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Dr Madhukar Mittal Medical Endocrinology

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Presentation on theme: "Dr Madhukar Mittal Medical Endocrinology"— Presentation transcript:

1 Dr Madhukar Mittal Medical Endocrinology
Nontoxic goitre Dr Madhukar Mittal Medical Endocrinology

2 Goitre Solitary Nodular Multinodular Toxic Nontoxic Diffuse

3 Goitre Solitary Nodular Multinodular Diffuse Nontoxic
Benign Malignant (20%) Multinodular Benign vs Malignant Diffuse Toxic Graves Simple autoimmune

4 Painful thyroid swelling
Subacute thyroiditis Acute thyroiditis Invasive malignancy Amiodarone induced thyrotoxicosis, type 1

5 Hard thyroid swelling Reidel’s thyroiditis Thyroid carcinoma
(firm : medullary CA, lymphoma)

6 Thyroid examination From behind with neck flexed slightly forward
Rt lobe is 25% larger than left lobe Palpable and smooth normally

7 Midline neck swellings
Goitre of thyroid isthmus & pyramidal lobe Thyroglossal cyst Suprasternal LN, lipoma Ludwig’s angina Submental LN Sublingual dermoid, lipoma

8 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

9 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

10 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

11 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

12 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

13 Examination Anemia BP Pulse rate Skin of hands (moist, hot/cold)
Tremors – hand, tongue LN Facies Eye signs Dermopathy Acropachy Vitiligo

14 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)

15 Treatment

16 Hyperthyroidism of Graves disease
Hypothyroidism Levothyroxine Hyperthyroidism of Graves disease Antithyroid drugs (Europe, Japan) Radioiodine (USA)

17 Acute thyroiditis Antibiotics Drainage of abscess

18 Subacute thyroiditis Aspirin – large doses 600mg 4-6 hrly
Prednisolone mg/d Thyrotoxic phase – β-blockers Hypothyroid phase – low dose levothyroxine

19 Silent thyroiditis Thyrotoxic phase – propranolol 20-40mg TDS/QID
Hypothyroid phase – LT4 for 6-9 months Annual followup for permanent hypothyroidism

20 Reidel’s thyroidits Surgery + tamoxifen

21 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

22 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

23 MNG - toxic Sx Radioiodine in elderly
Antithyroid drugs – often stimulate growth of goitre

24 MNG nontoxic Radioiodine Sx
T4 suppressive therapy (rarely effective for decreasing goitre size)

25 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

26 STN Hyperfunctioning Radioiodine ablation – esp >45yr
Sx resection – esp <45yr Enucleation Lobectomy Ethanol injection

27 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

28 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

29 MNG

30 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

31 Risk Factors Iodine deficiency Radiation exposure
Exposure to iodine from contrast dyes or other sources may precipitate or exacerbate thyrotoxicosis in MNG

32 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

33 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

34 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

35 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

36 Endemic goitre More common in mountainous regions
Diffuse goitre caused by I2 deficiency affecting >5% of population comprising children

37 Thank You

38 Iodine Deficiency

39 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

40 IDD: clinical spectrum
Goiter (all ages) Primary hypothyroidism Cretinism Neurological Myxoedematous Mixed Learning disability Goiter and Cretinism

41 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.

42 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

43 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

44 Global picture of IDD WHO Global Database on IDD

45 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. 

46 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

47 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

48 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

49 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),

50 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 +

51 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

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