LIVER CIRRHOSIS

Viral Infection- caused by certain viruses. Hepatitis virus.

Hepatitis A:
• Acute infectious hepatitis
• Oral-faecal route from contaminated H20 & food
• Time of infection and symproms appearance (2-6 weeks)
• 28 days inc. period
• s/s: fatigue, fever, jaundice, abdominal pain, nausea, vomiting, loss of appetite, R upper
quadrant pain, weight loss, itching.

Hepatitis B:

Acute Infection:

• An illness that begins with general ill-health, loss of appetite, nausea, vomiting, body
aches, mild fever, dark urine, and then progresses to development of jaundice. It has
been noted that itchy skin has been an indication as a possible symptom of all
hepatitis virus types. The illness lasts for a few weeks and then gradually improves in
most affected people.

Chronic Infection:

• Asymptomatic or may be associated with a chronic inflammation of the liver (chronic

hepatitis), leading to cirrhosis over a period of several years. This type of infection
dramatically increases the incidence of hepatocellular carcinoma (liver cancer).
Chronic carriers are encouraged to avoid consuming alcohol as it increases their risk
for cirrhosis and liver cancer.

Hepatitis C:

Acute Infection:
 • First 6 mos. After infection

• 6070% of people have no symptoms during this phase.

• s/s: dec. appetite, jaundice, abdominal pain, itching, and flu-like symptoms.

Chronic Infection:

• Asymptomatic in this phase

• Can be seen through biopsy/ultrasound for inflammation, liver scarring
• Untreated clients develops liver cirrhosis in less than 20 years
• s/s: ascites (fluid in the abdomen), jaundice.

Laennec's Cirrhosis:

Three stages. The pathologic features of this form of cirrhosis change with time. Therefore,
it is helpful to break the disease down into three stages: 1) the fatty liver stage, 2) the
fibrotic liver stage and 3) the nodular liver stage.

In early stages the liver is large and fatty. In this early stage, fat accumulates in the liver
cells around the central vein (fatty change). The liver becomes large, even huge
(hepatomegaly). The normal liver weighs about 1,200 grams. By comparison, fatty livers
can weigh in at over 6,000 grams and may, in the living patient, fill the abdominal cavity
(remember that the normal liver extends 2-3 finger breadths below the right costal margin).
At autopsy, the fatty liver is greasy and a cut surface is yellow. As dramatic as these
changes are, the fatty change is reversible.

In later stages, the liver becomes scarred (fibrotic). In this stage, the liver returns to a more
normal size; however, it does not return to normal in any other way. In fact, the changes
that develop during this stage are irreversible. The fatty change subsides and is replaced by
fibrosis (scarring) and some chronic inflammation. No doubt the retreat of fatty change and
the shrinking effect of scar tissue is responsible for the over-all decrease in liver size.
In the final stage, the liver becomes lumpy (nodular). In this stage, the liver shrinks even
further. It may not extend below the costal margin at all. Liver cells attempt to regenerate
in an increasingly fibrotic setting. They find it difficult to do so and form "regenerative
nodules" that only partially carry out normal liver function. This shrunken, nodular texture
has been dubbed the "hob-nail" or "cobble stone" effect.

Steatosis:

In cellular pathology, steatosis (also called fatty change, fatty degeneration or adipose
degeneration) is the process describing the abnormal retention of lipids within a cell. It
reflects an impairment of the normal processes of synthesis and elimination
of triglyceride fat. Excess lipid accumulates in vesicles that displace the cytoplasm. When
the vesicles are large enough to distort the nucleus, the condition is known
as macrovesicular steatosis, otherwise the condition is known as microvesicular steatosis.
Whilst not particularly detrimental to the cell in mild cases, large accumulations can disrupt
cell constituents, and in severe cases the cell may even burst. The risk factors associated
with steatosis are varied, and include diabetes mellitus,[1] protein malnutrition, hypertension,
cell toxins, obesity, andanoxia. As the liver is the primary organ of lipid metabolism it is
most often associated with steatosis, however it may occur in any organ, commonly the
kidneys, heart, and muscle.

Hepatomegaly:

Is the condition of having an enlarged liver. It is a nonspecific medical sign having many
causes, which can broadly be broken down into infection, direct toxicity, hepatic tumours,
or metabolic disorder. Often, hepatomegaly will present as an abdominal mass. Depending
on the cause, it may sometimes present along with jaundice.

What is liver fibrosis?

Liver fibrosis is the scarring process that represents the liver’s response to injury. In the
same way as skin and other organs heal wounds through deposition of collagen and other
matrix constituents so the liver repairs injury through the deposition of new collagen. Over
time this process can result in cirrhosis of the liver in which the architectural organization of
the functional units of the liver becomes so disrupted that blood flow through the liver and
liver function become disrupted. Once cirrhosis has developed the serious complications of
liver disease may occur including portal hypertension, liver failure and liver cancer.

Parenchyma:

The key elements of an organ essential to its functioning, as distinct from the capsule that
encompasses it and other supporting structures. The parenchyma is thus opposed to the
connective tissue framework, or stroma, of an organ. The parenchyma of the testis consists
of what are called the seminiferous tubules.
The pathological hallmark of cirrhosis is the development of scar tissue that replaces
normal parenchyma, blocking the portal flow of blood through the organ and disturbing
normal function. Iredale (2003) summarises the pivotal role of stellate cell, a cell type that
normally stores vitamin A, in the development of cirrhosis. Damage to the
hepatic parenchyma leads to activation of the stellate cell, which becomes contractile and
obstructs blood flow in the circulation. In addition, it secretes TGF-β1, which leads to a
fibrotic response and proliferation of connective tissue. Furthermore, it disturbs the balance
between matrixmetalloproteinases and the naturally occurring inhibitors (TIMP 1 and 2),
leading to matrix breakdown and replacement by connective tissue-secreted matrix.

Hepatic stellate cells (here HSC), also known as Ito cells (earlier lipocytes or fat-storing
cells), are pericytes found in the perisinusoidal space (a small area between
the sinusoids and hepatocytes) of the liver also known as the space of Disse. The stellate
cell is the major cell type involved in liver fibrosis, which is the formation of scar tissue in
response to liver damage.

The fibrous tissue forms nodes, which eventually replace the entire liver architecture,
leading to decreased blood flow throughout. The spleen becomes congested, which leads
to hypersplenism and increased sequestration of platelets. Portal hypertension is
responsible for most severe complications of cirrhosis.
The hepatic portal vein is not a true vein, because it does not conduct blood directly to the
heart. It is a vessel in the abdominal cavity that drains blood from the gastrointestinal
tract and spleen to capillary beds in the liver. It is usually formed by the confluence of
the superior mesenteric and splenic veins and also receives blood from the inferior
mesenteric, gastric, and cystic veins. The hepatic portal vein is a major component of
the hepatic portal system, and it is one of only two portal venous systems in the body. The
other is the Hypophyseal portal system.

Conditions involving the hepatic portal vein cause considerable illness and death. An
important example of such a condition is elevated blood pressure in the hepatic portal vein.
This condition, called portal hypertension, is a major complication of cirrhosis.