Hepatic Flashcards
function of the liver
synthesizes glucose via gluconeogenesis
sotres excess glucose as glycogen
synthesizes cholesterol and proteins into hormones and vitamins
metabolizes fats, protiens, and carbs to generate energy
metabolizes drugs via CYP450 and other enzyme pathways
detoxifies blood
involved in the acute phase of immune support
processes HGB and stores iron
synthesizes coagulation factors
aids in volume control as a blood reservoir
what coagulation factors are not synthesized by the liver
Factor III, IV, VIII, vWF
T/F liver dysfunction can lead to multi-organ failure
true, nearly every organ is impacted by liver function
what seperates the right and left lobe of the liver
falciform ligament
how many segments are in the liver
8 based on blood supply and bile drainage
which vessels branch into each segment of the liver
portal vein and hepatic artery
how many hepatic veins empty into IVC
3- right, middle, left hepatic veins
where does the bile duct travel
along portal veins
bile drains through the _____ ________ into ______ & _______
bile drains through the hepatic duct into gall bladder and common bile duct
bile enters duodenum via
ampulla of vater
how much of the cardiac output goes to the liver
25%
1.25-1.5L/min
highes proprotionate CO of all organs
where does the portal vein arise from
splenic vein and superior mesenteric vein
portal vein contains deoxygenated blood from which organs
GI organs (stomach, intestine), pancreas, spleen
portal vein provides how much of hepatic blood flow (%)
75%
hepatic artery, which branches off the aorta, provides how much hepatic blood flow (%)
25%
oxygen delivery sources to the liver
50% portal vein (deoxygenated)
50% hepatic artery
hepatic arterial blood flow is inversely related to
portal venous blood flow
T/F hepatic blood is not autoregulated
false, hepatic artery dilates in response to low portal venous flow; keeping consistent HBF
portal venous pressure reflects what?
splanchnic arterial tone and intrahepatic pressure
normal hepatic venous pressure gradient
HVPG 1-5 mmHg
what hepatic venous pressure gradient is clincally significant for portal HTN, i.e chirroshis, esophageal varices
HVPG > 10 mmHg
increasing portal venous pressure causes
blood to back up in systemic circulation
*esophagel and gastric varices
what hepatic venous pressure gradient is associated with variceal rupture
HPVG > 12 mmHg
risk factors for liver disease
family history
heavy ETOH
lifestyle
DM
obesity
illicit drug use
multiple partners
tattoss (basement tattoos)
blood transfusions (in the 80s)
rely heavily on “risk factors” for degree of suscpicion
when do liver symptoms begin to appear
late-stage liver disease
often asymptomatic until late-stage liver disease
physical exam findings of liver disease
pruritis
jaundice
ascites
asterixis (flapping tremor)
hepatomegaly
splenomegaly
spider nevi
hepato-biliary function tests
BMP, CBC
PT/INR
Aspartate aminotransferase (AST)
Alanine Aminotransferase (ALT)
bilirubin
alkaline phosphatase
ɣ-glutamyl-transferase (GGT)
*imaging includes: ultrasound, doppler US (portal blood flow), CT, MRI
most liver-specific enzyme
alanine aminotransferase (ALT)
which labs are elevated in late-stage liver disease
ɣ-glutamyl-transferase (GGT)
Alkaline phosphatase
labs suggesting hepatocellular injury
elevated AST/ALT (hepatocyte enzymes)
labs suggesting reduced synthetic function
decreased albumin
increased PT/INR
labs suggesting cholestasis
increased alkaline phosphatase
increrased GGT
increased bilirubin
3 groups of hepatobiliary disease
hepatocellular injury
reduced synthetic function
cholestasis
3 subclasses of hepatocellar injury and lab findings
Acute Liver Failure (ALF): hepatic enzymes may be elevated 25x
Alcoholic Liver Disease (ALD): AST:ALT ratio is usually 2:1
Non-Alcoholic Fatty Liver Disease (NALFD): AST:ALT ratio usually 1:1
bile pathway
hepatocytes secrete bile through bile ducts into common hepatic duct and go through gall bladder and common bile duct
GallBladder stores bile to deliver during ________ , Common Bile Ducts secretes bile directly into _____
GB stores bile to deliver during meals, CBD secretes bile directly into duodenum
risk factors for cholelithiasis “gallstones”
obesity, increased cholesterol, DM, pregnancy, female, family Hx
80% asymptomatic
symptoms and treatment of cholelithiasis “gallstones”
S/S: RUQ referred to shoulders, N/V, indigestion, fever (acute, obstruction)
Tx: IVF, ABX, pain management
Lab Choleysectomy
what is choledocolithiasis?
inital symptoms?
cholangitis?
treatment?
stone obstructing common bile duct > biliary colic
initial symptoms: N/V, cramping, RUQ pain
Cholangitis symptoms: fever, rigors, jaundice
Treatment: endoscopic removal of stone via ERCP
how is Endoscopic Retrograde Cholangiopancreatography (ERCP) done
guidewire through Sphincter of Oddi into Ampulla of Vater to retrieve stone from pancreatic duct or common bile duct
treatment for Spincter of Oddi Spasm
glucagon
1.
what anesthetic is done with ERCP and what postion is the patient in
GA
patient prone with left tilt, head of patient to the right
Tape ETT to the left
what is bilirubin
end product of heme- breakdown
unconjugated “indirect” vs “conjugated “direct” bilirubin
unconjugated bilirubin is protein bound to albumin, transported to the liver
conjugated bilirubin is water soluble, and excreted in the bile
what is unconjugated hyperbilirubinemia and some causes?
caused by an imbalance between bilirubin synthesis and conjugation
which hepatitises are most common
and which are more chronic
common: A,B,C,D,E
chronic: B,C
what is conjugated hyperbilirubinemia and some causes?
causes by an obstruction, causing reflux of conjugated bilirubin into the circulation
T/F VH is on the decline d/t vaccines and newer treatments
True!
which type of viral hepatitis requires liver transplant in the US
Hep C Virus
what newer tx has significantly reduced HCV in the US population
Tx b/o HCV genotype (75% type 1), HCV stage, +/- cirrhosis
12-week course Sofosbuvir/Velpatasvir
Provides 98-99% clearance of genotype 1A/1B
characteristics of viral hepatitis
what is most common cause of cirrohisis
alcoholic liver disease (ALD)
*top indication for liver transplants in the US
national prevalence of liver transplants for ALD is 2%
treatment for alcoholic liver disease
centered around abstinence
manage symptoms of liver failure
platelet cound < 50K requires blood transfusion
liver transplant if criteria is met
symptoms and labs of alcoholic liver disease
symptoms:
malnutrition, muscle wasting, parotid gland hypertrophy, jaundice, thrombocytopenia, ascites, hepatosplenomegaly, pedal edema
symptoms of ETOH withdrawal (DTs) may occur 24-72 hr after stopping
Labs:
increased mean corpuscular volume (MCV)
increased liver enzymes, ɣ-glutamyl-transferase (GGT), bilirubin
blood ethanol (acute intoxication)
risk factors for non-alcoholic fatty liver disease
obesity, insulin resistance, DM2, metabolic syndome
diagnosis of non-alcoholic fatty liver disease
hepatocytes contain > 5%
imaging and histology
*liver biopsy= gold standard in distinguishing NAFLD from other liver disease
non-alcoholic fatty liver disease can progress to
non-alcoholic steatohepatitis, cirrhosis, hepatocellular carcinoma
treatment of non-alcoholic fatty liver disease
diet, exercise
liver transplant for advanced fibrosis, cirrohiss, and related complications
prevalence of non-alcoholic fatty liver disease
non-alcoholic fatty liver disease (NAFLD) vs alcoholic fatty liver disease (AFLD)
autoimmune hepatitis predominantly affects who
women
autoimmune hepatitis
may be asymptomatic, acute, or chronic
+ autoantibodies and hypergammaglobuninemia
AST/ALT may be 10-20x normal in acute AIH
treatment: steroids, azathioprine
60-80% achieve remission, relapse is common
refractory disease requires immunosuppession
liver transplant when treatment fails or Acute liver failure ensues
most common cause of drug induced liver injury
acetaminophen OD
*normally reversible after the drug is removed
inborn errors of metabolism
groups of rare, genetically inheritied disorders that lead to a defect in the enzymes that breakdown and store protien, carbs, and fatty acid
occurs in 1: 2500 births
onset varies from birth to adolescence
most severe forms appear in the neonatal period and carry a high degree of mortality
inborn errors of metabolism - 3 specific disorders
Wilson’s Disease
Alpha-1 Antitrypsin Deficiency
Hemochromatosis
what is wilson’s disease
AKA hepatolenticular degeneration
autosomal recessive disease characterized by impaired copper metabolism
excessive copper buildup leads to oxidative stress in the liver, basal ganglia, and cornea
symptoms, diagnosis, and treatment for wilsons disease
symptoms: range from asymptomatic to sudden-onset liver failure with neurologic and pyschiatric manifestations
Diagnosis: Lab tests serum ceruloplasmin,
aminotransferases,urine copper level
Possible liver biopsy for copper level
treatment: copper-chelation therapy & oral znic to bind copper in the GI tract
what is alpha-1 antitryspin deficency
genetic disorder resulting in defective alpha-1 antitryspin protein.
alpha-1 antitryspin proteins protect the liver and lungs from neutrophil elastase
*neutrophil elastase is an enzyme that causes disruption of connective tissues leading to inflammation, cirrhosis, and hepatocellular carcinoma
alpha-1 antitryspin
incidence
diagnosis
treatment
incidence 1:16K to 1:35K (likely to be underdiagnosed)
Diagnosis: confirmed with alpha-1 antitryspin phenotyping
treatment: pooled alpha-1 antitryspin is effective for pulmonary symptoms; however it doesnt help with liver disease
liver transplant is the only curative treatment
hemochromatosis
excess iron in the body, leading to mutli-organ dysfunction
causes of hemochromatosis
repetitive blood transfusion, high dose iron tranfusion
genetic - excessive intestinal absorption
patient presentation of hemochromatosis
cirrohsis, heart failure, diabetes, adrenal insufficiency, or poly-arthopathy
excess iron accumulates in organs and causes damage to the tissues
labs, diagnosis, treatment of hemochromatosis
Labs: elevated AST/ALT, transferrin saturation and ferritin
Diagnosis: genetic mutation test, ECHO and MRI to diagnose cardiomyopathies and liver abnormalities
-liver biopsy may quantify iron levesl in the liver and assess damage
treatment: weekly phlebotomy, iron-chelating drugs, liver transplant
what is primary biliary cholangitis
previosuly known as biliary cirrhosis
autoimmune, progressive destruction of bile ducts with periportal inflammation and cholestasis
leads to liver scarring, firbosis, cirrhosis
who is more at risk to develop primary biliary cholangitis
Females > males; diagnosed in middle ages
thought to be caused by exposure to environmental toxins in genetically susceptible individuals
symptoms, Labs, imaging, and treatment for primary biliary cholangitis
symptoms: fatigue, jaundice, itching
Labs: increased Alk Phos, increased GGT, + antimitochrondrial antibodies
Imaging: CT/MRI/MRCP to rule out bile duct obtructions
Liver biopsy to reveal bile duct destruction and infiltration with lymphocytes
treatment: no cure, but exogenous bile acids slow progression
what is Primary Sclerosing Cholangitis (PSC)
autoimmune, chronic inflammation of the larger bile ducts
intrahepatic and extrahepatic
fibrosis in biliary tree leading to strictures -> cirrhosis, ESLD
Primary Sclerosing Cholangitis (PSC) affects men or women more? what age of onset
men, onset ~40s
symptoms of Primary Sclerosing Cholangitis (PSC)
fatigue, itching, deficency of fat soluble vitamins (A,D,E,K), cirrhosis
↑alkaline phosphatase and ɣ-glutamyl-transferase, +auto-antibodies
diagnosis and treatment of Primary Sclerosing Cholangitis (PSC)
diagnosis: MRCP/ERCP showing biliary strictures with dilated bile ducts
liver biopsy reinforces diagnosed (not always performed)
treatment:
no drug treatment proven to be effective
liver transplant - long term treatment
re-occurence is common after transplant due to to autoimmne nature
acute liver failure
life threatening severe liver injury occuring with days to 6 months after insult
rapid increase in AST/ALT, AMS, coagulopathy
massive hepatocyte necrosis causes cellular swelling and membrane disruption
causes of acute liver failure
50% of cases are drug-induced (majority acetaminophen)
viral hepatitis, autoimmune, hypoxia, ALF of pregnancy, HELLP
symptoms and treatment of acute liver failure
jaundice, nausea, RUQ pain, cerebral edema, encephalopathy, multi-organ failure, death
treatment: treat the cause, supportive care, liver transplant
what is the final stage of liver disease
cirrhosis - normal liver parenchyma replaced with scar tissue
symptoms/labs of cirrhosis
jaundice, ascites, varices, coagulopathy, encephalopathy
elevated AST/ALT, bilirubin, alkaline phosphatase, PT/INR, thrombocytopenia
causes of cirrhosis
alcoholic fatty liver, NAFL, HCV, HBV
transplant is the only cure
cirrhosis complications
portal HTN (HVPG > 5 mmHg)
ascites (most common complication)
spontaneous bacterial peritonitis (requires ABX)
varices
hepatic encephalopathy
hepatorenal syndrome
hepatopulmonary syndrome
portopulmonary HTN
ascites
caused by portal HTN leading to increased blood volume and peritoneal accumulation of fluid
management: low salt diet, albumin replacement
transjugular intrahepatic portosystemic shunt (TIPS)
reduces portal HTN and ascites
varices
present in ~50% of cirrhosis patients
hemorrhage is the most lethal complication
*beta blockers help reduce risk
*prophylactic endoscopic variceal banding and ligation
*refractory bleeding»_space; balloon tamponande
hepatic encephalopathy
build up of nitrogenous waste due to poor liver detoxification
neuropyschiatric symptoms (cognitive impairment to coma)
Tx: Lactulose, Rifaximin to decrease ammonia producing bacteria in the gut
hepatorenal syndrome
excess endogenous vasodilators (NO, Prostacylin) decreasing systemic MAP and renal blood flow
tx: midodrine, octeoride, albumin
hepatopulmonary syndrome
triad of chronic liver disease, hypoxemia, intrapulmonary vascular dilation
platypnea (hypoxemia when upright) due to R to L intrapulmonary shunt
portopulmonary HTN
Pulmonary HTN accompanied by portal HTN
systemic vasodilation triggers the production of pulmonary vasoconstrictors
treatment: PD-I, NO, prostacylcin analogs, and endothelin receptor antagonists
transplant is the only cure
2 scoring systems to determine severity and prognosis of liver disease
CTP: points based on bilirubin, albumin, PT, enceophalopathy, ascites
MELD: score on bilirubin, INR, creatinine, sodium
elective surgery is contraindicated in
acute hepatitis, severe chronic hepatitis, ALF
anesthesia in liver disease- if the patient has cirrhosis what is the next step
Risk stratification with MELD or CTP score
anesthetic considerations in liver disease
- careful H&P
- standard preop labs: CBC, BMP, PT/INR
- low treshold for invasive monitoring
- risk for aspiration, hypotension, hypoxemia
- colloids > crystalloids
- alcoholism increases MAC of VA
- drugs may have slow onset/prolonged Duration of Action
- bleeding/coagulation management
- Succ and ciastracurium ideal
- plasma cholinestase may be decreased in servere liver disease
what NMBs are desired in pts with liver disease
Succinycholine and Ciastracurium
*plasma cholineserase may be decreased in servere liver disease
Transjugular Intrahepatic Portosystemic Shunt (TIPS)
used to manage portal HTN
stent between the hepatic vein and the portal vein
shunt portal flow to the systemic circualtion
reducing the portosystemic pressure gradient
partial hepatectomy
resection to remove neoplasms, leaving adequate tissue for regernation
tolerable amount of resection d/o preexisting liver disease and function
indications and contraindications to TIPS
Indications:
refractory variceal hemorrhage, refractory ascites
contraindications:
Heart failure, tricupsid regurgitation, severe pulmonary HTN
anesthetic considerations for partial hepatectomy
anesthetic considerations
*invasive monitoring
blood products available
adequate vascular access for blood/pressors
surgeon may clamp the IVC or hepatic artery to control blood loss
maintain low CVP by fluid restriction prior to resection to reduce blood loss
Post op PCA
may cause posop coagulation disturbances
liver transplant
definitive treatment for ESLD
alcoholic liver disease the most common indication > fatty liver, HCC
*living donor: surgies timed together for minimal ischemia time
brain dead donor: kept hempodynamically stable for organ perfusion
intraop management for liver transplant
maintain hemodynamics (pressors/inotropes readily available)
ALine, CVC, PA CATH, TEE
control coagulation
Liver transplant table of surgical and anesthetic considerations
Anesthesia and liver disease - what MELD or CTP score should other alternatives be considered and work up for transplant
MELD> 16
Child Class C
MELD score <10 or CTP A
Proceed to OR
A patient with a MELD score 10-15 or CTP B. Should have what assessed next
Assess for Portal HTN
No: proceed to OR careful postop monitoring
Yes: consider preop TIPS procedure to optimize patient
