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Liver and Friends > Alcoholic liver disease > Flashcards

Alcoholic liver disease Flashcards

1
Q

What is alcoholic liver disease

A

liver damage caused by excess alcohol intake

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2
Q

Epedemiology of alcoholic liver diease

A
  • M>F prevalence
  • ArLD is the foremost health risk in developing countries and ranks third in developed countries.
  • The mortality related to liver cirrhosis increases with age.
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3
Q

stepwise progression of alcoholic liver disease

A

1 alcohol related fatty liver ( steatosis)
2 alcoholic hepatitis
3 cirrhosis

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4
Q

2 main pathways of alcohol metabolisation

A

alcohol dehydrogenase and cytochrome P450 2E1

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5
Q

Alcohol dehydrogenase pathway

A

alcohol dehydrogenase (hepatic enzyme) > converts alochol to acetaldehyde > metabolised to acetate by acetaldehyde dehydrogenase

Both enzymes reduce NAD to NADH > inhibits gluconeogenesis and increase fatty acid oxidation which promotes fatty infiltration liver

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6
Q

cytochrome P450 2E1 pathway

A

generates free radicals through the oxidation of NADPH to NADP. Chronic alcohol use upregulates cytochrome P450 2E1 and produces more free radicals.

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7
Q

What does chronic alcohol exposure also do

A

activate hepatic macrophages> produce (TNF)-alpha and induce the production of reactive oxygen species in the mitochondria.

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8
Q

Alcoholic hepatitis pathophysiology

A

acetaldehyde formed from metabolism of alcohol can react with molecules in the liver, forming acetaldehyde adducts

Recognised as foreign > attacked by immune system > inflammation + hepatitis

Leads to activation of stellate cells which causes deposition of extracellular matrix proteins, generation of portal hypertension and fibrosis.

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9
Q

Risk factors of ALD

A

hep c
chronic alcohol
obesity
age
female

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10
Q

uk recommended alcohol consumption

A

14 units a week
spread evenly over 3 or more days

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11
Q

describe the CAGE questionnare

A

C – CUT DOWN? Ever thought you should?
A – ANNOYED? Do you get annoyed at others commenting on your drinking?
G – GUILTY? Ever feel guilty about drinking?
E – EYE OPENER? Ever drink in the morning to help your hangover/nerves

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12
Q

1st line investigations for ALD

A
  • serum AST ; ALT
  • serum alkaline phosphotase
  • serum bilirubin
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13
Q

Other investigations for ALD

A
  • Full blood count
  • Urea & electrolytes
  • Liver function tests
  • C-reactive protein
  • Liver ultrasound
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14
Q

complications of alcohol

A
  • Alcoholic Liver Disease
  • Cirrhosis and the complications of cirrhosis including hepatocellular carcinoma
  • Alcohol Dependence and Withdrawal
  • Wernicke-Korsakoff Syndrome (WKS)
  • Pancreatitis
  • Alcoholic Cardiomyopathy
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15
Q

signs of liver disease

A

Jaundice
Hepatomegaly
hand signs
ascites
spider naevi
confusion

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16
Q

What hand signs may occur in ALLD

A

-palmar erythema
- dupuytrens contracture

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17
Q

What symptoms may be present in alcoholic liver disease

A
  • malaise
  • weakness
  • weight loss
  • abdo pain
  • pruritus
18
Q

What would LFT’s SHOW IN ALD

A
  • raised bilirubin
  • AST> ALT ratio
  • low albumin
19
Q

what would bloods show for ALD

A

elevated bilirubin
decrease in albumin
increase PT
increase ggt

20
Q

what would fbc show for ALD

A

-Macrocytic non megaloblastic anaemia
- thrombocytopenia

21
Q

general management of ALD

A
  • Stop drinking alcohol permanently
  • Consider a detoxication regime
  • Nutritional support with vitamins
  • Steroids improve short term outcomes
  • Treat complications of cirrhosis
  • Referral for liver transplant in severe disease however they must abstain from alcohol for 3 months prior to referral
  • IV Thiamine to prevent Wernicke-Korsakoff encephalopathy
22
Q

timeline of alcohol withdrawal symptoms

A

6-12 hours: tremor, sweating, headache, craving and anxiety
12-24 hours: hallucinations
24-48 hours: seizures
24-72 hours: “delirium tremens”

23
Q

how is thiamine deficiency linked to alcohol

A

-thiamine is poorly absorbed in the presence of alcohol
-alcoholics tend to have poor diets and rely on the alcohol for their calories

24
Q

what can thiamine deficiency cause

A

wernickes encephalopathy
korsakoffs syndrome

25
Q

Features of Wernicke’s encephalopathy

A
  • Confusion
  • Oculomotor disturbances (disturbances of eye movements)
  • Ataxia (difficulties with coordinated movements
26
Q

Features of Korsakoffs syndrome

A

Memory impairment (retrograde and anterograde)
Behavioural changes

27
Q

what is non alcoholic fatty liver disease

A

It is characterised by fat deposited in liver cells. These fat deposits can interfere with the functioning of the liver cells

28
Q

stage of NAFLD

A

1-Non-alcoholic Fatty Liver Disease
2-Non-Alcoholic Steatohepatitis (NASH)
3-Fibrosis
4-Cirrhosis

29
Q

Epidemiology of NAFLD

A
  • Commonest liver disorder in industrialised western countries
  • Affects around 3/4’s of all obese individuals
30
Q

Aetiology of NAFL

A
  • Obesity
  • Hypertension
  • Diabetes
  • Hypertriglyceridemia
  • Hyperlipidemia
31
Q

How does insulin play a role in NAFLD

A
  • insulin receptors are less responsive to insulin so
  • excess fat is deposited in liver- less secretion of FA in blood stream
  • steatosis occurs (increased synthesis of FFA from blood)
32
Q

What happens as fat droplets form within hepatocytes

A
  • hepatocytes to swell up with fat and push nuclei to edge of cell.
  • Liver appears large, soft, yellow and greasy.
  • Unsat FA vulnerable to ROS > form FA radicals which can react with non-radicals like O2
33
Q

What does the reaction of radicals and non radicals cause?

A

This ultimately damages lipid membrane, leading to mitochondrial dysfunction and cell death. This generates inflammation. Inflammation + steatosis = steatohepatitis.

34
Q

S + S of NAFLD

A

Sometimes symptoms are vague:

  • Fatigue
  • Malaise

Sufficient damage presents with:

  • Hepatomegaly
  • Pain in RUQ
  • Jaundice
  • Ascites
35
Q

RISK FACTORS FOR nafld

A

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

36
Q

Investigation in Non-Alcoholic Fatty Liver Disease

A

Serum AST and ALT: Increase in ALT and sometimes AST. (Different to alcoholic liver disease where AST>ALT)

LFT: raised bilirubin, ALP, GGT, prothrombin time, low serum albumin

FBC: anemia and thrombocytopenia due to hypersplenism

Imaging: US, CT, MRI to look for fatty infiltrates

Biopsy: used to diagnose and assess severity

  • Differential diagnosis
37
Q

what would liver US show for NAFLD

A

WILL show the diagnosis of hepatic steatosis

38
Q

DDs of NAFLD

A
  • Alcoholic liver disease
  • Autoimmune hepatitis
  • Hepatitis B and C
  • Hemochromatosis
  • PSC
  • PBC
39
Q

conservative management of NAFLD

A
  • Weight loss , approx 0.5- 1.0 kg a week through diet and exercise
  • limit alcohol intake
  • optimise blood pressure
40
Q

medical management of NAFLD

A
  • orlisat - enteric lipase inhibitor which prevents absorption of fat
  • metformin - to improve insulin sensitivity
  • antihyperlipidaemics - for patients with hyperlipidaemia
41
Q

Complications of NAFLD

A
  • Ascites
  • Varices and variceal haemorrhage
  • Encephalopathy
  • Hepatocellular carcinoma

Liver and Friends (17 decks)

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