Cirrhosis Flashcards

1
Q

what is cirrhosis

A

end stage of liver damage due to chronic, heavy alcohol intake

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2
Q

histology of cirrhosis

A

normal liver architecture is replaced with diffuse fibrosis and nodules of regenerating hepatocytes

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3
Q

what is decompensated cirrhosis

A

acute deterioration of someone with cirrhosis

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4
Q

what complications lead to decompensation

A

ascites, jaundice, encephalopathy and GI bleeding

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5
Q

what can decompensation be precipitated with

A

infection, GI bleeding, constipation, high-protein meal, electrolyte imbalance, alcohol, drugs, tumour development or portal vein thrombosis

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6
Q

aetiology of cirrhosis

A

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

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7
Q

what are inherited causes of cirrhosis

A

haemochromatosis, Wilsons disease, galactosaemia, cystic fibrosis, alpha 1- antitrypsin deficiency

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8
Q

non-alcohol related steatohepatitis (NASH)

A

obesity and diabetes

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9
Q

presenting symptoms (early, non-specific)

A

anorexia, nausea, fatigue, weakness and weight loss

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10
Q

why weight loss in cirrhosis

A

liver can’t process nutrients, and vomitting?

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11
Q

presenting symptoms (liver synthetic functions decreased)

A

easy bruising, abnormal swelling, ankle oedema

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12
Q

presenting symptoms (liver detoxification functions decreased)

A

jaundice, personality change, altered sleep pattern, amenorrhoea, galactorrhea

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13
Q

presenting symptoms (portal hypertension)

A

abdominal swelling, haematemesis (vomiting blood) and PR bleeding

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14
Q

epidemiology

A

one of top 10 causes of death worldwide

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15
Q

physical examination findings

A

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

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16
Q

investigations

A

bloods; FBC, LFT’s, clotting and serum AFP (alpha fetoprotein)

17
Q

what would you see in FBC

A

low platelet (thrombocytopenia) and low Hb due to portal hypertension- leads to hypersplenism

18
Q

what would you see in LFT’s

A

high ALP, ALT, GGT, AST and bilirubin. low albumin

19
Q

what would you expect to see regarding Prothrombin Time (PT)

A

prolonged in cirrhosis

20
Q

why is alpha fetoprotein important

A

its a marker for liver cancer so high levels may suggest hepatocellular carcinoma

21
Q

management (TREAT THE CAUSE)

A

Avoid alcohol, sedatives, opiates, NSAIDs and drugs that affect the liver
Nutrition is important
Enteral supplements should be given
NG feeding may be indicated

22
Q

treating encephalopathy

A

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

23
Q

treating ascites

A

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

24
Q

treating spontaneous bacterial peritonitis

A

Antibiotics (e.g. cefuroxime and metronidazole)

Prophylaxis against recurrent SBP with ciprofloxacin

25
Q

surgical treatment

A

TIPS (trans jugular intrahepatic portosystemic shunt)

liver transplant is only CURE

26
Q

possible complications

A
Portal hypertension with ascites  
Hepatic encephalopathy 
Variceal haemorrhage  
SBP 
HCC 
Renal failure (hepatorenal syndrome)  
Pulmonary hypertension (hepatopulmonary syndrome)
27
Q

prognosis?

A

Generally poor prognosis
Overall 5 year survival = 50%
If ascites, 2 year survival = 50%