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?

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

Portal veing posteriorly, common bile duct laterally, hepatic artery medially

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13
Q

What are the borders of the foramen of Winslow?

A

Anterior: portal traid, posterior: IVC, inferior: duodenum, superior: liver

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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

Urea

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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

What 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 to what?

A

Taurine or glycine, improves water solubility; primary bile acids: cholic and chenodeoxycholic, secondary: 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 sotrabe ability; high conjugated bilirubin

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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 elevaated 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

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

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

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

Impaired hepatic metabolism and impaired GFR

58
Q

What is hepatorenal syndrome? Treatment?

A

Same appearance as prerenal azotemia; stop diuretics, give volume

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? Treatment?

A

Angio, CT scan; liver biopsy shows sinusoidal dilation, congestion, centrilobular congestion; portacaval shunt

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 with show positive serology for what?

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?

A

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

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?

A

Echinococcus

87
Q

Labs with show what with echinococcus?

A

Casoni skin test, positive indirect hemagglutination

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

Preop albendazole, surgical removal; can inject cyst with alcohol at time of removal to kill organisms; need to get all of cyst wall

92
Q

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 abscesses are what?

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 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 (cole); 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, embolization if multiple and unresectable

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, then surgery, ?embolization, XRT and steroids for unresectable disease

114
Q

Rare complications of hemangiomas?

A

Consumptive coagulopathy (Kasabach-Merritt syndrome), CHF

115
Q

Characteristic 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 most common cancer worldwide?

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