The 12th leading cause of death in the United

States
pathologic features
- development of fibrosis
- architectural distortion
- formation of regenerative nodules.
Results :
- decrease hepatocellular mass, & function,
- an alteration of blood flow

End result of injury that leads to both
fibrosis and nodular regeneration.
May be reversible if cause is removed.
The clinical features result from
- hepatic cell dysfunction
- portosystemic shunting
- portal hypertension


The most common histologic
classification :
- micronodular,
- macronodular, and
- mixed forms

regenerating nodules are no larger than the
original lobules, ie, 1 mm in diameter
larger nodules (>3mm) ,may contain
central veins

Weakness, fatigability, disturbed sleep, muscle
cramps, and weight loss common.
advanced cirrhosis anorexia with associated
nausea and occasional vomiting.
Abdominal pain
Menstrual abnormalities (usually amenorrhea)
Impotence, loss of libido, sterility, and gynecomastia
in men
Hematemesis (1525%.)
70% the liver is enlarged, palpable and firm
spider nevi (invariably on the upper half of the
body),
palmar erythema
Dupuytren's contractures.



Jaundiceusually not an initial signis mild at first,
increasing in severity during the later stages of the
disease
Ascites, pleural effusions, peripheral edema, and
ecchymoses late findings.
Encephalopathy
Fever (35% of patients )and usually reflects :
- associated alcoholic hepatitis,
- spontaneous bacterial peritonitis,
- or intercurrent infection.
Splenomegaly (3550%) .
The superficial veins of the abdomen and thorax are
dilated, reflecting the intrahepatic obstruction to
portal blood flow, as do rectal varices.
significant complicating feature of
decompensated cirrhosis
development of ascites and bleeding
from esophagogastric varices
Loss of hepatocellular
- jaundice
- coagulation disorders,
- hypoalbuminemia
- portosystemic encephalopathy


Ascites
Spontaneous Bacterial Peritonitis
Hepatorenal syndrome
Variceal hemorrhage
Hepatopulmonary syndrome
Other Pulmonary syndromes
Hepatic hydrothorax
Portopulmonary HTN
Hepatic Encephalopathy
Hepatocellular carcinoma

early or compensated cirrhosis absent or minimal
abnormality
Anemia, often macrocytic;
Low white blood cell count reflecting hypersplenism,
or high suggesting infection;
Thrombocytopenia
Prolongation of the prothrombin time
Blood chemistries hepatocellular injury and
dysfunction
- modest elevations of AST and alkaline phosphatase
- progressive elevation of the bilirubin.
- low Serum albumin
- globulin , may be as high as in autoimmune
hepatitis.
Risk of diabetes mellitus

alcoholic cirrhosis elevated troponin I
and brain natriuretic peptide levels.
Blunted cardiac inotropic and chronotropic
responses to exercise, stress, and drugs, as
well as reduced ventricular function
("cirrhotic cardiomyopathy") and
prolongation of the QT interval common
in cirrhosis of all causes, but overt heart
failure is rare in the absence of alcoholism.
Liver biopsy inactive cirrhosis (fibrosis with
regenerative nodules) with no specific
features to suggest the underlying cause.

Ultrasound liver size , ascites or hepatic
nodules, including small hepatocellular
carcinomas.
Doppler ultrasound patency of the
splenic, portal, and hepatic veins
Hepatic nodules are characterized
further by contrast-enhanced CT scan or
MRI.
ASCITES
Increased echogenicity in the liver
most important principle abstinence from alcohol.
Diet adequate calories
- 2535 kcal/kg/day compensated cirrhosis
- 3540 kcal/kg/d (malnutrition)
protein
-11.2 g/kg/d (compensated cirrhosis)
-1.5 g/kg/d (malnutrition)
Sodium restriction if there is fluid retention
Hepatic encephalopathy protein intake 6080 g/d.
Vitamin supplementation
HAV, HBV, and pneumococcal vaccines and a yearly
influenza vaccine.

Ascites and edema :
- paracentesis
- diuretics
- Transjugular intrahepatic portosystemic
shunt (TIPS)
- Peritoneovenous shunts

Mild symptoms abdominal pain, increasing ascites,
fever, and progressive encephalopathy
Paracentesis ascitic fluid with :
- white cell count up to 500 cells/mcL ,
- PMNs > 250/mcL
- protein concentration of 1 g/dL or less
Dipsticks detect leukocyte esterase in ascitic fluid.
Cultures of ascites 8090% positive Common
isolates : Escherichia coli and pneumococci.
Antibiotic therapy (iv) cefotaxime, 2 g every 812
hours for at least 5 days.
Ceftriaxone and amoxicillin-clavulanic acid are
alternatives.
10% of patients with advanced cirrhosis and
ascites
Typical features :
- azotemia in the absence of shock or
- significant proteinuria
- failure of renal function to improve following
intravenous infusion of 1.5 L of isotonic saline.
-Oliguria, hyponatremia, and low urinary
sodium
other causes of renal failure (including prerenal
azotemia and acute tubular necrosis) have
been excluded.
Intravenous infusion of albumin in
combination with one of the following for
714 days:
- long-acting vasoconstrictor ornipressin
- ornipressin and dopamine
- terlipressin
- norepinephrine
- somatostatin analog octreotide,
- midodrine, an -adrenergic drug,

daynight reversal, asterixis, tremor, dysarthria,
delirium, drowsiness, and ultimately coma
occurs late except when precipitated by an
acute hepatocellular insult or an episode of
gastrointestinal bleeding.
Monitoring for events likely to precipitate HE
[i.E.- variceal bleeding, infection (such as SBP), the
administration of sedatives, hypokalemia, and
hyponatremia]
Reduction of ammoniagenic substrates
Lactulose / lactitol
Dietary restriction of protein
Zinc and melatonin