Ronald Chrisbianto Gani405090223
Faculty of Medicine 2009Tarumanagara University
ENDOCRINE SYSTEM BLOCK
CASE 4
HISTOLOGY OF THYROID
Junqueira’s Basic Histology 12th Ed
HISTOLOGY OF THYROID• composed of millions of rounded epithelial
structures called thyroid follicles• Follicles epithelium + gelatinous substance
(coloid) contains Thyroglobulin
C : CapsuleS : Septa
L : Lumen C : C cells
Junqueira’s Basic Histology 12th Ed
HISTOLOGY
C : C cellF : Folicullar Cell
Junqueira’s Basic Histology 12th Ed
HISTOLOGY
F : Follicular CellL : LumenBM : Basal MembraneC : Parafollicular Cell / C Cell
G : Golgi Apparatus
Junqueira’s Basic Histology 12th Ed
THYROID SYNTHESIS
Junqueira’s Basic Histology 12th Ed
PHYSIOLOGY OF THYROID
HORMON TIROID
• Bentuk kelenjar tiroid nya seperti pita• Letaknya tepat di tempat kita biasa memasang
dasi kupu• Sel sekretorik utama tiroid tersusun menjadi
gelembung berongga yang disebut folikel• Folikel berisi lumen yang disebut koloid• Konstituen utama koloid adalah tiroglobulin• Sel folikel akan menghasilkan hormon tiroid, yaitu
T3 dan T4
Sherwood’s Human Physiology From Cell’s to System 2nd Ed
FOLLICULAR CELL
Sherwood’s Human Physiology From Cell’s to System 7th Ed
HORMON TIROID
• Proses pembentukan hormon tiroid– TGB dihasilkan di RE sel folikel tiroid, lalu
dimasukkan ke koloid– Tiroid menangkap iodium dari darah lalu
dimasukkan ke dalam koloid melalui iodine-trapping mechanism.
– Dalam koloid, Iodium melekat pada tirosin. 1 iodium + tirosin MIT (Monoiodotirosin) 2 iodium + tirosin DIT (Diiodotirosin)
– MIT + DIT T3 dan DIT + DIT T4, tidak ada reaksi MIT + MIT
Sherwood’s Human Physiology From Cell’s to System 2nd Ed
Sherwood’s Human Physiology From Cell’s to System 7th Ed
HORMON TIROID
• Sel folikel memfagositosiskan koloid berisi TGB untuk melakukan sekresi hormon tiroid
• Di luar tiroid, sebagian besar T4 dirubah menjadi T3 karena T3 adalah bentuk hormon tiroid yang secara biologis aktif di tingkat sel, namun tiroid lebih banyak mengeluarkan T4
• Di dalam darah, hormon tiroid diikat di :– T3 : thyroxine-binding globulin 65%, albumin 35%– T4 : thyroxine-binding globulin 55%, albumin 10%,
thyroxine-binding prealbumin 35%
Sherwood’s Human Physiology From Cell’s to System 2nd Ed
HORMON TIROID
• Efek dari hormon tiroid– Meningkatkan laju metabolik basal tubuh keseluruhan– Efek kalorigenik– Tiroid sedikit, glukosa glikogen, dan sebaliknya– Diperlukan dalam sintesis protein pertumbuhan, tapi jika
berlebih katabolisme protein– Efek simpatomimetik– Meningkatkan denyut jantung, merangsang vasodilatasi perifer– Merangsang GH, mendorong efek GH, jika kurang kelainan,
jika berlebih tidak ada pertumbuhan berlebih.– Penting dalam pembentukan dan segala aktivitas SSP
Sherwood’s Human Physiology From Cell’s to System 2nd Ed
KONTROL HORMON TIROID
Sherwood’s Human Physiology From Cell’s to System 7th Ed
HORMON TIROID• Kelainan fungsi tiroid :
– Hipotiroidisme• terjadi krn :
– Kegagalan primer kelenjar tiroid– Kegagalan sekunder defisiensi TRH, TSH, atau keduanya– Defisiensi iodium
• Gejala :– Penurunan laju metabolik dasar– Tidak ada efek kalorigenik– Terjadi penambahan berat– Mudah lelah– Denyut nadi lambat dan lemah– Perlambatan refleks dan gangguan mental– Berkurangnya kewaspadaan, bicara melambat, gangguan
ingatanSherwood’s Human Physiology From Cell’s to System 2nd Ed
HORMON TIROID• Pembengkakan pada tangan, kaki, dan wajah disebut miksedema• Jika hipotiroidisme sejak lahir kretinisme• Kerusakan SSP dapat dicegah dengan terapi
– Hipertiroidisme• Paling sering disebabkan oleh penyakit grave• Gejala :
– Keringat berlebih– Penurunan toleransi thdp panas– Nafsu makan meningkat, tapi berat badan menurun– Degradasi netto simpanan karbo, lemak, protein– Penurunan massa otot rangka– Jantung berdebar– Emosional, mudah tersinggung, tegang, dan cemas
Sherwood’s Human Physiology From Cell’s to System 2nd Ed
HORMON TIROID• Pada penyakit grave, terjadi eksoftalmos• Pengobatan :
– Pengangkatan sebagian kelenjar tiroid yg hipersekresif– Pemberian iodium radioaktif– Penggunaan obat anti-tiroid
– Gondok (goiter) dapat menyertai pada hipotiroid dan hipertiroid
Sherwood’s Human Physiology From Cell’s to System 2nd Ed
HYPOTYROIDISM
HYPOTYROIDISM• Lebih dominan pada wanita• Secara klinis, dibagi menjadi
– Hipotiroidisme sentral• kerusakan hipotalamus / hipofisis
– Hipotiroidisme primer (paling banyak)• Kerusakan kelenjar tiroid
– Hipotiroidisme krn sebab lain• Farmakologis, kekurangan / kelebihan yodium, resistensi perifer
• Klasifikasi perjalanan penyakit– Hipotiroidisme klinis (TSH ↑, fT4 ↓)– Hipotiroidisme subklinis (TSH ↑, fT4 Normal)
• Hipotiroid intrauterin dan neonatal retardasi mental & fisik yg ireversibel jika tdk diberi terapi
• Hipotiroid pada usia remaja –dewasa reversibel• Hipotiroid pd usia lanjut gejala klinis tdk spesifik
Buku Ajar Ilmu Penyakit Dalam Ed V
ETIOLOGI• Hiportiroidisme Sentral
– Kegagalan hipofisis hipotiroidisme sekunder– Kegagalan hipotalamus hipotitoidisme tertier– 50% kasus tumor hipofisis
• Hipotiroidisme Primer– Pasca operasi : stromektomi subtotal M.grave, dalam 10 th, 40%
hipotiroidisme– Pascaradiasi : RAI pd hipertiroidisme, 40-50% menjadi hipotiroidisme dalam
10th. RAI pada nodul toksik 5% menjadi hipotiroidisme– Tiroiditis Autoimun– Tiroiditis pascapartum : silih berganti hipo & hipertiroid, Marker : antibodi anti
TPO dan anti Tg, prevalensi 5,5%– Tiroiditis subakut (De Quervain) : nyeri di kelenjar, demam, menggigil. Etio : virus
nekrosis jaringan hormon masuk ke sirkulasi– Dishormogenesis : defek pd enzim hormogenesis– Karsinoma – Hipotiroidisme sepintas / transien : pasca pengobatan RAI, pascatiroidektomi
subtotalBuku Ajar Ilmu Penyakit Dalam Ed V
Harrison’s Principle of Medicine 18th Ed
PENGARUH FARMAKOLOGIS
• OAT berlebih hipotiroidism• Menghambat sintesis tiroid : tionamid,
peklorat, sulfonamid, iodida.• Meningkatkan katabolisme tiroid : fenitoin,
fenobarbital• Menghambat jalur enterohepatik hormon
tiroid di usus ↑ : kolestipol, kolestiramin
Buku Ajar Ilmu Penyakit Dalam Ed V
SIGN & SYMPTOMS
Harrison’s Principle of Medicine 18th Ed
MYXEDEMA
Pathophysiology of Disease : Introduction to Clinical Medicine 6th Ed
ALGORITHM
Harrison’s Principle of Medicine 18th Ed
DIFFERENTIAL DIAGNOSIS
• Hashimoto’s thyroiditis• Multinodular Goiter• Thyroid Carcinoma
Harrison’s Principle of Medicine 18th Ed
TREATMENT• No residual thyroid function levothyroxine 1,6 μg/kg
body weight (100-150 μg/d)• Adult patient <60yo start with 50-100 μg/d levothyroxine,
adjusted on the basis of TSH level• TSH level measured per 2 months• Levothyroxine + Liothyronine effect has not been
confirmed yet• Once normal TSH achieved, interval of follow up of TSH
level may be extended to 2-3 years if the results are stable• Problems : self-discontinuation after symptoms reliefs• Elevated TSH after 200μg/d or fluctuating TSH poor
adherence to treatment Harrison’s Principle of Medicine 18th Ed
THYROTOXICOSIS
THYROTOXICOSIS
• Thyrotoxicosis : state of thyroid hormone excess
• Hyperthyroidism : result of excessive thyroid function
• Major etiologies of thyrotoxicosis are hyperthyroidism caused by Grave’s disease (60-80%) , toxic MNG, and toxic adenoma
Harrison’s Principle of Medicine 18th Ed
EPIDEMIOLOGY
• Varies among populations• High iodine intake higher prevalence of
Grave’s disease• Grave disease 2% of women• Onset occurs between age 20-50, or elder
Harrison’s Principle of Medicine 18th Ed
ETIOLOGY
Harrison’s Principle of Medicine 18th Ed
SIGNS & SYMPTOMS
Harrison’s Principle of Medicine 18th Ed
Signs & SymptomsA . Grave’s Opthalmopathy (Periorbital edema, lid retraction, conjunctival injection, proptosis)B . Thyroid DermopathyC . Thyroid Acropachy
Harrison’s Principle of Medicine 18th Ed
PATHOGENESIS
Pathophysiology of Disease : Introduction to Clinical Medicine 6th Ed
GRAVE’S OPTHALMOPATHY
Harrison’s Principle of Medicine 18th Ed
DIFFERENTIAL DIAGNOSIS
n engl j med 348;26
ALGORITHM
Harrison’s Principle of Medicine 18th Ed
TATA LAKSANA
• Tirostatika• Tiroidektomi• Iodium Radioaktif
Buku Ajar Ilmu Penyakit Dalam Ed V
Kelompok Obat Efek Indikasi
Obat Anti Tiroid Menghambat sintesis hormon tiroid dan berefek imun non supresif (PTU menghambat konversi T4 T3)
Pengobatan lini pertama pada Graves.Obat jangka pendek prabedah /pra-RAI
Propiltiourasil (PTU) Metimazol (MMI) Karbimazol (CTZ MMI) Antagonis Adrenergik β
β-blocker Mengurangi dampak hormon tiroid pd jaringan
Obat tambahan, kadang sebagai obat tunggal pd tiroiditis
Propanolol Metoprolol Atenolol Nadolol
Bahan mengandung iodine Menghambat keluarnya T4 dan T3Menghambat T4 dan T3 serta menghambat produksi T3 ektratiroidal
Persiapan tiroidektomi. Pada krisis tiroid.Bukan untuk penggunaan rutin Kalium Iodida
Solusi Lugol Natrium Ipodat Asam Lopanoat
Obat Lain Menghambat traspor iodium, sintesis dan keluarnya hormonMemperbaiki efek hormon di jaringan dan sifat imunologis
Bukan indikasi rutinPada subakut tiroiditis berat dan krisis tiroid Kalium Perklorat
Litium Karbonat Glukokortikoid
Buku Ajar Ilmu Penyakit Dalam Ed V
TIROIDEKTOMI
• Dikerjakan saat pasien dalam keadaan eutiroid baik scr biokimia maupun klinis
• Operasi menyisakan jaringan sebesar ibu jari, atau lobektomi total termasuk ismus, dan tiroidektomi subtotal lobus lain
Buku Ajar Ilmu Penyakit Dalam Ed V
IODIUM RADIOAKTIF• Belum ada petunjuk baku untuk dosis, ada 2 cara
– Pemberian dosis bertahap hingga pasien mencapai eutiroid– Langsung dosis besar, hipotiroid dikoreksi dengan substitusi
• Pemberian dosis (185mBq / 5mCi – 555 mBq / mCi) mempertimbangkan– Tingkat keparahan penyakit (↑)– Ukuran goiter (↑)– Level of radioiodine uptake (↓)
• Hiportiroidisme terjadi 10-20% dalam 1 tahun, 5% dalam 1 tahun
• Pasien disarankan untuk tidak hamil selama 6 bulan pascaradiasi
Buku Ajar Ilmu Penyakit Dalam Ed V
THYROIDITIS
ETIOLOGY & CLASSIFICATION
Harrison’s Principle of Medicine 18th Ed
THYROIDITIS SYNDROMES
n engl j med 348;26
ACUTE THYROIDITIS• Most common cause : presence of piriform sinus• Sign & Symptoms :
– thyroid pain, referred to throat or ears– small, tender, asymetric goiter– Fever, dysphagia, erythema
• Differential Diagnosis : Subacute or Chronic Thyroiditis, Hemmorhage into a cyst, malignancy, amiodarone-induced thyroiditis or amyloidosis
• Lab : ESR & WBC ↑, Thyroid function N, FNA Infiltration of PMN, Culture to identify organism
• Treatment : Antibiotic treatment (guided by gram stain or culture from FNA biopsy), surgery (draining abscess)
• Complication : Tracheal obstruction, septicemia, retropharingeal abscess, mediastinitis, jugular venous thrombosis
Harrison’s Principle of Medicine 18th Ed
SUBACUTE THYROIDITIS• De Quervain’s thyroiditis, granulomatous thyroiditis, viral thyroiditis (mumps,
coxsackie, influenza, adenovirus, echovirus)• Peak incidence age 30-50, F : M = 3 : 1• Clinical Manifestations : painful & enlarged thyroid, fever (sometimes), features of
thyrotoxicosis or hypothyroidism, malaise, Upper respiratory tract infections, sore throat, small & tender goiter, pain referred jaw or ear
• Lab : Thyrotoxic phase :– T4 & T3 ↑, TSH ↓, ESR ↑, Radioiodine uptake ↓. – Thyroid antibodies (-), – FNA biopsy to distunguish unilateral involvement from bleeding into a cyst or
neoplasm• Treatment :
– Large dose of Aspirin (600mg/4-6h) or NSAID relief symptoms, if not successful glucocorticoid (prednisone 40-60mg) tappered in 6-8 weeks.
– Monitor thyroid function every 2-4 weeks (TSH & fT4)– Low dose Levothyroxine (50-100 μg) if hypothyroid prolonged
Harrison’s Principle of Medicine 18th Ed
PATHOPHYSIOLOGY
Harrison’s Principle of Medicine 18th Ed
SILENT THYROIDITIS• Painless post-partum thyroiditis.• Occurs in patient with underlying autoimmune thyroid disease• Clinical course similiar to subacute, except there’s little or no
thyroid tenderness.• Occurs in 5% of post-partum women• Phases : Throtoxicosis (2-4 weeks), hypothyroidism (4-12
weeks), resolution• 3 times more common in women with T1DM.• Normal ESR & presence of TPO antibodies• Treatment : Glucocorticoid not recommended, thyrotoxicosis
propanolol 20-40mg,3-4x/d, hypothyroid levothyroxine. Annual follow up, may develop permanent hypothyroidism
Harrison’s Principle of Medicine 18th Ed
CHRONIC THYROIDITIS
• Hashimoto’s Thyroiditis• Supurative Thyroiditis• Riedel’s Thyroiditis
Harrison’s Principle of Medicine 18th Ed
HASHIMOTO’S THYROIDITIS
• Most common type of thyroiditis
• High-serum thyroid antibodies & goiter
• Most frequent cause of hypothyroidism & goiter in iodine sufficient areas
• 2 types : goitrous (90%), athropic (10%) thyroid failure
G : Germinal CenterP : Small Lymphocytes & Plasma CellsH : Hurthe Cell MetaplasiaC : Minimal Coloid Materials
n engl j med 348;26
PATHOGENESIS OF HASHIMOTO
Robbins Basic Pathology 8th Ed
HASHIMOTO’S THYROIDITIS
• F : M = 7 : 1• Firm, bumpy, symmetric, painless goiter• Natural History : Hyperthyroidism (inflammation)
hypothyroidism (permanent)• 4 antigents : TGB, Thyroid peroxidase, TSH receptor,
sodium iodine symporter• Thyroid appears hypoechogenic in USG• Treatment : Levothyroxine euthyroid, after 6
months goiter size decreased by 30%. FNA to distunguish limphoma or carcinoma
n engl j med 348;26
SUPPURATIVE THYROIDITIS• Rarely happens, because thyroid has encapsulation, high
iodide content, rich blood supply, and extensive lymphatic drainage
• Occurs in patients with preexisting thyroid disease (cancer, hashimoto, MNG), pyriform sinus fistula, AIDS, elderly
• Signs : fever, dysphagia, dysphonia, anterior neck pain and erythema, and a tender thyroid mass. Predeced by acute respirary tract infection
• Lab : Thyroid function : N (but hypo/hyper is possible), WBC & ESR ↑, Cold in radioactive-iodine scan, FNA to identify organism
• Treatment : antibiotics and surgery to drain abscessn engl j med 348;26
DRUG-INDUCED THYROIDITIS
• Amiodarone • Lithium• Interferon α and Interleukin 2
n engl j med 348;26
AMIODARONE-INDUCED THYROIDITIS
n engl j med 348;26
MONITORING OF THYROID FUNCTION IN PATIENT WITH AMIODARONE THERAPY
n engl j med 348;26
RIEDEL’S THYROIDITIS
• Fibrosis of tyroid gland that may extend to surrounding tissue, unknown cause, requiring surgery
• High serum thyroid antibodies in 67% patient.• Signs & Symptoms : rock-hard, fixed, painless
goiter tracheal or esophageal compression, extended fibrosis hypoparathyroidism
• Lab : euthyroid progress to hypothyroid. • Treatment : Surgery, glucocorticoid useful in
early stagesn engl j med 348;26
GOITER AND THYROID NODULES
GOITER & THYROID NODULES
• Diffuse Nontoxic Goiter• Nontoxic Multinodular Goiter• Toxic Multinodular Goiter• Hyperfunctioning Solitary Nodule
Harrison’s Principle of Medicine 18th Ed
DIFFUSE NONTOXIC GOITER
• Diffuse enlargement of thyroid occurs in the absence of nodules and hyperthyroidism
• Also called simple goiter or colloid goiter• Most common cause : iodine deficiency, called endemic
goiter if affects >5% population• More common in women• Iodine deficiency compensatory to trap more iodine to
produce more hormones• TSH level : N or slightly ↑, indicate increased sensitivity to
TSH or other pathways that lead to thyroid growth• Goitrogens : cassava roots, cruciferae family, milk from
areas where goitrogen present in grassHarrison’s Principle of Medicine 18th Ed
DIFFUSE NONTOXIC GOITER
• Sign & Symptoms : asymptomatic. Hemmorhage to cyst or nodule pain & swelling. symmetrically enlarged thyroid, nontender without any palpable nodules. Tracheal / esophageal compression. Pemberton’s sign
• Lab : Thyroid function: fT4 ↓, fT3 & TSH (N), Urinary iodine level ↓ (<10 μg/dL).Thyroid scan increased iodine uptake, USG indicated only if there’s any palpable mass in PE
• Treatment : – Levothyroxine goiter size regression within 3-6month, dose :
young start at 100 μg, elder start at 50 μg– Surgery : Rare, only when compression is documented– Radioiodine
Harrison’s Principle of Medicine 18th Ed
NONTOXIC MULTINODULAR GOITER
• Occurs in up to 12% in population• More common in women, higher age, iodine-
deficiency areas• Hypercellular regions to cystic area filled with
colloid, extensive fibrosis, hemmorhage, lymphocyte infiltration
• Clinical Manifestation : asymptomatic, euthyroid, large goiter compression (rare). Sudden pain hemmorhage or malignancy. Hoarseness laryngeal nerve involvement or malignancy
Harrison’s Principle of Medicine 18th Ed
NONTOXIC MULTINODULAR GOITER
• Diagnosis : – thyroid architecture
distorted, multiple nodules, Thyroid function N,
– Tracheal deviation – Pulmonary function testing
assess compression or tracheomalacia.
– CT & MRI anatomy of goiter.
– Barium meal asses esophageal compression.
– Biopsy malignancy screening
• Treatment : – Avoid contrast agent or
other iodine containing substance
– Radioiodine with increasing frequency goiter size regression 40-50%
– Acute compression glucocorticoid or surgery
– Surgery : Effective ↑, risk ↑, especially in elder with cardiopulmonary underlying disease
Harrison’s Principle of Medicine 18th Ed
TOXIC MULTINODULAR GOITER• Similiar to Nontoxic MNG, difference is presence of functional
autonomy in toxic MNG• Many nodules are polyclonal• Genetic abnormalities, TSH-R and Gsα mutation• Clinical presentation : goiter, subclinical hyperthyroidism or mild
thyrotoxicosis, patient usually elderly with atrial fibrilation,• Lab : TSH ↓, T3 ↑ ↑ & T4 ↑, 24h uptake of radioiodine not
increased• Thyroid scan : heterogenous uptake with increased and decreased
uptake• Treatment :
– Antithyroid drugs & beta blockers normalize thyroid function– Radioiodine decrease the mass of goiter– Surgery effective to goiter, last choice after drugsHarrison’s Principle of Medicine 18th Ed
MULTINODULAR GOITER
Pathophysiology of Disease : Introduction to Clinical Medicine 6th Ed
MULTINODULAR GOITER
Robbins Basic Pathology 8th Ed
HYPERFUNCTIONING SOLITARY NODULE
• A solitary, autonomously functionung thyroid nodule• acquired somatic activating mutation in TSH-R or Gsα in 90%
patient• Clinical Sign : mild thyrotoxicosis, presence of palpable nodule,
absence of clinical features to Grave.• Thyroid scan : focal uptake in hyperfunctioning nodule,
diminished uptake in remainder gland• Treatment :
– Radioiodine ablation. Large dose correct 75% of patient in 3 month. <10% develop hypothyroidism in 5 years.
– Surgery resection– Antithyroid drugs & beta blockers not suggested for long term therapy
Harrison’s Principle of Medicine 18th Ed
Harrison’s Principle of Medicine 18th Ed
BENIGN NEOPLASM
CLASSIFICATION OF THYROID NEOPLASM
Harrison’s Principle of Medicine 18th Ed
THYROID CANCER
THYROID CARCINOMA
• Most common malignancy in the endocrine system
• Incidence ~9/100.000 per year, incrases with age, plateuing in age ~50
• Bad prognosis in age <20 or >45• F : M = 2 : 1, but male has worse prognosis
Harrison’s Principle of Medicine 18th Ed
AGE OF INCIDENCE
Harrison’s Principle of Medicine 18th Ed
RISK FACTOR
Harrison’s Principle of Medicine 18th Ed
PATHOGENESIS• Radiation
– External radiation predispose to chromosomal breaks genetic rearrangement loss of tumor supressor genes
– Radiation risk of benign and malign nodules ↑– Radiation from iodine therapy contribute minimal increased
risk of thyroid cancer• TSH & Growth factor
– Residual expression of TSH-R allows TSH stimulated uptake of iodine
• Oncogenes & Tumor supressor genes– Increased rate of proliferation– Exhibit impaired apoptosis and features that enchances
invasion, angiongenesis, and metastasisHarrison’s Principle of Medicine 18th Ed
CLASSIFICATION
Harrison’s Principle of Medicine 18th Ed
WELL DIFFERENTIATED THYROID CANCER
• Papillary Thyroid Cancer• Follicular Thyroid Cancer
Harrison’s Principle of Medicine 18th Ed
PAPILLARY THYROID CARCINOMA
• Most common type of thyroid cancer (70-90%)• Present in 25% of autopsy• Small lesion, not clinically significant• Diagnosis by FNA or surgical resection• Multifocal, invade locally to the gland and adjacent tissue• Spread via lymphatic system, metastasize to bone and
lung• Mostly identified in early stages (80%) excelent
prognosis• Identified in stage IV (~1%) poor prognosis
Harrison’s Principle of Medicine 18th Ed
PAPILLARY CARCINOMA
Robbins Basic Pathology 8th Ed
FOLLICULAR THYROID CARCINOMA
• More common in iodine deficient regions• Difficult to diagnosed by FNA• Spread hematogenous to bone, lung and CNV• Mortality risk is higher than PTC• Mostly identified in later stage• Poor prognostic factor : distant metastases, age
>50, tumor size >4cm, Hurthe Cell histology, presence of marked vascular invasion
Harrison’s Principle of Medicine 18th Ed
FOLLICULAR CARCINOMA
Robbins Basic Pathology 8th Ed
TREATMENT OF WELL DIFFERENTIATED THYROID CANCER
• Surgery– Surgery to remove the cancer and involed tissue
or lymph node• TSH supression Therapy– Levothyroxine
• Radioiodine Treatment
Harrison’s Principle of Medicine 18th Ed
FOLLOW UP
Harrison’s Principle of Medicine 18th Ed
ANAPLASTIC AND OTHER THYROID CARCINOMA
• Anaplastic Thyroid Cancer– Poorly differentiated, agressive cancer– Patient died in 6 month after diagnosis– Chemotherapy or External beam radiation
• Thyroid Lymphoma– Arises in the background of Hashimoto’s disease– Highly sensitivie to external radiation– Surgical resection is avoided, treatment follow guideline from other
lymphoma• Meduallry Thyroid Carcinoma
– 5-10% of all Thyroid carcinioma– 3 types : MEN 2A, MEN 2B, Familial MTC– MEN 2B more aggresive than MEN 2A, Familial MTC is more aggresive
than sporadic– Management : surgical, it doesn’t uptake radioiodine
Harrison’s Principle of Medicine 18th Ed
MEDULLARY CARCINOMA
Robbins Basic Pathology 8th Ed
Harrison’s Principle of Medicine 18th Ed
REFERENCES
• Harrison’s Principle of Medicine 18th Ed• Buku Ajar Ilmu Penyakit Dalam Edisi V• Junqueira Basic Histology 12th Ed• Robbin’s Basic Pathology 8th Ed• McPhee SJ, Hammer GD, Pathophysiology of
Disease : Introduction to Clinical Medicine 6th Ed• Sherwood’s Physiology from cells to system 7th Ed• New England Journal of Medicine