Hepatic and biliary systems Flashcards

1
Q

List the functions of the liver (this card sucks)

A
  • Synthesizes glucose via gluconeogenesis
  • Stores excess glucose as glycogen
  • Synthesizes cholesterol & proteins into hormones and vitamins
  • Metabolizes fats, proteins, carbs to generate energy
  • Metabolizes drugs via CYP-450 and other enzyme pathways
  • Detoxifies blood
  • Involved in the acute-phase of immune support
  • Processes HGB and stores iron
  • Synthesizes coagulation factors (all except factors III, IV, VIII, vWF)
  • Aids in volume control as a blood reservoir
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2
Q

Liver dysfunction can lead to:

A

Multi-organ failure

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3
Q

How many segments does the liver have?

What is this based on?

A

8
- blood supply and bile drainage

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4
Q

What are the R & L lobes of the liver separated by?

A

Falciform ligament

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5
Q

What vessels branch into each segment of the liver?

A

Portal Vein
Hepatic artery

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6
Q

What 3 veins empty into the IVC from the liver?

A

Right, middle, left hepatic veins

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7
Q

Bile ducts travel along ______

A

Portal veins

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8
Q

Bile drains though _____ into what 2 things?

A

Hepatic duct

Gallbladder
Common bile duct

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9
Q

Bile enters the duodenum via what?

A

Ampulla of vater

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10
Q

Liver perfusion receives how much of COP?

Through what?

What is the flow rate?

A

25%

Via portal vein and hepatic artery

1.25-1.5 L/min

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11
Q

What does the portal vein arise from?

A

Splanchnic vein
Superior mesenteric vein

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12
Q

Portal vein blood is partially deoxygenated after perfusing what 3 organs?

A

GI organs
Pancreas
Spleen

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13
Q

What does the hepatic artery branch off of?

A

Aorta

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14
Q

How is O2 delivery split in the liver?

A

50% via portal vein (partially deoxygenated)
50% via hepatic artery

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15
Q

T/F
The liver receives the highest proportionate COP of all organs

A

True

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16
Q

Portal vein provides _____% of hepatic blood flow; hepatic artery provides ___% of hepatic blood flow

A

75%
25%

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17
Q

Hepatic arterial blood flow is inversely related to what?

A

Portal venous blood flow

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18
Q

Hepatic blood flow is ____

Hepatic artery ___ in response to low portal venous flow, keeping consistent HBF

A

Autoregulated
Dilates

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19
Q

Portal venous pressure reflects what 2 things?

A

Splanchnic arterial tone
Intrahepatic pressure

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20
Q

Increased portal venous pressure means what?

What does this put you at risk for?

A

Blood backs up into systemic circulation

  • esophageal varices, gastric varices
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21
Q

Hepatic venous pressure gradient picture
What is this used to determine?

A

Severity of portal HTN

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22
Q

T/F
Pts develop symptoms early with liver disease

A

False!
Often asymptomatic until late-stage liver disease; even later stages may only have age sx (disrupted sleep, loss of appetite)

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23
Q

Risk factors for liver dysfunction

A

Family hx
Heavy ETOH
Lifestyle
DM
Obesity
Illicit Drug use
Multiple partners
Tattoos
Transfusion

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24
Q

Physical exam of liver dysfunction

A

Pruritis
Jaundice
Ascites
Asterixis (flapping tremor)
Hepatomegaly
Splenomegaly
Spider nevi

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25
Q

Hepato-biliary labs

A
  • 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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26
Q

Hepato-biliary imaging

A

US
Dopple US (portal blood flow)
CT
MRI

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27
Q

What are the 3 groups of hepatobiliary disease?

A

Hepatocellular injury: ↑AST/ALT (hepatocyte enzymes)
- Acute Liver Failure (ALF): may be elevated 25x
- Alcoholic Liver Dz (ALD): AST:ALT ratio usually at least 2:1
- NAFLD: ratio usually 1:1

Reduced synthetic function: ↓Albumin, ↑PT/INR

Cholestasis:↑AlkPhosphatase,↑GGT,↑bilirubin

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28
Q

Liver blood test and differential diagnosis of HB disorders chart

A
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29
Q

What is cholelithiasis?
What is this caused by?

A

Gallstones

  • Hepatocytes secrete bile through bile ducts, into CHD→ GB & CBD
  • GB stores bile to deliver during meals, CBD secretes bile directly into duodenum
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30
Q

Risk factors of cholelithiasis

A

Obesity, ↑cholesterol, DM, pregnancy, female, family hx

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31
Q

What percent of pts with cholelithiasis are asymptomatic?

A

80%

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32
Q

S/S of cholelithiasis

What’s the treatment?

A

RUQ pain, referred to shoulders
N/V, indigestion
fever (acute obstruction)

IVF, abx, pain management, lap chole

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33
Q

What is Choledocolithiasis?

A

Stone obstructing CBD→ biliary colic

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34
Q

Initial symptoms of Choledocolithiasis

A

N/V, cramping, RUQ pain

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35
Q

Cholangitis symptoms

A

Fever, rigors, jaundice

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36
Q

Treatment for choledocolithiasis

A

Endoscopic removal of stone via ERCP

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37
Q

What does ERCP stand for?
What is it?

A

Endoscopic Retrograde Cholangiopancreatography

  • Endoscopist threads guidewire through Sphincter of Oddi, into Ampulla of Vater to retrieve stone from pancreatic duct or CBD
    -GA, usually prone w/left tilt (tape ETT to left)
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38
Q

What med may be required during ERCP for oddi spasm?

A

Glucagon

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39
Q

Difference in conjugated and unconjugated hyperbilirubinemia chart

A
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40
Q

What is bilirubin?

A

end product of heme-breakdown

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41
Q

What is unconjugated hyperbilirubinemia?

A

imbalance between bilirubin synthesis & conjugation

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42
Q

What is conjugated hyperbilirubinemia?

A

caused by anobstruction, causing reflux of conjugated bilirubin into the circulation

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43
Q

What are the 5 most common types of viral hepatitis?

A

A, B, C, D, E

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44
Q

T/F
Viral hepatitis is on the decline

Why or why not?

A

True
Vaccines, new treatments

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45
Q

What 2 types of viral hepatitis are more chronic?

A

B and C

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46
Q

____ is most common viral hepatitis requiring _____ in US

A

Hep C
Liver transplant

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47
Q

Hep C picture

A
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48
Q

Acute and chronic hepatitis common symptoms picture

A
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49
Q

What med can you give a 12 week course of for hep C?

This provides ____% clearance of genotype ____

A

Sofosbuvir/Velpatasvir

98%-99% of GT 1A/1B

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50
Q

Characteristic features of viral hepatitis picture

A
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51
Q

What is the most common cause of cirrhosis?

A

Alcoholic liver disease (ALD)

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52
Q

What is the top indication for liver transplant in the US?

A

ALD

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53
Q

What is treatment for ALD centered around?

A

Abstinence
- Management sx of liver failure
- Platelet count <50,000 requires blood transfusion
- Liver transplant an option if criteria is met

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54
Q

Unconjugated “indirect”bilirubin is protein bound to _____, transported to ____, conjugated into to its _____, excreted into _____

A

Albumin
Liver
H20-soluble “direct” state
Bile

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55
Q

ALD symptoms

A

Malnutrition
Muscle wasting
Parotid gland hypertrophy
Jaundice
thrombocytopenia
Ascites
Hepatosplenomegaly
Pedal edema
*Sx of ETOH withdrawal may occur 24-72h after stopping

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56
Q

ALD lab values

A

↑Mean corpuscular volume (MCV)
↑Liver enzymes
↑ɣ-glutamyl-transferase (GGT)
↑Bilirubin
Blood ethanol (acuteintox)

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57
Q

How is non alcoholic fatty liver disease diagnosed?

A

Hepatocytes contain >5% fat

  • Done by imaging and histology
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58
Q

Risk of Non-Alcoholic Fatty Liver Disease

A

Obesity, Insulin resistance, DM2, Metabolic syndrome

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59
Q

Treatment of hep C is based on what?

A

Genotype (75% of people are type 1)
HCV stage
+/- cirrhosis

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60
Q

What does non-alcoholic fatty liver disease progress to?

A

non-alcoholic steatohepatitis (NASH)
cirrhosis
hepatocellular carcinoma

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61
Q

____ and ____ have come additional leading causes of liver transplant in the US

A

NAFLD
NASH

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62
Q

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

A

Liver biopsy

63
Q

Treatment of NAFLD

A

Diet, exercise

64
Q

Liver transplant is indicated in what?

A

advanced fibrosis, cirrhosis, related complications

65
Q

More than ___ diabetics and ___ severe obese people out of 10 have NAFLD

___ out of 4 people have NAFLD regardless of weight

A

6 diabetics, 9 severe obese
1

66
Q

Types of fatty liver picture

67
Q

Autoimmune hepatitis primarily effects who?

68
Q

Autoimmune hepatitis lab values

A

+autoantibodies & hypergammaglobulinemia
AST/ALT may be 10-20x norm in acute AIH

69
Q

Treatment of autoimmune hepatitis

A

steroids, azathioprine (immunosuppressant)

70
Q

What percent of pts with autoimmune hepatitis achieve remission?

Is relapse common?

A

60%-80%
Yes

71
Q

When is liver transplant indicated in autoimmune hepatitis?

A

When treatment fails or acute liver failure ensues

72
Q

Most common cause of drug induced liver injury

Is this reversible?

A

Acetaminophen OD

Normally reversible after drug is removed

73
Q

What are the 3 specific disorders of metabolism?

What are these?

A

Wilsons Disease
Alpha-1 Antitrypsin Deficiency
Hemochromatosis

  • Group of rare, genetically inherited disorders that lead to a defect in the enzymes that breakdown and store protein, carbohydrates &fatty acids
74
Q

What is the ratio of occurrence in inborn errors of metabolism?

When is onset?

A

Occurs in 1:2500 births

Varies from birth to adolescence

75
Q

When does the most severe form of inborn error of metabolism appear?

A

Neonatal period
These carry a high degree of mortality

76
Q

What is Wilsons disease?

A

AKA hepatolenticular degeneration
- Autosomal recessive disease characterized by impaired copper metabolism
- Copper buildup leads to oxidative stress in the liver,basal ganglia, and cornea

77
Q

Symptoms of Wilsons disease

A

range from asymptomatic to sudden-onset liver failure along with neurologic & psychiatricmanifestations

78
Q

Diagnosis of Wilsons disease

A

Lab tests (serum ceruloplasmin,aminotransferases,urine copper level)
Possible liver biopsy for copper level

79
Q

Treatment of Wilsons disease

A

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

80
Q

What is Alpha-1 Antitrypsin Deficiency?

A

Gentetic disorder resulting in a defectiveα-1 antitrypsin protein

81
Q

What does Alpha-1 Antitrypsin do?

A

proteins protect the liver & lungs from neutrophil elastase
- neutrophil elastase isan enzyme that disrupts tissues of the lungs and liver
- Incidence1: 16,000 to1: 35,000, although it is likely underdiagnosed

82
Q

Alpha-1 Antitrypsin Deficiency is the #1 genetic cause of ______ in children

A

Liver transplant

83
Q

Diagnosis of Alpha-1 Antitrypsin Deficiency

A

confirmed w/α-1 antitrypsin phenotyping

84
Q

Treatment of Alpha-1 Antitrypsin Deficiency

A

Liver transplant is only curative treatment
- pooledα-1 antitrypsin is effective for pulmonary sx; however, it doesn’t help with liver disease

85
Q

What is hemochromatosis?

A

Excessive intestinal absorption of iron
- Maybe genetic or caused by repetitive blood transfusions or iron infusions
- Excess iron accumulates in organs and causes damage to the tissues

86
Q

What may pts with hemochromatosis present with?

A

cirrhosis, heart failure,diabetes, adrenal insufficiency,or polyarthropathy

87
Q

What do labs look like in hemochromatosis?

A

elevated AST/ALT, transferrin saturation, and ferritin

88
Q

How do you diagnosis hemochromatosis?

A

Genetic mutation testing
- echo and MRI to diagnose cardiomyopathies and liver abnormalities

89
Q

What can you do to quantify iron levels in the liver and assess level of damage of hemochromatosis?

A

Liver biopsy

90
Q

Treatment of hemochromatosis

A

weekly phlebotomy, iron-chelating drugs, liver transplant

91
Q

What is PSC?

A

Primary Sclerosing Cholangitis
- Autoimmune, chronic inflammation of the larger bile ducts
- Intrahepatic and extrahepatic
- Fibrosis in biliarytree→strictures (beads on string appearance)→ cirrhosis, ESLD

92
Q

Who is PSC more common in? When is the onset?

A

Males>females
Onset is around 40s

93
Q

Symptoms of PSC?

A

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

94
Q

What do labs look like in PSC?

A

↑alkaline phosphatase andɣ-glutamyl-transferase, +auto-antibodies

95
Q

Diagnosis of PSC?

A

MRCP or ERCP showing biliary strictures w/ dilated bile ducts
- liver biopsy reinforces dx, but isn’t always done

96
Q

Treatment of PSC?

A
  • no drug treatment is proven effective
  • liver transplant is only long term treatment
97
Q

_____ is common in PSC after transplant d/t autoimmune nature

A

Re-occurence

98
Q

What is PBC?

A

Primary Biliary Cholangitis
- Previously known as biliary cirrhosis
- Autoimmune, destruction of bile ducts withperiportal inflammation & cholestasis
- Can lead to liver scarring, fibrosis, cirrhosis

99
Q

Who is PBC more common in? When is onset?

A

Females>males
Often diagnosed in Middle Ages

100
Q

What is PBC thought to be caused by?

A

Exposure to environmental toxins in genetically susceptible individuals

101
Q

Symptoms of PBC

A

Jaundice, fatigue, itching

102
Q

Labs in PBC

A

↑Alk Phos,↑GGT, + Antimitochondrial antibodies

103
Q

Imaging in PBC

A

CT,MRI, & MRCP to r/o bile duct obstructions
- Liver biopsy reveals bile duct destruction andinfiltration w/lymphocytes

104
Q

Treatment of PBC

A

No cure, but exogenous bile acids slow progression

105
Q

PSC vs PBC picture

106
Q

What is acute liver failure?

A
  • Life-threatening severe liver injury occurring within days to 6 months after insult
  • Rapid increase in AST/ALT, AMS, coagulopathy
  • Massive hepatocyte necrosis→ cellular swelling &mbrndisruption
107
Q

What percent of acute liver failure cases are drug induced?

Which drug usually?

A

50%
Tylenol

108
Q

Other causes of acute liver failure

A

Viral hepatitis, autoimmune, hypoxia, ALF of pregnancy, HELLP

109
Q

Symptoms of acute liver failure

A

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

110
Q

Treatment of acute liver failure

A

Treat the cause, supportive care, liver transplant

111
Q

What is the final stage of liver disease called?

A

Cirrhosis
- Normal liver parenchyma replaced with scar tissue

112
Q

With cirrhosis, what do the symptoms progress to?

A

jaundice, ascites, varices, coagulopathy, encephalopathy, thrombocytopenia

113
Q

Most common causes of cirrhosis?

A

ALD, NAFL, HCV, HBV

114
Q

What are the elevated labs in cirrhosis?

A

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

115
Q

_____ is the only cure for cirrhosis

A

Transplant

116
Q

Cirrhosis complications include:

A

Portal HTN
Ascites
Bacterial peritonitis
Varicose
Hepatic encephalopathy
Hepatorenal syndrome
Hepatopulmonary syndrome
Portopulmonary HTN

117
Q

What does portal HTN cause?
What is the HVPG level?

A

↑vascular resistance within the portal venous system
HVPV >5

118
Q

What is the most common complication of cirrhosis?

119
Q

In ascites, portal HTN leads to increased _______ and __________

A

blood volume & peritoneal accumulation of fluid

120
Q

Management of ascites

A
  • ↓Salt diet
  • albumin replacement
  • Transjugular Intrahepatic Portosystemic Shunt (TIPS): Reduces P-HTN and ascites
121
Q

What is the most common infection peritonitis related to cirrhosis?

What does this require?

A

Bacterial peritonitis
Abx

122
Q

What percent of cirrhosis pts have varices?

123
Q

What is the most lethal complication of varices?

A

Hemorrhage
- Beta blockers help reduce risk
- Prophylactic endoscopic variceal banding & ligation
- Refractory bleeding → balloon tamponade

124
Q

What is hepatic encephalopathy?

A

Buildup of nitrogenous waste d/t poor liver detoxification

125
Q

What are symptoms associated with hepatic encephalopathy?

A

Neuropsychiatric symptoms
- cognitive impairment → coma

126
Q

Treatment of Hepatic Encephalopathy

A

Lactulose, Rifaximin to ↓ammonia-producing bacteria in gut

127
Q

What is hepatorenal syndrome?

A

Excess production of endogenous vasodilators (NO, PGs)→↓SVR→↓RBF

128
Q

Treatment of hepatorenal syndrome?

A

Midodrine, octreotide, albumin

129
Q

What is hepatopulmonary syndrome?

A
  • Triad of chronic liver dz, hypoxemia, intrapulmonary vascular dilation
  • Platypnea (hypoxemia when upright) d/t R to L intrapulmonary shunt
130
Q

What is portopulmonary HTN?

A
  • Pulmonary HTN accompanied by portal HTN
  • Systemic vasodilation triggers production of pulmonary vasoconstrictors
131
Q

What is the treatment of portopulmonary HTN?

A

PD-I’s, NO, prostacyclin analogs, and endothelin receptor antagonists
Transplant is only cure

132
Q

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

A

Child-turcotte-pugh (CT)
- points based on bilirubin, albumin, PT, encephalopathy, ascites
Model for end stage liver disease (MELD)
- scorebased on bilirubin, INR, creatinine, sodium

133
Q

CTP scoring picture

134
Q

MELD scoring picture

135
Q

Anesthesia in liver disease flow chart

136
Q

Standard preop labs in liver disease

A

CBC, BMP, PT/INR

137
Q

Pts with liver disease have a ____ threshold for invasive monitoring

138
Q

Pts with liver disease are at risk for what with anesthesia?

A

↑Risks aspiration, hypotension, hypoxemia

139
Q

Would you use colloids or crystalloids for resuscitation in liver disease?

A

Colloids preferred

140
Q

____ increases MAC of volatile anesthetics in liver disease pts

A

Alcoholism

141
Q

What 2 paralytics are preferred in liver disease?
Why?

A

Succs and Cisatracurium
- not liver-metabolized (plasmacholinesterasemay be decreased in severe liver dz)

142
Q

What does TIPS stand for?
What is this used to manage?

A

Transjugular Intrahepatic Portosystemic Shunt
- Portal HTN

143
Q

What happens in a TIPS procedure?

A
  • Stent or graft placed btw hepatic vein and portal vein
  • Shunts portal flow to systemic circulation
  • Reduces the portosystemic pressure gradient
144
Q

Indications for TIPS

A

Refractory variceal hemorrhage
Refractory ascites

145
Q

Contraindications of TIPS

A

Heart Failure
Tricuspid regurgitation
Severe pulmonary HTN

146
Q

What is a partial hepatectomy?

A
  • Resection to remove neoplasms, leaving adequate tissue for regeneration
  • Tolerable amount of resection d/o preexisting liver disease and function
147
Q

Up to what percent of liver removal is tolerated in pts with normal liver function?

148
Q

Anesthetic considerations for partial hepatectomy

A
  • Invasive monitoring
  • Blood products available
  • Adequate vascular access for blood/pressors
149
Q

______ is the definitive treatment for end stage liver disease

A

Transplant

150
Q

What is the different considerations for living/brain dead liver donors?

A

Living donor: surgeries timed together, minimal ischemic time
Brain dead donors: kept HD stable to for organ perfusion

151
Q

Intraop management of liver transplant

A

Maintain hemodynamics (Pressors/Inotropes readily available)
- A-line, CVC, PA cath, TEE

Control coagulation

152
Q

Special considerations for liver transplant picture