What Is Graves Disease? A Step-by-Step Biology Explanation
It is also termed as Exophthalmic goitre or toxic diffuse goitre.
What is Graves Disease?
Exophthalmic Goitre Definition: Graves disease is an immune system disorder characterised by excessive thyroid hormone production (hyperthyroidism). Graves' disease is a general cause of hyperthyroidism, but it may be caused by a variety of conditions.
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Exophthalmic Goitre Symptoms
Graves disease has a wide range of signs and symptoms because thyroid hormones affect many different body systems. Graves disease can affect anyone, but it is more prevalent in women and those under the age of 40. Following are the symptoms:
Anxiety and irritability
A fine tremor of the hands or fingers
Heat sensitivity and an increase in perspiration or warm, moist skin
Weight loss, despite normal eating habits
Enlargement of the thyroid gland (goitre)
Change in menstrual cycles
Erectile dysfunction or reduced libido
Frequent bowel movements
Bulging eyes (Graves' ophthalmopathy)
Fatigue
Thick, red skin usually on the shins or tops of the feet (Graves' dermopathy)
Rapid or irregular heartbeat (palpitations)
Sleep disturbance
Graves' Ophthalmopathy
Graves' ophthalmopathy is present in about 30% of people with Graves' disease. Inflammation and other immune system events damage muscles and other tissues around the eyes in Graves' ophthalmopathy.
The Following are Possible Signs and Symptoms:
Bulging eyes
Gritty sensation in the eyes
Pressure or pain in the eyes
Puffy or retracted eyelids
Reddened or inflamed eyes
Light sensitivity
Double vision
Vision loss
Graves' Dermopathy
Graves' dermopathy is a rare manifestation of Graves' disease that causes reddening and thickening of the skin, most often on the shins or tops of the feet.
Exophthalmic Goitre Cause
Researchers are uncertain as to why certain people develop autoimmune diseases like Graves' disease. These diseases are most likely caused by a combination of genes and an external trigger, such as a virus.
The immune system produces an antibody called thyroid-stimulating immunoglobulin (TSI) that binds to thyroid cells in Graves' disease. Thyroid-stimulating hormone (TSH) is a hormone produced by the pituitary gland that instructs the thyroid gland on how much thyroid hormone to produce. The thyroid produces too much thyroid hormone as a result of TSI.
How is Exophthalmic Goitre Diagnosed?
Based on your symptoms and results during a physical exam, your doctor may suspect Graves' disease. Hyperthyroidism may be confirmed by one or more blood tests, and Graves' disease can be the cause.
Other Clues That Hyperthyroidism is Caused by Graves’ Disease are:
An Enlarged Thyroid
Signs of Graves’ eye disease, present in about one out of three people with Graves’ disease4
A history of other family members with thyroid or autoimmune problems
If your doctor is unsure about the diagnosis, he or she can order additional blood or imaging tests to confirm Graves' disease as the cause.
TSI can be detected by a blood test. In mild cases of Graves' disease, however, TSI may not be detected in the blood. One of two imaging tests that use small, safe doses of radioactive iodine may be the next step. Your thyroid absorbs iodine from your blood and uses it to produce thyroid hormones, and it can do the same for radioactive iodine.
Radioactive Iodine Uptake Test - This test determines how much iodine the thyroid absorbs from the blood. Graves' disease is a condition in which the thyroid accumulates a lot of iodine.
Thyroid Scan - The distribution of iodine in the thyroid is seen in this scan. Graves' disease affects the entire thyroid, so iodine accumulates in the gland. Some causes of hyperthyroidism, such as nodules (small lumps in the thyroid gland), produce a particular pattern of iodine.
How Can Exophthalmic Goitre be Treated?
Medicine, radioiodine therapy, and thyroid surgery are the three treatment choices. The most popular treatment for Graves' disease is radioiodine therapy, but physicians are starting to use the medicine more often than in the past. Your doctor can prescribe a particular treatment based on factors such as your age, whether you are pregnant, or whether you have other medical conditions, and may help you determine which one is best for you.
Radioiodine Therapy
Radioactive iodine-131 (I-131) is taken by mouth as a tablet or a liquid for radioiodine therapy. The thyroid gland's cells that contain thyroid hormone are steadily destroyed by I-131 at a higher dose than that used for imaging studies. Other body tissues are unaffected by the I-131 dose used in radioiodine therapy.
Since the thyroid hormone-producing cells are killed, almost everybody who receives radioactive iodine therapy develops hypothyroidism or an underactive thyroid. Hypothyroidism, on the other hand, is less difficult to manage and causes fewer long-term health issues than hyperthyroidism. With daily thyroid hormone, people with hypothyroidism can fully regulate their condition.
Doctors should not use radioiodine therapy to treat pregnant or breastfeeding mothers. The thyroid of a foetus may be harmed by radioactive iodine, which can be transmitted from mother to child by breast milk.
Medicines
Beta-Blockers: Beta-blockers don't stop the thyroid from developing thyroid hormone, but they can help you feel better as you wait for other medications to kick in. Many of the signs of hyperthyroidism, such as shaking, rapid heartbeat, and nervousness, are relieved rapidly with these medications. The majority of people feel better after taking beta-blockers within a few hours.
Antithyroid Medicines: The most straightforward treatment for hyperthyroidism is antithyroid therapy. Antithyroid medications reduce the amount of thyroid hormone produced by your thyroid gland. These drugs rarely have a lasting cure, but their effects can last for a long time in some people after they stop taking them. Methimazole, an antithyroid medication, is most often prescribed by doctors.
Antithyroid medication is often prescribed to pregnant and breastfeeding women because it is thought to be better for the baby than other medications. Since methimazole can damage the foetus, doctors prefer to use propylthiouracil NIH external connection over methimazole during the first three months of pregnancy.
Propylthiouracil may also damage the foetus in extreme cases, although any side effects are much less dangerous than getting untreated hyperthyroidism throughout pregnancy.
Your thyroid hormone levels may not return to normal for several weeks or months after you start taking antithyroid medication. The average recovery time is 12 to 18 months, but in people who don't want radioiodine or surgery to cure their Graves' disease, treatment can last for years.
Antithyroid Medicines Can Cause Side Effects in Some People, Including
allergic reactions such as rashes and itching
a decrease in the number of white blood cells in your body, which can lower resistance to infection
liver failure, in rare cases
Thyroid Surgery
Surgery to suppress the thyroid gland is the least-used procedure for Graves' disease. Surgery is often used to treat massive goitres or pregnant women who are allergic to or experiencing side effects from antithyroid medications.
Your doctor will prescribe antithyroid medications to get the thyroid hormone levels back into the normal range before surgery. This procedure avoids a disorder known as thyroid storm, which occurs when people with hyperthyroidism undergo general anaesthesia and experience a sudden, extreme worsening of symptoms.
You will experience hypothyroidism after your thyroid is removed, and you will need to take thyroid hormone medication every day for the rest of your life. Your doctor will monitor your thyroid hormone levels after surgery and change your dosage as required.
FAQs on Graves Disease: Key Facts, Causes, Symptoms, and Treatments
1. What is Graves' disease and how is it related to hyperthyroidism?
Graves' disease is an autoimmune disorder and the most common cause of hyperthyroidism. Hyperthyroidism is the medical term for an overactive thyroid gland. In this condition, the immune system mistakenly attacks the thyroid, causing it to produce an excessive amount of thyroid hormones (T3 and T4), which leads to a widespread increase in the body's metabolic rate.
2. What is the underlying autoimmune cause of Graves' disease?
The primary cause of Graves' disease is the production of abnormal antibodies called Thyroid-Stimulating Immunoglobulins (TSI). Unlike in a normal immune response that fights pathogens, these antibodies target the body's own tissues—specifically, the thyroid gland. Genetic predisposition and environmental factors, such as stress or infection, are believed to trigger this autoimmune response.
3. How do the antibodies in Graves' disease mimic TSH and cause the thyroid to become overactive?
The mechanism involves a process called molecular mimicry. The TSI antibodies have a structure very similar to the body's own Thyroid-Stimulating Hormone (TSH), which is normally released by the pituitary gland. These antibodies bind to the TSH receptors on thyroid cells, tricking the gland into continuously producing and releasing high levels of thyroid hormones (thyroxine and triiodothyronine), independent of the body's actual needs. This leads to a state of chronic hyperthyroidism.
4. What are the common symptoms of Graves' disease, explained biologically?
The excess thyroid hormones accelerate the body's metabolism, causing a range of symptoms. Key examples include:
- Unintentional weight loss: Occurs despite an increased appetite, due to a highly elevated basal metabolic rate (BMR).
- Rapid or irregular heartbeat (tachycardia): Thyroid hormones increase the sensitivity of heart muscle cells to catecholamines like adrenaline.
- Heat intolerance and excessive sweating: Caused by the increase in metabolic heat production.
- Enlarged thyroid gland (goitre): Results from the constant stimulation of thyroid tissue by TSI antibodies.
- Anxiety and tremors: Stems from the overstimulation of the central nervous system.
5. Why is Graves' ophthalmopathy, or "bulging eyes," a characteristic sign of this condition?
Graves' ophthalmopathy, also known as thyroid eye disease, is an autoimmune manifestation of the disease. The same antibodies that target the thyroid gland can also attack the tissues and muscles behind the eyes. This triggers an inflammatory response, causing the retro-orbital muscles and fatty tissues to swell. The increased pressure from this swelling pushes the eyeballs forward, resulting in the characteristic bulging appearance known as exophthalmos.
6. How is Graves' disease different from Hashimoto's thyroiditis?
Both are autoimmune thyroid disorders, but they have opposite effects based on the type of antibody produced:
- Graves' Disease: Involves stimulatory antibodies (TSI) that bind to TSH receptors and cause the thyroid to overproduce hormones, leading to hyperthyroidism (an overactive thyroid).
- Hashimoto's Thyroiditis: Involves destructive antibodies that attack and destroy thyroid cells. This damage impairs the gland's ability to produce hormones, leading to hypothyroidism (an underactive thyroid).
7. From a biological perspective, how is a diagnosis of Graves' disease confirmed?
A diagnosis is confirmed by identifying specific biological markers in blood tests. An analysis will typically show:
- Low levels of Thyroid-Stimulating Hormone (TSH), as the pituitary gland reduces its output in response to high thyroid hormone levels in the blood.
- High levels of free Thyroxine (T4) and Triiodothyronine (T3), the active thyroid hormones.
- The presence of Thyroid-Stimulating Immunoglobulin (TSI) antibodies in the blood, which is the definitive marker that confirms the autoimmune cause is Graves' disease.
