Alcohol Hepatitis Flashcards

1
Q

define alcoholic hepatitis?

A

inflammatory liver injury caused by chronic heavy intake

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2
Q

what are the 3 forms of liver disease caused by excessive alcohol intake?

A

alcoholic fatty liver ( steatosis)

alcoholic hepatitis

chronic cirrhosis

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3
Q

what are the histopathological features of alcohol hepatitis?

A

centrilobular ballooning degeneration and necrosis of hepatocytes steatosis

fatty change neutrophillic

inflammation cholestasis- condition in which bile cannot flow from liver to duodenum mallor

hyaline inclusions ( eosinophilic intracytoplasmic aggregates of cytokeratin) giant mitochondria

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4
Q

summarise the epidemiology of alcoholic hepatitis?

A

occurs in 10-35% of heavy drinkers

patients with Hep C have more severe symptoms

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5
Q

what are the presenting symptoms of alcoholic hepatitis?

A

may remain asympyomatic and undetected

may be mild illness symptoms

  • nausea
  • malaise
  • epigastric pain
  • right hypochondrial pain
  • low grade fever

sever presenting symptoms

  • jaundice
  • abdominal discomfort or swelling
  • swollen
  • GI bleeding-> Haematemesis + melaena
  • long history of heavy drinking is required for the development of alcoholic hepatitis ( around 15-20 years)
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6
Q

What are the signs of alcoholic hepatitis on physical examination?

A

Signs of Alcohol Excess

  • Malnourished => fatigue
  • Palmar erythema
  • Dupuytren’s contracture
  • Facial telangiectasia– red lines appear due to widened venules
  • Parotid enlargement
  • Spider naevi
  • Gynaecomastia
  • Testicular atrophy
  • Hepatomegaly
  • Easy bruising

Signs of Severe Alcoholic Hepatitis

  • Febrile (in 50% of patients)
  • Tachycardia
  • Jaundice
  • Bruising
  • Encephalopathy(e.g. liver flap, drowsiness, disorientation) – caused by build up of ammonia in blood (which is normally removed by the liver) – crosses blood-brain barrier
  • Ascites
  • Hepatomegaly
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7
Q

what are the appropriate investihations for alcoholic hepatitis?

A

FBC

LFTs

U and E

ultrasound- check for liver impairment ( malignancy)

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8
Q

What can be seen in a full blood count for alcoholic hepatitis?

A

low hb High MCV High WCC Low plate

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9
Q

what is encephalopathy in alcoholic hepatitis caused by?

A

liver flap, drowsiness, disorientaiton-> caused by build up of ammonia in blood ( which is normally removed by liver)- crosses blood-brain barrier

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10
Q

What will LFTs look like in alcoholic hepatitis?

A

High AST + ALT – ratio if AST/ALT is >2% (if ALT>AST then it may suggest viral hepatitis or NASH)

High bilirubin

High ALP + GGT

Low albumin

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11
Q

describe U and E in alcoholic hepatitis?

A

Urea and K+ tend to be low

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12
Q

what happens to clotting in alcoholic hepatitis?

A

prolonged PT->sensitive marker for significant liver damage

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13
Q

What investigations should you consider?

A
  • Upper GI Endoscopy - investigate varices
  • Serum antibodies (e.g. AMA, ANA, ASMA) to rule out AI hepatitis
  • Viral hepatitis serology may be conducted to rule it out
  • Liver Biopsy - can help distinguish from other causes of hepatitis
  • EEG - slow-wave activity indicates encephalopathy
  • CT/MRI abdomen – may show hepatomegaly, splenomegaly, ascites, portal vein engorgement
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14
Q

outline a management plant for alcoholic hepatitis?

A

Acute

  • Thiamine
  • Vitamin C and other multivitamins(can be given as Pabrinex)
  • Monitor and correct K+, Mg2+ and glucose
  • Ensure adequate urine output
  • Treat encephalopathy with oral lactulose or phosphate enemas – decrease ammonia generation by bacteria
  • Ascites - manage with diuretics(spironolactone with/without furosemide)
  • Therapeutic paracentesis(removing fluid)
  • Glypressin and N-acetylcysteine for hepatorenal syndrome

Nutrition

  • Alcohol abstinence and alcohol withdrawal
  • Via oral or NG feedingis important
  • Protein restriction should be avoided unless the patient is encephalopathic
  • For the ascites => Na restricted diet(when progresses –> diuretics also added)
  • Nutritional supplementation and vitamins (B group, thiamine and folic acid) should be started parenterally initially, and continued orally

Imms – Influenza, pneumococcal, hep all recommended

Steroid Therapy (e.g. prednisolone)- reduce short-term mortality for severe alcoholic hepatitis

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15
Q

summatise the prognosis for patients with alcohol hepatitis?

A

Mortality:

  • First month = 10%
  • First year = 40%

If alcohol intake continues, most will progress to cirrhosis within 1-3 years

To calculate prognostic score can use Maddrey’s discriminant function or Glasgow alcoholic hepatitis score

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16
Q

what is hepatorenal syndrome?

A
  • development of renal failure in patients secondary to advanced chronic liver disease though to arise because of abnormalities in blood vessel tone in the kidneys blood vessels in the kidney constrict because of the dilatation of blood vessels in the spanchnic circulation ( Supplying the intestines)-> which is mediated by factors released by liver disease-> eg nitric oxide, prostaglandins
  • splanchnic vasodilation leads to reduced effective volume of blood detected by juxtaglomerular apparatus-> leading to activation of the RAS and vasoconstriction of vessels in the kidney –> leads to kidney failure HRS- cirrhosis + Ascites + renal failure ( if other causes of renal impairement excluded)
17
Q

what are the possible complications of alcoholic hepatitis?

A

acute liver decompensaition

hepatorenal syndrome

cirrhosis

oesophageal varices->haematemesis not stoppign in large volumes-> may be in shock or hypotension

peptic ulcers

18
Q

describe oesophageal varices as a complication of alcoholic hepatitis and how this is managed?

A

○ Macrocytic Anaemia, low plts, high GGT/bili, low albumin

○ Found in lower 1/3rd of oesophagus

  1. Terlipressin + AB (cefuroxime or ciprofloxacin should always be given as variceal bleeding is associated with a high risk of infection)
  2. Band ligation/ injection sclerotherapy
  3. Non-cardioselective beta-blokers are the first line treatment of prevention of variceal bleeding. Where a beta-blocker is not tolerated or if there is a singificant contra-indication to their usage, then regular endoscopy with variceal band ligation would be the second-line managment.

○ If above don’t work and still haematemesis then Sengstaken tube and /or TIPS is considered

Band ligation or sclerotherapy is used to eliminate the oesophageal varies to prevent further bleeding. IV Terlipressin reduces portal venous pressure and is usually given for at least 3 days after banding.