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HYPERTHYROIDISM HYPERTHYROIDISM

Pait New Hyperthyroid

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  • HYPERTHYROIDISM

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  • IntroductionWhat is Hyperthyroidism?Hyperthyroidism refers to overactivity of the thyroid gland leading to excessive synthesis of thyroid hormones and accelerated metabolism in the peripheral tissues. The secretion of thyroid hormone is no longer under the regulatory control of the hypothalamic-pituitary center.

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  • EPIDEMIOLOGYAll thyroid diseases occur more frequently in women than in men.Autoimmune thyroid diseases have a peak incidence in people aged 20-40 years.Graves disease is the most common form of hyperthyroidism in the United States, causing approximately 60-80% of cases of thyrotoxicosis.

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  • PATHOPHYSIOLOGY

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  • Causes of HyperthyroidismGraves Disease Diffuse Toxic GoiterPlummers Disease Toxic MNGToxic phase of Sub Acute Thyroiditis - SATToxic Single Adenoma STAPituitary Tumours excess TSHMolar pregnancy & Choriocarcinoma ( HCG)Metastatic thyroid cancers (functioning)Struma Ovarii (Dermoid and Ovarian tumours)Thyrotoxicosis Factitia ; INF, Amiodarone, SSRIs

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  • Graves DiseaseThe most common cause of thyrotoxicosis (50-60%). Organ specific auto-immune diseaseThe most important autoantibody is Thyroid Stimulating Immunoglobulin (TSI) or TSATSI acts as proxy to TSH and stimulates T4 and T3Anti thyro peroxidase (anti-TPO) antibodies Anti thyro globulin (anti-TG) Anti Microsomal and other Autoimmune diseases - Pernicious Anemia, T1DM RA, Myasthenia Gravis, Vitiligo, Adrenal insufficiency.

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  • Toxic Multinodular Goiter (TMG)TMG is the next most common hyperthyroidism - 20% More common in elderly individuals long standing goiterLumpy bumpy thyroid glandMilder manifestations (apathetic hyperthyroidism)Mild elevation of FT4 and FT3Progresses slowly over timeClinically multiple firm nodules (called Plummers disease)Scintigraphy shows - hot and normal areas

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  • Toxic Multinodular Goiter (TMG)

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  • Sub Acute Thyroiditis (SAT)SAT is the next most common hyperthyroidism 15%T4 and T3 are extremely elevated in this conditionImmune destruction of thyroid due to viral infectionDestructive release of preformed thyroid hormoneThyroid gland is painful and tender on palpationNuclear Scintigraphy scan - no RIU in the glandTreatment is NSAIDs and Corticosteroids

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  • Toxic Single Adenoma (TSA)TSA is a single hyper functioning follicular thyroid adenoma.Benign monoclonal tumor that usually is larger than 2.5 cmIt is the cause in 5% of patients who are thyrotoxicNuclear Scintigraphy scan shows only a single hot noduleTSH is suppressed by excess of thyroxines So the rest of the thyroid gland is suppressed

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  • Age and SexAgeGraves disease 20 to 40Toxic MNG > 50 yrsToxic Single Adenoma 35 to 50Sub Acute Thyroiditis Any ageSex M : F ratio Graves Disease 1: 5 to 1:10Toxic MNG 1: 2 to 1: 4

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  • Common SymptomsNervousnessAnxietyIncreased perspirationHeat intoleranceTremorHyperactivityPalpitationsWeight loss despite increased appetiteReduction in menstrual flow or oligo-menorrhea

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  • Common SignsHyperactivity, Hyper kinesisSinus tachycardia or atrial arrhythmia, AF, CHFSystolic hypertension, wide pulse pressureWarm, moist, soft and smooth skin- warm handshakeExcessive perspiration, palmar erythema, OnycholysisLid lag and stare (sympathetic over activity)Fine tremor of out stretched hands format's signLarge muscle weakness, Diarrhea, Gynecomastia

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  • Specific to Graves DiseaseDiffuse painless and firm enlargement of thyroid glandThyroid bruit is audible with the bell of stethoscopeOphthalmopathy Eye manifestations 50% of casesSand in eyes, periorbital edema, conjunctival edema (chemosis), poor lid closure, extraocular muscle dysfunction, diplopia, pain on eye movements and proptosis.Dermoacropathy Skin/limb manifestations 20% of casesDeposition of glycosamino glycans in the dermis of the lower leg non pitting edema, associated with erythema and thickening of the skin, without pain or pruritus - called (pre tibial myxedema)

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  • History TakingChief complain and history of present illness:symptoms of sympathetic activation, such as anxiety, hyperactivity, and tremor, in older patients have more cardiovascular symptoms, including dyspnea and atrial fibrillation with unexplained weight loss.Common symptoms of thyrotoxicosis include the following:excessive sweating especially at night, in cold weatherAnxiety and nervousnessIncreased perspirationHeat intoleranceHyperactivityPalpitationsweight loss despite good appetiteextent and duration of symptoms,

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  • Past medical history, certain conditions (eg, atrial fibrillation, osteoporosis, or hypercalcemia) may suggest the possibility of thyrotoxicosis. Social medical history,Radiation exposure increases the risk of benign and malignant nodular thyroid diseases, especially with the higher radiation levels used in radiation therapy.list of medications and dietary supplements (including expectorants, amiodarone, iodinated contrast dyes, and health food supplements containing seaweed or thyroid gland extractscontain large amounts of iodine) Family history, For example, Graves disease is an autoimmune disease, and patients often have a family history or past medical history of autoimmune disease (eg, rheumatoid arthritis, vitiligo, pernicious anemia). strong family history of nontoxic goiter (Toxic multinodular goiters )Thyroid disease

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  • Physical examinationInspectionGeneral examinationPosition patient sitting on a chair and expose the neck.Inspect neck before & after swallowingInspect for any obvious goitres or swellings,scars,signs of thyrotoxicosis include the following:Warm, moist, smooth skinHand tremorTachycardiaLid lagStareperiorbital edema, diplopia, or proptosis (Graves disease )Muscle weaknessWeight loss despite increased appetite

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  • PalpationExamine with neck in relaxed positionPalpate from behind the patientUse the tips of 3 middle fingers below the chin and move down towards the thyroid (assess for enlargement/nodules)Check for : enlarged and slightly firm thyroid gland, toxic multinodular goiters generally occur when the thyroid gland is enlarged to at least 2 to 3 times the normal size. Also check for enlarged and pain at thyroid, subacute pain or granulomatous thyroiditis .Swallow test.Lymph node examination.Trachea deviation.Percussion Percuss the sternum for dullness of retrosternal extension of a goitre.Auscultation Listen on goitre for thyroid bruit can be heard by using the bell of the stethoscope.

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  • Where to look for Thyroid ?

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  • Clinical Anatomy of Thyroid

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  • Clinical Exam of Thyroid

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  • Clinical Exam of Thyroid

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  • Clinical Exam of Thyroid

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  • Thyromegaly

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  • Clinical Presentations

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  • MNG and GravesHuge Toxic MNGDiffuse Graves Thyroid

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  • Higher grades of GoiterToxic MNG(Diffuse) Graves

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  • Grade IV Toxic MNGHuge Toxic MNGHuge Toxic MNG

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  • ProptosisLid lagThyroid Ophthalmopathy

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  • Ophthalmopathy in GravesPeriorbital edema and chemosis

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  • Ophthalmopathy in GravesOccular muscle palsy

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  • Severe Exophthalmia

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  • Thyroid DermopathyPink and skin coloured papules, plaques on the shin

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  • Graves with AcropathyGraves GoiterAcropathy

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  • Clubbing andOsteoarthropathyThyroid Acropathy

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  • Onycholysis

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  • Non specific changesHyperglycemia, GlycosuriaOsteoporosis and hypercalcemia LDL and Total CholesterolsAtrial fibrillation, LVH, LV EFHyper dynamic circulatory stateHigh output heart failureH/o excess Iodine, amiodarone, contrast dyes

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  • LOW NORMAL HIGHTHYROID STIMULATING HORMONE - TSH LOW NORMAL HIGHFREE THYROXINE or FT4PRIMARYHYPERTHYROIDNine Square Approach

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  • LOW NORMAL HIGHTHYROID STIMULATING HORMONE - TSH LOW NORMAL HIGHFREE THYROXINE or FT4Nine Square ApproachSUB CLINICALHYPERTHYROID

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  • DiagnosisTypical clinical presentationMarkedly suppressed TSH (
  • Algorithm for HyperthyroidismMeasure TSH and FT4 TSH, FT4Measure FT3Primary (T4) ThyrotoxicosisHighPituitary AdenomaFNAC, N ScanNormal TSH, FT4 N TSH, FT4N TSH, FT4 NT3 ToxicosisSub-clinical HyperFeatures of GravesYesRx. GravesNoSingle Adenoma, MNGLow RAIU RAIUSub Acute Thyroiditis, I2, Thyroxine F/u in 6-12 wks

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  • www.drsarma.inAlgorithm for Thyroid NoduleThyroid NoduleLow TSHNormal TSHTC 99 Nuclear ScanFNAC or US guided biopsyHot NoduleCold NoduleRAI Ablation, Surgery or ATDNon diagnostic repeat FNACSurgery or CytologyCystBenignT4 suppressionSuspicious or follicular CaMalignantSurgery4%10%69%17%

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  • Treatment OptionsSymptom relief medicationsAnti Thyroid Drugs ATDMethimazole, CarbimazolePropylthiouracil (PTU)Radio Active Iodine treatment RAI Rx.Thyroidectomy Subtotal or TotalNSAIDs and Corticosteroids for SAT

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  • Symptom ReliefRehydration is the first step blockers to decrease the sympathetic excess Propranalol, Atenelol, MetoprololRate limiting CCBs if blockers contraindicatedTreatment of CHF, ArrhythmiasCalcium supplementationSSKI or Lugol solution for vascularity of the gland

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  • Anti Thyroid Drugs (ATD)

    Imp. considerationsMethimazole PropylthiouracilEfficacyVery potentPotentDuration of actionLong acting BID/ODShort acting QID/TIDIn pregnancyContraindicatedSafely can be givenMechanism of actionIodination, CouplingIodination, CouplingConversion of T4 to T3No actionInhibits conversionAdverse reactionsRashes, NeutropeniaRashes, NeutropeniaDosage20 to 40 mg/ OD PO100 to 150mg qid PO

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  • Dietary Advice Avoid Iodized salt, Sea foodsExcess amounts of iodide in someExpectorants, x-ray contrast dyes, Seaweed tablets, and health food supplementsThese should be avoided becauseThe iodide interferes with or complicates the management of both ATD and RAI Rx.

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  • Summary of HyperthyroidismTSH is markedly low, FT4 is elevated

    HyperthyroidismAge% EnlargedPainRAIUTreatmentGraves (TSI Abeye, dermo, bruit)20 - 4060%DiffuseNoneATD 18 mToxic MNG> 5020%LumpyPressureRAI, SurgerySingle Adenoma35 - 505%SingleNoneRAI, ATDS Acute ThyroiditisAny age15%NoneYesNSAID, Ster.

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