Cirrhosis Flashcards
(18 cards)
Definition
Irreversible liver damage
Loss of normal architecture
Fibrosis, nodular regeneration
Most common causes (3)
Hepatitis C
Alcohol
Non-alcoholic fatty liver
Hepatitis B
Other causes
Obesity Haemachromatosis Wilson's Alpha 1 ATD Glycogen storage diseases Cholestatic Primary biliary cirrhosis PSC Autoimmune hepatitis Buddchiari, veno-occlusive, right sided heart failure Amiodarone, methotrexate
Pathogenesis
Hepatocyte death ECM deposition Vascular reorganisation Collagen deposition->stellate cells +++ Chronic inflammation
Clinical features
Leukoniychia, clubbing, palmar erythema, gynaecomastia Abdominal distension Jaundice and pruritus Melaena, coffee ground vomitus Telangiectasia Spider naevi Anorexia, weakness, weight loss Endocrine: loss of hair, loss of libido, breast atrophy, irregular menses, impotence, testicular atrophy, gynaecomastia Hepatomegaly
Aim of investigations
- Detect hepatic abnormality
- Measure severity
- Pattern of function test abnormality
- Identify cause
- Possible complications
Investigations
LFTs GGT Serum albumin EUC->low sodium Clotting PLT Albumin
To find the cause: Hepatitis C, hepatitis B serology, HIV Ferritin, TIBC, transferrin, ferritin ANA->AIH anti-smooth muscle->AIH anti-mitochondrial->PBC Serum caeruloplasmin alpha 1 anti-trypsin
Abdominal CT/MRI
Upper GI->varices, portal hypertensive gastropathy
Liver biopsy
Ascitic tap
What does low PLT and low WCC indicate
Hypersplenism
Management
- Treat underlying cause
- Good nutrition, physical activity
- Alcohol avoidance, hepatotoxic drugs (NSAID, high dose paracetamol)
- Weight loss
- Monitor for complications->ascites, varices, hepatorenal, portal HTN, HCC->USS, upper GI, CT, aFP
- Salt restriction, daily weights, bed rest + frusemide + spirinolactone for ascites
- Cholestyramine for pruritis
- Immunisation for hepatitis A and B
- Monitor for SBP, variceal bleeding, renal failure
- Consider spontaneous bacterial peritonitis if ascites and deteriorates
Complications
Coagulopathy + confusion/coma, hypoalbuminemia, asterixis Sepsis SBP Ascites Splenomegaly Varices HCC + risk
Prognosis
5yr survival 50%
Encephalopathy, hyponatremia, hypoalbuminemia and coagulopathy are poor prognostic factors
Common causes of SBP
Klebsiella, E. coli, Strep
Child pugh C
1. Bilirubin 3 mg/dL (>50 µmol/L)+3 2. Albumin >3.5 g/dL (>35 g/L)+1 2.8-3.5 g/dL (28-35 g/L))+2 2.2+3 4. Ascites No Ascites+1 Ascites, Medically Controlled+2 Ascites, Poorly Controlled+3 5. Encephalopathy No Encephalopathy+1 Encephalopathy, Medically Controlled+2 Encephalopathy, Poorly Controlled+3
MELD score
Dialysis at least twice in past week
Creatinine
Bilirubin
INR
Interpreting CPC score
Grade A= 5-6
Grade B = 7-9
Grade C= >10
Cirrhosis and deteriorating renal function
- Negative clearance of IgA-> IgA nephropathy +/= hepatic glomerulosclerosis
- HCV can cause cryoglobulinaemia +/- membranoproliferative GN
- HBV membranous nephropathy +/ PAN
- Hepatorenal syndrome
- MembranoP glomeruloN in a1 antitrypsin deficiency
Define hepatorenal syndrome
Management of hepatorenal syndrome
Hepatorenal syndrome (HRS) is functional renal failure->may be precipitated by infection (particularly spontaneous bacterial peritonitis), diuretics, nephrotoxic drugs, gastrointestinal bleeding or large-volume paracentesis.
a. Type 1 HRS is associated with a rapidly rising serum creatinine concentration, and has a poor prognosis.
b. Type 2 HRS is usually a slowly progressive deterioration in renal function that develops over weeks, and may be reversible with correction of precipitants and/or therapeutic intervention.
Management of hepatorenal
- Monitor diuretic use and reduce in accordance to renal impairment
- IV albumin for those at risk of SBP
- Prophylaxtic antibiotics for those with GIT bleed
- Avoid nephrotoxic medications
Terlipressin + albumin
