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 frecvente: Cauze mai rare:

• Chronic viral hepatitis (hepatitis
B, C)
• Alcoholic liver disease
• Hemochromatosis
• Nonalcoholic fatty liver disease
• Autoimmune hepatitis
• Primary and secondary biliary cirrhosis
• Primary sclerosing cholangitis
• Medications (eg, methotrexate, isoniazid)
• Wilson disease
• Alpha-1 antitrypsin deficiency
• Celiac disease
• Granulomatous liver disease
• Idiopathic portal fibrosis
• Polycystic liver disease
• Infection (eg, brucellosis, syphilis,
echinococcosis, schistosomiasis)
• Right-sided heart failure
• 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

Cresterea rezistentei intrahepatice

-modificari anatomice (ireversibile)
-cresterea tonusului vascular
(reversibil)
Cresterea
rezistentei la
Cresterea rezistentei prehepatic flux
(inclusiv rezistenta vaselor
colaterale, daca exista)

Cresterea rezistentei
posthepatice
(semnificativa numai daca exista o Hipertensiune
afectare hepatica concomitenta) portala

Vasodilatatie sistemica
Sindrom
hiperdinamic

Expansiunea volumului
plasmatic
Modificari morfologice hepatice in ciroza
Relatia cu Ciroza Vase Relatia cu ficatul
sinusoidele

NU Macrovascular Pre(infra)hepatic
Presinusoidal (vena porta)

Microvascular
(vena porta)
DA
Sinusoidal
Sinusoidal Intrahepatic

Microvascular
(vena hepatica)
Postsinusoidal
NU
Macrovascular
(vena hepatica) Post(supra)hepatic
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
 Modificari morfologice hepatice in ciroza

• 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

DEFICIT DE NO
INTRAHEPATIC

LIPSA DE AFECTAREA
CRESTE CONTRABALANSARE A VASORELAXARII SI CRESTE CRESTE
TROMBOGENEZA EFECTULUI REGLARII SINTEZA DE STRESS-UL
VASOCONSTRICTOR FLUXULUI COLAGEN? OXIDATIV

CRESTE RVIH
 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
Functia hepatica < 50% → retentie sodiu
Functia hepatica < 60% → ascita
 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

• 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
Scopuri:
• 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 > 12mmHg

• Teorii – factor declansator:

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

• Febra
• Durere abdominala (spontala 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%
• Cauza specifica necunoscuta
• 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 ϒ-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.
 Mecanismul hipoxemiei arteriale in SHP

La o perLa o persoana sanatoasa

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

• Incidenta 20% • Incidenta 4-5%

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

* cauza biliara – durere mai localizata si cu debut mai abrupt
* hereditara, metabolica, alcool – durere mai prost localizata
si cu debut mai lent
• 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 – 25-30% (node-negative)
- 10% (node-positive)
• 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
Stadializarea
Rezecabilitatea