10/22/15 Morning Report Hyperthyroidism

  • Pathophysiology of T4 secretion: TSH secreted in the anterior pituitary and stimulates the TSH receptor in the thyroid to secrete thyroid hormone
  • Clinical presentation of Hyperthyroidism: Hyperdefecation (not diarrhea), osteoporosis, oligomenorrhea in pre-menopausal females, hair changes, palpitations, arrhythmias
  • Etiologies of hyperthyroidism
    • Grave’s Disease (most common cause of hyperthyroidism)
    • Destructive thyroiditis (subacute, silent, postpartum)
    • Multinodular Goiter/Toxic Adenoma
    • Medication-induced (amiodarone, lithium, IFN-a, etc)
    • Factitious
  • Antibodies
    • Anti-TPO and anti-thyroglobulin Ab seen with Hashimoto’s Disease (hypothyroidism)
    • TSI (thyroid stimulating immunoglobulin) and TBII associated with Graves Disease.
      • TSI binds to TSH receptors on thyroid gland, stimulating production of thyroid hormone.
      • TSI also binds to TSH receptors located on fibroblasts, stimulating proliferation and glycosaminoglycan production in retro-orbital space.
  • Clinical Presentation specific to Graves include pretibial myxedema (5% patients with Graves), exophthalmos (25% of patients with Graves)
  • Work-up of Hyperthyroidism
    • If evidence for Graves Disease, then GD likely diagnosis.
    • Evidence of nodules on physical Exam:
      • If None: Perform RAI uptake scan and antibody studies.
        • If increased uptake, elevated thyroid hormone due to over-synthesis
          • If diffuse uptake, think Graves Disease
          • If patchy uptake, think toxic multinodular goiter
        • If decreased uptake, think of factitious or destructive causes (subacute, silent, postpartum.
      • If Present: Get RAIU scan and thyroid ultrasound to distinguish TNG vs TA and/or evidence of cold nodules. Check for any concerning factors for thyroid cancer.
    • Thyroglobulin: Precursor to thyroid hormone production. Combined with iodine to produce T4.
      • May be used to differentiate factitious vs destructive thyroiditis, surveillance for thyroid cancer.
  • Treatment Options:
    • Thionamides – Methimazole versus PTU
      • Watch for drug rash and/or agranulocytosis
    • Radioactive iodine ablation
      • Do not use in patients with Graves Disease with severe ophthalmopathy as this can worsen symptoms.
    • Surgery
  Grave’s Disease Multinodular Goiter Subacute Thyroiditis
Clinical Course/Exam




Pre-tibial Myxedema

Hyperthyroid symptoms

Palpable nodules

Preceded by URI sx, Pain around the neck, pain with palpation, initially hyperthyroid (6 weeks) but progresses to hypothyroid (6 weeks), then normalizes
Diagnosis Tests





High Free T4





Thyroid US

TSH, Free T4

RAI – low uptake

Thyroid US – diffuse enlargement






Methimazole (don’t use in 1st trimester of pregnancy). Watch for agranulocytosis.

RAIA, then will require

Surgical. Don’t use RAIA for patients with exophthalmos.

If compressive sx (dysphagia, etc) then surgery

If no compressive symptoms, can treat with RAIU. Toxic patients can also be treated with thionamides

NSAIDS, supportive

Then Prednisone if poor response

Symptomatic treatment, such as propranolol or beta blockers

Thionamides not indicated

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