bile: produced by hepatyocyes and stored in ___________ __________ drain bile > into bile ducts and the bile ducts converge to form the _____________ in the GB the cystic duct and pancreatic duct joint the CHD before emptying into the _______________ the ________________ controls bile flow from the CHD

gall bladder canaliculi common hepatic duct duodenum sphincter of oddi

lymphatic drains into space of ______ and empties into lypactic duct

disse

liver receives _____% CO

30%

portal vein map

aorta > splancnic organs > portal vein > liver

portal vein % liver blood flow

75%

portal vein % oxygen content and O2 sat

50 and lower than hepatic artery

receptors of portal vein

A1 vasocon D1 vasodilation

portal vein normal pressure and pHTN

normal 7-10mmHG pHTN 20-20mmHg

hepatic artery map

aorta > hepatic arty > liver

hepatic arty % liver blood flow

hepatic arty %oxygen content and O2 sat

50% and higher

receptors of hepatic artery

A1 vasocon B2 D1 vasodilation

hepatic artery buffer response

when portal vein decreases flow the hepatic artery compensates by increasing flow by washing out vasodilators (adenosine)

causes decrease hepatic blood flow

hypoxia, pain, SNS activation> increase in splanchnic vascular resistance hemorrhage > blood diverts elsewhere anesthesia > decrease MAP PPV, increase volume, CHF> increase CVP

hematologist properties of liver

procoagulants: all clotting facotrs (except for 8) anticoag: antithrombin, protein C, S, Z fibrinolytics: plasminogen thrombopoetin: stimulates plt production

metabolic of liver

carbs: regulate glucose, clears insulin liver failur: hypoglycemia

liver and proteins:

AA deamination: proteins> carbs/fats produces ammonia > urea hepatic encephalopathy albumin

lipids and the liver

triglycerides = energy storage synthesis of: cholesterol phospholipids lipoproteins

liver and bilirubin

aged RBC >> unconj bilir in spleen >> liver conjugation with glucagon in acid > conj bilir excreted in bile

3 main functions of bile

1. req for fat and fat soluble vitamin absorption 2. excretion pathway for bilirubin and metabolic products 3. alkalication of duodenum

hepatitis: excretion pathway interruption:

hemolysis > unconj bilir > neurotoxic and jaundice

hepatitis; vascular; decreased hepatic blood flow will cause what to hepatic extraction ratio

increase = perfusion depended clearance

hepatitis; valscuar: intrahepatic obstruction of blood flow: 3 dooms

portal HTN varicies ascites

hepatitis and the spleen

splenomegaly; plt sequestration; thrombocytopenia

hepatitis and hematologic

loss of hemostasis decrease: clotting factors, plts anemia: increase bleeding, increase RBC destruction, nutritional def

hepatitis and metabolic

bio transformation impaired decrease amount and quality of albumin > ascites, edem, altered drug kinetics increase protein bound drugs will have high VOD

drug induced hepatitis’s 5

Tylenol- consumes livers glutathione NSAIDS ETOH- no fatty acid metabolism and hepatmegly toxins halothene

what is hepatitis

liver inflammation hepatocellura injury with vary necrosis degree most common cause of liver cancer and trampsoant

chronic hepatitis most commonly

ETOH hep 3

chronic lobular hepatitis

recurrent exacerbation of acute inflammation rarely get to cirrhosis

chronic active hepatitis; define clinical and sx

progressive heptoctye destruction and cirrhosis clinical: mult organ failure, enceph, variceis rupture sx: jaundice, fatigue, throbotyov, neuropathy, myocarditis, PT prolong, arthritis, glomnephritis, low albumin

cirrhosis CNS effects:

+ammonia +ICP> somnolence and encephalahty impaired BBB> coma neuro transmission alteration > increase uptake of benzos

cirrhosis patients INTOLERANT to: and why

HYPOXEMIA from anemia and low blood viscosity HYPOVOLEMIA from decrease PRV and increase CO

cirrhosis cardiac: AV shunt limits > less responsive to =

CO cats

cirrhosis: cell death replaced with ______ and ________ less functional hepatocytes and (increase or decrease) of sinusoids? less blood vessels and more nodules with increase hepatic vascular reisstance and lead to: ________ compensation by: ___________ that bypasss liver and this is called: __________ drugs and toxins like ammonia will stay in liver longer all of this leads to:

nodules and fibrotic tissue increase sinusoids portal HTN collateral vessels >> portostytemic shunt EXTENSIVE DISORGANIZATION OF LOBULAR STRUCTURE MULTISYSTEM ORGAN FAILURE

cirrhosis and GI: main big star: malabasorbution will leads to _________ low albumin>> ______ and _______ peptic ulcers >> ______ gallstones>> ______ portal HTN >>> ______ and causes this electrolyte imbalance

reduces esophageal sphincter tone > aspiration > RSI malnutrition bowel edem, less drug bound and more free drug GI bleed jaundice ascites and dilutional hyponatremia

cirrhosis and Pulm: intrapulm AV shunt and pleural effusions>> ________ hypoxia >>> 2,3 DPG >> _______ ascites >> ________ high ammonia >_______ increased circulating vasodilators>> ____

hypoxemia, R to L shunt, VQ mismatch decrease oxygen affinity for hgb shifts R decrease FRC, compliance > atelectasis hyperventilation impairs HPV

cirrhosis and renal: what happens with RAAS decrease RBF >> increase ADH>> hepatorenal syndrome:

increase RAAS > increase aldosterone and water retention > hypokalemia, dilutional hyponatremia dilutional hyponatremia relative hypovolemia and ascites cirrhosis + portal htn + ascites = intense renal vasoconstriction; decrease RBF decrease UO with almost no Na+ increase BUN/Cr

how to optimize sx for chronic hepatitis:

volume oxygen: VQ mismatch and ascites electrolytes heme

chronic hepatitis and sx: how to maintain HBF gas of choice avoid: others:

ISO - not halothane avoid PEEP normocapnia liberal IVF regional OK if coags ok

hepatotoic drugs and CYP450 inhibitors

Tylenol halothene amio penicillin and tetracycline

chronic hepatitis and sx: GA what to avoid other

avoid: splanchnic resistance, light anesthesia , hypoxia, hypercarbia full. stomach, RSI maintain HBF and oxygenation

chronic hepatitis and sx: volatiles

avoid: high concentration, high flow sevo, halothene, N2O bc of bowel distention and alters splanchnic flow

chronic hepatitis and sx: and regional

reduces polypharm requirement avoid low BP coags okay? decreases AMIDE local anesthesia metabolism so use ESTERS

chronic hepatitis and sx: IV anesth and metabolism concerns

small incremental dose impaired metabolism: protein binding high VOD hepatic ext ratios

chronic hepatitis and sx: and muscle relaxants

reduced biliy excretion: roc risk succ and less pseudo NDNMB may require large initial dose less skeletal mass then less maintence does required good: cis, atricurium

chronic hepatitis and sx: and fluids

maintain UO crystalloids albumin 25% blood, FFP, cryo, plt, vit K

chronic hepatitis and sx: ventilation what will hypercarbia cause >> high intrathoracic pressure >>

hypercarbia>> SNS stimuli of splanchnic casvulature and decrease portal hepatic blood flow increase intrthorcic pressure with decreation HBF

ETOH withdrawal: onset: peak:

onset: 6-8 hours after blood is normal peak: 24-36 hours early signs: tremor, disorientation late: increase SNS, NV, insomnia, agitation tx: alcohol, BB, A2 agonist 2-4 days signs: DTs, seizure, tachy, up or down BP, combative tx: diazepam, BB other tx: vit B (thiamine) and disulfiramin (hepatotoxic)

ETOH withdrawal signs early late 2-4 days

ETOH withdrawal tx of early/late then treatment of 2-4 days

active drunk: MAC will be less or more required

less

chronic drunk not drunk at moment with do what to MAC

more MAC req

alcohol: _________ GABA so >> inhibits: _________ impairs: ___________ >>

potentials GABA so increase effect of benzos inhibit NMDA receptor impaires pharyngeal reflex > aspiration

best indicators of liver function: labs which is more sensitive to acute injury

PT: 12-14 sec albumin: 2.5-5 bilirubin: 0-11 also: AST/ALT: 10-40 CBC, plt

most common reason for liver transplant

hep C then ETOH

preop consideration to liver transplant

blood bank coagupathy for lining if encephalitic then no anti anxiety med do not correct hyponatremia too fast- central pontine

MELD

predict 90 day mortality facotrs: bilirubin, INR, creatinine

child Pugh

facors: albumin pt bilirubin ascites encephalotphy

liver transplant: first phase

preanaheptic

liver transplant: pre-anaheptic:

incision to cross clamp of portal vein, hepatic artery, IVC RSI CV instability massive transfusion CVP normal then increase to 10 right before clamping careful not give too much fluid to cause dilutional coagulapathy prevent hypothermia

transfusion goals liver transplant:

hgb 7 plt 40 fib 100 TEG 45

liver transplant: anahepatic:

removal of native liver to implantation of donor 3 methods: biocaval clamp piggy back venovenous bypass vascular clamping with cause decrease preload and CO (lowest here) no liver function worse coagulpahty, blood loss, lactic acidosis, hypoglycemia

liver transplant: neohepatic

reperfusion to biliary anastomosis complications: HYPERKALEMIA hypocal cytokine relae Lacie acid embolism debri hypothermia pulmHTN avoid high CVP

good graft function post liver transplant: immediately:

normal glucose normothermia acid base balance

post reperfusion syndrome: liver transplant

neohepatic phase hypotension for at least 1 min for first 5 min of reperfusion (under 30% baseline) pressers, correct electrolytes, acid base

postop liver transplant poor graft signs

hemodynamic instability lack of bile output

postop considerations liver transplant

poor graft: hemodynamic instability and lack of bile output no epidruel pain PCA anti rejection med- infection risk steroids might req insulin gtt

liver resection surgical risks depend on _________ up to what % can be resected steps:

preop liver function 75 1. control of vessels 2. parenchymal transection 3. Pringle maneuver- 60-90 min max clamp

total vascular exclusion:

large resection or tumor in IVC entire area of IVC is clamped risk tearing IVC, VAE

liver resection anesthesia consideration

vol and CV stability blood loss VAE extubate ?

TIPS

transjugular intrahepatic portosystemic shunt temporary tx for hepatorenal syndrome bypass portion of hepatic circulation by shunting blood from port vein to hepatic vein will decrease portal pressure, less bleed from esophageal varies, and less ascites risk: hemorrhage

cholesystokinin:

stimulates GB to contract

gallstone risk factors

obesity increase age rapid wt loss prego women>men

gallstone signs

leukoytosis fever RUQ pain muphys sign: worst with inspiration

gallstone obstruction to cystic duct:

GB distention edema perf risk jaundice

gallstone obstruction to common hepatic duct

cholesystis jaundice pancreatitis peritonitis

choledochlithiasis: what and tx

gallstone in commonheptic duct and ERCP

cholelithiaiss and tx

stones in gall bladder and cholecystectomy

cholecycsemty/gall bladder procudures; anesthesia consideration

laposcopic avoid N2O if liver dysfunction use cisatricurium avoid opioids bc sphincter of oddi relax sphincter: glucagon, NGT, atropine