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