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Medical dictionary.
Cirrhosis is a consequence of chronic
liver disease, characterised by
replacement of liver tissue by fibrosis,
scar tissue and regenerative nodules
leading to loss of liver function.
Cirrosisis scaring of liver caused by
many forms of liver disease and
conditions, such as hepatitis and chronic
alcohol abuse.
Types:
a. Alcoholic Cirrhosis ( Laennec’s Cirrhosis)
Most common type of liver cirrhosis
Caused by chronic alcoholism
b. Postnecrotic cirrhosis
Late result of a previous bout of acute viral hepatitis
c. Biliary cirrhosis
MTCAT '10
Resulted from chronic biliary obstruction and infection
Least common type
The liver is a very hardy organ and is normally able to regenerate damaged
cells. Cirrhosis develops when the factors that damage the liver (such as
alcohol and chronic viral infections) are present over a long period of time.
When this happens, the liver becomes injured and scarred. A scarred liver
can’t function properly, and ultimately this may result in cirrhosis.
Cirrhosis causes the liver to shrink and harden. This makes it difficult for
nutrient-rich blood to flow into the liver from the portal vein. The portal vein
carries blood from the digestive organs to the liver. The pressure in the
portal vein rises when blood can’t pass into the liver. The end result is a
serious condition called portal hypertension, in which the vein develops high
blood pressure. The unfortunate consequence of portal hypertension is that
this high-pressure system causes a backup, which leads to esophageal
varices (like varicose veins), which can then burst and bleed.
CLINICAL FEATURES
CT scan or Ultrasound– show shrinkage or abnormal
appearance of the liver.
Laboratory studies – bilirubin, albumin, alanine transaminase
(ALT), aspartate transaminase (AST), prothrombin time, and
serum ammonia- to check for elevated values, which indicate
hepatic cell destruction.
Laparoscopy and liver biopsy-direct visualization of the liver
Paracentesis-to examine ascetic fluid for cell, protein and
bacterial counts.
Esophagoscopy– to determine the presence of esophageal
varices.
PROMOTION OF REST
IMPROVE NUTRITION; Dietary restriction of
protein, salt, water.
SKIN CARE
REDUCE RISK FOR INJURY
MONITERING AND MANAGING POTENTIAL
COMPLICATIONS
HEPATIC ENCEPHALOPATHY
FLUID VOL EXCESS
TREATMENT OF UNDERLYING CAUSE
PREVENT INFECTION: ANTIBIOTICS . eg;
cephalosporine
ASITIS; FRUSAMIDE(40-80 mg/day)
HEPATO RENAL SYNDROME; DIEURITICS
HEPATIC ENCEPHALOPATHY; NEOMYCINE (1 mg
6th hrly), METRONIDAZOLE(250mg 8th hrly)
TRANS JUGULAR INTRAHEPATIC
PROTOSYSTEMIC SHUNT (TIPS)
DISTAL SPLENORENAL SHUNT (DSR)
ENDOSCOPIC SCLEROTHERAPY
BANDING OR LIGATION
SCLEROTHERAPY AND BANDING
BALLOON TAMPONADE
LIVER TRANSPLANTATION
PORTAL HYPERTENSION
ESOPHAGEAL VERISES
GASTRIC VARICIES
PEREPHERAL EDEMA
ASCITIS
HEPATIC ENCEPHALOPATHY/ COMA
HEPATORENAL SYNDROME
PERITONITIS
Monitor vital signs, intake and output and electrolyte levels to determine fluid volume status.
Maintain some periods of rest wtih legs elevated to mobilize edema and ascites.Alternate rest
periods with ambulation.
To assess fluid retention, measure and record abdominal girth every shift. Weight the patient daily
and document his weight.
Administer diuretics,potasium and protein or vitamin supplements as ordered. Restrict sodium and
fluid intake as ordered.
Observe and document for bleeding gums,ecchymoses,epistaxis,petechiae and degree of sclerae,
skin jaundice. Remain with the patient during the hemorrhagic episodes.
Inspect stools for ammount,color and consistency. Test stools and vomitus for occult blood as
ordered.
Watch for signs of anxiety,epigastric fullness, restlessness and weakness.
Observe closely for signs of behavioral or personality changes. Report increasing
stupor,lethargy,hallucinations or neuromuscular dysfunction. Arouse the patient periodically to
determine level of consciouness. Watch for asterixis, a sign of developing encephalopathy.
Allow the patient to express his feelings about having cirrhosis.Offer psychological support and
encouragement,when appropriate.