ORGANELE ANEXE ALE TUBULUI DIGESTIV

ANATOMIE
FIZIOLOGIE
MORFOPATOLOGIE
FIZIOPATOLOGIE
SINDROAME
FICATUL - ANATOMIE
VASCULARIZATIE
SISTEMUL PORT SI ANASTOMOZELE PORTO-CAVE
LOBULUL HEPATIC
SPATIUL SINUSOIDAL
CELULELE SINUSOIDALE
 SANGE
A. Hepatica
(circ. nutritiva) Lobul hepatic
VCI
V. Porta (capilar sinusoid)
(circ. functionala)

v. centrolobulara vv. suprahepatice

Spatiul port BILA

Lobul hepatic
(canalicule biliare
(hepatocit)
interlobulare)

Canal hepatic dr/stg Canal hepatic comun colecist

 STROMA FICATULUI
(tesutul conjunctiv)

Capsula ficatului contine ramuri din nervul frenic, vase de sange,

vase limfatice si canaliculi biliari
Tesutul conjunctiv perivascular
Tractul portal
Reteaua de reticulina pe suprafata hepatocitelor; serveste ca suport
mecanic pentru capilarele sinusoide
 HISTOPATOLOGIE
Hepatite cronice

Gradul de activitate histopatologica (necroinflamatorie)

Gradul de progresie stagiul (gradul de fibroza)

 Activitatea necroinflamatorie

Inflamatie portala
Necroza periportala piecemeal necrosis
Necroza confluenta bridging necrosis
Degenerare hepatocitara si necroza focala in lobul
 Gradul de fibroza stagiul
(progresia bolii)

Fibroza portala
Fibroza periportala
Bridging fibrosis (fibroza septala)
Ciroza
 Hepatita alcoolica

Risk drinking :
Barbati: 15 standard
drinks/sapt sau 5/ocazie
( ~ 30g alcool/zi sau 70g/ocazie)

Femei/ > 65 ani: 8 standard

drinks/sapt sau 4/ocazie
( ~ 16g alcool/zi sau 56g/ocazie)

1 standard drink = 14g etanol

 Steatoza hepatica acumulare de grasime in hepatocitele
perivenulare (centrolobular)

Steatohepatita alcoolica inflamatie perivenulara; extindere

spre tracturile portale; infiltrat PMN; corpi Mallory-Denk
(acumulari de eozinofile in citoplasma hepatocitelor)

Hepatita alcoolica balonizarea hepatocitelor, spotty necrosis,

infiltrat PMN si fibroza perivenular si in spatiul Disse (necroza
hialina) panlobulara (reversibila)

Ciroza micro/macronodulara (ireversibila)

 FUNCTIILE FICATULUI

Metabolismul carbohidratilor
- sinteza si degradarea glicogenului
- sinteza si degradarea glucozei
Metabolismul proteinelor (sinteza de aminoacizi, albumina,
factori de coagulare, s.a.)
Metabolismul lipidelor (sinteza de colesterol, trigliceride)
Metabolismul bilirubinei
Metabolismul hormonilor (steroizi, tiroidieni)
Metabolismul vitaminelor si al mineralelor
 FUNCTIILE FICATULUI

Degradare si detoxifiere hormoni, alcool, toxice,

medicamente, amoniac

Imunitate si protectie impotriva infectiilor

 Metabolismul carbohidratilor
This reserve is sufficient to maintain glucose homoeostasis in the
organism for up to 10 hours or, in conjunction with
Glicogeneza stocare de glicogen gluconeogenesis, up to 20 hours.

Glicogenoliza cu formare de glucoza

Gluconeogeneza
Glucoliza degradarea glucozei in glicerol si mai departe in
lipide

FICATUL FUNTIONEAZA A UN GLUCOSTAT

In a person with poor liver function, blood glucose concentration after a meal
rich in carbohydrates may rise two to three times as much as in a person with
normal liver function.
 Metabolismul lipidelor

Oxidarea acizilor grasi- energie

Sinteza de colesterol, fosfolipide si lipoproteine
Sinteza de lipide din proteine si carbohidrati

LIPOLIZA SI LIPOGENEZA
energie

energie
 Metabolismul proteinelor

Dezaminarea aminoacizilor
Sinteza ureei din amoniac (indepartarea amoniacului)
Sinteza de proteine plasmatice
Sinteza anumitor aminoacizi si sinteza de compusi chimici din
aminoacizi

90% din totalul proteinelor plasmatice sunt sintetizate de ficat

Metabolismul bilirubinei
 Alte functii metabolice

Stocarea vitaminelor (A, D, B12)

Stocarea fierului sub forma de feritina

Sinteza factorilor de coagulare: fibrinogen (I), protrombina (II), factorii VII,

IX si X (dependent de vitamina K)

Detoxifiere si excretie in bila de medicamente (sulfonamide, penicilina,

ampicilina, eritromicina), hormoni (tiroxina, hormonii steroizi estrogen,
cortizol, aldosteron), calciu
inflamatie BOALA CRONICA DE FICAT colestaza
cronica Cauze

Cauze mai rare:

Cauze frecvente:
Autoimmune hepatitis
Primary and secondary biliary cirrhosis
Primary sclerosing cholangitis
Chronic viral hepatitis Medications (eg, methotrexate, isoniazid)
Wilson disease
(hepatitis B, C) Alpha-1 antitrypsin deficiency
Celiac disease
Alcoholic liver disease Granulomatous liver disease
Idiopathic portal fibrosis
Hemochromatosis Polycystic liver disease
Infection (eg, brucellosis, syphilis,
Nonalcoholic fatty echinococcosis, schistosomiasis)
Right-sided heart failure
liver disease Hereditary hemorrhagic telangiectasia
Veno-occlusive disease
 Ciroza micronodulara (alcoolica)
- macronodulara (virala)

- Nespecifica
- Aspectul se schimba (micro macro)
- Markeri serologici pt diagnosticul etiologic
- Aspectul macroscopic invaziv (interventie chirurgicala,
laparascopie, autopsie)

INUTILA !
 Semne si simptome nespecifice

Inapetenta
Scadere in greutate
Fatigabilitate si slabiciune
Crampe musculare
Hepatomegalie
Contractura Dupuytren

boala hepatica compensata

 Ciroza decompensata semne si simptome date de

- insuficienta hepatica
- hipertensiunea portala
 Semne si simptome ale insuficientei hepatice

Icter (colestatic), prurit

Eritroza palmara, buze carminate, stelute vasculare
Fetor hepatic (cresterea concentratiei de dimetil-sulfid)
Amenoree/oligomenoree/metroragii
Hipogonadism (impotenta, infertilitate, disfunctii sexuale, atrofie
testiculara, diminuarea pilozitatii) in ciroza alcoolica sau hemocromatoza
Ginecomastie
Sindrom hemoragipar cutaneomucos (echimoze, sangerari gingivale,
epistaxis)
 Insuficienta hepatica acuta

Development of severe acute liver injury with

encephalopathy and impaired synthetic function (INR of
1.5) in a patient without cirrhosis or preexisting liver disease

Time course that differentiates acute liver failure from chronic

liver failure < 26 weeks (~ 6 months)
 Cauze frecvente

Acetaminophen (paracetamol) >4g/zi

Idiosyncratic drug reactions

- AINS
- antibiotice: amoxicilina, ciprofloxacina, sulfonamide, teraciclina, doxiciclina, nitrofurantoin
- allopurinol
- amiodarona, labetalol, metildopa, fenitoina
- anticonvulsivante, antidepresive triciclice
- tuberculostatice
- statine
- Herbalife
- cocaina

Viral hepatitis (hepatitis A, B, C, D, and E., herpes simplex virus, varicella zoster virus, Epstein-
Barr virus, adenovirus, and cytomegalovirus )
 Alte cauze de IHA

Alcoholic hepatitis (acute-on-chronic liver failure)

Autoimmune hepatitis
Wilson disease
Ischemic hepatopathy
Budd-Chiari syndrome
Veno-occlusive disease
Acute fatty liver of pregnancy/HELLP (hemolysis, elevated liver enzymes,
low platelets) syndrome
Malignant infiltration (most often breast cancer, small cell lung cancer,
lymphoma, melanoma, or myeloma)
Toxin exposure, including mushroom poisoning
Sepsis
 Clinic

Encefalopatie hepatica (edem cerebral)

Grade I: Changes in behavior, mild confusion, slurred speech, disordered sleep

Grade II: Lethargy, moderate confusion
Grade III: Marked confusion (stupor), incoherent speech, sleeping but wakes with
stimulation
Grade IV: Coma, unresponsive to pain
asterixis
alte semne de HT intracraniana : HTA, bradicardie, depresie respiratorie,
convulsii

Coagulopatie (INR 1,5)

 HIPERTENSIUNEA PORTALA

Presiune in vena porta mai mare de 5-10 mmHg

P = Q x R

P = gradientul de presiune portal

Q = fluxul portal
R = rezistenta vasculara in sistemul port
Factorii care contribuie la aparitia hipertensiunii portale
Modificari morfologice hepatice in ciroza
 Modificari morfologice ce determina cresterea
rezistentei vasculare intrahepatice

Compresia venelor hepatice de catre nodulii de regenerare

Distorsiunea vaselor prin procesul de fibroza

Ingustarea sinusoidelor hepatice prin hipertrofierea

hepatocitelor, depunere de tesut fibros in spatiul Disse
 Cresterea tonusului vascular intrahepatic

Vasoconstrictie concomitenta la nivelul vaselor intrahepatice

- la nivelul sinusoidelor hepatice (prin intermediul celulelor stelate si al
celulelor endoteliale sinusoidale)
- extrasinusoidal, la nivelul venulelor portale mici (celule musculare
netede)
 Dezechilibru intre mediatorii vasoconstrictori (endotelina, norepinefrina,
angiotensina II si vasopresina) si cei vasodilatatori oxidul nitric
- reducera eliberarii de NO de la nivelul endoteliului vascular hepatic joaca
rolul esential in aparitia vasoconstrictiei intrahepatice si, deci, in cresterea
rezistentei vasculare intrahepatice
 Statusul hiperdinamic

Vasodilatatie sistemica
Expansiunea volumului plasmatic

Debit cardiac crescut

Rezistenta vasculara sistemica scazuta
Flux splanhnic crescut

Paradoxuri:
- vasoconstrictie intrahepatica si cresterea rezistentei la flux
- vasodilatatie sistemica cu scaderea rezistentei vasculare sistemice
 Patogeneza modificarilor hemodinamice in ciroza

Sunturi porto-sistemice Translocare bacteriana

Endotoxemia
Scaderea activitatii SRE
PG si NO
Scaderea RVS
Vasodilatatie
splanhnica si sistemica Scaderea TA
Dezechilibru intre
TRIGGERI capacitatea vasculara si
Abuz de diuretice volumul plasmatic
Paracentaza evacuatorie larga Activarea sistemelor
Infectii vasoactive
Sangerare digestiva
Progresia bolii hepatice Insuficienta renala functionala
Medicamente (AINS, IEC) (prerenala)
Vasoconstrictie renala

Sindrom
hepatorenal
Functia hepatica < 50% retentie sodiu
Functia hepatica < 60% ascita
Hepatic venous pressure gradient (HVPG)
HPVG = WHVP - FHVP
 HVPG = 1 - 5 mmHg
8 mmHg collateral circulation
- ascites
10 mmHg - oesophageal varices
12 mmHg bleeding of oesophageal
varices
 Diagnosticul clinic al hipertensiunii portale
(semne si simptome)

Asimptomatica ani de zile

Hipertensiune portala clinic manifesta:

- circulatie colaterala
- splenomegalie
complicatii
 Complicatiile hipertensiunii portale

Sangerare digestiva (hemoragia variceala)

Gastropatie portal-hipertensiva
Ascita
Peritonita bacteriana spontana
Hidrotorax
Encefalopatie hepatica (EPH)
..
Sindrom hepatorenal (SHR)
Sindrom hepatopulmonar (SHP)
Hipertensiunea portopulmonara (HTPP)
Cardiomiopatia cirotica
 Sangerarea variceala

25-40% din pacientii cu ciroza; se coreleaza cu HVPG

Hematemeza si melena
Favorizeaza aparitia EPH si a SHR
Tratament endoscopic ligaturare, scleroterapie, TIPS (transjugular
intrahepatic portosystemic shunt )
Mortaliate mare 15-30% la 30 zile
Scopul tratamentului
Pacientii la risc varice voluminoase cu pete rosii (red spots)
Profilaxia primara (a primului episod)
Tratamentul sangerarii active
Preventia secundara ( a resangerarii)
 Ascita

Cea mai frecventa complicatie a cirozei

Presiunea in vena porta > 8mmHg

Teorii factor declansator:

- retentia de sodiu overflow theory
- scaderea volumului vascular efectiv underfilling theory
- vasodilatatia arteriolara
Patogeneza ascitei
 Peritonita bacteriana spontana

Febra
Durere abdominala (spontana si la palpare)
Alterarea statusului mental (EPH)
Diaree, ileus paralitic
Asimptomatica

Diagnostic PMN 250 cells/mm3

- culturi pozitive din lichidul de ascita
- absenta unei cauze de peritonita secundara

In ciroza avansata EPH, SHR

 Encefalopatia hepatica

30-45%
Factori implicati: disfunctia hepatica severa (alterarea functiei de
detoxifiere) + sunturile intra/extrahepatice (by-pass-area ficatului)
Amoniacul se formeaza in intestin de catre flora bacteriana
colonica din proteine, uree; topirea masei musculare; dezvoltarea
microflorei intestinale
Alte neurotoxine: mercaptani (metabolismul metioninei), acizi
grasi cu lant scurt, fenol
Falsi neurotransmitatori (octopamina) se formeaza din
aminoacizii cu lant ramificat si din aminoacizii aromatici
GABA (acid -aminobutiric) neurotransmitator inhibitor
- scade nivelul de constienta
 Sindrom hepato-renal

IRA la bolnavul cu ciroza avansata, HTPo si ascita

Diagnostic de excludere
Prognostic prost
Type 1 hepatorenal syndrome at least a twofold increase in serum
creatinine (reflecting a 50 percent reduction in creatinine clearance) to a
level greater than 2.5 mg/dL during a period of less than two weeks
Type 2 hepatorenal syndrome renal impairment that is less severe than
that observed with type 1 disease. The major clinical feature in patients
with type 2 hepatorenal syndrome is ascites that is resistant to diuretics.
Factori precipitanti: infectii, sangerare digestiva
Prezentare clinica

A progressive rise in serum creatinine

An often normal urine sediment
No or minimal proteinuria (less than 500 mg per day)
A very low rate of sodium excretion (ie, urine sodium concentration less than 10
meq/L)
Oliguria

Atentie la masa musculara; se calculeaza RFG

Lack of improvement in renal function after volume expansion with intravenous

albumin (1 g/kg of body weight per day up to 100 g/day) for at least two days
and withdrawal of diuretics.
 Sindromul hepato-pulmonar
Mecanismul hipoxemiei arteriale

La o perLa o persoana sanatoasa

(panelul A) diametrul capilarului
pulmonar este intre 8-15 m, oxigenul
difuzeaza normal in vas si V/Q este
normal. La pacientii cu SHP (panelul
B) multe capilare sunt dilatate si
perfuzia este neuniforma.
Dezechilibrul V/Q este principalul
mecanism indiferent de severitate, cu
sau fara sunt intrapulmonar, la care se
asociaza o scadere a difuziunii
oxigenului in centrul capilarelor
dilatate in stadiile cele mai avansate
(sagetile ingrosate).

soana sanatoasa (panelul A) diametrul

capilarului pulmonar este intre 8-15
m, oxigenul difuzeaza normal in vas
si V/Q este
*Roberto Rodriguez-Roisin,Michael J. Krowka: Hepatopulmonary Syndrome A Liver-Induced normal.
Lung Vascular La pacientii
Disorder, N Englcu
J Med 2008
SHP (panelul B) multe capilare sunt
dilatate si perfuzia este neuniforma.
 SHP HTPP

Incidenta 20% Incidenta 4-5%

Vasodilatatie pulmonara Vasoconstrictie pulmonara si
Dezechilibru V/Q remodelare vasculara pulmonara
Cresterea RVP si HTP
Consecinte: scaderea PaO2 si
cresterea PA-a,O2
Vasculopatie proliferativa:
Sunturi intrapulmonare - proliferare/ingrosare intimala
Afectarea difuziunii alveolo-capilare a - hipertrofia musculaturii netede
O2 - fibroza
Tromboze in situ
 Manifestari clinice

SHP HTPP

Dispnee Dispnee
Cianoza Semne de HTP:
Stelute vasculare - Z2 intarit
Hipocratism digital - suflu sistolic de RT
 Cardiomiopatia cirotica

50% din bolnavii cu ciroza avansata au disfunctie cardiaca

Modificari morfologice HVS, dilatare AS

Disfunctie diastolica tip relaxare intarziata
Incapacitatea adaptarii functiei sistolice la conditiile de stress
Modificari ECG prelungire interval QT

Factor de prognostic prost

 Laborator

Teste functionale hepatice (LFTs) - AST, ALT, fosfataza alcalina, GGT,

bilirubina, albumina, timp de protrombina, INR
Biochimia creatinina, ionograma (hiponatremie)
Anomalii hematologice trombocitopenie, anemie*,
leucopenie/leucocitoza
*Anemia is usually multifactorial in origin; acute and chronic gastrointestinal blood loss, folate deficiency, direct toxicity due to
alcohol, hypersplenism, bone marrow suppression (as in hepatitis-associated aplastic anemia), the anemia of chronic disease
(inflammation), and hemolysis may all contribute

Alte modificari: hiper/hipoglicemie, sideremie crescuta,

hipocolesterolemie, fibrinogen scazut, inflamatie (VSH, PCR, feritina
crescute), hipergamaglobulinemie
Lichidul de ascita SAAG > 1,1 g/dl
Ecografia
 Diagnostic

Biopsie hepatica
Evaluarea noninvaziva a fibrozei hepatice scorul METAVIR:
-F0: No fibrosis
-F1: Portal fibrosis without septa
-F2: Few septa
-F3: Numerous septa without cirrhosis
-F4: Cirrhosis

Elastogafia (FibroScan, ARFI - Acoustic Radiation Force Impulse imaging, SWE -

real-time Shear Wave Elastography)
Teste serologice Fibrotest (assessment of alpha-2-macroglobulin, alpha-2-
globulin (haptoglobin), gamma globulin, apolipoprotein A1, GGT, and total bilirubin;
patient's age and sex) mild fibrosis (F0 to F1), significant fibrosis (F2 to F4), or an
indeterminate stage of fibrosis (Sb 60-75%, Sp 80-90%)
 Carcinomul hepatocelular

Complicatie a bolii cronice de ficat de etiologie virala

Media de viata dupa diagnostic este de 6-20 luni
Dimensiunea mare, statusul functional prost al pacientului, invazia
vasculara si metastazele ganglionare - factori de prognostic prost

Tablou clinic nimic particular; decompensarea bolii hepatice de baza

(ascita, EPH, icter, sangerare variceala)
Alte simptome (nespecifice): durere abdominala superioara, scadere
ponderala, satietate precoce, formatiune tumorala abdominala palpabila,
febra (necroza tumorii), sd. paraneoplazice (hipoglicemie, eritrocitoza,
hipercalcemie, diaree apoasa)
 Diagnostic

Teste imagistice ecografie (Sb 78%, Sp 89%), CT spiral, RMN

Markeri serologici alpha-fetoproteina lipsita de specificitate (mai creste
in sarcina, tumori de origine gonadala, cancer gastric, hepatite virale
acute/cronice)
Biopsie percutana cand rezultatul testelor imagistice este incert iar
rezultatul are impact pe tratament
Ghidul EASL
For nodules seen on ultrasound that are <1 cm, the EASL guidelines recommend:
Repeat ultrasound at four months. If the nodule grows, additional investigation is required and dictated by
the size of the nodule. If the nodule is stable, ultrasound is repeated at four-month intervals for one year, after
which time it can be performed every six months.
For nodules between 1 and 2 cm:
Obtain a 4-phase CT scan and/or dynamic contrast-enhanced MRI. Only one imaging study is recommended
in centers of excellence with high-end radiologic equipment. Otherwise, both studies should be obtained.
If there are radiologic hallmarks of HCC (arterial hypervascularity and venous/late phase washout), then a
diagnosis of HCC is made.
If the radiologic hallmarks of HCC are not seen, a biopsy should be obtained and assessed by an expert
pathologist. If the biopsy results are inconclusive a second biopsy is recommended. If the results are still
inconclusive, ultrasound should be repeated at four-month intervals to monitor for growth, with a repeat biopsy
if there is growth or changes in the nodule's enhancement pattern.
For nodules >2 cm:
Obtain a 4-phase CT scan or dynamic contrast-enhanced MRI.
If there are radiologic hallmarks of HCC (arterial hypervascularity and venous/late phase washout), then a
diagnosis of HCC is made.
If the radiologic hallmarks of HCC are not seen, then a biopsy should be obtained to confirm the diagnosis. If
the biopsy results are inconclusive, ultrasound should be repeated at four-month intervals to monitor for growth.
Progresia bolii hepatice
 BOLILE COLECISTULUI SI ALE CAILOR BILIARE

Colica biliara durere severa, cu debut brusc

- cvasipermanenta
- in epigastru si HD, iradiaza interscapular, in
scapula dr/umarul dr
- durata 30 min- 5h
- insotita de grata si varsaturi
- poate fi provocata de o masa bogata in grasimi,
de o masa copioasa dupa o perioada de post
- frecvent nocturna
 Colecistita acuta

Durere cu debut brusc in HD > 5-6h

Febra
Leucocitoza NU ICTER!

Semn Murphy
Aparare musculara

Laborator: fosfataza alcalina, bilirubina, amilaza/lipaza,

transaminaze
Diagnostic - Ecografie
 Colangita (angiocolita)

Obstructia CBP cu infectie/inflamatie

Durere
Febra cu frisoane Triada Charcot
Icter

Laborator: leucocitoza cu neutrofilie, markeri de inflamatie

(VSH, PCR), bilirubina, fosfataza alcalina, transaminaze
crescute, hemoculturi pozitive.
Diagnostic: ecografie, ERCP
ERCP
Calculi in colecist ci cistic
A: calculi pe CBP B: dupa sfinterotomie si
indepartarea calculilor
 Colangiocarcinomul
Cancer de cai biliare intrahepatice, perihilare sau distale
 Prezentare clinica:
Icter obstructiv (prurit, urini hipercrome, scaune
decolorate) colangiocarcinom extrahepatic
Durere abdominala (30-50%)
Scadere in greutate (30-50%)
Febra (20%)
Slabiciune, oboseala, transpiratii nocturne

Laborator: bilirubina (BD), fosfataza alcalina, transaminaze

Diagnostic: ecografie, colangio-RMN, ERCP

 BOLILE PANCREASULUI

Secretia acida gastrica

Acizi grasi cu lant lung Aciditatea gastrica
Aminoacizii

SNPS
n. vag
duoden/jejun

+ secretina
+CCK
Sarurile biliare

+ secretia pancreatica + secretia pancreatica

enzimatica de apa si electroliti

Pancreasul secreta 1500-3000 ml fluid alcalin (pH>8) izoosmotic/zi, ce contine 30 enzime

 Pancreatita acuta (PA)

Clasificare
PA usoara (edematoasa) forma usoara, autolimitata;
absenta insuficientei de organ/complicatiilor locale sau
sistemice
PA moderat severa insuficienta de organ tranzitorie (max
48h) si/sau complicatii locale/sistemice
PA severa insuficienta organica persistenta (ce implica
unul sau mai multe organe)
30% - cauza necunoscuta !
 Manifestari clinice

Durere epigastrica (HD) severa si persistenta, cu debut acut

50% din cazuri iradiere in spate
Persista ore zile
Ameliorata de ridicarea in picioare sau aplecarea in fata
Insotita de greata si varsaturi (90%)
5-10% - fara durere
 Examen fizic

Abdomen dureros in epigastru/difuz abdomen acut

Distensie abdominala, meteorism (ileus paralitic)
Icter (obstructiv) litiaza biliara, edem de cap de pancreas
Formele severe febra, tahipnee, hipotensiune, hipoxemie
Semnul Turner echimoza pe flanc, si Cullen echimoza
periombilicala (3%) hemoragie retroperitoneala (necroza
pancreatica)
Rar paniculita (noduli rosietici durerosi localizati de obicei
distal pe extremitati)
 Laborator

Amilaza serica
- creste in 6-12h
- T1/2 10h
- revine la normal in 3-5 zile
omiterea diagnosticului la prezentarile tardive (>24h)
- valori > 3x N Sb = 67-83% si Sp = 85-98%
- in PA alcoolica (20%)sau determinata de hipertrigliceridemie
(50%) valorile amilazei serice pot fi < 3xN
 Lipaza serica
- Sb si Sp = 82-100%
- creste in 4-8h, peak la 24h, revine la normal in 8-14 zile
- permite un diagnostic mai tardiv
- este mai sensibila la pacientii cu alcoolism
- exista si cresteri nespecifice
Reactanti de faza acuta PCR se coreleaza cu severitatea
Leucocitoza, Ht crescut (hemoconcentratie), retentie azotata,
hipocalcemie, hiper/hipoglicemie
 Imagistica

Rx. abdominala simpla distensie aerica (ileus)

Rx. toracica ascensionarea hemidiafragmului, revarsat
lichidian pleural, infiltrate pulmonare,atelectazie bazala
Ecografia abdominala
CT, RMN abdominal
 Diagnostic

Two of the following three criteria:

1. acute onset of persistent, severe, epigastric pain often
radiating to the back,
2. elevation in serum lipase or amylase to three times or
greater than the upper limit of normal,
3. characteristic findings of acute pancreatitis on imaging
(contrast-enhanced computed tomography [CT], magnetic
resonance imaging [MRI], or transabdominal
ultrasonography
 Evolutie si prognostic

85% - PA edematoasa (usoara) remitere spontana in 3-5 zile

fara complicatii
Complicatii locale colectii peripancreatice, pseudochist de
pancreas, necroza si hemoragie, infectie
Complicatii sistemice - MSOF
 Pancreatita cronica

Proces fibroinflamator progresiv ce duce la o afectare

structurala permanenta a pancreasului, cu disfunctie
endocrina si exocrina
Diferentiere de PA
afectare pancreatica progresiva si ireversibila
- evolutie indelungata asimptomatica/insuficienta pancreatica
fara durere
- enzime pancreatice (amilaza, lipaza) in limite normale
 Etiologie

Alcohol abuse
Idiopathic pancreatitis (25-40%)
Genetic causes (mutations in the cystic fibrosis gene,
hereditary pancreatitis)
Ductal obstruction (eg, trauma, pseudocysts, stones, tumors,
possibly pancreas divisum)
Systemic disease such as systemic lupus erythematosus,
hypertriglyceridemia, possibly hyperparathyroidism
Autoimmune pancreatitis
 Manifestari clinice

Durerea abdominala
epigastrica, cu iradiere in spate
- greata, varsaturi
- la 15-30 min dupa masa
- cvasipermanenta
2 pattern-uri de durere:
- perioade dureroase < 10 zile, urmate de perioade nedureroase de
luni - > 1 an
- perioade prelungite de durere zilnica, uneori severa, ce necesita
spitalizari frecvene
20% fara durere (doar insuficienta pancreatica)
 Insuficienta pancreatica exocrina
- manifesta cand se pierde > 90% din functia pancreatica
Malabsorbtia grasimilor steatoree
Malabsrbtie de vitamine liposolubile (A,D,E,K) si vitamina B12
(rareori clinic manifeste)
Malabsorbtie de proteine scadere in greutate
Intoleranta la glucoza
 Diagnostic

Dificil
Simptome nespecifice/absente
Teste de laborator normale
Triada clasica: calcificari pancreatice, steatoree, DZ rar si
tardiv
Imagistica calcificari pancreatice, Wirsung dilatat si
neregulat, pseudochiste
ERCP de electie; in scop terapeutic
Diagnostic diferential cu cancerul de pancreas !
 Cancerul de pancreas

Prezentare tardiva
15-20% - candidati pentru pancreatectomie
Prognostic prost supravietuirea la 5 ani dupa
duodenopancreatectomie max 30%
95% adenocarcinom ductal provine din pancreasul exocrin
5% tumori pancreatice neuroendocrine
60-70% localizate la nivelul capului, 20-25% la corp/coada
 Manifestari clinice

Cele mai frecvente simptome la diagnostic

Asthenia 86 percent
Weight loss 85 percent
Durere Anorexia 83 percent
Abdominal pain 79 percent
Icter
Epigastric pain 71 percent
Scadere in greutate Dark urine 59 percent
Jaundice 56 percent
Nausea 51 percent
Back pain 49 percent
Diarrhea 44 percent
Vomiting 33 percent
Steatorrhea 25 percent
Thrombophlebitis 3 percent
 Durerea debut insidios (1-2 luni)
- in epigastru, cu iradiere in bara/spate
- caracter visceral
- intermitenta
- agravata dupa masa, pozitie culcata, noaptea
- ameliorata in pozitie fetala
Icterul progresiv
- obstructiv
- precoce in cancerul de cap de pancreas, mai tardiv in
cancerul de corp/coada (metastaze hepatice)
Icter obstructiv fara durere malign
Diabet zaharat cu debut recent
 Tromboflebita superficiala migratorie (Trousseau's syndrome)
Complicatii tromboembolice arteriale si venoase (in cancerul
de corp/coada)
Manifestari cutanate paraneoplazice: pemfigus bulos,
paniculita
 Cele mai frecvente semne:

Jaundice 55 percent
Hepatomegaly 39 percent
Right upper quadrant mass 15 percent
Cachexia 13 percent
Courvoisier's sign (nontender but palpable distended
gallbladder at the right costal margin) 13 percent
Epigastric mass 9 percent
Ascites 5 percent
 Diagnostic

Tablou clinic

Laborator: transaminaze, bilirubina, fosfataza alcalina, lipaza

Imagistica : ecografie abdominala, ERCP/colangioRMN (icter),

CT/RMN abdominal cu substanta de contrast (durere)
 Markeri tumorali CA 19-9

Sensibilitatea depinde de dimensiunea tumorii

Specificitate mica creste si in alte cancere si in afectiuni
pancreatice benigne
VPP mica (mai ales la asimptomatici)
La pacientii simptomatici, CA19-9 > 37 U/ml
Sb 80% Sp 85% VPP 72%
Nu se recomanda pentru screening !
La pacientii la care a fost de la inceput crescut are valoare
prognostica si este un indicator al activitatii bolii