Question
A 74-year-old man who has end stage cardiac failure with an ejection fraction of 32% and recurrent ventricular tachycardia comes to the Emergency department for review. He has been losing weight and suffering from increasing palpitations over the past few weeks.Medication of note includes amiodarone. On examination his blood pressure is 95/70 mmHg, his pulse is 130 beats per minute, (atrial fibrillation), and there is evidence of left ventricular failure.
His GP has checked his thyroid function tests, the results of which are shown below:
TSH <0.05 mU/l
Free T3 10.3 pmol/l
Free T4 29.0 pmol/l
What is the most appropriate treatment?
Carbimazole > Perchlorate Prednisolone Propylthiouracil Thyroxine
This patient has amiodarone-induced thyrotoxicosis, which exists as two distinct type, Type 1 which is usually treated with high doses of thionamides, and Type 2 which is treated with corticosteroids as the primary intervention. For this case, due to the poor cardiac status, there is limited time to gain control of thyroid function. Perchlorate is the intervention of choice because it rapidly treats the symptoms of thyrotoxicosis by blocking entry of iodide into the gland whilst other interventions take effect.
Prednisolone, carbimazole and propylthiouracil may all also be appropriate interventions, but won’t gain control of thyroid function rapidly enough to impact on cardiac status. Thyroxine will of cause further exacerbate thyrotoxicosis.
Subacute Thyroiditis - Example Question
A 29-year-old woman comes to the clinic with feelings of anxiety, palpitations and a resting tremor present over the past 2 weeks. She also has symptoms of a flu-like illness and pain over her anterior neck. On examination,you reveal tenderness over the thyroid. Her blood pressure is 115/88 mmHg, she has a fine tremor at rest, sweaty palms and a tachycardia of 88 beats per minute. TSH is <0.05 U/ml.
Which of the following is the most appropriate intervention?
Thyroxine Carbimazole Propylthiouracil Carbimazole and thyroxine > Propranolol
The short history of flu-like symptoms, coupled with pain over the thyroid gland is consistent with a diagnosis of subacute thyroiditis. The presentation with thyrotoxicosis is caused by a transient increase in thyroid hormone release, rather than over production, hence anti-thyroid drugs are not indicated. Symptomatic relief with propranolol is indicated, as are non-steroidal anti-inflammatory agents for management of pain and inflammation. A period of hypothyroidism may follow, with later recovery to normal thyroid function.
Anti-thyroid drugs are not needed, carbimazole and propylthiouracil are therefore incorrect, as is the block-replace regimen option. Although a transient period of hypothyroidism may be seen after the thyrotoxicosis subsides, thyroxine replacement is usually not needed.
Subacute Thyroiditis - Example Question
A 28-year-old woman presents with flu-like symptoms, palpitations and pain over the anterior neck over the past 2-3 weeks. She has also suffered rapid weight loss and feels increasingly anxious that there may be something seriously wrong with her. Her thyroid-stimulating hormone has been measured at <0.05 IU by her GP. On examination her blood pressure is 128/82 mmHg, her pulse is 95 beats per minute and regular, and she has a fine tremor. There is mild tenderness over the anterior neck. Body mass index is 22 kg/m²
Which of the following would you also expect to find?
Erythema nodosum Exophthalmos Multiple small thyroid nodules on ultrasound scan Positive anti-thyroid antibodies > Reduced uptake on thyroid scintigraphy
The most likely diagnosis, given the history of 2-3 weeks of flu-like symptoms and suppressed TSH, is subacute thyroiditis where thyroid inflammation drives increased release of stored thyroid hormone, rather than the clinical picture being due to overproduction of T3 and T4. Symptoms of hyperthyroidism should be managed with beta blockade as required, and there is no role for thioamides. Pain over the thyroid can be managed with non-steroidal anti-inflammatory drugs. After a period of hyperthyroidism, rebound hypothyroidism may be seen, followed by a recovery to euthyroidism.
Erythema nodosum is not associated with subacute thyroiditis. Exophthalmos and positive anti-thyroid antibodies are associated with autoimmune thyroid disease. Multiple small thyroid nodules are a feature of multinodular goitre.
Toxic Multinodular Goitre
- A thyroid gland containing a number of irregular nodules > Thyrotoxicosis
- Nuclear scintigraphy reveals patchy uptake
- Treatment of choice = RADIOIODINE
Sick Euthyroid Syndrome
Pathology postulated = Down regulation of type 1 deiodinase, reducing the peripheral conversion of T4 to T3 and thus reducing the basal metabolic rate during periods of stress. Upregulation of type 3 deiodinase to inactive (reverse) T3 also aids in reducing basal metabolic rate
TFTs - everything is characteristically LOW
= Reversible state of abnormal thyroid function due to non-thyroidal illness, without pre-existing hypothalamic-pituitary or thyroid gland dysfunction
In majority of cases, TSH level is within the normal range (inappropriately normal given low thyroxine and T3)
By definition, TFTs revert back to N after recovery
Causes of Sick Euthyroid Syndrome:
- MI
- DKA
- Starvation
- Burns
- Trauma
- Surgery
- Malignancy
- Organ Failure
- Inflammatory conditions
Hashimoto’s Thyroiditis
Hypothyroidism + Goitre + Anti-thyroid Peroxidase antibodies
Graves Disease
NB Most common cause of Thyrotoxicosis
Typically seen in women aged 30-50
Features:
- typical features of thyrotoxicosis
- eye signs in 30% patients (exophthalmos, ophthalmoplegia)
- pretibial myxoedema
- thyroid acropachy
Autoantibodies:
- anti-TSH receptor stimulating antibodies (90%)
- anti-thyroid peroxidase antibodies (50%)
Thyroid Eye Disease - Emergency Ophthalmology Situations
For patients with established thyroid eye disease, the following Sx/signs should indicate need for urgent R/V by ophthalmologist:
- unexplained deterioration in vision
- awareness of a 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 eyelids are closed
- disc swelling
Subclinical Hypothyroidism
Basics:
- TSH raised but T3, T4 normal
- No obvious Sx
Significance:
- Risk of progressing to overt hypothyroidism is 2.5% per year
- Risk increased by presence of thyroid autoantibodies
Treat IF:
- TSH > 10
- Thyroid autoantibodies +ve
- Other autoimmune disorder
- Prev treatment of Graves
Worsening Thyroid Eye symptoms after treatment for Graves?
Radio iodine treatment may lead to development/worsening of thyroid eye disease in up to 15% of patients with Graves e.g. eye pain, decreased visual acuity
Diabetic patients found to be Hypothyroid
NB in diabetic patients starting on thyroxine, doses of antidiabetic drugs including insulin may need to be increased
Hashimoto’s Thyroiditis
= Hypothyroidism + non-tender goitre
= an autoimmune disorder of the thyroid gland, typically assoc with hypothyroidism although there may be a transient thyrotoxicosis in acute phase
x 10 more common in women
Features:
- features of Hypothyroidism
- Goitre - firm, non-tender
- Anti-thyroid peroxidase and also anti-Tg antibodies
NB De Quervain’s thyroiditis typically causes a PAINFUL goitre
Graves Disease - Autoantibodies
Anti-TSH receptor stimulating antibodies (90%)
Anti-thyroid peroxidase antibodies (50-75%)
NB Anti-thyroid peroxidase antibodies also seen in 90% of patients with Hashimoto’s thyroiditis however this is generally associated with Hypothyroidism
Skin Manifestations of Thyroid Disease
Hypothyroidism:
- Dry (anhydrosis), cold, yellow skin
- Eczema
- Non-pitting oedema e.g. hands, face
- Xanthomata
- Dry, coarse scalp hair, loss of lateral aspect of eyebrows
Hyperthyroidism:
- Pretibial myxoedema: erythematous, oedematous, lesions above lateral malleoli
- Thyroid acropachy: clubbing
- Scalp hair thinning
- Increased sweating
NB Pruritis can occur with both
Differentiating between T1 and T2 Amiodarone-induced Thyrotoxicosis
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 Type 2 AIH, a colour flow Doppler sonography of the thyroid would show absent vascularity and gland destruction.
In patients where the diagnosis is uncertain, radioiodine uptake, (which is low in type 2 disease) may further help differentiating between the two
Thyroid Eye Disease - Emergency
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
Goitre with low TSH - Ix with Thyroid Technetium scan
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.
Thyrotoxicosis in Pregnancy and Carbimazole
If patient is stable on Carbimazole this can be increased to up to 20mg once daily during pregnancy. Propylthiouracil can be started instead of the carbimazole if the increased carbimazole dose does not adequately control the patients hyperthyroidism.
During early pregnancy, propylthiouracil should be used.
The block and replace strategy is not advised as it can lead to problems in the fetus and radioactive iodine is contraindicated.
Thyrotoxicosis Facticia (i.e. taking thyroxine unnecessarily)
Thyrotoxicosis factitia
Evidenced by the reduced thyroid uptake on radioisotope scanning, along with easy access to thyroxine.
De Quervains thyroiditis can present with symptoms similar to factitious thyroiditis and a decreased uptake on radioisotope scan.
Thyrotoxic Periodic Paralysis
Thyrotoxic periodic paralysis is a rare condition associated with hyperthyroidism. It is more common in males of oriental descent and presents between the second to third decade of life. There is an association with the HLA-DRw8 genotype. It is characterised by recurrent episodes of proximal muscle weakness and can vary from mild weakness to quadriplegia. Bulbar, respiratory muscles and cranial nerves are rarely affected.
Patients are hypokalaemic during attacks as thyrotoxicosis leads to an intracellular potassium shift, which resolves when potassium returns to the extracellular space. Patients may also have hypophosphataemia and hypomagnesaemia.
Treatment for acute attacks is potassium replacement, but patients should be monitored closely for hyperkalaemia. Definitive management includes the management of thyrotoxicosis with pharmacological, surgical or radioactive iodine management.
TSH-Secreting Pituitary Tumour = Thyrotropinoma
Thyrotropinoma is a rare type of pituitary tumour accounting for approximately less than 1% of cases of pituitary tumours. 90% are macroadenomas.
Presentation is typically with features of thyrotoxicosis and include weight loss, sweating, fatigue and tachycardia. There may also be signs of hypopituitarism.
TFTs: High TSH, High T3, T4
Thyroxine Therapy - SE and Interactions
Side-effects of thyroxine therapy hyperthyroidism: due to over treatment reduced bone mineral density worsening of angina atrial fibrillation
Interactions
iron: absorption of levothyroxine reduced, give at least 2 hours apart
Myxoedema Coma - Mx
Myxoedema coma is rare but has a high mortality rate. Presentation: Hypothermia Sinus bradycardia ?Unresponsive
Mx:
Administration of both liothyronine (T3) and levothyroxine (T4) is the most appropriate treatment. Liothyronine (T3) has a greater biologic activity and faster onset than levothyroxine (T4) and should be continued until there is clinical improvement. The administration of hydrocortisone is also important as patients there may be coexisting adrenal insufficiency (primary or secondary).
Supportive measures are important such as re-warming, fluid resuscitation, electrolyte correction and vasopressors if required.
Hashimoto’s Thyroiditis
Hashimoto’s thyroiditis is a chronic, destructive lymphocytic infiltration of the thyroid gland, which is mainly seen in patients with concurrent autoimmune diseases. Early on in the disease, T4 and TSH levels can be normal. Later on the thyroid function tests adopt a hypothyroid picture. A goitre is classical for Hashimoto’s thyroiditis. Anti-thyroid peroxidase is almost always present in Hashimoto’s thyroiditis (note, can also be detected in Graves and silent lymphocytic thyroiditis)
Thyroid Storm - Mx
Example Presentation:
Sudden onset heart failure associated with sinus tachycardia, pyrexia and thyrotoxicosis: this represents a thyroid storm and is an endocrinological emergency.
The treatment comprises of four aims: resuscitation, treat the sympathetic consequences of thyrotoxicosis, block underlying hyperthyroidism and treat any heart failure present.
The first step involved intravenous followed by oral beta-blockade. Diltiazem is an appropriate alternative if the patient cannot tolerate beta blockers.
In cases of simultaneous poor ventricular function and thyroid storm, intravenous infusions of short-acting beta blockers such as esmolol are also appropriate, which can be switched off immediately at the earliest sign of worsening cardiac function secondary to beta blockade.
Thyroid blockers can be instituted after this immediate therapy.
Oral corticosteroids are also important to reduce peripheral T4 to T3 conversion. However, both treatments can be instituted after achieving haemodynamic stability.
Lithium-induced Hypothyroidism
Lithium increases intrathyroidal iodine content, inhibits the coupling of iodotyrosine residues to form iodothyronines (thyroxine and triiodothyronine), and it also inhibits release of T4 and T3 leading to hypothyroidism, the clinical picture seen here. The most appropriate intervention is thyroxine supplementation.
There is no need acutely to stop lithium therapy, although substitution may eventually be considered after discussion with the patient’s psychiatrist. Due to the fact that lithium prevents coupling of iodotyrosine, iodine supplementation is ineffective.
T3 Toxicosis
In approximately 5% of patients with clinical and biochemical hyperthyroidism T3 may be elevated prior to T4. This is known as T3 toxicosis.
When both free hormones are normal but TSH is low, the term subclinical thyrotoxicosis can be applied
Mx: Same as for Hyperthyroidism
TFTs
Hyperthyroidism: Low TSH, High T3, T4
Hypothyroidism: High TSH, Low T3, T4
Subclinical Hyperthyroidism: Low TSH, Normal T3, T4
Secondary Hypothyroidism: Low TSH, Low T3, T4
Sick Euthyroid Syndrome: Low TSH, Low T3, T4 = Everything characteristically LOW. TSH inappropriately low-normal given low T3, T4
Non-compliance with Thyroxine: High TSH, Normal T3, T4
Excessive thyroxine e.g. Thyrotoxicosis Facticia: Low TSH, Normal T3, T4
TSH Secreting Pituitary Tumour: High TSH, High T3, T4
De Quervain’s thyroiditis: Post Flu/URTI
INITIALLY Low TSH, High T3, T4, followed by Hypothyroid phase
Subclinical Hypothyroidism: High TSH, Normal T3, T4
Causes of Hypothyroidism with brief initial Hyperthyroid Phases
Hashimotos Thyroiditis:
- V brief thyrotoxic phase initially
Subacute Thyroiditis (De Quervain's): - initial brief hyperthyroid phase followed by longer hypothyroid phase
Postpartum Thyroiditis:
- initial brief hyperthyroid phase followed by longer hypothyroid phase
Other Causes of Hypothyroidism:
- Riddle’s thyroid’s
- Iodine deficiency
- Lithium
NB Amiodarone causes both
