.Thyrotoxicosis
Biochemical and physiological manifestation of Excessive thyroid hormone (irrespective of source).
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Thyrotoxicosis need not be due to hyperthyroidism.But hyperthyroidism mostly produce thyrotoxicosis.
.Hyperthyroidism
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Disorder that result in over production of hormone by the thyroid gland.
In short, hyperthyroidism the pathology is in the thyroid gland itself.
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Thyrotoxicosis Vs HyperthyroidismHYPERTHYROIDISM
TOXICOSIS WITHOUT HYPERTHYROIDISM
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Subacute thyroiditisGrave's disease
Ectopic functioning thyroid
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Multi-nodular toxic goitre
Silent thyroiditis
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Toxic adenomaStruma ovarii
Jod ? Basedow's disease
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Metastatic follicular carcinoma
Trophoblastic tumours
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Postpartum thyroiditisThyrotoxicosis factitia
Diffuse toxic goitre....
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.Also known as Graves' disease after Robert Graves, an Irish physician who described three patients in 1835..An autoimmune disease with a strong familial predisposition.
.Female preponderance (5:1).
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.Peak incidence between the ages of 40 to 60 years.
.Characterized by:
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ThyrotoxicosisDiffuse goitre
Extrathyroidal conditions - Ophthalmopathy/ Dermopathy (Pretibial Myxoedema)/ Thyroid Acropachy/ Gynecomastia.
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Diffuse toxic goitre....
.Etiology:
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Exact etiology of the initiation of the autoimmune process is not known.Possible triggering events:
o Postpartum state
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o Iodine excesso lithium therapy
o and bacterial and viral infections.
Genetic factors also play a role-HLA-B8, HLA-DR3 and HLADQA1*0501.
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Diffuse toxic goitre.....Pathogenesis:
Stimulate B lymphocytes, which produce antibodies directed against the TSH-receptor.
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Thyroid stimulating Igs (TSIs) or antibodies that stimulate the TSH-R, as wel as TSH-binding inhibiting
immunoglobulins or antibodies have been described.
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Thyroid-stimulating antibodies stimulate the thyrocytes to grow and synthesize excess thyroid hormone(hal mark of Graves' disease).
Graves' disease also is associated with other autoimmune conditions such as-
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o type I diabetes mel itus, Addison's disease, pernicious anaemia, and myasthenia gravis.
Diffuse toxic goitre....
Diffuse toxic goitre
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.Pathology:
Macroscopical y:-
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o Thyroid gland is diffusely and smoothly enlargedo With a concomitant increase in vascularity.
Microscopical y:-
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o Gland is hyperplastico Epithelium is columnar with minimal col oid present.
o Nuclei exhibit mitosis
o And papil ary projections of hyperplastic epithelium are common.
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Diffuse toxic goitre.....Clinical manifestation: Divided into-
Related to hyperthyroidism.
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And specific to Graves' disease.
Diffuse toxic goitre....
.Hyperthyroid symptoms:
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Heat intolerance.
Increased sweating and thirst.
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Weight loss despite adequate caloric intake.Symptoms of increased adrenergic stimulation- palpitations, nervousness, fatigue, emotional lability, hyperkinesia, and
tremors.
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Most common GI symptoms include increased frequency of bowel movements and diarrhea.
Female patients- amenorrhea, decreased fertility, and an increased incidence of miscarriages.
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Children- experience rapid growth with early bone maturation.Older patients -cardiovascular complications such as atrial fibrillation and congestive heart failure.
Diffuse toxic goitre....
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.Other manifestation of Grave's:
Approximately 50% of patients also develop clinical y evident ophthalmopathy.
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Eye signs:(due to catecholamine excess)o Lid lag (von Graefe's sign)
o Spasm of the upper eyelid revealing the sclera above the corneo-scleral limbus (Dalrymple's sign)
o And prominent stare.
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Diffuse toxic goitre....Diffuse toxic goitre
. True infiltrative eye disease results in:
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Periorbital edema.
Conjunctival swelling and congestion (chemosis).
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Proptosis.Limitation of upward and lateral gaze (from involvement of the
inferior and medial rectus muscles, respectively).
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Keratitis.
And even blindness due to optic nerve involvement.
Diffuse toxic goitre....
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.Other manifestation of Grave's:
Dermopathy occurs in 1 to 2% of patients.
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Rare bony involvement leads to subperiostealbone formation and swel ing in the
metacarpals (Thyroid Acropachy).
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Onycholysis, or separation of fingernails fromtheir beds.
Diffuse toxic goitre
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.Clinical signs:
Weight loss and facial flushing may be evident.
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Skin- warm and moist and darkening of skin.Cardiovascular:
o Tachycardia or atrial fibril ation.
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o Cutaneous vasodilation leading to a widening of the pulse pressure and a rapid fal off in the transmitted pulse wave (col apsing pulse).Diffuse toxic goitre
.Clinical signs:
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Musculoskeletal:o Fine tremor, muscle wasting.
o and proximal muscle group weakness with hyperactive tendon reflexes often are present.
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Thyroid:o Diffusely and symmetrical y enlarged, as evidenced by an enlarged pyramidal lobe.
o Overlying bruit or thril and loud venous hum in the supraclavicular space.
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Diffuse toxic goitre.....Diagnostic Tests:
Suppressed TSH with elevated free T4 or T3 level.
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If eye signs are present- other tests are general y not needed.
In the absence of eye findings- an I-131 uptake and scan should be performed.
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o An elevated uptake, with a diffusely enlarged gland- confirms the diagnosis.o It helps to differentiate it from other causes of hyperthyroidism.
Anti-Tg and anti-TPO antibodies are elevated in up to 75% of patients.
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Elevated TSH-R or thyroid-stimulating antibodies (TSAb) are diagnostic of Graves' disease (about 90% ofpatients).
Diffuse toxic goitre....
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.Management:Treated by any of three treatment modalities-
o Anti-thyroid drugs.
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o Thyroid ablation with radioactive I-131.o Thyroidectomy.
Diffuse toxic goitre....
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.Anti Thyroid Drugs:General y are administered in preparation for RAI ablation or surgery.
Drugs commonly used are-
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o Propylthiouracil (PTU, 100 to 300 mg three times daily)
o and methimazole (10 to 30 mg three times daily, then once daily).
Both drugs reduce thyroid hormone production by inhibiting the organic binding of iodine and the
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coupling of iodo-tyrosines (mediated by TPO).
PTU also inhibits the peripheral conversion of T4 to T3, so useful for the treatment of thyroid storm.
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PTU has a lower risk of transplacental transfer.Diffuse toxic goitre
.Anti Thyroid Drugs:
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Side effects of treatment include-o Reversible granulocytopenia.
o Skin rashes, fever.
o Peripheral neuritis, polyarteritis, vasculitis.
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o Rarely, agranulocytosis and aplastic anemia.Catecholamine response of thyrotoxicosis can be al eviated by administering beta- blocking agents.
o Propranolol is the most commonly prescribed medication in doses of about 20 to 40 mg four times daily.
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Diffuse toxic goitre....
.Radioactive Iodine Therapy (I-131):
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RAI forms the mainstay of Graves' disease treatment in North America.Major advantages- avoidance of a surgical procedure and its risks.
Dose - usual y consists of 8 to 12 mCi administered orally.
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Most patients become euthyroid within 2 months.
About 50% of patients treated with RAI are euthyroid 6 months after treatment.
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And remaining are stil hyperthyroid or already hypothyroid.Diffuse toxic goitre....
.Radioactive Iodine Therapy (I-131):
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RAI therapy is most often used in-Older patients with small or moderate-sized goiters
Those who have relapsed after medical or surgical therapy.
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Contraindication:
Absolute : Women who are pregnant or breastfeeding.
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Relative : Young patients (i.e., especially children and adolescents), those with thyroid nodules, and those withophthalmopathy.
Diffuse toxic goitre....
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.Surgical Treatment:
Recommended when RAI is contraindicated:
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Have confirmed cancer or suspicious thyroid nodules.Young and Pregnant or desire to conceive soon after treatment.
Severe reactions to anti-thyroid medications
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Large goitres causing compressive symptoms.
Reluctant to undergo RAI therapy.
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What surgical Procedure ?-(Solely based on discretion of surgeon and their experience.)Near total thyroidectomy
Subtotal thyroidectomy
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Total thyroidectomy
Toxic MNG....
.Usual y occur in older individuals, who often have a prior history of a nontoxic multinodular goitre.
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.Over several years, thyroid nodules become autonomous to cause hyperthyroidism.
.Hyperthyroidism also can be precipitated by iodide-containing drugs such as contrast media and the anti-
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arrhythmic agent amiodarone (jod-basedow hyperthyroidism)..Symptoms and signs of hyperthyroidism are similar to Graves' disease, but extra-thyroidal manifestations
are absent.
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Toxic MNG....
.Blood tests- similar to Graves' disease with a suppressed TSH level and elevated free T4 or T3 levels.
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.RAI uptake also is increased, showing multiple nodules with increased uptake and suppression of theremaining gland.
.Treatment ? After adequately controlling hyperthyroid state Total Thyroidectomy is treatment of choice.
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Toxic Adenoma (Plummer's Disease).Hyperthyroidism from a single hyper-functioning nodule.
.Typical y occurs in younger patients who note recent growth of a long-standing nodule along with
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the symptoms of hyperthyroidism.
.Most hyper-functioning or autonomous thyroid nodules have attained a size of at least 3 cm before
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hyperthyroidism occurs.Toxic Adenoma (Plummer's Disease)
.Physical examination- usually reveals a solitary thyroid nodule without palpable thyroid tissue
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on the contralateral side.
.RAI scanning shows a "hot" nodule with suppression the rest of the thyroid gland.
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.Surgery (lobectomy and isthmusectomy) is preferred.Thyroid Storm
.A condition of hyperthyroidism accompanied by-
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Fever, central nervous system agitation or depression, cardiovascular dysfunction..May be precipitated by infection, surgery or trauma.
Thyroid Storm
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.Management:
Beta blockers- given to reduce peripheral T4 to T3 conversion and decrease the hyperthyroid symptoms.
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Oxygen supplementation and hemodynamic support should be instituted.Non-aspirin compounds can be used to treat pyrexia.
Lugol's iodine or sodium ipodate (intravenously) should be administered to decrease iodine uptake and thyroid hormone
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secretion.
PTU therapy blocks the formation of new thyroid hormone and reduces peripheral conversion of T4 to T3.
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Corticosteroids often are helpful to prevent adrenal exhaustion and block hepatic thyroid hormone conversion.