Chapter 31: Liver

Question 1

What is the #1 hepatic artery variant?

Answer 1

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

Question 2

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

Answer 2

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

Question 3

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

Answer 3

Common hepatic off of SMA

Question 4

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

Answer 4

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

Question 5

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

Answer 5

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

Question 6

What separates the right and left lobe of the liver?

Answer 6

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

Question 7

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

Answer 7

Glisson’s capsule

Question 8

What are the triangular ligaments?

Answer 8

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

Question 9

The portal triad enters what segments?

Answer 9

IV and V

Question 10

Gallbladder lies under what segments?

Answer 10

IV and V

Question 11

What is contained in the hepatoduodenal ligament?

Answer 11

Bile duct, portal vein, hepatic artery

Question 12

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

Answer 12

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

Question 13

What are the borders of the foramen of Winslow?

Answer 13

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

Question 14

Portal veins carry what % of blood to the liver?

Answer 14

2/3 of hepatic blood flow

Question 15

The middle hepatic artery most commonly branches from where?

Answer 15

Left hepatic artery

Question 16

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

Answer 16

Hepatic artery

Question 17

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

Answer 17

80%; other 20% go directly to IVC

Question 18

Blood supply to the caudate lobe?

Answer 18

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

Question 19

Alkaline phosphatase normally located where?

Answer 19

Canalicular membrane

Question 20

Where does nutrient uptake occur?

Answer 20

Sinusoidal membrane

Question 21

What is the normal energy source for liver?

Answer 21

Ketones; glucose is converted to glycogen and stored

Question 22

Where is urea synthesized?

Answer 22

Urea

Question 23

What factors are NOT made in the liver?

Answer 23

VonWillebrand and factor VIII

Question 24

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

Answer 24

B12

Question 25

What are the most common complications of hepatic resection?

Answer 25

Bleeding and bile leak

Question 26

What zone is most susceptible to ischemia?

Answer 26

Acinar zone III, hepatocytes

Question 27

What % of the liver can be safely resected?

Answer 27

75%

Question 28

What is the breakdown of Hgb?

Answer 28

Hgb –> heme –> biliverdin –> bilirubin

Question 29

Bilirubin is conjugated to what in the liver?

Answer 29

Glucuronic acid by glucuronyl transferase; improves water solubility

Question 30

Where does urobilinogen come from? Reabsorbed and released where?

Answer 30

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

Question 31

Components of bile?

Answer 31

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

Question 32

Bile acids are conjugated to what?

Answer 32

Taurine or glycine, improves water solubility; primary bile acids: cholic and chenodeoxycholic, secondary: deoxycholic and lithocholic

Question 33

What is lecithin?

Answer 33

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

Question 34

Where is the 1st place jaundice is evident?

Answer 34

Under the tongue

Question 35

What is the ddx for elevated unconjugated bilirubin?

Answer 35

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

Question 36

What is the ddx for elevated conjugated bilirubin?

Answer 36

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

Question 37

What is Gilbert’s disease?

Answer 37

Abnormal uptake; mildly high unconjugated bilirubin

Question 38

What is Crigler-Najjar?

Answer 38

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

Question 39

What is physiologic jaundice of newborn?

Answer 39

Immature glucuronyl transferase

Question 40

What is Rotor’s syndrome?

Answer 40

Deficiency in sotrabe ability; high conjugated bilirubin

Question 41

What is Dubin-Johnson syndrome?

Answer 41

Deficiency in secretion ability; high conjugated bilirubin

Question 42

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

Answer 42

Post-vaccination

Question 43

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

Answer 43

Had infection with recovery and subsequent immunity

Question 44

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

Answer 44

Hepatitis C (RNA)

Question 45

What hepatitis type is a cofactor for hepatitis B?

Answer 45

Hepatitis D

Question 46

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

Answer 46

Hepatitis E

Question 47

What is the most common cause of liver failure?

Answer 47

Cirrhosis

Question 48

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

Answer 48

PT

Question 49

What is the mortality of acute fulminant hepatic failure?

Answer 49

80%

Question 50

What is hepatic encephalopathy caused by?

Answer 50

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

Question 51

Causes of encephalopathy other than liver failure?

Answer 51

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

Question 52

Treatment for hepatic encephalopathy?

Answer 52

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

Question 53

What is the mechanism of cirrhosis?

Answer 53

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

Question 54

Treatment for ascites from hepatic/splanchnic lymph?

Answer 54

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

Question 55

Complications of peritoneovenous shunts?

Answer 55

DIC

Question 56

What is the prophylaxis for SBP?

Answer 56

Cipro 750mg/wk

Question 57

What is the cause of elevated aldosterone in liver failure?

Answer 57

Impaired hepatic metabolism and impaired GFR

Question 58

What is hepatorenal syndrome? Treatment?

Answer 58

Same appearance as prerenal azotemia; stop diuretics, give volume

Question 59

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

Answer 59

Hepatic vein thrombosis; SMA arteriogram with venous phase contrast

Question 60

How is the diagnosis of SBP made?

Answer 60

PMNs >250 in fluid, (+)cultures

Question 61

What are the bacteria that cause SBP?

Answer 61

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

Question 62

Risk factors for SBP?

Answer 62

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

Question 63

Treatment of SBP?

Answer 63

3rd generation cephalosporins

Question 64

Treatment for esophageal varices?

Answer 64

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

Question 65

Use of propranolol for esophageal varices?

Answer 65

May help prevent rebleeding, no good role acutely

Question 66

Treatment for refractory variceal bleeds?

Answer 66

TIPS

Question 67

Mortality with bleeding varices?

Answer 67

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

Question 68

Causes of presinusoidal obstruction causing portal hypertension?

Answer 68

Schistosomiasis, congenital hepatic fibrosis, portal vein thrombosis

Question 69

Most common cause of portal HTN in children?

Answer 69

Portal vein thrombosis

Question 70

Cause of sinusoidal obstruction leading to portal HTN?

Answer 70

Cirrhosis

Question 71

Cause of postsinusoidal obstruction causing portal HTN?

Answer 71

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

Question 72

What is the normal portal vein pressure?

Answer 72

<12mmHg

Question 73

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

Answer 73

Coronary veins

Question 74

Use of TIPS? Complications?

Answer 74

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

Question 75

What patients are candidates for splenorenal shunt? Contraindications?

Answer 75

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

Question 76

What does the Child’s class correlate with?

Answer 76

Mortality after shunt

Question 77

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

Answer 77

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

Question 78

What is Budd-Chiari syndrome? Presentation?

Answer 78

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

Question 79

How is Budd-Chiari diagnosed? Treatment?

Answer 79

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

Question 80

Where do primary infection which cause amebic liver abscess occur?

Answer 80

Amebic colitis

Question 81

Risk factors for amebic liver abscess?

Answer 81

Travel to Mexico, ETOH, fecal-oral transmission

Question 82

Amebic abscess with show positive serology for what?

Answer 82

Entamoeba histolytica

Question 83

Symptoms of amebic abscess?

Answer 83

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

Question 84

What will cultures of amebic abscess show? Aspiration?

Answer 84

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

Question 85

Diagnosis of amebic abscess? Treatment?

Answer 85

Based on CT findings; flagyl, aspiration if refractory or contaminanted; surgery only for free rupture

Question 86

Hydatid cyst formed by what?

Answer 86

Echinococcus

Question 87

Labs with show what with echinococcus?

Answer 87

Casoni skin test, positive indirect hemagglutination

Question 88

What can happen with aspiration of echinococcal cyst?

Answer 88

Anaphylaxis

Question 89

Diagnosis of echinococcus?

Answer 89

Abdominal CT shows ectocyst (calcified) and endocyst

Question 90

When do you need a preop ERCP for echinococcus?

Answer 90

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

Question 91

Treatment for hydatid cyst?

Answer 91

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

Question 92

Characteristics of schistosomiasis?

Answer 92

Maculopapular rash, eosinophilia

Question 93

Findings in sigmoid colon with schistosomiasis?

Answer 93

Fine granulation tissue, petechiae, ulcers

Question 94

Treatment of schistosomiasis?

Answer 94

Praziquantel and control of variceal bleeding

Question 95

80% of all abscesses are what?

Answer 95

Pyogenic abscess

Question 96

Symptoms of pyogenic abscess?

Answer 96

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

Question 97

1 organism in pyogenic abscess?

Answer 97

E. coli

Question 98

Pyogenic abscess commonly secondary to what?

Answer 98

Contiguous infection from biliary tract; can also occur following bacteremia from other infections

Question 99

Diagnosis of pyogenic abscess? Treatment?

Answer 99

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

Question 100

Hepatic adenomas occur in what patients?

Answer 100

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

Question 101

% of hepatic adenomas that are symptomatic?

Answer 101

20%, risk of significant bleeding

Question 102

Hepatic adenomas are more common in which lobe?

Answer 102

Right

Question 103

Symptoms of hepatic adenoma?

Answer 103

Pain, elevated LFTs, hypotension, palpable mass

Question 104

Diagnosis of hepatic adenoma?

Answer 104

No Kupffer cells in adenomas, therefore no uptake on sulfur colloid scan (cole); MRI shows hypervascular tumor, has periphreral blood supply

Question 105

Treatment for hepatic adenomas?

Answer 105

Asymptomatic: stop OCPs, if no regression needs resection; symptomatic: resectioin for bleeding and malignancy risk, embolization if multiple and unresectable

Question 106

Characteristics of focal nodular hyperplasia?

Answer 106

Central stellate scar that may look like cancer

Question 107

Malignancy risk with focal nodular hyperplasia?

Answer 107

No malignancy risk

Question 108

Diagnosis of focal nodular hyperplasia?

Answer 108

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

Question 109

Treatment for focal nodular hyperplasia?

Answer 109

Conservative therapy

Question 110

What is the most common benign hepatic tumor?

Answer 110

Hemangiomas

Question 111

Should hemangiomas be biopsied?

Answer 111

No, risk of hemorrhage

Question 112

Diagnosis of hemangiomas?

Answer 112

MRI and CT show periphreal to central enhancement; hypervascular lesion

Question 113

Treatment of hemangiomas?

Answer 113

Conservative unless symptomatic, then surgery, ?embolization, XRT and steroids for unresectable disease

Question 114

Rare complications of hemangiomas?

Answer 114

Consumptive coagulopathy (Kasabach-Merritt syndrome), CHF

Question 115

Characteristic wall finding of solitary cysts?

Answer 115

Blue hue

Question 116

Mets:primary ratio for malignant liver tumors?

Answer 116

20:1

Question 117

What is the most common cancer worldwide?

Answer 117

HCC

Question 118

Risk factors for HCC?

Answer 118

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

Question 119

What are the types of HCC?

Answer 119

Clear cell, lymphocyte infiltrative, fibrolamellar

Question 120

HCC tumor size correlates with what?

Answer 120

AFP

Question 121

What is the 5y survival of HCC?

Answer 121

30%

Question 122

Margins needed for HCC resection?

Answer 122

1cm

Question 123

What are risk factors for hepatic sarcoma?

Answer 123

PVC, thorotrast, arsenic; rapidly fatal

Question 124

Risk factors for cholangiosarcoma?

Answer 124

Clonorchiasis infection, UC, hemochormatosis, PSC, choledochal cysts

Question 125

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

Answer 125

20%

Question 126

Primary liver tumors are hyper or hypovascular? Mets?

Answer 126

Primary: hypervascular; mets: hypovascular

Question 127

Which kind of liver abscess usually appears as a single abscess in the right lobe of the liver and is associated with elevated LFTs?

Answer 127

Amebic liver abscess

[UpToDate: Amebic liver abscesses are most commonly found in the right lobe; 70% to 80% are solitary subcapsular lesions, although multiple lesions can be present. Localization in the left lobe predisposes to extension into the pericardial sac.

On ultrasound, the abscess appears as a round, well-defined hypoechoic mass. On CT scan, it appears as a low-density mass with a peripheral enhancing rim. On MRI, the abscess appears as low-signal intensity on T1-weighted images and high-signal intensity on T2-weighted images. After healing, the periphery of the abscess may calcify as a thin, round ring.

On gallium citrate and technetium-labeled sulfur colloid radionuclide liver scans, amebic abscesses are “cold” (with a bright rim in some cases), whereas pyogenic abscesses are “hot.” Radiographic findings must be interpreted in the appropriate clinical context with consideration of the differential diagnoses, including pyogenic abscess and malignancy.

Serial imaging is generally not helpful since lesions may appear to increase in size or number on ultrasound following initiation of treatment, even with appropriate therapy and clinical improvement. Treated lesions may become anechoic, calcified, or may persist as cystic-appearing lesions. Complete radiologic resolution may take two years or more. Therefore, persistent abnormalities on ultrasound imaging should not prompt retreatment or additional testing in a patient who is clinically well.

A chest radiograph abnormality will be observed in approximately 50% of patients with an amebic liver abscess, most commonly elevation of the right hemidiaphragm. This finding does not necessarily signal pulmonary involvement in the infection.]

Question 128

What is the sequence of breakdown products of hemoglobin?

Answer 128

Hemoglobin -> Heme -> Biliverdin -> Bilirubin

Question 129

What is the treatment for focal nodular hyperplasia of the liver?

Answer 129

Conservative therapy (No resection)

[UpToDate: The natural history of FNH is one of stability and lack of complications. Lesions generally do not change over time, although they occasionally become smaller. However, as mentioned above, enlargement of FNH in the setting of OCPs and during pregnancy have been reported. There is no evidence for malignant transformation of FNH.

Patients who are suspected of having FNH based upon the evaluation described above should be managed conservatively. If a diagnosis remains unclear, a liver biopsy may be helpful, but may also be misleading since only resection will be definitive. Follow-up studies at three and six months will often be sufficient to confirm the stability of the lesion and its benign nature, after which no long-term follow-up is required routinely. Surgery should be reserved for the rare, very symptomatic FNH lesion, and the highly suspicious lesion, which has eluded diagnosis by all other modalities.

We generally do not insist that oral contraceptives and other estrogen containing preparations should be discontinued. However, it is reasonable to obtain a follow-up imaging study in 6 to 12 months in women who continue taking these drugs. Small FNH do not appear to pose a significant risk to a successful pregnancy, although close observation is strongly recommended and resection may be prudent for large (>8 cm) FNH.]

Question 130

Diagnose:

• HBsAg: -
• Anti-HBs: +
• HBeAg: -
• Anti-HBe: -
• Anti-HBc: -

Answer 130

Immunized against HBV

Question 131

According to Couinaud’s nomenclature, which numbered liver segment is the superior right posterolateral segment?

Answer 131

Segment VII

Question 132

What is the treatment for hepatorenal syndrome?

Answer 132

Stop diuretics and give volume

[No good therapy other than a liver transplant]

[UpToDate: The ideal therapy for hepatorenal syndrome is improvement of liver function from recovery of alcoholic hepatitis, treatment of decompensated hepatitis B with effective antiviral therapy, recovery from acute hepatic failure, or liver transplantation. The ability of liver function to improve with abstinence from alcohol and effective antiviral therapy of hepatitis B is remarkable.

However, when improvement of liver function is not possible in the short term, we recommend that medical therapy be instituted in an attempt to reverse the acute kidney injury associated with hepatorenal syndrome. Our suggestions regarding the choice of medical therapy depend upon several factors, including: whether the patient is admitted to the intensive care unit; the availability of certain drugs, for which there is national and regional variability; and whether the patient is a candidate for liver transplantation:

In patients with hepatorenal syndrome who are critically ill, we suggest initial treatment with norepinephrine in combination with albumin. Norepinephrine is given intravenously as a continuous infusion (0.5 to 3 mg/hr) with the goal of raising the mean arterial pressure by 10 mmHg, and albumin is given for at least two days as an intravenous bolus (1 g/kg per day [100 g maximum]). Intravenous vasopressin may also be effective, starting at 0.01 units/min and titrating upward as needed to raise the mean arterial pressure as noted below.

In patients with hepatorenal syndrome who are not critically ill, our suggestions depend upon the availability of certain drugs:

• Where terlipressin therapy is available, we suggest initial treatment with terlipressin in combination with albumin. Terlipressin is given as an intravenous bolus (1 to 2 mg every four to six hours), and albumin is given for two days as an intravenous bolus (1 g/kg per day [100 g maximum]), followed by 25 to 50 grams per day until terlipressin therapy is discontinued.
• Where terlipressin therapy is not available (principally the United States), we suggest initial treatment with a combination of midodrine, octreotide, and albumin. Midodrine is given orally (starting at 7.5 mg and increasing the dose at eight-hour intervals up to a maximum of 15 mg by mouth three times daily), octreotide is either given as a continuous intravenous infusion (50 mcg/hr) or subcutaneously (100 to 200 mcg three times daily), and albumin is given for two days as an intravenous bolus (1 g/kg per day [100 g maximum]), followed by 25 to 50 grams per day until midodrine and octreotide therapy is discontinued.

In highly selected patients who fail to respond to medical therapy with the above regimens and who are considered well enough to undergo the procedure, transjugular intrahepatic portosystemic shunt (TIPS) is sometimes successful. However, this procedure is associated with numerous complications and, because of the need for intravenous contrast, it may cause acute kidney injury. For this reason, some experts prefer dialysis as a first option (continuous renal replacement therapy) in most cases, particularly for patients whose serum creatinine remains above 1.5 mg/dL despite medical therapy.

In patients who fail to respond to the above therapies, develop severely impaired renal function, and either are candidates for liver transplantation or have a reversible form of liver injury and are expected to survive, we recommend dialysis as a bridge to liver transplantation or liver recovery.]

Question 133

What is the usual energy source for the liver?

Answer 133

Ketones

[α-Ketoacids derived from the degradation of amino acids are the liver’s own fuel. In fact, the main role of glycolysis in the liver is to form building blocks for biosyntheses. Furthermore, the liver cannot use acetoacetate as a fuel, because it has little of the transferase needed for acetoacetate’s activation to acetyl CoA. Thus, the liver eschews the fuels that it exports to muscle and the brain.]

Question 134

Cultures of an amebic liver abscess typically show what?

Answer 134

Nothing

[Cultures of abscess often sterile -> Protozoa (Entamoeba Histolytica) exist only in peripheral rim]

Question 135

Most primary and secondary liver tumors are supplied by which artery?

Answer 135

Hepatic artery

Question 136

Which Hepatitis Virus causes high mortality in pregnant women

Answer 136

HEV

Question 137

Diagnose:

• HBsAg: +
• Anti-HBs: -
• HBeAg: +
• Anti-HBe: -
• Anti-HBc: IgM

Answer 137

Acute HBV

Question 138

What are the 4 boundaries of the Foramen of Winslow?

Answer 138

• Anterior: Portal triad
• Posterior: IVC
• Inferior: Duodenum
• Superior: Liver

Question 139

The portal triad (common bile duct, portal vein, and proper hepatic artery) enters which numbered segment(s) of the liver?

Answer 139

Segments IV and V

Question 140

What is the # 1 cause of hepatocellular carcinoma worldwide?

Answer 140

Hepatitis B

Question 141

Jaundice occurs when the total bilirubin reaches what level?

Answer 141

Greater than 2.5

Question 142

What is the treatment for postpartum liver failure with ascites?

Answer 142

Heparin and antibiotics

Question 143

A liver abscess caused by an infection with which organism is associated with a maculopapular rash, increased eosinophils, and variceal bleeding?

Answer 143

Schistosomiasis

[UpToDate: Manifestations of chronic infection are generally observed among individuals with ongoing exposure in endemic regions. Disease is caused by the host immune response to migrating eggs. In the bowel, inflammation can result in ulceration, blood loss, and scarring. In the liver, periportal fibrosis (Symmers’ pipestem fibrosis) can lead to portal hypertension and subsequent esophageal varices. In the bladder, granulomatous inflammation can result in development of pseudopolyps and/or urinary tract obstruction leading to renal failure.]

Question 144

What conjugates bilirubin to glucuronic acid in the liver?

Answer 144

Glucuronyl transferase

[Improves water solubility]

Question 145

What is a direct contraindication to a splenorenal shunt in a cirrhotic patient?

Answer 145

Refractory ascites

[This procedure can worsen ascites]

Question 146

Which numbered segments of the liver are fed by the left portal vein?

Answer 146

Segments II, III, and IV

Question 147

Best marker for chronic HBV infection

Answer 147

HBsAg longer than 6 months but no anti-HBs antibodies

Question 148

How is Budd-Chiari syndrome diagnosed?

Answer 148

Angiogram with venous phase, CT angiogram

[Liver biopsy shows sinusoidal dilatation, congestion, and centrilobular congestion]

Question 149

Which vein(s) act as collaterals between the portal vein and the systemic venous system of the lower esophagus (azygous vein)

Answer 149

Coronary veins

Question 150

What are the King’s College criteria of poor prognostic indicators for non-acetaminopen-induced acute liver failure?

Answer 150

INR > 6.5

Or any 3 of the following:

• Age less than 10 or greater than 40
• Drug toxicity or undetermined etiology
• Jaundice greater than 7 days before encephalopathy
• INR greater than 3.5
• Bilirubin greater than 17 mg/dL

Question 151

What is the treatment for symptomatic splenic vein thrombosis?

Answer 151

Splenectomy

Question 152

What role does propranolol have in treating esophageal varices?

Answer 152

May help prevent re-bleeding

[No good role acutely]

[UpToDate: Nonselective beta blockers lower portal pressure and reduce the risk of first bleeding in patients with esophageal varices. For these reasons, they are the treatment of choice for primary prophylaxis in patients at high risk for variceal bleeding.

Multiple clinical trials have compared beta blockers with placebo for the prevention of recurrent variceal hemorrhage. Approximately 75% of the patients enrolled had Child-Pugh class A cirrhosis. Alcohol was the most common cause of liver disease and many patients were excluded from participation due to contraindications to use of beta blockers. The most important variation among studies was the timing of entry into the studies from the index bleed (one day to one month). The doses of the drug used were also variable (10 to 480 mg/day of propranolol); the dose was generally titrated to achieve a 25% decrease in resting heart rate.

With a few exceptions, an overall improvement in rebleeding rate was noted, but a survival advantage was only shown in one study. Meta-analysis of these data suggests that the risk of bleeding is decreased by approximately 40%, while the risk of death is decreased by 20%. Propranolol has also decreased recurrent bleeding (35% vs 62% at one year) from portal hypertensive gastropathy.]

Question 153

What are the 2 primary bile acids (salts)?

Answer 153

Cholic and chenodeoxycholic

Question 154

Which type of benign liver tumor has a central stellate scar that may look like cancer?

Answer 154

Focal nodular hyperplasia

Question 155

What is the Pringle maneuver?

Answer 155

Clamping the porta hepatis

[Will not stop hepatic vein bleeding]

Question 156

The entrance to the lesser sac of the abdomen is called what?

Answer 156

Foramen of Winslow

Question 157

What is the only DNA hepatitis virus?

Answer 157

Hepatitis B

Question 158

What is the treatment for a pyogenic liver abscess?

Answer 158

CT-guided drainage and antibiotics

[Surgical drainage for unstable condition and continued signs of sepsis]

Question 159

According to Couinaud’s nomenclature, which numbered liver segment is the inferior left lateral segment?

Answer 159

Segment III

Question 160

Which syndrome is characterized by a mild defect in glucuronyl transferase, leading to abnormal conjugation of bilirubin?

Answer 160

Gilbert’s disease

Question 161

Conjugated bilirubin is broken down by bacteria in which portion of the digestive tract?

Answer 161

Terminal ileum

Question 162

What are the 5 scoring criteria for calculating the Child-Pugh Score?

Answer 162

• Albumin: Greater than 3.5 (1 ), 3-3.5 (2), Less than 3 (3)
• Bilirubin: Less than 2.5 (1), 2.5-4 (2), Greater than 4 (3)
• Encephalopathy: None (1), Minimal (2), Severe (3)
• Ascites: None (1), Treatable with meds, (2), Refractory (3)
• INR: Less than 1.7 (1), 1.7-2.3 (2), Greater than 2.3 (3)

(# of points)

Question 163

How is a pyogenic liver abscess diagnosed?

Answer 163

Aspiration

[UpToDate: The diagnosis of pyogenic liver abscess is made by history, clinical examination, and radiographic imaging followed by aspiration and culture of the abscess material.]

Question 164

80% of all liver abscesses fall into which category of abscess?

Answer 164

Pyogenic abscess

[15% mortality with sepsis]

Question 165

What percent of symptomatic HBV infected individuals develop acute vs chronic disease

Answer 165

• Acute: 90%
• Chronic: 10%

Question 166

Schistosomiasis, congenital hepatic fibrosis, and portal vein thrombosis are all causes of portal hypertension from what kind of obstruction (pre-sinusoidal, sinusoidal, post-sinusoidal)?

Answer 166

Pre-sinusoidal obstruction

[50% of portal HTN in children]

Question 167

What does elevated conjugated bilirubin signify?

Answer 167

Secretion defects into bile ducts or excretion defects into GI tract

[Stones, strictures, tumors]

Question 168

What is the associated percent mortality following shunt placement in each of the 3 categories of cirrhotic patients according to the Child-Pugh criteria?

Answer 168

• Child’s A: 2% mortality
• Child’s B: 10% mortality
• Child’s C: 50% mortality

Question 169

What is hepatorenal syndrome?

Answer 169

Progressive renal failure with same lab findings as prerenal azotemia

[Usually a sign of end-stage renal disease]

[UpToDate: Arterial vasodilatation in the splanchnic circulation, which is triggered by portal hypertension, appears to play a central role in the hemodynamic changes and the decline in renal function in cirrhosis. The presumed mechanism is increased production or activity of vasodilators, mainly in the splanchnic circulation, with nitric oxide thought to be most important.

As the hepatic disease becomes more severe, there is a progressive rise in cardiac output and fall in systemic vascular resistance; the latter change occurs despite local increases in renal and femoral vascular resistance that result in part from hypotension-induced activation of the renin-angiotensin and sympathetic nervous systems. Thus, the reduction in total vascular resistance results from decreased vascular resistance in the splanchnic circulation, perhaps in part under the influence of nitric oxide derived from the endothelium. Bacterial translocation from the intestine into the mesenteric lymph nodes may play an important role in this process. A review of the hemodynamic changes seen with progressive cirrhosis can be found in a separate topic review.

The decline in renal perfusion in this setting is associated with reductions in glomerular filtration rate (GFR) and sodium excretion (often to less than 10 meq/day in advanced cirrhosis) and a fall in mean arterial pressure, despite the intense renal vasoconstriction. The importance of splanchnic vasodilatation in these changes can be indirectly illustrated by the response to ornipressin, an analog of antidiuretic hormone (arginine vasopressin) that is a preferential splanchnic vasoconstrictor.]

Question 170

What are two rare complications of a liver hemangioma?

Answer 170

1. Consumptive coagulopathy (Kasabach-Merritt syndrome)
2. Congestive heart failure

[These complications are usually seen in children]

Question 171

Which 3 types of hepatocellular carcinoma have the best prognosis?

Answer 171

1. Clear cell
2. Lymphocyte infiltrative
3. Fibrolamellar

[UpToDate: Well-differentiated clear cell and fibrolamellar tumors and the presence of tumor encapsulation have been associated with a better prognosis. Some suggest the utility of using tumor grade to select patients for treatment (eg, liver transplantation), although this has not yet been accepted into practice.]

Question 172

Splenic vein thrombosis is most often caused by what?

Answer 172

Pancreatitis

Question 173

In order to perform a splenorenal shunt, which 5 veins must be ligated?

Answer 173

1. Left adrenal vein
2. Left gonadal vein
3. Inferior mesenteric vein
4. Coronary vein
5. Pancreatic branches of splenic vein

Question 174

What size margin is required in the resection of hepatocellular carcinoma?

Answer 174

1 cm margin

[UpToDate: The importance of wide resection margins is debated. In a study of 225 patients who underwent resection for HCC, three-year survival was significantly better when a >1 cm tumor-free margin was achieved (77% vs 21%, respectively). However, larger series suggest that a negative margin of <1 cm is acceptable.]

Question 175

According to Couinaud’s nomenclature, which numbered liver segment is the left medial segment (quadrate lobe)?

Answer 175

Segment IV

Question 176

What are the 5 main components of bile?

Answer 176

1. Bile salts
2. Proteins
3. Phospholipids
4. Cholesterol
5. Bilirubin

[Phospholipids include lecithin.]

Question 177

Best markers for past HBV infection

Answer 177

IgG anti-HBs & IgG anti-HBc In the absence of HBsAg

Question 178

Which treatment is required for refractory variceal bleeding?

Answer 178

Transjugular Intrahepatic Portosystemic Shunt (TIPS)

Question 179

What causes hepatic encephalopathy?

Answer 179

Liver loses ability to metabolize waste, leading to a build up of ammonia, mercantanes, and false neurotransmitters

Question 180

What is a normal portal vein pressure?

Answer 180

Less than 12mmHg

Question 181

According to Couinaud’s nomenclature, which numbered liver segment is the caudate lobe?

Answer 181

Segment I

Question 182

Recurrent flapping tremor of the arms, like the action of a bird’s wings, that occurs as a result of a brain condition associated with liver failure is called what?

Answer 182

Asterixis

[A sign that liver failure is progressing]

Question 183

What is the treatment for an amebic liver abscess?

Answer 183

Flagyl

[Aspiration only if refractory and surgery only if free rupture]

[UpToDate: For circumstances in which amebic liver abscess is suspected based on epidemiology, clinical manifestations, and radiographic findings, it is reasonable to initiate empiric treatment pending further diagnostic evaluation (including confirmatory antigenic or serologic testing and evaluation for the parasite in stool and liver abscess pus).

In general, amebic liver is managed with a tissue agent and a luminal agent (to eliminate intraluminal cysts).

• Tissue agents — Patients with an amebic liver abscess should be treated with metronidazole (500 to 750 mg orally three times daily for 7 to 10 days) or tinidazole (2 g once daily for 5 days). The cure rate with this therapy is >90%. Shorter duration of metronidazole is not generally recommended. Metronidazole is well absorbed from the gastrointestinal tract; intravenous therapy offers no significant advantage as long as the patient can take oral medications and has no major defect in small bowel absorption. Alternatives to metronidazole or tinidazole include ornidazole and nitazoxanide. Nitazoxanide (500 mg twice daily for 10 days) has been shown to be effective in a small case series. In the setting of slow response to metronidazole or relapse following therapy, therapeutic aspiration, percutaneous catheter drainage, and/or a prolonged course of metronidazole may be warranted.
• Luminal agents — Following therapy for invasive amebiasis, treatment with a luminal agent to eliminate intraluminal cysts is warranted, even if stool microscopy is negative. Intraluminal infection can be treated with one of the following regimens: paromomycin (25 to 30 mg/kg per day orally in three divided doses for 7 days), diiodohydroxyquin (650 mg orally three times daily for 20 days for adults and 30 to 40 mg/kg per day in three divided doses for 20 days for children), or diloxanide furoate (500 mg orally three times daily for 10 days for adult and 20 mg/kg per day in three divided doses for 10 days for children).

Uncomplicated amebic liver abscess has a mortality rate of <1% if diagnosed and treated early. In one study of 135 patients with amebic liver abscess in India with overall mortality rate of 17%, independent risk factors for increased mortality included bilirubin level >3.5 mg/dL, serum albumin <2.0 g/dL, large volume of the abscess cavity, multiple abscesses, and encephalopathy.]

Question 184

Which clotting factors are not made in the liver?

Answer 184

Von Willebrand factor and factor VIII

[Some factor VIII is produced in liver sinusoidal cells, but much of it is produced by endothelial cells outside of the liver throughout the body]

Question 185

What runs within the falciform ligament?

Answer 185

Remnant of the umbilical vein

Question 186

Diagnose:

• HBsAg: +
• Anti-HBs: -
• HBeAg: +
• Anti-HBe: -
• Anti-HBc: IgG

Answer 186

High infectivity Chronic HBV

Question 187

What is the main biliary phospholipid?

Answer 187

Lecithin

Question 188

Urine turns dark because of excess of what?

Answer 188

Urobilinogen

Question 189

Which part of the liver receives separate right and left portal and arterial blood flow and drains directly into the IVC via separate hepatic veins?

Answer 189

Caudate lobe (Segment I)

Question 190

What does the Child-Pugh score correlate with?

Answer 190

Mortality after open shunt placement

[These classes correlate with one- and two-year patient survival: class A: 100 and 85 percent; class B: 80 and 60 percent; and class C: 45 and 35 percent.]

[UpToDate: The Child-Pugh classification has been used to assess the risk of non-shunt operations in patients with cirrhosis. It is a modification of the Child-Turcotte classification, which incorporated five variables that were designed to stratify the risk of portacaval shunt surgery in patients with cirrhosis. The variables included the serum albumin and bilirubin, ascites, encephalopathy, and nutritional status. The Child-Pugh classification replaces nutritional status with prothrombin time. The score ranges from 5 to 15. Patients with a score of 5 or 6 have Child-Pugh class A cirrhosis (well-compensated cirrhosis), those with a score of 7 to 9 have Child-Pugh class B cirrhosis (significant functional compromise), and those with a score of 10 to 15 have Child-Pugh class C cirrhosis (decompensated cirrhosis).

In a review of 92 patients with cirrhosis who underwent abdominal surgery, the mortality rate was 10% for patients with Child-Pugh class A cirrhosis, 30% for patients with Child-Pugh class B cirrhosis, and 82% for patients with Child-Pugh class C cirrhosis. Other studies have validated the utility of the Child-Pugh classification for the assessment of surgical risk.

The Child-Pugh classification system also correlates with survival in patients not undergoing surgery; 1-year survival rates for patients with Child-Pugh class A, B, and C cirrhosis are approximately 100%, 80%, and 45%, respectively. Child-Pugh class is also associated with the likelihood of developing of complications of cirrhosis. As an example, patients with Child-Pugh class C cirrhosis are much more likely to develop variceal hemorrhage than those with Child-Pugh class A cirrhosis.]

Question 191

What is the treatment for an asymptomatic hepatic adenoma?

Answer 191

Stop OCPs (or any causative agent), If no regression, patient needs resection of the tumor

[UpToDate: Hepatic adenomas are uncommon benign epithelial liver tumors that develop in an otherwise normal-appearing liver. They are seen predominantly in young women (20 to 44 years old), are frequently located in the right hepatic lobe, and are typically solitary (70% to 80%), although multiple adenomas have been described in patients with prolonged contraceptive use, glycogen storage diseases, and hepatic adenomatosis. Adenomas range in size from 1 to 30 cm. Symptoms such as abdominal pain are more likely with larger lesions.

We recommend resection of all symptomatic hepatic adenomas and adenomas >5 cm (Grade 1C). Adenomas that do not resolve or enlarge after discontinuation of steroid medication should also be considered for surgical resection after discussion with the patient. In women taking oral contraceptives, we suggest repeating the imaging study six months after stopping oral contraceptives. If there is no change, or if the presumed adenoma has grown in size, we suggest surgery.]

Question 192

Which two pharmaceutical agents can be used to temporize actively bleeding esophageal varices?

Answer 192

1. Vasopressin (Splanchnic artery contriction)
2. Octreotide (Decrease portal pressure by decreasing blood flow)

[UpToDate: The first step in stopping variceal bleeding is the initiation of pharmacologic therapy. Pharmacologic therapy should be started in all patients with upper gastrointestinal bleeding who have varices or who are at risk for having varices (eg, patients with advanced cirrhosis). Pharmacologic therapy should not be delayed pending confirmation that the source of bleeding is indeed from varices. In the United States, pharmacologic therapy typically consists of an octreotide bolus (50 mcg intravenous [IV]) followed by a continuous infusion (50 mcg IV per hour). Where available, terlipressin is often used. Terlipressin is administered at an initial dose of 2 mg IV every four hours and can be titrated down to 1 mg IV every four hours once hemorrhage is controlled. Pharmacologic therapy is typically continued for three to five days following cessation of bleeding.

For patients with esophageal varices, acute bleeding is typically managed with endoscopic variceal ligation, though occasionally endoscopic sclerotherapy is used. The goal should be to perform an upper endoscopy within 12 hours of presentation. If the bleeding cannot be controlled endoscopically, treatment options include transjugular intrahepatic portosystemic shunt (TIPS) placement or surgical shunting. For bleeding gastric varices, treatment is with cyanoacrylate injection where available. If cyanoacrylate injection is not an option, TIPS placement is typically used. Balloon tamponade is an option for temporarily stopping bleeding from esophageal or gastric varices while definitive treatment is being arranged, but it is associated with serious complications including esophageal rupture. Bleeding ectopic varices may be managed with TIPS placement or surgery.

Vasoactive medications decrease portal blood flow and are used for the treatment of acute variceal hemorrhage. They include vasopressin, somatostatin, and their analogs (terlipressin and octreotide, respectively). As a group, vasoactive medications have been shown to decrease mortality and improve hemostasis in patients with acute variceal bleeding. However, terlipressin is the only agent individually shown to reduce mortality. Pharmacologic therapy should be started at the time of presentation in a patient who has known varices or is at risk for varices. It should not be held pending confirmation of the diagnosis. Terlipressin is the preferred agent in many countries outside of the United States. It is initially given as 2 mg intravenous (IV) bolus every four hours. Octreotide is the agent available in the United States and is given as a 50 mcg IV bolus, followed by a continuous infusion at a rate of 50 mcg per hour. Pharmacologic therapy should be continued for three to five days.]

Question 193

What percent of bile is composed of bile salts?

Answer 193

85%

Question 194

Can a benign focal nodular hyperplasia become malignant?

Answer 194

No

[Also very unlikely to rupture]

[UpToDate: Focal nodular hyperplasia (FNH) is the most common non-malignant hepatic tumor that is not of vascular origin. It is now generally accepted to be a hyperplastic (regenerative) response to hyperperfusion by the characteristic anomalous arteries found in the center of these nodules.

FNH is most often solitary (80% to 95%) and usually less than 5 cm in diameter. Only 3% are larger than 10 cm.

The majority of reports have found that symptoms or signs directly attributable to FNH are infrequent.

The diagnosis of FNH is usually made by demonstrating its characteristic features on imaging tests and excluding other lesions. The latter can typically be accomplished by assessing the context in which FNH is detected and by obtaining specific radiologic and laboratory testing.

The natural history of FNH is one of stability and a lack of complications. Thus, we suggest that patients who are suspected of having FNH based upon the evaluation described above be managed conservatively (Grade 2B).

FNH may be responsive to exogenous estrogens. We generally do not insist that oral contraceptives and other estrogen-containing preparations should be discontinued. However, it is reasonable to obtain a follow-up imaging study in 6 to 12 months in women who continue taking these drugs.]

Question 195

Which numbered segments of the liver are drained by the left hepatic vein?

Answer 195

Segment II, III, and superior portion of IV

Question 196

How effective are banding and sclerotherapy at treating esophageal varices?

Answer 196

95% effective

Question 197

What is the treatment for a liver abscess caused by Schistosomiasis?

Answer 197

Praziquantel

[Control any variceal bleeding]

[UpToDate: Treatment of schistosomiasis serves three purposes: reversing acute or early chronic disease, preventing complications associated with chronic infection, and preventing neuroschistosomiasis. The goal of treatment is reduction of egg production via reduction of worm load.

We recommend that patients with schistosomiasis be treated promptly with praziquantel, in the presence or absence of clinical manifestations (Grade 1B). A single dose of praziquantel reduces the parasite burden substantially though is not curative for moderate or severe infection.

Dosing of praziquantel for treatment of infection due to S. haematobium, S. mansoni, or S. intercalatum consists of 40 mg/kg (in one or two divided doses). Praziquantel dosing for treatment of infection due to S. japonicum or S. mekongi consists of 60 mg/kg (in two divided doses).

Follow-up after treatment includes monitoring of clinical manifestations, eosinophilia, and microscopy evaluation for eggs in stool or urine. In endemic areas, follow-up microscopy should be performed no sooner than six weeks following treatment. In nonendemic areas, follow-up microscopy may be performed three to six months after treatment. Persistence of viable eggs after treatment with praziquantel warrants repeat treatment.]

Question 198

Which Hepatitis viruses carry a risk of Hepatocellular Carcinoma

Answer 198

HBV, HCV, & HDV

Question 199

In which 4 circumstances is Transjugular Intrahepatic Portosystemic Shunt (TIPS) indicated?

Answer 199

1. Protracted bleeding
2. Progression of coagulopathy
3. Visceral hypoperfusion
4. Refractory ascites

Question 200

When would you consider surgery to treat an amebic liver abscess?

Answer 200

Free rupture of the abscess

Question 201

What correlates with tumor size in hepatocellular carcinoma?

Answer 201

AFP level

[UpToDate: A rise in serum AFP in a patient with cirrhosis or hepatitis B should raise concern that HCC has developed. It is generally accepted that serum levels greater than 500 mcg/L (normal in most laboratories is between 10 and 20 mcg/L) in a high-risk patient is diagnostic of HCC. However, HCC is often diagnosed at a lower AFP level in patients undergoing screening.]

Question 202

What percent of the liver can be safely resected?

Answer 202

75%

Question 203

What is the treatment for an asymptomatic liver hemangioma?

Answer 203

Conservative treatment

[UpToDate: Asymptomatic patients, particularly those with lesions <1.5 cm, can be reassured and observed. As discussed above, long-term follow-up of hemangiomas in such patients has confirmed that most do not grow or develop complications. We do not recommend follow-up imaging in patients with hemangiomas ≤5 cm in size, provided there is certainty of the diagnosis based on radiologic and on clinical details. On the other hand, rapid growth of a hemangioma has been reported, justifying radiologic follow-up of patients with lesions >5 cm, particularly those in a sub capsular location.]

Question 204

What is the second most common hepatic artery variant?

Answer 204

Left hepatic artery off left gastric artery

[Found in gastrohepatic ligament medially]

Question 205

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

Answer 205

B12

Question 206

Which numbered segments of the liver are fed by the right portal vein?

Answer 206

Segments V, VI, VII, and VIII

Question 207

What is the cause of sinusoidal obstruction leading to portal hypertension?

Answer 207

Cirrhosis

Question 208

Hepatic adenomas are more commonly found in which lobe?

Answer 208

Right lobe

[UpToDate: Seen predominantly in young women (20 to 44 years old), are frequently located in the right hepatic lobe, and are typically solitary (70% to 80%), although multiple adenomas have been described in patients with prolonged contraceptive use, glycogen storage diseases, and hepatic adenomatosis.]

Question 209

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

Answer 209

Glisson’s capsule

Question 210

Best markers for current acute HBV infection

Answer 210

IgM anti-HBc & HBsAg

Question 211

Which test should be performed pre-operatively in a patient with an echinococcal liver abscess (hydatid cyst) who has jaundice, increased LFTs, or cholangitis?

Answer 211

ERCP to check for communication with biliary system

Question 212

Which numbered segments of the liver are drained by the right hepatic vein?

Answer 212

Segment VI, VII, and VIII

Question 213

What is the serious complication of Transjugular Intrahepatic Portosystemic Shunt (TIPS)?

Answer 213

Encephalopathy

[UpToDate: The primary complication due to shunting of blood from the portal to systemic circulation is the development of portosystemic encephalopathy (PSE). In addition, transjugular intrahepatic portosystemic shunt (TIPS) placement has also been associated with acute pulmonary edema and heart failure.

The incidence of PSE following TIPS is approximately 30% to 35% and is similar to that reported after surgical portal diversion. In one study, for example, 9 of 30 patients receiving TIPS had 24 episodes of PSE during follow-up; in comparison, only six episodes of PSE occurred in 25 concurrent controls treated only with sclerotherapy. Increasing age, advanced liver failure, the presence of minimal hepatic encephalopathy at the time of TIPS placement, and a history of overt hepatic encephalopathy prior to TIPS placement have all been associated with an increased risk of developing PSE after TIPS.

The diameter of the shunt may influence the development of PSE. The resistance to flow through the shunt decreases exponentially with increasing shunt diameter, resulting in increases in shunt flow and portosystemic shunting. The probability of PSE increases dramatically at shunt diameters above 10 mm. However, one randomized trial that assigned 45 patients to receive either 8 or 10 mm diameter stents failed to show an increased incidence of PSE in the patients with larger diameter shunts. At one year, the probability of being free of PSE was 43% in the 8 mm stent arm and 47% in the 10 mm stent arm. In addition, the trial was stopped prior to enrolling its goal of 114 patients because of a significantly higher portosystemic pressure gradient in patients who received the smaller shunts (8.9 vs 6.5 mmHg). This correlated with a decrease in the probability of remaining free from complications due to portal hypertension at one year in the 8 mm group compared with the 10 mm group (42% vs 83%).]

Question 214

What is the mortality rate for acute liver failure (fulminant hepatic failure)?

Answer 214

80% mortality

[Outcome determined by the course of encephalopathy]

[UpToDate: Overall, survival rates in patients treated for acute liver failure are greater than 60%. Approximately 55% of patients will survive without needing a liver transplantation.

The prognosis of patients who are listed for transplantation is variable and cannot always be predicted accurately. An illustrative study from the United States included 308 patients with acute liver failure, of whom 67% survived. Of 135 patients who had been listed for transplantation, 66% received a transplantation, 22% died while awaiting transplantation, and 12% recovered without transplantation. In other series, death rates among patients listed for transplantation are as high as 40%.

Following liver transplantation, the one-year survival rate is approximately 80%. The majority of deaths among patients who undergo liver transplantation are due to neurologic complications or sepsis and occur within three months of the transplantation.]

Question 215

What percent of symptomatic HCV infected individuals develop acute vs chronic disease

Answer 215

• Acute: 20%
• Chronic: 80%

Question 216

Which Hepatitis viruses are transmitted by fecal oral route

Answer 216

HAV & HEV

Question 217

Diagnose:

• HBsAg: -
• Anti-HBs: -
• HBeAg: -
• Anti-HBe: +
• Anti-HBc: IgM

Answer 217

HBV Window Period

Question 218

Which syndrome is characterized by a deficiency in secretion ability that leads to high conjugated bilirubin?

Answer 218

Dubin-Johnson syndrome

[UpToDate: Dubin-Johnson syndrome is characterized clinically by mild icterus. Otherwise, patients are asymptomatic, although mild constitutional complaints such as vague abdominal pains and weakness can occur. Icterus can be so mild as to be noted only during intercurrent illnesses, pregnancy, or consumption of oral contraceptives. Pruritus is not seen in this condition. Physical examination is usually normal except for the icterus, although hepatosplenomegaly is seen occasionally.

Routine clinical laboratory tests, including the complete blood count, serum albumin, cholesterol, alanine and aspartate aminotransferases, alkaline phosphatase, and prothrombin time, are normal. Fasting and postprandial bile acid levels, which are sensitive indices of liver disease, are normal, reflecting the fact that the genetic abnormality does not affect the transport of most bile acids. Serum bilirubin concentrations are usually between 2 and 5 mg/dL but may decline to normal levels or be as high as 20 to 25 mg/dL. Approximately 50% of the serum bilirubin is conjugated. Of the conjugated bilirubin, a major fraction is bilirubin diglucuronide. In addition, covalently albumin-bound fraction is found in plasma. Bilirubinuria is common.]

Question 219

What are 6 strategies to treat ascites in the cirrhotic patient?

Answer 219

1. Water restriction (1-1.5L/d)
2. Decrease NaCl (1-2 g/d)
3. Diuretics (spironolactone counteracts hyperaldosteronism seen with liver failure)
4. Paracentesis
5. TIPS
6. Prophylactic antibiotics (norfloxacin) to prevent spontaneous bacterial peritonitis (used if previous SBP or current UGI bleed)

Question 220

What can lead to isolated gastric varices without elevation of pressure in the rest of the portal system?

Answer 220

Splenic vein thrombosis

Question 221

Which organism is most commonly responsible for pyogenic liver abscess?

Answer 221

E.Coli (Most pyogenic abscesses are from gram negative rods)

[UpToDate: Most pyogenic liver abscesses are polymicrobial; mixed enteric facultative and anaerobic species are the most common pathogens. Anaerobes are probably under-reported because they are difficult to culture and characterize in the laboratory.]

Question 222

How is focal nodular hyperplasia of the liver diagnosed?

Answer 222

Abdominal CT (hypervascular tumor)

[Has kupffer cells, so will take up sulfur colloid on liver scan as opposed to a hepatic adenoma which does not take up sulfur colloid]

[UpToDate: U/S is able to identify the central scar in only 20 percent of cases. A properly timed dynamic, triphasic, helical CT scan performed without contrast, and with contrast during the hepatic arterial and portal venous phases, will often be highly suggestive of the diagnosis. There may be little to distinguish FNH from normal liver on standard MRI, since it is composed of the same elements as normal liver.]

Question 223

Which Hepatitis virus requires infection with which other hepatitis virus

Answer 223

HDV requires HBV infection

Question 224

Where is jaundice first evident?

Answer 224

Under the tongue

Question 225

Which animals harbor echinococcus?

Answer 225

Sheep are carriers, Dogs are definitive hosts

Question 226

What does elevated un-conjugated bilirubin signify?

Answer 226

Prehepatic cause such as hemolysis or hepatic deficiencies in uptake or conjugation of bilirubin

Question 227

Can an isolated colon cancer metastasis to the liver be resected?

Answer 227

Yes, if enough liver will remain for the patient to survive

[35% 5-year survival after resection for cure]

[UpToDate: Resection offers the greatest likelihood of cure for patients with liver-isolated colorectal cancer (CRC). In surgical case series, 5-year survival rates after resection range from 24% to 58%, averaging 40%, and surgical mortality rates are generally <5%. Subgroups with advanced age, comorbid disease, and synchronous hepatic and colon resection may have higher procedure-related mortality and worse long-term outcomes. As an example, 5-year survival rate was only 25% in a population-based retrospective report of 3957 US Medicare enrollees undergoing hepatic resection for CRC liver metastases. Even so, 5-year survival rates with the most active systemic chemotherapy regimens are only 10% to 11%, only about one-fifth of whom have a sustained disease remission.

Approximately one-third of 5-year survivors suffer a cancer-related death, while those who survive 10 years appear to be cured. In an analysis of 612 consecutive patients who underwent resection of CRC liver metastases and were followed for at least 10 years, there were 102 actual 10-year survivors (17%), and only one patient experienced a disease-specific death after 10 years of survival.

Because of its clear survival impact, surgical resection is the treatment of choice when feasible. The percentage of patients with isolated hepatic metastases who are amenable to potentially curative resection is a bit of a moving target since surgeons may have different interpretations of “resectable.” It is safe to say that a majority of patients, with metastatic disease are not curative surgical candidates because of tumor size, location, multifocality, or inadequate hepatic reserve.]

Question 228

What is the name of the ligament that carries the 3 structures of the portal triad?

Answer 228

Hepatoduodenal ligament (porta hepatis)

Question 229

What is the most common type of benign liver tumor?

Answer 229

Hemangioma (Most are asymptomatic)

[UpToDate: Hepatic hemangiomas are the most common benign mesenchymal hepatic tumors. In one series 72 percent were hemangiomas.]

Question 230

Where is the primary infection in a patient with an amebic liver abscess?

Answer 230

The colon (amebic colitis)

[Reaches liver via portal vein]

[UpToDate: Amebiasis is caused by the protozoan Entamoeba histolytica. Most infections are asymptomatic; clinical manifestations include amebic dysentery and extraintestinal disease. Extraintestinal manifestations include amebic liver abscess and other more rare manifestations such as pulmonary, cardiac, and brain involvement. Amebic liver abscess is the most common extraintestinal manifestation of amebiasis. Amebae establish hepatic infection by ascending the portal venous system.]

Question 231

What does a positive Casoni skin test indicate?

Answer 231

Echinococcal liver abscess (hydatid cyst)

[Wikipedia: The Casoni test is an immediate hypersensitivity skin test used in the diagnosis of hydatid disease introduced by casoni. The test involves the intradermal injection of 0.25 ml of sterilised fluid from hydatid cysts/human cyst and sterilised by Seitz filtration on forearm and equal volume of saline injected on the other forearm. Observations made for next 30 mins and after 1 to 2 days. A wheal response occurring at the injection site within 20 minutes is considered positive. (Immediate hypersensitivity). Delayed hypersensitivity reaction usually read after 18-24 hours. The test is positive in about 90% of cases of hydatid disease affecting the liver, but positive in less than 50% of patients with hydatid disease elsewhere in the body; false positive results are also common. Being a type I hypersensitivity reaction, anaphylactic reaction tray must be kept ready before carrying out the test. Consequently, serological tests are now generally used.]

Question 232

What is the treatment for a symptomatic hepatic adenoma?

Answer 232

Tumor resection for bleeding and malignancy risk (Embolization if multiple and unresectable)

[UpToDate: Surgical resection should be recommended for all patients with symptoms attributable to the adenoma and those with large lesions >5 cm. Liver transplantation should be reserved for patients in whom surgical resection is not possible due to tumor size/location and those with adenomatosis. Mortality from elective surgical resection is <1 percent, and resection of some peripherally located adenomas can even be accomplished laparoscopically.]

Question 233

What are the 3 risk factors for spontaneous bacterial peritonitis?

Answer 233

1. Prior SBP
2. UGI bleed (variceal hemorrhage)
3. Low-protein ascites

Question 234

What is the treatment for spontaneous bacterial peritonitis?

Answer 234

3rd-generation cephalosporins

[patients usually respond within 48 hours]

[UpToDate: In patients with suspected spontaneous bacterial peritonitis (SBP), empiric therapy should be initiated as soon as possible to maximize the patient’s chance of survival. However, antibiotics should not be given until ascitic fluid has been obtained for culture. Most cases of SBP are due to gut bacteria such as Escherichia coli and Klebsiella, though streptococcal and staphylococcal infections can also occur. As a result, broad-spectrum therapy is warranted until the results of susceptibility testing are available. We prefer cefotaxime 2 g intravenously every eight hours because it has been shown to produce excellent ascitic fluid levels. In addition to antibiotic therapy, patients with SBP who are taking a nonselective beta blocker should have the medication discontinued.]

Question 235

What extends from the falciform ligament and carries the obliterated umbilical vein to the undersurface of the liver?

Answer 235

Ligamentum Teres

Question 236

Can a benign hepatic adenoma become malignant?

Answer 236

Yes

[UpToDate: The risk of malignant transformation to hepatocellular carcinoma is difficult to ascertain from the literature. Two small studies reported the development of malignant transformation in 8% to 13% of patients, suggesting that it is not a rare occurrence. An increase in size on sequential imaging studies or a rise in serum AFP levels should raise concern that malignant transformation has developed.]

Question 237

What is the most common cause of liver failure?

Answer 237

Cirrhosis

[Palpable liver, jaundice, and ascites]

Question 238

Which hepatocytes are most sensitive to ischemia?

Answer 238

Central lobular (Acinar zone III)

Question 239

Pyogenic liver abscess is most commonly secondary to what?

Answer 239

Contiguous infection from biliary tract

[UpToDate: A considerable proportion of pyogenic liver abscesses follow one or more episodes of portal vein pyemia, usually related to bowel leakage and peritonitis. Another important route is direct spread from biliary infection. Underlying biliary tract disease such as gallstones or malignant obstruction is present in 40% to 60% of cases.]

Question 240

Budd-Chiari syndrome, constrictive pericarditis, and CHF are all causes of portal hypertension from what?

Answer 240

Post-sinusoidal obstruction

Question 241

Should an echinococcal cyst be aspirated?

Answer 241

No

[Can cause leakage and anaphylactic shock]

Question 242

Which life-threatening syndrome is characterized as a severe deficiency in glucuronyl transferase (inability to conjugate bilirubin), leading to high unconjugated bilirubin?

Answer 242

Crigler-Najjar disease

Question 243

What is the treatment for an echinococcal liver abscess (hydatid cyst)?

Answer 243

Pre-op albendazole for 2 weeks followed by surgical removal

[Intra-op can inject cyst with alcohol to kill organisms, then aspirate out. Must get entire cyst wall]

[UpToDate: Management options for cystic echinococcosis (CE) include surgery, percutaneous management, drug therapy, and observation. Surgery has been the traditional approach for treatment of CE; subsequently, alternative approaches have been introduced and have replaced surgery as the treatment of choice in some cases.

In general, clinical approach depends on the World Health Organization (WHO) diagnostic classification. Stage CE1 and CE3a cysts have a single compartment; such cysts that are <5 cm may be treated with albendazole alone. In settings where albendazole treatment with follow-up monitoring is not feasible, definitive management with percutaneous treatment via puncture, aspiration, injection, and reaspiration (PAIR) is an acceptable alternative approach. Stage CE1 and CE3a cysts that are >5 cm may be treated with albendazole in combination with PAIR. In situations where albendazole treatment is not feasible, percutaneous treatment with PAIR (in the absence of adjunctive drug therapy) is an acceptable alternative approach. Issues related to drug therapy are discussed below.

Stage CE2 and CE3b cysts have many compartments that require individual puncture; patients with such cysts commonly relapse after PAIR. Therefore, management of these cysts requires either modified catheterization technique (eg, non-PAIR percutaneous therapy) or surgery (with adjunctive drug therapy). The optimal choice between these approaches is uncertain and further study is needed.

Stages CE4 and CE5 are inactive cysts that may be managed with observation.

There are few randomized trials comparing different treatments, and the level of evidence supporting the use of one therapeutic modality over another is low. In one study of 32 patients with hepatic cysts comparing percutaneous drainage alone, albendazole alone, and percutaneous drainage in combination with albendazole, those who received combination therapy had the greatest size reduction observed ultrasonographically. Subsequently, a randomized trial performed among 50 patients demonstrated that outcomes among those who underwent percutaneous drainage (in combination with albendazole) were comparable to outcomes among patients who underwent surgery (with no albendazole therapy).]

Question 244

Portal hypertension in children is usually caused by what?

Answer 244

Extra-hepatic portal vein thrombosis

Question 245

What is the mechanism of ascites in cirrhosis?

Answer 245

Hepatocyte destruction –> Fibrosis and scarring of liver –> Increased hepatic pressure –> Portal venous congestion –> Lymphatic overload –> Leakage of splanchnic and hepatic lymph into peritoneum –> Ascites

Question 246

Cirrhosis is a cause of what kind of portal hypertension (pre-sinusoidal, sinusoidal, post-sinusoidal)?

Answer 246

Sinusoidal obstruction

Question 247

What are the 2 secondary bile acids (salts)?

Answer 247

Deoxycholic and lithocholic

[Dehydroxylated primary bile acids by bacteria in gut]

Question 248

What is the treatment for Budd-Chiari syndrome?

Answer 248

Porta-caval shunt

[Needs to connect to the IVC above the obstruction]

[UpToDate:

Initial treatment includes:

• Correcting underlying disorders that predisposed to the development of Budd-Chiari syndrome (when possible)
• Initiating anticoagulation unless there are contraindications
• Treating complications of portal hypertension (if present)

Additional treatments that may be appropriate for some patients include:

• Thrombolysis for patients with acute Budd-Chiari syndrome if a well-defined clot is present
• Angioplasty/stenting for symptomatic patients with venous obstructions that are amenable to angiographic treatment
• Liver transplantation for patients with acute liver failure; patients with acute liver failure should be referred to a liver transplantation center if possible for evaluation and management

If initial treatments fail, options include:

• TIPS placement or surgical shunting to decompress the liver
• Liver transplantation]

Question 249

Which category of cirrhotic patient according to the Child-Pugh criteria may be considered for splenorenal shunt?

Answer 249

Child’s A cirrhotics who present just with bleeding

[Rarely used anymore]

Question 250

What causes physiologic jaundice of the newborn?

Answer 250

Immature glucuronyl transferase resulting in high unconjugated bilirubin

Question 251

What percent of hepatic adenomas are symptomatic?

Answer 251

80%

[20% risk of significant bleeding (rupture)]

[UpToDate: Hepatic adenomas are uncommon benign epithelial liver tumors that develop in an otherwise normal-appearing liver. They are seen predominantly in young women (20 to 44 years old), are frequently located in the right hepatic lobe, and are typically solitary (70% to 80%), although multiple adenomas have been described in patients with prolonged contraceptive use, glycogen storage diseases, and hepatic adenomatosis. Adenomas range in size from 1 to 30 cm. Symptoms such as abdominal pain are more likely with larger lesions. Adenomas are typically diagnosed because of abdominal pain localized to the epigastrium or right upper quadrant, during an imaging study done for unrelated reasons, and (less commonly) because of detection of a mass on clinical examination or as a sudden, life-threatening hemodynamic collapse associated with rupture and intraabdominal bleeding.]

Question 252

According to Couinaud’s nomenclature, which numbered liver segment is the inferior right posterolateral segment?

Answer 252

Segment VI

Question 253

What is the 5-year survival rate with resection of hepatocellular carcinoma?

Answer 253

30%

[UpToDate: There is a wide variability in outcomes after resection for HCC, attributable to both tumor-related factors and the underlying liver disease.

Long-term overall survival rates of ≥40% can be achieved with limited hepatic resections for small tumors (<5 cm) in patients with Child-Pugh class A cirrhosis. The best outcomes are reported in carefully selected patients who have solitary lesions without intrahepatic metastasis or vascular invasion (gross or microscopic invasion of branches of the portal or hepatic veins), tumor diameter ≤5 cm, and a negative surgical margin of >1 cm; 5-year survival rates are as high as 78%. Recent series demonstrate prolonged survival for more advanced HCC with proper patient selection despite major hepatectomy.

In contrast, studies with lower long-term survival rates usually include populations of patients with severe cirrhosis (Child-Pugh class B or C) or tumors greater than 8 cm in diameter, which require resection of more hepatic parenchyma. These patients have higher operative morbidity and mortality, and their intrinsic liver disease is a major contributor to reduced long-term survival.

Several staging systems have been developed to prognostically stratify outcomes from treatment of HCC. Some, like the tumor node metastasis (TNM) staging system of the American Joint Committee on Cancer (AJCC), are based entirely upon pathologic disease extent, while others, such as that of the Cancer of the Liver Italian Program (CLIP), take underlying liver function into account. There is ongoing debate as to which staging system is optimal for use in patients who do not undergo hepatic resection. Among hepatologists, the Barcelona Clinic Liver Cancer (BCLC) staging classification, is the most widely used staging system other than the AJCC staging classification, but many groups challenge the validity of the system because of good results in selected higher stage BCLC patients treated with surgery (where BCLC advises nonsurgical therapy).]

Question 254

What is the treatment for hepatic encephalopathy?

Answer 254

1. Lactulose titrated to 2-3 stools daily (it is a cathartic that gets rid of bacteria in the gut and acidifies the colon to prevent NH3 uptake by converting it to ammonium)
2. Limit protein intake (less than 70 g/day)
3. Branched-chain amino acids (metabolized by skeletal muscle, may be of some value)
4. Neomycin (gets rid of ammonia-producing bacteria from the gut)

Question 255

The liver stores large amounts of water-soluble or fat-soluble vitamins?

Answer 255

Fat-soluble vitamins

Question 256

What are the 3 risk factors for hepatic sarcoma?

Answer 256

1. Polyvinyl chloride (PVC)
2. Thorotrast (radiocontrast agent in medical radiography in the 1930s and 1940s)
3. Arsenic (rapidly fatal)

[UpToDate: Angiosarcoma is a high-grade malignant vascular neoplasm, and it is the most common sarcoma arising in the liver. It occurs in older patients (>60 years old) and is more common in men. It can be caused by exposure to vinyl chloride, arsenic, anabolic steroids, radiation, and thorium dioxide. Patients typically present with abdominal pain, fatigue, jaundice, ascites, and weight loss. Rarely, patients present with Budd-Chiari syndrome. Hepatomegaly with or without splenomegaly and thrombocytopenia are common findings. Metastases occur frequently and rapidly to the spleen, lymph nodes, lung, bone, and adrenals. Liver failure and intraabdominal bleeding due to liver rupture are common causes of death.

Angiosarcoma forms numerous poorly defined variably sized nodules that are soft, spongy, hemorrhagic, and necrotic. The entire liver is frequently involved. The tumor is composed of pleomorphic spindle or epithelioid cells, often with bizarre or multinucleated forms; mitoses are evident. Better-differentiated areas may show large cavernous spaces that are lined by atypical endothelial cells. The tumor cells grow along and into sinusoids, peliotic areas, and branches of portal and hepatic veins. Immunostaining shows positivity for vascular markers, such as the ERG transcription factor, CD31, CD34, and Factor VIII antigen.]

Question 257

What is Budd-Chiari syndrome?

Answer 257

Occlusion of hepatic veins or IVC

[This leads to RUQ pain, hepatosplenomegaly, ascites, fulminant hepatic failure, muscle wasting, and variceal bleeding]

Question 258

What portion of hepatic blood flow is supplied by the portal vein?

Answer 258

2/3

Question 259

Diagnose:

• HBsAg: +
• Anti-HBs: -
• HBeAg: -
• Anti-HBe: +
• Anti-HBc: IgG

Answer 259

Low infectivity Chronic HBV

Question 260

What are the two most common problems with hepatic resection?

Answer 260

1. Bleeding
2. Bile leak

Question 261

Where in the hepatocytes of the liver is alkaline phosphatase normally located?

Answer 261

In the canalicular membrane

[The highly specialized canalicular (or apical) membrane of the hepatocyte is rich in microvilli and comprises 10-15% of the membrane surface area of the hepatocyte]

[UpToDate: Increased serum alkaline phosphatase is derived from tissues whose metabolism is either functionally disturbed (the obstructed liver) or greatly stimulated (placenta in the third trimester of pregnancy and bone in growing children). The cause in hepatobiliary disease has been debated. Two theories were proposed in the past: the damaged liver regurgitates hepatic alkaline phosphatase back into serum; and the damaged liver, particularly if due to obstructive jaundice, fails to excrete the alkaline phosphatase made in bone, the intestines, and the liver. This long-standing debate was resolved in favor of the regurgitation of liver alkaline phosphatase into serum. The data supporting this theory include the following:

• Only hepatic alkaline phosphatase is found in the serum of patients with liver disease, particularly cholestasis.
• The clearance rates of infused placental alkaline phosphatase are the same in patients with bile duct obstruction and healthy controls.
• In experimental bile duct obstruction in rats, the entire increase in serum alkaline phosphatase activity is due to the leakage of hepatic alkaline phosphatase into serum. The increased serum activity is paralleled by a striking elevation in hepatic alkaline phosphatase activity and is not accounted for by biliary retention of alkaline phosphatase.

Thus, the elevation in serum alkaline phosphatase in hepatobiliary disease results from increased de novo synthesis in the liver followed by release into the circulation. Retained bile acids appear to play a central role in this process; they induce the synthesis of the enzyme and may cause it to leak into the circulation, perhaps by disruption of hepatic organelles and solubilization of phosphatase bound to such membranes.

The precise manner in which the alkaline phosphatase reaches the circulation is unclear. In some patients with cholestasis, small vesicles that contain many basolateral (sinusoidal) membrane enzymes still bound to these membranes, including alkaline phosphatase, have been found in serum.]

Question 262

What would an abdominal CT of a patient with an echinococcal liver abscess (hydatid cyst) reveal?

Answer 262

Ectocyst (calcified) and endocyst (double-walled cyst)

Question 263

Which Hepatitis viruses are transmitted by blood or sexual contact

Answer 263

HBV, HCV, & HDV

Question 264

Where in the hepatocytes of the liver does nutrient uptake occur?

Answer 264

Sinusoidal membrane

Question 265

Conjugated bilirubin is broken down by bacteria in the terminal ileum and free bilirubin is reabsorbed and converted to what?

Answer 265

Urobilinogen

[Urobilinogen is eventually released in the urine as urobilin]

Question 266

What is the difference in vascularity of primary liver tumors and metastatic liver tumors?

Answer 266

• Primary liver tumors are hypervascular
• Metastatic liver tumors are hypovascular

Question 267

The middle hepatic artery is most commonly a branch of which artery?

Answer 267

Left hepatic artery

Question 268

Fulminant hepatitis (acute liver failure) can occur with which types viral hepatitis?

Answer 268

B, D, and E

[Very rare with hepatitis A and C]

Question 269

Which types of viral hepatitis can cause chronic hepatitis and hepatoma (hepatocellular carcinoma)?

Answer 269

B, C, and D

Question 270

Diagnose:

• HBsAg: -
• Anti-HBs: +
• HBeAg: -
• Anti-HBe: +
• Anti-HBc: IgG

Answer 270

Recovery from HBV infection

Question 271

What are some (10) risk factors for hepatocellular carcinoma?

Answer 271

1. Hepatitis B (#1 cause worldwide)
2. Hepatitis C
3. Ethanol
4. Hemochromatosis
5. Alpha-1-antitrypsin deficiency
6. Primary sclerosing cholangitis
7. Alfatoxins
8. Hepatic adenoma
9. Steroids
10. Pesticides

[Primary biliary cirrhosis and Wilson’s disease are not risk factors]

Question 272

How are hepatic adenomas diagnosed?

Answer 272

Sulfur colloid scan (no Kupffer cells in adenomas, thus no uptake (cold) on sulfur colloid scan)

[U/S characteristics are often non-specific and may mimic other benign or malignant liver lesions. CT imaging often reveals areas of hemorrhage, necrosis, or fibrosis, giving adenomas a heterogeneous appearance. MRI demonstrates a hypervascular tumor]

[UpToDate: The diagnosis should be made based upon the clinical setting, a combination of imaging studies, and/or surgical resection. Percutaneous liver biopsy or fine-needle aspiration are usually not indicated because adenomas have a tendency to bleed following biopsy and because the amount of tissue obtained using these methods is frequently insufficient for establishing a diagnosis.]

Question 273

How do you diagnose a liver hemangioma?

Answer 273

MRI and CT scan show peripheral to central enhancement (Appears as a hypervascular lesion)

[UpToDate: The lesions classically opacify on CT after a delay of three or more minutes and remain isodense or hyperdense on delayed scans. MRI has emerged as a highly accurate, noninvasive technique for diagnosing hemangiomas with a sensitivity of approximately 90 percent and a specificity of 91 to 99 percent. The typical MRI appearance is a smooth, well-demarcated, homogeneous mass that has low signal intensity on T1-weighted images and is hyperintense on T2-weighted images. The presence of intratumoral fibrosis results in areas of low intensity on T2-weighted images.]

Question 274

The gallbladder lies under which numbered segment(s) of the liver?

Answer 274

Segments IV and V

Question 275

What are the King’s College criteria of poor prognostic indicators for acetaminopen-induced acute liver failure?

Answer 275

Arterial pH less than 7.3

Or all of the following:

• INR greater than 6.5
• Creatinine greater than 3.4mg/dL
• Grade III/IV encephalopathy

Question 276

What is a Sengstaken-Blakemore esophageal tube used for?

Answer 276

It has a balloon used to control variceal bleeding

[Risk of rupture of the esophagus so hardly used anymore]

Question 277

According to Couinaud’s nomenclature, which numbered liver segment is the superior left lateral segment?

Answer 277

Segment II

Question 278

What is the best indicator of synthetic function of the liver in a cirrhotic patient?

Answer 278

Prothrombin time (PT)

Question 279

Which two vessels join to form the portal vein?

Answer 279

1. Superior mesenteric vein
2. Splenic vein

Question 280

What are the 3 most common bacteria causing spontaneous bacterial peritonitis?

Answer 280

1. E. Coli
2. Pneumococci
3. Streptococci

[Most commonly mono-organism infection; if not, need to worry about bowel perforation]

Question 281

Into which vessel does the inferior mesenteric vein empty?

Answer 281

Splenic vein

Question 282

Which three structures make up the portal triad?

Answer 282

1. Common bile duct
2. Portal vein
3. Proper hepatic artery

Question 283

What markers will be present in an HBV vaccinated individual

Answer 283

IgG anti-HBs but no anti-HBc

Question 284

What are 3 causes of pre-sinusoidal obstruction leading to portal hypertension?

Answer 284

1. Schistosomiasis
2. Congenital hepatic fibrosis
3. Portal vein thrombosis

[UpToDate: Schistosomiasis is one of the most common causes of noncirrhotic portal hypertension worldwide. Of the three main Schistosoma species, S. japonicum and S. mansoni are known to cause liver disease. S. hematobium affects mainly the urinary tract, although at advanced stages the liver can develop portal fibrosis. The acute stage of schistosomiasis mimics acute bacterial infection and is accompanied by marked eosinophilia. Chronic hepatic schistosomiasis is characterized by features of portal hypertension: esophageal varices, hepatomegaly, and splenomegaly with hypersplenism. The diagnosis of schistosomiasis can be made by the detection of schistosomal ova in the stool. Management includes treating underlying parasitic infection and preventing or treating the consequences of portal hypertension.

S. japonicum is distributed widely throughout the world, predominantly in Asia. S. mansoni is endemic in Egypt, Africa, the Middle East, and South America. Two other species (S. mekongi and S. intercalatum) also cause hepatic infections in endemic areas in Southeast Asia and Western Africa, respectively.

Pathophysiology — The infection occurs when the schistosomal cercariae enter the body through the skin. Adult worms eventually find their way to inhabit tributaries of the inferior (S. mansoni) or superior (S. japonicum) mesenteric veins, where they produce hundreds to thousands eggs per day for several years before the end of their lifespan. Some of these eggs pass through the intestinal mucosa and are excreted in the urine or feces to continue their life cycle. Others flow into the portal vein tributaries and become trapped in the terminal portal venules, where they induce chronic inflammation that is subsequently followed by marked fibrosis. S. japonicum is capable of producing far more eggs than S. mansoni and thus causes more severe liver disease.

In the early stages of infection, the portal resistance is mainly presinusoidal. However, as the fibrotic changes in the portal tracts progress, lobular distortion at the sinusoidal level occurs. This results in an increase in resistance to portal venous flow, as evidenced by an increased wedged hepatic venous pressure in advanced cases. Hemodynamic studies in patients with hepatic schistosomiasis have demonstrated a hyperdynamic systemic and splanchnic circulation with normal hepatic venous pressure gradient and total hepatic blood flow.

Praziquantel and oxamniquine are active against all forms of human schistosomiasis and are effective in eradicating the worms in the acute stage of the disease. Cure rates vary from 60% to 90% for S. mansoni and 60% to 80% for S. japonicum. Even if treatment does not kill all the worms, it will result in a sharp reduction in egg laying. In patients with chronic schistosomiasis, the worms no longer lay eggs and the patient may not require any specific antihelminthic treatment.]

Question 285

Fever, abdominal pain, ascites with PMNs > 250, positive culture of ascites fluid are all indicative of what?

Answer 285

Spontaneous bacterial peritonitis

Question 286

Where is urea synthesized?

Answer 286

In the liver

Question 287

How much albumin should be replaced following paracentesis for ascites?

Answer 287

1 gram of albumin for every 100cc removed

Question 288

Which hormone is elevated in liver failure patients?

Answer 288

Aldosterone

[Secondary to impaired hepatic metabolism and impaired GFR]

Question 289

Which benign liver tumor has walls with a characteristic blue hue?

Answer 289

Solitary cyst

[Congenital, seen in women, right lobe, most can be left alone because rarely cause complications]

Question 290

Which numbered segments of the liver are drained by the middle hepatic vein?

Answer 290

Segment V and inferior portion of IV

Question 291

What are the 3 categories of cirrhosis patients according to the Child-Pugh Score?

Answer 291

• Child’s A: 5-6 points
• Child’s B: 7-9 points
• Child’s C: 10+ points

Question 292

What is the treatment for a symptomatic liver hemangioma?

Answer 292

Surgery +/- pre-op embolization (Steroids, possible XRT for unresectable disease)

[UpToDate: Asymptomatic patients, particularly those with lesions <1.5 cm, can be reassured and observed. Long-term follow-up of hemangiomas in such patients has confirmed that most do not grow or develop complications. We do not recommend follow-up imaging in patients with hemangiomas ≤5 cm in size, provided there is certainty of the diagnosis based on radiologic and on clinical details. On the other hand, rapid growth of a hemangioma has been reported, justifying radiologic follow-up of patients with lesions >5 cm, particularly those in a sub capsular location. Our approach is to repeat imaging in 6 to 12 months for such lesions, using the imaging modality that best showed the hemangioma previously (eg, computed tomography scan or magnetic resonance imaging). If there is no change in the size of the lesion, we do not perform additional imaging. In the absence of symptoms, the risk of bleeding is too low to justify prophylactic resection.

Patients who have pain or symptoms suggestive of extrinsic compression of adjacent structures should be considered for surgical resection. However, it is important that all other causes of pain have been evaluated and excluded prior to surgery. This approach is supported in one report in which 25% of patients had persistence of symptoms after surgical resection. Overall, indications for surgical intervention have decreased to approximately 2% and include the development of complications such as rupture and intraperitoneal bleeding, which has a 20% mortality rate, incapacitating symptoms due to large hemangiomas, or failure to exclude a malignancy by radiologic studies. Giant hemangiomas only rarely turn out to be malignant vascular tumors when resected.]

Question 293

According to Couinaud’s nomenclature, which numbered liver segment is the inferior right anteromedial segment?

Answer 293

Segment V

Question 294

What are 3 causes of post-sinusoidal obstruction leading to portal hypertension?

Answer 294

1. Budd-Chiari syndrome (hepatic vein occlusive disease)
2. Constrictive pericarditis
3. CHF

Question 295

What should immediately be considered if a patient meets King’s College criteria for liver failure?

Answer 295

Urgent liver transplant listing

Question 296

What is the most common cancer worldwide?

Answer 296

Hepatocellular carcinoma

Question 297

Which syndrome is characterized by a deficiency in storage ability that leads to high conjugated bilirubin?

Answer 297

Rotor’s syndrome

[UpToDate: The syndrome is characterized by chronic conjugated and unconjugated hyperbilirubinemia without evidence of hemolysis. Although Rotor syndrome had been thought previously to be a variant of Dubin-Johnson syndrome, the two conditions are now understood to be different entities. In Rotor syndrome, there is a defect in hepatic storage of conjugated bilirubin, which leaks into the plasma, resulting in hyperbilirubinemia. Rotor syndrome is also a benign condition.

As in Dubin-Johnson syndrome, Rotor syndrome does not require treatment. However, the diagnosis is important to avoid confusion with other hepatobiliary diseases.]

Question 298

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

Answer 298

Portal hypertension

[Usually due to extra-hepatic portal vein thrombosis]

Question 299

What does Cantlie’s line separate?

Answer 299

The right and left lobes of the liver

Question 300

What is the most common hepatic artery variant?

Answer 300

Right hepatic artery off superior mesenteric artery

[Courses behind pancreas, posterolateral to the common bile duct]

Question 301

According to Couinaud’s nomenclature, which numbered liver segment is the superior right anteromedial segment?

Answer 301

Segment VIII

Question 302

What causes postpartum liver failure with ascites?

Answer 302

Hepatic vein thrombosis

[Has an infectious component]

Question 303

Which type of benign liver tumor is common in women (especially those taking OCPs) and in individuals with a history of steroid use?

Answer 303

Hepatic adenoma

[UpToDate: Hepatic adenoma is a benign epithelial liver tumor that usually occurs in a noncirrhotic liver. It is most commonly seen in premenopausal women older than 30 years of age. The majority of patients have used oral contraceptives for more than two years prior to diagnosis. Hepatic adenoma has also been noted in patients with type 1 glycogen storage diseases. Hepatic adenoma has a small risk of neoplastic transformation.]

Question 304

What are bile acids conjugated to in the production of bile salts?

Answer 304

Taurine and Glycine

[Improves water solubility]

[Wikipedia: Prior to secreting any of the bile acids (primary or secondary, see below), liver cells conjugate them with one of two amino acids, glycine or taurine, to form a total of 8 possible conjugated bile acids. These conjugated bile acids are often referred to as bile salts because of their physiologically-important acid-base properties. The pKa of the unconjugated bile acids are between 5 and 6.5, and the pH of the duodenum ranges between 3 and 5, so when unconjugated bile acids are in the duodenum, they are almost always protonated (HA form), which makes them relatively insoluble in water. Conjugating bile acids with amino acids lowers the pKa of the bile-acid/amino-acid conjugate to between 1 and 4. Thus conjugated bile acids are almost always in their deprotonated (A-) form in the duodenum, which makes them much more water-soluble and much more able to fulfil their physiologic function of emulsifying fats.]