gds137 slide hyperthyroidism
TRANSCRIPT
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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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