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Flashcards in Cirrhosis & its Consequences Deck (76)
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1

What is cirrhosis?

 

What is the end result of this process?

it is a diffuse process that results from liver cell necrosis followed by fibrosis and nodule formation

 

the end result is impairment of liver cell function and gross distortion of the liver architecture, leading to portal hypertension

2

What is the most common cause of cirrhosis?

  • alcohol is the most common cause in the western world

 

  • viral hepatitis is the most common cause worldwide

3

What are the 3 most common causes of cirrhosis and what are non-invasive markers of aetiology?

Alcohol:

  • history of excess alcohol consumption

 

Chronic hepatitis B:

  • HBsAg +/- HBeAg/DNA in serum

 

Chronic hepatitis C:

  • HCV antibodies and HCV RNA in serum

4

What are 4 other conditions that are commonly seen in clinical practice that can cause cirrhosis?

 

What are non-invasive markers of aetiology?

Haemochromatosis:

  • family history
  • raised serum ferritin + transferrin saturation

 

Non-alcoholic fatty liver disease:

  • features of the metabolic syndrome
  • hyperechoic liver on ultrasound

 

Primary biliary cirrhosis:

  • presence of serum antimitochondrial antibodies

 

Sclerosing cholangitis (primary & secondary):

  • most patients have IBD and serum pANCA
  • multifocal stricturing and dilatation of bile ducts on cholangiography (MRCP or ERCP)

5

What are non-invasive markers of aetiology for autoimmune hepatitis and cystic fibrosis, which can cause cirrhosis?

Autoimmune hepatitis:

  • circulating autoantibodies 
  • hypergammaglobulinaemia

 

Cystic fibrosis:

  • presence of extrahepatic manifestations of CF

6

What non-invasive markers of aetiology are present in Budd-Chiari syndrome, causing cirrhosis?

  • presence of known risk factors 

 

  • caudate lobe hypertrophy

 

  • abnormal flow in major hepatic veins on USS

7

What non-invasive markers of aetiology are present in Wilson's disease, leading to cirrhosis?

  • young age

 

  • reduced serum caeruloplasmin and total copper

 

  • increased 24-hour urinary copper excretion

 

  • Kayser-Fleisher rings 

8

What are non-invasive markers of aetiology in a1-antitrypsin (AAT) deficiency, leading to cirrhosis?

  • young age

 

  • associated emphysema

 

  • reduced serum AAT

9

What are the 2 different types of cirrhosis histologically?

  • micronodular cirrhosis

 

  • macronodular cirrhosis

 

  • there is a mixed picture, with both small and large nodules 

10

What is micronodular cirrhosis and when is this often seen?

  • characterised by uniform, small nodules up to 3mm in diameter

 

  • this is often caused by alcohol damage 

11

What is macronodular cirrhosis and what is this associated with?

  • this involves large nodules that are up to several centimetres in diameter

 

  • this often occurs following hepatitis B infection

12

What are the clinical features of cirrhosis a result of?

clinical features are secondary to portal hypertension and liver cell failure

13

What is the difference between compensated and uncompensated cirrhosis?

Uncompensated cirrhosis:

  • cirrhosis with the complications of encephalopathy, ascites or variceal haemorrhage

 

Compensated cirrhosis:

  • cirrhosis without any of these complications

14

Why are investigations carried out in cirrhosis?

  • to assess the severity of the liver disease

 

  • to identify the aetiology

 

  • to screen for complications 

15

What do liver biochemistry and liver function tests usually show in cirrhosis?

Liver biochemistry:

  • may be normal
  • in most people there is at least a slight elevation in serum alkaline phosphatase (ALP) and aminotransferase 

 

Liver function:

  • serum albumin is reduced
  • prothrombin time is prolonged 
  • these reflect reduced hepatic synthesis

16

What will serum electrolytes show in cirrhosis?

  • low sodium concentration indicates severe liver disease secondary to either impaired free water clearance or excess diuretic therapy

17

What is serum a-fetoprotein (AFP) and why is this test performed?

  • usually undetectable after foetal life, but raised levels may occur in chronic liver disease

 

  • measured to screen for complications of hepatocellular carcinoma (HCC)

 

  • normal range is 10-20 ng/mL

 

  • a level > 400 ng/mL is regarded as diagnostic of HCC

18

How is the aetiology of cirrhosis confirmed?

the cause is determined by the history combined with laboratory investigations

 

a liver biopsy is performed to confirm the severity and type of liver disease

19

What further investigations may be carried out in cirrhosis?

  • oesophageal varices are sought with endoscopy

 

  • USS is useful for detection of hepatocellular carcinoma (HCC)

 

  • USS is used to assess the patency of the portal and hepatic veins 

20

21

What is involved in the management of cirrhosis?

 

How are the underlying causes commonly corrected?

  • cirrhosis is irreversible, so treatment is aimed at treating the complications seen in decompensated cirrhosis as they arise

 

  • venesection is used to correct haemochromatosis

 

  • abstinence from alcohol is used to correct alcoholic hepatitis

 

  • correcting the underlying cause may halt the progression of liver disease

22

What 5 variables are used to grade the severity and prognosis of liver disease?

 

What is 5-year survival like?

  • encephalopathy

 

  • ascites

 

  • prothrombin time

 

  • serum bilirubin

 

  • serum albumin

 

  • overall the 5-year survival rate without transplantation is 50%

23

What are the 7 most common complications of cirrhosis?

  • portal hypertension and variceal haemorrhage

 

  • ascites
    • this can become infected ascites (spontaneous bacterial peritonitis)

 

  • portosystemic encephalopathy

 

  • acute renal failure (hepatorenal syndrome)

 

  • hepatocellular carcinoma (HCC)

 

  • malnutrition

 

  • osteoporosis

24

What is the role of the portal vein?

 

 

  • it carries blood from the gut and the spleen to the liver

 

  • it accounts for 75% of hepatic vascular inflow
    • the other 25% comes from the hepatic artery

25

How does blood enter and leave the liver?

  • blood enters the liver via the hepatic artery and the portal vein

 

  • these blood vessels enter the liver via the hilum (porta hepatis)

 

  • blood passes into the hepatic sinusoids via the portal tracts 

 

  • blood leaves the liver via the hepatic veins, which join the inferior vena cava

 

  • the vena cava returns blood to the right side of the heart

26

What is normal portal pressure?

 

What happens in portal hypertension?

  • normal portal pressure is 8 - 10 mmHg

 

  • portal hypertension occurs when there is an increase in pressure within the portal vein and its branches

 

  • these are draining blood from the intestines, stomach, pancreas etc. to the liver 

27

What happens when the inflow of portal blood to the liver is obstructed?

 

What site is the most significant for collateral formation?

  • the inflow of portal blood to the liver can be partially or completely obstructed at a number of sites

 

  • this leads to high blood pressure proximal to the obstruction and the diversion of blood into portosystemic collaterals

 

  • the most important site for collateral formation is at the gastro-oesophageal junction (varices)

 

  • here the collaterals are superficial and liable to rupture, causing massive gastrointestinal haemorrhage 

28

What are the 3 main sites of obstruction to the inflow of portal blood to the liver?

Prehepatic:

  • obstruction of the portal vein before it reaches the liver

 

Intrahepatic:

  • this results from distortion of the liver architecture

 

Posthepatic:

  • this results from obstruction of the hepatic veins

29

What is the main prehepatic cause of portal hypertension?

portal vein thrombosis

30

What are the main causes of intrahepatic portal hypertension?

  • cirrhosis

 

  • alcoholic hepatitis

 

  • idiopathic non-cirrhotic portal hypertension

 

  • schistosomiasis