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Medicine > Gastro - Liver Cirrhosis > Flashcards

Gastro - Liver Cirrhosis Flashcards

1
Q

What is liver cirrhosis a result of?

A

Chronic inflammation
Damage to hepatocytes

Functional cells replaced with scar tissue

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2
Q

What effect does fibrosis have in the liver?

A

Structural
Blood flow

Leads to an increase in resistance

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3
Q

What effect does increased resistance have on hepatic vasculature?

A

Portal hypertension

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4
Q

What are the common causes of liver cirrhosis?

A

Alcohol-related liver disease
Non-alcoholic fatty liver disease
Hepatitis B
Hepatitis C

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5
Q

What are the rarer causes of liver cirrhosis?

A
  • Autoimmune hepatitis
  • Primary biliary cirrhosis
  • Haemochromatosis
  • Wilson’s disease
  • Alpha-1 antitrypsin deficiency
  • Cystic fibrosis
  • Amiodarone, methotrexate and sodium valproate
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6
Q

What are the examination findings of liver cirrhosis?

A

ALCOHOLICS
Ascites
Liver flap (asterixis)
Cachexia
Oversized spleen
Hand signs - palmar erythema, leukonychia
Oversized liver
Long INR and bruising
Itching
Caput medusae
Spider naevi

Jaundice
Gynaecomastia and testicular atrophy

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7
Q

What causes small nodular liver, splenomegaly and palmar erythema?

A

Small nodular liver
As the liver becomes more cirrhotic and covered in nodules it atrophies

Splenomegaly
Portal hypertension

Palmar erythema
Raised oestrogen levels

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8
Q

What causes gynaecomastia and testicular atrophy?

A

Endocrine dysfunction

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9
Q

What causes bruising, excoriations, caput medusae, leukonychia and asterixis?

A

Bruising
Abnormal clotting

Excoriations
Extreme itching as the liver loses function

Caput medusae
Portal hypertension

Leukonychia
Hypoalbuminaemia

Asterixis
Decompensated liver disease

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10
Q

When is a non-invasive liver screen carried out?

A

Abnormal lfts with no clear cause

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11
Q

What does a non-invasive liver screen involve?

A

Ultrasound liver (diagnose fatty liver)
Hepatitis B and C serology
Autoantibodies
Immunoglobulins
Caeruloplasmin
Alpha-1 antitrypsin levels
Ferritin and transferrin saturation

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12
Q

What autoimmune conditions are looked at in a non-invasive liver screen?

A

Autoimmune hepatitis
Primary biliary cirrhosis
Primary sclerosing cholangitis

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13
Q

What immunoglobulins are looked at in a non-invasive liver screen?

A

Autoimmune hepatitis
Primary biliary cirrhosis

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14
Q

What is caeruloplasmin a marker of?

A

Wilson’s disease

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15
Q

Why do you look at ferritin and transferrin saturation?

A

Hereditary haemochromatosis

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16
Q

What autoantibodies 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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17
Q

What is the difference between cirrhosis and decompensated cirrhosis?

A

May have normal LFTs cirrhosis

In decompensated all liver markers are deranged with raised
Bilirubin, ALT,AST and ALP

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18
Q

What other blood test results indicate decompensated liver disease?

A

Low albumin
Increased prothrombin time
Thrombocytopenia
Hyponatraemia
Urea and creatinine (hepatorenal syndrome)
Alpha-fetoprotein (hepatocellular carcinoma tumour marker)

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19
Q

What is the enhanced liver fibrosis test used for?

A

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

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20
Q

What markers are looked at in enhanced liver fibrosis blood test?

A

HA
P3NP
TIMP-1

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21
Q

What do difference scores in enhanced liver fibrosis test indicate?

A

10.51 or above- advanced fibrosis

Under 10.51- unlikely advanced fibrosis

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22
Q

How often should an enhanced liver fibrosis test be carried out in NAFLD?

A

Every 3 years

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23
Q

How does NAFLD appear on ultrasound?

A

Fatty changes appear as increased echogenicity

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24
Q

In liver cirrhosis what does an ultrasound show?

A
  • Nodularity of liver surface
  • Corkscrew appearance to hepatic arteries with increased flow as they compensate for reduced portal flow
  • Enlarged portal vein with reduced flow
  • Ascites
  • Splenomegaly
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25
Q

What can be used to screen for hepatocellular carcinoma?

A

Ultrasound
Alpha-fetoprotein

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26
Q

What is a transient elastography used for?

A

AKA FibroScan

Used to assess stiffness of the liver using high-frequency sound waves

Helps determine degree of fibrosis to test for liver cirrhosis

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27
Q

Who is transient elastrography used for?

A

Patients at risk of cirrhosis:
- Alcoholic-related liver disease
- Heavy alcohol drinkers (men drinking over 50 units, women over 35 units)
- NAFLD and advanced liver fibrosis (score over 10.51)
- Hepatitis C
- Chronic hepatitis B

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28
Q

What other investigations are used for liver cirrhosis?

A

Endoscopy
Assess and treat oesophageal varices when portal hypertension suspected

CT and MRI
Looked for hepatocellular carcinoma

Liver biopsy
Confirm cirrhosis diagnosis

29
Q

What is a MELD score?

A

Model for End-Stage Liver Disease

Use every 6 months in patients with compensated cirrhosis

Gives estimated 3-month mortality as a percentage

30
Q

What is the Child-Pugh score?

A

Uses 5 factors to assess cirrhosis severity and prognosis

A-Albumin
B-Bilirubin
C-Clotting (INR)
D-Dilatation (ascites)
E-Encephalopathy

31
Q

What are the principles of general management of liver cirrhosis?

A

Treat underlying cause

Monitoring complications
Managing complications
Liver transplant

32
Q

What does monitoring for complications involve?

A
  • MELD score every 6 months
  • Ultrasound and alpha-fetoprotein every 6 months for hepatocellular carcinoma
  • Endoscopy every 3 years for oesophageal varices
33
Q

When is liver transplantation considered?

A

Features of decompensated liver disease

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

34
Q

What is the 5-year prognosis once cirrhosis has developed?

35
Q

What are the important complications of cirrhosis?

A
  • Malnutrition and muscle
    wasting
  • Portal hypertension, oesophageal varices and bleeding varices
  • Ascites and spontaneous bacterial peritonitis
  • Hepatorenal syndrome
  • Hepatic encephalopathy
  • Hepatocellular carcinoma
36
Q

Why does cirrhosis lead to malnutrition and muscle wasting?

A
  • Loss of appetite
  • Affected protein metabolism in liver, reduced amount of protein liver produces
  • Disrupted ability to store glycogen and release it when required
  • Less protein available for maintaining muscle tissue
  • Muscle tissue broken down for fuel
37
Q

How is malnutrition managed?

A
  • Regular meals
  • High protein and calorie intake
  • Reduced sodium intake to minimise fluid retention
  • Avoiding alcohol
38
Q

Where does the portal vein come from?

A

Superior mesenteric vein
Splenic veins

39
Q

What is the purpose of the portal vein?

A

Delivers blood to the liver

40
Q

What happens to the portal vein in cirrhosis?

A

Increased resistance to blood flow in the liver

Increased back-pressure on the portal system

Splenomegaly

41
Q

What does back pressure in the portal system cause?

A

Swollen and tortuous vessels where collaterals form between portal systemic venous systems

42
Q

Where do collaterals form?

A

Distal oesophagus - Oesophageal varices

Anterior abdominal wall - caput medusae

43
Q

What do patients with varices experience?

A

Asymptomatic until the varices start bleeding

Due to high blood flow patients can exsanguinate (bleed out) very quickly

44
Q

What prophylaxis can be used for bleeding in stable oesophageal varices?

A

Non-selective beta blockers, propranolol- first line

Variceal band ligation (if beta blockers are contraindicated)

45
Q

What does variceal band ligation involve?

A

Rubber band wrapped around base of the varices

Cuts off blood flow through the vessels

46
Q

How are bleeding oesophageal varices managed?

A

Life-threatening emergency

  • Immediate senior help
  • Blood transfusion (activate major haemorrhage protocol)
  • Treat coagulopathy (fresh frozen plasma)
  • Vasopressin analogues (terlipressin or somatostatin)
  • Prophylactic broad-spectrum antibiotics
  • Urgent endoscopy with variceal band ligation
  • Consider intubation and intesive care
47
Q

What other options to control bleeding are there?

A

Sengstaken-Blakemore tube
Inflatable tube inserted into the oesophagus to tamponade bleeding varices

Transjugular intrahepatic portosystemic shunt (TIPS)

48
Q

What is a transjugular intrahepatic portosystemic shunt (TIPS)?

A

Wire inserted into jugular vein (under x-ray guidance)

Down vena cava into liver via hepatic vein

Connection made through liver between hepatic vein and portal vein and stent inserted

49
Q

What does a transjugular intrahepatic portosystemic shunt do?

A

Allows blood flow directly from portal vein to hepatic vein

Relieves pressure in portal system

50
Q

What are the main indications of a transjugular intrahepatic portosystemic shunt?

A

Bleeding oesophageal varices
Refractory ascites

51
Q

What is ascites?

A

Fluid in the peritoneal cavity

52
Q

What causes ascites?

A

Increased pressure in portal system causes fluid to leak out of capillaries in liver and other organs into peritoneal cavity

53
Q

Why does blood pressure decrease in the kidneys in ascites?

A

Drop in circulating volume caused by fluid loss into peritoneal cavity

54
Q

How do the kidneys respond to decreased blood pressure secondary to liver cirrhosis?

A

Renin release

RAAS

Causes a transudative ascites

55
Q

What are the management options of ascites?

A

Low sodium diet
Aldosterone antagonists
Paracentesis (ascitic tap or ascitic drain)
Prophylactic antibiotics (ciprofloxacin)
Transjugular intrahepatic portosystemic shunt (refractory ascites)
Liver transplant

56
Q

What is spontaneous bacterial peritonitis?

A

Infection develops in ascitic fluid and peritoneal lining without clear source of infection

57
Q

How often does spontaneous bacterial peritonitis occur?

A

10-20% of time in patients with ascites

Mortality of 10-20%

58
Q

How does spontaneous bacterial peritonitis present?

A

Fever
Abdominal pain
Deranged bloods
Ileus
Hypotension

59
Q

What are the most common causative organisms of spontaneous bacterial peritonitis?

A

Escherichia coli
Klebsiella pneumoniae

60
Q

What does management of spontaneous bacterial peritonitis involve?

A

Sample of ascitic fluid cultured
IV broad-spectrum antibiotics e.g. tazocin

61
Q

What is hepatorenal syndrome?

A

Impaired kidney function caused by reduced blood flow to the kidney due to liver cirrhosis and portal hypertension

Poor prognosis unless patient has liver transplant

62
Q

What causes hepatorenal syndrome?

A

Portal hypertension causes portal vessels to release vasodilators causing vasodilation in the splanchnic circulation

Vasodilation causes reduced blood pressure

Kidneys activate RAAS

Vasoconstriction of renal vessels, combined with low systemic pressure resulting in kidneys being starved of blood and significantly reduced kidney function

63
Q

What is hepatic encephalopathy?

A

AKA portosystemic encephalopathy

Caused by build up of neurotoxic substances affecting the brain

Especially ammonia

64
Q

Why does ammonia build up in patients with cirrhosis?

A

Hepatocyte impairment prevents them from metabolising ammonia into harmless waste products

Collateral vessels between portal and systemic circulation mean ammonia bypasses the liver and enters the systemic system directly

65
Q

How does hepatic encephalopathy present?

A

Acutely
Reduced consciousness
Confusion

Chronically
Personality changes
Memory and mood changes

66
Q

What factors trigger or worsen hepatic encephalopathy?

A

Constipation
Dehydration
Electrolyte disturbance
Infection
GI bleeding
High protein diet
Sedative medications

67
Q

How is hepatic encephalopathy managed?

A

Lactulose (aim for 2-3 soft stools daily)
Antibiotics (rifaximin) reduce number of intestinal bacteria producing ammonia
Nutritional support (NG tube)

68
Q

How does lactulose work to reduce ammonia?

A

Speeds up transit time and reduces constipation
- Clearing ammonia before absorption

Promotes bacterial uptake of ammonia for protein synthesis

Changes pH of intestines contents
- More acidic, kills ammonia-producing bacteria

69
Q

Why is Rifaximin the choice of antibiotic for hepatic encephalopathy?

A

Poorly absorbed, stays in GI tract

Neomycin and metronidazole are alternatives

Medicine (111 decks)

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