A Case Study on Liver Cirrhosis

Group Members:
Andres, Kimberly Joy C.
Cabaron, Fern Angelo E.
Cacanado, Cyrille B.
Sierra, Ma. Patricia B.
Valenciano, Ma. Emilet E.

Presented To:
Ms. Catherine Bautista, RND
TABLE OF CONTENTS:

I. Theoretical Consideration
A. Disease Condition
B. Classification
C. Etiology and Pathology
D. Clinical Manifestations
II. The Patient
A. Physician’s Data
III. Evaluation and Implications
A. Dietary Computations
1. Determine the following:
a. BMI Classification
b. DBW
c. Dietary Management
d. TER Determination
e. Diet Rx
f. Sample Meal Plan For One Day
g. Distribution Changes and Plan a Diet
IV. Nutritional Implications/ Analysis and Recommendations
V. References / Literature

Disease Condition

Liver disease (also called hepatic disease) is a broad term describing

any single number ofdiseases affecting the liver. Many are
accompanied by jaundice caused by increased levels ofbilirubin in the
system. The bilirubin results from the breakup of the hemoglobin of
dead red blood cells; normally, the liver removes bilirubin from the
blood and excretes it through bile.

Cirrhosis (pronounced /sɪˈroʊsɪs/) is a consequence of

chronic liver disease characterized by replacement of
liver tissue by fibrosis, scar tissue and regenerative nodules (lumps
that occur as a result of a process in which damaged tissue is
regenerated),[1][2][3] leading to loss of liver function. Cirrhosis is most
commonly caused by alcoholism, hepatitis B and C, and fatty liver
disease but has many other possible causes. Some cases
are idiopathic, i.e., of unknown cause.

Ascites (fluid retention in the abdominal cavity) is the most

common complication of cirrhosis and is associated with a poor quality
of life, increased risk of infection, and a poor long-term outcome. Other
potentially life-threatening complications are hepatic
encephalopathy (confusion and coma) and bleeding from esophageal
varices. Cirrhosis is generally irreversible, and treatment usually
focuses on preventing progression and complications. In advanced
stages of cirrhosis the only option is a liver transplant.

The word "cirrhosis" derives from Greek κίρῥος, meaning tawny (the
orange-yellow colour of the diseased liver). While the clinical entity
was known before, it was René Laennec who gave it the name
"cirrhosis" in his 1819 work in which he also describes the stethoscope.

Classification
 Alcoholic liver disease is the major cause of liver
disease in Western countries, (in Asian countries,
viral hepatitis is the major cause). It arises from the excessive
ingestion of alcohol. Even though millions of individuals drink
alcohol on a regular basis, only a few heavy drinkers develop
liver damage. How alcohol damages the liver is not completely
understood. It is known that alcohol produces toxic chemicals
like acetaldehyde which can damage liver cells, but why this
occurs in only a few individuals is still in debate. When alcohol
damages the liver, the function of the organ is not immediately
compromised as the liver has a tremendous capacity
toregenerate and even when 75% of the liver is damaged, it
continues to function as normal. When alcohol is consumed for
a long time, it eventually results in liver scarring or what is
known as cirrhosis or end-stage alcoholic liver disease.

RISK FACTORS:
The risk factors presently known are: quantity of alcohol
taken, type of alcohol (beer and spirits have increased risk),
gender (females are twice as susceptable to alcohol related
liver disease, presently explained by the difference in the
ability to metabolize it), hepatitis C infection, genetic factors
(changes in the profiles of various enzymes involved in the
metabolism of alcohol, such as ADH, ALDH, CYP4502E1 ,
mitochondrial dysfunction, and cytokine polymorphism) and
malnutrition and diet (particularly vitamin A and E
deficiencies). Generally it is believed that
certain genes increase metabolism of alcohol, which may
increase risk of cirrhosis and even alcohol related cancers.
Alcohol-induced liver injury can be worsened by hepatitis. If
one has hepatitis B or hepatitis C and consumes alcohol,
cirrhosis occurs sooner. Alcohol-induced liver disease is also
worsened in people who have iron overload. Malnutrition can
worsen alcohol-induced liver damage. Most alcoholics tend to
eat poorly and often substitute alcohol as a meal. The liver has
a great capacity to regenerate, but without proper nutrition, it
quickly fails.

Treatment:
The first treatment of alcohol-induced liver disease is cessation of
alcohol consumption. This is the only way to reverse liver damage or
prevent liver injury from worsening. Without treatment, most patients
with alcohol-induced liver damage will develop liver cirrhosis. Other
treatment for alcoholic hepatitis include:

Nutrition:
Doctors recommend a calorie-rich diet to help the liver in its
regeneration process. Dietary fat must be reduced
because fat interferes with alcohol metabolism. The diet is usually
supplemented with vitamins and dietary
minerals (including calcium and iron).

Many nutritionists recommend a diet high in protein, with

frequent small meals eaten during the day , about 5-6 instead of the
usual 3. Nutritionally, supporting the liver and supplementing with
nutrients that enhance liver function is recommended. These include
carnitine, which will help reverse fatty livers, and vitamin C, which is
an antioxidant, aids in collagen synthesis, and increases the production
of neurotransmitters such as norepinephrine and serotonin, as well as
supplementing with the nutrients that have been depleted due to the
alcohol consumption. Eliminating any food that may be manifesting as
an intollerance and alkalizing the body is also important. There are
some supplements that are recommended to help reduce cravings for
alcohol, including choline, glutamine, and vitamin C. As research shows
glucose increases the toxicity of centrilobular hepatotoxicants by
inhibiting cell division and repair, it is suggested fatty acids are used
by the liver instead of glucose as a fuel source to aid in repair; thus, it
is recommended the patient comsumes a diet high in protein and
essential fatty acids, eg. omega 3. Cessation of alcohol consumption
and cigarette smoking, and increasing exercise are lifestyle
recommendations to decrease the risk of liver disease caused by
alcoholic stress.

Etiology
 This disease is the ending of a life of debauchery. It comes from
indulging the senses by way of eating and drinking, and gratifying lust.
Lust enters into this derangement as a factor by bringing on enervation
and helping to derange digestion and nutrition. There are several
leading etiological factors given by medical authorities: the toxic,
coming from the use of alcoholics; the infectious, which is said to come
from specific fevers, syphilis, etc.; a type that comes from the
congestion following heart disease, known as cardiac liver; and one
that comes from obstruction of the bile-duct. There is a vascular
cirrhosis, which is brought on from irritation, engorgement, and the
developing of new tissue because of an oversupply of nutritive material
in the organ. The causes most commonly met with are overeating and
alcohol-drinking.

Pathology
Cirrhosis leading to hepatocellular carcinoma (autopsy specimen).

Macroscopically, the liver is initially enlarged, but with

progression of the disease, it becomes smaller. Its surface is irregular,
the consistency is firm and the color is often yellow (if
associatessteatosis). Depending on the size of the nodules there are
three macroscopic types: micronodular, macronodular and mixed
cirrhosis. In micronodular form (Laennec's cirrhosis or portal cirrhosis)
regenerating nodules are under 3 mm. In macronodular cirrhosis (post-
necrotic cirrhosis), the nodules are larger than 3 mm. The mixed
cirrhosis consists in a variety of nodules with different sizes.

However, cirrhosis is defined by its pathological features on

microscopy: (1) the presence of regenerating nodules of hepatocytes
and (2) the presence of fibrosis, or the deposition ofconnective
tissue between these nodules. The pattern of fibrosis seen can depend
upon the underlying insult that led to cirrhosis; fibrosis can also
proliferate even if the underlying process that caused it has resolved or
ceased. The fibrosis in cirrhosis can lead to destruction of other normal
tissues in the liver: including thesinusoids, the space of Disse, and
other vascular structures, which leads to altered resistance to blood
flow in the liver and portal hypertension.

As cirrhosis can be caused by many different entities which

injure the liver in different ways, different cause-specific patterns of
cirrhosis, and other cause-specific abnormalities can be seen in
cirrhosis. For example, in chronic hepatitis B, there is infiltration of the
liver parenchyma with lymphocytes; in cardiac cirrhosis there
are erythrocytes and a greater amount of fibrosis in the tissue
surrounding the hepatic veins; in primary biliary cirrhosis, there is
fibrosis around the bile duct, the presence of granulomas and pooling
of bile; and in alcoholic cirrhosis, there is infiltration of the liver
with neutrophils.

INJURY
↓
DEGENERATION
↓
FIBROSIS
↓
FORMATION OF FIBRO-VASCULAR MEMBRANES
↓
PARENCHYMAL DISSECTION INTO NODULES
↓
REARRANGEMENT OF BLOOD CIRCULATION
↓
CIRRHOSIS

II. The Patient

A. Physician’s Data

Name: Fernando Di Magiba

Age: 57 years old
Sex: Male
Place of Resident: Tondo, Manila
Weight: 57lbs.
Height: 5.6’