Cirrhosis Flashcards

1
Q

Aetiology? 4 most common

A
  • Alcoholic liver disease
  • NAFLD
  • Hep B
  • Hep C
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2
Q

Signs?

A

as per alcoholic liver disease:

  • Jaundice
  • HSM
  • Caput medusae
  • Ascites
  • Palmar erythema
  • Spider naevi
  • Gynaecomastia –> due to endocrine dysfunction
  • Asterixis
  • Bruising
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3
Q

Ix?

A
  • Bloods
    • Glucose
    • PT raised
    • Albumin low
    • FBC
    • U&E
      • deranged in hepatorenal syndrome
      • hyponatraemia
    • LFTs
      • in decompensated, all markers deranged
    • if cause unknown:
      • viral markers & auto-antibodies
    • Enhanced Liver Fibrosis (ELF) blood test 1st line in assessing fibrosis in NAFLD
  • US
  • FibroScan
  • Endoscopy
  • CT/MRI
  • Liver biopsy
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4
Q

what changes may be seen on US?

A
  • nodularity of liver surface
  • “corkscrew appearance” of hepatic arteries
  • enlarged portal vein w reduced flow
  • ascites
  • splenomegaly
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5
Q

how do you determine prognosis?

A

Child-Pugh score

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6
Q

Mx?

A
  • Screening for hepatocellular carcinoma - US & alpha fetoprotein every 6 months
  • Endoscopy every 3 years in pts without known varices
  • High protein, low sodium diet
  • Liver transplant
  • Manage complications
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7
Q

Complications?

A
  • malnutrition
  • portal HT, varices & variceal bleeding
  • ascites & spontaneous bacterial peritonitis
  • hepatorenal syndrome
  • hepatocellular carcinoma
  • hepatic encephalopathy
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8
Q

what are varices?

A

swollen, tortuous vessels that occur at junction between portal system and systemic venous system:

  • gastro-oesophageal junction
  • ileocaecal junction
  • rectum
  • anterior abdo wall (caput medusae)
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9
Q

Mx of varices?

A

if varices stable - bleed prevention:

  1. beta blockers
  2. endoscopic ligation
  3. TIPS
    • used if medical and endoscopic treatment fails
    • makes connection between hepatic vein and portal vein, allowing blood to flow directly from portal vein to hepatic vein bypassing liver
  • surveillance by endoscopy
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10
Q

Pathophysiology of Ascites?

A
  • low oncotic pressure (low albumin) & increased pressure in portal system causes increased capillary permeability & fluid to leak out into peritoneal cavity
  • this causes drop in circulating blood volume = low BP= RAAS kicks in
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11
Q

what kind of ascites does cirrhosis cause?

A

transudative (low protein content)

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12
Q

Ix of ascites?

A

paracentesis (ascitic tap) & send for protein, cell count, microscopy / culture, cytology

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13
Q

pathophysiology of hyponatraemia in ascites

A

dilutional hyponatraemia due to ADH response in kidneys

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14
Q

Mx of ascites?

A
  • low sodium diet
  • anti-aldosterone diuretics ie spironolactone
  • prophylactic abx against SBP
  • consider TIPS
  • consider liver transplant
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15
Q

Epidemiology of SBP

A
  • occurs in around 10% of pts w ascites secondary to cirrhosis
  • infection develops in ascitic fluid with no clear cause
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16
Q

presentation of SBP?

A
  • Can be asymptomatic
  • Fever
  • Abdo pain / tenderness
  • Deranged bloods
  • Ileus (reduced movement in intestines)
  • Hypotension
17
Q

most common organisms for SBP?

A
  • E.Coli
  • Klebsiella pneumoniae
  • Gram positive cocci
18
Q

Mx of SBP?

A

Ascitic culture prior to giving Abx:

  • IV Cephalosporin ie Cefotaxime
19
Q

pathophysiology of hepatorenal syndrome?

A

RAAS activation –> renal vasoconstriction –> starvation of blood to kidneys –> fatal within a week or so unless liver transplant performed

20
Q

PATHOPHYSIOLOGY OF hepatic encephalopathy?

A
  • Gut bacteria break down product = ammonia
  • Ammonia absorbed into blood stream and usually goes to liver where broken down into harmless waste product.
  • In cirrhosis, not able to do this and therefore build- up of ammonia. It also bypasses liver and goes directly into systemic circulation.
  • Presentation:
    • Acutely–> confusion & reduced consciousness
    • Chronically –> changes to personality, memory and mood
21
Q

Mx of hepatic encephalopathy?

A

laxatives (excretion of ammonia) & Abx (reduce gut bacteria)