Graves’ Disease Symptom Quiz
This Graves’ disease symptom quiz gives you a weighted score that combines hyperthyroid symptoms with the Graves’-specific tells (eye signs, autoimmune family history, and antibody status) that distinguish Graves’ from other causes of an overactive thyroid. It’s designed for adults asking “do I have Graves’ disease?” and trying to figure out whether antibody testing or specialist referral is the right next step.
Here’s how to use it:
Check every symptom you’ve had for the last 2 months, flag the risk factors that apply, and add antibody results if you have them. Your total is given out of a possible 56 points and drops you into one of four tiers with a clear next step. It’s that easy.
Note: This quiz is a screening tool, not a diagnosis. A confirmed diagnosis of Graves’ disease requires lab confirmation. If you’re experiencing severe symptoms (rapid or irregular heartbeat, chest pain, severe weakness, fever, confusion, or sudden vision loss), seek medical care immediately.
General Hyperthyroid Signals
Eye Signs (Graves’ Eye Disease)
Thyroid Gland
Autoimmune Onset Pattern
Risk Modifiers
Written and medically reviewed by Dr. Westin Childs, D.O. Last reviewed: April 26, 2026.
How to Use This Quiz
Step #1: Check the Symptoms That Apply to You
The quiz is organized into four sections: general hyperthyroid signals, eye signs (highly indicative of Graves’), thyroid gland findings, and autoimmune symptoms. Go through each section and check every symptom you’ve had for at least 2 months.
Don’t over-check. A symptom that comes and goes occasionally, or that’s clearly tied to something else (caffeine, anxiety, perimenopause, hot weather), doesn’t belong.
Step #2: Add Your Risk Factors and Antibody Results
The Risk Modifiers section captures factors that raise your baseline Graves’ risk: female age 20 to 50, a family history of Graves’ or autoimmune thyroid disease, a family history of any other autoimmune disease, a personal history of another autoimmune condition, recent pregnancy, and known elevated Graves’ antibodies (TSI or TRAb).
Graves’ disease is roughly 7 to 8 times more common in women than men, peaks at age 30 to 50, and has the strongest familial clustering of any thyroid condition outside of Hashimoto’s[4]. It also clusters with other autoimmune diseases like type 1 diabetes, celiac, vitiligo, and rheumatoid arthritis.
The antibody modifier carries the most weight in the entire quiz. Positive TSI or TRAb antibodies are essentially diagnostic of Graves’ disease[2], and the quiz reflects that by auto-flooring your tier to Moderate when antibodies are checked, regardless of symptom score.
Step #3: Read Your Score and Follow the Next Step
Click “Calculate My Score” and your total appears out of a possible 56 points. Your total places you into one of four tiers: Low Likelihood (0 to 9), Mild Pattern (10 to 19), Moderate Pattern (20 to 29), or Strong Pattern (30 and above).
A Low score means your pattern doesn’t strongly suggest Graves’. A Mild score means baseline TSH plus Free T3, Free T4, and TSI/TRAb antibodies are reasonable. A Moderate or Strong score means antibody testing is the immediate next step. Anyone who checks the antibody modifier is automatically placed at Moderate or higher because confirmed antibodies are diagnostic by themselves.
If your score is Moderate or higher, request TSH, Free T3, Free T4, plus TSI and TRAb antibodies. If you have eye signs, evaluation by an ophthalmologist familiar with thyroid eye disease is also appropriate. Plug any lab results you have into the Optimal Thyroid Lab Test Calculator to see where they fall against optimal ranges.
Understanding Your Results
Your Score
Your score is the sum of weighted symptoms and risk modifiers you checked. The maximum possible total is 56 points: 36 from 23 weighted symptoms and 20 from 6 modifiers (5 risk factors plus the antibody item).
Symptoms carry a weight of 1, 2, or 3 depending on how specifically they point at Graves’ versus other causes of hyperthyroidism. Highly specific Graves’ findings (bulging eyes, double vision, vision changes from optic nerve involvement) count 3 points each. Moderately specific findings (lid lag, eye pressure, diffuse goiter, sudden symptom onset) count 2 points. Generic hyperthyroid signs that occur in any cause of overactive thyroid (palpitations, heat intolerance, weight loss, tremor) count 1 point each.
The antibody modifier alone is weighted 8 points, which is why a single positive antibody result lifts the tier even when symptoms are mild.
Your Symptom Pattern Breakdown
Below your score, the quiz shows the categories where your strongest pattern sits. Heavy scoring in the Eye Signs section is the most predictive single finding for Graves’ disease specifically (versus toxic nodular goiter, thyroiditis, or iatrogenic over-replacement). Strong scoring in the Autoimmune Onset Pattern section (sudden onset, postpartum onset, post-stress trigger) is also highly Graves’-suggestive.
Heavy scoring only in the General Hyperthyroid Signals section without Graves’-specific findings suggests hyperthyroidism with a non-Graves’ cause is also possible. The Hyperthyroid Symptom Quiz covers the broader differential when the cause isn’t yet clear.
Your Risk Tier
The four tiers are calibrated conservatively. A Low score (0 to 9) means symptoms don’t strongly suggest Graves’. A Mild score (10 to 19) means some Graves’ signal worth investigating with antibody testing. A Moderate score (20 to 29) means a clear pattern that warrants the full thyroid panel plus TSI/TRAb. A Strong score (30 or higher) means a high-probability Graves’ pattern that warrants prompt evaluation, especially if eye signs are present.
The antibody floor overrides the base score. Anyone who checks the TSI or TRAb item is auto-placed at Moderate tier or higher because confirmed antibodies are diagnostic of Graves’ disease by themselves[2], regardless of symptom severity.
Your Recommended Next Step
Next steps scale with tier and antibody status. A Low or Mild tier without labs suggests requesting baseline TSH, Free T3, Free T4, and TSI/TRAb antibodies if symptoms persist. A Moderate or Strong tier without antibody confirmation calls for the full panel including TSI and TRAb. If antibodies are negative but TSH is suppressed and Free T3/T4 are elevated, a thyroid uptake scan distinguishes Graves’ (high uptake) from toxic nodular goiter (patchy uptake) or thyroiditis (low uptake).
If antibodies are confirmed positive, the goal shifts from diagnosis to management. Treatment options include antithyroid medication (methimazole or propylthiouracil), radioactive iodine ablation, or surgical thyroidectomy. The choice depends on age, severity, eye disease status, pregnancy plans, and patient preference. Endocrinology care is appropriate for Graves’ management.
If you have any eye signs (bulging eyes, double vision, vision changes, eye pain or pressure), evaluation by an ophthalmologist familiar with thyroid eye disease is also warranted. Active-phase thyroid eye disease is treatable; the burned-out phase is not.
Thyroid Eye Disease Severity
Thyroid eye disease (also called Graves’ ophthalmopathy or Graves’ orbitopathy) develops in about 25 to 50 percent of Graves’ disease patients[3]. Severity varies from mild dry eyes to sight-threatening optic nerve compression, and treatment options differ meaningfully across the severity spectrum. The table below maps the four levels and the recommended action for each.
| Severity | Eye Findings | Vision Impact | Recommended Care |
|---|---|---|---|
| Mild TED | Lid retraction, mild lid lag, dry or gritty eyes, occasional redness | None or minimal | Lubricating drops, stop smoking, monitor every 3 to 6 months with a TED-aware specialist |
| Moderate TED | Mild bulging eyes (proptosis), intermittent double vision, soft tissue swelling, eye pressure or pain | Occasional double vision, especially when looking up or sideways | Refer to ophthalmologist familiar with thyroid eye disease. Consider teprotumumab, IV steroids, or orbital radiotherapy during the active phase. |
| Severe TED | Marked proptosis, persistent double vision, exposure keratopathy, significant pain | Persistent double vision, blurry vision | Urgent specialist care. Immunomodulator therapy plus consideration of surgical orbital decompression. |
| Sight-Threatening TED | Optic nerve compression (color vision changes, central vision loss), corneal ulceration, exposure injury | Vision loss possible if untreated | Emergency ophthalmology referral. IV high-dose steroids and urgent surgical decompression. |
Active-phase thyroid eye disease (the inflammatory window) typically lasts 6 to 24 months. During the active phase, immunomodulator treatment can prevent permanent damage. Once the active phase burns out, residual proptosis or double vision becomes structural and requires surgical correction rather than medication. Catching active-phase TED early is therefore critical.
Smoking dramatically accelerates and worsens thyroid eye disease at every severity level. Stopping smoking is the single most impactful patient-controlled action for protecting eye outcomes in Graves’.
Frequently Asked Questions
The early signs of Graves’ disease combine classic hyperthyroid symptoms with the autoimmune-specific tells that distinguish Graves’ from other causes. The most common early signs are unexplained weight loss despite eating normally or more, heart palpitations or a fast pulse, heat intolerance with sweating in cool environments, anxiety or feeling “wired,” hand tremor, and lighter or skipped menstrual periods[1].
The Graves’-specific early tells are subtle eye changes (mild lid retraction, slight eye prominence, dry or gritty sensation), a smooth and even swelling in the front of the neck (a diffuse goiter, not a single nodule), and an abrupt onset over weeks rather than the slow progression typical of hypothyroidism.
Onset frequently follows a major life stressor, infection, or pregnancy. Many patients can pinpoint the rough month their symptoms started, which is a clinical pattern more characteristic of Graves’ than other thyroid conditions.
Graves’ disease is the autoimmune cause of about 70 to 80 percent of all hyperthyroidism cases[1]. Said simply: hyperthyroidism is the functional state of having too much thyroid hormone, and Graves’ disease is the most common underlying disease that produces it.
The other 20 to 30 percent of hyperthyroidism is caused by toxic multinodular goiter, toxic adenoma (Plummer’s disease), thyroiditis (subacute, postpartum, or silent), or thyroid hormone over-replacement from too much medication. Each behaves differently and requires different treatment, which is why identifying the cause matters as much as identifying the hyperthyroid state.
Graves’ is distinguished from those other causes by positive TSI or TRAb antibodies, the presence of a diffuse (not nodular) goiter, eye involvement (thyroid eye disease), and a relatively rapid symptom onset. If your suspicion isn’t yet specific to Graves’, take the broader Hyperthyroid Symptom Quiz first.
Graves’ disease is diagnosed by a combination of suppressed TSH, elevated Free T3 or Free T4, and positive TSI or TRAb antibodies[2]. The antibody tests are the part that confirms Graves’ specifically rather than just hyperthyroidism in general.
If antibodies are negative but the hyperthyroid pattern is clear, a thyroid uptake scan helps distinguish causes. Graves’ shows diffuse high uptake, toxic nodular goiter shows patchy uptake, and thyroiditis shows low uptake. Imaging is also useful when eye signs are present, where orbital MRI or CT can show muscle thickening characteristic of thyroid eye disease.
Many providers stop at TSH and Free T4. That’s the most common reason Graves’ patients (or hyperthyroid patients with a non-Graves’ cause) end up undertreated or misdirected. If your symptoms suggest hyperthyroidism, ask specifically for the full panel: TSH, Free T3, Free T4, TSI, and TRAb together.
Thyroid eye disease (also called Graves’ ophthalmopathy or Graves’ orbitopathy) is the autoimmune attack on the tissues behind the eye that develops in 25 to 50 percent of Graves’ disease patients[3]. The same immune process that attacks the thyroid also targets the connective tissue, fat, and muscles in the eye socket.
Bulging eyes (medically called proptosis or exophthalmos) happen because the eye-socket tissue swells and the eyeball is physically pushed forward. The eye sockets are bony cavities with no room to expand. When the surrounding tissue inflames and grows, the only direction the eye can go is outward.
The eye disease can occur before, during, or after the thyroid hyperactivity (occasionally even years apart), so eye signs in someone without obvious thyroid symptoms still warrant antibody testing. Active-phase thyroid eye disease is treatable with medications like teprotumumab, IV steroids, or orbital radiotherapy, but the inactive (burned-out) phase only responds to surgery. Catching active disease early is critical, which is why any new eye changes in a Graves’ patient should be evaluated promptly.
Two antibody tests confirm Graves’ disease: TSI (thyroid-stimulating immunoglobulin) and TRAb (TSH receptor antibody)[2]. Both detect antibodies that target the TSH receptor on thyroid cells, which is the mechanism behind Graves’ (the antibodies stimulate the receptor and drive the thyroid into hormone overproduction).
TSI specifically detects the stimulating subset of these antibodies, which are the ones causing disease. TRAb is a broader test that detects all antibodies binding the TSH receptor (stimulating, blocking, or neutral). Both are useful, and most labs offer either as a Graves’ confirmation test. TSI is increasingly preferred for monitoring disease activity and predicting relapse.
One important detail: positive antibodies confirm Graves’ regardless of titer. A barely-elevated TSI is just as diagnostic as a dramatically-elevated one. The titer correlates with disease activity but not with the diagnosis itself. Don’t accept “your antibodies are barely elevated, that’s not concerning” as a reason to skip the diagnosis if your symptoms fit.
Yes. Graves’ disease has a strong genetic component. Having a parent, sibling, or child with Graves’ disease or any autoimmune thyroid disease meaningfully raises your own risk[5].
The genetic susceptibility extends beyond thyroid disease itself. Graves’ clusters with other autoimmune conditions including type 1 diabetes, celiac disease, vitiligo, rheumatoid arthritis, lupus, Sjögren’s syndrome, and Addison’s disease. A family history of any autoimmune disease (not just thyroid) raises Graves’ risk, which is why the quiz weights both family thyroid history and family non-thyroid autoimmune history as separate modifiers.
Genes set the susceptibility, but environmental triggers usually pull the trigger. Most patients can identify a specific period when symptoms started, often after a major life stressor, infection, or pregnancy. The onset story is part of what makes Graves’ clinically distinguishable from slower-developing thyroid disease.
Yes. Pregnancy and the postpartum period are well-recognized triggers for new-onset Graves’ disease and for relapse in women who previously had Graves’ in remission[6].
The mechanism involves shifts in immune tolerance during pregnancy followed by a rebound in immune activity postpartum. About 5 to 10 percent of women experience some form of postpartum thyroid dysfunction in the year after childbirth, and Graves’ is one of the patterns that can present that way. New-onset thyroid symptoms in the months following delivery should always trigger a workup that includes both thyroid hormones and Graves’ antibodies.
Graves’ during an active pregnancy is a special situation. Treatment options are constrained (radioactive iodine is contraindicated in pregnancy, methimazole has different risks per trimester, and propylthiouracil is preferred in the first trimester). Anyone who suspects new Graves’ during pregnancy should work with both an endocrinologist and an obstetrician familiar with thyroid disease in pregnancy.
Treated Graves’ disease is generally manageable. Untreated or undertreated Graves’ can be dangerous, and severe cases can progress to a medical emergency[2].
The chronic risks of untreated Graves’ are atrial fibrillation (especially in adults over 65), heart failure, accelerated bone loss leading to osteoporosis, significant unintentional weight loss with muscle wasting, and the eye complications of thyroid eye disease (vision loss in severe cases). Bone density measurably drops within months when TSH stays suppressed.
The acute risk is thyroid storm, a rare but life-threatening complication where untreated Graves’ is pushed past a critical threshold by a trigger such as severe infection, surgery, trauma, childbirth, or stopping antithyroid medication abruptly. Symptoms include very high fever, severe tachycardia or arrhythmia, agitation or confusion, vomiting, diarrhea, and altered consciousness. Anyone experiencing this picture needs emergency room care immediately. Mild Graves’ does not progress to thyroid storm without a major trigger, but the possibility is the reason untreated Graves’ is taken seriously.
References
- Smith TJ, Hegedüs L. Graves’ Disease. New England Journal of Medicine. 2016;375(16):1552-1565. View on PubMed
- Ross DS, Burch HB, Cooper DS, et al. 2016 American Thyroid Association Guidelines for Diagnosis and Management of Hyperthyroidism and Other Causes of Thyrotoxicosis. Thyroid. 2016;26(10):1343-1421. View on PubMed
- Bartalena L, Kahaly GJ, Baldeschi L, et al. The 2021 European Group on Graves’ Orbitopathy (EUGOGO) clinical practice guidelines for the medical management of Graves’ orbitopathy. European Journal of Endocrinology. 2021;185(4):G43-G67. View on PubMed
- Vanderpump MP. The epidemiology of thyroid disease. British Medical Bulletin. 2011;99:39-51. View on PubMed
- Tomer Y, Davies TF. Searching for the autoimmune thyroid disease susceptibility genes: from gene mapping to gene function. Endocrine Reviews. 2003;24(5):694-717. View on PubMed
- Alexander EK, Pearce EN, Brent GA, et al. 2017 Guidelines of the American Thyroid Association for the Diagnosis and Management of Thyroid Disease During Pregnancy and the Postpartum. Thyroid. 2017;27(3):315-389. View on PubMed