Professional Documents
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Hepatitis
Dr. Lubna Dwerij
HEPATIC CIRRHOSIS
Cirrhosis is a chronic disease characterized by
replacement of normal liver tissue with diffuse fibrosis
that disrupts the structure and function of the liver.
There are three types of cirrhosis or scarring of the liver:
Alcoholic cirrhosis, in which the scar tissue
characteristically surrounds the portal areas. This is most
frequently caused by chronic alcoholism and is the most
common type of cirrhosis.
Postnecrotic cirrhosis, in which there are broad bands of
scar tissue. This is a late result of a previous bout of acute
viral hepatitis.
HEPATIC CIRRHOSIS
Biliary cirrhosis, in which scarring occurs
in the liver around the bile ducts. This
type of cirrhosis usually results from
chronic biliary obstruction and infection
(cholangitis); it is much less common
than the other two types.
Pathophysiology
Although several factors have been implicated in the
etiology of cirrhosis, alcohol consumption is considered
the major causative factor.
Although nutritional deficiency with reduced protein
intake contributes to liver destruction in cirrhosis,
excessive alcohol intake is the major causative factor in
fatty liver and its consequences.
However, cirrhosis has also occurred in people who do not
consume alcohol and in those who consume a normal diet
and have a high alcohol intake.
Pathophysiology
Some people appear to be more susceptible than others to
this disease, whether or not they have alcoholism or are
malnourished.
Other factors may play a role, including exposure to
certain chemicals carbon tetrachloride, chlorinated
naphthalene, arsenic, or phosphorus) or infectious
schistosomiasis.
Women are at greater risk for development of alcohol-
induced liver disease.
Pathophysiology
Alcoholic cirrhosis is characterized by episodes of necrosis
involving the liver cells, which sometimes occur
repeatedly throughout the course of the disease.
The destroyed liver cells are gradually replaced by scar
tissue. Eventually, the amount of scar tissue exceeds that
of the functioning liver tissue.
The disease usually has an insidious onset and a
protracted course, occasionally proceeding over a period
of 30 or more years.
Clinical Manifestations
Signs and symptoms of cirrhosis increase in severity as the
disease progresses.
Their severity is used to categorize the disorder as
compensated or decompensated cirrhosis.
Compensated cirrhosis, with its less severe, often vague
symptoms, may be discovered secondarily at a routine
physical examination.
The hallmarks of decompensated cirrhosis result from
failure of the liver to synthesize proteins, clotting factors,
and other substances and manifestations of portal
hypertension.
Clinical Manifestations
Liver Enlargement
Early in the course of cirrhosis, the liver tends to be large,
and the cells are loaded with fat. The liver is firm and has
a sharp edge that is noticeable on palpation.
Abdominal pain may be present because of recent, rapid
enlargement of the liver, which produces tension on the
fibrous covering of the liver (Glisson’s capsule).
Later in the disease, the liver decreases in size as scar
tissue contracts the liver tissue. The liver edge, if
palpable, is nodular.
Clinical Manifestations
Portal Obstruction and Ascites
Portal obstruction and ascites, late manifestations of
cirrhosis, are caused partly by chronic failure of liver
function and partly by obstruction of the portal
circulation.
Because a cirrhotic liver does not allow free blood
passage, blood backs up into the spleen and the GI tract
They are stagnant with blood and therefore cannot
function properly. Indigestion and altered bowel function
result.
Fluid rich in protein may accumulate in the peritoneal
cavity, producing ascites
Clinical Manifestations
Infection and Peritonitis
Bacterial peritonitis may develop in patients with cirrhosis
and ascites in the absence of an intra-abdominal source of
infection or an abscess.
This condition is referred to as spontaneous bacterial
peritonitis (SBP).
Bacteremia due to translocation of intestinal flora is
believed to be the most likely route of infection.
Clinical signs may be absent, necessitating paracentesis
for diagnosis.
Clinical Manifestations
Antibiotic therapy is effective in the treatment and
prevention of recurrent episodes of SBP.
The most severe complication of SBP is hepatorenal
syndrome, a form of renal failure unresponsive to
administration of fluid or diuretics.
Clinical Manifestations
Gastrointestinal Varices
The obstruction to blood flow through the liver
caused by fibrotic changes also results in the
formation of collateral blood vessels in the GI
system and shunting of blood from the portal
vessels into blood vessels with lower pressures.
As a result, the patient with cirrhosis often has
prominent, distended abdominal blood vessels,
which are visible on abdominal inspection (caput
medusae) and distended blood vessels throughout
the GI tract.
Clinical Manifestations
The esophagus, stomach, and lower rectum are common
sites of collateral blood vessels.
These distended blood vessels form varices or
hemorrhoids, depending on their location.
Because these vessels were not intended to carry the high
pressure and volume of blood imposed by cirrhosis, they
may rupture and bleed.
Therefore, assessment must include observation for occult
and frank bleeding from the GI tract.
Clinical Manifestations
Edema
Another late symptom of cirrhosis is edema, which is
attributed to chronic liver failure.
reduced plasma albumin concentration predisposes the
patient to the formation of edema.
Although edema is generalized, it often affects the lower
extremities, the upper extremities, and the presacral
area.
Facial edema is not typical
Clinical Manifestations
Vitamin Deficiency and Anemia
Because of inadequate formation, use, and storage of
certain vitamins (notably vitamins A, C, and K), signs of
deficiency are common, particularly hemorrhagic
phenomena associated with vitamin K deficiency.
Chronic gastritis and impaired GI function, together with
inadequate dietary intake and impaired liver function,
account for the anemia that is often associated with
cirrhosis.
Clinical Manifestations
Mental Deterioration
Additional clinical manifestations include deterioration of
mental and cognitive function with impending hepatic
encephalopathy and hepatic coma.
Assessment and Diagnostic Findings
The extent of liver disease and the type of treatment are
determined after review of the laboratory findings.
The functions of the liver are complex, and many
diagnostic tests provide information about liver function.
In severe parenchymal liver dysfunction, the serum
albumin level tends to decrease, and the serum globulin
level rises.
Enzyme tests indicate liver cell damage: serum alkaline
phosphatase, AST, ALT, and GGT levels increase, and the
serum cholinesterase level may decrease.
Assessment and Diagnostic Findings
Bilirubin tests are performed to measure bile excretion or
retention; increased levels of bilirubin can occur with
cirrhosis and other liver disorders. Prothrombin time is
prolonged.
Ultrasound scanning is used to measure the difference in
density of parenchymal cells and scar tissue.
CT, MRI, and radioisotope liver scans give information
about liver size and hepatic blood flow and obstruction.
Diagnosis is confirmed by liver biopsy.
Medical Management
The management of the patient with cirrhosis is usually
based on the presenting symptoms.
For example, antacids or histamine-2 (H2) antagonists are
prescribed to decrease gastric distress and minimize the
possibility of GI bleeding.
Vitamins and nutritional supplements promote healing of
damaged liver cells and improve the patient’s general
nutritional status.
Potassium-sparing diuretics such as spironolactone or
triamterene (Dyrenium) may be indicated to decrease
ascites, if present;
Medical Management
An adequate diet and avoidance of alcohol are essential.
Although the fibrosis of the cirrhotic liver cannot be
reversed, its progression may be halted or slowed by such
measures.
Some of these medications include angiotensin system
inhibitors, statins, diuretics, immunosuppressants, and
glitazones.
Medical Management