THYROTOXICOSIS AND HYPERTHYROIDISM

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THYROTOXICOSIS ANDHYPERTHYROIDISM

• An overview
• DR PRAVEEN SHETTY
• DEPARTMENT OF INTERNAL MEDICINE

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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,thyrotoxicosi
  s can originate in a variety of ways.
• RAIU is subnormal

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Hyperthyroidism

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

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Varieties of Thyrotoxicosis

• Associated with thyroid hyperfunction
• Excess production of TSH(rare)
• Abnormal thyroid stimulator-EgGraves disease
• Intrinsic thyroid autonomy-EgHyperfunctioning
  adenoma, Toxic multinodular goitre

• Not associated with thyroid hyperfunction
• Disorders of hormone storage-EgSubacute
  thyroiditis, chronic thyroiditis
• Extrathyroid source of hormone- Thyrotoxicosis
  factitia,ectopic thyroid tissue- struma ovarii,
  functioning follicular Ca.

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HyperthyroidismGraves disease

• Also known as Parrys or Basedows 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.

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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(71)
• Genetic factors play a important role
• An overlap exsists with other autoimmune diseases
  suggesting Graves is also a autoimmune thyroid
  disease

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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(TSIs) of IgG class and
  inhibition of the binding of TSH to its
  receptors(TBIIs).These factors represent TRAbs.

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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

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Clinical features

• The clinical manifestations include those that
  reflect the associated thyrotoxicosis and those
  specifically related to Graves disease

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Clinical features of thyrotoxicosis

• Neuromuscular
• Nervousness,irritability,emotional
  liability,psychosis
• Tremor
• Hyperreflexia,ill sustained clonus
• Muscle weakness,proximal myopathy,bulbar myopathy
• ReproductiveAmenorrhoea,Oligomenorrhoea
• Infertility,impotence

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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

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Thyrotoxicosis..

• Others
• Heat intolerance
• Increased sweating
• Fatigue
• Gynaecomastia
• Palmar erythema, Onycholysis

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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 Gravess

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Goiter

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

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Ophthalmopathy

• Signs of Gravess 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,conjunctivit
  is,periorbital swelling and the potential
  complications of corneal ulceration,optic
  neiritis and optic atrophy.

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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 appearanceit 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

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Differential diagnosis

• Anxiety
• Pheochromocytoma
• Hydatidiform mole
• Ectopic thyroid tissue(struma ovarii)
• Factitious thyrotoxicosis

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Investigations

• Thyroid function test
• TSH- Undetectable
• T4 - Raised
• T3 - Raised
• RAIU- Raised
• TSH-receptor antibodies(TRAb)-elevated in
  Gravess disease
• Isotope scanning- Increased uptake

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Other non specific findings

• Hepatic dysfunction- Raised AST,ALT
• Mild hypercalcemia
• Glycosuria- Associated diabetes mellitus

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Treatment of Hyperthyroidism
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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

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Duration of treatment

• 18-24 months
• Side effects- Rash
• Leukopenia
• Agranulocytosis

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Control of adrenergic symptoms

• Adrenergic antagonists
• Propranolol-40-120mg/day

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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

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Complications of ablative therapy

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

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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 41C or
  more,tachycardia,restlessness,hypotension,vomiting
  and diarrhea.

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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.

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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

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