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MET3a > Diseases of the Liver > Flashcards

Diseases of the Liver Flashcards

1
Q

2 presentations of liver disease

A

Acute liver failure

Chronic Liver disease/cirrhosis

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2
Q

What presentation of liver disease is more common?

A

Chronic/cirrhosis

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3
Q

What are the causes of acute liver failure?

A 
Drugs - paracetamol
Infections
Ischaemia
Toxins
Metabolic 
Vascular
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4
Q

What is the commonest cause of acute liver failure in the UK?

A

Paracetamol

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5
Q

What are the causes of chronic liver disease?

A 
Alcohol
Viral Hepatitis B and C
Non alcoholic fatty liver disease
Auto immune hepatitis
Primary biliary cirrhosis
Primary sclerosing cholangitis
Haemochromatosis & Wilson's Disease
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6
Q

What are the 3 commonest causes of cirrhosis?

A

Alcohol
Viral Hepatitis B and C
Non alcoholic fatty liver disease

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7
Q

What are the 2 phases of liver disease?

A

Asymptomatic - 20-40 years

Symptomatic - 1 to 5 years

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8
Q

What are the complications of cirrhosis?

A 
Ascites
Haemorrhage
Encephalopathy
Jaundice
HCC
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9
Q

Extra-hepatic impacts of alcohol

A 
HTN
Coronary Heart Disease
Ischaemic Stroke
Haemorrhagic stroke
Oral pharyngeal cancer
Pancreatitis
Liver Disease
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10
Q

Pathway of alcohol induced liver injury

A

Normal liver can becomes a fatty liver -> steatohepatitis -> fibrosis/cirrhosis -> HCC

Or normal liver can go straight to steatohepatitis or fibrosis/cirrhosis and continue from there

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11
Q

What does a fatty liver look like?

A

Fat laden globules on microscopy

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12
Q

What does steatohepatitis look like?

A

Fat and inflammation (purple infiltrates -> inflammatory mediators)

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13
Q

What can you see on fibrosis?

A

Reticulin staining shows collagen = area of scarring

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14
Q

How does HCC occur from fibrosis?

A

Constant regeneration and scarring can mean some cells undergo changes and form dysplastic nodules

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15
Q

How is HCC monitored in those with cirrhosis?

A

Regular 6 months ultrasound of liver and AFP tumour marker blood test to spot dysplastic nodules before HCC becomes untreatable

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16
Q

What is the commonest biopsy finding/stage in alcohol related liver diseases? (most to least common)

A

Steatosis
Steatohepatitis
Fibrosis/cirrhosis
HCC

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17
Q

3 mechanisms of alcohol injury to the liver

A

Metabolic
Inflammatory
genetic

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18
Q

Metabolic mechanism of alcohol injury to liver

A

High alcohol intake often comes with obesity and insulin resistance which both also damage the liver

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19
Q

Inflammatory mechanism of alcohol injury to the liver

A

Lipid signals - attract chemokines, cytokines, Kupffer cells, Stellate cells, endothelial cells

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20
Q

Genetic mechanism of alcohol injury to the liver

A

Some genes are associated with steatosis - explains why some individuals who drink the same volume are more predisposed than others to liver injury

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21
Q

Protocols of managing alcohol related liver disease

A

Identify Risk
Address dependence
Manage disease

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22
Q

How to identify risk of alcohol related liver disease

A

Calculate units per week
Low risk = 14U
Increasing = 15-50 for men, 15-35 for women
Higher = More than 8U/day or 50 per week for men, more than 6U/day or 35 per week for women

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23
Q

What is the alcohol limit?

A

No more than 14U per week and spread over 3 days

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24
Q

AUDIT scores

A

Scores risk of alcohol dependence

Can determine level of intervention required

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25
Q

Types of alcohol withdrawal syndromes

A

Minor = 6-36 hrs after last drink
Seizures = 6-48 hours
Alcoholic hallucinosis = 12-48 hours
Delirium tremens = 48-96 hours

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26
Q

Medications for alcohol withdrawal

A

Chlordizepoxide
Lorazepan if underlying cirrhosis as effects more easily reversible
Fixed dose or symptom triggered dose

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27
Q

Symptom triggered dose vs. fixed

A

Shorted
Lower dose
Need training with CiWAr

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28
Q

2 phases of alcoholic related liver disease

A

Alcoholic Hepatitis

Alcohol related liver cirrhosis

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29
Q

Features of alcoholic hepatitis

A 
Recent onset jaundice 
With or without ascites
Alcohol abuse ongoing for less than 2 months
Fever
Not really fibrosis
Potentially reversible
30
Q

What is the gold standard test for alcoholic hepatitis?

A

Liver biopsy

31
Q

Ix findings in alcoholic hepatitis

A

May have raised WCC, platelets
AST:ALT>1
Negative liver screen
Liver biopsy = steatosis, hepatocyte ballooning, inflammatory infiltrate

32
Q

Tx for alcoholic hepatitis

A 
Sepsis Tx as high risk
Nutrition - NG feed
Maddrey's Criteria = prognostic criteria
Alcohol abstinence determines LT prognosis
Liver transplant?
Steroids?
33
Q

What is NAFLD?

A
  • NASH = steatohepatitis
    OR
  • NAFLD
34
Q

Features of NASH?

A

Features of alcohol hepatitis on biopsy but absence on alcohol excess on history

35
Q

Pathways/spectrum of NAFLD?

A

Normal -> fatty liver -> NASH -> fibrosis/cirrhosis

Or normal straight to NASH

36
Q

Pathogenesis of NAFLD?

A

Accumulation of hepatic triglyceride
Free fatty acids released from lipid stores
Oxidative stress
Inflammatory mediators -> fibrosis -> cirrhosis -> HCC/failure

37
Q

NASH or NAFLD - which has worse prognosis?

A

NASH - higher risk of cirrhosis and liver death

38
Q

Presentation of NAFLD

A
  • abnormal LFTs
  • ALT:AST>1
  • if develop fibrosis ^ratio may not be present
  • fatigue
  • RUQ
  • hepatomegaly
  • no other symptoms unless cirrhosis
39
Q

Associated conditions with NAFLD

A 
Obesity - central/visceral
T2DM
Hypertriglyceridemia
HTN
Liver manifestation of insulin resistance metabolic syndrome
CV risk profile
40
Q

Commonest cause of death in patient of NAFLD

A

CV death

41
Q

Associations with NAFLD

A 
Drugs = steroids, Amiodarone, MTX
Genetic predisposition
Weight reducing surgery - jejuno-ileal bypass
Protein calories malnutrition
Total parenteral nutrition
Iron overload
42
Q

How is NAFLD diagnosed?

A

Exclude other liver diseases = liver screen
Screen for metabolic syndrome
Liver biopsy
Fibroscan - measures liver stiffness (non invasive, fibrosis detect)

43
Q

What is metabolic syndrome?

A

Impaired glucose tolerance
Central Obesity
Elevated S. trigylcerides, Low HDL
HTN

44
Q

NAFLD Treatment

A

Weight loss address - bariatric surgery?

Treat metabolic factors = HTN, diabetes, lipid lowering drugs

45
Q

Which hepatitis infection type is associated with acute hepatitis?

A 
Hep A and E
Both RNA viruses
Both faecal-oral route of transmission
Incubation between 2-6 weeks
Dx = IgM association
46
Q

Which hepatitis infection type is associated with chronic hepatitis?

A

Hep B and C
Hep B is DNA and C is RNA virus
Body fluids exposure is route of transmission
1 month - 6 month incubation
Hep C rarely acute but Hep B can be but self limiting in healthy
Worldwide burden of both

47
Q

How is hepatitis B transmitted?

A

Maternal (vertical) - neonates more common to remain chronically infected and increased risk of HCC in 30-40s
Blood contact
Sexual - acute infection with jaundice, healthy can often clear it

48
Q

Hepatitis D

A

Rare
IVDU
Requires Hep S surface antigen so need to have Hep B

49
Q

Prognosis of Hep B

A

Most patients asymptomatic -> recover
Others have acute hepatitis -> recover
Minority -> chronic infection as weak immune response -> asymptomatic chronic carriers but very small number get cirrhosis -> HCC?

50
Q

Diagnosis of Hepatitis B

A
  • Hepatitis B surface antigen (HbsAg) = positive means active infection
  • HbsAb (antibody to surface antigen) = marker of immunity if no other markers present
  • HbcAb = another AB
  • HbeAg/Ab = natural history of disease
  • HBV DNA = confirms virus presence and used to monitor treatment
  • HDV IgG and HDV RNA = check for hepatitis delta
51
Q

What is a marker of chronic hepatitis B?

A

> 6 months HbsAg

52
Q

HbcAb

A
  • another antiody, IgG, shows previous exposure to virus if surface antigen is not present
  • another one is IgM = shows acute infection
53
Q

Stages of Hepatitis B

A

Tolerance = high HBV DNA, HbeAg presence, liver enzyme elevated/normal suggesting tolerance to virus
Clearance = can fight virus, HBV DNA disappears, HBsAg, ALT levels improved
Latency = unable to clear, HbeAb appears, persistence of surface antigen
Reactivation - fluctuation of liver tests, HbeAb, resurface of HBV DNA

54
Q

When is ALT normal in Hep B?

A

HBeAg positive infection

vs. HBeAg positive hepatitis when enzymes raised

55
Q

Treatment of Hepatitis B

A
  • reduce viral replication = nucleoside/nucleotide analogues = entecavir, tenofovir
  • improve immunological response = PEG-IFN
  • reduce progression to cirrhosis
  • reduce risk of HCC
56
Q

What is the main difference between Hep B and Hep c?

A

Hep C has large risk of becoming chronic Therefore increased risk of cirrhosis and HCC

57
Q

RF of Hep C

A

High Risk = IVDU, clotting factors received before 1987
Moderate = haemodialysis, blood/organ transplant before 1992, undiagnosed liver problems, infants born to infected mothers
Low = occupational exposure, sexual practices

58
Q

How is Hep C diagnosed?

A
  • IgG test screened
  • if IgG positive then check Hep C RNA (viral load and genotype)
  • LFTs
  • Liver US
  • AFP for HCC risk (tumour marker associated with HCC)
  • Fibroscan for fibrosis
59
Q

Co-morbidities of Hep C

A

Alcohol
High BMI
Mood disorder
Lifestyle

  • higher risk of reinfection
60
Q

Tx of Hep C

A

8-12 weeks therapy
Very successful
Antiviral agents
Combination depends on genotype (6 possible genotypes) and fibrosis stage

61
Q

What is the WHO target with Hep C?

A

Eradicate by 2025

62
Q

Haemochromatosis features

A 
Excess iron absorption and deposition
Multi organ involvement
Autosomal recessive
More males than females
High HCC risk
63
Q

Ix results of haemochromatosis

A 
Increased ferritin
Increased transferrin saturation
HFE gene mutations
Liver biopsy
MRI (ferriscan)
64
Q

What organs are involved in haemochromatosis?

A

Pancreas
Pituitary
Cardiac
Skin & Joints

65
Q

Treatment for haemochromatosis

A

Venesection

Iron chelation therapy

66
Q

Wilson’s Disease Features

A 
Autosomal Recessive
ATP7B gene
Dysregulated copper metabolism
Rare
Acute liver failure rarely
Cirrhosis often
67
Q

Diagnosis Ix of Wilson’s

A

Liver biopsy
MRI brain
Reduced Ceruloplasmin -> then asses urinary copper which is elevated

68
Q

Associations of Wilsons disease

A

Kayser-Fleischer rings
haemolytic anaemia
Neurological - movement disorders, psychiatric

69
Q

treatment of Wilson’s disease

A

Copper chelation therapy

Liver Transplant

70
Q

HCC

A

Major risk factor is cirrhosis as can progress to HCC

- particularly if cirrhosis where cause is HepB/c, haemochromatosis

71
Q

What happens if on screening there is possible HCC?

A

Further Dx needed
CT triple phase
MRI
Biopsy

72
Q

Treatment of HCC

A

Curative Early Stages

  • surgical resection
  • transplant
  • radiofrequency ablation

Palliative Later

  • Transcatheter Arterial Chemoembolisation
  • radioembolization
  • Sorafenib
  • Radiofrequency ablation

MET3a (38 decks)

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