Thyroid Gland Diseases - Presentation

THYROID GLAND DISEASES Presented by Mohammed Safwat Shahine Associate Professor of Maxillofacial Surgery Faculty of Medicine, Assiut University Embrology  The thyroid originates between the first and second pharyngeal pouches near the base of the tongue. In th...

THYROID GLAND DISEASES Presented by Mohammed Safwat Shahine Associate Professor of Maxillofacial Surgery Faculty of Medicine, Assiut University Embrology  The thyroid originates between the first and second pharyngeal pouches near the base of the tongue. In the third week of gestation, around day 20- 24, endodermal cells of the primitive pharynx proliferate, creating the thyroid diverticulum. Beginning in the fifth week of gestation, the thyroid diverticulum migrates caudally along the midline, crossing anteriorly to the hyoid bone and laryngeal cartilage. During migration, the thyroid remains attached to the tongue via the thyroglossal duct. Division of the thyroid into right and left lobes occurs in the fifth week of gestation. Also, during the fifth week, the ultimobranchial bodies arise from the fourth/fifth pharyngeal pouches. The ultimobranchial bodies ultimately differentiate into the parafollicular C-cells, which play an essential role in calcium homeostasis. Traditionally, the parafollicular C-cells were thought to arise from neural crest cells, but recent works have disputed this by suggesting they arise from endoderm.The ultimobranchial bodies fuse with the superior dorsolateral aspect of the developing thyroid, forming Zuckerkandl's tubercle. By the seventh week of gestation, the thyroid has reached its final destination in the neck. Normally, the thyroglossal duct degenerates by the tenth week of gestation with only the foramen cecum to indicate its former existence. Surgical anatomy - Present in thyroid region. - Formed of 2 lobes and isthmus. - Surrounded by fibrous capsule and invested by pretracheal fascia which attached to thyroid cartilage and hyoid bone so move with delegation. - Arterial supply: Superior thyroid artery from external carotid artery and inferior thyroid artery from thyrocervical trunk a branch of subclavian artery and thyroid ima artery from aorta or innominate artery. - Venous drainage: Superior, middle thyroid veins drainage to internal jugular vein and inferior thyroid veins drain to left nominate vein Nerves related to the thyroid gland 1- Superior laryngeal nerve divided into: a. Internal laryngeal nerve: supply mucous membrane of larynx above vocal cord (its injury cause chocking). b. External laryngeal nerve (motor) supply tensors of vocal cord (cricothyroid muscles) responsible for high pitch voice (its injury cause loss of high pitched tone). 2- Recurrent laryngeal nerve(mixed): a. Motor fibers supply intrinsic muscles of the larynx except cricothyroid. b. Sensory to mucous membrane of larynx below vocal cords. Lymphatic drainage of the thyroid gland There are extensive lymphatic plexus within the gland drained by ascending &descending lymphatics. The ascending vessels: medial to prelaryngeal lymph glands lateral to upper deep cervical lymph glands. The descending vessels: medial to pretracheal lymph glands lateral to RLN & lower deep cervical lymph glands. Histology: The thyroid gland formed of acini lined by cuboidal epithelium and central colloid material, the acini surrounded by Para follicular cells which secrete calcitonin. Physiology:  The thyroid gland secrete T3, T4 (Thyroxin) and calcitonin.  The formation of T3, T4 (Thyroid hormones) from iodine in the following steps: 1- Iodine trapping by thyroid iodine pump. 2- Binding of iodine to tyrosine amino acid after conversion of inorganic iodine to organic iodine by peroxidase enzyme. 3. Coupling of mono and diiodotyrosine to form T3 (triiodothyronine) and T4 (thyroxin which stored in acini as thyroglobulins). 4. Release: thyroglobulins splits by protease to T3, T4 to the circulation.  Effects of thyroid hormones: 1- Stimulation of oxygen consumption and oxidation in all tissues. 2- Stimulate glucose utilization & glycogenolysis in liver. 3- Increase protein catabolism. 4- Lower serum cholesterol. 5- Sensitize heart to catecholamine. 6- Stimulate skeletal& sexual, mental development, growth and maturation. Calcitonin lowering serum calcium. Pituitary thyroid axis: This is thyroid- pituitary- hypothalamus Synthesis and release of thyroxin is controlled by TSH (thyroid stimulating hormone or thyrotrophic) from pituitary gland TH secretion is controlled by level of thyroxin in blood and lower level of thyroxin also stimulate hypothalamus receptors to release TRH (thyrotropin releasing hormone) from hypothalamus stimulate anterior-pituitary to secrete TSH. Increase size of gland, vascularity and hormones production. feedback mechanism  Thyroid enlargement (Goiter) Enlargement of the thyroid gland. Classifications of thyroid swellings: 1- Simple goiter (euthyroid): i. Diffuse hypertrophy: Physiological e.g. pubertal pregnancy. - Colloid. ii. Nodular: - Multinodular. - Solitary nodule. 2- Toxic: - Primary: diffuse (grave's disease) on top of normal gland. - Secondary on to top of Multinodular gland. - Rare causes. 3- Inflammatory: autoimmune e.g. Hashimoto's disease. - Granulomatous: de-Quervian's disease - Fibrosing: Riedel's thyroiditis - Infective: e.g. sub acute bacterial thyroiditis. - Other e.g. amyloid. 4- Neoplastic: - Begin. - Malignant 5- Hypothyroidism  Simple goiter Aetiology: Usually due to chronically low level of circulating thyroid hormones due to. A- Iodine deficiency: (daily requirement 0.1 – 0.15 mg). 1- Absolute deficiency in water and food (endemic goiter). 2- Relative deficiency: as the need of body exceed the supply of iodine e.g. adolescence, pregnancy and lactation (physiological). 3- Failure of intestinal absorption of iodine. B- Defects in synthesis of thyroid hormones (sporadic) 1- Goitergenic substances as: - Dietary: as cabbage & cauliflower which contain thiocyanate. - Water pollution. - Drugs: anti thyroid drugs 2- Enzyme deficiency e.g. peroxidase Pathophysiology: 1- Persistent stimulation with TSH causes diffuse hyperplasia (evolution) and diffuse hyper plastic goiter results. It is reversible as stimulation ceases (involution). 2- Continuous repetition of this process results in nodular goiter. 3- Colloid goiter result from involution beyond normal when iodine given in large dose to diffuse hyper plastic goiter. Clinical presentation: 1- Diffuse goiter. Physiological goiter. More common in females as result of relative iodine deficiency of iodine. The patients present by painless mobile diffuse symmetrical enlargement of the whole gland (Venus neck). Treatment: - Reassurance. - L- Thyroxin suppresses TSH and decreases gland growth. 2- Colloid goiter:  N.E: Diffuse smooth large goiter.  Cut section: golden brown glistening.  Microscopic view: large acini filed by colloid lined by flat epithelium clinically presented enlargement of the gland and soft consistency.  May be complicated by: - Pressure on trachea. - Disfigurement. - Turn into nodular goiter.  Treatment: as physiological  If large and huge: sub total thyroidectomy. 3- Nodular goiter May be multinodular or solitary nodule.  Clinical presentation: 1- Painless slowly growing swelling in neck may cause disfigurement or dyspnea. 2- Complications. On examination: - The gland is butter fly or U shaped nodular and well defines edges. - Trachea may be compressed unilaterally or bilaterally or tracheomalacia may occur. Complications: 1- Cyst formation and Hemorrhage inside cyst cause sudden compression on trachea and suffocation may occur. 2- Secondary toxic goiter. 3- Calcification. 4- Carcinoma: follicular type. 5- Retrosternal extension. 6- Compression on : - Trachea dyspnea. - Esophagus dysphagia. - Jugular vein Congestion. - Carotid artery  syncope. - RLN  hoarseness. - Arnold's nerve  pain refer to ear - Sympathetic chainHorner's syndrome.  Investigations: - Laryngoscope: vocal cords examination. - Thyroid functions T3, T4, TSH in suspicion of toxic goiter  Treatment: only surgical ttt. - For single Nodule: hemi thyroidectomy. - For Multinodular: subtotal thyroidectomy (Leave posteromedial part of gland equal to normal lobe (distal phalanx of thumb). - Postoperative – L- thyroxin.  Toxic goiter (Thyrotoxicosis) Clinical types and Aetiology: 1- Diffuse toxic goiter (primary- grave's disease): It autoimmune disease due to TSH receptors antibodies (the whole gland is hyper function) 2- Toxic nodular goiter (secondary): on top of simple nodular goiter, the nodules is inactive and internodular tissue is over active. 3- Toxic nodule: it autonomous and surrounding tissue is inactive. 4- Rare causes: on top of carcinoma – thyrotoxicosis Facticia - Hashimoto's disease Clinical picture:  Symptoms: 1- Metabolic: - Asthenia. - Loss of weight in spite of increased appetite. - Intolerance to hot weather. - Slight pyrexia. - Increase sweating. 2- Nervous: anxiety, insomnia. - Hand tremors. - Weakness, wasting of muscles of limbs. 3- CVS: palpitation, exertional dyspnea. 4- Urinary: polyuria. 5- Gonadal: increase libido - Polymenorrhea, menorrhagia and later amenorrhea. 6- Skeletal: osteoporosis and bone aches. 7- Locally: gland swelling 8. Eye: Diplopia. Signs: 1- General: weight loss inspite of good appetite. 2- Skin: sweating, moist warm palms. - Loss of hair. - Pretibial myxodema with primary toxic goiter. 3- Nerves: Irritability and anxiety. - Fine tremors of hands, tongue. 4- CVS: - Tachycardia. - Big pulse volume (Water hammer pulse). - Arrhythmia except heart block. - BL.P: increase systole, diastole is low or normal. 5- Hepato-splenomegaly may present 6- Eye: exophthalmoses (true in primary toxic goiter) 7- Locally: - Diffuse toxic goiter, gland enlarged symmetrical, soft skin over it is warm and pulsation at upper pole may detected. - In Nodular goiter: Gland enlarged, nodular and asymmetrical. Investigations: 1- Laboratory: - Serum T3, T4 Total and free is increased. - TSH is decreased. - Low cholesterol - TH Receptors antibodies. 2- Imaging. A) Radioactive Iodine,I123 studies: - Radioactive iodine uptake increase N: 15-35% of dose after 24h. - Thyroid scan: Differentiate diffuse from nodular, the nodule appear hyperactive (hot) B) Thyroid ultrasound: differentiate diffuse from nodular and solid from cystic. C) CT and MRI. D) Laryngoscope. Treatment: - Non specific: Physical, mental rest, Sedation & Tranquilizers. -Specific: 1- Medical treatment: indicated in: In all cases of diffuse toxic goiter. -In nodular toxic goiter as preoperative preparation. - In children and young age. - In recurrence postoperative cases.  The medical Treatment: 1- Beta – adrenergic blocking drugs. e.g. propranolol (indral) 2. Anti thyroid drugs: A- Thiouracil or its derivatives – Carbimazol: 10 mg /6h until euthyroid then 5 mg/8h. For 12- 18 month in diffuse goiter. Complication of drug:  enlargement of gland. Increase exophthalmos.  Blood – aplastic anemia  Agranulocytosis: presented by fever and sore throat) it treated by stop drug, hospitalization, antibiotic, vit B6 and Blood picture each 2 weeks. B- Propylthiouracil: potassium per chlorate 2- Surgical treatment:  In toxic nodular and Multinodular goiter is considered the main line of treatment as nodules is irreversible  In diffuse toxic goiter if medical treatment is failed. or large goiter or retrosternal goiter ,uncontrolled toxicity and recurrent  the preoperative medication or preparation by: 1) Lugol's iodine drops (5 % lodine – 10% KCL inwater) 5-15 drops for 2 weeks. 2) Antithyroid drugs till euthyroid last dose evening prior to operation. The operation is subtotal thyroidectomy left posteromedial part of gland equal to terminal phalanx of little finger. 3) Radioactive iodine therapy I131for Toxic nodule.  Poor surgical patient or recurrent.  Hypothyroidism Deficiency of circulating thyroid hormones. Due to: A- Primary in thyroid gland. e.g. 1- Autoimmune thyroiditis. 2- After thyroidectomy, or radioactive iodine. 3- Congenital e.g. hormone deficiency. 4- Iodine deficiency. 5- Goitergenic substances. 6- Inflammatory e.g. fibrous thyroiditis. B- Secondary e.g. hypopituitarism. Clinical picture: 1- Cretinism (infantile Hypothyroidism): - Sporadic or endemic cause neurological and mental retardation. Assessed by TSH level (high) by heal prick blood sample. - Treated by thyroxin with few days afterbirth. - Juvenile hypothyroidism usually in childhood. - Adult hypothyroidism. Presented by tiredness, mental lethargy, cold intolerance weight gain, constipation, menstrual disturbances and carpal tunnel syndrome. On examination: bradycardia, cold extremities, dry skin hoarse voice, puffiness. 2- Myxodema: sever hypothyroidism in adult 1- Lethargy, weakness, loss of appetite, weight gain, cold intolerance. 2- Sluggish reaction. 3- Face puffy and supra clavicular pad of fat deposition. 4- Skin: rough, dry. 5- Hard cold skin. 6- Hypercholesterolemia and may coma on stress.  Investigation: - T SH, T3,  T4 - antithyroid antibodies.  Treatment: thyroxin replacement.  Malignant tumors Predisposing factors: 1- External irradiation. 2- Mutation of certain oncogen. 3- Nodular goiter. 4- Hashimoto's disease predisposing to lymphoma, papillary cancer. 5- Endemic goiter increase risk of follicular type. Clinical picture: 1- Malignant goiter with typical symptoms and signs e.g. rapidly growing, painful, hard, fixed, and infiltrating surrounding e.g. RLN case hoarseness, dysphagia, dyspnea and Horner's syndrome. 2- Malignancy on suspicious, on top of multinodular goiter as goiter rapidly enlarged, associated with voice changes and dysphagia. 3- Solitary thyroid nodule. 4- Regional lymph nodes enlargement. 5- Distant metastasis e.g. bone or skull metastasis. Investigations: 1- Laboratory: - Calcitonin in serum: for Medullary carcinoma. - Serum thyroglobulin for differentiated carcinoma. 2- Imaging: - Thyroid ultrasound: differentiate solid, cystic. o Multicenteric. o lymph nodes enlargement. - RadioactivelodineI128 scanning show cold nodule. 3- Biopsy: - FNAC -True cut needle biopsy. - Incisional biopsy. - Lymph node biopsy. 4- Laryngoscopy. 5- Metastatic work up: - plain x-ray chest. -Abdominal ultrasound. - Bone scan. Treatment: Operable:  Papillary- Total or near total thyroidectomy.  Hemi thyroidectomy for thyroid nodule.  Follicular carcinoma: Total thyroidectomy.  Therapeutic radioactive iodine.  Postoperative: radioactive iodine for functioning tumors. Inoperable cases - Radiotherapy for nonfunctioning tumors. For inoperable tumors or anaplastic type. - Palliative isthmectomy. - Radioactive iodine therapy. Post thyroidectomy complications 1- Hemorrhage: primary, reactionary or secondary. a. Treated by opening the wound and relieve tension, control source of Bleeding. b. Small hematoma: aspiration. 2- Respiratory obstruction due to a. Laryngeal edema. b. RLW paralysis. Treated by endotracheal intubation or tracheostomy. 3- Recurrent laryngeal nerve Injury cause: 1- Unilateral injury: - Partial (adduction of cords): Dyspnea on excretion. - Complete: hoarseness of voice. 2- Bilateral: - Partial (adduction of both cords to mid line): Cause stridor and suffocation. - Complete: Loss of voice (aphonia). 4- Thyrotoxic crisis: improper prepared Thyrotoxic goiter and excessive manipulation of the gland during operation. 5- Hypo parathyroidism. 0.5% in 2-5 day postoperative due to removal or devascularization of gland presented by hypocalcaemia and tetany and treated by calcium. 6- Hypothyroidism. 7- Wound complication: a. Infection, granuloma. b. Keloid. 8- Recurrent goiter due to: a. Incomplete removal of gland. b. Malignancy. c. Not take post operative thyroxin. Thank you