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Paeds: Gastro and Growth > Liver + Jaundice > Flashcards

Liver + Jaundice Flashcards

1
Q

When should you investigate jaundice in the neonate to identify liver disease?

A

>2 weeks if term, >3 weeks if preterm

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2
Q

What are 9 symptoms of hepatic dysfunction in children?

A
  1. Encephalopathy
  2. Jaundice
  3. Epistaxis
  4. Varices with portal hypertension
  5. Hypersplenism
  6. Hepatorenal failure
  7. Loss of fat stores secondary to malnutrition
  8. Rickets secondary to vitamin D deficiency
  9. Peripheral neuropathy
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3
Q

What are 8 signs on examination of hepatic dysfunction in children?

A
  1. Clubbing
  2. Bruising and petechiae
  3. Splenomegaly from portal hypertension
  4. Spider naevi
  5. Palmar erythema
  6. Muscle wasting from malnutrition
  7. Ascites
  8. Hypotonia
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4
Q

What are 5 signs of cholestasis?

A
  1. Fat malaborption
  2. Deficiency of fat-soluble vitamins
  3. Pruritus
  4. Pale stools
  5. Dark urine
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5
Q

What proportion of neonatal jaundice will have resolved by 2 weeks (3 weeks if preterm)?

A

90%

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6
Q

What must you first investigate in prolonged neonatal jaundice and why?

A

Is it conjugated or unconjugated; unconjugated resolves spontaneously, conjugated indicates liver disease

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7
Q

What are 6 differentials for unconjugated neonaal jaundice in infancy?

A
  1. Breastmilk jaundice (contains substances which reduce gastric movements and increase enterohepatic circulation)
  2. Infection, particularly UTI
  3. Haemolytic anaemia e.g. G6PD deficiency, spherocytosis, ABO/Rh incompatibility
  4. Hypothyroidism
  5. High gastrointestinal obstruction
  6. Crigler-Najjar syndrome
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8
Q

What defines pathological conjugated hyperbilirubinaemia?

A

>25 micromol/L of conjugated bilirubin

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9
Q

What are 13 causes of conjugated hyperbilirubinaemia in infants?

A
  1. Biliary atresia
  2. Choledochal cyst
  3. Congenital infection
  4. Inborn errors of metabolism
  5. Alpha-1 anti-trypsin deficiency
  6. Galactosaemia
  7. Prolonged parenteral nutrition (can cause neonatal hepatitis syndrome)
  8. Tyrosinaemia (type 1)
  9. Errors of bile acid synthesis
  10. Progressive familial intrahepatic cholestasis
  11. Cystic fibrosis
  12. Intestinal failure-associated liver disease - long-term parenteral nutrition
  13. Alagille syndrome - intrahepatic biliary hypoplasia
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10
Q

What 3 categories can causes of conjugated hyperbilirubinaemia in infants be divided into?

A
  1. Bile duct obstruction: biliary atresia, choledochal cyst.
  2. Neonatal hepatitis syndrome: congenital infection,alpha-1 antitrypsin deficiency, galactosaemia, PFIC, CF etc.
  3. Intrahepatic biliary hypoplasia: Alagille syndrome
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11
Q

What is biliary atresia?

A

PRogressive fibrosis and obliteration of the extrahepatic and intrahepatic biliary tree

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12
Q

What will happen in biliary atresia if no treatment is given?

A

Chronic liver failure develops, death occurs within 2 years

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13
Q

What are 5 features of biliary atresia?

A
  1. Mild jaundice
  2. Pale stools (increasingly pale)
  3. Normal birthweight followed by faltering growth
  4. Hepatomegaly often present initially
  5. Splenomegaly - due to portal hypertension
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14
Q

What is the aetiology of biliary atresia?

A

Exact aetiology unknown

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15
Q

What are 5 investgiations in biliary atresia and what will they show?

A
  1. Blood tests: raised conjugated bilirubin, abnormal LFTs
  2. Fasting abdominal ultrasound: contracted or absent gallbladder (or may be normal)
  3. ERCP: confirm diagnosis, fails to outline normal biliary tree
  4. Liver biopsy: initially neonatal hepatitis with features of extrahepatic biliary obstruction developing with time
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16
Q

What is the treatment for biliary atresia?

A
  • Palliative surgery with a Kasai hepatoportoenterostomy (loop of jejunum anastomosed to cut surface of porta hepatis) bypasses fibrotic ducts and acilitates drainage of bile from any remaining patent ductules
  • Disease still likely to progress: nutrition and fat-soluble vitamin (ADEK) supplementation essential
  • If Kasai unsuccessful, consider liver transplantation
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17
Q

What is the prognosis of biliary atresia following treatment with a Kasai hepatoportoenterostomy?

A

Early surgery increases success rate with 80% clearing jaundice if performed before 60 days. With successful clearance, disease progresses in most children who may develop cholangitis and cirrhosis with portal hypertension

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18
Q

What is the single most common indication for liver transplantation in paediatric age group?

A

Biliary atresia

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19
Q

What are choledochal cysts?

A

Cystic dilatations of the extrahepatic biliary system

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20
Q

What are 3 ways that choledochal cysts may present?

A
  1. Detected on antenatal ultrasound scan
  2. Neonatal jaundice
  3. Older children: abdominal pain, palpable mass, jaundice, cholangitis
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21
Q

What are 2 ways that a diagnosis of choledochal cysts can be established?

A
  1. Abdominal ultrasound or
  2. magnetic resonance cholangiopancreatography (MRCP)
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22
Q

What is the treatment of choledochal cysts?

A

Surgical excision of the cyst with formation of Roux-en-Y anastomosis to the biliary duct

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23
Q

What are 2 possible complications of choledochal cysts?

A
  1. Cholangitis
  2. 2% risk of malignancy - may develop in any part of biliary tree
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24
Q

What is neonatal hepatitis syndrome?

A

Prolonged neonatal jaundice and hepatic inflammation

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25
Q

What is the typical presentation of neonatal hepatitis syndrome? 3 possible features

A
  1. Low birthweight
  2. faltering growth
  3. Jaundice - may be severe
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26
Q

What is it important to differentiate neonatal hepatitis syndrome from?

A

Biliary atresia - due to severe jaundice that it may present with

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27
Q

What investigation can be performed in suspected neonatal hepatitis syndrome and what might it show?

A

Liver biopsy - often nonspecific, shows giant cell arteritis

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28
Q

What is the cause of Alagille syndrome? What is the inheritance pattern? Varying penetrance even within families

A

Genetic - rare autosomal dominant condition

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29
Q

What are 8 features of the presentation of Alagille syndrome?

A
  1. Characteristic triangular facies
  2. Skeletal abnormalities including butterfly vertebrae
  3. Congenital heart disease (classicaly peripheral pulmonary stenosis)
  4. Renal tubular disorders
  5. Defects in the eye
  6. May be profoundly cholestatic
  7. Severe pruritis
  8. Faltering growth
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30
Q

How is a diagnosis of Alagille syndrome confirmed?

A

Identifying gene mutations

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31
Q

What is the treatment of Alagille syndrome? 4 aspects.

A
  1. Nutrition
  2. Fat-soluble vitamins
  3. Pruritis management - very difficult to manage, profound
  4. Liver transplant in small number
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32
Q

What is the prognosis of Alagille syndrome?

A

Most survive into adult life. Motality most likely secondary to the cardiac disease

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33
Q

What are 3 features of the typical facies of Alagille syndrome?

A
  1. Wide spaced eyes
  2. Pointed chin
  3. Prominent forehead
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34
Q

What is the inheritance pattern of progressive familial intrahepatic cholestasis?

A

Autosomal recessive

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35
Q

What is progressive familial intrahepatic cholestasis (PFIC)?

A

Autosomal recessive disorders that affect bile salt transport

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36
Q

What are 7 possible features of progressive familial intrahepatic cholestasis?

A
  1. Jaundice
  2. Intense pruritus
  3. Faltering growth
  4. Rickets
  5. Diarrhoea
  6. Hearing loss
  7. Older children: gallstones
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37
Q

How is diagnosis of progressive familial intrahepatic cholestasis confirmed?

A

Identifying mutations in bile salt transport genes

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38
Q

What is the treatment of progressive familial intrahepatic cholestasis? 3 aspects

A
  1. Nutritional support and fat-soluble vitamins
  2. Managing pruritus - severe
  3. Liver transplantation usually required due to progression of fibrosis
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39
Q

What is the inheritance pattern of neonatal metabolic liver disease: alpha 1 antitrypsin deficiency?

A

Autosomal recessive disorder

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40
Q

What phenotype is liver disease due to alpha-1 antitrypsin deficiency primary associated with?

A

Protease inhibitor coded on chromosome 14 (Pi), in liver disease = protein phenotype PiZZ

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41
Q

How does alpha-1 antitrypsin deficiency cause liver disease?

A

Abnormal folding of protease alpha-1 antitryptsin associated with accumulation of protein within the hepatocytes and hence liver disease in infancy and childhood

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42
Q

What lung disease can alpha-1 antitrypsin deficiency cause and when?

A

Lack of circulating alpha-1 antitrypsin results in emphyesma in adults

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43
Q

What are 4 features of the presentation of alpha-1 antitrypsin deficiency?

A
  1. Prolonged neonatal jaundice
  2. Bleeding due to vitamin K deficiency (haemorrhagic disease of the newborn, HDN)
  3. Hepatomegaly
  4. Splenomegaly - due to cirrhosis and portal hypertension
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44
Q

How is the diagnosis of neonatal metabolic liver disease due to alpha-1 antitrypsin deficiency made?

A

Estimating level of alpha-1 antitrypsin in plasma and identifying protein phenotype

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45
Q

What is the prognosis of alpha-1 antitrypsin deficiency?

A

Approximately 50% of children have good prognosis

Remainder will develop liver disease and may require transplantation

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46
Q

When can alpha-1 antitrypsin deficiency be diagnosed?

A

Antenatally

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47
Q

What are 2 aspects of the management of alpha-1 antitrypsin deficiency causing metabolic liver disease?

A
  1. Liver transplant in those 50% with poor prognosis
  2. Advice to avoid smoking (active and passive) due to risk of pulmonary disease develpoing in adult life
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48
Q

How common is galactosaemia?

A

very rare - incidence 1 in 23 000 to 1 in 44 000

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49
Q

What is the cause of gaalctosaemia?

A

Autosomal recessive inborn error of metabolism caused by deficiency of enzyme galactose-1-phosphate uridyltransferase

Genes affected: GALE, GALK1, GALT (most common)

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50
Q

What is galactosaemia?

A

Inability to metabolise galactose; builds up in tissues and blood, toxic

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51
Q

What are 4 presenting symptoms of galactosaemia?

A
  1. Poor feeding
  2. Vomiting
  3. Jaundice
  4. Hepatomegaly

when fed milk

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52
Q

What are 6 possible complications of galactosaemia if left untreated?

A
  1. Liver failure
  2. Cataracts
  3. Developmental delay
  4. Shock
  5. Haemorrhage
  6. Disseminated intravescular coagulation, often due to Gram-negative sepsis
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53
Q

How can investigations be used to diagnose galactosaemia? 2 things.

A
  1. Detecting galactose in the urine
  2. Measure enzyme galactose-1-phosphate uridyl transferase in red cells = definitive diagnosis
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54
Q

What can mask the diagnosis of galactosaemia?

A

recent blood transfusion

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55
Q

What is the management of galactosaemia?

A

A galactose free diet - prevents progression of liver disease

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56
Q

What are 2 developments of galactosaemia later in life that can occur despite prevention of liver disease progression?

A
  1. Ovarian failure
  2. Learning difficulties
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57
Q

What congenital infections cause conjugated jaundice? How can they be remembered?

A

TORCH: toxoplasmosis, rubella, cytomegalovirus, herpes simplex virus

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58
Q

How can cystic fibrosis cause conjugated hyperbilirubinaemia in infants?

A

Dysfunction of CFTR transporter interferes with chloride transportation across apical membranes of cells forming the biliary epithelium (cholangiocytes) so causes sticky mucus to build up in liver ducts. Prevents bile from leaving liver, causes inflammation and fibrosis

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59
Q

What are 5 key clinical features of viral hepatitis in children?

A
  1. Nausea
  2. Vomiting
  3. Abdominal pain
  4. Lethargy
  5. Jaundice
  6. Large tender liver
  7. Splenomegaly - 30%
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60
Q

What are 2 key liver blood tests to perform in viral hepatitis and what do they show?

A
  1. Liver transaminase: usually markedly elevated
  2. Coagulation usually normal
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61
Q

What proportion of children do not develop jaundice from viral hepatitis?

A

30-50%

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62
Q

What type of virus is hepatitis A and how is it spread?

A

RNA; faecal-oral transmission

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63
Q

What is the recent trend in hepatitis A virus?

A

fallen as socioeconomic conditions have improved

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64
Q

How may hepatitis A present in children? 4 ways

A
  1. Asymptomatic
  2. Mild illness and recover in 2-4 weeks
  3. Prolonged cholestatic hepatitis (self-limiting)
  4. Fulminant hepatitis
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65
Q

Can chronic liver disease occur in hepatitis A?

A

No

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66
Q

How is diagnosis of hepatitis A confirmed?

A

Detecting IgM antibody to the virus

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67
Q

What are 4 aspects of the management of hepatitis A?

A
  1. No treatment
  2. No evidence bed rest or change of diet effective
  3. Close contacts vaccinated within 2 weeks of onset of illness
  4. If increased risk e.g. chronic liver disease: HNIG (human normal immunoglobulin) should be considered
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68
Q

What type of virus is hepatitis B and how is it transmitted?

A

DNA virus, transmitted by:

  1. perinatal transmission from carrier mothers or horizontal spread within families
  2. inoculation with infected blood via blood transfusion, needlestick injuries, or renal dialysis
  3. among adults can be transmitted sexually
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69
Q

What are 2 regions of the world where there are high prevalence and carrier rates of hepatitis B virus?

A
  1. sub-Saharan Africa
  2. Far East
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70
Q

What happens to infants who contract HBV perinatally?

A

Asymptomatic but at least 90% become chronic carriers

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71
Q

What are 2 things that can happen to older children (not infants) who contract HBV?

A
  1. Asymptomatic
  2. Classical features of acute hepatitis (nausea, vomiting, jaundice, abdominal pain, lethargy)
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72
Q

What are 3 possible outcomes of developing acute hepatitis due to hepatitis B virus?

A
  1. Majority will resolve spontaneously
  2. 1-2%: fulminant hepatic failure
  3. 5-10%: chronic carriers
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73
Q

How is hepatitis B virus diagnosed?

A

Detecting HBV antigens and antibodies:

IgM antibodies ot the core antigen (anti-HBc) positive in acute infection

Hepatitis B surface antigen (HBsAg) denotes ongoing infectivity

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74
Q

The presence of what in the blood indicates acute hepatitis B viral infection?

A

core antigen antibodies: anti-HBc

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75
Q

The presence of what in the blood indicates ongoing infectivity?

A

Hepatitis B surface antigen (HBsAg)

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76
Q

Is there treatment for acute HBV infection?

A

no

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77
Q

What proportion of asymptomatic carrier children of hepatitis B virus will develop chronic HBV liver disease? What proportion will progress to cirrhosis?

A

30-50%

10% may progress to cirrhosis

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78
Q

What is the long term risk of being an asymptomatic carrier of chronic hepatitis B?

A

hepatocellular carcinoma

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79
Q

How effective is current treatment for chronic hepatitis B virus (interferons/antivirals) ?

A

poor efficacy: interferon/pegylated interferon successful in 50% of children infected horizontally (sputum, blood, excretions etc.) and 30% of children infected perinatally

oral antivirals (lamivudine, adefovir) effective in 25%, may be limited by development of resistance

newer drugs may be more effective (entecavir, tenofovir, telbivudine)

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80
Q

What are 4 treatment options for chronic hepatitis B virus in children?

A
  1. Interferon
  2. Pegylated interferon (long-acting formulation)
  3. Oral antiviral therapy e.g. lamivudine, adefovir
  4. Newer drugs: entecavir, tenofovir, telbivudine
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81
Q

What may limit the effectiveness of oral antivirals e.g. lamivudine, adefovir to treat chronic hepatitis B virus?

A

Development of resistance

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82
Q

What are 5 elements of prevention of hepatitis B virus (HBV) infection?

A
  1. All pregnant women screened antenatally for HBsAg (sign of infectivity)
  2. Babies of all HBsAg-positive mothers should receive course of hepatitis B vacination
  3. Hepatitis B immunoglobulin given if mother is hepatitis B e antigen (HBeAg)-positive
  4. Antibody response to vaccination in baby checked in high-risk infants at 12 months
  5. Other members of family also vaccinated
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83
Q

What proportion of high-risk infants for HBV require further vaccination after having antibodies checked following HBV vaccination?

A

5%

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84
Q

What evidence is there for the effectiveness of neonatal HBV vaccination?

A

Evidence it reduces incidence of HBV-related cancer

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85
Q

Why is it so important to vaccinate at-risk babies against hepatitis B virus?

A

treatments for chronic HBV liver disease show limited efficacy

chornic liver disease may progress to cirrhosis and HCC

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86
Q

What type of virus is hepatitis C virus and what are 3 ways it is transmitted?

A

RNA virus

  • blood transfusion
  • intravenous drug use
  • vertical transmission - mother to child
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87
Q

What is the most common cause of HCV transmission in children?

A

Vertical transmission

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88
Q

What increases the likelihood of vertical transmission of HCV to a baby?

A

coinfection with HIV

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89
Q

What type of disease does infection with hepatitis C virus typically cause?

A

Seldom causes acute infection

Majority become chronic carriers with 20-25% risk of progression to cirrhosis or HCC

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90
Q

What proportion of cases of chronic carriers of HCV develop cirrhosis or hepatocellular carcinoma?

A

20-25%

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91
Q

What treatment is available for hepatitis C virus infection? 2 options

A
  1. Combination of pegylated interferon and ribavirin - successful
  2. Recent development with oral antivirals e.g. sofosbuvir - likely to be 100% curative
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92
Q

What children should be screened for hepatitis C virus?

A

High risk children e.g. children of drug abusers

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93
Q

What age of children can be treated for hepatitis C infection and why?

A

3 years and older; no younger than 3 years as HCV may resolve spontaneously following vertically acquired infections

94
Q

What type of virus is hepatitis D and how is it transmitted?

A

defective RNA virus, depends on hepatitis B for replication. Occurs as coinfection with hepatitis B virus or superinfection causing acute exacerbation of chronic hepatitis B virus infection

95
Q

What long term risk is associated with hepatitis D virus and how common is it?

A

Cirrhosis, 50-70% of those who develop chronic HDV infection

96
Q

What type of virus is hepatitis E and how is it transmitted? 3 ways

A

RNA virus,

  1. enterally transmitted, usually by contaminated water
  2. blood transfusion
  3. eating pork
97
Q

What are the 2 ways that hepatitis D virus can infect a person?

A
  1. coinfection with hepatitis B virus infection
  2. superinfection in chronic hepatitis B virus infection causing acute exacerbation of chronic hepatitis B virus infection
98
Q

Where is hepatitis E virus most prevalent?

A

Low-income countries (but found worldwide)

99
Q

What can hepatitis E virus cause in pregnant women?

A

Fulminant hepatic failure with high mortality rate

100
Q

What is seronegative (non-A to G) hepatitis?

A

clinical presentation similar to hepatitis A; when viral aetiology of hepatitis suspected but not identified, konwn as seronegative hepatitis

101
Q

In addition to hepatitis A-E viruses, what is another viral cause of hepatitis?

A

Epstein-Barr virus

102
Q

What are 3 possible features of the presentation of Epstein-Barr virus?

A
  1. Asymptomatic - usually
  2. 40%: hepatitis with marked hepatosplenomegaly. may become fulminant
  3. <5%: jaundiced
103
Q

What is another term for fulminant hepatitis?

A

Acute liver failure

104
Q

What is acute liver failure (fulminant hepatitis)?

A

Development of massive hepatic necrosis with subsequent loss of liver function, with or without hepatic encephalopathy

105
Q

What are 5 causes of acute liver failure/ fulminant hepatitis in children <2 years old?

A
  1. Infection - most common is herpes simplex
  2. Metabolic disease
  3. Seronegative hepatitis
  4. Drug-induced
  5. Neonatal haemochromatosis
106
Q

What are 5 causes of fulminant hepatitis/ acute liver failure in children >2 years?

A
  1. Seronegative hepatitis
  2. Paracetamol overdose
  3. Mitochondrial disease
  4. Wilson disease
  5. Autoimmune hepatitis
107
Q

What are 5 features of presentation of acute liver failure/ fulminant hepatitis?

A
  1. Jaundice
  2. Encephalopathy
  3. Coagulopathy
  4. Hypoglycaemia
  5. Electrolyte disturbance
108
Q

What do early signs of encephalopathy in acute liver failure/ fulminant hepatitis include?

A

Periods of irritability and confusion with drowsiness

109
Q

What are 4 complications of acute liver failure/ fulminant hepatitis?

A
  1. Cerebral oedema
  2. Haemorrhage from gastritis or coagulopathy
  3. Sepsis
  4. Pancreatitis
110
Q

What are 6 investgiations to perform in suspected acute liver failure/ fulminant hepatitis?

A
  1. Blood tests - LFTs: bilirubin, transaminases, ALP, coagulation abnormal, plasma ammonia elevated
  2. Monitor acid-base balance
  3. Monitor blood glucose
  4. Monitor coagulation times
  5. EEG - will show hepatic encephalopathy
  6. CT scan - may demonstrate cerebral oedema
111
Q

What are 7 blood tests to perform in fulminant hepatitis/ acute liver failure and what are they likely to show?

A
  1. Bilirubin - may be normal in early stages
  2. Transaminases - greatly elevated
  3. Alkaline phosphatase - increased
  4. Coagulation - abnormal (monitor)
  5. Plasma ammonia - elevated
  6. Monitor acid-base balance
  7. Monitor blood glucose
112
Q

What are 5 aspects of the management of fulminant hepatitis/ acute liver failure?

A
  1. Early referral to national paediatric liver centre
  2. Maintain blood glucose >4mmol/L with IV dextrose
  3. Prevent sepsis with broad-spectrum abx and antifungal agents
  4. Prevent haemorrhage, particularly from GI tract, with IV vitamin K and H2-blocking drugs or PPIs
  5. Prevent cerebral oedema by fluid restriction and mannitol diuresis if oedema develops
  6. Liver transplant?
113
Q

What are 4 features of fulminant hepatitis/ acute liver failure?

A
  1. Shrinking liver
  2. Rising bilirubin with falling transaminases
  3. Worsening coagulopathy
  4. Progression to coma
114
Q

What proportion of children with acute liver failure/ fulminant hepatitis who progress to coma will die without liver transplantation?

A

70%

115
Q

What are the 3 most common causes of chronic liver disease in older children?

A
  1. Postviral hepatitis B, C
  2. Autoimmune hepatitis and sclerosing cholangitis
  3. Non-alcoholic fatty liver disease
116
Q

What are 6 possible features of presentation of chronic liver disease in older children?

A
  1. Apparent acute hepatitis
  2. Hepatosplenomegaly
  3. Cirrhosis
  4. Portal hypertension
  5. Lethargy
  6. Malnutrition
117
Q

What are 8 causes of chronic liver disease in older children?

A
  1. Postviral hepatitis B, C
  2. Autoimmune hepatitis and sclerosing cholangitis
  3. Drug-induced liver disease (NSAIDs)
  4. Cystic fibrosis
  5. Wilson disease
  6. Fibropolycystic liver disease
  7. Non-alcoholic fatty liver disease
  8. Alpha-1 antitrypsin deficiency
118
Q

What is the mean age of presentation of autoimmune hepatitis and sclerosing cholangitis?

A

7-10 years

119
Q

In which gender is autoimmune hepatitis and sclerosing cholangitis more common?

A

Female

120
Q

What are 3 ways that autoimmune hepatitis and sclerosing cholangitis may present?

A
  1. Acute hepatitis
  2. Fulminant hepatic failure
  3. Chronic liver disease

+autoimmune features (rash, arthritis, haemolytic anaemia, nephritis)

121
Q

What are 4 autoimmune features that may be present in autoimmune hepatitis and sclerosing cholangitis?

A
  1. Skin rash
  2. Arthritis
  3. Haemolytic anaemia
  4. Nephritis
122
Q

What is the diagnosis of both autoimmune hepatitis and sclerosing cholangitis based upon? 5 things

A
  1. Elevated total protein
  2. Hypergammaglobulinaemia (IgG>20g/L)
  3. Positive autoantibodies
  4. Low serum complement (C4)
  5. Typical histology
123
Q

What are 3 key autoantibodies present in primary sclerosing cholangitis?

A
  1. Perinuclear antineutrophil cytoplasmic antibodies (p-ANCA): 84%
  2. Anticardiolipin (aCL) antibodies: 66%
  3. Antinuclear antibodies (ANA): 53%
124
Q

What disease is primary sclerosing cholangitis commonly associated with?

A

Inflammatory bowel disease, in particular ulcerative colitis

125
Q

What are 3 things that autoimmune hepatitis may occur in association with?

A
  1. Inflammatory bowel disease
  2. Coeliac disease
  3. Other autoimmune diseases (

(or in isolation)

126
Q

What is the management of autoimmune hepatitis?

A

Prednisolone and azathioprine

127
Q

What proportion of children with autoimmune hepatitis will respod to azathioprine and prednisolone?

A

90%

128
Q

What is the treatment for sclerosing cholangitis?

A

Ursodeoxycholic acid

129
Q

How significant a cause of death in cystic fibrosis is liver disease?

A

Second most common cause of death after respiratory disease

130
Q

What is the most common liver abnormality in cystic fibrosis? What are 2 things this may be in association with?

A

Hepatic steatosis - fatty liver

  1. protein energy malnutrition
  2. micronutrient deficiencies
131
Q

Does steatosis caused by cystic fibrosis tend to progress?

A

No

132
Q

What is the management of hepatic steatosis in cystic fibrosis?

A

Ensuring optimal nutritional support (steatosis does not generally progress)

133
Q

What causes more significant liver disease that steatosis to arise in cystic fibrosis?

A

Thick tenacious bile wiht abnormal bile acid concentration leading to progressive biliary fibrosis

134
Q

What 2 complications of liver disease in CF develop in 20% of children by mid-adolescence?

A
  1. Cirrhosis
  2. Portal hypertension
135
Q

What is the best way to assess early liver disease in cystic fibrosis?

A

Liver histology

Biochemistry, ultrasound or radioisotope scanning unlikely to show a lot early on

136
Q

What are 3 things that liver histoloy is likely to show in cystic fibrosis?

A
  1. Fatty liver
  2. Focal biliary fibrosis
  3. Focal nodular cirrhosis
137
Q

What are 4 aspects of management of liver disease caused by cystic fibrosis?

A
  1. Endoscopic treatment of varices
  2. Nutritional therapy
  3. Treatment with ursodeoxycholic acid
  4. Liver transplantation - if end-stage liver disease (alone or with heart-lung transplant)
138
Q

What is the inheritance pattern and cause of Wilson disease?

A

Autosomal recessive; many mutations identified. Basic genetic defect is combination of reduced synthesis of caeruloplasmin (copper-binding protein) and defective excretion of copper in the bile, leading to accumulation of copper in liver, brain, kidney and cornea

139
Q

What are 4 places where copper accummulates in Wilson’s disease?

A
  1. Liver
  2. Brain
  3. Kidney
  4. Cornea
140
Q

At what age does Wilson’s disease present?

A

Rarely below age of 3; >3y

141
Q

What type of presentation of Wilson disease is most likely when presenting in childhood?

A

Hepatic presentation

142
Q

What are 4 ways that Wilson disease with a hepatic presentatino may present?

A
  1. Acute hepatitis
  2. Fulminant hepatitis (acute liver failure)
  3. Cirrhosis
  4. Portal hypertension
143
Q

In addition to hepatic presentations of Wilson disease (acute/ fulminant hepatitis, portal hypertension, cirrhosis), what are 5 further possible features (more likely if presenting from second decade onwards)?

A
  1. Neuropsychiatric features - mood and behaviour change
  2. Deterioration in school performance
  3. Extrapyramidal signs - incoordination, tremor, dysarthria
  4. Renal tubular dysfunction - vitamin D-resistant rickets
  5. Haemloytic anaemia
  6. Kayser-Fleischer rings
144
Q

What is the youngest age at which Kayser-Fleischer rings appear in Wilson disease?

A

don’t appear before 7 years

145
Q

What are 5 investigations and findings in Wilson disease?

A
  1. Low serum caeruloplasmin
  2. Low serum copper
  3. Urinary copper excretion increased
  4. Liver biopsy - elevated hepatic copper
  5. Gene mutation identified
146
Q

What is the definitive investigation to diagnose Wilson disease?

A

Elevated hepatic copper on liver biopsy OR identification of gene mutation

147
Q

What are 3 aspects of management of Wilson disease and how do they each work?

A
  1. Penicillamine or trientine: promote urinary copper excretion
  2. Zinc: reduces copper absorption
  3. Pyridoxine: prevents peripheral neuropathy
148
Q

How long may it take for neurological improvement from therapy to show in Wilson disease?

A

up to 12 months

149
Q

When is zinc used in children asymptomatic from Wilson disease?

A

used in asymptomatic children identified by screening families with an index case

150
Q

What is the prognosis of Wilson disease if left untreated?

A

30% of children will die from hepatic complications

151
Q

When is liver transplantation considered in Wilson disease?

A

For children with acute liver failure or severe end-stage liver disease

152
Q

What is fibropolcystic liver disease (aka ciliopathies)?

A

Range of inherited conditions affecting the development of the intrahepatic biliary tree

153
Q

What are 2 ways that fibropolycystic liver disease (aka ciliopathies) may present?

A
  1. Liver cystic disease or fibrosis
  2. Renal disease
154
Q

At what age does congenital hepatic fibrosis (form of fibropolycystic liver disease) present?

A

Children over 2 years old

155
Q

What are 3 key features that children with congenital hepatic fibrosis may present with?

A
  1. Hepatosplenomegaly
  2. Abdominal distension
  3. Portal hypertension
156
Q

How does congenital fibrosis differ from cirrhosis in terms of investigations?

A

in congenital hepatic fibrosis, liver function tests may be normal in early stage

157
Q

What will liver histology show in congenital liver fibrosis?

A

Large bands of hepatic fibrosis containing abnormal bile ductules

158
Q

What are 2 key complicatios of congenital liver fibrosis?

A
  1. Portal hypertension with varices
  2. Recurrent cholangitis
159
Q

What type of disease may coexist with congenital fibropolycystic liver disease?

A

Cystic renal disease

160
Q

What are 2 possible implications of coexistent cystic renal disease in fibropolycystic liver disease?

A
  1. Hypertension
  2. Renal dysfunction
161
Q

What are 2 indications for liver transplant in congenital fibropolycystic liver disease?

A
  1. Severe recurrent cholangitis
  2. Deterioration of renal function requiring renal transplant - combined transplant would be offered
162
Q

What is the single most common cause of chronic liver disease in the high income world?

A

Non-alcoholic fatty liver disease

163
Q

What does the range of non-alcoholic fatty liver disease span between?

A

from simple fatty deposition (steatosis) through to inflammation (steatohepatitis), fibrosis, cirrhosis, and end-stage liver failure

164
Q

What are 2 things that non-alcoholic fatty liver disease may be associated with in childhood?

A
  1. Metabolic syndrome
  2. Obesity
165
Q

What is the progonosis of non-alcoholic fatty liver disease in children?

A

Uncertain; few develop cirrhosis in childhood, in contrast to 8-17% of adults

166
Q

What are 3 ways that non-aloholic fatty liver disease in children may present?

A
  1. may be asymptomatic
  2. vague RUQ pain
  3. lethargy
  4. incidental echogenic liver on USS
  5. mildly elevated transaminases (ALT/AST) carried out for different reason
167
Q

What are 5 key autoantbodies found in autoimmune hepatitis?

A
  1. Antinuclear antibodies (ANA) type 1
  2. Smooth muscle antibodies (SMA) type 1
  3. Anti-liver-kidney microsomal antibodies (anti-LKM1) type 2
  4. anti-liver cytosol (anti-LC) antibodies type 2
  5. Anti-soluble liver antigen (anti-SLA) type 3
168
Q

What will liver biopsy show in non-alcoholic fatty liver disease?

A

marked steatosis with or without inflammation (NASH) - steatohepatitis or fibrosis

169
Q

What is the pathogenesis of NAFLD?

A

not fully understood, may be linked to insulin resistance

170
Q

What is the treatment for non-alcoholic fatty liver disease (NAFLD)?

A

Targets weight loss through diet and exercise, which may lead to liver function tests returning to normal

171
Q

What are 9 complications of chronic liver disease in children?

A
  1. Nutrition problems
  2. Fat-soluble vitamins
  3. Pruritus
  4. Encephalopathy
  5. Cirrhosis and portal hypertension
  6. Oesophageal varices
  7. Ascites
  8. Spontaneous bacterial peritonitis
  9. Renal failure
172
Q

What are 3 barriers to effective nutrition in children with chronic liver disease?

A
  1. Fat malabsorption
  2. Protein malnutrition - poor intake + high catabolic rate of diseased liver
  3. Anorexia - unwell child cannot take required amount of nutrition
173
Q

What causes fat malabsorption in chronic liver disease?

A

Long chain fat not effectively absorbed without bile; reduction in bile-salt pool in advanced liver disease (is particularly a problem in cholestatic liver disease)

174
Q

How can fat malabsorption in chronic liver disease be managed? 3 things

A
  1. medium chain triglyceride-containing milk (specialist formula) is required if children are persistently cholestatic, as it does not require bile micelles for absorption
  2. Up to 40% of fat needs to be long chain fat to prevent essential fatty acid deficiency
  3. Falt-soluble vitamin supplmentation
175
Q

Why do fat-soluble vitamins need to be supplemented?

A

Due to fat malabsorption in chronic liver disease; fat-soluble vitamins are carried on long chain fats and hence deficiency common unless these vitamins are supplemented

176
Q

What are the 2 things that make protein malnutrition common at presentation of liver disease?

A
  1. Poor intake
  2. High catabolic rate of diseased liver - using more energy
177
Q

When should protein restriction be considered in chronic liver disease?

A

should not be restriction (risk of protein malnutrition) unless child is encephalopathic

178
Q

How may the anorexia caused by chronic liver disease be managed?

A

Many require nasogastric tube feeding or occasionally parenteral nutrition

179
Q

What are 2 ways that fat-soluble vitamin supplements can be given in chronic liver disease?

A
  1. Orally
  2. IM - if severe deficiency
180
Q

What are the 4 fat-soluble vitamins?

A

ADEK

181
Q

What is the effect of vitamin K deficiency?

A

Bleeding diathesis including intracranial bleeding

182
Q

What is the effect of vitamin A deficiency?

A

Retinal changes in infants and night blindness in older children

183
Q

What are 3 effects of vitamin E deficiency?

A

Peripheral neuropathy, haemolysis, ataxia

184
Q

What is the effect of vitamin D deficiency in children with chronic liver disease?

A

Rickets and fractures

185
Q

What is the cause of pruritus in hepatic disease?

A

Severe pruritus associated with cholestasis although aetiology not clear

186
Q

What are 5 aspects of the management of severe pruritus in liver disease?

A
  1. Loose cotton clothing
  2. Avoiding overheating
  3. Keep nails short (excoriation)
  4. Moisturise with emollients
  5. Medication: phenobarbital, cholestyramine, ursodeoxycholic acid, rifampicin, sertraline, ondansetron
187
Q

How easy is it to treat pruritus associated with liver disease?

A

very difficult

188
Q

What are 6 medications that can be used to treat pruritus in liver disease?

A
  1. Phenobarbital: stimulates bile flow
  2. Cholestyramine: bile salt resin to absorb bile salts
  3. Ursodeoxycholic acid: oral bile acid to solubilise bile
  4. Rifampicin: enzyme inducer
  5. Sertraline
  6. Ondansetron
189
Q

When does encephalopathy occur in liver disease?

A

End-stage liver disease

190
Q

What are 5 things that may precipitate encephalopathy in end-stage livere disease?

A
  1. GI haemorrhage
  2. Sepsis
  3. Sedatives
  4. Renal failure
  5. Electrolyte imbalance
191
Q

Why is encephalopathy in liver disease hard to diagnose in children?

A

As level of consciouness may vary throughout day

192
Q

What are 2 ways that encephalopathy may present in infants?

A
  1. Irritability
  2. Sleepiness
193
Q

What are 4 ways that older children may present with encephalopathy?

A
  1. Abnormalities in mood
  2. Sleep rhythm abnormalities
  3. Intellectual performance changes
  4. Behaviour change
194
Q

What are 2 investigations that will detect findings to help diagnose encephalopathy in end stage liver disease?

A
  1. Plasma ammonia may be elevated
  2. EEG - always abnormal
195
Q

What are 2 drugs that can be used to treat encephalopathy in end-stage liver disease and how do they work to do this?

A
  1. Oral lactulose (osmotic laxative)
  2. Nonabsorbable oral antibiotic (e.g. rifaximin)

help reduce ammonia by lowering colonic pH and increasing gut transit time

196
Q

What is the definition of cirrhosis?

A

end result of many forms of liver disease, defined pathologically as extensive fibrosis with regenerative nodules

197
Q

What are 2 things which may cause cirrhosis?

A
  1. secondary to hepatocellular disease
  2. chronic bile duct obstruction - biliary cirrhosis
198
Q

What are the 3 main pathophysiological effects of cirrhosis?

A
  1. Diminished hepatic function
  2. Portal hypertension: splenomegaly, varices, ascites
  3. May develop hepatocellular carcinoma
199
Q

What are 3 effects of portal hypertension?

A
  1. Splenomegaly
  2. Varices
  3. Ascites
200
Q

What might be the clinical picture in chidren with compensated cirrhosis?

A

May be asymptomatic if liver function is adequate

May not be jaundiced, normal liver function tests

201
Q

What are 9 physical signs of decompensated cirrhosis?

A
  1. Jaundice
  2. Palmar and plantar erythema
  3. Telangectasia and spider naevi
  4. Malnutrition
  5. Hypotonia
  6. Dilated abdominal veins (caput medusa) - portal hypertension
  7. Splenomegaly - portal hypertension
202
Q

Are you likely to feel hepatomegaly in cirrhosis? Why/why not?

A

No - more likely to be shrunken and impalpable

203
Q

What are 4 investigations that should be performed liver cirrhosis?

A
  1. Screen for known causes of chronic liver disease
  2. Upper GI endoscopy
  3. Abdominal ultrasound
  4. Liver biopsy
204
Q

What are 2 things that upper GI endoscopy may detect in liver cirrhosis?

A
  1. oesophageal varices
  2. erosive gastritis
205
Q

What might abdominal ultrasound show in liver cirrhosis?

A

Shrunken liver and splenomegaly with gastric and oesophageal varices

206
Q

What can a liver biopsy show in cirrhosis?

A

May indicate the aetiology e.g. typical changes in congenital hepatitic fibrosis, copper storage

207
Q

Why might a liver biopsy in cirrhosis be difficult?

A

increased fibrosis

208
Q

What might biohemical tests show as cirrhosis decompensates?

A

may demonstrate elevation of aminotransferases (alanine aminotransferase and aspartate aminotransferase) and alkaline phosphatase. plasma albumin falls and prothrombin time becomes increasingly prolonged

209
Q

What is the difference between what is show by aminotransferases and ALP, and what is shown by albumin and prothrombin time

A

ALT, AST, ALP: indicate inflammation

albumin and prothrombin time: indicate liver function

prothrombin time = indication of clotting function

210
Q

What can hypersplenism show on blood tests?

A

Thrombocytopenia - low platelets

211
Q

How are oesophageal varices best diagnosed?

A

Upper gastrointestinal endoscopy

212
Q

How is acute bleeding from oesophageal varices treated?

A

Conservatively, with blood transfusions and H2-blockers (e.g. ranitidine) or omeprazole

213
Q

What are 4 options for treatment of oesophageal varices if bleeding persists?

A
  1. Octreotide infusion (reduces portal venous pressure)
  2. Vasopressin analogues (vasoconstrictor activity)
  3. Endoscopic band ligation
  4. Sclerotherapy
214
Q

What are 2 ways to manage oesophageal varices if trying to avoid liver transplantation/ in the lead up to it?

A
  1. Portacaval shunts - may preclude
  2. Radiological placement of stent between hepatic and portal veins - can be used as temporary measure if transplant being considered
215
Q

What is the pathophysiology of ascites in chronic liver disease?

A

it is uncertain, but contributory factors include hypoalbuminaemia, sodium retention, renal impairment and fluid redistribution

216
Q

What are 4 ways to treat ascites?

A
  1. Sodium and fluid restriction
  2. Diuretics
  3. if refractory: albumin infusions or
  4. Paracentesis
217
Q

What is a possible complication of ascites?

A

Spontaneous bacterial peritonitis - ifnection of ascitic fluid

218
Q

What are 4 symptoms that should make you suspect spontaneous bacterial peritonitis?

A
  1. Undiagnosed fever
  2. Abdominal pain
  3. Tenderness
  4. Unexplained deterioration in hepatic or renal function
219
Q

What are the 2 steps of management of spontaneous bacterial peritonitis?

A
  1. Diagnostic paracentesis performed and sent for WCC and differential and culture
  2. Treatment with broad-spectrum antibiotics
220
Q

What are 3 things that renal failure can be secondary to in chronic liver disease?

A
  1. Renal tubular acidosis
  2. Acute tubular necrosis
  3. Functional renal failure (hepatorenal syndrome)
221
Q

What are 3 situations when liver transplantation is an accepted therapy?

A
  1. Acute liver failure
  2. Chronic end-stage liver failure
  3. Some hepatic malignancy (hepatoblastoma or hepatocellular carcinoma)
222
Q

What are 4 indications for transplantation in chronic liver failure?

A
  1. Severe malnutrition unresponsive to intensive nutritional therapy
  2. Complications refractory to medical management (bleeding varices, resistant ascites)
  3. Failure of growth and development
  4. Poor quality of life
223
Q

What must be done prior to liver transplant and what 2 things does this involve?

A

Liver transplant evaluation

  1. Assessment of vascular anatomy of liver
  2. Exclusion of irreversible disease in other organ systems
224
Q

What are 3 absolute contraindications for liver transplantation?

A
  1. Sepsis
  2. Untreated cadiopulmonary disease
  3. Cerebrovascular disease
225
Q

What are 2 options for transplanted livers in children and why?

A

Considerable difficulty obtaining small organs for children. Most receive part of an adult’s liver:

  1. Cadaveric graft - reduced to fit child’s abdomen (reduction hepatectomy) or split (shared between adult and child)
  2. Living related donor
226
Q

What are 5 complications post-liver transplantation?

A
  1. Primary non-function of liver (5%)
  2. Hepatic artery thrombosis (10-20%)
  3. Biliary leaks and strictures (20%)
  4. Rejection (30-60%)
  5. Sepsis
227
Q

What is the commonest cause of death post liver transplant?

A

Sepsis

228
Q

What is 1) the overall 1 year survival in large national centres following liver translpant?

2) What is the overall 20-year survival?

A
  1. 90%
  2. >80%
229
Q

What is the time period when most post-operative deaths following liver transplant occur?

A

within first 3 months (if survive initial postoperative period, usually do well)

230
Q

What is the pattern of deranged LFTs in hepatocellular vs cholestatic disease?

A

Hepatocellular: ALT or AST > ALP

Cholestatic: ALP > ALT or AST

Gamma GT: cholestasis

Paeds: Gastro and Growth (14 decks)

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