Lec#15+16 Thyroid Disorders

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Thyroid disorders

Murad Shatnawi, MD
Assistant Professor of Endocrinology , Diabetes and Metabolism.
YU
01/11/2021
Hypothalamus make TRH

Anterior pituitary makes TSH

Thyroid Gland makes T4 and T3

Iodine enters thyroid gland and is used for T3 and T4 production


Hormones are released from the thyroid and vast majority are protein bound (TBG) and deposited in peripheral cells
T4 has 4 iodine atoms, removal of one produces T3 , thyroid hormones functions are to :
• Facilitate normal growth and development
• Increase metabolism
• Increase catecholamine effects
TSH : Most useful marker of thyroid hormone function , Released in a pulsatile diurnal rhythm- highest at night
Disorders of the thyroid gland
• Hypothyroidism
• Hyperthyroidism
• Thyroid nodules
• Thyroid cancer
Hypothyroidism
• Hypothyroidism is a common condition with various causes but
autoimmune disease (Hashimoto’s thyroiditis) and thyroid failure
following 131I or surgical treatment of thyrotoxicosis account for over
90% of cases, except in areas where iodine deficiency is endemic.
• Women are affected approximately six times more frequently than
men.
Hypothyroidism
• Insufficient thyroid hormone
1. Primary: thyroid gland failure
2. Secondary: pituitary gland failure
3. Tertiary: hypothalamus failure
Primary hypothyroidism etiology
• Iodine deficiency- most common cause worldwide
• Congenital
• Autoimmune mediated
• Hashimoto’s thyroiditis- B lymphocytes invade thyroid
• Iatrogenic- post-thyroidectomy or radio-iodine treatment
• Drug-induced – Anti-thyroid, lithium, amiodarone
• Severe infection
• Trauma to thyroid/pituitary/hypothalamus
• Pituitary tumour
Clinical assessment
• The clinical presentation depends on the duration and severity of the hypothyroidism.
• A consequence of prolonged hypothyroidism is the infiltration of many body tissues by the
mucopolysaccharides, hyaluronic acid and chondroitin sulphate, resulting in a low-pitched
voice, poor hearing, slurred speech due to a large tongue, and compression of the median
nerve at the wrist (carpal tunnel syndrome).
• Infiltration of the dermis gives rise to nonpitting oedema (myxoedema), which is most
marked in the skin of the hands, feet and eyelids. The resultant periorbital puffiness is
often striking and may be combined with facial pallor due to vasoconstriction and
anaemia, or a lemon-yellow tint to the skin caused by carotenaemia, along with purplish
lips and malar flush.
• Most cases of hypothyroidism are not clinically obvious, however, and a high index of
suspicion needs to be maintained so that the diagnosis is not overlooked in individuals
complaining of non-specific symptoms such as tiredness, weight gain, depression or carpal
tunnel syndrome.
Common symptoms and signs
• Cold intolerance
• Fatigue, somnolence
• Dry skin
• Dry hair
• Menorrhagia
• Weight gain
Less common
• Constipation
• Hoarseness
• Carpal tunnel syndrome
• Alopecia
• Aches and pains
• Muscle stiffness
• Deafness
• Depression
• Infertility
• Hoarse voice
• Facial features:
• Purplish lips
• Malar flush
• Periorbital oedema
• Loss of lateral eyebrows
• Anaemia
• Carotenaemia
• Erythema ab igne
• Bradycardia
• hypertension
• Delayed relaxation of reflexes
• Dermal myxoedema
Rare
• Psychosis (myxoedema madness)
• Galactorrhoea
• Impotence
• Ileus, ascites
• Pericardial and pleural effusions
• Cerebellar ataxia
• Myotonia
Investigations
• In the vast majority of cases, hypothyroidism results from an intrinsic disorder of the thyroid gland
(primary hypothyroidism). In this situation, serum T4 is low and TSH is elevated, usually in excess of 20
mU/L. Measurements of serum T3 are unhelpful since they do not discriminate reliably between
euthyroidism and hypothyroidism.
• Secondary hypothyroidism is rare and is caused by failure of TSH secretion in an individual with
hypothalamic or anterior pituitary disease.
• In severe, prolonged hypothyroidism, the electrocardiogram (ECG) classically demonstrates sinus
bradycardia with low-voltage complexes and ST segment and T-wave abnormalities.
• Measurement of thyroid peroxidase antibodies is helpful but further investigations are rarely required
• Serum enzymes: raised creatine kinase, aspartate aminotransferase, lactate dehydrogenase (LDH)
• Hypercholesterolaemia
• Anaemia: normochromic normocytic or macrocytic
• Hyponatraemia
• hyperprolactinemia
Management
• Treatment is with levothyroxine replacement. It is customary to start with a low dose
of 50 μg per day for 3 weeks, increasing thereafter to 100 μg per day for a further 3
weeks and finally to a maintenance dose of 100–150 μg per day.
• In younger patients, it is safe to initiate levothyroxine at a higher dose (for example,
100 μg per day), to allow a more rapid normalisation of thyroid hormone levels.
• Levothyroxine has a half-life of 7 days so it should always be taken as a single daily
dose and at least 6 weeks should pass before repeating thyroid function tests and
adjusting the dose, usually by 25 μg per day.
• Patients feel better within 2–3 weeks.
• Reduction in weight and periorbital puffiness occurs quickly, but the restoration of
skin and hair texture and resolution of any effusions may take 3–6 months.
• life-long levothyroxine therapy
• The dose of levothyroxine should be adjusted to maintain serum TSH
within the reference range. To achieve this, serum T4 often needs to be in
the upper part of the reference range or even slightly raised, because the
T3 required for receptor activation is derived exclusively from conversion
of T4 within the target tissues, without the usual contribution from
thyroid secretion.
• Some patients remain symptomatic despite normalisation of TSH and
may wish to take extra levothyroxine, which suppresses TSH. However,
suppressed TSH is a risk factor for osteoporosis and atrial fibrillation
(subclinical thyrotoxicosis), so this approach cannot be recommended
• Target TSH is 0.5-2.5 mU/L
• It is important to measure thyroid function every 1–2 years once the
dose of levothyroxine is stabilised.
• persistent elevation of serum TSH despite an ostensibly adequate
replacement dose of levothyroxine; most commonly, this is a
consequence of suboptimal compliance with therapy.
• Levothyroxine absorption is maximal when the medication is taken
before bed and may be further optimised by taking a vitamin C
supplement.
Levothyroxine replacement in ischaemic
heart disease
• exacerbation of myocardial ischaemia, infarction and sudden death
are recognised complications of levothyroxine replacement, even
using doses as low as 25 μg per day. In patients with known ischaemic
heart disease, thyroid hormone replacement should be introduced at
low dose and increased very slowly under specialist supervision
• Coronary angioplasty or bypass surgery may be required if angina is
exacerbated by levothyroxine replacement therapy
Hypothyroidism in pregnancy
• Most pregnant women with primary hypothyroidism require an increase in
the dose of levothyroxine of approximately 25–50 μg daily to maintain normal
TSH levels. This may reflect increased metabolism of thyroxine by the
placenta and increased serum thyroxine binding globulin during pregnancy,
resulting in an increase in the total thyroid hormone pool to maintain the
same free T4 and T3 concentrations.
• Inadequate maternal T4 therapy may be associated with impaired cognitive
development in an unborn child and so women are usually advised to
increase their daily levothyroxine dose by 25 μg when pregnancy is
confirmed.
• Serum TSH and free T4 should be measured during each trimester and the
dose of levothyroxine adjusted to maintain a target TSH (0.1-2.5)
Myxoedema coma
• This is a very rare presentation of hypothyroidism in which there is a
depressed level of consciousness, usually in an elderly patient who
appears myxoedematous.
• Body temperature may be as low as 25°C, convulsions are not
uncommon and cerebrospinal fluid (CSF) pressure and protein
content are raised. The mortality rate is 50% and survival depends on
early recognition and treatment of hypothyroidism and other factors
contributing to the altered consciousness level, such as medication,
cardiac failure, pneumonia, dilutional hyponatraemia and respiratory
failure.
• Myxoedema coma is a medical emergency and treatment must begin before
biochemical confirmation of the diagnosis. Suspected cases should be treated
with an intravenous injection of 20 μg triiodothyronine, followed by further
injections of 20 μg 3 times daily until there is sustained clinical improvement. In
survivors, there is a rise in body temperature within 24 hours and, after 48–72
hours, it is usually possible to switch patients to oral levothyroxine in a dose of 50
μg daily. Unless it is apparent that the patient has primary hypothyroidism, the
thyroid failure should also be assumed to be secondary to hypothalamic or
pituitary disease and treatment given with hydrocortisone 100 mg IM 3 times
daily, pending the results of T4, TSH and cortisol measurement .Other measures
include slow rewarming ,cautious use of intravenous fluids, broad-spectrum
antibiotics and high-flow oxygen. Occasionally, assisted ventilation may be
necessary
Symptoms of hypothyroidism with normal
thyroid function tests
• The classic symptoms of hypothyroidism are, by their non-
specific .There is a wide differential diagnosis for symptoms such as
‘fatigue’, ‘weight gain’ and ‘low mood’.
• serum TSH is an excellent measure of a individual’s thyroid hormone
status.
• Normal TSH necessiate looking for an alternative diagnosis
Subclinical hypothyroidism
• Serum TSH is raised, with normal serum T3 and T4 concentrations

• there is a risk of progression to overt thyroid failure, particularly if


antibodies to thyroid peroxidase are present or if the TSH rises above 10
mU/L. In patients with non-specific symptoms, a trial of levothyroxine
therapy may be appropriate. In those with positive autoantibodies or
TSH greater than 10 mU/L, it is better to treat the thyroid failure early
rather than risk loss to follow-up and subsequent presentation with
profound hypothyroidism. Levothyroxine should be given in a dose
sufficient to restore the serum TSH concentration to normal.
Thyrotoxicosis
• Thyrotoxicosis describes a constellation of clinical features arising
from elevated circulating levels of thyroid hormone.
• The most common causes are Graves’ disease, multinodular goitre
and autonomously functioning thyroid nodules (toxic adenoma)
• Thyroiditis is more common in parts of the world where relevant viral
infections occur, such as North America.
Clinical assessment
• The clinical manifestations of thyrotoxicosis are variable
• The most common symptoms are weight loss with a normal or
increased appetite, heat intolerance, palpitations, tremor and
irritability.
• Tachycardia, palmar erythema and lid lag are common signs. Not all
patients have a palpable goitre, but experienced clinicians can
discriminate the diffuse soft goitre of Graves’ disease from the
irregular enlargement of a multinodular goitre.
• All causes of thyrotoxicosis can cause lid retraction and lid lag, due to
potentiation of sympathetic innervation of the levator palpebrae
muscles, but only Graves’ disease causes other features of
ophthalmopathy, including periorbital oedema, conjunctival irritation,
exophthalmos and diplopia.
• Pretibial myxoedema and the rare thyroid acropachy (a periosteal
hypertrophy, indistinguishable from finger clubbing) are also specific
to Graves’ disease
Common symptoms and signs
• Weight loss despite normal or increased appetite
• Heat intolerance, sweating
• Palpitations, tremor
• Dyspnoea, fatigue
• Irritability, emotional lability
• Weight loss
• Tremor
• Palmar erythema
• Sinus tachycardia
• Lid retraction, lid lag
Less common
• Osteoporosis (fracture, loss of height)
• Diarrhoea, steatorrhoea
• Angina
• Ankle swelling
• Anxiety, psychosis
• Muscle weakness
• Periodic paralysis
• Pruritus, alopecia
• Amenorrhoea/oligomenorrhoea
• Infertility, spontaneous abortion
• Loss of libido, impotence
• Excessive lacrimation
• Goitre with bruit
• Atrial fibrillation
• Systolic hypertension/ increased pulse pressure
• Cardiac failure
• Hyper-reflexia
• sustained clonus
• Proximal myopathy
• Bulbar myopathy
Rare
• Vomiting
• Apathy
• Anorexia
• Exacerbation of asthma
• Gynaecomastia
• Spider naevi
• Onycholysis
• Pigmentation
Investigations
• The first-line investigations are serum T3, T4 and TSH. If abnormal values are
found, the tests should be repeated and the abnormality confirmed in view of the
likely need for prolonged medical treatment or destructive therapy.
• In most patients, serum T3 and T4 are both elevated, but T4 is in the upper part
of the reference range and T3 raised (T3 toxicosis) in about 5%.
• Serum TSH is undetectable in primary thyrotoxicosis, but values can be raised in
the very rare syndrome of secondary thyrotoxicosis caused by a TSH-producing
pituitary adenoma. When biochemical thyrotoxicosis has been confirmed, further
investigations should be undertaken to determine the underlying cause, including
measurement of TSH receptor antibodies (TRAb, elevated in Graves’ disease, and
isotope scanning, Other non-specific abnormalities are common.
• An ECG may demonstrate sinus tachycardia or atrial fibrillation
• Radio-iodine uptake tests measure the proportion of isotope that is trapped in the
whole gland, but have been largely superseded by 99mtechnetium scintigraphy scans,
which also indicate trapping, are quicker to perform with a lower dose of radioactivity,
and provide a higher-resolution image. In low-uptake thyrotoxicosis, the cause is usually
a transient thyroiditis
• Occasionally, patients induce ‘factitious thyrotoxicosis’ by consuming excessive amounts
of a thyroid hormone preparation, most often levothyroxine. The exogenous thyroxine
suppresses pituitary TSH secretion and hence iodine uptake, serum thyroglobulin and
release of endogenous thyroid hormones. The T4:T3 ratio (typically30 : 1 in
conventional thyrotoxicosis) is increased to above 70 : 1 because circulating T3 in
factitious thyrotoxicosis is derived exclusively from the peripheral monodeiodination of
T4 and not from thyroid secretion. The combination of negligible iodine uptake, high
T4:T3 ratio and a low or undetectable thyroglobulin is diagnostic
• Serum enzymes: raised alanine aminotransferase, γ-glutamyl
transferase (GGT), and alkaline phosphatase from liver and bone
• Raised bilirubin
• Mild hypercalcaemia
• Glycosuria: associated diabetes mellitus, ‘lag storage’ glycosuria
Establishing the differential diagnosis in
thyrotoxicosis
• Any features of Graves’ disease?
• Diffuse goitre with bruit
• Ophthalmopathy
• Pretibial myxoedema
• Positive TSH receptor antibodies

If No : Thyroid scintigraphy
If Yes : Graves
Management
Definitive treatment of thyrotoxicosis depends on the underlying cause and may
include
antithyroid drugs : Carbimazole, propylthiouracil (50% relapse) Risk of
agranulocytosis ,
radioactive iodine
surgery.
• A non-selective β-adrenoceptor antagonist (β-blocker), such as
propranolol will alleviate but not abolish symptoms in most patients
within 24–48 hours. Beta-blockers should not be used for long-term
treatment of thyrotoxicosis .
Atrial fibrillation in thyrotoxicosis
• Atrial fibrillation occurs in about 10% of patients with thyrotoxicosis. The
incidence increases with age, so that half of all males with thyrotoxicosis
over the age of 60 are affected. Moreover, subclinical thyrotoxicosis is a
risk factor for atrial fibrillation. Characteristically the ventricular rate is
little influenced by digoxin, but responds to the addition of a β-blocker.
• Thromboembolic vascular complications are particularly common in
thyrotoxic atrial fibrillation so that anticoagulation with warfarin is
required, unless contraindicated. Once thyroid hormone and TSH
concentrations have been returned to normal, atrial fibrillation will
spontaneouslyrevert to sinus rhythm in about 50% of patients, but
cardioversion may be required in the remainder
Thyrotoxic crisis (‘thyroid storm’)
• Life threatening emergency (rare) – 30% mortality even with early recognition and
management

• Exacerbation of thyrotoxicosis precipitated by stress i.e.


• Surgery
• Infection
• Trauma

• Signs
• Fever
• Agitation and confusion
• Tachycardia +/- AF
• Management
• IV fluids
• Broad spectrum antibiotics
• Propanolol, digoxin
• Antithyroid drugs – sodium ipodate, Lugol’s solution, carbimozole
Subclinical thyrotoxicosis
• Serum TSH is undetectable, and serum T3 and T4 are at the upper end
of the reference range. This combination is most often found in older
patients with multinodular goitre. These patients are at increased risk
of atrial fibrillation and osteoporosis, and hence the consensus view is
that they have mild thyrotoxicosis and require therapy, usually with
131I. Otherwise, annual review is essential, as the conversion rate to
overt thyrotoxicosis with elevated T4 and/or T3 concentrations is 5%
each year.
Thyroid lump or swelling
• A lump or swelling in the thyroid gland can be a source of considerable anxiety for
patients. There are numerous causes but, broadly speaking, a thyroid swelling is either a
solitary nodule, a multinodular goitre or a diffuse goitre
• Nodular thyroid disease is more common in women and occurs in approximately 30% of
the adult female population. The majority of thyroid nodules are impalpable but may be
identified when imaging of the neck is performed for another reason, such as during
Doppler ultrasonography of the carotid arteries or computed tomographic pulmonary
angiography. Increasingly, thyroid nodules are identified during staging of patients with
cancer with computed tomography (CT), magnetic resonance imaging (MRI) or positron
emission tomography (PET) scans.
• Palpable thyroid nodules occur in 4–8% of adult women and 1–2% of adult men, and
classically present when the individual (or a friend or relative) notices a lump in the neck.
Multinodular goitres and solitary nodules sometimes present with acute painful
enlargement due to haemorrhage into a nodule.
• Patients with thyroid nodules often worry that they have cancer, but
the reality is that only 5–10% of thyroid nodules are malignant. A
solitary nodule presenting in childhood or adolescence, particularly if
there is a past history of head and neck irradiation, or one presenting
in the elderly should heighten suspicion of a primary thyroid
malignancy
• The presence of cervical lymphadenopathy also increases the
likelihood of malignancy. Rarely, a secondary deposit from a renal,
breast or lung carcinoma presents as a painful, rapidly growing,
solitary thyroid nodule. Thyroid nodules identified on PET scanning
have an approximately 33% chance of being malignant.
Causes of thyroid enlargement
Diffuse goitre
• Simple goitre
• Hashimoto’s thyroiditis1
• Graves’ disease
• Drugs Iodine, amiodarone, lithium
• Iodine deficiency (endemic goitre)
• Suppurative thyroiditis
• Transient thyroiditis
• Dyshormonogenesis
• Infiltrative : Amyloidosis, sarcoidosis ..etc.
• Riedel’s thyroiditis
Solitary nodule or part of MNG
• Colloid cyst
• Hyperplastic nodule
• Follicular adenoma
• Papillary carcinoma
• Follicular carcinoma
• Medullary cell carcinoma
• Anaplastic carcinoma
• Lymphoma
• Metastasis
Clinical assessment and investigations
• Swellings in the anterior part of the neck most commonly originate in
the thyroid and this can be confirmed by demonstrating that the
swelling moves on swallowing
• It is often possible to distinguish clinically between the three main
causes of thyroid swelling.
• There is a broad differential diagnosis of anterior neck swellings, which
includes lymphadenopathy, branchial cysts, dermoid cysts and
thyroglossal duct cysts (the latter are classically located in the midline
and move on protrusion of the tongue).
• An ultrasound scan should be performed urgently, if there is any doubt
as to the aetiology of an anterior neck swelling.
• Serum T3, T4 and TSH should be measured in all patients with a goitre
or solitary thyroid nodule.
• The finding of biochemical thyrotoxicosis or hypothyroidism (both of
which may be subclinical) should necessiate further investigations
Thyroid scintigraphy
• Thyroid scintigraphy with 99m technetium should be performed in an
individual with a low serum TSH and a nodular thyroid to confirm the
presence of an autonomously functioning (‘hot’) nodule
• In such circumstances, further evaluation by fine needle aspiration is
not necessary. ‘Cold nodules’ on scintigraphy have a much higher
likelihood of malignancy, but the majority are benign and so
scintigraphy is not routinely used in the evaluation of thyroid nodules
when TSH is normal.
Thyroid ultrasound
• If thyroid function tests are normal, an ultrasound scan will determine
the nature of the thyroid swelling. Ultrasound can establish whether
there is generalised or localised swelling of the thyroid. Inflammatory
disorders causing a diffuse goitre, such as Graves’ disease and
Hashimoto’s thyroiditis, demonstrate a diffuse pattern of
hypoechogenicity and, in the case of Graves’ disease, increased
thyroid blood flow may be seen on colour flow Doppler.
• The presence of thyroid autoantibodies will support the diagnosis of
Graves’ disease or Hashimoto’s thyroiditis, while their absence in a
younger patient with a diffuse goitre and normal thyroid function
suggests a diagnosis of ‘simple goitre’
• Ultrasound can also readily determine the size and number of nodules
within the thyroid and can distinguish solid nodules from those with a
cystic element.
• It cannot reliably distinguish benign from malignant nodules but, in
experienced hands, there are some ultrasound characteristics which are
associated with a higher likelihood of malignancy. These include:
hypervascularity of the nodule, the presence of microcalcification and
irregular, infiltrative margins.
• A pure cystic nodule is highly unlikely to be malignant and a
‘spongiform’ appearance is also highly predicative of a benign aetiology.
Fine needle aspiration
• Cytological examination of a thyroid nodule, following fine needle
aspiration, is recommended for most thyroid nodules over 1 cm in
size. Smaller nodules should be aspirated if there is a high suspicion of
malignancy on clinical or ultrasound grounds, while some clinicians
will be happy to observe a nodule up to 2 cm in size with a
spongiform appearance. Individuals with a multinodular goitre have
the same risk of malignancy as those with a solitary nodule.
Sometimes, one of the nodules in a multinodular goitre is much larger
than any other (a ‘dominant’ nodule), but ultimately the choice of
nodule to biopsy should be based on ultrasound characteristics.
• Fine needle aspiration of a thyroid nodule can be performed in the outpatient
clinic using a standard 21-gauge needle and a 20 mL syringe, usually making
several passes through different parts of the lesion. Ultrasound-guided needle
aspiration is necessary for impalpable nodules and to permit targeting of the
solid component of a mixed cystic/solid nodule. Aspiration may be
therapeutic in the small proportion of patients in whom the swelling is a cyst,
although recurrence on more than one occasion is an indication for surgery.
• Cytological examination can differentiate benign (80%) from definitely
malignant or indeterminate nodules (20%), of which 25–50% are confirmed as
cancers at surgery. The limitations of fine needle aspiration are that it cannot
differentiate between follicular adenoma and carcinoma, and that in 10–20%
of cases an inadequate specimen is obtained.
Subacute (de Quervain’s)
thyroiditis
• In its classical painful form, subacute thyroiditis is a transient
inflammation of the thyroid gland occurring after infection with
Coxsackie, mumps or adenoviruses.
• There is pain in the region of the thyroid that may radiate to the angle
of the jaw and the ears, and is made worse by swallowing, coughing and
movement of the neck.
• The thyroid is usually palpably enlarged and tender. Systemic upset is
common. Affected patients are usually females aged 20–40 years.
Painless transient thyroiditis can also occur after viral infection and in
patients with underlying autoimmune disease. The condition can also
be precipitated by drugs, including interferon-α and lithium.
• Irrespective of the clinical presentation, inflammation in the thyroid
gland occurs and is associated with release of colloid and stored
thyroid hormones, but also with damage to follicular cells and
impaired synthesis of new thyroid hormones. As a result, T4 and T3
levels are raised for 4–6 weeks until the pre-formed colloid is
depleted. Thereafter, there is usually a period of hypothyroidism of
variable severity before the follicular cells recover and normal thyroid
function is restored within 4–6 months
• In the thyrotoxic phase, the iodine uptake is low, because the
damaged follicular cells are unable to trap iodine and because TSH
secretion is suppressed. Low-titre thyroid autoantibodies appear
transiently in the serum, and the erythrocyte sedimentation rate (ESR)
is usually raised.
• High-titre autoantibodies suggest an underlying autoimmune
pathology and greater risk of recurrence and ultimate progression to
hypothyroidism.
• The pain and systemic upset usually respond to simple measures such
as non-steroidal anti-inflammatory drugs (NSAIDs). Occasionally,
however, it may be necessary to prescribe prednisolone 40 mg daily
for 3–4 weeks. The thyrotoxicosis is mild and treatment with a β-
blocker is usually adequate. Antithyroid drugs are of no benefit
because thyroid hormone synthesis is impaired rather than enhanced.
Careful monitoring of thyroid function and symptoms is required so
that levothyroxine can be prescribed temporarily in the hypothyroid
phase. Care must be taken to identify patients presenting with
hypothyroidism who are in the later stages of a transient thyroiditis,
since they are unlikely to require life-long levothyroxine therapy
Post-partum thyroiditis
• The maternal immune response, which is modified during pregnancy
to allow survival of the fetus, is enhanced after delivery and may
unmask previously unrecognised subclinical autoimmune thyroid
disease.
• Surveys have shown that transient biochemical disturbances of
thyroid function occur in 5–10% of women within 6 months of
delivery
• Those affected are likely to have anti-thyroid peroxidase antibodies in
the serum in early pregnancy. Symptoms of thyroid dysfunction are
rare and there is no association between postnatal depression and
abnormal thyroid function tests. However, symptomatic thyrotoxicosis
presenting for the first time within 12 months of childbirth is likely to
be due to post-partum thyroiditis and the diagnosis is confirmed by a
negligible radio-isotope uptake. The clinical course and treatment are
similar to those of painless subacute thyroiditis (see above).
Postpartum thyroiditis tends to recur after subsequent pregnancies,
and eventually patients progress over a period of years to permanent
hypothyroidism.
Amiodarone
• The anti-arrhythmic agent amiodarone has a structure that is analogous to that of T4
(and contains huge amounts of iodine; a 200 mg dose contains 75 mg iodine, compared
with a daily dietary requirement of just 125 μg. Amiodarone also has a cytotoxic effect
on thyroid follicular cells and inhibits conversion of T4 to T3. Most patients receiving
amiodarone have normal thyroid function, but up to 20% develop hypothyroidism or
thyrotoxicosis and so thyroid function should be monitored regularly.
• The ratio of T4:T3 is elevated and TSH provides the best indicator of thyroid function.
• The thyrotoxicosis can be classified as either:
• type I: iodine-induced excess thyroid hormone synthesis in patients with an underlying
thyroid disorder, such as nodular goitre or latent Graves’ disease
• type II: thyroiditis due to a direct cytotoxic effect if amiodarone administration results
in a transient thyrotoxicosis.
• These patterns can overlap and can be difficult to distinguish clinically,
as iodine uptake is low in both
• Antithyroid drugs may be effective in patients with the type I form,
but are ineffective in type II thyrotoxicosis. Prednisolone is beneficial
in the type II form.
MEN Syndrome
• MEN1 : parathyroid , pituitary & Pancreatic tumors.
• MEN2A : Parathyroid hyperplasia, MTC & PHE
• MEN2B : MTC , PHE & mucosal neuroma
APS
• 1 : addison , hypoparathyroid and ch candidiasis
• 2 : addison , hypothyroidism and diabetes
Selenium
• Selenium supplementation in people with Hashimoto's thyroiditis
might reduce antibody levels and result in a decreased dosage of
levothyroxine (LT4) and may provide other beneficial effects (e.g. on
mood and health-related quality of life).
• They found that treatment with selenium, but not with
pentoxifylline, was associated with improved quality of life, less eye
involvement, and delayed progression of Graves' orbitopathy at 6
months

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