1 / 36

HIPERTIROIDII

HIPERTIROIDII. HYPERTHYROIDISM. Increased serum levels of thyroid hormones, - Surgical correction is frequently appropriate. NORMAL THYROID FUNCTION. The follicular cells- T3, T4 T3, T4 bind with thyroglobulin, stored on the gland until released onto the bloodstream

parry
Download Presentation

HIPERTIROIDII

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript


  1. HIPERTIROIDII

  2. HYPERTHYROIDISM • Increased serum levels of thyroid hormones, - Surgical correction is frequently appropriate

  3. NORMAL THYROID FUNCTION • The follicular cells- T3, T4 • T3, T4 bind with thyroglobulin, stored on the gland until released onto the bloodstream • Release is under the control of TSH and TRH • A feed-back mechanism regulating T3, T4 release is related to the level of circulating T3, T4.

  4. HORMONAL ACTION • The thyroid hormones: - increase the metabolic rate, - increase the O2 consumption, - increase glycogenolysis, - enhance the actions of catecholamines • The result is: • Increase in the PR, CO. • Nervousness, irritability, muscular tremor, muscle wasting These effects can be blocked by the use of beta-blockers

  5. HORMONAL ACTION • The parafollicular or C-cells- produce thyrocalcitonin • Thyrocalcitonin action: - to lower serum calcium and phosphate concentration, - reduces bone resorption - in the kidney accelerates calcium and phosphate excretion:

  6. THYROID GLANDCLINICAL EXAMINATION • Hyperthyroidism • Symptoms: dyspnea on effort, palpitation, tiredness, preferance for cold, sweating, nervousness, weight loss, good appetite • Signs: palpable thyroid, exophtalmos, lid lag, hyperkinesis, finger tremor, hot and moist hands, rapid PR

  7. INVESTIGATIONS • TSH- raised in primary hypothyroidism and after treatment of thyrotoxicosis by surgery or radioiodine, - reduced in hyperthyroidism • Free T3, T4- radioimmunoassays, • Radioiodine uptake, • Thyroid isotope scanning • Ultrasonography, CT, MRI • Fine needle aspiration cytology • Thyroid autoantibodies (ab.tothyroglobulin)

  8. Thyroid scintigram • Autonomous adenoma in the right lobe of the struma. • The test substance accumulates almost exclusively in the range of the autonomous adenoma. • The other areas of the struma show a considerable reduced accumulation of activity.

  9. GOITERENLARGEMENT OF THE THYROID GLAND • Simple goiter - diffuse hyperplastic goitre, - nodular goitre • Toxic goiter - diffuse (Grave’s disease), - toxic multinodular goitre, - toxic solitary nodule • Neoplastic goiter - benign, - malignant • Thyroiditis - subacute (de Quervain’s), - autoimmune(Hashimoto’s), - invasive fibrous thyroiditis (Riedel’s) - acute suppurative

  10. HYPERTHYROIDISM • Common causes: - diffuse toxic goitre (Graves’s disease), - toxic multinodular goitre (Plummer’s disease), - toxic solitary nodule, - exogenous thyroid hormone excess, - thyroiditis

  11. HYPERTHYROIDISM • Rare causes: - metastatic thyroid carcinoma, - pituitary tumour secreting TSH

  12. GRAVE’S DISEASE • The most common cause of hyperthyroidism • It is an immunological disorders • Thyroid stimulating antibodies (IgG type) bind to the TSH receptor of the thyroid cells- excess of the thyroid hormones • The thyroid gland hypertrophies • Diffuse enlargement

  13. GRAVE’S DISEASEClinical Diagnosis • Symptoms and signs of thyrotoxicosis result from excess thyroid hormones: • Cardio vascular • Neurological • Metabolic • Exophtalmos • Diffuse enlargement of the thyroid

  14. GRAVE’S DISEASE • Ophthalmopathy- two major components: -Non-infiltrating ophthalmopathy-sympathetic activity: - upper lid retraction, - a stare, - infrequent blinking -Infiltrative ophthalmopathy- edema of the orbital contents, lids, periorbital tissue, cellular infiltration within the orbit

  15. HYPERTHYROIDISMPREOPERATIVE PREPARATION • Surgery must be done in the euthyroid state • ATD for a period then discontinue • Betablockers to control cardiac symptoms • Lugol’s solution, 10 days, will diminish the peroperative hemorrhagic risk

  16. GRAVES’ DISEASETREATMENT • To restore the euthyroid state: • Antithyroid drugs + beta-blockers • Radioactive iodine - distroys overactive tissue • Surgery - bilateral subtotal/total thyroidectomy

  17. Grave’s diseaseMultiple nodules and hypervascularity

  18. Grave’s diseasePressure symptoms

  19. Recurrent Grave’s disease after subtotal thyroidectomy, nodule at the piramidal lobe

  20. Right thyroid nodules after subtotal thyroidectomy

  21. Nodules with cystic degeneration after subtotal thyroidectomy

  22. Left upper nodule with cystic degeneration

  23. MULTINODULAR GOITREMANAGEMENT • Hyperthyroid- iodine scan • Large- ATD & surgery • Small- iodine therapy • Euthyroid • No dominant nodule-observe • Dominant nodule-FNAC • Benign, no sy-observe • Malignant- surgery • Suspicious- surgery • Inadequate- repeat FNAC • Retrosternal- surgery • Cosmetic- surgery

  24. SOLITARY THYROID NODULEMANAGEMENT • Hyperthyroid- FNAC & isotope scan • Greater than 3 cm.- surgery • Less than 3 cm.- iodine therapy • Euthyroid- FNAC • Benign-no pressure sy.-observe, repeat FNAC in 6 months • Benign- with pressure sy.- surgery • Thyoiditis- T4 treatment • Suspicious- surgery • Malignant- surgery • Inadequate FNAC- repeat • Cystic benign- observe, review in 6 weeks • Cystic malignant- surgery

  25. TOXIC SOLITARY NODULETREATMENT • This condition is caused by a single autonomous thyroid nodule • Best option- surgery- unilateral thyroid lobectomy

  26. Toxic compressive goiter

  27. POSTOPERATIVE COMPLICATIONS • 1. Postoperative bleeding • 2.Postoperative thyrotoxic crisis • 3.Postoperative voice changes • 4. Hypoparathyroidism • 5. Hypothyroidism

  28. POSTOPERATIVE BLEEDING • Postoperative bleeding • there is always a risk of postop .bleeding, • it is rare but sometimes dramatic • The bleeding may occur in one of two sites, • deep to the myofascial layer in relation to thyroid vessels-evacuation must be done quickly - deep to the skin flaps, from veins • Compressive hematoma- respiratory embarrasment- evacuation is mandatory

  29. POSTOPERATIVETHYROTOXIC CRISIS • Serious complication-where there has not been adequate preop.preparation • It occurs within the first 24 hours of thyroidectomy • Symptoms: confusion, hyperactive, fever, profuse sweating, rapid PR. • Treatment: beta-blockers, iv steroids, iodine

  30. POSTOPERATIVE VOICE CHANGES • Rare due to any damage to recurrent laryngeal nerves- this occurs in less than 1% • Probably minor changes in the muscles around the cricoid and thyroid cartilages are the most important, inevitable with the mobilization of the gland • Trauma to external laryngeal nerve- cricothyroid muscle- voice change- difficulty in achieving vocal cord tension • Trauma t the internal laryngeal nerve can occur where there is difficulty in mobilizing the superior pole

  31. POSTOPERATIVE HYPOPARATHYROIDISM • Hypocalcemia- usually a consequance of a metabolic changes- re-entry of calcium into bone demineralized by hyperthyroidism (“hungry bones”) • Parathyroids are small and are not always easy to identify • The incidence of hypoparathroidism after surgery shoud be less than 1%

  32. POSTOPERATIVE HYPOTHYROIDISM • All forms of treatment for thyrotoxicosis will produce a population of patients prone to develop hypothyroidism • Greatest risk after radioiodine therapy

More Related