KELENJAR THYROID

Chairul Sandro
 THYROID
 Kelenjar thyroid berasal dari bahasa Yunani ;
thyreoeides yang berarti berbentuk perisai
 EMBRIOLOGI
 Asal : Proliferasi sel epithel dasar pharing

 Minggu ke 4 masa kandungan : gl. tiroid

muncul.

 Minggu ke 7 : kelenjar thyroid migrasi ke

posisi sebenarnya, yaitu di anterior dari
trachea

 Minggu ke 10 : Ductus thyroglossus

regresi (menghilang) menjadi lobus
piramidalis thyroid

 Minggu ke 12 : Kelenjar thyroid janin

secara fungsional mulai mandiri
ANATOMI
 BATAS-BATAS
Batas Anterolateral :
1. M. Sternothyroidea
2. M. Omohyoidea venter superior
3. M. Sternohyoidea
4. Tepi anterior M. Sternocleidomastoideus

Batas Posterolateral :
Carotid Sheath
 Art. Carotis Communis
 V. Jugularis Interna
 N. Vagus

Batas Medial :
1. Laring
2. Trachea (cincin trachea ke 2, 3 & 4)
3. M. Constrictorpharingeus Inferior
VASKULARISASI dan NERVUS
Relationship of recurrent laryngeal nerve to the inferior thyroid
artery
 SISTEM LIMFATIK
• Ascending Lymphatic
 Media, mengalir ke prelaryngeal lymph node yang
terletak pada membrane cricothyroidea
 Lateral, mengalir ke Jugulo-digastric grup dari deep
cervical lymph node.

• Descending Lymphatic
 Medial, mengalir ke pretracheal grup di trachea
 Lateral, mengalir ke Gl. Recurrent chain pada Nervus
Laryngeus recurrent.
 Parathyroid
Warna kekuningan, diameter 4-7 mm, berat 100 mgr
Biasanya ditemukan 4 buah
Vaskularisasi : A. thyroidea inferior
Drainase vena : vena thyroidea superior, media, inferior
Bila vaskularisasi terganggu, autograft m. SCM, strap
muscles
Terdiri dari sel utama (mensisntesis dan mensekresi
PTH) dan sel oksifil
PTH : meningkatkan absorbsi kalsium dan fosfat dari
tulang
Thyroid gland structure
Struktur thyroid
Colloid Basal membrane of epithelial cells
(glycoprotein)
Apical membrane of epithelial cells

Thyroid C-cell

Capillary
(Rich blood supply)

Cuboidal epithelial cells

Basement
membrane
 Each follicle is filled with pink-staining proteinaceous
material called colloid.

● When the gland is INACTIVE:

colloid is abundant, follicles are large, & lining cells
are flat.

● When the gland is ACTIVE:

follicles are small, lining cells are cuboid or columnar,
& the edge of colloid is scalloped, forming many small
“reabsorption lacunae”.
Thyroid gland secretions
● 2 important thyroid hormones:
● Thyroxine (T4) or tetraiodothyronine
● Triiodothyronine (T3)
- Secreted by Follicular cells.
- Can be stored in thyroid gland for couple of months
(2-3 months).
- Having significant effect on  metabolic rate of the body.

● Calcitonin
- Secreted by Parafollicular cells.
- Important hormone for Ca2+ metabolism & homeostasis.
Thyroid hormones
 Amount secreted:
- Thyroxine (T4) or tetraiodothyronine …93%
- Triiodothyronine (T3) …7%
 Almost all T4 is converted to T3 in tissues.

T4 T3
T4 T4
Capillary Reverse T3
(Rich blood supply)

Target cell
 T3 is the active form of T4.
 T3  4 times > potent (active/important) than T4 in
tissue, but it present in much smaller quantities
in
blood, & persists for a much shorter time than
does T4.
 T3 has great affinity to nuclear receptors than T4.

 Reverse T3 (RT3) is inactive.

 Transfer
of
thyroid hormones
in blood
Transfer of thyroid hormones in blood

 Almost all THs are carried in the blood, mostly in an

inactive form, bound to 3 different types of proteins:

a. Thyroxine binding globulin … 80%

b. Thyroxine binding pre-albumin …  10%
c. Plasma albumin (serum albumin) …  10%
N.B. T4 has greater affinity to bind proteins than T3.

 Only very little T3 (0.25-0.3%) & T4 (0.03%) are carried

in the blood in the free active form.
 Synthesis
of
thyroid hormones
Hypothalamic-pituitary-thyroid hormone axis
 T3 & T4 are synthesized in the colloid by:

1. Iodine formation.
2. Thyroglobulin formatiom.
3. Iodination.
4. Condensation (coupling).
5. Thyroid hormones secretion.
6. Deiodination.
How thyroid hormones are synthesized?
3. Iodination:
 Iodine attach to tyrosine within thyroglobulin chain.
 Iodinase enzyme is found in the apical membrane 
Colloid  start iodination process.

1 Iodine + 1 tyrosine  Mono-iodo-tyrosine (MIT)

iodinase
2 Iodine + 1 tyrosine  Di-iodo-tyrosine (DIT)

Colloid
4. Condensation (coupling):
 MIT & DIT or 2 DIT molecules coupled together.
MIT + DIT = T3
DIT + DIT = T4

N.B.
- Not all DIT & MIT  thyroid hormones.
- Only 25% of DIT & MIT give rise to thyroid hormones.
- T3 can also be formed by de-iodination (removing 1
iodine atom) of T4 by deiodinase enzyme.
5. Thyroid hormones secretion:

 After formation of THs, they remain bound to thyroglobulin

in the colloid until secreted.
 Hormones are surrounded in colloid by acid pool, then
converted into ‘colloid droplet’.
 TSH stimulates pinocytosis of thyroglobulin into the
follicular cell.
 Lysozome enzymes hydrolyze peptide bonds & release T3
& T4 from thyroglobulin.
 T3 & T4 will be discharged freely & secreted into the
capillaries (blood), attaching to TBG.
6. Deiodination:

 Inside follicular cells, DIT & MIT forms are NOT

secreted into the blood.

 DIT & MIT will be deiodinized to (Io) & tyrosine.

 Deiodized tyrosine will recycled back to synthesize

New MIT & DIT.
How thyroid hormones are synthesized?
 Control of
thyroid hormones
secreations
Control of thyroid hormones secretions
 Hypothalamus (TRH)  Anterior pituitary gland (TSH) 
(+) thyroid gland  (+) THs via cAMP dependent mechanism.
 THs  -ve feed back mechanism to Hypothalamus inorder
to inhibit (TRH) secretion to anterior pituitary gland.
Control of thyroid hormones secretions

 THs  also -ve feed back mechanism to Anterior pituitary gland

in order to inhibit responsiveness to Hypothalamus (TRH).
 Functions
of
thyroid hormones
Functions of thyroid hormones
 Generally, THs:
1. Increases metabolic rate.
 Stimulates increased consumption of glucose,
fatty acids and other molecules.
2. Increases metabolic heat, by  mitochondrial no &
activity   ATP,
3. Stimulates rate of cellular respiration by:
 Production of uncoupling proteins.
 Increase active transport by Na+/K+ pumps.
 Stimulates O2 consumption of most of cells in
the body.
Functions of thyroid hormones
4. Necessary for normal growth & maturation.
5. Promotes maturation of nervous system.
6. Stimulates protein synthesis.
7. Help regulating lipid & CHO metabolism.
 Abnormal
thyroid hormones
secretions
I: Hyperthyroidism (thyrotoxicosis)
 Hyperthyoidism   THs.
 Could be:
1ry hyperthyroidism … (diseases is in the gland),
e.g. Grave’s disease
Exerts TSH-like effects on thyroid.
Not affected by negative feedback.
 T3 & T4  reflex  TSH.

2ry hyperthyroidism … (disease is higher

up)
 TRH   TSH   T3 & T4.
 Follicular
 Females > malescells become overactive.
(4:1).
I: Hyperthyroidism … ‘Grave’s disease’
 90% of hyperthyoidism is due to “Grave’s disease”.
 GD is an autoimmune disease   thyroid stimulating antibodies IgG
 Symptoms of GD:
- Exophthalmous, due to retro-orbital oedema (irreversible).
- Lid lag, due to weakness of extraoccular muscles (reversible).
- Anxiety & restlessness.
- Sleeplessness.
-  appetite,  weight & diarrhea.
- Intolerence to heat.

 Treatment:
- drugs to  iodination process, such as PTU ‘Propylthiouracil’; MMI
‘methylmercaptoimidazole’.
 II: Hypothyroidism Adult (Myxedema)
 Hypothyroidism in adults   THs.
 Could be:
1ry hypothyroidism … (diseases is in the gland)
- autoimmune disease such as “Hashimoto’s throiditis”.
- lack of iodine.
- absence of deiodination enzyme.
 T3 & T4  reflex  TSH.
2ry hypothyroidism … (disease is higher up)
 TRH   TSH   T3 & T4.

 Follicular cells become less active.

 If No Iodine   T3 & T4   TRH   TSH
 growth (size) of the gland  simple goiter.
How goiter ‘swollen neck’ is formed?
With lack of iodine …
COLD
Hypothalamus
TRH
+

Anterior
pituitary

TSH +
NO or low Thyroid Lack of
feedback iodine
gland
inhibition
Poor +++
Low T3 or T4 ­ Growth of
release the gland
 If there is absence of deionization enzyme 
NO recycle synthesis of DIT & MIT  accumulate.

 DIT & MIT will not be used for new THs formation
  THs.
II: Hypothyroidism (myxedema).

 Symptoms of Hypothyroidism:
- Decreased metabolic rate.
- Slow heart rate & pulse.
- Slow muscle contractions
-  appetite,  weight gain, & constipation.
- Prolonged sleep, & dizziness.
- Coarse skin.
- Slow thinking, lethargy, & mask face.
- Intolerence to cold ( ability to adapt cold).
- Myxoedema  swollen & puffy appearance of body,
due to deposition of protein-carbohydrate complexes
‘mucopolysaccharides’ & fluid in subcutaneous tissue.
 II: Hypothyroidism
Children (Cretinism)
 Hypothyroidism in children  THs.
• Hypothyroid from end of 1st trimester to 6 months
postnatally, or in the 1st few years of life.
 T3 & T4  reflex  TSH.

 Additional Signs & Symptoms:

- Severe mental retardation.
- Short stature (due to  growth of bones, muscle, &
brain).
 Treatment: Thyroxine.
KELAINAN2 PD KEL.THYROID

Di bagi atas 2 tipe :

1. Berdasarkan fungsi ( Hipertiroid/hipo)

2. Massa tiroid (Neoplasma)

 KELAINAN KELENJAR TIROID

Ggn perkembangan Kista tiroglossus

Tiroid lingual
Radang/autoimun Graves disease
Hashimoto disease
Hiperplasia/ggn Meta- Struma koloid
bolik Struma endemik
Neoplasma Adenoma
Adeno Ca
A. Abnormalitas dari penurunan tiroid
- Penurunan abnormal ektopik jar.tiroid
dalam lidah, pd grs tengah leher dan
mediastinum
B. Tiroid Glottis ( Lidah )
- Tiroid tidak turun,tetap di dasar lidah
- gejala : obstruksi atau kesulitan bicara
- Th/ Supresi TSH
- Koreksi bedah bila gej.obstruksi (+)
C. KISTA DAN SINUS DUKTUS
TIROGLOSSUS
- Lokasi : antara tlg hyoid dan isthmus
Tanda dan gejala
- Solid atau kistik
- Paling sering pd anak-anak
- infeksi kista pada 1/3 kasus
Penanganan :
- Eksisi dg prosedur Sistrunk
D. DISFUNGSI TIROID YG MEMERLUKAN
PEMBEDAHAN
a. Penyakit Graves (Goiter non noduler
toksik-difus)
- Penyakit autoimun
- > wanita
- Dewasa muda ( 20-40 thn)
- Sindroma klinik hipermetabolisme
- Klinis : Palpitasi,berkeringat,tdk takut
panas,iritabilitasi,insomnia,
gelisah,berat badan turun dan
kelelahan
- Tanda “Bruit” yg terdengar diatas
kelenjar tiroid,gemetar pd tangan
dan lidah,aritmia jantung,dan
pelebaran fissura palpebra mata.
- Deposisi abnormal mukopolisaka-
rida dan infiltrasi sel sekitar di
jaringan  eksoftalmus,edema
kelopak mata,kemosis dan edema
pretibial
Diagnosis Penyakit Graves
- Dikonfirmasi dgn adanya peningkatan T4
serum total,dan peningkatan T3 resin up take (T3RU)
dan peningkatan T3 dgn radio immuno assay
- Scan tiroid menunjukkan tiroid yg membesar
- Kadar kolesterol serum menurun dan Gula
darah,fosfatase alkalin meningkat
Pengobatan Medis Peny. Graves
1. Radioiodine (131 I) secara oral
2. Propiltheourasil dan methymazole,
- bekerja inhibisi kompetitif thdp
peroksidase
- memblok oksidasi dr yodida ke iodin
elemental
- berperan dlm konversi perifer T4 ke T3
3. TH/ Bedah  Indikasi :
(1) Bila th/ medis gagal
(2) Pasien menolak u/ diobati
(3) Pasien mengalami reaksi merugikan
thdp obat anti tiroid
Jenis operasi : Tiroidektomi sub total
bilateral
Syarat : harus euthyroid
b. Penyakit Plummers ( Goiter
Multinoduler Toksik )
- Beberapa nodul hiperfungsi
- Sering pd ♀ usia > 50 th
- Biasanya dg riwayat goiter
multinoduler non toksik
- Sering pada daerah endemik
- Klinis : Gejala hipertiroidisme
Dugaan peny plummers:
aritmia,kelelahan otot dan
adanya Goitermultinoduler
- Laboratorium ;
(1) T3 dan T4 meningkat
(2) Penyerapan Radioiodin  pd
nodul yg hiperfungsi
- Pengobatan
(1) Medis : Radioiodin
(2) Bedah; lobectomy
E. Pembesaran Glandula Tiroid (Goiter)

(1) Goiter non nodular difus atau fungsi

yg me↓ kr sebab jinak

(2) Goiter Fokal atau Noduler dgn fungsi

normal (SNNT), mungkin ok
neoplasma tiroid
 NEOPLASMA TIROID
Faktor Resiko
Curiga maligna bila :
1. Umur : Usia > 40 th
2. Riwayat Keluarga
MEN 2A, MEN 2B dan Carsinoma tiroid
meduler  MTC dan PTC
Mutasi gen RET diturunkan
3. Paparan Radiasi (9%)
> 20 Gy. Radiasi pada anak-anak
Radioth. Di daerah kepala  insiden
kanker tiroid
4. Sindroma genetik
Garner sindrome, cadwens disease
Ca mammae, ovarium , ginjal dan SSP  PTC
tiroiditis hashimoto  Ca medulare dan
lymfoma
5. Diet
Mentega, keju dan daging > sayuran dan buahan
rendah iodin
 DIAGNOSIS
Anamnesis :
Riwayat radiasi
Pertumbuhan cepat
Suara serak
Riwayat keluarga (+)
Riwayat keluarga dengan MEN
Ggn sumbatan jalan nafas
Usia < 20 th > 50 th
 Pemeriksaan fisik
Nodul padat dan keras
Pembesaran KGB regional
Metastase tulang dan paru
Terfiksasi pada jaringan sekitar
Paralisi pita suara
 Pemeriksaan Penunjang
a. Lab : TSH dan T4
Tumor marker : Human tyroglobulin
Calcitonin pada Ca Medulare

b. Rad : - Foto polos leher metode “ soft tissue

technique” mikrokalsifikasi
- CT-Scan dan MRI ;
Menilai adanya perluasan struma
substernal atau kompresi trakea

c. USG : - Menilai ukuran dan jlh nodul

 - menilai nodul solid, kistik atau campuran

d. Sidik tiroid
Scanning (sidik) tiroid dpt menilai nodul
dingin (cold),panas (hot) & hangat (warm)
Nodul dingin ; - Insiden 80 - 85 %
- 20-30% ganas
Nodul panas ; - Insiden 5 %
- resiko ganas plg rendah
Nodul hangat; - insiden 10 - 15 %
- resiko ganas paling ↓
e. Needle Biopsi : - Needle core Biopsy
- FNAB,akurasi 88-95%
PTC,MTC dan UTC

f. Pemeriksaan Potong Beku (VC) :75-83%

Folikuler <<

g. Pemeriksaan Histopatologi
PTC Struktur papiler, Psomoma bodies
varian folikuler  ground glass nuclear
FTC  infiltrasi kapsul dan vaskuler
TNM
KLASIFIKASI
Mc. Kenzie membagi atas
4 tipe :
1. Ca papilare
2. Ca folikulare
3. Ca medulare
4. Ca anaplastik

penatalaksanaan
Adeno Ca Papiler /PTC (80%)
tumbuh lambat
Well dif
Penyebaran lymfogen
Metastase KGB regional– Paru, tulang
Infiltrasi esofagus dan trakea
Adeno Ca Folikuler /FTC
10-20% dari keganasan tiroid
Iodium yang kurang
Wanita : laki = 2:1
Usia >40 th
Hematogen, jarang KGB regional. Metastase jauh
Tipe dibagi berdasarkan invasi
1. minimal : encapsulated
2. moderate : angioinvasi
3. luas : encapsulated + angioinvasi
Adeno Ca Medular /MTC
5,1 % keganasan tyroid
solidum
Berasal dari sel parafolikuler
Atas dan tengah tyroid
Mengandung amiloid
kadar kalsitonin
Sifat tidak nenyengat I 131
Metastase cepat
Adeno Ca Anaplastik /UTC
Jarang, 5%
Sangat ganas
Gangguan mekanik leher
Metastase cepat. Lymfogen dan jauh
Tipe histopatology
Anaplastik spindle cell, giant cell dan small cell
PENATALAKSANAAN NODUL THYROID
Bila tidak ada VC
 INDIKASI OPERASI THYROID
1. Curiga ganas/keganasan kelenjar thyroid
2. Struma yang menyebabkan kompresi / gejala penekanan
berupa :
◦ Gangguan menelan
◦ Gangguan pernafasan
◦ Suara parau
3. Struma nodus dan difusa toxica
4. Struma retrosternal yang menyebabkan kompresi
5. Kosmetik
 KONTRA INDIKASI OPERASI
THYROID
 Terdapat suatu keadaan kondisi medis yang
menyebabkan penderita tidak dapat menerima
pembiusan dan/atau operasi.

 Bila angka harapan hidup sangat kecil.

KOMPLIKASI
 Komplikasi Dini :
Perdarahan
Cedera n. laryngeus superior
Cedera n. laryngeus recurrent

 Komplikasi yg terjadinya lambat:

Hipocalsemia
 PERAWATAN PASCA
BEDAH
Monitor jalan nafas dan vital signs
Posisi penderita elevasi kepala 30° bila telah sadar
penuh atau setengah duduk
Pengukuran kadar kalsium dalam darah
Drain dilepas bila produksi < 10 cc/hari
Angkat jahitan hari ke 7
 RAWAT JALAN
 Kriteria pasien dipulangkan dari rumah sakit (biasanya
hari ke 4 post op) :
Tidak ada kesulitan bernafas
Tidak ada perdarahan post op atau hematoma pada
leher
Pasien sudah mobilisasi
Tanda vital baik
Kadar kalsium serum > 2,0 mmol/L
TERIMA KASIH