PANCREATITE CRONICE
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PANCREATITE CRONICE
Prof.Dr.Radu VoiosuUniversitatea de Medicină şi Farmacie Carol Davila Bucureşti
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DIAGNOSTICUL
E uşor la cei suferinzi de mult timp Paradigma actuală plasează acut şi
cronic la extremităţile aceluiaşi spectru Ce înseamnă precoce = Se poate reveni/încetini dezvoltarea
P.C ?
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PLANUL DISCUŢIEI
1.Datele normale structură şi funcţie 2.Conceptul de pancreatită cronică 3.Imagistica pancreatitei cronice 4.Clasificarea etiologică a pancreatitei 5.Tratamente specifice 6.Tratamente comune
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… nothing short of a surgical exploration
will unearth
the thick spongy worm
buried deep in the viscera
silent behind the curtain
of peritoneum
with a head, a body and a tail.
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Ecce viermele…
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ANATOMIA
Formă paralelipipedică 6/4/3 cm Procesul uncinat Canalul principal 4,3,2 mm Canalul accesoriu cranial de ampula
Vater Vase din hepatica, splenică, AMS Raporturi strânse cu v.portă
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Structura acinară
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Membrana conţine receptori
CCK Bombesină Neuromedina B Secretină VIP
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SECREŢIA ESTE DEPENDENTĂ DE METABOLISM
Activare : faza cefalică
faza gastricăfaza intestinală
Inhibare : stimuli adrenergicisomatostatinaPP
secreţia intestinală de peptidaze
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Reglarea secreţiei
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ENZIME
Proteolitice - tripsinogen
- chemotripsinogen
- elastaza
- carboxipeptidaza A,B
- kallikreina
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ENZIME
Lipolitice - colipaza
- lipaza
- carboxihidrolaza
Glicolitice – amilaza 1,4α
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Celulele acinare
Produc
Stocheză
Eliberează enzimele
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AUTOLIZA E PREVENITĂ :
Sinteza de precursori inactivi
Enzimeanvelopate în organele
Antiproteaze intracelulare
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ANTIPROTEAZE CONTROLATE GENETIC
PRSS1 menţine enzimele inactive
SPINK1menţine integritatea inhibitorilor
CFTR reglează secreţia de bicarbonat
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Etiologie Mutaţie genetică
Alcoolică SPINK 1
CFTR
Tropicală PRSS 1
SPINK 1
CFTR
Idiopatică SPINK 1
CFTR
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ROLUL FIZIOLOGIC
Bernard HENDERSON 1856
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Definiţie:
Inflamaţie cronică caracterizată
prin alterări morfologice ireversibile,
ducând la: a)dureri abdominale
b)alterarea permanentă a funcţiilor pancreasului
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EVOLUŢIA CONCEPTELOR
1. SARLES , MARSEILLE 1963 Definiţie anatomo-patologică bazată pe 5
anomalii şi anume : Fibroză Celule inflamatorii Pierderea parenchimului Dilataţii canaliculare Litiaza căii principale
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EVOLUŢIA CONCEPTELOR
GEORGE ORWELL
1984
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EVOLUŢIA CONCEPTELOR
2. Conceptului anatomo patologic i se adaugă :
Obstrucţia Funcţia Clinica , durerea ca simptom princeps
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EVOLUŢIA CONCEPTELOR
3. Clasificarea Cambridge incorporează :
Date echografice Date tomografice Date E.R.C.P
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EVOLUŢIA CONCEPTELOR
Apare clasificarea japoneză etiologică
cunoscută azi sub numele
TIGAR-O
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Modificări morfologice
Distrugerea parenchimului exocrin Focală Segmentară Difuză
prin: anomalii ductale infiltrat inflamator fibroza
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Macroscopie
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Microscopie
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INSUFICIENŢELE MORFOLOGIEI
1.Eşantioane obţinute chirurgical, deci faze avansate.
2.Nu are cuantificare 3.Nu are ierarhizare
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Puţină istorie
1856 – Claude Bernard face modelul animal al PA
1878 – Fridreich incriminează alcoolul 1896 – Chiari postulează autodigestia 1946 – Comfort elaborează teoria
necroză/fibroză 1970 – Sarles – ipoteza dopurilor proteice 1996 – Whitcomb defineşte leziunea
cromozomială C 7 q 35
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The molecular basis of pancreatic disease arose from the pioneering work of Claude, DeDuve, Palade and Porter, who used the molecular biologic techniques to study the process of cellular protein synthesis.
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CLASIFICARE ETIOLOGICĂ
T (toxica-metabolică) I (idiopatică) G (genetică) A (autoimună) R (recidivantă,acută) O (obstructivă)
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I. Pancreatite toxic- metabolice
1. alcoolice
2. tabagism
3. hipercalcemie / hiperparatiroidie
4. hiperlipemie
5. medicamentoase – fenacetina
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II. Idiopatice
1. debut precoce
2. debut tardiv
3. tropicale
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III. Genetice
1.Transmisie autozomal dominantă- gena tripsinogenului cationic (codon 29,122)
2. Transmisie autozomal recesivă - gena SPINK 1 cromozom 5q
- gena CFTR
- gena tripsinogenului cationic (6,22,23)
- deficit α1 AT
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ROLUL GENEI SPINK 1 (PSTI)
Situată pe C5 Inhibă 20% din tripsina Substituţia asp/ser (N43S) e mutaţia
cea mai frecventă (1-2 %) E factor de susceptibilitate !
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ROLUL GENEI CFTR
Codeză proteina canalelor de clor Sunt cunoscute > 1200 mutaţii 4% din populaţie e heterozigotă 6 clase de mutaţii 1: neexprimată
2+3 nefuncţională
4 canal alterat
5+6 proteină instabilă
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IV. Autoimune
1. Izolate
2. Asociate : - S.Gougerot –Sjogren
- B.I.I.
- C.B.P
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V. Pancreatite acute severe recidivante
Pancreatita acută necrotică
Pancreatita acută recidivantă
Pancreatita acută ischemică
Pancreatita acută dupa iradiere
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VI. Obstructive
1. obstructţe canaliculară
2. stenoza canaliculară cicatrizantă
3. pancreas divisum
4. diskinezie sfincter Oddi
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Pancreatita cu eosinofile
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Formă rară
Se asociază GEC cu eozinofile
Sindrom hipereozinofilic
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Experienţă
Sunt cunoscute 16 cazuri certe
Alergie la 50% din cazuri
Ig E crescut la 80% din cazuri
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Pancreatite Autoimune
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Sarles 1961 a făcut primele observaţii
Yashida 1995 a mai descris 11 cazuri
2% pancreatite
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Caractere
1. Cresterea γglobulinelor (IgG)
2. Prezenta de auto-anticorpi
3. Absenţa calcificărilor şi pseudochistelor
4. Asocierea cu alte afecţiuni
5. Infiltrat limfocitar
6. Răspuns la corticoterapie
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Criterii de diagnostic
1. Creşterea IgG 4 (6,6 g/L fata de 0,51 g/L N)
2. Anticorpi antinucleari 75%3. Anticorpi antilactoferina 75%4. Anticorpi antianhidraza carbonica II
60%5. Factor reumatoid 30%6. Anticorpi antifibra netedă 20%
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Mecanisme propuse
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Imunitate umorală
Coexistenţa atingerii pancreatice cu: S Gougerot – Sjogren CSP CBP LES
a generat ideea “dry gland syndrome” / “autoimmune epithelitis”
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Imunitate umorală
Antigene ţintă:
1. Anhidraza carbonică II
2. Lactoferina
3. Anhidraza carbonică IV
Nashimori Gut 2005
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Imunitate celulară
Limfocite citotoxice CD 8
Intervenţia IL2, TNF α, IFN γ
(profil Th1)
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Pancreatite asociate B.I.I.
Diferenţiată de 1. Pancreatita medicamentoasă
1. Sigura 5 ASA2. Probabilă la prednison şi metronidazol3. Improbabilă la tacrolimus şi ciclosporină
2. Pancreatita litiazică 1. Atingere ileala2. Nutriţie parenterală
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Prevalenţă 1,2 – 1,5 %
C.U. 56% (42% pancolită)
BC 33%
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Manifestări
a) PA 24%
b) Icter 14%
c) Insuficienţa pancreatică 20-80%
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Cadru Nosologic
Este de discutat în cadrul etiologiei
- Alcoolice- Medicamentoase
relaţia pancreatită acută -> cronică
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Problema care se pune
1. Pancreatita acută survine pe fond cronic (subînţeles : până atunci latentă! )
2. Pancreatita acută este o entitate
3. Pancreatita acută recurentă produce leziunea cronica
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Teoria SAPE
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Fenomene celulare în cursul Pancreatitei acute
Stress( taurocolat, ceruleina)
Inhibarea genelor care codează enzime
Supraexpresia proteinelor de stress
Diminuarea acestora concomitent cu
Creşterea expresiei genelor de regenerare
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Histologie
Creşterea Apoptozei = Necroza
imposibilitatea declanşează
întoarcerii la homeostazie inflamaţia
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În Pancreatita cronică :
1. Agresiune mai slabă ca în PA
2. Răspunsul acinar
→ reducerea funcţiei exocrine → inducerea genelor de
supravieţuire
3. Continuarea agresiunii → apoptoza
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Derivă
1.Agresiune nonfatală
→ întoarcerea la program de homeostazie
→ regenerare
→ restitutio ad integrum
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REZULTĂ CĂ TREBUIE GĂSITĂ EXPLICAŢIA DIFERENŢEI DE PREDISPOZIŢIE => GENE ?
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Au fost demonstrate :
Asocierile cu SPINK 1
Anomalii ale raportului tripsinogen / inhibitorul tripsinei
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Diferenţa PA – PC este fără obiect căci mecanismele puse în joc sunt IDENTICE.
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Se poate afirma că PC = PA benignă prelungită.
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• Greu de diferenţiat de PA
• Timp de certitudine 5 ani
Pancreatita Cronică Alcoolică:
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Criterii
DEFINITĂ:
Calculi pancreatici
Leziuni la ERCP
Steatoree > 7g / zi (in absenţa altor cauze)
Piesa operatorie
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PROBABILĂ:
Leziuni minime ERCP
Chiste persistente, recurente
Test patologic la secretină
Insuficienţa pancreatică endocrina
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Opinia curenta
Alcoolul este responsabil de atingerea
CRONICĂ
dar descoperirea clinică poate fi :
ACUTĂ, ZGOMOTOASĂ, PRECOCE
sau, dimpotrivă:
DISCRETĂ ŞI TARDIVĂ !
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Pancreatita alcoolică
Relaţia abuz alcool-pancreatită este STABILITĂ.
Dar:
1.Majoritatea pacienţilor sunt alcoolici
2.Majoritatea alcoolicilor nu au pancreatită
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Barach’s Rule :
An alcoholic is a person who drinks more than his own physician.
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5-10 % din alcoolicii “heavy” dezvoltă boala.
Aceasta subliniază încă o dată relaţia
factori exogeni- factori genetici .
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Patogenia pancreatitei alcoolice
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1. Mecanisme celulare
Creşterea enzimelor (lipaza, amilaza, proteaze)
Scăderea inhibitorilor
Interferenţa cu transportul intracelular
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2. Mecanisme canaliculare
Hipervâscozitate prin hexozamine
Hipoproducţie litostatina
Anomalii ale proteinei GP 2
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Intervenţia UDPG transferazei
Risc crescut de 2,2 ori la cei care au gena UGTI A7
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Alte teorii patogenetice
a) Teoria permeabilizării ductale
b) Teoria metaboliţilor toxici
c) Teoria ischemică
d) Teoria leziunii mitocondriale
e) Teoria activării celulelor stelate
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Pancreatite Genetice
1. Pancreatite cronice ereditare
2. Deficitul α1 AT
3. Fibroza chistica a pancreasului
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Pepsinogenul cationic (PRSS I = serine proteinase 1) :
se autoactivează mai usor
e rezistent la autocataliză
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Patogenie
1. Creşterea activării intrapancreatice a tripsinogenului depăşind capacitatea PSTI (pancreas secreted tripsine inhibitor)
2. Stabilizarea tripsinei –mecansim accesoriu
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Teoria refluxului
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Teoria obstructiva
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Litogeneza
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ASPECTE CLINICE
Durere abdominală :tip A, B
Maldigestie
Diabet zaharat
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MECANISMELE DURERII ÎN PANCREATITA CRONICĂ
I. Durerea extrapancreatică
a) stenoza căii biliare principale
b) stenoza duodenului (groove pancreatitis )
Explică durerea postprandială(20%)
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II. Durerea pancreatică
A. Teoria creşterii presiunii intraductale
- decompresia influenţează durerea
- suplimentele enzimatice scad CCK
- insuficienţa e indoloră !
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Contraargumente
- Durerea există şi la insuficienţii pancreatici
- Octreoctidul e ineficient- Persistă la decomprimaţii chirurgical în
30% cazuri
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B. Teoria ischemică
Hipertensiunea ductală şi parenchimalî comprimă vasele producând ischemie
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C. Teoria fibrozei
Creşte presiunea intraductală.
Nu există corelaţie fibroză-durere
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D.Teoria inflamaţiei neurogene
Substanţa P se leagă de receptorii de neurokinină (NK-R1) generând inflamaţie.
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DIAGNOSTICUL IMPUNE ASOCIEREA CU
TESTE IMAGISTICE
TESTE FUNCŢIONALE
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IMAGISTICA
Radiografie simplă Echografie Tomografie computerizată Colangiopancreatografia RM+secretină Echoendoscopia Colangiopancreatografia retrogradă per
endoscopică Elastografia per endoscopică
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Valoarea diagnostică a echografiei de suprafaţă
Echografie abdominală
Sensibilitate 50-95%
Specificitate 75-95%
1.Atrofia glandei
2.Contur neregulat
3.Căi dilatate
4.Calcificări
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Pancreatita cronică - CT
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Pancreatita cronică calcificantă
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Pseudochist pancreatic - CT
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Condiţii de efectuare
Ct Spiral Substanţă de contrast
Grosimea cupelor 5 mm
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Valoarea diagnostică a T.C.
Tomografie computerizată
Sensibilitate 55-95%
Specificitate 85-100%
1. Atrofie
2.Contur neregulat
3.Ducte dilatate
4.Calcificări
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Pancreatita cronica - ERCP
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COLANGIO-RMN
Colangio RMN Sensibilitate 90%
Specificitate 92-98%
1.Atrofie
2.Mărire localizată
3.Contur neregulat
4.Dilataţii
5.Modificări de semnal
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Pancreatita obstructivă -ERCP
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CRITERIILE CAMBRIDGE
Clasa I < 3 ramuri afectate
Clasa II >3 ramuri sau DUCTUL PRINCIPAL
Defecte de umplere, stenoze/dilataţii.calcificări
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Pancreatita autoimună – CT, ERCP
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TESTE BIOCHIMICE STATICE
ENZIME SERICE
SEMNE DE COLESTAZĂ
STEATOREEA
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ECHOENDOSCOPIA
Avantaje .
poate preleva eşantioane cito/histo
poate TRATA
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ECHOENDOSCOPIA
DEZAVANTAJE
E invazivă
Impune pregătire specifică
Necesită echoendoscop linear
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CLASIFICAREA ROSEMONT
ANOMALII PARENCHIMATOASE
ANOMALII DUCTALE
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ANOMALII PARENCHIMALECaracter Descriere Criteriu major Criteriu minor Grad Histologie
Zone hiperecho cu con de umbră
Structuri echogene>2mm
A 1 Calcificări
Lobularitate Structuri>5mm cu inel hiperechoic
2 N/A
A Aspecte de fagure
>3lobuli BB fără aspect de fagure
Lubuli necontigui
Da
Zone hiperechogene fără con umbră
> 2mm Da 3 N/A
Chist Da 4 Pseudochist
Stranding Da 5 N/A
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ASPECTE DUCTALE
Caracter Definiţie Criteriu major Criteriu minor Grad Histologie
Calculi duct principal
Structuri echogene
A 1 litiază
Contur neregulat
Calibru neregulat
Da 2 N/A
Dilataţii colaterale
>3anormale Da 3 Ectazii
Dilataţii cale principală
>3,5mm Da 4 Dilataţii
Cale principală hiperechogenă
Pereţi echogeni
Da 5 Fibroză ductală
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DIAGNOSTIC CONSISTENT
1. Un criteriu major A +> 3 minore
2.Un criteriu major A + major B
3. 2 criterii majore A
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ASPECT NORMAL AL ELASTOGRAFIEI PANCREAS
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ENZIME
Tripsina serică
Chemotripsina fecală
INSENSIBILE!
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STEATOREE - Sudan
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TESTE DINAMICE-caracteristici:
Sensibile Specifice Uşor de realizat Neinvazive Ieftine
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TESTUL CCK-SECRETINĂ
Standardul de aur Complex Consumă timp Neplăcut Greu de suportat Centre terţiare Nestandardizat Recent înlocuite cu dozarea Zn
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TESTE DE DIGESTIE
Prânzul Lundh
PABA(specificitate 90% în prezenţa steatoreei, 65 % I.E.P. Moderată)
Lauratfloresceină
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TESTE ELISA
SENSIBILITATE LIMITATĂ
Elastază <100µg/g
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Teste respiratorii
Colesteroloctanoatul (+ D-xiloză)
Trigliceride
Utilizează C13
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Şi atunci de ce teste de funcţie?
Atât Grupul ZURICH cât şi MAYO consideră că pancreatita cronică= I.P.E., indiferent de etiologia pancreatitei !
Steatoreea este apanajul extremei insuficienţe!
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EXCEPŢII :
Deficitul izolat de lipază/colipază produse de leziuni C10/C8
Deficitul de enterokinază
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Arbore decizional
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TRATAMENT
Dietă 2000-3000 cal/zi
Acizi graşi cu catenă medie
Antioxidanţi
Somatostatină 50-200µg/zi
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TRATAMENT ENDOSCOPIC
Sfincterotomia +/- stentare Complicaţii : pancreatită acută 2-7%
sângerări 3%
perforaţii < 3%
stenoze < 1%
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DILATAŢIE, STENTARE
Fir ghid Dilatare : cateter /balon Stentare 3-10 F
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Necunoscute
Durata stentării
Diametrul stentului
Gradul de dilatare cu balonul
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Complicaţii
Migrarea stentului 10%
Ocluzia stentului 20%
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LITOTRIPSIE
Extracţie cu balon/coşuleţ
ESWL
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ALTELE
OBSTRUCŢIA BILIARĂ
PANCREAS DIVIZUM
BLOCAREA ŞI NEUROLIZA CELIACĂ
DRENAJUL PSEUDOCHISTELOR
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PREPARATE ENZIMATICE
Capsule acidorezistente
Conţinut variabil în lipază
Când trebuie începută administrarea lor ?
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Combaterea durerii
Trepte progresive
Neuroliza
Decompresia
Pancreactectomia
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METODE ENDOSCOPICE
Decompresia
Stentarea
Extragerea litiazei
Drenajul pseudochistelor
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