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Liver Cirrhosis Flashcards

1
Q

What is liver cirrhosis?

A

Liver cirrhosis is the result of chronic inflammation and damage to liver cells.
The functional liver cells are replaced with scar tissue (fibrosis).
Nodules of scar tissue form within the liver

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2
Q

How does fibrosis affect liver function?

A

Fibrosis affects the structure and blood flow through the liver, increasing the resistance in the vessels leading into the liver.

This increased resistance and pressure in the portal system is called portal hypertension

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3
Q

What are the 4 common causes of liver cirrhosis?

A

Alcohol-related liver disease
Non-alcoholic fatty liver disease (NAFLD)
Hepatitis B
Hepatitis C

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4
Q

What are some of the rarer causes of cirrhosis?

A

Autoimmune hepatitis
Primary biliary cirrhosis
Haemochromatosis
Wilsons disease
Alpha-1 antitrypsin deficiency
Cystic fibrosis
Drugs (e.g., amiodarone, methotrexate and sodium valproate)

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5
Q

What are some of the findings on examination which would suggest liver cirrhosis?

A

Cachexia (wasting of the body and muscles)
Jaundice (raised bilirubin)
Hepatomegaly
Small nodular liver (as it becomes more cirrhotic
Splenomegaly (due to portal hypertension)
Spider naevi
Palmar erythema
Gynaecomastia and testicular atrophy
Bruising (abnormal clotting)
Excoriations (scratches on the skin due to itching)
Ascites (fluid in the peritoneal cavity)
Caput medusae (distended paraumbilical veins due to portal hypertension)
Leukonychia (white fingernails associated with hypoalbuminemia)
Asterixis “flapping tremor” in decompensated liver disease

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6
Q

When would you do a non-invasive liver screen?

A

When there are abnormal liver function tests without a clear cause

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7
Q

What tests are involved in the non-invasive liver screen?

A
  • Ultrasound liver (used to diagnose fatty liver)
  • Hepatitis B and C serology
  • Autoantibodies (autoimmune hepatitis, primary biliary cirrhosis and primary sclerosing cholangitis)
  • Immunoglobulins (autoimmune hepatitis and primary biliary cirrhosis)
  • Caeruloplasmin (Wilsons disease)
  • Alpha-1 antitrypsin levels (alpha-1 antitrypsin deficiency)
  • Ferritin and transferrin saturation (hereditary haemochromatosis)
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8
Q

What are the autoantibodies with are relevant to liver disease?

A

Antinuclear antibodies (ANA)
Smooth muscle antibodies (SMA)
Antimitochondrial antibodies (AMA)
Antibodies to liver kidney microsome type-1 (LKM-1)

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9
Q

What will the LFT results show in decompensated cirrhosis?

A

Raised:
Bilirubin
Alanine transaminase (ALT)
Aspartate transferase (AST)
Alkaline phosphatase (ALP)

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10
Q

What other blood tests should be done in suspected liver cirrhosis and what would they show for certain causes?

A
  • Low albumin due to reduced synthetic function of the liver
  • Increased prothrombin time due to reduced synthetic function of the liver (reduced production of clotting factors)
  • Thrombocytopenia (low platelets) is a common finding and indicates a more advanced disease
  • Hyponatremia (low sodium) occurs with fluid retention in severe liver disease
  • Urea and creatinine become deranged in hepatorenal syndrome
  • Alpha-fetoprotein is a tumor marker for hepatocellular carcinoma
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11
Q

What does the enhanced liver fibrosis blood test do?

A

it is the first-line investigation for assessing fibrosis in NAFLD.

It measures three markers (HA, PIIINP and TIMP-1) and uses an algorithm to provide a result that indicated whether they have advanced fibrosis of the liver?

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12
Q

What enhanced liver fibrosis blood test score indicates they have advanced fibrosis?

A

10.51 or above

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13
Q

What would an ultrasound scan show in liver cirrhosis?

A

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

Also used as a screening tool for hepatocellular carcinoma

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14
Q

What is transient elastography?

A

Transient elastography “FibroScan” is used to assess the stiffness of the liver using high-frequency sound waves. It helps determine the degree of fibrosis (scarring) to test for liver cirrhosis.

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15
Q

A fibro scan is used to assess patients at risk of cirrhosis, what groups of people are included in this?

A

Alcohol-related liver disease
Heavy alcohol drinkers (men more than 50 units or women more than 35 units)
NAFLD and advanced liver fibrosis (more than 10.51)
Hepatitis C
Chronic hep B

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16
Q

What other investigations would you perform with someone with liver cirrhosis?

A

Endoscopy can be used to assess for and treat oesophageal varices when portal hypertension is suspected.

CT and MRI can be used to look for hepatocellular carcinoma, hepatosplenomegaly, abnormal blood vessel changes, and ascites.

Liver biopsy can be used to confirm the diagnosis of cirrhosis.

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17
Q

What is the MELD score>

A

(Model for End-Stage Liver Disease) the score should be calculated every 6 months in patients with compensated cirrhosis.

The formula considers the bilirubin, creatinine, INR, and sodium and whether they require dialysis, giving an estimated 3-month mortality as a percentage.

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18
Q

What is the child-pugh score?

A

The Child-Pugh scores use 5 factors to assess the severity of cirrhosis and the prognosis. Each factor is considered and scored 1, 2, or 3. The minimum overall score is 5 (scoring 1 for each factor), and the maximum is 15 (scoring 3 for each factor). You can remember the features with the “ABCDE” mnemonic:

A – Albumin
B – Bilirubin
C – Clotting (INR)
D – Dilation (ascites)
E – Encephalopathy

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19
Q

What are the four principles which underlie the general management of liver cirrhosis?

A
  1. Treating the underlying cause
  2. Monitoring for complications
  3. Managing complications
  4. Liver transplant
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20
Q

What are examples of treating the underlying cause?

A
  1. Stop drinking alcohol
  2. Lifestyle changes for non-alcohol fatty liver disease
  3. Antiviral drugs for hepatitis C
  4. Immunosuppressants for autoimmune hepatitis
21
Q

What monitoring can be conducted for monitoring complications of liver cirrhosis?

A

MELD score every 6 months
Ultrasound and alpha-fetoprotein every 6 months for hepatocellular carcinoma
Endoscopy every 3 years for oesophageal varices

22
Q

When is liver transplantation considered?

A

When there are features of decompensated liver disease. AHOY mnemonic

A - Ascites
H - Hepatic encephalopathy
O - oesophageal varices bleeding
Y - Yellow (jaundice)

23
Q

What are the important complications of liver cirrhosis?

A

Malnutrition and muscle wasting
Portal hypertension, oesophageal varices and bleeding varices
Ascites and spontaneous bacterial peritonitis
Hepatorenal syndrome
Hepatic encephalopathy
Hepatocellular carcinoma

24
Q

Why is malnutrition a complication of liver cirrhosis?

A

Patients often have a loss of appetite resulting in reduced intake.
Cirrhosis affects protein metabolism in the liver and reduced the amount of protein the liver produces
It also disrupts the ability of the liver to store glucose as glycogen and release it when required.
Less protein is available for maintaining muscle tissue and muscle tissue is broken down for use as fuel.

25
Q

What are the management options for malnutrition as a complication of liver cirrhosis?

A

Nutritional support guided by a dietician with
- Regular meals
- High protein and calorie intake
- Reduced-sodium intake to minimise fluid retention
- Avoiding alcohol

26
Q

How is portal hypertension a complication of liver cirrhosis?

A

Liver cirrhosis increases the resistance to blood flow in the liver. As a result, there is increased back pressure on the portal system. This is called portal hypertension. The back pressure of blood results in splenomegaly.

27
Q

What effects does portal hypertension have at the PVS and SVS collaterals?

A

Back pressure forms at several locations
- Distal esophagus -> causing esophagus varices
- Anterior abdominal wall -> causing esophageal varices
- Rectum -> causing rectal hemorrhages

28
Q

What are the dangers of esophageal varices?

A

Varices are asymptomatic until they start bleeding. Due to the high blood flow, bleeding from varices can cause patients to exsanguinate (bleed out) very quickly.

29
Q

What are the management options for stable esophageal varices?

A

Non-selective beta blockers (e.g., propranolol) first-line
Variceal band ligation (if beta blockers are contraindicated)

Variceal band ligation involves a rubber band wrapped around the base of the varices, cutting off the blood flow through the vessels.

30
Q

What are the management options for bleeding esophageal varices?

A
  • Immediate senior help
  • Consider blood transfusion (activate the major haemorrhage protocol)
  • Treat any coagulopathy (e.g., with fresh frozen plasma)
  • Vasopressin analogues (e.g., terlipressin or somatostatin) cause vasoconstriction and slow bleeding
  • Prophylactic broad-spectrum antibiotics (shown to reduce mortality)
  • Urgent endoscopy with variceal band ligation
  • Consider intubation and intensive care
31
Q

What other options are there to control the bleeding in oesophageal varices?

A

Sengstaken-Blakemore tube
Transjugular intrahepatic portosystemic shunt (TIPS)

32
Q

What is a Sengstaken-Blakemore tube?

A

An inflatable tube inserted into the oesophagus to tamponade the bleeding varices

33
Q

What is a Transjugular intrahepatic portosystemic shunt (TIPS)?

A

TIPS is a technique where an interventional radiologist inserts a wire under x-ray guidance into the jugular vein, down the vena cava and into the liver via the hepatic vein. A connection is made through the liver between the hepatic vein and portal vein, and a stent is inserted. This allows blood to flow directly from the portal vein to the hepatic vein, relieving the pressure in the portal system.

The two main indications are:
- Bleeding oesophageal varices
- Refractory ascites

34
Q

What are ascites?

A

Ascites refer to fluid in the peritoneal cavity.

35
Q

How do ascites form?

A

The increased pressure in the PVS causes fluid to leak out of the capillaries in the liver and other abdominal organs into the peritoneal cavity.

The drop in circulating volume caused by fluid loss into the peritoneal cavity causes reduced blood pressure in the kidneys.

The kidneys sense this lower pressure and release renin, which leads to increased aldosterone secretion via the renin-angiotensin-aldosterone system.

Increased aldosterone causes the reabsorption of fluid and sodium in the kidneys, leading to fluid and sodium retention.

Cirrhosis causes transudative (low protein content) ascites)

36
Q

What are the management options for ascites?

A
  • Low sodium diet
  • Aldosterone antagonists (e.g., spironolactone)
  • Paracentesis (ascitic tap or ascitic drain)
  • Prophylactic antibiotics (ciprofloxacin or norfloxacin) when there is <15 g/litre of protein in the ascitic fluid
  • Transjugular intrahepatic portosystemic shunt (TIPS) is considered in refractory ascites
  • Liver transplantation is considered in refractory ascites
37
Q

What is spontaneous bacterial peritonitis?

A

Spontaneous bacterial peritonitis (SBP) occurs in 10-20% of patients with ascites. It has a mortality of 10-20%. It involves an infection developing in the ascitic fluid and peritoneal lining without a clear source of infection (e.g., an ascitic drain or bowel perforation).

38
Q

What are the presenting features of spontaneous bacterial peritonitis?

A

It can be asymptomatic, but presenting features include
- Fever
- Abdominal pain
- Deranged blood (raised WBC, CRP, creatinine, or metabolic acidosis)
- Ileus (reduced movement in the intestines)
- Hypotension

39
Q

What are the most common organisms which cause spontaneous bacterial peritonitis?

A

Escherichia coli
Klebsiella pneumoniae

40
Q

What are the management options for spontaneous bacterial peritonitis?

A
  • Taking a sample of ascites fluid for culture before giving antibiotics
  • Intravenous broad-spectrum antibiotics according to local policies (eg piperacillin with tazobactam)
41
Q

What is hepatorenal syndrome?

A

Impaired kidney function is caused by changes in the blood flow to the kidneys relating to liver cirrhosis and portal hypertension.

42
Q

What is the pathophysiology of hepatorenal syndrome?

A

Portal hypertension causes the portal vessels to release vasodilators, which cause significant vasodilation in the splanchnic circulation (the vessels supplying the gastrointestinal organs).

Vasodilation leads to reduced blood pressure - kidneys respond by activating the renin-angiotensin-aldosterone system, which leads to vasoconstriction of the renal vessels.

Renal vasoconstriction combined with low systemic pressure results in the kidneys being starved of blood and significantly reduced kidney function.

It has a poor prognosis unless the patient has a liver transplant.

43
Q

What is hepatic encephalopathy?

A

It is the build-up of neurotoxic substances that affect the brain.

44
Q

What is the effect of ammonia on hepatic encephalopathy?

A

Ammonia is produced by intestinal bacteria when they break down proteins. Ammonia is absorbed in the intestines.

In liver cirrhosis:
- The liver cells functional impairment prevents them from metabolising the ammonia into harmless waste products.
- Collateral vessels between the PVS and the SVS mean that the ammonia bypasses the liver and enters the SVS directly

45
Q

How does hepatic encephalopathy present?

A

Acutely it presents with reduced consciousness and confusion
It can also present more chronically with changes to personality, memory and mood.

46
Q

What factors can worsen hepatic encephalopathy?

A

Constipation
Dehydration
Electrolyte disturbance
Infection
GI bleeding
High protein diet
Medications (particularly sedative medications)

47
Q

What are the management options for hepatic encephalopathy?

A

Lactulose (aiming for 2-3 soft stools daily)
Antibiotics (eg, rifaximin to reduce the number of intestinal bacteria producing ammonia)
Nutritional support (nasogastric feeding may be required)

48
Q

How does lactulose work to reduce ammonia?

A
  • It speeds up transit time and reduces constipation (the laxative effect cleaning the ammonia before it is absorbed)
  • Promotes bacterial uptake of ammonia to be used for protein synthesis
  • Changes the pH of the contents of the intestine to become more acidic, killing ammonia-producing bacteria

GI (13 decks)

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