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*Medicine: Gastrointestinal > Chronic Liver Disease > Flashcards

Chronic Liver Disease Flashcards

1
Q

What is chronic liver failure?

A
  • liver failure may be recognised by development of coagulopathy (INR >1.5) + encephalopathy
  • occur suddenly in prev healthy liver → acute liver failure
  • more often it occurs on background of cirrhosis → chronic liver failure
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2
Q

What are symptoms of chronic liver disease?

A

patients may be asymptomatic or experience non-specific symptoms, particularly weakness, anorexia and fatigue, specific symptoms include:

  • right hypochondrial pain due to liver distension
  • abdo distension due to ascites
  • ankle swelling due to fluid retention
  • haematemesis + melaena from GI haemorrhage
  • pruritus due to cholestasis - often an early symptom of PBC
  • gynaecomastia, loss of libido + amenorrhoea due to endocrine dysfunction
  • portosystemic encephalopathy
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3
Q

What is chronic liver disease?

A
  • a disease process of the liver that involves progressive destruction + regeneration of liver parenchyma leading to fibrosis and cirrhosis
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4
Q

there are a lot

What are the potential signs of chronic liver disease?

A
  1. General: jaundice, pyrexia, hair loss, anaemia
  2. Compensated: palmar erythema, clubbing, dupuytren’s, xanthomas, xanthelasmas, parotid enlargement, spider naevi, gynaecomastia, hepatomegaly or smaller liver (late), splenomegaly, scratch marks, testicular atrophy, purpura + pigmented ulcers
  3. Decompensated: leuconychia, confusion + encephalopathy, drowsy/coma, hepatic flap, loss of proximal bulk, ascites, caput medusae, oedema
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5
Q

What are the infective causes of chronic liver disease?

A
  • Hep B
  • Hep C
  • Hep D
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6
Q

What are the non-infective causes of chronic liver disease?

A
  • autoimmune chronic hep
  • alcoholic liver disease
  • drugs: methyldopa, nitrofurantoin
  • wilson’s disease
  • a1-antitrypsin deficiency
  • haemochromatosis
  • primary biliary cirrhosis
  • primary sclerosing cholangitis
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7
Q

Liver cirrhosis implies irreversible liver damage. Histologically, there is loss of normal hepatic architecture with bridging fibrosis and nodular regeneration.

What are the common causes of liver cirrhosis?

A
  • Alcohol
  • Non-alcoholic fatty liver disease
  • Viral hep (B + C)
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8
Q

What are features of hepatic failure, as a result of cirrhosis?

A
  • Coagulopathy
  • Encephalopathy
  • Hypoalbuminaemia → oedema
  • Sepsis → pneumonia, septicaemia
  • Spontaneous bacterial peritonitis
  • Hypoglycaemia
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9
Q

Liver cirrhosis can also lead to portal hypertension where portal vein pressure is >15mmHg.

What are features of portal hypertension?

A
  • Ascites
  • Splenomegaly
  • Portosystemic shunt incl oesophageal varices
  • Caput medusae
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10
Q

What investigations can be done for liver cirrhosis?

A
  • New recommended techniques include transient elastography (fibroscan) and acoustic radiation force impulse imaging
  • NAFLD → enhanced liver fibrosis score
  • Upper endoscopy for varices
  • Liver USS every 6 months (+/- alpha-feto protein) to check for hepatocellular cancer
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11
Q

What is the general management of liver cirrhosis?

A
  • good nutrition
  • alcohol abstinence
  • avoid NSAIDs, sedatives + opiates
  • colestyramine helps pruritus (4g/12h PO, 1hr after other drugs)
  • consider USS + alpha-fetoprotein every 6 months to screen for HCC
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12
Q

What is the treatment for ascites?

A
  • fluid restriction (<1.5L/d) + low salt diet​
  • spironolactone 100mg/24h PO
    • dose increased as tolerated as it counters deranged RAAS axis
  • chart daily weight + aim for weight loss of <1/2kg per day
  • if response poor → add furosemide <120mg/24hr PO
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13
Q

How is liver transplant prioritisation calculated in the UK and what is the immediate management of it?

A
  • Prioritisation based upon UKELD score, calc from:
    • serum Na
    • creatinine
    • bilirubin
    • INR
  • Post op = 12-48hr on ITU w/ enteral feeding starting ASAP + close monitoring of LFTs
  • immunosuppression examples → tacrolimus +/- mycophenolate mofetil + prednisolone
  • acute rejection = pt feels unwell w/ pyrexia + tender hepatomegaly
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14
Q

What is hepatic encephalopathy?

A
  • XS absorption of ammonia + glutamine from bacterial breakdown of proteins in gut → builds up and passes to brain
  • XS glutamine causes osmotic imbalance → cerebral oedema
  • associated w/ acute liver failure AND chronic disease
  • mild cognitive impairment may precede
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15
Q

What are features of hepatic encephalopathy?

A
  • confusion; altered GCS
  • asterix: liver flap
  • constructional apraxia (can’t draw 5 pointed star)
  • triphasic slow waves on EEG
  • raised ammonia level
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16
Q

How is hepatic encephalopathy graded?

A
  1. Irritability
  2. Confusion, inappropriate behaviour
  3. Incoherent, restless
  4. Coma
17
Q

How is hepatic encephalopathy managed?

A
  • treat underlying precipitating cause
  • first-line → lactulose
  • addition of rifaximin for secondary prophylaxis
  • lactulose promotes excretion of ammonia + inc metabolism of ammonia by gut bacteria
  • rifaximin modulates gut flora → reduced ammonia production
  • other options → embolisation of portosystemic shunts + liver transplantation
18
Q

What is primary biliary cholangitis (PBC)?

A
  • chronic liver disorder
  • middle-aged females (9:1)
  • interlobular bile ducts damaged by chronic autoimmune granulomatous inflammation causing cholestasis → fibrosis, cirrhosis + portal hypertension
  • often asymptomatic + diagnosed after incidental high ALP
  • lethargy, sleepiness, pruritus may precede jaundice

Signs → jaundice / skin pigmentation / xanthelasma / xanthomata / hepatosplenomegaly

19
Q

What do investigations for PBC show?

A
  • ANTIMITOCHRONDRIAL ANTIBODIES (AMA)
  • ALP + GGT high
  • USS to exclude extrahepatic cholestasis
20
Q

What is the management for PBC?

A
  • pruritus → cholestyramine 4-8g/24h PO
  • fat-soluble vitamin supplementation (ADEK)
  • high-dose ursodeoxycholic acid → may improve survival + delay transplantation
  • monitoring regular LFT + USS
  • liver transplant → for end-stage disease or intractable pruritus
21
Q

What is primary sclerosing cholangitis (PSC)?

A
  • progressive cholestasis w/ bile duct inflammation and strictures
  • associated w/ ulcerative colitis (80% of pts w/ PSC have UC)
  • bile duct, gallbladder, liver + colon cancers are more common so do yearly colonoscopy + USS
  • liver transplant mainstay for end-stage disease; recurrence occurs in up to 30%
  • prognosis worse for those w/ IBD as 5-10% develop colon cancer post-transplant
22
Q

What are the clinical features of PSC?

A
  • cholestasis → jaundice + pruritus
  • RUQ pain
  • fatigue

Investigations → ERCP (diagnostic, beaded appearance), ANCA positive, onion skin on biopsy

23
Q

What is non-alcoholic fatty liver disease (NAFLD)?

A
  • most common cause of liver disease in developed world
  • caused by obesity
  • spectrum of disease:
    • steatosis → fat in liver
    • steatohepatitis → fat w/ inflammation (aka NASH)
    • progressive disease may cause fibrosis + cirrhosis
24
Q

What are clinical features of NAFLD?

A
  • usually asymptomatic
  • hepatomegaly
  • ALT typically greater than AST
  • increased echogenecity on USS
25
Q

What is the investigation and treatment for NAFLD?

A
  • incidental findings on liver USS → enhanced liver fibrosis (ELF) blood test to check for advanced fibrosis
  • mainstay of Rx is lifestyle changes (weight loss) + monitoring
26
Q

What is Wilson’s disease?

A
  • rare inherited autosomal recessive disorder characterised by excessive copper deposition in tissues
  • it is treatable, so screen all for cirrhosis
  • onset symptoms between 10-25yrs
  • children usually present with liver disease whereas first sign of disease in young adults is often neurological disease
27
Q

What are the clinical features of Wilson’s disease?

A
  • Liver → hepatitis / cirrhosis
  • Neuro → basal ganglia degeneration / speech / behaviour + psych problems
  • Kayser-Fleischer rings
  • Renal tubular acidosis
28
Q

What is the diagnosis and treatment of Wilson’s disease?

A
  • Diagnosis → reduced serum caeruloplasmin / reduced serum copper
  • Management → penicillamine (chelates copper) 1st line

*Medicine: Gastrointestinal (29 decks)

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