Hepatic 1 Flashcards
what are the overall functions of the liver?
- removes toxic byproducts of certain medications
- metabolizes or breaks down nutrients from food to produce energy
- helps your body fight infection by removing bacteria from the blood
- produces substances that regulate blood clotting
- produces bile which is needed to digest fat and absorb vitamins A, D, E and K
- produces most proteins needed by the body
- prevents shortages of nutrients by storing vitamins, minerals, and sugar
how big is the liver?
2.5-3 lbs
largest organ in the body
what is the basic functional unit of the liver
- lobule
- cylindrical shape
- several mm long and 0.8-2 mm wide
how many lobules are in the liver
50,000-100,000
what are the basic structures of a liver lobule (9)?
- portal vein
- sinusoids
- central vein
- hepatic artery
- bile canaliculi and bile duct (“capillaries” that transport bile)
- space of disse and lymphatic duct
- hepatic cellular plates
- kuppfer cells (macrophages in liver)
- interlobular septa
Space of Disse
space around the endothelial cells; plasma goes through large gaps of endothelial cells and into this space; eventually drains into lymphatics
what is the portal triad?
-portal vein
-hepatic artery
-bile duct
these are the components of a typical portal canal
celiac trunk artery
- important for hepatic blood flow
- gives rise to hepatic artery so supplies blood to liver
where does the liver receive blood flow from?
- the portal vein and the hepatic artery
- both supply about 50% of the liver’s O2 requirement
SvO2 of portal vein
85%
SaO2 of hepatic artery
98-100%
what is normal hepatic blood flow?
1500 mL/min
about 25-30% of CO
how much hepatic blood flow comes from portal vein and hepatic artery respectively?
- portal vein - 1100 mL (75%)
- hepatic artery - 400 mL (25%)
what is the avg portal vein pressure?
9 mmHg
resistance to blood flow through the liver
- portal vein pressure on avg is 9 mmHg
- pressure in hepatic vein leaving liver and entering IVC normally averages 0 mmHg
- small pressure difference demonstrates that resistance to flow in hepatic sinusoids is VERY low
- resistance MUST be low given than 1500 mL of blood flows through the liver each minute
- calculate resistance using ohm’s law
how long does it take for blood to traverse from the portal vein to the central vein?
- 8 to 9 seconds
- promotes sufficient time for the blood to be in contact with the hepatocytes and kupffer cells
what is hepatic arterial blood flow dependent on?
- autoregulation
- metabolic demand
- constriction and dilation dependent on local conditions
what is hepatic portal vein blood flow dependent on?
-blood flow to the GI tract and the spleen
Liver blood flow compensation
- change in blood flow from one source will produce a reciprocal (but somewhat limited) compensatory change in the blood flow from the other source
- decrease in hepatic arterial blood flow produces an increase in portal venous blood flow
cirrhosis and hepatic blood flow
- cirrhosis greatly increases the resistance to blood flow
- destruction of the liver parnechymal cells results in replacement with fibrous tissue that contracts around the blood vessels (bridging fibrosis)
- bridging fibrosis = fibrotic tissue bridges across sinusoids and cuts them off
- greatly impedes portal vein blood flow
most common cause of cirrhosis
alcoholism
other common causes of cirrhosis
- viral hepatitis
- obstruction of bile ducts
- infection in the bile ducts
- ingestion of poisons (carbon tetrachloride - formerly used in dry cleaning)
- non-alcoholic fatty liver disease
fatty liver
- deposits of fat cause liver enlargement
- strict abstinence can lead to a full recovery
liver fibrosis
- scar tissue forms
- recovery is possible but scar tissue remains
cirrhosis
- growth of connective tissue destroys liver cells
- damage is irreversible
NAFLD
- non-alcoholic fatty liver disease
- hepatocytes accumulate excess fat (a process known as steatosis)
- such fat can come from the diet, be made in the liver, or be released by insulin resistance fatty adipose tissue
- 25% of population has NAFLD
common causes of NAFLD
- obesity
- DMTII
- metabolic syndrome
- nutrition
- medication
NASH
- non-alcoholic steatohepatitis
- develops when accumulated fat causes stress and injury to hepatocytes
- bloated hepatocytes swell further and start to die causing inflammation
- scarring occurs as collagen fibers replace dead cells
- 30% of those with NAFLD get NASH
what percentage of those with NASH develop cirrhosis?
20%
hepatic artery blood vessel receptors
- alpha 1 adrenergic receptors - vasoconstriction
- beta 2 adrenergic, dopaminergic D1 receptors, and cholinergic receptors - produce vasodilation
portal vein blood vessel receptors
- alpha 1 adrenergic receptors - vasoconstriction
- d 1 dopaminergic receptors - produces vasodilation (but not to the same extent as the arterial system
SNS activation + hepatic blood flow
- hepatic artery and mesenteric vessel vasoconstriction
- decreased hepatic blood flow
liver as blood reservoir
- expandable organ
- large quantities of blood can be stored in its blood vessels
- liver normal blood volume including what is in the veins and sinusoids = 450 mL
- acts as blood reservoir when there is excess blood volume and can supply extra volume when blood volume is diminished
High pressure in RA + Liver blood reservoir
high pressure in RA produces back pressure in liver –> expands 0.5-1L can be stored
(happens in CHF)
low pressure in body + liver blood reservoir
blood shifts from hepatic veins and sinusoids into central circulation
as much as 300 mL
does blood from the portal vein have bacteria
- yes!!
- almost always grows gram negative rods when cultured
- blood from intestinal capillaries has bacteria from the gut
- HOWEVER we don’t grow bacilli from a systemic blood sample bc kupffer cells
kupffer cells function
- line hepatic and venous sinusoids
- cleanse blood as it passes through these sinuses
- phagocytose cellular debris, viruses, proteins, and particulate matter
- release various enzymes, cytokines, and other chemical mediators
liver + lymph production
- liver has very high lymph flow
- pores in sinusoids are VERY permeable and allow easy passage of fluid and protein into the spaces of disse
- this permits large amounts of lymph with a protein concentration similar to plasma to form
how much of the body’s lymph comes from the liver?
about 1/2 of all lymph
what does high hepatic vascular pressure cause?
fluid transudation into the abdominal cavity
3-7 mmHg increase in hepatic venous pressure
- causes excessive amounts of lymph fluid
- can leak through the outer surface of the liver capsule into the abdominal cavity
10-15 mmHg increase in hepatic venous pressure
- can cause lymph flow to be 20x normal
- produces sweating from a liver surface with large amounts of free fluid entering the abdominal cavity
- this is ASCITES
blockage of portal vein + lymph flow
- creates high pressure in the GI tract
- transudation of fluid through the gut into the abdominal cavity
- MORE ascites
anabolic reaction
- involves the building of larger, complex molecules from smaller, simpler ones
- require input of energy
catabolic reaction
- opposite of anabolic reaction
- break the chemical bonds in larger, more complex molecules
hepatic metabolism in GENERAL
- liver = large chemically reactant pool of cells
- have HIGH rate of metabolism
- share substrates and energy from one system to another
- processes and synthesizes multiple substances that are transported throughout the body (numerous enzymatic pathways)
what are the final products of carbohydrate (CHO) metabolism?
- glucose
- fructose
- galactose
- AKA the monosaccharides
what is the final common pathway of CHO metabolism?
glucose
-this is because fructose and galactose are converted into glucose by the liver
what do all cells use to make ATP?
GLUCOSE (duh!) = ATP = energy
what are the four specific liver functions associated with CHO metabolism?
- conversion of galactose and fructose to glucose
- storage of large amounts of glycogen
- gluconeogenesis
- formation of many chemical compounds from intermediate products of CHO metabolism
chemical formula of the monosaccharides
C6H12O6
glycogen
- branched polymer of glucose
- how most glucose is stored following a meal
- readily available source of glucose that does not contribute to intracellular osmolality
- storage as glycogen allows the liver to remove excess glucose from the blood, store it, and return it to the blood when BG concentration decreases
glucose buffer function
- allows the liver to remove excess glucose from the blood, store it, and return it to the blood when BG concentration decreases
- have glucose available, but maintain osmotic homeostasis
what happens when glycogen storage capacity is exceeded?
glucose is converted to FAT
what in the body can store significant amounts of glycogen?
- liver
- muscle
insulin
enhances glycogen storage
epinephrine and glucagon
enhance glycogen breakdown (glycogenolysis)
24 hour fast
- amount of time it takes for hepatic glycogen stores to be exhausted
- after this gluconeogenesis is necessary to provide an uninterrupted supply of glucose (and remember glucose = ATP = energry)
gluconeogenesis
- occurs only when BG concentration falls below normal
- V important in maintenance of normal BG concentration
- convert amino acids, glycerol, pyruvate, and lactate to glucose
- can be done by liver and kidneys
agents that increase gluconeogenesis
- glucocorticoids
- catecholamines
- glucagon
- thyroid hormone
agents that decrease gluconeogenesis
-insulin
fat metabolism by liver
- CHO storage capacity is saturated the liver converts the excess ingested CHOs to fat
- fatty acids are used for fuel or stored in the adipose tissue and liver for later use
- most cells can directly use FAs as an energy source
- RBCs and renal medulla can only use glucose
- neurons normally use glucose but can use ketone bodies produced in the liver by the breakdown of FAs following a few days of starvation
specific functions of liver associated with fat metabolism
- oxidation of fatty acids to supply energy for other body functions
- synthesis of large amounts of cholesterol, phospholipids and lipoproteins
- synthesis of fat from CHO and proteins
oxidation of fatty acids
- fats must be split into glycerol and FAs
- FAs are then split by beta oxidation into 2-carbon acetyl radicals that form acetyl coenzyme A
- acetyl CoA enters citric acid cycle and is oxidized to liberate LOTS of energy (in form of ATP)
beta oxidation
- oxidation = give/donate electrons
- occurs in all cells of the body but especially rapidly in liver cells
what does the liver do with the Acetyl Co-A it cannot use
- convert to acetoacetic acid (combo of two acetyl Co-A molecules)
- acetoacetic acid is highly soluble so leaves hepatocytes and is absorbed by other tissues
- tissues reconvert acetoacetic acid back into acetyl CoA to enter citric acid cycle and oxidize it for energy
- liver responsible for a MAJOR part of fat metabolism
synthesis of cholesterol, phospholipids, and lipoproteins from fat metabolism by liver
-acetyl Co-A also used by liver to synthesize cholesterol and phospholipids
cholesterol
- 80% synthesized in the liver is converted to bile salts and secreted in the bile
- remainder is packaged in lipoproteins and carried by the blood to all tissues of the body
phospholipids
also synthesized by liver and transported predominantly in lipoproteins
lipoproteins
like semi trucks that carry/deliver things throughout the body
what are cholesterol and phospholipids used by body cells for?
- cell membranes
- intracellular structures
- chemical substances important to cell function (like hormones)
synthesis of fat from proteins and carbs
- almost all synthesis of fat from CHO and proteins occurs in the liver
- after fat is synthesized it is transported in lipoproteins to the adipose tissue to be stored
specific liver functions associated with protein metabolism
- deamination of proteins (aka removal of nitrogen)
- formation of urea for removal of ammonia from the body fluids
- formation of plasma proteins
- synthesis of amino acids and synthesis of other compounds from amino acids
deamination of proteins
- essentially removal of nitrogen or amine group
- this is required of AAs before they can be used for energy or before they can be converted to CHO or fats
- enzymatic process which converts AAs into their respective keto acids and results in production of ammonia as a byproduct
- cleaving of N and converts back to C=O group (carbonyl)
what is the principle site of deamination
- the liver
- liver deaminates most of the AAs derived from dietary protein consumption
deamination of alanine
plays a major role in hepatic gluconeogenesis
transaminase
- enzymes that catalyze a transamination reaction between an amino acid and an keto acid
- or removal of an amine group and replacement with keto acid group
formation of urea from ammonia
- allows for removal of ammonia from body fluids
- urea readily diffuses out of liver and excreted by kidneys
- if liver does NOT do this –> increased plasma ammonia –> hepatic coma –> death
how are large amounts of ammonia formed?
- deamination process
- bacteria in gut with subsequent absorption into the blood
porta-caval shunt
- causes greatly reduced blood flow or bypassed blood flow to the liver
- excessive ammonia in the blood
- toxicity results
formation of plasma proteins by liver
-essentially all of the plasma proteins with exception of immunoglobulins are formed by hepatocytes (accounts for about 90% of all plasma proteins)
how many plasma proteins does the liver form/day
15-50 g/day
if you lose 1/2 of your plasma proteins how long does it take the liver to replace them
1-2 weeks
quantitatively the most important plasma proteins are…
- albumin - responsible for maintaining a normal plasma osmotic pressure and the principal binding site for FAs, hormones, and drugs
- alpha1 antitrypsin - prevents breakdown of other proteins by trypsin
qualitatively the most important plasma proteins are
-coagulation factors
synthesis of AAs and other compounds by liver
- one of the most important hepatic functions
- non-essential AAs can be synthesized in liver by interconversion of one AA to another
- keto acid formed that has the same chemical composition as AA to be formed except at the keto oxygen
- next amino radical is transferred from an available AA to the keto acid to take the place of the keto oxygen (transamination)
phase I recations
-modify substances through cytochrome P450 enzymes and mixed function oxidases
oxidation
- 90% of all reactions
- primarily via P450 enzymes and secondarily by mixed function oxidases
- often generates reactive oxygen species because carboxyl, epoxy, and hydroxyl groups are introduced into the parent compound
reduction
-mainly catalyzed by P450 enzymes
enzyme induction
- results in an increase in the production of the enzymes that metabolize these drugs; so reduction in the available amount of drug
- can lead to tolerance to other drugs metabolized by the same enzymes
CYP 450 inducers
- ethanol
- barbiturates
- ketamine
- benzodiazepines
enzyme inhibition
- causes inhibition of enzymes to metabolize drugs
- ranitidine, amiodarone, ciprofloxacin
drugs that have a high rate of hepatic extraction
- lidocaine
- morphine
- verapamil
- labetalol
- propranolol
- decrease in clearance is usually a product of reduced hepatic blood flow and not hepatic dysfunction
phase II reaction
- may or may not follow a phase 1 reaction
- involves conjugation of a substance with a water soluble metabolite
- conjugated substances excreted in urine or bile
water soluble metabolites involved in conjugation
- glucuronide (most common)
- sulfate
- taurine
- glycine
phase I reactions (CYP450)
- oxidation
- reduction
- hydrolysis
- hydration
- dehalogenation (volatile anesthetics)
phase II reactions (conjugation pathways)
- sulfation
- glucoronidation
- glutathione conjugation
- acetylation
- amino acid conjugation
- methylation
liver as storage site for vitamins
- stores large quantities of vitamin A, B12, D, E, and K
- A –> prevent Vit A deficiency for 10 months
- B12 –> prevent B12 deficiency for 1 or more years
- D –> prevent D deficiency for 3-4 months
liver + iron storage
- liver stores iron as ferritin (a globular protein)
- apoferritin + iron = ferritin
- ferritin is stored in hepatocytes until the iron is needed elsewhere in the body
- low iron in body - ferritin releases iron
- apoferritin-ferritin system therefore acts as an iron storage and buffer system
apoferritin
protein that can bind excess iron in body fluids
Transferrin
carries in the blood
liver + coagulation factors
- liver produces most of the coagulation factors
- vitamin K required cofactor for synthesis of 2, 7, 9, 10
vitamin K deficiency
coagulopathy due to impaired function of 2, 7, 9 and 10
factors not produced by the liver
8 and vWF
what hormones are degraded in the liver?
- TH
- insulin
- steroid hormones (cortisol, aldosterone, estrogen)
- glucagon
- ADH
bile canaliculi
where hepatocytes continuously secrete bile salts, cholesterol, phospholipids, and conjugated bilirubin into
L and R hepatic ducts
bile ducts from hepatic lobules eventually form these
common bile duct
- hepatic duct + cystic duct = common bile duct
- hepatic duct is from the R and L hepatic ducts
- cystic duct is from the gallbaldder
sphincter of oddi
controls flow of bile from the common bile duct
gallbladder
- reservoir for bile
- concentrates biliary fluid through active transport of Na+ and passive water reabsorption
cholecystokinin
hormone released from the intestinal mucosa in response to fat and protein that causes contraction of the gallbladder, relaxation of the spinchter of oddi, and ejection of bile into the small intestine
bilirubin
- major end product of Hgb degradation
- one of the many substances excreted in the bile and eliminated in the feces
- provides a valuable tool for diagnosing hemolytic blood diseases and various types of liver disease
how long does a typical RBC last?
120 days
process of bilirubin formation
- RBC lyses –> released Hgb is phagocytized by tissue macrophages
- Hgb split into globin and heme
- heme ring opened and Fe released and transported in the blood by transferrin
- 4 pyrrole rings of the porphyrin structure are converted to biliverdin
- biliverdin is rapidly converted to free bilirubin and released from macrophages
- free bilirubin immediately combines with plasma albumin
Hgb to bilirubin simplified
Hgb –> globin + heme –> Fe + pyrrole rings –> biliverdin –> free bilirubin (combines with albumin in blood “free”)
unconjugated or indirect bilirubin
- free bilirubin
- bound to plasma albumin but still considered free
- absorbed by hepatocytes eventually and released from albumin
conjugation of bilirubin back in liver
- glucuronide (80%)
- sulfate (10%)
conjugated or direct bilirubin
- excreted from hepatocytes by an active transport process into the bile canaliculi and then into the intestines
- toxic to hepatocytes
urobilinogen
- 1/2 of conjugated bilirubin converted by bacteria in the intestines to this
- urobilinogen is reabsorbed back into the blood
- some excreted in urine
- majority reexcreted by LIVER back into intestines and eliminated in feces
SUMMARY formation and excretion of bilirubin
- hgb phagocytized by macrophage
- free bilirubin released by macrophage to circulate in blood
- absorbed by hepatocytes, release unconjugated bilirubin from albumin and conjugate it (conjugated = toxic to hepatocytes)
- conjugated bili excreted into biliary tract and enters intestines
- bacteria in intestines converts half conjugated bili into urobilinogen
- urobilinogen reabsorbed back into blood
- some urobilinogen passes through kidneys and excreted in urine
- MOST urobilinogen passes through liver and excreted in feces
jaundice
- excess bilirubin in ECF
- could be unconjugated or conjugated
hemolytic jaundice
- increased destruction of RBCs
- large hematoma
- RBCs hemolyzed rapidly
- increase production of bilirubin by macrophages
- increase unconjugated bilirubin (free/indirect) in blood, hepatocytes cannot process or conjugate all the bilirubin
- primary increase in unconjugated bilirubin in the blood
- secondary increase in conjugated (direct) bilirubin
- total bili HIGH
- excretory function of liver NOT IMPAIRED
- formation of urobilinogen in intestines increases and urinary excretion increases
obstructive jaundice
- obstruction of bile ducts or damage to hepatocytes preventing usual amounts of bilirubin from being excreted into the GI tract
- making normal amount but it cannot go anywhere
- most often obstruction of common bile duct due to gallstone or malignancy
- can also be due to damage to hepatic cells (as in hepatitis)
- unconjugated bili enters hepatocytes and conjugated in usual way
- rate of conjugated bilirubin formation is normal but it cannot pass from the liver into the intestines
- conjugated bilirubin enters the blood most likely by rupture of the bile canaliculi and direct emptying of bile into the lymph system
- most bilirubin in plasma is CONJUGATED (unlike hemolytic jaundice)
diagnostic differences between hemolytic and obstructive jaundice
- hemolytic = almost all bilirubin in plasma is unconjugated (i.e. free bilirubin)
- obstructive = bilirubin in plasma is mainly in conjugated form
TOTAL obstruction of bile flow
- no conjugated bilirubin can reach intestines
- bacteria cannot convert to urobilinogen
- so no urobilinogen reabsorbed into blood and excreted by kidney
- urine urobilinogen is NEGATIVE = diagnostic
serum transaminase measurements
- AST and ALT
- not very sensitive or specific
- reflect hepatocellular integrity as apposed to liver function
- released when hepatocytes destroyed (similar to troponin with cardiomyocytes)
tests that measure liver synthetic function
- serum albumin
- PT or INR
- cholesterol
- psucdocholinesterase
- LIVER HAS TO PRODUCE THESE
parynchymal disorders
hepatocellular dysfunction
obstructive disorders
biliary excretion
when is jaundice evident
total bili > 3.0 mg/dL
conjugated hyperbilirubinemia + increased urobilinogen
- intrahepatic cholestasis (bile caniculi blocked)
- extrahepatic biliary obstruction
- the two above can lead to hepatocellular dysfunction
unconjugated hyperbilirubinemia
- hemolysis
- congenital or acquired defects in bilirubin conjugation
which form of bilirubin is toxic to cells
conjugated
serum aminotransferases (transaminases)
-enzymes released into the circulation as a result of hepatocellular damage
AST
- aspartate aminotransferase
- present in many tissues in addition to liver (non-specific)
- heart, skeletal muscle, kidney
ALT
- alanine aminotransferase
- primarily located in liver, more specific
AST/ALT levels
- normie below 35-45 IU/L
- mild elevation = cholestasis or metastatic disease
- absolute level poorly correlate with degree of hepatic injury in CLD
- absolute level of value in acute liver disease (drug OD, ischemic injury, fulminant hepatitis)
serum alkaline phosphatase
- produced by liver, bone, small bowel, kidneys, and placenta, excreted into bile
- most circulating comes from bone
- in presence of external biliary obstruction, more alk phos synthesized and released into circulation
2x normal alk phos
hepatocellular injury or hepatic metastatic disease
HIGH alk phos
- intrahepatic cholestasis
- biliary obstruction (diagnostic)
serum albumin
- normie = 3.5-5.5
- long half life, so prob normal level with acute liver disease
hypoalbuminemia causes
- chronic liver disease (diagnostic)
- acute stress
- malnutrition
- increased loss of albumin in urine (nephrotic syndrome)
- increased loss of albumin in the GI tract (enteropathy with protein loss)
blood ammonia
- normie 47-65
- increased ammonia usually reflects disruption of hepatic urea synthesis
- marked elevation = severe hepatocellular damage
prothrombin time
- normal = 11-14 seconds
- PT > 3-4 seconds from control is considered significant (corresponds to INR of 1.5)
PT measures activity of which coagulation factors?
- fibrinogen
- factor 2 (prothrombin)
- factor 5
- factor 7
- factor 10
factor 7
- short half life
- PT useful in evaluating hepatic synthetic function of patients with acute or chronic liver disease
prolonged PT
- usually reflects severe liver disease because only 20-30% of normal factor activity is necessary for NL coagulation
- true unless vit K deficiency present
- PT does not correct with IV admin of vit K (requires 24 hrs) then severe liver disease likely present
Pre-hepatic liver dysfunction lab values
bilirubin overload
- bilirubin = increased unconjugated fraction
- AST/ALT = no change
- Alk Phos = no change
- PT = no change
- albumin = no change
pre-hepatic liver dysfunction causes
- hemolysis
- hematoma reabsorption
- bilirubin overload from whole blood
intrahepatic liver dysfunction lab values
parenchymal/hepatocellular dysfunction
- bilirubin = increased conjugated fraction
- AST/ALT = markedly increased
- Alk Phos = no change to slightly increased
- PT = prolonged
- albumin = decreased
intrahepatic liver dysfunction causes
- viruses
- drugs
- sepsis
- arterial hypoxemia
- CHF
- cirrhosis
post-hepatic liver dysfunction lab values
cholestasis
- bilirubin = increased conjugated fraction
- AST/ALT = normal to slightly increased
- Alk Phos = markedly increased
- PT = no change to prolonged
- albumin = no change to decreased
post-hepatic liver dysfunction causes
- stones
- cancer
- sepsis
anesthesia effect on hepatic blood flow
-usually decreased during general and regional due to direct and indirect effects of anesthetic agents themselves, type of ventilation, surgical procedure
volatile agents + hepatic blood flow
decrease hepatic blood flow
- most with halothane
- least with isoflurane
anesthetic agents + hepatic blood flow
- indirectly decrease hepatic blood flow in proportion to any decrease in CO or MAP
- decrease CO also reduces hepatic blood flow by reflex SNS stimulation and vasoconstriction of the arterial and venous splanchnic vasculature
spinal + epidural anesthesia + hepatic blood flow
decrease primarily by decreasing BP
general anesthesia + hepatic blood flow
decreases by decreaseing BP and CO –> SNS stimulation –> vasoconstriction
PPV with high MAP + hepatic blood flow
- decrease VR and CO
- compromises hepatic blood flow
- PEEP can accentuate this
surgical procedure + hepatic blood flow
-procedures on or near the liver can reduce hepatic blood flow up to 60% most likely by SNS activation, local vascular reflexes, direct compression of vessels of hepatic circulation
drugs that decrease hepatic blood flow
- beta adrenergic blockers
- alpha 1 adrenergic agonist
- vasopressin
effect of anesthesia on hepatic metabolic function
- effect on CHO, protein and fat metabolism poorly understood
- endocrine stress response secondary to fasting and surgical stress –> increased catecholamines, glucagon, and cortisol
- CHO and protein stores metabolized resulting in hyperglycemia and negative nitrogen balance
anesthesia/opioids + biliary tract function
- all opioids can potentially cause spasm of sphincter of Oddi and increase biliary pressure
- less likely to occur if opioid is given slowly and in small increments
sphincter of Oddi spasm + opioids worst –> least
- fentanyl/alfenta/sufenta/remi
- morphine
- meperidine
- butorphanol
- nalbuphine
spincter of oddi spasm treatment
- naloxone
- glucagon
most common cause of post-op jaundice
over production of bilirubin due to reabsoprtion of a large hematoma or RBC breakdown following transfusion
