Thyroid disorders Part 1

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Thyroid Disorders

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  • Extra notes:
    The thyroid is supplied with arterial blood from the superior thyroid artery, a branch of the external carotid artery, and the inferior thyroid artery, a branch of the thyrocervical trunk, and sometimes by the thyroid ima artery, branching directly from the subclavian artery.
    The venous blood is drained via superior thyroid veins, draining in the internal jugular vein, and via inferior thyroid veins, draining via the plexus thyreoideus impar in the left brachiocephalic vein.
    Lymphatic drainage passes frequently the lateral deep cervical lymph nodes and the pre- and parathracheal lymph nodes. The gland is supplied by parasympathetic nerve input from the superior laryngeal nerve and the recurrent laryngeal nerve.
  • Reverse t3:
    On top of the chronic stresses of your life, there are three common physiological reasons patients have noted, with the first two related to your adrenals (low cortisol, high cortisol), and the third related to your iron levels. Even low B12 and other chronic inflammation and other health issues can cause it.
    When biological stress is excessive, such as being on the inadequate treatment of T4-only or being held hostage to the lousy TSH lab test (both which keep you underdosed or hypo), your adrenal glands produce high amounts of cortisol to help you cope with ongoing hypothyroidism and lingering symptoms and conditions. The excess cortisol inhibits the conversion of T4 to T3, and instead produces even larger amounts of RT3, creating an RT3 problem.
    When biological stress is ongoing, your adrenals will eventually produce less cortisol (ask “adrenal fatigue” or “adrenal insufficiency”), dropping from high cortisol to a mix of high and low, the to all low. And those low levels can cause chronic anxiety, poor coping skills, paranoia, easy nausea, sensitivity to light or sounds, psychological issues, etc. When you don’t make enough cortisol, thyroid hormones can pool high in your blood. So your body responds by converting the T4 to excess RT3.
    When iron goes low, which is quite common in thyroid patients due to low stomach acid, your red blood cells become less plentiful (or you have enough, but they are weak and pale), and carrying thyroid hormones via your blood becomes inadequate, causing thyroid hormones to pool in your blood. The body responds by producing excessive amounts of RT3 to clear out the excess T4.
  • Extranotes:
    A radioactive iodine uptake (RAIU) test uses a radioactive tracer and a special probe to measure how much tracer the thyroid gland camera.gif absorbs from the blood. The test can show how much tracer is absorbed by the thyroid gland and if it is evenly spread in the gland.
    A radioactive iodine uptake (RAIU) test is done to:Find the cause of an overactive thyroid gland (hyperthyroidism).
    The normal uptake is between 15 and 25 percent.
    131I sodium iodide, 123I sodium iodide.  But the use of131 I for routine diagnosis is discouraged because the radiation dose is about 100 times stronger than that of123 I.
    I131 Used to treat hyperthyroidism by destroying follicular cells of the thyroid gland.
    The test is inappropriate for patients who are pregnant or breastfeeding
    In thyroiditis:
    Several thyroid disorders that cause inflammation of the thyroid, or thyroiditis, may cause leakage of thyroid hormone and iodine out of the thyroid into the bloodstream, which can lead to high T4 levels. When the thyroid is inflamed, it does not take up the radioactive iodine given as part of the thyroid uptake test. For example, hyperthyroidism seen in Graves’ disease would be marked by high blood T4 and a high thyroid uptake reading. In thyroiditis, temporary hyperthyroidism may exist because of the release of T4 into the blood; however, the thyroid uptake reading is low because of the inflammation. Temporary hyperthyroidism in thyroiditis is often followed by a period of hypothyroidism before the thyroid heals.
    Causes of increased uptake include the following:
    Hyperthyroidism
    Iodine deficiency
    Pregnancy
    Recovery phase of subacute, silent, or postpartum thyroiditis
    Rebound after suppression of thyrotropin
    Rebound after withdrawal of antithyroid medication
    Lithium carbonate therapy
    Hashimoto thyroiditis
    Congenital defects of thyroid hormogenesis apart from trapping defect
    Causes of decreased uptake include the following:
    Primary hypothyroidism
    Destructive thyroiditis (subacute thyroiditis, silent thyroiditis, postpartum thyroiditis)
    Post-thyroidectomy,131 I treatment, or external neck radiation
    Central hypothyroidism
    Thyroid hormone
    Excess iodine
    Dietary variations and supplements
    Radiological contrast
    Amiodarone
    Topical iodine
    Medications other than those containing iodine (eg, antithyroid drugs, perchlorate, thiocyanate, sulphonamides, sulphonylurea, high-dose glucocorticosteroids)
  • Extranotes:
    Antithyroid Antibody Test
    Antithyroid antibodies are markers in the blood that are extremely helpful in diagnosing Hashimoto’s disease. Two principal types of antithyroid antibodies are
    anti-TG antibodies, which attack a protein in the thyroid called thyroglobulin
    anti-thyroperoxidase, or anti-TPO, antibodies, which attack an enzyme in thyroid cells called thyroperoxidase
    Thyroid-stimulating immunoglobulin
    Thyroid-stimulating immunoglobulin is an autoantibody present in Graves’ disease. TSI mimics TSH by stimulating the thyroid cells, causing the thyroid to secrete extra hormone.
    TSH receptor antibody IS SAME AS Thyroid stimulating immunoglobulin
    TSH receptor antibodies activate adenylate cyclase by binding to the TSH receptor. This causes the production of thyroid hormones and subsequent growth and vascularisation of the thyroid. TRAbs are also useful in the diagnosis of Graves' Ophthalmopathy. Although the exact mechanism of how TRAbs induce Graves' Ophthalmopathy is unknown, it is likely that the antibodies bind to TSH receptors in retro-orbital tissues, causing infiltration of lymphocytes. This inflammatory response leads to cytokine production that causes fibroblasts to produce glycosaminoglycans, leading to ophthalmopathy.
  • Extranotes:
    TSH is normally low when the thyroid gland is functioning properly, the failure of TSH to rise when circulating thyroid hormones are low is an indication of impaired pituitary function.
    Secondary hyperthyroidism is rare. The pathology is at the level of the pituitary. TSH, T3 and T4 are all very high. TRH stimulation tests are used in the diagnosis and result in a flat response curve.Causes include:
    TSH-secreting pituitary adenoma.
    Thyroid hormone-resistance syndrome.
    HCG-secreting tumour.
    Gestational thyrotoxicosis.
    Both pregnancy and taking oral contraceptives increase levels of binding protein in the blood. In either of these cases, although a woman may have a high total T4 level, she may not have hyperthyroidism. Severe illness or the use of corticosteroids—a class of medications that treat asthma, arthritis, and skin conditions, among other health problems—can decrease binding protein levels. Therefore, in these cases, the total T4 level may be low, yet the person does not have hypothyroidism.
  • Thyrotoxicosis refers to the biochemical and physiological manifestations of excessive thyroid hormone. 
    Hyperthyroidism is a term reserved for disorders that result in the over production of hormone by the thyroid gland. Thyrotoxicosis need not be due to hyperthyroidism
  • Extra notes:
    hCG has intrinsic thyrotropic activity.
    A struma ovarii (literally: goitre of the ovary) is a rare form of monodermal teratoma that contains mostly thyroid tissue, which may cause hyperthyroidism
    Causes of hyperthyroidismGrave's diseaseJod - Basedow's diseaseToxic nodular goiterToxic adenomaCauses of thyrotoxicosis without hyperthyroidismSubacute thyroiditisEctopic functioning thyroid tissueStruma ovariiPostpartum thyroiditisSilent thyroiditisMetastatic follicular carcinomaTrophoblastic tumors
  • Extranotes:
    The Jod-Basedow effect typically occurs with comparatively small increases in iodine intake, in people who have thryoid abnormalities that cause the gland to function without the control of the pituitary (i.e., a thyroid gland that is not normally suppressed bythyroid hormone driven loss of TSH secretion from the pituitary). In some ways the Jod-Basedow phenomenon is the opposite of the Wolff-Chaikoff effect, which refers to the short period of thyroid-hormone suppression which happens in normal persons and in persons with thyroid disease, when comparatively large quantities of iodine or iodide are ingested. However, unlike the Wolff-Chaikoff effect, the Jod-Basedow effect does not occur in persons with normal thyroid glands, as thyroid hormone synthesis and release in normal persons is controlled by pituitary TSH secretion, which does not allow hyperthyroidism when extra iodine is ingested.
    The Wolff–Chaikoff effect (pronounced "woolf' cha'kof"), discovered by Drs. Jan Wolff and Israel Lyon Chaikoff at the University of California, is a reduction in thyroid hormone levels caused by ingestion of a large amount of iodine.[2] In 1948, Wolff and Chaikoff reported that injection of iodine in rats almost completely inhibited organification (oxidation of iodide) in the thyroid gland. Patients with Graves' disease are more sensitive than euthyroid patients,and iodine has been used to manage Graves' disease.
    The Wolff–Chaikoff effect is an autoregulatory phenomenon that inhibits organification in the thyroid gland, the formation of thyroid hormones inside the thyroid follicle, and the release of thyroid hormones into the bloodstream. This becomes evident secondary to elevated levels of circulating iodide. The Wolff - Chaikoff effect is an effective means of rejecting a large quantity of imbibed iodide, and therefore preventing the thyroid from synthesizing large quantities of thyroid hormone. The Wolff–Chaikoff effect lasts several days (around 10 days), after which it is followed by an "escape phenomenon", which is described by resumption of normal organification of iodine and normal thyroid peroxidase function. "Escape phenomenon" is believed to occur because of decreased inorganic iodine concentration secondary to down-regulation of sodium-iodide symporter (NIS) on the basolateral membrane of the thyroid follicular cell.
    The Wolff–Chaikoff effect can be used as a treatment principle against hyperthyroidism (especially thyroid storm) by infusion of a large amount of iodine to suppress the thyroid gland. Iodide was used to treat hyperthyroidism before antithyroid drugs such as propylthiouracil and methimazole were developed. Hyperthyroid subjects given iodide may experience a decrease in basal metabolic rate that is comparable to that seen after thyroidectomy. The Wolff–Chaikoff effect also explains the hypothyroidism produced in some patients by several iodine-containing drugs, including amiodarone. The Wolff–Chaikoff effect is also part of the mechanism for the use of potassium iodide in nuclear emergencies.
  • Extranotes:
    Hyperthyroidism is the most common feature of Graves' disease, affecting nearly all patients, and is caused by autoantibodies to the thyrotropin (TSH) receptor (TSHR-Ab) that activate the receptor, thereby stimulating thyroid hormone synthesis and secretion as well as thyroid growth (causing a diffuse goiter). The presence of TSHR-Abs in serum and orbitopathy on clinical examination distinguishes the disorder from other causes of hyperthyroidism.
  • The therapeutic approach to Graves' hyperthyroidism consists of both rapid amelioration of symptoms with a beta-blocker and measures aimed at decreasing thyroid hormone synthesis: 
    The choice of therapy is determined by individual consideration of the risks and benefits of the three treatment modalities
    Regardless of the choice of treatment, all patients will require lifelong monitoring.
    Surgery — Surgery is an unpopular therapy for Graves' hyperthyroidism, being selected by only 1 percent of thyroid specialists . It is primarily indicated in patients who have an obstructive goiter or a very large goiter, in patients with active ophthalmopathy who desire definitive therapy for their hyperthyroidism, in pregnant women who are allergic to antithyroid drugs, and in patients who have allergies or poor compliance on antithyroid drugs but refuse radioiodine. Surgery would also be indicated if there was a coexisting suspicious or malignant thyroid nodule or primary hyperparathyroidism.
  • Extranotes:
    hyperthyroidism is associated with an increased number of ß-adrenergic receptors . The ensuing increase in ß-adrenergic activity is responsible for many of the symptoms associated with this disorder. It also explains the ability of ß-blockers to ameliorate rapidly many of the symptoms, including palpitations, tachycardia, tremulousness, anxiety, and heat intolerance .
    Propranolol in high doses (above 160 mg/day) also slowly decreases serum triiodothyronine (T3) concentrations by as much as 30 percent , via inhibition of the 5'-monodeiodinase that converts thyroxine (T4) to T3.
    We typically start with atenolol 25 to 50 mg daily, and increase the dose as needed (up to 200 mg daily) to reduce pulse to under 90 beats per minute if blood pressure allows.
    Patients should have their thyroid function assessed at four to six week intervals until stabilized on maintenance thionamide therapy.
  • Extrantes:
    Patients who have severe hyperthyroidism or are allergic to thionamides may benefit from alternative medical therapies. The oral radiocontrast agents sodium ipodate and iopanoic acid are potent inhibitors of the peripheral conversion of T4 to T3. They are not used as primary therapy because of possible induction of resistant hyperthyroidism. However, when given in combination with methimazole (at doses of 500 to 1000 mg/day), they can rapidly ameliorate severe hyperthyroidism and can also be used to prepare a hyperthyroid patient for early surgery.
     Iodine solutions, such as saturated potassium iodide solutions (SSKI) or potassium iodide-iodine (Lugol's solution),. Iodine has several effects on thyroid function. In hyperthyroid patients, iodine acutely inhibits hormonal secretion within hours , but the responsible mechanisms are uncertain. This is the most acute effect of iodine on thyroid status, occurring within one to two days of the start of therapy.
    A second effect involves inhibition of thyroid hormone synthesis. In normal subjects, the administration of pharmacologic amounts of iodine leads to temporary inhibition of iodine organification in the thyroid gland, thereby diminishing thyroid hormone biosynthesis, a phenomenon called the Wolff-Chaikoff effect . However, within two to four weeks of continued exposure to excess iodine, organification and thyroid hormone biosynthesis resume in a normal fashion. This is called escape from the Wolff-Chaikoff effect.
    Glucocorticoids inhibit peripheral T4 to T3 conversion and, in patients with Graves' hyperthyroidism, reduce thyroid secretion. They have been used in patients with severe hyperthyroidism and thyroid storm,
    Radioiodine is widely used for the treatment of Graves' hyperthyroidism. It has been the therapy of choice in the United States, We usually recommend radioiodine therapy. Although a thionamide provides control of hyperthyroidism as long as the drug is taken, the persistent remission rate when the drug is discontinued one to two years later averages only about 30 percent.
    Radioiodine is administered as a capsule or, less commonly, an oral solution of sodium 131I, which is rapidly absorbed from the GI tract and concentrated in thyroid tissue. It induces extensive tissue damage, resulting in ablation of the thyroid within 6 to 18 weeks.
    The goal of radioiodine therapy is destruction of the gland, with the early development of hypothyroidism. This eliminates the risk of recurrent hyperthyroidism. On the other hand, some clinicians prefer lower doses of radioiodine with the aim of achieving a euthyroid state while lowering the risk of early hypothyroidism 
  • Thyrotoxicosis should be treated with antithyroid drugs which cross the placenta and also treat the fetus, whose thyroid gland is exposed to the action of maternal TRAb.
  • Thyroid disorders Part 1

    1. 1. Thyroid disorders..Part 1 Pratap Sagar Tiwari, MD Lecturer, NMCTH
    2. 2. Anatomy http://khalidalomari.weebly.com/blood-supply-and-venous-drainage.htm
    3. 3. Vascular/Neural Anatomy Superior thyroid artery  external carotid artery, Inferior thyroid artery  thyrocervical trunk, Thyroid ima artery  subclavian artery. superior thyroid veins internal jugular vein, Middle thyroid vein internal jugular vein inferior thyroid veins  left brachiocephalic vein. Lymphatic drainage : the lateral deep cervical lymph nodes and the pre- and parathracheal lymph nodes. Parasympathetic nerve input  superior laryngeal nerve and recurrent laryngeal nerve.
    4. 4. Thyroid Histology http://www.studyblue.com/notes/note/n/anatomy-lab-shit/deck/7511240
    5. 5. Histology Follicles The thyroid is composed of spherical follicles Inside the follicles there is follicular lumen. It is surrounded by follicular cells and filled with colloid. Colloid is rich in a protein called thyroglobulin. Thyroid epithelial cells (or "follicular cells") The follicles are surrounded by a single layer of thyroid epithelial cells, which secrete T3 and T4. Parafollicular cells (or "C cells") Scattered among follicular cells and in spaces between the spherical follicles are another type of thyroid cell, parafollicular cells, which secrete calcitonin.
    6. 6. Thyroid hormone synthesis
    7. 7. Thyroid hormone synthesis • The thyroid secretes predominantly T4 and only a small amount of T3. • Approximately 85% of T3 in blood is produced from T4 by a family of monodeiodinase enzymes which are active in many tissues including liver, muscle, heart and kidney. • T4 can be regarded as a pro-hormone, since it has a longer half-life in blood than T3 (approx. 1 wk compared with approx. 18 hrs). • T4 binds and activates thyroid hormone receptors less effectively than T3. • T4 can also be converted to the inactive metabolite, reverse T3.
    8. 8. Thyroid Binding Globulin • Most of the thyroid hormones in the blood are attached to a protein called thyroid binding globulin (TBG). • If there is an excess or deficiency of this protein it alters the T4 or T3 measurement but does not affect the action of the hormone. • If a patient appears to have normal thyroid function, but an unexplained high or low T4, or T3, it may be due to an increase or decrease of TBG.
    9. 9. Radioactive iodine uptake (RAIU) test • A low uptake of tracer by the thyroid gland: hyperthyroidism is caused by inflammation of the thyroid gland (thyroiditis) or taking too much thyroid medicine. • A high uptake of tracer (spread evenly in the thyroid gland): hyperthyroidism is caused by Graves' disease. • An uneven spread of tracer in the thyroid gland (with either low or high areas of uptake) :hyperthyroidism is caused by a multinodular goiter or a noncancerous (benign) tumor called a toxic adenoma.
    10. 10. • Thyroid Ultrasound: solid vs cyctic • Thyroid Scan: hot vs cold • Thyroid Needle Biopsy • Thyroid Antibodies(anti-TG, anti-TPO): hashimoto • TSI Test: Graves’ disease
    11. 11. Interpretation T3 T4 TSH State ↔ ↔ ↔ Euthyroid ↑ ↑ ↓ Primary hyperthyroidism ↓ ↓ ↑ Primary hypothyroidism ↓ ↓ ↓ Secondary hypothyroidism ↑ ↑ ↑ Secondary hyperthyroidism ↔/↑ ↔/↑ ↔ Euthyroid hyperthyroxinemia ↔/↓ ↔/↓ ↔ Euthyroid hypothyroxinema ↔ ↔ ↑ Subclinical hypothyroidism ↔ ↔ ↓ Subclinical hyperthyroidism
    12. 12. Thyrotoxicosis • Thyrotoxicosis describes a constellation of clinical features arising from elevated circulating levels of thyroid hormone. • The most common causes are Graves' disease, multinodular goitre and autonomously functioning thyroid nodules (toxic adenoma).
    13. 13. Interpretation
    14. 14. Thyrotoxicosis: causes Common causes Graves' disease Iodide-induced (amiodarone, contrast) Multinodular goitre Extrathyroidal source Factitious thyrotoxicosis Struma ovarii Solitary thyroid adenoma TSH-induced TSH-secreting pituitary adenoma Choriocarcinoma and hydatidiform mole Thyroiditis (de Quervain's or Postpartum) Follicular carcinoma ± metastases
    15. 15. Thyrotoxicosis Symptoms SIgns Weight loss despite normal or increased appetite Weight loss Tremor Heat intolerance Palmar erythema Palpitations Sinus tachycardia Dyspnoea Lid retraction, lid lag Irritability, emotional lability Fatigue, Sweating, Tremor Less common Osteoporosis, Diarrhoea, steatorrhoea Goitre with bruit, Atrial fibrillation, HF Muscle weakness, Pruritus, Ankle swelling Alopecia Systolic hypertension/increased pulse pressure Amenorrhoea/oligomenorrhoea Infertility, spontaneous abortion Hyper-reflexia, Ill-sustained clonus, Proximal myopathy
    16. 16. Jod-Basedow phenomenon • is hyperthyroidism following administration of iodine or iodide, either as a dietary supplement or as contrast medium. • This phenomenon is thus iodine-induced hyperthyroidism, typically presenting in a patient with endemic goiter (due to iodine deficiency).
    17. 17. Graves' disease • is a syndrome that may consist of hyperthyroidism, goiter, eye disease (orbitopathy), and occasionally a dermopathy referred to as pretibial myxedema. • Hyperthyroidism is the mc feature of GD, affecting nearly all patients, and is caused by autoantibodies to the thyrotropin (TSH) receptor (TSHR-Ab) • TSHR-Ab activate the receptor, thereby stimulating thyroid hormone synthesis and secretion as well as thyroid growth (causing a diffuse goiter). • The presence of TSHR-Abs in serum and orbitopathy on clinical examination distinguishes the disorder from other causes of hyperthyroidism.
    18. 18. Treatment options Therapy Advantages Disadvantages Thionamides Methimazole Carbimazole Propylthiouracil Chance of permanent remission rash, arthralgias, GI, agranulocytosis, vasculitis (lupus-like syndrome), hepatitis (PTU) Radioiodine Permanent resolution of hyperthyroidism Permanent hypothyroidism oncogenic effects of radiation Surgery Rapid, permanent cure of hyperthyroidism Permanent hypothyroidism Risk of hypoparathyroidism, recurrent laryngeal nerve damage.
    19. 19. Antithyroid drugs 1. carbimazole 2. methimazole 3. Propylthiouracil • reduce the synthesis of new thyroid hormones by inhibiting the iodination of tyrosine. • Carbimazole also has an immunosuppressive action, leading to a reduction in serum TSHRAb concentrations. • CI: Breastfeeding (propylthiouracil suitable)
    20. 20. B blockers • HT is a/w an increased number of ß-adrenergic receptors . The ensuing increase in ß-adrenergic activity is responsible for many of the symptoms . • It also explains the ability of ß-blockers to ameliorate rapidly many of the symptoms, including palpitations, tachycardia, tremulousness, anxiety, and heat intolerance . • Propranolol in high doses (above 160 mg/day) also slowly decreases T3 concentrations by as much as 30 % , via inhibition of the 5'-monodeiodinase that converts T4 to T3. • Start with atenolol 25 to 50 mg daily, and increase the dose as needed (up to 200 mg daily) to reduce pulse to under 90 bpm if bp allows. • Patients should have their thyroid function assessed at 4-6 wks intervals until stabilized on maintenance thionamide therapy.
    21. 21. Iodinated contrast agents and iodine • The oral radiocontrast agents sodium ipodate and iopanoic acid are potent inhibitors of the peripheral conversion of T4 to T3. • When given in combination with methimazole (at doses of 500 to 1000 mg/day), they can rapidly ameliorate severe hyperthyroidism and can also be used to prepare a hyperthyroid patient for early surgery.
    22. 22. Thyrotoxicosis in pregnancy • Propylthiouracil may be preferable to carbimazole since the latter might be associated with a skin defect in the child, known as aplasia cutis. • In order to avoid fetal hypothyroidism and goitre, it is important to use the smallest dose of antithyroid drug (optimally < 150 mg /d) that will maintain maternal (and presumably fetal) free T4, T3 and TSH WNR.
    23. 23. Graves' ophthalmopathy (orbitopathy) • The eye disease often associated with Graves' thyroid disease is referred to as Graves' ophthalmopathy. • This condition is immunologically mediated. • Within the orbit (and the dermis) there is cytokine-mediated proliferation of fibroblasts which secrete hydrophilic glycosaminoglycans. • The resulting increase in interstitial fluid content, combined with a chronic inflammatory cell infiltrate, causes marked swelling and ultimately fibrosis of the extraocular muscles and a rise in retrobulbar pressure. • The eye is displaced forwards (proptosis/ exophthalmos) and in severe cases there is optic nerve compression.
    24. 24. Features • Ptosis, pseudo ptosis, strabismus (hypotropia, esotropia)
    25. 25. Mobius sign (poor convergence)Mobius sign (poor convergence)
    26. 26. 26 Ballet signBallet sign – restriction of one or more extra ocular musclesrestriction of one or more extra ocular muscles – Initially due to edema , later fibrosisInitially due to edema , later fibrosis – All 4 recti are involved but mainly IR and MRAll 4 recti are involved but mainly IR and MR
    27. 27. 27 Restrictive myopathy Elevation defect Abduction defect Depression defect Adduction defect
    28. 28. 28 • Upper lid retraction (Dalrymple sign)Upper lid retraction (Dalrymple sign) -90%-90%
    29. 29. 29 Mechanisms for upper lid retraction Up gaze restriction Proptosis Fibrotic contracture of LPS Secondary over action of LPS-SR complex Muller muscle over action
    30. 30. 30 Signs of eyelid retraction • Bilateral lid retraction • No associated proptosis • Bilateral lid retraction • Bilateral proptosis • Lid lag in downgaze• Unilateral lid retraction • Unilateral proptosis
    31. 31. 31 Lid lag on down gaze (von Graefe’s sign)
    32. 32. 32 Glabellar furrows Eyelid edema
    33. 33. 33  Stellwag sign (incomplete and infrequent blinking)Stellwag sign (incomplete and infrequent blinking)  Goffroy sign (absent creases in the forehead on superior gaze)Goffroy sign (absent creases in the forehead on superior gaze)  Enroth’s sign (eyelid fullness)Enroth’s sign (eyelid fullness) Gifford’s signGifford’s sign (difficulty in upper lid eversion )(difficulty in upper lid eversion )
    34. 34. 34 Minimal staining Ulceration perforation Corneal signs
    35. 35. Assessment of severity • Class 0 — No symptoms or signs • Class I — Only signs, no symptoms (eg, lid retraction, stare, lid lag) • Class II — Soft tissue involvement • Class III — Proptosis • Class IV — Extraocular muscle involvement • Class V — Corneal involvement • Class VI — Sight loss (optic nerve involvement)
    36. 36. End of slides References: •Davidson 21st •Uptodate 20.3 •Medscape •Wikipedia •Eye signs pics taken from slides of : THYRIOD EYE DISEASEDr. Gyanendra Lamichhane,Lumbini Eye Institute,Bhairahawa ,Nepal

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