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APEX > Unit 10 - Liver/Gallbladder > Flashcards

Unit 10 - Liver/Gallbladder Flashcards

1
Q

structure responsible for eliminating bacteria from the liver

A

Kupffer cells

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2
Q

functional unit of the liver

A

acinus

otherwise known as the liver lobule

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3
Q

functional unit of the liver

A

acinus

otherwise known as the liver lobule

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4
Q

where do sinusoids receive blood flow

A

hepatic artery
portal vein

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5
Q

where are Kupffer cells located

A

in sinusoids

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6
Q

collect bile produced by hepatocytes

A

bile canaliculi

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7
Q

SNS innervation of the liver

A

T3-T11

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8
Q

how are hepatocytes organized in acinus

A

in zones according to proximity to portal triad & central vein

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9
Q

what part of acinus are O2 and nutrient gradients the highest

A

zone 1
lowest in zone 3

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10
Q

what part of acinus is most susceptible to injury

A

zone 3

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11
Q

where in the acinus is the highest concentration of CYP450 enzymes

A

zone 3

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12
Q

how is bile produced

A

hepatocytes

stored in gallbladder

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13
Q

path of bile to duodenum

A

canniculi → bile duct → common hepatic duct → common bile duct → ampulla of Vater → duodenum

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14
Q

3 Key Functions of Bile:

A

1) Absorption of fat and fat-soluble vitamins (AEDK)
2) Excretory pathway for bilirubin and products of metabolism
3) Alkalinization of duodenum

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15
Q

where is Cholecystokinin produced

A

duodenum

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16
Q

how is CCK production stimulated

A

Eating fat and protein increases release

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17
Q

effect of CCK release

A

stimulates gallbladder contraction and ↑ flow of bile into duodenum

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18
Q

function of space of Disse

A

Lymph and proteins drain into before emptying into lymphatic duct

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19
Q

organ responsible for about ½ of lymph production in the body

A

liver

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20
Q

how much CO does liver receive

A

~30% of CO (1500 mL/min)

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21
Q

blood supply to liver

A

Dual blood supply from portal vein and hepatic artery

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22
Q

liver blood flow and O2 supply from portal vein

A

75% blood flow, 50% O2 supply

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23
Q

liver blood flow and O2 supply from hepatic artery

A

25% blood flow, 50% O2 supply

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24
Q

how does splanchnic vascular resistance affect portal vein blood flow

A

↑ splanchnic vascular resistance = ↓ portal vein blood flow (SNS stim, pain, hypoxia, hypercarbia)

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25
Q

Portal Perfusion Pressure =

A

Portal Vein Pressure – Hepatic Vein Pressure

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26
Q

portal vein and sinusoid pressure in portal HTN

A

portal vein: > 20-30 mmHg
sinusoid: > 5 mmHg

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27
Q

normal portal vein and sinusoid pressure

A

portal vein: 7-10 mmHg
sinusoid: 0 mmHg

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28
Q

physiologic consequences of portal hypertension

A
  • esophageal varices, hemorrhage
  • ascites
  • spider angiomas
  • hemorrhoids
  • encephalopathy
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29
Q

compensation for reduced portal vein flow

A

hepatic arterial buffer response compensates by increasing flow through hepatic artery

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30
Q

why are pts with severe liver disease at increased risk for inadequate hepatic blood flow

A

Severe liver disease abolishes the hepatic arterial buffer response

portal vein flow is not autoregulated (and hepatic arterial flow can’t r

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30
Q

why are pts with severe liver disease at increased risk for inadequate hepatic blood flow

A

Severe liver disease abolishes the hepatic arterial buffer response

portal vein flow is not autoregulated (and hepatic arterial flow can’t r

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31
Q

how does anesthesia affect liver blood flow

A

Both GA & neuraxial anesthesia reduce MAP and CO = dose-dependent ↓ in liver blood flow

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32
Q

how does propranolol affect liver blood flow

A

↓ CO and increases splanchnic vascular resistance
(hepatic artery constriction)

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33
Q

how do intraabd surgeries affect liver blood flow

A

reduce d/t retraction and release of vasoactive substances

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34
Q

what 2 major blood vessels supply blood to the liver

A
  1. hepatic artery
  2. portal vein
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35
Q

celiac artery provides blood flow to which 3 organs

A
  1. liver
  2. spleen
  3. stomach
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36
Q

superior mesenteric artery provides blood flow to which 3 organs

A
  1. pancreas
  2. small intestine
  3. colon
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37
Q

1 organ that receives blood flow from inferior mesenteric artery

A

colon

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38
Q

4 examples of things that increase splanchnic vascular resistance

A
  1. SNS stim
  2. hypoxia
  3. pain
  4. propranolol
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39
Q

why is PT an early indicator of synthetic dysfunction

A

factor 7 has the shortest half life of all procoagulants

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40
Q

vitamin K dependent clotting factors

A

factors 2, 7, 9, 10

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41
Q

The absorption of vitamin K is dependent on:

A

bile in the gut

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42
Q

where is alpha-1 acid glycoprotein produced

A

liver
(hepatocytes)

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43
Q

where is von willebrand factor produced

A

vascular endothelial cells

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44
Q

where is factor 3 produced

A

vascular endothelial cells

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45
Q

where is factor 8 produced

A

liver sinusoidal cells and endothelial cells

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46
Q

the liver produces all plasma proteins except:

A

immunoglobulins

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47
Q

function of thrombopoietin

A

stim plt production

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48
Q

most abundant plasma protein

A

albumin

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49
Q

why are pts with liver failure at increased risk of hypoglycemia

A

Liver is an important regulator of serum glucose & clears insulin from circulation

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50
Q

body’s compensation for hyperglycemia

A
  • insulin released from pancreatic beta cells (glycogenesis)
  • glucose converted to glycogen for storage
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51
Q

body’s response to hypoglycemia

A
  • release of glucagon from pancreatic alpha cells & epi from adrenal medulla (glycogenolysis & gluconeogenesis)
  • glycogen from storage and non-carbohydrates (amino acids, pyruvate, lactate, glycerol) turned to glucose
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52
Q

what is amino acid deamination

A

allows the body to convert proteins to carbohydrates and fats.
Some of these are utilized in the Krebs cycle to produce ATP

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53
Q

how is urea eliminated from the body

A
  • liver converts ammonia to urea
  • urea is eliminated by kidneys
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54
Q

MOA of hepatic encephalopathy

A

Failure to clear ammonia (hepatic failure or portosystemic shunting)

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55
Q

blood reservoir for acidic drugs

A

albumin

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56
Q

blood reservoir for basic drugs

A

alpha 1 acid glycoprotein

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57
Q

erythrocyte life cycle

A

120 days

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58
Q

where are old RBCs broken down

A

by the reticuloendothelial cells in the spleen

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59
Q

byproduct of hgb metabolism

A

bilirubin

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60
Q

how is unconjugated bilirubin transported to liver

A

bound to albumin

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61
Q

how is unconjugated bilirubin excreted

A
  • lipophilic - transported to liver bound to albumin
  • liver conjugates with glucuronic acid - increases water solubility
  • conjugated bilirubin excreted into bile
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62
Q

how is conjugated bilirubin metabolized & eliminated

A

by intestinal bacteria
eliminated in stool

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63
Q

normal PT values

A

12-14 seconds

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64
Q

LFT very sensitive for acute injury

A

PT

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65
Q

how does vitamin K deficiency affect PT

A

prolongs

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66
Q

normal value for albumin

A

3.5-5 g/dL

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67
Q

half life of albumin

A

21days
poor indicator of acute liver injury

poor specificity for liver disease

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68
Q

causes of decreased albumin level

A

impaired synthesis or ↑ consumption

Conditions that ↓: infection, nephrotic syndrome, malnutrition, malignancy, burns

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69
Q

coagulation factors NOT synthesized in liver

A

vWF
factor 3
factor 4

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70
Q

what is glycogenesis

A

glucose stored as glycogen

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71
Q

what is glycogenolysis

A

glycogen cleaved into glucose

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72
Q

gluconeogenesis

A

glucose created from non-carb sources

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73
Q

what does marked elevation of both AST & ALT indicate

A

hepatitis

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74
Q

AST/ALT ratio > 2 suggests:

A

cirrhosis, alcoholic liver disease

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75
Q

normal values for AST & ALT

A

AST: 10-40 units/L
ALT: 10-50 units/L

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76
Q

LFTs that assess synthetic function

A

PT, albumin

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77
Q

LFTs that assess hepatocellular injury

A

AST, ALT

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78
Q

LFTs that assess hepatic clearance

A

bilirubin

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79
Q

LFTs that assess biliary tract obstruction

A

Alkaline phosphatase
Y Glutamyl transpeptidase
5’-Nucleotidase

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80
Q

most specific indicator of biliary obstruction

A

5’-NT

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81
Q

normal values:

Alkaline phosphatase
Y Glutamyl transpeptidase
5’-Nucleotidase

A

Alkaline phosphatase: 45-115 units/L
Y Glutamyl transpeptidase: 0-30 units/L
5’-Nucleotidase : 0-11 units/L

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82
Q

albumin levels assoc. with hepatocellular injury

A

acute injury: no change
chronic: decreased

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83
Q

causes of prehepatic liver injury

A

Hemolysis
Hematoma reabsorption

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84
Q

causes of hepatocellular injury

A

Cirrhosis
Alcohol abuse
Drugs
Viral infection
Sepsis
Hypoxemia

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85
Q

causes of cholestatic liver injury

A

Biliary tract obstruction
Sepsis

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86
Q

what aspect of hepatic function is assessed by alkaline phosphatase

A

cholestatic
(biliary duct obstruction)

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87
Q

Most common cause of liver cancer

A

hepatitis

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88
Q

most common indicator for liver transplantation in adults

A

hepatitis

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89
Q

etiologies of hepatitis

A

viruses, hepatotoxins, and autoimmune responses

also herpes simplex, CMV, Epstein-Barr

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90
Q

how does hepatitis A typically present

A

usually silent for 1-2 weeks after infection

then malaise, N/V, jaundice that generally last 2-12 weeks

91
Q

transmission of hepatitis A

A

oral-fecal

92
Q

serum markers of hepatitis A

A

early = IgM
late = IgG

93
Q

hepatitis viruses assoc with cirrhosis and hepatocellular carcinoma

A

B, C

**B: **adults: 1-5%
children: 80-90%
C: up to 75%

94
Q

transmission of hepatitis B

A

percutaneous
sexual contact

95
Q

serum markers of hepatitis B

A

HBsAg
Anti-HBcAg

96
Q

transmission of hepatitis C

A

percutaneous

97
Q

transmission of hepatitis D

A

percutaneous

98
Q

serum markers of hep C

A

anti-HCV (1.5-9 months)

99
Q

hep C viruses that can be transmitted via blood

A

B, C

100
Q

co-infection that occurs with hep B

A

hepatitis D

101
Q

etiologies of drug-induced hepatitis

A
  • tylenol
  • halothane
  • alcohol
102
Q

most common cause of acute liver failure in US

A

tylenol

103
Q

substrate for many phase 2 conjugation reactions

A

glutathione

104
Q

function of glutathione in phase 2 conjugation reactions

A

increases a substance’s water solubility so that the substance can be excreted in the bile or by the kidney

105
Q

patho of liver toxicity with tylenol overdose

A
  • toxic metabolite = NAPQI
  • NAPQI normally conjugated with glutathione to nontoxic form
  • OD consumes liver’s glutathione supply
  • NAPQI concentration increases, leads to hepatocellular injury
106
Q

treatment of tylenol OD

A

mucomyst (N-acetylcysteine) within 8 hours of OD

107
Q

MOA of halothane hepatitis

A
  • liver metabolizes to TFA
  • halothane up to 20% metabolism produces large amount of TFA

believed to be immune-mediated reaction r/t TFA

107
Q

MOA of halothane hepatitis

A
  • liver metabolizes to TFA
  • halothane up to 20% metabolism produces large amount of TFA

believed to be immune-mediated reaction r/t TFA

108
Q

MOA of halothane hepatitis

A
  • liver metabolizes to TFA
  • halothane up to 20% metabolism produces large amount of TFA

believed to be immune-mediated reaction r/t TFA

109
Q

risk factors for halothane hepatitis

A
  • Age > 40
  • female gender
  • > 2 exposures
  • genetics
  • obesity
  • CYP2E1 induction (alcohol, isoniazid, phenobarbital)
110
Q

most common cause of drug-induced hepatitis

A

ETOH

111
Q

MOA of alcohol-induced hepatitis

A

ETOH impairs fatty acid metabolism, which causes fat accumulation in the liver and leads to hepatomegaly

112
Q

2 most common causes of chronic hepatitis

A
  1. alcohol
  2. hep C
113
Q

how is chronic hepatitis characterized

A

hepatic inflammation that exceeds 6 months

114
Q

how is chronic hepatitis diagnosed

A

Increased liver enzymes and bilirubin + histologic evidence of liver inflammation

115
Q

s/s chronic hepatitis

A
  • jaundice
  • fatigue
  • thrombocytopenia
  • glomerulonephritis
  • neuropathy
  • arthritis
  • myocarditis
116
Q

propranolol decreases portal pressure by what 2 mechanisms

A
  1. decreased CO (beta-1)
  2. splanchnic vasoconstriction (beta-2)
117
Q

AIs for hepatitis

A

maintain hepatic blood flow
* avoid PEEP
* liberal IVF
* normocapnia
* avoid hepatotoxic drugs/CYP450 inhibitors

118
Q

drugs to avoid in pts with hepatitis

A

Hepatotoxic Drugs or those that Inhibit CYP450
* Acetaminophen
* Halothane
* Amiodarone
* Antibiotics: PCN, tetracycline, and sulfonamides

119
Q

MAC considerations for EOTH

A

acute intoxication = decreased MAC

chronic user, not acutely intoxicated = increased MAC

120
Q

how does alcoholism affect benzos

A

potentiates GABA
increased effect of benzos

121
Q

receptors affected by ETOH

A

potentiates GABA
inhibits NMDA

122
Q

early s/s alcohol withdrawal syndrome

A

Tremors and disordered perception (hallucinations, nightmares)

123
Q

when do s/s alcohol withdrawal begin

A

6-8 hrs after the BAC returns to near normal

(peaks at 24 - 36 hours)

124
Q

late s/s alcohol withdrawal

A
  • Increased SNS activity (tachycardia, hypertension, dysrhythmias)
  • N/V
  • insomnia
  • confusion
  • agitation
125
Q

treatment of alcohol withdrawal

A
  • Alcohol
  • beta-blockers
  • alpha-2 agonists
126
Q

typical onset of delirium tremens after an alcoholic stops drinking

A

2 - 4 days without alcohol

127
Q

s/s Delirium tremens

A
  • Grand mal seizures
  • tachycardia
  • hyper- or hypotension
  • combativeness
128
Q

delirium tremens treatment

A

Diazepam (or another benzo) and beta-blockers

129
Q

what vitamin deficiency causes Wernicke-Korsakoff syndrome

A

B1

thiamine

130
Q

what is Wernicke-Korsakoff syndrome

A

characterized by a loss of neurons in the cerebellum brought on by thiamine deficiency

131
Q

treatment for alcoholics in recovery

A
  • Disulfiram
  • hepatotoxic and inhibits dopamine beta-hydroxylase (NE synthesis) = hypotension
132
Q

characteristics of cirrhosis

A
  • cell death
  • healthy hepatic tissue is replaced by nodules and fibrotic tissue
  • Reduces # of functional hepatocytes & sinusoids
133
Q

etiologies of cirrhosis

A
  • NAFLD
  • ETOH abuse
  • alpha 1 antitrypsin deficiency
  • biliary obstruction
  • chronic hepatitis
  • R heart failure
  • hemochromatosis
  • wilson disease
134
Q

2 genetic causes of cirrhosis

A
  • alpha 1 antitrypsin deficiency
  • wilson disease
135
Q

why do pts with cirrhosis develop portal HTN

A
  • Blood can’t flow past nodules
  • increased hepatic vascular resistance d/t less blood vessels passing through liver
136
Q

what defines end stage liver disease

A

End-stage liver disease exists when the liver is unable to carry out its synthetic, metabolic, and clearance functions

137
Q

MELD and Child-Pugh scores that increase risk of periop M&M

A

MELD > 15
Child-Pugh 10-15

138
Q

what is the MELD score used for

A
  • Predicts 90-day mortality in patients with ESLD
  • More commonly used for patients with end-stage liver disease who require transplantation
139
Q

what does the MELD score examine

A

3 factors of hepatic function: bilirubin, INR, and serum creatinine

140
Q

MELD Scores:
low risk
intermediate risk
high risk

A
  • Low risk = < 10
  • Intermediate risk = 10-15
  • High risk = > 15
141
Q

what does the Child-Pugh score examine

A

five factors of hepatic function: albumin, PT, bilirubin, ascites, and encephalopathy

142
Q

Child-Pugh score:
class A
class b
class C

A
  • Class A (5-6 points) = 10% risk of perioperative mortality
  • Class B (7-9 points) = 30% risk of perioperative mortality
  • Class C (10-15 points) = 80% risk of perioperative mortality
143
Q

child-pugh class score that should be managed medically before surgery until hepatic function improves

A

class C

144
Q

circulation changes in cirrhosis

A

hyperdynamic circulation
* decreased SVR and BP
* increased CO
* increased blood volume (inc RAAS activation)
* R-L shunting
* increased SvO2

145
Q

affects of ascites with cirrhosis

A

↓ Oncotic pressure
↓ Protein binding
↑ Vd

Drainage = hypotension

146
Q

affects of ascites with cirrhosis

A

↓ Oncotic pressure
↓ Protein binding
↑ Vd

Drainage = hypotension

147
Q

affects of ascites with cirrhosis

A

↓ Oncotic pressure
↓ Protein binding
↑ Vd

Drainage = hypotension

148
Q

respiratory effects of cirrhosis

A

Restrictive defect
Respiratory alkalosis
Hepatopulmonary synd.
Portopulmonary HTN

149
Q

what causes restrictive defect in cirrhosis

A

Ascites & pulmonary effusion = ↓ compliance & atelectasis

150
Q

why do pts with cirrhosis have resp alkalosis

A

hyperventilation to compensate for hypoxemia

151
Q

what is hepatopulmonary syndrome

A

complication of cirrhosis
Pulmonary vasodilation = R-L shunt = hypoxemia

152
Q

what defines portopulmonary HTN in cirrhosis

A

PAP > 25 mmHg in setting of portal HTN

153
Q

how is increased ammonia treated

A

lactulose, abx, ↓ protein intake

154
Q

MOA of hepatic encephalopathy in cirrhosis

A

↓ hepatic clearance = ↑ ammonia = cerebral edema = ↑ ICP

Bleeding = reabsorption = ↑ nitrogen load = ↑ ammonia

155
Q

mechanism of thrombocytopenia in cirrhosis

A
  • splenomegaly = increased platelet consumption
  • decreased thrombopoietin and bone marrow suppression
156
Q

renal effects of cirrhosis

A

decreased GFR
* renal hypoperfusion
* dilutional hyponatremia
* renal failure

157
Q

definitive treatment of hepatorenal syndrome

A

liver tx

158
Q

why do pts with cirrhosis have decreased CaO2

A

hemorrhage, folic acid deficiency, hemolysis, bone marrow suppression

159
Q

what is the TIPS procedure

A

Bypasses a portion of the hepatic circulation by shunting blood from the portal vein (hepatic inflow vessel) to the hepatic vein (hepatic outflow vessel)

160
Q

effects of TIPS procedure

A

reduces portal pressure and minimizes back pressure on the splanchnic organs

reduces the likelihood of bleeding from esophageal varices and reduces the volume of ascites

161
Q

effects of TIPS procedure

A

reduces portal pressure and minimizes back pressure on the splanchnic organs

reduces the likelihood of bleeding from esophageal varices and reduces the volume of ascites

162
Q

effects of TIPS procedure

A

reduces portal pressure and minimizes back pressure on the splanchnic organs

reduces the likelihood of bleeding from esophageal varices and reduces the volume of ascites

163
Q

significant risk during the TIPS procedure

A

hemorrhage

164
Q

temporary treatment. of hepatorenal syndrome

A

TIPS procedure

165
Q

indications for liver transplant

A

hep C (most common)
alcoholic liver disease, malignancy

166
Q

can TEE be used during liver transplant

A

reasonably safe so long as transgastric views are avoided

167
Q

when does pre-anhepatic stage begin and end

A
  • Begins with surgical incision
  • ends with cross clamping of portal vein, hepatic artery, and IVC/hepatic vein
168
Q

lab used to guide replacement therapy in liver transplant

A

TEG or ROTEM

169
Q

lab goals in pre-anhepatic stage of liver tx

A
  • Hgb > 7 g/dL
  • platelets > 40,000
  • fibrinogen > 100 mg/dL
  • and MA (TEG) >45
170
Q

causes of CV instability in pre-anhepatic stage of liver tx

A
  • drainage of ascites
  • compression of vascular structures
  • ongoing blood loss
171
Q

how can biliary obstruction contribute to cirrhosis

A

inflammation & tissue destruction

172
Q

how can chronic hepatitis contribute to cirrhosis

A

inflammation & tissue destruction

173
Q

how can right sided heart failure contribute to cirrhosis

A

increased hepatic vascular resistance

174
Q

which stage of liver tx is assoc with regurgitation and aspiration

A

pre-anhepatic stage

175
Q

stage of liver tx assoc with hyperkalemia

A

neohepatic stage

176
Q

stage of liver tx assoc. with profound decrease in CO

A

anhepatic stage

177
Q

stage of liver tx with no liver function

A

anhepatic

178
Q

when does the anhepatic stage of liver tx begin and end

A

Begins with removal of native liver & ends with implantation of donor liver

179
Q

technique used during anhepatic stage of liver tx assoc with reduced operating and warm ischemic time

A

piggyback technique

180
Q

technique used in anhepatic stage assoc with significantly reduced preload

A

bicaval clamp

181
Q

where is the bicaval clamp placed when used in liver tx

A

to IVC above/below liver

full obstruction of IVC flow

182
Q

where is the bicaval clamp placed when used in liver tx

A

to IVC above/below liver

full obstruction of IVC flow

183
Q

option if patient doesn’t tolerate piggyback technique during liver tx

A

VV bypass

184
Q

liver tx:
outflow cannulas (towards pump)

A

femoral vein = systemic blood flow
portal vein = splanchnic blood flow

185
Q

liver tx with VV bypass:
cannula with return to body

A

axillary vein (blood returns to IVC - heart)

186
Q

benefits of piggyback technique over bicaval clamp in liver tx

A
  • Reduced operating and warm ischemic time
  • Fewer blood products required
  • less preload reduction vs. bicaval clamp
187
Q

complications assoc with VV bypass in liver tx

A

air embolism, thromboembolism, decannulation

188
Q

common problems during anhepatic stage of liver tx

A
  • worsening coagulopathy
  • ongoing blood loss
  • lactic acidosis
  • hypoglycemia
189
Q

how often should labs be checked during anhepatic stage of liver tx

A

q 15-30 min

190
Q

when does warm ischemic time begin in liver tx

A

begins when donor liver is removed from ice and ends when reperfused

191
Q

max warm ischemic time in liver tx

A

should not exceed 30-60 minutes

192
Q

6 methods to treat increased K+ with reperfusion after liver tx

A
  • hyperventilation
  • D50 + insulin
  • bicarb
  • albuterol
  • Lasix
  • CVVHD
193
Q

when does the neohepatic stage of liver tx begin and end

A

Begins with reperfusion of donor liver & ends with biliary anastomosis (or transport to ICU)

194
Q

objectives of neohepatic stage of liver tx

A
  • reperfusion of donor liver
  • anastomosis of hepatic artery
  • anastomosis of biliary structures
195
Q

key complications of neohepatic stage of liver tx

A
  • hyperkalemia
  • hypocalcemia
  • cytokine release
  • lactic acidosis
  • embolic debris
  • hypovolemia
  • systemic hypotension (decreased SVR)
  • pulmonary hypertension (increased PVR)
  • hypothermia
  • cardiac arrest
196
Q

CVP goal in neohepatic stage of liver tx

A

Avoid an elevated CVP, as this will cause congestion in the graft

197
Q

findings that suggest good graft function in neohepatic stage of liver tx

A
  • stabilization of serum glucose and acid-base status
  • prompt return to normothermia
198
Q

how is post-reperfusion syndrome defined

A

systemic hypotension > 30% below baseline for at least 1 minute during the first 5 minutes of reperfusion of donor liver

199
Q

incidence of post reperfusion syndrome after liver tx

A

common (incidence 10-60%)

200
Q

treatment of post-reperfusion syndrome in liver tx

A

vasopressors, correct hyperkalemia/hypocalcemia, correct acid-base

201
Q

consequences of crystalloid resuscitation in neohepatic stage of liver tx

A

dilutional coagulopathy
thrombocytopenia

202
Q

consequences of large blood volume admin in neohepatic stage of liver tx

A
  • lactic acidosis
  • hyperkalemia
  • hypocalcemia

r/t citrate toxicity

203
Q

s/s poorly functioning graft after liver tx

A

continued HD instability and lack of bile output

204
Q

can epidural analgesia be used in liver tx

A

contraindicated because of the patient’s coagulation status

205
Q

most common gallbladder diseases are caused by:

A

obstruction or inflammation

206
Q

s/s biliary stone obstruction in cystic duct

A
  • gallbladder distension
  • edema
  • risk of perforation
  • jaundice
207
Q

s/s biliary stone obstruction in common bile duct

A
  • cholecystitis
  • jaundice
  • pancreatitis
  • peritonitis
208
Q

factors that increase incidence of biliary stones

A
  • obesity
  • aging
  • rapid weight loss
  • pregnancy
  • women > men
209
Q

s/s biliary stones

A
  • Leukocytosis
  • fever
  • RUQ pain
  • Murphy’s sign (pain worse with inspiration)
210
Q

biliary pathology of biliary stones
(LFTs)

A
  • ↑alkaline phosphatase
  • ↑ conjugated bilirubin
  • ↑ amylase
  • ↑ Y glutamyl transpeptidase
  • ↑ 5’-nucleotidase
211
Q

why does prolonged NPO time increase likelihood of gallstones

A

lack of CCK release contributes to biliary stasis

212
Q

treatment for cholecystitis

A

cholecystectomy

(Cholecystitis = gallbladder inflammation)

213
Q

treatment for cholelithiases

A

cholecystectomy

(cholelithiases = gallstones)

214
Q

treatment of Choledocholithiasis

A

ERCP

(Choledocholithiasis = stones in common bile duct)

215
Q

drugs that relax the sphincter of Oddi and decrease biliary pressure

A
  • glucagon
  • glyco
  • atropine
  • naloxone
  • nitroglycerin

some debate that octreotide can cause

216
Q

consequences of sphincter of Oddi spasm

A

**increased biliary pressure
**
can cause biliary colic and false positive of intraop cholangiogram

217
Q

patho of biliary stones

A

obstructive defect that impedes flow of bile & pancreatic enzymes

218
Q

what 2 hepatic structures converge at ampulla of Vater

A
  • pancreatic duct
  • common bile duct
219
Q

location of portal vein

A

between splanchnic circulation and liver

220
Q

why does blood that arrives to the liver via portal vein have a lower O2 content

A

this blood has already oxygenated the splanchnic organs
(spleen, intestine, stomach, gallbladder, pancreas)

221
Q

receptors that line the hepatic artery

A

alpha 1
beta 2

222
Q

receptors that line portal vein

A

alpha 1

223
Q

which types of hepatitis are most likely to be contracted during blood transfusion

A

A, C

224
Q

management of esophageal varices

A
  • decrease hepatic venous pressure to < 10 mmHg
  • TIPS procedure
  • propranolol
  • moderate fluid resuscitation
  • balloon tamponade
225
Q

drugs that relax the sphincter of Oddi

A
  • glucagon
  • glycopyrrolate
  • atropine
  • narcan
  • nitro

APEX (54 decks)

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