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Cirrhosis

Petrus J. Hasibuan


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Definition

Cirrhosis is a chronic,

degenerative disease in whichnormal liver cells are damaged

and are then replaced by scar

tissue


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Description

Cirrhosis changes the structure of the

liver and blood vessels that nourish it.

The disease reduces the livers ability tomanufacture proteins and process

hormones, nutrients, medications, and

poisons.


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Cirrhosis gets worse over time and canbecome potentially life threatening. Thisdisease can cause: Excessive bleeding (hemorrhage) Impotence Liver cancer Coma due to accumulated ammonia and body

wastes (liver failure) Death


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Early symptoms of cirrhosis include:

Fatigue & weaknessrelated to anemia & alterrednutrient metabolism

Poor appetite Nausea Weight loss

In men : Impotence Reduced testicle size Enlarged, tender breasts Loss of interest in sexdue to altered liver metabolism of sex

hormones Small, red spider-like blood vessels under the

skincaused by increased pressure in the tiny bloodvessels due to liver congestion

Increased sensitivity to drugs due to reduced ability ofliver to inactivate them.


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Later symptoms, some of which are

due to complications, include:

Reddened or blotchy palms Loss of body hair

Sleep disturbances Insulin resistance Ulcers Fever and other signs of infectiondue to

altered immune function Gallstoneif cirrhosis prevents bile from

reaching the gallbladder


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Pale or clay-colored stoolscaused by a

reduction in excreted bile pigments Frequent nosebleeds, skin bruising or bleeding

gums resulting from decreased liver synthesis

of clotting factors

Asciteswater retention and swelling in the legsand abdomen caused by obstructed blood flow

through the liver and reduced synthesis of the

protein albumin Bacterial peritonitisinfection of ascites causing

abdominal pain and fever


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Itching: caused by deposition of bile products inthe skin

Jaundice : yellowing of the skin or eyes due tobuild-up of bile pigments (bilirubin)

Vomiting blood due to swollen veins theesophagus that burst

Encephalopathy and coma mental changes,including forgetfulness, trouble concentrating,confusion, and agitation, caused by the build-up of ammonia in the blood

Decreased urine output and dark urine causedby kidney dysfunction or failure

Liver cancer


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Other symptoms of cirrhosis

include: Anemia

Bleeding gums Decreased interest in

sex Fever

Fluid in the lungs

Hallucinations lethargy

Lighteadedness

Muscle weakness Musty breath

Painful nerve

inflammation

(neuritis)

Slurred speech tremors


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Table Sequelale of cirrhosis1 Portal hypertension: bleeding from varices in esophagus/stomach (most

common), duodenum, rectum, or surgical stomas; bleeding fromcongestive gastropathy; splenomegaly with hypersplenism

2 Ascites; spontaneous bacterial peritonitis; hepatic hydrothorax,abdominal hernia

3 Hepatorenal syndrome

4 Hepatic encephalopathy

5 Synthetic dysfunction/coagulopathy

6 Hepatopulmonary syndrome

7 Hepatocellular carcinoma

8 Feminization

9 Altered drug metabolism

10 Hepatic osteodystrophy


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Variceal hemorrhage

Hemorrhage from gastroesophageal varices is

often the initial complication of portal

hypertension. Less commonly, variceal

hemorrhage occurs from other sites of

portosystemic collateral vessels, including the

duodenum, rectum, or sites of prior abdominal

surgery.


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Esophageal cariceal hemorrhage typically

occurs as painless, large-volume hematemesis

or melena with minimal abdominal pain. Signs

of significant volume depletion, including

orthostasis and paloor, are common. Mortality

from variceal hemorrhage is more a function

of underlying liver disease than severity ofhemorrhage per se.


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In a patient with known varices, risk factors that

correlate with increased likelihood of bleeding

include (1) variceal size (large varices have increased

wall tension and greater thinning of the vessel wall);

(2) endoscopic signs known as red wales or cherry-red spots overlying the varix, which are believed to

represent hemorrhage within the vessel wall; (3)

WHPG greater than 12 mmHg; and (4) poor

liverfunction with ascites and/or jaundice. Gastricacid plays little role in the pathogenesis of bleeding.


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Table. Management of gastroesophageal variceal

hemorrhage

1. Hemodynamic stabilization

2. Emergent diagnostic endoscopy

3. Initial control of hemorrhage (option)a. Endoscopic sclerotherapyb. Endoscopic variceal band ligationc. Intravenous vasopressin/nitroglycerin or octreotided. Balloon tamponadee. Transjugular intrahepatic potacaval shunt (TIPS)

4. Prevention of initial or recurrent cariceal hemorrhage (option)a. Prophylactic beta-blockers in high-risk patients who have not

bledb. Beta-Blockers after initial bleeding episodec. Chronic obliterative endoscopic sclerotherapy or band

ligationd. Portacaval shunt surgerye. Liver transplantation


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Diagnosis

A patientss medical history can reveal illnesses orlifestyles likely to lead to cirrhosis. liver changes can

be seen during a physical examination. A doctor whosuspects cirrhosis may order blood and urine tests tomeasure liver function.

Computed tomography scans (CT), ultrasound, andother imaging techniques can be used duringdiagnosis.

Liver biopsy is usually needed to confirm a diagnosisof cirrhosis.


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Treatment

The goal of treatment is to cure or reduce the

condition causing cirrhosis, prevent or delay

disease progression, and prevent or treat

complication.

Salt and fluid intake is often limited, and

activity is encouraged. A diet high in calories

and moderately high in proten can benefitsome patient.


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Medication

Diuretic, fluid retention, and ammonia accumulation

associated with cirrhosis.

Laxatives help the body absorb toxins and accelerate

their removal from the digestive tract. Beta blockers may be prescribed to control cirrhosis

induced portal hypertension.

Interferon medicines may be used by patients withchronic hepatitis B and C to prevent post-hepatic

cirrhosis (before chirrosis take place)

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