0227 - Cirrhosis and its complications Flashcards
Define cirrhosis
A condition in which the liver responds to death of hepatocytes by producing interlacing strands of fibrous tissue between nodules of regenerating cells.
What are the most common causes of cirrhosis?
Alcohol (60-70%)
Chronic viral hepatitis B/C (10%)
Fatty liver (10-15%)
Biliary disorders: Primary Biliary Cirrhosis, Primary Sclerosing Cholangitis (5-10%)
Haemochomatosis (5%)
Others (autoimmune hepatitis, Wilson’s disease, drugs)
What is the course of alcoholic cirrhosis
Normal liver ->fatty liver
8-20% will progress directly to cirrhosis
10-35% will get alcoholic hepatitis, of which 40% will progress to cirrhosis
Briefly outline NAFLD
Nonalcoholic Fatty liver disease
Spectrum - Steatosis; Steatohepatitis; Cirrhosis
Common (<30% popn), but is a major risk factor for liver disease, CV risk, diabetes and HCC
What are the outcomes of NAFLD?
5% develop cirrhosis, 1.7% die within 7 years
Simple steatosis - benign
NASH - ⅓ will progress (fibrosis), cirrhosis 5-8% over 5 years with poor outcome.
What are the major consequences of cirrhosis?
Portal Hypertension, leading to:
Oesophageal/gastric/hemorrhoids
Ascites and spontaneous bacterial peritonitis
Hepatorenal syndrome
Also Liver cancer (HCC) - injury, repair, chronic inflammation
How is ascitic fluid analysed? How can analysis indicate portal HTN?
Diagnostic aspiration (cell count, albumin, culture, cytology) 250 neutrophils/mm3 - Spontaneous bacterial peritonitis Serum albumin-ascitic fluid albumin gradient (SAAG) >11g/L = portal HTN
What are the two forms of pathophysiology of ascites?
1 - Increased hydrostatic (HTN) pressure and low oncotic (albumin) leads to increased lymph flow. Portal pressure localises leak to abdomen, hence ascites.
2 - Low effective arterial blood volume activates RAA, SY, ADH, leading to Na+, H2O retention and increased plasma volume.
How is ascites managed?
Salt restriction (2g/day)
Spironolactone (antagonise RAA), then frusemide
Monitor weight, paracentesis if resistant to diuretics (but replace the albumin)
Briefly outline spontaneous bacterial peritonitis
Few/no signs/symptoms, diagnose by ascitic fluid (neutrophils >250/mm3)
IV antibiotics - 5 days
Prophylactic ABs if history of SBP or if GI bleed
Briefly outline hepatic encephalopathy
Worse sign even than ascites.
Signs - Asterixis, number connection tests, personality changes, altered sleep and memory
Believed caused by ammonia.
How do you treat hepatic encephalopathy?
Aim to treat precipitating factors (infection, drugs, constipation etc)
Lactulose to acidify gut (neutralise NH3, kill bacteria) and keep it moving
High protein diet
Antibiotics to sterilise gut
Briefly outline hepatorenal syndrome
Functional renal failure in patients with cirrhosis (nothing wrong with the kidney itself)
Acute/chronic liver disease + low GFR/creatinine >130
No other causes of renal failure
No response to fluid challenge.
How do you treat hepatorenal syndrome?
Exclude/treat other causes of acute renal failure
Vasoconstrictors to reduce systemic vasodilation (promote renal flow)
Dialysis if transplant is planned.
What is the management plan for varices?
Prevent first bleed (band/ligate them, beta blockers)
Control active bleeding (emergency balloon tamponade, band, drugs)
Prevent rebleed (banding)
