Cirrhosis Flashcards
what is cirrhosis
end stage of liver damage due to chronic, heavy alcohol intake
histology of cirrhosis
normal liver architecture is replaced with diffuse fibrosis and nodules of regenerating hepatocytes
what is decompensated cirrhosis
acute deterioration of someone with cirrhosis
what complications lead to decompensation
ascites, jaundice, encephalopathy and GI bleeding
what can decompensation be precipitated with
infection, GI bleeding, constipation, high-protein meal, electrolyte imbalance, alcohol, drugs, tumour development or portal vein thrombosis
aetiology of cirrhosis
mainly chronic alcohol misuse, chronic viral hepatitis (unproductive sex, sharing needles - body fluid exchange)
autoimmune hepatitis, drugs, inherited, vascular, chronic biliary diseases, not known or non-alcohol related steatohepatitis
what are inherited causes of cirrhosis
haemochromatosis, Wilsons disease, galactosaemia, cystic fibrosis, alpha 1- antitrypsin deficiency
non-alcohol related steatohepatitis (NASH)
obesity and diabetes
presenting symptoms (early, non-specific)
anorexia, nausea, fatigue, weakness and weight loss
why weight loss in cirrhosis
liver can’t process nutrients, and vomitting?
presenting symptoms (liver synthetic functions decreased)
easy bruising, abnormal swelling, ankle oedema
presenting symptoms (liver detoxification functions decreased)
jaundice, personality change, altered sleep pattern, amenorrhoea, galactorrhea
presenting symptoms (portal hypertension)
abdominal swelling, haematemesis (vomiting blood) and PR bleeding
epidemiology
one of top 10 causes of death worldwide
physical examination findings
abdominal distension, jaundice, haematemesis (blood in vomit), black stool (melaena), hand and nail features (clubbing, spider naevi, palmar erythema), hepatomegaly, splenomegaly, muscle wasting and peripheral oedema
investigations
bloods; FBC, LFT’s, clotting and serum AFP (alpha fetoprotein)
what would you see in FBC
low platelet (thrombocytopenia) and low Hb due to portal hypertension- leads to hypersplenism
what would you see in LFT’s
high ALP, ALT, GGT, AST and bilirubin. low albumin
what would you expect to see regarding Prothrombin Time (PT)
prolonged in cirrhosis
why is alpha fetoprotein important
its a marker for liver cancer so high levels may suggest hepatocellular carcinoma
management (TREAT THE CAUSE)
Avoid alcohol, sedatives, opiates, NSAIDs and drugs that affect the liver
Nutrition is important
Enteral supplements should be given
NG feeding may be indicated
treating encephalopathy
Treat infections
Exclude GI bleed
Use lactulose and phosphate enemas
Normally, the liver breaks down ammonia that is absorbed in the GI tract, however, in Cirrhosis the ammonia can go through the liver without being broken down and exert toxic effects on the brain
IMPORTANT: lactulose reduces the absorption of ammonia from the gut
This helps prevent encephalopathy caused by ammonia reaching the brain
Avoid sedation
treating ascites
Diuretics (spironolactone with/without furosemide)
Dietary sodium restriction
Therapeutic paracentesis (with human albumin replacement)
Monitor weight
Fluid restrict if plasma sodium < 120 mmol/L
Avoid alcohol and NSAIDs
treating spontaneous bacterial peritonitis
Antibiotics (e.g. cefuroxime and metronidazole)
Prophylaxis against recurrent SBP with ciprofloxacin
surgical treatment
TIPS (trans jugular intrahepatic portosystemic shunt)
liver transplant is only CURE
possible complications
Portal hypertension with ascites Hepatic encephalopathy Variceal haemorrhage SBP HCC Renal failure (hepatorenal syndrome) Pulmonary hypertension (hepatopulmonary syndrome)
prognosis?
Generally poor prognosis
Overall 5 year survival = 50%
If ascites, 2 year survival = 50%
