– Liver

  Hepatic artery variants


•  Right hepatic artery off superior mesenteric artery (#1 hepatic artery variant; 20%) courses behind pancreas, posterolateral to the common bile duct


•  Left hepatic artery off left gastric artery (about 20%) – found in gastrohepatic ligament medially


  Falciform ligament – separates medial and lateral segments of the left lobe; attaches liver to anterior abdominal wall; extends to umbilicus and carries remnant of the umbilical vein


  Ligamentum teres – carries the obliterated umbilical vein to the undersurface of the liver; extends from the falciform ligament


  Line drawn from the middle of the gallbladder fossa to IVC (portal fissure or Cantlie’s line) separates the right and left liver lobes




  Segments


•  I – caudate


•  II – superior left lateral segment


•  III – inferior left lateral segment


•  IV – left medial segment (quadrate lobe)


•  V – inferior right anteromedial segment


•  VI – inferior right posterolateral segment


•  VII – superior right posterolateral segment


•  VIII – superior right anteromedial segment


  Glisson’s capsule – peritoneum that covers the liver


  Bare area – area on the posterior-superior surface of liver not covered by Glisson’s capsule


  Triangular ligaments – lateral and medial extensions of the coronary ligament on the posterior surface of the liver; made up of peritoneum


  Portal triad enters segments IV and V


  Gallbladder lies under segments IV and V



  Kupffer cellsliver macrophages


  Portal triadcommon bile duct (lateral), portal vein (posterior), and proper hepatic artery (medial); come together in the hepatoduodenal ligament (porta hepatis)


  Pringle maneuver – porta hepatis clamping; will not stop hepatic vein bleeding


  Foramen of Winslow (entrance to lesser sac)


•  Anterior – portal triad


•  Posterior – IVC


•  Inferior – duodenum


•  Superior – liver


  Portal vein


•  Forms from superior mesenteric vein joining splenic vein (no valves)


•  Inferior mesenteric vein – enters splenic vein


•  Portal veins – 2 in liver; ⅔ of hepatic blood flow


  Left – goes to segments II, III, and IV


  Right – goes to segments V, VI, VII, and VIII


  Arterial blood supply


•  Right, left, and middle hepatic arteries (follows hepatic vein system below)


•  Middle hepatic artery MC a branch off the left hepatic artery


•  Most primary and secondary liver tumors are supplied by the hepatic artery


  Hepatic veins – 3 hepatic veins; drain into IVC


•  Left – II, III, and superior IV


•  Middle – V and inferior IV


•  Right – VI, VII, and VIII


•  Middle hepatic vein comes off left hepatic vein in 80% before going into IVC; other 20% goes directly into IVC


•  Accessory right hepatic veins – drain medial aspect of right lobe directly to IVC


•  Inferior phrenic veins – also drain directly into the IVC


  Caudate lobe – receives separate right and left portal and arterial blood flow; drains directly into IVC via separate hepatic veins


  Alkaline phosphatase – normally located in canalicular membrane


  Nutrient uptake – occurs in sinusoidal membrane


  Ketones – usual energy source for liver; glucose is converted to glycogen and stored


•  Excess glucose converted to fat


  Urea – synthesized in the liver


  Not made in the liver – von Willebrand factor and factor VIII (endothelium)


  Liver stores large amount of fat-soluble vitamins


  B12 – the only water-soluble vitamin stored in the liver


  Bleeding and bile leak – most common problems with hepatic resection


  Hepatocytes most sensitive to ischemia – central lobular (acinar zone III)


  75% of normal liver can be safely resected


BILIRUBIN


  A breakdown product of hemoglobin (Hgb → heme → biliverdin → bilirubin)


  Conjugated to glucuronic acid (glucuronyl transferase) in the liver → improves water solubility


  Conjugated bilirubin is actively secreted into bile


  Urobilinogen


•  Breakdown of conjugated bilirubin by bacteria in the terminal ileum occurs


•  Free bilirubin is reabsorbed, converted to urobilinogen, and eventually released in the urine as urobilin (yellow color)


•  Excess urobilinogen turns urine dark like cola


BILE


  Contains bile salts (85%), proteins, phospholipids (lecithin), cholesterol, and bilirubin


  Final bile composition determined by active (Na/K ATPase) reabsorption of water in gallbladder


  Cholesterol – used to make bile salts/acids


  Bile salts are conjugated to taurine or glycine (improves water solubility)


•  Primary bile acids (salts) – cholic and chenodeoxycholic


•  Secondary bile acids (salts) – deoxycholic and lithocholic (dehydroxylated primary bile acids by bacteria in gut)


  Lecithin – main biliary phospholipid


  Bile solubilizes cholesterol and emulsifies fats in the intestine, forming micelles, which enter enterocytes by fusing with membrane


JAUNDICE


  Occurs when total bilirubin > 2.5; 1st evident under the tongue


  Maximum bilirubin is 30 unless patient had underlying renal disease, hemolysis, or bile duct–hepatic vein fistula


  Elevated un-conjugated bilirubin – prehepatic causes (hemolysis); hepatic deficiencies of uptake or conjugation


  Elevated conjugated bilirubin – secretion defects into bile ducts; excretion defects into GI tract (stones, strictures, tumor)


  Syndromes


•  Gilbert’s disease – abnormal conjugation; mild defect in glucuronyl transferase


•  Crigler–Najjar disease – inability to conjugate; severe deficiency of glucuronyl transferase; high unconjugated bilirubin → life-threatening disease


•  Physiologic jaundice of newborn – immature glucuronyl transferase; high unconjugated bilirubin


•  Rotor’s syndrome – deficiency in storage ability; high conjugated bilirubin


•  Dubin–Johnson syndrome – deficiency in secretion ability; high conjugated bilirubin


VIRAL HEPATITIS


  All hepatitis viral agents can cause acute hepatitis


  Fulminant hepatic failure can occur with hepatitis B, D, and E (very rare with A and C)


  Hepatitis B, C, and D can cause chronic hepatitis and hepatoma


  Hepatitis A (RNA) – serious consequences uncommon


  Hepatitis B (DNA)


•  Anti-HBc-IgM (c = core) is elevated in the first 6 months; IgG then takes over


•  Vaccination – have ↑ anti-HBs (s = surface) antibodies only


•  ↑ anti-HBc and ↑ anti-HBs antibodies and no HBs antigens (HBsAg) → patient had infection with recovery and subsequent immunity


  Hepatitis C (RNA) – can have long incubation period; currently most common viral hepatitis leading to liver TXP


  Hepatitis D (RNA) – cofactor for hepatitis B (worsens prognosis)


  Hepatitis E (RNA) – fulminant hepatic failure in pregnancy, most often in 3rd trimester


LIVER FAILURE


  Most common cause of liver failurecirrhosis (palpable liver, jaundice, ascites)


  Best indicator of synthetic function in patient with cirrhosis – prothrombin time (PT)


  Acute liver failure (fulminant hepatic failure) – 80% mortality


•  Outcome determined by the course of encephalopathy


•  Consider urgent liver TXP listing if King’s College criteria are met


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Jun 24, 2017 | Posted by in GENERAL SURGERY | Comments Off on – Liver

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