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  • 1. Benign ThyroidBenign ThyroidDiseasesDiseasesUniversity of Texas Medical BranchDept of OtolaryngologyGrand Rounds PresentationAlan Cowan, MDShawn Newlands, MD, PhDMay 2006
  • 2. HistoryHistory GoiterGoiter– Fist described in China in 2700 BCFist described in China in 2700 BC Thyroid FunctionThyroid Function– Da Vinci – thyroid is designed to fill empty spaces in the neckDa Vinci – thyroid is designed to fill empty spaces in the neck– Parry – thyroid works as a buffer to protect the brain from surgesParry – thyroid works as a buffer to protect the brain from surgesin blood flowin blood flow– Roman physicians – thyroid enlargement is a sign of pubertyRoman physicians – thyroid enlargement is a sign of puberty CuresCures– ““application of toadapplication of toad’’s blood to the necks blood to the neck””– ““stroking of the thyroid gland with a cadaverous handstroking of the thyroid gland with a cadaverous hand””
  • 3. Surgical advancesSurgical advances 500 AD500 AD– Abdul Kasan Kelebis Abis performed the first goiter excision inAbdul Kasan Kelebis Abis performed the first goiter excision inBaghdad.Baghdad.– Procedure: unknownProcedure: unknown 12001200’’s ADs AD– Advancements in goiter procedures included applying hot ironsAdvancements in goiter procedures included applying hot ironsthrough the skin and slowly withdrawing them at right angles. Thethrough the skin and slowly withdrawing them at right angles. Theremaining mass or pedicled tissue was excised.remaining mass or pedicled tissue was excised.– Patients were tied to the table and held down to prevent unwantedPatients were tied to the table and held down to prevent unwantedmovement.movement.– Most died from hemorhage or sepsisMost died from hemorhage or sepsis .. 1646 AD1646 AD– Wilhelm Fabricus performed a thyroidectomy with standard surgicalWilhelm Fabricus performed a thyroidectomy with standard surgicalscalpels.scalpels.– The 10 y/o girl died, and he was imprisonedThe 10 y/o girl died, and he was imprisoned 1808 AD1808 AD– Guillaume Dupuytren performed a total thyroidectomy.Guillaume Dupuytren performed a total thyroidectomy.– The patient died postoperatively ofThe patient died postoperatively of ““shockshock””
  • 4. Surgical advancesSurgical advances 18661866– ““If a surgeon should be so foolhardy as to undertake itIf a surgeon should be so foolhardy as to undertake it[thyroidectomy] … every step of the way will be[thyroidectomy] … every step of the way will beenvironed with difficulty, every stroke of his knife willenvironed with difficulty, every stroke of his knife willbe followed by a torrent of blood, and lucky will it bebe followed by a torrent of blood, and lucky will it befor him if his victim lives long enough to enable him tofor him if his victim lives long enough to enable him tofinish his horrid butchery.finish his horrid butchery.””–– Samuel David GrossSamuel David Gross
  • 5. Surgical advancesSurgical advances 18831883KocherKocher’’s performs a retrospective reviews performs a retrospective review 5000 career thyroidectomies5000 career thyroidectomies Mortality rates decreasedMortality rates decreased– 40% in 1850 (pre-Kocher & Bilroth)40% in 1850 (pre-Kocher & Bilroth)– 12.6% in 187012.6% in 1870’’s (Kocher begins practice)s (Kocher begins practice)– 0.2% in 1898 (end of Kocher0.2% in 1898 (end of Kocher’’s career)s career) Many patients developed cretinism or myxedemaMany patients developed cretinism or myxedemaHis conclusions ….His conclusions ….
  • 6. Surgical advancesSurgical advancesIn presentation to the German SurgicalIn presentation to the German SurgicalCongress …Congress …““ ……the thyroid gland in fact had a function….the thyroid gland in fact had a function….””- Theodor Kocher, 1883- Theodor Kocher, 1883
  • 7. Medical AdvancesMedical Advances 1820 AD1820 AD– Johann Straub and Francois Coindet found that useJohann Straub and Francois Coindet found that useof seaweed (iodine) reduced goiter size andof seaweed (iodine) reduced goiter size andvascularityvascularity 1830 AD1830 AD– Graves and von Basedow describe a toxic goiterGraves and von Basedow describe a toxic goitercondition they referred to ascondition they referred to as ““Merseburg TriadMerseburg Triad”” ––goiter, exopthalmos, palpitations.goiter, exopthalmos, palpitations.
  • 8. Thyroid PhysiologyThyroid Physiology
  • 9. Iodine transportIodine transport NaNa++/I/I--symport proteinsymport proteincontrols serum Icontrols serum I--uptakeuptake Based on NaBased on Na++/K/K++antiport potentialantiport potential Stimulated by TSHStimulated by TSH Inhibited byInhibited byPerchloratePerchlorate
  • 10. Thyroid hormone formationThyroid hormone formation Thyroid Peroxidase (TPO)Thyroid Peroxidase (TPO)– Apical membrane proteinApical membrane protein– Catalyzes Iodine organification to tyrosine residues ofCatalyzes Iodine organification to tyrosine residues ofthyroglobulinthyroglobulin– Antagonized by methimazole, PTUAntagonized by methimazole, PTU Iodine coupled to ThyroglobulinIodine coupled to Thyroglobulin– Monoiodotyrosine (Tg + one IMonoiodotyrosine (Tg + one I--))– Diiodotyrosine (Tg + two IDiiodotyrosine (Tg + two I--)) Pre-hormones secreted into follicular spacePre-hormones secreted into follicular space
  • 11. Wolff-Chaikoff EffectWolff-Chaikoff Effect Increasing doses of IIncreasing doses of I--increase hormone synthesisincrease hormone synthesisinitiallyinitially Higher doses causeHigher doses causecessation of hormonecessation of hormoneformation.formation. This effect is countered byThis effect is countered bythe Iodide leak from normalthe Iodide leak from normalthyroid tissue.thyroid tissue. Patients with autoimmunePatients with autoimmunethyroiditis may fail to adaptthyroiditis may fail to adaptand becomeand become hypohypothyroid.thyroid.
  • 12. Jod-Basedow EffectJod-Basedow Effect Opposite of the Wolff-Chaikoff effectOpposite of the Wolff-Chaikoff effect Excessive iodine loads induceExcessive iodine loads induce hyperhyperthyroidismthyroidism Observed in hyperthyroid disease processesObserved in hyperthyroid disease processes– GravesGraves’’ diseasedisease– Toxic multinodular goiterToxic multinodular goiter– Toxic adenomaToxic adenoma This effect may lead to symptomatic thyrotoxicosis inThis effect may lead to symptomatic thyrotoxicosis inpatients who receive large iodine doses frompatients who receive large iodine doses from– Dietary changesDietary changes– Contrast administrationContrast administration– Iodine containing medication (Amiodarone)Iodine containing medication (Amiodarone)
  • 13. Thyroid Hormone ControlThyroid Hormone Control
  • 14. TRHTRH Produced by HypothalamusProduced by Hypothalamus Release is pulsatile, circadianRelease is pulsatile, circadian Downregulated by TDownregulated by T33 Travels through portal venous system toTravels through portal venous system toadenohypophysisadenohypophysis Stimulates TSH formationStimulates TSH formation
  • 15. TSHTSH Produced by Adenohypophysis ThyrotrophsProduced by Adenohypophysis Thyrotrophs Upregulated by TRHUpregulated by TRH Downregulated by TDownregulated by T44, T, T33 Travels through portal venous system toTravels through portal venous system tocavernous sinus, body.cavernous sinus, body. Stimulates several processesStimulates several processes– Iodine uptakeIodine uptake– Colloid endocytosisColloid endocytosis– Growth of thyroid glandGrowth of thyroid gland
  • 16. TSH ResponseTSH Response
  • 17. Thyroid HormoneThyroid Hormone Majority of circulating hormone is TMajority of circulating hormone is T44– 98.5% T98.5% T44– 1.5% T1.5% T33 Total Hormone load is influenced by serum bindingTotal Hormone load is influenced by serum bindingproteinsproteins– Albumin 15%Albumin 15%– Thyroid Binding Globulin 70%Thyroid Binding Globulin 70%– Transthyretin 10%Transthyretin 10% Regulation is based on the free component of thyroidRegulation is based on the free component of thyroidhormonehormone
  • 18. Hormone Binding FactorsHormone Binding Factors Increased TBGIncreased TBG– High estrogen states (pregnancy, OCP, HRT, Tamoxifen)High estrogen states (pregnancy, OCP, HRT, Tamoxifen)– Liver disease (early)Liver disease (early) Decreased TBGDecreased TBG– Androgens or anabolic steroidsAndrogens or anabolic steroids– Liver disease (late)Liver disease (late) Binding Site CompetitionBinding Site Competition– NSAIDNSAID’’ss– Furosemide IVFurosemide IV– Anticonvulsants (Phenytoin, Carbamazepine)Anticonvulsants (Phenytoin, Carbamazepine)
  • 19. Thyroid EvaluationThyroid Evaluation TRHTRH TSHTSH Total TTotal T33, T, T44 Free TFree T33, T, T44 RAIURAIU ThyroglobulinThyroglobulin Antibodies: Anti-TPO, Anti-TSHrAntibodies: Anti-TPO, Anti-TSHr
  • 20. Thyroid EvaluationThyroid Evaluation
  • 21. RAIURAIU Scintillation counter measures radioactivity after IScintillation counter measures radioactivity after I123123administration.administration. Uptake varies greatly by iodine statusUptake varies greatly by iodine status– Indigenous diet (normal uptake 10% vs. 90%)Indigenous diet (normal uptake 10% vs. 90%)– Amiodarone, Contrast study, Topical betadineAmiodarone, Contrast study, Topical betadine Elevated RAIU with hyperthyroid symptomsElevated RAIU with hyperthyroid symptoms– GravesGraves’’– Toxic goiterToxic goiter Low RAIU with hyperthyroid symptomsLow RAIU with hyperthyroid symptoms– Thyroiditis (Subacute, Active HashimotoThyroiditis (Subacute, Active Hashimoto’’s)s)– Hormone ingestion (Thyrotoxicosis factitia, HamburgerHormone ingestion (Thyrotoxicosis factitia, HamburgerThyrotoxicosis)Thyrotoxicosis)– Excess IExcess I--intake in Gravesintake in Graves’’ (Jod-Basedow effect)(Jod-Basedow effect)– Ectopic thyroid carcinoma (Struma ovarii)Ectopic thyroid carcinoma (Struma ovarii)
  • 22. Iodine statesIodine states Normal ThyroidNormal Thyroid Inactive ThyroidInactive Thyroid Hyperactive ThyroidHyperactive Thyroid
  • 23. Common ThyroidCommon ThyroidDisordersDisorders
  • 24. GoiterGoiter GoiterGoiter: Chronic enlargement of the thyroid gland not due: Chronic enlargement of the thyroid gland not dueto neoplasmto neoplasm Endemic goiterEndemic goiter– Areas where > 5% of children 6-12 years of age have goiterAreas where > 5% of children 6-12 years of age have goiter– Common in China and central AfricaCommon in China and central Africa Sporadic goiterSporadic goiter– Areas where < 5% of children 6-12 years of age have goiterAreas where < 5% of children 6-12 years of age have goiter– MultinodularMultinodular goitergoiter in sporatic areas often denotes the presencein sporatic areas often denotes the presenceof multiple nodules rather than gross gland enlargementof multiple nodules rather than gross gland enlargement FamilialFamilial
  • 25. GoiterGoiter EtiologyEtiology– HashimotoHashimoto’’s thyroiditiss thyroiditis Early stages only, late stages show atrophic changesEarly stages only, late stages show atrophic changes May present with hypo, hyper, or euthyroid statesMay present with hypo, hyper, or euthyroid states– GravesGraves’’ diseasedisease Due to chronic stimulation of TSH receptorDue to chronic stimulation of TSH receptor– DietDiet Brassica (cabbage, turnips, cauliflower, broccoli)Brassica (cabbage, turnips, cauliflower, broccoli) CassavaCassava– Chronic Iodine excessChronic Iodine excess Iodine excess leads to increased colloid formation and can preventIodine excess leads to increased colloid formation and can preventhormone releasehormone release If a patient does not develop iodine leak, excess iodine can lead to goiterIf a patient does not develop iodine leak, excess iodine can lead to goiter– MedicationsMedications Lithium prevents release of hormone, causes goiter in 6% of chronicLithium prevents release of hormone, causes goiter in 6% of chronicusersusers– NeoplasmNeoplasm
  • 26. GoiterGoiter PathogenesisPathogenesis– Iodine deficient areasIodine deficient areas Heterogeneous response to TSHHeterogeneous response to TSH Chronic stimulation leads to multiple nodulesChronic stimulation leads to multiple nodules– Iodine replete areasIodine replete areas Thyroid follicles are heterogeneous in their growth and activityThyroid follicles are heterogeneous in their growth and activitypotentialpotential Autopsy series show MNG >30%.Autopsy series show MNG >30%. Thyroid function evaluationThyroid function evaluation– TSH, T4, T3TSH, T4, T3– Overt hyperthyroidism (TSH low, T3/T4 high)Overt hyperthyroidism (TSH low, T3/T4 high)– Subclinical hyperthyroidism (TSH low, T3/T4 normal)Subclinical hyperthyroidism (TSH low, T3/T4 normal) Determination of thyroid state is key in determining treatmentDetermination of thyroid state is key in determining treatment
  • 27. Non-Toxic GoiterNon-Toxic Goiter Cancer screening in non-toxic MNGCancer screening in non-toxic MNG– Longstanding MNG has a risk of malignancy identical toLongstanding MNG has a risk of malignancy identical tosolitary nodules (<5%)solitary nodules (<5%)– MNG with nodules < 1.5 cm may be followed clinicallyMNG with nodules < 1.5 cm may be followed clinically– MNG with non-functioning nodules > 4cm should be excisedMNG with non-functioning nodules > 4cm should be excised No FNA needed due to poor sensitivityNo FNA needed due to poor sensitivity Incidence of cancer (up to 40%)Incidence of cancer (up to 40%)– FNA in MNGFNA in MNG Sensitivity 85% - 95%Sensitivity 85% - 95% Specificity 95%Specificity 95% Negative FNA can be followed with annual USNegative FNA can be followed with annual US Insufficient FNAInsufficient FNA’’s should be repeateds should be repeated Incoclusive FNA or papillary cytology warrants excisionIncoclusive FNA or papillary cytology warrants excision– Hyperfunctioning nodules may mimic follicular neoplasm onHyperfunctioning nodules may mimic follicular neoplasm onFNAFNA
  • 28. Non-Toxic GoiterNon-Toxic Goiter Treatment optionsTreatment options (no compressive symptoms)(no compressive symptoms)– US follow-up to monitor for progressionUS follow-up to monitor for progression– Thyroid suppression therapyThyroid suppression therapy May be used for progressive growthMay be used for progressive growth May reduce gland volume up to 50%May reduce gland volume up to 50% Goiter regrowth occurs rapidly following therapy cessationGoiter regrowth occurs rapidly following therapy cessation– SurgerySurgery Suspicious neck lymphadenopathySuspicious neck lymphadenopathy History of radiation to the cervical regionHistory of radiation to the cervical region Rapid enlargement of nodulesRapid enlargement of nodules Papillary histologyPapillary histology Microfollicular histology (?)Microfollicular histology (?)
  • 29. Non-Toxic GoiterNon-Toxic Goiter Treatment optionsTreatment options (compressive symptoms)(compressive symptoms)– RAI ablationRAI ablation Volume reduction 33% - 66% in 80% of patientsVolume reduction 33% - 66% in 80% of patients Improvement of dysphagia or dyspnea in 70% - 90%Improvement of dysphagia or dyspnea in 70% - 90% Post RAI hypothyroidism 60% in 8 yearsPost RAI hypothyroidism 60% in 8 years Post RAI GravesPost RAI Graves’’ disease 10%disease 10% Post RAI lifetime cancer risk 1.6%Post RAI lifetime cancer risk 1.6%– SurgerySurgery Most commonly recommended treatment for healthyMost commonly recommended treatment for healthyindividualsindividuals
  • 30. Toxic GoiterToxic Goiter Evaluate forEvaluate for– GravesGraves’’ diseasedisease Clinical findings (Pretibial myxedema, Opthalmopathy)Clinical findings (Pretibial myxedema, Opthalmopathy) Anti-TSH receptor AbAnti-TSH receptor Ab High RAUIHigh RAUI– ThyroiditisThyroiditis Clinical findings (painful thyroid in Subacute thyroiditis)Clinical findings (painful thyroid in Subacute thyroiditis) Low RAUILow RAUI– Recent Iodine administrationRecent Iodine administration AmiodaroneAmiodarone IV contrastIV contrast Change in dietChange in diet FNA evaluationFNA evaluation– Not indicated in hyperthyroid nodules due to low incidence ofNot indicated in hyperthyroid nodules due to low incidence ofmalignancymalignancy– FNA of hyperthyroid nodules can mimic follicular neoplasmsFNA of hyperthyroid nodules can mimic follicular neoplasms
  • 31. Toxic GoiterToxic Goiter Risks of hyperthyroidismRisks of hyperthyroidism– Atrial fibrillationAtrial fibrillation– Congestive Heart FailureCongestive Heart Failure– Loss of bone mineral densityLoss of bone mineral density– Risks exist for both clinical or subclinical diseaseRisks exist for both clinical or subclinical disease Toxic GoiterToxic Goiter– Toxicity is usually longstandingToxicity is usually longstanding– Acute toxicity may occur in hyperthyroid states (Jod BasedowAcute toxicity may occur in hyperthyroid states (Jod Basedoweffect) witheffect) with Relocation to iodine replete areaRelocation to iodine replete area Contrast administrationContrast administration Amiodarone (37% iodine)Amiodarone (37% iodine)
  • 32. Toxic GoiterToxic Goiter Treatment for Toxic MNGTreatment for Toxic MNG– Thionamide medicationsThionamide medications Not indicated for long-term use due to complicationsNot indicated for long-term use due to complications May be used for symptomatic individuals until definitiveMay be used for symptomatic individuals until definitivetreatmenttreatment..– RadioiodineRadioiodine Primary treatment for toxic MNGPrimary treatment for toxic MNG Large ILarge I131131dose required due to gland sizedose required due to gland size Goiter size reduction by 40% within 1 yearGoiter size reduction by 40% within 1 year Risk of hypothyroidismRisk of hypothyroidism 11% - 24%11% - 24% May require second doseMay require second dose– SurgerySurgery Used for compressive symptomsUsed for compressive symptoms Hypothyroidism occurs in up to 70% of subtotal thyroidectomyHypothyroidism occurs in up to 70% of subtotal thyroidectomypatientspatients Pre-surgical stabilization with thionamide medicationsPre-surgical stabilization with thionamide medications Avoid SSKI due to risk for acute toxic symptomsAvoid SSKI due to risk for acute toxic symptoms
  • 33. GravesGraves’’ DiseaseDisease Most common cause of thyrotoxicosis in the industrialized worldMost common cause of thyrotoxicosis in the industrialized world Autoimmune condition with anti-TSHr antibodiesAutoimmune condition with anti-TSHr antibodies Onset of disease may be related to severe stress which alters theOnset of disease may be related to severe stress which alters theimmune responseimmune response DiagnosisDiagnosis– TSH, TTSH, T44, T, T33 to establish toxicosisto establish toxicosis– RAIU scan to differentiate toxic conditionsRAIU scan to differentiate toxic conditions– Anti-TPO, Anti-TSAb, fTAnti-TPO, Anti-TSAb, fT33 if indicatedif indicatedRAIU in Hyperthyroid StatesRAIU in Hyperthyroid StatesHigh UptakeHigh Uptake Low UptakeLow UptakeGravesGraves’’ Subacute ThyroiditisSubacute ThyroiditisToxic MNGToxic MNG Iodine ToxicosisIodine ToxicosisToxic AdenomaToxic Adenoma Thyrotoxicosis factitiaThyrotoxicosis factitia
  • 34. GravesGraves’’ DiseaseDisease TreatmentTreatment– Beta blockers for symptomsBeta blockers for symptoms– Thionamide medicationsThionamide medications May re-establish euthyroidism in 6-8 weeksMay re-establish euthyroidism in 6-8 weeks 40% - 60% incidence of disease remission40% - 60% incidence of disease remission 20% incidence of allergy (rash, itching)20% incidence of allergy (rash, itching) 0.5% incidence of potentially fatal agranulocytosis0.5% incidence of potentially fatal agranulocytosis– Radioiodine ablationRadioiodine ablation 10% incidence of hypothyroidism at 1 year10% incidence of hypothyroidism at 1 year 55% - 75% incidence of hypothyroidism at 10 years55% - 75% incidence of hypothyroidism at 10 years Avoid RAI in children and pregancyAvoid RAI in children and pregancy– SurgerySurgery Large goiters not amenable to RAILarge goiters not amenable to RAI Compressive symptomsCompressive symptoms Children, pregnancyChildren, pregnancy 50% - 60% incidence of hypothyroidism50% - 60% incidence of hypothyroidism
  • 35. Toxic AdenomaToxic Adenoma ThyrotoxicosisThyrotoxicosis– Hyperfunctioning nodules <2 cm rarely lead toHyperfunctioning nodules <2 cm rarely lead tothyrotoxicosisthyrotoxicosis– Most nodules leading to thyrotoxicosis are >3 cm.Most nodules leading to thyrotoxicosis are >3 cm. Treatment IndicationsTreatment Indications– Post-menopausal femalePost-menopausal female Due to increased risk of bone lossDue to increased risk of bone loss– Patients over 60Patients over 60 Due to high risk of atrial fibrillationDue to high risk of atrial fibrillation– Adenomas greater than 3 cm (?)Adenomas greater than 3 cm (?)
  • 36. Toxic AdenomaToxic Adenoma TreatmentsTreatments– Antithyroid medicationsAntithyroid medications Not used due to complications of long-term treatmentNot used due to complications of long-term treatment– RadioiodineRadioiodine Cure rate > 80% (20 mCi I131)Cure rate > 80% (20 mCi I131) Hypothyroidism risk 5% - 10%Hypothyroidism risk 5% - 10% Second dose of I131 needed in 10% - 20%Second dose of I131 needed in 10% - 20% Patients who are symptomatically toxic may require control withPatients who are symptomatically toxic may require control withthionamide medications before RAI to reduce risk of worseningthionamide medications before RAI to reduce risk of worseningtoxicity.toxicity.– SurgerySurgery Preferred for children and adolescentsPreferred for children and adolescents Preferred for very large nodules when high I131 doses neededPreferred for very large nodules when high I131 doses needed Low risk of hypothyroidismLow risk of hypothyroidism– Ethanol InjectionEthanol Injection Rarely done in the USRarely done in the US May achieve cure in 80%May achieve cure in 80%
  • 37. HypothyroidismHypothyroidism Symptoms – fatigability, coldness, weight gain,Symptoms – fatigability, coldness, weight gain,constipation, low voiceconstipation, low voice Signs – Cool skin, dry skin, swelling ofSigns – Cool skin, dry skin, swelling offace/hands/legs, slow reflexes, myxedemaface/hands/legs, slow reflexes, myxedema Newborn – Retardation, short stature, swelling ofNewborn – Retardation, short stature, swelling offace/hands, possible deafnessface/hands, possible deafness Types of HypothyroidismTypes of Hypothyroidism– Primary – Thyroid gland failurePrimary – Thyroid gland failure– Secondary – Pituitary failureSecondary – Pituitary failure– Tertiary – Hypothalamic failureTertiary – Hypothalamic failure– Peripheral resistancePeripheral resistance
  • 38. HypothyroidismHypothyroidism Cause is determined by geographyCause is determined by geography– HashimotoHashimoto’’s in industrialized countriess in industrialized countries– May be due to iodine excess in some costal areasMay be due to iodine excess in some costal areas DiagnosisDiagnosis– Low FTLow FT44, High TSH (Primary, check for antibodies), High TSH (Primary, check for antibodies)– Low FTLow FT44, Low TSH (Secondary or Tertiary, TRH, Low TSH (Secondary or Tertiary, TRHstimulation test, MRI)stimulation test, MRI) TreatmentTreatment– Levothyroxine (TLevothyroxine (T44) due to longer half life) due to longer half life– Treatment prevents bone loss, cardiomyopathy,Treatment prevents bone loss, cardiomyopathy,myxedemamyxedema
  • 39. HypothyroidismHypothyroidism AgenesisAgenesis Thyroid destructionThyroid destruction– HashimotoHashimoto’’s thyroiditiss thyroiditis– SurgerySurgery– II131131 ablationablation– Infiltrative diseasesInfiltrative diseases– Post-laryngectomyPost-laryngectomy Inhibition of functionInhibition of function– Iodine deficiencyIodine deficiency– Iodine administrationIodine administration– Anti-thyroid medications (PTU, Methimazole, Lithium, Interferon)Anti-thyroid medications (PTU, Methimazole, Lithium, Interferon)– Inherited defectsInherited defects TransientTransient– PostpartumPostpartum– ThyroiditisThyroiditis
  • 40. HashimotoHashimoto’’ss(Chronic, Lymphocytic)(Chronic, Lymphocytic) Most common cause of hypothyroidismMost common cause of hypothyroidism Result of antibodies to TPO, TBGResult of antibodies to TPO, TBG Commonly presents in females 30-50 yrs.Commonly presents in females 30-50 yrs. Usually non-tender and asymptomaticUsually non-tender and asymptomatic Lab valuesLab values– High TSHHigh TSH– Low TLow T44– Anti-TPO AbAnti-TPO Ab– Anti-TBG AbAnti-TBG Ab Treat with LevothyroxineTreat with Levothyroxine
  • 41. ThyroiditisThyroiditis
  • 42. HashimotoHashimoto’’s Thyroiditiss Thyroiditis Most common cause of goiter and hypothyroidism in the U.S.Most common cause of goiter and hypothyroidism in the U.S. PhysicalPhysical– Painless diffuse goiterPainless diffuse goiter Lab studiesLab studies– HypothyroidismHypothyroidism– Anti TPO antibodies (90%)Anti TPO antibodies (90%)– Anti Thyroglobulin antibodies (20-50%)Anti Thyroglobulin antibodies (20-50%)– Acute Hyperthyroidism (5%)Acute Hyperthyroidism (5%) TreatmentTreatment– Levothyroxine if hypothyroidLevothyroxine if hypothyroid– Triiodothyronine (for myxedema coma)Triiodothyronine (for myxedema coma)– Thyroid suppression (levothyroxine) to decrease goiter sizeThyroid suppression (levothyroxine) to decrease goiter size ContraindicationsContraindications Stop therapy if no resolution notedStop therapy if no resolution noted– Surgery for compression or pain.Surgery for compression or pain.
  • 43. Silent ThyroiditisSilent ThyroiditisPost-partum ThyroiditisPost-partum Thyroiditis Silent thyroiditis is termed post-partum thyroiditis if it occurs withinSilent thyroiditis is termed post-partum thyroiditis if it occurs withinone year of delivery.one year of delivery. ClinicalClinical– Hyperthyroid symptoms at presentationHyperthyroid symptoms at presentation– Progression to euthyroidism followed by hypothyroidism for up to 1 year.Progression to euthyroidism followed by hypothyroidism for up to 1 year.– Hypothyroidism generally resolvesHypothyroidism generally resolves DiagnosisDiagnosis– May be confused with post-partum GravesMay be confused with post-partum Graves’’ relapserelapse TreatmentTreatment– Beta blockers during toxic phaseBeta blockers during toxic phase– No anti-thyroid medication indicatedNo anti-thyroid medication indicated– Iopanoic acid (Telopaque) for severe hyperthyroidismIopanoic acid (Telopaque) for severe hyperthyroidism– Thyroid hormone during hypothyroid phase. Must withdraw in 6 monthsThyroid hormone during hypothyroid phase. Must withdraw in 6 monthsto check for resolution.to check for resolution.
  • 44. Subacute ThyroiditisSubacute ThyroiditisDeQuervainDeQuervain’’s, Granulomatouss, Granulomatous Most common cause of painfulMost common cause of painfulthyroiditisthyroiditis Often follows a URIOften follows a URI FNA may reveal multinuleatedFNA may reveal multinuleatedgiant cells or granulomatousgiant cells or granulomatouschange.change. CourseCourse– Pain and thyrotoxicosis (3-6Pain and thyrotoxicosis (3-6weeks)weeks)– Asymptomatic euthyroidismAsymptomatic euthyroidism– Hypothyroid period (weeks toHypothyroid period (weeks tomonths)months)– Recovery (complete in 95%Recovery (complete in 95%after 4-6 months)after 4-6 months)
  • 45. Subacute ThyroiditisSubacute ThyroiditisDeQuervainDeQuervain’’s, Granulomatouss, Granulomatous DiagnosisDiagnosis– Elevated ESRElevated ESR– Anemia (normochromic, normocytic)Anemia (normochromic, normocytic)– Low TSH, Elevated T4 > T3, Low anti-TPO/TgbLow TSH, Elevated T4 > T3, Low anti-TPO/Tgb– Low RAI uptake (same as silent thyroiditis)Low RAI uptake (same as silent thyroiditis) TreatmentTreatment– NSAIDNSAID’’s and salicylates.s and salicylates.– Oral steroids in severe casesOral steroids in severe cases– Beta blockers for symptoms of hyperthyroidism, Iopanoic acid for severeBeta blockers for symptoms of hyperthyroidism, Iopanoic acid for severesymptomssymptoms– PTU not indicated since excess hormone results from leak instead ofPTU not indicated since excess hormone results from leak instead ofhyperfunctionhyperfunction– Symptoms can recur requiring repeat treatmentSymptoms can recur requiring repeat treatment– GravesGraves’’ disease may occasionally develop as a late sequellaedisease may occasionally develop as a late sequellae
  • 46. Acute ThyroiditisAcute Thyroiditis CausesCauses– 68% Bacterial (S. aureus, S. pyogenes)68% Bacterial (S. aureus, S. pyogenes)– 15% Fungal15% Fungal– 9% Mycobacterial9% Mycobacterial May occur secondary toMay occur secondary to– Pyriform sinus fistulaePyriform sinus fistulae– Pharyngeal space infectionsPharyngeal space infections– Persistent Thyroglossal remnantsPersistent Thyroglossal remnants– Thyroid surgery wound infections (rare)Thyroid surgery wound infections (rare) More common in HIVMore common in HIV
  • 47. Acute ThyroiditisAcute Thyroiditis DiagnosisDiagnosis– Warm, tender, enlarged thyroidWarm, tender, enlarged thyroid– FNA to drain abscess, obtain cultureFNA to drain abscess, obtain culture– RAIU normal (versus decreased in DeQuervainRAIU normal (versus decreased in DeQuervain’’s)s)– CT or US if infected TGDC suspectedCT or US if infected TGDC suspected TreatmentTreatment– High mortality without prompt treatmentHigh mortality without prompt treatment– IV AntibioticsIV Antibiotics Nafcillin / Gentamycin or Rocephin for empiric therapyNafcillin / Gentamycin or Rocephin for empiric therapy– Search for pyriform fistulae (BA swallow, endoscopy)Search for pyriform fistulae (BA swallow, endoscopy)– Recovery is usually completeRecovery is usually complete
  • 48. RiedelRiedel’’s Thyroiditiss Thyroiditis Rare disease involving fibrosis of the thyroid glandRare disease involving fibrosis of the thyroid gland DiagnosisDiagnosis– Thyroid antibodies are present in 2/3Thyroid antibodies are present in 2/3– Painless goiterPainless goiter ““woodywoody””– Open biopsy often needed to diagnoseOpen biopsy often needed to diagnose– Associated with focal sclerosis syndromes (retroperitoneal,Associated with focal sclerosis syndromes (retroperitoneal,mediastinal, retroorbital, and sclerosing cholangitis)mediastinal, retroorbital, and sclerosing cholangitis) TreatmentTreatment– Resection for compressive symptomsResection for compressive symptoms– Chemotherapy with Tamoxifen, Methotrexate, or steroids mayChemotherapy with Tamoxifen, Methotrexate, or steroids maybe effectivebe effective– Thyroid hormone only for symptoms of hypothyroidismThyroid hormone only for symptoms of hypothyroidism