MULTINODULAR GOITRE
INTRODUCTION
Multinodular goitre or thyroid follicular nodular disease is the most common disease of thyroid. It is characterized by asymmetric or nodular enlargement of thyroid gland causing distortion of its outer surface. Majority of the patient is asymptomatic and euthyroid. There is slight increase in the risk of malignancy.
CASE SENARIO
A 55-year-old female presents with a painless neck swelling. She also complained of palpitations and weight loss. On further questioning, she occasionally experiences dyspnea and difficulty swallowing.
High-Order Thinking Criteria:
i.Requires understanding of the pathophysiology of multinodular goiter, knowledge of risk factors, and ability to differentiate between various causes.
ii.Involves critical thinking about diagnostic strategies, appropriate laboratory tests (e.g., thyroid function tests, ultrasound), and interpretation of results.
iii.Requires weighing treatment options, considering patient-specific factors, and understanding the risks and benefits of medical therapy versus surgical intervention.
Location : Neck (anterior triangle).
Special features:
The thyroid gland is a butterfly-shaped endocrine gland located centrally in the front of the neck. It spans from the level of the 5th cervical vertebra (C5) to the first thoracic vertebra (T1) and typically weighs between 15-25g, making it the largest of the endocrine glands. Encased within the deep cervical fascia's pretracheal region, the gland consists of a central isthmus connecting its right and left pear-shaped lobes. Each lobe's apex points upward towards the oblique line of the thyroid cartilage, while the base is positioned below at the level of the 4th or 5th tracheal ring. The isthmus stretches across the midline anteriorly to the 2nd, 3rd, and 4th tracheal rings. Additionally, a pyramidal lobe maybe present extending upward from the isthmus, typically located to the left of the midline, a developmental remnant of the thyroglossal duct from embryonic stages.
Gross
Enlarged and multilobulated thyroid gland showing variegated cut surface, cystic and haemorrhagic with gelatinous appearance.
Histopathology
Section shows thyroid tissue composed of variable sized thyroid follicles lined by bland cuboidal to flattened epithelium containing variable amount of colloid. Adjacent area shows cystic degeneration characterized by haemorrhage and hemosiderin laden macrophages.
Thyroid hormones act on every organ system in the human body. Thyroid hormones act synergistically with growth hormone and somatomedins to promote bone formation; they increase basal metabolic rate (BMR) by increasing oxygen consumption and heat production; they alter cardiovascular and respiratory systems to increase blood flow and oxygen delivery to the tissues. In the nervous system, thyroid hormones are essential for normal CNS maturation during perinatal period; they interact with sympathetic nervous system as they display similar effects as those produced by catecholamines via Beta-adrenergic receptors on BMR, heat production, heart rate and stroke volume. Thyroid hormones also increase glucose absorption, gluconeogenesis, lipolysis, and proteolysis. They increase both protein synthesis and degradation, but overall their effect is catabolic, which results in decreased muscle mass.
Chemical properties of thyroid hormones
The two main thyroid hormones are thyroxine (T4) and triiodothyronine (T3), are iodine-containing hormones derived from amino acid tyrosine. They are lipophilic, largely protein-bound in the bloodstream, and play crucial roles in regulating metabolism, growth, and development. In the bloodstream, both hormones are primarily bound to plasma proteins, with only a small fraction existing in the free form. The main binding proteins include thyroxine-binding globulin (TBG), transthyretin (TTR), and albumin. The free forms are biologically active and can enter cells to exert their effects. T4 serves as a stable prohormone that is converted to the more active T3 in target tissues. T3 and T4 exert their physiological effects by binding to thyroid hormone receptors (TRα and TRβ) located in the nucleus of target cells. These receptors function as transcription factors, regulating the expression of genes involved in metabolism, growth, and development.
Treatment of hypothyroidism: Thyroid Hormone Supplement (Levothyroxine)
Treatment of hyperthyroidism: anti-thyroid medications:
1. Thioamides e.g. carbimazole, propylthiouracil MOA: Inhibit the synthesis of thyroid hormone by inhibiting the thyroid peroxidase enzymes
2. Iodide salts e.g. potassium iodide, Lugol's solution MOA: Inhibit the release of thyroid hormone from the gland.
3. Radioactive iodine (sodium iodide I 131) MOA: emits beta particles that could destroy the thyroid follicular cells.
Computed Tomography image of the neck in axial view shows enlarged thyroid gland with multiple nodules in bilateral thyroid lobes.
Three most common aetiologies of hyperthyroidism:
1) Graves disease (GD)
2) Toxic multinodular goiter (TMNG)
3) Toxic adenoma (TA)
Clinical symptoms: nervousness, heat intolerance, palpitations, fatigue and weight loss
Clinial signs: agitation, sinus tachycardia, fine tremor and hyper-reflexia, atrial fibrillation
Management:
1) Anti-thyroid drugs: Carbimazole, propylthiouracil (PTU)
2) Radioactive
Surgical Management Of Multinodular Goitre indication For Surgery
i. MNG with obstructive symptoms
ii. Presence of suspicious nodule
iii. MNG with refractory hyperthyroidism
iv. Request for cosmetic purpose
v. Huge MNG with retrosternal extension
Surgical Option
i. Hemithyroidectomy – removal 1 lobe of the thyroid gland including the isthmus
ii. Total Thyroidectomy – removal the whole thyroid glands
Post Total Thyroidectomy Complications
i. Bleeding & Hematoma
ii. Flap Necrosis
iii. Recurrent & Superior Laryngeal nerve injury
iv. Hypocalcemia
v. Trachea/Oesophageal Injury
