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Yr 4 - CCC > GI: Liver Disease > Flashcards

GI: Liver Disease Flashcards

1
Q

How does liver cirrhosis lead to portal hypertension?

A

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

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

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2
Q

What are the 4 most common causes of liver cirrhosis?

A

1) Alcohol related liver disease
2) Hep B
3) Hep C
4) Non-alcoholic fatty liver disease (NAFLD)

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3
Q

What 2 infections can lead to cirrhosis?

A

Hep B and C

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4
Q

Give some rarer causes of cirrhosis

A

1) Autoimmune hepatitis
2) Alpha 1 antitrypsin deficiency
3) Primary biliary cirrhosis
4) Haemochromatosis
5) Wilsons disease
6) Cystic fibrosis
7) Drugs (e.g., amiodarone, methotrexate and sodium valproate)

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5
Q

Give 3 drugs that can cause cirrhosis

A

1) methotrexate
2) amiodarone
3) sodium valproate

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6
Q

Signs of cirrhosis on examination?

A

1) Cachexia
2) Jaundice (raised bilirubin)
3) Hepatomegaly
4) Small nodular liver as it becomes more cirrhotic
5) Spider naevi
6) Caput medusae
7) Gynaecomastia & testicular atrophy in males
8) Splenomegaly (due to portal hypertension)
9) Palmar erythema (increased oestrogen)
10) Bruising (abnormal clotting)
11) Excoriations
12) Ascites
13) Leukonychia (white fingernails) associated with hypoalbuminaemia
14) Asterixis (“flapping tremor”) in decompensated liver disease

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7
Q

What is leukonychia associated with?

A

Hypoalbuminaemia

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8
Q

Abnormal liver function tests without a clear cause require a non-invasive liver screen.

What does this include?

A

1) US liver (used to diagnose fatty liver)

2) Hep B & C serology

3) Autoantibodies (autoimmune hepatitis, primary biliary cirrhosis and primary sclerosing cholangitis)

4) Immunoglobulins (autoimmune hepatitis and primary biliary cirrhosis)

5) Caeruloplasmin (Wilsons disease)

6) Alpha-1 antitrypsin levels (alpha-1 antitrypsin deficiency)

7) Ferritin and transferrin saturation (hereditary haemochromatosis)

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9
Q

What test is used to assess for Wilson’s disease?

A

Caeruloplasmin

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10
Q

What is caeruloplasmin?

A

a serum copper transport protein.

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11
Q

Describe caeruloplasmin levels in liver disease?

A

Low

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12
Q

Investigations in Wilson’s disease?

A

If suspicion of Wilson disease is high, order a ceruloplasmin level. It will be less than 20 mg/dL (normal 20 mg/dL to 40 mg/dL). Urinary copper levels will be raised more than 100 mcg/dL.

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13
Q

What autoantibodies are relevant to liver disease

A

1) Antinuclear antibodies (ANA)

2) Smooth muscle antibodies (SMA)

3) Antimitochondrial antibodies (AMA)

4) Antibodies to liver kidney microsome type-1 (LKM-1)

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14
Q

How does liver disease affect albumin?

A

Low albumin due to reduced synthetic function of the liver

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15
Q

How does liver disease affect prothrombin time?

A

Increased prothrombin time due to reduced synthetic function of the liver (reduced production of clotting factors)

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16
Q

How does liver disease affect platelets?

A

Thrombocytopenia (low platelets) is a common finding and indicates more advanced disease

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17
Q

How does liver disease affect sodium?

A

Hyponatraemia (low sodium) occurs with fluid retention in severe liver disease

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18
Q

What is a tumour marker for HCC?

A

alpha-fetoprotein (AFP)

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19
Q

1st line investigation for assessing fibrosis in non-alcoholic fatty liver disease?

A

The enhanced liver fibrosis (ELF) blood test

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20
Q

Is the ELF test used in other types of liver disease?

A

No - only non-alcoholic fatty liver disease

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21
Q

What does the ELF test measure?

A

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

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22
Q

What ELF test result indicates advanced fibrosis?

A

10.51 or above

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23
Q

What ELF test result indicates unlikely advanced fibrosis?

A

Under 10.51

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24
Q

What is used to diagnose non-alcoholic fatty liver disease (once other causes are excluded)?

A

US

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25
Q

How do fatty changes in NAFLD appear on US?

A

appear as increased echogenicity.

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26
Q

What may an US show in NAFLD?

A

1) nodularity of the surface of the liver

2) a ‘corkscrew’ appearance to the hepatic arteries with increased flow as they compensate for reduced portal flow

3) Enlarged portal vein with reduced flow

4) Ascites

5) Splenomegaly

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27
Q

What is used as a screening tool for HCC?

A

US + AFP

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28
Q

What is a transient elastography (i.e. FibroScan)?

Purpose?

A

Can be used to assess the stiffness of the liver using high-frequency sound waves.

It helps determine the degree of fibrosis (scarring) to test for liver cirrhosis.

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29
Q

When would a transient elastography be used?

A

It is used in patients at risk of cirrhosis:

1) Alcohol-related liver disease
2) Heavy alcohol drinkers (men drinking more than 50 units or women drinking more than 35 units per week)
3) Non-alcoholic fatty liver disease and advanced liver fibrosis (score 10.51 or more on the ELF blood test)
4) Hepatitis C
5) Chronic hepatitis B

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30
Q

What can be used to assess for and treat oesophageal varices when portal hypertension is suspected?

A

Endoscopy

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31
Q

What test is used to confirm the diagnosis of cirrhosis?

A

Liver biopsy

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32
Q

What is an MELD (Model for End-Stage Liver Disease) score?

A

Gives an estimated 3-month mortality as a percentage for patients with compensated cirrhosis.

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33
Q

How often should the MELD score be used?

A

NICE recommend using the MELD score every 6 months in patients with compensated cirrhosis.

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34
Q

What is involved in the MELD score?

A

The formula considers the bilirubin, creatinine, INR and sodium and whether they require dialysis,

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35
Q

What is the Child-Pugh score?

A

Uses 5 factors to assess the severity of cirrhosis and the prognosis.

Each factor is considered and scored 1, 2 or 3.

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36
Q

What is involved in the Child-Pugh score?

A

ABCDE:

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

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37
Q

How are complications monitored for in cirrhosis?

A

1) MELD score every 6 months

2) Ultrasound and alpha-fetoprotein every 6 months for hepatocellular carcinoma

3) Endoscopy every 3 years for oesophageal varices

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38
Q

When is liver transplantation generally considered?

A

when there are features of decompensated liver disease.

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39
Q

What are the 4 key features of decompensated liver disease?

A

AHOY:

1) Ascites
2) Hepatic encephalopathy
3) Oesophageal varices bleeding
4) Yellow (jaundice)

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40
Q

What is 5-year survival after cirrhosis have developed?

A

Approx 5 years

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41
Q

What are some complications of cirrhosis?

A

1) Malnutrition and muscle wasting

2) Portal hypertension, oesophageal varices and bleeding varices

3) Ascites and spontaneous bacterial peritonitis

4) Hepatorenal syndrome

5) Hepatic encephalopathy

6) Hepatocellular carcinoma

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42
Q

How can cirrhosis lead to malnutrition?

A

1) Patients often have a loss of appetite

2) Cirrhosis affects protein metabolism in the liver and reduces the amount of protein the liver produces.

3) Disrupts the ability of the liver to store glucose as glycogen and release it when required

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43
Q

How does cirrhosis lead to muscle wasting?

A

Overall, less protein is available for maintaining muscle tissue and muscle tissue is broken down for use as fuel.

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44
Q

Nutritional guidance in liver cirrhosis?

A
  • Regular meals
  • High protein and calorie intake
  • Reduced sodium intake to minimise fluid retention
  • Avoiding alcohol
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45
Q

What is the portal vein?

A

Comes from the superior mesenteric and splenic veins and delivers blood to the liver.

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46
Q

How does cirrhosis cause portal hypertension?

A

Liver cirrhosis increases the resistance to blood flow in the liver.

As a result, there is increased back pressure on the portal system (portal hypertension).

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47
Q

How does cirrhosis lead to splenomegaly?

A

Portal hypertension - back pressure of blood results in splenomegaly.

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48
Q

How does cirrhosis lead to a) oesophageal varices, b) caput medusae?

A

Back pressure in the portal system causes swollen and tortuous vessels at sites where collaterals form between the portal and systemic venous systems.

These collaterals can occur in:
a) Distal oesophagus (oesophageal varices)
b) Anterior abdominal wall (caput medusae)

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49
Q

Complications of varices?

A

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

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50
Q

1st line prophylaxis of bleeding in stable oesophageal varices?

A

Non-selective beta blockers (e.g., propranolol)

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51
Q

If beta blockers are contraindicated, what is the next option for prophylaxis of bleeding in stable oesophageal varices?

A

Variceal band ligation

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52
Q

What is variceal band ligation?

A

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

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53
Q

Management of bleeding oesophageal varices?

A

Life threatening - ABCDE

1) Immediate senior help

2) Consider blood transfusion (activate the major haemorrhage protocol)

3) Treat any coagulopathy (e.g., with fresh frozen plasma)

4) Vasopressin analogues (e.g., terlipressin or somatostatin) cause vasoconstriction and slow bleeding

5) Prophylactic broad-spectrum antibiotics (shown to reduce mortality)

6) Urgent endoscopy with variceal band ligation

7) Consider intubation and intensive care

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54
Q

What is given in bleeding oesophageal varices to cause vasoconstriction and slow bleeding?

A

Vasopressin analogues (e.g., terlipressin or somatostatin)

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55
Q

What are 2 other options to control the bleeding in bleeding oesophageal varices?

A

1) Sengstaken-Blakemore tube

2) Transjugular intrahepatic portosystemic shunt (TIPS)

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56
Q

What is a Sengstaken-Blakemore tube?

A

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

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57
Q

What is a transjugular intrahepatic portosystemic shunt (TIPS)?

A

1) An interventional radiologist inserts a wire under x-ray guidance into the jugular vein, down the vena cava and into the liver via the hepatic vein.

2) A connection is made through the liver between the hepatic vein and portal vein, and a stent is inserted.

3) This allows blood to flow directly from the portal vein to the hepatic vein, relieving the pressure in the portal system.

58
Q

What 2 veins are connected in a TIPS?

A

Hepatic and portal vein

59
Q

What are the 2 main indications for TIPS?

A

1) Bleeding oesophageal varices
2) Refractory ascites

60
Q

what is refractory ascites?

A

ascites which cannot be mobilized by low sodium diet and maximal doses of diuretics

61
Q

What is ascites?

A

Fluid in the peritoneal cavity

62
Q

How does cirrhosis lead to ascites?

A

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

63
Q

How does cirrhosis lead to fluid and sodium retention?

A

1) Loss of fluid to peritoneal cavity (ascites)

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

3) Kidneys release renin in response

4) This causes increased aldosterone secretion via the renin-angiotensin-aldosterone system.

5) Increased aldosterone causes the reabsorption of fluid and sodium in the kidneys

64
Q

Does cirrhosis cause transudative or exudative ascites?

A

Transudative (low protein count)

65
Q

Management options for ascites in cirrhosis?

A

1) Low sodium diet

2) Aldosterone antagonists e.g. spironolactone

3) Paracentesis (ascitic tap or drain)

4) Prophylactic antibiotics e.g. ciprofloxacin or norfloxacin

5) TIPS is considered in refractory ascites

6) Liver transplantation is considered in refractory ascites

66
Q

When are prophylactic antibiotics indicated in ascites in cirrhosis?

A

when there is <15 g/litre of protein in the ascitic fluid

67
Q

What is spontaneous bacterial peritonitis (SBP)?

A

It involves an infection developing in the ascitic fluid and peritoneal lining without a clear source of infection (e.g., an ascitic drain or bowel perforation).

Occurs in 10-20% of patients with ascites.

68
Q

Features of spontaneous bacterial peritonitis?

A
  • Can be asymptomatic
  • Fever
  • Abdominal pain
  • Deranged bloods (raised WBC, CRP, creatinine or metabolic acidosis)
  • Ileus (reduced movement in the intestines)
  • Hypotension
69
Q

What are the 2 most common organisms causing spontaneous bacterial peritonitis (SBP)?

A

1) E. coli
2) Klebsiella pneumoniae

70
Q

Management of spontaneous bacterial peritonitis (SBP)?

A

1) Taking a sample of ascitic fluid for culture before giving antibiotics

2) Intravenous broad-spectrum antibiotics according to local policies (e.g., piperacillin with tazobactam)

71
Q

What is hepatorenal syndrome?

A

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

72
Q

What is hepatic encephalopathy?

A

It is thought to be caused by the build-up of neurotoxic substances that affect the brain.

73
Q

What is most important toxin that can build up in cirrhosis?

A

Ammonia

74
Q

Where is ammonia produced/absorbed?

A

Produced by intestinal bacteria when they break down proteins and is absorbed in the intestines.

75
Q

What are the 2 reasons that ammonia builds up in cirrhosis?

A

1) The liver cells’ functional impairment prevents them from metabolising the ammonia into harmless waste products

2) CPollateral vessels between the portal and systemic circulation mean that the ammonia bypasses the liver and enters the systemic system directly.

76
Q

Presentation of hepatic encephalopathy?

A

Reduced consciousness and confusion

77
Q

Factors that can trigger or worsen hepatic encephalopathy?

A
  • Constipation
  • Dehydration
  • Electrolyte disturbance
  • Infection
  • Gastrointestinal bleeding
  • High protein diet
  • Medications (particularly sedative medications)
78
Q

Management of hepatic encephalopathy?

A

1) Lactulose (aiming for 2-3 soft stools daily)

2) Abx e.g. rifaximin –> to reduce the number of intestinal bacteria producing ammonia

3) Nutritional support (nasogastric feeding may be required)

79
Q

How does lactulose reduce ammonia (3 ways)?

A

1) Speeds up transit time and reduces constipation (the laxative effect clearing the ammonia before it is absorbed)

2) Promotes bacterial uptake of ammonia to be used for protein synthesis

3) Changes the pH of the contents of the intestine to become more acidic, killing ammonia-producing bacteria

80
Q

What is Abx of choice in hepatic encephalopathy?

A

Rifaximin

81
Q

What is Rifaximin abx of choice in hepatic encephalopathy?

A

it is poorly absorbed and stays in the gastrointestinal tract.

82
Q

Give 2 alternatives to rifaximin in hepatic encephalopathy?

A

Neomycin and metronidazole

83
Q

What is alcohol related liver disease?

A

Alcohol-related liver disease results from long-term excessive consumption of alcohol.

84
Q

What 2 factors may increase risk of alcoholic related liver disease?

A

1) obesity
2) viral hepatitis

85
Q

What are the 3 stages of alcohol related liver disease?

A

1) Alcoholic fatty liver (also called hepatic steatosis)

2) Alcoholic hepatitis

3) Cirrhosis

86
Q

What occurs in alcohol fatty liver?

A

Drinking leads to a build-up of fat in the liver. This process is reversible with abstinence.

87
Q

What is alcoholic hepatitis?

A

Drinking alcohol over a long period causes inflammation in the liver cells (binge drinking is associated with the same effect)

88
Q

Is mild alcoholic hepatitis reversible?

A

Usually with permanent abstinence

89
Q

Is cirrhosis reverisble?

A

No. Stopping drinking can prevent further damage. Continued drinking has a very poor prognosis.

90
Q

Weekly units of alcohol recommendations?

A

14 - this should be spread evenly over 3 or more days and not more than 5 units in a single day.

91
Q

Define binge drinking

A

6 or more units for women and 8 or more for men in a single session.

92
Q

What can alcohol in pregnancy lead to?

A

1) Miscarriage
2) Small for dates
3) Preterm delivery
4) Fetal alcohol syndrome

93
Q

Complications of alcohol?

A

1) Alcohol-related liver disease

2) Cirrhosis and its complications (e.g., hepatocellular carcinoma)

3) Alcohol dependence and withdrawal

4) Wernicke-Korsakoff syndrome (WKS)

5) Pancreatitis

6) Alcoholic cardiomyopathy

7) Alcoholic myopathy, with proximal muscle wasting and weakness

8) Increased risk of cardiovascular disease (e.g., stroke or myocardial infarction)

9) Increased risk of cancer, particularly breast, mouth and throat cancer

94
Q

Examination findings in excessive alcohol consumption?

A
  • Signs of cirrhosis e.g. caput medusae, ascites
  • Smelling of alcohol
  • Slurred speech
  • Bloodshot eyes
  • Dilated capillaries on the face (telangiectasia)
  • Tremor
95
Q

What may be seen in LFTs in alcohol-related liver disease?

A

1) Raised alanine transaminase (ALT)

2) Raised aspartate transferase (AST)

3) Raised alkaline phosphatase (ALP) (later in disease)

4) AST:ALT ratio above 1.5 particularly suggests alcohol-related liver disease

5) Low albumin

6) Raised bilirubin (in cirrhosis)

7) Raised gamma-glutamyl transferase (gamma-GT) (particularly notable with alcohol-related liver disease)

96
Q

What AST:ALT ratio particularly suggests alcohol-related liver disease?

A

AST:ALT ratio above 1.5

97
Q

How is a diagnosis of alcohol-related hepatitis or cirrhosis made?

A

Liver biopsy

98
Q

Management of alcohol-related liver disease?

A

1) Stop drinking alcohol permanently (drug and alcohol services are available for support)

2) Psychological interventions (e.g., motivational interviewing or cognitive behavioural therapy)

3) Consider a detoxication regime

4) Nutritional support with vitamins (particularly thiamine – vitamin B1) and a high-protein diet

5) Corticosteroids

6) Treat complications of cirrhosis (e.g., portal hypertension, varices, ascites and hepatocellular carcinoma)

7) Liver transplant in severe disease (generally 6 months of abstinence is required)

99
Q

How are corticosteroids used in alcohol related liver disease?

A

Corticosteroids may be considered to reduce inflammation in severe alcoholic hepatitis to improve short-term outcomes (but not long-term outcomes)

100
Q

The CAGE questions can be used to quickly screen for harmful alcohol use.

What is this?

A

C - Cut down –> Do you ever think you should cut down?

A - Annoyed –> Do you get annoyed at others commenting on your drinking?

G - Guilty –> Do you ever feel guilty about drinking?

E - Eye opener –> Do you ever drink in the morning to help your hangover or nerves?

101
Q

What score can be used to screen people for harmful alcohol use?

A

Alcohol Use Disorders Identification Test (AUDIT)

102
Q

What AUDIT score indicates harmful drinking?

A

8 or more

103
Q

Describe symptoms during first 6-12 hours of alcohol withdrawal

A

Tremor, sweating, headache, craving and anxiety

104
Q

Describe symptoms during 12-24 hours of alcohol withdrawal

A

Hallucinations

105
Q

Describe symptoms during 24-48 hours of alcohol withdrawal

A

seizures (peak incidence of seizures at 36 hours)

106
Q

When is peak incidence of seizures in alcohol withdrawal?

A

36 hours

107
Q

When is the peak incidence of delirium tremens in alcohol withdrawal?

A

48 to 72 hours

108
Q

Mechanism of alcohol withdrawal?

A

Chronic alcohol consumption enhances GABA mediated inhibition in the CNS (similar to benzodiazepines) and inhibits NMDA-type glutamate receptors.

Alcohol withdrawal is thought to be lead to the opposite (decreased inhibitory GABA and increased NMDA glutamate transmission)

108
Q

What is delirium tremens?

A

Delirium tremens is a medical emergency associated with alcohol withdrawal (5% mortality rate if left untreated)

108
Q

What receptors does alcohol stimulate?

A

GABA receptors in the brain (relaxing effect)

109
Q

What tools can be used to score the patient on their alcohol withdrawal symptoms and guide treatment?

A

CIWA-Ar (Clinical Institute Withdrawal Assessment for Alcohol)

109
Q

How does chronic alcohol use affect the GABA system?

A

Results in the GABA system becoming down-regulated and the glutamate system becoming up-regulated to balance the effects of alcohol.

When alcohol is removed, the GABA system under-functions and the glutamate system over-functions, causing extreme excitability of the brain and excessive adrenergic (adrenalin-related) activity.

109
Q

Symptoms of delirium tremens?

A
  • Coarse tremor
  • Confusion
  • Delusions
  • Auditory & visual hallucinations
  • Fever
  • Tachycardia
109
Q

Management of alcohol withdrawal?

A

1) Chlordiazepoxide (Librium)

2) High-dose B vitamins (Pabrinex)

3) Followed by long term oral thiamine

109
Q

What receptors does alcohol inhibit?

A

Glutamate (NMDA receptors) –> causes a further relaxing effect

109
Q

What is an alternative to chlordiazepoxide (or diazepam) in patients with hepatic failure?

A

Lorazepam

109
Q

What can thiamine deficiency lead to?

A

Wernicke’s encephalopathy & Korsakoff syndrome

109
Q

Triad of symptoms seen in Wernicke’s?

A

1) Confusion
2) Oculomotor disturbances (disturbances of eye movements)
3) Ataxia (difficulties with coordinated movements)

110
Q

Features of Korsakoff syndrome?

A

1) Memory impairment (retrograde and anterograde)
2) Behavioural changes

Often irreversible with patients requiring full time institutional

110
Q

What is often used during acute episodes of alcoholic hepatitis?

A

Glucocorticoids e.g. prednisolone

111
Q

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

A

Characterised by excessive fat in the liver cells, specifically triglycerides.

These fat deposits interfere with the functioning of the liver cells.

112
Q

What % of adults are estimated to have non-alcoholic fatty liver disease?

A

25%

113
Q

Progression of NAFLD?

A

The early stages of NAFLD can be asymptomatic. However, it can progress to hepatitis and liver cirrhosis.

114
Q

Stages of NAFLD?

A

1) Non-alcoholic fatty liver disease
2) Non-alcoholic steatohepatitis (NASH)
3) Fibrosis
4) Cirrhosis

115
Q

Risk factors for NAFLD?

A

Same as CVS disease:

  • Middle age onwards
  • Obesity
  • Poor diet and low activity levels
  • Type 2 diabetes
  • High cholesterol
  • High blood pressure
  • Smoking
116
Q

NAFLD is associated with metabolic syndrome. What is this?

A

A combination of hypertension, obesity and diabetes.

117
Q

What is often first indication in LFTs that a patient has NAFLD?

A

Raised alanine aminotransferase (ALT)

118
Q

How can hepatic steatosis (fatty liver) be diagnosed?

A

On an US –> seen as increased echogenicity

119
Q

1st line investigation for assessing fibrosis in non-alcoholic fatty liver disease?

A

The enhanced liver fibrosis (ELF) blood test

120
Q

What are 2 other options for assessing liver fibrosis in NAFLD?

A

1) NAFLD Fibrosis Score (NFS)

2) Fibrosis 4 (FIB-4) score

121
Q

What is the NFS score based on ?

A

It is based on an algorithm of age, BMI, liver enzymes (AST and ALT), platelet count, albumin and diabetes.

122
Q

What can be used to assess the stiffness of the liver?

A

Transient elastography (“FibroScan”)

123
Q

When would transient elastography be used?

A

It is used where the enhanced liver fibrosis (ELF) test indicates advanced fibrosis.

124
Q

What is the normal AST:ALT ratio?

A

Less than 1

125
Q

What AST:ALT ratio indicates advanced fibrosis in NALFD?

A

> 0.8 in NALFD

126
Q

What does an AST:ALT ratio >1.5 (i.e. a disproportionately high AST) indicate?

A

Indicates alcohol-related liver disease rather than NAFLD.

127
Q

Gold standard test for diagnosing NAFLD?

A

Liver biopsy

128
Q

Management of NAFLD?

A
  • Weight loss
  • Healthy diet (Mediterranean diet is recommended)
  • Exercise
  • Avoid/limit alcohol intake
  • Stop smoking
  • Control of diabetes, blood pressure and cholesterol
  • Refer patients where scoring tests indicate liver fibrosis to a liver specialist
  • Specialist management may include vitamin E, pioglitazone, bariatric surgery and liver transplantation
129
Q

Features of NAFLD?

A

1) usually asymptomatic
2) hepatomegaly
3) ALT is typically greater than AST
4) increased echogenicity on ultrasound

130
Q

ALT vs AST in NAFLD?

A

ALT is typically greater than AST

131
Q
A

Yr 4 - CCC (53 decks)

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