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24 Physical & Health Assessment > Hepatic Biliary Systems > Flashcards

Hepatic Biliary Systems Flashcards

1
Q

Which vein is located in the posterior section of the liver?

A

Hepatic vein

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2
Q

What structure lies in the lateral section of the liver?

A

Middle hepatic vein

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3
Q

What does the cystic duct connect?

A

Gallbladder and Bile duct

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4
Q

What is the liver responsibe for synthesizing?

A

The Liver synthesizes glucose via gluconeogenesis, synthesizes cholesterol and proteins into hormones and vitamins, and also synthesizes coagulation factors (all except factors III, IV, VIII, vWF).

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5
Q

What does the liver do with excess glucose?

A

Stores it as glycogen

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6
Q

What does liver metabolize? Which enzymes in the liver are involved in metabolizing drugs?

A

Liver metabolizes fats, proteins, carbs and drugs. Liver uses CYP-450 and other enzymes to metabolize drugs.

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7
Q

What is a function of the liver in immune support?

A

Involved in the acute-phase of immune support

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8
Q

What does the liver do with iron?

A

Processes HGB and stores iron

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9
Q

What is the role of the liver in blood volume control?

A

Aids in volume control as a blood reservoir

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10
Q

What can liver dysfunction lead to?

A

Can lead to multi-organ failure

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11
Q

How many segments does the liver have?

A

8

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12
Q

What separates the right and left lobes of the liver?

A

Falciform Ligament

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13
Q

Where does bile drain through?

A

Bile drains through Hepatic duct into Gallbladder & common bile duct

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14
Q

Where does bile enter duodenum?

A

Ampulla of Vater

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15
Q

What are the three hepatic veins and where do they empty into?

A

right hepatic vein, middle hepatic vein, left hepatic vein. All of which empty into the IVC.

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16
Q

What percentage of cardiac output does the liver receive? How much blood flow does this represent in L/min.

A

25% of CO; 1.25-1.5 L/min

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17
Q

Where does the portal vein arise from? How much of the hepatic blood flow is derived from portal vein?

A

Splenic vein and superior mesenteric vein.
Provides 75% hepatic blood flow.

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18
Q

The Portal vein blood provides partially deoxygenated blood from what areas?

A

GI organs (Stomach, intestines), pancreas and spleen.

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19
Q

Where does the hepatic artery branch off from? What percent of Hepatic blood flow does hepatic artery provide?

A

hepatic artery branches off of the Aorta and provides 25% of the hepatic blood flow.

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20
Q

How is the oxygen delivery split between the portal vein and hepatic artery?

A

50% via Portal vein, 50% via Hepatic artery

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21
Q

What is the relationship between hepatic arterial blood flow and portal venous blood flow?

A

Heptic arterial blood flow and portal venous blood flow are inversely related

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22
Q

How Is hepatic blood flow regulated?

A

Hepatic blood flow is autoregulated. The hepatic artery dilates in response to low portal venous flow (portal venous flow 75% HBF), to keep the HBF consistent.

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23
Q

What does ↑Portal venous pressure lead to?

A

Blood backing up into systemic circulation

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24
Q

Splanchnic arterial tone and intrahepatic pressure contribute to what?

A

Portal venous pressure

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25
Q

What can high portal venous pressures lead to?

A

The blood backs up into the systemic circulation. If severe enough can lead to esophageal and gastric varices.

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26
Q

What is Hepatic Venous Pressure Gradient (HVPG) used to determine?

A

Determines the severity of portal hypertension

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27
Q

Regarding HVPG what signs and symptoms are related to the following levels: HVPG 1-5 mmHg, HVPG >10mmHg, HVPG >12 mmHg?

A

HVPG 1-5 mmHg: normal portal venous pressure
HVPG >10mmHg: clinically significant portal HTN, i.e., cirrhosis, esophageal varices
HVPG >12 mmHg: Variceal rupture

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28
Q

When will liver dysfunction symptoms be apparent?

A

Often asymptomatic until late stage liver disease.
Late stages may only have vague symptoms. (sleep disruption, decreased apetite)
For this reason we rely heavily on risk factors when liver dysfunction suspected.

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29
Q

What are risk factors for liver disease?

A

family hx, heavy ETOH, lifestyle, DM, Obesity, Illicit Drug use, Multiple partners, Tattoos, Transfusion (more so for transfusions in the 1980’s before blood was screened)

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30
Q

What are common physical examination findings in liver disease?

A

Pruritis, Jaundice, Ascites, Asterixis (flapping tremor), Hepatomegaly, Splenomegaly, Spider nevi (spider veins on face)

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31
Q

What blood tests are used to assess hepato-biliary function?

A

BMP, CBC, PT/INR, AST/ALT, Bilirubin, alkaline phosphatase, gamma glutamyl-transferase (GGT)

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32
Q

Which enzyme is most liver-specific?

A

Alanine aminotransferase (ALT)

present mainly in the cytosol of the liver and in low concentrations elsewhere.

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33
Q

Which imaging methods are commonly used to evaluate hepato-biliary issues?

A

Ultrasound, Doppler U/S (portal blood flow) CT, MRI

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34
Q

What are the 3 groups of Hepatobiliary Disease

A

Hepatocellular Injury
- high AST/ALT
Reduced synthetic function
- low albumin, high PT/INR (low clotting factors)
cholestasis
- high Alk phos, GGT & bilirubin

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35
Q

What are the characteristics of Hepatocellular injury

A

increased AST/ALT (hepatocyte enzymes)
- Acute Liver Failure (AST:ALT x25 elevated)
- Alcoholic liver disease (AST:ALT usually 2:1)
- Non-alcoholic fatty liver disease: (AST:ALT usually 1:1)

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36
Q

What is cholelithiasis also known as?

A

Gallstones

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37
Q

What are the risk factors for cholelithiasis?

A

Obesity, high cholesterol, diabetes, pregnancy, female gender, family history

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38
Q

What are the common symptoms of cholelithiasis? What percent of patients with gallstones are asymptomatic?

A

RUQ pain, referred to shoulders, N/V, indigestion, fever in acute obstruction.
80% are asymptomatic

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39
Q

What is the treatment for cholelithiasis?

A

IV fluids, antibiotics, pain management, Lap Cholecystectomy (surgical removal of gall bladder)

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40
Q

Where does the bile flow through s/p cholecystectomy?

A

All bile flows through the common bile duct straight into the duodenum after cholecystectomy.

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41
Q

What is choledocolithiasis?

A

A stone obstructing the common bile duct l/t biliary colic.

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42
Q

What is the initial presentation of choledocholithiasis?

A

N/V, cramping, RUQ pain

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43
Q

What are the symptoms of cholangitis?

A

Fever, rigors, jaundice

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44
Q

What is the treatment for choledocolithiasis?

A

Endoscopic stone removal via ERCP (Endoscopic Retrograde Cholangiopancreatography)

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45
Q

How is the stone retrieved during an ERCP?

A

Guidewire fed through Sphincter of Oddi into Ampulla of Vater then retrieved form pancreatic duct or common bile duct.

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46
Q

What is commonly used to manage Oddi Spasm during ERCP?

A

Glucagon 2mg IV slow

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47
Q

What is the preferred patient positioning during ERCP?

A

Patient is prone, head to patients right, tape ETT to left.

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48
Q

What is the function of the gallbladder?

A

Stores bile

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49
Q

What connects the gallbladder to the common bile duct?

A

Cystic duct

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50
Q

What are solid particles that form in the gallbladder called?

A

Gallstones

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51
Q

What is bilirubin? How is unconjugated bilirubin transported to the liver?

A

Bilirubin is the end product of heme-breakdown.
Unconjugated bilirubin is transported to the liver bound to albumin.

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52
Q

What happens to bilirubin in the liver?

A

Conjugated into its water soluble direct state then excreted into bile

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53
Q

What causes unconjugated (indirect) hyperbilirubinemia?

A

Imbalance between synthesis and conjugation (liver having issues conjugating lol)

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54
Q

What causes conjugated (direct) hyperbilirubinemia?

A

Obstruction leading to reflux of conjugated bilirubin

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55
Q

What are the 5 most common types of viral hepatitis?

A

A, B, C, D, E

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56
Q

Which types of viral hepatitis are chronic? Which is most chronic? How are these transmitted?

A

B & C are chronic. C is the most chronic (75% will develop chronic hepatitis).
B &C are both bloodborne and have long incubation periods.

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57
Q

Which type of viral hepatitis is most common in the US requiring liver transplant?

A

Hepatitis C Virus (HCV)

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58
Q

What is the standard 12-week treatment for Hepatitis C Virus (HCV)?

A

Sofosbuvir/Velpatasvir

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59
Q

What percentage of genotype 1A/1B clearance does Sofosbuvir/Velpatasvir provide?

A

98-99%

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60
Q

What are some common symptoms of acute and chronic hepatitis?

A

Fatigue, jaundice, nausea or vomiting, lack of appetite, bleeding/bruising, dark urine.

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61
Q

What are potential complications of chronic HCV infection?

A

Cirrhosis, Hepatocellular Carcinoma

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62
Q

What is the most common cause of cirrhosis?

A

Alcoholic Liver Disease (ALD)

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63
Q

What is the top indication for liver transplants in the US? What is the national prevalence of liver transplant for ALD?

A

Alcoholic Liver Disease is the top indication for liver transplants in the US. The prevalence of liver transplant for ALD is 2%.

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64
Q

What is the initial presentation of ALD?

A

Asymptomatic

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65
Q

What is the main focus of treatment for ALD?

A

Alcohol abstinence

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66
Q

At what platelet count does ALD management require a blood transfusion?

A

<50,000

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67
Q

Symptoms of alcoholic liver disease

A
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68
Q

Symptom of alcoholic liver disease associated with immune response

A

Parotid gland hypertrophy

(large the salivary glands. Each parotid is wrapped around the mandibular ramus, and secretes serous saliva through the parotid duct into the mouth, to facilitate mastication and swallowing and to begin the digestion of starches.)

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69
Q

Lab value indicating red blood cells are larger than normal in alcoholic liver disease

A

↑Mean (cell) corpuscular volume (MCV)

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70
Q

Which enzyme’s increase is a specific marker for alcoholic liver disease?

A

↑MCV, ALT/ALT (2:1), ɣ-glutamyl-transferase (GGT), bilirubin.

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71
Q

What might occur 24-72 hours after stopping alcohol in someone with alcoholic liver disease?

A

Symptoms of ETOH withdrawal

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72
Q

What is Non-Alcoholic Fatty Liver Disease?

A

Hepatocytes contain >5% fat

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73
Q

What are some risk factors for Non-Alcoholic Fatty Liver Disease?

A

Obesity, Insulin resistance, DM2, Metabolic syndrome

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74
Q

How does Non-Alcoholic Fatty Liver Disease progress?

A

Progresses to Non-steatohepatitis (NASH), then cirrhosis, and finally hepatocellular carcinoma

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75
Q

Aside from Alcoholic Liver Disease what are other leading causes of liver transplant in the US?

A

NAFLD & NASH

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76
Q

What is the gold standard in distinguishing NAFLD from other liver diseases?

A

Liver biopsy

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77
Q

When is a liver transplant indicated for Non-Alcoholic Fatty Liver Disease?

A

Advanced fibrosis, cirrhosis, related complications

78
Q

What are the types of fatty liver disease?

A

Non-alcoholic Fatty Liver Disease (NAFLD), Alcoholic Fatty Liver Disease (AFLD)

79
Q

What are the subtypes of Non-alcoholic Fatty Liver Disease (NAFLD)?

A

Non-alcoholic Fatty Liver (NAFL), Non-alcoholic Steatohepatitis (NASH), Liver Fibrosis, Cirrhosis of the Liver

80
Q

What are the subtypes of AFLD?

A

Alcoholic Fatty Liver/Steatosis, Alcoholic Hepatitis, Alcoholic Cirrhosis

81
Q

What is the most common cause of drug induced liver injury? Is this reversible?

A

Acetaminophen OD. Normally acetaminophen overdose is reversible after drug is removed.

82
Q

What demographic is predominantly affected by Autoimmune Hepatitis? What is the treatment for autoimmune hepatitis? How many patients receiving treatment achieve remission?

A

Predominantly affects women.
Steroids, azathioprine
60-80% achieve remission however relapse is common.

83
Q

What may be elevated significantly in acute autoimmune hepatitis (AIH)?

A

AST/ALT may be 10-20 times higher in acute AIH

84
Q

When is a liver transplant indicated in autoimmune hepatitis?

A

When treatment fails or acute liver failure ensues

85
Q

What is the definition of Inborn Errors of Metabolism? What is the prevalence of Inborn Errors of Metabolism?

A

Rare, genetically inherited disorders affecting enzymes that breakdown/store protein, carbs & fatty acids.
Prevalence: occurs in 1:2500 births

86
Q

When can the onset of Inborn Errors of Metabolism occur? When do the most severe forms of Inborn Errors of Metabolism typically appear?

A

Onset varies from birth to adolescence.
The most severe forms appear in the neonatal period and carry high degree of mortality.

87
Q

Name three specific disorders classified as Inborn Errors of Metabolism.

A

Wilson’s Disease (AKA hepatolenticular degeneration), Alpha-1 Antitrypsin Deficiency, Hemochromatosis

88
Q

How is Wilsons Disease inherited?

A

Wilson’s Disease is an autosomal recessive.

89
Q

What is the main characteristics of Wilsons Disease? What can this lead to?

A

Wilson’s Disease is characterized by impaired copper metabolism.
Excess copper leads to oxidative stress in the liver, basal ganglia, and cornea.

90
Q

What are the possible symptoms of Wilsons Disease?

A

Range from asymptomatic to sudden-onset liver failure along with neurologic and psychiatric manifestations.

91
Q

How is Wilsons Disease diagnosed?

A

Lab tests (serum ceruloplasmin, aminotransferases, urine copper level and possible liver biopsy for copper level

92
Q

What is the treatment for Wilsons Disease?

A

Copper-chelation therapy & oral zinc to bind copper in the GI tract.

93
Q

What is Alpha-1 Antitrypsin Deficiency? What do α-1 antitrypsin proteins protect the liver & lungs from?

A

Genetic disorder with defective α-1 antitrypsin protein.
α-1 antitrypsin protein protects liver and lungs from neutrophil elastase.

94
Q

What can neutrophil elastase cause?

A

Inflammation, cirrhosis, and HCC

95
Q

What is the incidence of Alpha-1 Antitrypsin Deficiency?

A

1:16,000 to 1:35,000

96
Q

What is the #1 genetic cause of liver transplant in children?

A

α-1 antitrypsin deficiency

97
Q

How is the diagnosis of Alpha-1 Antitrypsin Deficiency confirmed?

A

α-1 antitrypsin phenotyping

98
Q

What treatment is effective for pulmonary symptoms in Alpha-1 Antitrypsin Deficiency?

A

Pooled α-1 antitrypsin

99
Q

What is the only curative treatment for liver disease in Alpha-1 Antitrypsin Deficiency?

A

Liver transplant

100
Q

What is hemochromatosis?

A

Disorder assoc w/ excess iron in the body leading to multi-organ dysfunction

101
Q

What are some causes of hemochromatosis?

A

Genetic, repetitive blood transfusions, high-dose iron infusions

102
Q

How does excess iron in hemochromatosis affect the body?

A

Causes damage to organs and tissues

103
Q

What are some possible presentations of hemochromatosis?

A

Cirrhosis, heart failure, diabetes, adrenal insufficiency, polyarthropathy

104
Q

What lab findings are seen in hemochromatosis?

A

Elevated AST/ALT, transferrin saturation, ferritin

105
Q

How is hemochromatosis diagnosed?

A

Genetic mutation testing

106
Q

How are cardiomyopathies and liver abnormalities diagnosed in hemochromatosis?

A

Echocardiogram & MRI

107
Q

How can iron levels in the liver and the level of damage be assessed in hemochromatosis?

A

Liver bx may quantify liver iron levels and assess level of damage.

108
Q

What are the treatment options for hemochromatosis?

A

Weekly phlebotomy to remove excess iron, iron-chelating drugs, liver transplant

109
Q

What is Primary Biliary Cholangitis (PBC)?
formerly known as biliary cirrhosis

A

Autoimmune, progressive destruction of bile ducts (intrahepatic ducts only) with periportal inflammation and cholestasis.

110
Q

What are common symptoms of PBC? What can PBC lead to?

A

Jaundice, fatigue, itching.
Can lead to liver scarring, fibrosis, cirrhosis.

111
Q

How is PBC diagnosed?

A

Elevated Alk Phos, GGT, + Antimitochondrial antibodies

112
Q

What is the typical demographic most affected by PBC?

A

Females > Males, middle-ages

113
Q

What is the suggested cause of PBC?

A

Exposure to environmental toxins in genetically susceptible individuals

114
Q

How can bile duct obstructions be ruled out in PBC?

A

Imaging: CT, MRI, MRCP

115
Q

What does a liver biopsy reveal in PBC?

A

Bile duct destruction and lymphocyte infiltration

116
Q

What is the treatment approach for PBC?

A

No cure (d/t alteration of stomach lining), however exogenous bile acids slow progression

117
Q

What is Primary Sclerosing Cholangitis (PSC)?

A

Autoimmune, chronic inflammation of larger bile ducts (both extrahepatic and intrahepatic ducts)

118
Q

What are the symptoms of Primary Sclerosing Cholangitis (PSC)?

A

Fatigue, itching, deficiency of fat-soluble vitamins (A,D, E, K), cirrhosis

119
Q

Who is mostly affected by Primary Sclerosing Cholangitis (PSC)? What is the typical age of onset for PSC?

A

Males are more affected than females. Onset Around 40’s

120
Q

What are the common lab findings in Primary Sclerosing Cholangitis (PSC)?

A

High alkaline phosphatase, high ɣ-glutamyl-transferase, positive auto-antibodies

121
Q

How is Primary Sclerosing Cholangitis (PSC) diagnosed?

A

MRCP or ERCP showing biliary strictures with dilated bile ducts

122
Q

What is the only long term treatment for Primary Sclerosing Cholangitis (PSC)?

A

Liver transplant

123
Q

Why is re-occurrence common after a liver transplant in PSC?

A

Due to its autoimmune nature

124
Q

What is the characteristic finding in primary sclerosing cholangitis?

A

Fibrosis in biliary tree with strictures that have “Beads on a string” appearance.

125
Q

What is acute liver failure?

A

Life-threatening severe liver injury occurring rapidly (within days to 6 months after insult). Will see rapid increase in ALT/AST, AMS, coagulopathy

126
Q

What are some common causes of acute liver failure?

A

Almost 50% are Drug-induced (mostly acetaminophen).
Other causes: viral hepatitis, autoimmune, hypoxia, Acute liver failure of pregnancy, HELLP.

127
Q

Why is cellular swelling and membrane disruption seen with acute liver failure?

A

This is caused by massive hepatocyte necrosis seen with ALF

128
Q

What are some symptoms of acute liver failure?

A

Jaundice, nausea, RUQ pain, cerebral edema, encephalopathy, multi-organ failure, and death.

129
Q

How is acute liver failure managed?

A

Treat the cause, supportive care, liver transplant

130
Q

What is the final stage of liver disease?

A

Cirrhosis

131
Q

What replaces normal liver parenchyma in cirrhosis?

A

Scar tissue

132
Q

What are early stage symptoms of cirrhosis?

A

Often asymptomatic

133
Q

List some progressed symptoms of cirrhosis.

A

Jaundice, ascites, varices, coagulopathy, encephalopathy

134
Q

What are the most common causes of cirrhosis?

A

Alcoholic fatty liver, NAFL, HCV (hep. C), HBV (hep. B)

135
Q

Which lab values are elevated in cirrhosis?

A

AST/ALT, bilirubin, Alk phosphatase, PT/INR

136
Q

What is a common blood disorder associated with cirrhosis?

A

Thrombocytopenia

137
Q

What is the only cure for cirrhosis?

A

Transplant

138
Q

What is the most common complication of cirrhosis?

A

Ascites

139
Q

How does Portal HTN contribute to ascites?

A

Portal HTN leads to ↑blood volume and peritoneal accumulaition of fluid which worsens ascites.

140
Q

What is the management approach for Ascites in cirrhosis?

A

↓Salt diet, albumin replacement

141
Q

What procedure can be done to reduce Portal-HTN and ascites?

A

Transjugular Intrahepatic Portosystemic Shunt (TIPS).

142
Q

What is the most common infection related to cirrhosis? How is this infection treated?

A

Spontaneous Bacterial Peritonitis. Requires Antibiotics.

143
Q

What percent of cirrhosis patients develop varices? What is the most lethal complication of varices in cirrhosis?

A

Approximately 50% (surprisingly) of cirrhosis patients develop varices. The most lethal complication of varices is Hemorrhage

144
Q

How can the risk of variceal hemorrhage be reduced in cirrhosis patients?

A

Beta blockers help reduce risk and prophylactic endoscopic vatical banding and ligation help prevent rupture.

145
Q

What is the treatment for refractory variceal bleeding in cirrhosis? The need for balloon tamponade will ___________ mortality

A

Balloon tamponade. Need for this device is indicative of a higher mortality rate. (Last resort to slow bleeding)

146
Q

Hepatic encephalopathy is caused by

A

Buildup of nitrogenous waste seoncdary to poor liver detoxification

147
Q

What are the neuropsychiatric symptoms seen in hepatic encephalopathy?

A

Cognitive impairment progessing to → coma

148
Q

How can ammonia-producing bacteria in the gut be reduced to manage hepatic encephalopathy?

A

Lactulose, Rifaximin

149
Q

Hepatorenal Syndrome is caused by what

A

excess endogneous vasodilators (NO/PGs) which decrease MAP thereby decreasing renal blood flow.

150
Q

What is the treatment for Hepatorenal Syndrome?

A

Midodrine, Octreotide, Albumin

151
Q

What is the triad seen with Hepatopulmonary Syndrome?

A

Chronic liver disease, hypoxemia, intrapulmonary vascular dilation

152
Q

What is Platypnea and what disease process is it associated with?

A

Hypoxemia when upright d/t R to L intrapulmonary shunt. This is seen in Hepatopulmonary Syndrome

153
Q

What is portopulmonary HTN

A

Pulmonary HTN accompanied with Portal HTN

154
Q

What triggers the production of pulmonary vasoconstrictors in Portopulmonary HTN?

A

Systemic vasodilation

155
Q

What is the treatment for Portopulmonary HTN?

A

PD-I’s, NO, prostacyclin analogs, endothelin receptor antagonists

156
Q

What is the only cure for Portopulmonary HTN?

A

Transplant

157
Q

When is elective surgery contraindicated in liver disease?

A

Acute hepatitis, severe chronic hepatitis, ALF

158
Q

What are the 2 scoring systems to determine severity and prognosis of liver disease?

A

Child-Turcotte-Pugh(CTP): based on bilirubin, albumin, PT, encephalopathy, and ascites.
(MELD): Model for End Stage Liver Disease: score based on bili, INR, creatinine, and sodium.

Slide 39

159
Q

What labs are standard preoperatively for patients with liver disease?

A

CBC, BMP, PT/INR

160
Q

What are some of the high risks associated with surgery in liver disease patients

A

↑Risks aspiration, HoTN, hypoxemia

161
Q

What type of fluids are preferred for resuscitation in patients with liver disease?

A

Colloids > crystalloids for resuscitation

162
Q

How does alcoholism affect volatile anesthetics in patients with liver disease?

A

Increases MAC

163
Q

How are drugs impacted by liver disease

A

Slower onset and longer duration can be seen with liver disease.

164
Q

Which muscle relaxants are ideal for patients with liver disease? Why are these ideal?

A

Succs, Cisatracurium since these are not metabolized by the liver.

165
Q

What may be decreased in severe liver disease impacting drug metabolism?

A

Plasma cholinesterase

166
Q

What is the purpose of a TIPS procedure? How does a TIPS procedure work?

A

To manage portal HTN
The TIPS procedure involves a Stent or graft placed between hepatic vein and portal vein. This shunts portal flow to systemic circulation (reducing portosystemic pressure gradient)

167
Q

What are the indications for a TIPS procedure?

A

Refractory variceal hemorrhage, Refractory ascites

168
Q

What are the contraindications for a TIPS procedure?

A

Heart Failure, Tricuspid regurgitation, Severe pulmonary HTN

169
Q

What is a partial hepatectomy?

A

Resection to remove neoplasms, leaving adequate tissue for regeneration

170
Q

How much removal is tolerated in patients with normal liver function?

A

Up to 75%

171
Q

What are some anesthetic considerations for partial hepatectomy?

A

Invasive monitoring, blood products available, adequate vascular access

172
Q

What is the standard practice to reduce blood loss during liver resection?

A

Maintain low CVP by fluid restriction prior to resection to reduce blood loss.

173
Q

What may the surgeon due intraoperatively to control blood loss

A

Surgeon may clamp IVC or hepatic artery to control blood loss.

174
Q

What may be required for pain management post partial hepatectomy?

A

Post op PCA

175
Q

What does liver resection often cause postoperatively? How is this resolved?

A

Coagulation disturbances occur post op and persist until liver re-equilibrates

176
Q

What is the definitive treatment for end-stage liver disease?

A

Liver transplant

177
Q

Which is the most common indication for liver transplant?

A

Alcoholic liver disease.
ALD>Fatty Liver>HCC

178
Q

How do living donor and brain dead donor transplants differ?

A

Living donor: surgeries are timed together to minimize ischemia time.
Brain Dead Donor: kept hemodynamically stable for organ perfusion.

179
Q

What should be readily available for maintaining hemodynamics during liver transplant?

A

Pressors/Inotropes

180
Q

What monitoring devices are commonly used during liver transplants?

A

A-line, CVC, PA cath, TEE

181
Q

What must be controlled during intraoperative management of liver transplants?

A

Control coagulation

182
Q

What should be evaluated before a liver transplant surgery?

A

MELD score, UNOS listing

183
Q

What should be considered when evaluating patients for a liver transplant?

A

Preoperative evaluation, vascular access, blood product availability

184
Q

What is done during the dissection phase of a liver transplant?

A

Mobilization of liver and vascular structures, isolation of bile duct

185
Q

What is done during the anhepatic phase of a liver transplant?

A

Clamping of hepatic artery and portal vein, removal of diseased liver

186
Q

What is done during the reperfusion phase of a liver transplant?

A

Anastomosis of hepatic artery and biliary system. Reperfusion of transplanted liver.

187
Q

What are the surgical considerations for posttransplantation?

A

Hemostasis, evaluation of graft function, ultrasound for vascular potency

188
Q

Hemodynamic compromise during dissection portion of liver transplant is related to

A

Ascites loss (ascites drained), hemorrhage during dissection, decreased venous return

189
Q

Complications of liver transplant seen during reperfusion phase

A

Hemodynamic instability, dysrhythmias, hyperkalemia, acidosis, pulmonary emboli, cardiac arrest

190
Q

Post-liver transplant anesthesia care involves

A

ICU admission, early or late extubation, hemodynamic management

24 Physical & Health Assessment (33 decks)

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