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N935 Advanced Pathophysiology > Hepatic Physiology > Flashcards

Hepatic Physiology Flashcards

1
Q

Anesthesia’s goals pertaining to the liver

A

maintain BP and oxygenation, keep the function that the patient does have

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2
Q

What does the liver do to drugs? (simplified)

A

makes them water soluble so they can be eliminated by the kidneys

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3
Q

What are the basic structures of a liver lobule?

A

portal vein, sinusoids, central vein, hepatic artery, bile canaliculi and bile duct, space of disse, lymphatic duct, hepatic cellular plates, kupffer cells, interlobular septa

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4
Q

What makes the structural shape of the liver lobule advantageous?

A

hexagonal shape that shares blood supply and bile ducts in multiple directions with abutting lobules

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5
Q

What are the two sources of blood supply to the liver?

A

portal vein

hepatic artery

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6
Q

What is the significance of the space of Disse?

A

drains into the lymph

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7
Q

What are sinusoids structurally/functionally similar to?

A

capillaries

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8
Q

What does the liver cell plate do?

A

collects bile into the bile canaliculi

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9
Q

What organ is a huge source of lymph?

A

the liver!

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10
Q

Where are the Kupffer cells and what do they do?

A

inside the sinusoids and are macrophages that remove bacteria

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11
Q

What is the best source of oxygenation to the liver?

A

the hepatic artery

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12
Q

How much of the livers O2 requirement does the portal vein supply?

A

50%

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13
Q

Portal vein SvO2

A

85%

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14
Q

How much of the livers O2 requirement does the hepatic artery supply?

A

50%

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15
Q

Hepatic artery SaO2

A

98-100%

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16
Q

The liver has ___ blood flow and ___ vascular resistance

A

high; low

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17
Q

normal hepatic blood flow

A

1500mL/minute (25-30% of CO)

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18
Q

How much of the hepatic blood flow comes from the portal vein?

A

1100 mL/ minute (75% of total)

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19
Q

How much of the hepatic blood flow comes from the hepatic artery?

A

400 mL/ minute (25% of total)

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20
Q

What is the average portal vein pressure as blood enters the liver?

A

9 mmHg

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21
Q

Pressure in the hepatic vein leaving the liver to the inferior vena cava is about

A

0 mmHg

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22
Q

If resistance increases (what can it lead to)

A

portal hypertension

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23
Q

Hepatic arterial blood flow is dependent on

A

metabolic demand (autoregulation)

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24
Q

Hepatic portal vein blood flow is dependent on

A

blood flow to the GI tract and spleen

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25
Q

A decrease in hepatic arterial blood flow produces an ___ portal venous blood flow

A

increase

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26
Q

If arterial pressure is decreased then

A

decreased pressure through the hepatic artery and the portal vein

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27
Q

The superior mesenteric artery supplies blood to ___ (which organs)

A

colon, small intestines, pancreas

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28
Q

The celiac artery supplies blood to ___ (which organs)

A

stomach, spleen, pancreas

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29
Q

The inferior mesenteric artery supplies blood to ___ (which organs)

A

the colon

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30
Q

The blood supply from portal vein comes from (which organs)

A

stomach, spleen, pancreas, small intestines, and colon

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31
Q

Cirrhosis ___ the resistance to blood

A

greatly increases!

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32
Q

Patho of cirrhosis

A

destruction of liver parenchymal cells = replacement with fibrous tissue that contracts around the blood vessels = impedes portal vein blood flow

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33
Q

Most common cause of cirrhosis ___

A

alcoholism

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34
Q

Causes of cirrhosis (besides alcoholism)

A

viral hepatitis, obstruction of bile ducts, infection in the bile ducts, ingestion of poisons, non-alcoholic fatty liver disease

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35
Q

stages of alcohol induced liver damage (3)

A
  1. fatty liver (deposits = liver enlargement) *is recoverable
  2. liver fibrosis (scar tissue forms) *recovery possible but with scar tissue
  3. cirrhosis (connective tissue destroys liver cells) *irreversible!!
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36
Q

micronodular cirrhosis

A

alcohol abuse can lead directly to cirrhosis from repeated exposure of the cells to toxins causing fibrosis and cirrhosis

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37
Q

What medications can cause liver disease?

A

TPN, amiodarone

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38
Q

What are the 3 most common causes of liver disease?

A

obesity, T2DM, metabolic syndrome

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39
Q

Metabolic syndrome

A

HTN, excess glucose and triglycerides, increased fat

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40
Q

NAFLD what does it stand for

A

non alcoholic fatty liver disease

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41
Q

25% of the US population has ___

A

NAFLD

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42
Q

NASH

A

nonalcoholic steatohepatitis (inflammation)

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43
Q

Up to 30% of people with NAFLD will develop

A

NASH

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44
Q

Up to 20% of people with NASH will develop

A

cirrhosis

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45
Q

Which receptors does the hepatic artery have?

A

alpha 1 (vasoconstriction), beta2 (vasodilation), dopa1 (vasodilation)

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46
Q

Which receptors does the portal vein have?

A

alpha 1, dopa1

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47
Q

sympathetic activation results in hepatic artery and mesenteric vessel ____ and ____ hepatic blood flow

A

vasoconstriction; decreased

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48
Q

beta 2 adrenergic stimulation ___ the hepatic artery

A

vasodilates

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49
Q

the liver’s normal blood volume including what is in the veins and sinusoids is

A

about 450mL

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50
Q

the liver can expand to hold how much blood (in liters)

A

up to 1 L

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51
Q

when low pressure exists (like in hemorrhage) how much blood can the liver shift into circulation?

A

as much as 300 mL

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52
Q

How is the bacteria in the blood from the portal vein “cleansed”?

A

Kupffer cells engulfs the bacteria and goes through phagocytosis

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53
Q

Pores in the sinusoids are ___

A

very permeable allowing passage of fluid and protein in to the spaces of disse

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54
Q

About how much lymph comes from the liver?

A

1/2

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55
Q

high hepatic vascular pressure causes ____

A

fluid transudation into the abdominal cavity

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56
Q

a _____ increase in hepatic venous pressure can increase lymph flow to 20x normal

A

10-15 mmHg

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57
Q

How does ascites occur?

A

a high pressure in hepatic venous pressure leads to increase in lymph flow and back up of fluid that leaks through the liver capsule into the abdominal cavity

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58
Q

carbohydrates, fats, and proteins all lead to

A

the citric acid cycle and ATP production

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59
Q

list some metabolic functions of the liver

A

carbohydrate, fat, protein, and drug metabolism

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60
Q

carbohydrate metabolism final products

A

glucose, fructose, and galactose

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61
Q

all cells utilize _____ to produce energy in the form of ATP

A

glucose

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62
Q

specific liver functions with carbohydrate metabolism

A

convert galactose and fructose into glucose, storage of glycogen, gluconeogenesis, formation of chemical compounds

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63
Q

What are glucose, fructose, and galactose? What do they have in common?

A

simple sugars or monosaccharides

have the same chemical formula (C6H12O6) but structural formulas differ

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64
Q

storage of glycogen allows

A

the liver to remove excess glucose from the blood, store it, and return it to the blood when BG is low (glucose buffer function)

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65
Q

Glucose buffer function

A

removed excess glucose that is stored in the liver and then returned to the blood when BG gets low

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66
Q

Does glycogen contribute to intracellular osmolality?

A

no

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67
Q

Structure of glycogen

A

a branched polymer of glucose (just a bunch hooked together)

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68
Q

when glycogen storage capacity is full, glucose is converted to

A

fat

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69
Q

insulin ___ glycogen storage

A

enhances

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70
Q

epinephrine and glucagon ___ glycogen breakdown (aka glycogenolysis)

A

enhances

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71
Q

hepatic glycogen stores are depleted after a ___

A

24 hours fast

gluconeogensis kicks in to provide an uninterrupted supply of glucose

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72
Q

gluconeogenesis only occurs when

A

BG concentration falls below normal

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73
Q

agents that increase gluconeogenesis

A

glucocorticoids, catecholamines, glucagon, thyroid hormoen

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74
Q

agents that decrease gluconeogenesis

A

insulin

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75
Q

when carbohydrate storage capacity is saturated the liver converts the excess carbs to

A

fat

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76
Q

RBCs and renal medulla can only use ___ for energy

A

glucose

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77
Q

specific liver functions with fat metabolism

A

oxidation of fatty acids to supply energy, synthesis of large amounts of cholesterol, phospholipids, and lipoproteins, synthesis of fat from carbs and proteins

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78
Q

to derive energy from fat (triglycerides)

A

they must be split into glycerol and fatty acids
fatty acids are then split by beta oxidation into 2 carbon acetyl radicals that form acetyl CoA which enters the citric acid cycle to create a lot of ATP

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79
Q

the liver cannot use all of the ___ it produces

A

acetyl CoA

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80
Q

unused Acetyl CoA is

A

converted to acetoacetic acid which is highly soluble and leaves the hepatocytes enters the blood and absorbed by other tissues which will reconvert into acetyl CoA to be used to produce energy

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81
Q

acetyl CoA can also be used to synthesize

A

cholesterol and phospholipids

82
Q

most of the cholesterol synthesized in the liver is converted to

A

bile salts and secreted into the bile

83
Q

a small amount of cholesterol is

A

packaged into lipoproteins and carried to other tissue cells

84
Q

cholesterol and phospholipids can be used to form

A

cell membranes, intracellular structures, chemical substances important to cell function

85
Q

if protein metabolism doesn’t occur

A

death will occur in a few days

86
Q

specific liver functions associated with protein metabolism include

A

deamination of proteins, formation of urea for removal of ammonia, formation of plasma proteins, synthesis of amino acids

87
Q

Deamination means

A

removal of nitrogen

88
Q

essential amino acids have to come from

A

our diet

89
Q

Deamination of _____ plays a major role in hepatic gluconeogenesis

A

alanine

90
Q

large amount of ammonia are formed by

A

deamination process

bacteria in gut with subsequent absorption into the blood

91
Q

essentially all of the plasma proteins with the exception of ____ are formed by ___

A

immunoglobulins; hepatocytes

92
Q

the liver can form plasma proteins at the rate of

A

15-50 g/day

93
Q

if someone loses 1/2 of their plasma proteins the liver can replace them in about

A

1-2 weeks

94
Q

quantitatively the most important plasma proteins are

A

albumin and alpha1- antitrypsin

95
Q

albumin is responsible for

A

maintaining a normal plasma osmotic pressure and is the principal binding and transporting protein

96
Q

qualitatively the most important plasma proteins are

A

coagulation factors

97
Q

transamination

A

amino radical is transferred from an available amino acid to the keto acid

98
Q

glycogenesis is

A

glucose stored as glycogen

99
Q

glycogenolysis

A

breakdown glycogen to make glucose

100
Q

end products of hepatic biotransformation are either

A

inactivated or are made more water soluble and excreted in urine or bile

101
Q

phase 1 reactions of hepatic biotransformation

A

modify substances through cytochrome p450 enzymes and mixed function oxidases

102
Q

oxidation generates

A

reactive oxygen species because carboxyl, epoxy, and hydroxyl groups are introduced into the parent compound

103
Q

the cytochrome p450 system can be induced by

A

ethanol, barbiturates, ketamine, benzodiazepines

104
Q

enzyme induction results in an

A

increase in the production of the enzymes that metabolize these drugs

105
Q

enzyme induction can lead to ___

A

tolerance of these drugs

106
Q

enzyme induction can promote

A

tolerance to other drugs metabolized by the same enzymes

107
Q

ranitidine, amiodarone, ciprofloxacin can

A

prolong the effects of other drugs by inhibiting these enzymes

108
Q

products of phase 1 reactions may be ___

A

more active than the parent compound or rendered cytotoxic

109
Q

drugs with very high rate of hepatic extraction from the circulation

A

lidocaine, morphine, verapamil, labetalol, propranolol

110
Q

a decrease in metabolic clearance of drugs that undergo high rate of hepatic extraction is from __

A

a reduced hepatic blood flow not hepatocyte dysfunction

111
Q

barbiturates and benzodiazepines are inactivated by

A

phase 1 reactions

112
Q

examples of poorly extracted drugs

A

tylenol, clindamycin, diazepam, digitoxin, warfarin

113
Q

if someone has liver disease and is given lidocaine what effect will it have on the pharmacokinetics?

A

the half life is prolonged and the clearance is less so the effect is decreased but stays in the body longer

114
Q

phase 2 reactions of biotransformation involve

A

conjugation of a substance with a water soluble metabolite

115
Q

water soluble metabolites

A

glucuronide, sulfate, taurine, glycine

116
Q

conjugated substances can be excreted in

A

the urine or bile

117
Q

types of phase 1 reactions

A

oxidation, reduction, hydrolysis, hydration, dehalogenation

118
Q

types of phase 2 reactions

A

sulfation, glucoronidation, glutathione conjugation, acetylation, amino acid conjugation, methylation

119
Q

the liver is a storage site for

A

vitamins A, B12, D, E, and K

120
Q

enough vitamin A can be stored for up to

A

10 months

121
Q

enough vitamin B12 can be stored for up to

A

1 or more years

122
Q

enough vitamin D can be stored for up to

A

3-4 months

123
Q

how does the liver store iron?

A

as ferritin

124
Q

hepatic cells produce and excrete ___ which can bind excess iron in body fluids

A

apoferritin

125
Q

apoferritin + iron =

A

ferritin

126
Q

iron is carried in the blood by

A

transferrin

127
Q

vitamin K is a required cofactor for the synthesis of

A

factor II, VII, IX, X

128
Q

vitamin k deficiency manifests as

A

coagulopathy d/t impaired formation of factors 2,7,9,10

129
Q

which factors are not produced by the liver?

A

factor VIII and vonwillebrand

130
Q

the liver is the primary site of degradation for

A

thyroid hormone, insulin, steroid hormones, glucagon, ADH

131
Q

hepatocytes continuously secrete ___ into the bile canaliculi

A

bile salts, cholesterol, phospholipids and conjugated bilirubin

132
Q

flow of bile from the common bile duct is controlled by

A

the sphincter of oddi

133
Q

gallbladder function

A

reservoir for bile, concentrates biliary fluid by active transport of Na+ and passive H2O reabsorption

134
Q

Cholecystokinin

A

is a hormone released from the intestinal mucosa in response to fat and protein that causes contraction of the gallbladder, relaxation of sphincter of oddi and ejection of bile into the small intestine

135
Q

what is the major end product of Hgb degradation?

A

bilirubin

136
Q

bilirubin provides a valuable tool for diagnosing

A

hemolytic blood diseases and various types of liver disease

137
Q

after about ___ days RBCs become fragile and their membranes rupture

A

120

138
Q

how Hgb is broken down

A

split into globin and heme, heme ring opened and Fe is released and transported by transferrin, the 4 pyrrole rings of the porphyrin structure are converted to biliverdin which is converted to free bilirubin which combines with plasma albumin

139
Q

bilirubin bound to plasma albumin is called

A

free bilirubin, unconjugated / indirect bilirubin

140
Q

bilirubin is conjugated with

A

glucuronide* and sulfate

141
Q

in the intestine 1/2 of the ____ is converted by bacteria to ___ which is reabsorbed back into the blood

A

conjugated bilirubin; urobilinogen

142
Q

What does excess bilirubin in the ECF cause?

A

jaundice

143
Q

Which kind of bilirubin will cause jaundice?

A

can be unconjugated or conjugated!

144
Q

Common causes of jaundice

A

increased destruction of RBCs (hemolytic jaundice), obstruction of the bile ducts or damage to hepatocytes (obstructive jaundice)

145
Q

Which kind of bilirubin is toxic?

A

conjugated

146
Q

What happens during hemolytic jaundice?

A

increased production of bilirubin by macrophages and unconjugated bilirubin in the blood

147
Q

When hepatocytes cannot process all of the bilirubin what happens?

A

primarily an increase in unconjugated bilirubin but also a secondary increase in conjugated bilirubin

148
Q

In hemolytic jaundice excretory function of the liver is

A

not impaired

149
Q

in hemolytic jaundice the rate of formation of urobilinogen in the intestines ___ and urinary excretion ___

A

increases; increases

150
Q

What most often causes obstruction of the common bile duct?

A

gallstones, malignancy but can also be caused by damage to hepatic cells from hepatitis

151
Q

in obstructive jaundice most of the bilirubin in the plasma is in the ____ form

A

conjugated

152
Q

in hemolytic jaundice majority of the bilirubin in the plasma is in the ____ form

A

unconjugated

153
Q

when there is total obstruction of bile flow

A

no conjugated bilirubin can reach the intestines to be converted so no urobilinogen is reabsorbed into the blood and excreted by the kidney

154
Q

with total obstruction of bile flow the test for urobilinogen in the urine is

A

completely negative

155
Q

serum transaminase measurements reflect

A

hepatocellular integrity

156
Q

tests that measure the liver’s synthetic function include

A

serum albumin, PT/INR, cholesterol, pseudocholinesterase

157
Q

liver abnormalities are typically divided into

A 
parenchymal disorders (hepatocellular dysfunction)
obstructive disorders (biliary excretion)
158
Q

normal total bilirubin

A

< 1.5 mg/dL

159
Q

what does the total bilirubin reflect?

A

balance between production and biliary excretion

160
Q

a predominately conjugated hyperbilirubinemia is associated with

A

an increased urobilinogen and reflect intrahepatic cholestasis, extrahepatic biliary obstruction which may lead to hepatocellular dysfunction

161
Q

a primarily unconjugated hyperbilirubinemia may be seen with

A

hemolysis or with congenital or acquired defects in bilirubin conjugation

162
Q

serum aminotransferases are

A

enzymes released in the circulation as a result of hepatocellular injury

163
Q

what are two commonly measured serum aminotransferases?

A

AST/ALT

164
Q

which serum aminotransferase is more specific?

A

ALT (primarily located in the liver)

165
Q

Alkaline phosphatase is produced by the ____ and excreted into the ___

A

liver, bone, small bowel, kidneys, and placenta; bile

166
Q

most of the circulating alk phos comes from ___

A

bone

167
Q

in the presence of biliary obstruction alk phos

A

is synthesized more and released into the circulation

168
Q

serum albumin has a ___ half life

A

long half life so its value may initially be normal with acute liver disease

169
Q

low serum albumin levels are indicative of

A

chronic liver disease, acute stress, malnutrition

170
Q

What can cause hypoalbuminemia?

A

increased loss in urine (nephrotic syndrome) and in the GI tract (enteropathy with protein loss)

171
Q

increased NH3 in the blood usually reflects disruption of

A

hepatic urea synthesis

172
Q

PT measures the activity of

A

fibrinogen, factor II, V, VII, X

173
Q

factor VII has a ____ half life

A

short half life so PT is useful in evaluating hepatic synthetic function of patients with acute or chronic liver disease

174
Q

if the PT doesn’t correct after IV vitamin K

A

severe liver disease is likely present

175
Q

how much time does it take for vitamin K to correct?

A

24 hours

176
Q

pre - hepatic classification

A

bilirubin overload/ increased unconjugated bilirubin

177
Q

causes of pre-hepatic dysfunction

A

hemolysis, hematoma reabsorption, bilirubin overload from whole blood (massive transfusion)

178
Q

intra-hepatic classification

A

parenchymal/hepatocellular dysfunction

179
Q

What lab values are affected by intra-hepatic dysfunction?

A

conjugated bilirubin, aminotransferase enzymes, PT (prolonged), albumin (decreased)

180
Q

what causes intra-hepatic dysfunction?

A

viruses, drugs, sepsis, arterial hypoxemia, congestive heart failure, cirrhosis

181
Q

post-hepatic classification

A

cholestasis (obstruction)

182
Q

what lab values are affected by post-hepatic dysfunction?

A

conjugated bilirubin, alk phos

183
Q

what causes post-hepatic dysfunction?

A

stones, cancer, sepsis

184
Q

how does general and regional anesthesia affect hepatic blood flow?

A

decreases it due to direct and indirect effects of anesthetic agents themselves, type of ventilation, and surgical procedure

185
Q

which volatile agent causes the greatest decrease in portal blood flow?

A

halothane

186
Q

which volatile agent is the agent of choice for hepatic disease?

A

isoflurane

187
Q

hypoxemia produces

A

increased SNS stimulation and decrease in hepatic blood flow

188
Q

surgical procedures on or near the liver can

A

decrease hepatic blood flow by 60% from SNS activation, autoregulation, and direct compression of vessels

189
Q

drugs that decrease hepatic blood flow

A

beta adrenergic blockers, alpha 1 agonists, vasopressin

190
Q

endocrine stress response secondary to fasting and surgical stress results in

A

increased circulating levels of catecholamines, glucagon, cortisol

191
Q

the endocrine stress response can be at least partially blunted by

A

regional anesthesia, deep general anesthesia, pharmacological block of the SNS

192
Q

all opioids can potentially cause

A

spasm of the sphincter of Oddi and increases biliary pressure

193
Q

which opioids cause the most “spasm” of the sphincter of oddi

A

the phenylpiperdines - fentanyl, sufentanil, alfentanil, remifentanil

194
Q

IV opioids can induce ___ or result in ____ cholangiograms

A

biliary colic or result in false positive cholangiograms

195
Q

persistent abnormalities in liver function test may be indicative of

A

viral hepatitis, sepsis, idiosyncratic drug reaction, surgical complications

196
Q

the most common cause of postoperative jaundice is

A

over production of bilirubin d/t reabsorption of a large hematoma or RBC breakdown following transfusion

197
Q

hepatitis has been associated with

A

methoxyflurane, enflurane, isoflurane, halothane

198
Q

potential mechanisms for halothane hepatitis

A

formation of hepatotoxic metabolites, immune hypersensitivity

199
Q

how much of halothane is metabolized?

A

20%

200
Q

how much of sevoflurane is metabolized?

A

1%

201
Q

halothane hepatitis is a diagnosis of

A

exclusion

202
Q

risk factors associated with halothane hepatitis

A

middle age, obesity, females, repeat exposure (within 28 days)

N935 Advanced Pathophysiology (15 decks)

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