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42 Cards in this Set
- Front
- Back
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LFTs - ENZYMES |
Alkphos and GGT = cholestatic, malignancy or alcohol abuse ALT/AST = hepatocellular damage; increased 1.5-3x in ALD/NAFLD or >3x in viral, drug and AI hepatitis Poor indicator as ALT often normal in NAFLD |
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LFTs - BILIRUBIN, CLOTTING AND PROTEINS
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Bilirubin >17 = abnormal; >30 = clinical jaundice Bilirubin is unconjugated in Gilbert's and haemolysis Low albumin is a bad prognostic feature Clotting profiles often near normal as liver produces pro and anti clotting factors |
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LFTs - AUTOANTIBODIES
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ANA + ASMA = AI hepatitis AMA = PBC (very sensitive and specific) pANCA - PSC |
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LFTs - IGS
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IgA = ALD or NAFLD IgG = AI hepatitis IgM = PBC |
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LFTs - SEROLOGY
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HAV: IgM is acute and IgG past infection HBV: sAg shows infection HCV: IgG is exposure and RNA PCR is active infection HEV: same as for HAV |
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LFTs - Fe AND Cu STUDIES
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Increased ferritin and transferrin saturation in Haemachromatosis Low caeruloplasmin in Wilson's |
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LFTs - TUMOUR MARKERS
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AFP in 50-80% of HCC patients CA19-9 in cholangiocarcinoma |
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IMAGING IN LIVER DISEASE
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USS is first line; good for obstructions, masses, gallstones, spleen and kidneys; doppler to assess HTN CT is more sensitive but needs contrast; good for focal lesions >5mm, liver architecture, varices MRI eg MRCP |
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LIVER BIOPSY |
Gold standard for diagnosis and staging of chronic disease Many complications Used post-transplant to assess rejection |
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PATHOPHYSIOLOGY OF JAUNDICE
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Hb breaks down in RES = unconjugated and albumin-bound bilirubin This is broken down in liver Bilirubin is conjugated with glucoronic acid and excreted in bile Colonic bacteria deconjugate bilirubin to colourless urobilinogen which is oxidised = stool colour |
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SIGNS OF LIVER DECOMPENSATION
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Jaundice Encephalopathy Ascites Asterixis |
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SCORING SYSTEMS
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Child-pugh: assess liver function and prognosis in cirrhosis; based on bilirubin, albumin, INR, ascites and encephalopathy MELD: prioritises patients for transplant; based on bilirubin, creatinine and INR |
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PORTAL HYPERTENSION
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Dilatation of smaller vessels in abdomen; vessels are thin-walled so can burst PVP >10mmHg (norm = 7) Prophylaxis via non-selective BB eg propanolol |
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MANAGEMENT OF ACUTE VARICEAL BLEEDING
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Resus AB prophylaxis (augmentin/cefuroxime) Terlipressin, somatostatin and octreotide Endoscopy Sengstaken-blakemore tube (catheter and balloon at OGJ) TIPS (Transjugular intrahepatic portal systemic shunt to decrease PVP) |
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ASCITES
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Caused by venous outflow obstruction leading to increased ECF which causes transudation of fluid into the abdomen Treat via cause management, salt/fluid restriction and paracentesis |
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PARACENTESIS
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Fluid drainage in <6h Replacement with 100ml 20% HAS for every 1.5L HAS to avoid hepatorenal syndrome |
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ASCITIC FLUID ASSESSMENT
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Serum ascites albumin gradient: high (>11) in cirrhosis, cardiac failure, alcoholic hepatitis and nephrotic syndrome WCC: 30% HCC pts have bloody ascites PMN high in SBP Ascites can be cultured in blood culture bottles (but not gram stain) |
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SALT AND FLUID RESTRICTION
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Na input should exceed output Salt 22-44mmol/d and fluid 1-1.5L/d Concurrent diuretics: spironolactone and furosemide both titrated up whilst monitoring kidney function Patients should lose 0.5kg/d |
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REFRACTORY ASCITES
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Diuretic-resistant or diuretic-intractable (diuretic-induced complications eg electrolytes off, renal impairment and hepatic enceph.) Treat via TIPS or paracentesis |
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SPONTANEOUS BACTERIAL PERITONITIS - CAUSES
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Cirrhosis causing immunological defects eg decreased complement and phagocytosis Portal HTN causing oedema which produces bacteria and allows bacteria to spread from other places |
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SBP - SYMPTOMS AND TREATMENT |
Fever, abdo pain, encephalopathy, diarrhoea, ileus, shock, hypothermia Tazocin and lifelong prophylaxis with ciprofloxacin |
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HEPATORENAL SYNDROME
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Renal failure with sever liver disease and no other cause of the renal pathology Often in patients with decompensated cirrhosis Multi-organ failure due to regional arterial vascon Manage via transplant and then albumin and terlipressin |
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HRS - TYPES |
TYPE 1: rapid; creatinine doubles and GFR halves in 24h; background of acute liver failure and causes renal failure TYPE 2: moderate renal failure which is slow and steady; causes refractory ascites |
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HEPATIC ENCEPHALOPATHY
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Graded 1-4 based on symptoms eg lack of awareness through to coma Due to ammonia, benzos, cytokines, hypoNa causing astrocyte swelling Triggers: acidosis, increased protein, infection, sedatives, diuretics Treat cause and give lactose/phosphate enemas and rifaximin (AB) |
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DAY TO DAY CIRRHOSIS MANAGEMENT
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6monthly screens for HCC 2yearly OGDs and BB for varices Immunise HAV/HBV Monitoring for ascites and vitamin deficiencies |
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ACUTE VS FULMINANT |
Fulminant is part of acute liver failure which implies encephalopathy and no pre-existing liver disease
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CLASSIFICATION OF LIVER FAILURE
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All have encephalopathy Hyperacute = 0-7d with cerebral oedema, raised PT, and slightly raised bilirubin Acute = 8-28d with oedema, raised PT and bilirubin Subacute = 1-3m with less raised PT and raised bilirubin |
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PARACETAMOL OD - PATHPHYSIOLOGY |
Normal metabolites (sulphate and glucoronide conjugates) become saturated Metabolism shifts to be via NAPQ1 which causes cell death |
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PARACETAMOL OD - TREATMENT
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N-acetylcysteine to detox via glutathione to non-toxic mercapturic acid conjugates Ensure no malnutrition Consider interaction of rifampicin and anti-epileptics |
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INDICATIONS FOR TRANSPLANT IN PARACETAMOL OD
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pH <7.25 post-resus PT >100 and creatinine >300 Lactate >3.5 after 24hr Life threatening deterioration |
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COMPLICATIONS OF ALF
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Loss of metabolic functions eg gluconeogenesis ARDS BM suppression Encephalopathy Increased CO and subclinical cardiac injury Pancreatitis Decreased GCC Renal dysfunction SIRS Impaired leukocytes |
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CEREBRAL OEDEMA |
Major cause of death and neuro injury Impaired urea synthesis causes astrocytes start to clear ammonia; produces glutamine which attracts water Treat via hypertonic saline, 20% mannitol and cooling body to 32-34deg |
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PBC - PATHOPHYSIOLOGY
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AMA plus raised ALP
Damage to small intrahepatic bile ducts causing inflammation, fibrosis and cirrhosis
Often in women (esp middle aged), NOT in children |
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PBC - SYMPTOMS & INVESTIGATIONS
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Asymptomatic Fatigue Itch Dry eyes/mouth Poor memory Symptoms of advanced liver disease USS Biopsy only if unsure, will show granulomatous picture |
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PBC - TREATMENT
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Ursodeoxycholic acid (hydrophilic bile acid; can cause wt gain, hair thinning and diarrhoea) Transplantation Treat itch (not antihistamines) Treat fatigue (exclude other causes) Monitor cirrhosis, HCC/varices screening, screen for osteoporosis |
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AI - PATHOPHYSIOLOGY |
ANA, ASMA and IgG Type 1 most common, Type 2 more in younger people and females; T2 is LKM-1 and LC1 antibodies Can be precipitated by drugs eg nitrofurantoin |
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AI - SYMPTOMS & INVESTIGATIONS
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Asymptomatic Fatigue Anorexia Nausea Arthralgia Acute hepatitis or complications of cirrhosis LFTS and liver biopsy needed (show inflam infiltrate) |
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AI - TREATMENT
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Immunosuppression eg prednisolone, azathioprine, MMF or tacrolimus Transplant Aim to normalise ALT and IgG |
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PSC - PATHOPHYSIOLOGY
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ALP and ANCA Inflammation and fibrosis of intra- and extrahepatic ducts with multifocal strictures Increased risk of cholangio- or gallbladder cancer |
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PSC - SYMPTOMS & INVESTIGATIONS
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Asymptomatic Fatigue Itch RUQ pain Weight loss Cholangitis Jaundice Cirrhosis Do LFTs, MRCP (beading) and biopsy (onion skin fibrosis) |
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PSC - TREATMENT
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No real treatment Monitor for IBD ERCP strictures/stenting Treat itch Monitor and treat osteoporosis Malignancy screens Transplantation (PSC can reoccur) |
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IgG4 DISEASE
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Similar to PSC but extrahepatic ducts only Raised IgG4 Multi-organ eg pancreatic Very steroid responsive |
