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Thyroid Anatomy

Thyroid Anatomy. Brownish-red, highly vascular gland Location: ant neck at C5-T1, overlays 2 nd – 4 th tracheal rings Avg. width: 12-15 mm (each lobe) Avg. height: 50-60 mm long Avg. weight: 25-30 g in adults (slightly more in women) **enlarges during menstruation and pregnancy**

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Thyroid Anatomy

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  1. Thyroid Anatomy

  2. Brownish-red, highly vascular gland • Location: ant neck at C5-T1, overlays 2nd – 4th tracheal rings • Avg. width: 12-15 mm (each lobe) • Avg. height: 50-60 mm long • Avg. weight: 25-30 g in adults (slightly more in women) **enlarges during menstruation and pregnancy** Pyramidal lobe: • often ascends from the isthmus or the adjacent part of either lobe (usu L) up to the hyoid bone • may be attached by a fibrous/fibromuscular band  “levator” of the thyroid gland

  3. Transverse view: relationship to other NB structures in neck

  4. Relation w/ Strap muscles • Lateral – sternothyroid • Anterior -omohyoid muscle • sternohyoid • Inferior - SCM (lower portion) ** careful - motor nerve supply from the ansacervicalis enters these muscles inferiorly.

  5. Vascular Anatomy ARTERIAL: • superior and inferior thyroid arteries (occthyroideaima) • ++ collateral anastomoses (ipsi and contralaterally) • thyroid ima (when pres) originates from aortic arch or innominate artery, enters the thyroid at inferior border of isthmus.

  6. Vascular anatomy VENOUS: 3 pairs of veins: • STV – asc along STA and becomes a tributary of the IJV • MTV – directly lateral  IJV • ITV (variable): • R – passes ant to innominate a  R BCV or ant trachea  L BCV • L – drainage  L BCV **occ – both inf veins form a common trunk “thyroid ima vein”  empties into L BCV

  7. Vascular Anatomy

  8. Relationship with RLN: • RLN ascends in the TE groove and enters the larynx b/w the inferior cornu of the thyroid cartilage and the arch of the cricoid • RLN can be found after it emerges from the superior thoracic outlet: • Sup: thyroid lobe • Lat: common carotid artery • Medial: trachea

  9. Lymphatics • Extensive, multidirectional flow • periglandular  prelaryngeal (Delphian)  pretracheal  paratracheal (along RLN)  brachiocephalic (sup mediastinum)  deep cervical  thoracic duct

  10. Structure • Under pretracheal thyroid inner true capsule  thin and closely adherent to the gland • capsule extensions within the gland form septae, dividing it into lobes and lobules • lobules are composed of follicles = structural units of the gland  layer epithelium enclosing a colloid-filled cavity • colloid (pink on H&E stain) contains an iodinated glycoprotein, iodothyroglobulin (precursor of thyroid hormones).

  11. Structure Epithelial cells = 2 types: • principal (ie: follicular) – formation of colloid (iodothyroglobulin) • parafollicular (ie: C cells -clear, light), lie adjacent to follicles w/in basal lamina  produce calcitonin

  12. THYROID GLAND HISTOLOGY http://arbl.cvmbs.colostate.edu/hbooks/pathphys/endocrine/thyroid/anatomy.html

  13. THYROID PHYSIOLOGY

  14. Thyroid Hormone Synthesis • 1. Iodide trapping • 2. Oxidation of iodide and iodination of thyroglobulin • 3. Coupling of iodotyrosine molecules within thyroglobulin (formation of T3 and T4) • 4. Proteolysis of thyroglobulin • 5. Deiodination of iodotyrosines • 6. Intrathyroidal deiodination of T4 to T3

  15. OH OH I I I I I O O NH2 NH2 I I OH OH O O 3,5,3’-Triiodothyronine (T3) THYROID HORMONES Thyroxine (T4)

  16. Hypothalamic Pituitary Axis

  17. THYROID HORMONES IN THE BLOOD • Approximately 99.98% of T4 is bound to 3 serum proteins: Thyroid binding globulin (TBG) ~75%; Thyroid binding prealbumin (TBPA or transthyretin) 15-20%; albumin ~5-10% • Only ~0.02% of the total T4 in blood is unbound or free. • Only ~0.4% of total T3 in blood is free.

  18. NH2 NH2 I OH I OH OH “Step up” “Step down” I O O O I T4 I I OH I R OH I R I O O I T3 rT3 I OH I R O 3,3’-T2 R = THYROID HORMONE METABOLISM

  19. Effects of Thyroid Hormone • Fetal brain and skeletal maturation • Increase in basal metabolic rate • Inotropic and chronotropic effects on heart • Increases sensitivity to catecholamines • Stimulates gut motility • Increase bone turnover • Increase in serum glucose, decrease in serum cholesterol • Increases oxygen consumption in most target tissues.

  20. Disorders of Thyroid: • Functional-Hyperthyroidism • Hypothyroidism • (Euthyroid) • Thyroiditis. • Neoplasms – adenoma/carcinoma. • Congenital – Thyroglossal cyst/duct.

  21. History • Period-Duration.Days.Weeks.Months.years • Progress-Rapid, slowly • Pressure symtopms.Dyspnea.Dysphagia • Palpitation.TG • Pain-Thyroiditis • Paralysis-Change of voice.Malignancy?

  22. Pertinent questions –clinical assessment of goiter • 1-is it Goiter-? • 2-Diffuse or Nodular? • 3-Single nodule –Solitary thyroid nodule or Dominant nodule in MNG 4- Function wise: Hyper, Hypo or euthyroid? 5-Thyroiditis? 6-Signs of malignancy? 7-Retrosternal Extension? 8-recurrent

  23. EXAMPLES OF THYROID DISEASES 1° Hypothyroidism Hyperthyroidism Congenital Hypothyroidism www.hsc.missouri.edu/~daveg/thyroid/thy_dis.html

  24. Thyroid Disease Spectrum Overt Hypothyroidism TSH >4.0 IU/mL, Free T4 Low Mild Thyroid Failure TSH >4.0 IU/mL, Free T4Normal Euthyroid TSH 0.4-4.0 IU/mL, Free T4 Normal Thyrotoxicosis TSH <0.4 IU/mL, Free T3/T4Normal or Elevated 10 0 5 TSH, IU/mL Braverman LE, et al. Werner & Ingbar’s The Thyroid. A Fundamental and Clinical Text. 8th ed. 2000. Canaris GJ, et al. Arch Intern Med. 2000;160:526-534. Vanderpump MP, et al. Clin Endocrinol (Oxf). 1995;43:55-68.

  25. Classification of goiter1-Simple nontoxic a-Diffuse hyperplastic-i-physiological-puberty.preg.ii-prim.Iodine def-Endemic G iii-Sec.Iodine def. *Goiterogens-of Brassica family-Cabbage,soya bean *Excess dietary flouride. *Drugs-PAS,Lithium,Phenylbutazone. Thiocyanates,potassium perchlorate. Antithyroiddrugs.radioactiveiodine.Dyshormonogenesis b-Colloid G c-MNG d-Solitary nontoxic nodule e-Recurrent nontoxic nodule

  26. 2-Toxic Ga-Diffuse-prim- Graves’ disb-MN(sec.)Plummer’s disc-Toxic nodule-Solitary-Tertiary-Toxic adenomad0 Recurrent toxic G3-Thyroiditisa-acuteb-subacutec-chronic-CLT4-neoplastic a.benignb-malign

  27. Solitary thyroid nodule(STN)Aims-1-Determine whether it is causing localized or systemic symptoms2-Whether it is benign or malignantDDX:1-Benign G2-Cyst(intrathyroidal)3-thyroiditis4-Benign tumor5-Malignant tumorHy- IND- Sex-STN-more likely to be Ca in a man than woman Age= = = in young (<20) & older >60Y Thyroid Ca occurs in 40% of children withSTN Residence(place of birth)-Benign nodule in endemic G areas 6 Ps Past Hy-Hyvof radiation to neck( most important)-Low –dose therapeutic radiation(6.5-2000cGy) in infancy & childhood—Increased incidence of benign G(35%), or thyroid cancer(13%) family Hy-Thyroid Ca is familial in 25% of patientswith Medullary Ca O/E- Palpate systematically – STN or MNG Solitary hard nodule-likely to be mailgnant Cervical LAP-?Investigations:US– Solid or cystic ? number of nodules Suspicious nodule? Coexistent suspicious LN?FNA + US guideCytological results: 1-Mailgnant 2-Benign 3-Suspicious 4-Inadequate repeat biopsy False +ive is rare 20% of suspicious- & 5% of benign reports-are actually malignant CXR—including neck-Tracheal displacement.calcification of nodule.Pul.metastasisIndications for surgery_1-suspicion or documented Ca.2-Pressure symptoms.3-TG4-Substernal extension5-Cosmetic deformityNon-op.Rx-1-small or moderately sized MNG2-CLT.unless suspicious area.3-Hy of radiation-4-Family Hy of Ca. thyroid

  28. Clinical assessment of G

  29. MNGPathogenesis:1-Persistent TSH stimulation---Diffuse hyperplasia of gland( all active lobules)---later with 2-fluctuation of TSH level-----mixed areas of active & inactive lobules develop-----3-active lobules become more vascular & hyperplastic4-Hage occur with necrosis in the center5- nodule formation6- center of nodule is inactive& only margin is active i.einternodular tissue is active----7- Formation of many nodules---MNG

  30. Colloid G-Due to long standing Iodine deficency + localized accumulation of significant colloid in the glandMNG: Clinical features-1-More common in middle aged females2-long Hy-many years. slowly progressive3-Many nodules. Dif.size, in both lobes , isthmus4- nodule- firm, nontender & moves with deglutition.5-Recent increase in size-short duration- hageweeks to months- malign transformation

  31. Complications of MNG1-Sec thyrotoxicosis2-Follicular Ca. of thyroid3-Hage in a nodule4-tracheal compression- -retrosternal extension/obstruction5-Cosmetic problemInvestigationsTFTs-TSH, F(T4)U/SFNAXR of neck- calcification. Position & compression of trachea.Rx Surgery S/TNear total thyroidectomyTotal T

  32. Solitary thyroid noduleCauses1-Thyroid cyst2-Thyoid adenomasa- Follicularb-Hurthle cell3- Papillary Ca4-Dominanent nodule in MNGTypes:1- Toxic adenoma2-Nontoxic Solitary nodulebased on radioactive study:a- Hot –autonomous toxic noduleb-Warm-normally functioning nodulec-Cold-nonfunctioning-thyroiditis, thyroid cyst, hage, malig

  33. Clinical features1-Single palpable nodule2- progress- rapid enlargement may be malig3-Age – extreme of life – can be malig.4-30 % are cystic4- up to 20 % of cold nodule –malig5-site- commonest site at junction of isthmus wit one of lat lobe.Clinical features suggesting malig:1-any nodule can be malig2-rapid onset/or recent increase in size.3-Pressure effects4-paralysis- hoarseness of voice5-hard, irregular, fixed nodule6-palpable significant cervical LAP

  34. Investigations1-TFTs2-neck U/S3-FNA4-Radioactive isotope study(Iodine 123,131, Tc 995-XR- neck- tracheal deviation.Rxindications for surgery:1-Cyst->4cm.Hagic,Malig or suspecios on FNA, Recurrent Cyst. Complex cyst (both solid & cystic component).2-follicular neoplasm3-malig nodule4-toxic adenoma in young patient5- pressure effects6- Cosmetic reason

  35. Rx-continuedA- Conservative- Colloid nodule- T4 Rx- respond in 50%if nodule: reappears,or enlarges rapidly or causes cosmetic problem—then -HT(hemithyroidectomyB-Surgery- minimal op.HT1-Nontoxic G- hemithyroidectomy including the isthmus.2-Papillary Ca. near total T.+suppression dose of T4(0.2-0.3mg/d)3-Toxic adenoma-age >45; radioactive iodine(131) 5 milli curie orally.Age <45Contro with antithyroid then surgery- hemithyrodectomy4-If FNA-follicular adenoma-hemithyroidectomyIf HPE- follicular Ca(capsular & vascular invasion) then complete total T( W/N1wk or after 3wks)5-if nodule in the isthmus- isthmusectomy + part of adjacent lat. lobes6-If FNA- Medullary Ca-Total T+bilat.neck nodal dissection including central compartment

  36. Thyroid cyst1- Tensly cystic swelling may be hard-2- common cause – colloid degeneration. 50%- absence of epithelial lining3- 30% of solitary nodules are cystic4- 15% cystic swellings- are malig5-cystic formation is common in papillary ca.6-complex cyst- contains both cystic & solid areas , more likely to be mlig7- FNAC may cause regression of simple cyst.8- Recurrence after 3 aspiration or if cyst hagic –surgery9-Complex cyst or > 4cm or malig or suspecious- surgery

  37. SOB in Goiter1-MNG- tracheal compression2- Retosternal G3- Sec toxic G- CHF4- Ca. infiltrating the trachea

  38. Thyrotoxicosis & HyperthyroidismThyrotoxicosis- symptoms complex caused by increased levels of thyroid hormones’Types:1-Diffuse toxic G- graves’ dis- Prim thyrotoxicosis.2-toxic MNG-Sec Thyrotoxicosis3- Toxic adenoma- nodule4- Others:a-thyrotoxicosisfactitia- drug induced . Excessive intake of T4 b-JodBasedowthyrotoxicosis- by large doses of iodine given to hyperplastic endemic Gc-Thyroiditis- de Quervain’s or Autoimmuned-Occ. Ca thyroide-Neonatal thyrotoxicosis- subsides in 3-4 wksf- Struma ovariig- Drugs-amiodarone- antiarrhythmic agent

  39. Clinical featuresIncidenceAge- anySex- F: M 8:1Prim. Commonly in younger age groupSec. is common in older gae groupGraves’ dis- may present without obvious goiterSuspect Graves’ disese In:1-Unexplained behavioural problem2-insomnia3-myopathy4-Unexplained diarrhea or wt loss5-Tachycardia6-menstrual changes or infertility

  40. Symptoms1-CNS-Irritability.Nervousness. Insomnia2-Neuromascular system:Undue fatigue & muscle weakness.Tremor3-Skeletal system: increase in linear growth in children4-Skin; hair loss . Pruritus.palmarerythema.5-CVS:tachycardai.SOB at rest or on mild exersion.Angina. Arrythmias.CHF(in elderly)6-GIT-Wt loss despite good appetite.diarrhea( due to increased activity at ganglionic level).7-GUT: oligo or amenorrhea.Occ. Urinary frequency

  41. Sympathetic overactivity:causes-SOB,Palpitation.tiredness.Heatintolerance.Sweating,nervousness,increased appetite & decrease in Wt.Because of increased catabolism they have increased appetite , decrease wt & also increased creatinine level which signifies myopathy due to more muscle catabolism.Fine tremor_ due to diffuse irritability of gray matter.Thrill & bruit are detected in upper pole as the Sup TA enters the gland superficially while ITA enters from deeper plane so the thrill cannot be felt in lower pole

  42. Hyper- thyroidism Features:

  43. THYROID EYE DISEASE • INFILTRATION • 1. soft tissue involvement :- chemosis, conjunctival injection over the recti insertions, puffy lids

  44. THYROID EYE DISEASE • Superior limbic keratoconjunctivitis (SLK)

  45. Clinical Characteristics of Exophthalmos • Proptosis • Corneal Damage • Periorbital edema • Chemosis • Conjunctival injection • Extraocular muscle impairment • Optic neuropathy

  46. Clinical Characteristics of Localized Myxedema • Raised surface • Thick, leathery consistency • Nodularity, sometimes • Sharply demarcated margins • Prominent hair follicles • Usually over pretibial area • Non-tender

  47. Margins sharply demarcated Margins sharply demarcated Graves’ Disease - Localized Myxedema Nodularity Thickened skin

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