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Other Considerations. Differential Diagnoses. Nodular Non-toxic Goiter Graves’ Disease Toxic Multinodular Goiter Toxic Adenoma Solitary Thyroid Nodule. Nodular Non-toxic Goiter. Enlargement of the thyroid gland No toxicity; no cancer

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differential diagnoses
Differential Diagnoses
  • Nodular Non-toxic Goiter
  • Graves’ Disease
  • Toxic MultinodularGoiter
  • Toxic Adenoma
  • Solitary Thyroid Nodule
slide4

Enlargement of the thyroid gland

  • No toxicity; no cancer
  • The following factors increase your chance of developing nontoxic goiter:
    • Sex: female (nontoxic goiter is more common in women than men)
    • Age: over 40 years

Reference: http://www.mbmc.org/healthgate/GetHGContent.aspx

symptoms
SYMPTOMS
  • Nontoxic goiters usually do not have noticeable symptoms.
  • Swelling on the neck
  • Breathing difficulties, coughing, or wheezing with large goiter
  • Difficulty swallowing with large goiter
  • Feeling of pressure on the neck
  • Hoarseness
management
MANAGEMENT
  • A goiter only needs to be treated if it is causing symptoms.
  • Treatments for an enlarged thyroid include:
    • Radioactive iodine to shrink the gland, particularly if the thyroid is producing too much thyroid hormone
    • Surgery (thyroidectomy) to remove all or part of the gland
    • Small doses of Lugol's iodine or potassium iodine solution if the goiter is due to iodine deficiency
    • Treatment with thyroid hormone supplements if the goiter is due to underactive thyroid

Reference: http://www.nlm.nih.gov/medlineplus/ency/article/001178.htm

indications for surgery
INDICATIONS FOR SURGERY
  • Huge goiter which is cosmetically unacceptable
  • Compression symptoms
  • Suspicion of malignancy
graves disease
GRAVES’ DISEASE
  • Atype of hyperthyroidism, is caused by a generalized overactivity of the entire thyroid gland.
  • An autoimmune disease; thyroid-stimulating antibodies directed at TSH receptors on follicular cells.
  • It is named for Robert Graves, an Irish physician, who was the first to describe this form of hyperthyroidism about 150 years ago.
etiology
ETIOLOGY
  • The trigger for auto-antibody production is not known.
  • Genetic predisposition – HLA DR3
  • Since Graves' disease is an autoimmune disease which appears suddenly, often quite late in life, it is thought that a viral or infection may trigger antibodies which cross-react with the human TSH receptor (a phenomenon known as antigenic mimicry, also seen in some cases of Type I diabetes).
    • Yersiniaenterocolitica

Reference: http://en.wikipedia.org/wiki/Graves%27_disease

clinical features
CLINICAL FEATURES
  • Triad:
    • Goiter including the pyramidal lobe
    • Thyrotoxicosis
    • Exophthalmos
  • Symptoms:
  • Heat intolerance
  • Thirst
  • Sweating
  • Weight loss despite adequate caloric intake
  • Amenorrhea
  • Tachycardia or atrial fibrillation
  • Congestive heart failure
slide11

PE:

  • Weight loss
  • Flushing
  • Warm and moist skin
  • Inappropriate sweating
  • Tachycardia
  • Widening of pulse pressure
  • Fine tremor
  • Muscle wasting
  • Hyperactive tendon reflexes
  • Pretibialmyexedema
  • Gynecomastia
  • Audible bruit over the gland
  • Laboratory Findings:
  • Decreased TSH
    • Increased circulating T3/T4 levels
    • Increased circulating thyroid autoantibodies
    • Thyroid stimulating immunoglobulins (TSI)
    • Tyhroid stimulating antibodies (TSAb)
  • Radioactive iodine scan shows diffuse uptake through the gland of 45-90 percent.
management1
MANAGEMENT
  • Medical:
    • Propylthiouracil (PTU)
    • Methimazole (Tapazole)
    • Carbimazole
    • Beta-blockers (Propanolol)
slide13

Relapse rate in 12-18 months

  • Risk for fetalgoiter, hypothyroidism
  • No morbidity related after surgery
  • Treatment of choice for small goiters and pregnant patients (PTU)
  • Euthyroid state is achieved in 4-6 weeks
slide14

Radioactive Iodine

    • Ease of treatment
    • Highly effective especially in diffuse goiters
    • No morbidity related to surgery
    • Treatment of choice for failed surgical management
    • The effect is seen in 1.5-4 months
    • Standard dose = 10 mCl = 8500 cGy
slide15

Surgery

    • Complete and permanent control of toxicity
    • Rapid control of symptoms
    • Removal of mass
    • Treatment of choice for huge goiters
    • Needs pre-operative preparation
    • Overall morbidity of 1-2%
toxic multinodular goiter
Toxic MultinodularGoiter
  • Usually occur in individuals older than 50 years of age who often have a prior history of a nontoxic multinodulargoiter
  • Over several years, enough thyroid nodules become autonomous to cause hyperthyroidism.
  • Similar to Graves’ disease, but symptoms and signs of hyperthyroidism are less severe and extrathyroidal manifestations are absent.
  • May present with atrial fibrillation or palpitations, tachycardia, nervousness, tremor or weight loss.
  • Low TSH, normal or minimally increased T4, elevated T3, T3>T4.
toxic multinodular goiter1
Toxic MultinodularGoiter
  • Thyroid scan – heterogenous uptake with multiple regions of increased and decreased uptake.
  • 24hr uptake of radioiodine may not be increased.
  • Management
    • Antithyroid drugs + beta blockers – normalize thyroid function and address the clinical features of thyrotoxicosis, but often stimulates the growth of the goiter; spontaneous remission does not occur.
    • Radioiodine – treat areas of autonomy, decrease the mass of the goiter
    • A trial of radioiodine should be considered before subjecting patients to surgery.
toxic multinodular goiter2
Toxic MultinodularGoiter
  • Surgery
    • Definitive treatment of underlying thyrotoxicosis and goiter.
    • Subtotal thyroidectomy is the standard procedure.
    • Patients should be rendered euthyroid using antithyroid drugs before operation.
toxic adenoma
Toxic Adenoma
  • A solitary, autonomously functioning thyroid nodule
  • Typically occurs in younger patients
  • (+) thyroid nodule with symptoms of hyperthyroidism
  • Size is at least 3cm before hyperthyroidism occurs.
  • Absent clinical features suggestive of Graves’ disease or other causes of thyrotoxicosis
toxic adenoma1
Toxic Adenoma
  • Thyroid scan – definitive diagnostic test
    • Focal uptake in the hyperfunctioning nodules
    • Diminished uptake in the remained of the gland
      • Suppression of the activity of the normal thyroid
toxic adenoma2
Toxic Adenoma
  • Radioiodine ablation – treatment of choice
    • 131I is concentrated in the hyperfunctioning nodule with minimal uptake and damage to normal thyroid tissue.
    • Relatively large doses – correct thyrotoxicosis in about 75% of patients within 3 months.
    • Hypothyroidism occurs in <10% of patients over the next 5 years.
toxic adenoma3
Toxic Adenoma
  • Surgical resection
    • Limited to enucleation of the adenoma
    • Lobectomy
    • Preservation of thyroid function
    • Low risk of hypoparathyroidism
    • Low risk of damage to the recurrent laryngeal nerve
toxic adenoma4
Toxic Adenoma
  • Medical therapy using antithyroid drugs and beta blockers – normalize thyroid function but is not an optimal long term treatment
  • Ethanol injection under ultrasound guidance
    • Repeated injections – often >5 sessions
    • Reduce nodule size
solitary thyroid nodule
Solitary Thyroid Nodule
  • Present in approximately 4 percent of the population
  • Pain is unusual. When present, it should raise suspicion for intrathyroidalhemorrhage in a benign nodule, thyroiditis, or malignancy.
  • History of hoarseness - may be secondary to malignant involvement of the recurrent laryngeal nerves
  • Risk factors for malignancy – exposure to ionizing radiation and family history of thyroid and other malignancies associated with thyroid cancer.
solitary thyroid nodule1
Solitary Thyroid Nodule
  • Mass moves with swallowing.
  • Hard, gritty of fixed nodules are more likely to be malignant.
  • Most are euthyroid.
  • If a patient with a nodule is found to be hyperthyroid, the risk of malignancy is approximately 1 percent.
  • FNAB – most important diagnostic test
    • Benign – 65% (includes cysts and colloid nodules)
    • Suspicious – 20%
    • Malignant – 5%
    • Nondiagnostic – 10%
solitary thyroid nodule2
Solitary Thyroid Nodule
  • Ultrasound
    • For detecting nonpalpable thyroid nodules
    • For differentiating solid from cystic nodules
    • For diagnosing suspicious nodules with microcalcifications
    • For identifying adjacent lymphadenopathy
  • CT and MRI – unnecessary in except for large, fixed, or substernal lesions.
  • 123I or 99mTc – rarely necessary, unless evaluating patients for “hot” or autonomous thyroid nodules
solitary thyroid nodule3
Solitary Thyroid Nodule
  • Malignant tumors – generally treated by total or near-total thyroidectomy
  • Simple thyroid cysts - resolve with aspiration in approximately 75 percent of cases
      • Unilateral thyroid lobectomy - if the cyst persists after three attempts at aspiration
  • Lobectomy
    • For cysts >4 cm in diameter
    • For complex cysts with solid and cystic components
solitary thyroid nodule4
Solitary Thyroid Nodule
  • Colloid nodule – should be observed with serial ultrasound and Tg measurements
    • Repeat FNAB if nodule enlarges
  • L-thyroxine – in doses sufficient to maintain a serum TSH level between 0.1 and 1.0 μU/mL.
    • 50% decrease in size
  • Thyroidectomy – if a nodule enlarges on TSH suppression, causes compressive symptoms, or for cosmetic reasons
    • Exceptions: Patient who has had previous irradiation of the thyroid gland or who has a family history of thyroid cancer.
    • In these patients total or near-total thyroidectomy is recommended.
      • High incidence of thyroid cancer (≥ 40%)
      • Decreased reliability of FNA biopsy