Hepatic and Biliary Flashcards

Exam 3

1
Q
A
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2
Q

How many hepatic veins are there? What do they drain into?

A

3 - right, middle, and left
Drain into vena cava

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3
Q

The right and left lobes of the liver are separated by the ____________

A

Falciform Ligament

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4
Q

There are __ total segments of the liver

A

8 - divided by blood supply and bile drainage

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5
Q

Bile ducts travel along _______, and bile drains through the _______ into _____ and _______

A

portal veins
hepatic duct
gall bladder and common bile duct

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6
Q

Bile enters the duodenum via the ______

A

Ampulla of Vater

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7
Q

The liver receives how much of CO?

A

25% - 1.25-1.5 L/min
- highest proportionate COP of all organs

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8
Q

The portal vein arises from what?

A

The splanchnic vein and superior mesenteric vein

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9
Q

Why is portal vein blood partially deoxygenated?

A

Perfuses GI organs, pancreas & spleen

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10
Q

The portal vein provides ___% of HBF, while the hepatic artery provides __%

A

75%, 25%

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11
Q

What percentage of oxygen delivered to the liver is via the portal vein vs the hepatic artery?

A

50% each

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12
Q

The hepatic artery branches off the _____

A

aorta

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13
Q

The hepatic artery _______ in response to low portal venous flow

A

dilates

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14
Q

What is the most common cause of portal HTN?

A

Cirrhosis

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15
Q

Portal HTN can result in _____ and ______

A

↑Portal venous pressure → blood backsupinto systemic circulation
- esophageal and gastric varices

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16
Q

What is a normal HVPG, portal HTN, and variceal rupture?

A

Normal 1-5 mmHg
HVPG > 10 mmHg
HVPG > 12 mmHg

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17
Q

What are the risk factors of liver disease (9)?

A

Family hx, ETOH, lifestyle, DM, obesity, illicit Drug use, mult sexual partners, tattoos, transfusion

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18
Q

What are the signs of liver disease on physical exam (7)?

A

Pruritis, jaundice, ascites, asterixis (flapping tremor), hepatomegaly, splenomegaly, spider nevi

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19
Q

What are the 7 liver 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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20
Q

Which imaging can detect portal blood flow?

A

Doppler US

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21
Q

What are the 3 groups of hepatobiliary disease?

A
  • Hepatocellular injury
  • Reduced synthetic function
  • Cholestasis
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22
Q

Which labs will be increased in hepatocellular injury?

A

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

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23
Q

Which lab values will be altered in reduced synthetic function?

A

↓Albumin, ↑PT/INR

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24
Q

Which lab values will be altered in cholestasis?

A

↑AlkPhosphatase,↑GGT,↑bilirubin

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25
Which lab values will be altered in bilirubin overload (hemolysis)?
Increased unconjugated and conjugated bilirubin
26
_______ secrete bile through bile ducts into the CHD
Hepatocytes
27
Which organ stores bile? What vessel secretes bile directly into the duodenum?
GB stores bile to deliver during meals, CBD secretes bile directly into duodenum
28
What are the risk factors of cholelithiasis “gallstones”?
Obesity, ↑cholesterol, DM, pregnancy, female, family hx
29
What are the S/S of cholelithiasis “gallstones”?
80% asymptomatic - RUQ pain, referred to shoulders - N/V, indigestion - fever (acute obstruction)
30
What is the treatment of gallstones?
IVF, abx, pain mgmt, and lap cholecystectomy
31
What is choledocolithiasis?
Stone obstructing CBD→ biliary colic
32
What are the initial vs cholangitis s/s of choledocolithiasis?
- Initial sx: N/V, cramping, RUQ pain - Cholangitis sx: fever, rigors, jaundice
33
What is the treatment for choledocolithiasis?
Endoscopic removal of stone via ERCP
34
How does an Endoscopic Retrograde Cholangiopancreatography (ERCP) work?
- 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 (head to R, tape ETT to left)
35
How is an oddi spasm treated during ERCP?
1 mg of glucagon
36
______ is the end product of heme-breakdown
Bilirubin
37
What is the difference between conjugated vs unconjugated bilirubin?
Unconjugated "indirect" bilirubin is PB to albumin, transported to liver, conjugated into to its H20-soluble “direct” state, excreted into bile
38
What is the patho of unconjugated vs conjugated hyperbilirubinemia?
- Unconjugated (indirect) hyperbilirubinemia: imbalance btw bilirubin synthesis & conjugation - Conjugated (direct) hyperbilirubinemia: caused by an obstruction, causing reflux of conjugated bilirubin into the circulation
39
What are the causes of unconjugated vs conjugated hyperbilirubinemia?
Unconjugated: physiologic jaundice of newborn, jaundice of prematurity, hgb disorders (sickle cell), hemolysis, hereditary defects in conjugation, drug-induced, sepsis Conjugated: intrahepatic cholestasis, hepatocellular injury, benign post-op jaundice, Dubin-Johnson syndrome, Rotor syndrome, obstructive jaundice, and biliary atresia
40
What are the 5 most common types of viral hepatitis? Which are more chronic?
A-E B and C
41
___ is most common viral hepatitis requiring liver transplant in US
HCV
42
What is the treatment for viral hepatitis?
12 week course Sofosbuvir/Velpatasvir
43
What happens if viral hepatitis goes untreated?
cirrhosis, then hepatocellular carcinoma
44
Differentiate between type B vs C viral hepatitis
B and C - transmitted percutaneously and sexually B incubation 60-110 days, C is 35-70 days Type C is worse for adults - chronic liver disease 75% of patients Type B worse for children - chronic liver disease in 80-90%
45
What is the most common cause of cirrhosis?
Alcoholic liver disease
46
What is the treatment for ALD?
- Treatment centered around abstinence - Management sx of liver failure - Platelet count <50,000 requires blood transfusion - Liver transplant an option if criteria is met (abstinence for 1 year)
47
What are the s/s of ALD (9)?
- Malnutrition - Muscle wasting - Parotid gland hypertrophy - Jaundice - thrombocytopenia - Ascites - Hepatosplenomegaly - Pedal edema - Sx of ETOH withdrawal may occur 24-72h after stopping
48
What are the differing lab values in patients with ALD?
- ↑Mean corpuscular volume (MCV) - ↑Liver enzymes - ↑ɣ-glutamyl-transferase (GGT) - ↑Bilirubin - Blood ethanol (acute intox)
49
How is non-alcoholic fatty liver disease diagnosed?
- hepatocytes contain >5% fat - Imaging and histology - Liver biopsy= gold standard in distinguishing NAFLD from other liver dx
50
What are the causes of non-alcoholic fatty liver disease?
Obesity, Insulin resistance, DM2, Metabolic syndrome
51
How does non-alcoholic fatty liver disease progress?
- Progresses to NASH, cirrhosis, hepatocellular carcinoma - NAFLD & NASH have become additional leading causes of liver transplant in US
52
What is the treatment for non-alcoholic fatty liver disease?
diet and exercise, liver transplant indicated for advanced fibrosis, cirrhosis, related complications
53
What is the prevalence of NAFLD?
1/4 regardless of weight 6/10 diabetics 9/10 obese people
54
Which progresses faster? alcoholic or non-alcoholic fatty liver disease?
Alcoholic
55
Autoimmune hepatitis effects women _____ than men
more
56
What are the expected lab values of autoimmune hepatitis?
- +autoantibodies & hypergammaglobulinemia - AST/ALT may be 10-20x norm in acute AIH
57
What is the treatment for autoimmune hepatitis?
steroids, azathioprine (immunosuppressant) - Liver transplant indicated when tx fails or acute liver failure ensues
58
What is the most common cause of drug-induced liver injury?
Acetaminophen OD - normally reversible after drug is removed
59
What are the 3 specific disorders of inborn errors of metabolism?
- Wilsons Disease - Alpha-1 Antitrypsin Deficiency - Hemochromatosis
60
Inborn Errors of Metabolism occur in 1:_____ births
2500
61
_______ are a group of rare, genetically inherited disorders that lead to a defect in the enzymes that breakdown and store protein, carbohydrates & fatty acids
Inborn errors of metabolism
62
Wilsons Disease is also known as _______ and is characterized by impaired ______ metabolism
hepatolenticular degeneration copper
63
Copper buildup leads to oxidative stress in the ______, _______, and _______
liver, basal ganglia, and cornea
64
What are the s/s of Wilsons disease? Lab values?
Sx: range from asymptomatic to sudden-onset liver failure along with neurologic & psychiatric manifestations Tx: Copper-chelation therapy & oral zinc to bind copper in the GI tract
65
How is Wilsons disease diagnosed?
Lab tests (serum ceruloplasmin, aminotransferases, urine copper level) - Possible liver biopsy for copper level
66
_______ is a genetic disorder resulting in a defective α-1 antitrypsin protein
Alpha-1 Antitrypsin Deficiency
67
α-1 antitrypsin proteins protect the _____ and _____ from _______
liver & lungs from neutrophil elastase
68
__________ is the #1 genetic cause of liver transplant in children
α-1 antitrypsin deficiency
69
How is α-1 antitrypsin deficiency diagnosed?
confirmed w/ α-1 antitrypsin phenotyping
70
How is α-1 antitrypsin deficiency treated?
pooled α-1 antitrypsin is effective for pulmonary sx; however, it doesn’t help with liver disease - Liver transplant is the only curative treatment for liver disease in α-1 antitrypsin deficiency
71
________ is the excessive intestinal absorption of iron
Hemochromatosis - Excess iron accumulates in organs and causes damage to the tissues
72
What causes Hemochromatosis? How is it diagnosed?
May be genetic or caused by repetitive blood transfusions or iron infusions Dx: genetic mutation testing
73
What are the expected lab values for patients with Hemochromatosis?
Labs reveal elevated AST/ALT, transferrin saturation, and ferritin Liver bx may quantify iron levels in the liver and assess the level of damage
74
What is the treatment for Hemochromatosis?
Tx: weekly phlebotomy, iron-chelating drugs, liver transplant
75
What is a common comorbidity of patients with Hemochromatosis?
cardiomyopathies
76
_______ is an autoimmune, chronic inflammation of the larger bile ducts, resulting in fibrosis in the biliary tree?
Primary Sclerosing Cholangitis (PSC)
77
How does PSC progress?
Fibrosis in biliary tree→strictures (beads on string appearance)→ cirrhosis, ESLD
78
Males are ____ likely to have PSC than women
more, onset 40s
79
What are the s/s of PSC?
Fatigue, itching, deficiency of fat-soluble vitamins (A,D,E,K), cirrhosis
80
How is PSC diagnosed?
- Dx: MRCP or ERCP showing biliary strictures w/ dilated bile ducts - Liver biopsy reinforces dx, but isn't always performed
81
What are the expected lab values of patients with PSC?
Labs: ↑alkaline phosphatase and ɣ-glutamyl-transferase, +auto-antibodies
82
What is the treatment for patients with PSC?
- No drug treatments are proven to be effective - Liver transplant is only long term treatment - Re-occurrence is common after transplant d/t autoimmune nature
83
_________ is the autoimmune, destruction of bile ducts with periportal inflammation & cholestasis
Primary Biliary Cholangitis (PBC)
84
Primary Biliary Cholangitis (PBC) is also known as
biliary cirrhosis
85
What are the s/s of PBC?
jaundice, fatigue, & itching
86
PBC can lead to...
liver scarring, fibrosis, cirrhosis
87
What causes PBC? What population typically has it?
- Females > Males; often dx'd in middle-ages - Thought to be c/b exposure to environmental toxins in genetically susceptible individuals
88
What are the expected lab values of patients with PBC?
Labs: ↑Alk Phos,↑GGT, + Antimitochondrial antibodies
89
How is PBC diagnosed?
- Imaging: CT, MRI, & MRCP to r/o bile duct obstructions - Liver biopsy reveals bile duct destruction and infiltration w/lymphocytes
90
What is the treatment for PBC?
No cure, but exogenous bile acids slow progression
91
Acute liver injury occurs within _____ after insult. 50% of cases are caused by ______
6 months drug-induced - acetaminophen
92
What are other causes of acute liver failure?
Viral hepatitis, autoimmune, hypoxia, ALF of pregnancy, HELLP
93
What are the s/s of acute liver failure?
Jaundice, nausea, RUQ pain, cerebral edema, encephalopathy, multi-organ failure, death Massive hepatocyte necrosis→ cellular swelling & mbrn disruption
94
What is the tx of acute liver failure?
Treat the cause, supportive care, liver transplant
95
What are the expected lab values of acute liver failure?
Rapid increase in AST/ALT, AMS, coagulopathy
96
_____ is final stage liver disease; characterized by normal _____ being replaced with ____
cirrhosis Normal liver parenchyma replaced with scar tissue
97
What are the s/s of cirrhosis?
- Often asymptomatic in early stages - Sx's progress to jaundice, ascites, varices, coagulopathy, encephalopathy
98
What are the most common causes of cirrhosis?
ALD, NAFL, HCV, HBV
99
What are the expected lab values of patients with cirrhosis?
Elevated labs: AST/ALT, bilirubin, Alk phosphatase, PT/INR - thrombocytopenia
100
_______ is the only cure for cirrhosis
transplant
101
What are the 8 complications from cirrhosis?
Portal HTN, ascites, bacterial peritonitis, varices, hepatic encephalopathy, hepatorenal syndrome, hepatopulmonary syndrome, and portopulmonary HTN
102
What is the most common complication of cirrhosis? Treatment?
ascities - ↓Salt diet, albumin replacement - Transjugular Intrahepatic Portosystemic Shunt (TIPS) - Reduces P-HTN and ascites
103
_______ is the most lethal complication of varicies; treatment?
Hemorrhage - Beta blockers help reduce risk - Prophylactic endoscopic variceal banding & ligation - Refractory bleeding → balloon tamponade
104
________ is a complication of cirrhosis in which there is buildup of nitrogenous waste d/t poor liver detoxification
Hepatic Encephalopathy
105
What are the s/s and tx for Hepatic Encephalopathy?
- Neuropsychiatric symptoms (cognitive impairment → coma) - Tx: Lactulose, Rifaximin to ↓ammonia-producing bacteria in gut
106
What is the patho of Hepatorenal Syndrome? Tx?
- Excess production of endogenous vasodilators (NO, PGs)→↓SVR→↓RBF - Tx: Midodrine, Octreotide, Albumin
107
_________ is a triad of chronic liver disease, hypoxemia, intrapulmonary vascular dilation
Hepatopulmonary Syndrome
108
What is the hallmark symptom of Hepatopulmonary Syndrome?
Platypnea (hypoxemia when upright) d/t R to L intrapulmonary shunt
109
What is the patho and tx for Portopulmonary HTN?
- Pulmonary HTN accompanied by portal HTN - Systemic vasodilation triggers production of pulmonary vasoconstrictors - Tx: PD-I’s, NO, prostacyclin analogs, and endothelin receptor antagonists; transplant is only cure
110
What are the 2 scoring systems for liver disease? What values are they based on?
- Child-Turcotte-Pugh (CTP): points based on bilirubin, albumin, PT, encephalopathy, ascites - Model for End-Stage Liver Disease (MELD): score based on bilirubin, INR, creatinine, sodium
111
Anesthesia considerations for patients with liver disease?
- ↑Risks aspiration, HoTN, hypoxemia - Colloids > crystalloids for resuscitation - Alcoholism increases MAC of volatile anesthetics - Drugs may have slow onset/prolonged DoA - Succs and Cisatracurium are ideal (not liver-metabolized)
112
What is the Transjugular Intrahepatic Portosystemic Shunt (TIPS) procedure?
- “TIPS” procedure to manage portal HTN - Stent or graft placed btw hepatic vein and portal vein - Shunts portal flow to systemic circulation - Reduces the portosystemic pressure gradient
113
What are the indications and contraindications for TIPS?
Indications: - Refractory variceal hemorrhage - Refractory ascites Contraindications: - Heart Failure - Tricuspid regurgitation - Severe pulmonary HTN
114
What is a partial hepatectomy?
- Resection to remove neoplasms, leaving adequate tissue for regeneration - Up to 75% removal is tolerated in pts with normal liver function
115
What are the anesthetic considerations of a patient undergoing a partial hepatectomy?
- Invasive monitoring - surgeon may clamp IVC or hepatic artery - Blood products available - postop coagulation disturbances - Adequate vascular access for blood/pressors - maintain low CVP by fluid restriction to reduce blood loss
116
What is the intra-op mgmt for liver transplant?
- Maintain hemodynamics (Pressors/Inotropes readily available) - A-line, CVC, PA cath, TEE - Control coagulation