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APEX-KLE > KLE-Liver > Flashcards

KLE-Liver Flashcards

1
Q

What are the ligaments that attach the liver to the abdominal wall

A

Falciform

Round

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2
Q

What are the ligaments that attach the liver to the diaphragm

A

Coronary ligament

Triangular ligament

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3
Q

What is the functional unit of the liver

A

Lobule

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4
Q

Describe the lobule structure

A

Hexagonal w/ central vein and portal veins at 6 corners

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5
Q

What are the liver components for the following:
Arterioles
Capillaries
Venules

A 
Arterioles= terminal branches of 
-hepatic artery
-Portal vein
Capillaries = sinusoids
Venules = central vein
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6
Q

What are the 3 zones of the acinus

A

divisions that correspond to the distance from arterial O2 supply
Zone 1 = closest, most oxygenated
Zone 2 = middle, middle oxygenation
Zone 3 = furthest, least oxygenated

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7
Q

What is significant about acinus zone 3

A

Most susceptible to ischemic injury

Contains highest concentration of CYP450 enzymes

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8
Q

What are Kupffer cells

A
  1. Part of the reticuloendothelial system

2. Remove bacteria before vena cava

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9
Q

What structure drains bile

A

Canaliculi

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10
Q

Where is bile produced and stored

A 
Produced = hepatocyte
Stored = gallbladder
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11
Q

How is bile drained to the gallbladder

A
  1. Canaliculi drain bile into bile duct
  2. Bile ducts converge to form hepatic duct
  3. Hepatic duct joined by cystic and pancreatic duct
  4. Empties into duodenum
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12
Q

What structure controls the flow of bile released from common hepatic duct

A

Sphincter of Oddi

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13
Q

What medication can increase biliary pressure and how

A

Opioids contract the sphincter of Oddi

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14
Q

What effect do opioids have on the common hepatic bile duct

A

Causes contraction of the sphincter of Oddi, increasing biliary pressure

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15
Q

What are 3 functions of bile

A
  1. Absorption of fat and fat-soluble vitamins (DAKE)
  2. Excretory pathway for bilirubin and products of metabolism
  3. Alkalization of duodenum
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16
Q

What vitamins are absorbed by bile

A

Fat-soluble vitamins = DAKE

Vitamins D, A, K, E

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17
Q

What is cholecystokinin (CCK)

A

it stimulates the gallbladder to contract increasing flow of bile into duodenum following fat and protein consumption

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18
Q

Where is cholecystokinin produced

A

duodenum

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19
Q

What is the lymphatic structure of the liver

A

Lymph and proteins drain into the space of Disse (between hepatocytes and sinusoids)
They then empty into lymphatic ducts

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20
Q

What organ is responsible for half of the lymph production in the body

A

Liver

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21
Q

What percent of CO and volume does the liver receive

A 
CO = 30% 
Volume = 1,500 mL/min
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22
Q

What percent of blood flow and O2 supply does the hepatic artery supply the liver

A

Blood flow = 25%

O2 supply = 50%

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23
Q

What percent of blood flow and O2 supply does the portal vein supply the liver

A

Blood flow = 75%

O2 supply = 50%

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24
Q

The hepatic artery is a branch of which artery

A

Celiac artery

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25
Q

How does splanchnic vascular resistance affect hepatic flow

A

Portal vein is a product of splanchnic circulation

Increased splanchnic vascular resistance reduces portal vein BF

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26
Q

What are examples of causes of decreased portal vein flow

A
  1. SNS stimulation
  2. Pain
  3. Hypoxia
  4. Hypercarbia
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27
Q

What is the equation of portal perfusion pressure

A

Portal perfusion pressure = portal vein pressure - hepatic vein pressure

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28
Q

What is the normal pressure for the following:
Portal vein
Sinusoid

A

Portal vein = 7-10 mmHg

Sinusoids = 0 mmHg

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29
Q

What are diagnostic pressure for portal HTN at the following sites:
Portal vein
Sinusoids

A

Portal vein = >20-30 mmHg

Sinusoids = >5 mmHg

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30
Q

How does the hepatic artery compensate for decreased portal vein flow

A

Washout of vasodilators (adenosine) increase hepatic artery flow

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31
Q

What is the equation for hepatic artery perfusion pressure

A

hepatic artery perfusion pressure = MAP - hepatic vein pressure

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32
Q

5 perioperative factors that reduce liver blood flow

A
  1. Increased splanchnic vascular resistance (SNS stim, pain)
  2. Factors increasing CVP (PPV, excess hydration)
  3. Some beta-blockers (propranolol)
  4. Intrabd procedures
  5. Laparoscopic surgery (pneumoperitoneum)
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33
Q

How does propranolol affect liver blood flow

A

reduces CO and increases splanchnic vascular resistance

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34
Q

The celiac artery provides blood flow to which 3 organs

A
  1. Liver
  2. Spleen
  3. Stomach
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35
Q

The superior mesenteric artery provides BF to which 3 organs

A
  1. Pancreas
  2. Small intestines
  3. Colon
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36
Q

What organ is supplied by the inferior mesenteric artery

A

colon

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37
Q

What is the liver responsible for synthesizing

A
  1. Coagulation proteins

2. Plasma proteins

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38
Q

What are 4 coagulation protein categories that the liver is responsible for synthesizing

A
  1. Procoagulants
  2. Anticoagulants
  3. Fibrinolytics
  4. Thrombopoietin
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39
Q

What procoagulants are NOT synthesized by the liver

A
  1. von Willebrand factor
  2. Factor 3
  3. Factor 4 (Ca++)
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40
Q

Where is factor 8 produced

A

Liver sinusoidal cells and endothelial cells (NOT hepatocytes)

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41
Q

Where are most protein coagulation factors produced

A

The hepatocytes of the liver

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42
Q

Vitamin K is required for synthesizing which factors

A

2, 7, 9, 10

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43
Q

What anticoagulant factors are synthesized in the liver

A
  1. Antithrombin

2. Proteins S, C, Z (vit K dependent)

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44
Q

What fibrinolytics and thrombopoietin factors are synthesized in the liver

A 
Fibrinolytics = plasminogen
Thrombopoietin = stimulates plt production
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45
Q

Which plasma protein is not produced by the liver

A

immunoglobulins

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46
Q

How does hepatic function affect protein binding of drugs

A

Protein synthesis is decreased, so drugs will have a higher Vd and free fraction

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47
Q

How is vascular oncotic pressure affected by liver dysfunction

A

Impaired protein synthesis reduces plasma proteins and ultimately vascular oncotic pressure

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48
Q

What are the metabolic responsibilities of the liver

A

Metabolism of

  1. CHO
  2. Proteins
  3. Lipids
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49
Q

What is the liver’s role in glucose and insulin regulation

A
  1. Utilizes glycogenesis and glycogenolysis to increase or decrease serum glucose
  2. Clears insulin from circulation
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50
Q

What is the liver’s response with hyperglycemia

A

Glycogenesis

Glucose => glycogen (storage)

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51
Q

What is the liver’s response to hypoglycemia

A

Glycogenolysis:
glycogen (storage) => glucose

Gluconeogenesis:
non-CHO => glucose (w/ AA, pyruvate, lactate, glycerol)

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52
Q

What does hyperglycemia stimulate the release of

A

insulin from pancreatic beta cells

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53
Q

What does hypoglycemia stimulate the release of

A

Glucagon from pancreatic alpha cells

Epi from adrenal medulla

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54
Q

How is protein processed by the liver

A
  1. AA deamination allows proteins conversion to CHO and fats
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55
Q

What is the result of protein metabolism

A

CHO and fats

Large quantities of ammonia

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56
Q

How is ammonia cleared

A

The liver converts it to urea which is eliminated by the kidneys

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57
Q

Metabolic processing of lipids by the liver

A
  1. Energy storage from triglycerides
  2. Energy release by beta-oxidation of fatty acids
  3. Synthesis of cholesterol, phospholipids, and lipoproteins
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58
Q

What is the process of bilirubin production

A

old hgb goes to spleen => turned to heme => becomes unconjugated bilirubin

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59
Q

How is bilirubin transported to the liver and from where

A

Unconjugated bilirubin is lipophilic and transported bound to albumin from spleen to liver

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60
Q

What does the liver do to unconjugated bilirubin

A

conjugates bilirubin to glucuronic acid, increasing water solubility

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61
Q

What is the ultimate fate of conjugated bilirubin

A

excretion into bile, metabolized by intestinal bacteria and elimination in stool

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62
Q

What liver function tests indicate synthetic function issues

A

PT

Albumin

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63
Q

What liver function tests indicate hepatocellular injury

A

AST

ALT

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64
Q

What liver function test indicates hepatic clearance effectiveness

A

Bilirubin

65
Q

What liver function tests indicates biliary duct obstruction

A
  1. Alkaline phosphatase
  2. Y glutamyl transpeptidase
  3. 5’-nucleotidase
66
Q

Which liver function test for synthetic function is very sensitive for acute hepatic injury

A

PT (half-life = 4-6 hrs)

67
Q

With which hepatocellular LFTs can hepatitis and cirrhosis be considered
Result interpretation

A
  1. Marked elevation of both = hepatitis

2. AST/ALT ratio >2 = cirrhosis or alcoholic liver disease

68
Q

What are confounding factors for elevated bilirubin

A

Hemolysis or hematoma absorption

69
Q

What is the most specific LFT for biliary obstruction

A

5’-nucleotidase

Bile duct obstructions increases systemic levels

70
Q

What are 3 categories of liver disease

A
  1. Prehepatic
  2. Hepatocellular injury
  3. Cholestatic
71
Q

Which LFTs are altered in prehepatic causes of liver dz

A
  1. unconjugated bilirubin increased
72
Q

Causes of prehepatic liver dz

A

hemolysis

hematoma absorption

73
Q

Which LFTs are altered in hepatocellular injury r/t liver dz

A
  1. bilirubin increased
  2. AST/ALT increased
  3. PT increased
  4. albumin dec chronic injury
  5. Alk phos increased
74
Q

What are 6 causes of liver dz r/t hepatocellular injury

A
  1. Cirrhosis
  2. Alcohol abuse
  3. Drugs
  4. Viral infxn
  5. Sepsis
  6. Hypoxemia
75
Q

Which 7 LFTs are altered in liver dz d/t cholestatic causes

A
  1. conj bili increased
  2. AST/ALT late inc
  3. PT late inc
  4. Albumin late dec
  5. Alk Phos always inc
  6. Y glutamyl transpeptidase inc
  7. 5’-nucleotidase
76
Q

What are causes of liver dz r/t cholestasis

A
  1. biliary tract obstruction

2. Sepsis

77
Q

Which hepatitis types cause cirrhosis

A

B and C

C most common

78
Q

When does drug-induced hepatitis typically present

A

2-6 weeks after insult

79
Q

What is the most common cause of acute liver failure

A

Acetaminophen

80
Q

How is acetaminophen metabolism affected by overdose

A

The OD consumes the liver’s supply of glutathione

Toxic metabolite concentration increases causing hepatocellular injury

81
Q

How is acetaminophen metabolized by the liver

A

The toxic metabolite N-acetyl-p-benzoquinoeimine is conjugated with glutathione increasing water solubility and a non-toxic compound

82
Q

What is the treatment for acetaminophen OD

A

N-acetylcysteine within 8 hours

83
Q

How does halothane cause hepatitis

A

20% is metabolized by the liver producing significant quantities of TFA
Hepatitis is an immune-mediated reaction to TFA

84
Q

What is chronic hepatitis

A

Inflammation that exceeds 6 months

Leads to destruction of hepatic parenchyma, cirrhosis, and ultimately causes failure

85
Q

What is the most common cause of chronic hepatitis

A

alcoholism

86
Q

How is chronic hepatitis diagnosed

A

Increased liver enzymes and bilirubin

Histologic evidence of liver inflammation

87
Q

What are 7 s/sx of chronic hepatitis

A
  1. Jaundice
  2. Fatigue
  3. Thrombocytopenia
  4. Glomerulonephritis
  5. Neuropathy
  6. Arthritis
  7. Myocarditis
88
Q

How does alcoholism contribute to liver disease

A

It impairs fatty acid metabolism causing fat accumulation in the liver and hepatomegaly

89
Q

What are 2 primary goals of anesthesia in liver failure pts

A
  1. Maintain hepatic BF

2. Avoid hepatotoxic drugs or inhibitors of CYP450

90
Q

6 methods to maintain hepatic flow during anesthesia

A
  1. Use iso or sevo
  2. Avoid halothane
  3. Avoid PEEP
  4. Ensure normocapnia
  5. Liberal IVF
  6. regional anesthesia ok if no coag defects
91
Q

What are 6 drugs to avoid in the liver dz pt that are hepatoxic

A
  1. Acetaminophen
  2. Halothane
  3. Amiodarone
  4. PCN
  5. Tetracycline
  6. Sulfonamides
92
Q

Why is NMJ monitoring important with liver dz

A
  1. Pseudocholinesterase activity may be decreased, prolonging succinylcholine
  2. Decreased rocuronium excretion
  3. Larger Vd
93
Q

What are 4 anesthetic considerations for alcoholism

A
  1. MAC is decreased in acutely intoxicated
  2. MAC increased in chronic etoh abuser
  3. Alcohol potentiates GABA increasing BZD effect
  4. Alcohol inhibits NMDA receptors
94
Q

Describe the aspiration risk of alcoholics

A
  1. Pharyngeal reflexes impaired by etoh

2. Assume acute intoxication = full stomach

95
Q

What are late s/sx of alcohol withdrawal

A
  1. increased SNS activity
  2. N/V
  3. Insomnia
  4. Confusion
  5. Agitation
96
Q

What are 3 treatments for early alcohol withdrawal

A
  1. Alcohol
  2. Beta-blockers
  3. alpha-2 agonists
97
Q

Treatment for delirium tremens

A

diazepam

beta-blocker

98
Q

What are deficiencies to consider in the alcoholic

A

Deficient vitamin B1 (thiamin) causing wernicke-korsakoff syndrome and loss of neurons in cerebellum

99
Q

What is a treatment for recovering alcoholics

Impact on liver

A 
Tx = hepatotoxic
Impact = hepatotoxic
100
Q

What is the pathology of cirrhosis

A

Cell death, where healthy hepatic tissue is replaced by nodules and fibrotic tissue reducing number of functional hepatocytes and sinusoids

101
Q

How does cirrhosis affect hepatic bf

A

blood can’t flow past the nodules causing increased vascular resistance
Leads to portal HTN
Pressure is then transmitted to splanchnic circulation

102
Q

How does the body compensate for portal HTN

A

Increased vascular resistance is partially offset by collateral vessels that bypass the liver
Portosystemic shunts

103
Q

What are the risks of postosystemic shunting

A

Blood bypasses the liver with drugs and toxins remaining in systemic circulation for longer

104
Q

What qualifies as end-stage liver disease

A

when the liver cannot carry out synthetic, metabolic, and clearance functions

105
Q

What is the MELD score

A

Predicts 90-day mortality in pts w/ ESLD

106
Q

What factors are used for the MELD score

A
  1. Bilirubin
  2. INR
  3. Serum Crt
107
Q

How does MELD scoring predict mortality

A

Low risk = <10
Intermediate risk = 10-15
High risk = >15

108
Q

What 5 factors are assessed with the modified child-pugh score

A
  1. Albumin
  2. PT
  3. Bilirubin
  4. Ascites
  5. Encephalopathy
109
Q

What are the classifications of the child-pugh scoring

A

Class A = 5-6 points = 10% mortality risk
Class B = 7-9 = 30% mortality risk
Class C = 10-15 = 80% mortality risk

110
Q

What are 5 reasons cirrhotic pts hyperdynamic

A
  1. dec SVR/BP => inc CO
  2. inc RAAS activation => inc volume
  3. inc peripheral BF (shunting) => inc SvO2
  4. dec vasopressor response
  5. Diastolic dysfunction
111
Q

What CV pathology is associated with portal HTN

A
  1. inc hepatic vascular resistance and backpressure
  2. esophageal varicies
  3. splenomegaly
112
Q

What are 4 effects of ascites

A
  1. dec oncotic pressure
  2. dec protein binding
  3. inc volume distribution
  4. drainage => HoTN
113
Q

What type of pulmonary defect is associated with cirrhosis

A

Restrictive

114
Q

Why do cirrhotic pts have restrictive pulmonary defects

A

Ascites and pulm effusion decrease compliance

115
Q

What acid-base imbalance is associated with cirrhosis

A

Respiratory alkalosis

d/t compensation for hypoxemia with hyperventilation

116
Q

How does hepatopulmonary syndrome affect pulmonary vasculature

A

Pulmonary vasodilation => intrapulmonary shunt (R to L) => hypoxemia

117
Q

How does cirrhosis affect airway pressure

A

PAP>25 mmHg in setting of portal HTN

118
Q

CNS effects of cirrhosis

A

Decreased hepatic clearance increase ammonia causing cerebral edema and ICP

119
Q

Treatment for increased ammonia

A

lactulose, abx, dec protein intake

120
Q

What are 3 autonomic effects of cirrhosis

A
  1. inc SNS
  2. inc RAAS
  3. ANS reflex dysfunction
121
Q

Renal effects of cirrhosis

A

dec GFR

122
Q

How does cirrhosis decrease GFR

A

By renal hypoperfusion and hepatorenal syndrome

123
Q

Result of decreased GFR from renal hypoperfusion

A

RAAS activation => Na+ and water retention

124
Q

Result of decreased GFR from hepatorenal syndrome

A

Renal failure

125
Q

How does splenomegaly affect coagulation status in cirrhosis

A

increases plt consumption

126
Q

What is the TIPS procedure

A

transjugular intrahepatic portosystemic shunt

bypasses a portion of hepatic circulation by shunting blood from portal vein to hepatic vein

Goal = reduce portal pressure and minimize back pressure

127
Q

What is the greatest risk with TIPS procedure

A

bleeding

128
Q

What are preoperative anesthetic considerations p/t liver transplant

A
  1. T&xmatch w/ plenty of blood
  2. Coagulopathies affecting invasive line placement
  3. TEE is safe w/ esophageal varices w/o transgastric views
  4. Avoid anxiolytic premed w/ encephalopathy
  5. Don’t correct hyponatremia rapidly
129
Q

What are the phases of transplant surgery

A
  1. pre-anhepatic
  2. anhepatic
  3. neohepatic
130
Q

What surgical objective occur during the pre-anhepatic phase

A
  1. Surgical incision
  2. mobilization of liver structures
  3. mobilization of vascular structures
  4. Isolation of bile duct
131
Q

What are surgical objectives during anhepatic phase

A
  1. removal of sick liver

2. implantation of donor liver

132
Q

What are surgical objective during neohepatic phase

A
  1. reperfusion of donor liver
  2. anastomosis of hepatic artery
  3. anastomosis of biliary structures
133
Q

Anesthetic considerations for pre-anhepatic phase

A
  1. increased risk for aspiration (RSI)
  2. risk of significant blood loss, use fluid warmer
  3. Anticipate CV instability (HoTN)
  4. Lower CVP to reduce blood loss
134
Q

Why is HoTN common during pre-anhepatic phase

A

d/t drainage of ascites and decompression of vascular structures compounded by blood loss

135
Q

Fluid consideration during the pre-anhepatic stage

A
  1. significant blood loss should be replaced with blood
  2. Large volume of blood products leads to lactic acidosis, hyperkalemia, hypocalcemia
  3. Crystalloid resus causes dilutional coagulopathy
136
Q

Hemodynamic considerations during pre-anhepatic phase

A
  1. Lower CVP reduces blood loss
  2. Increase CVP before IVC clamping
  3. HoTN is common d/t relief of ascites and pressure from vasculature
137
Q

What are blood related lab goals during liver transplant

A

Hgb >7 g/dl
Plt >40,000
Fibrinogen >100 mg/dl
MA TEG >45

138
Q

What are the differences in hepatic isolation that surgeons use

A

Bicaval = full IVC flow obstruction
Piggyback = Partial IVC flow obstruction
Venovenous bypass = cannulation of fem ven to ax vein

139
Q

Considerations for bicaval clamp (complete IVC obstruction)

A

Preload reduction causing HoTN and tachycardia

Aggressive fluids can lead to overload when clamp released

140
Q

Considerations with piggyback technique (partial IVC obstruction)

A

Less preload reduction

Fewer blood products required

141
Q

Considerations for venovenous bypass

A

Used if pt doesn’t tolerate piggyback technique
Less hemodynamic instability and blood loss
Higher complication rate w/ air embolism or thromboembolism

142
Q

How should preload reduction with IVC clamping be addressed in the liver transplant pt

A

Use sympathomimetics

143
Q

Common problems during anhepatic phase

A
  1. worsening coagulopathy
  2. blood loss
  3. lactic acidosis
  4. hypoglycemia (no glycogen stores)
144
Q

How is acidosis combated during liver transplant

A

NaHCO3

145
Q

What is warm ischemic time

A

Begins when donor liver is removed from ice until it is reperfused
Should not exceed 30-60 minutes

146
Q

How is serum K+ affected by donor liver perfusion

A

It will increase

147
Q

What happens once donor liver is reperfused

A

D/t ischemia, restored BF washes out metabolic substances that accumulated

148
Q

What are 10 complications associated with donor liver reperfusion

A
  1. Hyperkalemia
  2. hypocalcemia
  3. cytokine release
  4. Lactic acidosis
  5. embolic debris
  6. hypovolemia
  7. HoTN
  8. Pulmonary HTN
  9. Hypothermia
    10 Arrest
149
Q

When is the risk of hyperkalemia highest during liver transplantation

What are first line treatments

A

During neohepatic phase

Tx=CaCl, NaHCO3

150
Q

What are indications that the donor liver is functioning

A

Stabilization of serum glucose and acid-base status

151
Q

What is the most important consideration during neohepatic phase and treatment

A

Post-perfusion syndrome

Tx=supportive including vasopressors, correcting lytes, correcting AB status

152
Q

Type of induction for liver transplant pts and why

A

RSI

seldom NPO and increased pressures from ascites increase aspiration risk

153
Q

Effects of obstruction of cystic duct

A
  1. gallbladder distension
  2. edema
  3. risk of perf
  4. jaundice
154
Q

Effects of obstruction of common bile duct

A
  1. cholecystitis
  2. jaundice
  3. pancreatitis
  4. peritonitis
155
Q

What are risk factors for increased incidence of gallstones

A
  1. obesity
  2. aging
  3. rapid weight loss
  4. pregnancy
  5. women > men
156
Q

S/Sx of cholecystitis

A
  1. Leukocytosis
  2. fever
  3. RUQ pain
157
Q

What is Murphy’s sign

A

pain that is worse with inspiration in abd

158
Q

Why does a prolonged NPO status increase likelihood of gallstone formation

A

Lack of CCK release contributes to biliary stasis

159
Q

Treatment to relax sphincter of Oddi

A
  1. glucagon
  2. naloxone
  3. NTG
  4. Atropine
  5. Glycopyrrolate

APEX-KLE (4 decks)

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