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.
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.
3
Q
How does the liver contribute to energy generation?
A
The liver metabolizes fats, proteins, and carbohydrates to generate energy.
4
Q
How does the liver contribute to drug metabolism?
A
The liver metabolizes drugs via various enzyme pathways, including the CYP-450 system
5
Q
What is the role of the liver in blood detoxification?
A
by processing and removing toxins and waste products.
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.
7
Q
How does the liver contribute to iron metabolism?
A
The liver processes hemoglobin (HGB) and stores iron.
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)
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.
10
Q
How does the liver aid in volume control?
A
by serving as a blood reservoir.
11
Q
How many segments does the liver have?
A
The liver has 8 segments.
12
Q
How are the right and left lobes of the liver separated?
A
by the Falciform Ligament.
13
Q
What branches into each segment of the liver?
A
The Portal Vein and Hepatic Artery branch into each segment of the liver.
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
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
16
Q
Through what structure does bile enter the duodenum?
A
via the Ampulla of Vater.
17
Q
A
The liver receives 25% of cardiac output (COP)
1.25 to 1.5 L/min
18
Q
Which organ has the highest proportionate COP?
A
The liver
19
Q
Where does the portal vein arise from?
A
the splenic vein and superior mesenteric vein.
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
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).
22
Q
Where does the hepatic artery branch off from?
A
the aorta.
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).
24
Q
How is oxygen delivered to the liver?
A
50% via the portal vein (deoxygenated)
50% via the hepatic artery (partially oxygenated).
25
How is hepatic arterial blood flow related to portal venous blood flow?
Hepatic arterial blood flow is **inversely** related to portal venous blood flow.
26
How is hepatic blood flow regulated?
Through what mechanism?
Hepatic blood flow is autoregulated
(The hepatic **artery dilates in response to low portal venous flow** to maintain consistent hepatic blood flow (HBF).)
27
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What does portal venous pressure reflect?
splanchnic arterial tone and intrahepatic pressure.
28
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What happens if portal venous pressure increases?
- Can lead to blood backing up into the systemic circulation, resulting in complications such as **esophageal and gastric varices**
29
Hepatic Venous Pressure Gradient is used for:
Determining the severity of portal hypertension
30
Video animation:
https://www.youtube.com/watch?v=LkXQTDb8g2U
31
What are some common risk factors for liver disease?
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.
32
What are some common symptoms of late-stage liver disease?
vague symptoms such as **disrupted sleep** and **decreased appetite**.
33
physical exam findings in liver disease?
Common physical exam findings in liver disease include
- Pruritus
- Jaundice
- Ascites
- **Asterixis (flapping tremor)**
- Hepatomegaly
- Splenomegaly
- Spider nevi.
34
Hepato-biliary Function Tests:
LABS:
- BMP
- CBC
- PT/INR
- Aspartate aminotransferase (AST)
- Alanine aminotransferase (ALT) most - liver-specific enzymes
- Bilirubin
- Alkaline Phosphatase
- ɣ-glutamyl-transferase (GGT)
35
Hepato-biliary Function Imaging:
Imaging
Ultrasound
Doppler U/S (Portal bld flow)
CT
MRI
36
What are the biomarkers for acute liver failure (ALF)?
In acute liver failure (ALF), AST and ALT levels may be elevated up to 25 times the normal range.
37
What is the typical AST:ALT ratio in alcoholic liver disease (ALD)?
In alcoholic liver disease (ALD), the AST:ALT ratio is usually at least 2:1.
38
What is the typical AST:ALT ratio in non-alcoholic fatty liver disease (NAFLD)?
In non-alcoholic fatty liver disease (NAFLD), the AST:ALT ratio is usually 1:1.
39
What biomarkers indicate reduced synthetic function of the liver?
decreased albumin levels and increased PT/INR.
40
What biomarkers indicate cholestasis?
Cholestasis is indicated by **increased** levels of:
- **Alkaline phosphatase (Alk Phosphatase)**
- **Gamma-glutamyl transferase (GGT)**
- **Bilirubin**
41
Look at this differential diagnosis of Hepatobiliary Disorders
Flash cards added at the end
42
What are the functions of hepatocytes in bile secretion?
Hepatocytes secrete bile through **bile ducts** into the **common hepatic duct (CHD)** which leads to the **gallbladder (GB)** and **common bile duct (CBD)**
43
How does the gallbladder (GB) function in bile storage?
The gallbladder (GB) stores bile to deliver it during meals
the common bile duct (CBD) secretes bile directly into the duodenum.
44
What are the risk factors for cholelithiasis?
obesity
high cholesterol levels
diabetes mellitus (DM)
pregnancy
being female
family history of gallstones.
45
What percentage of cases of cholelithiasis are asymptomatic?
Approximately 80% of cases of cholelithiasis are asymptomatic.
46
What are the common symptoms of cholelithiasis?
Common symptoms of cholelithiasis include
- **Right upper quadrant (RUQ) pain** **referred to the shoulders**,
- Nausea & vomiting
- Indigestion
- Fever in cases of acute obstruction.
47
What are the treatment options for cholelithiasis?
Treatment options for cholelithiasis include
- Intravenous fluids (IVF)
- Antibiotics (abx)
- Pain management
- Laparoscopic cholecystectomy (removal of the gallbladder).
48
Types of Cholecystectomy:
49
What is choledocolithiasis?
Choledocolithiasis refers to the presence of gallstones (calculi) **_in the common bile duct (CBD)_**. Biliary colic.
50
What is the initial presentation of a stone obstructing the common bile duct (CBD)?
nausea,
vomiting,
cramping,
right upper quadrant (RUQ) = **biliary colic**
51
What are the symptoms of cholangitis?
Symptoms of cholangitis (inflammation of the CBD)
- fever
- rigors (shaking chills)
- jaundice.
52
What is the preferred treatment for stone removal in cases of CBD
The preferred treatment is endoscopic removal of the stone via **endoscopic retrograde cholangiopancreatography (ERCP)**
53
What does ERCP stand for?
ERCP stands for Endoscopic Retrograde Cholangiopancreatography.
54
Describe the procedure of ERCP.
threads a guidewire through the Sphincter of Oddi into the Ampulla of Vater to retrieve the stone from the pancreatic duct or CBD.
55
What position is typically used during ERCP, and why?
prone position with left tilt
The endotracheal tube (ETT) may be taped to the left side to prevent displacement.
56
What medication may be required during ERCP in the event of Oddi Spasm?
Glucagon may be required to manage Oddi Spasm during ERCP.
57
Common bile duct obstruction picture:
58
ERCP Procedure picture:
59
What is bilirubin?
Bilirubin is the end product of heme breakdown.
60
Describe unconjugated bilirubin.
- 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.
61
What causes unconjugated (indirect) hyperbilirubinemia?
imbalance between bilirubin synthesis and conjugation.
62
What causes conjugated (direct) hyperbilirubinemia?
an **obstruction in the biliary system**leading to the **reflux of conjugated bilirubin into the circulation**.
63
What are the five most common types of viral hepatitis?
The five most common types are hepatitis A, B, C, D, and E.
64
How has the overall prevalence of viral hepatitis changed over time?
Overall, viral hepatitis is on the decline due to vaccines and newer treatments
65
Which types of viral hepatitis are more chronic?
Hepatitis B and C are more chronic compared to other types.
66
What is the most common viral hepatitis requiring liver transplant in the United States?
Hepatitis C virus (HCV) (75% type 1)
67
What is the recommended treatment for hepatitis C?
regimen is a 12-week course of sofosbuvir/velpatasvir, which provides 98-99% clearance of genotype 1A/1B.
68
HCV Cycle Picture
69
Acute and Chronic Hepatitis Symptoms image:
70
Hepatitis 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%
71
Hepatitis B
* 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%
72
Hepatitis C
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
73
Hepatitis D
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%
74
Hepatitis E
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
75
ALD and Liver Transplants
Alcoholic liver disease
* Leading reason for liver transplants in the U.S.
* 2% of liver transplants nationwide are for ALD.
76
Reporting of ALD
Underreporting of ALD is common due to stigma.
77
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Progression of ALD
* Initially may show no symptoms.
* Symptoms of liver failure emerge as it progresses.
78
Treating ALD
Abstinence from alcohol is central to treatment.
79
Management of ALD Symptoms
Treatment includes managing symptoms of liver failure.
80
ALD and Platelet Count
Plt count <50,000 requires transfusion
81
Liver Transplant for ALD
Patients with ALD may be eligible for a liver transplant if they meet specific criteria.
82
What symptom of ALD is a result of poor dietary habits and absorption?
Malnutrition
83
What symptom of ALD is due to malnutrition and altered metabolism?
Muscle wasting
84
Which gland enlargement is associated with chronic ALD?
Parotid gland hypertrophy
85
What symptom of ALD results from liver dysfunction and causes yellowing of the skin and eyes?
Jaundice
86
What term describes a low platelet count often associated with chronic liver disease?
Thrombocytopenia
87
What is the term for the accumulation of fluid in the abdomen, indicating advanced liver disease?
Ascites
88
What is the term for the enlargement of the liver and spleen seen in ALD?
Hepatosplenomegaly
89
What term describes the swelling of the feet and ankles due to fluid retention in ALD?
Pedal edema
90
When may symptoms of alcohol withdrawal occur after stopping drinking?
24-72 hours after cessation of alcohol intake
91
Which lab value is typically elevated in ALD and indicates a change in red blood cells?
Mean corpuscular volume (MCV)
92
Which lab values are typically elevated due to liver damage in ALD?
Liver enzymes
93
What enzyme, often elevated in ALD, can indicate liver disease and heavy alcohol use?
Gamma-glutamyl transferase (GGT)
94
What lab value, when elevated, indicates impaired liver function in ALD?
Bilirubin
95
What lab test measures acute alcohol intoxication?
Blood ethanol level
96
What is the trend of non-alcoholic fatty liver disease (NAFLD) in the US?
AFLD is on the rise in the United States.
97
How is non-alcoholic fatty liver disease (NAFLD) diagnosed?
hepatocytes contain more than 5% fat.
98
What are the primary risk factors associated with non-alcoholic fatty liver disease (NAFLD)?
Obesity
insulin resistance
type 2 diabetes mellitus (DM2)
metabolic syndrome.
99
What conditions can NAFLD progress to?
non-alcoholic steatohepatitis (NASH)
cirrhosis
hepatocellular carcinoma.
100
What has NAFLD and its progression, NASH, become in the context of liver transplants in the US?
NAFLD and NASH have become additional leading causes of liver transplant in the United States.
101
What methods are used for the diagnosis of NAFLD?
Diagnosis is made through imaging and histology.
102
What is the gold standard for distinguishing NAFLD from other liver diseases?
Liver biopsy is the gold standard
103
What are the primary treatments for non-alcoholic fatty liver disease (NAFLD)?
The primary treatments include diet and exercise.
104
When is a liver transplant indicated for NAFLD?
advanced fibrosis, cirrhosis, and related complications.
105
NAFLD Prevalence: diabetics and severely obese people?
More than 6 diabetics and 9 out of 10 severely obese people have NAFLD
106
NAFLD: Non-diabetics/obese people
1 in 4 people have NAFLD regardless of weight
107
Types of Fatty Liver Image:
108
Who is predominantly affected by autoimmune hepatitis (AIH)?
Predominantly affects women.
109
How does autoimmune hepatitis (AIH) present symptomatically?
May be asymptomatic, acute, or chronic.
110
What are common laboratory findings in autoimmune hepatitis (AIH)?
Positive autoantibodies & hypergammaglobulinemia.
111
How elevated are AST/ALT levels in acute autoimmune hepatitis (AIH)?
AST/ALT may be 10-20 times the normal level in acute AIH.
112
What is the typical treatment for autoimmune hepatitis (AIH)?
Treatment includes steroids and azathioprine.
113
What is the rate of remission and risk of relapse in autoimmune hepatitis (AIH)?
60-80% achieve remission; however, relapse is common.
114
How is refractory autoimmune hepatitis (AIH) managed?
Refractory disease requires increased immunosuppression.
115
When is a liver transplant indicated in autoimmune hepatitis (AIH)?
Indicated when treatment fails or acute liver failure ensues.
116
What is the most common cause of drug-induced liver injury (DILI)?
The most common cause is acetaminophen overdose.
117
What is the prognosis for drug-induced liver injury (DILI) when the drug is removed?
Normally reversible after the drug is removed
118
What are **inborn errors of metabolism (IEM)?**
A group of rare, genetically inherited disorders leading to **defects in the enzymes that break down and store proteins, carbohydrates, and fatty acids.**
119
How common are inborn errors of metabolism?
They occur in 1 out of every 2500 births.
120
When does the onset of inborn errors of metabolism typically occur?
Onset varies from birth to adolescence.
121
What is the prognosis of severe forms of inborn errors of metabolism?
high degree of mortality.
122
What is Wilson's Disease?
Wilson's Disease is an inborn **error of metabolism characterized** by **excessive copper accumulation in the body**
123
What is Alpha-1 Antitrypsin Deficiency?
A deficiency in the alpha-1 antitrypsin enzyme, which can lead to liver and lung disease.
124
What is Hemochromatosis?
A metabolic disorder causing **excessive iron storage in various organs, potentially leading to organ damage**
125
What is Wilson's Disease and its other name?
Wilson's Disease, also known as **hepatolenticular degeneration**
is an autosomal recessive disease characterized by **impaired copper metabolism**
126
What does excessive copper buildup cause in Wilson's Disease?
It leads to **oxidative stress** in the liver, basal ganglia, and cornea.
127
What is the range of symptoms in Wilson's Disease?
asymptomatic
sudden-onset liver failure
neurologic
psychiatric manifestations.
128
How is Wilson's Disease diagnosed?
lab tests such as
- serum ceruloplasmin
- aminotransferases
- urine copper level
- possible liver biopsy for copper level.
129
What are the treatment options for Wilson's Disease?
copper-chelation therapy and oral zinc to bind copper in the gastrointestinal tract.
130
What is alpha-1 antitrypsin deficiency?
A genetic disorder resulting in defective alpha-1 antitrypsin protein.
131
What does alpha-1 antitrypsin protein protect against?
It protects the liver and lungs from **neutrophil elastase** an enzyme that can disrupt connective tissues and cause inflammation.
132
What damage does neutrophil elastase cause if not regulated?
It can lead to **inflammation, cirrhosis, and hepatocellular carcinoma (HCC)**
133
How common is alpha-1 antitrypsin deficiency?
The incidence ranges from 1 in 16,000 to 1 in 35,000, but is likely underdiagnosed.
134
What is the significance of **alpha-1 antitrypsin deficiency** in pediatric liver transplants?
It is the #1 genetic cause of liver transplant in children.
135
How is alpha-1 antitrypsin deficiency diagnosed?
alpha-1 antitrypsin phenotyping.
136
What treatment is effective for the pulmonary symptoms of alpha-1 antitrypsin deficiency?
Pooled alpha-1 antitrypsin
137
What is the only curative treatment for liver disease caused by alpha-1 antitrypsin deficiency?
Liver transplant
138
What is hemochromatosis?
excess iron in the body, leading to multi-organ dysfunction.
139
How can hemochromatosis occur?
It may be genetic, causing **excessive intestinal absorption of iron, or caused by repetitive blood transfusions or high-dose iron infusions**.
140
What happens when excess iron accumulates in the body?
t accumulates in organs and causes damage to the tissues.
141
What conditions might patients with hemochromatosis present with?
cirrhosis
heart failure
diabetes
adrenal insufficiency
polyarthropathy.
142
What lab findings are indicative of hemochromatosis?
Elevated AST/ALT
transferrin saturation
ferritin levels.
143
How is hemochromatosis diagnosed?
genetic mutation testing
echocardiogram
MRI
potentially liver biopsy to quantify iron levels and assess damage.
144
Which imaging techniques are used to diagnose cardiomyopathies and liver abnormalities in hemochromatosis?
Echocardiogram and MRI.
145
How can iron levels in the liver be quantified?
Liver biopsy
146
What are the treatment options for hemochromatosis?
weekly phlebotomy
iron-chelating drugs
potentially a liver transplant.
147
# ```
What is Primary Biliary Cholangitis (PBC)?
An autoimmune disease
previously known as biliary cirrhosis
involving the
- progressive destruction of bile ducts
- periportal inflammation
- cholestasis.
148
What are the possible long-term consequences of PBC?
Can lead to liver scarring, fibrosis, and ultimately, cirrhosis.
149
Who is most commonly affected by PBC?
Females
often diagnosed in middle-aged individuals.
150
What is thought to contribute to the development of PBC?
Thought to be caused by exposure to environmental toxins in genetically susceptible individuals.
151
What are common symptoms of PBC?
Symptoms include jaundice, fatigue, and itching.
152
What lab findings are typically elevated in PBC?
Labs reveal **increased**
- Alkaline Phosphatase (Alk Phos),
- Gamma-Glutamyl Transferase (GGT), and
- Positive Antimitochondrial antibodies.
153
Which imaging tests are used in PBC to rule out bile duct obstructions?
CT scan, MRI, and Magnetic Resonance Cholangiopancreatography (MRCP).
154
What can a liver biopsy reveal in a patient with PBC?
Liver biopsy reveals bile duct destruction and infiltration with lymphocytes.
155
How is PBC treated?
There is **no cure**, but treatment with **exogenous bile acids can slow the progression** of the disease.
156
What is Primary Sclerosing Cholangitis (PSC)?
PSC is an autoimmune, chronic disease that causes **inflammation and fibrosis of both intrahepatic and extrahepatic bile ducts**.
157
# ```
How does PSC affect the biliary system?
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
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Who is more likely to develop PSC and at what age?
Males are more commonly affected than females, typically diagnosed around their 40s.
159
What are the symptoms of PSC?
fatigue
itching
deficiencies of fat-soluble vitamins (A, D, E, K)
complications from cirrhosis.
160
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Which lab findings are associated with PSC?
**Elevated alkaline phosphatase** and **gamma-glutamyl-transferase, and the presence of auto-antibodies**.
161
What imaging techniques are used to diagnose PSC?
Magnetic Resonance Cholangiopancreatography (MRCP) or Endoscopic Retrograde Cholangiopancreatography (ERCP) showing biliary strictures with dilated bile ducts.
162
Is a liver biopsy always necessary for diagnosing PSC?
A liver biopsy can reinforce the diagnosis but isn't always performed due to its invasive nature and potential complications.
163
What are the treatment options for PSC?
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
What is a concern after a liver transplant for PSC?
The autoimmune nature of PSC may lead to recurrence after liver transplantation.
165
Sclerosing cholangitis v. biliary cholangitis image:
166
What is acute liver failure?
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
# [](http://)
hat is the most common cause of acute liver failure?
Almost 50% of cases are drug-induced, with the majority due to acetaminophen overdose.
168
What are other causes of acute liver failure besides drugs?
viral hepatitis,
autoimmune disorders,
hypoxia,
acute fatty liver of pregnancy,
HELLP syndrome.
169
What symptoms can present in acute liver failure?
jaundice,
nausea,
right upper quadrant pain,
cerebral edema,
encephalopathy,
multi-organ failure
potentially death.
170
How is acute liver failure treated?
Treatment involves addressing the underlying cause, providing supportive care, and potentially a liver transplant.
171
Definition of Cirrhosis
Cirrhosis is the final stage of liver disease where **normal liver parenchyma is replaced with scar tissue**
172
Early Stages of Cirrhosis
Often asymptomatic in early stages, making it difficult to detect without specific testing.
173
Symptoms as Cirrhosis Progresses
jaundice,
ascites,
varices,
coagulopathy,
encephalopathy as the condition worsens.
174
# **
Common Causes of Cirrhosis
alcoholic fatty liver disease
non-alcoholic fatty liver disease (NAFL),
hepatitis C virus (HCV)
hepatitis B virus (HBV).
175
Laboratory Findings in Cirrhosis
Elevated labs include
AST/ALT,
bilirubin,
alkaline phosphatase,
(PT/INR).
176
Hematologic Changes in Cirrhosis
Thrombocytopenia, a reduction in platelet count, is a common complication.
177
Cure for Cirrhosis
The only cure for cirrhosis is a liver transplant.
178
What is portal hypertension in the context of cirrhosis, and what is a significant indicator of its presence?
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
Which complication is the most common in cirrhosis and what leads to its development?
Ascites
developed due to **portal hypertension** which leads to **increased blood volume and fluid accumulation** in the peritoneal cavity.
180
How is ascites managed in patients with cirrhosis?
low-sodium diet and albumin replacement therapy.
181
What is TIPS and its role in the management of cirrhosis complications?
The Transjugular Intrahepatic Portosystemic Shunt (TIPS) is a procedure that **reduces portal hypertension and can help manage ascites**
182
What is the most common infection related to cirrhosis, and how is it treated?
Spontaneous Bacterial Peritonitis (SBP)
requiring prompt antibiotic treatment.
183
How common are varices in patients with cirrhosis?
Varices are present in approximately 50% of patients with cirrhosis.
184
What is the most lethal complication associated with varices in cirrhosis patients?
Hemorrhage
185
How can the risk of hemorrhage from varices be reduced?
Beta-blockers help reduce the risk, and prophylactic endoscopic variceal banding and ligation can also be employed.
186
What is the treatment for refractory bleeding from varices?
Refractory bleeding may be managed with balloon tamponade.
187
What causes hepatic encephalopathy in patients with cirrhosis?
It is due to the buildup of nitrogenous waste because of poor liver detoxification.
188
What are the neuropsychiatric symptoms associated with hepatic encephalopathy?
Symptoms can range from cognitive impairment to coma.
189
How is hepatic encephalopathy treated?
Lactulose and Rifaximin to decrease ammonia-producing bacteria in the gut.
190
How common are varices in cirrhosis patients and what is the most lethal complication?
Varices are present in approximately 50% of patients with cirrhosis, and hemorrhage from these varices is the most lethal complication.
191
What is the mechanism behind **hepatorenal syndrome** in cirrhosis?
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
What are the treatment options for hepatorenal syndrome?
Treatment includes midodrine, octreotide, and albumin.
193
What is hepatopulmonary syndrome and what unique symptom does it present with?
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
What is portopulmonary hypertension and what triggers it?
Portopulmonary hypertension is pulmonary hypertension that occurs in conjunction with portal hypertension.
Systemic vasodilation triggers the production of pulmonary vasoconstrictors.
195
What are the treatment options for portopulmonary hypertension?
PD-I’s (phosphodiesterase inhibitors)
nitric oxide (NO),
prostacyclin analogs
endothelin receptor antagonists.
196
What is the only cure for these complications of cirrhosis?
A liver transplant is the only cure.
197
When is elective surgery contraindicated for patients with liver disease?
acute hepatitis, severe chronic hepatitis, and acute liver failure (ALF).
198
What are the two scoring systems used to determine the severity and prognosis of liver disease?
Child-Turcotte-Pugh (CTP)
Model for End-Stage Liver Disease (MELD).
199
What parameters are included in the Child-Turcotte-Pugh (CTP) scoring system?
The CTP score is based on bilirubin, albumin, prothrombin time (PT), presence of encephalopathy, and ascites.
200
What factors are considered in the Model for End-Stage Liver Disease (MELD) score?
bilirubin,
international normalized ratio (INR),
creatinine,
sodium levels.
201
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?
The 1-year survival rate for Class A is 100%, and the 2-year survival rate is 85%.
202
Child-Turcotte-Pugh Class B Prognosis
What is the survival prognosis for Class B liver disease as per the Child-Turcotte-Pugh score?
Class B liver disease has a 1-year survival rate of 81% and a 2-year survival rate of 57%.
203
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?
For Class C liver disease, the 1-year survival rate is 45%, and the 2-year survival rate is 35%.
204
MELD Score Under 10 Prognosis
What is the observed mortality rate for a patient with a MELD score under 10?
The observed mortality rate for a MELD score under 10 is between 1.9% and 3.7%.
205
MELD Score 10-19 Prognosis
What is the observed mortality rate for a MELD score between 10 and 19?
or a MELD score between 10 and 19, the observed mortality rate is between 6% and 20%.
206
MELD Score 20-29 Prognosis
What is the observed mortality rate for a MELD score between 20 and 29?
The observed mortality rate for a MELD score between 20 and 29 is between 19.6% and 45.5%.
207
MELD Score 30-39 Prognosis
How does a MELD score of 30 to 39 affect 3-month survival?
A MELD score of 30 to 39 correlates with an observed mortality rate between 52.6% and 74.5%.
208
MELD Score 40 or Above Prognosis
What does a MELD score of 40 or above indicate about 3-month survival?
A MELD score of 40 or above is associated with an observed mortality rate of 71.3% to 100%.
209
Anesthesia in Liver disease
Initial Assessment for Liver Disease
How do you begin preoperative risk assessment in a patient undergoing elective surgery?
Slide 40
First, determine if the patient has cirrhosis.
210
Anesthesia in Liver disease
Risk Stratification in Cirrhosis
What scoring systems are used for risk stratification in patients with cirrhosis?
Slide 40
Use the MELD or Child-Turcotte-Pugh (CTP) score for risk stratification.
211
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
Yes, patients with MELD <10 or Child class A can proceed to the operating room (OR) with careful postoperative monitoring.
212
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
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
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
Consider alternatives to surgery and workup for transplantation due to high risk.
214
Anesthesia in Liver disease
Handling Portal Hypertension Preoperatively
What is the suggested management for patients with cirrhosis and portal hypertension?
Slide 40
Consider preoperative TIPS placement and discuss specific risks and patient-specific optimization before the operation.
215
What should be emphasized during preoperative evaluation for a patient with liver disease?
A careful history and physical examination are crucial.
216
Which standard preoperative labs are essential for patients with liver disease?
Complete blood count (CBC),
basic metabolic panel
(PT/INR)
217
What is the recommendation regarding invasive monitoring in patients with liver disease?
There is a low threshold for employing invasive monitoring due to increased risks.
218
What are the increased risks during anesthesia in patients with liver disease?
Patients have higher risks of aspiration, hypotension (HoTN), and hypoxemia.
219
Between colloids and crystalloids, which is preferred for fluid resuscitation in liver disease, and why?
Colloids are preferred over crystalloids for resuscitation to optimize intravascular volume without worsening ascites.
220
How does alcoholism affect the minimum alveolar concentration (MAC) of volatile anesthetics?
Alcoholism can increase the MAC of volatile anesthetics, possibly requiring higher doses.
221
What should be considered when selecting anesthetic drugs for patients with liver disease?
medications not metabolized by the liver, such as **succinylcholine** and **cisatracurium** are ideal.
222
How might severe liver disease affect plasma cholinesterase levels?
Plasma cholinesterase activity may be decreased, affecting the metabolism of certain drugs.
223
How is bleeding and coagulation managed in patients with liver disease under anesthesia?
Bleeding and coagulation should be closely monitored, and management might include transfusion of blood products and administration of coagulation factors.
224
Primary Indications for TIPS
refractory variceal hemorrhage and refractory ascites.
225
Contraindications for TIPS
patients with heart failure
tricuspid regurgitation
severe pulmonary hypertension.
226
What is the definitive treatment for End-Stage Liver Disease (ESLD)?
Liver transplant is the definitive treatment for ESLD.
227
What are the most common indications for liver transplant?
**Alcoholic liver disease is the most common** indication
followed by **fatty liver disease** and **hepatocellular carcinoma (HCC)**
228
How is a living donor liver transplant typically conducted?
Surgeries are timed together, and there is minimal ischemia time for the donated liver.
229
How are brain-dead donors managed to preserve organ viability?
Hemodynamic stability is maintained to ensure organ perfusion.
230
What are the key aspects of intraoperative management during liver transplant?
Maintain hemodynamics with readily available
- pressors/inotropes,
- utilize arterial lines,
- central venous catheters,
- pulmonary artery catheters,
- transesophageal echocardiography (TEE),
- control coagulation.
231
What are preoperative surgical considerations for liver transplantation?
Preoperative surgical considerations include transplantation evaluation, which covers psychological evaluation, MELD score assessment, and UNOS listing.
232
What are preoperative anesthetic considerations for liver transplantation?
evaluation,
establishing vascular access,
ensuring blood product availability.
233
What are the surgical considerations during the dissection phase of liver transplantation?
surgical incision,
mobilization of liver and vascular structures,
isolation of bile duct.
234
What are the anesthetic considerations during the dissection phase of liver transplantation?
managing hemodynamic compromise from
- loss of ascites,
- hemorrhage during dissection,
- decreased venous return.
235
: What surgical considerations are made during the anhepatic phase of liver transplantation?
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
What are the anesthetic considerations during the anhepatic phase of liver transplantation?
focus on hemodynamic compromise from full or partial IVC clamping,
metabolic acidosis,
hypocalcemia from citrate intoxication,
hyperkalemia,
hypothermia
hypoglycemia.
237
What occurs during the reperfusion phase of liver transplantation from a surgical standpoint?
The reperfusion phase involves anastomosis of the hepatic artery and biliary system, and reperfusion of the transplanted liver.
238
What are the anesthetic considerations during the reperfusion phase of liver transplantation?
Anesthetic considerations during reperfusion include managing hemodynamic instability, dysrhythmias, hyperkalemia, acidosis, pulmonary emboli, and cardiac arrest.
239
What are post-transplantation surgical considerations in liver transplantation?
Post-transplantation surgical considerations include hemostasis, evaluation of graft function, and ultrasound for vascular patency.
240
What are the post-transplantation anesthetic considerations in liver transplantation?
Post-transplantation anesthetic considerations include ICU admission, timing of extubation (early or late), and ongoing hemodynamic management.
241
Lab: Aminotransferases
Predominant abnormality in:
- Bilirubin overlad
- Hepatocellular Injury
- Cholethiasis
- Bilirubin Overload (Hemolysis): Normal
- Hepatocellular Injury: Increased; May be normal or decreased in advanced stages
- Cholestasis: Normal; May be increased in advanced stages
242
Lab: Serum albumin
Predominant abnormality in:
- Bilirubin overlad
- Hepatocellular Injury
- Cholethiasis
- Bilirubin Overload (Hemolysis): Normal
- Hepatocellular Injury: Decreased; May be normal in acute fulminant hepatic failure
- Cholestasis: Normal; May be decreased in advanced stages
243
Lab: Prothrombin time
Predominant abnormality in:
- Bilirubin overlad
- Hepatocellular Injury
- Cholethiasis
- Bilirubin Overload (Hemolysis): Normal
- Hepatocellular Injury: Prolonged
- Cholestasis: Normal; May be prolonged in advanced stages
244
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
- Bilirubin Overload (Hemolysis): Unconjugated (also mild increase in conjugates)
- Hepatocellular Injury: Conjugated
- Cholestasis: Conjugated
245
Lab: Alkaline phosphatase
Predominant abnormality in:
- Bilirubin overlad
- Hepatocellular Injury
- Cholethiasis
- Bilirubin Overload (Hemolysis): Normal
- Hepatocellular Injury: Normal; May be increased by hepatic infiltrative disease
- Cholestasis: Increased
246
Lab: γ-Glutamyl transpeptidase (GGT)
Predominant abnormality in:
- Bilirubin overlad
- Hepatocellular Injury
- Cholethiasis
- Bilirubin Overload (Hemolysis): Normal
- Hepatocellular Injury: Normal
- Cholestasis: Increased
247
Lab: Blood urea nitrogen
Predominant abnormality in:
- Bilirubin overlad
- Hepatocellular Injury
- Cholethiasis
- 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
Lab: BSP/ICG (dye)
Predominant abnormality in:
- Bilirubin overlad
- Hepatocellular Injury
- Cholethiasis
- Bilirubin Overload (Hemolysis): Normal
- Hepatocellular Injury: Retention of dye
- Cholestasis: Normal or retention of dye
249
Alcoholic Liver Disease (ALD) in America
* ALD is increasing in prevalence.
* Most common cause of cirrhosis.
