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Document Details

Fakeeh College for Medical Sciences

Tags

thyroid disorders medical science endocrinology

Summary

This document is a set of notes detailing thyroid disorders. It covers various aspects such as clinical scenarios, questions, objectives, and student learning outcomes. The document also includes detailed information on embryology, anatomy, and physiology of the thyroid gland.

Full Transcript

Thyroid gland disorders Clinical Scenario A 30-Year-old female patient referred to the general surgery clinic for neck swelling she describes her symptoms as intolerance to heat, fast heart rate and sweaty palms, she complained of swelling on her neck getting...

Thyroid gland disorders Clinical Scenario A 30-Year-old female patient referred to the general surgery clinic for neck swelling she describes her symptoms as intolerance to heat, fast heart rate and sweaty palms, she complained of swelling on her neck getting bigger over time, and she suffers from palpitations irritability and anxiety she started to feel difficulty in swallowing and breathing specially when she lies down to sleep and her symptoms are not getting any better Past History: Irrelevant Family history: Irrelevant When the doctor examined the patient: Vital signs: - O2 Saturation:94% - Respiratory Rate: 25/min - Pulse: 130/min - BP: 125/90 Examination: - Alert and conscious - Talking (maintained airway) - The swelling moving up with deglutition - Butterfly shaped swelling multinodular on the Anterior triangle of the neck bilaterally extending to retrosternal area Questions: What is the normal anatomical mechanism of goiter moving up with deglutition? What is the pathophysiology of goiter? What are the common presentations of goiter? Identify the different modalities of investigations for the above case? Explain the complications of long-standing goiter? Explain the medical and the surgical management options for the above complicated case of goiter? Objectives 1) Review the embryology, anatomy, and physiology of the thyroid gland 2) Approach history and physical examination of patients with thyroid pathology 3) Discuss diagnostic investigations for thyroid diseases 4) Discuss the medical and surgical approaches in the management of patients with thyroid disorders Student learning outcome By the end of this session, you will be able to : 1) Recognize anatomy of thyroid 2) Explain physiology of thyroid hormones 3) Classify thyroid swellings 4) Differentiate different types of thyroid nodules 5) Plan for management for simple goitre 6) Plan for management for toxic goitre Embryology Develops from: The median bud of the pharynx at the foramen cecum (junction between anterior two-thirds and posterior third of the tongue) Descends in the neck passing close to or through the hyoid bone then the track obliterates to form the thyroglossal duct The remaining part of the lobes develop from ultimobranchial body (4th pharyngeal pouch) which gives rise to the superior parathyroid glands also The inferior parathyroid glands develop from the (3rd pharyngeal pouch) Para follicular C cells develop from the neural crest Anatomy Situated in the neck opposite to the 5th, 6th, & 7th cervical vertebrae. Made up of 2 lobes joined by thin band of tissues; the isthmus. Its apex lies below the oblique line of the thyroid cartilage while the base is at the level of 6th tracheal cartilage Covered by true capsule and false capsule from the pretracheal fascia (attachment!!) Arterial supply: Superior thyroid artery: The 1st branch of the external carotid artery. Related to the external laryngeal nerve (injury during ligature) Inferior thyroid artery: branch from thyrocervical trunk of subclavian artery Related to recurrent laryngeal nerve (injury during ligation) Accessory esophageal and tracheal branches Thyroid ima (from aortic arch-only in 1-3%) Venous drainage: Superior thyroid vein: into Internal jugular vein Middle thyroid vein: into Internal jugular vein (1st to be ligated in thyroidectomy) Inferior thyroid vein: into left innominate vein Lymphatic drainage: Lateral part:. To the upper & lower deep cervical lymph nodes (Levels: II,III,IV,Vb). Medial parts of both lobes 1) Pre-laryngeal LNs over cricothyroid membrane. 2) Pre-tracheal LNs (Delphi). 3) Para-tracheal LNs (mediastinal). Related nerves: External laryngeal nerve: from sup. Laryngeal from vagus Supplies cricothyroid + inferior constrictor Injury: loss of high pitched voice + voice fatigue Recurrent laryngeal nerve: from Vagus nerve Physiology + Hypothalamus - TRH Pituitary TSH Thyroid T4-TBG T4 T3 T3-TBG Developmental disorders ❖ Lingual thyroid: Ectopic thyroid tissue at the base of the tongue Due to failure of descent of the thyroglossal duct Ectopic thyroid tissue can occur at other sites (along course of descent) Investigation: Thyroid scan to exclude that it is the only thyroid tissue Treatment: Excision.. if leading to symptoms (dysphagia, dyspnea) ❖ Thyroglossal cyst and fistula Due to failure of obliteration of part of thyroglossal duct Commonest site is the subhyoid in midline Common in children and adolescents Hallmark in examination: moves with tongue protrusion and with deglutition Symptoms: painless midline neck swelling May become painful if infected May rupture or inadequately managed leading to fistula. Investigations: U/S Treatment: Sistrunk operation Goitre: Enlargement of the thyroid gland Pathophysiology: 1) Deficiency of Thyroid hormones, either relative or absolute, stimulates the hypothalamus to produce TRH, which in turn stimulate TSH secretion. 2) Persistent TSH stimulation leads to diffuse hyperplasia & hypertrophy of the thyroid gland → If one of the following occurs: 1) When the stress is over, Involution of the gland occur, and the gland may return to its normal size. 2) If the stress is persistent, hyperplasia persists → Physiological Goiter. 3) Sudden fall of TSH (as in shock dose of iodine), will lead to inactivation of most of the follicles, and the acini become distended with colloid → Colloid goiter. 4) Fluctuation of TSH levels will lead to cycles of hyperplasia and involution. A mixed pattern develops with areas of hyperplasia mixed with areas of hyperinvolution → Nodular goitre Simple diffuse goitre (physiological goitre) Common in females (stress of puberty, pregnancy, lactation) Due to relative increased body demands than thyroid hormones.. Increased TSH.. goitre C/P: Diffuse smooth symmetrical enlargement of the gland (Venus Neck) Investigations: Normal profile U/S : Normal enlarged gland Treatment: Assurance L-thyroxine supplementation!! Colloid goitre A late stage of diffuse hyperplasia when TSH stimulation has fallen of and when many follicles are inactive and full of colloid C/P: Diffuse symmetrically enlarged gland Compression manifestations might occur (dyspnea, dysphagia..) Treatment: Assurance unless there is compression manifestations Simple nodular goitre The commonest disease of thyroid gland Etiology: fluctuation of TSH level.. Mixed pattern of active and inactive thyroid follicles.. repetition of fluctuation of TSH will lead to nodular goitre C/P: common in females 30-50 years No thyrotoxic manifestations Painless swelling in the front of the neck (cosmetic) Pain is uncommon Complications(in huge goitre): Compression manifestations (trachea, oesophagus, RLN, IJV, CA) Cancer in 5 % !!! If long standing !! → follicular carcinoma. Calcifications Cystic degeneration and haemorrhage into a cyst. Secondary thyrotoxicosis Investigations: Normal thyroid profile Neck U/S: Assessment of thyroid nodule (TIRADS !!!) Assessment of LNs status Guides for FNAC (impalpable/small) FNAC: if suspicious (TIRADS !!!) Indirect laryngoscopy (asymptomatic vocal cord paralysis 4%) Treatment: Indications of surgery: Suspicion of malignancy Compression manifestation Cosmetic Types of surgery: Hemithyroidectomy (STN or localized to one lobe) Subtotal thyroidectomy !! Near total thyroidectomy !! Total thyroidectomy Approach: Open Endoscopic Thyrotoxicosis Is a clinical syndrome in which free T3 or free T4 or both are elevated and peripheral tissues are hypermetabolic, irrespective of source of the excess hormones Etiology: Thyrotoxic goitre Other causes: Thyroiditis (Hashimoto thyroiditis/ De Queirvan thyroiditis) Thyrotoxic facticia ( intake of Eltroxin) Functioning thyroid carcinoma TSH secreting pituitary adenoma Struma ovarii (ovarian cancer secreting tumor) Toxic goitre Goitre with increased thyroid hormones Either: Diffuse toxic goitre (1ry/Grave’s disease) Toxic nodular goitre (2ry/Plummer’s disease) Toxic adenoma Primary toxic goitre Autoimmune disease due to thyroid stimulating antibodies (TSAb). Common in young females (20-30 years) Disease has abrupt onset with remission and exacerbation 50% of patients have family hx of autoimmune endocrine disorders True exophthalmos is characteristic May be complicated by heart failure Diffuse thyroid swelling without nodules Toxic thyroid profile with high thyroid autoantibodies Treatment is mainly medical if failed Surgery or RAI Treatment: Medical treatment: Antithyroid drugs (Neomercazol/propyl thiouracil) : propyl thiouracil is safe in pregnancy B-blockers: to minimize the tachycardia. Diazepam: if aggressive CNS manifestation. Medical treatment could be used for a period up to 2 years.. If failed!! Surgical treatment: Subtotal thyroidectomy!! Or total thyroidectomy Indications: failure of medical treatment, RSE, compression manifestations Preoperative preparation is a must to avoid thyrotoxic crisis RAI: (teratogenic/ carcinogenic): Used in old patients (˃ 45 years) after failure of medical treatment or recurrence after thyroidectomy Thyrotoxic crisis Severe postoperative hyperthyroidism due to inadequate preoperative preparation Clinical picture: Hyperpyrexia, Hypertension, Delirium & Convulsions. Treatment: Cooling + lV ( lndral, Corticosteroid, Propylthiouracil, Antipyretics ) Secondary toxic goitre Occurs in older females (30-50 years) On top of long standing nodular goitre. No exophthalmos. Thyroid gland is enlarged and nodular. Thyroid hormones are elevated but antibodies are within normal Treatment: - Surgery after preoperative preparation. - RAI might have a role. Toxic nodule Excess secretion of thyroid hormone from autonomous hyperactive thyroid nodule Manifested by thyrotoxic manifestations Elevated thyroid hormones, no elevated autoantibodies. By U/S: solitary thyroid nodule with increased vascularity Thyroid scan : hot nodule with suppression of the uptake of surrounding thyroid tissue. Treatment : Surgery & RAI might have a role in elderly To sum up Choice the line of treatment 1- 1ry toxic goiter:- > 45yr → Radio iodine. < 45yr → small goiter → Antithyroid drugs. → Large goiter → Surgery. 2- 2ry toxic goiter:- Surgery 3- Toxic nodule:- > 45yr → Radio iodine. < 45yr → Surgery (lobectomy or hemithyroidectomy). 4- Recurrence after adequate surgery:- > 45yr → Ablation by radio iodine. < 45yr → Antithyroid drugs. 5- Failure of treatment with antithyroid drugs:- Surgery or Radio-iodine Thyroiditis: Hashimoto’s thyroiditis Most common form of thyroiditis Autoimmune thyroiditis due to anti-thyroglobulin antibodies & thyroid peroxidase antibodies (TPO). Common in middle aged females. Initial manifestations of thyrotoxicosis. Later on →manifestations of myxedema. FNAC is diagnostic May predispose to Papillary thyroid carcinoma or thyroid lymphoma. Treatment : - Medical - Surgical treatment in large goitre, compression manifestations or suspicion of malignancy. Retrosternal goitre ▪ More common in males (tough neck muscles) ▪ Manifestations is mainly compression manifestations ▪ Mediastinal syndrome?! ▪ CT is important ▪ Treatment is mainly surgical (sternotomy may be required) Solitary thyroid nodule Solitary thyroid nodule vs dominant nodule of Multinodular goiter. May be clinically STN but by U/S reveals MNG HISTORY CLINICAL LABORATORY IMAGING PATHOLOGY MANAGEMENT EXAMINATION TESTS REVIEW Solitary thyroid nodule How to investigate??? ✓ Ultrasound ✓ FNAC ✓ TFT ✓ Thyroid scan

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