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Adv. Health Assessment (Spring 2024) > Spring 2024 (Exam III) Hepatic and Biliary > Flashcards

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
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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

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3
Q

T/F liver dysfunction can lead to multi-organ failure

A

True, nearly every organ is impacted by liver function

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4
Q

Right and left lobe of the liver are separated by the ______ ______.

A

Falciform ligament

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5
Q

How many segments are in the liver?

A
  • 8 based on blood supply and bile drainage
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6
Q

______ and ______ vessels branch into each segment of the liver.

A
  • Portal vein and Hepatic artery
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7
Q

How many hepatic veins empty into IVC?

A

Three
* Right, Middle, and Left hepatic veins

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8
Q

Bile ducts travel along ____ and drain through the ____ ____ into the gallbladder and common bile duct

A
  • Portal Veins
  • Hepatic duct
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9
Q

Bile enters duodenum via

A

Ampulla of vater

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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

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11
Q

Where does the portal vein arise from?

A

Splenic vein and superior mesenteric vein

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12
Q

Portal vein contains deoxygenated blood from which organs

A

GI organs (stomach, intestine), pancreas, spleen

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13
Q

How does the liver get perfusion?

A
  • 75% from portal vein
  • 25% from hepatic artery
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14
Q

Oxygen delivery sources to the liver

A

50% portal vein (deoxygenated)
50% hepatic artery

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15
Q

Hepatic arterial blood flow is inversely related to

A

Portal venous blood flow

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16
Q

T/F hepatic blood is not autoregulated

A

False:
Hepatic artery dilates in response to low portal venous flow; keeping consistent HBF

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17
Q

Portal venous pressure reflects ____ and ____.

A

Splanchnic arterial tone and intrahepatic pressure

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18
Q

Normal hepatic venous pressure gradient is

A

HVPG 1-5 mmHg

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19
Q

What happens at a HVPG >10 and >12?

A
  • > 10- Clinically significant PHTN
    -i.e. Cirrhosis, esophageal varices
  • > 12- Variceal rupture
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20
Q

Increase in portal venous pressure

A

Blood backs up in systemic circulation
* Esophageal and gastric varices

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21
Q

When do liver symptoms begin to appear

A

Late-stage liver disease
*often asymptomatic until late-stage liver disease

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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
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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
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24
Q

Physical exam finidngs of liver disease:

A
  • Pruritis
  • Jaundice
  • Ascites
  • Aasterixis (flapping tremor)
  • Hepatomegaly
  • Splenomegaly
  • Spider nevi
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25
Q

Hepato-biliary function tests

A

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

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26
Q

What is the most liver-specific enzyme

A

Alanine aminotransferase (ALT)

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27
Q

Which labs are elevated in late-stage liver disease

A

ɣ-glutamyl-transferase (GGT)
Alkaline phosphatase

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28
Q

What are the 3 groups of hepatobiliary disease?

A
  • Hepatocellular Injury
  • Reduced Synthetic Function
  • Cholestasis
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29
Q

What labs suggest hepatocellular injury?

A

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

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30
Q

What labs suggest reduced synthetic function?

A

↓Albumin
↑PT/INR

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31
Q

What labs suggest cholestasis?

A

↑AlkPhosphatase
↑GGT
↑Bilirubin

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32
Q

3 subclasses of hepatocellar injury and lab findings

A

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

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33
Q

Blood test differentials

A
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34
Q

____ secrete bile through bile ducts, into the common hepatic duct and go through gall bladder and common bile duct

A

Hepatocytes

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35
Q

The gallbladder stores bile to deliver during ________
Common Bile Ducts secretes bile directly into ______.

A
  • Meals
  • Duodenum
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36
Q

Risk factors for cholelithiasis “gallstones”

A
  • Obesity
  • Increased cholesterol
  • DM
  • Pregnancy
  • Female
  • Family Hx
    *80% asymptomatic
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37
Q

Symptoms and treatment of cholelithiasis “gallstones”

A

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

Tx: IVF, ABX, pain management

Lap Choleysectomy

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38
Q

What is choledocolithiasis and the
inital symptoms?
Cholangitis?
Treatment?

A

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

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39
Q

Endoscopic Retrograde Cholangiopancreatography (ERCP)

A
  • Guidewire through Sphincter of Oddi into Ampulla of Vater to retrieve stone from pancreatic duct or common bile duct
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40
Q

Treatment for Spincter of Oddi Spasm

A

Glucagon

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41
Q

____ ____ is done with ERCP; usually in ____ with left tilt (Tape ETT to the left)

A
  • General anesthesia
  • Prone
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42
Q

What is bilirubin?

A
  • End product of heme- breakdown
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43
Q

Whats the difference between unconjugated and conjugated bilibubin?

A
  • Unconjugated bilirubin is protein bound to albumin, transported to the liver
  • Conjugated bilirubin is water soluble, and excreted in the bile
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44
Q

What is unconjugated hyperbilirubinemia and some causes?

A
  • “Indirect” hyperbilirubinemia is caused by an imbalance between bilirubin synthesis and conjugation
45
Q

What is conjugated hyperbilirubinemia and some causes?

A
  • “Direct” hyperbilirubminemia is caused by an obstruction, causing reflux of conjugated bilirubin into the circulation
46
Q

What are the 5 most common types of Hepatitis?

A

A, B, C, D, E

47
Q

Of the 5 types of hepatitis, which are the more chronic?

A
  • B and C
    *HCV is the most common viral hepatitis requiring liver transplant in US
48
Q

T/F HCV is on the decline d/t vaccines and newer treatments

49
Q

Treatment for HCV is based on

A
  • Genotype (75% Type-1)
  • HCV stage
  • +/- Cirrohsis
50
Q

What newer treatment has significantly reduced HCV in the US population?

A
  • 12-week course Sofosbuvir/Velpatasvir
    *Provides 98-99% clearance of genotype 1A/1B
51
Q

Characteristics of hepatitis A, B, C, D, E?

A

B & C are bloodborne and chronic
C is the most chronic (75%)
Long incubation periods

52
Q

What is most common cause of cirrohisis

A

Alcoholic liver disease (ALD)
top indication for liver transplants in the US
national prevalence of liver transplants for ALD is 2%

53
Q

Treatment for alcoholic liver disease

A

Centered around abstinence
* Manage symptoms of liver failure
* Platelet count < 50K requires blood transfusion
* liver transplant if criteria is met

54
Q

Symptoms and labs of alcoholic liver disease

A

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)

thats my dad

55
Q

Risk factors for non-alcoholic fatty liver disease

A
  • Obesity
  • Insulin resistance
  • DM2
  • Metabolic syndome
56
Q

How is non-alcoholic fatty liver disease diagnosed?

A
  • Hepatocytes contain > 5% fat
  • Imaging
  • Histology
    Liver biopsy= gold standard in distinguinging NAFLD from other liver disease
57
Q

Non-alcoholic fatty liver disease can progress to

A
  • Non-alcoholic steatohepatitis (NASH) , cirrhosis, hepatocellular carcinoma
    *NAFLD & NASH have become additional leading causes of liver transplants in US
58
Q

Treatment of non-alcoholic fatty liver disease

A
  • Diet & Exercise
  • Liver transplant for advanced fibrosis, cirrhosis, and related complications
59
Q

Prevalence of non-alcoholic fatty liver disease

60
Q

Non-alcoholic fatty liver disease (NAFLD) vs alcoholic fatty liver disease (AFLD)

61
Q

Autoimmune hepatitis predominantly affects who

62
Q

Autoimmune hepatitis facts

A
  • 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
Q

What is the most common cause of drug induced liver injury?

A

Acetaminophen OD
*normally reversible after the drug is removed

64
Q

Inborn errors of metabolism

A
  • 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
Q

What are the 3 specific disorders of inborn errors of metabolism?

A
  • Wilson’s Disease
  • Alpha-1 Antitrypsin Deficiency
  • Hemochromatosis
66
Q

What is Wilson’s Disease?

AKA hepatolenticular degeneration

A
  • autosomal recessive disease characterized by impaired copper metabolism
  • excessive copper buildup leads to oxidative stress in the liver, basal ganglia, and cornea
67
Q

Symptoms, diagnosis, and treatment for Wilson’s Disease

A

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
Q

what is alpha-1 antitryspin deficency

A

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
Q

alpha-1 antitryspin
incidence
diagnosis
treatment

A

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
Q

hemochromatosis

A

excess iron in the body, leading to mutli-organ dysfunction

71
Q

causes of hemochromatosis

A

repetitive blood transfusion, high dose iron tranfusion
genetic - excessive intestinal absorption

72
Q

patient presentation of hemochromatosis

A

cirrhosis, heart failure, diabetes, adrenal insufficiency, or poly-arthopathy

excess iron accumulates in organs and causes damage to the tissues

73
Q

labs, diagnosis, treatment of hemochromatosis

A

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
Q

what is primary biliary cholangitis

previosuly known as biliary cirrhosis

A
  • autoimmune, progressive destruction of bile ducts with periportal inflammation and cholestasis
  • leads to liver scarring, firbosis, cirrhosis
75
Q

who is more at risk to devlop primary biliary cholangitis

A

Females > males; diagnosed in middle ages
thought to be caused by exposure to environmental toxins in genetically susceptible individuals

76
Q

symptoms, Labs, imaging, and treatment for primary biliary cholangitis

A

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
Q

what is Primary Sclerosing Cholangitis (PSC)

A

autoimmune, chronic inflammation of the larger bile ducts
intrahepatic and extrahepatic
fibrosis in biliary tree leading to strictures -> cirrhosis, ESLD

78
Q

Primary Sclerosing Cholangitis (PSC) affects men or women more? what age of onset

A

men, onset ~40s

79
Q

symptoms of Primary Sclerosing Cholangitis (PSC)

A

fatigue, itching, deficency of fat soluble vitamins (A,D,E,K), cirrhosis
↑alkaline phosphatase andɣ-glutamyl-transferase, +auto-antibodies

80
Q

diagnosis and treatment of Primary Sclerosing Cholangitis (PSC)

A

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
Q

acute liver failure

A

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
Q

causes of acute liver failure

A

50% of cases are drug-induced (majority acetaminophen)
viral hepatitis, autoimmune, hypoxia, ALF of pregnancy, HELLP

83
Q

symptoms and treatment of acute liver failure

A

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

treatment: treat the cause, supportive care, liver transplant

84
Q

what is the final stage of liver disease

A

cirrhosis - normal liver parenchyma replaced with scar tissue

85
Q

symptoms/labs of cirrhosis

A

jaundice, ascites, varices, coagulopathy, encephalopathy
elevated AST/ALT, bilirubin, alkaline phosphatiase, PT/INR, thrombocytopenia

86
Q

causes of cirrhosis

A

alcoholic fatty liver, NAFL, HCV, HBV
transplant is the only cure

87
Q

cirrhosis complications

A
  • portal HTN (HVPG > 5 mmHg)
  • ascites (most common complication)
  • spontaneous bacterial peritonitis (requires ABX)
  • varices
  • hepatic encephalopathy
  • hepatorenal syndrome
  • hepatopulmonary syndrome
  • portopulmonary HTN
88
Q

ascites

A
  • 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
Q

varices

A

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
Q

hepatic encephalopathy

A

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
Q

hepatorenal syndrome

A

excess endogenous vasodilators (NO, Prostacylin) decreasing systemic MAP and renal blood flow
tx: midodrine, octreotide, albumin

92
Q

hepatopulmonary syndrome

A

triad of chronic liver disease, hypoxemia, intrapulmonary vascular dilation
platypnea (hypoxemia when upright) due to R to L intrapulmonary shunt

93
Q

portopulmonary HTN

A

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
Q

2 scoring systems to determine severity and prognosis of liver disease

A

CTP: points based on bilirubin, albumin, PT, enceophalopathy, ascites
MELD: score on bilirubin, INR, creatinine, sodium

95
Q

elective surgery is contraindicated in

A

acute hepatitis, severe chronic hepatitis, ALF

96
Q

anesthesia in liver disease

97
Q

anesthetic considerations in liver disease

A
  • 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
Q

what NMBs are desired in pts with liver disease

A

Succinycholine and Ciastracurium
*plasma cholineserase may be decreased in servere liver disease

99
Q

Transjugular Intrahepatic Portosystemic Shunt (TIPS)

A

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
Q

partial hepatectomy

A

resection to remove neoplasms, leaving adequate tissue for regeneration
tolerable amount of resection d/o preexisting liver disease and function

101
Q

indications and contraindications to TIPS

A

Indications:
refractory variceal hemorrhage, refractory ascites
contraindications:
Heart failure, tricupsid regurgitation, severe pulmonary HTN

102
Q

anesthetic considerations for partial hepatectomy

A

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
Q

liver transplant

A

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
Q

intraop management for liver transplant

A

maintain hemodynamics (pressors/inotropes readily available)
ALine, CVC, PA CATH, TEE
control coagulation

105
Q

Liver transplant table of surgical and anesthetic considerations

106
Q

risk factors for liver disease

A

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
Q

what hepatic venous pressure gradient is associated with variceal rupture

A

HPVG > 12 mmHg

108
Q

what hepatic venous pressure gradient is clincally significant for portal HTN, i.e chirroshis, esophageal varices

A

HVPG > 10 mmHg

Adv. Health Assessment (Spring 2024) (25 decks)

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