Download - 6. Curs Nodulul Tiroidian
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GUSA ENDEMICA
- Curs pentru studentii la Medicina-
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TIROIDA- ANATOMIE
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TIROIDA- ANATOMIE SI IMAGISTICA
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TIROIDA- MICROSCOPIE OPTICA
Foliculi tiroidieni cu coloid
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CELULA FOLICULARA TIROIDIANA
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IODUL SI HORMONII TIROIDIENI
- iodul: 66% din T4 si 58% din T3
- depozitele intratiroidiene de iod: 5-10 mg
- concentrare iod tiroida:ser= 30:1 (NIS, transport activ)
- aportul optim de iod: 150 µg/zi adulti, 200 µg/zi gravide
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BIOSINTEZA HORMONILOR TIROIDIENI
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SECRETIA DE HORMONI TIROIDIENI
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RECEPTORUL NUCLEAR AL HORMONILOR TIROIDIENI
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REGLAREA SECRETIEI TIROIDIENEAXA HIPOTALAMO-HIPOFIZO-TIROIDIANA
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DEIODAZELE TIROIDIENE SI HIPOFIZARE
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Dupa Williams, 2003
Carbimazol
MetimazolIodul in exces: KI/NaI sol
saturata, solutie Lugol, acid iopanoic
Ablatia tiroidei: 131I, tiroidectomie
Propiltiouracil (PTU)
Deriv. de imidazol
Deriv. de tiouree
Iodul
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RECEPTORUL PENTRU TSH
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INDICATORI DE EFICIENTANORMALUL FUNCTIEI TIROIDIENE
PRODUCTIA SANGVINA: T4, T3 T4 liber
EFECTUL TISULAR TSH
CARE ESTE NIVELUL NORMAL AL TSH?
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FIZIOLOGIE
T4:T3= 14:1 la om
T4:T3= 6:1 la soarece
Pilo A, Am J Physiol, 1990; 258:E715
Rata zilnica a prod.tiroidiene:
101 µg T4 + 6 µg T3
Conversia T4 T3 = 20 µg T3
Creier- T4:T3= 1,17:1
Miocard- T4:T3= 2,25:1
Secretia tiroidiana Tisular
Escobar-Morreale HF, Endocrinology, 1996; 137(6):2490
Rata absorbtiei: T4 - 80%
T3 - 90%
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NOUL INTERVAL DE NORMALITATE A TSH-ului
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- Definitie
- Clasificare
- Clinica
- Paraclinic
- Diagnostic pozitiv
- Diagnostic diferential
- Etiologie
- Patogenie
- Anatomie patologica
- Fiziopatologie
- Evolutie
- Complicatii
- Tratament
- Prognostic
GUSA ENDEMICA
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DEFINITIE• Marire de volum a tiroidei + modificari
distrofice intratiroidiene
• Datorata deficitului de iod
• apare la >5% din scolari 6-12 ani
• In zone geografice cu cantitati mici de iod in apa si alimente
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- Definitie
- Clasificare
- Clinica
- Paraclinic
- Diagnostic pozitiv
- Diagnostic diferential
- Etiologie
- Patogenie
- Anatomie patologica
- Fiziopatologie
- Evolutie
- Complicatii
- Tratament
- Prognostic
GUSA ENDEMICA
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a. Clinica:- oligosimptomatic- endocrinopat: Hiper, hipo- neuropat
b. In functie de gravitatea deficitului de iod:
CLASIFICARE
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NormalDeficit iodat uşor
Deficit iodat
moderat
Deficit iodat sever
Prevalenţa guşii (%) < 5% 5-20% 20-30% > 30%
Mediana iodului urinar (μg/l) > 100 50-99 20-49 < 20
TSH neonatal > 5 mU/l (%) < 3% 3-20% 20-40% > 40%
INDICATORI AI SEVERITĂŢII DEFICIENŢEI IODATE
CLASIFICARE
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Delange F Top End, 1996, 2:2
EPIDEMIOLOGIE
- P: prevalenta
- U: urgenta
- I: interv. eficienta
- G: gravitate
- E: educare
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- Definitie
- Clasificare
- Clinica
- Paraclinic
- Diagnostic pozitiv
- Diagnostic diferential
- Etiologie
- Patogenie
- Anatomie patologica
- Fiziopatologie
- Evolutie
- Complicatii
- Tratament
- Prognostic
GUSA ENDEMICA
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CLINICA- IDDPerioada fetală Avort, naşteri premature, anomalii congenitale, creşterea
mortalităţii perinatale, cretinism endemic: formaNeurologică şi cea mixedematoasă
Nou-născut Guşă oligosimptomatică, hipotiroidism neonatal clinic manifest sau subclinic, retard mental endemic, creşterea susceptibilităţii tiroidiene la radiaţii
Copil şi adolescent Guşă oligosimptomatică, hipotiroidism subclinic, întârzierea dezvoltării intelectuale şi fizice, creşterea susceptibilităţii tiroidiene la radiaţii
Adult Guşă oligosimptomatică/ cu fenomene compresive, hipotiroidism, retard mental endemic, hipertiroidismspontan la vârstnici, hipertiroidism iod-indus, scădereafertilităţii, creşterea susceptibilităţii tiroidiene la radiaţii
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FAZA OLIGOSIMPTOMATICA: hiperplazia tiroidei FAZA ENDOCRINOPATA FAZA NEUROPATA
CLINICA
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Gradul guşii -Clasificare DescriereGradul 0 Fără guşă vizibilă sau palpabilăGradul 1 Guşă palpabilă, dar nevizibilă cu
gatul în poziţi e normală (tiroida nu este vizibil mărită). Nodulii
tiroidieni într-o tiroidă de dimensiuni normale aparţin acestei
categorii.Gradul 2 Guşă vizibilă cu gâtul în poziţie
normală
CLASIFICAREA GUSEI- OMS 2001
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Faza oligosimptomatica:
-Gusi difuze: copiii si adolescentii
- gusi nodulare: adultii si varstnicii
CLINICA
± semne de compresie (esofag, trahee, simpatic cervical, vasculara- semnul Pemberton)
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CLINICA-Faza endocrinopata
- Faza neuropata: endemie severa
CRETINISMUL ENDEMIC
Definitie: Forma cea mai severa a IDD la descendentii mamei cu gusa endemica
A. Epidemiologic: deficit iodat sever (iodurie < 20 µg/l)
B. Clinic: retard mental + sd. Neurologic si/sau mixedem
C. Profilactic
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CRETINISMUL ENDEMIC- global
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Forma mixedematoasă Forma neurologicăRetardare mentală
Severă severă
Statură deficit statural sever cvasinormalăGuşă de regulă absentă nodulară
Surdomutitate Rară Prezentă/hipoacuzie cu dizartrie
Diplegie spastică
Absentă prezentă, tulburări deechilibru şi coordonare
ROT Diminuate exagerateMaturaţie osoasă şi sexuală
marcat întârziate, disgenezie
epifizară a capului femural
normale
Funcţie tiroidiană
Hipotiroidism sever (TSH marcat crescut,T4, T3 scăzute)
Eutiroidism/hipotirodism subclinic (TSH uşor crescut,
FT4 normal)
CRETINISMUL ENDEMIC- FORME CLINICE
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- Definitie
- Clasificare
- Clinica
- Paraclinic
- Diagnostic pozitiv
- Diagnostic diferential
- Etiologie
- Patogenie
- Anatomie patologica
- Fiziopatologie
- Evolutie
- Complicatii
- Tratament
- Prognostic
GUSA ENDEMICA
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- ecografia tiroidiana
- ioduria recoltata in zona endemica (N: 100-199 µg/l)
- RIC: crescuta moderat la 2 h, marcat la 24 ore
- nivele N/crescute de TSH
- nivele N/scazute de T4, free T4
- nivele N/crescute de T3
- Ac anti TPO, anti Tg: absenti
- scintigrama tiroidiana cu iod/technetiu
PARACLINIC
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VOLUME TIROIDIENE DE REFERINTA FUNCTIE DE VARSTA, SEX, SUPRAFATA CORPORALA
Zimmermann et al, 2004
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IMAGISTICA: EFECTE COMPRESIVE
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Gusa polinodulara: nodul transformat chistic
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GUSA MEDIASTINALA
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Mediana iodului urinar
(μg/l)Aport iodat Status iodat nutriţional
< 20 insuficient deficit iodat sever20-49 insuficient deficit iodat moderat50-99 insuficient deficit iodat uşor
100-199 adecvat optim
200-299 Uşor crescutrisc de hipertiroidism iod-indus la
5-10 ani după introducerea iodării sării la persoanele susceptibile
> 300 excesiv risc de hipertiroidism iod-indus,boli tiroidiene autoimune
CRITERII EPIDEMIOLOGICE DE EVALUAREA A STATUSULUI IODAT PE BAZA MEDIANEI CONCENTRAŢIILOR IODULUI URINAR
LA COPII ŞCOLARI
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- Definitie
- Clasificare
- Clinica
- Paraclinic
- Diagnostic pozitiv
- Diagnostic diferential
- Etiologie
- Patogenie
- Anatomie patologica
- Fiziopatologie
- Evolutie
- Complicatii
- Tratament
- Prognostic
GUSA ENDEMICA
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DIAGNOSTIC POZITIV-Individual:
prezenta gusei deficit geoclimatic de iod criteriu epidemiologic
-Endemia: prevalenta gusei >5% la scolari TSH neonatal > 5 mUI/l la > 3% nou nascuti deficit geoclimatic de iod (iodurie < 100 µg/L)
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- Definitie
- Clasificare
- Clinica
- Paraclinic
- Diagnostic pozitiv
- Diagnostic diferential
- Etiologie
- Patogenie
- Anatomie patologica
- Fiziopatologie
- Evolutie
- Complicatii
- Tratament
- Prognostic
GUSA ENDEMICA
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DIAGNOSTIC DIFERENTIAL 1. Gusa dishormonala
2. Gusa autoimuna
3. Neoplasme tiroidiene (TB)
4. Gusa sporadica indusa de Li, amiodarona, factori gusogeni
5. Gusa prin mutatii activatoare ale receptorului de TSH
6. Tiroidita subacuta
7. Gusa din sarcina
8. Rezistenta generalizata la hh. tir
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RECEPTORUL PENTRU TSH
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- Definitie
- Clasificare
- Clinica
- Paraclinic
- Diagnostic pozitiv
- Diagnostic diferential
- Etiologie
- Patogenie
- Anatomie patologica
- Fiziopatologie
- Evolutie
- Complicatii
- Tratament
- Prognostic
GUSA ENDEMICA
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ETIOLOGIE
1.Deficitul de iod
2.Factori gusogeni
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90 μg/zi pentru copii preşcolari (0-59 luni)120 μg/zi pentru copiii şcolari (6-12 ani)
150 μg/zi pentru adulţi (peste 12 ani)200 μg/zi pentru gravide şi pentru femeile care
alăptează
RECOMANDĂRILE OMS PENTRU APORTUL ZILNIC MINIM DE IOD
Grupe tinta pentru profilaxia iodata: femeile gravide si in perioada de alaptare, nou-nascuti, copiii mici
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A. Poluarea bacteriană: progoitrin -inhibă organificarea iodului B. Factori alimentari:- Tiocianat, izotiocianat (din rădăcinile de cassava-manioc)- inhibă captarea tiroidiană a iodului - Flavonoizi (polifenoli) – inhibă peroxidaza tiroidiană (oxidarea intratiroidiană a iodului şi cuplarea lui) - Goitrina (guşogen vegetal) - inhibă organificarea iodului - Soia – guşogen prin acţiune indirectă, întrerupe circuitul enterohepatic al T4, cu creşterea eliminările digestive de T4
- Malnutriţia – determină deficit de vitamina A, cu o structură anormala a Tg - Litiul – interferă cu proteoliza, deiodarea şi eliberarea hormonală- Deficitul de seleniu – alterarea deiodazei de tip I (o selenoproteină) care are rol major în deiodarea periferică a T4
FACTORI GUSOGENI
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- Definitie
- Clasificare
- Clinica
- Paraclinic
- Diagnostic pozitiv
- Diagnostic diferential
- Etiologie
- Patogenie
- Anatomie patologica
- Fiziopatologie
- Evolutie
- Complicatii
- Tratament
- Prognostic
GUSA ENDEMICA
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PATOGENIEAport scazut de iod
Scaderea productiei de T4, T3
Cresterea sensibil. Tisulare la TSH/cresterea secr. TSH
Hiperplazie tiroidiana difuza nodulara
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PATOGENIE
Mecanisme adaptative la deficitul de iod
cresterea captarii intratiroidiene a iodului sinteza si secretia preferentiala de T3 cresterea conversiei T4 in T3 periferic si in cortexul cerebral
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Morreale G, Top End, 1996, 2:3
PATOGENIE CRETINISM
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PATOGENIE CRETINISM
Forma neurologica:
- leziunile apar precoce in utero (T1)
- hipotiroidismul matern
- deficit iodat sever hipotiroxinemia materna
- cohlee surdomutitate
- neocortex cerebral retard mental
- tract corticospinal diplegie spastica
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PATOGENIE CRETINISM
Forma mixedematoasa:
- leziunile apar tardiv in sarcina, postnatal
- deficit iodat postnatal
- tiocianati
- deficit de seleniu
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- Definitie
- Clasificare
- Clinica
- Paraclinic
- Diagnostic pozitiv
- Diagnostic diferential
- Etiologie
- Patogenie
- Anatomie patologica
- Fiziopatologie
- Evolutie
- Complicatii
- Tratament
- Prognostic
GUSA ENDEMICA
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ANATOMIE PATOLOGICA
“ Distrofie endemica tireopata” – St. Milcu
Hiperplazie/ atrofie/ fibroza
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- Definitie
- Clasificare
- Clinica
- Paraclinic
- Diagnostic pozitiv
- Diagnostic diferential
- Etiologie
- Patogenie
- Anatomie patologica
- Fiziopatologie
- Evolutie
- Complicatii
- Tratament
- Prognostic
GUSA ENDEMICA
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FIZIOPATOLOGIEExcitarea subliminala prin TSH
Foliculi activi/atrofici
Crestere noduli autonomi (TSH indep) masa critica
Mutatii activatoare ale recept. TSH
Gusa endemica hipertirodizata
± suplim/exces de iod
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PROGNOSTIC
quod ad vitam, quod ad integrum: bune sub profilaxie corecta
quod ad functionem: rezervat in forma neuropata, ireversibila
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- Definitie
- Clasificare
- Clinica
- Paraclinic
- Diagnostic pozitiv
- Diagnostic diferential
- Etiologie
- Patogenie
- Anatomie patologica
- Fiziopatologie
- Evolutie
- Complicatii
- Tratament
- Prognostic
GUSA ENDEMICA
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EVOLUTIE- COMPLICATII
fenomenul Jod-Basedow: hipertiroidism iod indus in gusile vechi cresterea prevalentei carcinomului tiroidian folicular dar NU creste prevalenta globala a K tir compresiuni: CBH
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- Definitie
- Clasificare
- Clinica
- Paraclinic
- Diagnostic pozitiv
- Diagnostic diferential
- Etiologie
- Patogenie
- Anatomie patologica
- Fiziopatologie
- Evolutie
- Complicatii
- Tratament
- Prognostic
GUSA ENDEMICA
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TRATAMENT
OBIECTIVELE TERAPIEI
substituirea deficitului iodat normalizarea hh. Tiroidieni inlaturarea fenomenelor compresive
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PRINCIPIILE TERAPIEI
PROFILAXIE PERMANENT tuturor persoanelor din zona endemica (doar gusi difuze) aportul iodat optim:
150 µg/zi adulti 200 µg/zi gravide/alaptare/pubertate
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TRATAMENTUL PROFILACTIC
sare iodata ulei iodat (Lipiodol) KI
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SAREA IODATA
metoda profilactica cea mai raspandita ieftina, eficienta, accesibila KI sau KIO3
20-40 mg KIO3/ kg sare
St. Milcu- 1957 Legea iodarii universale a sarii (2003): 40 mg KIO3/kg sare
disparitia cazurilor de cretinism
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ULEIUL IODAT
inj (480 mg iod), cps (190 mg iod) adulti: 1 cps/3 luni
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IODURA DE POTASIU
KI 1 mg/saptamana Jodid 100, 1 cp/zi –adulti Jodid 200, 1 cp/zi gravide, pubertate
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EFECTELE PROFILAXIEI IODATE
corectia deficitului de iod elimina retardul mental, gusa, hipotir si morbiditatatea perinatala scade incidenta hipertiroidismul neautoimun scade morbiditatea prin cancer tiroidian (creste rap papilar/folicular)
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REACTII ADVERSE ALE PROFILAXIEI IODATE
1.Hipertiroidismul iod-indus (varstnici, exces de iod)
2. Creste frecventa tiroiditei autoimune Hashimoto
TERAPIE EFICIENTA SI SIGURA
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TRATAMENTUL CURATIV
HH. TIROIDIENI supresia gusei difuze, corectarea hipotiroidismului CHIRURGIA: tiroidectomie subtotala (gusi mari, fenomene compresive, cervico-toacice) 131I 20-40 mCi (controvesat): CI ale chirurgiei
METODE
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CHIRURGIA tiroidei
A. Incizie transversala, simetrica, la 1 cm sub cartilajul cricoid prin muschiul platysma
B. Incizie pe linia mediana pentru aducerea tiroidei in prim planul campului operator
C. Disecarea cat mai aproape de tiroida pentru a evita injuria filetelor nervoase si ligaturarea vaselor
A B C
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TRATAMENTUL CU IOD RADIOACTIV
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- Definitie
- Clasificare
- Clinica
- Paraclinic
- Diagnostic pozitiv
- Diagnostic diferential
- Etiologie
- Patogenie
- Anatomie patologica
- Fiziopatologie
- Evolutie
- Complicatii
- Tratament
- Prognostic
GUSA ENDEMICA
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NODULUL TIROIDIAN SI CANCERUL TIROIDIAN
- Curs pentru studentii la Medicina-
Dr. Raluca Alexandra Trifanescu
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NODULUL TIROIDIAN
nodulii tiroidieni: 4% din populatie (femei:barbati= 4:1)
<5% din nodulii tiroidieni sunt cancer tiroidian
EPIDEMIOLOGIE
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ETIOLOGIA NODULILOR TIROIDIENI BENIGNI
tiroidita focala nodul dominant in gusa polinodulara chist tiroidian, paratiroidian, de tireoglos agenezia unui lob tiroidian hiperplazie de bont posttiroidectomie/postradioiod adenoame tiroidiene benigne
folicular rare: teratoame, lipoame, hemangioame
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Probabil BENIGN Probabil MALIGN
Anamneza
AHC de gusa benignaRezidenta in zona
endemica
AHC de carcinom medular tiroidianIradiere terapeutica a capului sau
gatuluiNodul cu crestere recenta si rapida
Difonie, disfagie, obstructie
Examenobiectiv
Femeie varstnicaNodul moale
Gusa multinodulara
Copil, adult tanar, barbatNodul solitar,dur, fixat de tes adiac.
Paralizie de corzi vocale, adenopatie dura, metastaze la
distanta
Paraclinic Ac antitiroidieni prezenti Calcitonina crescuta
Scintigrama Nodul “cald” Nodul “rece”
Ecografie Chist pur Solid sau semichistic
Biopsie Citologie benigna Citologie maligna
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ECOGRAFIA
Chist pur Chist impur
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SCINTIGRAMA TIROIDIANA
Nodul “cald” Nodul “rece”
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PUNCTIA BIOPSIE- ASPIRATIE CU AC FIN (FNA)
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Nodul tiroidian unic/noduli multipli
Anamneza, examen obiectiv tiroidian si cervical
Diametru < 1 cm
Nesuspect
TSH normal
Urmarire
Diametru 1cm sau 1 cm ,dar suspect
Punctie tiroidiana cu ac fin
Scintigrafie tiroidiana
Nodul “rece”
Ecografie TSH, FT4, FT3, ATPO
Nodul solid/mixt Calcitonina
TSH supresat sau gusa multinodulara
Benign Malign, suspect sau neoplasm folicular
Chirurgie
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DIAGNOSTICUL CITOLOGIC PRIN PUNCTIE BIOPSIE CU AC FIN
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TRATAMENTLeziune benigna (FNA) LT4
Regresie
Continua LT4
NU regreseaza Creste
Rebiopsiere
Chirurgie
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TERAPIA SUPRESIVA CU LEVOTHYROXINA IN NODULUL TIROIDIAN
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Urmarire ± LT4
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- Definitie
- Clasificare
- Clinica
- Paraclinic
- Diagnostic pozitiv
- Diagnostic diferential
- Etiologie
- Patogenie
- Anatomie patologica
- Fiziopatologie
- Evolutie
- Complicatii
- Tratament
- Prognostic
CANCERUL TIROIDIAN
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DEFINITIE• proces malign ce intereseaza tiroida
• D.p.d.v al celulei de origine:
» primar
» metastatic (cancer gastric, renal, pulmonar, limfom)
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EPIDEMIOLOGIE
cea mai frecventa neoplazie maligna endocrina cancer rar (1% din totalul cancerelor) curabilitate mare
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CLASIFICAREA.PRIMAR:
1. Origine in celulele foliculare tiroidiene
- carcinom diferentiat
- papilar (70-75%)
- folicular (10-15%)
- carcinom nediferentiat (anaplastic) 5%
2. Origine in celulele C (parafoliculare)
- carcinom medular tiroidian 5%
3. Origine in alte celule: sarcom, limfom tiroidita Hashimoto, carcinom cu celule scuamoase
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B. SECUNDAR
1. Metastazele cancerelor solide: pulmonar, san, rinichi
2. Limfom
CLASIFICARE
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CARCINOMUL TIROIDIAN DIFERENTIATCARCINOMUL PAPILAR
forma cea mai frecv: 75% neend, 50% end mai frecv la tineri < 40 ani cancer inalt diferentiat capteaza 131I
evolutie lenta cancer TSH dependent secreta tireoglobulina
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CLINICA
nodul ferm solitar/ dominant in gusa polinodulara clar delimitat de restul glandei 10% (mai ales la copii): debut ca meta gg.
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NODUL “RECE SCINTIGRAFIC”
- hipocaptant
- dar capteaza 131I > alte cancere tiroidiene terapie
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ECOGRAFIA
- nodul dens
- uneori cu arii de ramolire sau hemoragie
- calcificari fine: corpii psammoma
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MARKER TUMORALTIREOGLOBULINA
- coloid invazie vasculara sange
- crestere= RECIDIVA SAU METASTAZARE
- utilitate: eficienta terapiei aparitia metastazelor NU preoperator
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DISEMINARE1. META
INTRAGLANDULARE
2. LIMFATICA precoce meta gg. nu modifica progn.
3. SANGVINA tardiva plaman, os, creier
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ANATOMIE PATOLOGICA
tireocite in struct. papilifere, centrate de o tija fibrovasculara
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patognomonici
mici sfere cu calcificari laminare
ANATOMIE PATOLOGICACORPII PSAMMOMA
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EVOLUTIE- COMPLICATII
foarte lenta mortalitate 5% la 15 ani meta ganglionare – precoce, frecvente meta la distanta – tardiv transformare anaplazica tardiva (varstnici) carcinom anaplazic invazie mm, trahee, esofag
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TRATAMENT1. leziuni < 1cm, incapsulate, fara meta, < 45 ani:
lobectomie + istmectomie + tratament supresiv cu LT4 (TSH: 0,1-0,4 mUI/l)
2. leziuni > 1cm, invazie capsulara, meta, > 45 ani, barbati: tiroidectomie cvasitotala + evidare ganglionara ablatie cu 131I a resturilor tiroidiene (30-100
mCi) tratament supresiv cu LT4 (TSH < 0,1 mUI/l)
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URMARIRE
oprire la 6 luni a LT4 4-6 sapt/ TSH-r dozare Tg scintigrama whole-body
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TERAPIA CU 131I
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CARCINOMUL TIROIDIAN DIFERENTIATCARCINOMUL FOLICULAR
prevalenta: 10-15% neend, 30-40% end mai frecv la 40-45 ani cancer inalt diferentiat capteaza 131I
dar evolutie mai agresiva decat cel papilar
cancer TSH dependent secreta tireoglobulina
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CLINICA
nodul ferm solitar/ dominant in gusa polinodulara clar delimitat de restul glandei
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NODUL TIROIDIAN “RECE”
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ANATOMIE PATOLOGICA
se mentine structura foliculara dg: invazie capsulara si vasculara greu de diferentiat la punctia biopsie de celulele normale
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DISEMINARE1. SANGVINA
precoce plaman, os, creier unele meta pot fi functionale (T3, T4)
2. LIMFATICA
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WBS- METASTAZE PULMONARE
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SCINTIGRAMA CU TC- METASTAZE OSOASE
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EVOLUTIE- COMPLICATII
lenta, dar mai agresiv decat papilarul mortalitate 8% la 10 ani meta la distanta – mai precoce meta functionale tireotoxicoza
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MARKER TUMORALTIREOGLOBULINA
- coloid invazie vasculara sange
- crestere= RECIDIVA SAU METASTAZARE
- utilitate: eficienta terapiei aparitia metastazelor NU preoperator
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TRATAMENT
- Indiferent de marime: tiroidectomie cvasitotala + evidare ganglionara ablatie cu 131I a resturilor tiroidiene (30-100
mCI); radiosensilitate > papilar tratament supresiv cu LT4 (TSH < 0,1 mUI/l)
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CARCINOMUL TIROIDIAN DIFERENTIATCARCINOMUL MEDULAR
origine: celulele parafoliculare C secreta calcitonina, Ag carcinoembrionar (ACE), ACTH NU secreta tireoglobulina NU capteaza iodul cancer TSH INdependent sporadic (33%)/ familial/ MEN (66%)
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CLINICA nodul ferm solitar/ dominant in gusa polinodulara clar delimitat de restul glandei sd. Cushing secretie ectopica de ACTH,
CRH diaree secr. ectopica de VIP NU hipocalcemie
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PARACLINIC
1. Dozare calcitonina bazal si dupa stimulare cu calciu /pentagastrina
2. Histologie: rosu de Congo
3. Imunohistochimie pozitiva pentru calcitonina
4. Mutatii specifice ale oncogenei ret
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MARKER TUMORALCALCITONINA
- clinic: nu determ hipocalcemie
- diagnostic (serica + IHC)
- screening la cei cu mutatii ale oncogenei ret
- eficienta terapiei: aparitia recidivelor metastazelor
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ANATOMIE PATOLOGICA
Dg: coloratie Rosu de Congo IHC + calcitonina
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DISEMINARE1.LIMFATICA:
gg. cervicali gg. mediastinali
2. SANGVINA ficat plaman os
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ASOCIERI IN SD. MEN
MEN II a (sd. Sipple)K. medular tiroidian feocromocitom hiperparatiroidism
MEN II bK. medular tiroidian feocromocitom anomalii neuroectodermale status marfanoid
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TRATAMENT
- Indiferent de marime: tiroidectomie cvasitotala + Disectie cervicala cu evidare ganglionara +/- radioterapie externa, chimioterapie NU ablatie cu 131I a resturilor tiroidiene
(radiorezistent) NU tratament supresiv cu LT4
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EVOLUTIE spontana lenta prognostic rezervat forma spradica: prognostic mai sever
SCREENING calcitonina calcemie, fosfatemie catecolamine urinare
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CARCINOMUL TIROIDIAN NEDIFERENTIAT (ANAPLAZIC)
rar mai frecv la varstnici nu capteaza 131I radiorezistenta recidive frecvente postoperatoriiprognostic prost: mortalitate 80% la 1 an
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CLINICA tumora mare cu crestere rapida fenomene compresive locale +/- tiroidita locala
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DIAGNOSTIC POZITIV• Clinica sugestiva• Ecografie: leziune solida/semisolida, adenopatii• Scintigrama: nodul “rece”• Citologie (punctie biopsie cu ac fin):
carcinom papilar carcinom anaplastic carcinom medular (Rosu de Congo) carcinom folicular daca are invazie
capsulara si/sau vasculara• Histologie (tip + extensie gg)
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DIAGNOSTIC DIFERENTIAL
Nodulul solitar benignGusi multinodulareHemiageneziiAl formei histopatologiceAl formei primare/secundareLimfom!!! Tiroidita HashimotoTiroidita Riedl (lemnoasa)
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ETIOPATOGENIE
expunerea la radiatii a regiunii cervicale/capului, mai ales in copilarie
mutatii oncogena ras K folicular mutatii oncogena ret K papilar mutatii oncogena ret K medular Pierderea genei supresor tumoral P53
transformarea anaplazica a K diferentiate
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FIZIOPATOLOGIE
Meta gg Meta sangvine pulmon, os, ficat, creier Invazie structuri locale Transformare anaplastica
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TRATAMENTOBIECTIVELE TERAPIEI
inlaturarea masei tumorale primare (terapie primara) prevenire recidive si metastazare (terapie adjuvanta) terapia supresiva si suportiva cu LT4
terapia recidivelor si metastazelor (terapie secundara)
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METODE1. Chirurgia: tiroidectomie totala
Complicatii: Hipoparatiroidism definitiv Paralizie de nv. Laringei recurenti
2. Ablatia cu 131I a resturilor tiroidiene Doze: 30-100 mCi
Distruge resturile postoperatorii Creste specificitatea Tg si scintigramei whole-
body postoperator
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METODE3. Terapia supresiva cu LT4
Doze: 2-2,2 µg/kg c
TSH tinta: - risc scazut: 0,1-0,4 µUI/ml- risc crescut < 0,1 µUI/ml
RA: osteoporoza, tahiaritmii, angina
- se opreste cu 4-6 saptamani anterior Tg, scinti whole body- sau inlocuire cu liotironina T3 50 µg/zi oprit cu 2 sapt. Ant- sau inlocuire cu TSH recombinant (hipopituitarism, IC, insuf. Renala severa)
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MONITORIZARE