95.Liver_biliary Flashcards

1
Q

pringle manuever

A

20 minutes occlusion of hepatic artery and portal veinfinger in epiploic foramen(dorsal–CVC, ventral–PV, cranial–liver, caudal–hepatic artery)

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2
Q

blood supply to liver

A

hepatic artery (br celiac artery): 20% blood 50% oxygenportal vein: 80% blood 50% oxygen

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3
Q

where does the cystic artery arise from

A

branch of the left branch of the hepatic artery

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4
Q

most proximal draining veins into the portal vein prior to liver branching (prehepatically)

A

splenic veingastroduodenal vein (most proximal–absent in cats)

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5
Q

T/Fthe most cranial hepatic vein entering the caudal vena cava arises from the left hepatic lobe

A

TRUEleft branches are the most cranial, then central branches and then the most caudal are right branches located within the parenchyma

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6
Q

lobes of the liver

A

6 lobesleft medialleft lateralright medialright lateralcaudate —caudate and papillary processesquadrate

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7
Q

biliary flow

A

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

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8
Q

functions of liver (6)

A

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

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9
Q

physiology of Hb breakdown

A

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

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10
Q

regenerative capacity of liver

A

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)

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11
Q

factors that impede liver regeneration

A

diabetes mellitus (decr insulin which is a major hepatotrophic hormone)male genderbile obstruction agemalnutrition

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12
Q

common location of trauma biliary tract rupture

A

–CBD (body)–hepatic ductsRARELY from GB itself

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13
Q

most common causes of EHBO in dogs

A

–GB mucocele–pancreatitis–neoplasia–cholangitis–cholelithiasis(can also have FB or mass in duodenum)

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14
Q

most common causes of EHBO in cats

A

–complex inflammatory dz (pancreatitis,cholangiohepatitis, cholecystitis with or without stones)–neoplasia(less common: parasites–flukes, diaphragmatic hernia)

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15
Q

after acute ligation of CBD in dogs, how long does it take for dilation to occur

A

dilation of CBD occurs within 24-48 hrs (along with an increase in serum bilirubin)dilation of lobar/interlobular ducts takes 4-6 days

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16
Q

pathophysiologic consequences of EHBO

A

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)

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17
Q

bile peritonitis causes in dogs

A

–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

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18
Q

pathophysiology bile peritonitis

A

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

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19
Q

T/Fwhen bile salts are not present in SI to bind endotoxin, systemic endotoxemia may develop

A

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

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20
Q

hepatobiliary imaging

A

–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

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21
Q

cholelithiasis composition in dogs and cats

A

50% opaque dogs (calcium bilirubinate)80% opaque cats (calcium carbonate)usually found near major duodenal papilla–can do sphincterotomycholecystectomy preferred after retrograde flushing stone back into GB and ensuring patency (recurrence is not reported if GB removed)other options (especially if CBD is not patent): cholodochotomy (dehisce! and stricture) or cholecystoenterostomy (recurrence seen)

22
Q

normal CBD diameter on ab US

A

CBD normal diameter dogs and cats 3-4 mm

23
Q

typical US appearance of GB mucocele

A

immobile stellate or finely striated GBkiwi fruit

24
Q

method to monitor EHBO with serial ab US

A

can give synthetic CCK (sincalide) IVnormally, GB should empty 40% within 1 hrEHBO if empty <20%

25
Q

coagulation testing of liver patients prior to surgery

A

CBC (blood smear, platelets), Chem, UAcoag panel (PT, aPTT, ACT)PIVKA (most SN)blood type cross match57% dogs with confirmed liver disease will have at least one abN coagulation parameterMayhew it al 2013 TEG for EHBO suggest HYPERCOAGincreased tendency for hemorrhage in dogs with natural liver disease has not been demonstrated

26
Q

surgical liver cultures

A

sx and lap liver cultures had sign more positive results than percutaneous needle biopsyintraop biliary culture was significantly more likely to have positive culture than liver culture (30 vs 7%)Ab recommendations1. fluoroquin, penicillin, metro2. fluoroquin, amoxi-clav3. fluoroquin, clindamycin

27
Q

methods to control extensive hemorrhage during liver surgery

A

maintenance of CVP < 5 cm H20 is essential for minimizing blood loss1. inflow occlusion–Pringle Manuever (hepatic artery and portal vein 20 min occlusion)–dogs have less collateral circulation than humans2. total hepatic vascular exclusion–simultaneous occlusion of cranial and caudal VC–with concurrent inflow (hepatic artery and portal vein) occlusion–dramatically reduces cardiac preload; brief occlusion only3. hepatic artery ligation–supplies only 20% to liver but generally it is the major (95%) supply to liver tumor–give ANTIBIOTICS–attempt to ligate lobar arteries if possible–consider cholecystectomy–ensure portal vein flow

28
Q

overall agreement with FNA and histopath of liver lesions in dogs and cats

A

dogs 30%cats 50%

29
Q

liver biopsy

A

punch biopsies bleed the mostligature and harmonic scalpel may bleed the least(other options: lap biopsy forceps, lap endoloop or extracorporeal loop ligature, biopsy needle/Trucut, vessel sealing device)obtain enough for histopathology, culture, and toxicology

30
Q

methods of exposure for partial or complete liver resection

A
  1. midline celiotomy—may extend into caudal thorax/median sternotomy2. puncture the diaphragm3. lap sponges btwn diaphragm and liver lobes to retract caudally4. cut triangular ligaments5. paracostal incision
31
Q

contributions of liver volume from each lobe

A

tolerate 65-70% resectionright lateral and caudate make up 28%right medial and quadrate make up 28%left lateral and left medial make up 44%

32
Q

methods of regional tumor control for diffuse or metastatic or not amenable to surgery tumors

A

percutaneous ablation techniques1. radiofrequency ablation2. microwave ablation3. laser thermal ablation4. cryoablation5. ethanol ablationintravascular tumor embolization/chemoembolizationintra-arterial (lesional) chemotherapy

33
Q

when is clinical icterus present

A

with serum bilirubin >1.5-2.0 mg/dL

34
Q

preparation of hepatic patient for liver surgery

A

–fluids–vitamin K 1-2 mg/kg SQ q 12 hr–FFP, whole blood, pRBC if needed–Ab perioperatively–GI protectants +/-(based on prep PE, imaging, and bloodwork/coag panel/blood typing)

35
Q

surgical decision making for extra hepatic biliary tree

A

–check patency (normograde or retrograde* choledochal flushing)–if NOT patent: reroute: cholecystoduodenostomy* (preferred), cholecystojejunostomy (suture or EndoGIA)–if PATENT and potential reversible disease (pancreatitis, cholangitis, +/- trauma to CBD) or palliation for malignancy: stent or cholecystotomy tube–if PATENT but NOT reversible disease (stones, neoplasia, GB mucocele, trauma to GB, necrosis of GB): cholecystectomy (open, laparoscopic)

36
Q

T/Fdiversion of bile from the duodenum (as with cholecystojejunostomy) can lead to duodenal ulceration in dogs

A

TRUEwithout bile in duodenum, duodenal ulcers occurnormally when bile is present in SI, gastric acid secretion is inhibitedif bile is gone and inhibitory feedback is loss, gastric over secretion may occur leading to ulcer formation in the duodenum

37
Q

stoma size created during a cholecystoenterostomy

A

antimesenteric SI incision with longitudinal incision in GBcreate stoma as long as possiblesmall stomas < 2.5 cm may predispose to obstruction and stricture formationeach side is sutured with simple continuous single layer+/- apical suture at each end to relieve tension3-0- 4-0 monofilament absorbable(double layer may invert and decrease lumen–stricture)

38
Q

possible complications following rerouting cholecystostomy

A

–hemorrhage–gastric/duodenal ulceration–stricture–re-obstruction–dehiscence/bile peritonitis–ascending cholangiohepatitis

39
Q

most common indication for surgery management of EHBO in dogs

A

GB mucocele–cystic mucosal hyperplasia and hypersecretionshetland sheepdogs (GB disease) predispositionhypoT (14% vs 5%)hyperadrenocorticism (risk 29x GB mucocele–21% vs 2%)cholecystectomy (check patency first!)

40
Q

ab US sensitivity for detecting GB rupture

A

86%

41
Q

medical mgmt for GB mucocele

A
  1. ursodial: choleretic, immunomodulatory2. S-adenosyl-L-methionine (SAM-e): anti-inflammatory, antioxidant3. famotidine: H2 receptor antagonist4. vitamin E: antioxidant, anti-inflammatory 5. Silymarin (milk thistle): anti-oxidant, choleretic, antifibrotic/anti-inflammatory
42
Q

complications following cholecystectomy for GB mucocele removal

A
  1. leakage/peritonitis2. pancreatitis3. reobstruction if congealed bile in CBD
43
Q

prognosis following cholecystectomy for GB mucocele

A

Worley et al JAVMA 2004 (22 dogs)70% survivalPike et al JAVMA 2004 (30 dogs)22% mortality (80% survival)GB rupture was NOT associated with increased mortality

44
Q

what constitutes “triaditis” in cats

A

–IBD–pancreatitis–cholecystitis

45
Q

4 types of primary hepatobiliary tumors

A
  1. hepatocellular adenomas and adenocarcinomas (massive, nodular, diffuse)2. cholangiocellular adenomas and adenocarcinomas3. neuroendocrine carcinomas (aggressive, diffuse, poor px)4. mesenchymal (HSA, leiomyosarcoma, OSA, FSA): poor px(mets to liver are more common than primary liver tumor #1 hematopoetic/lymphoid #2 epithelial/mesenchymal)
46
Q

paraneoplastic condition related to variety of hepatic neoplasms

A

hypoglycemia

47
Q

T/Fcorrelation with ultrasound live appearance and tissue histopathology is poor

A

TRUEways to enhance correlation:contrast enhanced harmonic US (microgas bubble)MRI

48
Q

hemorrhage/hematoma formation complication rate following percutaneous needle core liver biopsy

A

<6%

49
Q

T/Flaparoscopic liver biopsy contains fewer portal triads and hepatic lobules than traditional open technique

A

true

50
Q

most common hepatocellular liver tumor in dogs

A

hepatocellular carcinoma 70%; 30% adenomas)–massive (60%)–usually L sided; favorable px with resection; MST 1400d–nodular (30%)–higher met rate–diffuse (10%)–higher met rate

51
Q

prognosis with liver resection and massive hepatocellular carcinoma according to Liptak 2004 JAVMA 48 cases

A

1400 days MSTperiop mortality 5%poor px associated with R sided tumors NOT with incomplete resection (10%)

52
Q

T/Fin cats, hepatocellular adenomas is more comma than hepatocellular carcinomas

A

truein cats, bile duct tumors are the most common primary hepatic neoplasm–benign cyst adenomas (good px) are TWICE as common as bile duct carcinomas (100% mortality)