🦋 Graves' Antithyroid Drug Simulator in 3D

Baseline Graves' Hyperthyroidism

Autoantibodies overdrive the thyroid, flooding the body with hormone — rendered here as a real 3D follicle you can orbit and zoom around.

• 4.6: Free T4 (baseline) (ng/dL, markedly high)
• 100%: TPO activity (unchecked iodination)
• Suppressed: TSH (negative feedback)
• ~1%: Prevalence (lifetime, women > men)

TSH-receptor antibodies

Autoantibodies mimic TSH, continuously stimulating the thyroid gland.

TPO-driven iodination

Thyroid peroxidase oxidizes iodide and attaches it to thyroglobulin tyrosines on the follicle membrane.

Clinical picture

Tachycardia, weight loss, heat intolerance, and tremor result from excess hormone.

Untreated Graves' disease can progress to thyroid storm, a medical emergency.

Antithyroid Drug Administered

Thionamide molecules enter the follicle in true 3D space and seek out TPO enzymes anchored on the membrane.

• Thionamide: Drug class (methimazole / PTU)
• TPO enzyme: Target (active-site inhibitor)
• Faster: Onset (methimazole) (longer half-life)
• Slower: Onset (PTU) (also blocks T4→T3)

Mechanism of inhibition

Drug molecules are oxidized by TPO, consuming the enzyme's catalytic capacity — visible as the enzyme fading from amber to grey.

Dose dependence

Higher doses saturate more TPO molecules on the follicle surface, blocking hormone synthesis faster.

Methimazole vs PTU

PTU also blocks peripheral T4-to-T3 conversion; methimazole is more potent overall and docks faster in this model.

Hormone Synthesis Progressively Blocked

With TPO inhibited, stored hormone depletes and free T4 declines over weeks — fewer red hormone particles escape the colloid sphere.

• 6–8 wks: Time to euthyroid (typical course)
• ~7 days: T4 half-life (gradual decline)
• Depleting: Colloid store (no new hormone made)
• Ongoing: Titration (dose adjusted to labs)

Depleting the reservoir

Existing stored hormone in colloid is released even as new synthesis halts.

Lab-guided titration

Free T4 and TSH are rechecked periodically to fine-tune the dose.

Symptom resolution

Heart rate, tremor, and weight trends normalize as hormone falls.

Agranulocytosis Surveillance

A separate 3D neutrophil swarm beside the follicle shrinks in real time as routine blood counts watch for a rare but dangerous crash.

• ~0.3%: Agranulocytosis risk (of treated patients)
• <500: Danger threshold (neutrophils/µL)
• First 90 days: Onset window (highest risk period)
• Stop drug: Action if crossed (immediate discontinuation)

What to watch for

Sore throat and fever are the classic warning symptoms to report urgently.

Dose-risk relationship

Higher doses correlate with steeper, faster neutrophil declines in the swarm.

Response protocol

Drug is stopped immediately and counts are monitored until recovery.

A neutrophil count under 500/µL is a medical emergency requiring drug cessation.

Outcome — Euthyroid State or Escalation

Most patients stabilize on therapy; some need definitive treatment instead.

• ~40-50%: Remission rate (after 12-18 month course)
• ~50%: Relapse rate (after stopping drug)
• RAI / surgery: Alternative (if adverse effects)
• Euthyroid: Goal (normal T4 and TSH)

Successful maintenance

Continued low-dose therapy keeps hormone levels in the normal range.

When to escalate

Agranulocytosis or poor control prompts a switch to RAI or surgery.

Long-term outlook

Many patients eventually taper off with sustained remission.

Definitive treatment options