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ABSITE Review: Fiser, Decker, SCORE, UpToDate, TrueLearn COPY > Chapter 31 - Liver+ > Flashcards

Chapter 31 - Liver+ Flashcards

1
Q

What is the #1 hepatic artery variant?

A

Right hepatic off of SMA, 20%; courses behind pancreas, posterolateral to CBD

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2
Q

What is the most common variant of the left hepatic artery?

A

Left hepatic off left gastric artery; found in gastrohepatic ligament medially

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3
Q

What is the most common variant of the common hepatic artery?

A

Common hepatic off of SMA

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4
Q

What is the course of the falciform ligament? What does it contain?

A

Separates medial and lateral segments of the left lobe; attaches liver to anterior abdominal wall; extends to umbilicus and carries remnant of the umbilical vein

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5
Q

What is the course of the ligamentum teres? What does it contain?

A

Extends from falciform ligament on the undersurface of the liver; carries the obliterated umbilical vein

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6
Q

What separates the right and left lobe of the liver?

A

Line drawn from the middle of the gallbladder fossa to IVC (Cantlie’s line)

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7
Q

What is the name of the peritoneum that covers the liver?

A

Glisson’s capsule

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8
Q

What are the triangular ligaments of the liver?

A

Lateral and medial extensions of the coronary ligament on the posterior surface of the liver

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9
Q

The portal triad enters what segments?

A

IV and V

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10
Q

Gallbladder lies under what segments?

A

IV and V

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11
Q

What is contained in the hepatoduodenal ligament?

A

Bile duct, portal vein, hepatic artery

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12
Q

What are the positions of the contents of the portal triad?

A

common bile duct laterally, hepatic artery medially, portal vein posteriorly

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13
Q

What are the borders of the foramen of Winslow?

A

Superior: liver

Anterior: portal traid posterior: IVC

Inferior: duodenum

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14
Q

Portal veins carry what % of blood to the liver?

A

2/3 of hepatic blood flow

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15
Q

The middle hepatic artery most commonly branches from where?

A

Left hepatic artery

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16
Q

Primary and secondary tumors of the liver are most commonly supplied by what blood vessel?

A

Hepatic artery

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17
Q

The middle hepatic vein joins the left hepatic vein in what % of patients?

A

80%; other 20% go directly to IVC

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18
Q

Blood supply to the caudate lobe?

A

Receives separate right and left portal and arterial flow; drains directly into IVC via separate hepatic veins

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19
Q

Alkaline phosphatase normally located where?

A

Canalicular membrane

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20
Q

Where does nutrient uptake occur?

A

Sinusoidal membrane

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21
Q

What is the normal energy source for liver?

A

Ketones; glucose is converted to glycogen and stored

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22
Q

Where is urea synthesized?

A

Liver.

Amino acid oxidation for energy yields urea and CO2. Ammonia also converted to urea. Done through the urea cycle w/ N-acetylglutamate to regulate. It is dissolved in the blood. Carries nitrogen. Excreted in kidneys.

Urea loss can be used to measure muscle mass loss by estimating nitrogen from urea, then protein, then muscle mass.

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23
Q

What factors are NOT made in the liver?

A

VonWillebrand and factor VIII

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24
Q

What is the only water-soluble vitamin stored in the liver?

A

B12

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25
Q

What are the most common complications of hepatic resection?

A

Bleeding and bile leak

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26
Q

Which acinar zone is most susceptible to ischemia?

A

Acinar zone III, hepatocytes

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27
Q

What % of the liver can be safely resected?

A

75%

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28
Q

What is the breakdown of Hgb?

A

Hgb –> heme –> biliverdin –> bilirubin

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29
Q

Bilirubin is conjugated to what in the liver?

A

Glucuronic acid by glucuronyl transferase; improves water solubility

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30
Q

Where does urobilinogen come from? Reabsorbed and released where?

A

Breakdown of bilirubin by bacteria in the terminal ileum; reabsorbed in blood, released in urine

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31
Q

Components of bile?

A

Bile salts, proteins, phospholipids (lecithin), cholesterol, bilirubin

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32
Q

Bile acids are conjugated with what two amino acids?

What are the primary and secondary conjugated bile acids?

A

Taurine or glycine, improves water solubility (form micelles)

Primary bile acids: cholic and chenodeoxycholic

Secondary bile acids: deoxycholic and lithocholic

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33
Q

What is lecithin?

A

Main biliary phospholipid, solubilizes cholesterol and emulsifies fats in the intestine

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34
Q

Where is the 1st place jaundice is evident?

A

Under the tongue

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35
Q

What is the ddx for elevated unconjugated bilirubin?

A

Prehepatic causes (hemolysis), hepatic deficiencies of uptake or conjugation

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36
Q

What is the ddx for elevated conjugated bilirubin?

A

Secretion defects into bile ducts; excretion defects into GI tract (stones, strictures, tumor)

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37
Q

What is Gilbert’s disease?

A

Abnormal uptake; mildly high unconjugated bilirubin

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38
Q

What is Crigler-Najjar?

A

Inability to conjugate; deficiency of glucuronyl transferase; high unconjugated bilis, life-threatening

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39
Q

What is physiologic jaundice of newborn?

A

Immature glucuronyl transferase

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40
Q

What is Rotor’s syndrome?

A

Deficiency in storage ability; high conjugated bilirubin. Liver looks normal.

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41
Q

What is Dubin-Johnson syndrome?

A

Deficiency in secretion ability; high conjugated bilirubin

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42
Q

What does it mean if you have elevated anti-HBs abs only?

A

Post-vaccination

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43
Q

What does it mean if you have elevated anti-HBc and anti-HBs antibodies, but no HBs antigen

A

Had infection with recovery and subsequent immunity

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44
Q

What is the most common viral hepatitis leading to liver transplant?

A

Hepatitis C (RNA)

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45
Q

What hepatitis type is a cofactor for hepatitis B?

A

Hepatitis D

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46
Q

What is the hepatitis which will cause fulminant hepatic failure in pregnancy?

A

Hepatitis E

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47
Q

What is the most common cause of liver failure?

A

Cirrhosis

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48
Q

What is the best indicator of synthetic function in patients with cirrhosis?

A

PT

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49
Q

What is the mortality of acute fulminant hepatic failure?

A

80%

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50
Q

What is hepatic encephalopathy caused by?

A

Liver failure that leads to inability to metabolize; causes buildup of ammonia, mercantanes, methane thiols, and false neurotransmitters

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51
Q

Causes of encephalopathy other than liver failure?

A

GI bleeding, infection (SBP), electrolyte imbalance, drugs

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52
Q

Treatment for hepatic encephalopathy?

A

Lactulose - cathartic that gets rid of bacteria in gut and acidifies colon (preventing NH3 uptake by converting it to ammonium), titrate to 2-3 stool/day; limit protein intake, branched chain amino acids, no abx, neomycin, dopamine receptor antagonists

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53
Q

What is the mechanism of cirrhosis?

A

Hepatocyte destruction –> fibrosis and scarring of liver –> increased hepatic pressure –> portal venous congestion –> lymphatic overload –> leakage of splanchnic and hepatic lymph into peritoneum –> ascites

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54
Q

Treatment for ascites from hepatic/splanchnic lymph?

A

Decrease NaCl, diuretics, paracentesis, TIPS, peritoneovenous shunts, prophylactic abx, water restriction

55
Q

Complications of peritoneovenous shunts?

A

DIC

56
Q

What is the prophylaxis for SBP?

A

Cipro 750mg/wk

57
Q

What is the cause of elevated aldosterone in liver failure?

A

Reduced effective blood volume 2/2 vasodilation and low albumin may lead to activation of the RAAS system.

58
Q

What is hepatorenal syndrome? Treatment?

A

Portal HTN -> splanchnic arterial dilation (nitric oxide) -> hypotension -> RAAS, sympathetics -> increased renal vascular resistance -> decreased renal perfusion -> decreased GFR

Same appearance as prerenal azotemia (RAAS, so low Na excretion); stop diuretics, give volume w/ albumin

  • ICU: neropinephrine
  • non-ICU: terlipressin or midodrine with octreotide
  • If nonresponsive to above: TIPS
59
Q

What is the cause of postpartum liver failure with ascites? Diagnosis?

A

Hepatic vein thrombosis; SMA arteriogram with venous phase contrast

60
Q

How is the diagnosis of SBP made?

A

PMNs >250 in fluid, (+)cultures

61
Q

What are the bacteria that cause SBP?

A

1 E. coli, pneumococci, streptococci; most commonly mono-organism (if not need to worry about bowel perforation)

62
Q

Risk factors for SBP?

A

Prior SBP, variceal hemorrhage, low-protein ascites, nephrotic syndrome, SLE in children

63
Q

Treatment of SBP?

A

3rd generation cephalosporins

64
Q

Treatment for esophageal varices?

A

Sclerotherapy (90% effective), vasopressin, octreotide, Sengstaken-Blakemore tube (to control, risk of rupture of esophagus), correct coags, blood transfusion

65
Q

Use of propranolol for esophageal varices?

A

May help prevent rebleeding, no good role acutely

66
Q

Treatment for refractory variceal bleeds?

A

TIPS

67
Q

Mortality with bleeding varices?

A

33% with 1st episode; 50% with each subsequent bleeding episodes

68
Q

Causes of presinusoidal obstruction causing portal hypertension?

A

Schistosomiasis, congenital hepatic fibrosis, portal vein thrombosis

69
Q

Most common cause of portal HTN in children?

A

Portal vein thrombosis

70
Q

Cause of sinusoidal obstruction leading to portal HTN?

A

Cirrhosis

71
Q

Cause of postsinusoidal obstruction causing portal HTN?

A

Budd-Chiari syndrome (hepatic vein occlusive disease), constrictive pericarditis, CHF

72
Q

What is the normal portal vein pressure?

A

<12mmHg

73
Q

What are the collaterals between the portal vein and systemic venous system of the lower esophagus?

A

Coronary veins

74
Q

Use of TIPS? Complications?

A

Used for protracted bleeding, progression of coagulopathy, visceral hypoperfusion, refractory ascites; development of encephalopathy

75
Q

What patients are candidates for splenorenal shunt? Contraindications?

A

Child’s A cirrhotics who present with bleeding only; contraindicated in refractory ascites (can worsen)

76
Q

What does the Child’s class correlate with?

A

Mortality after shunt

77
Q

What is the most common cause of massive hematemesis in children?

A

Portal HTN (most commonly from extrahepatic thrombosis of portal vein)

78
Q

What is Budd-Chiari syndrome? Presentation?

A

Occlusion of hepatic veins and IVC; RUQ pain, hepatosplenomegaly, ascites, fulminant hepatic failure, muscle wasting, variceal bleeding

79
Q

How is Budd-Chiari diagnosed?

A
  • Doppler US - hep V outflow obsx w/o cardiac dz
  • Venography can rule out if Doppler neg but high suspx
  • CT scan or MRI helps confirm and plan op
  • Biopsy (not required) - sinusoidal dilation, centrilobular congestion
  • ID underlying d/o and treat
80
Q

Where do primary infection which cause amebic liver abscess occur?

A

Amebic colitis

81
Q

Risk factors for amebic liver abscess?

A

Travel to Mexico, ETOH, fecal-oral transmission

82
Q

Amebic abscess will show positive serology for what organism?

A

Entamoeba histolytica

83
Q

Symptoms of amebic abscess?

A

Fever, chills, RUQ pain, elevated WBCs, jaundice, hepatomegaly

84
Q

What will cultures of amebic abscess show? Aspiration looks like?

A

Often sterile; protozoa exist only in peripheral rim; anchovy paste

85
Q

Diagnosis of amebic abscess? Treatment?

A

Based on CT findings

Flagyl

Aspiration if refractory or contaminanted

Surgery only for free rupture

86
Q

Hydatid cyst formed by what organism?

A

Echinococcus

87
Q

CBC and serology show what with echinococcus? What is the name of the skin test?

A
  • Eosinophilia
  • positive indirect hemagglutination
  • Casoni skin test
88
Q

What can happen with aspiration of echinococcal cyst?

A

Anaphylaxis

89
Q

Diagnosis of echinococcus?

A

Abdominal CT shows ectocyst (calcified) and endocyst

90
Q

When do you need a preop ERCP for echinococcus?

A

In patients with jaundice, increased LFTs, cholangitis to check for communication with biliary system

91
Q

Treatment for hydatid cyst?

A

Source control, carefully:

  • Preop albendazole
  • Surgical removal
    • Can inject cyst with alcohol to kill organisms
  • Need to get all of cyst wall
92
Q

Derm and lab characteristics of schistosomiasis?

A

Maculopapular rash, eosinophilia

93
Q

Findings in sigmoid colon with schistosomiasis?

A

Fine granulation tissue, petechiae, ulcers

94
Q

Treatment of schistosomiasis?

A

Praziquantel and control of variceal bleeding

95
Q

80% of all hepatic abscesses are what type?

A

Pyogenic abscess

96
Q

Symptoms of pyogenic abscess?

A

Fever, chills, wt loss, RUQ pain, elevated LFTs/WBCs, sepsis

97
Q

1 organism in pyogenic abscess?

A

E. coli

98
Q

Pyogenic abscess commonly secondary to what?

A

Contiguous infection from biliary tract; can also occur following bacteremia (portal vein if gut, hepatic artery if systemic) from other infections

99
Q

Diagnosis of pyogenic abscess? Treatment?

A

Aspiration; CT guided drainage and antibiotics, surgical drainage for unstable condition and continued signs of sepsis

100
Q

Hepatic adenomas occur in what patients?

A

Women, steroid use, OCPs, type I collagen storage disease

101
Q

% of hepatic adenomas that are symptomatic?

A

20%, risk of significant bleeding

102
Q

Hepatic adenomas are more common in which lobe?

A

Right

103
Q

Symptoms of hepatic adenoma?

A

Pain, elevated LFTs, hypotension, palpable mass

104
Q

Diagnosis of hepatic adenoma?

A

No Kupffer cells in adenomas, therefore no uptake on sulfur colloid scan (cold)

MRI shows hypervascular tumor, has periphreral blood supply

105
Q

Treatment for hepatic adenomas?

A

Asymptomatic: stop OCPs, if no regression needs resection

Symptomatic: resectioin for bleeding and malignancy risk

Multiple and unresectable: embolization

106
Q

Characteristics of focal nodular hyperplasia?

A

Central stellate scar that may look like cancer

107
Q

Malignancy risk with focal nodular hyperplasia?

A

No malignancy risk

108
Q

Diagnosis of focal nodular hyperplasia?

A

CT; has Kupffer cells, will take up sulfur colloid on liver scan; CT/MRI shows hypervascular tumor

109
Q

Treatment for focal nodular hyperplasia?

A

Conservative therapy

110
Q

What is the most common benign hepatic tumor?

A

Hemangiomas

111
Q

Should hemangiomas be biopsied?

A

No, risk of hemorrhage

112
Q

Diagnosis of hemangiomas?

A

MRI and CT show periphreal to central enhancement; hypervascular lesion

113
Q

Treatment of hemangiomas?

A

Conservative unless symptomatic

If symptomatic, rule out other causes first. Then intervention - surgery, embolization, XRT and steroids for unresectable disease

114
Q

Rare complications of hemangiomas?

A

Consumptive coagulopathy (Kasabach-Merritt syndrome - childhood, tx w/ radiotherapy), CHF

115
Q

Characteristic descriptive/gross/macroscopic wall finding of solitary cysts?

A

Blue hue

116
Q

Mets:primary ratio for malignant liver tumors?

A

20:1

117
Q

What is the 6th most common cancer worldwide with the 2nd highest mortality?

A

HCC

118
Q

Risk factors for HCC?

A

1 worldwide Hep B, HCV, ETOH, hemochromatosis, alpha-1-antitrypsin deficiency, PSC, aflatoxins, hepatic adenoma, steroids, pesticides

119
Q

What are the types of HCC?

A

Clear cell, lymphocyte infiltrative, fibrolamellar

120
Q

HCC tumor size correlates with what?

A

AFP

121
Q

What is the 5y survival of HCC?

A

30%

122
Q

Margins needed for HCC resection?

A

1cm

123
Q

What are risk factors for hepatic sarcoma?

A

PVC, thorotrast, arsenic; rapidly fatal

124
Q

Risk factors for cholangiosarcoma?

A

Clonorchiasis infection, UC, hemochormatosis, PSC, choledochal cysts

125
Q

What is the 5yr survival rate for colon cancer mets to the liver that are resected?

A

20%

126
Q

Primary liver tumors are hyper or hypovascular? Mets?

A

Primary: hypervascular; mets: hypovascular

127
Q

How is Budd-Chiari managed?

A
  • ID underlying d/o and treat
  • Anticoagulation + EGD to find varices
  • If new clot (<1 mo) - thrombolytic vs angioplasty + stent
  • If above fails - TIPS, surgical shunt, transplant
128
Q

What is the typical presentation of HCC?

A

abdominal pain, weight loss, anorexia, jaundice, and malaise;

physical exam may include hepatomegaly and ascites

129
Q

What imaging is needed to diagnose HCC? What are HCC’s characteristics?

A

US first, >1 cm gets either CT or MRI (more sensitive) w/ four-phase study: hyperintense during arterial phase and hypodense/washout during delayed phase

130
Q

Patients with normal hepatic parenchyma can tolerate what functional liver remnant volume?

What about those with cirrhosis?

A

Normal: 20-30%

Cirrhosis: 40-50%

131
Q

What can be done to increase FLRV?

A

Usually indicated in patients with cirrhosis and FLRV <40%: Portal vein embolization - induces hypertrophy

132
Q

Describe steps in right hepatectomy

A
  • right subcostal hockey-stick incision
  • dissect falciform until hepativ veins seen inserting into IVC
  • dissect coronal ligaments
  • dissect right hepatic vein
  • fundus first cholecystectomy
  • dissect hepatic artery, ligate it
  • dissect CBD, dissect portal vein, ligate right portal vein
  • find transection line, do parenchymal resection
  • dissect right bile duct and ligate it
133
Q

Give a differential for liver cancer?

A
  • HCC
  • cholangiocarcinoma
  • metastatic CRC
  • metastatic NET
134
Q

What patients with liver metastasis of NET can undergo resection?

A
  • unilobar disease
  • select bilobar disease - may need 2 stage operation
  • diffuse disease - may require transplant

ABSITE Review: Fiser, Decker, SCORE, UpToDate, TrueLearn COPY (49 decks)

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