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Hyperthyroidism PowerPoint Presentation

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Description : Check out this medical PowerPoint presentation titled "Hyperthyroidism"by Dr Swaapnika.

This medical PowerPoint presentation talks about hyperthyroidism, a condition in which the thyroid gland produces an excessive amount of thyroid hormones. The thyroid gland is a small, butterfly-shaped gland located in the front of the neck, and it plays a crucial role in regulating the bodys metabolism. Thyroid hormones control the rate at which the body uses energy, affects the heart rate, and influences the functioning of other organs.

There are several causes of hyperthyroidism, including Graves disease, toxic nodular goiter, and thyroiditis. Graves disease is an autoimmune disorder in which the immune system produces antibodies that stimulate the thyroid gland to produce too much thyroid hormone. Toxic nodular goiter is a condition in which nodules on the thyroid gland produce too much thyroid hormone. Thyroiditis is inflammation of the thyroid gland that can cause temporary hyperthyroidism.

Symptoms of hyperthyroidism include weight loss, increased appetite, rapid heartbeat, nervousness, irritability, sweating, heat intolerance, tremors, fatigue, and difficulty sleeping. If left untreated, hyperthyroidism can lead to serious complications, such as heart problems, bone loss, and a thyroid storm, which is a life-threatening condition.

Treatment for hyperthyroidism depends on the cause of the condition and the severity of the symptoms. Options include medications that block the production of thyroid hormone, radioactive iodine therapy to destroy part of the thyroid gland, or surgery to remove the thyroid gland. In some cases, hyperthyroidism may resolve on its own without treatment.

Tags : hyperthyroidism, thyroid gland, thyroid hormones, Graves disease, toxic nodular goiter, thyroiditis, endocrinology, endocrinology PowerPoint presentation

Published on : Apr 18, 2023 | Views : 3055 | Downloads : 16

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Slide 1-

Hyperthyroidism Dr Swaapnika
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Hyperthyroidism- is the result of excessive thyroid function. Thyrotoxicosis is defined as the state of thyroid hormone excess. The major etiologies of thyrotoxicosis are hyperthyroidism caused by Graves’ disease, toxic MNG, and toxic adenomas.
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GRAVES’ DISEASE Graves’ disease accounts for 60–80% of thyrotoxicosis. As in autoimmune hypothyroidism, a combination of environmental and genetic factors, including polymorphisms in HLADR, CTLA-4, and PTPN22 (a T cell regulatory gene), contribute to Graves’ disease susceptibility. Smoking is a minor risk factor for Graves’ disease and a major risk factor for the development of ophthalmopathy. The hyperthyroidism of Graves’ disease is caused by TSI (thyroid stimulating immunoglobulin) that are synthesized in the thyroid gland as well as in bone marrow and lymph nodes.
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Graves’ patients in whom high levels of TSI can cross the placenta and cause neonatal thyrotoxicosis. Cytokines appear to play a major role in thyroid-associated ophthalmopathy. There is infiltration of the extraocular muscles by activated T cells; the release of cytokines such as IFN-gamma, TNF, and IL-1 results in fibroblast activation and increased synthesis of glycosaminoglycans that trap water, thereby leading to characteristic muscle swelling.
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Increased fat is an additional cause of retrobulbar tissue expansion. The increase in intraorbital pressure can lead to proptosis, diplopia, and optic neuropathy. Late in the disease, there is irreversible fibrosis of the muscles.
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Clinical manifestations
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In the elderly, features of thyrotoxicosis may be subtle or masked, and patients may present mainly with fatigue and weight loss, a condition known as apathetic thyrotoxicosis. Thyrotoxicosis may cause unexplained weight loss, despite an enhanced appetite, due to the increased metabolic rate.
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Fine tremor is a frequent finding, best elicited by having patients stretch out their fingers while feeling the fingertips with the palm. Thyrotoxicosis is sometimes associated with a form of hypokalemic periodic paralysis. Common neurologic manifestations include hyperreflexia, muscle wasting, and proximal myopathy without fasciculation.
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The direct effect of thyroid hormones on bone resorption leads to osteopenia in longstanding thyrotoxicosis; mild hypercalcemia occurs in up to 20% of patients, but hypercalciuria is more common. In Graves’ disease the thyroid is usually diffusely enlarged to two–three times its normal size. Lid retraction, causing a staring appearance, can occur in any form of thyrotoxicosis and is the result of sympathetic overactivity.
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The earliest manifestations of ophthalmopathy are usually a sensation of grittiness, eye discomfort, and excess tearing. Scoring system to gauge the extent and activity of the orbital changes in Graves’ disease-The “NO SPECS” scheme
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0 = No signs or symptoms 1 = Only signs (lid retraction or lag), no symptoms 2 = Soft tissue involvement (periorbital edema) 3 = Proptosis (>22 mm) 4 = Extraocular muscle involvement (diplopia) 5 = Corneal involvement 6 = Sight loss
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Thyroid dermopathy occurs in <5% of patients with Graves’ disease , almost always in the presence of moderate or severe ophthalmopathy. Thyroid acropachy refers to a form of clubbing found in <1% of patients with Graves’ disease
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TSH level is suppressed and total and unbound thyroid hormone levels are increased in Graves disease. Measurement of TBII(TSH binding inhibitor immunoglobulin) or TSI will confirm the diagnosis but is not needed routinely. Elevation of bilirubin, liver enzymes, and ferritin. Microcytic anemia and thrombocytopenia may occur.
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Clinical features of thyrotoxicosis can mimic certain aspects of other disorders, including panic attacks, mania, pheochromocytoma, and weight loss associated with malignancy. The diagnosis of thyrotoxicosis can be easily excluded if the TSH and unbound T3 levels are normal.
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There may be fluctuation between hypo and hyperthyroidism due to changes in the functional activity of TSH-R antibodies. Ophthalmopathy typically worsens over the initial 3–6 months, followed by a plateau phase over the next 12–18 months, with spontaneous improvement, particularly in the soft tissue changes.
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Diplopia may appear late in the disease due to fibrosis of the extraocular muscles. Thyroid dermopathy, when it occurs, usually appears 1–2 years after the development of Graves’ hyperthyroidism; it may improve spontaneously.
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Treatment The hyperthyroidism of Graves’ disease is treated by reducing thyroid hormone synthesis, using antithyroid drugs, or reducing the amount of thyroid tissue with radioiodine (131I) treatment or by thyroidectomy. The main antithyroid drugs are the thionamides, such as propylthiouracil, carbimazole, and the active metabolite of the latter, methimazole. All inhibit the function of TPO, reducing oxidation and organification of iodide. Propylthiouracil inhibits deiodination of T4 to T3.
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There are many variations of antithyroid drug regimens. The initial dose of carbimazole or methimazole is usually 10–20 mg every 8 or 12 h. Propylthiouracil is given at a dose of 100–200 mg every 6–8 h, and divided doses are usually given throughout the course. High doses may be given combined with levothyroxine supplementation (block-replace regimen) to avoid drug-induced hypothyroidism.
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Thyroid function tests and clinical manifestations are reviewed 3–4 weeks after starting treatment, and the dose is titrated based on unbound T4 levels. It takes 6 – 8 weeks to achieve euthyroidism after the initiation of the treatment. The usual daily maintenance doses of antithyroid drugs in the titration regimen are 2.5–10 mg of carbimazole or methimazole and 50–100 mg of propylthiouracil.
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The common side effects of antithyroid drugs are rash, urticaria, fever, and arthralgia (1–5% of patients). Need to watch for symptoms of possible agranulocytosis (e.g., sore throat, fever, mouth ulcers)
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Propranolol (20–40 mg every 6 h) or longer-acting beta blockers such as atenolol, may be helpful to control adrenergic symptoms, especially in the early stages before antithyroid drugs take effect. The need for anticoagulation with coumadin should be considered in all patients with atrial fibrillation.
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Radioiodine causes progressive destruction of thyroid cells and can be used as initial treatment or for relapses after a trial of antithyroid drugs. Propylthiouracil has a prolonged radioprotective effect and should be stopped several weeks before radioiodine is given.
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131I dosage generally ranges between 185 MBq (5 mCi) to 555 MBq (15 mCi). Hyperthyroidism can persist for 2–3 months before radioiodine takes full effect. For this reason, beta-adrenergic blockers or antithyroid drugs can be used to control symptoms during this interval.
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Persistent hyperthyroidism can be treated with a second dose of radioiodine, usually 6 months after the first dose. Pregnancy and breast feeding are absolute contraindications to radioiodine treatment, but patients can conceive safely 6 months after treatment.
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Subtotal or near-total thyroidectomy is an option for patients who relapse after antithyroid drugs and prefer this treatment to radioiodine. Careful control of thyrotoxicosis with antithyroid drugs, followed by potassium iodide (3 drops orally tid), is needed prior to surgery to avoid thyrotoxic crisis and to reduce the vascularity of the gland.
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Propylthiouracil is usually used because of relatively low transplacental transfer and its ability to block T4 to T3 conversion.
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Thyrotoxic crisis, or thyroid storm, is rare and presents as a life-threatening exacerbation of hyperthyroidism, accompanied by fever, delirium, seizures, coma, vomiting, diarrhea, and jaundice. Large doses of propylthiouracil (600 mg loading dose and 200–300 mg every 6 h) should be given orally or by nasogastric tube or per rectum; the drug’s inhibitory action on T4 to T3 conversion makes it the antithyroid drug of choice.
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One hour after the first dose of propylthiouracil, stable iodide is given to block thyroid hormone synthesis via the Wolff-Chaikoff effect (the delay allows the antithyroid drug to prevent the excess iodine from being incorporated into new hormone). Ophthalmopathy requires no active treatment when it is mild or moderate, as there is usually spontaneous improvement.
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THYROIDITIS A clinically useful classification of thyroiditis is based on the onset and duration of disease. The patient presents with thyroid pain, often referred to the throat or ears, and a small, tender goiter that may be asymmetric. The erythrocyte sedimentation rate (ESR) and white cell count are usually increased, but thyroid function is normal. FNA biopsy shows infiltration by polymorphonuclear leukocytes; culture of the sample can identify the organism
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The differential diagnosis of thyroid pain includes Subacute thyroiditis Chronic thyroiditis Hemorrhage into a cyst Malignancy including lymphoma Amiodarone-induced thyroiditis or Amyloidosis.
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Antibiotic treatment is guided initially by Gram stain and subsequently by cultures of the FNA biopsy. Surgery to drain the abscess.
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SUBACUTE THYROIDITIS This is also termed de Quervain’s thyroiditis, granulomatous thyroiditis, or viral thyroiditis. Viral etiology-mumps, coxsackie, influenza. Symptoms can mimic pharyngitis. During the initial phase of follicular destruction, there is release of Tg and thyroid hormones, leading to increased circulating T4 and T3 and suppression of TSH. Later stages shows increase in TSH and increased radio iodine uptake.
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Clinical Manifestations Painful and enlarged thyroid, sometimes accompanied by fever. Malaise and symptoms of an upper respiratory tract infection may precede the thyroid-related features by several weeks. The patient typically complains of a sore throat, and examination reveals a small goiter that is exquisitely tender.
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The diagnosis is confirmed by a high ESR and low radioiodine uptake. Relatively large doses of aspirin (e.g., 600 mg every 4–6 h) or NSAIDs are sufficient to control symptoms in many cases. Glucocorticoids -The usual starting dose is 40–60 mg prednisone, depending on severity.
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SILENT THYROIDITIS Painless thyroiditis, or “silent” thyroiditis, occurs in patients with underlying autoimmune thyroid disease. Typically, patients have a brief phase of thyrotoxicosis lasting 2–4 weeks, followed by hypothyroidism for 4–12 weeks, and then resolution.
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In addition to the painless goiter, silent thyroiditis can be distinguished from subacute thyroiditis by a normal ESR and the presence of TPO antibodies. Glucocorticoids are not indicated for silent thyroiditis. Severe thyrotoxic symptoms can be managed with a brief course of propranolol, 20–40 mg three or four times daily.
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SICK EUTHYROID SYNDROME Any acute, severe illness can cause abnormalities of circulating TSH or thyroid hormone levels in the absence of underlying thyroid disease. Cause is the release of cytokines such as IL-6.
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The most common hormone pattern in sick euthyroid syndrome (SES) is a decrease in total and unbound T3 levels (low T3 syndrome) with normal levels of T4 and TSH. Very sick patients may exhibit a dramatic fall in total T4 and T3 levels (low T4 syndrome). This state has a poor prognosis
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History is vital No laboratory investigations needed. Treatment is usually not required and subsequent thyroid functions need to be moitored.
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THYROID FUNCTION IN PREGNANCY Five factors alter thyroid function in pregnancy (1) the transient increase in hCG during the first trimester, which stimulates the TSH-R. (2) the estrogen-induced rise in TBG during the first trimester, which is sustained during pregnancy. (3) alterations in the immune system, leading to the onset, exacerbation, or amelioration of an underlying autoimmune thyroid disease. (4) increased thyroid hormone metabolism by the placenta. (5) increased urinary iodide excretion, which can cause impaired thyroid hormone production in areas of marginal iodine sufficiency.
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hCG-induced changes in thyroid function can result in transient gestational hyperthyroidism and/or hyperemesis gravidarum, a condition characterized by severe nausea and vomiting and risk of volume depletion. Thyroid hormone requirements are increased by 25–50 mic g/d during pregnancy.
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GOITER AND NODULAR THYROID DISEASE Goiter refers to an enlarged thyroid gland. Biosynthetic defects, iodine deficiency, autoimmune disease, and nodular diseases can each lead to goiter, though by different mechanisms. In Graves’ disease, the goiter results mainly from the TSH-R–mediated effects of TSI. The goitrous form of Hashimoto’s thyroiditis occurs because of acquired defects in hormone synthesis, leading to elevated levels of TSH and its consequent growth effects.
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Nodular disease is characterized by the disordered growth of thyroid cells, often combined with the gradual development of fibrosis. When diffuse enlargement of the thyroid occurs in the absence of nodules and hyperthyroidism, it is referred to as a diffuse nontoxic goiter. This is sometimes called simple goiter, because of the absence of nodules, or colloid goiter.
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Most patients with thyroid nodules have normal thyroid function tests. TSH is suppressed, a radionuclide scan is indicated to determine if the identified nodule is “hot,” as lesions with increased uptake are almost never malignant and FNA is unnecessary.
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Thank you