THYROTOXICOSIS vs HYPERTHYROIDISM
Thyrotoxicosis is an umbrella term for clinical syndrome that results from excess thyroid hormone (usually T3), regardless of whether or not the thyroid is the primary source.
- Causes: Graves disease, thyroiditis, thyroid nodules, excessive iodine, medications, recent contrast load (Jod Basedow effect)
Hyperthyroidism refers to excess thyroid hormone synthesis by the thyroid gland.
- Top 3 causes: Graves disease, thyroiditis, thyroid nodules
- Risk factors: female gender, history, age (20-40yo), smoking, trauma to thyroid gland, major stress, etc
GRAVES DISEASE (GD)
GD is the most common cause of hyperthyroidism (more than half.) In GD, TSH receptor antibodies (TRAb) activate autonomous production of T4/T3 and often stimulate thyroid growth (i.e. diffuse goiter.)
Pemberton’s sign evaluates venous obstruction in patients with goiter.
Unrelated to excess thyroid hormone, Graves’ ophthalmopathy (GO) and infiltrative dermopathy (localized or pretibial myxedema) only occur in GD.
- 25-50% of all patients with GD have GO
- The most common site of infiltrative dermopathy is the skin overlying the shins, where it presents as raised, hyperpigmented, violaceous, orange-peel-textured papules.
Fun fact: Ask about biotin use (eg Sugar Bear Hair!)–biotin mimics GD on labs but without symptoms!
NEONATAL GRAVES DISEASE (NGD)
Newborns born to mothers with GD have increased risk of growth retardation, craniosynostosis, hyperactivity, and developmental/behavioral problems.
NGD affects ~1-5% of at-risk pregnancies, and is worse if 3rd trimester maternal TRAb >5x UNL. NGD is typically self-limited (~3-12 weeks) but MUST BE TREATED with methimazole ASAP to avoid long-term sequelae!
DDx includes germline mutations in TSH receptor and McCune-Albright syndrome.
- Labs: TSH, Free T4, Total T3
- Free T3 assays not reliable yet and not routinely ordered
- Consider TRAb (TSH receptor autoantibodies) and imaging depending on examination/labs–RAIU (contraindicated in pregnancy!), thyroid ultrasound with doppler flow, MRI brain, and/or pelvic ultrasound
Beta blockers for symptom control (blocks adrenergic effects!)
- Atenolol once daily > Propranolol TID, Metoprolol TID for outpt (+ATDs)
- Esmolol gtt for thyroid storm
Antithyroid drugs (ATDs):
- PTU – watch out for liver failure
- methimazole – watch out for agranulocytosis, teratogenic
- MOA: inhibit synthesis of thyroid hormones, block conversion of T4 to T3; takes 3-6 months for full effect
- Pregnancy: PTU preferred in 1T; PTU or methimazole acceptable in 2T/3T
- Breastfeeding: PTU or methimazole okay in breastfeeding moms
- Radioactive iodine (RAI) is indicated for GD but contraindicated in pregnancy, lactation, malignancy, or pts with GO
- RAI concentrates in thyroid gland and destroys thyroid tissue; takes 3-6 months for full effect
Thyroid storm = thyrotoxicosis + systemic decompensation
- Use Burch-Wartofsky Point Scale >45
- Treat via all pathways!
- Preferential use of PTU > methimazole due to more effective dampening of T4 conversion, blocks new hormone synthesis
- BB (esmolol gtt) to block adrenergic effects
- Iodine solution to block new hormone synthesis
- Hydrocortisone to reduce T4 conversion, improve vasomotor tone
Subclinical hyperthyroidism → repeat labs in 3 months, treat if >65 yo with comorbidities
*Blog post based on Med-Peds Forum talk by Vivian Shi, PGY3