Alcoholic Liver Disease and Cirrhosis Flashcards

1
Q

What is the aetiology of alcoholic liver disease?

A

Alcohol, duh.

  • Heavy, prolonged consumption needed to affect damage
  • c. 40-80g/day M; 20-40g/day F; for 10-12yrs is sufficient to cause liver damage in the absence of other liver diseases

Other risk factors:

  • Drinking outside meal times
  • Female sex (due to lower consumption required)
  • Genetics - relating to propensity for addiction and metabolism pathways for alcohol
  • Hep C
  • Smoking
  • Vitamin A+E deficiencies
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2
Q

What is the pathophysiology of alcoholic liver disease?

A

Chronic ethanol intake:
- Acetalhydrate -> NADH production + oxidative stress + lipid peroxidation -> 3 stages

3 stages:

1) Alcoholic steatosis = fatty liver
- c. 90% of drinkers
- Process is reversible
- LFTs can be affected - LOOK LIKE?
2) Alcoholic hepatitis = inflammation and necrosis
- c.25% of drinkers
3) Alcoholic liver cirrhosis = fibrosis of parenchyma
- c.15% of drinkers

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3
Q

What is the pathophysiology of alcoholic liver disease?

A

Chronic ethanol intake - metabolised by alcohol dehydrogenase into
acetalhydrate -> increased NADH production + oxidative stress + lipid peroxidation -> 3 stages

3 stages:

1) Alcoholic steatosis = fatty liver
- c. 90% of drinkers, can begin after a few days of heavy drinking
- Process is reversible
2) Alcoholic hepatitis = inflammation and necrosis
- c.25% of drinkers
3) Alcoholic liver cirrhosis = fibrosis of parenchyma
- c.15% of drinkers

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4
Q

What is cirrhosis and what causes it? (general)

A

A diffuse hepatic process involving fibrosis and conversion of normal liver architecture into structurally abnormal nodules

  • Hepatic vasculature distorts > increased intrahepatic resistance and portal HTN > varices + renal hypoperfusion (> salt and water retention, fluid overload and increased cardiac output)
  • Damage to parenchyma > impaired detox and synthesis

It is the final histological progression of multiple liver diseases:

  • *Alcohol
  • *Hepatitis B and C
  • *Non alcoholic fatty liver disease
  • Haemochromatosis
  • Primary biliary cirrhosis
  • Biliary obstruction
  • Autoimmune hepatitis
  • Wilsons, porphyria, A1AT-deficiency
  • Sarcoidosis
  • Budd-Chiari syndrome
  • Drugs and toxins e.g. methotrexate, amiodarone, isoniazid
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5
Q

How does alcoholic liver disease present? (by stage)

A

Fatty liver:

  • Asymptomatic
  • May show up as an incidental finding on LFTs (mild AST/ALT derangement) or liver USS

Acute alcoholic hepatitis:

  • Fever
  • Jaundice
  • Hepatomegaly +/- tender
  • Possible signs of decompensation (ascites, varices, encephalopathy etc. SEE ACUTE LIVER FAILURE DECK)

Cirrhosis:

  • A significant portion will be asymptomatic - again showing up incidentally on LFTs/USS (or post mortem)
  • Possible signs of decompensation
  • CHRONIC SIGNS SEE NEXT CARD
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6
Q

How does cirrhosis present chronically?

A

Cutaneous features:

  • Jaundice
  • Scratch marks secondary to pruritus
  • Spider naevi (found on trunk and face) and other telangiectasias
  • Palmar erythema
  • Bruising
  • Petechiae or purpura
  • Hair loss
  • White nails = Terry’s nails (horizontal white bands or a proximal white nail plate = signs of hypoalbuminaemia
  • Finger clubbing
  • Dupuytren’s contracture
  • Caput medusae (veins radiating from umbilicus in portal HTN)

Other:

  • Gynaecomastia
  • Hypogonadism

Other signs depending on aetiology e.g. Kayser-Fleischer ring in Wilsons

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7
Q

What blood tests are required when assessing alcoholic liver disease? (and cirrhosis more broadly) (think of at least 10)

A

LFTs:

  • AST, ALT, ALP, GGT
  • AST:ALT ratio >2:1 suggest alcoholic liver disease; <1 suggest NAFLD/NASH
  • GGT raised in active alcoholism

Albumin:
- Hypo in advanced cirrhosis

FBC:

  • Occult bleeding may produce anaemia (iron deficient)
  • Macrocytosis may suggest alcohol abuse (B12 deficiency)
  • Hypersplenism may cause thrombocytopaenia

U+E:

  • Hyponatraemia - from increased ADH activity
  • Poor renal function may indicate hepatorenal syndrome

B12/folate:
- Often low in alcoholism as malnutrition

Coagulation:

  • Sensitive test of liver synthetic function
  • PT time is reduced in advanced cirrhosis

Ferritin:

  • Low may indicate Fe deficiency from diet or blood loss
  • (raised in haemochromatosis)

Viral screen:
- Hep B/C

Fasting glucose/insulin/triglycerides + uric acid levels:

  • Should be measured if non-alcoholic steatohepatitis (NASH) suspected
  • Gluconeogenesis is one of the last functions to become impaired in the context of liver failure

Anti-mitochondrial Abs in PBC; A1AT levels; ceruloplasmin and copper for Wilsons

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8
Q

What is hepatorenal syndrome?

A

Rapid deterioration of kidney function in someone with cirrhosis or ongoing hepatic failure
- Usually fatal unless liver transplant

Caused by changes in circulation suppling intestines, affecting blood flow and tone to the kidneys - Can lead to a diuretic resistant ascites

Can be managed with a transjugular intrahepatic portosystemic shunt (TIPS) - to reduce the pressure in the portal vein - whilst awaiting transplant
- Haemodialysis may be required

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9
Q

What imaging is used when assessing alcoholic liver disease/cirrhosis?

A

Liver USS:

  • Surface nodularity - coarse and heterogenous echotexture
  • Segmental hypertrophy (caudate and lateral left) and atrophy (posterior left)
  • Doppler - signs of portal hypertension e.g. portal vein dilatation, slow flow, ?portal venous thrombosis etc
  • Can also be used to guide biopsy for diagnostic histology

Sonoelastography/fibroscan:
- Low amplitude waves propagated through internal organs and vibrations sensed giving a reading of the various densities and stiffnesses present within the organ

CT/MRI
- Less sensitive than above but can be used to find complications, including HCC

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10
Q

What is the Child-Pugh classification system?

A

Used to estimate prognosis in cirrhosis

Mnemonic = ABCDE

Serum Albumin (g/dL)

  • > 35 = 1 point
  • 28-35 = 2 points
  • <28 = 3 points

Serum total Bilirubin (mg/dL)

  • <2 = 1 point
  • 2-3 = 2 points
  • > 3 = 3 points

INR (Clotting)

  • <1.7 = 1 point
  • 1.7-2.2 = 2 points
  • > 2.2 = 3 points

Ascites (Distension)

  • Absent = 1 point
  • Controlled medically = 2 points
  • Poorly controlled = 3 points

Encephalopathy

  • Absent = 1 point
  • Controlled medically = 2 points
  • Poorly controlled = 3 points

Points = life expectancy

  • 5-6 = 15-20yrs
  • 7-9 = 4-14yrs
  • 10-15 = 1-3yrs
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11
Q

How do you manage alcoholic liver disease and cirrhosis?

A

STOP DRINKING = MOST IMPORTANT
- Support people with inpatient detox and intensive outpatient alcohol service follow up

Treat any other underlying causes of cirrhosis i.e. infection

Corticosteroids - when severe liver inflammation is present

Ensure adequate nutrition (calories, protein and micronutrients)

  • Zn deficiency is common so supplementation may be helpful
  • B12/folate
  • Iron

Itching:
- Cholestyramine

Osteoporosis:
- Vit D and Ca supplementation +/- bisphosphonates

Prophylactic Abx in those with cirrhosis and UGIB

Vaccination
- Hep A, influenza and pneumococcal

Modification to drug prescribing

Liver transplantation for end stage

Manage any acute complications of decompensation

  • Band ligation of varices
  • Furosemide and spironolactone for ascites
  • TIPS
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12
Q

What are the complications of cirrhosis?

A

Oesophageal varices:

  • Dilatation of oesophageal veins which become prone to bleeding
  • Upper endoscopy on Dx then surveillance every 3yrs

Ascites:

  • Free fluid in the peritoneal cavity
  • Can be treated with diuretics, but may become resistant if advanced liver disease/hepatorenal syndrome
  • Also puts patients at risk of spontaneous bacterial peritonitis

Splenomegaly and subsequent thrombocytopaenia

Coagulopathy - from reduced hepatic synthesis of factors II VII IX X ; possible DIC

Hepatocellular carcinoma:

  • Most commonly following Hep C cirrhosis
  • Patients with cirrhosis should be scanned with USS, CT or MRI 6/12-annually as part of screening
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22
Q

What is Budd-Chiari syndrome?

A
Rare disorder (0.1-10/million/yr) caused by hepatic vein obstruction with a number of different aetiologies 
- So should always be considered in patients with acute or chronic liver disease 

At least >1 vein to be obstructed to appear symptomatic

23
Q

What are some potential causes of Budd-Chiari syndrome?

A

Haematological:

  • Polycythaemia vera + of the myeloproliferative disorders
  • Antiphospholipid syndrome
  • Post bone marrow transplant

Reduced blood flow:

  • Vena cava abnormalities
  • Right heart failure
  • Constrictive pericarditis

Drugs:
- COCP, HRT

Chronic infection:

  • Hydatid disease, amoebic abscesses, aspergillosis
  • Syphilis, TB

Malignancy:

  • Hepatocellular carcinoma
  • Renal cell carcinoma
  • Wilms’ tumour
  • Adrenal carcinoma

Inflammatory conditions:

  • IBD
  • Sarcoid
  • SLE

Trauma
Surgery
Pregnancy
Idiopathic

24
Q

How does Budd-Chiari syndrome present?

A

Classical triad:

  • RUQ pain
  • Ascites
  • Hepatomegaly

+/- Jaundice +/- AKI +/- fulminant hepatic failure

25
Q

How do you investigate Budd-Chiari syndrome?

A

Ascitic fluid:
- Usually high protein content

LFTs:
- Mild elevation

PTT:
- Possibly prolonged

MRI, Doppler USS

26
Q

How do you manage Budd-Chiari syndrome?

A

Treat the underlying cause

Anticoagulation

Ascites:

  • Fluid + salt restriction
  • Spironolactone

Angioplasty/stenting/local thrombolysis/TIPS
Liver transplant