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Y4 - CCC & PC > Liver Cirrhosis > Flashcards

Liver Cirrhosis Flashcards

1
Q

Why does liver cirrhosis occur?

A
  • it is the result of chronic inflammation that damages the liver cells
  • damaged liver cells are replaced with scar tissue (fibrosis)
  • nodules of scar tissue form within the liver
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2
Q

Why does portal hypertension occur in cirrhosis?

A
  • fibrosis affects the structure and blood flow through the liver
  • there is increased resistance in the vessels leading to the liver
  • this results in an increased pressure in the portal system
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3
Q

What are the most common causes of cirrhosis?

A
  • hepatitis B
  • hepatitis C
  • alcoholic liver disease
  • non alcoholic fatty liver disease
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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

it is important to consider these as some of them are potentially reversible

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5
Q

Which drugs can potentially cause cirrhosis?

A
  • S - sodium valproate
  • A - amiodarone
  • M - methotrexate

remember - SAM

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6
Q

What are the signs of cirrhosis?

A
  • jaundice (raised bilirubin)
  • caput medusae (portal HTN)
  • palmar erythema (hyperdynamic circulation)
  • gynaecomastia / testicular atrophy (endocrine dysfunction)
  • bruising (abnormal clotting)
  • ascites
  • spider naevi
  • hepatomegaly (but liver then shrinks as it becomes more cirrhotic)
  • splenomegaly (portal HTN)
  • asterixis (in decompensated disease)
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7
Q

What are spider naevi?

A

telangiectasia with a central arteriole and small vessels radiating away

telangiectasia (“spider veins”) - dilated / broken blood vessels near the surface of the skin

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8
Q

What blood tests are performed in cirrhosis?

A

LFTs:
* usually normal

  • all markers become deranged in decompensated disease (ALP, AST, ALT + bilirubin)

albumin + prothrombin time:

  • markers of synthetic function
  • low albumin and raised PTT is seen

U&Es:

  • hyponatraemia indicates fluid retention in severe disease

urea + creatinine:

  • deranged in hepatorenal syndrome

alpha-fetoprotein:

  • tumour marker for HCC
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9
Q

Why is alpha-fetoprotein (AFP) measured in cirrhosis?

A
  • it is a tumour marker for hepatocellular carcinoma
  • it should be checked every 6 months with USS
  • this is a screening test for HCC
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10
Q

What is the enhanced liver fibrosis (ELF) blood test?

When is it used?

A
  • first line investigation for assessing fibrosis in NAFLD
  • cannot be used for diagnosing cirrhosis of other causes

it is currently not available in many areas

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11
Q

How can the ELF score be used to determine whether fibrosis is present?

A
  • a score < 7.7 indicates no or mild fibrosis
  • a score 7.7 - 9.8 indicates moderate fibrosis
  • a score of 9.8 or higher indicates severe fibrosis

it measures 3 markers - HA, PIIINP and TIMP-1

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12
Q

What may be seen on ultrasound in cirrhosis?

A
  • nodularity of the surface of the liver
  • “corkscrew” appearance of arteries with increased flow
  • enlarged portal vein with reduced flow
  • ascites
  • splenomegaly
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13
Q

When is a patient with cirrhosis offered an USS?

A
  • NICE recommend AFP + USS every 6 months in patients with cirrhosis
  • this screens for HCC
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14
Q

What is FibroScan and what does it test for?

A
  • it checks the elasticity of the liver by sending high frequency sound waves into it
  • this assesses the degree of cirrhosis

it is called “transient elastography”

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15
Q

How frequently should a FibroScan be performed?

A
  • it should be performed every 2 years in patients at risk of cirrhosis
  1. hepatitis C
  2. heavy alcohol drinkers
  3. NAFLD + evidence of fibrosis on ELF test
  4. alcoholic liver disease
  • it should be performed yearly in chronic hepatitis B

heavy alcohol drinkers = > 50 units for men and > 35 units for women per week

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16
Q

When is endoscopy performed in cirrhosis?

A

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

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17
Q

When may CT and MRI scans be performed in cirrhosis?

A

to look for:

  • hepatocellular carcinoma
  • hepatosplenomegaly
  • ascites
  • abnormal blood vessel changes
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18
Q

What test is needed to make a definitive diagnosis of cirrhosis?

A

liver biopsy

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19
Q

What score is used to indicate the severity of cirrhosis?

A

Child-Pugh score

indicates severity of cirrhosis and prognosis

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20
Q

What parameters are used to calculate the Child-Pugh score?

A
  • encephalopathy
  • INR
  • bilirubin
  • albumin
  • ascites
  • each parameter is given a score of 1, 2 or 3

(remember parameters as EIBAA)

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21
Q

What is the MELD score and when is it used?

A
  • it is used every 6 months in patients with compensated cirrhosis
  • it assesses whether they require dialysis
  • it gives a 3-month estimated mortality which helps guide referral for liver transplant
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22
Q

What parameters are included in the MELD score?

A
  • bilirubin
  • INR
  • creatinine
  • sodium

remember parameters as BICS

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23
Q

What stages are involved in the general management of cirrhosis?

A
  • USS + AFP every 6 months to assess for HCC
  • MELD score every 6 months
  • high protein and low sodium diet
  • endoscopy every 3 years (in patients without known varices)
  • consider liver transplant
  • manage complications
24
Q

How is the prognosis of cirrhosis estimated?

A
  • through use of the Child-Pugh and MELD scores
  • disease course is variable
  • 5-year survival is around 50%
25
Q

What are the potential complications of cirrhosis?

A
  • malnutrition
  • hepatorenal syndrome
  • ascites + spontaneous bacterial peritonitis
  • hepatic encephalopathy
  • hepatocellular carcinoma
  • portal hypertension, varices + bleeding
26
Q

Why is a liver biopsy no longer recommended by NICE as a diagnostic tool for cirrhosis?

A
  • the procedure is associated with adverse effects, such as bleeding and pain
  • FibroScan and imaging are used instead
  • ELF score is used in NAFLD
27
Q

Why does malnutrition occur in cirrhosis and what are the consequences of this?

A
  • cirrhosis affects metabolism of proteins in the liver, reducing the amount of protein produced
  • it affects the ability to store glucose as glycogen, leading to use of muscle tissue as fuel
  • this leads to muscle wasting + weight loss
28
Q

How is malnutrition as a result of cirrhosis managed?

A
  • regular meals (every 2-3 hours)
  • low sodium diet (to minimise fluid retention)
  • high protein + high calorie diet
  • avoid alcohol
29
Q

What is the portal vein formed from?

What happens in portal hypertension?

A
  • the portal vein is formed from the superior mesenteric vein and splenic vein
  • in cirrhosis there is increased resistance to blood flow in the liver
  • this leads to increased back-pressure in the portal system
30
Q

How does portal hypertension result in varices?

A
  • there is increased back-pressure in the portal system
  • this causes the vessels to become swollen / tortuous at the sites where the portal system anastomoses with the systemic venous system
  • varices are swollen, tortuous vessels
31
Q

At which sites do varices develop?

A
  • gastro-oesophageal junction
  • ileocaecal junction
  • rectum
  • anterior abdominal wall via the umbilical vein (caput medusae)
caput medusae
32
Q

What are the symptoms associated with varices?

A
  • varices do not produce symptoms until they start bleeding
  • there is a high blood flow through varices
  • patients can exsanguinate (bleed out) very quicky
33
Q

What are the 3 main options for the treatment of stable varices?

A

propanolol:

  • acts as a non-selective beta blocker to reduce portal HTN

elastic band ligation

injection of sclerosant:

  • less effective than band ligation
34
Q

What is involved in the transjugular intra-hepatic portosystemic shunt (TIPS) procedure?

A
  • a wire is inserted under XR guidance
  • the wire passes through the jugular vein, down the vena cava and into the liver via the hepatic vein
  • a connection is made between the hepatic vein and portal vein
  • a stent is put into place
  • this allows blood to flow directly from the portal vein into the hepatic vein to relieve the pressure in the portal system + varices
35
Q

When is a TIPS procedure performed?

A
  • if medical and endoscopic treatment of varices fails

OR

  • there are bleeding varices that cannot be controlled in other ways
36
Q

What are the 4 stages involved in resuscitation when there are bleeding oesophageal varices?

A

terlipressin:
* or other vasopressin analogue

  • causes vasoconstriction and slows bleeding

correct coagulopathy:

  • with vitamin K and FFP

broad spectrum abx:

  • prophylactic abx reduces mortality

intubation / ICU:

  • consider ICU as patients can become life-threateningly unwell

FFP = fresh frozen plasma which contains many clotting factors

37
Q

What is required urgently when oesophageal varices are bleeding?

A
  • following resuscitation, urgent endoscopy is required
  • there may be injection of sclerosant into the varices to cause “inflammatory obliteration”
  • or elastic band ligation of varices
38
Q

What is done if endoscopy fails to control bleeding varices?

A

Sengstaken-Blakemore tube

  • an inflatable tube inserted into the oesophagus to tamponade the bleeding varices
39
Q

Why does ascites occur as a result of cirrhosis?

A
  • increased pressure in the portal system causes fluid to leak out of the capillaries in the liver / bowel
  • fluid enters the peritoneal cavity
40
Q

How does ascites affect the kidneys?

A
  • there is a drop in circulating volume as fluid is lost into the peritoneal space
  • kidneys secrete renin as a result of lower BP
  • renin leads to increased aldosterone secretion
  • there is increased reabsorption of fluid + sodium in the kidneys
41
Q

What type of ascites is caused by cirrhosis?

A

transudative ascites

i.e. low protein content

42
Q

What is involved in the management of ascites?

A
  • low sodium diet
  • anti-aldosterone diuretics (spironolactone)
  • paracentesis (ascitic tap / drain)
  • consider TIPS procedure / transplantation in refractory ascites
  • prophylactic antibiotics
43
Q

Why are prophylactic antibiotics given in ascites?

What antibiotics are given?

A
  • to reduce the risk of spontaneous bacterial peritonitis (SBP)
  • ciprofloxacin or norfloxacin are given
  • given to all patients with < 15g/L protein in the ascitic fluid
44
Q

When does ascites become clinically detectable?

A

it is not detectable until there is at least 500ml fluid present

45
Q

What are the clinical features of ascites?

A
  • abdominal distension / discomfort
  • weight gain
  • reduced appetite
  • shortness of breath (due to diaphragmatic splinting in large volume ascites)
46
Q

How is a sample of ascitic fluid obtained?

What colour would this be in cirrhosis?

A
  • a sample is obtained using a neddle and syringe
  • this is called “ascitic tap” or “paracentesis”
  • fluid is clear / straw coloured in cirrhosis
47
Q

What is spontaneous bacterial peritonitis (SBP)?

A

an infection developing in the ascitic fluid + peritoneal lining without any clear cause

(e.g. not secondary to ascitic drain / bowel perforation)

occurs in around 10% of patients with ascites secondary to cirrhosis

48
Q

How does SBP present?

A
  • it can be asymptomatic
  • fever
  • abdominal pain
  • deranged bloods (raised WCC, CRP, creatinine / metabolic acidosis)
  • ileus
  • hypotension

as it can be asymptomatic, there should be a low threshold for ascitic fluid culture

49
Q

What are the most common causative organisms of SBP?

A
  • Escherichia coli
  • Klebsiella pneumoniae
  • Gram positive cocci (staphylococcus / enterococcus)
50
Q

What is involved in the management of SBP?

A
  • take an ascitic culture prior to giving antibiotics
  • usually treated with IV cephalosporin - e.g. cefotaxime
51
Q

What is hepatorenal syndrome and why does it occur?

A
  • hypertension in the portal system leads to dilation of portal blood vessels
  • blood pools in the portal vessels
  • there is a loss of blood volume in other areas of circulation
  • there is activation of the RAAS due to reduced kidney BP
  • this results in renal vasoconstriction
  • renal vasoconstriction and low circulatory volume starves the kidneys of blood
  • there is rapidly deteriorating kidney function
52
Q

What is the treatment for hepatorenal syndrome?

A

liver transplant

hepatorenal syndrome is fatal within 1 week if transplant is not performed

53
Q

What causes hepatic encephalopathy?

A
  • a build up of toxins in the blood - particularly ammonia
  • ammonia is produced by intestinal bacteria when they break down proteins and is absorbed in the gut
54
Q

Why does ammonia build up in the blood in cirrhosis?

A
  • functional impairment of hepatocytes prevents metabolism of ammonia into harmless waste products
  • collateral vessels between the portal / systemic circulation means ammonia can bypass the liver and directly enter the systemic circulation
55
Q

How does hepatic encephalopathy present?

A

acute presentation:

  • reduced consciousness
  • confusion

chronic presentation:

  • changes to personality / mood
  • memory disturbances
56
Q

What are the precipitating factors for hepatic encephalopathy?

A
  • constipation
  • electrolyte disturbances
  • infection
  • GI bleeding
  • high protein diet
  • medications (sedatives)

Y4 - CCC & PC (34 decks)

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