liver section Flashcards
where is bile produced and stored
produced by hepatocytes and stored in gallbladderr
what drains bile into bile duct
canaliculi
bile ducts converge to form
hepatic duct
what two ducts join the common hepatic duct before it empties into the gallbladde
the cystic duct and the pancreatic duct
sphincter of oddi role
controls flow of bile released from common hepatic duct
contraction of sphincter of oddi increases
biliary pressure
3 key functions of bile
- absorption of fat soluble vitamins (DAKE)
- excretory pathway for bilirubin and products of metabolism
- alkalization of duodenum
where is cholecystokinin produced
duodenum
lymph and proteins drain into
space of disse (between hepatocyte and sinusoid)
how much CO does the liver receive
~30% (1500mL/min)
is flow through the portal vein auto regulated
no
what does increased splanchnic vascular resistance do to portal vein blood flow
reduces portal vein blood flow
normal portal vein pressure
7-10mmHg
portal vein pressure diagnostic for portal HTN
> 20-30mmHg
normal pressure in sinusoids
0mmHg
pressure in sinusoids diagnostic for portal HTN
> 5mmHg
how does the hepatic arterial buffer respond when theres a reduction of portal vein blood flow
washout of vasodilators such as adenosine, increase BF through hepartic artery
hepatic artery perfusion pressure=
MAP-hepatic vein pressured
preoperative factors that reduce liver BF (5)
- increased splanchnic vascular resistance (SNS, stimulation, pain, hypoxia)
- things that increase CVP (PPV, excessive hydration, CHF)
- some beta blockers (propranolol reduces CO and increases splanchnic vascular resistance)
- intraabdominal surgical procedures
- laparoscopic surgery (pneumoperitoneum)
what do hepatocytes produce (3)
thrombopoeitin
alpha 1 acid glycoprotein
factor 7
why is PT an early indicator of synthetic liver dysfunction
factor 7 has the shortest t1/2 of all procoagulant proteins
what does the liver not produce?
factors 3 (produced by vascular endothelial cells) and 4 (calcium comes from diet)
vWF (endothelial cells and megakaryocytes)
liver produces all plasma proteins except for
immunoglobulins (gamma globulins)
albumin is a reservoir for
acidic drugs
alpha 1 acid glycoprotein is a reservoir for
basic dugs
what does impaired plasma protein synthesis do to vascular oncotic pressure
reduces vascular oncotic pressure
what happens to pseudocholinesterase production with liver failure
reduced, so increased DOA of succ and possibly DOA of esters.
during hyperglycemia, how does the liver respond?
releases insulin from pancreatic beta cells. glycogenesis
during hypoglycemia, how does the liver respond?
release of glucagon from pancreatic alpha cells, epi from adrenal medulla. glycogenolysis and gluconeogenesis.
what is the amino acid deamination process
allows body to convert proteins to carbs and fats. some are utilized in krebs cycle to produce ATP.
-produces large quantity of ammonia. liver converts this to urea, which is eliminated by kidney
role of lipids in the liver (3)
-energy storage in the form of triglycerides
-energy release by beta oxidation of fatty acids
-synthesis of cholesterol, phospholipids, lipoproteins
life cycle of an erythrocyte
120 days
what are old RBCs broken down by
reticuloendothelial cells in spleen
precursors of unconjugated bilirubin
hemoglobin->heme
is unconjugated bilirubin hydrophilic or lipophilic
lipophilic
how is unconjugated bilirubin transported to the liver
bound to albumin
what does liver conjugate bilirubin with to increase water solubility
glucoronic acid
metabolism of conjugated bilirubin
excreted into bile, metabolized by intestinal bacteria, eliminated in stool
liver function tests to assess synthetic function
PT (sensitive for acute injury) and albumin (not sensitive for acute injury(
liver function tests that assess hepatocellular injurry
AST (10-40 units/L)
ALT (10-50 units/L)
-marked elevation of both suggests hepatitis
-AST/ALT ratio >2 suggests cirrhosis or alcoholic liver disease
liver function tests that assess hepatic clearance
bilirubin (0-11 units/L)
- confounding factors: hemolysis or hematoma reabsorption
liver function test that assess biliary duct obstruction
alkaline phosphatase (45-115 units/L)
y glutamyl transpeptidase (0-30 units/L)
5 nucleotides (0-11 units/L)
-AP is not very specific
most specific indicator of biliary duct obstruction
5 nucleotidase
pre hepatic liver disease
bilirubin
aminotransferase (AST and ALT)
prothrombin time
albumin
alkaline phosphatase
y glutamyl transpeptidase
5 nucleotidase
causes
bilirubin (increased in conjugated)
aminotransferase (AST and ALT) 0
prothrombin time 0
albumin 0
alkaline phosphatase 0
y glutamyl transpeptidase 0
5 nucleotidase 0
pre hepatic lier disease causes
hemolysis
hematoma reabsorption
hepatocellular injury/ liver disease
bilirubin
aminotransferase (AST and ALT)
prothrombin time
albumin
alkaline phosphatase
y glutamyl transpeptidase
5 nucleotidase
bilirubin increased conjugated
aminotransferase (AST and ALT) increased
prothrombin time increased
albumin not changed for acute injury, decreased for chronic injury
alkaline phosphatase 0 or increased
y glutamyl transpeptidase 0
5 nucleotidase 0
causes of hepatocellularr injury
cirrhosis
alcohol abuse
durgs
viral infection
sepsis
hypoxemia
after the liver (cholestatic) liver injury
bilirubin
aminotransferase (AST and ALT)
prothrombin time
albumin
alkaline phosphatase
y glutamyl transpeptidase
5 nucleotidase
bilirubin increased conjugated
aminotransferase (AST and ALT) 0 or increased during late disease
prothrombin time 0 or increased during late disease
albumin 0 or decreased during late disease
alkaline phosphatase increased
y glutamyl transpeptidase increased
5 nucleotidase increased
causes of cholestatic liver injury
biliary tract obstruction
sepsis
most common form of viral hepatitis
hepatitis A
which forms of hepatitis can cause cirrhosis
hepatitis B and C
how can halothane produce hepatitis
metabolized to inorganic fluoride ions and trifluoroacetic acid (TFA). can produce immune mediated response leading to hepatitis
hepatitis A
transmission route
prophylaxis after exposure
serum markers
does it cause cirrhosis and hepatocellular carcinoma
transmission route: oral fecal
prophylaxis after exposure: pooled gamma globulin, hep A vaccine
serum markers: IgM (early) IgG (late)
does it cause cirrhosis and hepatocellular carcinoma: no
hepatitis B
transmission route
prophylaxis after exposure
serum markers
does it cause cirrhosis and hepatocellular carcinoma
transmission route: percutaneous, sexual contact
prophylaxis after exposure: hep B immunoglobulin, hep B vaccine
serum markers: HBsAg, anti HBcAg
does it cause cirrhosis and hepatocellular carcinoma: yes
hepatitis C
transmission route
prophylaxis after exposure
serum markers
does it cause cirrhosis and hepatocellular carcinoma
transmission route: percutaneous
prophylaxis after exposure: interferon and ribavirin
serum markers: Anti HCV (1.5-9 months)
does it cause cirrhosis and hepatocellular carcinoma: yes in up to 75%
hepatitis D (co infection with type B)
transmission route
prophylaxis after exposure
serum markers
transmission route: percutaneous
prophylaxis after exposure: unclear
serum markers: anti HDV (late)
most common cause of acute liver failure in US
aceta overdose
toxic metabolite of acetaminophen
n acetyl p benzoquinoneimine (NAPQI)
chronic hepatitis diagnosis
hepatic inflammation that exceeds 6 months. increased liver enzymes and bilirubin, histologic evidence of liver inflamamtion
- PT is prolonged and albumin is decreased
s/sx of chronic hepatitis
jaundice, fatigue, thrombocytopenia, glomerulonephritis, neuropathy, arthritis, myocarditis
ways to maintain hepatic BF during anesthesia
-use iso or sevo but avoid halothane
-avoid PEEP
-ensurer normocapnia
-administer liberal IVF
-regional is ok if no coat defects
hepatic drugs that should be avoided due to inhibiting CYP450 (4)
-aceta
-halothane
-amio
-abx (PCN, tetracycline, sulfonamides)
what does alcohol potentiate the effect of
GABA, so increased effect of benzos
also inhibits NMDA receptors
how does ETOH cause an aspiration risk
impairs pharyngeal reflexes
assume acutely intoxicated patient has full stomach
s/sx of withdrawal begin at ____ hours and peaks at _______ hours
begin 6-8h after BAC is back to normal and peaks at 24-36 hours
early s/sx alcohol withdrawal syndrome
tremors, disordered perception (hallucinations, nightmares)
late s/sx alcohol withdrawal syndeome
increased SNS activity (tachycardia, HTN, dysrhythmias), n/v, insomnia, confusion, agitation
treatment of alcohol withdrawal syndrome
alcohol, beta blockers, alpha 2 agonists
disulfiram
treatment for alcoholics in recovery. hepatotoxic, inhibits beta hydroxylate (NE synthesis) -> HoTN
etiologies of cirrhosis
- non alcoholic fatty liver disease (most common cause of liver disease)
- alcohol abuse
- alpha 1 antitrypsin deficiency
- biliary obstruction
- chronic hepatitis
-right sided heart failure (increased hepatic vascular resistance) - hemochromatosis (iron overload)
- wilsons disease
MELD score
predicts 90 day mortality in patients with ESLD
- low risk <10
- intermediate risk 10-15
- high risk >15
modified child pugh score
examines five factors of hepatic function: albumin, bilirubin, ascites, encephalopathy
-class A (5-6 points) 10% risk of periop mortality
-class B (7-9) 30% risk of periop mortality
-class C (10-15 points) 80% risk of periop mortality
which child pugh scores are ok to proceed with surgery after optimization
classes A and B
ESLD manifestations: CV
hyper dynamic circulation
portal HTN
ascites
how does ESLD hyper dynamic circulation present
portosystemic shunt and vasodilator release, decreased SVR and BP-> increased CO
increased RAAS activation, increased BV)
decreased peripheral blood flow -> increased SVO2
decreased response to vasopressors
diastolic dysfunction
how does ESLD portal hypertension present
increased hepatic vascular resistance, increase back pressure to proximal organs
esophageal varices -> bleeding
splenomegaly -> thrombocytopenia
how does ESLD ascites present
decreased oncotic pressure, decreased protein binding, increased Vd, drainage-> HoTN
pulmonary effects of ESLD include
restrictive defect (ascites and perfusion decreases compliance and atelectasis)
respiratory alkalosis (hypoxemia-> compensatory hyperventilation)
hepatopulmonary syndrome (pulmonary vasodilation -> intrapulmonary shunt (R to L) -> hypoxemia)
portopulmonary HTN (PAP >25mmHg in the setting of portal HTN)
how ESLD affects CNS
hepatic encephalopathy r/t decreased hepatic clearance, increased ammonia, cerebral edema, increased ICP, increased ammonia treated with lactulose, abx, and decreased protein intake
-bleeding-> blood reabsorption -> increrase in nitrogen load-> increase in ammonia
how ESLD affects ANS
increased SNS, increased RAAS, ANS reflex dysfunction
how ESLD affects renal
renal hypoperfusion (decreased GFR, RAAS, Na/H2O retention)
hepatorenal syndrome (decreased GFR, renal failure)
how ESLD effects hematologic status
anemia (decreased CaO2 d/t hemorrhage, folic acid deficiency, hemolysis, bone marrow depression.
reduced factor production (decreased procoagulants and anticoagulants, bleeding or clot risk.
thrombocytopenia- decreased thrombopoeitin and bone marrow depression decreases platelet production
splenomegaly increases platelet consumption
what is the TIPS procedure
transjugular intrahepatic portosystemic shunt. bypasses portion of hepatic circulation by shunting blood from portal vein (hepatic inflow vessel) to hepatic vein (hepatic outflow vessel). this reduces portal pressure and minimizes back pressure on splanchnic organs. reduces likelihood of bleeding from esophageal varies and reduces volume of ascites.
most common indication of liver trransplant
hepatitis C
if the patient suffers from hepatic encephalopathy, avoid
anxiolytic premedication
three phases of liver transplantation
- pre an hepatic phase
- an hepatic phase
- neohepatic phase
preanhepatic phase time course and surgical objectives
begins with surgical incision, ends with cross clamping of portal vein, hepatic artery, and IVC
objectives: surgical incision, mobilization of liver structures and vascular structures, isolation of bile duct
an hepatic phase time course and surgical objectives
begins with removal of native liver and ends with implantation of donor liver
objectives: removal of sick liver, implantation of donor liver (allograft)
neohepatic phase time course and surgical objectives
begins with reperfusion of donor liver and ends with biliary anastomosis (for transport to ICU)
objectives: reperfusion of donor liver
anastomosis of hepatic artery and biliary structures
HGB, platelet, fibrinogen, TEG goals during pre an hepatic phase
HGB >7g/dL
platelets >40,000
fibrinogen >100
TEG >45
an hepatic phase: bicaval clamp and special considerations
clamps applied to IVC (above and below liver). full obstruction of IVC flow)
-significant preload reduction (HoTN, tachycardia)
aggressive fluid administration to combat HoTN can lead to volume overload when clamps are released
anhepatic phase: piggyback technique and special considerations
side clamping of IVC. partial obstruction to IVC flow
- allows for some amount of BF
-less preload reduction when compared to bicaval clamping
-reduced OR and warm ischemic times
-fewer blood products required
an hepatic phase venovenous bypass and special considerations
sites of cannulation (outflow: femoral vein and portal vein)
(return to body: axillary vein: blood returns to IVC- heart)
-piggyback technique has reduced the need for VVB.
-associated with less hemodynamic instability, blood loss, and prevention of portal and splanchnic congestion. higher complication rate though.
neo hepatic phase key complications include
hyperkalemia (highest risk in neo hepatic phase, give CaCl or bicarb), hypocalcemia, cytokine release, lactic acidosis, embolic debris, hypovolemia, systemic HoTN, pHTN, cardiac arrest.
-avoid elevated CVP as this will cause graft complications
-
most important consideration during neohepaticc phase
post reperfusion syndrome (PRS). defined as systemic HoTN more than 30% below baseline for at least one minute during first 5 minutes of reperfusion of donor liver
s/sx of poorly functioning graft post:
hemodynamic instability and lack of bile output (if the implant is taking, the patient should start to stabilize in neo hepatic phase)
obstruction of cystic duct s/sx (4)
gallbladder distention, edema, risk of perforation, jaundice
obstruction of common bile duct s/sx (4)
cholecystitis, jaundice, pancreatitis, peritonitis
s/sx of gall stones
leukocytosis, fever, RUQ pain, worse with inspiration (murphys sign)
biliary pathology includes
increase alkaline phosphatase, conjugated bilirubin, amylase, y glutamyl transpeptidate, 5- nucleotidase
surgical tx for choledocholithiasis (stones in common bile duct)
ERCP
drugs that relax sphincter of oddi
glucagon, naloxone, NTG. glycopyrrolate and atropine may help as well
