Sandbox:Aakash

Aakash Hans, MD[1]

Sandbox

Hyperthyroidism

Pathogenesis

• Grave's disease
  • TSI or TSH receptor antibodies are directed against TSH receptors on follicular cells, which stimulate thyroid hormone production.
  • Immunologically activated fibroblasts in the skin and eye cause the dermopathy and ophthalomopathy.
  • Genetic factors play a minor role, with HLA-DR3 being the only documented risk factor.
  • Viral or bacterial infections can also trigger hyperthyroidism as the antibodies against the cell membrane of E coli and Y enterocolitica cross react with TSH receptors.
• Drug induced
  • Iodine can cause hyperthyroidism due to excess oral intake or due to exposure to radiographic contrast material containing iodine.
  • Generally occurs in people with underlying autonomously functioning thyroid gland, but can also occur in patients with endemic goiter who are treated with iodine. This is known as Jod-Basedow phenomenon.
  • Anti-arrhythymic drug amiodarone contains more iodine than the recommended daily allowance, and therefore can precipitate hyperthyroidism.

Clinical Features

1. Thyroid : enlargement can be nodular or diffuse
2. Gastrointestinal : weight loss, vomiting, diarrhea and increase appetite.
3. Cardio-respiratory : palpitations, angina, sinus tachycardia and wide pulse pressure.
4. Neuro-muscular : nervousness, tremors, psychosis and hyper-reflexia.
5. Dermatological : increased sweating, palmar erythema, pigmentation and alopecia.

Investigations

• TSH
  • Is decreased or not present in majority of cases.
  • This is the primary test performed, as if it tests normal, it virtually rules out hyperthyroidism.
• Serum T3 and T4
  • Is increased in almost all cases.
• I-131 Uptake
  • Not required in most patients.
  • Uptake is usually increased.
• Antibodies
  • Thyroid peroxidase antibody levels are raised.