Liver Cirrhosis Flashcards

1
Q

4 most common causes of liver cirrhosis?

A
  1. ALD
  2. NAFLD
  3. Hepatitis B
  4. Hepatits C
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2
Q

Rarer causes of liver cirrhosis

A

Autoimmune hepatitis

Primary biliary cirrhosis

Haemochromatosis

Wilsons disease

Alpha- 1 antitrypsin deficiency

Cystic fibrosis

Drugs (e.g. amiodarone, methotrexate, sodium valporate)

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3
Q

Pathophysiology of liver cirrhosis?

A
  • result of chronic inflammation and damage to liver cells
  • when the liver cells are damaged they are replaced with scar tissue (fibrosis) and nodules of scar tissue form within the liver
  • this fibrosis affects the structure and blood flow through the liver → causes increased resistance in the vessels leading in to the liver → this is called portal hypertension.
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4
Q

Signs of Cirrhosis on examination?

A
  • Jaundice → caused by raised bilirubin
  • Hepatomegaly → however the liver can shrink as it becomes more cirrhotic
  • Splenomegaly → due to portal hypertension
  • Spider Naevi → these are telangiectasia with a central arteriole and small vessels radiating away
  • Palmar erythema → caused by hyperdynamic circulation
  • Gynaecomastia (enlargement to male breasts) and testicular atrophy in males due to endocrine dysfunction
  • Bruising → due to abnormal clotting
  • Ascites
  • Caput medusae → distended paraumbilical veins due to portal hypertension
  • Asterixis → “flapping tremor” in decompensated liver disease
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5
Q

Blood test results would show: liver cirrhosis?

A
  • liver biochemistry is often normal, however in
    decompensated cirrhosis - All the markers (ALT, AST, ALP and bilirubin) become elevated.
  • Albumin and prothrombin time are useful markers of the “synthetic function” of the liver. The albumin levels drop and the prothrombin time increases as the synthetic function become worse.
  • Hyponatraemia indicates fluid retention in severe liver disease
  • Urea and creatinine become deranged in the hepatorenal syndrome
  • Further bloods can help establish the cause of the cirrhosis if unknown (such as viral markers and autoantibodies)
  • Alpha-fetoprotein is a tumour marker for hepatocellular carcinoma and can be checked every 6 months as a screening test in patients with cirrhosis along with ultrasound
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6
Q

First line test for assessing fibrosis in non-alcoholic fatty liver disease?

A

Enhanced liver fibrosis (ELF) blood test
- not currently available in many areas and cannot be used for diagnosing cirrhosis of other causes

  • measures 3 markers (HA, PIIINP and TIMP-1) and uses an algorithm to provide a result that indicates the fibrosis of the liver
  • < 7.7 indicatesnone to mild fibrosis
  • ≥ 7.7 to 9.8 indicatesmoderate fibrosis
  • ≥ 9.8 indicatessevere fibrosis
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7
Q

Apart from blood tests, what other investigations would I carry out for suspected liver cirrhosis?

A

Ultrasound

Fibroscan

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8
Q

Ultrasound: liver cirrhosis may show:

A
  • Nodularity of the surface of the liver
  • A “corkscrew” appearance to the arteries with increased flow as they compensate for reduced portal flow
  • Enlarged portal vein with reduced flow
  • Ascites
  • Splenomegaly

Ultrasound is also used as a screening tool for hepatocellular carcinoma. NICE recommend screening patients with cirrhosis for HCC every 6 months.

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9
Q

Firbsocan: liver cirrhosis

A

can be used to check the elasticity of the liver by sending high frequency sound waves into the liver. It helps assess the degree of cirrhosis. This is called “transient elastography” and should be used to test for cirrhosis. NICE recommend retesting every 2 years in patients at risk of cirrhosis:

  • Hepatitis C
  • Heavy alcohol drinkers (men drinking > 50 units or women drinking > 35 units per week)
  • Diagnosed alcoholic liver disease
  • Non alcoholic fatty liver disease and evidence of fibrosis on the ELF blood test
  • Chronic hepatitis B (although they suggest yearly for hep B)
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10
Q

when may endoscopy be used in terms of liver cirrhosis?

A

to assess for and treat oesophageal varices when portal hypertension is suspected

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11
Q

when may CT and MRI scans be used for liver cirrhosis?

A

to look for hepatocellular carcinoma, hepatosplenomegaly, abnormal blood vessel changes and ascites

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12
Q

when may liver biopsy be used: liver cirrhosis:

A

can be used to confirm the diagnosis of cirrhosis

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13
Q

What scoring would I use for liver cirrhosis severity?

A

Child-Pugh score for cirrhosis

Each factors is taken into account and given as score of 1, 2 or 3. Therefore the minimum score is 5 and the maximum score is 15. The score then indicates the severity of the cirrhosis and the prognosis.

Bilirubin: score 1 = <34, score 2 = 34-50, score 3 = >50

Albumin: score 1 = >35, score 2 = 28-35, score 3 = <28

INR: score 1 = <1.7, score 2 = 1.7-2.3, score 3 >2.3

Ascites: score 1= none, score 2 = mild, score 3 = moderate or severe

Encephalopathy: score 1 = none, score 2 = mild, score 3 = moderate or severe

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14
Q

General management of liver cirrhosis?

A
  • Ultrasound and alpha-fetoprotein every 6 months for hepatocellular carcinoma
  • Endoscopy every 3 years in patients without known varices
  • High protein, low sodium diet
  • MELD score every 6 months
  • Consideration of a liver transplant
  • Managing complications
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15
Q

Management of malnutrition:

A
  • Regular meals (every 2-3 hours)
  • Low sodium (to minimise fluid retention)
  • High protein and high calorie (particularly if underweight)
  • Avoid alcohol
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16
Q

Complications of liver cirrhosis

A
  • 5 year survival is overall about 50% once cirrhosis has developed

Malnutrition
Portal hypertension, Varices and Vieal Bleeding
Ascites
Spontaneous Bacterial Peritonitis (SBP)
Hepato-renal Syndrome
Hepatic Encephalopathy
Heptocellular Carinoma

17
Q

Explain why portal hypertension, varices and vieal bleeding are complications of liver cirrhosis

A

The portal veincomes from the superior mesenteric vein and thesplenic vein and delivers blood to the liver.

Liver cirrhosisincreases the resistance of blood flow in the liver. As a result, there is increased back-pressure into theportal system. This is called “portal hypertension”. This back-pressure causes the vessels at the sites where the portal systemanastomoseswith thesystemic venous systemto become swollen and tortuous. These swollen, tortuous vessels are calledvarices. They occur at the:

  • Gastro oesophageal junction
  • Ileocaecal junction
  • Rectum
  • Anterior abdominal wall via the umbilical vein (caput medusae)

Varices do not cause symptoms or problems until they start bleeding. Due to the high blood flow through varices, once they start bleeding patients canexsanguinate(bleed out) very quickly.

18
Q

Why do you get ascites with liver cirrhosis?

A

Ascites is basically fluid in the peritoneal cavity. The increased pressure in the portal system causes fluid to leak out of the capillaries in the liver and bowel and in to the peritoneal cavity.

The drop in circulating volume caused by fluid loss into the peritoneal space causes a reduction in blood pressure entering the kidneys.

The kidneys sense this lower pressure and releaserenin, which leads to increasedaldosteronesecretion (via therenin-angiotensin-aldosterone system) and reabsorption of fluid and sodium in the kidneys. Cirrhosis causes atransudative, meaning low protein content, ascites.

19
Q

Management of ascites?

A
  • Low sodium diet
  • Anti-aldosterone diuretics (spironolactone)
  • Paracentesis (ascitic tap or ascitic drain)
  • Prophylactic antibiotics against spontaneous bacterial peritonitis (ciprofloxacin or norfloxacin) in patients with less than 15g/litre of protein in the ascitic fluid
  • Consider TIPS procedure in refractory ascites
  • Consider transplantation in refractory ascites
20
Q

Management of SBP: complication of liver cirrhosis?

A

Management:

  • Take an ascitic culture prior to giving antibiotics
  • Usually treated with an IV cephalosporin such as cefotaxime
21
Q

Hepato-renal syndrome: complication of cirrhosis

A

Hepatorenal syndrome occurs inliver cirrhosis
Hypertension in theportal system leads to dilation of the portal blood vessels, stretched by large amounts of blood pooling there. This leads to a loss of blood volume in other areas of the circulation, including the kidneys. This leads hypotension in the kidney and activation of therenin-angiotensin system. This causes renalvasoconstriction, which combined with low circulation volume leads to starvation of blood to the kidney. This leads to rapid deteriorating kidney function.Hepatorenal syndrome is fatal within a week or so unless liver transplant is performed.

22
Q

Hepatic encephalopathy: complication of cirrhosis:

A
  • This is also known asportosystemic encephalopathy. It is thought to be caused by the build up of toxins that affect the brain. One toxin that is particularly worth remembering isammonia, which is produced by intestinal bacteria when they break down proteins and is absorbed in the gut. There are two reasons that ammonia builds up in the blood in patients with cirrhosis: Firstly, the functional impairment of the liver cells prevents them metabolising the ammonia into harmless waste products. Secondly, collateral vessels between the portal and systemic circulation mean that the ammonia bypasses liver altogether and enters the systemic system directly.
  • By giving laxatives we help clear the ammonia from the gut before it is absorbed and by giving antibiotics we reduce the number of bacteria in the gut producing ammonia.
  • Acutely, it presents with reduced consciousness and confusion. It can present in a more chronically with changes to personality, memory and mood.