CHAPTER I

INTRODUCTION
1.1 Background
Cirrhosis is a pathological condition that describes the stageend of
progressive hepatic fibrosis characterized by distortionfrom liver architecture and
regenerative nodule formation. This picture occursdue to hepatocellular necrosis.
Reticuline supporting tissues experience collapsesaccompanied by connective
tissue deposits (Nurdjanah, 2006).
This disease is the final pathological journey of various diseasesliver, where
in the liver many liver damage is found which is indicated byfibrosis. The fibrosis
response to liver damage is reversible but atmost patients with cirrhosis are non-
reversible (Kusumobroto, 2007).

1.2 Formula For Problem

1. UnderstandingLiver Cirrhosis
2. Anatomy and Physiology
3. Etiology
4. Pathophysiology
5. Clinical manifestations
6. Management
7. Complication
8. Assessment
9. Pathway
10. Nursing diagnoses and Intervention

1.3 Purpose
So that students are able to understand what we have discussed about liver
cirrhosis.

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 CHAPTER II
DEBATE

2.1 UnderstandingLiver cirrhosis

Liver cirrhosis is a disease characterized by the presence of diffuse and
chronic inflammation of the liver, followed by the proliferation connective tissue,
degeneration and regeneration of liver cells, so that riot in the composition of the
liver parenchyma (Mansjoer, Faculty of Medicine, 2001).
Liver Cirrhosis is a chronic liver disease characterized diffuse with the
formation of connective tissue with nodules. Usually begins with the
inflammation process liver cell necrosis large. Formation of connective tissue and
the regeneration effort nodules. Architectural distortion liver will cause changes in
circulation micro and macro become irregular due to the addition of network belt
and the nodule (Smeltzer and Bare, 2001).
Liver cirrhosis is a chronic liver disease of unknown the cause with
certainty. It is known that this disease an end stage of chronic liver disease and the
occurrence hardening of the liver (Sujono, 2002). Based on some of the above
understanding can be concluded that liver cirrhosis is a chronic liver disease
characterized by the presence diffuse inflammation of the liver, followed by
connective tissue proliferation, degeneration and regeneration of liver cells and is
accompanied nodules end stage of chronic liver disease and the hardening of
heart.

2.2 Anatomy and Physiology

The liver is the largest organ in the body, weighing about 1500 g. It is
dikuadaran upper right abdomen, below diaphragm and protected by the ribs
(costae). hearts divided into four lobes and each lobe of the liver encased by a thin
layer connective tissue that stretches into the lobe itself and liver mass split into
small units, called lobules.
The anatomy of the human heart when viewed with the naked eye, consists
of four lobes (parts) of different sizes.

2
1. The right lobe is the largest part of the liver that is 5 to 6 times larger than the
left lobe.
2. The left lobe is the part of the heart that has a more pointed and smaller shape
than the right lobe. The left and right lobes are separated by the falciform
ligaments.
3. The caudate lobe is smaller than the previous two lobes, located extending
from the back of the right lobe and wrapping the main reverse vein (inferior
vena cava).
4. The quadratic lobe is lower than the caudate lobe and is located from the back
side of the right lobe to the gallbladder. The squared lobe and caudate are
rarely seen in anatomical images because they are located behind the left and
right lobes.
The blood circulation in and out of the heart is essential in organization of
liver function. The liver receives its blood supply from two different sources.
Most of the blood supply comes from a vein porta that drain blood rich in
nutrients from the tract gastrointestinal. Another part of the blood supply into the
liver via the hepatic artery and contains a lot of oxygen. Both sources The blood
flows into the liver called sinusoidal capillaries Hepatic. Thus, liver cells
(hepatocytes) will be submerged by a mixture of venous and arterial blood. From
the sinusoidal blood flow to theEach lobule central vein, and from all the lobules
to the vein Hepatic. Hepatic veins drain the contents into the vena cava inferior.
So there are two sources that drain blood into in the liver and there is only one
path out.
Besides hepatocytes, the cells phagocytosis included in reticuloendothelial
system is also found in the liver. Other organs containing reticuloendothelial cells
are spleen, bone marrow, lymph nodes and lungs. In the liver, these cells are
called cell Kupffer. The main function of Kupffer cells are consuming particle
objects (Such as bacteria) that goes into the liver via the portal blood. Liver
metabolic functions:
1. Glucose metabolism After a meal blood glucose is taken from the portal vein
by liver and converted into glycogen stored in the hepatocytes. Furthermore,

3
 glycogen is converted back to glucose and if needed is released into the
bloodstream to maintain normal glucose levels. additional glucose can be
synthesized by the liver through a process called gluconeogenesis. For this
process the liver using acids amino result of protein breakdown or lactate
produced by muscles work.
2. Conversion of ammonia The use of amino acids for gluconeogenesis will
forming ammonia as a byproduct. liver change ammonia generated by this
metabolic process into urea. Ammonia is produced by bacteria in the intestine
also will removed from the portal blood for urea synthesis. With This means
careful changing ammonia is a dangerous toxin into urea are compounds that
can be excreted into urine.
3. Protein metabolism This organ synthesize almost the entire plasma protein
including albumin, blood clotting factors transport protein specific and most of
the plasma lipoproteins. vitamin K required liver to synthesize protombin and
some of the factors Other freezing. Amino acids serve as elements builder for
protein synthesis.
4. Fat metabolism The fatty acids can be broken down to produce energy and
ketones. Ketones are compounds small that it can fit into the bloodstream and
become a source of energy for muscles and other body tissues. acid solution fat
into ketones material mainly occurs when availability Glucose metabolism is
very limited as the famine or uncontrolled diabetes.
5. Storage of vitamins and iron
6. Drug metabolism Metabolism generally eliminate drug activity that although in
some cases, activation of the drug may occur. One of the critical path for drug
metabolism include conjugation (binding) of the drug with a number of
compounds, to form more soluble substance. Results conjugation it can be
excreted in the faeces or urine as excretion of bilirubin.
7. The formation of bile Bile is formed by hepatocytes and collected in
canaliculus and bile ducts. The function of bile is ekskretorik such as excretion
of bilirubin and as a helper process digestion through fat emulsification by bile
salts.

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8. Excretion of bilirubin Bilirubin is a pigment that comes from the breakdown
hemoglobin by cells in the reticuloendothelial system include Kupffer cells of
the liver. hepatocytes secrete bilirubin from the blood, and through a chemical
reaction to change it via glucuronide conjugation into acid that makes bilirubin
more soluble in aqueous solution. conjugated bilirubin excreted by the
hepatocytes into the bile canaliculus nearby were brought in bile into the
duodenum. The concentration of bilirubin in the blood can be increased if
There are heart disease, when bile flow is blocked or in case destruction of red
blood cells is excessive. obstruction bile ducts, bilirubin enters the intestine and
as Consequently, there is no urobilinogen in the urine. (Smeltzer & Bare, 2001)

2.3 Etiology
According to the School of Medicine (2001), the causes of cirrhosis include:
1. Malnutrition
2. Alcoholism
3. Viral hepatitis
4. Heart failure that causes hepatic vein dam
5. Wilson's disease (copper accumulation of excessive default)
6. Hemochromatosis (iron overload)
7. Toxic substances

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There are 3 types of cirrhosis or scar formation in the heart:
1. Laennec cirrhosis (alcoholism, nutritional), where scarring typically surrounds
the portal area. Often caused by chronic alcoholics.
2. Cirrhosis pascanekrotik, where there is a band of scar tissue Further widening
as a result of acute viral hepatitis that occurs previous.
3. Biliary cirrhosis, which occurs in the formation of scar tissue around the liver
bile ducts.Which occurs due to biliary obstruction Chronic infections (cholangit).

2.4Pathophysiology
Although there are several factors involved in the etiology of cirrhosis,
consumption of alcoholic beverages is considered as a causal factor main.
Cirrhosis occurs with the highest frequency in the drink liquor. Despite the
decrease in the intake of nutritional deficiency protein contributed to the liver
damage in cirrhosis, but the intake Excessive alcohol is a major contributory
factors fatty liver and the consequences thereof. however Thus, cirrhosis also have
occurred in individuals who do not have drinking liquor and in individuals who
diet normal but with high alcohol consumption (Smeltzer & Bare, 2001).
Most people seem to be more prone to this disease compared to other
individuals without determined whether the individual is have the habit of
drinking liquor or suffer malnutrition. Other factors may play a role, including
Exposure to certain chemicals (carbon tetrachloride, naphthalene chlorinated, asen
or phosphorus) or schistosomiasis infections that contagious. The number of male
patients with cirrhosis is twice more than women, and the majority of cirrhotic
patients aged 40-60 year (Smeltzer and Bare, 2001).
Alcoholic cirrhosis or historically called cirrhosis Laennec characterized by
diffuse scarring, loss of cell-liver cells were uniform, and a bit of regenerative
nodules. so Now and sometimes called micronodular cirrhosis. Micronodular
cirrhosis can also injuries caused by other liver. Three major lesions induced
alcohol is an alcoholic fatty liver, alcoholic hepatitis, and alcoholic cirrhosis
(Tarin, 2001).

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2.5 Clinical manifestations
According to Smeltzer & Bare (2001) clinical manifestations of liver
cirrhosis among others:
1. Enlarged Heart
At the beginning of the trip to liver cirrhosis, liver tend to enlarge and the
cells filled with fat. The liver becomes hard and have sharp edges that can be
detected through palpation. Abdominal pain can occur as a result of the
enlargement of the liver fast and just happened resulting strain the liver fibrous
sheath (kapsula Glissoni). on a trip more advanced disease, liver size will be
reduced after scar tissue causes contraction of the heart tissue. If can be
palpated, the surface of the heart will be felt bumpy (Nodular).
2. Obstruction Portal and Ascites
Manifestations in part caused by a failure Chronic liver function and partly
by the obstruction of circulation portal. All blood from the digestive organs
practically gathered in the portal vein and carried to the liver. Because heart
cirrhotic not allow passage of free blood, then The blood flow will return to the
spleen and tracts Gastrointestinal with the consequence that these organs a
place of chronic passive congestion; in other words, the second The organ will
be filled with blood and thus do not can work well. Patients with these
circumstances tend to suffer from chronic dyspepsia and constipation or
diarrhea. The patient's weight is gradually decreased.
Protein-rich fluid and accumulate dirongga Peritoneal will cause ascites.
This is demonstrated through perfusion of the existence of shifting dullness or
a fluid wave. Splenomegaly also occur. Nets telangiectasia, or dilatation
Superficial arteries causing reddish blue nets, which can often be seen through
the inspection of the face and whole body.
3. varicose Gastrointestinal
Obstruction of blood flow through the liver caused by fibrotic changes
also resulted in the formation of vessel collateral blood in the gastrointestinal
system and pemintasan ( shunting) of blood vessels into the portal vein with a

7
 lower pressure. As a result, sufferers cirrhosis often exhibit abdominal
distension of blood vessels A striking and visible on inspection of the abdomen
(caput medusae), and distention of blood vessels throughout the tract
gastrointestinal. Esophagus, stomach and lower rectum an area that is often
experienced vessels formation collateral blood. Distension of the blood vessels
will form varicose veins or hemorrhoids depending on the location.
Because its function is not to bear the blood volume and a high pressure
due to cirrhosis, the blood vessels of this can rupture and cause bleeding.
Therefore, assessment should include observation to determine bleeding real
and hidden from tract gastrointestinal. Approximately 25% of patients
hematemesis light; the rest will undergo massive hemorrhage from variceal
rupture of the stomach and esophagus.
4. Edema
More advanced symptoms in liver cirrhosis caused by chronic liver failure.
Plasma albumin concentration decline so that predisposes to edema. Production
excessive aldosterone will cause sodium retention and water and potassium
excretion.
5. Vitamin Deficiency and Anemia
Since the formation, use and storage Inadequate certain vitamins
(especially vitamin A, C and K), then the signs of vitamin deficiency are often
found, especially as hemorrhagic phenomena associated with the Chronic
Gastritis vitamin K deficiency and disfunction Gastrointestinal together
inadequate dietary intake and impaired liver function contributed to the anemia
that often accompanies cirrhosis of the liver. Symptoms of anemia and
nutritional status as well as the patient's poor health will lead to severe fatigue
which impairs the ability to perform routine activities daily.
6. Mental setback
Other clinical manifestations are setback function mental with hepatic
encephalopathy and coma membakat. Therefore, a neurological examination
needs to be done in cirrhosis hepatic and covers the general behavior of the
patient, the ability cognitive, orientation to time and place, and speech patterns.

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2.6 Management
Management according to Tarin (2001) are:
1. The patient is in good heart compensation is done Regular control, adequate
rest, diet composition high high calorie protein, fat taste.

2. Cirrhotic patients with known causes such as:

a. Alcohol and drugs recommended stop use. Alcohol reduces protein intake into
the body. With a high-calorie diet (300 calories), protein content of about 70-
90 grams of food a day for hinder the development of kolagenik can be tried
with Award D penicilamine and Cochicine.
b. Hemokromatis Discontinued use of preparations containing iron / therapy
flatfoot (desferioxamine). Sexy veins do 2x a week as much as 500cc for a
year.
c. In chronic autoimmune hepatitis corticosteroids.

3. Treatment of complications arising

a. ascites Bed rest and begin a low-salt diet, salt intake 5.2 g/day. Low-salt diet
combined with diuretic drugs. Initially the administration spironolactone at a
dose of 100-200 mg once daily. responses diuretics can be monitored with a
weight loss of 0.5 kg/day, without edema feet or 1 kg/day with their leg
edema. When giving spironolactone inadequate could be combined with
furosemide at a dose of 20-40 m /day. Provision of furosemide can be
increased dosage if not no response, the maximum dose is 160 mg/day.
paracentesis done when ascites is very large. Spending could ascites up to 4-6
liters and covered with albumin administration.
b. Esophageal variceal bleeding (haematemesis, hematemesis with melena or
melena only)
1) Perform aspiration of gastric fluid containing blood to determine whether
the bleeding
has stopped or is still underway.

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 2) When bleeding a lot, the systolic pressure below 100 mmHg, pulse above
100 x/min
or Hb below 99% administration of IVFD by administering dextrose/copy
and blood
transfusions to taste. 3) Given vasopressin 2 amps 0.1 g in 500cc D5% or
administration of normal saline for 4 hours can be repeated three times. 15
c. Encephalopathy
1) Correction of precipitating factors such as the provision of KCL in
hypokalaemia.
2) Reducing protein intake of food to give appropriate diet.
3) Aspiration of gastric fluid for patients who have bleeding on varicose veins.
4) Antibiotics campisilin / cephalosporin in state systemic infection.
5) Liver transplantation.
d. Spontaneous bacterial peritonitis
Given the antibiotic of choice such as cefotaxime, amoxicillin,
aminoglycosides.
e. Hepatorenal syndrome / nefropatik hepatic Regulate the balance of fluids and
salts.

2.7 Complication
Complications of liver cirrhosis according to Tarin (2001) are:
1. Portal hypertension
2. Coma / ensefalopaty hepatic
3. Hepatoma
4. Ascites
5. Spontaneous bacterial peritonitis
6. Failure of the liver (hepatocellular)
7. Hepatorenal syndrome

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2.8Assessment
Assessment in patients with cirrhosis according Doenges (2000) as follows:
1. Demography
a. Age: over 30 years
b. Men are at greater risk than women
c. Occupation: history of exposure to toxins
2. Medical history
a. A history of chronic hepatitis
b. Metabolic disorders: DM
c. Chronic obstructive ductus coleducus
d. Severe congestive heart failure and chronic
e. Autoimmune diseases
f. A history of chronic malnutrition, especially PEM
3. Functional patterns
a. Activity / rest
Symptoms: Weakness, fatigue.
Symptoms: Lethargy, decreased muscle mass / tone.
b. Circulation
Symptoms: A history of congestive heart failure (CHF) infection, pericarditis,
rheumatic
heart disease, cancer (liver malfunctions cause liver failure), dysrhythmias,
extra hear
sounds, DVJ; abdominal venous distension.
c. Elimination
Symptoms: Flatus.
Symptoms: Abdominal distention (hepatomegaly, splenomegaly, ascites), a
decrease
absence of bowel sounds, stool color of the soil clay, melena, dark urine,
concentrated.

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 d. Food / fluid
Symptoms: Anorexia, food intolerance / can not be digesting, nausea /
vomiting.
Symptoms: Weight loss / increase (liquid), skin dry, poor turgor, jaundice:
spider
angioma, bad breath / fetor hepaticus, bleeding gums.
e. Neurosensori
Symptoms: The nearest person to report changes personality, mental
deterioration.
Signs: mental changes, confusion hallucinations, coma, talking slow / obscure.
f. Pain / Comfort
Symptoms: Abdominal pain / right upper quadrant pain.
Signs: Behavior careful / distractions, focus on yourself.
g. Respiratory
Symptoms: Dyspnea.
Signs: Tachypnea, shallow breathing, additional breath sounds, limited lung
expansion (ascites), hypoxia.
h. Security
Symptoms: pruritus.
Symptoms: Fever (more common in cirrhosis alkohlik), jaundice, ecchymosis,
petechiae.
i. Sexuality
Symptoms: menstrual disorders, impotence.
Signs: testicular atrophy, gynecomastia, loss of hair (chest,under the arm,
pubis) .

4. Physical examination
a. looks weak
b. Increased temperature, increased blood pressure (when theweakexcess fluid)
c. Sclera jaundice, conjunctival pallor
d. Jugular venous distention dileher

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 e. chest:
1) Gynecomastia (enlarged breasts in males)
2) Decreased lung expansion
3) The use of accessory muscles of respexpansion
4) Dysrhythmias, gallop
5) Abnormal lung sound (rales)
f. Abdomen:
1) Belly bulge, increased abdominal girth
2) Decreased bowel sounds
3) Ascites / tension in the upper right abdomen, liver palpable hard
4) Tenderness heartburn
g. Urogenital:
1) testicular Atrophy
2) Hemorrhoids (dilation of the veins around the rectum)
h. Integument:
Jaundice, palmar erythema, spider naevi, alopecia, ecchymosis
i. Extremities:
Edema, decreased muscle strength

5. Supporting investigation
a. Laboratory examination
According to Smeltzer & Bare (2001), namely:
1) complete blood
Hb / Ht and HR may decline because of bleeding.
HR damage and anemia seen with hypersplenismand iron deficiency.
Leukopenia may exist as a resultHiperplenisme.
2) The increase in SGOT, SGPT
3) Decreased serum albumin
4) The level of the electrolyte: hypokalemia
5) Elongation period protombin
6) Serum glucose: hypoglycemia

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7) decreased fiincreased
8) BUN increased

b. diagnostic studies
According to Smeltzer & Bare (2001), namely:
1) Radiology
Can be seen to confirm the presence of esophageal varices
portal hypertension.
2) Esofagoskopi
May indicate the presence of esophageal varices.
3) Ultrasound
4) Angiography
To measure the pressure of the portal vein.
5) Skan / liver biopsy
Detecting fat infiltrates, fibrosis, tissue damage heart.
6) Percutaneous transhepatic Partografi
Circulation shows the portal venous system.

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 2.9 Pathway

Alcohol Consumption Hepatic Virus Bacteria Drugs Stress

Hepatosite Damage
Intake Decreases

Dx : Nutrional Disorderc Less Than

Inflamantion Of The Liver Needed

Weakness

Changes In Blood Flow Hypothalamic Chemoreption Stimulus Dx : Activity intolerance

Set Point Changes

Lliver Necrosis

Increase In Body Heak

Dx : High Risk Of Bilirubin Decreases Hypertermia

Infection

Hyperbilirubinemia Nauseuous vomit

Anorexia
15
Jaundice
2.10 Nursing Diagnoses And Intervention
No. Diagnoses NOC NIC
1. Risk of infection After nursing action for 2x24  Infection
Susceptible to invasion hours, the severity of infection protection
and multiplication of with the criteria - Monitor signs
pathogenic organisms No Indikator A T and symptoms
that can interfere with 1. The pulse is 3 5 of sischemic and
weak
health. local infection.
- Monitor
2. Anxiety 3 5
vulnerability to
3. Dizzy 2 5
infection.
4 fatigue 3 5
- Follow
Information:
1 = weight neutropenia
2 = quite heavy prevention
3 = medium
4 = light measures, as
5 = none appropriate.
- Limit the number
of visitors,
accordingly
2. Nutritional imbalance is After nursing action for 2x 24  Management of
less than the body's hours nutritional status with food disorders
needs, Less food intake criteria nutrition
20% or more below the No Indikator A T - Management
ideal weight range is 1. Nutrition 3 5 nutrition.
intake
proven by expressing a - Help increase.
2. Food supply 3 5
desire to improve - weight Monitor
3. Ratio of 2 5
nutrition daily food calorie
weight / height
Information: intake.
1 = weight
2 = quite heavy
3 = medium

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 4 = light
5 = none

3. Activity intolerance After nursing measures 2x24  Energy

Definition: hours " Level of fatigue " with management
Psychological or the results criteria: - Assess the patient's
physiological NOC: Level of fatigue physiological
insufficiency to maintain NO. INDIKATOR A T status which
or completedaily life 1. Lethargy 3 5 causes fatigue in
activitiesthat must or 2. Disorders of accordance with
should be done. concentration 3 5 the age and
Limitation of 3. Symptoms of development
characteristics: chronic context.
• Dispnea after the fatigue 3 5 - Choose
move syndrome interventions to
• Inconvenience reduce fatigue both
after activity Information: pharmacologically
• ECG changes 1 = weight and non-
• Response of 2 = quite heavy pharmacologically,
abnormal heart 3 = medium appropriately.
frequency to 4 = light - Encourage rest
activity 5 = none periods and
• Abnormal blood activities in turn.
pressure response - Gradually
to activity evaluating the
Related factors: level of activity of
• Lifestyle patients.
lacksmovement
• Immobility
• Imbalance
between supply
and oxygen
demand
• Bed rest

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 CHAPTER III

FINALE

3.1 Conclusions
Given the treatment of liver cirrhosis is only symptomatic and treats complications, the
prognosis of hepatic cirrhosis can be poor. However, the discovery of compensated liver
cirrhosis has a good prognosis. Therefore the accuracy of the diagnosis and proper handling is
needed in the management of liver cirrhosis,

3.2 Suggestions
1. Suggestion of the author to the reader, namely multiply read literature related to internal
medicine, especially those discussing liver organs so that this material can be better
understood.
2. If there is an error, you usually give advice or criticism so that ordinary writers make better
papers.

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 BIBLIOGRAPHY

Nurdjanah, 2006. Medical Surgery Nursing 2 (Ed 8) Jakarta: publisher of Medical Books
(ECG).
Kusumobroto, 2007. Internal Medicine volume 1, Jakarta: FKUI.
Amirudin, 2007. Pathophysiology, Clinical Concepts of the Processes of the Disease Process.
Jakarta: EGC Publisher.
Smeltzer and Bare, 2000. Medical Surgery Nursing 2 (Ed 8) Jakarta: Medical Book
publishers (ECG).
Mansjoer, Faculty of Medicine, 2001. Jakarta: Penerbit EGC.
Smeltzer & Bare 2001. Medical Surgery Nursing 2 (Ed 8) Jakarta: Medical Book publishers
(ECG).
Tarin, 2001. Medical Surgery Nursing 2 (Ed 8) Jakarta: publisher of Medical Books (ECG).
Bulechek M. Gloria, 2016. Nursing Intervention Classification, Elsevier Singapore : Pte Ltd.
Keliat Anna Budi, 2015. Nursing Diagnoses, Jakrta : Buku Kedokteran EGC.
Moorhead Sue, 2016. Nursing Outcomes Classificaton, Elsevier Singapore : Pte Ltd.

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