PEMICU II

Dian Sri Utami

405100286

ANATOMI

GLANDULA TIROID
Terdapat dibagian bawah leher
ikut bergerak ketika menelan
Bentuk seperti kupu-kupu, terdiri atas 2 lobus
yang dihubungkan oleh isthmus yang
menyilang digaris tengah setinggi cincin
cartilage tracea 2,3,4. Lebih kurang 40% akan
terdapat lobus piramidalis, muncul dari bagian
permukaan atas isthmus, yang lebih sering dari
bagian kiri garis tengah.
Bagian atas dari lobus piramidalis dapat berupa
fibromuscular : Levator Glandula tiroid yang
menuju ke os hyoid. Pada kasus dimana lobus
piramidalis tidak ada, pita fibromuscular ini
terdapat di bagian atas isthmus.

 Glandula thyroid merupakan organ yang

sangat vascular
Dibungkus oleh : Fascia Pretrachealis
yang melekatkan organ ini pada larynx dan
trachea
Fascia ini ikut membentuk dan membatasi
pembagian lobus-lobusnya.
Setiap lobus berbentuk buah advokat
dengan puncaknya mengarah ke atas
sampai ke linea oblig cartilagenis trachea.
Basisnya terdapat di bawah, setinggi cincin
trachea ke 4 5.

Alat-alat disekitarnya
Anterolateral :
o m. sternothyroid
o venter superior m.
omohyooideus
o m. sternohyoideus
o tepi anterior m.
sternocleidomastoide
us

Alat-alat disekitarnya
Posterolateral :
o A.carotis communis
o V. jugularis interna
o N. vagus

Alat-alat disekitarnya
Medial :
o Larynx-trachea
o m. constrictor
pharyngis inferior
o Oesophagus
o antara oesophagus
dan trachea
terdapat
N.Laryngeus
Posterior :
recurrens
o Glandula
parathyroid
superior dan
anterior
o Anastomose antara
A. thyroidea
superior dan

Perdarahan
Berasal
dariThyroidea
:
1.A.
superior
cabang A. carotis externa
2.A. Thyroidea inferior
cabang truncus thyrocervicalis
berjalan naik di belakang kelenjar sampai setinggi
cartilage cricoidea, kemudian membelok ke
medial bawah mencapai batas posterior kelenjar.
N. laryngicus recurrens melintasi bagian depan
atau bagian belakang arteri ini.
3.A. Thyroidea Ima
Jika ada merupakan cabang A. Brachiocephalica
atau arcus aorta
Berjalan naik di depan trachea menuju isthmus

Pembuluh balik
1.V. Thyroidea superior : mencurahkan
isinya ke vena jugularis interna
2.V. thyroidea media : bermuara ke vena
jugularis interna
3.V. Thyroidea inferior : menampung darah
dari isthmus dan polus bawah kelenjar,
Vena ini dari kedua sisi akan
beranastomose sewaktu berjalan turun ke
bawah di depan trachea dan bermuara ke
V. brachiocephalica

Pembuluh
limfe
Limfe akan dialirkan ke lateral, ke NnLl.
Cervicalis profunda. Beberapa pembuluh
menuju NnLl. Paratrachealis
Pembuluh
saraf
Disarafi oleh serabut post ganglionik simpatis
yang berasal dari ganglion cervicalis superior,
media, dan inferior. Serabut-serabut ini
mengikuti pinggir arteri, didistribusikan
terutama pada pembuluh darah, hanya sedikit
ke sel folikel. Beberapa serabut N. vagus juga
mengikuti arteri ke kelenjar ini.

KELENJAR PARATHYROID

Bentuk :
o Pipih, oval, ukuran 3 8 mm x 2 5 mm
x 0,5 2 mm. Warna kuning kemerahan

 Letak :
o permukaan posterior lobus lateralis glandula thyroid,
biasanya berjumlah 4 buah.
o Kelenjar parathyroid superior : terletak di belakang pars
superior glandula thyroid
o Kelenjar parathyroid inferior : terletak di dekat tempat
masuknya A. Thyroidea inferior, posisi dan jumlahnya
bervariasi. Kelenjar parathyroid dapat tertanam pada
kelenjar thyroid

 Perdarahan :
Cabang-cabang A. Thyroidea terutama
dari A. Thyroidea inferior, juga dari
anastomose cabang yang mendarahi m.
prevertebralis, pharynx dan oesophagus.
Persarafan :
o Berasal dari sistim simpatis yang
menyertai arteri, terbanyak berasal dari
ganglion C6
o Pars inferior berhubungan erat dengan N.
recurrens laryngeal

FISIOLOGI

Fisiologi Kelenjar Tiroid

Kontrol Terhadap Kelenjar Tiroid
Hipotalamus

Gondok berkembang

TRH

Tiroid

Pituitari anterior
_

TSH

Tdk memenuhi
penyedianan tiroksin
TSH

Tiroid
T3

Hiperplasi &
hipertrofi
T4

 Fungsi Tiroid
- Memacu metabolisme
Berkaitan dengan suhu lingkungan
- Kalorigenesis
Stres
ACTH sumber Kalorigenesis
Metabolisme Lemak & karbohidrat

-Hipertiroidisme
- suhu tubuh tinggi, banyak berkeringat, penurunan
bobot tubuh, iritabilitas, dan tekanan darah tinggi
- Hipotiroidisme
- bobot tubuh meningkat, lamban dan tidak ada
toleransi terhadap udara dingin pada waktu
dewasa.
-Perkembangan

Paratiroid
Bentuk pipih, oval / seperi buah pear, letak
permukaan posterior lobus lateralis tiroid
Paratiroid, kalsitonin dan dihidroksikolekalsiferol
merupakan hormon utama berkaitan dengan
metabolisme seperti :
Kalsium
Pirofosfat
Magnesium
Pengaturan metabolisme tulang
Dan komponen organik

Metabolisme Kalsium
99% ion Ca++ berupa kristal mineral tulang
Kalsium memiliki 3 fungsi dalam sel
- Komponen kunci dalam membran sel,
permeabilitas serta sifat listriknya
- Sebagai faktor perangkai selama ekksitasi dan
kontraksi semua jenis otot.
- Stadium awal untuk merangkai tanggapan sel
sasaran terhadap hormon.
Kalsium diserap diusus dibantu oleh 1,25Dihidroksikolekalsiferol metabolit Vit D3 diginjal
yang dikontrol oleh paratiroid.

Biosintesis PTH
PTH sapi, manusia dan babi
polipeptida linier
dengan BM 9500 dan 84 residu aa
PTH disintesis sbg prapro-PTH (115 residu aa)
Prapro-PTH masuk RE
25 residu aa
dikeluarkan dr terminal N Pro-PTH (90 residu aa)
Di aparatus golgi 6 residu aa dari terminal N
dikeluarkan lagi
PTH ( 84 residu aa)
Kadar normal PTH dlm plasma ; 10-55 pg/ml
Waktu paruh kurang dari 20 mnt
Polipeptida disekresikan akan diuraikan oleh selsel kuffer di hati mjd 2 polipeptida
Fragmen terminal C yang tdk aktif BM 7000 dan
fragmen terminal N yang aktif dgn BM 2500

Hipoparatiroidisme
Pengambilan tiroid
kadar kalsium turun
Hipokalsemia
hilang kemampuan
mobilisasi kalsium oleh tulang, ginjal dan usus
Ion kalsiun turun pada ekstrasel hiperiritabilitas
neuromuskuler
tetani, kejang otot,
kematian
Transport kalsium usus turun
1,25dihidroksikolekalsiferol tidak terbentuk krn PTH
tidak ada

Hiperparatiroidisme
Meningkatkan resropsi dan mobilisasi
kalsium, shg kalsium plasma meningkat
dan fosfat plasma menurun
PTH meningkatkan ekskresi fosfat dalam
urin ( reabsropsi fosfat ditubulus
proksimal menurun dan reabsropsi ion
kalsium meningkat ditubulus distal.
Peningkatan reabsropsi kalsium oleh usus
Menyebabkan kelumpuhan pada tulang
karena tingginya deposisi kalsium
sehingga menghilangkan mineral

Kalsitonin
Rantai polipeptida td 32 residu aa ,
BM 3000
Dilepaskan jika kalsium serum tinggi
Bekerja di tulang dan ginjal
Penghambat reabsropsi
Mencegah pelunakan tulang

Fungsi 1,25Dihidroksikolekalsiferol
Bereaksi seirama dgn PTH, mengontrol
mineralisasi tulang
Meningkatkan reabsropsi kalsium dan fosfat oleh
tubuli ginjal
Meningkatkan transport kalsium dan fosfat yang
melintasi sel-sel mukosa usus.

BIOKIMIA

Thyroid Regulation
Somatostatin,
Glucocorticoid
Dopamine

Thyroid hormone synthesis

1) Iodide pump
Rate limiting step in thyroid hormone synthesis
which needs energy
Follicles have in their basement membrane an
iodide trapping mechanism which pumps dietary I
into the cell
Normal thyroid: serum iodine is 30-40:1
Iodide uptake enhancers:
TSH
Iodine deficiency
TSH receptors antibody

Iodide uptake inhibitors

Iodide ion
Drugs
Digoxin
Thiocynate
perchlorate

Thyroid hormone synthesis

2) Iodide oxidation to iodine and
Organification
Inside the cells, iodide is oxidized by
peroxidase system to more reactive
iodine
Iodine immediately reacts with tyrosine
residue on a thyroid glycoprotein called
thyroglobulin to form :
T1= mono-iodotyrosyl thyroglobulin
T2= di-iodotyrosyl thyroglobulin

Both processes are catalyzed by thyroid

peroxidase enzyme

Thyroid hormone synthesis

3) Coupling
T1& T2 couple together to form T3&T4
MIT +DIT = T3 (Tri-iodothyronine)
DIT + DIT = T4 (Thyroxin)
All attached to thyroglobulin and stored
in the colloid Thyroglobulin molecule
This process is stimulated by TSH

Production of Thyroid Hormones

NIS (Na+/I- Sympoter)

TPO

Effects of thyroid hormones

Fetal brain & skeletal maturation

Increase in basal metabolic rate
Inotropic & chronotropic effects on heart
Increases sensitivity to catecholamines
Stimulates gut motility
Increase bone turnover
Increase in serum glucose, decrease in
serum cholesterol
Conversion of carotene to vitamin A
Play role in thermal regulation

Increase BMR ( Basal Metabolic Rate )

cellular metabolic activity by :

size, total membrane surface & number of mitochondria

ATP formation

active transport of ions ( Na+, K+ )

Promote growth & development of the brain during

fetal life and for the first few years of postnatal life

Carbohydrate metabolism

enhanced glycolysis, gluconeogenesis,

GI absorption & insulin secretion

Fat metabolism

enhanced fat metabolism

Accelerates the oxidation of free fatty acids by the cells

plasma cholesterol, phospholipids & triglycerides

Body weight

the appetite, food intake, GI motility but

the body weight

Cardiovascular system

vasodilatation

blood flow

cardiac output

heart rate
Respiratory

the rate and depth respiration

CNS

extreme nervous & psychoneurotic tendency

Muscle

make the muscles react with vigor ----->

muscle tremor ( 10-15 times/sec )

Sleep: extreme fatigue but is difficult to sleep

KELAINAN TIROID

Causes , Clinical Features

& Consequences of
Hypothyroidism
Congenital Hypothyroidism
Acquired Hypothyroidism

Etiology
Congenital
Acquired
Primary
Secondary
Tertiary

Congenital Hypothyroidism
Occurs in about 1/4000 live birth
Thyroxin is important for CNS development
and postnatal growth
The most frequent cause is congenital
absence of the thyroid gland (athyrosis)
Presentations may include cyanosis,
prolonged hyperbilirubinemia, poor feeding,
hoarse cry, umbilical hernia, respiratory
distress, macroglossia, large fontanelle, and
delayed skeletal maturation
Rarely, neonatal hypothyroidism is transient

Congenital Hypothyroidism
Etiology
1) Thyroid dysgenesis
Idiopathic:
Commonest cause in 95% of cases
Athyreosis (40%)
Hypoplasia (40%)
Ectopia (base of tongue, midline) (20%)

2) Thyroid dyshormonogenesis (A.R) (10%)

3) Hypothalamic-pituitary hypothyroidism
Anencephaly, holoprosencephaly, S.O.D
idiopathic

Congenital
Hypothyroidism
4) Transient hypothyroidism
Maternal TRAB
Maternal ingestion of goitrogen

5) Drugs
6) Iodine excess
7) Iodine deficiency

Anti-thyroid Drugs and

fetus

Thionamides
PTU & MZT

Iodide
Lithium
Amiodarone
Radioiodine

After 10-12 wk gestation can

damage
fetal thyroid gland

Presentations of congenital
hypothyroidism
Macroglosia
Prolonged hyperbilirubinemia
Poor feeding
Hoarse cry
Decreased activity
Constipation
Umbilical hernia
Dry yellow skin
large fontanelle
Delayed skeletal maturation

Neonatal screening for congenital

hypothyroidism
Routine in most countries worldwide
Filter paper blood spot measuring TSH

Why ??
Clinical manifestations at birth, usually are subtle or
even absent (passive transplacental maternal
thyroxin)
At birth, surge of TSH (stress of delivery) up to 30 -40
u/ml
Early detection will prevent mental retardation or
decreasing IQ of affected neonates
Thyroxin is important for CNS development from birth
till 3 years of life
Screening program will miss 2ry/ tertiary cases
The program is hampered by a high rate of false
positive results

Acquired Hypothyroidism
More common than hyperthyroidism
99% is primary (< 1% due to TSH deficiency)
Hashimotos
most common thyroid problem (4% of
population)
most common cause in iodine-replete
areas
chronic lymphocytic thyroiditis
Associated with TPO antibodies (90%), less
commonly Tg antibodies
Iatrogenic Hypothyroidism from radioactive
iodine therapy

Acquired Hypothyroidism
Subacute thyroiditis

Painful, often radiates to the ear

c/o malaise, pharyngitis, fatigue, fever, neck pain/swelling
Viral etiology (URI/ pharyngitis)
self-limited. Can tx inflammation w/ ASA, NSAIDs or
steroids

Suppurative/ Acute Infectious thyroiditis

Infections of the thyroid are rare
normally protected from infection by its thick capsule
Bacterial >> fungal, mycobacterial or parasitic
Pts are acutely ill w/ a painful thyroid gland
assoc w/ fever/chills, anterior neck pain/swelling,
dysphagia and dysphonia

Acquired Hypothyroidism

Symptoms
General Slowing Down
Lethargy/somnolence
Depression
Modest Weight Gain
Cold Intolerance
Hoarseness
Dry skin
Constipation ( peristaltic activity)
General Aches/Pains
Arthralgias or myalgias
(worsened by cold temps)

Brittle Hair
Menstrual irregularities
Excessive bleeding
Failure of ovulation

Libido

Acquired Hypothyroidism
Examination

Dry, pale, course skin with yellowish tinge

Periorbital edema
Puffy face and extremities
Sinus Bradycardia
Diastolic HTN
Body temperature
Delayed relaxation of reflexes
Megacolon ( peristaltic activity)
Pericardial/ pleural effusions
Congestive heart failure
Non-pitting edema
Hoarse voice
Myopathy

Goiter
A swollen thyroid
gland
Assessment;
how big, how
quickly has it
developed, is it
smooth or nodular,
is it painful, any
associated lymph
nodes, any sudden
changes, is it big
enough to cause
local symptoms (e.g.
breathing
problems)

Myxedema

Hypothyroidism --- loss of scalp hair

A Color Atlas of Endocrinology p70

Hypothyroidism with short

stature

Diagnosis
Congenital hypothyroidism
Thyroid hormone level
TSH
Thyroid scan
Acquired Hypothyroidism
TSH
fT4
Thyroid antibodies
Thyroid ultrasound
TSH: low in secondary hypothyroidism
high in primary hypothyroidism
TRH test: to differentiate between
secondary & Tertiary hypothyroidism

Euthyroid sick syndrome

Abnormalities in thyroid function tests
observed with systemic non thyroidal illness
Cytokine mediated
Reduced TRH release, TSH response, T4
production/release, T4 to T3 conversion and
TBG production
Increased somatostatin secretion
Inhibitory effects of dopamine and
glucocorticoid on TRH action
Very low T4 values have a poor prognosis

Causes , Clinical Features

& Consequences of
Hyperthyroidism

Hyperthyroidism (Thyrotoxicosis)
Definition
Excessive secretion of T3 & T4
Affects metabolic processes in all
body organs
Hyperthyroidism is 4-10 times more
prevalent in women
Most common endocrine disease
second only to diabetes as the most
occurring endocrine disease

Thyrotoxicosis
Causes
Transient
1.Neonatal thyrotoxicosis
2.Infectious : Acute & subacute thyroiditis
3.Drug induced: Amiodarone, interferon
&interleukin
4.Iatrogenic

Thyrotoxicosis
Causes
Persistent
1.Graves disease
2.Toxic multinodular goiter
3.Toxic solitary adenoma
4.Central (pituitary origin)

Neonatal Thyrotoxicosis

Only occur with 5% of thyrotoxic mothers

Severity consistent in future pregnancies
20% mortality if untreated
Evolves rapidly, evident by day 7 of life,
unless TRAB blocking antibody is present
Associate with cranial synostosis and
learning difficulties, if not treated
Fetal thyrotoxicosis in rats leads to
abnormal CNS myelination
Parents should be aware of potential
learning problems (early school years
should be monitored)

Neonatal hyperthyroidism born to mother

with Graves disease

A Color Atlas of Endocrinology p51

Graves disease
Pathogenesis
T-cell dependent autoimmune disease
60% have HLA association with A1,
B8, DR3,DR4,DR5
Autoimmune disorder that results in
production of antibodies directed
against thyroid antigens:
TSH receptors
Thyroglobulin
Thyroid peroxidase

Subacute Thyroiditis
Clinical course lasts weeks to months
Acute phase (2-6/52) with clinical and
biochemical hyperthyroidism
Recovery phase (weeks-months) transient
hypothyroidism then euthyroidism
Clinically, history of sore throat, fever,
tender goiter, cervical lymphadenopathy
High ESR, negative antibodies and absent
radioactive I131 uptake

Hyperthyroidism
May result in significant
morbidity, mortality & even death

Symptoms

Jittery, shaky, nervous

Difficulty concentrating
Emotional lability
Insomnia
Rapid HR, palpitations, Feeling
Hot
Weight Loss
Diarrhea
Fatigue
Menses : lighter flow, shorter
duration

Hyperthyroidism

Exam

Eye findings (20%)

Goiter
Thyroid bruit or thrill
Tachycardia: Sinus Tachycardia,
Atrial Fibrillation
Flow murmur
Systolic hypertension
Hyperreflexia
Tremors
Proximal muscle weakness
Clubbing
Onycholysis (<1%)
separation of nail from the
nailbed

Dermopathy (1%)

Thyrotoxicosis
Heart: Increased heart rate, contractility
and cardiac output
Skeletal muscles: Proximal myopathy, easy
fatigability and muscle atrophy
Gonads: Irregular menstrual cycles,
impotence
Liver: Low cholesterol LDL &
apolipoprotein
Bone: Increased bone turnover,
osteoporosis & increased risk of fracture

Grave's ophthalmopathy
The pathogenesis of infiltrative
ophthalmopathy is poorly understood
It may occur before the onset of
hyperthyroidism or as late as 15 to 20 years
The clinical course of ophthalmopathy is
independent of the clinical course of
hyperthyroidism
Infiltrative ophthalmopathy may result from
immunoglobulins directed to specific
antigens in the extraocular muscles &
orbital fibroblasts
The antibodies are distinct from those
initiating Graves'-type hyperthyroidism

Hyperthyroid Eye Disease

Hyperthyroidism (any cause)
Lid lag, lid retraction and stare
Due to increased adrenergic
tone stimulating the levator
palpebral muscles.
True Graves Ophthalmopathy
Proptosis
Diplopia
Inflammatory changes
Conjunctival injection
Periorbital edema
Chemosis
Due to thyroid autoAbs that
cross-react w/ Ags in
fibroblasts, adipo-cytes, +
myocytes behind the eyes.

Graves ophthalmopathy

Hyperthyroid Eye Disease

Graves Dermopathy

Thyroid Dermopathy
Thickening and redness
of the dermis
Due to lymphocytic
infiltration

Thyroid Acropachy

Thyroid acropachy. This is most marked in the index fingers and

thumbs

Tremor of the hand

A Color Atlas of Endocrinology p49

Diagnosis
TSH level usually < 0.05 u / ml
95 % of cases, high FT4 & FT3
In 5% high FT3 with normal T4 (T3
Thyrotoxicosis)
Thyroid receptor (TRAB) are usually
elevated at diagnosis
Antibodies against thyroglobulin,
peroxidase or both are present in
the majority of patients

Thyrotoxicosis- Treatment

Three modalities for more than last 50 years

Radioactive iodine,antithyroid drugs&surgery
None is optimal
None interrupts the autoimmune process
Each has a drawbacks
There is no treatment for underlying cause
No other research options so far

Neonatal Thyrotoxicosis
Treatment
1) Lugols iodine
1 drop tid for 1-2 / 7
Dramatic coarse therapy
Blocks T4 release, synthesis and I uptake
(Wolf Chaikoff effect)
2) Propranolol
3) Carbimazole
will take several days to have an effect
on T4 synthesis

Hyperthyroidism (Treatment)
1) -blockers (symptom control)

Propranolol (Inderal )
Atenolol (Tenormin )
Metoprolol (Lopressor )

2) 131-RAIA (70% thyroidologists prefer)

Dosing
Graves: 10-15 mCi
Toxic MNG/Adenoma: 20-30 mCi
Absolute contraindications

Pregnancy and lactation (excreted in breast milk)!

Pregnancy should be deferred for at least 6 months following

therapy with radio-active 131
It is advisable to avoid 131-Rdio-active iodine therapy in
patients with active moderate severe Graves
ophthalmopathy.

Hyperthyroidism (Treatment)
3) Antithyroid Drugs (30% thyroidologists prefer)

Propylthiouracil (PTU)
100 mg bid-tid to start
Methimazole
10X more potent the PTU
10 mg bid-tid to start
Complications of ATDs
Agranulocytosis (1/200-500)
usually presents w/ acute pharyngitis/ tonsilitis or
pneumonia.

Rash
Hepatic necrosis, Cholestatic jaundice
Arthralgia

Hyperthyroidism (Treatment)
4) Surgery (sub-total thyroidectomy)

Indications
Patient preference
Large or symptomatic goiters
When there is question of malignancy
Need to be euthyroid prior to surgery
To the risk of arrhythmias during induction of
anesthesia
To the risk of thyroid storm post operatively
ATDs + -blockers
Risks
Permanent hypoparathyroidism
Recurrent laryngeal nerve problems
Permanent hypothyroidism

GAKI

=DIFUS NON TOXIC GOITER=ENDEMIC GOITER

GAKI
merupakan suatu masalah gizi yang
disebabkan karena kekurangan
iodium.
Gejala
Reterdasi mental
Gangguan pendengaran
Gangguan bicara
Kretinisme biasanya pada anakanak

Klasifikasi
1. Grade 0 : Normal
Dengan inspeksi tidak terlihat, baik datar maupun tengadah
maksimal, dan dengan palpasi tidak teraba.
2. Grade IA
Kelenjar Gondok tidak terlihat, baik datar maupun penderita
tengadah maksimal, dan palpasi teraba lebih besar dari
ruas terakhir ibu jari penderita.
3. Grade IB
Kelenjar Gondok dengan inspeksi datar tidak terlihat, tetapi
terlihat dengan tengadah maksimal dan dengan palpasi
teraba lebih besar dari Grade IA.
4. Grade II
Kelenjar Gondok dengan inspeksi terlihat dalam posisi datar
dan dengan palpasi teraba lebih besar dari Grade IB.
5. Grade III
Kelenjar Gondok cukup besar, dapat terlihat pada jarak 6
meter atau lebih.

Gangguan Akibat GAKY

1. Pada Fetus
- Abortus
- Steel Birth
- Kelainan Kematian
Perinatal
- Kretin Neuroligi
- Kretin
Myxedematosa
- Defek Psikomotor
2. Pada Neonatal
- Hipotiroid
- Gondok Neonatal

3. Pada Anak dan

Remaja
- Juvenile
Hipothyroidesm
- Gondok Gangguan
Fungsi Mental
- Gangguan
Perkembangan Fisik
- Kretin
Myxedematosa dan
Neurologi
4. Pada Dewasa
- Gondok dan segala
Komplikasinya

Dosis Pemberian Kapsul Yodium

1. Anak SD (daerah endemik berat) :
1 kapsul/tahun
2. Daerah endemik sedang dan berat :
- Wanita Usia Subur : 2 Kapsul/tahun
@ 200 mg
- Ibu hamil : 1 Kapsul
/tahun
- Ibu Menuyusui : 1 Kapsul
selama menyusui

Kecukupan iodium yang dianjurkan

untuk orang Indonesia antara lain :
1. Bayi (12 bulan pertama) 50
mikrogram/hari
2. Anak (usia 2-6 tahun) 90
mikrogram/hari
3. Anak usia sekolah (usia 7-12 tahun)
120
mikrogram/hari
4. Dewasa (diatas usia 12 tahun) 150
mikrogram/hari
5. Ibu hamil 175 mikrogram/hari
6. Ibu menyusui 200 mikrogram/hari

TIROIDITIS
AKUT ( SUPURATIF )
Disebut juga infective thyroiditis, infeksi
oleh bakteri / jamur.
Contoh kuman : pneumococcus,
streptococcus hemolyticus, dll.
Gejala Klinis : nyeri dileher mendadak,
malaise, demam, menggigil dan takikardi.
Pemeriksaan Lab : leukositosis, LED
meningkat, sidikan tiroid menunjukkan
nodul dingin.
Pengobatan : utama :antibiotik
kokus gram + : penisilin, tetrasiklin.
jika ada abses : lobektomi.

 SUB AKUT

Umumnya diduga karena virus

MK : pasien mengeluh dileher bagian
depan menjalar ke telinga, demam,
malaise.
Pem.fisik : tiroid membesar, nyeri
tekan,takikardi berkeringat, tremor, dll
Pem. Lab : leukositosis, LED meningkat,
pada 2/3 kasus hormon tiroid meninggi.
Pengobatan : biasanya sembuh sendiri
sehingga pengobatan yang
diberikan
simptomatis.
- asetosal untk mengurangi nyeri
- pada keadaan berat :
glukokortikoid

 MENAHUN
1.LIMFOSITIK (HASHIMOTO)
Suatu tiroiditis autoimun dgn nama lain struma
limfomatosa
Menyerang wanita berumur 30-50 th
Kelenjar tiroid biasanya membesar lambat, tdk
terlalu besar, simetris, reguler, & padat. Kadangkadang ada nyeri spontan & nyeri tekan. Bisa
eutiroid/hipotiroid dan jarang hipertiroid.
Histopatologi : infiltrasi limfosit yg difus, obliterasi
folikel tiroid dan fibrosis.
Diagnosis : hanya dapat ditegakkan secara histologi
melalui biopsi.
Pengobatan : bila kelenjar tiroid sangat besar
pengangkatan.
2. Non spesifik

STRUMA NON TOKSIK

SIMPLEKS

ETIOLOGI DAN PATOGENESIS

a. Sintesis hormon tiroid yg tganggu, misal krn
def.yodium, masukan goitrogen dr mknan atau
defek pd jalur biosintetik hormon.
b. Yodinisasi yg tidak sempurna dr tiroglobulin
c. Antibodi yg menstimulasi pertumbuhan tiroid
PATOLOGI
- pd stadium awal, kelenjar mmperlihatkan
hipertropi seragam, hiperplasia, dan
hipervaskularisasi
- sebagian kelenjar mmperlihatkan involusi atau
hiperinvolusi yg seragam dg akumulasi koloid

 MANIFESTASI KLINIS
- pembesaran tiroid
- muka sembab, pusing, dan sinkop
(tanda Pemberton)
- suara parau
DIAGNOSIS
- T4 dan T3 serum mendekati batas
normal
- RAI normal namun mungkin dpt
meningkat pd def.yodium atau defek
biiosintesis

 TATA LAKSANA
- untuk mengurangi ukuran struma
bs dg menyediakan hormon eksogen
dlm jumlah cukup untuk
menghambat sekresi TSH
- pemberian hormon tiroid:
Levotiroksin dg dose: 100 g stp
hari dan dosis ditingkatkan bulan
berikutnya sampai maksimal 150
atau 200 g/hari.