Dr Madhukar Mittal Medical Endocrinology Nontoxic goitre Dr Madhukar Mittal Medical Endocrinology
Goitre Solitary Nodular Multinodular Toxic Nontoxic Diffuse
Goitre Solitary Nodular Multinodular Diffuse Nontoxic Benign Malignant (20%) Multinodular Benign vs Malignant Diffuse Toxic Graves Simple autoimmune
Painful thyroid swelling Subacute thyroiditis Acute thyroiditis Invasive malignancy Amiodarone induced thyrotoxicosis, type 1
Hard thyroid swelling Reidel’s thyroiditis Thyroid carcinoma (firm : medullary CA, lymphoma)
Thyroid examination From behind with neck flexed slightly forward Rt lobe is 25% larger than left lobe Palpable and smooth normally
Midline neck swellings Goitre of thyroid isthmus & pyramidal lobe Thyroglossal cyst Suprasternal LN, lipoma Ludwig’s angina Submental LN Sublingual dermoid, lipoma
Lateral neck swellings Carotid triangle Thyroid Branchial cyst Carotid body tumor Carotid artery aneurysm Submandibular triangle LN Enlarged submandibular salivary gland Post triangle Cystic hygroma Pharyngeal pouch Subclavian aneurysm Cervical rib
Thyroid 12-20g Between cricoid cartilage & suprasternal notch Develops during 3rd week of GA from floor of primitive pharynx Hormone synthesis begins at 11 weeks GA Parathyroid glands located in posterior region of each pole of thyroid C cells : interspersed throughout thyrod gland
Thyroid examination Normally Pizillo’s method On swallowing Hands clasped behind head and push On swallowing Thyroid moves up Thyroglossal cysts Subhyoid bursitis Fixed prelaryngeal/pretracheal LN For retrosternal goitre Raise both arms till they touch ears Pemberton’s sign
Thyroid examination From behind with neck flexed Lahey’s method With both hands Crile’s method With thumb Kocher’s test Slight push on lat lobes produces stridor To exclude retrosternal prolongation
History Age Residence Pain Sleep Compressive symp Others Family H/O Young – colloid goitre, STN Middle age – hashimoto’s, follicular CA Residence Pain Sleep Compressive symp Others Respiratory Myopathy Cardiac Neurologic Family H/O
Examination Anemia BP Pulse rate Skin of hands (moist, hot/cold) Tremors – hand, tongue LN Facies Eye signs Dermopathy Acropachy Vitiligo
Malignancy Hard swelling Local signs LN – papillary, anaplastic Dyspnea, dysphagia, hoarseness of voice Carotid pulsations cannot be felt LN – papillary, anaplastic Metastases – follicular (bone, lungs) Recent increase in size of swelling with pain Diarrhea – medullary CA Prior h/o irradiation STN Male Solid nodule Large nodule >4cm Cold nodule (least imp sign)
Treatment
Hyperthyroidism of Graves disease Hypothyroidism Levothyroxine Hyperthyroidism of Graves disease Antithyroid drugs (Europe, Japan) Radioiodine (USA)
Acute thyroiditis Antibiotics Drainage of abscess
Subacute thyroiditis Aspirin – large doses 600mg 4-6 hrly Prednisolone 40-60 mg/d Thyrotoxic phase – β-blockers Hypothyroid phase – low dose levothyroxine
Silent thyroiditis Thyrotoxic phase – propranolol 20-40mg TDS/QID Hypothyroid phase – LT4 for 6-9 months Annual followup for permanent hypothyroidism
Reidel’s thyroidits Surgery + tamoxifen
Amiodarone induced Hypothyroidism Thyrotoxicosis type 1 LT4 Thyrotoxicosis type 1 Stop amiodarone if possible High doses of ATD Thyrotoxicosis type 2 Oral contrast agents (Na ipodoate, Na tyropanoate) K perchlorate Glucocorticoids Lithium Near total thyroidectomy
Simple goitre I2 or suppressive thyroxine therapy (young patients with soft goitre for 3-6 months) Radioiodine (decreases goitre size by 50%) Sx – for tracheal compression
MNG - toxic Sx Radioiodine in elderly Antithyroid drugs – often stimulate growth of goitre
MNG nontoxic Radioiodine Sx T4 suppressive therapy (rarely effective for decreasing goitre size)
Thyroid Cancer Lymphoma MTC Follicular Papillary External radiation Total thyroidecctomy Follicular Near total thyroidectomy f/b radioiodine & LT4 suppression Papillary Stage 1 – Sx f/b LT4 suppression Neck dissection only if LN involved
STN Hyperfunctioning Radioiodine ablation – esp >45yr Sx resection – esp <45yr Enucleation Lobectomy Ethanol injection
STN Examination / USG → MNG / STN TSH if low → thyroid scan → hot nodule – RAIA /Sx FNAC ← cold or indeterminate (if <1cm/difficult, then USG guided FNAC) FNAC report
FNAC report Benign Cyst Suspicious or malignant (10%) NonDx (20%) Suppressive therapy with LT4 for 6-12 months (30% decrease in size) Monitor by USG (Sx if increase in size or suspicious cytology) Cyst Reaspirate and follow by USG Suspicious or malignant (10%) Sx NonDx (20%) Repeat FNA
MNG
Nontoxic MNG Occurs in up to 12% of adults More common in females Increased prevalence with age More common in iodine deficient regions Most nodules are polyclonal in origin
Risk Factors Iodine deficiency Radiation exposure Exposure to iodine from contrast dyes or other sources may precipitate or exacerbate thyrotoxicosis in MNG
Etiology Pathogenesis of MNG is multifactorial. Genetic Autoimmune Environmental Major difference between toxic and nontoxic MNG Toxic MNG evolves from nontoxic MNG as part of the natural history of the disease Stages of nodular transformation of the thyroid Goitrogenic stimuli (iodine deficiency, autoimmunity, or nutritional goitrogens) cause diffuse thyroid hyperplasia In the proliferating thyroid, growth factor expression is increased, stimulating cellular division and formation of independent clones Most nodules in MNG are polyclonal in origin, but monoclonal nodules also occur
Diagnosis Detection of MNG by physical examination depends on goiter and nodule size, location, and anatomy of the patient’s neck Laboratory evaluation Determination of serum TSH will distinguish nontoxic MNG from toxic MNG Diagnostic imaging is indicated in following situations: To verify hyperfunctioning nodules in a patient with a MNG and concomitant clinical and/or laboratory evidence of hyperthyroidism To evaluate the degree of obstruction in large MNG Fine-needle aspiration (FNA) biopsy A dominant or enlarging nodule within MNG Nonfunctioning (cold) nodules ≥1–1.5 cm in diameter Nodules found to have microcalcifications, hypoechogenicity, complex architecture, or increased vascularity on ultrasonography FNA should not be used to evaluate autonomous (warm/hot) nodules
Imaging X-ray, CT, or MRI of the neck/chest indicated only when necessary for: Goiter anatomy Substernal extension Extent of tracheal compression Iodinated contrast agents should be administered cautiously to persons with a low TSH level May precipitate or exacerbate underlying hyperthyroidism Consider pretreatment with antithyroid drug therapy before imaging with contrast agents
Imaging Thyroid scintigraphy (123iodine or 99mtechnetium) Limited to patients with a low TSH level to verify the clinical diagnosis of toxic MNG Unnecessary in the setting of a normal TSH level. Toxic MNG shows heterogeneous iodine uptake with multiple regions of increased and decreased uptake Ultrasonography Recommended for all patients with known or suspected thyroid nodules Useful for accurate monitoring of nodule size or for guiding FNA biopsy of suspicious nodules
Endemic goitre More common in mountainous regions Diffuse goitre caused by I2 deficiency affecting >5% of population comprising children
Thank You
Iodine Deficiency
Iodine Deficiency Iodine is an essential micronutrient T4 synthesis Brain growth and development Daily requirement (adult) 150 ug/day 1 teaspoonful of iodine is sufficient for lifetime Iodine deficiency causes a wide spectrum of illness collectively termed iodine deficiency disorders (IDD) Iodine is an essential micronutrient required for synthesis of thyroid hormone, normal brain growth and development, maintenance of metabolism and thermo regulation
IDD: clinical spectrum Goiter (all ages) Primary hypothyroidism Cretinism Neurological Myxoedematous Mixed Learning disability Goiter and Cretinism
IDD Mild iodine deficiency causes, in children, poor school performance, reduced intellectual ability and impaired work capacity1,2 Results Compromised human potential Poor socio-economic development On a worldwide basis, iodine deficiency is the single most important preventable cause of brain damage This not only compromises the human potential but also results in poor socio-economic development of populations residing in endemic iodine deficient areas Tiwari BD, Godbole MM, et al. Learning disabilities and poor motivation to achieve due to prolonged iodine deficiency. Am J Clin Nutr 1996;63:782– 6. Kochupillai N., The impact of iodine deficiency on human resource development. Prog Food Nutr Sci. 1989;13(1):1-15. Review.
IDD: Causes Low dietary iodine contents Soil with low iodine content due to past glaciations or the repeated leaching effects of snow, water (floods) and heavy rainfall Crops grown in this soil, therefore, do not provide adequate amounts of iodine when consumed Iodine deficiency disorders (IDD) continue to be the major nutritional deficiency disorders throughout India
Global magnitude of IDD WHO data: IDD is a public health problem in 130 of 191 countries, Data insufficient to categorize 41 Only 20 countries free from IDD Globally, 740 million people with goiter, 13% of world’s population Over 2 billion people are exposed to the risk of IDD 35.2% of populations with urinary iodine excretion (UIE)< 100 µg/L
Global picture of IDD WHO Global Database on IDD
Magnitude of iodine deficiency - India Total districts in india: 587 321 districts surveyed 260 (81%) districts endemic for IDD 200 million people are at risk 71 million with goiter >8 million have neurological deficit National Iodine Deficiency Disorders Control Program: National Health Program Series 5. Published by Department of Communication, National Institute of Health and Family Welfare, New Delhi, 2003; 99.
IDD: National Health Problem IDD is still a significant public health problem in India As per recommendation of Central Council of Health (1984), the GOI took policy decision for “Universal Iodization of Salt” to be achieved by year 1992. UP: USI started 2 Oct, 1987 Realizing the importance of iodine deficiency in relation to human resource development, National IDD Control Program has been included in 20-point program of prime minister
Shift in policies in salt iodination 1992: sale of non-iodized salt declared as punishable offence 2000: Punitive clause removed through Central notification 2005, Nov: Punitive clause restored
Non-uniform Iodized salt distribution in India The use of iodized salt varies dramatically from one state to another Why: number of factors scale of salt production, transportation requirements, enforcement efforts, differences in state regulations, the pricing structure, and storage patterns Adequately iodized salt is uniformly high (>72 %) in Northeast Region, in most states in the North region, and in Kerala, reaching a high of 94 percent in Manipur Lowest (<40%) in AP, MP, UP and Orissa
Presence of iodized salt in household Background characteristic None (0 ppm) Inadequate (<15 ppm) Adequate* (15+ ppm) India Urban 12.8 15.7 71.5 Rural 29.3 29.5 41.2 Uttar Pradesh 23.4 40.2 36.4 Numbers expressed as % *Adequate iodine contents in salt >15ppm National Family Health Survey 3 (NFHS-3), 2005-06
IDD: Epidemiological criteria Iodine Deficiency None Mild Moderate Severe Median urine iodine, µg/L >100 50-99 20-49 <20 Goiter prevalence <5% 5-20% 20-30% >30% Neonatal TSH, >5 IU/L whole blood <3% 3-20% 20-40% >40% Cretinism +
Goitrogens Environmental Drugs Cassava root (contains thiocyanate) Cegetables cruciferae family (cabbage, cauliflower, brussel sprouts) Milk from regions where goitrogens are present in grass Others Drugs Iodides Amiodarone, aminoglutethemide, Lithium Cobalt Diiodoquinone Ethionamide PAS