5. Alcoholic Liver Disease Flashcards

1
Q

What is alcoholic liver disease?

A

The long-term excessive consumption of alcohol on the liver

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2
Q

What may be the cause behind alcoholic liver disease having a variable onset and progression between people?

A

Genetic predisposition

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3
Q

List the stepwise progression of ALD?

A
  1. Alcohol related fatty liver
  2. Alcoholic hepatitis
  3. Cirrhosis
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4
Q

What stage of ALD is alcoholic related fatty liver?

Can it be reversed, and how?

A

The first stage of ALD

If drinking stops, it can be reversed (takes around 2 weeks)

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5
Q

What stage of ALD is alcoholic hepatitis?

What causes it?

Can it be reversed and if so how?

A

Second stage of ALD

Drinking over a long period or bing drinking

If mild can be reversed with permanent abstinence

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6
Q

What stage of ALD is cirrhosis?

Describe the cirrhotic liver.

Can it be reversed?

Prognosis?

A

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

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7
Q

OH consumption limits?

Who should avoid completely?

A

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

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8
Q

OH consumption increases?

A

Risk of any cancer (especially mouth, throat and breast)

ALD (cirrhosis increases risk of hepatocellular carcinoma)

Pancreatitis

Alcoholic Cardiomyopathy

Wernicke-Korsakoff syndrome

Addiction

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9
Q

How do you screen for harmful OH use?

A

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

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10
Q

List at least 7 signs of liver disease

A

Losing liver function:

  1. Edema (no protein)
  2. Bruising (no clotting factors)
  3. Palmar erythema, gynaecosmastia, spider naevi (high estrogen, not metabolised)
  4. Toxins (asterixis)
  5. Jaundice and itch (bilirubin not metabolised)

Portal vein hypertension:

  1. Ascites and caput medusa (portal hypertension causes fluid in peritoneal cavity and engorged epigastric veins)

Fatty, inflamed liver:

  1. Hepatomegaly
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11
Q

In ALD, what would the bloods show (spit into what happens to blood, liver and kidneys in ALD)?

A

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

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12
Q

Investigations for suspected ALD?

A

Bedside: obs and GI exam

Bloods: FBC, UE, TFT, LFT, CRP, ESR

Imaging: US, Fibroscan, CT, MRI

Procedure: endoscopy and liver biopsy

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13
Q

General management of ALD

A
  1. OH cessation (consider detoxication regime)
  2. Nutritional support with vitamins (thiamine) and a high protein diet
  3. Steroids improve short term outcomes (over 1 month) but infection and GI bleeding need to be managed first and do not improve outcomes
  4. Treat complications of cirrhosis
  5. Refer for liver transplant in severe disease, but must abstain from OH for 3m prior to referral
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14
Q

Describe the range and timeframe of alcohol withdrawal syndromes

A

6-12h: H/A, tremor, sweating, anxiety, craving

12-24h: hallucinations

24-48h: seizures

24-72h: delirium tremens

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15
Q

Why is delirium tremens a medical emergency?

A

35% mortality if left untreated

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16
Q

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?

A

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

17
Q

How is OH withdrawal managed?

A

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)

18
Q

Describe Wernicke-Korsakoff Syndrome

A

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

19
Q

What is Fibroscan used to asses

A

Elasticity and degree of cirrhosis

20
Q

What indicated fatty changes on ultrasound of the liver?

A

Increased echogenicity

21
Q

What procedure is used to look for esophageal varices?

A

Endoscopy

22
Q

What 5 changes can CT and MRI visualise in a patient with ALD?

A

Fatty changes

Hepatocellular carcinoma

Hepatosplenomegaly

Blood vessel changes

Ascites

23
Q

How is the diagnosis of ALD confirmed?

A

Liver biopsy

24
Q

Before administrating steroids to a patient with ALD, what must be done?

A

Liver biopsy to confirm ALD

25
Q

SS of delirium tremens?

A

Extreme excitability and adrenergic activity:

Severe, sudden hypertension

Acute confusion

Severe agitation

Delusions

Hallucinations

Tremor
Tachycardia
Hyperthermia
Ataxia (difficult with co-ordinated mvmts)
Arrhythmia