Alcoholic Liver Disease Flashcards
(32 cards)
Causes of liver disease
Alcohol consumption Viral infections e.g. hepatitis Inherited disease e.g. Wilson's Vascular abnormalities Toxins, cancer, biliary tract disorders, infections, etc.
What is the recommended number of units per week in UK?
14 units
What classifies as ‘binge drinking’
> 6 units in a single session
- major cause for A&E admissions
What are the short term affects of alcohol on the body?
1) Loss of inhibition (impaired judgement)
2) Decreased respiratory rate
3) GI disturbances
4) Loss of consciousness
5) Impotence (inability to take effective action)
6) Acute poisoning
7) Complexion/effect on appearance
8) Unintentional injuries
What are the long term effects of alcohol on the body?
1) Liver disease
2) Cancer
3) Pancreatitis
4) GI ulceration
5) Osteoporosis (malabsorption)
6) Infertility
7) Heart disease and stroke due to cholesterol
8) Increased blood pressure
9) Obesity
10) Dementia
Stages of liver disease
Healthy liver
Fatty liver (steatosis)
Fibrosis
Cirrhosis
How is alcohol metabolised?
Alcohol dehydrogenase to acetaldehyde
Acetaldehyde dehydrogenase to acetic acid
Further metabolised to fatty acids
What happens to alcohol metabolism in chronic consumption?
Impaired efficiency of aldehyde dehydrogenase
1) Build up of acetaldehyde = inflammation, necrosis (inflammatory immune response- protein function)
2) Acetaldehyde = inhibits alcohol dehydrogenase (increased levels of circulating alcohol- causes effects to persist for longer)
Upregulation of CYP450 2E1
- Microsomal ethanol oxidising system responsible for ~10% in low consumption
- High consumption = increased free radicals produced causing further damage
What is fatty liver?
Is it reversible? What does it effect?
Accumulation of fat in the hepatocytes
- due to disruption of metabolic pathways
Reversible and rarely symptomatic
- doesn’t effect metabolism of food/drugs
What is the form of acute alcoholic hepatitis that is commonly caused by alcohol consumption? (AAH)
Steatohepatitis
What is steatohepatitis?
Accumulation of fat + hepatocellular injury
- inflammation and fibrosis
- can cause liver pain, vomiting, confusion
- improves with abstinence (though many will still develop cirrhosis despite)
What is thought to be the mechanisms of injury for steatohepatitis?
Poorly understood
- oxidative stress
- aldehyde accumulation
- altered protein function
What is fibrosis/cirrhosis?
Inflammation + fibrogenesis + collagen deposition
- the more episodes of inflammation, the more likely it is to develop
- irreversible, unlike acute episodes
- direct injury from free radicals and expression of inflammatory cytokines
- may exhibit signs of decompensation
- abstinence is key in management
Will cirrhosis occur in all patients with multiple episodes of inflammation?
No, dependent on individuals
Increased susceptibility depends on:
- genetics
- age
- gender
- BMI
- race
- consumption patterns
Give the outline of the management plan for patients admitted with AAH
1) Treat withdrawal symptoms and seizures if they occur
2) Treat the inflammatory component of AAH
3) Treat any complications of both liver disease and alcohol use
4) Treat malnutrition/malabsorption
5) Abstinence
Treatment (AAH) for malnutrition and behavioural changes (delusions, agitation, confusion)
Sedatives and vitamin supplement
- e.g. Chlordiazepoxide (BZ) + Pabrinex (injection)
Chlordiazepoxide
- anti-convulsant and sedative
- slow onset means lower risk of dependency
- symptom triggered dosing
- if chronic end stage patients, give oxazepam/lorazepam (shorter t1/2)
Why might shorter-acting BZs be used?
BZs are metabolised by the liver
- effects may last much longer than desired
Why is Pabrinex used?
Many patients will have poor diet
- vitamin deficient (high carbs, low protein, vitamins and minerals)
- malabsorption in intestinal mucosa (corrosion of lining)
- thiamine deficiency (vitamin B = polyneuritis- motor/sensory effects)
What can thiamine deficiency lead to?
1) Wernicke’s encephalopathy (mimics dementia)
- vitamin B reserves used up
- leads to nstagmus (involuntary rapid eye movements), ataxia (loss control of body movements), learning/memory impairment
2) Korsakoff syndrome
Dosing for Pabrinex?
1-3 pairs BD/TDS
- Avoid IM if coagulopathic
- IV also available
What are the typical signs of acute alcoholic hepatitis?
Signs of decompensation
Enlarged liver (hepatomegaly)
Fever
Leucocytosis (increased WBC)
Lab signs of AAH
Increased: WBC Neutrophil count AST INR Bilirubin
If signs indicate AAH, but also raised creatinine?
Hepato-renal syndrome
- indication for liver transplant (poor prognostic marker)
Scoring systems used for AAH
MELD
Lille
- albumin, bilirubin, INR, creatinine
- recalculate as treatment progresses
