Spring 2024 (Exam III) Hepatic and Biliary Flashcards
1
Q
Function of the liver (10)
A
- Synthesizes glucose via gluconeogenesis
- Stores excess glucose as glycogen
- Synthesizes cholesterol and proteins into hormones and vitamins
- Metabolizes fats, protiens, and carbs to generate energy
- Metabolizes drugs via CYP450 and other enzyme pathways
- Detoxifies blood
- Involved in the acute phase of immune support
- Processes HGB and stores iron
- Synthesizes coagulation factors
- Aids in volume control as a blood reservoir
2
Q
Which coagulation factors are not synthesized by the liver?
A
Factor III, IV, VIII, vWF
*Calcium is factor IV and comes from our diet
3
Q
T/F liver dysfunction can lead to multi-organ failure
A
True, nearly every organ is impacted by liver function
4
Q
Right and left lobe of the liver are separated by the ______ ______.
A
Falciform ligament
5
Q
How many segments are in the liver?
A
- 8 based on blood supply and bile drainage
6
Q
______ and ______ vessels branch into each segment of the liver.
A
- Portal vein and Hepatic artery
7
Q
How many hepatic veins empty into IVC?
A
Three
* Right, Middle, and Left hepatic veins
8
Q
Bile ducts travel along ____ and drain through the ____ ____ into the gallbladder and common bile duct
A
- Portal Veins
- Hepatic duct
9
Q
Bile enters duodenum via
A
Ampulla of vater
10
Q
How much of the cardiac output goes to the liver?
A
25%
1.25-1.5L/min
*highest proprotionate CO of all organs
11
Q
Where does the portal vein arise from?
A
Splenic vein and superior mesenteric vein
12
Q
Portal vein contains deoxygenated blood from which organs
A
GI organs (stomach, intestine), pancreas, spleen
13
Q
How does the liver get perfusion?
A
- 75% from portal vein
- 25% from hepatic artery
14
Q
Oxygen delivery sources to the liver
A
50% portal vein (deoxygenated)
50% hepatic artery
15
Q
Hepatic arterial blood flow is inversely related to
A
Portal venous blood flow
16
Q
T/F hepatic blood is not autoregulated
A
False:
Hepatic artery dilates in response to low portal venous flow; keeping consistent HBF
17
Q
Portal venous pressure reflects ____ and ____.
A
Splanchnic arterial tone and intrahepatic pressure
18
Q
Normal hepatic venous pressure gradient is
A
HVPG 1-5 mmHg
19
Q
What happens at a HVPG >10 and >12?
A
- > 10- Clinically significant PHTN
-i.e. Cirrhosis, esophageal varices - > 12- Variceal rupture
20
Q
Increase in portal venous pressure
A
Blood backs up in systemic circulation
* Esophageal and gastric varices
21
Q
When do liver symptoms begin to appear
A
Late-stage liver disease
*often asymptomatic until late-stage liver disease
22
Q
Assessment of liver function should
A
- Rely heavily on “risk factors” for degree of suspicion
*Even later stages may only have vague sx such as disrupted sleep or decreased appetite
23
Q
What are the risk factors for liver disease (9)?
A
- Family hx
- Heavy ETOH
- Lifestyle
- DM
- Obesity
- Illicit Drug Use
- Multiple Partners
- Tattoos
- Transfusion
24
Q
Physical exam finidngs of liver disease:
A
- Pruritis
- Jaundice
- Ascites
- Aasterixis (flapping tremor)
- Hepatomegaly
- Splenomegaly
- Spider nevi
25
Hepato-biliary function tests
**LABS**
BMP, CBC
PT/INR
Aspartate aminotransferase (AST)
Alanine Aminotransferase (ALT)
Bilirubin
Alkaline phosphatase
ɣ-glutamyl-transferase (GGT)
**Imaging**
US, doppler US (portal blood flow), CT, MRI
26
What is the most liver-specific enzyme
Alanine aminotransferase (ALT)
27
Which labs are elevated in late-stage liver disease
ɣ-glutamyl-transferase (GGT)
Alkaline phosphatase
28
What are the 3 groups of hepatobiliary disease?
* Hepatocellular Injury
* Reduced Synthetic Function
* Cholestasis
29
What labs suggest **hepatocellular injury**?
**Elevated 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
30
What labs suggest **reduced synthetic function**?
↓Albumin
↑PT/INR
31
What labs suggest **cholestasis**?
↑Alk Phosphatase
↑GGT
↑Bilirubin
32
3 subclasses of hepatocellar injury and lab findings
Acute Liver Failure (ALF): hepatic enzymes may be **elevated 25x**
Alcoholic Liver Disease (ALD): AST:ALT **ratio is usually 2:1**
Non-Alcoholic Fatty Liver Disease (NALFD): AST:ALT **ratio usually 1:1**
33
Blood test differentials
34
____ secrete bile through bile ducts, into the common hepatic duct and go through gall bladder and common bile duct
Hepatocytes
35
The gallbladder stores bile to deliver during ________
Common Bile Ducts secretes bile directly into ______.
* Meals
* Duodenum
36
Risk factors for cholelithiasis "gallstones"
* Obesity
* Increased cholesterol
* DM
* Pregnancy
* Female
* Family Hx
*80% asymptomatic
37
Symptoms and treatment of cholelithiasis "gallstones"
S/S: RUQ referred to shoulders, N/V, indigestion, fever (acute, obstruction)
Tx: IVF, ABX, pain management
Lap Choleysectomy
38
What is choledocolithiasis and the
inital symptoms?
Cholangitis?
Treatment?
A stone obstructing common bile duct→ biliary colic
* Initial symptoms: N/V, cramping, RUQ pain
* Cholangitis symptoms: fever, rigors, jaundice
* Treatment: Endoscopic Retrograde Cholangiopancreatography (ERCP) stone removal
39
Endoscopic Retrograde Cholangiopancreatography (ERCP)
* Guidewire through Sphincter of Oddi into Ampulla of Vater to retrieve stone from pancreatic duct or common bile duct
40
Treatment for Spincter of Oddi Spasm
Glucagon
41
____ ____ is done with ERCP; usually in ____ with left tilt (**Tape ETT to the left**)
* General anesthesia
* Prone
42
What is bilirubin?
* End product of heme- breakdown
43
Whats the difference between unconjugated and conjugated bilibubin?
* Unconjugated bilirubin is protein bound to albumin, transported to the liver
* Conjugated bilirubin is water soluble, and excreted in the bile
44
What is unconjugated hyperbilirubinemia and some causes?
* "Indirect" hyperbilirubinemia is caused by an imbalance between bilirubin synthesis and conjugation
45
What is conjugated hyperbilirubinemia and some causes?
* "Direct" hyperbilirubminemia is caused by an obstruction, causing reflux of conjugated bilirubin into the circulation
46
What are the 5 most common types of Hepatitis?
A, B, C, D, E
47
Of the 5 types of hepatitis, which are the more chronic?
* B and C
*HCV is the most common viral hepatitis requiring liver transplant in US
48
T/F HCV is on the decline d/t vaccines and newer treatments
True!
49
Treatment for HCV is based on
* Genotype (75% Type-1)
* HCV stage
* +/- Cirrohsis
50
What newer treatment has significantly reduced HCV in the US population?
* 12-week course Sofosbuvir/Velpatasvir
*Provides 98-99% clearance of genotype 1A/1B
51
Characteristics of hepatitis A, B, C, D, E?
*B & C are bloodborne and chronic*
*C is the most chronic (75%)
Long incubation periods*
52
What is most common cause of cirrohisis
Alcoholic liver disease (ALD)
*top indication for liver transplants in the US
national prevalence of liver transplants for ALD is 2%*
53
Treatment for alcoholic liver disease
**Centered around abstinence**
* Manage symptoms of liver failure
* Platelet count < 50K requires blood transfusion
* liver transplant if criteria is met
54
Symptoms and labs of alcoholic liver disease
**Symptoms:**
* Malnutrition
* Muscle wasting
* Parotid gland hypertrophy
* Jaundice
* Thrombocytopenia
* Ascites
* Hepatosplenomegaly
* Pedal edema
* **Symptoms of ETOH withdrawal (DTs) may occur 24-72 hr after stopping**
**Labs:**
* ↑Mean corpuscular volume (MCV)
* ↑Liver enzymes
* ↑ɣ-glutamyl-transferase (GGT)
* ↑Bilirubin
* Blood ethanol (acute intoxication)
## Footnote
thats my dad
55
Risk factors for non-alcoholic fatty liver disease
* Obesity
* Insulin resistance
* DM2
* Metabolic syndome
56
How is non-alcoholic fatty liver disease diagnosed?
* Hepatocytes contain > 5% fat
* Imaging
* Histology
*Liver biopsy= gold standard in distinguinging NAFLD from other liver disease*
57
Non-alcoholic fatty liver disease can progress to
* Non-alcoholic steatohepatitis (NASH) , cirrhosis, hepatocellular carcinoma
*NAFLD & NASH have become additional leading causes of liver transplants in US
58
Treatment of non-alcoholic fatty liver disease
* **Diet & Exercise**
* Liver transplant for advanced fibrosis, cirrhosis, and related complications
59
Prevalence of non-alcoholic fatty liver disease
60
Non-alcoholic fatty liver disease (NAFLD) vs alcoholic fatty liver disease (AFLD)
61
Autoimmune hepatitis predominantly affects who
Women
62
Autoimmune hepatitis facts
* May be asymptomatic, acute, or chronic
* (+) Autoantibodies and hypergammaglobuninemia
* AST/ALT may be 10-20x normal in acute AIH
**Treatment: steroids, azathioprine**
* 60-80% achieve remission, relapse is common
* Refractory disease requires immunosuppession
* Liver transplant when treatment fails or Acute liver failure ensues
63
What is the most common cause of **drug induced liver injury**?
Acetaminophen OD
*normally reversible after the drug is removed
64
Inborn errors of metabolism
* Groups of rare, genetically inheritied disorders that lead to a defect in the enzymes that breakdown and store protein, carbs, and fatty acid
* Occurs in 1: 2500 births
* Onset varies from birth to adolescence
**Most severe forms appear in the neonatal period and carry a high degree of mortality**
65
What are the 3 specific disorders of inborn errors of metabolism?
* Wilson's Disease
* Alpha-1 Antitrypsin Deficiency
* Hemochromatosis
66
What is Wilson's Disease?
| AKA hepatolenticular degeneration
* autosomal recessive disease characterized by impaired copper metabolism
* excessive copper buildup leads to oxidative stress in the liver, basal ganglia, and cornea
67
Symptoms, diagnosis, and treatment for Wilson's Disease
Symptoms: range from asymptomatic to sudden-onset liver failure with neurologic and pyschiatric manifestations
Diagnosis: Lab tests serum ceruloplasmin,
aminotransferases, urine copper level
Possible liver biopsy for copper level
**treatment: copper-chelation therapy & oral zinc to bind copper in the GI tract**
68
what is alpha-1 antitryspin deficency
genetic disorder resulting in defective alpha-1 antitryspin protein.
alpha-1 antitryspin proteins protect the liver and lungs from neutrophil elastase
*neutrophil elastase is an enzyme that causes disruption of connective tissues leading to inflammation, cirrhosis, and hepatocellular carcinoma
69
alpha-1 antitryspin
incidence
diagnosis
treatment
incidence 1:16K to 1:35K (likely to be underdiagnosed)
Diagnosis: confirmed with alpha-1 antitryspin phenotyping
treatment: pooled alpha-1 antitryspin is effective for pulmonary symptoms; however it doesnt help with liver disease
**liver transplant is the only curative treatment**
70
hemochromatosis
excess iron in the body, leading to mutli-organ dysfunction
71
causes of hemochromatosis
repetitive blood transfusion, high dose iron tranfusion
genetic - excessive intestinal absorption
72
patient presentation of hemochromatosis
cirrhosis, heart failure, diabetes, adrenal insufficiency, or poly-arthopathy
| excess iron accumulates in organs and causes damage to the tissues
73
labs, diagnosis, treatment of hemochromatosis
Labs: elevated AST/ALT, transferrin saturation and ferritin
Diagnosis: genetic mutation test, ECHO and MRI to diagnose cardiomyopathies and liver abnormalities
-liver biopsy may quantify iron levels in the liver and assess damage
treatment: weekly phlebotomy, iron-chelating drugs, liver transplant
74
what is primary biliary cholangitis
| previosuly known as biliary cirrhosis
* autoimmune, progressive destruction of bile ducts with periportal inflammation and cholestasis
* leads to liver scarring, firbosis, cirrhosis
75
who is more at risk to devlop primary biliary cholangitis
Females > males; diagnosed in middle ages
thought to be caused by exposure to environmental toxins in genetically susceptible individuals
76
symptoms, Labs, imaging, and treatment for primary biliary cholangitis
symptoms: fatigue, jaundice, itchingh
Labs: increased Alk Phos, increased GGT, + antimitochrondrial antibodies
Imaging: CT/MRI/MRCP to rule out bile duct obtructions
**Liver biopsy to reveal bile duct destruction and infiltration with lymphocytes**
treatment: no cure, but exogenous bile acids slow progression
77
what is Primary Sclerosing Cholangitis (PSC)
autoimmune, chronic inflammation of the larger bile ducts
intrahepatic and extrahepatic
fibrosis in biliary tree leading to strictures -> cirrhosis, ESLD
78
Primary Sclerosing Cholangitis (PSC) affects men or women more? what age of onset
men, onset ~40s
79
symptoms of Primary Sclerosing Cholangitis (PSC)
fatigue, itching, deficency of fat soluble vitamins (A,D,E,K), cirrhosis
↑alkaline phosphatase and ɣ-glutamyl-transferase, +auto-antibodies
80
diagnosis and treatment of Primary Sclerosing Cholangitis (PSC)
diagnosis: MRCP/ERCP showing biliary strictures with dilated bile ducts
liver biopsy reinforces diagnosed (not always performed)
treatment:
no drug treatment proven to be effective
liver transplant - long term treatment
*re-occurence is common after transplant due to to autoimmne nature*
81
acute liver failure
life threatening severe liver injury occuring with days to 6 months after insult
rapid increase in AST/ALT, AMS, coagulopathy
massive hepatocyte necrosis causes cellular swelling and membrane disruption
82
causes of acute liver failure
50% of cases are drug-induced (majority acetaminophen)
viral hepatitis, autoimmune, hypoxia, ALF of pregnancy, HELLP
83
symptoms and treatment of acute liver failure
jaundice, nausea, RUQ pain, cerebral edema, encephalopathy, multi-organ failure, death
treatment: treat the cause, supportive care, liver transplant
84
what is the final stage of liver disease
cirrhosis - normal liver parenchyma replaced with scar tissue
85
symptoms/labs of cirrhosis
jaundice, ascites, varices, coagulopathy, encephalopathy
elevated AST/ALT, bilirubin, alkaline phosphatiase, PT/INR, thrombocytopenia
86
causes of cirrhosis
alcoholic fatty liver, NAFL, HCV, HBV
transplant is the only cure
87
cirrhosis complications
* portal HTN (HVPG > 5 mmHg)
* ascites (most common complication)
* spontaneous bacterial peritonitis (requires ABX)
* varices
* hepatic encephalopathy
* hepatorenal syndrome
* hepatopulmonary syndrome
* portopulmonary HTN
88
ascites
* Caused by portal HTN leading to increased blood volume and peritoneal accumulation of fluid
* management: low salt diet, albumin replacement
* transjugular intrahepatic portosystemic shunt (TIPS)
*reduces portal HTN and ascites*
89
varices
present in ~50% of cirrhosis patients
hemorrhage is the most lethal complication
*beta blockers help reduce risk
*prophylactic endoscopic variceal banding and ligation
*refractory bleeding --> balloon tamponande
90
hepatic encephalopathy
build up of nitrogenous waste due to poor liver detoxification
neuropyschiatric symptoms (cognitive impairment to coma)
Tx: Lactulose, Rifaximin to decrease ammonia producing bacteria in the gut
91
hepatorenal syndrome
excess endogenous vasodilators (NO, Prostacylin) decreasing systemic MAP and renal blood flow
tx: midodrine, octreotide, albumin
92
hepatopulmonary syndrome
triad of chronic liver disease, hypoxemia, intrapulmonary vascular dilation
platypnea (hypoxemia when upright) due to R to L intrapulmonary shunt
93
portopulmonary HTN
Pulmonary HTN accompanied by portal HTN
systemic vasodilation triggers the production of pulmonary vasoconstrictors
treatment: PD-I, NO, prostacylcin analogs, and endothelian receptor antagonists
**transplant is the only cure**
94
2 scoring systems to determine severity and prognosis of liver disease
CTP: points based on bilirubin, albumin, PT, enceophalopathy, ascites
MELD: score on bilirubin, INR, creatinine, sodium
95
elective surgery is contraindicated in
acute hepatitis, severe chronic hepatitis, ALF
96
anesthesia in liver disease
97
anesthetic considerations in liver disease
* careful H&P
* standard preop labs: CBC, BMP, PT/INR
* low treshold for invasive monitoring
* risk for aspiration, hypotension, hypoxemia
* **colloids > crystalloids**
* alcoholism increases MAC of VA
* drugs may have slow onset/prolonged Duration of Action
* bleeding/coagulation management
* Succ and ciastracurium ideal
* plasma cholinestase may be decreased in servere liver disease
98
what NMBs are desired in pts with liver disease
Succinycholine and Ciastracurium
*plasma cholineserase may be decreased in servere liver disease
99
Transjugular Intrahepatic Portosystemic Shunt (TIPS)
used to manage portal HTN
stent between the hepatic vein and the portal vein
shunt portal flow to the systemic circualtion
reducing the portosystemic pressure gradient
100
partial hepatectomy
resection to remove neoplasms, leaving adequate tissue for regeneration
tolerable amount of resection d/o preexisting liver disease and function
101
indications and contraindications to TIPS
Indications:
refractory variceal hemorrhage, refractory ascites
contraindications:
Heart failure, tricupsid regurgitation, severe pulmonary HTN
102
anesthetic considerations for partial hepatectomy
anesthetic considerations
*invasive monitoring
blood products available
adequate vascular access for blood/pressors
surgeon may clamp the IVC or hepatic artery to control blood loss
maintain low CVP by fluid restriction prior to resection to reduce blood loss
Post op PCA
may cause posop coagulation disturbances
103
liver transplant
definitive treatment for ESLD
alcoholic liver disease the most common indication > fatty liver, HCC
*living donor: surgies timed together for minimal ischemia time
brain dead donor: kept hempodynamically stable for organ perfusion
104
intraop management for liver transplant
maintain hemodynamics (pressors/inotropes readily available)
*ALine, CVC, PA CATH, TEE*
control coagulation
105
Liver transplant table of surgical and anesthetic considerations
106
risk factors for liver disease
family history
heavy ETOH
lifestyle
DM
obesity
illicit drug use
multiple partners
tattoos (basement tattoos)
blood transfusions (in the 80s)
| rely heavily on "risk factors" for degree of suscpicion
107
what hepatic venous pressure gradient is associated with variceal rupture
HPVG > 12 mmHg
108
what hepatic venous pressure gradient is clincally significant for portal HTN, i.e chirroshis, esophageal varices
HVPG > 10 mmHg
