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216 Cards in this Set
- Front
- Back
What enzyme is most specific to liver function?
|
ALT
|
|
Which clotting factor is not manufactured in the liver?
|
factor 8
|
|
What is the hallmark sign of acute liver failure?
|
elevated PT
|
|
What lab for hepatic dysfunction is related to the biliary tract?
|
alk phos
|
|
Which vein does not contribute to hepatice blood flow?
|
portal vein
|
|
The largest internal organ in the body is
|
the liver
weighs 1500 g |
|
Significant hepatic dysfunction following anesthesia and surgery is...
|
uncommon -- limited to pts w preexisting hepatic impairment and those w rare reactions to volatile agents
|
|
When a pt has elevated alk phos levels, in order to differentiate the diagnosis of biliary obstruction, what lab test must be ordered?
|
5 ' NT
also GGT is similar to alk phos- most sensitive indicator of hepatobiliary disease |
|
The ______ divides the liver nito right and left lobes, and is remnant of the umbilical cord.
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falciform ligament
|
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What lobe is largest in the liver?
|
larger right lobe (w 2 additional smaller lobes)
|
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What is the functional unit of the liver?
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acinus
|
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What is the structural unit of the liver?
|
lobules (50,000-100,000)
|
|
The liver is supplied by sympathetic nerve fibers T____ through T _____, as well as parasympathetic fibers from the ____ and _____ nerve.
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T6-T11, vagus, R phrenic (innervates diaphragm)
|
|
For epidual in liver surgery, you must have a block at least at the level of
|
T6.
|
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In the liver, zone ____ is better oxygenated than zone _____.
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1 more O2 than zone 3
|
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What composes the portal triad?
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bile duct, hepatic artery, portal vein
|
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The _______ is where blood is filtered and plasma is removed.
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space of disse
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The _____ receive blood from the hepatic artery and portal vein to bring blood into the liver.
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sinusoids
|
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The _____ cells act as macrophages in the liver.
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kuppfer cells
|
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A hepatic lobule (Structural unit) consists of liver cells arranged in a radial pattern around a _____.
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central vein
|
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_____ are endothelial lined spaces located between the liver cells. They are partly lined w kupfer cells.
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sinusoids
|
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What are the 5 components of a portal tract?
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1. hepatic arterioles
2. portal venules 3. lymphatics 4. bile canaliculi 5. nerves |
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______ originate between hepatocytes and join to form bile ducts.
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bile canaliculi
|
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Venous drainage from the central veins of hepatic lobules combine to form the hepatic veins, which eventually empty into the ....
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inferior vena cava.
|
|
Which cells are better oxygenated? closest to the portal tract or closest to central veins?
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closest to portal tract better oxygenated
|
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_____ is stored in the gallbladder. Its function is to digest ___ and ___.
|
Bile, fats and cholesterol
|
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_____ triggers the release of bile when you have a fatty meal.
|
CCK hormone
|
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Bile is released from the _____ and released into the duodenum for digestion.
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sphincter of odi
|
|
The liver is perfused by ____% of CO.
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25-30%
|
|
What is the pressure, blood supply and O2 supply to the hepatic artery?
|
autoreg at MAP 50-150
25% total blood supply 50% O2 supply |
|
What is the pressure, blood supply and O2 supply of the portal vein?
|
low pressure system <10mmHg (portal HTN if higher)
75% total blood supply 50% O2 supply |
|
Normal cardiac output is
|
4-6 L/min
|
|
Normal cardiac index is
|
2-4 L/min
|
|
The _______ branches from the aorta. It contains alpha 1 (vasoconstrictor), beta and dopamine (Vasodilator) receptors.
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hepatic artery
|
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The _____ Delivers blood from the spleen and GI tract into the liver. The blood is nutrient rich but also contains bacteria.
|
portal vein
|
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The ______ only has alpha (vasoconstrictor) and dopamine (vasodilator) receptors, no beta receptors. Therefore beta blockers will not affect the tone of this vessel.
|
portal vein
|
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After blood comes through the liver, it travels through the ______, and then the hepatic vein carries it back to the inferior vena cava (Deoxygenated blood).
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central vein
|
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Hepatic metabolism of carbohydrates uses glucose to form _____ in the _____ cycle. Large amounts of frutose are broken down into ____.
|
ATP, citric acid cycle, lactate
|
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In the liver, fats are metabolized via ______ into acetyl CoA to form ATP in the citric acid cycle.
|
fatty acid oxidation
|
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All cells can use fat as energy except for...
|
RBCs and renal medulla
|
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In the liver, proteins are broken down via ______ of amino acids. The byproducts of protein metabolism are ___ and ____.
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deamination/transamination, ketoacids and ammonia
|
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____ formation helps to break down ammonia, because buildup of ammonia leads to _____.
|
Urea, encephalopathy
|
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The liver is responsible for biosynthesis of non essential _______ and _____ protein formation.
|
amino acids, plasma protein
|
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The liver makes all plasma proteins except for
|
IGs
|
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A buildup of lactate results in
|
lactic acidosis
|
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Of the proteins made in the liver, 50% is ____, which is necessary for oncotic pressure and drug binding w acidic drugs.
|
albumin
|
|
Alpha 1 glycoprotein (AAG) binds _____ drugs.
|
basic
|
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If the liver is compromised and you cant break down carbs....this results in...
|
low glucose - hypoglycemia,
low ATP formation so anaerobic metabolism more predominant |
|
If the liver is compromised and cant break down fat, this results in...
|
fatty stools
|
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If the liver is compromised and cant break down protein, this results in...
|
abundance of ammonia and cant form enough urea to get rid of ammonia (coma)
not enough albumine leads to incr capillary leak and edema/ascites/congestion and toxicity from drug because albumin not able to bind drugs and toxic metabolite formation (ex: meperidine to normeperidine causes seizures, morphine toxic metabolite is more potent than drug) |
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If the liver is dysfunctional, and cannot assist w coagulation...
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incr bleeding during surgery
|
|
If the liver is dysfunctional, and canot store glycogen or break it down...
|
there will be further hypoglycemia -- high insulin without any glucose to break down
|
|
If the liver is dysfunctional and it cannot cleanse blood...
|
toxins from GI tract can enter the IVC and cause sepsis
|
|
If the liver is dysfunctional and cannot provide its usual buffer response because the portal vein is impaired...
|
hepatic artery will try to compensate, but under anesthesia it is less able to compensate due to vasodilation from anesthetic agents
|
|
If the liver is dysfunctional and cannotmaintain aldosterone and electrolyte balance...
|
incr aldosterone, incr K, micturition, swelling, dilutional electrolyte imbalance
|
|
What are the phase one drug metabolism functions of the liver?
|
HOR+MDD to inactivate metabolites
hydrolysis, oxidation, reduction, methylation, dealkylation, and deamination |
|
Most drugs are metabolized by what liver enzyme?
|
CYP3A4
|
|
What are the phase two drug metabolism functions of the liver?
|
conjugation/glucuronidation to prepare for kidney excretion, makes the drug water soluble
|
|
This enzyme system can either be induced or inhibited.
|
CYP450
|
|
CYP450 ______ increase metabolism speed, and the provider may need to give more drug.
|
inducers (ketamine, barbs, etoh, anti-seizure meds, benzos)
|
|
CYP450 _______ cause more drug to be present wtihout being metabolized, increasing risk of toxicity.
|
inhibitors (cimetidine, propranolol, chloramphenicol abx)
|
|
What does it mean if liver extraction ratio is > 0.7?
|
high and dependent on hepatic blood flow
ex: fentanyl, morphine, ketamine, propofol, labetalol if you have cirrhosis, then you have a problem! |
|
What does it mean if liver extraction ratio is <0.3?
|
low,
ex: diazepam, lorazepam really dependent on microsomal enzymes |
|
All coagulation factors except ______ are manufactured in the liver.
|
3, 4 (tissue factors for calcium) and 8 (von willenbrand)
|
|
What fat soluble vitamins does the liver store?
|
ADEK and B12 (not fat sol.)
K (2,7,9,10 factors) |
|
The liver stores glycogen from postprandial glucose consumption. In the fasting person, the liver can access glucose stores through a process called
|
glycogenolysis
|
|
When glycogen stores are max'ed at 70 g, excess glucose is converted to
|
fat
|
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The liver serves as a reservoir for ____ % of TBV (5 L).
|
10-15%
|
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The liver filters blood received from the _____, which contains bacteria and nutrients from the GI tract and spleen, with macrophages called _____.
|
portal vein, kuppfer cells
|
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Coumadin works on which part of clotting to inhibit it?
|
vitamin K
|
|
Clotting factors range from number ___ through number ____ with no number ____.
|
1-13, no factor 6
|
|
What are the steps to forming a platelet plug?
|
DC GOVT!
aDhesion aCtivation aGgregation |
|
This occurs when the portal vein becomes compromised, and the hepatic artery can dilate to shunt more blood (Can compensate).
|
arterial buffer response
|
|
The liver forms bile, as well as formation and excretion of bilirubin, which is the byproduct of ____ breakdown, present in incr levels w hemolytic anemia.
|
Hgb
|
|
The liver metabolizes hormones, such as thyroxine, which is the precursor to
|
T3
|
|
The liver is the major site of degradation of these hormones:
|
1. insulin
2. steroid hormones (aldosterone, cortisol, estrogen, testosterone) 3. glucagon 4. antidiuretic hormone |
|
____ is the primary secretion of the liver, producing 1 L/day.
|
bile
|
|
Functions of bile
|
fat and cholesterol digestion
excretion of bilirubin (giving bile its color), cholesterol, many drugs |
|
Hepatocytes continuously secrete _____(several things)___ into the bile canaliculi.
|
bile salts, cholesterol, phospholipids, conjugated bilirubin
|
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What 2 paralytics have biliary metabolism and excretion?
|
vec and roc
|
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The ______ combine to form the common bile duct.
|
R and L bile ducts
|
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The bile ducts from lobules join and form ____.
|
hepatic ducts
|
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Biliary flow into the duodenum is controlled by the _____. Some drugs cause spasm here, namely _____.
|
sphincter of odi, fentanyl, morphine and other narcotics
|
|
The ______ serves as a reservoir for bile. Biliary fluid is concentrated here between meals, and the hormone _____ releases bile into the duodenum.
|
gallbladder, CCK hormone
|
|
What are the characteristics of hyperparathyroidism?
|
bones, stones and groans!
elevated Ca causes brittle bones, formation of stones from Ca, and pain (Groans) |
|
Bile acids are essential for ____ the insoluble components of bile and facilitating the intestinal absorption of _____.
|
emulsifying, lipids
|
|
Bile acids represent the major route of ____ elimination.
|
cholesterol
|
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Defects in the formation or secretion of _____ interfere with the absorption of fats and fat-soluble vitamins.
|
bile salts
|
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This lab test is used to reveal biliary obstruction. When it is elevated in the present of also elevated LFTs, it is likely to show a biliary obstruction rather than hepatic.
|
alk phos (ALP)
|
|
Normal alk phos?
|
25-85 iu/L
|
|
Bilirubin is primarily the end product of ____ metabolism.
|
hemoglobin
|
|
Following metabolism of Hgb and eventual conversion to bilirubin, it is then released into the blood where it readily binds to ____.
|
albumin
|
|
Binding to intracellular proteins traps bilirubin inside hepatocytes, where it is ____ and actively excreted into bile canaliculi and eventually into the ________.
|
conjugated, small intestine
|
|
In the intestines, bilirubin is converted to ____ by bacterial enzymes, mostly excreted through feces.
|
urobilinogen
|
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A small amt of bile is excreted via ____ or reexcreted in the bile.
|
urine
|
|
What will the bilirubin levels be to differentiate between a liver problem vs a kidney problem?
|
liver problem: high unconjugated bilirubin
kidney problem: high conjugated bilirubin |
|
The most commonly performed liver lab tests are neither ___ nor ____. The don't determine liver function, but instead determine _____.
|
sensitive nor specific,
liver dysfunction/integrity tests reflect hepatocellular integrity rather than hepatic fcn |
|
Secondary to the liver's large functional reserves, ____ may be present with few or no lab abnormalities.
|
cirrhosis
|
|
Liver abnormalities are divided into either _____ or _____ disorders.
|
parenchymal or obstructive
|
|
Cholesterol and pseudocholinesterase are valuable in assessing _____ function.
|
liver
|
|
The liver can still function until ____% cirrhotic (no lab changes yet).
|
70-80%
|
|
Normal total bilirubin concentration is <
|
1.5 mg/dL
|
|
Serum bilirubin reflects the balance between ____.
|
production and excretion of bilirubin
|
|
Jaundice is usually clinically obvious when total bilirubin exceeds ____
|
3 mg/dL
|
|
Predominantly conjugated hyperbilirubinemia is associated with ____.
|
urinary urobilinogen
|
|
Predominantly unconjugated hyperbilirubinemia may be seen with ...
|
hemolysis or with congenital or acquired defects in bilirubin conjugation
|
|
Normal ammonia levels are
|
80-110 mg/dL
|
|
Significant elevations in ammonia usually reflect disruption of ____. Marked elevations reflect ______.
|
hepatic urea synthesis,
severe hepatocellular damage |
|
Normal PT is _____. It measures the activity of ________.
|
11-14 sec,
fibrinogen (1), prothrombin (2), factors 5,7, and 10 |
|
Factor _____ has the shortest half life, of 4-6 hrs.
|
7
|
|
____ is useful in evaluating hepatic function in acute or chronic liver disease.
|
PT
|
|
Normal albumin level is ____, and it evaluates the function of the ____. A decrease is also seen in _____.
|
3-5 g/dL, liver, malnutrition
|
|
The half life of albumin is
|
2-3 wks
|
|
____ lab tests assess liver injury, not function.
|
LFTs (transaminases)
|
|
____ LFT is more liver specific, also called SGOT.
|
ALT
|
|
_____ LFT is also found in RBC, cardiac and skeletal muscle cells, also called SGPT.
|
AST
|
|
When the AST:ALT ratio is > 2:1, this suggests _____
|
etoh abuse
|
|
During regional/general anesthesia, hepatic blood flow decreases due to...
|
vasodilation from decr sympathetic outflow and blunted baroreceptor response
|
|
All volatile anesthetics reduce ______ blood flow in proportion to decreases in MAP and CO.
|
portal hepatic blood flow
HEIDS halothane (20% metab in liver), enflurane (2%), iso (0.2%), des (0.02%), sevo (3-4%) |
|
Controlled positive pressure ventillation with high mean airway pressures (high PEEP and APRV) causes what liver changes?
|
congestion of blood in hepatic vessels
|
|
Surgical procedures near the liver can reduce hepatic blood flow up to ___%, (abd surgery).
|
60%
|
|
Hypercapnia during anethesia leads to _____ blood flow.
|
incr (due to vasodilation)
|
|
Beta 2 _____ causes vasodilation, and beta 2 _____ can further complicate hepatic blood flow in cirrhosis.
|
agonist, blocker
|
|
There is an _____ Response to fasting and surgical trauma.
|
endocrine
|
|
The _____ response may be partially blunted by regional anesthesia, deep general, or pharmacologic blockade of the SNS.
|
stress response
|
|
Altered pharmacokinetics of drugs during anesthesia is most likely attributable to...
|
decr hepatic blood flow assoc w anesthetic agents (esp drugs w high liver extraction ratios)
|
|
All _____ can potentially cause spasm of the sphincter of odi and incr biliary pressure. IV administration of these drugs can induce biliary colic or result in false-positive cholangiograms (have glucagon, NTG or narcan available!).
|
opioids (morphine and fentanyl esp)
|
|
Mild post op liver dysfunction in healthy persons is not ____.
|
uncommon
persistent abnormalities in liver tests and post op jaundice require further investigation |
|
Halogenated anesthetics, such as halothane, lead to hepatitis due to ...
|
production of toxic metabolites --> hepatocyte hypoxia
|
|
Halothane hepatitis is a diagnosis of exclusion. You must first rule out...
|
hep A/B/C, epstein barr, CMV
|
|
Severity of halothane hepatitis can vary from...
|
asymptomatic elevation of LFTs to fulminant hepatic necrosis
|
|
Hepatitis due to these 2 halogenated anesthetics is very rare.
|
enflurane, isoflurane
(never in des or sevo) |
|
What are the risk factors associated with developing hepatitis from halogenated anesthetics?
|
middle age, obesity, female sex, repeat exposure
|
|
_____ of the liver is a major cause of death in men in their 40s-50s.
|
cirrhosis
|
|
Clinical manifestations of hepatic dysfunction are often ______ until extensive damage has occurred.
|
absent
|
|
Effects from anesthetics and surgery can precipitate further hepatic decompensation in...
|
marginal patients w little reserve
|
|
______ is the #1 reason for liver transplant.
|
hepatitis
|
|
Acute hepatitis is usually the result of
|
- a viral infection, drug reaction, or exposure to hepatotoxin
|
|
_____ represents acute hepatocellular injury with variable amts of cell necrosis
|
acute hepatitis
|
|
Mild inflammatory reactions may present as asymptomatic elevations in serum _____.
|
transaminases
|
|
Massive necrosis presents as acute ______ hepatitis.
|
fulminant
|
|
Viral hepatitis is most commonly due to
|
hepatitis a, b, or c
|
|
Hepatitis ____ and ____ are transmitted by oral-fecal route.
|
A and E
|
|
Hepatitis ___ and ____ are transmitted primarily percutaneously/parenterally and by contact w body fluids.
|
B and C
|
|
Hepatitis ____ may be transmitted by either route and requires the presence of ____.
|
D, hepatitis B required
|
|
Epstein Barr, HSV, CMV, and coxsachieviruses may all cause
|
hepatitis
|
|
Hepatitis ___ has the highest chronic infective rate.
|
C
|
|
You cannot get chronic hepatitis from strains __ and __.
|
A and E
|
|
What are the bilirubin levels for hep A, B, and C?
|
a <2, normal
b 2-3 C >3, high |
|
What are the albumin levels for hep A, B, and C?
|
a, >3.5, normal
b 3-3.5 C <3, low |
|
Vaccines are available for which strains of hepatitis?
|
A and B
|
|
Rejection of a liver transplant occurs ____ weeks after surgery.
|
1-6 wks
|
|
The highest fatality rate is associated w which strain of hepatitis?
|
D
|
|
All hepatitis strains arise from RNA genome except for...
|
B- DNA
|
|
Drug-induced hepatitis can result from...
|
1. direct dose-dependent toxicity
2. idiosyncratic drug rxn |
|
Drug-induced hepatitis course resembles..
|
viral hepatitis course
|
|
Alcohol consumption related liver damage is known as _____ hepatitis, which causes ____ infiltrates in the liver and heart.
|
Laenacc's, fatty
|
|
The max dose of tylenol to prevent liver injury is
|
3-4 g/day
|
|
3 potent drugs that can be ingested and cause drug-induced hepatitis are
|
CCl4 and mushrooms, volatile anesthetics
|
|
_____ is persistent hepatic inflammation for longer than 6 montes, as evidenced by elevated LFTs.
|
chronic hepatitis
|
|
Chronic hepatitis is classified as having a distinct syndrome based on liver biopsy, which will reveal one of these 3 types:
|
1. chronic persistent- confined, benign
2. chronic lobular- intermittent exacerbations 3. chronic active- cirrhosis |
|
In pts w hepatitis, elective surgeries should be postponed until...
|
acute episode resolved, labs in normal range
|
|
How will hepatitis affect intraoperative management?
|
1. prolonged duration of action w large or repeated doses of IV agents (esp benzos)
2. iso IA of choice 3. avoid factors known to reduce hepatic blood flow 4. regional can be used if no coagulopathy and avoid hypotension |
|
___ is a serious and progressive disease that eventually results in hepatic failure.
|
cirrhosis
|
|
The most common cause of cirrhosis is...
|
Laennac's (Etoh)
active DTs= 50% mortality |
|
Causes of cirrhosis:
|
1. laennacs (Etoh)
2. chronic active hep 3. chronic biliary inflammation or obstruction 4. chronic right-sided CHF (congestion, blood backing up) 5. hemochromatosis (incr Fe, causes organ damage) 6. wilson's disease- incr Copper for bilirubin metab 7. antitrypsin deficiency - genetic or related to emphysema |
|
Hepatocyte necrosis is followed by ____ and ____. There is no further blood/nutrient/O2 flow or exchange.
|
fibrosis and nodular regeneration
|
|
In cirrhosis, eventually portal venous flow is obstructed leading to..
|
portal HTN
|
|
Do cirrhosis s/s clinically correlate w disease severity?
|
nope
|
|
2 key s/s of cirrhosis
|
jaundice, ascites
|
|
What complications of cirrhosis are usually fatal?
|
hemorrhage, hepatorenal syndrome, encephalopathy
|
|
3 major complications of cirrhosis
|
1. variceal hemorrhage from portal HTN (give vasopressin 0.1-0.4 u/min or octreotide 50 mcg/hr
2. intractable fluid retention - ascites 3. hepatic encephalopathy - coma |
|
Some cirrhosis pts may present with spontaneous ______, and some may develop hepatocellular ______.
|
bacterial peritonitis, carcinoma
|
|
What are the GI symptoms of cirrhosis?
|
portal HTN, ascites, esophageal varices, hemorrhoids, GI bleed, splenomegaly
|
|
What are the circulatory symptoms of cirrhosis?
|
hyperdynamic state (incr CO and HR), systemic arteriovenous shunts (Develop thin-walled vessels that rupture easily)
|
|
What are the pulmonary symptoms of cirrhosis?
|
incr intrapulm. shunt (R to L), V/Q mismatch (normal is 0.8), decr FRC (normal is 2500), pleural effusions, atelectasis, restritive ventilatory defect
|
|
What are the renal symptoms of cirrhosis?
|
incr proximal/distal reabsorption of Na, impaired free H20 clearance, decr renal perfusion d/t portal HTN, hepatorenal syndrome
|
|
The only definitive treatment for hepatorenal syndrome is ____.
|
liver transplant
|
|
What are the manifestations of hepatorenal syndrome?
|
- decr renal perfusion
- incr reabsorption of Na - incr ADH/Aldosterone |
|
In hepatorenal syndrome, it is important to avoid NSAIDs because...
|
inhibits prostaglandin synthesis in an already dysfunctional kidney
|
|
What are the hematologic symptoms of cirrhosis?
|
anemia, coagulopathy (due to decr factors and decr functioning platelets), splenomegaly causes thrombocytopenia and leukopenia
|
|
What are the heme value goals for cirrhosis pts?
|
- HCT 30%
- plt >100k - better to transfuse FFP, Plt, and cryo (factor 1,8,13) |
|
What is the primary infectious complication of cirrhosis?
|
spontaneous bacterial peritonitis
|
|
What are the metabolic consequences of cirrhosis? (electrolyte imbalances)
|
HYPO:
Na, K, Mg, albumin, glucose |
|
What are the neuro consequences of cirrhosis?
|
encephalopathy, coma
|
|
How is cirrhosis encephalopathy treated?
|
lactulose binds ammonia, then you poop it out
|
|
Gynecomastia, spider angiomata, palmar erythema, and asterixis (wrist tremor on extension) can all be symptomatic of....
|
cirrhosis
|
|
For cirrhosis pts undergoing anesthesia, there is an increased risk for deterioration of
|
liver function
|
|
Patients with post-necrotic cirrhosis due to hep B or C may be ______.
|
infectious
|
|
How will cirrhosis affect dosing of NMBs?
|
smaller than normal maint dosing (those Dependent on hepatic elimination), prolonged duration of succ due to low AChesterase levels
|
|
The liver is highly dependent on _____ perfusion.
|
hepatic arterial
|
|
The half-life of ____ are often significantly prolonged in cirrhosis.
|
opioids
|
|
What is the NMB of choice in cirrhosis pts? What is the potential metabolite of this agent?
|
cisatracurium, laudanosine metabolite can cause seizures
|
|
Because of the abdominal distension associated with ascites, what is the induction technique?
|
RSI
|
|
Why not use nasal trumpets or NGTs in cirrhosis pts?
|
impaired coags, incr bleeding
|
|
What are the preferred IAs in cirrhosis pts?
|
des and iso
|
|
It is important to monitor ____ and _____ balance in cirrhosis pts intraoperative.
|
acid/base and fluid/electrolyte -- check ABGs
|
|
Why isnt N20 tolerated in some cirrhosis pts?
|
sympathomimetic effects, filling gas spaces if abdominal surgery
|
|
Intraoperative preservation of intravascular fluid and urine output in cirrhosis takes priority, and _____ fluids are used. _____ may be preferable to avoid Na overload and incr oncotic pressure.
|
isotonic, colloids
|
|
In cirrhosis pts, fluid replacement should take into account excessive _____ and _____ shifts.
|
bleeding, fluid
|
|
Which albumin product is preferred in cirrhosis pts?
|
25%
|
|
In cirrhosis pts, removal of ascitic fluid and volume replacement may create drastic fluid shifts causing potential...
|
BP changes
|
|
When giving cirrhosis pts RBCs, you should be on the look out for...
|
RBC breakdown byproducts
|
|
Hepatobiliary disease is most often characterized by _____. It is the most common cause of ____ obstruction in the biliary tract.
|
cholestasis (impaired bile flow), extrahepatic
|
|
Patients with hepatobiliary disease present with...
|
progressive jaundice, dark urine, pale stool, pruritis
|
|
_____ cholestasis most commonly results from viral hepatitis or an idiosyncratic drug rxn.
|
intrahepatic
|
|
What is the treatment for intra or extra hepatic cholestasis?
|
surgical removal of the gall bladder or placement of a stent to promote drainage
|
|
Patients with hepatobiliary disease present to the OR for...
|
cholecystectomy, relief of extrahepatic biliary obstruction, or both
|
|
In an extrahepatic biliary obstruction pt, it is important to assess what lab?
|
PT
|
|
What can complicate anesthetic mgmt and further compromise venous return/compress vessels in hepatobiliary disease pts?
|
insufflation of CO2 into abdomen, pt positioning
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How is biliary spasm at the sphincter of odi treated?
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narcan, NTG, glucagon
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4 common hepatic surgical procedures
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repair of lacs, drainage of abcesses, resection for tumors, liver transplant
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what are the 3 phases during a liver transplant?
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1. preanhepatic- dissection phase
2. anhepatic- liver completely removed from body 3. neohepatic- revascularization (trouble comes in this stage beause metabolites, toxins and radicals are released, causing hemodynamic instability -- give Ca, HCO3 to stabilize) |
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What are the anesthetic mgmt considerations during liver transplant cases?
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- consider potential large EBL (10-15% TBV in liver)
- invasive hemodynamic monitoring - large bore IVs |
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Post op jaundice can result from a variety of factors:
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- gilberts disease (Cant process bili)
- cholelithiasis - cholestasis - acute hepatitis - hemolytic anemia - transfusion rxn - G6PD deficiency (Avoid nsaids, asa, fava beans, sulfa drugs, use tiva w propofol) |
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Causes of post op jaundice (3):
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1. prehepatic- incr bili production, unconjugated high
2. hepatic- hepatocellular dysfunction, both conj and unconj high 3. posthepatic- biliary obstruction, conjugated high |