Liver cirrhosis
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LIVER CIRRHOSIS. DEFINITION : pathological condition with the development of fibrosis to the point that there is architectural distorsion with formation of regenerative nodules. CAUSES : Alcoholism Chronic viral hepatitis (Hepatitis B, Hepatitis C) Autoimmune hepatitis

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LIVER CIRRHOSIS

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Liver cirrhosis

LIVER CIRRHOSIS


Liver cirrhosis

DEFINITION: pathological condition with the development of fibrosis to the point that there is architectural distorsion with formation of regenerative nodules

CAUSES:

  • Alcoholism

  • Chronic viral hepatitis (Hepatitis B, Hepatitis C)

  • Autoimmune hepatitis

  • Nonalcoholic steatohepatitis

  • Billiary cirrhosis

  • Primary billiary cirrhosis

  • Primary sclerosing cholangitis

  • Autoimmune cholangiopathy

  • Cardiac cirrhosis

  • Metabolic liver disease:

  • Hemocromatosis

  • Wilson’s disease

  • L1 Antitrypsin deficiency

  • Cystic fibrosis

  • Cryptogenic cirrhosis


Alcoholic cirrhosis

ALCOHOLIC CIRRHOSIS

14 milion adults in US -alcohol abuse or dependence

10th most common cause of death in adults

alcoholic cirrhosis accounts 40% of deaths due to cirrhosis


Clinical features

CLINICAL FEATURES

  • NON SPECIFIC SYMPTOMS:

  • vague right upper quadrant pain

  • fever

  • nausea and vomiting

  • diarrhea

  • anorexia

  • malaise

  • LATER , SPECIFIC COMPLICATIONS:

  • ascites

  • edema

  • bleeding (UDH)

  • jaundice/encephalopathy

  • incidentally at the time of autopsy or elective surgery

PHYSICAL EXAMINATION

  • liver and spleen enlarged with the liver edge firm and nodular

  • scleral icterus

  • palmar erythema

  • spider angiomas

  • parothid gland enlargement

  • digital clubbing

  • muscle wasting

  • edema and ascites

  • decreased body hair, gynecomastia

  • testicular atrophy

  • menstrual irregularities/ amenorrheic women

    These changes are often reversible following cessation of alcohol


Liver cirrhosis

LABORATORY TESTS

- normal in patients with early compensated alcoholic cirrhosis

- in advanced liver disease many abnormalities are present:

  • anemia (chronic GI blood lose, nutritional deficiencies, hipersplenism related to portal hypertension , hemolytic anemia- ZIEVE’S syndrome)

  • platelets counts are often reduced early (PHT)

  • total direct bilirubin- N/ elevated

  • protrombin times prolonged

  • AST>ALT2:1ratio

DIAGNOSIS

  • Clinical features + physical examination findings + laboratory studies

  • Liver biopsy,ultrasonography, UDE,CT ( dg. dif. Cancer)

    (abstinence maintained 6 months--> residual, nonreversible disease)

    Patients who have had complications and who continue to drink have a <50% 5-year survival in contrast with those who remain abstinent -->prognosis improved and LIVER TRANSPLANTATION - VIABLE OPTION


Treatment

TREATMENT

  • Abstinence- cornerstone therapy

  • Good nutrition and long term medical supervision

  • Glucocorticoids are occasionally used(DF>32)

  • Oral PENTOXIFYLINE decrease tumour necrosis factor alpha (TNF-alpha) and other proinflamatory cytokines

  • Parenterally adm. of inhibitors of TNF-alpha (INFLIXIMAB/ ETANERCEPT)

  • Medication that reduce craving for alcohol ACAMPROSATE CALCIUM

  • Vit.B1,B6,B12+SG10%,Arginine,Aminohepa,Aspatofort


Cirrhosis due to chronic viral hepatitis b or c

CIRRHOSIS DUE TO CHRONIC VIRAL HEPATITIS B OR C

patients exposed to the hepatitis C (HCV) - 80% develop chronic hepatitis C and ,of those,-20-30% will develop cirrhosis over 20-30 years

world wide , 170 million individuals have hepatitis C

progression of liver disease due to chronic HC is characterized by :

portal- based fibrosis with brindging fibrosis and nodularity developing --> cirrhosis

inflammatory infiltrate in portal areas

lobular hepato-cellular injury and inflammation

HCV genotype 3, steatosis is often present

Hepatitis B exposure : 5% develop chronic hepatitis B, 20% will go to develop cirrhosis

in US 1,25 million carriers of HB; Asia, Africa 15%aquires the infection vertically (at birth) and 25% may develop cirrhosis


Liver cirrhosis

CLINICAL FEATURES

  • fatigue

  • malaise

  • right upper quadrant pain

    LABORATORY EVALUATION

  • HCV-RNA,genotype

  • AgHBS

  • anti HBS

  • HBe Ag

  • anti HBe

  • HBV-DNA levels

TREATMENT IN HEPATITIS B

  • LAMIVUDINE100mg/day

  • ADEFOVIR

  • ENTECAVIR 0.5mg/day

  • TENOFOVIR

    INTERFERON ALFA should not be used in decompensated cirrhotics

    with EV,ascites,jaundice


Cirrhosis from autoimmune hepatitis

CIRRHOSIS FROM AUTOIMMUNE HEPATITIS

Positive autoimmune markers ANA,ASMA

Active inflammation - elevated liver enzimes-->immunosuppresive therapy

Obesity in western countries - patients with nonalcoholic fatty liver disease

Management of complications of cirrhosis due to AIH or NASH is similar to that for other forms of cirrhosis


Billiary cirrhosis

BILLIARY CIRRHOSIS

Cholestatic liver disease result from necroinflammatory lesions :

congenital

metabolic processes

external bile duct compresion

2 broad categories reflect the anatomic sites of abnormal bile retention :

intrahepatic -- different approach

extrahepatic--surgical/endoscopic biliary tract decompression


Pbc primary biliary cirrhosis

PBC (primary biliary cirrhosis)

100-200 / million(female preponderence / median age - 50 years )-at the time of diagnosis

Cause: unknown

It is characterized by portal inflammation and necrosis of cholangiocytes in small and medium size bile ducts

Lab findings: elevated bilirubine level

progressive liver failure

LIVER TRANSPLANTATION- treatment of choice for patients with decompensated cirrhosis

URSODEOXYCHOLIC ACID (UDCA)

AMA - 90% patients with PBC - useful markers for PBC


Pbc primary biliary cirrhosis1

PBC (primary biliary cirrhosis)

CLINICAL FEATURES

  • fatigue

  • pruritus 50% - bothersome in the evening; prior to jaundice (severe disease and poor prognosis)

    PHYSICAL EXAMINATION

  • JAUNDICE

  • hepatomegaly

  • splenomegaly

  • ascites

  • edema

  • hiperpigmentation-trunk,arms

  • xantelasma (xanthomata)

  • bonepain : osteopenia/osteoporosis

  • scratching lesions

LABORATORY FINDINGS :

  • augmentation of GGT, ALP, ALT, AST, IgM

  • hiperbilirubinemia

  • trmobocytopenia , leucopenia, anemia -- PHT, hipersplenism

  • LIVER BIOPSY - 10% AIH, “overlap” syndrome

    DIAGNOSIS

    Patients with chronic colestatic liver enzyme abnormalities in middle-aged women

    AMA +/- (10%) --> biopsy


Treatment1

TREATMENT

  • UDCA (early initiated 13-15 mg/kg/day) improve bichemical and histological features; it does not reverse and cure the disease; side effects: diarrhea, headache

  • LIVER TRANSPLANTATION –decompensated disease

  • Antihistamines

  • Narcotic receptor antagonist (naltrexone)

  • Rifampin

  • Cholestyramine-bile salt sequestering agent

  • Plasmapheresis intractable pruritus

  • Bisphosphonate should be instituted when bone disease is identified (bone density testing)


Primary sclerosing cholangitis

PRIMARY SCLEROSING CHOLANGITIS

Definition: chronic cholestatic syndrome – diffuse inflamation, fibrosis involving the entire biliary treeobliteration of both intra and extrahepatic biliary tree, leading to biliary cirrhosis / portal hipertension/ liver failure

Cause: unknown

bile duct proliferation, ductopenia, pericholangitis

liver biopsy : periductal fibrosis


Primary sclerosing cholangitis1

PRIMARY SCLEROSING CHOLANGITIS

CLINICAL FEATURES :

  • fatigue profound and nonspecific

  • pruritus

  • steatorrhea

  • deficiencies of fat – soluble vitamins

  • metabolic bone disease

    LABORATORY FINDINGS:

  • abnormal liver enzymes (>2 ALP and ↑ AST,ALT)

  • albumin levels ↓

  • TP↑

  • overlap syndrome between PSC and AIH

  • autoantibodies + in overlap syndrome , - in PSC alone (only); P-ANCA is + in 65% of those with PSC; in PSC50% patients have UCcolonoscopy


Primary sclerosing cholangitis2

PRIMARY SCLEROSING CHOLANGITIS

DIAGNOSIS

  • colangiographic imaging-multifocal stricturing and beading

  • MRCP-initial evaluation

  • ERCP-whether or not a dominant stricture is present

    The strictures are typically short with intervening segments of normal or slightly dilated bile ducts diffusely distributed beaded appearance

    Gallbladder, cystic duct involved in 15% of cases;evolution gradually to biliary cirrhosis decompensation with ascites , esophageal variceal hemorrhage , encephalopathy

    TREATMENT

  • nonspecific

  • high-dose (20mg/kg/day) UDCA

  • endoscopic dilatation of strictures

  • LIVER TRASPLANTATION (LT) ; Cholangiocarcinoma relative CI for LT


Hemochromatosis

HEMOCHROMATOSIS

DEFINITION: inherited disorder of iron metabolism that results in a progressive increase in hepatic iron deposition whitch , over time, can lead to a portal-based fibrosis progressing to cirrhosis / liver failure/ hepatocellular cancer

Serum iron studies :

  • elevated transferin saturation

  • ↑ feritine level

  • HFE mutation analysis

    TREATMENT is straight forward with regular therapeutic phlebotomy


Wilson s disease

WILSON’S DISEASE

DEFINITION: inherited disorder of cooper homeostasis with failure to excrete excess amounts of cooper , leading to accumulation in the liver.

1/30000 individuals; affects adolescents and young adults

DIAGNOSIS:

  • ceruloplasmin levels

  • 24-hours urine cooper levels

  • liver biopsy

    PHYSICAL EXAMINATION - KAYSER-FLEICHER corneal ring

    TREATMENT : cooper chelating medication (D-PENICILLAMINE/TRIENTINE/Zn)


Alfa1 at deficiency

ALFA1-AT DEFICIENCY

DEFINITION: inherited disorder that causes abnormal folding of the alfa-1AT PROTEIN-->failure of secretion of that protein from the liver

22 genotype / 10-20% - chronic liver disease

DIAGNOSIS:

  • determining of alfa1 AT levels/ genotype

  • liver biopsy : PAS+ ; diastase- resistant globules

    TREATMENT: LT is curative


Complications of cirrhosis

COMPLICATIONS OF CIRRHOSIS

  • Portal hypertension:

    -GE varices

    -portal hypertensive gastropathy

    -splenomegaly, hypersplenism

    -ascites

    -SBP

  • Hepatorenal syndrome I,II

  • Hepatic encephalopaty

  • Hepatopulmonary syndrome

  • Portopulmonary hypertension

  • Malnutrition

  • Bone disease:

    -osteopenia

    -osteoporosis

    -osteomalacia

  • Hematologic abnorm.:

    -anemia

    -hemolysis

    -neutropenia

    -trombocytopenia

    - coagulopathy


Treatment for variceal hemorrhage 1 primary prophylaxis 2 prevention of recurrent bleeding

TREATMENT FORVARICEAL HEMORRHAGE :1. PRIMARY PROPHYLAXIS2. PREVENTION OF RECURRENT BLEEDING

1. PRIMARY PROPHYLAXIS

- screening by endoscopy of all patients with cirrhosis

-non-selective betabloblokers or variceal band ligation / sclerotherapy ((PROPRANOLOL, NADOLOL)

-hepatic vein pressure >12 mmHg

ACUTE BLEEDING :

  • fluid and blood product replacement

  • prevention of subsequent bleeding with EVL

  • vasoconstrictive agenta : SOMATOSTATIN , OCTREOTIDE 50-100 ug/h by continuous infusion (VASOPRESIN -in the past)

  • BALLON TAMPONADE (Sengstaken-Blakemore tube / Minnesota tube)--> stabilisation prior to endoscopic therapy

  • esophageal varices extended into the proximal stomach - TRANSJUGULAR INTRAHEPATIC PORTOSYSTEMIC SHUNT (angiographic guidance)


2 prevention of recurrent bleeding

2. PREVENTION OF RECURRENT BLEEDING

  • repeated VBL until varices are obliterated

  • betablockade- recurrent VBL

  • portosystemic shunt surgery , TIPS for patients with good hepatic synthetic function who could benefit by having portal decompressive surgery.


Liver cirrhosis

MANAGEMENT OF RECURRENT VARICEAL HEMORRHAGERECURENT ACUTE BLEEDING ENDOSCOPIC THERAPY +/- PHARMACOLOGIC THERAPYCONTROL OF BLEEDING 

COMPENSATED CIRRHOSIS(CHILD’S CLASS A)

SURGICAL SHUNT VS. TIPS

LIVER TRANSPLANTATION

DECOMPENSATED CIRRHOSIS( CHILD’S CLASS B,C)

TRANSPLANT EVALUATION

ENDOSCOPIC THERAPY OR BETA-BLOKERS

TIPS

LIVER TRANSPLANTATION


Ascites treatment

ASCITES TREATMENT

  • 1.Dietary sodium restriction-small amounts of ascites 6-8g/day ,<2g/day in>ascites

  • Fresh, frozen foods

  • 2.Diuretic therapy-moderate amounts of ascites:Spironolactone100-200mg/day,4-600mg/day+Furosemide40-80mg/day(peripheral edema);120-160mg/day-necompliant patients.

  • 3.Repeated large volume paracentesis,TIPS,liver transplantation(<50% survive 2years after the onset of ascites).


Hepatic encephalopathy

HEPATIC ENCEPHALOPATHY

  • Ammonia levels>,mercaptans

  • 1.Hydration and correction of electrolyte imbalance

  • 2.Replacing animal-based protein with vegetable-based protein

  • 3.Lactulose-elimination of nitrogenous products(2-3soft stools/day)

  • 4. Nonabsorbed antibiotics:Neomicine/Metronidazole(renal failure,ototoxicity,peripheral neuropathy),RIFAXIMINE-NORMIX,NO side effects.

  • 5. ZN supplementation


Spontaneous bacterial peritonitis

SPONTANEOUS BACTERIAL PERITONITIS

  • Neutrophil count>250/mm3

  • Occur in 30%of patients with SBP and25% in hospital mortality rate

  • Escherichiacoli/gram+bacteria(Streptococcus viridans,Staphilococcus aureus,Enterococcus

  • Second –generation cephalosporin-CEFOTAXIM 4g/day

  • In those with UDB,the frecquency of SBP is

    increased and prophylaxis against it is recommended


Hepato renal syndrome

HEPATO-RENAL SYNDROME

  • Functional renal failure without renal pathology that occurs in 10% of patients with advanced cirrhosis or acute liver failure

  • Step-wise progressive increase in creatinine in those with large amount of ascites

  • TYPE 1 HRS:progressive impairment in renal function and >reduction in creatinine clearance within 1-2 weeks of presentation

  • TYPE 2 HRS: reduction in glomerular filtration rate with >serum creatinine level(better outcome than type 1 HRS!)

  • Dopamine,PG analogs

  • Midodrine(alpha-agonist)

  • Octreotide

  • Albumine i.v.

  • LIVER TRANSPLANTATION


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