Chronic Liver Disease Flashcards
Describe Cirrhosis
Liver cirrhosis is the 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, which causes increased resistance in the vessels leading in to the liver. This is called portal hypertension.
Most common causes of liver cirrhosis?
Alcoholic liver disease
Non Alcoholic Fatty Liver Disease
Hepatitis B
Hepatitis C
Rarer causes
Autoimmune hepatitis Primary biliary cirrhosis Haemochromatosis Wilsons Disease Alpha-1 antitrypsin deficiency Cystic fibrosis Drugs (e.g. amiodarone, methotrexate, sodium valproate)
Signs of cirrhosis
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 cirulation
Gynaecomastia 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
Liver biochemistry results
Liver biochemistry is often normal, however in decompensated cirrhosis all of the markers (ALT, AST, ALP and bilirubin) become deranged.
Albumin and prothrombin
Albumin and prothrombin time are useful markers of the “synthetic function” of the liver. The albumin level drops and the prothrombin time increases as the synthetic function becomes worse.
what does hyponatraemia indicate?
Hyponatraemia indicates fluid retention in severe liver disease.
Urea and Cr
Urea and creatinine become deranged in hepatorenal syndrome.
What is alpha-fetoprotein and when is it tested?
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.
Ultrasound in cirrhosis
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.
Fibroscan
“FibroScan” 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)
endoscopy
Endoscopy can be used to assess for and treat oesophageal varices when portal hypertension is suspected.
CT and MRI
CT and MRI can be used to look for hepatocellular carcinoma, hepatosplenomegaly, abnormal blood vessel changes and ascites.
Liver biopsy
Liver biopsy can be used to confirm the diagnosis of cirrhosis.
What makes up the child-pugh score?
Bilirubin
<34
34-50
>50
Albumin
>35
28-35
<28
INR
<1.7
1.7-2.3
>2.3
Ascites
None
Mild
Moderate or severe
Encephalopathy
None
Mild
Moderate or severe
MELD score
The MELD score is recommended by NICE to be used every 6 months in patients with compensated cirrhosis. It is a formula that takes into account the bilirubin, creatinine, INR and sodium and whether they are requiring dialysis. It gives a percentage estimated 3 month mortality and helps guide referral for liver transplant.
Management
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 as below
Complications of cirrhosis
Malnutrition
Portal Hypertension, Varices and Variceal Bleeding
Ascites and Spontaneous Bacterial Peritonitis (SBP)
Hepato-renal Syndrome
Hepatic Encephalopathy
Hepatocellular Carcinoma
Malnutrition in cirrhosis
Cirrhosis leads to malnutrition and muscle wasting. A simplified explanation of this is that it leads to increased use of muscle tissue as fuel and reduces the protein available in the body for muscle growth. Cirrhosis affects the metabolism of proteins in the liver and reduces the amount of protein produced. It also disrupts the livers ability to store glucose as glycogen and release it when required. This results in the body using muscle tissue as fuel leading to muscle wasting and weight loss.
managing malnutrition
Regular meals (every 2-3 hours) Low sodium (to minimise fluid retention) High protein and high calorie (particularly if underweight) Avoid alcohol
Ascites
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 release renin, which leads to increased aldosterone secretion (via the renin-angiotensin-aldosterone system) and reabsorption of fluid and sodium in the kidneys.
What kind of ascites does cirrhosis cause?
Cirrhosis causes a transudative, meaning low protein content, ascites.
Managing ascites
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
What is SBP?
Spontaneous Bacterial Peritonitis (SBP)
This occurs in around 10% of patients with ascites secondary to cirrhosis and can have a mortality of 10-20%. It involves an infection developing in the ascitic fluid and peritoneal lining without any clear cause (e.g. not secondary to an ascitic drain or bowel perforation).
How does SBP present?
Can be asymptomatic so have a low threshold for ascitic fluid culture
Fever
Abdominal pain
Deranged bloods (raised WBC, CRP, creatinine or metabolic acidosis)
Ileus
Hypotension
How does SBP present?
Can be asymptomatic so have a low threshold for ascitic fluid culture
Fever
Abdominal pain
Deranged bloods (raised WBC, CRP, creatinine or metabolic acidosis)
Ileus
Hypotension
most common organisms in SBP?
Escherichia coli
Klebsiella pnuemoniae
Gram positive cocci (such as staphylococcus and enterococcus)
managing SBP
Take an ascitic culture prior to giving antibiotics
Usually treated with an IV cephalosporin such as cefotaxime
What is hepatorenal syndrome?
Hepatorenal syndrome occurs in liver cirrhosis. Hypertension in the portal 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 the renin-angiotensin system. This causes renal vasoconstriction, 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.
What causes hepatic encephalopathy?
thought to be caused by the build up of toxins that affect the brain. One toxin that is particularly worth remembering is ammonia, which is produced by intestinal bacteria
How does ammonia build up
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.
How does hepatic encephalopathy present?
Acutely, it presents with reduced consciousness and confusion. It can present in a more chronically with changes to personality, memory and mood.
Hepatic encephalopathy precipitating factors
Constipation Electrolyte disturbance Infection GI bleed High protein diet Medications (particularly sedative medications)
Management of hepatic encephalopathy
Laxatives (i.e. lactulose) promote the excretion of ammonia. The aim is 2-3 soft motions daily. They may require enemas initially.
Antibiotics (i.e. rifaximin) reduces the number of intestinal bacteria producing ammonia. Rifaximin is useful as it is poorly absorbed and so stays in the GI tract.
Nutritional support. They may need nasogastric feeding.
