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Presenting problems in thyroid disease

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Sadia Shabbir
Sadia Shabbir

This document summarizes information about hyperthyroidism and hypothyroidism, including their common causes, symptoms, signs, investigations, and treatment approaches. The most common causes are Graves' disease, multinodular goiter, and solitary thyroid adenomas. Common symptoms include weight loss, heat intolerance, palpitations, and tremors. Diagnostic testing involves measuring T3, T4, and TSH levels. Treatment depends on the underlying cause, and may include antithyroid drugs, radioactive iodine, surgery, or beta-blockers to control symptoms.

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Presenting problems in thyroid disease
Hyperthyroidism(thyrotoxicosis) Hypothyroidism Enlargement of thyroid (goitre or thyroid nodule)
The most common causes are Graves disease Multinodular goitre Solitary thyroid adenoma Iodide-induced Drugs (amiodarone) Radiographic contrast media Iodine prophylaxis programme2
Extrathyroidal source of thyroid hormone Factitious thyrotoxicosis Struma ovarii TSH-induced TSH-secreting pituitary adenoma Choriocarcinoma and hydatidiform mole Follicular carcinoma 賊 metastases
COMMON Symptoms Weight loss despite normal or increased appetite Heat intolerance, sweating Palpitations, tremor Dyspnoea, fatigue Irritability, emotional lability Signs Weight loss Tremor Palmar erythema Sinus tachycardia Lid retraction, lid lag
Less common Symptoms Osteoporosis (fracture, loss of height) Diarrhoea, steatorrhoea Angina Ankle swelling Anxiety, psychosis Muscle weakness Periodic paralysis (predominantly in Chinese) Pruritus, alopecia Amenorrhoea/oligomenorrhoea Infertility, spontaneous abortion Loss of libido, impotence
SIGNS Excessive lacrimation Goitre with bruit Atrial fibrillation Systolic hypertension/increased pulse pressure Cardiac failure Hyper-reflexia Ill-sustained clonus Proximal myopathy Bulbar myopathy
The first-line investigations are serum T3, T4 and TSH In most patients, serum T3 and T4 are both elevated Serum TSH is undetectable in primary thyrotoxicosis, but values can be raised in the very rare syndrome of secondary thyrotoxicosis caused by a TSH-producing pituitary adenoma.
When biochemical thyrotoxicosis has been confirmed, further investigations should be undertaken to determine the underlying cause, including Measurement of TSH receptor antibodies (TRAb, elevated in Graves disease) isotope scanning
Non-specific laboratory abnormalities in thyrotoxicosis: Serum enzymes: raised alanine aminotransferase, 粒- glutamyl transferase (GGT), and alkaline phosphatase from liver and bone Raised bilirubin Mild hypercalcaemia Glycosuria: associated diabetes mellitus, lag storage glycosuria An ECG may demonstrate sinus tachycardia or atrial fibrillation.
Occasionally, patients induce factitious thyrotoxicosis by consuming excessive amounts of a thyroid hormone preparation, most often levothyroxine. The exogenous thyroxine suppresses pituitary TSH secretion and hence iodine uptake, serum thyroglobulin and release of endogenous thyroid hormones. The T4:T3 ratio (typically 30 : 1 in conventional thyrotoxicosis) is increased to above 70 : 1 because circulating T3 . The combination of negligible iodine uptake, high T4:T3 ratio and a low or undetectable thyroglobulin is diagnostic.
Definitive treatment of thyrotoxicosis depends on the underlying cause and may include antithyroid drugs, radioactive iodine or surgery. A non-selective 硫-adrenoceptor antagonist (硫- blocker), such as propranolol (160 mg daily) or nadolol (4080 mg daily), will alleviate but not abolish symptoms in most patients within 2448 hours. Beta-blockers should not be used for long- term treatment of thyrotoxicosis
Graves disease can occur at any age but is unusual before puberty and most commonly affects women aged 3050 years
Pathophysiology The thyrotoxicosis results from the production of IgG antibodies directed against the TSH receptor on the thyroid follicular cell, which stimulate thyroid hormone production and proliferation of follicular cells, leading to goitre in the majority of patients. These antibodies are termed thyroid-stimulating immunoglobulins or TSH receptor antibodies (TRAb) and can be detected in the serum of 8095% of patients with Graves disease.
For patients under 40 years of age, most clinicians adopt the empirical approach of prescribing a course of carbimazole and recommending surgery if relapse occurs, while 131I is employed as first- or second-line treatment in those aged over 40.
Antithyroid drugs:should be introduced at high doses (carbimazole 4060 mg daily or propylthiouracil 400600 mg daily). Usually, this results in subjective improvement within 1014 days and renders the patient clinically and biochemically euthyroid at 34 weeks. At this point, the dose can be reduced and titrated to maintain T4 and TSH within their reference range. In most patients, carbimazole is continued at 520 mg per day for 1218 months in the hope that remission will occur. Patients with thyrotoxicosis relapse in at least 50% of cases, usually within 2 years of stopping treatment. Rarely, T4 and TSH levels fluctuate between those of thyrotoxicosis and hypothyroidism at successive review appointments, despite good drug compliance, presumably due to rapidly changing concentrations of TRAb. In these patients, satisfactory control can be achieved by blocking thyroid hormone synthesis with carbimazole 3040 mg daily and adding levothyroxine 100150 袖g daily as replacement therapy
Thyroid surgery: Patients should be rendered euthyroid with antithyroid drugs before operation. Potassium iodide, 60 mg 3 times daily orally, is often added for 2 weeks before surgery to inhibit thyroid hormone release and reduce the size and vascularity of the gland, making surgery technically easier.
Radioactive iodine: 131I is administered orally as a single dose, and is trapped and organified in the thyroid. Although 131I decays within a few weeks, it has long-lasting inhibitory effects on survival and replication of follicular cells. This regimen is effective in 75% of patients within 412 weeks. During the lag period, symptoms can be controlled by a 硫-blocker or, in more severe cases, by carbimazole. However, carbimazole reduces the efficacy of 131I therapy because it prevents organification of 131I in the gland, and so should be avoided until 48 hours after radio-iodine administration. If thyrotoxicosis persists after 6 months, a further dose of 131I can be given.
This condition is immunologically mediated but the autoantigen has not been identified. 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.
The most frequent presenting symptoms are related to increased exposure of the cornea, resulting from proptosis and lid retraction. There may be excessive lacrimation made worse by wind and bright light, a gritty sensation in the eye
Presenting problems in thyroid disease
Severe inflammatory episodes are treated with glucocorticoids (e.g. daily oral prednisolone or pulsed IV methylprednisolone) and sometimes orbital radiotherapy.Loss of visual acuity is an indication for urgent surgical decompression of the orbit. In burnt- out disease, surgery to the eyelids and/or ocular muscles may improve conjunctival exposure, cosmetic appearance and diplopia.
Atrial fibrillation occurs in about 10% of patients with thyrotoxicosis. The incidence increases with age, so that almost half of all males with thyrotoxicosis over the age of 60 are affected. Moreover, subclinical thyrotoxicosis is a risk factor for atrial fibrillation. Characteristically, the ventricular rate is little influenced by digoxin, but responds to the addition of a 硫-blocker. Thromboembolic vascular complications are particularly common in thyrotoxic atrial fibrillation so that anticoagulation with warfarin is required, unless contraindicated. Once thyroid hormone and TSH concentrations have been returned to normal, atrial fibrillation will spontaneously revert to sinus rhythm in about 50% of patients, but cardioversion may be required in the remainder.
This is a rare but life-threatening complication of thyrotoxicosis. The most prominent signs are fever, agitation, confusion, tachycardia or atrial fibrillation and, in the older patient, cardiac failure. It is a medical emergency, which has a mortality of 10% despite early recognition and treatment. Thyrotoxic crisis is most commonly precipitated by infection in a patient with previously unrecognised or inadequately treated thyrotoxicosis. It may also develop shortly after subtotal thyroidectomy in an ill-prepared patient or within a few days of 131I therapy, when acute irradiation damage may lead to a transient rise in serum thyroid hormone levels.
Patients should be rehydrated and given propranolol, either orally (80 mg 4 times daily) or intravenously (15 mg 4 times daily). Sodium ipodate (500 mg per day orally) will restore serum T3 levels to normal in 4872 hours. This is a radiographic contrast medium which not only inhibits the release of thyroid hormones, but also reduces the conversion of T4 to T3 and is, therefore, more effective than potassium iodide or Lugols solution.Oral carbimazole 4060 mg daily should be given to inhibit the synthesis of new thyroid hormone.After 1014 days the patient can usually be maintained on carbimazole alone.

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Presenting problems in thyroid disease

  • 2. Hyperthyroidism(thyrotoxicosis) Hypothyroidism Enlargement of thyroid (goitre or thyroid nodule)
  • 3. The most common causes are Graves disease Multinodular goitre Solitary thyroid adenoma Iodide-induced Drugs (amiodarone) Radiographic contrast media Iodine prophylaxis programme2
  • 4. Extrathyroidal source of thyroid hormone Factitious thyrotoxicosis Struma ovarii TSH-induced TSH-secreting pituitary adenoma Choriocarcinoma and hydatidiform mole Follicular carcinoma 賊 metastases
  • 5. COMMON Symptoms Weight loss despite normal or increased appetite Heat intolerance, sweating Palpitations, tremor Dyspnoea, fatigue Irritability, emotional lability Signs Weight loss Tremor Palmar erythema Sinus tachycardia Lid retraction, lid lag
  • 6. Less common Symptoms Osteoporosis (fracture, loss of height) Diarrhoea, steatorrhoea Angina Ankle swelling Anxiety, psychosis Muscle weakness Periodic paralysis (predominantly in Chinese) Pruritus, alopecia Amenorrhoea/oligomenorrhoea Infertility, spontaneous abortion Loss of libido, impotence
  • 7. SIGNS Excessive lacrimation Goitre with bruit Atrial fibrillation Systolic hypertension/increased pulse pressure Cardiac failure Hyper-reflexia Ill-sustained clonus Proximal myopathy Bulbar myopathy
  • 8. The first-line investigations are serum T3, T4 and TSH In most patients, serum T3 and T4 are both elevated Serum TSH is undetectable in primary thyrotoxicosis, but values can be raised in the very rare syndrome of secondary thyrotoxicosis caused by a TSH-producing pituitary adenoma.
  • 9. When biochemical thyrotoxicosis has been confirmed, further investigations should be undertaken to determine the underlying cause, including Measurement of TSH receptor antibodies (TRAb, elevated in Graves disease) isotope scanning
  • 10. Non-specific laboratory abnormalities in thyrotoxicosis: Serum enzymes: raised alanine aminotransferase, 粒- glutamyl transferase (GGT), and alkaline phosphatase from liver and bone Raised bilirubin Mild hypercalcaemia Glycosuria: associated diabetes mellitus, lag storage glycosuria An ECG may demonstrate sinus tachycardia or atrial fibrillation.
  • 11. Occasionally, patients induce factitious thyrotoxicosis by consuming excessive amounts of a thyroid hormone preparation, most often levothyroxine. The exogenous thyroxine suppresses pituitary TSH secretion and hence iodine uptake, serum thyroglobulin and release of endogenous thyroid hormones. The T4:T3 ratio (typically 30 : 1 in conventional thyrotoxicosis) is increased to above 70 : 1 because circulating T3 . The combination of negligible iodine uptake, high T4:T3 ratio and a low or undetectable thyroglobulin is diagnostic.
  • 12. Definitive treatment of thyrotoxicosis depends on the underlying cause and may include antithyroid drugs, radioactive iodine or surgery. A non-selective 硫-adrenoceptor antagonist (硫- blocker), such as propranolol (160 mg daily) or nadolol (4080 mg daily), will alleviate but not abolish symptoms in most patients within 2448 hours. Beta-blockers should not be used for long- term treatment of thyrotoxicosis
  • 13. Graves disease can occur at any age but is unusual before puberty and most commonly affects women aged 3050 years
  • 14. Pathophysiology The thyrotoxicosis results from the production of IgG antibodies directed against the TSH receptor on the thyroid follicular cell, which stimulate thyroid hormone production and proliferation of follicular cells, leading to goitre in the majority of patients. These antibodies are termed thyroid-stimulating immunoglobulins or TSH receptor antibodies (TRAb) and can be detected in the serum of 8095% of patients with Graves disease.
  • 15. For patients under 40 years of age, most clinicians adopt the empirical approach of prescribing a course of carbimazole and recommending surgery if relapse occurs, while 131I is employed as first- or second-line treatment in those aged over 40.
  • 16. Antithyroid drugs:should be introduced at high doses (carbimazole 4060 mg daily or propylthiouracil 400600 mg daily). Usually, this results in subjective improvement within 1014 days and renders the patient clinically and biochemically euthyroid at 34 weeks. At this point, the dose can be reduced and titrated to maintain T4 and TSH within their reference range. In most patients, carbimazole is continued at 520 mg per day for 1218 months in the hope that remission will occur. Patients with thyrotoxicosis relapse in at least 50% of cases, usually within 2 years of stopping treatment. Rarely, T4 and TSH levels fluctuate between those of thyrotoxicosis and hypothyroidism at successive review appointments, despite good drug compliance, presumably due to rapidly changing concentrations of TRAb. In these patients, satisfactory control can be achieved by blocking thyroid hormone synthesis with carbimazole 3040 mg daily and adding levothyroxine 100150 袖g daily as replacement therapy
  • 17. Thyroid surgery: Patients should be rendered euthyroid with antithyroid drugs before operation. Potassium iodide, 60 mg 3 times daily orally, is often added for 2 weeks before surgery to inhibit thyroid hormone release and reduce the size and vascularity of the gland, making surgery technically easier.
  • 18. Radioactive iodine: 131I is administered orally as a single dose, and is trapped and organified in the thyroid. Although 131I decays within a few weeks, it has long-lasting inhibitory effects on survival and replication of follicular cells. This regimen is effective in 75% of patients within 412 weeks. During the lag period, symptoms can be controlled by a 硫-blocker or, in more severe cases, by carbimazole. However, carbimazole reduces the efficacy of 131I therapy because it prevents organification of 131I in the gland, and so should be avoided until 48 hours after radio-iodine administration. If thyrotoxicosis persists after 6 months, a further dose of 131I can be given.
  • 19. This condition is immunologically mediated but the autoantigen has not been identified. 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.
  • 20. The most frequent presenting symptoms are related to increased exposure of the cornea, resulting from proptosis and lid retraction. There may be excessive lacrimation made worse by wind and bright light, a gritty sensation in the eye
  • 22. Severe inflammatory episodes are treated with glucocorticoids (e.g. daily oral prednisolone or pulsed IV methylprednisolone) and sometimes orbital radiotherapy.Loss of visual acuity is an indication for urgent surgical decompression of the orbit. In burnt- out disease, surgery to the eyelids and/or ocular muscles may improve conjunctival exposure, cosmetic appearance and diplopia.
  • 23. Atrial fibrillation occurs in about 10% of patients with thyrotoxicosis. The incidence increases with age, so that almost half of all males with thyrotoxicosis over the age of 60 are affected. Moreover, subclinical thyrotoxicosis is a risk factor for atrial fibrillation. Characteristically, the ventricular rate is little influenced by digoxin, but responds to the addition of a 硫-blocker. Thromboembolic vascular complications are particularly common in thyrotoxic atrial fibrillation so that anticoagulation with warfarin is required, unless contraindicated. Once thyroid hormone and TSH concentrations have been returned to normal, atrial fibrillation will spontaneously revert to sinus rhythm in about 50% of patients, but cardioversion may be required in the remainder.
  • 24. This is a rare but life-threatening complication of thyrotoxicosis. The most prominent signs are fever, agitation, confusion, tachycardia or atrial fibrillation and, in the older patient, cardiac failure. It is a medical emergency, which has a mortality of 10% despite early recognition and treatment. Thyrotoxic crisis is most commonly precipitated by infection in a patient with previously unrecognised or inadequately treated thyrotoxicosis. It may also develop shortly after subtotal thyroidectomy in an ill-prepared patient or within a few days of 131I therapy, when acute irradiation damage may lead to a transient rise in serum thyroid hormone levels.
  • 25. Patients should be rehydrated and given propranolol, either orally (80 mg 4 times daily) or intravenously (15 mg 4 times daily). Sodium ipodate (500 mg per day orally) will restore serum T3 levels to normal in 4872 hours. This is a radiographic contrast medium which not only inhibits the release of thyroid hormones, but also reduces the conversion of T4 to T3 and is, therefore, more effective than potassium iodide or Lugols solution.Oral carbimazole 4060 mg daily should be given to inhibit the synthesis of new thyroid hormone.After 1014 days the patient can usually be maintained on carbimazole alone.