SECTION 5 — Thyroid Eye Disease (TED) Medications

1⃣ What is TED?

Thyroid eye disease (Graves orbitopathy)

2⃣ What type of disease is TED?

Autoimmune

3⃣ What tissues are affected?

Retro-orbital tissues

4⃣ What exacerbates TED?

Stress, pregnancy, radioactive iodine therapy

5⃣ What are mild symptoms of TED?

Dry eye, gritty sensation

6⃣ What are severe symptoms of TED?

Proptosis (exophthalm os), vision loss, diplopia

7⃣ What is the first treatment step?

Restore euthyroid state

8⃣ What lifestyle change is critical?

Smoking cessation

9⃣ What is the first-line pharmacologic treatment?

IV methylprednisolone

10⃣ What is the glucocorticoid used?

IV methylprednisolone

11⃣ What is the initial dose schedule of IV methylprednisolone?

500 mg IV weekly weeks 1–6

12⃣ What is the second dose schedule of IV methylprednisolone?

250 mg IV weekly weeks 7–12

13⃣ What is the total cumulative dose of IV methylprednisolone?

4.5–5 g over 12 weeks

14⃣ How soon is improvement seen?

Within 4 weeks

15⃣ What % of patients respond in 6 months?

~50%

16⃣ What long-term risk is associated with glucocorticoids?

Osteoporosis/fractures

17⃣ What assessment is needed for long-term steroid use?

Skeletal assessment (bone density)

18⃣ What is the biologic used for TED?

Teprotumumab

19⃣ What is the dosing for teprotumumab?

10 mg/kg initial, then 20 mg/kg IV every 3 weeks x 8 doses

20⃣ What is the MOA of teprotumumab?

Reduces orbital inflammation

21⃣ What are adverse effects of teprotumumab?

Nausea, muscle spasms, hyperglycemia, hearing impairment

22⃣ What comorbidity requires caution with teprotumumab?

Type 2 diabetes

23⃣ Why?

May impair glycemic control

24⃣ What is the IL-6 inhibitor used in TED?

Tocilizumab

25⃣ When is tocilizumab used?

When steroids fail

26⃣ What does tocilizumab target?

Interleukin-6 (IL-6)

27⃣ What B-cell depleting antibody is used?

Rituximab

28⃣ What is rituximab’s MOA?

Depletes B cells and reduces TSH receptor antibodies

29⃣ What is a key risk with high-dose rituximab?

Severe immunosuppression

30⃣ How is TED dosing of rituximab different?

Lower dose used — less immunosuppression

31⃣ Does teprotumumab cure TED?

No — reduces inflammation, symptoms

32⃣ What happens if TED progresses untreated?

Vision loss, permanent fibrosis

33⃣ What should patients avoid during RAI therapy?

Triggers of TED (smoking, stress)

34⃣ What organ function must be monitored on glucocorticoids?

Bone (skeletal)

35⃣ What labs should be monitored on tocilizumab?

Liver enzymes, neutrophil count

36⃣ What labs should be monitored on rituximab?

CBC, immune markers

37⃣ What symptom may suggest steroid toxicity?

Hyperglycemia

38⃣ Why are biologics considered second-line?

Cost, risk of adverse effects

39⃣ How are TED treatments typically sequenced?

Steroids → teprotumumab → tocilizumab/rituximab

40⃣ What patient education is critical for TED?

Smoking cessation

41⃣ What non-drug therapy can help TED?

Lubricating eye drops

42⃣ What is the goal of TED therapy?

Preserve vision, reduce symptoms

43⃣ What is a key monitoring parameter during teprotumumab?

Hearing assessment

44⃣ Why is hearing monitoring needed?

Hearing loss is a side effect

45⃣ What is an urgent TED complication?

Optic neuropathy

46⃣ What is the goal of using glucocorticoids in TED?

Decrease retro-orbital inflammation

47⃣ What is the role of IV administration of methylprednisolone?

Higher efficacy with lower risk than oral steroids

48⃣ Why is TED worse after RAI?

Transient rise in TSH receptor antibodies

49⃣ What group is at higher risk for TED?

Smokers

50⃣ Why is early treatment of TED critical?

To prevent permanent vision loss