parati roid
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PARATIROID
Dr.Hj.Resmi Kartini,MS
Bagian Patologi Anatomi
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FUNGSI :
1. PTH → Mobilisasi Ca DR Tulang 2. Reabsorpsi tubulus ginjal ↑ (Ca) 3. Promotes Prod Ginjal : 1,25 (OH)2 D3 → Active in intestinal Absorpsion of Ca 4. Kadar posfat Serum ↓ →Posfaturi ↑ PTH Resorpsi tulang → Ca + P ↑ (darah)
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Hiper Paratiroid
Primer → Krsk pd kelenjar → Hiper sekresi hormon. Paratir → Hiper Kalsemi Hipo Posfatemi Sekunder Hipo Kalsemi → PTH ↑ Hipo Paratiroid
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Primary Hiper ParatiroidPTH ↑ →1. Resorpsi tulang ↑ , mobilisasi Ca Skelet ↑2. Renal Tub. Reabsorpsi ↑
Retensi Ca3. Sintesis 1,25 (OH)2 D3 renal ↑
− Absorpsi C it ?? ↑
Hiper Kalsemia ← Hiper paratir ↑ (90%) / Cancer
- Adenoma 75-80%- Primary Hyperplasia (difuse / NOD) 10-15%- Ca Paratir < 5%
Kad Ca serum ↑ tidak mbr efek pd fungsi autunom tumor, Adenoma, Ca,Hiperplasia kel. Trs ?? Hiperfungsi akibat defek mekanisme reseptor Ca chief
cell –normal → Kad. Ca Serum.
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USA ♀ 3:1
EROPA Dekade ? →
Asimptomatik
D/ Weakness
Mudah Lelah
Disfungsi Afektif
Hiper Calseuria 10% penderita
Osteitis Fibrosa Cystica
(Hiperaktif Osteoclas)
MEN
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Adenoma
Soliter 0,5 – 5 cm , soft , merah, tan kapsul, kel inferior
Kel yg tidak terkena supresi, kecil
↑ Chief cell sheet, trabekula, folikuler oxyphil cell variasi ukuran inti.
Transitional cell
Infark , nekrosis
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Hiperplasia Primer
Sporadik/ Men Syndr I II aKeseluruh Kel terkena 7% , dpt 2 kel asimetris, >> 0,5 –1GR m ↑ chief cell difus, nodul(water, oxifil)Jr, fibrous mengelilingi
→ Solid sheets, nest , trabekula, foll cell bi nukl Sel lemak
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Karcinoma Abu 2 putih,masa irreg,io gr Biasa pada I kel Histol : Uniform,pleo, nod,trabekuler,solid Khas kapsul jar fibrosa MALIGNANCY invasi lokal,metastase rekuren lokal 1/3 kasus Metastase 2/3 kasus Kematian komplikasi hiperparatir
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Perjalanan penyakit :Klinik :Ginjal : nefrolitiasis nefrokalsinosisSkeletal : osteitis fibrosa cyctica ostoe porosisGit : n,v, ulcus peptikum pankreatitisCVS : sakit kepala,lethargy,depresi,memori negatif,seizureOtot :kelemahan umum.Perubahan kulit dan mataD/ ← hipercalcemia,hipoposfatemi,fatig
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Hipoparatiroidism
1.Op.tiroidektomi 2.Kel.Kong.Paratir - →Di Georges’s Syndr. 3Py Autoimun→Polyglandular autoimun sy Adrenal, ovarian failure,kandidiasis
muko kutaneus,An.Pernisiosa
4.Sundry ,Familial autosomal dan metabolic syndr .( hipomagnesemia )
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Klinik : Neuromuscular exitability← kad Ca ion
serum ↓ N VII →kontraksi otot mata,mulut hidung
→ ( Chvostek’ Sign ) Oklusi aliran darah lengan ,tangan Spasme karpal ( Trousseaun’s sign ) Titani,spasme karpo pedal Stidor laring,convulsi
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ADRENAL
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Normal adrenal steroid biosynthesis
cholesterol
↓
pregnenolone 3 17α L
Progesteron → 17α-hydroxyprogesterone → dehydroepiandrosterone
↓21 ↓21 ↓3 A
Deoxycorticosterone deoxycortisol androstenedione → estrone
↓11 ↓11 ↓17β
Corticosterone cortisol testosterone
↓18
aldosterone
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ADRENAL
Stress akut → lipid depletion → berat↓ Prolong stress Penyakit kronik → Hiperplasia dan hipertropi sel korteks
Zona glomerulosa → mineralokortikoid Zona fasciculata → Zona retikularis → glukokortikoid Medula katekholamin
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MINERALOKORTIKOID Aldosteron reabsorbsi Na ekskresi K
GLICOCORTICOID Cortisol
Inhibisi efek uptake glukosa jaringan Glukosa intolerance Hiperglisemi DM
Absorbsi Ca & P ginjal ↓→ osteoporosis
TESTOSTERON
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HIPERFUNGSIHIPER ADRENALISM Sindroma cushing, cortisol ↑ Hiper aldosteronism Adreogenital syndrome : androgen ↑
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SINDROMA CUSHING Hipercorticolism Klinik :
Obesitas 85-90% Moon face 85% Weakness, fatigability 85% Hirsutism 75% Hipertensi 75% Plethora 75% Glucose intolerance / DM 75/20 % Osteoporosis 75% Neuropsichiatric abnormal 75-80% Menstruasi abnormal 70% Skin striae (lower abdomen) 50%
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Patogenesis1. Pemakaian glukokortikoid
imunosupresi pd transplantasi
2. ACTH pituitary 65-70% ♀3. Non endokrin neoplasma ♂ dekade 5-6
prod ektopik ACTH / CRH → hiperplasia↑ →small cell Cacarcinoid bronchiolus, pankreasmalignant thymomafeokhromocytomamedullary ca tiroidgastrinoma
4. Adenoma, ca, nod hiperplasia → 20-25%ACTH indepentLesi adrenal auto → autonomous secresi kortisol (hiper)
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Adenoma, Ca → adult Ca → children Ca→↑ hipercortisolism → Neoplasma unilat kelenjar lain atropi ← ACTH Supresi → Adrenal cushing syndr →
Cortisol ↑ACTH ↓
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MORFOLOGI : Lesi2 dasar cushing syndrome
Pituitary adrenal
PITUITARY :Cortical efek feed back corticotrofNon tumor (tumor)→ Crooke’s deg.hialin basofil
Basophilic microadenoma Bosophilic macro adenoma Granulated chromophobic adenoma Hiperplasia difus corticotrof
ADRENAL Diffuse hiperplasia Nod hiperplasia Adenoma, Ca jarang Atropi korteks
bilateral : glucocorticoid exogen
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DIFFUSE HYPERPLASIA
60 -70 % KASUS Kel adrenal >> 25-40 gr Korteks melebar Lipid poor retikularis Sel-sel fasikulata normal
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NOD Hyperplasia 15-20% Bilateral 0,5 – 2cm, kuning nod tersebar Dipisahkan daerah korteks luas Sel lipid laden, lipid poor Inti variasi, binukleus 20-50 gr ACTH ↑→ autoantibodi reseptor ACTH Diffuse micronodul
Unilat, nod hitam pigmen, kecil : lipofusin, neuromelanin
Sel kecil, kompak, pleo, rgn Dapat familial, autosomal dominan
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CUSHING’S SYNDROME Hipersekresi kortisol, banyak terjadi pada wanita, dapat pula
mengenai laki2dan anak. Manifestasi klinik : cortisol >>
Deposisi lemak→striae katabolisme protein →muscle wasting, weakness→striae Protein sintesis <<→muscle wasting, weakness→striae Gluconeogenesis →hiperglikemia dan glukosuria Depresi reaksi imun → tendensi infeksi bakteri Supresi growth hormon → pertumbuhan anak ↓ Adipositas pada wajah, leher Osteoporosis→ khyposis Hypertension Virilism pada wanita
Penyebab : Adenoma korteks adrenal, adenokarsinoma Pituitary adenoma → acth ↑ Bronchial carcinoma, carcinoids, pancreatic tumours Pemakaian lama glukokortikoid atau terapi ACTH
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Hiperaldosteronism Primer1. Sekresi aldosteron independent khronik (↑↑)2. Sistem renin angiotensin independen
iskemi ginjal, edema kroniksekunder hiperaldosteronism
Khas : aktifitas renin plasma supresi hipokalemia retensi Na hipertensi
ETIOLOGI :- Adenoma soliter conn’s syndrome 65 %- hiperplasia bilateral idiopatik adrenal 30 %- Glukokortikoid supressible hyperaldosteronism- Familial non glukokortikoid supresPenyebab ini temukan pd 0,05 - 0,2% penderita hipertensi
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ADENOMA dan CARCINOMA ADENOMA
Kapsul tipis, <30gr Mikroskopis :
Sel kortikal lipid rich, lipid poor Variasi sel rgn True neoplasma ? Nod hiperplasia /
CARCINOMA kapsul (-), besar 200-300gr, sel anaplastik Perjalanan penyakit :
D/ kortisol ↑ → hidroksikortikoid T/ ?
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GLUCOCORTICOID SUPPRESSIBLE HYPER ALDOSTERONISM Jarang, familial, pengaruh ACTH Supresi ← pemakaian dexametazon exogen Perjalanan penyakit :
Hipertensi, hipokalemi ← K ginjal sekresi Manifest neuromuskuler (weakness, parestesi, ggn
visual, tetani) Retensi Na -- edem → hipertensi → Decom cordis
Diagnosa : PHA : aldosteron ↑renin ↓
Causa ? Adenoma → T/ Hiperplasia
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HIPERPLASIA ADRENAL KONGENITAL / ADRENOGENITAL SYNDROME Jarang, D/ sukar Hermaproditism Pseudohermaproditism Virilium (♀) Prekok (♂) Androgen syndr → adrenal virilium ← Ca adrenal sekresi androgen
Kong metab errors (enz biosintesis) Steroid cortical (cortisol)
Cortisol ↓→ ACTH ↑ (hiperplasia adr) Enzim terganggu → aldosteron
→ cortisol N
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Morfologi
ALDOSTERON PRODUCING ADENOMA Soliter, kecil < 2cm,
kiri, kapsul, ♀ dekade 4-5
Ø yellow, terang, tdd sel korteks, lipid laden
~ sel fasiculata, uniform
Pleomorfik, anaplasia (-)
HIPERPLASIA IDIOPATIK BILATERALSel zona
glomerulosa hiperpla difus ? Fokal dg diselingi nodul adrenocortical kecil (lipid laden)
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HIPOFUNGSI KORTEKS ADRENAL (HIPOADRENALISM) Cause : lesi anatomik
metabolik → Steroid ↓ ACTH ↓ (sekunder)1. insuf adrenocortical akut primer (adrenal crisis)2. insuf adrenocortical kronik primer (addison”s
dissease)3. insuf adrenocortical sekunder
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INSUFISIENSI ADRENOCRTICAL ACUTE PRIMER JARANG:1. Krisis penderita ionsuf adrenal kronik ← stress
→ steroid ↑, respons ↓2. pemakaian steroid → adrenal ↓
adrenalektomi → stress, adr supres 3. Destruksi adrenal masif
- neonatus partus lama/sukar, trauma, hipoksia →hemoragik adrenal- post op dilatasi infeksi → hemor adrenal- bakteriemi → hemoragik masif adrenal → water house frederick syndrome
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MORFOLOGI
Tergantung penyebab Adrenalitis autoimun Norm : leaf like structure Histologi:
Atropi difus zone2, sel lipid <<, kecil, keriput, Lipofusin sitoplasma ↑ sebukan sel limfosit, plasma, makrofag Medula adrenal (-)
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PERJALANAN PENYAKIT
Glukokortikoid ↓ Mineralokortikoid ↓ klinik :
Weakness, fatty, anorexia, BB ↓ Hipotensi, hiperpigmentasi kulit
Na Cl Bikarbonat Insuf adr, cor, primer : ACTH
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WATERHOUSE-FRIDERICHSEN SYNDROME Jarang Catastrophic syndr :
1. meningokok, gonokok, pneumokok, stafilokok → septikemia
2. Hipotensi progresif → shock3. DIC → purpura skin4. Insuf adrenocortical (rapid) → hemor adr bilat masif
Bacterial seeding → P.D kecil (adr) → DIC,endotoxin → vaskulitis
hipersensitivity vaskulitis Histologi : hemoragik medula
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Insufisiensi Adrenocortical Kronik Primer ( Addison’s Disease ) Jarang ←Destruksi kronik kortex adrenal Insidious → sampai 90% destruksi Adult, white, ♀ Etiologi & patogenesis: peny yg mengenai korteks adrenal :
limfoma, amiloidosis, sarcoiodosis, hemokhromatosis, jamur, hemor adr
Adrenalitis autoimun 60-70%TBC kort, med poliglandular syndr, tipe :Metas Ca
1. candidiasis, hipoparatiroid, insuf adrenal2. Adrenal, insulin dependen, DM, Tiroid disease (Schmidt synd)3. Poligland adrenal (-)Anti adrenal antibodi ↑
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Insufisiensi adrenocortical sekunderMetastatic cancerInflamasi → hipotalamus → ACTH ↓ →Infark pituit hipoadrIrradiasiGlukokortikoid pemakaian lama→ACTH ↓Adrenal fungsi ↓Hiperpigmentasi of addison’s disease (-)Hor melanotropic↓Cortisol ↓, androgen ↓, aldosteron sintesis N→Malfungsi pituit No mark hiponatremi,hiperkalemi
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Hipofungsi Korteks Adrenal Defisiensi mineralokortikoid dan glukokortikoid Hipofungsi akut:
Acute failure reabsorpsi Na dan ekskresi K Kegagalan glukoneogenesis → hipoglikemia dan
sensitifitas insulin ↑ Kematian disebabkan oleh :
Hipovolemia syok Hiperkalemia cardiac irregularity
Destruksi medula dan defisiensi katekolamin → syok
Penyebab kematian yg plg sering adalah septikemi krn meningococcus → nekrosis korteks dan gross hemoragis pada medulla
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MEDULA ADRENAL Sel neuroendokrin
Katekholamine Epinefrin Norepinefrin Dopamin Histamin Serotonin Renin Khromogranin A Neuropeptide hormon
Extra adrenal system Paraganglion :
Bronchiomeric Ontravagal aorticosimpatetik
Patologi : tumor Pheochromocytoma Neuroblastoma ganglioneuroma
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PHEOCHROMOCYTOMA Jarang Catecholamine induced hypertension → T/ op Hipertensi → 0,1-0,3% akan pheochromocytoma ~ Cushing syndrome
Endocrinopathy 85 % medula adrenal
Extra adrenal paraganglia → Paraganglioma
95% sporadik 10% autosomal dominant Familial – men – anak ♂ , bilateral Non familial 40-60 th ♀
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MORFOLOGI
Pada MEN syndrome : adrenal difus / noduler hiperplasia / neoplasma
Dikatakan berasal dr hiperplasia 100 gr (1-400 gr) Batas jelas, fibrous trabekula, vaskularisasi (+),
lob patern Ø Abu pucat, coklat Hemor nekrosis, kista - T besar
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HISTOLOGI
Sel tumor sitoplasma > Inti kecil, sentral di batas septa fibrovasc ~ Trabekula , cluster Pleiomorfik ~ alveol, bizzare, giant Sel tumor dapat pada sinusoid dan kapsul →
bukan indikasi malignant Kriteria malignancy – metastasis → KGB, hati,
paru, tulang Syrvival metast < 3th
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PERJALANAN PENYAKIT
Klinik : hipertensi paroxysmal attack ← stress, exercise, change of postureDHR tumor palpation
→ katekolamine→ cong heart failure, edem pulmo, MCI, fibrilasi ventrikel, hemor serebri → †
Katekolamine cardiopathy/catecholamine heart muscle disease
D/: urine : Ca, metanefrin, VMA → iskemik ← vasokonstriksi , direct toxicity
→ sakit kepala, ansietas, takut , tremor, fatique, nausea, vomitus, nyeri abdomen
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THYMUS1. Development disorders
1. hipoplasia/aplasia2. kista
2. Hiperplasia 3. Thymoma
HIPERPLASIA :Thymic foll hyperplasiaKGBPD : inflamasi kronik
imunologikmiastenia gravis 65-75% kasus
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THYMOMA Sel epitel thymus Benign thymoma cito & biol benign Malignant thymoma
Tipe I : sitologi benign biological agresif, invasi lokal, jarang distant spread
Tipe II : “thymic Ca” sitol malignant
Adult, > 40 th, ♀~♂Mediastinum ant, sup or
Kadang leher, tiroid, hilus paru20-30% dari tumor anterosuperior mediastinum
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MORFOLOGI
Lobulated, abu2 putih, 15-20 cm
Nekrosis kistik, kalsifikasi (→ biological benign)
Encapsulated, 20-25% penetrasi kapsul → infiltrasi jar peritimik
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MIKROSKOPIS Sel epitelial, infiltratif, limfosit non
neoplastik Benign:
Sel epitelial sel medulla, elongated, spindelProd “ medullaey thymoma”Sel epitelial plump, bulat, cortical typeMarsall’s corpuscle jar
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MalignantTipe I :
Lokal invasive, metast 20-25% of thymoma Sel epitelial: cortical cell, sitoplasma >> Inti vesikuler bulat, spindel Palisade P.DPenetrasi → invasi capsul
5 th surv rate 50 %- 90% excisi komplit
Tipe II :Makros : fleshy, invasif → metast- ↑ Squamous Ca, well, poorly dif- Limfoepitelioma : sel anaplastik kortikal, limfosit N- Sarcomatoid- Basaloid- Clear cell
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PERJALANAN PENYAKIT
Insidentil Clinical attention :
40 % imaging study Simp local pressure 50 % miastenia gravis 10% sindroma paraneoplastik sistemik
(grave’s disease, an pernisiosa, dermatomiositis-poliomiositis, sindroma cushing) ?
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PINEAL GLAND
PinealomaPinealoblastomaPineositoma
Morfologi :
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PINEOBLASTOMA Young Soft, friable, abu, hemor, nekrosis Invasi struktur sekitar Histologi :
Sel pleomorfik, Ø 2-4 x RBC Inti besar hiperkromatik, mitosis Large/poorly rosette
Metastasis CSF
→ Hidrosefalus
Survival jarang 1-2 th
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PINEOCYTOMA Adult, slowly, batas tegas Massa abu2, hemor Histologi :
Glial, neural difLargely astrosimatous, pineosit (bulat,oval)Pseudorossette, dibatasi sel pineosit →Sentral massa eosinofil, fibrovascPerjalanan penyakit - 7 thKlinik penekanan → ggn visual, sakit kepalaMental deterioration, demensia
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DEFISIENSI 21 HIDROXILASE
1. Salt wasting adrenogenitalism
2. Simple virilizing adrenogen
3. Nonclassic adrenogenasimtomatik
androgen ↑ anak / pubertas
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1. in utero Lahir → salt wasting Hiponatremia Hiperkalemia → Asidosis Hipotensi Cardiovasc collaps †
2. aldosteron↓ RGNtestosteron ↑
hiperplasia adrenal
3. D/ defek biosintesis steroidogenesis
genetik
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AUTOSOMAL RECESSIVE
MORFOLOGI ;Defek sintesis cortisol →ACTH ↑→ hiperplasia bilateral adrenalBerat 10-15 kØ Korteks lebar, coklatLipid depletion 2 retic/glom→Nod kecil
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FAMILIAL SYNDROME WITH PHEOCHROMOCYTOMA MEN tipe II atau IIA
Medullary thyroid carcinima dan Ccell hyperplasia Pheocromocytoma dan Adrenal meduillary hyperplasia Parathyroid hiperplasia
MEN tipe III atau IIB Medullary thyroid carcinima dan Ccell hyperplasia Pheocromocytoma dan Adrenal meduillary hyperplasia Mucosal neuromas Marfanoid features
Von Hippel-Lindau Renal hepatic, pancreatic, and adrenal medullary hyperplasia Renal cell Ca Pheocromocytoma Angiomatosis Cerebellar hemangioblastoma
Von Recklinghausen Neurofibromatosis Café ua lait skin spoil Schwannomas, meningiomous gliomas Pheocromocytoma
Sturge-Weber Cavernous hei Cavernous hemangioma pada cranial nerve pheocromocytoma