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Liver Conditions Flashcards

1
Q

What duration defines chronic liver disease?

A

Disease greater than 6 months

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2
Q

What is the clinical pathway of cirrhosis?

A

1) Causes of chronic liver disease - presents as signs and symptoms of the causal disease
2) Recurrent inflammation and process of fibrosis
3) Compensated cirrhosis - presents with stigmata of cirrhosis
4) Decompensated cirrhosis leading to chronic liver failure or acute-on-chronic liver disease

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3
Q

What are the 4 cells of the liver?

A

Hepatocytes, Endothelial cells, Kupffer cells and Hepatic stellate cells

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4
Q

What is the function of hepatic stellate cells?

A

Storage of vitamin A as retinol

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5
Q

What is the function of Endothelial cells in the liver?

A

Regulate the passage of molecules from the blood to the liver

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6
Q

What is the function of Kupffer cells?

A

Liver’s own immune system

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7
Q

What is liver fibrosis?

A

The accumulation of tough, fibrous scar tissue in the liver as a result of injury healing process going wrong

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8
Q

What is the pathophysiology of progression of fibrosis to cirrhosis?

A

1) Hepatocytes are injured due to infection with a virus, heavy alcohol consumption, toxins, trauma etc, and activates the immune system.
2) Hepatocyte injury stimulates inflammatory immune cells to release cytokines, growth factors etc which direct hepatic stellate cells (source of most ECM) to activate and produce collagen type I and III, glycoproteins, proteoglycans, and other substances
3) These substances are deposited in the hepatic parenchyma and space of disse of the liver, the latter causing capillarisation - where capillaries lose fenestration which blocks exchange (portal hypertension)
4) At the same time, the process of breaking down or degrading collagen is impaired so regeneration is limited to small nodules

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9
Q

What is Chronic Liver Disease, and what is it not?

A

Chronic liver disease is a disease process resulting in cirrhosis – not a disease in itself

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10
Q

How long does it normally take to get from a healthy liver to chronic liver disease?

A

20 years

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11
Q

What are the main causes of cirrhosis?

A

Common: - Alcohol - NAFLD - Hep C/B - PBC/PSC - Autoimmune hep Less common: -Haemachromotosis - Wilson’s -alpha 1 antitrypsin

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12
Q

What actually is cirrhosis?

A

Pathological end-stage of any chronic liver disease. Irreversible liver damage with loss of normal liver architecture histologically with bridging fibrosis and nodular regeneration

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13
Q

What is steatosis?

A

Infiltration of liver cells with fat, associated with disturbance of the metabolism by, for example, alcoholism, malnutrition, pregnancy, or drug therapy.

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14
Q

What is the most common cause of chronic liver disease in the western world?

A

NAFLD

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15
Q

What is the 2 Hit Paradigm for the pathophysiology of NAFLD?

A

First hit: Most likely insulin resistance leading to accumulation of triglycerides in the liver and hepatic steatosis development Second hit: additional oxidative injury required to manifest the nectro-inflammatory component

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16
Q

True or False: NAFLD and metabolic syndrome aren’t associated

A

False, nice try

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17
Q

What is the relationship between NASH and NAFLD?

A

NAFLD is an umbrella term which encompasses simple steatosis (fatty liver) without liver inflammation, and Non-alcohol steatohepatitis (NASH) where there is inflammation as a result of fatty infiltration with risk of fibrosis and cirrhosis

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18
Q

How would you differentiate between simple steatosis and NASH?

A

US and Liver biopsy

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19
Q

Which conditions does auto-immune liver disease cover?

A

• Primary Biliary Cholangitis (Cirrhosis) • Auto-immune Hepatitis • Primary Sclerosing Cholangitis

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20
Q

What is Primary Biliary Cholangitis?

A

Chronic autoimmune disease where the epithelial cells of the small intrahepatic bile ducts are damaged by the immune system. Characterised by progressive bile duct damage (and eventual fibrosis/loss)

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21
Q

What is the underlying aetiology of PBC?

A

There is a very high incidence of autoantibodies, most characteristically directed against mitochondrial antigens (antimitochondrial antibody).

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22
Q

What is the pathophysiology of PBC?

A

Process in PBC is damage to, and progressive destruction of, the biliary epithelial cells lining the small intrahepatic bile ducts. Bile ducts are damaged in the context of portal tract inflammation, further supporting the concept of an autoimmune component to the disease. Loss of bile duct cross-sectional area within the liver leads to cholestasis with progressive bile acid retention. Bile acid pooling can cause secondary damage within the liver, further contributing to progressive bile duct loss

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23
Q

Which is more common in women: PBC or PSC?

A

PBC (B for burds)

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24
Q

What are the symptoms of PBC?

A

Asymptomatic initially, then fatigue, itch without rash, xanthesalma and xanthomas

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25
Q

How would you diagnose PBC?

A

• Positive AMA (anti-mitochondrial antibody) • Cholestatic liver function tests (LFTs) • Liver Biopsy

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26
Q

What is the treatment for PBC?

A

Urseo deoxycholic acid (UDCA)

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27
Q

What is the beneficial effects of UDCA on PBC?

A

1) it increases the rate of bile flow from the hepatocytes, thereby combating cholestasis and diluting toxic bile acids in bile. 2) it inhibits the body’s production of toxic bile acids, thereby preventing further injury to the hepatocytes. 3) it inhibits apoptosis of the hepatocytes 4) it mildly inhibits the immune response in the liver, thereby possibly reducing immunological injury to the bile ducts and liver.

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28
Q

What is auto-immune hepatitis characterised by?

A

Characterised by the presence of circulating auto-antibodies with a high serum globulin concentration and inflammatory changes on liver histology,

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29
Q

Who is affected by autoimmune hepatitis more, men or women?

A

Women (of course)

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30
Q

Who is affected by Type 1 and Type 2 auto-immune hepatitis?

A

Type 1 - adults

Type 2 - children and young adults

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31
Q

Which antibodies characterised Type 1 auto-immune hepatitis?

A

• ANA (anti-nuclear antibodies) • ASMA • SLA severity • IgG • AMA • pANCA

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32
Q

Which antibodies characterised Type 2 auto-immune hepatitis?

A

Just LKM -1 and AMA

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33
Q

How does auto-immune hepatitis present?

A
  • Hepatomegaly - Jaundice - Stigmata of chronic liver disease - Splenomegaly - Elevated AST and ALT - Elevated PT - Non-specific symptoms: malaise, fatigue, lethargy, nausea, abdominal pain, anorexia
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34
Q

How is autoimmune hepatitis diagnosed?

A
  • Elevated AST and ALT - Elevated IgG - Rule out other causes - Presence of autoimmune antibodies - Liver biopsy
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35
Q

What is the hallmark histological finding of autoimmune hepatitis?

A

Interface hepatitis, neutrophils everywhere

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36
Q

What is the treatment for auto-immune hepatitis?

A

Prednisolone and Azathioprine (steroids and immunosuppressants)

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37
Q

What is cholestasis?

A

When bile can’t flow from the liver to the duodenum

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38
Q

What is Primary Sclerosing Cholangitis?

A

Cholestatic autoimmune liver disease causing continued inflammation, fibrosis and strictures of the intra and extra hepatic bile ducts, leading to cirrhosis, and end-stage liver disease.

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39
Q

Which is more common in men: PBC or PSC?

A

PSC

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40
Q

What is haemochromotosis?

A

Genetic iron overload syndrome. Specifically: autosomal-recessive disorder leading to dysregulated intestinal absorption of dietary iron and increased iron release from macrophages.

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41
Q

Which genes are associated with haemochromotosis?

A

C282Y or H63D, mutations in HFE gene on short arm of chromosome 6 (according to Zack anyway..)

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42
Q

What is the treatment for haemochromotosis?

A

Venesection (regular blood transfusion)

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43
Q

What is Wilson’s disease?

A

Autosomal-recessive disease of copper accumulation and toxicity caused by a defect in an enzyme involved in the biliary excretion of excess copper. Loss of function of caeruplasmin (copper binding protein).

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44
Q

What is lenticulo-hepatic degeneration in Wilson’s?

A

Get copper deposition in liver and basal ganglia

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45
Q

How does Wilson’s clinically present?

A

• Neurological- chorea-atheitoid movements • Hepatic – cirrhosis or sub-fulminant liver failure • Kaiser Fleisher rings

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46
Q

What is the treatment for Wilson’s?

A

Copper chelation drugs

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47
Q

What is Alpha 1 Anti-trypsin Deficiency?

A

Mutation in the A1AT gene causing deficient of aloha 1 anti-trypsin

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48
Q

What does alpha 1 anti-trypsin normally do?

A

Breaks down proteases to stop them breaking down proteins of membranes

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49
Q

What are the clinical pathologies of Alpha 1 Anti-trypsin Deficiency?

A

• Lung emphysema (as the proteins of membranes are broken down) • Liver deposition of mutant protein, cell damage

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50
Q

What is the management for Alpha 1 Anti-trypsin Deficiency?

A

Supportive

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51
Q

What is Budd Chiari Syndrome?

A

Hepatic venous outflow obstruction at any level from the small hepatic veins to the inferior vena cava and the right atrium, regardless of the cause of the obstruction. (blockage of drainage of liver)

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52
Q

Hows does Budd Chiari present?

A

• Acute: Jaundice and tender hepatomegaly • Chronic- Ascites

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53
Q

How would you diagnose Budd Chiari?

A

US visualisation of hepatic veins

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54
Q

How would you treat Budd Chiari?

A

Recanalization or TIPS

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55
Q

What is a TIPS procedure?

A

Transjugular intrahepatic portosystemic shunt - An artificial channel within the liver that establishes communication between the inflow portal vein and the outflow hepatic vein. Mostly used in portal hypertension and Budd chair

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56
Q

What is methotrexate and which implications can it have for the liver?

A

Drug used for rheumatoid arthritis and psoriasis. Can be toxic to the liver causing fibrosis

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57
Q

What is cardiac cirrhosis?

A

Cirrhosis secondary to high right heart pressures

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58
Q

What is Acute Liver Disease?

A

Rapid development of hepatic dysfunction without prior liver disease. Due to any insult to the liver causing damage

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59
Q

What is acute hepatic encephalopathy?

A

Occurs when the liver stops being able to filter blood so get neurological effects, confusion and a flap

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60
Q

What is the limit to the proportion of hepatocytes which can die and the liver will still regenerate?

A

90%

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61
Q

What are the clinical features of acute liver disease?

A
  • None (common) - Jaundice - Lethagy - Nausea - Anorexia - Itch - Abnormal LFTs
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62
Q

With acute liver disease, what does high ALTs make you think of?

A

Paracetamol

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63
Q

What are some of the main causes of acute liver disease?

A

Viral A-E, Ebstein-barr, drugs, shock liver (suddenly hypotensive), cholagnitis, alcohol, malignancy, chronic liver disease, budd chiari

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64
Q

What is the management of acute liver disease?

A
  • Rest with fluids and no booze - Increase calories (but not high fat) - sodium bicarbonate bath, for itch
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65
Q

What is Fulminant Hepatic Failure?

A

Sub-group of acute liver disease. A clinical syndrome resulting in massive necrosis of liver cells leading to severe impairment of liver function

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66
Q

What are the characteristics of Fulminant Hepatic Failure?

A

Jaundice and encephalopathy in a patient with a previously normal liver

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67
Q

What is the treatment for Fulminant Hepatic Failure?

A
  • Supportive
  • Inotropes & Fluids
  • Renal replacement
  • Management of raised ICP
  • Transplant
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68
Q

What should the liver look like normally?

A

light, tan in colour with a smooth surface

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69
Q

What is the main rule of pathogenesis of almost any liver disease?

A

Any insult causes death of hepatocytes, which causes inflammation results in activation of fibroblasts which causes scarring. This recurring results in cirrhosis

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70
Q

Which two ways can jaundice be classified?

A

By site (pre-hepatic ec) and by type of bilirubin (conjugated vs. unconjugated)

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71
Q

What is the underlying cause of pre-hepatic jaundice?

A

Too much haem to break down e.g. haemolytic anaemia

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72
Q

What is the underlying cause of hepatic jaundice?

A

Liver cells injured or dead e.g. acute liver failure, alcoholic hepatitis, decompensated cirrhosis

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73
Q

What is the underlying cause of post-hepatic jaundice?

A

Bile cannot escape into the bowel e.g. gallstones, tumours of head of pancreas

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74
Q

What is cirrhosis?

A

A special type of fibrosis that occurs as an end-point as a result of repeated insult

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75
Q

What are the 3 main complications of cirrhosis?

A

Portal hypertension, ascites and liver failure

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76
Q

What are the 3 main sites of portal-systemic anastomoses?

A

Oesophageal varices, caput medusa and haemorrhoids

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77
Q

How is alcohol normally metabolised in the liver?

A

By 2 main pathways: alcohol dehydrogenase and cytochrome P-450 2E1. Alcohol is metabolised to acetaldehyde by alcohol dehydrogenase, which then is metabolised to acetate by the mitochondrial enzyme acetaldehyde dehydrogenase. Alcohol dehydrogenase and acetaldehyde dehydrogenase reduce nicotinamide adenine dinucleotide (NAD) to NADH (reduced form of NAD).

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78
Q

How can excess alcohol then cause damage to the liver, considering alcohol metabolism?

A

Excessive NADH in relation to NAD inhibits gluconeogenesis and increases fatty acid oxidation, which in turn promotes fatty infiltration in the liver. Results in an inflammatory response and fibroblast activation

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79
Q

What duration of drinking causes which outcome - and is it reversible?

A

.

80
Q

**What happens to the liver after heavy drinking for 2-3 days?

A

Acute fatty liver injury-Once the liver has been forced to store excessive fat, then it is taking up functional units so reduction in function. Willl appear bright yellow and fat/slimy

81
Q

What happens to the liver after heavy drinking for weeks-months?

A

Presence of hepatocyte necrosis, neutrophils, mallory bodies and periceullar fibrosis. Bile starts to accumulate

82
Q

What happens to the liver after heavy drinking for months-years?

A

Collagen is laid down around cells (blue) and scarring/fibrosis starts to occur. Once the collagen gets cross-linked it becomes irreversible.

83
Q

What happens to the liver after heavy drinking for years?

A

Micronodular cirrhosis with abundant white scarring. Irreversible - All of the functional reserve has been used up and scarred

84
Q

What is the main type of investigation used with viral hepatitis?

A

Serology

85
Q

How is hepatitis A spread?

A

Faecal-oral spread (from the bile ducts into the faeces)

86
Q

Does Hep A have a short or long incubation period?

A

Short

87
Q

How is hepatitis B spread?

A

Spread by blood, blood products, sexually or vertically (in utero) - basically via the dance-with-no-pants

88
Q

Does Hep B have a short or long incubation period?

A

Long

89
Q

How is hepatitis C spread?

A
  • Spread by blood, blood products, possibly sexually
90
Q

Does Hep C have a short or long incubation period?

A

Short

91
Q

What is the clinical definition of chronic hepatitis?

A

Abnormal LFTs for more than 6 weeks

92
Q

What are some of the main causes of chronic hepatitis?

A
  • Hepatitis B - Hepatitis C - Autoimmune hepatitis - Primary Biliary Cirrhosis - Drug induced hepatitis - Primary Sclerosing Cholangitis
93
Q

What might you see on biopsy with PBC?

A

Granulomas and bile duct loss

94
Q

PBC affects the -?- bile ducts, while PSC can affect the -?- bile ducts

A

1) intrahepatic 2) intrahepatic and larger extra-hepatic bile ducts

95
Q

True or False: Haemochromatosis predisposes to carcinoma

A

True

96
Q

True or False: Haemochromatosis eventually deposits iron in the portal connective tissue and stimulates fibrosis

A

True (getting lazy now)

97
Q

What links Parkinson’s symptoms and jaundice?

A

Wilson’s Disease

98
Q

What links cirrhosis and emphysema?

A

Alpha-1-antitrypsin deficiency

99
Q

True or False: Primary tumours of the liver are more common than secondary

A

False, secondary metastases are more common in the liver

100
Q

What are the 2 main types of primary tumour of the liver?

A

Hepatocellular adenoma and Hepatocellular carcinoma (hepatoma)

101
Q

What is hepatocellular carcinoma associated with?

A

Hep B/C, alcohol and cirrhosis

102
Q

What is the difference between fibrosis and cirrhosis?

A

Fibrosis is the first stage of scarring, and can occur from any insult. While cirrhosis is the end-stage of scarring characterised by nodular regeneration, and is when this scar tissue builds up and takes over most of the liver and prevents function

103
Q

Portal hypertension

A

Portal vein pressure above the normal range of 5-8 mmHg (Portal vein-hepatic vein pressure gradient greater than 5mmHg)

104
Q

What two main factors contribute to portal hypertension?

A

1) Increased resistance to portal inflow 2) Increased portal inflow

105
Q

What can the causes of portal hypertension be divided into?

A

Pre-hepatic: blockage of the portal vein before the liver; due to portal vein thrombosis or occlusion

Intrahepatic: disruption of the change in hepatic architecture - pre sinusoidal e.g. schistosomiasis or post-sinusoidal e.g cirrhosis

Post-hepatic: blockage in the venous system leaving the liver eg. budd chiari

106
Q

Which two environments present in cirrhosis can predispose the liver to hepatocellular carcinoma?

A

• Mitogenic environment (rapid turnover) due to recurrent hepatocyte death • Mutogenic environment (those which are made are damaged) due to inflammation

107
Q

What are the 3 commonest causes of cirrhosis?

A

Alcohol, HCV and NASH

108
Q

What is the difference between compensated and decompensated cirrhosis?

A

Compensated cirrhosis means that the liver is heavily scarred but can still perform many important bodily functions. While decompensated cirrhosis means that the liver is extensively scarred and unable to function properly, resulting in liver failure

109
Q

What are the signs of compensated cirrhosis?

A

May be asymptomatic, Spider nave, Plamar erythema, clubbing, gynaecomastia, Hepatomegaly(?), Splenomegaly

110
Q

**What are spider naevi and what amount is normal?

A

A type of telangiectasis (swollen blood vessels) found slightly beneath the skin surface, often containing a central red spot and reddish extensions which radiate outwards like a spider’s web. If you press on them then they blanche out to the legs, then on release the fill out again centrally.

111
Q

What are the signs of decompensated cirrhosis?

A

• Jaundice • Ascites • Encephalopathy • Easy bruising

112
Q

Which 4 mechanisms cause ascites?

A

• Decreased plasma colloid pressure • Increased hepatic lymph production • Reduced hepatic venous flow • Decreased albumin production

113
Q

How do you diagnose ascites?

A

Shifting dullness and ascites

114
Q

True or False: Appearance of ascites is a marker of a good outcome

A

False, unfortunately unicorns aren’t real either

115
Q

Which diuretic should you use first for ascites?

A

Spironolactone (add loop diuretic if recurrent)

116
Q

How do you manage ascites?

A
  • Improve underlying liver disease - Reduce salt intake - Diuretics - Paracentesis - TIPSS - Transplant
117
Q

True or False: Encephalopathy is a complication of cirrhosis

A

True

118
Q

What is the underlying cause of hepatic encephalopathy?

A

The occurrence of confusion, altered level of consciousness, and coma as a result of liver failure. It is caused by accumulation in the bloodstream of toxic substances that are normally removed by the liver, e.g. ammonia which can cross the BBB.

119
Q

What does primary/secondary prophylaxis of bleeding varies entail?

A

B-blockers • Non-selective ones as we need the Beta-2 effect • Propranolol • Carvideolol •Cause vasodialtion Variceal Ligation • Can go in prophylactically and treat them

120
Q

What endoscopic interventions can be used in the treatment of acute vatical bleeding?

A
  • Sclerotherapy - injection into the vessels to make them shrink
  • TIPSS - reduce the portal pressure
  • Varicieal ligation ‘banding’
  • Balloon tamponade - balloon inflated to apply pressure and stop bleed
121
Q

Why are vatical bleeds so severe?

A

As they have a large blood supply

122
Q

What are the 3 main basis for making a decision of liver transplant?

A

Events e.g. vatical bleed or ascites LFTs Quality of life

123
Q

Which score do you use to calculate the pts and therefore need for liver transplant?

A

UKELD score

124
Q

What are the 3 major mechanisms of complications of cirrhosis?

A

Reduced liver blood flow, reduced metabolic function and reduced plasma proteins

125
Q

What is an important effect of cirrhosis which is relevant to drugs?

A

Portal-systemic shunting - Shunting of blood to by-pass the liver, so drugs are no longer metabolised by the liver (no first pass metabolism so large concentrations of the drug), and there is also general reduced metabolic capacity

126
Q

What is the first pass effect?

A

A phenomenon of drug metabolism whereby the concentration of a drug is greatly reduced by the liver before it reaches the systemic circulation.

127
Q

What circulation changes occur in liver disease?

A

1) Low albumin so low plasma volume detected 2) Kidney therefore puts out renin to keep more salt and water retained via the renin-angiotensin-aldosterone system 3) Aldosterone cant get metabolised by the liver as it is a complicated steroid and livers can metabolise these when damaged 4) So aldoterone remains in the system and we get secondary aldosteronism

128
Q

What effect can occur, particularly to men, relating to hormones in liver disease?

A

Men lose their secondary sex attributes as they cant break down oestrogen

129
Q

What analgesics would you use if needed in liver disease and why?

A

Paracetamol, 1g twice daily - not exceeding 3g daily. NSAIDs worsen renal impairment and cause peptic ulcers. Opiates aren’t fully metabolised so the amines cause encephalopathy. Paracetamol toxicity occurs with normal doses in liver disease, due to reduced glutathione stores. So if use it at lower doses, is the lesser of evils

130
Q

What consequences does liver disease have on the kidney?

A
  • Increased angiotensin II, aldosterone, SNS and ADH results in: • Potassium loss • Sodium retention • Water retention
131
Q

What is hecto-renal syndrome?

A

Rapid deterioration in kidney function in individuals with cirrhosis or fulminant liver failure.

132
Q

What happens in paracetamol toxicity?

A

Metabolism of paracetamol involves the conversion to highly reactive intermediates which interacts with glutathione in your system and inactivates it to sage cysteine and mercapturic acid conjugates. However if you take too large a dose, then you have used up all of the glutathione so the highly reactive intermediates are left to necrose your liver

133
Q

Which drugs are associated with drug induced liver disease?

A

Amoxicillin and Clavulanic acid

134
Q

What is the most common acute viral hepatitis?

A

Hepatitis E

135
Q

What is the most commonly diagnosed viral hepatitis (including chronic)?

A

Hepatitis C

136
Q

What conditions are Hep A associated with?

A

Poor hygiene/overcrowding (e.g. travelling)

137
Q

Is Hep A an acute or chronic infection?

A

Acute

138
Q

What are the first antibodies to be produced in an infection?

A

IgM (e.g. Hep A IgM)

139
Q

When is Hep D only found?

A

With Hep B (either as co infection - infection eat the same time, or superinfection - Hep B then Hep D later)

140
Q

Who are at a higher risk of Hep B in the UK?

A

SE Asians or sub-saharan Africans,, Multiple sex partners, IVDUs and children of infected mothers

141
Q

In lab, hat does Hep B surface antigen (HBsAg) indicate?

A

Present in all infectious individuals (current infection)

142
Q

In lab, what does Hep B IgMs indicate?

A

Recent infection

143
Q

In lab, what does Hepatitis B Surface Antibody (HBsAb) indicate?

A

Immunity - either from being vaccinated, or if you have recovered from a hepatitis B infection.

144
Q

In lab, what does Hepatitis B Core Antibody (HBcAb or anti-abc) indicate?

A

This antibody does not provide any protection or immunity against the hepatitis B virus. A positive test indicates that a person may have been exposed to the hepatitis B virus.

145
Q

If you were immune to Hep B, what would you’re lab results show?

A

HBsAg= Negative (-) HBsAb = Positive (+) HBcAb = Negative or positive (-/+)

146
Q

If you had a current acute or chronic current Hep B infection, what would your lab results show?

A

HBsAg= Positive (+) HBsAb = Negative (-) HBcAb = Negative or Positive (-/+)

147
Q

In lab, what does Hepatitis B e-antigen (HBeAG) indicate?

A

Infectivity

148
Q

In general, what does the presence of Hep B antigens indicate?

A

Current infectious

149
Q

In general, what does the presence of Hep B antibodies indicate?

A

Previous infection

150
Q

In lab, what does presence of Hep B virus DNA?

A

High infectivity - active replication of virus

151
Q

True or False: there is a vaccine for Hep B

A

True

152
Q

True or False: there is a vaccine for Hep C

A

False

153
Q

**What is the general natural history of Chronic infection?

A

Infection > acute hepatitis > chronic infection > chronic hepatitis > cirrhosis > cancer

154
Q

Are Hep B/C acute or chronic infections?

A

Chronic (are asymptomatic until the point of chronic)

155
Q

What is the management for acute viral hepatitis?

A
  • Symptomatic - No antivirals given - Monitor for encephalopathy or resolution - Notify Public Health - Immunisation of contacts
156
Q

What is the management for chronic viral hepatitis?

A
  • Antivirals -Vaccination against other hepatitis viruses or influenza, pneumococcal - Infection control - Alcohol↓ - Hepatocellular carcinoma awareness/screening  
157
Q

What are examples of anti-vitals used in chronic viral hepatitis?

A

Interferon alpha (peginterferon), ribavirin, telaprevir, tenofovir

158
Q

What is the most common solid liver tumour on non-cirrhotic patients?

A

Heaemangioma

159
Q

What are the 4 main benign lesions of the liver?

A

• Haemangioma • Focal nodular hyperplasia • Adenoma • Liver cysts

160
Q

What are the 2 main primary malignant lesions of the liver?

A

Hepatocelullar carcinoma and intrahepatic cholangiocarcinoa

161
Q

What treatment is required for haemangioma?

A

None

162
Q

What is a liver haemiangioma?

A

A benign tumour of blood vessels

163
Q

What is Focal Nodular Hyperplasia (FNH)?

A

Benign nodule formation of normal liver tissue. Occurs as a hyper plastic response to abnormal arterial flow

164
Q

What treatment is required for FNH?

A

None

165
Q

What is a hepatic adenoma?

A

Benign neoplasm composed of normal hepatocytes no portal tract, central veins or bile ducts

166
Q

True or False: Hepatic adenomas are associated with contraceptive pill

A

True

167
Q

What is the management for hepatic adenoma?

A
  • Stop hormones - Observe every 6m for 2y - If no regression then surgical excision
168
Q

What are simple cystic lesions?

A

Liquid collection lined by an epithelium

169
Q

What are hydatid cystic lesions?

A

Parasitic zoonosis caused by the Echinococcus tape worm. Causes multiple cysts in the liver

170
Q

What is the management for hydatid cystic lesions?

A

Surgery: Conservative (Open cystectomy) or Radical (Pericystectomy,or lobectomy) Medical: Albendazole Percutaneous drainage: Puncture Aspiration Injection Reaspiration (PAIR) •

171
Q

What is PAIR?

A

Puncture Aspiration Injection Respiration - PAIR is performed using either ultrasound or CT guidance, involves aspiration of the cyst contents via a special cannula, followed by injection of a scolicidal agent for at least 15 minutes, and then reaspiration of the cystic content

172
Q

What is Polycystic Liver Disease (PLD)?

A

Rare condition that causes cysts to grow throughout the liver

173
Q

What are the 3 types associated with Polycystic Liver Disease?

A

• Von Meyenburg complexes (VMC) • Polycystic Liver disease • Autosomal dominant Polycystic Kidney disease

174
Q

What are the clinical features of liver abscesses?

A
  • High fever - Leukocytosis - Abdominal Pain - Complex liver lesion - History • Abdominal or biliary infection • Dental procedure
175
Q

What is the management of liver abscesses?

A
  • Initial empiric broad spectrum antibiotics -Aspiration/drainage percutaneously -Echocardiogram – check for bacterial endocarditis - Operation if no clinical improvement: • Open drainage • Resection - 4 weeks antibiotic therapy with repeat imaging
176
Q

What are the clinical features of hepatocellular carcinoma?

A
  • Wt loss and RUQ pain (most common) - Asymptomatic - Worsening of pre-existing chronic liver disease - Acute liver failure - O/E: • Signs of cirrhosis • Hard enlarged RUQ mass • Liver bruit (rare
177
Q

What is a tumour marker for hepatocellular carcinoma (HCC)?

A

Alpha fetoprotein (AFP) (>100ng/ml suggest HCC)

178
Q

What are the treatment options for hepatocellular carcinoma?

A
  • Transplant - resection, local ablation, chemo embolisation (TACE) and systemic therapies e.f. Sorafenib
179
Q

What is TACE?

A

Trans Arterial Chemo Embolisation - inject chemo into hepatic artery

180
Q

What is bilirubin, and what happens to it before and in the liver?

A

Bilirubin is made from the haem part of haemoglobin when red blood cells are destroyed, usually in the reticuloendothelial system. In its insoluble unconjugated form, it is transported to the liver albumin bound. Liver enzymes then conjugate it to form bilirubin glucuronide (conjugated/direct bilirubin), which is secreted in bile into the gut to be excreted in both urine and faeces.

181
Q

What level of bilirubin is required to cause jaundice?

A

over 35micromol/l

182
Q

What are ALT and AST?

A

Alanine transaminase (ALT) and aspartate transaminase (AST) are together referred to as the aminotransferases or transaminases

183
Q

Which is more specific to the liver: ALT or AST?

A

ALT

184
Q

What are some causes of pre-hepatic jaundice?

A

haemolytic anaemia or internal haemorrhage

185
Q

What are some causes of intra-hepatic jaundice?

A

Cirrhosis and viral hepatitis

186
Q

What are some causes of post-hepatic jaundice?

A

Obstruction e.g. gallstones or pancreatic tumour

187
Q

What are the true liver function tests?

A

Bilirubin, albumina and prothrombin time

188
Q

What are the liver damage tests?

A

ALT/AST, Alk phos and GGT

189
Q

Which liver damage tests are associated with bile duct damage?

A

GGT and Alk Phos

190
Q

Which liver damage tests are associated with the hepatocytes?

A

ALT (+AST, though less specific)

191
Q

What would abnormal PT, bilirubin and albumin levels, and normal (wish) liver damage tests indicate?

A

Chronic liver failure

192
Q

What 3 patterns of pathology are you most likely to be asked about?

A

1) Hepatocyte damage e.g. hepatitis 2) Cholestatic e.g. gall stones 3) Mixed e.g chronic cirrhosis

193
Q

What would hepatitis look like on LFTs?

A

Raised unconjugatd bilirubin, very raised ALT/AST and normal Alk Phos and GGT

194
Q

What would cholestatic pattern look like on LFTs?

A

Raised unconjugated bilirubin, normal ALT/AST and very raised Alk Phos and GGT

195
Q

Stereotypically, what are you thinking with a 50y patient (>40y basically) of chinese background with jaundice?

A

Hep B

196
Q

What would the clinical features of post-hepatic jaundice be?

A

Itchy, with dark urine and pale stools

197
Q

What would the clinical features of intra-hepatic jaundice be?

A

Hepatomegaly possibly

RW Gastroenterology (13 decks)

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