DIAN P2 Endokrin

8/20/2019 DIAN P2 Endokrin

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ANATOMI


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GLANDULA TIROID

Terdapat dibagian bawah leherikut bergerak ketika menelanBentuk seperti kupu-kupu, terdiri atas 2 lobusyang dihubungkan oleh isthmus yang

menyilang digaris tengah setinggi cincincartilage tracea 2,3,4. Lebih kurang 40 akanterdapat lobus piramidalis, muncul dari bagianpermukaan atas isthmus, yang lebih sering daribagian kiri garis tengah.Bagian atas dari lobus piramidalis dapat berupa!bromuscular : Levator Glandula tiroid yangmenu"u ke os hyoid. #ada kasus dimana lobuspiramidalis tidak ada, pita !bromuscular initerdapat di bagian atas isthmus.


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• $landula thyroid merupakan organ yangsangat %ascular

• &ibungkus oleh ' Fascia Pretrachealisyang melekatkan organ ini pada laryn( dantrachea

• )ascia ini ikut membentuk dan membatasipembagian lobus-lobusnya.

• *etiap lobus berbentuk buah ad%okatdengan puncaknya mengarah ke atassampai ke linea oblig cartilagenis trachea.Basisnya terdapat di bawah, setinggi cincintrachea ke 4 + .


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Alat-alat disekitarnya

Anterolateral :o m. sternoth roido venter su!erior m.

omoh ooideuso m. sternoh oideus

o te!i anterior m.sternocleidomastoideus


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Posterolateral :

o A.carotis commu

niso ". #u$ularis internao N. va$us


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Medial :o Lar n%&tracheao m. constrictor

!har n$is in'erioro Oeso!ha$uso antara oeso!ha$us

dan tracheaterda!atN.Lar n$eusrecurrens Posterior :

o Glandula!arath roidsu!erior dananterior

o Anastomose antara

A. th roideasu!erior dan


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#erdarahan

. . Thyroidea superior• cabang . carotis e(terna

2. . Thyroidea in/erior• cabang truncus thyrocer%icalis

• ber"alan naik di belakang kelen"ar sampai setinggicartilage cricoidea, kemudian membelok kemedial bawah mencapai batas posterior kelen"ar.

• . laryngicus recurrens melintasi bagian depanatau bagian belakang arteri ini.

3. . Thyroidea 1ma• ika ada merupakan cabang . Brachiocephalicaatau arcus aorta

• Ber"alan naik di depan trachea menu"u isthmus

(erasaldari :


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Pem)uluh )ali*

. . Thyroidea superior ' mencurahkanisinya ke %ena "ugularis interna

2. . thyroidea media ' bermuara ke %ena

"ugularis interna3. . Thyroidea in/erior ' menampung darahdari isthmus dan polus bawah kelen"ar,

ena ini dari kedua sisi akan

beranastomose sewaktu ber"alan turun kebawah di depan trachea dan bermuara ke. brachiocephalica


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Pem)uluhlim'eLim/e akan dialirkan ke lateral, ke nLl.

er%icalis pro/unda. Beberapa pembuluhmenu"u nLl. #aratrachealis

Pem)uluhsara' &isara! oleh serabut post ganglionik simpatisyang berasal dari ganglion cer%icalis superior,media, dan in/erior. *erabut-serabut ini

mengikuti pinggir arteri, didistribusikanterutama pada pembuluh darah, hanya sedikitke sel /olikel. Beberapa serabut . %agus "ugamengikuti arteri ke kelen"ar ini.


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+,L,N-AR PARAT /ROID

(entu* :o #ipih, o%al, ukuran 3 + 5 mm ( 2 + mm

( 0, + 2 mm. 6arna kuning kemerahan


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Leta* :o permukaan posterior lobus lateralis glandula thyroid,

biasanya ber"umlah 4 buah.

o 7elen"ar parathyroid superior ' terletak di belakang parssuperior glandula thyroid

o 7elen"ar parathyroid in/erior ' terletak di dekat tempatmasuknya . Thyroidea in/erior, posisi dan "umlahnyaber%ariasi. 7elen"ar parathyroid dapat tertanam padakelen"ar thyroid


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Perdarahan :

abang-cabang . Thyroidea terutamadari . Thyroidea in/erior, "uga darianastomose cabang yang mendarahi m.pre%ertebralis, pharyn( dan oesophagus.

Persara'an :o Berasal dari sistim simpatis yang

menyertai arteri, terbanyak berasal dariganglion 8

o #ars in/erior berhubungan erat dengan .recurrens laryngeal


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FI0IOLOGI


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)isiologi 7elen"ar Tiroid

+ontrol Terhada! +elen#ar Tiroid

9ipotalamus

T:9

#ituitari anterior

T*9

Tiroid

T3 T4

1

;

$ondok berkembang

Tiroid

Tdk memenuhipenyedianan tiroksin

T*9

9iperplasi <hipertro!


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• Fun$si Tiroid&=emacu metabolismeBerkaitan dengan suhu lingkungan- 7alorigenesis*tres T9 sumber 7alorigenesis =etabolisme Lemak < karbohidrat

-9ipertiroidisme- suhu tubuh tinggi, banyak berkeringat, penurunan

bobot tubuh, iritabilitas, dan tekanan darah tinggi

- 9ipotiroidisme- bobot tubuh meningkat, lamban dan tidak adatoleransi terhadap udara dingin pada waktudewasa.

-#erkembangan


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#aratiroid

• Bentuk pipih, o%al > seperi buah pear, letakpermukaan posterior lobus lateralis tiroid

• #aratiroid, kalsitonin dan dihidroksikolekalsi/erolmerupakan hormon utama berkaitan denganmetabolisme seperti '

» 7alsium» #iro/os/at» =agnesium» #engaturan metabolisme tulang» &an komponen organik


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Meta)olisme +alsium

• ?? ion a@@ berupa kristal mineral tulang• 7alsium memiliki 3 /ungsi dalam sel

- 7omponen kunci dalam membran sel,permeabilitas serta si/at listriknya- *ebagai /aktor perangkai selama ekksitasi dankontraksi semua "enis otot.- *tadium awal untuk merangkai tanggapan selsasaran terhadap hormon.

7alsium diserap diusus dibantu oleh ,2 -&ihidroksikolekalsi/erol metabolit it &3 digin"alyang dikontrol oleh paratiroid.


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Biosintesis #T9• #T9 sapi, manusia dan babi polipeptida linier

dengan B= ? 00 dan 54 residu aa• #T9 disintesis sbg prapro-#T9 A residu aa• #rapro-#T9 masuk :C 2 residu aa

dikeluarkan dr terminal #ro-#T9 A?0 residu aa

• &i aparatus golgi 8 residu aa dari terminal dikeluarkan lagi #T9 A 54 residu aa• 7adar normal #T9 dlm plasma D 0- pg>ml• 6aktu paruh kurang dari 20 mnt

• #olipeptida disekresikan akan diuraikan oleh sel-sel kuEer di hati m"d 2 polipeptida

• )ragmen terminal yang tdk akti/ B= F000 dan/ragmen terminal yang akti/ dgn B= 2 00


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9ipoparatiroidisme

• #engambilan tiroid kadar kalsium turun• 9ipokalsemia hilang kemampuan

mobilisasi kalsium oleh tulang, gin"al dan usus

• 1on kalsiun turun pada ekstrasel hiperiritabilitasneuromuskuler tetani, ke"ang otot,kematian

• Transport kalsium usus turun ,2 -dihidroksikolekalsi/erol tidak terbentuk krn #T9tidak ada


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9iperparatiroidisme

• =eningkatkan resropsi dan mobilisasikalsium, shg kalsium plasma meningkatdan /os/at plasma menurun

• #T9 meningkatkan ekskresi /os/at dalamurin A reabsropsi /os/at ditubulusproksimal menurun dan reabsropsi ionkalsium meningkat ditubulus distal.

• #eningkatan reabsropsi kalsium oleh usus• =enyebabkan kelumpuhan pada tulang

karena tingginya deposisi kalsiumsehingga menghilangkan mineral


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7alsitonin

:antai polipeptida td 32 residu aa ,B= 3000

&ilepaskan "ika kalsium serum tinggi Beker"a di tulang dan gin"al

#enghambat reabsropsi =encegah pelunakan tulang


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)ungsi ,2 -&ihidroksikolekalsi/erol

• Bereaksi seirama dgn #T9, mengontrolmineralisasi tulang

• =eningkatkan reabsropsi kalsium dan /os/at olehtubuli gin"al

• =eningkatkan transport kalsium dan /os/at yangmelintasi sel-sel mukosa usus.


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(IO+IMIA


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Thyroid :egulation

Somatostatin,Glucocorticoid

Do!amine


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Thyroid hormone synthesis 1odide pump

• :ate +limiting step in thyroid hormone synthesiswhich needs energy• )ollicles ha%e in their basement membrane an

iodide trapping mechanism which pumps dietary 1 - into the cell

• ormal thyroid' serum iodine is 30-40' – 1odide uptake enhancers'• T*9• 1odine de!ciency• T*9 receptors antibody

– 1odide uptake inhibitors• 1odide ion• &rugs

– &igo(in – Thiocynate – perchlorate


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Thyroid hormone synthesis

2 1odide o(idation to iodine andGrgani!cation

• 1nside the cells, iodide is o(idiHed by

pero(idase system to more reacti%eiodine• 1odine immediately reacts with tyrosine

residue on a thyroid glycoprotein calledIthyroglobulinJ to /orm '

– T K mono-iodotyrosyl thyroglobulin – T2K di-iodotyrosyl thyroglobulin

• Both processes are catalyHed by thyroidpero(idase enHyme


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Thyroid hormone synthesis

3 oupling• T < T2 couple together to /orm T3


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CEects o/ thyroid hormones

• )etal brain < skeletal maturation• 1ncrease in basal metabolic rate• 1notropic < chronotropic eEects on heart• 1ncreases sensiti%ity to catecholamines• *timulates gut motility• 1ncrease bone turno%er• 1ncrease in serum glucose, decrease in

serum cholesterol• on%ersion o/ carotene to %itamin • #lay role in thermal regulation


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Increase BMR ( Basal Metabolic Rate )• ↑cellular metabolic activity by :

• ↑ si e, total membrane sur!ace " number o! mitoc#ondria

• ↑ $%& !ormation

• ↑ active trans'ort o! ions ( a , * )

&romote +ro t# " develo'ment o! t#e brain durin+!etal li!e and !or t#e !irst !e years o! 'ostnatal li!e

-arbo#ydrate metabolism


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arbo#ydrate metabolism

• en#anced +lycolysis, +luconeo+enesis,

• GI absor'tion " insulin secretion

.at metabolism

• en#anced !at metabolism

• $ccelerates t#e o/idation o! !ree !atty acids by t#e cells

• 'lasma c#olesterol, '#os'#oli'ids " tri+lycerides

Body ei+#t

↑ t#e a''etite, !ood inta0e, GI motility but 1 t#e body ei+#t


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• Cardiovascular system

• vasodilatation

• ↑ blood lo!

• ↑ cardiac output

• ↑ "eart rate

• #espiratory

↑ t"e rate and dept" respiration

• CNS

e$treme nervous % psyc"oneurotic tendency

• &uscle

ma'e t"e muscles react !it" vi or -----muscle tremor ( * -*, times/sec )

• Sleep e$treme ati ue but is di icult to sleep


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+,LAINAN TIROID


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auses , linical )eatures< onse uences o/

9ypothyroidism

ongenital 9ypothyroidism

c uired 9ypothyroidism


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Ctiology

• ongenital• c uired

– #rimary – *econdary – Tertiary


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ongenital 9ypothyroidism• Gccurs in about >4000 li%e birth

• Thyro(in is important /or * de%elopmentand postnatal growth

• The most /re uent cause is congenitalabsence o/ the thyroid gland Aathyrosis

• #resentations may include cyanosis,prolonged hyperbilirubinemia, poor /eeding,hoarse cry, umbilical hernia, respiratory

distress, macroglossia, large /ontanelle, anddelayed skeletal maturation• :arely, neonatal hypothyroidism is transient


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ongenital 9ypothyroidismCtiology

Thyroid dysgenesis 1diopathic'• ommonest cause in ? o/ cases

– thyreosis A40

– 9ypoplasia A40 – Cctopia Abase o/ tongue, midline A20

2 Thyroid dyshormonogenesis A .: A 0

3 9ypothalamic-pituitary hypothyroidism – nencephaly, holoprosencephaly, *.G.& – idiopathic


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ongenital


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ongenital9ypothyroidism

4 Transient hypothyroidism – =aternal T: B – =aternal ingestion o/ goitrogen &rugs

8 1odine e(cessF 1odine de!ciency

i h id & d


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nti-thyroid &rugs and/etus

• Thionamides – #TM < =NT

• 1odide• Lithium• miodarone• :adioiodine

– /ter 0- 2 wk gestation candamage

/etal thyroid gland

#resentations o/ congenital


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#resentations o/ congenitalhypothyroidism

• =acroglosia• #rolonged hyperbilirubinemia• #oor /eeding• 9oarse cry• &ecreased acti%ity• onstipation• Mmbilical hernia

• &ry yellow skin• large /ontanelle• &elayed skeletal maturation

t l i g / g it l


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eonatal screening /or congenitalhypothyroidism

• :outine in most countries worldwide

• )ilter paper blood spot measuring T*9• 6hy OO

• linical mani/estations at birth, usually are subtle ore%en absent Apassi%e transplacental maternalthyro(in

• t birth, surge o/ T*9 Astress o/ deli%ery up to 30 -40Pu>ml

• Carly detection will pre%ent mental retardation ordecreasing 1Q o/ aEected neonates

• Thyro(in is important /or * de%elopment /rom birthtill 3 years o/ li/e

• *creening program will miss 2ry> tertiary cases• The program is hampered by a high rate o/ /alse

positi%e results


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• =ore common than hyperthyroidism• ?? is primary AR due to T*9 de!ciency• 9ashimoto ’ s

– most common thyroid problem A4 o/

population – most common cause in iodine-replete

areas – chronic lymphocytic thyroiditis – ssociated with T#G antibodies A?0 , less

commonly Tg antibodies• 1atrogenic 9ypothyroidism /rom radioacti%e

iodine therapy


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• *ubacute thyroiditis – #ain/ul, o/ten radiates to the ear – c>o malaise, pharyngitis, /atigue, /e%er, neck pain>swelling – iral etiology AM:1> pharyngitis – sel/-limited. an t( inSammation w> * , * 1& s or

steroids

• *uppurati%e> cute 1n/ectious thyroiditis – 1n/ections o/ the thyroid are rare

• normally protected /rom in/ection by its thick capsule

– Bacterial UU /ungal, mycobacterial or parasitic – #t s are acutely ill w> a pain/ul thyroid gland

• assoc w> /e%er>chills, anterior neck pain>swelling,dysphagia and dysphonia


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• *ymptoms – $eneral *lowing &own – Lethargy>somnolence – &epression – =odest 6eight $ain – old 1ntolerance – 9oarseness – &ry skin – onstipation A 2 peristaltic acti%ity – $eneral ches>#ains

• rthralgias or myalgias

Aworsened by cold temps – Brittle 9air – =enstrual irregularities

• C(cessi%e bleeding• )ailure o/ o%ulation

– 2 Libido

i d 9 h idi


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C(amination• &ry, pale, course skin with yellowish tinge• #eriorbital edema• #uEy /ace and e(tremities• *inus Bradycardia•

&iastolic 9T• 2 Body temperature• &elayed rela(ation o/ reSe(es• =egacolon A 2 peristaltic acti%ity• #ericardial> pleural eEusions• ongesti%e heart /ailure• on-pitting edema• 9oarse %oice• =yopathy


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$oiter

• swollen thyroid

gland• ssessmentD

– how big, howuickly has it

de%eloped, is itsmooth or nodular,is it pain/ul, anyassociated lymphnodes, any sudden

changes, is it bigenough to causelocal symptoms Ae.g.breathing

problems


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Myxedema

Hypothyroidism --- loss of scalp hair


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Hypothyroidism --- loss of scalp hair

$ -olor $tlas o! 2ndocrinolo+y '34

9 h idi i h h


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9ypothyroidism with shortstature

&i i


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&iagnosis ongenital hypothyroidism

• Thyroid hormone le%el• T*9• Thyroid scan


• T*9• /T4• Thyroid antibodies• Thyroid ultrasound• T0 ' low in secondary hypothyroidism

high in primary hypothyroidism• TR test: to diEerentiate between

secondary < Tertiary hypothyroidism


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auses , linical )eatures< onse uences o/

9yperthyroidism


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9yperthyroidism AThyroto(icosis

&e!nition• C(cessi%e secretion o/ T3 < T4• Eects metabolic processes in all

body organs• 9yperthyroidism is 4- 0 times more

pre%alent in women

• =ost common endocrine diseasesecond only to diabetes as the mostoccurring endocrine disease


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Thyroto(icosisauses

Transient . eonatal thyroto(icosis

2.1n/ectious ' cute < subacute thyroiditis3.&rug + induced' miodarone, inter/eron


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Thyroto(icosis

auses

#ersistent.$ra%es disease

2.To(ic multinodular goiter3.To(ic solitary adenoma

4. entral Apituitary origin

eonatal Thyroto(icosis


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eonatal Thyroto(icosis• Gnly occur with o/ thyroto(ic mothers

• *e%erity consistent in /uture pregnancies• 20 mortality i/ untreated• C%ol%es rapidly, e%ident by day F o/ li/e,

unless T: B blocking antibody is present

• ssociate with cranial synostosis andlearning diVculties, i/ not treated

• )etal thyroto(icosis in rats leads toabnormal * myelination

• #arents should be aware o/ potentiallearning problems Aearly school yearsshould be monitored

eonatal #y'ert#yroidism born to mot#er


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eonatal #y ert#yroidism born to mot#erit# Graves5 disease


$ra%e s disease


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$ra%e s disease#athogenesis• T-cell dependent autoimmune disease• 80 ha%e 9L association with ,

B5, &:3,&:4,&:

• utoimmune disorder that results inproduction o/ antibodies directedagainst thyroid antigens' – T*9 receptors – Thyroglobulin – Thyroid pero(idase

* b t Th iditi


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*ubacute Thyroiditis• linical course lasts weeks to months• cute phase A2-8> 2 with clinical and

biochemical hyperthyroidism• :eco%ery phase Aweeks-months transient

hypothyroidism then euthyroidism• linically, history o/ sore throat, /e%er,

tender goiter, cer%ical lymphadenopathy• 9igh C*:, negati%e antibodies and absent

radioacti%e 1 3 uptake

9yperthyroidism


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9yperthyroidism

• =ay result in signi!cant

morbidity, mortality < e%en death• *ymptoms – ittery, shaky, ner%ous – &iVculty concentrating

– Cmotional lability – 1nsomnia – :apid 9:, palpitations, )eeling

9ot

– 6eight Loss – &iarrhea – )atigue – =enses ' lighter Sow, shorter

duration


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9yperthyroidism

• C(am – Cye !ndings A20 – $oiter – Thyroid bruit or thrill – Tachycardia' *inus Tachycardia,

trial )ibrillation – )low murmur – *ystolic hypertension – 9yperreSe(ia – Tremors

– #ro(imal muscle weakness – lubbing – Gnycholysis AR

• separation o/ nail /rom thenailbed

– &ermopathy A

Th t (i i


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Thyroto(icosis

• 9eart' 1ncreased heart rate, contractilityand cardiac output• *keletal muscles' #ro(imal myopathy, easy

/atigability and muscle atrophy

• $onads' 1rregular menstrual cycles,impotence• Li%er' Low cholesterol L&L <

apolipoprotein

• Bone' 1ncreased bone turno%er,osteoporosis < increased risk o/ /racture

$ % W h h l h


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$ra%eWs ophthalmopathy• The pathogenesis o/ in!ltrati%e

ophthalmopathy is poorly understood• 1t may occur be/ore the onset o/hyperthyroidism or as late as to 20 years

• The clinical course o/ ophthalmopathy isindependent o/ the clinical course o/hyperthyroidism

• 1n!ltrati%e ophthalmopathy may result /romimmunoglobulins directed to speci!cantigens in the e(traocular muscles <

orbital !broblasts• The antibodies are distinct /rom thoseinitiating $ra%esW-type hyperthyroidism


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9 th id C &i


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9yperthyroid Cye &isease

• 9yperthyroidism Aany cause

– Lid lag, lid retraction and stare – &ue to increased adrenergic

tone stimulating the le%atorpalpebral muscles.

• True $ra%es’

Gphthalmopathy – #roptosis – &iplopia – 1nSammatory changes

• on"uncti%al in"ection

• #eriorbital edema• hemosis – &ue to thyroid auto b s that

cross-react w> g s in!broblasts, adipo-cytes, @myocytes behind the eyes.

Grave5s o'#t#almo'at#y


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y

9 th id C &i


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9yperthyroid Cye &isease

$ra%es &ermopathy


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$ra%es &ermopathy

Thyroid &ermopathy – Thickening and redness

o/ the dermis• &ue to lymphocytic

in!ltration

h d h

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Thyroid cropachy

Th roid acro!ach . This is most mar*ed in the inde% 3n$ers andthum)s


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%remor o! t#e #and



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&i i


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&iagnosis• T*9 le%el usually R 0.0 µ u > ml• ? o/ cases, high )T4 < )T3• 1n high )T3 with normal T4 AT3

Thyroto(icosis• Thyroid receptor AT: B are usuallyele%ated at diagnosis

• ntibodies against thyroglobulin,pero(idase or both are present inthe ma"ority o/ patients


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Thyroto(icosis- Treatment


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Thyroto(icosis Treatment

• Three modalities /or more than last 0 years• :adioacti%e iodine,antithyroid drugs


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eonatal Thyroto(icosis Treatment

Lugol s iodine• drop tid /or -2 > F• &ramatic coarse therapy• Blocks T4 release, synthesis and 1 uptake

A6ol/ haikoE eEect2 #ropranolol3 arbimaHole

will take se%eral days to ha%e an eEecton T4 synthesis


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9 th idi AT t t


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9yperthyroidism ATreatment

3 ntithyroid &rugs A30 thyroidologists pre/er – #ropylthiouracil A#TM• 00 mg bid-tid to start

– =ethimaHole• 0Z more potent the #TM

• 0 mg bid-tid to start – omplications o/ T& s

• granulocytosis A >200- 00 – usually presents w> acute pharyngitis> tonsilitis or

pneumonia.

• :ash• 9epatic necrosis, holestatic "aundice• rthralgia

9 th idi AT t t


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9yperthyroidism ATreatment

4 *urgeryAsub-total thyroidectomy

– 1ndications• #atient pre/erence• Large or symptomatic goiters• 6hen there is uestion o/ malignancy

– eed to be euthyroid prior to surgery• To [ the risk o/ arrhythmias during induction o/

anesthesia• To [ the risk o/ thyroid storm post operati%ely• T& s @ X-blockers

– :isks• #ermanent hypoparathyroidism• :ecurrent laryngeal ner%e problems• #ermanent hypothyroidism


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$ 71

K&1)M* G TGZ1 $G1TC:KC &C=1 $G1TC:


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GA+I

merupakan suatu masalah giHi yangdisebabkan karena kekuranganiodium .

Ge#ala\ :eterdasi mental

\ $angguan pendengaran\ $angguan bicara\ +retinisme )iasan a !ada ana*&

ana*


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+lasi3*asi. $rade 0 ' ormal

&engan inspeksi tidak terlihat , baik datar maupun tengadahmaksimal, dan dengan palpasi tidak teraba.

2. $rade 17elen"ar $ondok tidak terlihat, baik datar maupun penderitatengadah maksimal, dan palpasi teraba lebih besar dariruas terakhir ibu "ari penderita.

3. $rade 1B7elen"ar $ondok dengan inspeksi datar tidak terlihat, tetapiterlihat dengan tengadah maksimal dan dengan palpasiteraba lebih besar dari $rade 1 .

4. $rade 117elen"ar $ondok dengan inspeksi terlihat dalam posisi datardan dengan palpasi teraba lebih besar dari $rade 1B .

. $rade 1117elen"ar $ondok cukup besar, dapat terlihat pada "arak 8meter atau lebih.

$angguan kibat $ 7^


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$angguan kibat $ 7^

. Pada Fetus- bortus- *teel Birth- 7elainan 7ematian

#erinatal- 7retin euroligi- 7retin

=y(edematosa

- &e/ek #sikomotor2. Pada Neonatal- 9ipotiroid- $ondok eonatal

3. Pada Ana* danRema#a- -uvenile

i!oth roidesm- $ondok Gan$$uan

Fun$si Mental- Gan$$uan

Per*em)an$an Fisi* - 7retin

=y(edematosa daneurologi4. Pada De6asa- $ondok dan segala

7omplikasinya-


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Dosis Pem)erian +a!sul /odium. nak *& Adaerah endemik berat '

7 *a!sul8tahun

2. &aerah endemik sedang dan berat '- 6anita Msia *ubur ' 2 7apsul>tahun_ 200 mg

- 1bu hamil ' 7apsul>tahun

- 1bu =enuyusui ' 7apsulselama menyusui


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7ecukupan iodium yang dian"urkanuntuk orang 1ndonesia antara lain '

. Bayi A 2 bulan pertama 0mikrogram>hari

2. nak Ausia 2-8 tahun ?0

mikrogram>hari3. nak usia sekolah Ausia F- 2 tahun20

mikrogram>hari4. &ewasa Adiatas usia 2 tahun 0

mikrogram>hari. 1bu hamil F mikrogram>hari

8 1bu menyusui 200 mikrogram>hari

T1:G1&1T1*


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• 7MT A *M#M: T1)

&isebut "uga in/ecti%e thyroiditis, in/eksioleh bakteri > "amur. ontoh kuman ' pneumococcus,streptococcus hemolyticus, dll.

$e"ala 7linis ' nyeri dileher mendadak,malaise, demam, menggigil dan takikardi. #emeriksaan Lab ' leukositosis, LC&meningkat, sidikan tiroid menun"ukkan

nodul dingin. #engobatan ' utama 'antibiotikkokus gram @ ' penisilin, tetrasiklin.

"ika ada abses ' lobektomi.

• *MB 7MT


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MB 7MT Mmumnya diduga karena %irus

=7 ' pasien mengeluh dileher bagiandepan men"alar ke telinga, demam,malaise. #em.!sik ' tiroid membesar, nyeritekan,takikardi berkeringat, tremor, dll #em. Lab ' leukositosis, LC& meningkat,pada 2>3 kasus hormon tiroid meninggi. #engobatan ' biasanya sembuh sendirisehingga pengobatan yang diberikansimptomatis.- asetosal untk mengurangi nyeri- pada keadaan berat ' glukokortikoid

• =C 9M


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• =C 9M7.LIMFO0ITI+ 9 A0 IMOTO

*uatu tiroiditis autoimun dgn nama lain strumalim/omatosa=enyerang wanita berumur 30- 0 th7elen"ar tiroid biasanya membesar lambat, tdkterlalu besar, simetris, reguler, < padat. 7adang-kadang ada nyeri spontan < nyeri tekan. Bisaeutiroid>hipotiroid dan "arang hipertiroid.9istopatologi ' in!ltrasi lim/osit yg di/us, obliterasi/olikel tiroid dan !brosis.&iagnosis ' hanya dapat ditegakkan secara histologimelalui biopsi.#engobatan ' bila kelen"ar tiroid sangat besar pengangkatan.

2. on spesi!k

*T:M= G TG7*17


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*1=#LC7*• CT1GLG$1 & # TG$C C*1*

a. *intesis hormon tiroid yg tganggu , misal krnde/.yodium, masukan goitrogen dr mknan ataude/ek pd "alur biosintetik hormon.b. ^odinisasi yg tidak sempurna dr tiroglobulin

c. ntibodi yg menstimulasi pertumbuhan tiroid

• # TGLG$1- pd stadium awal, kelen"ar mmperlihatkan

hipertropi seragam, hiperplasia, danhiper%askularisasi- sebagian kelen"ar mmperlihatkan in%olusi atauhiperin%olusi yg seragam dg akumulasi koloid

• = 1)C*T *1 7L1 1*


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= 1)C T 1 7L1 1- pembesaran tiroid

- muka sembab, pusing, dan sinkopAtanda #emberton- suara parau

• &1 $ G*1*- T4 dan T 3 serum mendekati batasnormal- : 1 normal namun mungkin dptmeningkat pd de/.yodium atau de/ekbiiosintesis


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• T T L 7*

- untuk mengurangi ukuran strumabs dg menyediakan hormon eksogendlm "umlah cukup untukmenghambat sekresi T*9- pemberian hormon tiroid' Le%otiroksin dg dose' 00 `g stphari dan dosis ditingkatkan bulanberikutnya sampai maksimal 0atau 200 `g>hari.

DIAN P2 Endokrin

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