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Chronic Liver Disease (Complications: (Hepato-renal syndrome (Poor…
Chronic Liver Disease
Complications:
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Anaemia
Due to malnutrition, poor bleeding control +/- chronic disease
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Encephalopathy
Decreased clearance of ammonia --> accumulation --> astrocytes try to clear by converting glutamate to glutamine --> excess glutamine --> osmotic imbalance and shift of fluid into cells --> cerebral oedema
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Pathophysiology:
Damaged heapatocytes release damage associated molecular patterns (DAMPs) --> stimulaiton of kupffer and stellate cells --> release of cytokines (e.g. TNF alpha, IL 6, TGF) --> immune mediated destruction and myofibroblast proliferation --> collagen deposition and fibrosis
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Defintion:
Cirrhosis: irreversible, progressive chronic liver condition where fibrous tissue replaces damaged hepatocytes with formation of regenerative nodules
Investigations:
Bloods:
Infective screening: Hep BsAg, Anti-HCV, EBV (monospit heterophile), CMV
Genetic: serum seruloplasmin, iron studies (transferrin low, total Fe high and TIBC low), alpha-1 antitrypsin levels,
LFT's (hepatic, mixed, cholestatic)
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Autoimmune: ANA & Anti-smooth muscle anti-bodies (autoimmune hepatits), antimitochondrial antibody* (primary biliary cirrhosis), p-ANCA (primary sclerosing cholangitis)
Toxins: BAC, paracetamol levels,
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Tests to consider: MRCP/ERCP*, liver biopsy (if no answer found)
Acute Ix
Ascitic tap:
LDH: increase suggests infection, bowel perforation or tumour
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Culture and sensitivity: look for E.coli, klebsiella and strep pneumoniae
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Management:
Acute/In hospital:
- Assess fluid status, if ascitie/or fluid over loaded: fluid restrict, low salt diet, diuretics e.g. spirnolactone +/- frusemide, therapeutic tap, daily weights
- Assess nutritional status: thiamine and folate supplementation, check BGL often (hepatic diabetes), if BGL <2: treat with 50mls 50% glucose IV
- Avoid hepatotoxic drugs e.g. NSAIDs, paracetamol, tetracycline, avoid constipating drugs e.g. opiods as they exacerbate encephalopathy
- Daily bloods: FBC, UEC, INR, LFTs
- Manage encephalopathy: lactulose (prevents GI absorption of ammonia), limit protein intake, neomycin (kills bowel flora to decrease ammonia production)
- SBP management: Rifaxamine and repeat paracentesis in 2-3 days to document decreased PMN's
Long Term:
- Slow disease progression, avoid ETOH, avoid hepatotoxic drugs
- Avoid superimposed insults to the liver (e.g. vaccinations)
- Symptom relief (e.g. cholestyramine for pruritis and performing therapeutic taps)
- Manage lab abnormalities e.g. thrombocytopaenia with FFP
- Prevent, identify and treat complications
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Clinical Features:
Abdo and trunk signs: spider naevi (oestrogen; fills inside out), caput medussa (vascular congestion), gynaecomastia (oestrogen), jaundice, pruritis, hepato/splenomegaly, ascites
Facial signs: jaundice, parotid enlargement
Peripheral signs: clubbing, leuconychia (hypoalbuminaema), asterixis (encephalopathy), palmar erythema (oestrogen), dupetryn's contracture (ETOH), oedema
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Risk factors: ETOH, sexual Hx, IVDU, obesity
Causes:
Autoimmune: Autoimmune hepatitis, primary biliary cirrhosis
Infectious: Hep B, Hep C, CMV, EBV
Drugs and toxins: ETOH, paracetamol
Genetic: Wilson's disease, haemochromatosis, alpha-1 antitrypsin deficiency
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Classification:
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Child Pugh: Predictor of 1 yr mortality which takes into account serum bilirubin, albumin, INR, ascites and encephalopathy
Compensated: The biochemical/histological/radiological findings are consistent with pathological process but hepatic synthetic function is preserved with no evidence of complications
- **: perform in both hepatic/mixed and cholecystatic patterns
- *: perform only in cholecystatic patterns