gds137 slide hyperthyroidism

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    HYPERTHYROIDISM

    GRAVES DISEASE

    Dr HAKIMI SpAK

    Dr MELDA DELIANA SpAK

    Dr SISKA MAYASARI LUBIS S A

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    Back round Hyperthyroidism : overactivity of the

    thyroid gland leading to excessive

    accelerated metabolism in the peripheraltissues

    Thyrotoxicosis : the clinical effects of anunbound thyroid hormone, whether orno e yro g an s e pr mary

    source

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    Causes of thyrotoxicosis in childhood Hyperthyroidism :

    Diffuse toxic goiter (Graves' disease)

    Nodular toxic goiter (Plummer disease)

    TSH-induced hyperthyroidism:

    TSH producing pituitary tumor

    e ec ve p u ary res s ance o yro ormone

    Thyrotoxicosis without hyperthyroidism:

    Subacute thyroiditis

    Thyroid hormone ingestion

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    Patho enesis Genetic clonal lack of suppressor T cells T helper cells

    multiply B cells produce TSH receptor antibodies:

    recep or an o es n o recep ors yrogland) T3 and T4 (Clinical presentation of hyperthyroidism) (Pituitary gland) TSH

    ? TSH receptor antibodies bind to TSH receptors in retro-orbital connective tissue T cells produce inflammatorycytokines Glycosaminoglycans / Eye muscle antibodies?

    Ophthalmopathy

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    Fre uenc In the US : because Graves' disease accounts for more than

    95% of childhood cases of hyperthyroidism, the frequency of

    Graves' disease approximates the frequency of all cases of

    Prevalence : 0,02% in childhood, accounting for fewer than 5%of the total cases of Graves' disease

    Associated with MHC locus (HLA-B8, HLA-DR-3, and possiblyHLA-DQA1*0501) and polymorphisms of cytotoxic lymphocyte

    - ,expressed on the surface of activated lymphocytes and inhibits

    T-lymphocyte activation

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    Mortalit / Morbidit Excellent prognosis

    Neonatal Graves' disease is self-limited, the prognosis is considerably.

    prematurity, airway obstruction and heart failure. The mortality rate :as high as 16%

    Female to male ratio = 6 to 8 : 1

    Prepubertal children tend to have more severe disease, require longermedical therapy and achieve a lower rate of remission compared with

    pubertal children. This appears to be particularly true in children whopresent at < 5 years of age

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    A e Incidence increases throughout childhood,

    with a peak incidence in children aged 10 -15 years

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    Predis osin factors Genetic susceptibility (including HLA alleles)

    Stress

    Smoking (especially associated with ophthalmopathy) Female sex sex steroid

    Postpartum period

    Iodine (including amiodarone)

    Lithium

    Rare factors : Interferon- thera

    Highly active antiretroviral therapy

    (HAART) for HIV infection

    Campath 1-H monoclonal antibody (for multiple sclerosis)

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    Clinical features* * Hyperthyroidism :

    Heat intolerance, sweating, palpitations, pruritus,,weight loss (with hyperphagia), weight gain (rarely),hyperdefecation, tremulousness and tremor,

    , , , ,thirst, anxiety, emotional lability, insomnia,restlessness, inability to concentrate,

    ,dysfunction/gynecomastia, dyspepsia, nausea,vomiting (rare)

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    Clinical features

    y

    Ophthalmopathy :Eye irritation, dryness, excessive tearing,

    visual blurring, diplopia, retro-orbital

    discomfort, pain on eye movement, visualloss

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    Clinical features*Signs*

    Hyperthyroidism :

    Warm, smooth, moist skin, onycholisis(loosening of the nail bed, Plummers nails),palmar erythema, thinning of the hair, stare,

    , , ,tachycardia, atrial fibrilation, widened pulsepressure, hyperdynamic circulation, tremor

    ngers , yperact ve re exes, prox ma

    myopathy

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    Clinical features

    p a mopa y :

    Periorbital edema, conjunctival erythema,

    , ,ophthalmoplegia, loss of colour vision (optic

    ,

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    Laboratory evaluation' , ,

    T3RU and low or undetectable levels of TSH

    If the diagnosis of Graves disease is unclear, TSH receptor Abs

    Tg and / or TPO Abs are often present but are less sensitive andspecific than TSH receptor Abs in the diagnosis of Graves disease in

    Radioactive iodine uptake and scan are necessary to confirm thediagnosis of Graves disease only in atypical cases (for example, ifmeasuremen o recep or s s nega ve an e yro ox cphase of either CLT or subacute thyroiditis or functioning thyroid

    nodule is suspected). In Graves disease, the uptake is elevated anddiffuse

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    Laborator evaluation Obtaining a CBC before the initiation of

    antithyroid medications may be valuable forseparating patients with underlying

    Leukopenia or thrombocytopenia from

    pa en s w o eve op rug ox c y

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    Thera The choice of which of the three therapeutic options

    (medical th/, radioactive iodine, or surgery) to use

    should be individualized and discussed with thepatient and his/her family

    Medical thera with one of the thiouracil derivates

    (PTU or MMI) is the initial choice of mostpediatricians, although radioiodine is gainingincreasing acceptance, particularly in non-complianta o escen s, n c ren w o are men a y re ar e ,and in those about to leave home

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    Thera PTU, MMI, and carbimazole (converted to MMI)

    exert their antithyroid effect by inhibiting the

    iodotyrosine residues on the Tg molecule to

    generate T3 and T4

    PTU but not MMI, inhibits the conversion of T4 to the

    more ac ve somer , a po en a a van age e

    thyrotoxicosis is severe

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    Thera The usual initial dosage of MMI is 0.5 mg/kg/day

    given once or twice daily and that of PTU is 5.

    given in a dose of 10-20 mg twice or thrice dailydepending on the concentration of free T4

    In severe cases, a beta-adrenergic blocker(propranolol, 0.5-2.0 mg/kg/day given every 8 h) cane a e o con ro e overac v y un a

    euthyroid state is obtained

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    Thera The serum concentrations of T4 and T3

    normalize in 3-6 weeks, but TSHconcen ra on may no re urn o norma unseveral months later

    Approximately 50% of children will go intolon -term remission within 4 ears, withcontinuing remission rate of 25% every 2

    years for up to 6 years of treatment

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    Thera Lower initial degree of hyperthyroxinemia

    (T4 < 20 ug/dL or 257.4 nmol/L, T3/T4 ratio< 20), BMI, and older age have been

    associated with an increased likelihood of

    permanen rem ss on

    ers stance o receptor s n cates a

    high likelihood of relaps

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    Thera Radioactive iodine therapy should be used

    with caution in children < 10 years of ageand particularly in those 5 years of age or

    less because of the increased susceptibility

    o e yro g an n e young o eproliferative effects of ionizing radiation

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    Although a dose of 50-200 uCi of 131 I /es ma e gram o yro ssue as een use ,the higher dosage is recommended, particularly

    the thyroid gland and thereby reduce the risk offuture neoplasia

    The formula used is: (estimated thyroid weight in- -

    uptake)

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    Thera One usually sees a therapeutic effect within

    6 weeks to 3 months

    If significant ophthalmopathy is present, RAI

    therapy should be used with caution, andtreatment with corticosteroid for 6-8 weeks

    a ter a m n strat on may e w se

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    Surgery is appropriate for patients who have failedme ca management, t ose w o ave mar e yenlarged thyroid, those whom refuse RAI, and for

    the rare patient with significant eye disease in whomRAI is contraindicated

    .

    (Lugols solution, 5-10 drops twice a day, orpotassium iodide, 2-10 drops daily) are added for 7-

    vascularity of the gland

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