4. • Excessive chronic alcohol use can cause several
different types of chronic liver disease, including
alcoholic fatty liver, alcoholic hepatitis, and alcoholic
cirrhosis.
•Chronic alcohol use can produce fibrosis in the absence
of accompanying inflammation and/or necrosis.
•Fibrosis can be centrilobular, pericellular, or periportal.
•When fibrosis reaches a certain degree, there is
disruption of the normal liver architecture and
replacement of liver cells by regenerative nodules.
Clinical features:
•nonspecific symptoms:
• such as vague right upper quadrant abdominal pain,
fever, nausea and vomiting, diarrhea, anorexia, and
malaise.
•Specific:
ascites, edema, or upper gastrointestinal (GI)
hemorrhage.
Jaundice or encephalopathy.
5. Physical examination:
Laboratory tests
•hemolytic anemia called Zieve’s syndrome
• Platelet counts =less with hypersplenism.
• Serum total bilirubin =normal or elevated with advanced
disease.
•Direct bilirubin = mildly elevated with a normal total bilirubin
•Prothrombin times = prolonged and do not respond to
parenteral vitamin K.
•Serum Na levels = normal (unless patients have ascites) and then
can be depressed, largely due to ingestion of excess free water.
6. Diagnosis
•Liver biopsy can be helpful to confirm a
diagnosis, but generally when patients
present with alcoholic hepatitis and are still
drinking, liver biopsy is withheld until
abstinence has been maintained for at least 6
months to determine residual, nonreversible
disease.
•computed tomography (CT)
•ultrasound
• magnetic resonance imaging (MRI)
TREATMENT
•Glucocorticoids (in pateitn with discriminant function (DF)
value of >32. there is improved survival at 28 days with the
use of glucocorticoids.
•oral pentoxifylline
• inhibitors of TNF-α such as infliximab or etanercept.
•e. medications that reduce craving for alcohol, such as
acamprosate calcium, has been favorable.
•contradicted
•Acetaminophen use is often discouraged in patients with
liver disease; however, if no more than 2 g of
acetaminophen per day are consumed, there generally are
no problems.
7. CIRRHOSIS DUE TO CHRONIC VIRAL HEPATITIS
B OR C
• the true incidence of cirrhosis due to hepatitis C alone is
unknown.
• The morbidity and mortality in chronic hepatitis B are linked to
the evolution to cirrhosis and hepatocellular carcinoma. The
progression of fibrosis is strongly associated with persistent
active viral replication When the diagnosis is made, the 5-year
cumulative incidence of developing cirrhosis ranges from 8% to
20%.
8. • Symptoms and signs of chronic liver disease:
i. Fatigue,
ii. malaise,
iii. vague right upper quadrant pain and laboratory abnormalities are
frequent presenting features
Diagnosis including :
i. quantitative HCV RNA testing
ii. analysis for HCV genotype, or
iii. hepatitis B serologies like (HBsAg, anti-HBs, HBeAg) (hepatitis B e
antigen), anti-HBe,
iv. quantitative HBV DNA levels.
9. TREATMENT
• Antiviral therapy
lamivudine, adefovir, telbivudine, entecavir, and tenofovir.
(which is effective at viral suppression, as evidenced by reducing
aminotransferase levels and HBV DNA levels, and improving
histology by reducing inflammation and fibrosis. )
• Interferon α can also be used for treating hepatitis B.
10. CARDIAC CIRRHOSIS
Definition: Patients with long-standing right-sided congestive heart failure may develop chronic liver injury and cardiac cirrhosis. This is an
increasingly uncommon, if not rare, cause of chronic liver disease given the advances made in the care of patients with heart failure.
Etiology and Pathology :
• long-term right-sided heart failure, there is an elevated venous pressure transmitted via the inferior vena cava and hepatic veins to the
sinusoids of the liver, which become dilated and engorged with blood. The liver becomes enlarged and swollen, and with long-term
passive congestion and relative ischemia due to poor circulation, centrilobular hepatocytes can become necrotic, leading to pericentral
fibrosis.
• Clinical Features:
• signs of congestive heart failure
• enlarged firm liver on physical examination.
• elevated levels of ALP, aminotransferase and AST usually higher than ALT.
• It is unlikely that patients will develop variceal hemorrhage or encephalopathy.
• DIAGNOSIS:
• Pateint with cardiac disease + elevated ALP and an enlarged liver.
• Liver biopsy shows a pattern of fibrosis that can be recognized by an experienced hepatopathologist.
• Differentiation from Budd-Chiari syndrome (BCS) can be made by seeing extravasation of red blood cells in BCS, but not in cardiac
hepatopathy.
• Venoocclusive disease can also affect hepatic outflow and has characteristic features on liver biopsy. Venoocclusive disease can be seen
under the circumstances of conditioning for bone marrow transplant with radiation and chemotherapy; it can also be seen with the
ingestion of certain herbal teas as well as pyrrolizidine alkaloids. This is typically seen in Caribbean countries and rarely in the United
States. Treatment is based on management of the underlying cardiac disease.
11.
12.
13.
14. HEPATIC ENCEPHALOPATHY
• defined as an alteration in mental status and cognitive function occurring in the presence of liver failure. In acute liver
injury with fulminant hepatic failure, the development of encephalopathy is a requirement for a diagnosis of fulminant
failure.
• Gut-derived neurotoxins that are not removed by the liver because of vascular shunting and decreased hepatic mass get
to the brain and cause the symptoms that we know of as hepatic encephalopathy.
• Ammonia levels are typically elevated in patients with hepatic encephalopathy, but the correlation between severity of
liver disease and height of ammonia levels is often poor, and most hepatologists do not rely on ammonia levels to make
a diagnosis. Other compounds and metabolites that may contribute to the development of encephalopathy include
certain false neurotransmitters and mercaptans.
Clinical Features
• changes in mental status can occur within weeks to months.
• Brain edema can be seen in these patients, swelling of the gray matter.
• Cerebral herniation is a feared complication patients with cirrhosis.
• hypokalemia, infection, an increased dietary protein load, or electrolyte disturbances.
• Patients may be confused or exhibit a change in personality.
• They may actually be quite violent and difficult to manage; alternatively, patients may be very sleepy and difficult to
rouse.
• Evidence of GI bleeding should be sought, and patients should be appropriately hydrated. Electrolytes should be measured
and abnormalities corrected.
