95.Liver_biliary Flashcards
pringle manuever
20 minutes occlusion of hepatic artery and portal veinfinger in epiploic foramen(dorsal–CVC, ventral–PV, cranial–liver, caudal–hepatic artery)
blood supply to liver
hepatic artery (br celiac artery): 20% blood 50% oxygenportal vein: 80% blood 50% oxygen
where does the cystic artery arise from
branch of the left branch of the hepatic artery
most proximal draining veins into the portal vein prior to liver branching (prehepatically)
splenic veingastroduodenal vein (most proximal–absent in cats)
T/Fthe most cranial hepatic vein entering the caudal vena cava arises from the left hepatic lobe
TRUEleft branches are the most cranial, then central branches and then the most caudal are right branches located within the parenchyma
lobes of the liver
6 lobesleft medialleft lateralright medialright lateralcaudate —caudate and papillary processesquadrate
biliary flow
canaliculiinterlobular ductslobar ductshepatic ducts (2-8)CBD*at the point where the first hepatic duct meets the cystic duct= CBDenter at major duodenal papilla, sphincter of Oddi (adjacent to but not conjoined to pancreatic duct—conjoined in cats)80% cats do NOT have minor duodenal papilla for accessory pancreatic duct
functions of liver (6)
dysfxn occurs with 70-80% loss of liver–protein synthesis (20% of TP)–CHO metabolism (glucose homeostasis)–Lipid metabolism (makes cholesterol, stores fat in the form of TG from free FA)–immune system:reticuloendothelial phagocytic function of harmful substances, Kuppfer cells (macros)–all coag factors including vit K dependent factors 2, 7, 9, 10 (liver does not make VIII, vWF) and vit K, TPO, fibrinogen–bile production: made up of bile acids, bilirubin (80% from Hb), cholesterol, phospholipids, water, bicarb, ions
physiology of Hb breakdown
reticuloendothelial function of liver (extravascular) breakdown of Hb–bilirubin is bound to alb and taken to liver–conjugated in liver to glucuronic acid and secreted into bile –combine with bile acids (taurine–cats, taurine or glycine–dogs WITH cholesterol)–conjugated bili and bile acids travel to GB for storage–SI stimulated release of CCK causes GB to contract and sphincter of Oddi to relax–bile salts emulsify fats (miscelle formation) and bind endotoxin to prevent their absorption–bilirubin is degraded to urobilinogen by bacT–urobilinogen is converted to urobilin or stercobilin (brwn color feces)–90% passage in feces; 10% re-circulation within portal system
regenerative capacity of liver
incredible regenerative capacity–begins within hours and peaks at 3 daystolerates removal of 65-70%BUT NOT >80%compensatory hypertrophy and hyperplasiahepatic arterial buffer response–change in portal pressure with massive resection will increase hepatic arterial perfusion (portal vein embolization can increase liver volumes 25-30%)cytokines also enhance regeneration (insulin, estrogen, growth factors, PG, etc)
factors that impede liver regeneration
diabetes mellitus (decr insulin which is a major hepatotrophic hormone)male genderbile obstruction agemalnutrition
common location of trauma biliary tract rupture
–CBD (body)–hepatic ductsRARELY from GB itself
most common causes of EHBO in dogs
–GB mucocele–pancreatitis–neoplasia–cholangitis–cholelithiasis(can also have FB or mass in duodenum)
most common causes of EHBO in cats
–complex inflammatory dz (pancreatitis,cholangiohepatitis, cholecystitis with or without stones)–neoplasia(less common: parasites–flukes, diaphragmatic hernia)
after acute ligation of CBD in dogs, how long does it take for dilation to occur
dilation of CBD occurs within 24-48 hrs (along with an increase in serum bilirubin)dilation of lobar/interlobular ducts takes 4-6 days
pathophysiologic consequences of EHBO
absence of bile salts in SI leads to increase bacT overgrowth and endotoxin absorption, impaired clearance of endotoxin through RE system of liver so systemic endotoxemia ensues–hypotension–coagulopathy (DIC)–GI bleeding (endotoxemia related gastric ischemia and incr acid production)–delayed wound healing (decr fibroplasia/angiogenesis)–decreased myocardial contractility –acute renal failure (endotoxemic = renal vasoconstrictor, acute tubular necrosis)
bile peritonitis causes in dogs
–trauma–necrotizing cholecystitis–ruptured GB mucoceleRARE in cats –think traumacan also have a proximal duodenal perf with bile peritonitis if near major duodenal papillabilirubin in ab fluid 2x > peripheral blood bilirubin
pathophysiology bile peritonitis
bile salts are hyperosmolar in ab cavity (fluid shifts)inflammation, necrosis, hemolysis occurnormally sterile but can have bacT from ascending GI, colonization of liver bacT, bacT translocation, or from direct inoculation with penetrating injury septic biliary effusions greatly worsen px
T/Fwhen bile salts are not present in SI to bind endotoxin, systemic endotoxemia may develop
TRUEin the GI, bile salts emulsify fats (miscelle formation) and bind endotoxin to prevent their absorptionwhen they are not available INCR bacT and INCR endotoxin
hepatobiliary imaging
–survey rads (not SN/SP: mineralization (may be incidental, gas, liver size, mass effect, stones)–ab US (FNA, biopsy, centesis, color flow doppler, contrast enhanced harmonic US w gas microbubbles)–hepatobiliary scintigraphy (quantifies liver function; technetium iminodiacetic acid accumulate within biliary tract; if not seen in SI in 3 hours== EHBO; limitation of mechanical vs functional obstruction and location)–CT/MRI–Endoscopic retrograde cholangiopancreatography (ERCP)–contrast, stone removal or stent placement