Flashcards in Cirrhosis Deck (18):
1
Definition
Irreversible liver damage
Loss of normal architecture
Fibrosis, nodular regeneration
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Most common causes (3)
Hepatitis C
Alcohol
Non-alcoholic fatty liver
Hepatitis B
3
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
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Pathogenesis
Hepatocyte death
ECM deposition
Vascular reorganisation
Collagen deposition->stellate cells +++
Chronic inflammation
5
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
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Aim of investigations
1. Detect hepatic abnormality
2. Measure severity
3. Pattern of function test abnormality
4. Identify cause
5. Possible complications
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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
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What does low PLT and low WCC indicate
Hypersplenism
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Management
1. Treat underlying cause
2. Good nutrition, physical activity
3. Alcohol avoidance, hepatotoxic drugs (NSAID, high dose paracetamol)
4. Weight loss
5. Monitor for complications->ascites, varices, hepatorenal, portal HTN, HCC->USS, upper GI, CT, aFP
6. Salt restriction, daily weights, bed rest + frusemide + spirinolactone for ascites
7. Cholestyramine for pruritis
8. Immunisation for hepatitis A and B
9. Monitor for SBP, variceal bleeding, renal failure
10. Consider spontaneous bacterial peritonitis if ascites and deteriorates
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Complications
Coagulopathy + confusion/coma, hypoalbuminemia, asterixis
Sepsis
SBP
Ascites
Splenomegaly
Varices
HCC + risk
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Prognosis
5yr survival 50%
Encephalopathy, hyponatremia, hypoalbuminemia and coagulopathy are poor prognostic factors
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Common causes of SBP
Klebsiella, E. coli, Strep
13
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
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MELD score
Dialysis at least twice in past week
Creatinine
Bilirubin
INR
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Interpreting CPC score
Grade A= 5-6
Grade B = 7-9
Grade C= >10
16
Cirrhosis and deteriorating renal function
1. Negative clearance of IgA-> IgA nephropathy +/= hepatic glomerulosclerosis
2. HCV can cause cryoglobulinaemia +/- membranoproliferative GN
3. HBV membranous nephropathy +/ PAN
4. Hepatorenal syndrome
5. MembranoP glomeruloN in a1 antitrypsin deficiency
17
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.
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