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N935 Advanced Pathophysiology > hepatic pathophysiology and anesthesia implications > Flashcards

hepatic pathophysiology and anesthesia implications Flashcards

1
Q

what typically causes liver carcinoma?

A

hepatitis c

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2
Q

clinical manifestations of hepatic disease are often

A

absent until extensive damage has occurred

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3
Q

acute hepatitis is usually the result of

A

viral infection, drug reaction, exposure to a hepatotoxin

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4
Q

clinical manifestation of acute hepatitis depends on

A

severity of the inflammatory reaction and amount of cellular necrosis

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5
Q

acute hepatitis caused by viral infection are due to

A

hepatitis a, b, or c viruses

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6
Q

hepatitis a is transmitted by the

A

oral-fecal route

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7
Q

hepatitis b and c are transmitted primarily

A

percutaneously and by contact with body fluids

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8
Q

hepatitis A

A

least severe, most recover in weeks to months, transmission through fecal contamination

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9
Q

hepatitis E

A

similar to A, mostly in 3rd world countries, transmission through fecal contamination

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10
Q

hepatitis D

A

does not produce hepatitis by itself

only occurs as a co-infection with acute hep B or super infection with chronic hep B

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11
Q

which hepatitis does not cause jaundice?

A

hepatitis B

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12
Q

hepatitis B can lead to

A

fulminant hepatic necrosis or chronic hepatitis

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13
Q

hepatitis C

A

antibodies not present for long periods, rarely produces fulminant hepatic failure

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14
Q

hepatitis C produces

A

asymptomatic carries

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15
Q

concerning acute hepatitis caused by viral infection patients often have a

A

prodromal illness for 1-2 weeks with fatigue, malaise, low grade fever, N/V

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16
Q

incidence of chronic active viral hepatitis is more common in

A

hepatitis C (50% at least)

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17
Q

things to consider if someone is an infectious carrier

A

avoid direct contact with blood and secretions
immunization is effective against hep b
prior infection with hep c does not mean they have immunity when re-exposed
post-exposure prophylaxis with hyperimmune globulin if effective for hep B

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18
Q

drug induced acute hepatitis results from

A

direct dose-dependent toxicity of a drug or a metabolite, idiosyncratic drug reaction, combination of the two

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19
Q

most common cause of drug induced acute hepatitis

A

alcohol

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20
Q

chronic alcohol ingestion can result in

A

fatty infiltration as a result of impaired fatty acid oxidation, increased uptake and esterification of fatty acids, diminished lipoprotein synthesis and secretion

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21
Q

drugs that can cause acute hepatitis

A

alcohol, acetaminophen, volatile anesthetics, sulfonamides, amiodarone

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22
Q

should patients with acute hepatitis have surgery?

A

no, d/t high mortality rate

should be postponed until resolved with normal liver function test

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23
Q

alcohol withdrawal during surgery is associated with

A

a mortality rate of as high as 50%

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24
Q

patients with hepatitis are at risk for further hepatic dysfunction and hepatic failure including

A

encephalopathy, coaguolopathy, hepatorenal syndrome

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25
Q

which lab values should be done for someone with acute hepatitis?

A

BUN/creat, bilirubin, albumin, PT/INR, electrolytes, glucose, transaminases, alk phos, platelet count

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26
Q

what electrolyte abnormality and acid base deficiency is most common with acute hepatitis?

A

hypokalemia and metabolic alkalosis usually d/t vomiting

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27
Q

chronic alcoholics may have which electrolyte disturbance?

A

hypomagnesemia which predisposes them to dysrhythmias

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28
Q

in acute hepatitis which is higher ALT or AST?

A

ALT

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29
Q

om alcoholic hepatitis which is higher ALT or AST?

A

AST

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30
Q

which lab is the best indicator of synthetic function of the liver with hepatitis?

A

PT prolonged >3-4 seconds (>1.5 INR) after administration of vitamin K = severe liver dysfunction

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31
Q

hypoalbuminemia is usually not present except in

A

protracted cases with severe malnutrition or chronic hepatitis

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32
Q

preop evaluation of emergent patient with acute hepatitis includes:

A

determining cause and degree of hepatic impairment, recording drug exposures (alcohol, recreational drugs, recent transfusions, prior anesthetics), N/V, correction of dehydration/electrolyte abnormalities, mental status changes, if alcoholic

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33
Q

acute intoxication of alcohol manifests as

A

inappropriate behavior or obtunded

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34
Q

withdrawal from alcohol manifestations

A

irritability, tremulousness, hypertension, tachycardia

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35
Q

goal of intraoperative management in acute hepatitis is to

A

preserve existing hepatic function, avoid factors that may be detrimental to the liver

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36
Q

acute viral hepatitis may produce increased ____ to anesthetics

A

CNS sensitivity

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37
Q

which anesthetic is typically preferred in acute hepatitis patients?

A

inhalational agents over IV agents d/t metabolism

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38
Q

things to avoid that reduce hepatic blood flow

A

hypotension, excessive SNS stimulation, high mean airway pressures during controlled ventilation

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39
Q

chronic hepatitis definition

A

persistent hepatic inflammation for longer than 6 months as evidenced by elevated serum aminotransferases

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40
Q

what are the 3 patient classifications of chronic hepatitis and how are they determined?

A

chronic persistent, chronic lobular, and chronic active

determined by liver biopsy

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41
Q

chronic persistent hepatitis present with

A

acute hepatitis (B or C) that has a protracted course but eventually resolves

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42
Q

chronic persistent hepatitis is characterized by

A

chronic inflammation of the portal tracts with preservation of the normal cellular architecture

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43
Q

which chronic hepatitis classification(s) DO(ES) NOT progress to cirrhosis?

A

chronic persistent and chronic lobular

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44
Q

chronic lobular hepatitis presents with

A

acute hepatitis that resolves but is followed by recurrent exacerbations

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45
Q

chronic lobular hepatitis is characterized by

A

foci of inflammation and cellular necrosis in the lobules

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46
Q

chronic active hepatitis occurs most commonly as

A

a sequela of hepatitis B or C

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47
Q

chronic active hepatitis is characterized by

A

chronic hepatic inflammation with destruction of cellular architecture (more global)

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48
Q

which chronic hepatitis classification(s) does lead to cirrhosis?

A

chronic active hepatitis

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49
Q

in hepatitis C antivirals can

A

cure more than 95% of affected patients

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50
Q

patients with chronic persistent or chronic lobular hepatitis should be treated similar to

A

those with acute hepatitis

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51
Q

patients with chronic active hepatitis should be treated as

A

that they have cirrhosis

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52
Q

most common causes of cirrhosis

A

alcohol abuse, NAFLD, chronic active hepatitis (B and C), chronic biliary inflammation or obstruction

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53
Q

Cirrhosis leads to

A

hepatocyte necrosis –> fibrosis and nodular regeneration

54
Q

destruction of the livers normal cellular and vascular architecture produces

A

obstruction of the portal venous flow leading to portal hypertension, impairment of normal synthetic and metabolic functions leading to multisystem disease

55
Q

what 2 things eventually develop in most patients with cirrhosis

A

jaundice and ascites

56
Q

other manifestations of cirrhosis include

A

spider angiomas, palmar erythema, gynecomastia, spleenomegaly

57
Q

3 major complications with cirrhosis

A

variceal hemorrhage from portal HTN
intractable fluid retention in the form of ascites
hepatic encephalopathy or coma

58
Q

approximately 10% of patients with cirrhosis have at least one episode of

A

bacterial peritonitis

59
Q

severity of hepatic impairment and surgical risk can be estimated using the

A

childs-turcotte -pugh scoring system which consists of 2 clinical features and 3 lab assessments

60
Q

Class A from Childs-Turcotte-Pugh Score

A

5-6 points
one year survival 100%
two year survival 85%

61
Q

Class B from Childs-Turcotte-Pugh Score

A

7-9 points
one year survival 80%
two year survival 60%

62
Q

Class C from Childs-Turcotte-Pugh Score

A

10-15 points
one year survival 45%
two year survival 35%

63
Q

sign of portal hypertension preoperatively is

A

dilated abdominal wall veins

64
Q

what is a major cause of morbidity and mortality of cirrhosis

A

massive bleeding from gastroesophageal varices

65
Q

medical treatment for variceal bleeding includes

A

replace blood loss with IV fluids and blood products, vasopressin, somatostatin, propranolol, balloon tamponade, endoscopic sclerosis or ligation of the varices, emergency surgery if continues to bleed

66
Q

hematological manifestations with cirrhosis

A

anemia, thrombocytopenia/coagulopathy, leukopenia

67
Q

thrombocytopenia/coagulopathy associated with

A

congestive spleenomegaly d/t portal hypertension
decreased hepatic synthesis of clotting factors
enhanced fibrinolysis d/t reduced elimination of factors that activate the fibrinolytic system

68
Q

leukopenia associated with

A

congestive spleenomegaly d/t portal hypertension

69
Q

cirrhosis is typically associated with a

A

hyperdynamic circulatory state

70
Q

cardiac output is often ___ in cirrhosis

A

increased and generalized peripheral vasodilation is present

71
Q

what kind of shunt can develop with cirrhosis

A

arteriovenous shunt can develop in the systemic and pulmonary circulation

72
Q

cirrhotic cardiomyopathy may be present due to

A

av shunt, decreased blood viscosity which both contribute to increased CO, above normal filling pressures, and below normal SVR

73
Q

respiratory manifestations with cirrhosis

A

hyperventilation is common leading to respiratory alkalosis
hypoxemia d/t R–> L shunt
decreased lung volume (especially FRC) d/t ascites elevating diaphragm leading to atelectasis

74
Q

When an AV shunt is involved with cirrhosis what are the consequences?

A

involves 40% of the CO!!

will have a V/Q mismatch and hypoxemia!

75
Q

what are some preop labs/tests that would be useful in someone with cirrhosis concerning respiratory manifestations?

A

chest xray, abg

76
Q

if someone has a large amount of ascites what would be something to consider preoperatively?

A

performing a paracentesis

77
Q

alterations in fluid and electrolyte balance are manifested as

A

ascites, edema, electrolyte abnormalities on lab results, hepatorenal syndrome

78
Q

mechanisms responsible for ascites include:

A

portal HTN
hypoalbuminemia
seepage of protein rich lymph from the surface of the liver
avid renal sodium retention and water reabsorption

79
Q

how does portal HTN lead to ascites?

A

increases hydrostatic pressure favors fluid transudation across the intestine into the peritoneum

80
Q

how does hypoalbuminemia lead to ascites?

A

decreases plasma osmotic pressure which favors fluid transudation

81
Q

patients with cirrhosis and ascites have

A

decreased renal perfusion
altered intrarenal hemodynamics
enhanced proximal and distal tubule Na+ reabsorption
impairment of free water clearance

82
Q

what electrolyte abnormalities are common with cirrhosis

A

hyponatremia (dilutional)

hypokalemia (excessive loss from hyperaldosteronism or diuretics)

83
Q

hepatorenal syndrome

A

is a functional deficit in patients with cirrhosis that usually follows GI bleeding, aggressive diuresis, sepsis, or major surgery

84
Q

hepatorenal syndrome is characterized by

A

progressive oliguria, avid Na+ retention, azotemia, intractable ascites, high mortality rate

85
Q

perioperative fluid management in someone with cirrhosis

A

be judicious

albumin or some kind of colloid is better choice

86
Q

loop diuretics should only be used

A

after bed rest, sodium restriction, and spironolactone have failed

87
Q

hepatic encephalopathy is characterized by

A 
alterations in mental status
fluctuating neurological status
asterixis, hyperreflexia
EEG changes
increased ICP potentially
88
Q

metabolic encephalopathy

A

related to the amount of hepatocellular damage and degree of shunting of portal blood directly into the systemic circulation so toxins from the GI tract that normally are metabolized in the liver will accumulate into systemic circulation

89
Q

factors known to precipitate hepatic encephalopathy include

A 
GI bleed
increased dietary protein intake
hypokalemic alkalosis from vomiting/diuresis
infection
worsening liver function
90
Q

response to medications is unpredictable due to changes in

A

CNS sensitivity, volume of distribution, protein binding, drug metabolism, drug elimination

91
Q

volume of distribution of highly ionized NMBAs is increased requiring

A

greater than normal loading doses

92
Q

hepatic elimination of NMBAs is decreased requiring

A

lower than normal maintenance doses

93
Q

in someone with cirrhosis the liver is very dependent on

A

hepatic arterial blood flow d/t reduced portal blood flow

94
Q

how do we preserve hepatic artery blood flow to the liver?

A

avoid anesthetic agents that potentially reduce the arterial blood flow (agents that cause hypotension)

95
Q

What is the most commonly used anesthetic for cirrhotic patients?

A

propofol induction and isoflurane maintenance

96
Q

What is NMBA of choice in someone who has cirrhossi?

A

cisatracurium

97
Q

opioid supplementation reduces the volatile agent requirement but will have a prolonged

A

T1/2 B (elimination) leading to prolonged respiratory depression

98
Q

if someone is having N/V, GI bleeding, and abd distention what will we probably have to do

A

RSI with cricoid pressure

99
Q

if a cirrhosis patient is cardiovascularly unstable and with active bleeding how should we proceed with inducing them?

A

awake intubation

RSI with cricoid pressure using ketamine or etomidate and succinylcholine

100
Q

why should you monitor someone with 5 leads that has cirrhosis?

A

to detect ischemia because if they are on vasopressin that will cause coronary vasoconstriction which can lead to ischemia

101
Q

someone who has a large Right to Left shunt

A

may not tolerate N2O and may require PEEP to treat V/Q mismatch

102
Q

intraabdominal procedures in cirrhotic patients are often associated with

A

excessive bleeding d/t venous engorgement from portal HTN, adhesions from previous surgeries, coagulopathy
fluid shifts from evacuation of ascites and prolonged procedure

103
Q

removal of large amounts of ascites may require

A

IV colloid solutions to prevent profound hypotension

104
Q

significant blood transfusions can result in

A

citrate toxicity

105
Q

explain citrate and why IV Ca++ is often necessary during a large amount blood transfusions

A

citrate is metabolized in the liver but if someone has cirrhosis that impairs that metabolism… the citrate binds to serum Ca++ and causes hypocalcemia which will decrease contractility soooo that’s why we give IV Ca++ to reverse the negative effects of the hypocalcemia

106
Q

typical dose for IV Calcium

A

1 gram

107
Q

primary cause of death in acute/fulminant liver failure?

A

cerebral edema d/t high levels of NH3 (ammonia) in the brain and accumulation of glutamate and neuronal swelling

108
Q

cirrhosis can lead to

A

portal HTN (ascites and varices) and/or hepatocellular cancer

109
Q

hepatocellular death causes

A

decreased synthesis, decreased clearance, and metabolic derangement leading to encephalopathy and coagulopathy

110
Q

cholestasis

A

stoppage of bile flow

111
Q

hepatobiliary disease is characterized by

A

cholestasis

112
Q

most common cause of cholestasis is

A

extrahepatic obstruction of the biliary tract (obstructive jaundice) d/t gallstone, stricture, tumor in common hepatic duct

113
Q

cholestasis can also be caused by _____ (not extrahepatic)

A

intrahepatic obstruction d/t suppression or stoppage of bile flow at hepatocyte or bile canaliculus from either viral hepatitis or idiosyncratic drug reaction

114
Q

treatment of extrahepatic obstruction is usually

A

surgical

115
Q

treatment of intrahepatic obstruction is usually

A

medical

116
Q

both extrahepatic and intrahepatic obstructions produce a predominately _____ hyperbilirubinemia and ____ alk phos

A

conjugated ; increased

117
Q

symptomatic gallstone disease (cholelithiasis) usually present with

A

biliary colic secondary to obstruction of the cystic duct

118
Q

when someone has biliary colic from obstruction and develops chills or high fever that is suggestive of

A

ascending bacterial infection of the biliary system = cholangitis

119
Q

medical treatment for someone with acute cholecystitis before going to the OR include

A

NG to suction, IV fluids, antibiotics, opioids

120
Q

patients with extrahepatic biliary obstruction from any cause readily develop

A

vitamin K deficiency so they should get vitamin K and may need FFP

121
Q

how long does it take to get a full response after administering vitamin K?

A

24 hours

122
Q

if someone who has cholecystitis has high bilirubin levels what might that indicate?

A

renal failure

123
Q

long standing extrahepatic biliary obstruction is associated with

A

secondary biliary cirrhosis and portal HTN

124
Q

what is a consideration regarding opioids and someone undergoing a lap cholecystetomy?

A

can induce spasm in sphincter of oddi which can result in a false positive on the cholangiogram
so pay attention in the case and don’t give opioid right before they do the cholangiogram

125
Q

agents dependent on what kind of excretion is preferable in someone with cholecystitis

A

renal excretion

make sure you monitor urine output through a catheter and maintain periop diuresis

126
Q

common hepatic surgeries include

A

repair of lacerations
drainage of abscesses
resection of tumors

127
Q

what things should you consider having or doing for a hepatic surgery?

A 
multiple large bore IVs
fluid and blood warmers
rapid infusion devices
direct arterial and CVP monitoring 
avoid hypotension
128
Q

administration of ____ may reduce blood loss

A

aprotinin
aminocaproic acid
tranexamic acid

129
Q

___glycemia may occur following large liver resections

A

hypo- glycemia

130
Q

postop complications of hepatic surgery include

A

bleeding, sepsis, hepatic dysfunction

131
Q

in someone who has cirrhosis what surgeries have the highest risk of mortality?

A

peptic ulcer surgery (54%), emergency abdominal surgery (57%), emergency cardiac surgery (80%), abdominal surgery for trauma (47%)

132
Q

in someone who has acute hepatitis and needs an exploratory laparotomy what is the mortality rate?

A

100% ……..

N935 Advanced Pathophysiology (15 decks)

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