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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
Types of alcohol withdrawal syndromes
Minor = 6-36 hrs after last drink Seizures = 6-48 hours Alcoholic hallucinosis = 12-48 hours Delirium tremens = 48-96 hours
26
Medications for alcohol withdrawal
Chlordizepoxide Lorazepan if underlying cirrhosis as effects more easily reversible Fixed dose or symptom triggered dose
27
Symptom triggered dose vs. fixed
Shorted Lower dose Need training with CiWAr
28
2 phases of alcoholic related liver disease
Alcoholic Hepatitis | Alcohol related liver cirrhosis
29
Features of alcoholic hepatitis
``` Recent onset jaundice With or without ascites Alcohol abuse ongoing for less than 2 months Fever Not really fibrosis Potentially reversible ```
30
What is the gold standard test for alcoholic hepatitis?
Liver biopsy
31
Ix findings in alcoholic hepatitis
May have raised WCC, platelets AST:ALT>1 Negative liver screen Liver biopsy = steatosis, hepatocyte ballooning, inflammatory infiltrate
32
Tx for alcoholic hepatitis
``` Sepsis Tx as high risk Nutrition - NG feed Maddrey's Criteria = prognostic criteria Alcohol abstinence determines LT prognosis Liver transplant? Steroids? ```
33
What is NAFLD?
- NASH = steatohepatitis OR - NAFLD
34
Features of NASH?
Features of alcohol hepatitis on biopsy but absence on alcohol excess on history
35
Pathways/spectrum of NAFLD?
Normal -> fatty liver -> NASH -> fibrosis/cirrhosis Or normal straight to NASH
36
Pathogenesis of NAFLD?
Accumulation of hepatic triglyceride Free fatty acids released from lipid stores Oxidative stress Inflammatory mediators -> fibrosis -> cirrhosis -> HCC/failure
37
NASH or NAFLD - which has worse prognosis?
NASH - higher risk of cirrhosis and liver death
38
Presentation of NAFLD
- abnormal LFTs - ALT:AST>1 - if develop fibrosis ^ratio may not be present - fatigue - RUQ - hepatomegaly - no other symptoms unless cirrhosis
39
Associated conditions with NAFLD
``` Obesity - central/visceral T2DM Hypertriglyceridemia HTN Liver manifestation of insulin resistance metabolic syndrome CV risk profile ```
40
Commonest cause of death in patient of NAFLD
CV death
41
Associations with NAFLD
``` Drugs = steroids, Amiodarone, MTX Genetic predisposition Weight reducing surgery - jejuno-ileal bypass Protein calories malnutrition Total parenteral nutrition Iron overload ```
42
How is NAFLD diagnosed?
Exclude other liver diseases = liver screen Screen for metabolic syndrome Liver biopsy Fibroscan - measures liver stiffness (non invasive, fibrosis detect)
43
What is metabolic syndrome?
Impaired glucose tolerance Central Obesity Elevated S. trigylcerides, Low HDL HTN
44
NAFLD Treatment
Weight loss address - bariatric surgery? | Treat metabolic factors = HTN, diabetes, lipid lowering drugs
45
Which hepatitis infection type is associated with acute hepatitis?
``` Hep A and E Both RNA viruses Both faecal-oral route of transmission Incubation between 2-6 weeks Dx = IgM association ```
46
Which hepatitis infection type is associated with chronic hepatitis?
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
How is hepatitis B transmitted?
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
Hepatitis D
Rare IVDU Requires Hep S surface antigen so need to have Hep B
49
Prognosis of Hep B
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
Diagnosis of Hepatitis B
- 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
What is a marker of chronic hepatitis B?
>6 months HbsAg
52
HbcAb
- another antiody, IgG, shows previous exposure to virus if surface antigen is not present - another one is IgM = shows acute infection
53
Stages of Hepatitis B
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
When is ALT normal in Hep B?
HBeAg positive infection | vs. HBeAg positive hepatitis when enzymes raised
55
Treatment of Hepatitis B
- reduce viral replication = nucleoside/nucleotide analogues = entecavir, tenofovir - improve immunological response = PEG-IFN - reduce progression to cirrhosis - reduce risk of HCC
56
What is the main difference between Hep B and Hep c?
Hep C has large risk of becoming chronic Therefore increased risk of cirrhosis and HCC
57
RF of Hep C
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
How is Hep C diagnosed?
- 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
Co-morbidities of Hep C
Alcohol High BMI Mood disorder Lifestyle - higher risk of reinfection
60
Tx of Hep C
8-12 weeks therapy Very successful Antiviral agents Combination depends on genotype (6 possible genotypes) and fibrosis stage
61
What is the WHO target with Hep C?
Eradicate by 2025
62
Haemochromatosis features
``` Excess iron absorption and deposition Multi organ involvement Autosomal recessive More males than females High HCC risk ```
63
Ix results of haemochromatosis
``` Increased ferritin Increased transferrin saturation HFE gene mutations Liver biopsy MRI (ferriscan) ```
64
What organs are involved in haemochromatosis?
Pancreas Pituitary Cardiac Skin & Joints
65
Treatment for haemochromatosis
Venesection | Iron chelation therapy
66
Wilson's Disease Features
``` Autosomal Recessive ATP7B gene Dysregulated copper metabolism Rare Acute liver failure rarely Cirrhosis often ```
67
Diagnosis Ix of Wilson's
Liver biopsy MRI brain Reduced Ceruloplasmin -> then asses urinary copper which is elevated
68
Associations of Wilsons disease
Kayser-Fleischer rings haemolytic anaemia Neurological - movement disorders, psychiatric
69
treatment of Wilson's disease
Copper chelation therapy | Liver Transplant
70
HCC
Major risk factor is cirrhosis as can progress to HCC | - particularly if cirrhosis where cause is HepB/c, haemochromatosis
71
What happens if on screening there is possible HCC?
Further Dx needed CT triple phase MRI Biopsy
72
Treatment of HCC
Curative Early Stages - surgical resection - transplant - radiofrequency ablation Palliative Later - Transcatheter Arterial Chemoembolisation - radioembolization - Sorafenib - Radiofrequency ablation

MET3a (38 decks)

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