5. Alcoholic Liver Disease Flashcards
What is alcoholic liver disease?
The long-term excessive consumption of alcohol on the liver
What may be the cause behind alcoholic liver disease having a variable onset and progression between people?
Genetic predisposition
List the stepwise progression of ALD?
- Alcohol related fatty liver
- Alcoholic hepatitis
- Cirrhosis
What stage of ALD is alcoholic related fatty liver?
Can it be reversed, and how?
The first stage of ALD
If drinking stops, it can be reversed (takes around 2 weeks)
What stage of ALD is alcoholic hepatitis?
What causes it?
Can it be reversed and if so how?
Second stage of ALD
Drinking over a long period or bing drinking
If mild can be reversed with permanent abstinence
What stage of ALD is cirrhosis?
Describe the cirrhotic liver.
Can it be reversed?
Prognosis?
Last stage
Liver is made up of scar tissue rather than healthy, functioning tissue
Irreversible but abstinence will prevent further damage
Continued drinking has a very poor prognosis
OH consumption limits?
Who should avoid completely?
No more than 14 units, spread evenly over 3 days at least and no more than 5 units in a day
If pregnant avoid compltetely
OH consumption increases?
Risk of any cancer (especially mouth, throat and breast)
ALD (cirrhosis increases risk of hepatocellular carcinoma)
Pancreatitis
Alcoholic Cardiomyopathy
Wernicke-Korsakoff syndrome
Addiction
How do you screen for harmful OH use?
CAGE screening tool:
Have you ever felt you should cut down?
Have you ever been annoyed by someone criticising your drinking?
Have you ever felt guilty about drinking?
Have you ever had an eye-opener in the morning to ease your hangover?
Or use the WHO’s AUDIT questionnaire: 10 questions and a score of 10 or + indicates harmful use
List at least 7 signs of liver disease
Losing liver function:
- Edema (no protein)
- Bruising (no clotting factors)
- Palmar erythema, gynaecosmastia, spider naevi (high estrogen, not metabolised)
- Toxins (asterixis)
- Jaundice and itch (bilirubin not metabolised)
Portal vein hypertension:
- Ascites and caput medusa (portal hypertension causes fluid in peritoneal cavity and engorged epigastric veins)
Fatty, inflamed liver:
- Hepatomegaly
In ALD, what would the bloods show (spit into what happens to blood, liver and kidneys in ALD)?
Blood:
Elevated PT time
FCB shows macrocytosis aka raised MCV
Liver:
LFT show raised ALT, AST (ALP is raised later in the disease) raised bilirubin and reduced albumin
Kidneys:
UE deranged in hepato-renal syndrome
Investigations for suspected ALD?
Bedside: obs and GI exam
Bloods: FBC, UE, TFT, LFT, CRP, ESR
Imaging: US, Fibroscan, CT, MRI
Procedure: endoscopy and liver biopsy
General management of ALD
- OH cessation (consider detoxication regime)
- Nutritional support with vitamins (thiamine) and a high protein diet
- Steroids improve short term outcomes (over 1 month) but infection and GI bleeding need to be managed first and do not improve outcomes
- Treat complications of cirrhosis
- Refer for liver transplant in severe disease, but must abstain from OH for 3m prior to referral
Describe the range and timeframe of alcohol withdrawal syndromes
6-12h: H/A, tremor, sweating, anxiety, craving
12-24h: hallucinations
24-48h: seizures
24-72h: delirium tremens
Why is delirium tremens a medical emergency?
35% mortality if left untreated
What acute and chronic effects does OH have on the receptors of the brain?
What medical emergency is caused by the chronic effects of OH on the brain?
Acutely: stimulates GABA receptors which have a relaxing effect and inhibits glutamate receptors, inhibiting electrical activity, causing a relaxing effect
Chronic OH use causes the GABA system to be down-regulated and the glutamate system to be upregulated so the effects of OH are balanced
On abstinance the GABA under functions and glutamate over functions causing extreme excitability and adrenergic activity causing delirium tremens
How is OH withdrawal managed?
Score the patient using CIWA-Ar tool
Chlordiazepoxide aka librium is used in medical treatment (titrated to required dose, on a reducing regimen for 5-7d)
Need IV high dose b-vitamins (pabrinex) and then oral b-vitamins (thiamine)
Describe Wernicke-Korsakoff Syndrome
Thiamine (aka B-vitamin) deficiency
Thiamine is poorly absorbed in the prescence of OH, so alcoholics are B-vitamin deficient
Wernicke’s Encephalopathy (medical emergency, high mortality rate if untreated) occurs first: confusion, oculomotor disturbances (eye mvmt disturbance) and ataxia
Korsakoff’s Syndrome: retrograde and anterograde memory impairment and behavioural changes, often irreversible and pts require full time institutionalised care
Prevention and management: Thiamine supplementation and abstain from OH
What is Fibroscan used to asses
Elasticity and degree of cirrhosis
What indicated fatty changes on ultrasound of the liver?
Increased echogenicity
What procedure is used to look for esophageal varices?
Endoscopy
What 5 changes can CT and MRI visualise in a patient with ALD?
Fatty changes
Hepatocellular carcinoma
Hepatosplenomegaly
Blood vessel changes
Ascites
How is the diagnosis of ALD confirmed?
Liver biopsy
Before administrating steroids to a patient with ALD, what must be done?
Liver biopsy to confirm ALD
SS of delirium tremens?
Extreme excitability and adrenergic activity:
Severe, sudden hypertension
Acute confusion
Severe agitation
Delusions
Hallucinations
Tremor Tachycardia Hyperthermia Ataxia (difficult with co-ordinated mvmts) Arrhythmia
