Exam 3 - Hepatic/Biliary Systems Flashcards

1
Q

Functions of the liver?

A
  • Glucose synthesis (gluconeogenesis)
  • Storage of glucose as glycogen
  • Synthesis of hormones and vitamins from cholesterol
  • Metabolism to create energy and drug metabolism (CYP450)
  • Iron storage
  • Makes coag factors (except III, IV, VIII, and vWF)
  • Blood reservoir
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2
Q

How many segments are there in the liver? What creates them?
What seperates the 2 lobes?

A
  • 8 segments (each has a branch of the portal vein and hepatic artery)
  • Falciform ligament
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3
Q

What veins return blood from the liver to the IVC?

A

Right, middle, and left hepatic veins

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4
Q

How does bile travel through and out of the liver?

A

Via bile ducts that travel along portal veins
Drains through hepatic duct into CBD and GB
Enters duodenum via Ampulla of Vater

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5
Q

The liver recieves how much of the CO?

A

25% or 1.25-1.5 L/min, highest portion of CO of all organs

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6
Q

The portal vein provides ____ of hepatic blood flow and is partially ____

A

75%, deoxygenated

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7
Q

The hepatic artery branches off the ____ and provides ____ of the hepatic blood flow

A

aorta, 25%

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8
Q

The liver obtains ____ of oxygen from both portal vein and hepatic artery

A

50%

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9
Q

How is hepatic blood flow regulated?
What can happen when this fails?

A

Hepatic blood flow is autoregulated; Hepatic artery dilates when portal blood flow is low
When portal venous pressure increases blood backs up in the systemic circulation and can cause varices

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10
Q

What is a normal HPVG?

A

1-5 mmHg

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10
Q

What HVPG correlates with cirrohsis and esophageal varices?

A

HVPG > 10 mmHg

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11
Q

What can happen at an HVPG >12 mmHg?

A

Variceal rupture

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12
Q

What risk factors may lead to liver disease?

A
  • Family hx
  • EtOH abuse
  • DM
  • Obesity
  • Illicit drug use
  • Multiple partners
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13
Q

Someone with liver failure may have what physical findings?

A
  • Pruritis (bilirubin excess)
  • Jaundice
  • Ascites
  • Asterixis (flapping tremor)
  • Hepatomegaly
  • Spleenomegaly
  • Spider nevi
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14
Q

What are the 3 groups of hepatobiliary disorders?

A
  • Bilirubin overload
  • Hepatocellular injury
  • Cholestasis
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15
Q

What abnormal lab findings are found with bilirubin overload?

A
  • Unconjugated bilirubin predominants
  • BUN may be slightly increased
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16
Q

What abnormal lab findings are found with hepatocellular injury?

A
  • Incrased aminotrasferases (AST/ALT)
  • Decreased albumin
  • Prolonged PT
  • Retention of dye
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17
Q

What abnormal lab findings are found with cholestasis?

A
  • Increased alkaline phosphatase
  • Increased Ɣ-Glutamyl transpeptidase
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18
Q

Risk factors, S/S, and treatments for cholelithiasis

A

Risk factors: Obesity, ↑cholesterol, DM, preganancy, female, family hx
S/S: RUQ pain referred to shoulders, N/V, indegestion, fever
Tx: IVF, abx, lap cholecystectomy

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19
Q

What is choledocolithiasis?

A

Stone obstructs the CBD causing retrograde flow of bile

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20
Q

Sx of choledocolithiasis?

A

N/V, cramping, RUQ pain
Can progress to cholangitis → fever, rigors, jaundice

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21
Q

Treatment for choledocolithiasis?

A

ERCP - Endoscopic Retrograde Cholangiopancreatography
Guidewire threaded through Sphincter of Oddi into Ampulla of Vater to retrieve stone

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22
Q

Anesthesia concerns for ERCP?

A
  • Pt is under GA
  • Usually prone with left tilt (tape ETT to the left)
  • Glucagon may be needed if sphincter of oddi spasm
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23
Q

What is bilirubin and the different forms?

A

Bilirubin - end product of heme breakdown
Unconjugated (indirect) bilirubin - protein bound to albumin; conjugated in the liver to “direct” state and excreted into bile (now water soluble)

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24
Q

What causes unconjugated hyperbilirubinema?

A

Imbalance between bilirubin synthesis and conjugation: drug induced, sepsis, sickle cell

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25
Q

What causes conjugated hyperbilirubinemia?

A

Caused by obstruction, causing reflux of bilirubin into circulation: intrahepatic cholelithiasis, hepatitis, drugs, cirrhosis

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26
Q

What type of hepatitis usually requires a liver transplant?
What treatments reduce HCV?

A
  • Hepatitis C
  • HCV genotyping and staging has improved
  • Sofosbuvir/Velpatasvir clear 99% of 1A/1B genotypes
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27
Q

How are the different viral hepatitis’ spread?

A

A, E: fecal-oral, contaminated water
B,C: Transfusion, percutaneous, sexual
D: Percutaneous

28
Q

Which viral hepatitis has the longest incubation period?

A

Type B: 60-110 days

29
Q

What viral hepatitis’ progress to chronic liver disease?

A

B: in 1-5% of adults and 80-90% of children
C: up to 75% of patients

30
Q

What is the most common cause of cirrhosis and liver transplants?

A

Alcholic liver disease

31
Q

S/S of Alcoholic LD?

A
  • Jaundice
  • Thrombocytopenia
  • Acites
  • Hepatosplenomegaly
  • EtOH withdrawl
32
Q

Abnormal lab values found in ALD?

A
  • ↑Mean corpuscular volume (MCV)
  • ↑Liver enzymes
  • ↑ɣ-glutamyl-transferase (GGT)
  • ↑Bilirubin
  • Blood ethanol (acuteintox)
33
Q

Diagnosis and causes of NAFLD?

A

Dx: hepatocytes contain >5% fat - requires liver biopsy
Causes: Obesity, insulin resistance, DM2, metabolic syndrome

34
Q

Treatments for NAFLD?

A

Diet, exercise, liver transplant for advanced fibrosis/cirrhosis

35
Q

Describe autoimmune hepatitis?
Treatments?

A
  • Predominantly effects women
  • Have autoantibodies and hypergammaglobulinemia
  • AST/ALT may be 10-20x normal in acute phase
  • Steroids and azathioprine (immunosuppressant)
  • Liver transplant for acute liver failure
36
Q

Most common cause of drug induced liver injury?

A

Acetaminophen OD

37
Q

What are the 3 cogenital hepatic disorders?

A
  • Wilsons disease
  • ⍺-1 Antitrypsin deficiency
  • Hemochromatosis
38
Q

Describe Wilsons Disease (hepatoenticular degneration)?

A
  • Autosomal recessive disease causing impaired copper metabolism (excess Cu buildup)
  • Leads to oxidative stress on liver, basal ganglia, and cornea
39
Q

S/S and treatmets for Wilsons disease?

A
  • Asymptomatic
  • Sudden onset liver failure
  • Neurologic and psychiatric manifestations
  • Tx: copper-chelation therapy and oral zinc to bind Cu in GI traact
40
Q

Describe ⍺-1 antitrypsin deficiency?

A
  • Defective ⍺-1 antitrypsin protein
  • Normally ⍺-1 antitrypsin protects the lung and liver from neutrophil elastase (enzyme disruptes tissues)
  • Leading genetic cause of liver transplants in children
41
Q

Treatments for ⍺-1 antitrypsin deficiency?

A
  • Pooled ⍺-1 antitrypsin for pulmonary symptoms
  • Liver transplant is the only curative treatment
42
Q

What is hemochromatosis?

A
  • Excessive GI absorption of iron → accumulates in organs and causes tissue damage
  • May be genetic or from blood/iron transfusion
43
Q

S/S and treatments for hemochromatosis?

A
  • Cirrhosis, heart failure, DM, adrenal insufficiency or polyarthropathy
  • ↑AST/ALT, transferrin saturation, and ferritin
  • Tx: weekly phlebotomy, iron-chelation, liver transplant
44
Q

What is Primary Sclerosing Cholangitis (PSC)?

A
  • Autoimmune inflammation of the large bile ducts
  • Leads to fibrosis in biliary tree causing a “beads on string” appearance
  • Can cause cirrhosis and ESLD

Intra and extrahepatic

45
Q

S/S of PSC?

A
  • Fatigue
  • Itching
  • Fat soluble vitamin deficiency (A,D,E,K)
  • Cirrhosis
  • ↑Alk phos, ɣ-glutamyl-transferase, +auto-antibodies
  • Males > females
46
Q

How is PSC diagnosed and treated?

A

MRCP/ERCP showing biliary strictures
Liver transplant is only long term treatment (re-occurence common)

47
Q

Describe Primary Biliary Cholangitis (PBC)?

A
  • Autoimmune destruction of bile ducts causing periportal inflammation and cholestasis
  • Can lead to fibrosis, scarring, and cirrhosis
  • Thought to be caused by enviornmental toxin exposure in genetically susceptible individuals

intrahepatic only

48
Q

S/S of PBC?

A
  • Jaundice
  • Fatigue
  • Itching
  • ↑Alk Phos,↑GGT, + Antimitochondrial antibodies
  • Bile duct destruction and infiltration w/ lymphocytes on biopsy
49
Q

Treatment for PBC?

A

No cure, bile acids slow progression (can damage stomach lining)

50
Q

Patho of acute liver failure?
S/S?
Treatment?

A
  • Massive hepatocyte necrosis leads to cellular swelling and membrane disruption
  • Sx: Jaundice, nausea, RUQ pain, cerebral edema, encephalopathy, MODS
  • Tx: fix underlying cause, suppoprtive care, liver transplant
51
Q

What is the final stage of liver disease?

A

Cirrhosis - normal liver parenchyma replaced with scar tissue

52
Q

What is the most common complication of cirrhosis and treatments?

A

Ascites - due to increase abdominal blood volume and peritoneal accumulation of fluid
Tx: ↓Salt diet, albumin replacement, Transjugular Intrahepatic Portosystemic Shunt (TIPS)

53
Q

Most common infection r/t cirrhosis?

A

Bacterial Peritonitis

54
Q

Cirrhotic varcies treatments?

A
  • BB reduce risk
  • Prophylactic banding and ligation
  • Balloon tamponade for refractory bleeding
55
Q

Causes, symptoms, and treatments for hepatic encephalopathy?

A
  • Buildup of nitrogenous waste d/t poor liver detoxification
  • Neuropsychiatric symptoms (cognitive impairment → coma)
  • Tx: Lactulose, Rifaximin to ↓ammonia-producing bacteria in gut
56
Q

What is hepatorenal syndrome?
Treatments?

A
  • Excess production of endogenous vasodilators (NO, PGs)→↓SVR→↓RBF
  • Tx: Midodrine, Octreotide, Albumin
57
Q

What is hepatopulmonary syndrome?
Symptom?

A
  • Triad of chronic liver dz, hypoxemia, intrapulmonary vascular dilation
  • Platypnea (hypoxemia when upright) d/t R to L intrapulmonary shunt
58
Q

What is portopulmonary HTN?
Treatments?

A
  • 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
59
Q

What is the Child-Turcotte-Pugh score and what is it based on?

A

Awards points based on bilirubin, albumin, PT, ascites, and encephalopathy

60
Q

What is the Model for End Stage Liver Disease score and what is it based on?

A

Score based on bilirubin, INR, creatinine, and sodium

61
Q

How does the MELD and CTP score influence preoperative decision making?

62
Q

Intraoperative anesthetic considerations for liver disease?

A
  • Invasive monitoring
  • Colloids preferred to crystalloids
  • Chronic alcholism increases MAC
  • Drugs may have prolonged DOA/slower onset
  • Incerased risk for bleeding
63
Q

What NMB is preferred for liver disease patients?

A

Sucinylcholine and cisatricurium (not liver metabolized)
Although plasma cholinesterases may also be decreased

64
Q

What is 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
65
Q

TIPS indications and contraindications?

A

Indications: Refractory variceal hemorrhage and ascities
CI: HF, Tricuspid regurgitation, severe pulmonary HTN.

66
Q

Indications for partial hepatectomy?
Anesthetic considerations?

A
  • Removal of neoplasms
  • Up to 75% can be removed (tissue can regenerate)
  • Need invasive monitoring, blood products, adequate IV access, maintain low CVP to reduce blood loss.
67
Q

Liver transplant anesthetic concerns?