THYROTOXICOSIS

1
THYROTOXICOSIS
ENCHILL Jacob
KUMI Derrick
OUTLINE 2
• Introduction
• Literature review
• Diagnosis
• Clinical manifestations
• Treatment
• Case presentation
INTRODUCTION 3
• Biochemical and physiological manifestation of excessive thyroid

hormone.
• Not all thyrotoxicosis are due to hyperthyroidism but all
hyperthyroidism produce thyrotoxicosis.
• Synthesis and release of thyroid hormone is controlled by TSH
released form the anterior pituitary
• TSH is controlled by the release of thyroid releasing hormone
(TRH) from the hypothalamus and a negative feedback loop to the
pituitary
• Thyroid hormone production is dependent on adequate iodine
intake
INTRODUCTION 4
• Hyperthyroidism resembles a state of increased adrenergic activity

despite a normal or low serum cortisol level
• Classic complaints include heat intolerance, palpitations, weight
loss, sweating, nervousness, and fatigue
LITERATURE REVIEW 5
LITERATURE REVIEW 6
• Thyroid hormone is reversibly bound to various proteins including

thyronine-binding globulin (TBG)
• Free unbound portions are biologically active
• T4 is the predominant circulating hormone
• T4 is deiodinated to t3
• T3 is biologically more active than T4 but has a shorter half-life
LITERATURE REVIEW 7
LITERATURE REVIEW 8
Clinical Types
• Primary thyrotoxicosis – Grave’s Disease
• Secondary Thyrotoxicosis
• Toxic nodule
• Rare causes for hyperthyroidism
LITERATURE REVIEW 9
Grave’s Disease
• This is the most common cause of
hyperthyroidism and has an autoimmune
basis.
• It is an autoimmune disease mediated by
antibodies that stimulate the TSH receptor,
leading to excess secretion of thyroid
hormones and hyperplasia of thyroid
follicular cells, resulting in
hyperthyroidism and diffuse goitre
LITERATURE REVIEW 10
• Secondary hyperthyroidism is the term used when the thyroid gland is
stimulated by excessive thyroid-stimulating hormone (TSH) in the
circulation.
• Secondary hyperthyroidism is rare. The pathology is at the level of the
pituitary. TSH, T3 and T4 are all very high. TRH stimulation tests are used
in the diagnosis and result in a flat response curve.
Causes include:
• TSH-secreting pituitary adenoma.

• Thyroid hormone-resistance syndrome.
• hCG-secreting tumour.
Toxic nodule
• It is autonomous nodule (not under the control of T.S.H or thyroid
antibodies).
• The remnant thyroid tissues surrounding that nodule are
suppressed due to low T.S.H level caused by high thyroxine
secreted from the nodule.
Hyperthyroidism due to rare causes":

• Thyrotoxicosis factitia: caused by thyroxine intake as a tonic.
• Jod-Basedow (Iodine-Goitre) Due to intake of large dose of iodine esp.
in endemic areas.
• In de Quervain's thyroiditis very mild in early stages due to liberation of
thyroid hormone from damaged tissues
• Neonatal thyrotoxicosis In babies born to hyperthyroid mother or
euthyroid mother with past history of thyrotoxicosis as the high
antibody titre may induce thyrotoxicosis in the baby
• Follicular carcinoma of the thyroid gland
• Drugs; These include amiodarone, lithium and exogenous iodine.
•
Risk Factors:
• Family history.
• High iodine intake.
• Smoking (particularly for thyroid-associated ophthalmopathy).
• Trauma to the thyroid gland (including surgery).
• Toxic multinodular goitre (which is especially associated with an
increased iodine intake, either from a change in diet or an acute dose
from iodine-containing agents (eg, amiodarone, contrast agents)).
• Childbirth.
• Highly active antiretroviral therapy (HAART).
DIAGNOSIS 14
Investigations
• TFTs: serum TSH can exclude primary thyrotoxicosis. Confirm the diagnosis with free
T4 levels. If TSH is suppressed but free T4 levels are normal then, if not previously
supplied, free T3 level is needed (T3 toxicosis occurs in 5% of patients).
• Autoantibodies - these are most commonly seen in Graves' disease:
• Antimicrosomal antibodies - against thyroid peroxidase. Thyroid peroxidase
antibodies are present in about 75% of cases of Graves' hyperthyroidism and can help
to differentiate autoimmune disease from toxic nodular hyperthyroidism.[3]
• Antithyroglobulin antibodies.
• TSH-receptor antibodies which are commonly present in Graves' disease. They have
been shown to have a sensitivity of 98% and a specificity of 99%.[9]However, this test
is not widely available.
DIAGNOSIS 15
Imaging:
• Thyroid ultrasound scan.
• Thyroid uptake scans: to locate hot (overactivity) and cold (no
activity) spots.
Inflammatory markers:
• In patients with subacute thyroiditis, CRP and ESR are often raised
Differential diagnosis of Phaeochromocytoma and any cause of

significant weight loss.
CLINICAL MANIFESTATIONS 16
TREATMENT 17
Carbimazole (methimazole) or propylthiouracil (Class: thionamides):
• These drugs act very quickly and inhibit the production of thyroid hormones. Full benefit may take 2-3 weeks to
become apparent.
• The recommended starting dose of carbimazole or methimazole is 10-20 mg per day.[3]
• There are two potential methods of treating hyperthyroid patients: 'block and replace' - where anti-thyroid drugs are
given with thyroxine replacement, and 'dose titration' - where only anti-thyroid drugs are used and doses are
adjusted to achieve normalisation of thyroid hormone production.
• A systematic review and meta-analysis suggest that both types of methods are equally effective. Furthermore, the
dose titration method was associated with a lower rate of side-effects.[11]
• Most patients with hyperthyroid Graves' disease are rendered euthyroid by 4-8 weeks of treatment with carbimazole
(20-40 mg daily).[4]
• TFTs are repeated every month and the dose altered according to the T4 level. TSH may remain suppressed for
months despite the T4 coming into the normal range and is, thus, unreliable.
• Once the patient is euthyroid, the dose of carbimazole is reduced until the patient is on the lowest amount
necessary to maintain the T4 and T3 within the normal range.
• Remission is usually achieved at 18-24 months, after which attempts may be made to stop anti-thyroid drugs.
• Minor side-effects include: nausea and a bitter taste after taking medication. Warn patients to come for FBC if they
TREATMENT 18
Radio-iodine
• Increasingly, the first-line treatment in teenagers.It is also usually the treatment of choice in relapsed Graves'
disease and in those patients with toxic nodular hyperthyroidism:
• Radioactive iodine is given to the patient as a drink and is taken up by the thyroid gland, leading to
destruction of the gland. It can take 3-4 months to take effect.
• Radio-iodine has the advantages that it is relatively inexpensive and a definitive method of treating
hyperthyroidism.
• Anti-thyroid drugs should be stopped 5-7 days before treatment with radio-iodine because continuous use
reduces thyroid iodide uptake and retention, which in turn reduces cure rates.
• It cannot be given to pregnant or breast-feeding females and females must be advised not to get pregnant for
at least six months.
• Radioactive iodine may also worsen eye disease in Graves' thyrotoxicosis; this is more marked in smokers.
• The patient does have to be informed that the radioactive iodine is cleared via the urine and thus can be
passed on. They are usually advised to avoid close contact with children and pregnant women for about three
weeks.
TREATMENT 19
Surgical
• Surgery is used infrequently in the treatment of thyrotoxicosis.[3]

• Patients should be returned to the euthyroid state with anti-thyroid drugs before
surgery to avoid thyroid storm.
• Subtotal or near total thyroidectomy achieves a 98% cure rate. It is indicated if
there is suboptimal response to anti-thyroid medication or radio-iodine, especially
in patients who are pregnant or who have Graves' orbitopathy.
• Complications are rare but include haemorrhage, hypoparathyroidism and vocal
cord paralysis.
• Patients who undergo surgery will need to be followed up over a number of years,
as they may develop hypothyroidism.
• Toxic adenoma or toxic multinodular goitre which is resistant to conservative
treatment or causing compression symptoms is best treated with surgical excision.
TREATMENT 20
• NB: thyrotoxicosis associated with thyroiditis is transient and

resolves spontaneously. Anti-thyroid drugs are not effective and
should therefore be avoided.
• All patients with new-onset thyrotoxicosis should be referred for
assessment in secondary care, to establish the cause and to agree
on a management plan.[4]
• Beta-blockers can be used for rapid symptom control whilst

waiting for thyroid function to normalise. Calcium-channel
blockers may be used if patients are intolerant of beta-blockers.

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1

• Biochemical and physiological manifestation of excessive thyroid

• Hyperthyroidism resembles a state of increased adrenergic activity

• Thyroid hormone is reversibly bound to various proteins including

• TSH-secreting pituitary adenoma.

Hyperthyroidism due to rare causes":

Differential diagnosis of Phaeochromocytoma and any cause of

• Surgery is used infrequently in the treatment of thyrotoxicosis.[3]

• NB: thyrotoxicosis associated with thyroiditis is transient and

• Beta-blockers can be used for rapid symptom control whilst

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