Comparison of Post-necrotic, Biliary, Cardiac, and Alcohol Cirrhosis

DEFINITION

ETIOLOGY

PATHOLOGY

POSTNECROTIC (MACRONODULAR) CIRRHOSIS

Most common
Post-acute viral
Liver small and
worldwide form
(types B and C)
nodular
Massive loss of
hepatitis
liver cells, with
Post-intoxication
irregular
with industrial
patterns of
chemicals
regenerating
Some infections
cells
and metabolic
disorders
BILIARY CIRRHOSIS
Bile flow
Primary
Early-stage biopsy
decreased with
Chronic stasis of bile
reveals
concurrent cell
in intrahepatic
inflammatory
damage to
ducts
process with
hepatocytes
Cause unknown
necrosis of cells
around bile
Autoimmune process
and ducts
ductules
implicated
Hepatocytes are lost
Secondary
and scar tissue
Obstruction of bile
remains
ducts outside of
End stage similar to
liver
post-necrotic type

CARDIAC CIRRHOSIS
Chronic liver
Atrioventricular
disease
valve disease
associated with
Prolonged
severe rightconstrictive
sided long-term
pericarditis
heart failure
Decompensated cor
(fairly rare)
pulmonale

ALCOHOLIC CIRRHOSIS
Alcoholic cirrhosis
Associated with
(Lannec,
alcohol abuse

ASSESSMENT DATA

DIAGNOSIS AND
PROGNOSIS

INTERVENTION(S)

As in alcoholic cirrhosis except

less muscle wasting and
more jaundice

Needle biopsy of the liver

establishes pathologic
processes
Within 5 years, 75% die
of complications
serum
aminotransferases
gamma globulins

Treat complication as
needed

Fatigue
Generalized pruritus
Dark urine
Jaundice
Impaired bile flow
Steatorrhea
absorption of fat-soluble
vitamins
Elevated serum lipids
cholesterol deposits in
subcutaneous tissues
Signs of portal hypertension

Elevated serum bilirubin

levels
Early: 3-10 mg/100 ml
Late: >50 mg/100 ml
High elevations of alkaline
phosphatase
gamma globulins
blood lipids
Presence of lipoprotein X
serum bile salts
Hypoprothrombinemia
antimitochondrial
antibody in primary
cases
serum copper in
primary cases

Primary
Ursodiol
Treatment is symptomatic
(e.g., high-calorie diet,
lower intake of fats by 30
40 g/day if problems
develop)
Cholestyramine for pruritus
Supplement of fat-soluble
vitamins
Secondary
Treatment to relieve
mechanical obstruction

Early
Dark-colored liver
enlarged by blood
and edema fluid
Late
Liver capsule
thickens and
nodular scarring
occurs

Slight jaundice, enlarged liver,

and ascites in person with
severe cardiac impairment
over 10-year span
RUQ pain during acute
congestion
Cachexia
Fluid retention
Circulatory problems

conjugated bilirubin in
serum
sulfobromophthalein
albumin in serum
serum
aminotransferases
Liver biopsy
Prognosis
Depends on course of
cardiac disease

Cause of chronic heart

failure is treated if
possible

Scarring and
collagen tissue

May produce no symptoms for

long periods

Liver biopsy; history of

alcohol abuse; high AST;

Primarily supportive
Correction of vitamin and

micronodular)
Small nodules
form as a result
of persistence of
some offending
agent

deposits
Regenerating
nodules are very
small
Normal lobular
structure is
destroyed

Onset of symptoms may be

insidious or abrupt
Early: Weakness, fatigue,
weight loss
Later: Anorexia, nausea, and
vomiting
Abdominal pain
Ascites
Menstrual irregularities
Impotence
Enlarged breasts in men
Hematemesis
Spider angiomas

high bilirubin (slight);

anemia
Prognosis depends on
presence of
complications and
continued abuse of
alcohol

mineral deficiencies if
any (e.g., folate,
thiamine, pyridoxine,
vitamin K, and minerals
[magnesium and
phosphate]); treat
complications as needed
(e.g., ferrous sulfate for
anemia, IV vasopressin
for esophageal varices,
reduce or withhold
dietary protein for
hepatic encephalopathy
or vitamin K for
hemorrhagic tendency)