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TX WES class of 2026 > T3 - Hepatic & Biliary Systems Assessment > Flashcards

T3 - Hepatic & Biliary Systems Assessment Flashcards

1
Q

What is the function of the liver in glucose metabolism?

A

The liver synthesizes glucose via gluconeogenesis and stores excess glucose as glycogen.

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2
Q

What role does the liver play in synthesizing hormones and vitamins?

A

The liver synthesizes cholesterol and converts proteins into hormones and vitamins.

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3
Q

How does the liver contribute to energy generation?

A

The liver metabolizes fats, proteins, and carbohydrates to generate energy.

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4
Q

How does the liver contribute to drug metabolism?

A

The liver metabolizes drugs via various enzyme pathways, including the CYP-450 system

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5
Q

What is the role of the liver in blood detoxification?

A

by processing and removing toxins and waste products.

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6
Q

What function does the liver serve in the acute-phase immune response?

A

The liver is involved in the acute-phase of immune support, producing proteins and factors necessary for the body’s defense mechanisms.

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7
Q

How does the liver contribute to iron metabolism?

A

The liver processes hemoglobin (HGB) and stores iron.

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8
Q

What is the role of the liver in coagulation?

A

The liver synthesizes coagulation factors, with the exception of factors 3/III, 4/IV, 8/VIII, and von Willebrand factor (vWF)

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9
Q

How does liver dysfunction impact overall health?

A

Liver dysfunction can lead to multi-organ failure as nearly every organ is impacted by liver function.

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10
Q

How does the liver aid in volume control?

A

by serving as a blood reservoir.

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11
Q

How many segments does the liver have?

A

The liver has 8 segments.

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12
Q

How are the right and left lobes of the liver separated?

A

by the Falciform Ligament.

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13
Q

What branches into each segment of the liver?

A

The Portal Vein and Hepatic Artery branch into each segment of the liver.

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14
Q

How many hepatic veins empty into the inferior vena cava (IVC)?

A

Three hepatic veins namely the Right, Middle, and Left hepatic veins

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15
Q

How does bile drainage occur in the liver?

A
  • Bile ducts travel along portal veins, and
  • Bile drains through the hepatic duct into the gallbladder (GB) and common bile duct (CBD)
  • Bile enters duodenum via ampulla of vater
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16
Q

Through what structure does bile enter the duodenum?

A

via the Ampulla of Vater.

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17
Q

What proportion of cardiac output (COP) does the liver receive?

How many liters per minute does it receive?

A

The liver receives 25% of cardiac output (COP)

1.25 to 1.5 L/min

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18
Q

Which organ has the highest proportionate COP?

A

The liver

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19
Q

Where does the portal vein arise from?

A

the splenic vein and superior mesenteric vein.

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20
Q

What is the oxygenation status of blood in the portal vein?

Where does it originate from?

A

Blood in the portal vein is deoxygenated originating from the gastrointestinal (GI) organs, pancreas, and spleen

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21
Q

What percentage of hepatic blood flow (HBF) does the portal vein provide?

A

The portal vein provides 75% of hepatic blood flow (HBF).

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22
Q

Where does the hepatic artery branch off from?

A

the aorta.

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23
Q

What percentage of hepatic blood flow (HBF) does the hepatic artery provide?

A

The hepatic artery provides 25% of hepatic blood flow (HBF).

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24
Q

How is oxygen delivered to the liver?

A

50% via the portal vein (deoxygenated)

50% via the hepatic artery (partially oxygenated).

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25
Q

How is hepatic arterial blood flow related to portal venous blood flow?

A

Hepatic arterial blood flow is inversely related to portal venous blood flow.

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26
Q

How is hepatic blood flow regulated?

Through what mechanism?

A

Hepatic blood flow is autoregulated

(The hepatic artery dilates in response to low portal venous flow to maintain consistent hepatic blood flow (HBF).)

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27
Q

What does portal venous pressure reflect?

A

splanchnic arterial tone and intrahepatic pressure.

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28
Q

What happens if portal venous pressure increases?

A
  • Can lead to blood backing up into the systemic circulation, resulting in complications such as esophageal and gastric varices
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29
Q

Hepatic Venous Pressure Gradient is used for:

A

Determining the severity of portal hypertension

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30
Q

Video animation:

A

https://www.youtube.com/watch?v=LkXQTDb8g2U

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31
Q

What are some common risk factors for liver disease?

A

Risk factors for liver disease include
- Family history
- Heavy alcohol consumption (ETOH)
- Lifestyle factors
- Diabetes mellitus (DM),
- Obesity,
- Illicit drug use,
- Multiple sexual partners
- Tattoos
- Transfusions.

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32
Q

What are some common symptoms of late-stage liver disease?

A

vague symptoms such as disrupted sleep and decreased appetite.

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33
Q

physical exam findings in liver disease?

A

Common physical exam findings in liver disease include
- Pruritus
- Jaundice
- Ascites
- Asterixis (flapping tremor)
- Hepatomegaly
- Splenomegaly
- Spider nevi.

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34
Q

Hepato-biliary Function Tests:

A

LABS:
- BMP
- CBC
- PT/INR
- Aspartate aminotransferase (AST)
- Alanine aminotransferase (ALT) most - liver-specific enzymes
- Bilirubin
- Alkaline Phosphatase
- ɣ-glutamyl-transferase (GGT)

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35
Q

Hepato-biliary Function Imaging:

A

Imaging
Ultrasound
Doppler U/S (Portal bld flow)
CT
MRI

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36
Q

What are the biomarkers for acute liver failure (ALF)?

A

In acute liver failure (ALF), AST and ALT levels may be elevated up to 25 times the normal range.

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37
Q

What is the typical AST:ALT ratio in alcoholic liver disease (ALD)?

A

In alcoholic liver disease (ALD), the AST:ALT ratio is usually at least 2:1.

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38
Q

What is the typical AST:ALT ratio in non-alcoholic fatty liver disease (NAFLD)?

A

In non-alcoholic fatty liver disease (NAFLD), the AST:ALT ratio is usually 1:1.

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39
Q

What biomarkers indicate reduced synthetic function of the liver?

A

decreased albumin levels and increased PT/INR.

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40
Q

What biomarkers indicate cholestasis?

A

Cholestasis is indicated by increased levels of:

  • Alkaline phosphatase (Alk Phosphatase)
  • Gamma-glutamyl transferase (GGT)
  • Bilirubin
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41
Q

Look at this differential diagnosis of Hepatobiliary Disorders

A

Flash cards added at the end

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42
Q

What are the functions of hepatocytes in bile secretion?

A

Hepatocytes secrete bile through bile ducts into the common hepatic duct (CHD) which leads to the gallbladder (GB) and common bile duct (CBD)

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43
Q

How does the gallbladder (GB) function in bile storage?

A

The gallbladder (GB) stores bile to deliver it during meals

the common bile duct (CBD) secretes bile directly into the duodenum.

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44
Q

What are the risk factors for cholelithiasis?

A

obesity
high cholesterol levels
diabetes mellitus (DM)
pregnancy
being female
family history of gallstones.

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45
Q

What percentage of cases of cholelithiasis are asymptomatic?

A

Approximately 80% of cases of cholelithiasis are asymptomatic.

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46
Q

What are the common symptoms of cholelithiasis?

A

Common symptoms of cholelithiasis include
- Right upper quadrant (RUQ) pain referred to the shoulders,
- Nausea & vomiting
- Indigestion
- Fever in cases of acute obstruction.

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47
Q

What are the treatment options for cholelithiasis?

A

Treatment options for cholelithiasis include
- Intravenous fluids (IVF)
- Antibiotics (abx)
- Pain management
- Laparoscopic cholecystectomy (removal of the gallbladder).

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48
Q

Types of Cholecystectomy:

A
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49
Q

What is choledocolithiasis?

A

Choledocolithiasis refers to the presence of gallstones (calculi) in the common bile duct (CBD). Biliary colic.

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50
Q

What is the initial presentation of a stone obstructing the common bile duct (CBD)?

A

nausea,
vomiting,
cramping,
right upper quadrant (RUQ) = biliary colic

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51
Q

What are the symptoms of cholangitis?

A

Symptoms of cholangitis (inflammation of the CBD)
- fever
- rigors (shaking chills)
- jaundice.

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52
Q

What is the preferred treatment for stone removal in cases of CBD

A

The preferred treatment is endoscopic removal of the stone via endoscopic retrograde cholangiopancreatography (ERCP)

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53
Q

What does ERCP stand for?

A

ERCP stands for Endoscopic Retrograde Cholangiopancreatography.

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54
Q

Describe the procedure of ERCP.

A

threads a guidewire through the Sphincter of Oddi into the Ampulla of Vater to retrieve the stone from the pancreatic duct or CBD.

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55
Q

What position is typically used during ERCP, and why?

A

prone position with left tilt

The endotracheal tube (ETT) may be taped to the left side to prevent displacement.

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56
Q

What medication may be required during ERCP in the event of Oddi Spasm?

A

Glucagon may be required to manage Oddi Spasm during ERCP.

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57
Q

Common bile duct obstruction picture:

A
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58
Q

ERCP Procedure picture:

A
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59
Q

What is bilirubin?

A

Bilirubin is the end product of heme breakdown.

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60
Q

Describe unconjugated bilirubin.

A
  • Unconjugated bilirubin, also known as “indirect” bilirubin, is bound to albumin in the plasma.
  • It is transported to the liver, where it is conjugated into its water-soluble “direct” state before being excreted into bile.
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61
Q

What causes unconjugated (indirect) hyperbilirubinemia?

A

imbalance between bilirubin synthesis and conjugation.

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62
Q

What causes conjugated (direct) hyperbilirubinemia?

A

an obstruction in the biliary systemleading to the reflux of conjugated bilirubin into the circulation.

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63
Q

What are the five most common types of viral hepatitis?

A

The five most common types are hepatitis A, B, C, D, and E.

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64
Q

How has the overall prevalence of viral hepatitis changed over time?

A

Overall, viral hepatitis is on the decline due to vaccines and newer treatments

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65
Q

Which types of viral hepatitis are more chronic?

A

Hepatitis B and C are more chronic compared to other types.

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66
Q

What is the most common viral hepatitis requiring liver transplant in the United States?

A

Hepatitis C virus (HCV) (75% type 1)

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67
Q

What is the recommended treatment for hepatitis C?

A

regimen is a 12-week course of sofosbuvir/velpatasvir, which provides 98-99% clearance of genotype 1A/1B.

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68
Q

HCV Cycle Picture

A
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69
Q

Acute and Chronic Hepatitis Symptoms image:

A
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70
Q

Hepatitis A

A
  • Mode of Transmission: Fecal-oral sewage-contaminated water or shellfish
  • Incubation Period: 20–37 days
  • Serum Antigen and Antibody Tests: IgM early, IgG appears during convalescence
  • Course: Acute, does not progress to chronic liver disease
  • Prevention after Exposure: Pooled γ-globulin, hepatitis A vaccine
  • Mortality: <0.3–0.6%
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71
Q

Hepatitis B

A
  • Mode of Transmission: Transfusions, percutaneous, sexual, perinatal
  • Incubation Period: 60–110 days
  • Serum Antigen and Antibody Tests: HBsAg and anti-HBcAg early and persist in carriers
  • Course: Chronic liver disease develops in 1–5% of adults and 80–90% of children
  • Prevention after Exposure: Hepatitis B immunoglobulin, hepatitis B vaccine
  • Mortality: 0.3–1.5%
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72
Q

Hepatitis C

A

Mode of Transmission: Transfusions, percutaneous, sexual, perinatal
Incubation Period: 35–70 days
Serum Antigen and Antibody Tests: Anti-HCV in 6 weeks to 9 months
Course: Chronic liver disease develops in up to 75%
Prevention after Exposure: Two protease inhibitors +/− interferon
Mortality: Unknown

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73
Q

Hepatitis D

A

Mode of Transmission: Percutaneous
Incubation Period: 60–110 days
Serum Antigen and Antibody Tests: Anti-HDV late; may be short lived
Course: Coinfection with type B
Prevention after Exposure: Unknown
Mortality: Acute icteric hepatitis: 2–20%

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74
Q

Hepatitis E

A

Mode of Transmission: Fecal-oral, contaminated water
Incubation Period: 15–60 days
Serum Antigen and Antibody Tests: IgM early, IgG appears shortly afterwards
Course: Usually acute, may cause chronic liver disease in those with weakened immune systems
Prevention after Exposure: Ribavirin in immunocompromised
Mortality: 1%, 10–30% among pregnant women

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75
Q

ALD and Liver Transplants

A

Alcoholic liver disease
* Leading reason for liver transplants in the U.S.
* 2% of liver transplants nationwide are for ALD.

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76
Q

Reporting of ALD

A

Underreporting of ALD is common due to stigma.

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77
Q

Progression of ALD

A
  • Initially may show no symptoms.
  • Symptoms of liver failure emerge as it progresses.
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78
Q

Treating ALD

A

Abstinence from alcohol is central to treatment.

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79
Q

Management of ALD Symptoms

A

Treatment includes managing symptoms of liver failure.

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80
Q

ALD and Platelet Count

A

Plt count <50,000 requires transfusion

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81
Q

Liver Transplant for ALD

A

Patients with ALD may be eligible for a liver transplant if they meet specific criteria.

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82
Q

What symptom of ALD is a result of poor dietary habits and absorption?

A

Malnutrition

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83
Q

What symptom of ALD is due to malnutrition and altered metabolism?

A

Muscle wasting

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84
Q

Which gland enlargement is associated with chronic ALD?

A

Parotid gland hypertrophy

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85
Q

What symptom of ALD results from liver dysfunction and causes yellowing of the skin and eyes?

A

Jaundice

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86
Q

What term describes a low platelet count often associated with chronic liver disease?

A

Thrombocytopenia

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87
Q

What is the term for the accumulation of fluid in the abdomen, indicating advanced liver disease?

A

Ascites

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88
Q

What is the term for the enlargement of the liver and spleen seen in ALD?

A

Hepatosplenomegaly

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89
Q

What term describes the swelling of the feet and ankles due to fluid retention in ALD?

A

Pedal edema

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90
Q

When may symptoms of alcohol withdrawal occur after stopping drinking?

A

24-72 hours after cessation of alcohol intake

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91
Q

Which lab value is typically elevated in ALD and indicates a change in red blood cells?

A

Mean corpuscular volume (MCV)

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92
Q

Which lab values are typically elevated due to liver damage in ALD?

A

Liver enzymes

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93
Q

What enzyme, often elevated in ALD, can indicate liver disease and heavy alcohol use?

A

Gamma-glutamyl transferase (GGT)

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94
Q

What lab value, when elevated, indicates impaired liver function in ALD?

A

Bilirubin

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95
Q

What lab test measures acute alcohol intoxication?

A

Blood ethanol level

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96
Q

What is the trend of non-alcoholic fatty liver disease (NAFLD) in the US?

A

AFLD is on the rise in the United States.

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97
Q

How is non-alcoholic fatty liver disease (NAFLD) diagnosed?

A

hepatocytes contain more than 5% fat.

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98
Q

What are the primary risk factors associated with non-alcoholic fatty liver disease (NAFLD)?

A

Obesity
insulin resistance
type 2 diabetes mellitus (DM2)
metabolic syndrome.

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99
Q

What conditions can NAFLD progress to?

A

non-alcoholic steatohepatitis (NASH)
cirrhosis
hepatocellular carcinoma.

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100
Q

What has NAFLD and its progression, NASH, become in the context of liver transplants in the US?

A

NAFLD and NASH have become additional leading causes of liver transplant in the United States.

101
Q

What methods are used for the diagnosis of NAFLD?

A

Diagnosis is made through imaging and histology.

102
Q

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

A

Liver biopsy is the gold standard

103
Q

What are the primary treatments for non-alcoholic fatty liver disease (NAFLD)?

A

The primary treatments include diet and exercise.

104
Q

When is a liver transplant indicated for NAFLD?

A

advanced fibrosis, cirrhosis, and related complications.

105
Q

NAFLD Prevalence: diabetics and severely obese people?

A

More than 6 diabetics and 9 out of 10 severely obese people have NAFLD

106
Q

NAFLD: Non-diabetics/obese people

A

1 in 4 people have NAFLD regardless of weight

107
Q

Types of Fatty Liver Image:

A
108
Q

Who is predominantly affected by autoimmune hepatitis (AIH)?

A

Predominantly affects women.

109
Q

How does autoimmune hepatitis (AIH) present symptomatically?

A

May be asymptomatic, acute, or chronic.

110
Q

What are common laboratory findings in autoimmune hepatitis (AIH)?

A

Positive autoantibodies & hypergammaglobulinemia.

111
Q

How elevated are AST/ALT levels in acute autoimmune hepatitis (AIH)?

A

AST/ALT may be 10-20 times the normal level in acute AIH.

112
Q

What is the typical treatment for autoimmune hepatitis (AIH)?

A

Treatment includes steroids and azathioprine.

113
Q

What is the rate of remission and risk of relapse in autoimmune hepatitis (AIH)?

A

60-80% achieve remission; however, relapse is common.

114
Q

How is refractory autoimmune hepatitis (AIH) managed?

A

Refractory disease requires increased immunosuppression.

115
Q

When is a liver transplant indicated in autoimmune hepatitis (AIH)?

A

Indicated when treatment fails or acute liver failure ensues.

116
Q

What is the most common cause of drug-induced liver injury (DILI)?

A

The most common cause is acetaminophen overdose.

117
Q

What is the prognosis for drug-induced liver injury (DILI) when the drug is removed?

A

Normally reversible after the drug is removed

118
Q

What are inborn errors of metabolism (IEM)?

A

A group of rare, genetically inherited disorders leading to defects in the enzymes that break down and store proteins, carbohydrates, and fatty acids.

119
Q

How common are inborn errors of metabolism?

A

They occur in 1 out of every 2500 births.

120
Q

When does the onset of inborn errors of metabolism typically occur?

A

Onset varies from birth to adolescence.

121
Q

What is the prognosis of severe forms of inborn errors of metabolism?

A

high degree of mortality.

122
Q

What is Wilson’s Disease?

A

Wilson’s Disease is an inborn error of metabolism characterized by excessive copper accumulation in the body

123
Q

What is Alpha-1 Antitrypsin Deficiency?

A

A deficiency in the alpha-1 antitrypsin enzyme, which can lead to liver and lung disease.

124
Q

What is Hemochromatosis?

A

A metabolic disorder causing excessive iron storage in various organs, potentially leading to organ damage

125
Q

What is Wilson’s Disease and its other name?

A

Wilson’s Disease, also known as hepatolenticular degeneration

is an autosomal recessive disease characterized by impaired copper metabolism

126
Q

What does excessive copper buildup cause in Wilson’s Disease?

A

It leads to oxidative stress in the liver, basal ganglia, and cornea.

127
Q

What is the range of symptoms in Wilson’s Disease?

A

asymptomatic
sudden-onset liver failure
neurologic
psychiatric manifestations.

128
Q

How is Wilson’s Disease diagnosed?

A

lab tests such as
- serum ceruloplasmin
- aminotransferases
- urine copper level
- possible liver biopsy for copper level.

129
Q

What are the treatment options for Wilson’s Disease?

A

copper-chelation therapy and oral zinc to bind copper in the gastrointestinal tract.

130
Q

What is alpha-1 antitrypsin deficiency?

A

A genetic disorder resulting in defective alpha-1 antitrypsin protein.

131
Q

What does alpha-1 antitrypsin protein protect against?

A

It protects the liver and lungs from neutrophil elastase an enzyme that can disrupt connective tissues and cause inflammation.

132
Q

What damage does neutrophil elastase cause if not regulated?

A

It can lead to inflammation, cirrhosis, and hepatocellular carcinoma (HCC)

133
Q

How common is alpha-1 antitrypsin deficiency?

A

The incidence ranges from 1 in 16,000 to 1 in 35,000, but is likely underdiagnosed.

134
Q

What is the significance of alpha-1 antitrypsin deficiency in pediatric liver transplants?

A

It is the #1 genetic cause of liver transplant in children.

135
Q

How is alpha-1 antitrypsin deficiency diagnosed?

A

alpha-1 antitrypsin phenotyping.

136
Q

What treatment is effective for the pulmonary symptoms of alpha-1 antitrypsin deficiency?

A

Pooled alpha-1 antitrypsin

137
Q

What is the only curative treatment for liver disease caused by alpha-1 antitrypsin deficiency?

A

Liver transplant

138
Q

What is hemochromatosis?

A

excess iron in the body, leading to multi-organ dysfunction.

139
Q

How can hemochromatosis occur?

A

It may be genetic, causing excessive intestinal absorption of iron, or caused by repetitive blood transfusions or high-dose iron infusions.

140
Q

What happens when excess iron accumulates in the body?

A

t accumulates in organs and causes damage to the tissues.

141
Q

What conditions might patients with hemochromatosis present with?

A

cirrhosis
heart failure
diabetes
adrenal insufficiency
polyarthropathy.

142
Q

What lab findings are indicative of hemochromatosis?

A

Elevated AST/ALT
transferrin saturation
ferritin levels.

143
Q

How is hemochromatosis diagnosed?

A

genetic mutation testing
echocardiogram
MRI
potentially liver biopsy to quantify iron levels and assess damage.

144
Q

Which imaging techniques are used to diagnose cardiomyopathies and liver abnormalities in hemochromatosis?

A

Echocardiogram and MRI.

145
Q

How can iron levels in the liver be quantified?

A

Liver biopsy

146
Q

What are the treatment options for hemochromatosis?

A

weekly phlebotomy
iron-chelating drugs
potentially a liver transplant.

147
Q

```

What is Primary Biliary Cholangitis (PBC)?

A

An autoimmune disease

previously known as biliary cirrhosis

involving the
- progressive destruction of bile ducts
- periportal inflammation
- cholestasis.

148
Q

What are the possible long-term consequences of PBC?

A

Can lead to liver scarring, fibrosis, and ultimately, cirrhosis.

149
Q

Who is most commonly affected by PBC?

A

Females

often diagnosed in middle-aged individuals.

150
Q

What is thought to contribute to the development of PBC?

A

Thought to be caused by exposure to environmental toxins in genetically susceptible individuals.

151
Q

What are common symptoms of PBC?

A

Symptoms include jaundice, fatigue, and itching.

152
Q

What lab findings are typically elevated in PBC?

A

Labs reveal increased
- Alkaline Phosphatase (Alk Phos),
- Gamma-Glutamyl Transferase (GGT), and
- Positive Antimitochondrial antibodies.

153
Q

Which imaging tests are used in PBC to rule out bile duct obstructions?

A

CT scan, MRI, and Magnetic Resonance Cholangiopancreatography (MRCP).

154
Q

What can a liver biopsy reveal in a patient with PBC?

A

Liver biopsy reveals bile duct destruction and infiltration with lymphocytes.

155
Q

How is PBC treated?

A

There is no cure, but treatment with exogenous bile acids can slow the progression of the disease.

156
Q

What is Primary Sclerosing Cholangitis (PSC)?

A

PSC is an autoimmune, chronic disease that causes inflammation and fibrosis of both intrahepatic and extrahepatic bile ducts.

157
Q

```

How does PSC affect the biliary system?

A

Fibrosis in the biliary tree leads to strictures

giving a “beads on a string” appearance on imaging

can progress to cirrhosis and end-stage liver disease (ESLD).

158
Q

```

Who is more likely to develop PSC and at what age?

A

Males are more commonly affected than females, typically diagnosed around their 40s.

159
Q

What are the symptoms of PSC?

A

fatigue
itching
deficiencies of fat-soluble vitamins (A, D, E, K)
complications from cirrhosis.

160
Q

Which lab findings are associated with PSC?

A

Elevated alkaline phosphatase and gamma-glutamyl-transferase, and the presence of auto-antibodies.

161
Q

What imaging techniques are used to diagnose PSC?

A

Magnetic Resonance Cholangiopancreatography (MRCP) or Endoscopic Retrograde Cholangiopancreatography (ERCP) showing biliary strictures with dilated bile ducts.

162
Q

Is a liver biopsy always necessary for diagnosing PSC?

A

A liver biopsy can reinforce the diagnosis but isn’t always performed due to its invasive nature and potential complications.

163
Q

What are the treatment options for PSC?

A

While no drug treatments have been proven to be effective

exogenous bile acids have been used to slow progression

Ultimately, liver transplantation may be necessary.

164
Q

What is a concern after a liver transplant for PSC?

A

The autoimmune nature of PSC may lead to recurrence after liver transplantation.

165
Q

Sclerosing cholangitis v. biliary cholangitis image:

A
166
Q

What is acute liver failure?

A

severe liver injury occurring within days to 6 months after an insult

characterized by a
- rapid increase in liver enzymes
- altered mental status
- coagulopathy.

167
Q

hat is the most common cause of acute liver failure?

A

Almost 50% of cases are drug-induced, with the majority due to acetaminophen overdose.

168
Q

What are other causes of acute liver failure besides drugs?

A

viral hepatitis,
autoimmune disorders,
hypoxia,
acute fatty liver of pregnancy,
HELLP syndrome.

169
Q

What symptoms can present in acute liver failure?

A

jaundice,
nausea,
right upper quadrant pain,
cerebral edema,
encephalopathy,
multi-organ failure
potentially death.

170
Q

How is acute liver failure treated?

A

Treatment involves addressing the underlying cause, providing supportive care, and potentially a liver transplant.

171
Q

Definition of Cirrhosis

A

Cirrhosis is the final stage of liver disease where normal liver parenchyma is replaced with scar tissue

172
Q

Early Stages of Cirrhosis

A

Often asymptomatic in early stages, making it difficult to detect without specific testing.

173
Q

Symptoms as Cirrhosis Progresses

A

jaundice,
ascites,
varices,
coagulopathy,
encephalopathy as the condition worsens.

174
Q

**

Common Causes of Cirrhosis

A

alcoholic fatty liver disease
non-alcoholic fatty liver disease (NAFL),
hepatitis C virus (HCV)
hepatitis B virus (HBV).

175
Q

Laboratory Findings in Cirrhosis

A

Elevated labs include
AST/ALT,
bilirubin,
alkaline phosphatase,
(PT/INR).

176
Q

Hematologic Changes in Cirrhosis

A

Thrombocytopenia, a reduction in platelet count, is a common complication.

177
Q

Cure for Cirrhosis

A

The only cure for cirrhosis is a liver transplant.

178
Q

What is portal hypertension in the context of cirrhosis, and what is a significant indicator of its presence?

A

Portal hypertension is an increase in blood pressure within the portal venous system,

hepatic venous pressure gradient (HVPG) greater than 5 is a significant indicator.

179
Q

Which complication is the most common in cirrhosis and what leads to its development?

A

Ascites

developed due to portal hypertension which leads to increased blood volume and fluid accumulation in the peritoneal cavity.

180
Q

How is ascites managed in patients with cirrhosis?

A

low-sodium diet and albumin replacement therapy.

181
Q

What is TIPS and its role in the management of cirrhosis complications?

A

The Transjugular Intrahepatic Portosystemic Shunt (TIPS) is a procedure that reduces portal hypertension and can help manage ascites

182
Q

What is the most common infection related to cirrhosis, and how is it treated?

A

Spontaneous Bacterial Peritonitis (SBP)

requiring prompt antibiotic treatment.

183
Q

How common are varices in patients with cirrhosis?

A

Varices are present in approximately 50% of patients with cirrhosis.

184
Q

What is the most lethal complication associated with varices in cirrhosis patients?

A

Hemorrhage

185
Q

How can the risk of hemorrhage from varices be reduced?

A

Beta-blockers help reduce the risk, and prophylactic endoscopic variceal banding and ligation can also be employed.

186
Q

What is the treatment for refractory bleeding from varices?

A

Refractory bleeding may be managed with balloon tamponade.

187
Q

What causes hepatic encephalopathy in patients with cirrhosis?

A

It is due to the buildup of nitrogenous waste because of poor liver detoxification.

188
Q

What are the neuropsychiatric symptoms associated with hepatic encephalopathy?

A

Symptoms can range from cognitive impairment to coma.

189
Q

How is hepatic encephalopathy treated?

A

Lactulose and Rifaximin to decrease ammonia-producing bacteria in the gut.

190
Q

How common are varices in cirrhosis patients and what is the most lethal complication?

A

Varices are present in approximately 50% of patients with cirrhosis, and hemorrhage from these varices is the most lethal complication.

191
Q

What is the mechanism behind hepatorenal syndrome in cirrhosis?

A

It is caused by excess endogenous vasodilators like nitric oxide (NO) and prostaglandins (PGs)

leading to decreased systemic mean arterial pressure (MAP) and renal blood flow (RBF)

192
Q

What are the treatment options for hepatorenal syndrome?

A

Treatment includes midodrine, octreotide, and albumin.

193
Q

What is hepatopulmonary syndrome and what unique symptom does it present with?

A

Hepatopulmonary syndrome is a triad of chronic liver disease, hypoxemia, and intrapulmonary vascular dilation with platypnea - hypoxemia when upright—due to a right-to-left intrapulmonary shunt.

194
Q

What is portopulmonary hypertension and what triggers it?

A

Portopulmonary hypertension is pulmonary hypertension that occurs in conjunction with portal hypertension.

Systemic vasodilation triggers the production of pulmonary vasoconstrictors.

195
Q

What are the treatment options for portopulmonary hypertension?

A

PD-I’s (phosphodiesterase inhibitors)
nitric oxide (NO),
prostacyclin analogs
endothelin receptor antagonists.

196
Q

What is the only cure for these complications of cirrhosis?

A

A liver transplant is the only cure.

197
Q

When is elective surgery contraindicated for patients with liver disease?

A

acute hepatitis, severe chronic hepatitis, and acute liver failure (ALF).

198
Q

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

A

Child-Turcotte-Pugh (CTP)

Model for End-Stage Liver Disease (MELD).

199
Q

What parameters are included in the Child-Turcotte-Pugh (CTP) scoring system?

A

The CTP score is based on bilirubin, albumin, prothrombin time (PT), presence of encephalopathy, and ascites.

200
Q

What factors are considered in the Model for End-Stage Liver Disease (MELD) score?

A

bilirubin,
international normalized ratio (INR),
creatinine,
sodium levels.

201
Q

Child-Turcotte-Pugh Class A Prognosis

What are the 1-year and 2-year survival rates for Class A liver disease according to the Child-Turcotte-Pugh score?

A

The 1-year survival rate for Class A is 100%, and the 2-year survival rate is 85%.

202
Q

Child-Turcotte-Pugh Class B Prognosis

What is the survival prognosis for Class B liver disease as per the Child-Turcotte-Pugh score?

A

Class B liver disease has a 1-year survival rate of 81% and a 2-year survival rate of 57%.

203
Q

Child-Turcotte-Pugh Class C Prognosis

What are the 1-year and 2-year survival rates for Class C liver disease based on the Child-Turcotte-Pugh score?

A

For Class C liver disease, the 1-year survival rate is 45%, and the 2-year survival rate is 35%.

204
Q

MELD Score Under 10 Prognosis

What is the observed mortality rate for a patient with a MELD score under 10?

A

The observed mortality rate for a MELD score under 10 is between 1.9% and 3.7%.

205
Q

MELD Score 10-19 Prognosis

What is the observed mortality rate for a MELD score between 10 and 19?

A

or a MELD score between 10 and 19, the observed mortality rate is between 6% and 20%.

206
Q

MELD Score 20-29 Prognosis

What is the observed mortality rate for a MELD score between 20 and 29?

A

The observed mortality rate for a MELD score between 20 and 29 is between 19.6% and 45.5%.

207
Q

MELD Score 30-39 Prognosis

How does a MELD score of 30 to 39 affect 3-month survival?

A

A MELD score of 30 to 39 correlates with an observed mortality rate between 52.6% and 74.5%.

208
Q

MELD Score 40 or Above Prognosis

What does a MELD score of 40 or above indicate about 3-month survival?

A

A MELD score of 40 or above is associated with an observed mortality rate of 71.3% to 100%.

209
Q

Anesthesia in Liver disease

Initial Assessment for Liver Disease

How do you begin preoperative risk assessment in a patient undergoing elective surgery?

Slide 40

A

First, determine if the patient has cirrhosis.

210
Q

Anesthesia in Liver disease

Risk Stratification in Cirrhosis

What scoring systems are used for risk stratification in patients with cirrhosis?

Slide 40

A

Use the MELD or Child-Turcotte-Pugh (CTP) score for risk stratification.

211
Q

Anesthesia in Liver disease

Proceeding to Surgery with Low MELD or CTP Score

Can patients with a low MELD or Child class A score proceed to surgery?

Slide 40

A

Yes, patients with MELD <10 or Child class A can proceed to the operating room (OR) with careful postoperative monitoring.

212
Q

Anesthesia in Liver disease

Considerations for Intermediate MELD or CTP Score

What should be considered for patients with a MELD score of 10-15 or Child class B?

Slide 40

A

Assess the presence of portal hypertension. If absent, proceed to the OR with careful postoperative monitoring. If present, consider preoperative TIPS placement and discuss procedure-specific risks.

213
Q

Anesthesia in Liver disease

High-Risk Patients with High MELD or CTP Score

What is the recommended approach for patients with a MELD score >16 or Child class C?

Slide 40

A

Consider alternatives to surgery and workup for transplantation due to high risk.

214
Q

Anesthesia in Liver disease

Handling Portal Hypertension Preoperatively

What is the suggested management for patients with cirrhosis and portal hypertension?

Slide 40

A

Consider preoperative TIPS placement and discuss specific risks and patient-specific optimization before the operation.

215
Q

What should be emphasized during preoperative evaluation for a patient with liver disease?

A

A careful history and physical examination are crucial.

216
Q

Which standard preoperative labs are essential for patients with liver disease?

A

Complete blood count (CBC),
basic metabolic panel
(PT/INR)

217
Q

What is the recommendation regarding invasive monitoring in patients with liver disease?

A

There is a low threshold for employing invasive monitoring due to increased risks.

218
Q

What are the increased risks during anesthesia in patients with liver disease?

A

Patients have higher risks of aspiration, hypotension (HoTN), and hypoxemia.

219
Q

Between colloids and crystalloids, which is preferred for fluid resuscitation in liver disease, and why?

A

Colloids are preferred over crystalloids for resuscitation to optimize intravascular volume without worsening ascites.

220
Q

How does alcoholism affect the minimum alveolar concentration (MAC) of volatile anesthetics?

A

Alcoholism can increase the MAC of volatile anesthetics, possibly requiring higher doses.

221
Q

What should be considered when selecting anesthetic drugs for patients with liver disease?

A

medications not metabolized by the liver, such as succinylcholine and cisatracurium are ideal.

222
Q

How might severe liver disease affect plasma cholinesterase levels?

A

Plasma cholinesterase activity may be decreased, affecting the metabolism of certain drugs.

223
Q

How is bleeding and coagulation managed in patients with liver disease under anesthesia?

A

Bleeding and coagulation should be closely monitored, and management might include transfusion of blood products and administration of coagulation factors.

224
Q

Primary Indications for TIPS

A

refractory variceal hemorrhage and refractory ascites.

225
Q

Contraindications for TIPS

A

patients with heart failure
tricuspid regurgitation
severe pulmonary hypertension.

226
Q

What is the definitive treatment for End-Stage Liver Disease (ESLD)?

A

Liver transplant is the definitive treatment for ESLD.

227
Q

What are the most common indications for liver transplant?

A

Alcoholic liver disease is the most common indication

followed by fatty liver disease and hepatocellular carcinoma (HCC)

228
Q

How is a living donor liver transplant typically conducted?

A

Surgeries are timed together, and there is minimal ischemia time for the donated liver.

229
Q

How are brain-dead donors managed to preserve organ viability?

A

Hemodynamic stability is maintained to ensure organ perfusion.

230
Q

What are the key aspects of intraoperative management during liver transplant?

A

Maintain hemodynamics with readily available
- pressors/inotropes,
- utilize arterial lines,
- central venous catheters,
- pulmonary artery catheters,
- transesophageal echocardiography (TEE),
- control coagulation.

231
Q

What are preoperative surgical considerations for liver transplantation?

A

Preoperative surgical considerations include transplantation evaluation, which covers psychological evaluation, MELD score assessment, and UNOS listing.

232
Q

What are preoperative anesthetic considerations for liver transplantation?

A

evaluation,
establishing vascular access,
ensuring blood product availability.

233
Q

What are the surgical considerations during the dissection phase of liver transplantation?

A

surgical incision,
mobilization of liver and vascular structures,
isolation of bile duct.

234
Q

What are the anesthetic considerations during the dissection phase of liver transplantation?

A

managing hemodynamic compromise from
- loss of ascites,
- hemorrhage during dissection,
- decreased venous return.

235
Q

: What surgical considerations are made during the anhepatic phase of liver transplantation?

A

clamping of the hepatic artery and portal vein,
removal of the diseased liver,
anastomosis of the IVC and portal vein of the donor liver.

236
Q

What are the anesthetic considerations during the anhepatic phase of liver transplantation?

A

focus on hemodynamic compromise from full or partial IVC clamping,
metabolic acidosis,
hypocalcemia from citrate intoxication,
hyperkalemia,
hypothermia
hypoglycemia.

237
Q

What occurs during the reperfusion phase of liver transplantation from a surgical standpoint?

A

The reperfusion phase involves anastomosis of the hepatic artery and biliary system, and reperfusion of the transplanted liver.

238
Q

What are the anesthetic considerations during the reperfusion phase of liver transplantation?

A

Anesthetic considerations during reperfusion include managing hemodynamic instability, dysrhythmias, hyperkalemia, acidosis, pulmonary emboli, and cardiac arrest.

239
Q

What are post-transplantation surgical considerations in liver transplantation?

A

Post-transplantation surgical considerations include hemostasis, evaluation of graft function, and ultrasound for vascular patency.

240
Q

What are the post-transplantation anesthetic considerations in liver transplantation?

A

Post-transplantation anesthetic considerations include ICU admission, timing of extubation (early or late), and ongoing hemodynamic management.

241
Q

Lab: Aminotransferases

Predominant abnormality in:

  • Bilirubin overlad
  • Hepatocellular Injury
  • Cholethiasis
A
  • Bilirubin Overload (Hemolysis): Normal
  • Hepatocellular Injury: Increased; May be normal or decreased in advanced stages
  • Cholestasis: Normal; May be increased in advanced stages
242
Q

Lab: Serum albumin

Predominant abnormality in:

  • Bilirubin overlad
  • Hepatocellular Injury
  • Cholethiasis
A
  • Bilirubin Overload (Hemolysis): Normal
  • Hepatocellular Injury: Decreased; May be normal in acute fulminant hepatic failure
  • Cholestasis: Normal; May be decreased in advanced stages
243
Q

Lab: Prothrombin time

Predominant abnormality in:

  • Bilirubin overlad
  • Hepatocellular Injury
  • Cholethiasis
A
  • Bilirubin Overload (Hemolysis): Normal
  • Hepatocellular Injury: Prolonged
  • Cholestasis: Normal; May be prolonged in advanced stages
244
Q

Lab: Bilirubin (main form present)Bilirubin Overload (Hemolysis): Unconjugated (also mild increase in conjugates)
Hepatocellular Injury: Conjugated
Cholestasis: Conjugated

Predominant abnormality in:

  • Bilirubin overlad
  • Hepatocellular Injury
  • Cholethiasis
A
  • Bilirubin Overload (Hemolysis): Unconjugated (also mild increase in conjugates)
  • Hepatocellular Injury: Conjugated
  • Cholestasis: Conjugated
245
Q

Lab: Alkaline phosphatase

Predominant abnormality in:

  • Bilirubin overlad
  • Hepatocellular Injury
  • Cholethiasis
A
  • Bilirubin Overload (Hemolysis): Normal
  • Hepatocellular Injury: Normal; May be increased by hepatic infiltrative disease
  • Cholestasis: Increased
246
Q

Lab: γ-Glutamyl transpeptidase (GGT)

Predominant abnormality in:

  • Bilirubin overlad
  • Hepatocellular Injury
  • Cholethiasis
A
  • Bilirubin Overload (Hemolysis): Normal
  • Hepatocellular Injury: Normal
  • Cholestasis: Increased
247
Q

Lab: Blood urea nitrogen

Predominant abnormality in:

  • Bilirubin overlad
  • Hepatocellular Injury
  • Cholethiasis
A
  • Bilirubin Overload (Hemolysis): Normal; May be increased by renal dysfunction
  • Hepatocellular Injury: Normal; May be decreased by severe liver disease and normal kidney function
  • Cholestasis: Normal
248
Q

Lab: BSP/ICG (dye)

Predominant abnormality in:

  • Bilirubin overlad
  • Hepatocellular Injury
  • Cholethiasis
A
  • Bilirubin Overload (Hemolysis): Normal
  • Hepatocellular Injury: Retention of dye
  • Cholestasis: Normal or retention of dye
249
Q

Alcoholic Liver Disease (ALD) in America

A
  • ALD is increasing in prevalence.
  • Most common cause of cirrhosis.

TX WES class of 2026 (18 decks)

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