Liver disease Flashcards

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1
Q

Symptoms of liver disease

A
Jaundice
Ascites
Pruritis 
Fat in faeces
Changes in colour of urine and faeces
Irregularities in clotting
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2
Q

What tests can be done to indicate liver disease?

A

Liver function tests - testing liver enzymes & proteins.

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3
Q

What enzymes/proteins etc are measured in LFTs?

A
Enzymes: ALT 
AST 
ALP 
GGT 
- Bilirubin 
- Albumin 
- Prothrombin (clotting) - INR
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4
Q

What are the AST/ALT?

A

Inflammation markers - damaged hepatocytes release these into the blood. ALT is more specific to the liver (AST may indicate muscle damage too).
Ratio >2 alcoholic liver disease indicator
Ratio <1 NAFLD indicator

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5
Q

If a AST/ALT ratio is >2 or <1 what liver diseases do they indicate?

A

> 2 alcoholic

<1 NAFLD

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6
Q

What do ALP and GGT indicate?

A

A blockage of the bile ducts. They help confirm that the liver is the source of the raised ALT. GGT is useful for detecting alcohol damage but be aware high GGT can indicate any form of liver disease.

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7
Q

What is INR? and why can it be used to detect liver disease?

A

Time taken for he blood to clot. “Prothrombin time”. The liver is responsible for producing prothrombin/clotting factors. So a longer PT (higher INR) may suggest a reduction in clotting factors/liver not working properly/ Vitamin K deficiency due to block of bile extraction/malnutrition

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8
Q

Why might a vitamin K injection be given following a high INR score?

A

Given to see if it affects clotting time because vitamin K is deficient in liver disease - block of bile extraction/malnutrition

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9
Q

In acute liver damage - how do these parameters change:

  1. Bilirubin
  2. ALT/AST
  3. ALP
  4. Albumin
  5. INR
A
Bilirubin normal or increased 
ALT/AST greatly increased (ALT >AST) 
ALP normal or slightly increased
Albumin is normal
INR is usually normal//increase
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10
Q

How does bilirubin indicate liver disease?

A

Protein - it is a breakdown of haemoglobin - measure of liver function as liver usually conjugates bilirubin - so bilirubin in blood predicts LD. Can also indicate blockage of bile ducts

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11
Q

How does albumin indicate liver disease

A

Albumin is produced by liver and responsible for oncotic pressure, transport/binding of nutrients and drugs.
Reduced albumin means not enough being produced by liver - results in fluid retention (note - total protein is usually normal in liver disease but changes may indicate malnutrition).

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12
Q

What is liver disease classified based on?

A

Duration - acute/ chronic

Damage type - Cholestatic/hepatocellular

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13
Q

Differentiate acute and chronic liver disease

A

Acute: self limiting, history <6 months e.g paracetamol overdose, viral infection

Chronic: Long term liver damage >6mnth. Could lead to permenant structural changes e.g due to alcoholic cirrhosis, NAFLD, non alcohol steatohepatitis, viral infection, hereditory

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14
Q

Differnentiate cholestatic and hepatocellular LD

A

Cholestatic - Bile flow reduced/blocked. Increased ALP, GGT, Bilirubin, bile acids, cholesterol

Hepatocellular - damage to hepatocytes - ALT and AST increase as released from damaged hepatocytes. Serum levels increased. - something outside liver is affecting function?

Both types lead to fibrosis - larger, whiter liver

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15
Q

What are the 5 main complications associated with severe liver disease?

A
fluid retention 
Ascites
Portal hypertension 
Jaundice 
Hepatic encephalopathy
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16
Q

What is the most common cause of cirrhosis

A

Alcoholic liver disease

17
Q

What is produced in alcoholic LD that causes inflammation/damage

A

Production of reactive oxygen species at every point in the metabolism of alcohol

18
Q

Stages of alcoholic LD?

A
  1. Alcoholic fatty LD - asymptomatic, rapid, reversible
  2. Alcoholic hepatitis - chronic use, can slow progression by stopping drinking
  3. Cirrhosis - Unlikely to survive <5 years unless permentantly stop drinking
19
Q

What is the management of alcoholic Fatty LD?

A

Stop drinking alcoholic - behaviour and support services
Treat the symptoms of alcohol withdrawal - Delirium Tremens (DTs), diazepam
- Treat the thiamine deficiency and malnutrition - can get wernickes encephalopathy so give IV thiamine and vitamins

20
Q

What is non alcoholic fatty liver disease?

A

Largest increase in fatty globules in NAFLD & changes in hormonal signalling around liver - inflammation forming sar tissue

21
Q

Stages of NAFLD

A
  1. fatty liver - asymptomatic, may be detected by LFts
  2. NASH - non alcoholic steatohepatitis - inflammation & pain
  3. fibrosis
  4. cirrhosis
22
Q

What are the risks of NAFLD

A
Type 2 diabetes
obesity 
Hypertension 
Hypercholesterolaemia 
Smokers
>50 y/o
23
Q

Treatment for NAFLD?

A

Increase exercise and diet.
Treat underlying cause eg diabetes, hypertension,
Avoid alcohol
If on statins for high lipids - stay on unless LFTs double within 3 months of starting

24
Q

name 3 types of viral hepatitis and transmission routes

A

Hep A - faecal oral route e.g contaminated foods, can also be sex, anal, sharing needles
Hep B - infected blood products / sexual intercourse unprotected Mainly
Hep C - infected blood products e.g IV drug users (rarely sex)

25
Q

Duration of Hep A and treatment?

A

Self limiting 3-6 weeks, no treatment but avoid alcohol, vaccination if high risk or travelling to high risk areas

26
Q

Does Hep C have symptoms?

A

Asymptomatic until et chronic liver disease - only really diagnosed at this stage via Hep C blood test.

27
Q

Hep C treatments?

A

Achieve sustained viral clearance and antiviral drugs - Ribavarin - but does not give immunity

28
Q

Symptoms of Hep B

A

May take 2-3 months to present, self limiting, diagnose using Hep B blood test.

29
Q

What is viral hepatitis?

A

Inflammation of the lier and increased ALT due to virus.
A generally contaminated foods
B sexual contact unprotected
C infected blood products mainly IV drug users

30
Q

What is the leading cause of acute liver failure?

A

Paracetamol poisoning

31
Q

In the case of paracetamol overdose, why is it important to know exactly how many tablets were consumed and when they were taken? (4)

A

Because after 24hours - there will be irreversible severe liver damage

  • Liver failure will occur 48-96 hours after OD.
  • If within 1 hour - can give activated charcoal which will absorb the drug in the GIT.
  • Acetylcysteine IV can be given if on or above treatment line and is 100% effective if given within 8 hours or less.
  • if its been 24hours from the OD to 1st presentation then must alert poisons authority.
32
Q

What happens in paracetamol overdose

A

usually metablised by conjugation - small % via CYP450 route to form NAPqI which is toxic, but usually conjugated by glutathione (GSH). In overdose, conjugation is saturated as more NAPQI forms which means it cannot be broken down.

33
Q

Treatment of paracetamol overdose

A

N-acetylcysteine - spares GSH glutathione

34
Q

What drugs should be avoided inliver damage - why?

A

Rifampicin
Liver damage
They are excreted unchanged by liver,

Also - NSAIDS, warfarin, sedative drugs (action could be increased so may mask hepatic encephalopathy)

35
Q

What happens to bioavailability of drugs in liver damage?

A

Hepatic blood flow is reduced so bioavailability of drugs undergoing first pass metabolism is increased.