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Assessment '24 - Mordecai > 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

The liver detoxifies the blood 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 III, IV, 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

The liver aids in volume control 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

The right and left lobes of the liver are separated 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, empty into the inferior vena cava (IVC).

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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

Bile enters the duodenum 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 has the highest proportionate COP of all organs.

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19
Q

Where does the portal vein arise from?

A

The portal vein arises from 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 hepatic artery branches off from 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

Oxygen delivery to the liver is divided: 50% via the portal vein (deoxygenated) and 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

Portal venous pressure reflects 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

Late-stage liver disease may present with vague symptoms such as disrupted sleep and decreased appetite.

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33
Q

What are some common 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:

Standard labs:
-BMP
- CBC
- PT/INR

Liver enzymes:
- 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

Reduced synthetic function of the liver is indicated by 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, while 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

Risk factors for cholelithiasis include obesity, high cholesterol levels, diabetes mellitus (DM), pregnancy, being female, and a 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

Initial symptoms include nausea, vomiting, cramping, and right upper quadrant (RUQ) pain, known as biliary colic.

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51
Q

What are the symptoms of cholangitis?

A

Symptoms of cholangitis (inflammation of the CBD) include fever, rigors (shaking chills), and 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

During ERCP, an endoscopist 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

Patients are usually placed in a prone position with left tilt during ERCP to facilitate the procedure. 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

Unconjugated hyperbilirubinemia occurs due to an imbalance between bilirubin synthesis and conjugation.

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62
Q

What causes conjugated (direct) hyperbilirubinemia?

A

Conjugated hyperbilirubinemia is caused by an obstruction in the biliary system, leading 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) is the most common viral hepatitis requiring liver transplant in the US.

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67
Q

What is the recommended treatment for hepatitis C?

A

Treatment for hepatitis C depends on factors such as genotype, stage of the disease, and presence of cirrhosis.

A common treatment 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

Alcoholic Liver Disease (ALD) in America

A
  • ALD is increasing in prevalence.
  • Most common cause of cirrhosis.
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75
Q

ALD and Liver Transplants

A
  • 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.
  • Stigma contributes to underreporting.
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77
Q

Reporting of ALD

A

Underreporting of ALD is common due to stigma.

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78
Q

Progression of ALD

A
  • Initially may show no symptoms.
  • Symptoms of liver failure emerge as it progresses.
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79
Q

Treating ALD

A

Abstinence from alcohol is central to treatment.

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80
Q

Management of ALD Symptoms

A

Treatment includes managing symptoms of liver failure.

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81
Q

ALD and Platelet Count

A

Plt count <50,000 requires transfusion

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82
Q
A

Platelet count below 50,000 may necessitate a blood transfusion.

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83
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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84
Q

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

A

Malnutrition

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85
Q

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

A

Muscle wasting

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86
Q

Which gland enlargement is associated with chronic ALD?

A

Parotid gland hypertrophy

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87
Q

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

A

Jaundice

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88
Q

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

A

Thrombocytopenia

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89
Q

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

A

Ascites

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90
Q

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

A

Hepatosplenomegaly

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91
Q

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

A

Pedal edema

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92
Q

When may symptoms of alcohol withdrawal occur after stopping drinking?

A

24-72 hours after cessation of alcohol intake

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93
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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94
Q

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

A

Liver enzymes

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95
Q

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

A

Gamma-glutamyl transferase (GGT)

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96
Q

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

A

Bilirubin

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97
Q

What lab test measures acute alcohol intoxication?

A

Blood ethanol level

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98
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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99
Q

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

A

NAFLD is diagnosed when hepatocytes contain more than 5% fat.

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100
Q

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

A

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

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101
Q

What conditions can NAFLD progress to?

A

NAFLD can progress to non-alcoholic steatohepatitis (NASH), cirrhosis, and hepatocellular carcinoma.

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102
Q
A
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103
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.

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104
Q

What methods are used for the diagnosis of NAFLD?

A

Diagnosis is made through imaging and histology.

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105
Q

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

A

Liver biopsy is the gold standard in distinguishing NAFLD from other liver diseases.

106
Q

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

A

The primary treatments include diet and exercise.

107
Q

When is a liver transplant indicated for NAFLD?

A

Liver transplant is indicated for advanced fibrosis, cirrhosis, and related complications.

108
Q

NAFLD Prevalence: diabetics and severely obese people?

A

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

109
Q

NAFLD: Non-diabetics/obese people

A

1 in 4 people have NAFLD regardless of weight

110
Q

Types of Fatty Liver Image:

A
111
Q

Who is predominantly affected by autoimmune hepatitis (AIH)?

A

Predominantly affects women.

112
Q

How does autoimmune hepatitis (AIH) present symptomatically?

A

May be asymptomatic, acute, or chronic.

113
Q

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

A

Positive autoantibodies & hypergammaglobulinemia.

114
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.

115
Q

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

A

Treatment includes steroids and azathioprine.

116
Q

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

A

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

117
Q

How is refractory autoimmune hepatitis (AIH) managed?

A

Refractory disease requires increased immunosuppression.

118
Q

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

A

Indicated when treatment fails or acute liver failure ensues.

119
Q

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

A

The most common cause is acetaminophen overdose.

120
Q

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

A

Normally reversible after the drug is removed

121
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.

122
Q

How common are inborn errors of metabolism?

A

They occur in 1 out of every 2500 births.

123
Q

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

A

Onset varies from birth to adolescence.

124
Q

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

A

Most severe forms appear in the neonatal period and carry a high degree of mortality.

125
Q

What is Wilson’s Disease?

A

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

126
Q

What is Alpha-1 Antitrypsin Deficiency?

A

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

127
Q

What is Hemochromatosis?

A

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

128
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.

129
Q

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

A

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

130
Q

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

A

ymptoms range from being asymptomatic to sudden-onset liver failure, as well as neurologic and psychiatric manifestations.

131
Q

How is Wilson’s Disease diagnosed?

A

Through lab tests such as serum ceruloplasmin, aminotransferases, and urine copper level, with a possible liver biopsy for copper level.

132
Q

What are the treatment options for Wilson’s Disease?

A

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

133
Q

What is alpha-1 antitrypsin deficiency?

A

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

134
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.

135
Q

What damage does neutrophil elastase cause if not regulated?

A

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

136
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.

137
Q

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

A

It is the number one genetic cause of liver transplant in children.

138
Q

How is alpha-1 antitrypsin deficiency diagnosed?

A

Diagnosis is confirmed with alpha-1 antitrypsin phenotyping.

139
Q

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

A

Pooled alpha-1 antitrypsin is effective for treating pulmonary symptoms.

140
Q

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

A

Liver transplant is the only curative treatment for the liver disease associated with this condition.

141
Q

What is hemochromatosis?

A

A disorder associated with excess iron in the body, leading to multi-organ dysfunction.

142
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.

143
Q

What happens when excess iron accumulates in the body?

A

It accumulates in organs and causes damage to the tissues.

144
Q

What conditions might patients with hemochromatosis present with?

A

Patients may present with cirrhosis, heart failure, diabetes, adrenal insufficiency, or polyarthropathy.

145
Q

What lab findings are indicative of hemochromatosis?

A

Elevated AST/ALT, transferrin saturation, and ferritin levels.

146
Q

How is hemochromatosis diagnosed?

A

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

147
Q

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

A

Echocardiogram and MRI.

148
Q

How can iron levels in the liver be quantified?

A

Liver biopsy may be performed to quantify iron levels and assess the level of damage.

149
Q

What are the treatment options for hemochromatosis?

A

Treatment includes weekly phlebotomy, iron-chelating drugs, and potentially a liver transplant.

150
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, and cholestasis.

151
Q

What are the possible long-term consequences of PBC?

A

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

152
Q

Who is most commonly affected by PBC?

A

Females are affected more than males; often diagnosed in middle-aged individuals.

153
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.

154
Q

What are common symptoms of PBC?

A

Symptoms include jaundice, fatigue, and itching.

155
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.

156
Q

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

A

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

157
Q

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

A

Liver biopsy reveals bile duct destruction and infiltration with lymphocytes.

158
Q

How is PBC treated?

A

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

159
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.

160
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, and can progress to cirrhosis and end-stage liver disease (ESLD).

161
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.

162
Q

What are the symptoms of PSC?

A

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

163
Q

Which lab findings are associated with PSC?

A

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

164
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.

165
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.

166
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.

167
Q

What is a concern after a liver transplant for PSC?

A

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

168
Q

Sclerosing cholangitis v. biliary cholangitis image:

A
169
Q

What is acute liver failure?

A

A life-threatening condition with severe liver injury occurring within days to 6 months after an insult, characterized by a rapid increase in liver enzymes, altered mental status, and coagulopathy.

170
Q

What is the most common cause of acute liver failure?

A

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

171
Q

What are other causes of acute liver failure besides drugs?

A

Other causes include viral hepatitis, autoimmune disorders, hypoxia, acute fatty liver of pregnancy, and HELLP syndrome.

172
Q

What happens at the cellular level during acute liver failure?

A

Hepatocyte necrosis, which leads to cellular swelling and membrane disruption.

173
Q

What symptoms can present in acute liver failure?

A

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

174
Q

How is acute liver failure treated?

A

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

175
Q

Definition of Cirrhosis

A

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

176
Q

Early Stages of Cirrhosis

A

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

177
Q

Symptoms as Cirrhosis Progresses

A

Symptoms progress to jaundice, ascites, varices, coagulopathy, and encephalopathy as the condition worsens.

178
Q

**

Common Causes of Cirrhosis

A

The most common causes include alcoholic fatty liver disease, non-alcoholic fatty liver disease (NAFL), hepatitis C virus (HCV), and hepatitis B virus (HBV).

179
Q

Laboratory Findings in Cirrhosis

A

Elevated labs include AST/ALT, bilirubin, alkaline phosphatase, and prolonged prothrombin time/international normalized ratio (PT/INR).

180
Q

Hematologic Changes in Cirrhosis

A

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

181
Q

Cure for Cirrhosis

A

The only cure for cirrhosis is a liver transplant.

182
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, and a hepatic venous pressure gradient (HVPG) greater than 5 is a significant indicator.

183
Q

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

A

Ascites is the most common complication of cirrhosis, developed due to portal hypertension which leads to increased blood volume and fluid accumulation in the peritoneal cavity.

184
Q

How is ascites managed in patients with cirrhosis?

A

Management of ascites typically involves a low-sodium diet and albumin replacement therapy.

185
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.

186
Q

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

A

Spontaneous Bacterial Peritonitis (SBP) is the most common infection related to cirrhosis, requiring prompt antibiotic treatment.

187
Q

How common are varices in patients with cirrhosis?

A

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

188
Q

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

A

Hemorrhage is the most lethal complication of varices.

189
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.

190
Q

What is the treatment for refractory bleeding from varices?

A

Refractory bleeding may be managed with balloon tamponade.

191
Q

What causes hepatic encephalopathy in patients with cirrhosis?

A

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

192
Q

What are the neuropsychiatric symptoms associated with hepatic encephalopathy?

A

Symptoms can range from cognitive impairment to coma.

193
Q

How is hepatic encephalopathy treated?

A

reatment includes the use of Lactulose and Rifaximin to decrease ammonia-producing bacteria in the gut.

194
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.

195
Q

What treatments help reduce the risk of hemorrhage from varices in cirrhosis?

A

Beta blockers are used to reduce the risk, along with prophylactic endoscopic variceal banding and ligation.

196
Q

What is the treatment for refractory bleeding from varices?

A

efractory bleeding may be treated with balloon tamponade.

197
Q

What leads to the development of hepatic encephalopathy in cirrhosis and what are the symptoms?

A

The buildup of nitrogenous waste due to poor liver detoxification leads to hepatic encephalopathy, with symptoms ranging from cognitive impairment to coma.

198
Q

How is hepatic encephalopathy treated?

A

Treatment includes lactulose and rifaximin to decrease ammonia-producing bacteria in the gut.

199
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).

200
Q

What are the treatment options for hepatorenal syndrome?

A

Treatment includes midodrine, octreotide, and albumin.

201
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.

202
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.

203
Q

What are the treatment options for portopulmonary hypertension?

A

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

204
Q

What is the only cure for these complications of cirrhosis?

A

A liver transplant is the only cure.

205
Q

When is elective surgery contraindicated for patients with liver disease?

A

Elective surgery is contraindicated in cases of acute hepatitis, severe chronic hepatitis, and acute liver failure (ALF).

206
Q

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

A

The two scoring systems are the Child-Turcotte-Pugh (CTP) and the Model for End-Stage Liver Disease (MELD).

207
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.

208
Q

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

A

The MELD score is based on bilirubin, international normalized ratio (INR), creatinine, and sodium levels.

209
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%.

CTP-A - 1= 100%
CTP-A - 2= 85%

210
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%.

211
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%.

CTP-C-1 = 45%
CTP-C-2 = 35%

212
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%.

213
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%.

214
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%.

215
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%.

216
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%.

217
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.

218
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.

219
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.

220
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.

221
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.

222
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.

223
Q

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

A

A careful history and physical examination are crucial.

224
Q

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

A

Complete blood count (CBC), basic metabolic panel (BMP), and prothrombin time/international normalized ratio (PT/INR) are standard.

225
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.

226
Q

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

A

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

227
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.

228
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.

229
Q

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

A

Drugs may have a slow onset and prolonged duration of action; medications not metabolized by the liver, such as succinylcholine and cisatracurium, are ideal.

230
Q

How might severe liver disease affect plasma cholinesterase levels?

A

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

231
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.

232
Q
A
233
Q

```

What is the TIPS Procedure?

A

TIPS is a procedure to manage portal hypertension where a stent or graft is placed between the hepatic vein and portal vein, shunting portal blood flow to the systemic circulation, thus reducing the portosystemic pressure gradient.

234
Q

Primary Indications for TIPS

A

The primary indications for TIPS are refractory variceal hemorrhage and refractory ascites.

235
Q

Contraindications for TIPS

A

TIPS is contraindicated in patients with heart failure, tricuspid regurgitation, or severe pulmonary hypertension.

236
Q

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

A

Liver transplant is the definitive treatment for ESLD.

237
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).

238
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.

239
Q

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

A

Hemodynamic stability is maintained to ensure organ perfusion.

240
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, and transesophageal echocardiography (TEE), and control coagulation.

241
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.

242
Q

What are preoperative anesthetic considerations for liver transplantation?

A

Preoperative anesthetic considerations include evaluation, establishing vascular access, and ensuring blood product availability.

243
Q

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

A

The surgical considerations during dissection include surgical incision, mobilization of liver and vascular structures, and isolation of bile duct.

244
Q

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

A

Anesthetic considerations during dissection involve managing hemodynamic compromise from loss of ascites, hemorrhage during dissection, and decreased venous return.

245
Q

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

A

Surgical considerations during the anhepatic phase include clamping of the hepatic artery and portal vein, removal of the diseased liver, and anastomosis of the IVC and portal vein of the donor liver.

246
Q

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

A

Anesthetic considerations during the anhepatic phase focus on hemodynamic compromise from full or partial IVC clamping, metabolic acidosis, hypocalcemia from citrate intoxication, hyperkalemia, hypothermia, and hypoglycemia.

247
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.

248
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.

249
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.

250
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.

251
Q

Lab: Aminotransferases

Predominant abnormality in:

  • Bilirubin overload
  • 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
252
Q

Lab: Serum albumin

Predominant abnormality in:

  • Bilirubin overload
  • 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
253
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
254
Q

Lab: Bilirubin (main form present)

Predominant abnormality in:

  • Bilirubin overload
  • Hepatocellular Injury
  • Cholethiasis
A
  • Bilirubin Overload (Hemolysis): Unconjugated (also mild increase in conjugates)
  • Hepatocellular Injury: Conjugated
  • Cholestasis: Conjugated
255
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
256
Q

Lab: γ-Glutamyl transpeptidase (GGT)

Predominant abnormality in:

  • Bilirubin overlad
  • Hepatocellular Injury
  • Cholethiasis
A
  • Bilirubin Overload (Hemolysis): Normal
  • Hepatocellular Injury: Normal
  • Cholestasis: Increased
257
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
258
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

BSP (Bromosulfophthalein) is a diagnostic dye used historically for liver function tests, now largely outdated. ICG (Indocyanine Green) is a dye still used for assessing liver function, cardiac output, and for imaging blood vessels in medical diagnostics.

259
Q

What is Partial Hepatectomy?

A

Resection to remove neoplasms

Ensures adequate liver tissue remains for regeneration

260
Q

Resection Parameters in Partial Hepatectomy

A

Depends on preexisting liver disease and function
Up to 75% removal tolerated with normal liver function

261
Q

Anesthetic Considerations for Hepatectomy

A

Invasive monitoring required
Blood products should be available
Ensure adequate vascular access for blood/pressors

262
Q

Managing Blood Loss During Hepatectomy

A

Surgeons may clamp IVC or hepatic artery
Low CVP maintained by fluid restriction to reduce blood loss

263
Q

Postoperative Care After Hepatectomy

A

Post-op patient-controlled analgesia (PCA) often required
Watch for postop coagulation disturbances

Assessment '24 - Mordecai (10 decks)

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