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T y r o i d
Dr. M a h a t m a SpPDSMF Penyakit Dalam FK UMS
SURAKARTAEAGLE FLIES ALONE, MHT
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The hypothalamic-hypophyseal-thyroid axis
Mind its feedback mechanism
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THIOCYANATES
(CYANOGENIC
GLYCOSIDES)
THIOGLYCOSIDES:
GOITRIN
ISOTHIOCYNATES
DISULFIDES
WATER BORNE
GOITROGENS
IODIDE(SEAWEEDS)
COAST GOITER
IODIDE
TRANSPORT
OXIDATIONORGANIC BINDING AND
COUPLING
PROTEOLYSISRELEASE AND
DEHALOGENATION
MITDIT
T4T3
MITDIT
I- I- (I )20
T4T3
I-
THYROGLOBULIN
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Schematic representation of timing of mature formative events in the human brain
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HORMON TIROID
HIPOFISIS
METABOLISMEPERTUMBUHAN
OTAK : - Kecerdasan
- Saraf
MASUKAN
IODIUM
PENGELUARAN
IODIUM
TSH
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PENDEKATANPENDERITA STRUMA
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Anamnesis Sejak kapan
Nyeri spontan/ tidak
Nyeri berpindah
Membesar cepat / lambat
Keluarga
Radioterapi Perubahan suara
Tanda toksik
Dx fisik Morfologi
Nodosa : multi/tunggal
Difusa
Nyeri
Keras, kenyal, kistik, berbenjol
Melekat dengan sekitar Pendorongan trakea
Pembertons sign
Bising (bruit)
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Struma difusaToksik: 1. Graves, 2. Hashimoto
Gejala dan tanda klinik toksik
Indeks New Castle
Indeks Wayne
Non toksik(hipotiroidisme atau eutiroidisme)
Struma endemik
Hashimoto
Dishormonogenesis
Iatrogenik
OAT
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Goitre associated with autoimmunity
Most with Graves disease
80% have a diffuse goitre
TSH receptor autoantibodies
15% with Hashimoto disease
Majority have atropic hypothyroidismAccumulation of lymphocytes in the thyroid
gland
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Multi nodular goitre
More prevalence in elderly, female,genetic background
Scintigram most varied, follicle withscattered necrotic area, connectivetissue strands, cyst and evencalcifications
Only few nodules have a true adenoma
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Tanda khas keganasan tiroid
Tumbuh dengan cepat dan sakit Riwayat keluarga kanker tiroid Riwayat radiasi leher masa anak-anak Suara serak Keras Melekat sekitar Limpadenopati Paralisis pita suara
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Pemeriksaan penunjang
Sidik tiroid (Scintigrafi)
USG (ultrasonografi) Biopsi jarum halus (FNA)
Petanda tumor (marker)
Biokimiawi
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Sidik tiroid
Yodium radioaktif
Menilai fungsi dan anatomi Nodul dingin :penangkapan yodium kurang dari sekitarnya
Nodul hangatpenangkapan yodium sama dengan sekitarnya
Nodul panaspenangkapan yodium lebih banyak dari sekitarnya
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Hot, warm and cold spots
Scintigraphy with radioIodine, shows the function
of the respective gland
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Ultrasonografi
Padat atau cair
Tidak bisa menilai fungsiKista tiroid
Adenoma tiroid / nodul padatTiroiditis
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Biopsi aspirasi jarum halusJarum suntik no 22 27
Aman, tidak nyeri,dilakukan di poliklinik
Kista : guna untuk diagnostiksekaligus terapeutik
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Biokimiawi
Kadar Free T4 plasma (peranantiroglobulin)
Kadar TSHs plasmaTiroglobulin plasma CalsitoninAntibodi mikrosomal (TPO) Antibodi tiroglobulin (TGO)
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Subtotal Thyroidectomy.
Isthmus and majority of the oppositelobe
Indikasi
small
non-aggressive thyroid cancers
substernal goiters
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Total Thyroidectomy.
Remove all of the thyroid gland.
Choice for all thyroid cancers
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IDD Global Magnitude (1996)
1. At least 1572 million were at risk of IDD
2. At least 655 million affected by goiter ( 27% SEA
15% Europe, 22% Western Pasific etc )
3. Est imated 43 m i l lion people affected by somedegree of IDD-related b rain damage
4. IDD is regarded as P.H. problem in 118 countries
5. IDD is the main cause of potential ly preventable
mental retardation .
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HORMON TIROID
HIPOFISIS
GONDOK METABOLISMEPERTUMBUHAN
OTAK : - Kecerdasan
- SarafKRETIN
HIPOTIROIDI
MASUKAN
IODIUM
PENGELUARAN
IODIUM
TSH
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Apakah GAKI itu ?
Gangguan Akibat Kekurangan Yodium /
Gondok endemik
Kekurangan yodium bukan hanya gondoksaja, namun ada efek yang lebih jauh
Gondok endemik : bukan hanya kekuranganyodium saja.
Misalnya ggn nutrisi, goitrogen, genetik
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Mengapa GAKI
dipermasalahkan ?
Gangguan yang ditimbulkannya sangat
banyak dan luas Jumlah penderita masih banyak
Penyakit ini sebenarnya
dapat dicegah
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Akibat GAKI
pada manusia ?
Yodium : bahan dasar mutlak hormon tiroksin
Tiroksin : pada masa pertumbuhan penting padaperkembangan fisik dan syaraf (otak) Penting saat masa fetus, masa kehamilan, masa
bayi, masa anak, masa remaja. Dampak kekurangan :
1. Kretin endemik2. Kretin neurologik
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Gambaran klinis kretinisme
A. Kretin endemik dan Kretin neurologik :Lahir di daerah kekurangan yodium, dngdua atau lebih dari :
1. Gangguan kecerdasan2. Tuli simetrik tipe sensorik3. Kelainan saraf (gangguan jalan,
gangguan bicara, refleks
patologik kelambatan jalan)B. Keduanya irreversibel, permanen, tidak
dapat diperbaiki dengan obat apapun.
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f DD
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Spectrum of IDD:
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SPEKTRUM GAKI
Fetus Anak dan remaja Abortus * Gondok Lahir mati * Hipotiroidisme juvenil Anomali kongenital * Ggn fungsi mental
Kematian perinatal * Ggn perkembangan fisik Kematian anak Kretin endemik Kretin miksedematosa Defek psikomotor
Neonatus Dewasa Gondok neonatus * Gondok dng akibatnya Hipotiroidisme neonatus * Hipotiroidisme
* Gangguan fungsi mental
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B h n b k
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Bahan bakuyodium manusia
Tanaman, air tanah yang mengandung yodium(kecuali terkikis)
Kebutuhan : 100-300 mikrogram sehari Harus cukup terus menerus sepanjang hidup
Makin berat kekurangannya, makin beratmanifestasi klinisnya
Tolok ukur :Kadar yodium urine
Kadar yodium dalam darahTangkapan radioaktif oleh leherJumlah klinik gondok di masyarakatJumlah kretin endemik di masyarakat
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KRITERIA ENDEMIK
ENDEMIK GRADE I (RINGAN)
UEI > 50 ug I/gr kreatinin
ENDEMIK GRADE II (SEDANG)UEI 25 - 50 ug I/gr kreatinin
ENDEMIK GRADE III (BERAT)UEI < 25 ug I/gr kreatinin
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SURVEY EPIDEMIOLOGI
KRITERIA PEREZ, 1960Grade O : tidak teraba
Grade I : teraba dan terlihat dengankepala ditengadahkan
I a : tidak teraba / jika terabatidak lebih besar dari tiroidnormal
I b : jelas teraba dan membesar,umumnya tidak terlihat walau
kepala tengadahGrade II : mudah dilihat dengan posisi
biasaGrade III : terlihat dari jarak tertentu
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Wanita hipotiroidisme hamil
bagaimana ?
Harus mendapat terapi substitusitiroksin
Dipantau dengan TSH bukan denganFT4
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Apakah ada hubungan antaraberatnya endemik dengan
beratnya gangguan ?
Ya Makin berat endemik, makin tinggi
prevalensi gondok, makin banyakkretinisme
Mengingat : kretinisme adalah
irreversibel Maka : harus garam beryodium Alasan : kebutuhan sehari-hari
konsumsinya tertentu
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Pemberian garam beryodium akanmerubah apa saja ?
Prevalensi gondok menurun Komplikasi metabolik membaik Hipotiroidisme normal kembali Gangguan pendengaran berkurang Tidak lahir bayi kretin lagi Putus sekolah menurun Refleks abnormal anak menghilang Rekaman otak membaik Angka kematian bayi menurun Perbaikan gangguan kecerdasan
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Berapa lama diberikan garam
beryodium ?
Terus menerus,sepanjang hidup
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ENDEMIC CRETINISM
1. Epidemiological aspect iod ine defic iency2. Clinical aspects neurolog ical and myxedematous3. Pathologic aspects intrauter ine and irreversible
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Table.2. Symptomatologyof endemiccretinism from Sengi and Papua NewGuinea (in%)
Sengi Papua
A. Hearing loss 93 93.6
Deaf-mutism 12 79.9
B. Mental retardation 95 >90
C. Neuromotor abnormalities 76 79.9
Impaired speech 37 13.7Specific gait 46 ?
Elevated reflexes 29 40
Babinsky sign 5
Squint 2 25.5
Later walker 22
D. Clinical hypothyroidism 29 0
Short stature 29 10-50E. Goiter 70 10-50
____________________________________________________
Djokomoeljanto 1974, Pharoah 1972.
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Endemic cretinism
a.Neurological endemic cretinism
Mental retardation , deaf-mutism
Hearing lo ss bi lateral percept ive
spast ic diplegia, squ int etc
b. Myxedematous endemic cretinism
Dwarf ism , mental retardat ion,
hypothyro id ism
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HypothyroidismClinical hypothyroidism
29% in cretins
17% in n on cretinous
Biochemical hypothyroidism
41% in cretins
27% in n on cretinous
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Spectrum of Iodine Deficiency Disorders (I)
Fetus Abortions, Stillbirths, Congenital
abnormalities, Increased perinatal mor
tality, Increased infant mortality,
Neurologicalcret in ism:mental def, deaf
mutism, spastic diplegia, squintMyxedematouscret in ism: dwarfism ,
mental deficiency, hypothyroidism
Psychomotor defects
Neonate Neonatal goiter, Neonatal hypothyroidism
Increased susceptibility to nuclear radiation
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One mililiter of iodinated oil injection reversed thefate of the whole family
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Diagnosis: fungsi, anatomi, etiologi
Sinonim :morbus Basedow , morbus Parry
Pengertian :
a. hipertiroidisme
b. tirotoksikosis
MORBUS GRAVES
Causes of Hyperthyroidism
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Main causesGraves disease and variants
toxic multinodular goitre
toxic nodule
Rarer causesJod-Basedowdisseminated thyroid autonomythyroiditis:
de Quervains
silentfactitioushypothalamicpituitary:
with or without apituitary tumour
post-partum:probably variant
of silentmolar pregnancyChoriocarninoma
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Organ-Spesific Autoimmune Disease
chronic hepatitis
Hashimotos disease
myxoedema
lymphocytic thyroidistis
Graves disease
pernicious anaemia
Addisons disease
hypoparathyroidism(some forms)
diabetes mellitus (some
forms)
vitiligo
premature ovarian failure
allergic alveolitis
Table of the organ-spesific autoimmune diseases. All of these disorderss
are characterised by the presence of circulating antibodies and lymphocytic
infiltration of the gland or tissue
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Hipertiroidisme
Tirotoksikosis
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A COOH
TSH
TSHR antibody
B COOH
TSH and TSHR-Ab induced activation. Although similar conformational changes are
assumed to apply in these cases, the extent of similarity with whole and cleaved
receptor remains to be established (Graves 2000)
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pathogenesis of Graves Opthalmopathy
Mechanism of IGO protrusion and oedema with fibrous tissues
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Gejalah serta tanda hipertiroidisme pada penyakit Graves
Sistem Gejala dan tanda Sistem Gejala dan tanda
Umur tak tahan hawa panas Susunan saraf pusat labil, intitabelHiperkinesis, bapai, berat badan psikosis, tremor, nervo-
Menurun, percepatan pertumbuhan sitasperiodic paralysis
Drug tolerance, youthfullness (*)
Gastrointestin hiperdefekasi, kelaparan, makan Cardiorespirasi dyspnoea, hipertensi
Banyak, haus, muntah aritmi, palpitasi, gagal
jantung
Muskular rasa lemah Darah / limfatik limfositosis, anemia
Genitourinaria oligomenoroe, amenoroe Splenomegali
Libido menurun pembesaran l.n.leher
Kulit rambut rontok, berkeringat Skelet osteoporosis
Kulit basah, onycholysis epifisis cepat menutup
Nyeri tulang
Spesifik untuk penyakit Graves, ditambah :
Optalmopati (50%) udema pretibial, kemosis, proptosis, diplopia, visus < ulkus kornea
Dermopati (0.5-4%)Akropaki ( 1 % )
Sumber McDougall.1991. Huruf miring jarang * hampir khusus bagi Oriental.
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Classical and the many faces of Graves disease
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Classical and the many faces of Graves disease
Asymmetrical opthalmopathy DD: retroblubar tumor
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Asymmetrical opthalmopathy, DD: retroblubar tumor
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Lid retractionExopthalmos
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Clinical signs Laboratory tests
diffuse goitre
eye signs thyroid-stimulating antibodies(TSAb)
localised myxoedema
acropachy thyroglobulin antibodies (TgAb)
(anti-Tg Ab)vitiligo
family history microsomal antibodies
(anti-M Ab)
Diagnosis of Graves Disease
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Diagnos is kl inis kecurigaanhipertiroidisme:
Indeks Wayne
Indeks New Castle
Diagnosis past idengan memeriksa :
kadar hormon beredar (T4, fT4, T3, fT3, TSH )
nilai tangkap yodium radioaktif leher ( )etiologi : antibodi, ultrasonografi, scintigrafi
I d k di tik kli ik WAYNE
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Indeks diagnostik klinik WAYNE
(eutiroidisme hipertiroidisme)
Gejala yang baru timbulatau bertambah berat
Skor Tanda tanda Skor
ada tidak ada tidak
Sesak bila bekerjaBerdebar debarKelelahanLebih suka udara panasLebih suka udara dinginTak dipengaruhi suhuKeringat berlebihanKeguguranNafsu makan bertambahNefasu makan kurangBerat badan naik
Berat badan turun
+1+2+2
+5-+3+2+3
+3
-5
-
-3-3
-
Kelenjar tiroid terabaBisig klenjar tiroidExophtha;mosKelopak mata tertinggalGerakan hiperkinetikTremor halus jariTangan yang panasTangan yang basahFibrilasi atriumNadi teratur- < 80 /menit
- 80-90 /menit- > 90 /menit
+3+2+2+1+4+1+2+1+4
0+3
-3-2
-2
-2-1
-3
0
Wayne EJ. Brit Med J 1:78, 1960. Hiper: >20,
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Indeks diagnostik klinik NEW CASTLE
Item Grade Score Item Grade Score
Age of onset 15-2425-3435-44
048
Age of onset 45-55> 55
1216
Psychologicalprecipitant
PresentAbsent
-50
Exopthalmos PresentAbsent
90
Frequent checking Present
Absent
-3
0
Lid retraction Present
Absent
2
0Severe anticipatory
anxietyPresentAbsent
-30
Hyperkinesia PresentAbsent
40
Increased appetite PresentAbsent
50
Fine finger tremor PresentAbsent
70
Goitre Present
Absent
3
0
Pulse rate > 90 / m 16
Thyroid bruit PresentAbsent
180
Pulse rate 80-90/m< 80/m
80
Euthyroid range11 to +23, doubtful range + 24 TO + 39, toxic range +40 to +80.
Gurney, Owen, Hall et al. Lancet ii: 1275, 1970.
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Membedakan morbus Graves dengan sebab lain
dengan menggunakan uji tangkap 1-131
Tinggi Rendah
Morbus Graves Masukan tiroksin berlebihan
Gondok Noduler toksik tunggal medikamentosa, faktisiaGondok Multinodulaer toksik health food, hamburger mix
Thyroiditis Silent, Postpartum,
De Quervain, Ca infiltratif
Sebab lain : mola, struma ovarii. TSH
Secreting tumor, metasis Ca follic
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Treatments available
For Graves disease
medical
surgical
radioiodine
Methods of treating Graves disease. Graves disease may be
treated with antithyroid drugs, by partial thyroidectomy or by
means ofradioiodine
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Indication for Medical
Treatment
patient preference
small goitre
mild disease
other disease
children
pregnancy
opthalmopathy
pre-operative
pre-radioiodine
thyrotoxic crisis
relapse after thyroidectomy
Antithyroid Drugs
carbimazole
methimazole
propylthiouracil (PTU)
potassium perchlorate
lithium
iodides
proppanolol
sodium ipodate
Indication for Medical Treatment in
Graves disease
Table of anthithyroid drugs.
Carbimazole is the drug of choice in Europe.Some clinicians add thyroxine to the
carbimazole in a blocking-replacement
regime, once the patient is clinically
euthyroid. Carbimazole is rapidly converted
to methimazole (10 mg carbimazole = 6 mg
methimazole)
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MMI, PTU
I- I+
transpor Oxidative
iodination
T1 T2
Coupling
T3 T4
release
I2
Li
Rantai peptid tiroglobulin
operasi SEL TIROID I131
T4
T3
PTUpropanlol
Na-ipodate
C.steroid
T3Sel somatik
Beta-blocker
Skema hormonogenesis dan efek pengobatan
M k i k j b t l ti id
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Mekanisme kerja obat golongan tionamide
INTRATIROIDAL
1. Menghambat yodinasi tiroglobulin dengan mencegah yodium
tiroksidasi dari residu tirosin
2. Menghambat reaksi coupling yodotirosin > yodotironin
3. Mengikat tiroglobulin dan merubah strukturnya (?)
4. Menghambat sintesis tiroglobulin (?)EXTRATIROIDAL
1. Menghambat konvesi T4 > T3 di perifer (hanya PTU)
2. Mempengaruhi sistem imun.
a. mengurangi respon limfosit in vitrob. mengurangi kadar titer autoantibodi tiroid
c. menormalkan aktifitas sel supresor
d. dapat langsung mengenai autoimunitas intratiroidal
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Guna beta blockers pada hipertiroidisme
Telah terbukti pada:pelengkap pengobatan OAT
pelengkap pengobatan radioiodine
pada krisis tiroid
selama dilakukan tes diagnostik
Kemungkinan penggunaan lain:
persiapan tiroidektomi
sebagai obat tunggal tirotoksikosis
sebagai obat tunggal pada kehamilan
pengobatan hiperkalsemia pada tirotoksikosis
pada hipertiroidi neonatal
- pengobatan /pencegahan thyrotoxic periodic paralysis
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Dosis awal dan maintenance OAT yang sering digunakan
Obat Dosis awal (mg) Maintenance (mg)
Neomercazol 30-60 5-20 (10)Methimazol 30-60 5-20 (10)
Propiltiourasil 200-600 50-200 (100)
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Metoda pemberianA. Decrementalcara tritasi, dosis makin menurun
sesuai dengan respons pasien
B. Block-suplemen.Obat diberi hingga ada supresi dan
Ablasi, kemudian diberi suplemen dosis fisiologis.
Cara ini tidak dianjurkan ada wanita hamil.
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Indications for surgical treatment
Abso lu te 1.suspicious of harboring malignancy
2.pregnant case uncontrolled with ATD/ allergy
3.wish to be pregnant soon after treatment
4.compressive symptoms, reject RAI exposure
Relative 1.poor compliance
2.rapid control is desired
3.patient with Graves opthalmopathy
4.larger/ goiter with low uptake
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Indication for, and Complications of, Radioiodine Treatmen
Indications
patient preference
patients over 45 years
treatment choice for recurrence afterthyroidectomy
severe uncontrolled disease
large goitre
poor patient cooperation
presence of other disease
Complications
permanent hypothyroidism
transient hypothyroidism
thyroiditis
sialadentis
thyrotoxic crisis
nodule formation
malignancy (not proven)
Indication for radioiodine therapy and associated complication. Radioiodine is the mosteffective treatment in cases of recurrence after surgery. It is suitable for older patients in severe disease,
and when patient cooperation is poor. Radioiodine is also useful in the presence of other disorders. The
only problematic complication is hypothyroidism, which is relatively easy to control.
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- high relapse rate
- longterm treatment with
tight control by doctor
- surgical expertise
necessary
- morbidity exist
- 40% hypothyroid within
10y
- slow clinical action
- 50% hypothyroids post-
radiation
Possibility to obtain
remission in the long run
without hypothyroidsm
- substantial number of
cases remit (euthyroid)
- relatively quick and
simple- relapse is relatively
scarce
- simple- rarely relapse (depends
on the dose)
Anti Thyroid Drugs
Thyroidectomy
Radio Active Iodine ( I131)
DisadvantagesAdvantagesMode of treatment
Advantages and disadvantages of treatment
modalities in Graves disease
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Graves dan kehamilan.
T4 ,T3 amat sedikit sedang TSAb dan PTU lewat plasenta
Hipotiroidisme fetus perlu dihindari
200 mg PTU masih tidak memberi dampak jelek
Deteksi hipotiroidisme fetus :
a. Nadi janin normal sekitar 120-150/m
b. >150 mungkin hiper dan < 120 mungkin hipotiroidi.
c. Dengan serial USG, melihat besar janind.Menentukan bone age
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Trias krisis tiroid hipertermi, kesadaran turun, gejala
toksikosis meningkatCheck dengan indeks klinik Burch-WartofskyTidak ada indikator kimiawi yang memadaiFaktor presipitas krisis tiroid
Medikal Surgikal
Infeksi Pembedahan tiroid
Emboli paru Operasi besar
Ketoasidosis diabetik Operasi minor
Kelebihan hormon tiroid Ekstraksi gigi
Terapi dengan 1- 131 MelahirkanIodium (obat. zat warna ) Dilatasi. kuretase
Strok
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Prinsip pengobatan krisis tiroid
1. Cairan dan oksigen
2. Menurunkan kadar hormon (sol Lugol, PTU)
3. Mengelola hipertermijangan asp ir in
4. Memberi corticosteroid
5. Inderal atau betablocker non spesifik lain
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Indeks klinik krisis tiroid BURCH WARTOFSKY
Thermoregulatory dysfunction
Temperature 99-99.9 F 5100-100.9 10
101-101.9 15
102-102.9 20103-103,9 25
140 30Central nervous system effects
Absent 0Mild (agitation) 10Moderate(delirium,psychosis,letargy 20Severe (seizure, coma) 30Gastrointestinal hepatic dysfunctionAbsent 0Moderate(diarrhea,vomit, abdpain) 10
Severe (unexplained jaundice) 20
Cardiovascular dysfunction
Tachycardia 99 109 5110 119 10120 - 129 15130 - 139 20
140 25Congestive heart failureAbsent 0
Mild (pedal edema) 5Moderate ( bibasilar rales) 10Severe (pulmonary edema) 15Atrial fibrillation Absent 0
Present 10Precipitant historyNegative 0Positive 10
For severe thyrotoxicosis award the highest score, with intercurrent illness choose which favor the
diagnosis of thyroid storm . Score 45 highly suggestive, 25-44 suggestive impendingand below 25 is
unlikely to respresent thyroid storm. Note: hyperthermia, consciousness, toxic signs
Burch HB, Wartofsky L., Endocrinol Metab Clin North Am, 22 : 263, 1993
Hypothyroidism
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yp y
1. decrease function of thyroid gland2. the effect of thyroid hormone in tissues
a. Central (secondary or tertiary)
b. Primary (thyroid gland itself)Primary: (a) postoperative, (b) postradiation (c)
autoimmune, (d) postpartum thyroiditis (e)
de Quervains, (f) dyshormonogenesis (g)carcinoma thyroid, (h) transient and (i)pharmacologic drugs.
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Hypothyroid cases as seen in IodineDeficiency Areas some belongs toendemic cretinism
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Characteristic feature of a hypothyroid woman
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Billewicz index (1969) for hypothyroidism
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Clinical index for hypothyroidism
Yes(score) No (score)
Symptoms Sweat scarcelyDry skin
Cold ntolerance
Weight gain
ConstipationHusky voice
Tingling sensation
Hearing loss
+6
+3
+4
+1
+2+4
+5
+2
-2
-6
-5
-1
-1-6
-1
-1
Physical signs Slow movementCoarse skin
Cold skin
Periorbital oedema
Heart rate < 60 / minutes
Slow Achilles reflex
+11
+7
+3
+4
+4
+15
-3
-7
-2
-6
-4
-6
Hypotiroid> 25, Not hypothyroid < - 30, Equivocal between
29 and +24
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