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THYROTOXICOSIS AND HYPERTHYROIDISM

THYROTOXICOSIS AND HYPERTHYROIDISM. An overview DR PRAVEEN SHETTY DEPARTMENT OF INTERNAL MEDICINE. Thyrotoxicosis. Defined as the clinical,physiologic,and biochemical findings that result when the tissues are exposed to,and respond to,excess thyroid hormone.

JasminFlorian
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THYROTOXICOSIS AND HYPERTHYROIDISM

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  1. THYROTOXICOSIS ANDHYPERTHYROIDISM An overview DR PRAVEEN SHETTY DEPARTMENT OF INTERNAL MEDICINE

  2. Thyrotoxicosis • Defined as the clinical,physiologic,and biochemical findings that result when the tissues are exposed to,and respond to,excess thyroid hormone. • Rather than being a specific disease,thyrotoxicosis can originate in a variety of ways. • RAIU is subnormal

  3. Hyperthyroidism • Denotes only those conditions in which sustained hyperfunction of the thyroid gland leads to thyrotoxicosis. • Increased RAIU is the hallmark.

  4. Associated with thyroid hyperfunction: Excess production of TSH(rare) Abnormal thyroid stimulator-Eg:Graves’ disease Intrinsic thyroid autonomy-Eg:Hyperfunctioning adenoma, Toxic multinodular goitre Not associated with thyroid hyperfunction: Disorders of hormone storage-Eg:Subacute thyroiditis, chronic thyroiditis Extrathyroid source of hormone- Thyrotoxicosis factitia,ectopic thyroid tissue- struma ovarii, functioning follicular Ca. Varieties of Thyrotoxicosis

  5. HyperthyroidismGraves’ disease • Also known as Parry’s or Basedow’s disease. • Graves’ disease is a disorder with three major manifestations: • 1)Hyperthyroidism with diffuse goitre • 2)Ophthalmopathy and • 3)Dermopathy. • These three manifestations may not appear together.

  6. Incidence and prevalence • Relatively common disease that can occur at any age • More common in the 3rd and 4th decade • Disease is more frequent in women(7:1) • Genetic factors play a important role • An overlap exsists with other autoimmune diseases suggesting Graves is also a autoimmune thyroid disease

  7. Etiology and Pathogenesis • Cause of Graves’ is unknown • No single factor is responsible for the entire syndrome • With respect to hyperthyroidism,the central disorder is a disruption of homeostatic mechanisms that normally control hormone secretion.This disruption results from the presence in the plasma of thyroid stimulating immunoglobulins(TSI’s) of IgG class and inhibition of the binding of TSH to its receptors(TBII’s).These factors representTRAb’s.

  8. Pathology • Thyroid gland is diffusely enlarged,soft and vascular. • There is parenchymatous hyperplasia and hypertrophy with lymphocytic infilteration. • The ophthalmopathy is characterized by an inflammatory infilterate of the orbital contents,with lymphocytes,mast cells and plasma cells • The dermopathy of Graves’ disease is characterized by thickening of the dermis,which is infilterated by lymphocytes and mucopolysaccharides

  9. Clinical features • The clinical manifestations include those that reflect the associated thyrotoxicosis and those specifically related to Graves’ disease

  10. Clinical features of thyrotoxicosis • Neuromuscular: • Nervousness,irritability,emotional liability,psychosis • Tremor • Hyperreflexia,ill sustained clonus • Muscle weakness,proximal myopathy,bulbar myopathy • Reproductive:Amenorrhoea,Oligomenorrhoea Infertility,impotence

  11. Thryotoxicosis.. • Gastrointestinal: • Weight loss despite increased appetite • Hyperdefecation • Diarrhoea and steatorrhoea • Vomiting • Cardiorespiratory: • Palpitations,Sinus tachycardia,Atrial fibrillation • Increased pulse pressure • Dyspnea on exertion • Angina,cardiomyopathy and heart failure

  12. Thyrotoxicosis.. • Others: • Heat intolerance • Increased sweating • Fatigue • Gynaecomastia • Palmar erythema, Onycholysis

  13. Manifestations of Graves’ disease • The distinctive manifestations-diffuse hyperfunctioning goiter,ophthalmopathy,and dermopathy-appear in varying combinations,and in varying frequencies,goiter being the most common. • Premature greying of hair and patchy vitiligo are non specific features of Graves’s

  14. Goiter • Is diffuse and toxic and maybe asymetric and lobular. • There may be presence of bruit over the goiter

  15. Ophthalmopathy • Signs of Graves’s ophthalmopathy are divided into two components: • 1) Spastic: Stare, lid lag and lid retraction which account for the “frightened” facies. • 2) Mechanical: Proptosis of varying degrees,ophthalmoplegia,and congestive occulopathy characterized by chemosis,conjunctivitis,periorbital swelling and the potential complications of corneal ulceration,optic neiritis and optic atrophy.

  16. Dermopathy • Usually occurs over the dorsum of the legs or feet and is termed localized or pretibial myxedema. • It is usually a late phenomenon • The affected area is usually demarcated from the normal skin by being raised andthickened and having a peau d’ orange appearance;it may be pruritic and hyperpigmented. • The most common presentation is non pitting oedema,but lesions maybe plaque like,nodular or polypoid. • Clubbing of the fingers and toes accompanies and is termed thyroid acropachy

  17. Differential diagnosis • Anxiety • Pheochromocytoma • Hydatidiform mole • Ectopic thyroid tissue(struma ovarii) • Factitious thyrotoxicosis

  18. Investigations • Thyroid function test: • TSH- Undetectable • T4 - Raised • T3 - Raised • RAIU- Raised • TSH-receptor antibodies(TRAb)-elevated in Graves’s disease • Isotope scanning- Increased uptake

  19. Other non specific findings • Hepatic dysfunction- Raised AST,ALT • Mild hypercalcemia • Glycosuria- Associated diabetes mellitus

  20. Treatment of Hyperthyroidism

  21. Anti thyroid drugs • Chemically block hormone synthesis • Enhance evolution to remission • Best indicated for children,adolescents,young adults and pregnant women. • Propylthiouracil-100-150mg every 6or 8 hrs • Carbimazole- 40-60mg daily initially for 3 weeks,then reduce to 20-40mg for another 8 weeks and maintain at 5-20mg daily for 18-24 months. • Methimazole-active metabolite of Carbimazole

  22. Duration of treatment • 18-24 months • Side effects- Rash Leukopenia Agranulocytosis

  23. Control of adrenergic symptoms • Adrenergic antagonists: • Propranolol-40-120mg/day

  24. Ablative therapy(Surgery & Iodine) • Indications: • Relapse or recurrance following drug therapy • A large goiter • Failure to follow medical regimen. • Radioactive iodine is simple,effective and economical

  25. Complications of ablative therapy • Immediate complications of surgery: • Bleeding,injury to recurrant laryngeal nerve and thyroid crises. • Other complications • Hypothyroidism • Radiation thyroiditis

  26. Complications of thyrotoxicosis • 1)Cardiac- Heart failure Atrial fibrillation • 2)Thyrotoxic crises: or ‘storm’: • Fulminating increase in signs and symptoms of thyrotoxicosis. • Occurs in medically untreated or inadequately treated patients.May be precipitated by surgery or sepsis • The syndrome is characterized by extreme irritability,delirium or coma,fever 41°C or more,tachycardia,restlessness,hypotension,vomiting and diarrhea.

  27. Treatment of thyroid crisis • Provide supportive care; • Treat dehydration • Administer glucose and saline • Vitamin B complex and glucocorticoids • Digitalization is required in those with atrial fibrillation • Immediate and large doses of anti thyroid agents(Eg-propylthiouracil 100mg every 2h) • Iodine intravenously or by mouth • Propranolol 40-80mg every 6h • Dexamethasone(2mg every 6h) and to be tapered later.

  28. Treatment of ophthalmopathy and Dermopathy • Methylcellulose eye drops • Tinted glasses • Persistant diplopia can be corrected by surgery • Papilloedema,loss of visual field or acuity requires urgent treatment with prednisolone 60 mg daily. • Majority of patients require no treatment other than reassurance. • Dermopathy of Graves rarely requires treatment

  29. THANK YOU

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