curs endo 1
DESCRIPTION
endocrinologyTRANSCRIPT
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Definiţia unui hormon
●Hormonii = molecule mesager ce transmit informatia biologica intre celule si tesuturi
– sediul secretiei
• glande endocrine
• sistemul endocrin difuz
Structura
• polipeptide: TRH, STH, ACTH, MSH, PRL, T3, T4, PTH
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Structura• glicoproteine: TSH, FSH, LH, HCG, renina,
angiotensina
• hormoni steroizi: cortizol, aldosteron, estrogeni, progesteron, testosteron, DHEA, androstendion
• monoamine: adrenalina, noradrenalina, dopamina
Circulaţie• hormoni liposolubili- proteine transportoare
• hormoni hidrosolubili- liber, solviti in plasma
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Catabolismul
• ficat• rinichi• receptori hormonali
Timpul de înjumătăţire
scurt (ex.h. hipofizari- minute)
lung (ex. Tiroxina- 8 zile)
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Receptorul hormonal= structură proteică cu specificitate pentru hormon si afinitate de legare
RECEPTOR DE MEMBRANARECEPTOR DE MEMBRANA
RECEPTOR CITOPLASMATICRECEPTOR CITOPLASMATIC
RECEPTOR NUCLEARRECEPTOR NUCLEAR
H TIROIDIENIH TIROIDIENI
H. PEPTIDICI
H. STEROIZIH. STEROIZI
ADNADN
RR
RR
RR
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Reglarea secreţiei hormonale
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Reglarea SE = feedback NEGATIV /POZITIV
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• BE CENTRALA
Etiopatogenia bolilor endocrine
HPTHPT HPTHPTHPTHPT
HPFHPF HPFHPF HPFHPF
GTGT GTGT GTGT
RBE PRIMARA
BE DE RECEPTOR
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Patologia hipotalamo-hipofizarăSindromul adipozo-genital
Sindrom caracterizat prin obezitate si infantilism genital
Forme• congenitală (sindr. Laurence-Moon-Biedle) -AR:
obezitate, infantilism genital, oligofrenie, talie mica, retinopatie pigmentară, polidactilie cu sindactilie, diabet insipid
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• tumorala (Babinski- Frolich)
• netumorala- traumatisme, procese inflamatorii
• idiopatic
Tablou clinic• obezitate cu evolutie progresivă, “ in trepte”
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• infantilism genital• pubertate
incompleta
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• talia• hiperlaxitate ligamentară• dezvoltare intelectuală normală dar cu complexe de
inferioritate
Diagnostic• clinic• paraclinic:
* examinari imagistice (RMN, CT)
*gonadotropi- scăzuţi
*hormonii sexuali- scăzuţi
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*cortizol, metaboliţi urinari- crescuţi
*T3, T4, TSH- normali / scăzuţi
*STH- normal / scăzut
Tratament
Chirurgical+/- radioterapie• Regim hipocaloric• Substituţie hormonală: STH, Tiroxină• Infantilism genital: - Pregnyl 2-3 cure
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Pubertatea fiziologica
• etapa fiziologica caracterizata prin dezvoltarea caracterelor sexuale secundare si accelerarea procesului de crestere (salt statural)
• Fetite: 8-13 ani • Baieti: 9-14 ani
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Pubertatea precoceDefinitie:
maturarea precoce a axului hipotalamo-hipofizo-gonadic ▬► sexualizare secundară precoce (sub vârsta de 10 ani) a indivizilor
Etiologia• tumorală• netumorală• : iradierea SNC, boli genetice• idiopatică
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Tablou clinic
*apariţia precoce a caracterelor sexuale secundare
*dezvoltarea organelor genitale
*apariţia menstrelor şi a erecţiilor
*scurt puseu de creştere- oprirea creşterii
*sindrom de dezadaptare neuro-psihică şi socială
* manifestări specifice etiologiei boli
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Diagnostic• FSH, LH , hormoni sexuali- crescuti• RMN, CT
Tratament
În formele tumorale- îndepărtarea tumorii
În formele netumorale- frenarea axului gonadotrop
• Medroxiprogesteron 5- 20mg/zi
• analogi de gonadoliberină -Decapeptil
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Diabetul insipidSindrom caracterizat prin:
- deficitul ADH
- insensibilitatea receptorilor renali la acţiunea lui
Clasificare
•DI Central
•DI Nefrogen
•DI Total
•DI Partial
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Etiologie
DI central:
*post- chirurgie hipotalamo-hipofizară
*traumatisme craniene
*tumori
*infecţii
*familial - AD
*genetic
*idiopatic
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DI nefrogen
*congenital -AR
*dobândit
Tablou clinic• poliurie >2,5-3 L/24 ore- 15-20 L (indicele potofilic)• nicturie• sete intensă, polidipsie• inapetenţă, scădere ponderală, dureri epigastrice
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• astenie• anxietate• alte semne hormonale, neurologice, oftalmologice
în funcţie de etiologie
Diagnostic• clinic• paraclinic:
*bilanţul hidric: cantitate > 2,5 l/zi, densitate< 1005 în toate eşantioanele
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*proba la sete: - restricţie hidrică 1-4 ore- eşantioane orare:
• Potomanie: scăderea cantităţii+ creşterea densităţii• DI: nemodificat
*proba la ADH: 2 pic. Adiuretin (instilaţie nazală):
• DI central =scăderea cantităţii urinii+ creşterea densităţii
• DI nefrogen= volum urinar, densitate nemodificateExaminări etiologice: RMN, investigarea
morfo- funcţională a rinichiului
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Diagnostic diferenţial• Diabetul zaharat- densitate urinară > 1020• Potomania- proba la sete• nefropatii cu insuficienţă renală• pielonefrita cronică• hiperaldosteronismul primar
Tratament• etiologic- rareori posibil• igieno-dietetic
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• patogenetic:
*În DI central:• Adiuretin 0,1 mg/ml 1-4 pic, în 1-2 prize• Minirin 0,2- 1,2 mg/zi+ sedative şi psihoterapie
*În DI nefrogen:• Diureticele tiazidice
- Hidroclorotiazida (Nefrix 25 mg/tb) în doza de 50-100mg/zi în 2-3 prize
- suplimentarea aportului de potasiu sau asocierea de Spironolactonă, Triamteren, Amilorid
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Sindromul tumoral hipofizar
Sindrom datorat unor procese expansive care evoluează în loja hipofizară sau în imediata ei vecinătate, caracterizat prin semne realizate de compresiunea formaţiunii asupra structurilor învecinate, asociate uneori cu semne de hipersecreţie hormonală
Etiologie• Adenoame hipofizare secretante sau nesecretante• Adenocarcinomul hipofizar
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• Tumori de vecinătate• Metastaze
Patogenie
*Compresiune asupra structurilor învecinate (chiasma optică, cortul hipofizar, sinusurile cavernoase)
*Compresiunea ţesutului hipofizar
*Particularităţi date de caracterul secretant al tumorii
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Tablou clinic• Semne neurologice
*cefaleea
*HTIC
*crize convulsive• Semne oftalmologice
*discromatopsia
*hemianopsia bitemporală
*scotoame
*edem papilar, stază papilară, atrofia nervilor optici
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• Sindroame endocrino-metabolice1.Sindroame de hipersecreţie hormonală2. Insuficienţă hipofizară
1.Sindroame de hipersecreţie hormonalăProlactinom:
La femei: galactoree+amenoreeLa bărbaţi: ginecomastie, hipogonadism
Adenom secretant de STHLa copii: gigantismLa adulţi: acromegalie
Adenom secretant de ACTHBoala Cushing
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Adenom gonadotrop
Semne de insuficienţă gonadică
La femei:
- bradimenoree- amenoree
- involuţia caracterelor sexuale secundare
- infertilitate
La bărbat:
- TDS
- atrofie testiculară
- involuţia caracterelor sexuale secundare
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- alterarea spermatogenezei
Adenom tireotrop
Hipertiroidism
2. Insuficienţă hipofizară, prin:
- comprimarea ţesutului hipofizar
- compresiunea tumorii asupra tijei hipofizare
Ordinea cronologică a instalării insuficienţelor trope: STH, FSH+LH, TSH, ACTH
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Diagnostic paraclinic
*explorarea morfologică a hipofizei
*dozări hormonale
Explorarea morfologică a hipofizei• Semne radiologice comune:
- modificări de formă, contur şi diametre ale şeii turcice
- semne radiologice de HTIC: “impresiuni digitiforme”, disjuncţia suturilor (la copii)
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• Semne radiologice cu valoare etiologică:
- craniofaringiom
- acromegalie
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• RMN sau CT
- evidenţiază microadenoamele
- permite stabilirea raporturilor tumorii cu structurile din jur
Explorarea tulburărilor vizuale
- câmp vizual
- FO
Dozari hormonale
PRL, STH, ACTH, FSH, LH, TSH
Tratament
1.Chirurgical
*Abord transfenoidal
*Abord “inalt” transparietal sau transfrontal
Complicatii: DI, insuficienta hipofizara globala, fistule LCR, tromboze venoase
2. Radioterapia:
*Rx terapie, accelerator de particole, cobaltoterapie
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Dozări hormonale• PRL, STH, ACTH-cortizol, FSH, LH-h. sexuali, TSH-
FT4
Tratament
1. Chirurgical
*abord transfenoidal
*abord “înalt” transparietal sau transfrontal
Complicaţii: DI, insuficienţă hipofizară globală, fistule LCR, tromboze venoase
2. Radioterapia
*Rx terapia clasica, cobaltoterapia, “gamma- knife”
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• 100- 120 Gy (10.000-12.000 razi)• Indicaţii:• refuzul intervenţiei chirurgicale• tumori “inoperabile”• recidiva TU după chirurgie• Complicaţii:• insuficienţa hipofizară• arahnoidita optochiasmatică
3. Medicamentos
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*Agonişti dopaminergici• Bromocriptina, 10-15 mg/zi• Dostinex, 0,5-1 mg/săpt
*Somatostatina• Octreotide (Sandostatin) 0,1 mg/fi, subcutan. 0,2-0,3
mg/zi în 2- 3 prize, Somatulin 1f la 14 zile
4. Tratament substitutiv
Insuficienţa somatotropă• STH (Norditropin fl. 12 UI, adm. sc. 0,1 UI/kg/zi
Insuficienţa gonadotropă• Estro- progestative la femei
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• Testosteron la bărbaţi
- Undestor 40 mg/tb x 3/zi, Nebido
Insuficienţa tireotropă• Tiroxina, 25-100mcg/zi
Insuficienţa corticotropă• Prednison 5 mg/tb, 1-3 tb/zi• Anabolizanţi, Decanofort, 25mg/fi, 1-2 fi/lună
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HiperprolactinemiileClasificare
Fiziologică: sarcina, alăptare
Patologică
Prolactinom
Hiperprolactinemii netumorale:
- medicamentoase
- sindromul de tija hipofizara
- hipotiroidismul primar
- IRC
- ciroza hepatica
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Tablou clinic• La femeie:
- galactoree- tulburări ale ciclului menstrual
• La bărbaţi: - TDS- diminuarea libidoului- involuţia caracterelor sexuale secundare- ginecomastie, foarte rar galactoree
• +/- semnele sindromului tumoral hipofizar
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Diagnostic paraclinic:
Dozari hormonale
Prolactina• valori normale: 2,3- 11,5 ng/ml la bărbat, 2,5- 14,6
ng/ml la femeie• valori > 150 ng/ml = prolactinom• valori moderat crescute –test la TRH
Explorarea morfologică• radiografia selară
• RMN, CT
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Alte explorări• CV, FO• STH• FSH, LH, hormoni sexuali• TSH, FT4• ACTH, cortizol
Tratament
1. Medicamentos: agonişti dopaminergici
*Bromocriptina, 10-15 mg/zi
*Dostinex, 0,5 mg/tb, 0,5- 1 mg/săpt
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Tratament
2. Chirurgical
* Abord transfenoidal
* Abord “înalt” transparietal sau transfrontal
3. Radioterapie
Indicaţii: recidiva TU după chirurgie
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AcromegaliaSindrom realizat de hipersecreţia permanentă si
nemodulată de STH apărută după vârsta pubertăţii
Efectele STH• Hiperplazia ţesuturilor mezenchimale- periost, os,
tegument, pereţi vasculari, viscere• Hiperglicemiant• Hiperlipemiant prin favorizarea lipolizei
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Etiologie• Adenom hipofizar secretant de STH• Adenom mixt secretant de STH, PRL• MEN I• Paraneoplazică
Tablou clinic• Dismorfism acrofacial• Visceromegalia
• Hipertensiunea arteriala
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• Alte simptome şi semne: astenia, tulburări de libidou, apatie, depresie, galactoree, ginecomastie
• Semnele sindromului tumoral hipofizar: neurologice, oftalmologice
• Semne de insuficienţă hipofizară
Diagnostic paraclinic:
* Semne radiologice:
- radiografia de profil de craniu
- radiografia de mâini
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- radiografia de coloană
- RMN sau CT
* Dozări hormonale:
- STH > 11,5 ng/ml
- testul de frenaj HGPO (STH 0-60-120 min)
- Somatomedina -IGF 1 crescut
- PRL
* Dozări biochimice
- fosfataza alcalină > 60mU/l
- fosfatemia > 4,5 mg/dl
- calciuria > 300 mg/24 ore
- calciul seric- normal sau uşor crescut
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* Repercursiuni oftalmologice, endocrine şi metabolice ale bolii:
- câmp vizual, FO
- FSH, LH, Testosteron, Estrogeni, Progesteron
- TSH, FT4
- ACTH, Cortizol
- Glicemie, HGPO
- Profil lipidic
* Ecografia tiroidiana, abdominala
* Colonoscopia
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Complicaţii:• Cardiovasculare: cardiomiopatie, HTA,
coronaropatie, IC• Diabet zaharat: NID- insulinodependent• Artropatia acromegalică• Neuropatii periferice: sindromul de tunel carpian• Litiaza renală• Compresiune chiasmatică, atrofie optică• HTIC• Insuficienţa hipofizară
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Tratament
1. Chirurgical
* Abord transfenoidal
* Abord “înalt” transparietal sau transfrontal
2. Radioterapia
3. Medicamentos
* Octreotide (Sandostatin) 0,1 mg/fi, sc. 0,2- 0,3 mg/zi în 2-3 prize
* Bromocriptina în adenoamele mixte
* Tratamentul HTA şi DZ
* Tratament hormonal substitutiv
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Evaluarea eficienţei terapiei• STH < 2 ng/ml• Normalizarea IGF 1, fosfatazei alcaline şi a
fosfaţilor
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Insuficienţa hipofizară
Distrugerea celulelor hipofizare sau stimularea lor insuficientă de către factorii hipotalamici- insuficienţe glandulare multilpe: gonadică, tiroidiană, CSR la care se adaugă efectele deficitului de STH, PRL, MSH
Etiologie
1. Distrugerea celulelor hipofizare
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1. Distrugerea celulelor hipofizare• leziune tumorală: adenoame secretante sau nesecretante,
carcinom hipofizar, metastaze
• leziuni netumorale: postchirurgie, radioterapie, traumatism
• cauze vasculare: necroza postpartum (Sd. Sheehan), anevrisme ale carotidei interne
• alte cauze: hipofizita autoimună, infecţii (TBC, sifilis), tulburări metabolice (hemocromatoza), “empty sella”
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2. Absenţa stimulării hipofizare prin leziune hipotalamică
• tumori: craniofaringiom, gliom, meningiom, astrocitom
• alte cauze: TBC, sifilis, histiocitoza, sarcoidoza hipotalamică
• absenţa congenitală a nucleilor hipotalamici (Sd. Kalman
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Deficitul trop:• partial / total• izolat / global
Tablou clinic
Panhipopituitarismul adultului:
* Insuficienţa gonadică• La bărbat:
- dispariţia libidoului şi impotenţa
- involuţia caracterelor sexuale secundare- pilozitate axilo- pubiană şi facială
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- testiculi scăzuţi în volum, OGE depigmentate
• La femeie:
- amenoree
- absenţa libidoului
- pilozitate axilo-pubiană diminuată sau absentă
- OGE depigmentate
- atrofia mucoasei vaginale
- atrofia glandelor mamare
- depigmentarea areolelor
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* Insuficienţa tiroidiană
- frilozitate
- apatie
- crampe musculare
- extremităţi reci
- tegumente uscate
- facies palid, uşor infiltrat
- bradicardie
* Insuficienţa CSR
- astenie
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* Insuficienţa CSR
- paloare
- depigmentarea tegumentelor
- hipotensiune
- hipoglicemie
* Deficitul somatotrop
- aspect atrofic al tegumentelor
- tendinţa la hipoglicemie
- constituirea unei anemii normo sau hipocrome
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* +/- Semnele sindromului tumoral hipofizar
Diagnostic paraclinic
* Dozări hormonale- bazale
- deficitele hormonale periferice: estrogeni, progesteron, respectiv testosteron, FT4, cortizol
- deficitul tropilor hipofizari: FSH, LH, TSH, ACTH, STH,PRL
* Teste dinamice
- testul la TRH, GnRH, CRH, GHRH
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*Explorarea morfologică• RMN sau CT
Evoluţie şi prognostic
- dependente de evoluţia procesului patologic
Complicaţii
Coma hipofizară (paloare intensă, hipotensiune, hipotermie, bradicardie, colaps cardiovascular)
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Tratament
Hormoni periferici
* Estroprogestative la femei
*Testosteron la bărbaţi (Undestor 40 mg/tb, 3x1 tb/zi, Nebido)
*Thyroxina 25-100 mcg/zi
* prednison 5mg/tb 1-3 tb/zi
Hormoni tropi
FSH, LH- în tentativa de stabilire a fertilităţii
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Forme particulareSindromul Sheehan
Necroza hipofizară postpartum
Etiopatogenie
naştere hemoragică- spasmul arterelor hipofizare superioare- necroza hipofizară +/- hipofizita
Tablou clinic
- agalactie + amenoree
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- instalarea progresivă a celorlalte semne de insuficienţă hipofizară
- tulburări psihocomportamentale
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Insuficienţa hipofizară a copilului
Microsomia hipofizară sau infantilonanismul hipofizar caracterizat prin retardare staturo- ponderală secundară deficitului de somatotrop asociat cu infantilism şi hipotiroidism
Tablou clinic
- debut în jurul vârstei de 2-3 ani
- creştere lentă cu absenţa puseelor de creştere
- talia definitivă: 110-120 cm
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- segmente corporale proporţionate
- întârzierea apariţiei nucleilor de osificare
- cap mic, cu masiv facial hipotrofic, triunghiular
- mandibula este slab dezvoltată cu retrognatie
- erupţie dentară vicioasă şi întârziată
- oase nazale slab dezvoltate
- extremităţi scurte, gracile- acromicrie
- tegumente cianotice, marmorate, geroderma
- infantilism genital la vârsta pubertăţii
-dezvoltare psihică normală, puerilism
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- asocierea hipotiroidismului, hipocorticismului
- eventual, semnele sindromului tumoral hipofizar
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Diagnostic paraclinic:
- vârsta osoasă
- dozarea STH bazal
- teste de stimulare prin: hipoglicemie provocată, efort fizic, arginina, glucagon
- dozarea IGF1
- determinarea fosfatemiei, fosfatazei alcaline
- dozarea tropilor hipofizari şi a hormonilor periferici corespunzători
- explorarea morfologică hipotalamo- hipofizară
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Diagnostic diferenţial
Nanisme endocrine:
* Hipotiroidism
* Pubertatea precoce
* Pseudopubertatea precoce
* Sindromul suprarenogenital
* Nanismul din Sd. Cushing
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* Nanismul din diabetul zaharat- Sd. Mauriac
Nanisme neendocrine
* Nanisme genetice: deficit de somatomedine- Sd. Laron, progeria
* Nanism osos: condrodistrofia, acondroplazia
* Nanismul din Sd. Turner
* Nanismul din pseudohipoparatiroidism
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* Nanisme din boli nutriţionale şi metabolice:
- boli digestive
- boli renale
- boli cardiace
- boli pulmonare cronice
• Tratament• etiologic• substitutiv: Norditropin, sc, 0,1 UI/kg/ zi la 2 zile• substituţia celorlalte linii deficitare:
- substituţia pe linie CSR, tiroidiană , gonadică
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TiroidaGuşa
Creşterea în volum a glandei tiroide
Clasificare
Etiologică:
- congenitală
- prin carenţă iodată
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Epidemiologică
- endemică
- sporadică
Funcţională
- normofuncţională
- hiperfuncţională
- hipofuncţională
Morfologică
- difuză
- nodulară
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Gradele de guşă
0. nu se vede, se palpează
1. (mică) vizibilă la extensia maximă a gâtului şi la deglutiţie, se palpează
2. (mijlocie) se vede, se palpează, nu depăşeşte ramura anterioară a sternocleidomastoidianului
3. (mare) se vede, se palpează, depăşeşte marginea anterioară a sternocleidomastoidienilor
4. (gigantă) depăşeşte marginile laterale ale gâtului
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Guşa prin carenţă iodatăNecesarul de iod= 100- 200 mcg/zi
Patogenie• carenţa de iod- sinteza scăzută a hormonilor
tiroidieni- defrenarea TSH- hiperplazie
Carenţa de iod=<50 μg/zi
> 10% din populatie= endemie
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Forme clinice• DET gr. I
* Gusa difuză- nodulară- compresivă• DET gr. II
* Guşa + hipofuncţie sau hiperfuncţie• DET gr. III ( neuropată)
* leziuni neurologice prin afectarea dezvoltării embrio- fetale
- cretinismul endemic
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Diagnostic paraclinic
- ecografia tiroidiană
- RIC crescută
- Ioduria < 25 mcg/zi
- T4 normal/scăzut
- T3 normal/crescut
- TSH crescut/ normal
- RX toracic
- CT cervico-mediastinal
- Examen ORL
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Profilaxia
• iodarea sării
• iodura de K 1 mg/săpt la copii şi gravide
Tratament
* Iodura de K 2 mg/săpt, în guşile mici, difuze
* Tiroxina 25- 50 mcg/zi în guşile medii difuze sau în nodulul unic parenchimatos
* Strumectomie subtotala în guşile mari şi gigante + terapie substitutivă
* Tratament adecvat în guşile endocrinopate
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HipertiroidismulSindrom cauzat de expunerea tesuturilor
organismului la concentratii excesive ale hormonilor tiroidieni
Forme etiopatogenetice
* Boala Basedow
* Adenomul toxic tiroidian
* Guşa hipertiroidizată
* Alte forme:hipertiroidismul indus de iod, tirotoxicoza factitia, adenomul hipofizar secretant de TSH
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Boala Basedow
Etiopatogenie
Clinic: guşă + exoftalmie + semne de impregnare cu hormoni tiroidieni
• Guşa: difuză, omogenă
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• Semne de hipertiroidism:
* neuropsihice
* cardiovasculare
* digestive
* renale
* musculare
* osoase
* endocrine
* metabolice
* tegumentare
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• Oftalmopatia
0 : fără semne şi simptome oculare
1. Semne: retracţia pleoapei superioare, privire fixă, lărgirea fantei palpebrale, asinergismul de convergenţă şi oculopalpebral
2. Semne + simptome: edem palpebral, conjunctival, secreţie lacrimală crescută, fotofobie, senzaţie de nisip în ochi + protruzie < 21 mm
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3. Semne + simptome (2) + protruzie > 21 mm
4. Diplopia
5. Lagoftalmie, leziuni cornee, protruzie < 32 mm
6. Atrofia nervului optic
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Adenomul toxic tiroidian
Clinic:
* Nodul unic
* Semne de hipertiroidism
* Absenţa exoftalmiei
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Guşa hipertiroidizată
Clinic
* Guşă simplă / nodulară
* Semne de hipertiroidism
* Absenţa exoftalmiei edematoase
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Evoluţie
Complicaţii
Visceralizările hipertiroidismului:
- cardiotireoza
- osteoporoza
- hepatotoxicoza
- diabet zaharat
Criza tireotoxică
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Diagnostic paraclinic
* dozări hormonale: FT4, FT3, TSH
* anticorpi TSI
* ecografia tiroidiană
* RIC şi scintigrafia tiroidiană
* teste biochimice
* EKG
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Tratament• ATS + betablocante + sedative• Chirurgical• Iod radioactiv
Tratamentul exoftalmiei
Exoftalmia benignă
* ATS
Exoftalmia malignă
* ATS + Corticoterapie
*ATS + Radioterapie antiinflamatorie orbitară
*ATS + Corticoterapie + Radioterapie + Decompresia chirurgicală a orbitei
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HIPOTIROIDISMULSindrom cauzat de imposibilitatea glandei tiroide de a
asigura organismului necesarul de hormoni tiroidieni
Etiopatogenie
Hipotiroidism primar 90- 95%
* autoimun
* post- tiroidectomie (chirurgicală, radioactivă)
* ATS
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* genetic:
- agenezie
- tulburări de hormonogeneză
* postinflamator- tiroidita subacută, acută, cronică
Secundar
* tumori
* necroza hipofizară
* traumatisme
* leziuni infiltrative
* infecţii: TBC, lues
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Hipotiroidism prin tulburări de receptivitate
Clasificare clinică
- Hipotiroidism frust
- Hipotiroidism clinic manifest
- Mixedem
Semne clinice
* tegumentare
* cardio- vasculare
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* respiratorii
* digestive
* musculare
* neuro- psihice
* metabolice
* endocrine
Complicaţii
Coma mixedematoasă ( flască, hipotermie, bradicardie, hipotensiune, bradipnee, ileus dinamic, oligurie, hipoglicemie, convulsii)
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Diagnostic paraclinic
* dozări hormonale
* ecografia tiroidiană
* RIC- testul la perclorat
* colesterol, trigliceride
* probe hepatice
* hemograma
* EKG, Eco cord
* anticorpi antitiroidieni
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Tratament
Thyroxina - doze progresive- 50-150 mcg/zi
Evaluarea eficacităţii tratamentului
* parametrii clinici
* dozări hormonale: FT4, TSH
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Tiroiditele
Procese inflamatorii ale glandei tiroide
Forme clinice
* Tiroidita acută
* Tiroidita subacută
* Tiroidita cronică Hashimoto
* Tiroidita cronică Riedl
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Tiroidita acută/Abcesul tiroidian
Etiologie• Stafilococ, Streptococ, germeni gram negativ • Fungii
Tablou clinic
- hipertrofie bruscă, foarte dureroasă
- disfonie, disfagie
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- tegumente calde, roşii
- adenopatie satelită
- febră mare, frison
- mialgii, altralgii
- cefalee, astenie
Paraclinic
- VSH foarte mare
- leucocitoză cu neutrofilie
- RIC- necaracteristică, nemodificată
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- Ecografia: zone hipoecogene, transonice (abces)
- puncţie, culturi
Evoluţie
- spontană spre abcedare- tegument/ mediastin
Tratament
* antibiotice
* antiiflamatorii
* drenaj chirurgical în forma abcedată
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Tiroidita subacută
Etiologie
- virală
- imun- alergică
Tablou clinic
* hipertrofie dureroasă, fermă
* disfagie, disfonie
* subfebrilităţi, mialgii, astenie
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* adenopatie laterocervicală
* semne de hipertiroidism pasager
Paraclinic
- VSH foarte mare
- leucocite normale cu limfocitoză
- RIC foarte scăzută
- ecografia: hipoecogenitate globală sau lobară
- tiroglobulina crescută
- FT3, FT4- crescuti, TSH- scăzut
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Evoluţie
- spontană spre vindecare 7- 8 săpt
- hipertiroidie- eutiroidie- hipotiroidie
- recidive posibile/ frecvente
Tratament• corticoterapie• AINS• strumectomie în formele recidivante
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Tiroidita cronică limfocitară- Hashimoto
Patogenie• autoimună
Tablou clinic
- hipertrofie variabilă, fermă, suprafaţă lobulată / atrofia glandei tiroide
- disfagie, uneori dispnee
- hipotiroidie/ eutiroidie/ hipertiroidie (Hashitoxicoza)
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Paraclinic
- VSH normal sau uşor crescut
- hiper gama- globulinemie
- RIC necaracteristică
- ecografia: hipoecogenitate globală
- anticorpi antitiroidieni (anti TPO, antitireoglobulina) mult crescuţi
- T3, T4, FT3, FT4 variabili
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Evoluţie
- spre hipotiroidie
Tratament
* substitutiv
* corticoterapie
* chirurgical în forma compresivă
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Tiroidita cronică fibroasă Riedl
Etiologie• necunoscută
Patogenie• proliferare de ţesut conjunctiv fibros
Tablou clinic
- hipertrofie variabilă, dură
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- disfagie, disfonie, dispnee
- hipotiroidie
- facultativ: fibroză retroperitoneală, mediastinală, a ţesutului retroorbitar sau a glandelor mamare
Paraclinic
* VSH normal
* RIC- scăzută, arii “ reci” scintigrafic
* T3, T4- scăzuţi, TSH crescut
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Evoluţie• spre invazia şi înglobarea structurilor învecinate• hipotiroidie
Tratament
* chirurgical
\* substitutiv
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Patologia paratiroidiana
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Hiperparatiroidismul primar
Etiologie
* adenom paratiroidian
* hiperplazie globală a paratiroidelor
* cancerul paratiroidian
Tablou clinic
Semne osteoarticulare
- dureri osoase
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- deformări osoase
- fracturi spontane
- altralgii prin artropatii erozive, calcifieri periarticulare, condrocalcinoza
Semne reno- urinare
- litiaza renala fosfo- calcică si oxalo- calcică
- nefrocalcinoza
Semne determinate de hipercalcemie
- sete cu poliurie si polidipsie
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- tulburări digestive: anorexie, greţuri, vărsături, constipaţie, ulcer gastro- duodenal, pancreatita
- tulburări neurologice: astenie, cefalee, deficit motor proximal, atrofie musculară, tulburări senzitive
- tulburări psihice: neuroastenie, manifestări psihotice, elemente depresive
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- tulburări cardiovasculare: palpitaţii, tahicardie, dispnee de efort, HTA
- depunere de calciu în ţesuturile moi:
- limb cornean
- cartilagii- condrocalcinoza
- tegument
- membrana bazală a tubilor renali- nefrocalcinoza
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Explorări paraclinice
A. Pentru afirmarea hiperparatiroidismului
- hipercalcemia
- hipercalciuria
- hipofosfatemia
- hiperfosfaturia
- fosfataza alcalină- crescută
- osteocalcina- crescută
- vitamina D - crescută
- cAMP urinar- crescut
- PTH - crescut
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- radiografii osoase
- biopsie de creastă iliacă
B. Pentru localizarea leziunii
- ecografia paratiroidiană
- tomografia computerizată
- arteriografia paratiroidiană
- cateterizarea venoasă selectivă
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Tratament
* chirurgical
* tratamentul hipercalcemiei
- furosemid
- calcitonina
* tratamentul hipocalcemiei postoperatorii: “hungry bones syndrome”
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Hiperparatiroidismul secundar
Etiologie• hipocalcemia• hiperfosfatemia• scăderea vitaminei D
Tablou clinic
- dureri osoase
- dureri articulare
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- deformări osoase şi fracturi patologice
- tasări vertebrale
- acro-osteoliza
- calcifieri la nivelul ţesuturilor moi
Explorări paraclinice
* hipocalcemie sau calcemie normală
* hipocalciurie
* hiperfosfatemie
* hipofosfaturie
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* fosfataza alcalină normală sau uşor crescută
* PTH mult crescut
* modificări radiologice
Tratament
* medical• reducerea aportului alimentar de fosfaţi• complexanţi intestinali ai fosfaţilor• vitamina D
*chirurgical
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HipoparatiroidismulDefiniţie
Etiologie
A. Insuficienţa secretorie
Primară
- absenţa congenitală a paratiroidelor
- lezarea autoimună
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Secundară
- postoperatorie
- după doză terapeutică de iod radioactiv
- hemosideroza
- leziuni metastatice
- hiperparatiroidism matern
B. Rezistenţa periferică la acţiunea PTH
- anomalii structurale
- anomalii ale receptorului de PTH
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Tablou clinic
* Criza de tetanie
* Semne şi simptome intercritice
- semne de hiperexcitabilitate neuro- musculară
- semnul Chwostek
- semnul Trousseau
- manifestări psihice: anxietate, nervozitate, sindrom depresiv
- manifestări neurologice
- comiţialitate
- edem papilar, HTA intracraniană
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- modificări ale fanerelor
- modificări dentare
- cataracta
- tulburări cardiovasculare
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Explorări paraclinice
- hipocalcemia
- hipocalciuria
- hiperfosfatemia
- hipofosfaturia
- magneziul seric şi urinar normal
- PTH scăzut
- electromiograma
- electroencefalograma
- modificări radiologice
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Tratament- URGENŢĂ MEDICALĂ
* preparate de calciu
- parenteral
- per os
* miorelaxante
* vitamina D
* suplimentarea aportului alimentar cu 0,5- 1 g calciu/zi
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Pseudo- hipoparatiroidismul
Etiologie
- boală genetică, A.D.- legată de cromozomul X
Tablou clinic
* Semne clinice şi biologice de hipoparatiroidism
*Sindrom dismorfic:
- talie mică
- facies rotund cu trăsături împăstate
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- obezitate
- brahimetacarpie
- brahimetatarsie
* Retard intelectual
* Modificări radiologice
- brahimetacarpie, brahimetatarsie
- calcifieri ale nucleilor cenuşii
- densificarea structurilor osoase
- noduli subcutanaţi calcificaţi
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Tratament
- identic cu hipoparatiroidismul
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Glandele suprarenaleCSR
• zona glomerulara-ALDOSTERON
•zona fasciculata- CORTIZOL
•zona reticulata- DHEA- DHEA-S- ANDROSTENDION
CRHCRH
ACTHACTH
CORTIZOLCORTIZOL
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Insuficienţa corticosuprarenală cronică
Boala Addison
Etiologie• suprarenalita TBC• suprarenalita autoimună
Tablou clinic
* Astenia , adinamie
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* Hiperpigmentarea tegumentelor şi a mucoaselor
* Hipotensiune arterială şi /sau hipotensiune ortostatică
* Tulburări digestive
* Scădere ponderală
* Tendinţa la hipoglicemie
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* Psihosindromul
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Explorări paraclinice
1. Confirmarea insuficienţei secretorii
2. Stabilirea formei etiologice
1. Confirmarea insuficienţei cortico- suprarenale
Deficitul glucocorticoid
- cortizolemie < 79 ng/ml la ora 8 dimineaţa
- 17 OHCS < 3 mg/24 ore la femei şi < 5 mg/24 ore la bărbat
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Deficitul de androgeni suprarenalieni
- 17 CS < 7 mg/24 ore la femeie şi < 9 mg/24 ore la bărbat
Deficitul mineralo- corticoid
- Na (p) < 135 mEq/L
- K (p) > 5 mEq/L
- Cl (p) < 93 mEq/L
Dozarea ACTH- valori crescute > 56 pg/ml
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Testul de stimulare cu Synacthen retad- negativ
Alte elemente paraclinice de diagnostic
- glicemia à jeun este scăzută < 70 mg %
- HGPO- aspect plat
- hemograma: discretă anemie şi eozinofilie moderată
- Rx toracic: umbra cardiacă micşorată, alungită, aspect de “ cord în picătură”
- EKG: complexe QRS microvoltate şi unda T difazică
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2. Stabilirea etiologiei
a. Pentru etiologia TBC
Clinic
- antecedente patologice de TBC pulmonar sau extrapulmonar
- antecedente de contagiune TBC intrafamilială
- vârsta 30- 40 ani
Elemente paraclinice
- IDR hiperergică
- radiografia toracică
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- radiografia abdominală
- explorarea CT: hipertrofie inomogenă
b. Pentru forma autoimună
Elemente clinice
- vârsta 20- 30 ani
- absenţa antecedentelor TBC
- coexistenţa altor boli autoimune
Paraclinic
- evidenţierea anticorpilor antisuprarenalieni
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- CT- atrofie corticală bilaterală
Diagnostic diferenţial
- Pigmentaţia etnică
- Intoxicaţia cu metale grele
- Hemocromatoza
- Neurastenia
Complicaţii
CRIZA ADDISONIANA
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Tratament
Substitutiv- ad vitam
* Glucocorticoid- Prednison 5- 20 mg/zi
+/-* Mineralocorticoid- Mincortid 1 fi im/săpt
- Astonin 1/2- 2 tb/zi
* Androgen- Decanofort 1 fi/lună
- Naposim 3x1 tb/zi
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Insuficienţa corticosuprarenală centrală (secundară)
Sindrom realizat de deficitul de hormoni glucocorticoizi, mineralocorticoizi şi androgeni ca urmare a unei stimulări insuficiente din partea axului hipotalamo- hipofizar
Etiologie
- procese distructive ale hipotalamusului şi hipofizei
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Clinic
- aceleaşi elemente ca şi în boala Addison cu excepţia hiperpigmentaţiei
Explorări paraclinice
- deficitul hormonilor glucocorticoizi, mineralocorticoizi şi androgeni - identic cu insuficienţa primară
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Elemente paraclinice de diferenţiere:
* nivel scăzut de ACTH
* testul de stimulare cu Synacthen retard este pozitiv
* explorarea CT/RMN a zonei hipotalamo- hipofizare permite localizarea leziunii
Tratament
- substitutiv
- etiologic
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Hiperfuncţia corticosuprarenală- Sindromul Cushing
Definiţie
Forme etio- patogenetice
Forme centrale • hipotalamică (hipersecreţie de CRF)• hipofizară (hipersecreţie de ACTH- boala Cushing)
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Forme periferice• adenomul corticosuprarenal• displazia nodulară• adenocarcinomul corticosuprarenal• forma paraneoplazică (secreţia unor substanţe
ACTH- like)• forma iatrogenă
Tablou clinic
* obezitate facio- tronculo- abdominală
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CRH
ACTH
CORTIZOL CORTIZOL
CRH
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CRH
ACTH
CORTIZOL CORTIZOL
ACTH
CRH
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ACTH
CORTIZOL
ACTH-LIKE
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Tablou clinic
* obezitate facio- tronculo- abdominală
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* leziuni cutanate
- eritroza facială
- vergeturi roşii- violacee
- atrofie tegumentară
- echimoze, peteşii
- infecţii micotice sau bacteriene
* hipertensiune arterială
* tulburări de glicoreglare
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* amiotrofie în special la rădăcina membrelor
* semne de hetero- sexualizare
* osteoporoza
* psihosindrom
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Diagnostic paraclinic• Etapa de confirmare a excesului secretor• Etapa stabilirii formei etio- patogenetice
Confirmarea hipersecreţiei cortico- suprarenale
Excesul glucocorticoid
- dispariţia ciclului de cortizol
- cortizolemie > 220 ng/ml la ora 8 dimineaţa şi > 145 ng/ml la ora 18
- 17 OHCS > 5 mg/24 ore la femeie şi > 7 mg/24 ore la bărbat
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Excesul de androgeni suprarenalieni
- 17 CS > 10 mg/24 ore la femeie şi > 15 mg/24 ore la bărbat
Excesul mineralocorticoid
- Na (p) > 145 mEq/L
- K (p) < 3,5 mEq/L
- Cl (p) > 105 mEq/l
Teste complementare uzuale
- glicemia à jeun - adesea crescută
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- discretă leucocitoză cu scăderea limfocitelor şi a eozinofilelor
- creştere a calciuriei > 250 mg/24 ore
- calcemie normală/crescută
- hipercolesterolemie
- hipertrigliceridemie
- hidroxiprolinurie crescută prin hipercatabolismul colagenului
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Diagnosticul formei etio- patogenetice
1. Dozarea ACTH
2. Testele de frenaj
- testul de frenaj Bricaire
- testul de mică inhibiţie (pe metaboliţii urinari- Liddle 2 x 2
- testul de mare inhibiţie (pe metaboliţii urinari- Liddle 2 x 8
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3. Explorarea morfologică
- ecografie
- CT
- RMN
Tratament
* Forma hipotalamică
* Forma hipofizară: chirurgie, radioterapie
* Forma periferică
Medicamentos: Ketoconazol
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Sindroame adrenogenitaleDeficitul de 21 hidroxilază
Etiologie• boli genetice cu transmitere autosomal recisivă
Patogenie
* sinteza gluco şi mineralocorticoidă blocată la 17 OH progesteron- cortizol scăzut- defrenare a secreţiei de ACTH- hiperplazie CSR- hipersecreţie de androgeni
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Tablou clinic
* Forma cu debut precoce
la fete • pseudohermafroditism feminin:
- hipertrofie clitoridiană- “aspect peniform”
- hipertrofia labiilor mari cu diferite grade de fuziune labioscrotală - aspect “ pseudoscrotal”
- OGI de tip feminin
la băieţi
- hipertrofie peniană
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După naştere
la fete
* pseudopubertate precoce heterosexuală
la băieţi
* pseudopubertate precoce izosexuală
- pubertate fiziologică tardivă şi incompletă
- prezenţa deficitului mineralocorticoid- pierdere de sare- deshidratare
- semne de insuficienţă CSR: inapetenţă, vărsături, hipotensiune, apatie, cianoză
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* Forma cu debut tardiv
la femei
* heterosexualizare:
- hirsutism
- hipertrofie clitoridiană
- acnee
- hipertrofia maselor musculare
- modificarea vocii
- dereglări ale ciclului menstrual
la bărbaţi- nesemnificativ
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Explorări paraclinice
* cortizol scăzut / normal
* 17 OHCS scăzuţi /normali
* 17 OH progesteron- mult crescut
* pregnandiolul urinar- crescut
* ACTH crescut- hiperplazie CSR bilaterală
* 17 CS crescuţi pe seama tuturor celor trei fracţii
* + / - aldosteron scăzut
* Na- scăzut
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* K - crescut
* stimularea cu Synacthen accentuează tulburările biochimice
* frenajul cu Dexametazonă ameliorează tulburările biochimice
Tratament
- Dexametazona 0,5 - 1 mg / zi
- suplimentare sodata
- chirurgia OGE
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Patologia endocrină a ovarelorInsuficienţa ovariană
Clasificare
După sediul leziunii
* Primară
* Secundară
După momentul apariţiei
* Prepubertală
* Postpubertală
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Insuficienţa ovariană primară cu debut prepuberal
Etiologie • Iatrogene
* chirurgical
* iradiere
* tratamente citostatice• Infecţii
* TBC, bruceloza, v. urlian
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• Autoimune
* anticorpi anti- ovar sau anticelule steroidiene
• Idiopatice
Tablou clinic• Infantilism genital:
* organe genitale hipotrofice, nedezvoltate
* glande mamare nedezvoltate
* pilozitate axilopubiană redusă
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* amenoree primară
* sterilitate primară
• Modificări somatice:
* retard statural ( sub vârsta de 7 ani )
* habitus eunucoid (după vârsta de 7 ani)
* aspect dizarmonic
* hiperlaxitate ligamentară
• Modificări psihice
* complexe de inferioritate
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Explorări paraclinice
* estrogenii şi progesteronul- absenţi
* gonadotropii- crescuţi
* explorări imagistice: ecografia, celioscopia cu biopsie de ovar
* anticorpi antiovar, anti- receptor steroizi
* testul Barr
* cariotipul
Tratament
* Estrogenizare progresivă (etinilestradiol 10- 50 mcg/ zi, 6- 12 luni)
*Asociere estro- progestativă
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Insuficienţa ovariană primară cu debut postpuberal
Etiologie• Iatrogene
* chirurgicale
* iradiere
* tratamente citostatice• Autoimune• Idiopatice
* climacteriul precoce
* sindromul ovarelor rezistente
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Tablou clinic
* Amenoree secundară
* Involuţia tractului genital şi a uterului
* Involuţia caracterelor sexuale secundare
- reducerea ţesutului glandular mamar
- reducerea pigmentării mamelonului
- reducerea pilozităţii axilopubiene
* Diminuarea libidoului
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* Tulburări neuro- vegetative
* Tulburări metabolice
- osteoporoza
- ateroscleroza
* Obezitate
Paraclinic
- estrogenii şi progesteronul- absenţi
- gonadotropii: FSH, LH- crescuţi
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- Anticorpi anti- ovar şi anti- celule steroidiene
- celioscopia cu biopsie de ovar (absenţa sau raritatea foliculilor)
Tratament
* Estro- progestativ
* Tratamentul osteoporozei
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Insuficienţa ovariană secundară (centrală) cu debut prepuberal
Etiologie• Hipotalamus
- tumorale
- netumorale
• Hipofiza
- tumorale
- netumorale
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• Tablou clinic
* hipoplazie genitală
* impuberism
* amenoree primară
* tablou complex (asocierea insuficienţei celorlalţi tropi- adesea nanism)
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Paraclinic
* estrogenii şi progesteronul- absenţi
* gonadotropii- scăzuţi sau absenţi
*explorări imagistice
- ecografia, celioscopia
- radiografia selară
- RMN, CT
* test la gonadotropi- integritatea ovarului
* test la GnRH- localizarea deficitului (hipotalamus- hipofiza)
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Tratament
* corectarea deficitului celorlalti tropi (STH, TSH)
* substituţie estrogenică- estroprogestativă
* GnRH sau gonadotropi
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Insuficienţa ovariană secundară (centrală) cu debut postpubertal
Etiologie• Hipotalamice
* Nelezionale
- amenoreea psihogenă
- anorexia mentală
- dieta severă, malnutriţie
- exerciţiu fizic intens, prelungit
- boli consumptive ( neoplazii, TBC, SIDA)
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* Lezionale
- tumorale
- infiltrative
- infecţii
• Hipofizare
- ischemice
- tumorale
- infiltrative
- traumatisme cranio- cerebrale cu secţionarea tijei hipofizare
- iatrogene (hipofizectomie, iradiere)
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Tablou clinic
* Amenoree secundară
* Tablou variabil în funcţie de cauză
Anorexia mentală:
* scădere în greutate -caşexie extremă
* amenoree secundară
* hirsutism discret
*involuţia caracterelor sexuale secundare
* bradicardie
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Paraclinic
- estrogenii şi progesteronul- scăzuţi sau absenţi
- gonadotropii- scăzuţi (peak- ul ovulator de LH absent)
- RMN, CT
- evaluarea secreţiei celorlalţi tropi hipofizari
- test cu GnRH pentru stabilirea nivelului deficitului (hipotalamic/ hipofizar)
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Tratament
* Etiologic (prolactinom, anorexia mentală)
* Dacă sunt prezente, se corectează celelalte deficite (ACTH, TSH)
*Substituţie estro- progestativă + /- tratament inductor de ovulaţie
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Insuficienţa ovariană parţială/ progesteronică
Sindromul de tensiune premenstruală
Etiopatogenie• hiperestrogenism relativ• hiperestrogenism absolut
- exacerbarea efectelor estrogenice
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Tablou clinic
* congestie mamară dureroasă (mastodinie)
* dureri abdominale
* edeme declive sau generalizate
* creştere în greutate
* modificări digestive: apetit capricios, balonări, greţuri
* manifestări cardio-vasculare subiective
* crize de migrenă
* tulburări neuro-psihice: iritabilitate, depresii, insomnii
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* tulburări ale ritmicităţii menstrelor
în hiperestrogenismul relativ
* bradimenoree
* oligomenoree
în hiperestrogenismul absolut
* tahimenoree
* polimenoree sau menoragie
* absenţa ovulaţiei
* +/- sterilitate
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Explorări paraclinice
în hiperestrogenismul relativ
* estrogeni- normali
* progesteron- scăzut
în hiperestrogenismul absolut
* estrogeni- crescuţi
* progesteron- normal
* FSH- normal
* absenţa peak-ului ovulator de LH
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* curba termică cu aspect monofazic
* frotiu cito-vaginal caracteristic
Complicaţii
*Mastoza fibro-chistică
* Neoplasm endometrial
* Fibrom uterin
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Tratament
* Patogenetic
- Medroxiprogesteron , Duphaston 10 mg/tb, 1-2 tb/ zi timp de 7-10 zile
* Simptomatic
- sedative, diuretice, AINS, preparate de calciu, magneziu, antispastice
- progestogel
- tratament inductor de ovulaţie
- anticoncepţionale
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Sindromul ovarelor polichisticeSindromul Stein-Leventhal
Etiopatogenie
excesul de androgeni suprarenalieni
maturare foliculară insuficientă
deficit progesteronic
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Tablou clinic
* obezitate moderată
* hirsutism
* tulburări ale ciclului menstrual: bradimenoree, oligomenoree, amenoree
* anovulaţie
* sterilitate
* semne de impregnare androgenică:
- modificarea vocii
- tendinţă la acnee
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- dezvoltarea maselor musculare
- androgenizare psiho-comportamentală
- modificări ale organelor genitale: - hipertrofie clitoridiană
- involuţia uterului şi a glandelor mamare
* complexe de inferioritate
Varianta HAIR- AN
* hiperandrogenism
* insulinorezistenţa
* acanthosis nigricans
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Explorări paraclinice
dozări hormonale
- estrogeni normali / crescuţi
- progesteron scăzut
- FSH scăzut
- LH crescut
- FSH / LH > 2
- testosteron normal / crescut
- 17 CS crescuţi
- insulinemia crescută in HAIR- AN
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explorări morfologice
- ecografia ovariană
- celioscopia
Tratament
* scădere ponderală
* tratamentul hirsutismului
- asocieri estroprogestative contraceptive
- Androcur
- Spironolactona 50- 100 mg/zi
- Finasterid
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Tratament
* progestative
* tratament inductor de ovulaţie
* tratament chirurgical
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Insuficienţa testiculară
Clasificare
după localizare
* primare
* secundare
după debut
* prepubertal
* postpubertal
Consecinţe
- deprivare hormonală + infertilitate
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Insuficienţa testiculară primară cu debut prepubertal
Etiologie• congenitală ( < săpt. 7 = feminizare)
• iradierea
• boli infecţioase (parotidita epidemică)
• citostatice
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Tablou clinic
* +/- criptorhidie
* intersexualitate sau hipoplazie genitală
* talie eunucoidă
* hiperlaxitate ligamentară
* impuberism (absenţa caracterelor sexuale secundare)
* infertilitate
* tulburări psihice (infantilism, complexe de inferioritate, depresie)
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Paraclinic
* testosteron scăzut sau absent
* gonadotropi: FSH, LH - crescuţi
* testul la Pregnyl- negativ
* biopsia testiculară
Tratament• Substitutiv androgenic- Testosteron• Chirurgical- în cazurile de intersexualitate• Feminizare fenotipică- lăsarea în sexul feminin +
estrogeni
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Insuficienţa testiculară primară cu debut postpubertal
Etiologie• infecţii orhitice• traumatisme• iradierea• îndepărtarea chirurgicală (seminom, carcinom de
prostată)
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Tablou clinic
* involuţia caracterelor sexuale secundare
* obezitate
* pseudoginecomastie
* TDS- impotenţă
* diminuarea, suprimarea libidoului
* infertilitate
* osteoporoza
* tulburări neuro-vegetative
* tulburări psihice: nevroza cenestopată, psihoze, izolare
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Paraclinic
* testosteron- scăzut sau absent
* gonadotropi: FSH, LH - crescuţi
* radiologie- osteoporoză difuză
Tratament• substitutiv androgenic (dacă nu există
contraindicaţii)
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Insuficienţa testiculară centrală (secundară) cu debut prepubertal
Etiologie• Hipotalamus
- tumorale
- netumorale • Hipofiza
- tumorale
- netumorale
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Tablou clinic
* testiculi prezenţi în scrot cu aspect infantil
* impuberism
* talie variabilă (nanism-talie înaltă)
* tulburări psihice
Paraclinic
* testosteron scăzut / absent
* gonadotropi scăzuti / absenţi
* test la GnRH
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* test la Pregnyl
* explorarea morfologică a zonei hipotalamo- hipofizare
Tratament• Substitutiv androgenic
• Inducerea spermatogenezei cu Clomifen, GnRH, FSH + LH
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Insuficienţa testiculară secundară (centrală) cu debut postpubertal
Etiologie• Hipotalamice
Nelezionale
- dieta severă, malnutriţie
- boli consumptive
- boli endocrine
- “Castrarea” hormonală pentru cancere hormonodependente
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Lezionale
- tumorale
- infiltrative
- infecţii • Hipofizare
- adenoame nesecretante sau secretante- prolactinom
- infiltrative
- iatrogene
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Tablou clinic
* testiculi prezenţi în scrot cu aspect involuat (micşoraţi, nedureroşi)
* involuţia caracterelor sexuale secundare
* osteoporoza
* TDS- impotenţa
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* diminuarea-dispariţia libidoului
* modificarea comportamentului, tulburări psihice
Paraclinic
- testosteron scăzut / absent
- gonadotropi scăzuti / absenţi
- test la GnRH- permite localizarea deficitului
- test la Pregnyl
- RMN, CT
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Tratament• substitutiv androgenic
• inducerea spermatogenezei cu Clomifen, GnRH, FSH + LH
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Sindromul Turner
• 45 XO• 46 XX / 45 XO • Anomalii de structură ale cromozomului X
Tablou clinic
* talie mică
* hipertelorism
* boltă palatină ogivală
* gât scurt
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* inserţie joasă “în trident” a părului pe ceafă
* “pterigium colli”
* torace “în platoşă”
* teleangiectazii
* malformaţii unghiale
* malformaţii osoase:
- semnul Kosowicz
- semnul Archibald
- semnul Mandelung
* malformaţii viscerale
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* anomalii senzoriale
* impuberismul
* dezvoltarea intelectuală
Paraclinic• Dozări hormonale
* estrogeni, progesteron- scăzuţi
* FSH, LH - crescuţi
* STH- normal / crescut
* somatomedine- scăzute
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• Teste genetice
* testul Barr
* cariotipul• Explorări imagistice
* radiografii osoase
* ecografia
* celioscopia
Tratament• substituţie estro-progestativă
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Sindromul Klinefelter
• Cariotip: 47 XXY
mozaicism
Tablou clinic
* întârziere în apariţia caracterelor sexuale secundare
- testiculi mici, duri, + / - criptorhidie
- scrot, penis: normale
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- pilozitate axilo-pubiană redusă
- diametrul biacromial =/ < diametrul bitrohanterian
- hipotrofie musculară
* depunere de ţesut adipos în jurul centurii pelviene
* hipertrofie staturală
* retard psihic uşor / moderat
* infertilitate
* ginecomastie
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Paraclinic
- testosteron la limita inferioară / scăzut
- DHT scăzut
- FSH, LH- crescuţi
- prolactina normală
- spermograma- azoospermie
- test Barr pozitiv
- cariotip: 47 XXY, 48 XXXY, 49 XXXXY, mozaicism
- biopsia testiculară
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Tratament• substitutiv cu androgeni
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HIPOTIROIDISMUL
• TABLOU CLINIC• tegumente• mucoase
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HIPOTIROIDISMUL
• TABLOU CLINIC• tegumente• mucoase
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HIPOTIROIDISMUL
• TABLOU CLINIC• tegumente• mucoase
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HIPOTIROIDISMUL
• TABLOU CLINIC• tegumente• mucoase
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HIPOTIROIDISMUL
• TABLOU CLINIC• tegumente• mucoase