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06 - absite > Chapter 31: Liver > Flashcards

Chapter 31: Liver Flashcards

1
Q

Right hepatic artery variants

A

Off SMA (#1 hepatic artery variant, 20%) courses behind pancreas, posterolateral to the common bile duct

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2
Q

1 hepatic artery variant

A

Right hepatic artery off SMA

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3
Q

Left hepatic artery variant

A

Off left gastric artery (about 20%) - found in gastrohepatic ligament medially

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4
Q

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

A

Falciform ligament

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5
Q

What does the falciform ligament contain?

A

Remnant of umbilical vein

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6
Q

Carries the obliterated umbilical vein to the undersurface of the liver; extends from the falciform ligament

A

Ligamentum teres

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7
Q

Line drawn from the middle of the gallbladder fossa to IVA ; separates right and left liver lobes

A

Portal fissure or Cantlie’s line

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8
Q

Liver segments

A

1: caudate
2: superior left lateral
3: inferior left lateral
4: left medial (quadrate lobe)
5: inferior right anteromedial
6: inferior right posterolateral
7: superior right posterolateral
8: superior right anteromedial

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9
Q

Liver segment: 1

A

Caudate

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10
Q

Liver segment: 2

A

Superior left lateral segment

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11
Q

Liver segment: 3

A

Inferior left lateral segment

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12
Q

Liver segment: 4

A

Left medial segment (quadrate lobe)

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13
Q

Liver segment: 5

A

Inferior right anteromedial segment

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14
Q

Liver segment: 6

A

Inferior right posterolateral segment

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15
Q

Liver segment: 7

A

Superior right posterolateral segment

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16
Q

Liver segment: 8

A

Superior right anteromedial segment

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17
Q

Peritoneum that covers the liver

A

Glisson’s capsule

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18
Q

Area on the posterior-superior surface of liver not covered by Glisson’s capsule

A

Bare area

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19
Q

Lateral and medial extensions of the coronary ligament on the posterior surface of the liver; made up of peritoneum

A

Triangular ligaments

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20
Q

Where does the portal triad enter?

A

Segments 4 and 5

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21
Q

Where does the gallbladder lie?

A

Segments 4 and 5

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22
Q

Liver macrophages

A

Kupffer cells

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23
Q

What composes the portal triad?

A

Common bile duct (lateral), portal vein (posterior), and proper hepatic artery (medial); come together in the hepatoduodenal ligament (porta hepatis)

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24
Q

Porta hepatis clamping; will not stop hepatic vein bleeding

A

Pringle maneuver

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25
Q

Entrance to lesser sac

A

Foramen of Winslow

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26
Q

Borders of Foramen of Winslow (entrance to lesser sac)

A
  • Anterior: portal triad
  • Posterior: IVC
  • Inferior: duodenum
  • Superior: liver
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27
Q

What forms the portal vein?

A

Forms from superior mesenteric vein joining splenic vein (no valves)

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28
Q

Where dose inferior mesenteric vein drain?

A

Enters splenic vein

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29
Q

2 in liver

- 2/3 of hepatic blood flow

A

Portal veins

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30
Q

Where are L / R portal vein located?

A

Left: goes to segment 2, 3, 4
Right: goes to segment 5, 6, 7, 8

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31
Q

Arterial blood supply of the liver

A

Right, left, and middle hepatic arteries (follows hepatic vein system below)

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32
Q

What is the middle hepatic artery a branch of?

A

MC a branch off the left hepatic artery

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33
Q

Arterial supply of most primary and secondary liver tumors

A

Hepatic artery

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34
Q

How many hepatic veins are there? Where do they drain?

A

3 hepatic veins

- Drain into IVC

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35
Q

Location left hepatic vein

A

2, 3 and superior 4 segments

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36
Q

Location of middle hepatic vein

A

5 and inferior 6 segments

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37
Q

Location of right hepatic vein

A

6, 7, and 8 segments

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38
Q

What does middle hepatic vein come off of?

A

Left hepatic vein in 80% before going to IVC; other 20% goes directly into IVC

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39
Q

Drain medial aspect of right lobe directly to IVC

A

Accessory right hepatic veins

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40
Q

Where do inferior phrenic veins drain?

A

Also drain directly into the IVC

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41
Q

Liver lobe: receives separate right and left portal and arterial blood flow; drains directly into IVC via separate hepatic veins

A

Caudate lobe

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42
Q

Where is alkaline phosphatase located?

A

Normally located in canalicular membrane

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43
Q

Where does nutrient uptake occur?

A

Sinusoidal membrane

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44
Q

Usual energy source for liver; glucose is converted to glycogen and stored.
- Excess glucose converted to fat

A

Ketones

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45
Q

Where is urea synthesized?

A

Liver

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46
Q

Coagulation factors not made in the liver

A

von Willebrand factor and factor 8 (endothelium)

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47
Q

Type of vitamins stored in the liver

A

Liver stores large amount of fat-soluble vitamins

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48
Q

The only water-soluble vitamin stored in the liver

A

b12

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49
Q

Most common problems with hepatic resection

A

Bleeding and bile leak

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50
Q

Hepatocytes most sensitive to ischemia

A

Central lobular (acinar zone 3)

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51
Q

How much of the liver can be safely resected?

A

75%

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52
Q

Breakdown product of hemoglobin (Hgb -> heme -> biliverdin -> bilirubin)

A

Bilirubin

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53
Q

What improves water solubility of bilirubin?

A

Conjugated to glucuronic acid (glucuronyl transferase) in the liver

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54
Q

Where is conjugated bilirubin secreted?

A

Bile

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55
Q
  • Breakdown of conjugated bilirubin by bacteria in the terminal ileum occurs
  • Free bilirubin is reabsorbed and converted to this
  • Excess turns urine dark like cola
A

Urobilinogen

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56
Q

What is urobilinogen released in the urine as?

A

Urobilin (yellow color)

free bilirubin -> urobilinogen -> urobilin

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57
Q

What does bile contain?

A

Bile salts (85%), proteins, phosopholipids (lecithin), cholesterol, and bilirubin

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58
Q

What determines the final bile composition?

A

Active (Na/K ATPase) reabsorption of water in gallbladder

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59
Q

Used to make bile salts / acids

A

Cholesterol

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60
Q

What improves water solubility of bile salts?

A

Bile salts are conjugated to taurine or glycine

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61
Q

What are primary bile acids (salts)?

A

Cholic and chenodeoxycholic

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62
Q

What are secondary bile acids (salts)?

A

Deoxycholic and lithocholic (dehydroxylated primary bile acids by bacteria in gut)

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63
Q

Main biliary phospholipid

A

Lecithin

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64
Q

Solubilizes cholesterol and emulsifies fats in the intestine, forming micelles, which enter enterocytes by fusing with membrane

A

Bile

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65
Q

When does jaundice occur?

A

When total bilirubin > 2.5

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66
Q

Where is jaundice first evident?

A

Under the tongue

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67
Q

What is the maximum bilirubin?

A

30: unless patient had underlying renal disease, hemolysis, or bile duct-hepatic vein fistula

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68
Q

Causes of elevated un-conjugated bilirubin

A

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

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69
Q

Causes of elevated conjugated bilirubin

A

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

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70
Q

Abnormal conjugation; mild defect in glucuronyl transferase

A

Gilbert’s disease

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71
Q

Inability to conjugate; sever deficiency of glucuronyl transferase; high unconjugated bilirubin -> life-threatening disease

A

Crigler-Najjar disease

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72
Q

Immature glucuronyl transferase; high unconjugated bilirubin

A

Physiologic jaundice of newborn

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73
Q

Deficiency in storage ability; high conjugated bilirubin

A

Rotor’s syndrome

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74
Q

Deficiency in secretion ability, high conjugated bilirbuin

A

Dubin-Johnson syndrome

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75
Q

All hepatitis viral agents can cause…

A

Acute hepatitis

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76
Q

What can cause fulminant hepatic failure in viral hepatitis?

A

Can occur with hepatitis B, D, and E (very rare with A and C)

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77
Q

Viral hepatitis: can cause chronic hepatitis and hepatoma

A

Hepatitis B, C, and D

78
Q

Consequences of hepatitis A (RNA)

A

Serious consequences uncommon

79
Q

Hepatitis B: elevated in the first 6 months; IgG then takes

A

Anti-HBc-IgM (c = core)

80
Q

Hepatitis B vaccination serum

A

Have increased anti-HBs (s=surface) antibodies only

81
Q

Hepatitis B: patient had infection with recovery and subsequent immunity

A

Increased anti-HBc and increased anti-HBs antibodies and no HBs antigens (HBsAg)

82
Q

Can have long incubation period; currently most common viral hepatitis leading to liver TXP

A

Hepatitis C (RNA)

83
Q

Cofactor for hepatitis B (worsens prognosis)

A

Hepatitis D (RNA)

84
Q

Viral hepatitis: fulminant hepatic failure in pregnancy, most often in 3rd trimester

A

Hepatitis E (RNA)

85
Q

MCC liver failure

A

Cirrhosis (palpable liver, jaundice, ascites)

86
Q

Best indicator of synthetic function in patient with cirrhosis

A

Prothrombin time (PT)

87
Q
  • 80% mortality
  • Outcome determined by the course of encephalopathy
  • Consider urgent liver TXP listing if King’s College criteria are emt
A

Acute liver failure (fulminant hepatic failure)

88
Q

King’s college criteria of poor prognostic indicators:

- Acetaminophen-induced ALF

A
  • Arterial pH 6.5, creatinine > 3.4 mg/dL (300 umol/L), grade 3/4 encephalopathy
89
Q

King’s college criteria of poor prognostic indicators:

- Non-Acetaminophen-induced ALF

A

-INR > 6.5
(or any three of the following)
- Age 40, drug toxicity or undetermined etiology, jaundice > 7 d before encephalopathy, INR > 3.5, bilirubin > 17 mg/dL (300umol/L)

90
Q

What causes hepatic encephalopathy?

A

Liver failure leads to inability to metabolize -> get buildup of ammonia, mercantanes, and false neurotransmitters

91
Q

Causes other than liver failure for encephalopathy

A

GIB, infection (SBP), electrolyte imbalances, drugs

92
Q

May need to do what in hepatic encephalopathy

A

May need to embolize previous therapeutic shunts or other major collaterals

93
Q

Treatment: hepatic encephalopathy

A
  • Lactulose

- Limit protein intake (

94
Q

Cathartic that gets rid of bacteria in the gut and acidifies colon (preventing NH3 uptake by converting it to ammonium), titrate to 2-3 stools/d

A

Lactulose

95
Q

Protein intake suggested for hepatic encephalopathy

A
96
Q

Hepatic encephalopathy: metabolized by skeletal muscle, may be of some value

A

Branched-chain amino acids

97
Q

Gets rid of ammonia-producing bacteria from gut

A

Neomycin

98
Q

Cirrhosis mechanism

A

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

99
Q

Management of albumin with paracentesis for ascites

A

Replace with albumin (1g for every 100 cc removed)

100
Q

Treatment: ascites (from hepatic/splanchnic lymph)

A

Water restriction (1-1.5 L/d), decreased NaCl (1-2 g/d), diuretics (spironolactone counteracts hyperaldosteronism seen with liver failure), paracentesis, TIPS, prophylactic antibiotics to prevent SBP (norfloxacin; used if previous SBP or current UGIB)

101
Q

Why is aldosterone elevated with liver failure?

A

Secondary to impaired hepatic metabolism and impaired GFR

102
Q

Progressive renal failure; same lab findings as preener azotemia; usually a sign of end-stage liver disease

A

Hepatorenal syndrome

103
Q

Treatment: hepatorenal syndrome

A

Stop diuretics, give volume; no good therapy other than liver TXP

104
Q

What are neurological changes seen with progressive liver failure?

A

Asterixis; sign that liver failure is progressing

105
Q

What causes postpartum liver failure with ascites?

A

From hepatic vein thrombosis; has an infectious component

106
Q

Dx / Tx: postpartum liver failure with ascites

A

Dx: SMA arteriogram with venous phase contrast

Tx: heparin and antibiotic

107
Q
  • Fever, abdominal pain, PMNs > 250 in fluid, positive cultures
  • Risk factors: prior SBP, UGIB, low-protein ascites
A

Spontaneous bacterial peritonitis

108
Q

MCC spontaneous bacterial peritonitis

A

E. coli (#1), pneumococci, streptococci

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

109
Q

Tx: spontaneous bacterial peritonitis

A

3rd-generation cephalosporins; patients usually respond within 48 hours

110
Q

How do esophageal varices bleed?

A

Bleed by rupture

111
Q

Treatment: esophageal varices

A
  • Banding and sclerotherapy (95% effective)
  • Vasopressin, octreotide
  • NGT (h/o CAD)
  • Propranolol (no good role acutely)
112
Q

Why is vasopressin good for esophageal varices?

A

Splanchnic artery constriction

113
Q

Why is octreotide good for esophageal varices?

A

Decreases portal pressure by decreasing blood flow

114
Q

Has a balloon used to control variceal bleeding; risk of rupture of the esophagus (hardly used anymore)

A

Sengstaken-Blakemore esophageal tube

115
Q

Esophageal varices: may help prevent re-bleeding; no good role acutely

A

Propranolol

116
Q

Esophageal varices: complication of sclerotherapy

A

Can get stricture from sclerotherapy; usually easily managed with dilatation

117
Q

Needed for refractory variceal bleeding

A

TIPS

118
Q

Portal hypertension: pre-sinusoidal obstruction

A

Schistosomiasis, congenital hepatic fibrosis, portal vein thrombosis (50% of portal HTN in children)

119
Q

What causes 50% of portal HTN in children?

A

Portal vein thrombosis

120
Q

Portal hypertension: sinusoidal obstruction

A

Cirrhosis

121
Q

Portal hypertension: post-sinusoidal obstruction

A

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

122
Q

Normal portal vein pressure

A
123
Q

Act as collaterals between the portal vein and the systemic venous system the lower esophagus (azygous vein)

A

Coronary veins

124
Q

Leads to esophageal variceal hemorrhage, ascites, splenomegaly, and hepatic encephalopathy

A

Portal HTN

125
Q

Can decompress portal system

A

Shunts

126
Q

Used for protracted bleeding, progression of coagulopathy, visceral hypo perfusion or refractory ascites
- Allows integrate flow

A

TIPS (transjugular intrahepatic portosystemic shunt)

127
Q

Low rate of encephalopathy; need to ligate left adrenal vein, left gonadal vein, inferior mesenteric vein, coronary vein, and pancreatic branches of splenic vein

A

Splenorenal shunt

128
Q

When do you use splenorenal shunt for hepatic encephalopathy?

A

Used only for Child’s A cirrhotics who present just with bleeding (rarely used anymore)

129
Q

When is splenorenal shunt contraindicated for hepatic encephalopathy?

A

Refractory ascites, as splenorenal can worsen ascites

130
Q

Child’s B or C with indication for shunt

A

TIPS

131
Q

Child’s A that just has bleeding as symptom

A

Consider splenorenal shunt (more durable); otherwise TIPS

132
Q

Correlates with mortality after open shunt placement

A

Child-Pugh Score

133
Q

What are the components of the Child-Pugh Score?

A

Albumin, bilirubin, encephalopathy, ascites, INR

134
Q

Mortality with shunt: Child’s A (5-6 pts)

A

2% mortality with shunt

135
Q

Mortality with shunt: Child’s B (7-9 pts)

A

10% mortality with shunt

136
Q

Mortality with shunt: Child’s C (10 pts or greater)

A

50% mortality with shunt

137
Q

Usually caused by extra-hepatic portal vein thrombosis

A

Portal HTN in children

138
Q

MCC massive hematemesis in children

A

Portal HTN in children

139
Q
  • Occlusion of hepatic veins or IVC

- RUQ pain, hepatomegaly, ascites, fulminant hepatic failure, muscle wasting, variceal bleeding

A

Budd-Chiari Syndrome

140
Q

Dx: budd-chiari syndrome

A

Angiogram with venous phase, CT angiogram; liver biopsy shows sinusoidal dilation, congestion, centrilobular congestion

141
Q

Tx: budd-chiari syndrome

A

Porta-caval shunt (needs to connect to the IVC above the obstruction)

142
Q

Can lead to isolated gastric varices without elevation of pressure in the rest of the portal system. These gastric varies can bleed.

A

Splenic vein thrombosis

143
Q

What causes splenic vein thrombosis?

A

Most often caused by pancreatitis

144
Q

Tx: Splenic vein thrombosis

A

Splenectomy if symptomatic

145
Q
  • Increased LFTs, increase in right lobe of liver, usually single
  • Symptoms: fever, chills, RUQ pain, increased WBCs, jaundice, hepatomegaly.
  • Can usually diagnose based on CT characteristics
A

Amebic liver abscess

146
Q

Where does primary infection occur in amebic liver abscess?

A

Colon - amebic colitis

147
Q

Risk factors: amebic liver abscess

A

Travel to Mexico, ETOH; fecal-oral transmission

148
Q

What is serology positive for in amebic liver abscess?

A

Entamoeba histolytica - 90% have infection

149
Q

How does ameba reach the liver to cause liver abscess?

A

Reaches liver via portal vein

150
Q

What does culture usually reveal in amebic liver abscess?

A

Cultures of abscess often sterile -> protozoa exist only in peripheral rim

151
Q

Tx: amebic liver abscess

A

Flagyl; aspiration only if refractory; surgery only if free rupture

152
Q
  • Forms cyst (hydatid cyst)
  • Positive Casoni skin test, positive serology
  • Sheep (carriers); dogs (human exposure); increase in right lobe of the liver
A

Echinococcus

153
Q

Why do you not aspirate a hydatid cyst (echinococcus)?

A

Do not aspirate -> can leak out and cause anaphylactic shock

154
Q

What does abdominal CT show in echinococcus (hydatid cyst)?

A

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

155
Q

When do you do pre op ERCP in echinococcus (hydatid cyst)?

A

Jaundice, increased LFTs or cholangitis to check for communication with the biliary system

156
Q

Treatment: echinococcus liver abscess

A

Pre-op albendazole (2 weeks) and surgical removal (intra-op can inject cyst with alcohol to kill organisms, then aspirate out); need to get all of cyst wall

157
Q

What happens if you spill cyst contents in echinococcus?

A

Anaphylactic shock

158
Q
  • Maculopapular rash, increased eosinophils
  • Sigmoid colon: primary infection, fine granulation tissue, petechiae, ulcers
  • Can cause variceal bleeding
A

Schistosomiasis

159
Q

Tx: schistosomiasis

A

Praziquantel and control of variceal bleeding

160
Q
  • account for 80% of liver abscess
  • Symptoms: fever, chills, weight loss, RUQ pain, increased LFTs/WBCs, sepsis
  • increase in right lobe; 15% mortality with sepsis
A

Pyogenic abscess

161
Q

1 organism in pyogenic liver abscess

A

E. coli (GNRs)

162
Q

What causes pyogenic abscess?

A

Most commonly secondary to contiguous infection form biliary tract
- Can occur following bacteremia from other types of infections (diverticulitis, appendicitis)

163
Q

Dx / Tx: pyogenic liver abscess

A
  • Dx: aspiration

- Tx: CT-guided drainage and antibiotics; surgical drainage for unstable condition and continued signs of sepsis

164
Q

What causes hepatic adenomas?

A

Women, steroid use, OCPs

165
Q
  • 80% are symptomatic, 20% risk of significant bleeding (rupture)
  • Can become malignant
  • More common in right lobe
  • Symptoms: pain, increased LFTs, hypotension (from rupture), palpable mass
A

Hepatic adenomas

166
Q

Dx: hepatic adenoma

A

No Kupffer cells in adenomas, thus no uptake on sulfur colloid scan (cold)
- MRI demonstrates a hypervascular tumor

167
Q

Tx: asymptomatic hepatic adenoma

A

Stop OCPs; if regression, no further therapy is needed; if no regression, patient needs resection of the tumor

168
Q

Tx: symptomatic hepatic adenoma

A

Tumor resection for bleeding and malignant risk; embolization if multiple and unresectable.

169
Q
  • Has central stellate scar that may look like cancer
  • No malignant risk; very unlikely to rupture
  • MRI / CT scan demonstrates a hypervascular tumor
A

Focal nodular hyperplasia

170
Q

Dx: focal nodular hyperplasia

A

Abdominal CT; has Kipper cells; so will take up sulfur colloid on liver scan

171
Q

Tx: focal nodular hyperplasia

A

Conservative therapy (No resection)

172
Q

Most common benign hepatic tumor

A

Hemangiomas

173
Q
  • Rupture rare; most asymptomatic; more common in women

- Avoid biopsy -> risk of hemorrhage

A

Hemangiomas

174
Q

Dx: hemangiomas

A

MRI and CT scan show peripheral to central enhancement

- Appears as hyper vascular lesion

175
Q

Tx: hemangiomas

A

Conservative unless symptomatic, then surgery +/ pre-op embolization; steroids (possible XRT) for unresectable disease

176
Q

Rare complications of hemangioma

A

Consumptive coagulopathy (Kasabach-Merritt syndrome) and CHF; these complications are usually seen in children

177
Q
  • Congenital; women, right lobe
  • Walls have a characteristic blue hue
  • Complications from these cysts are rare; most can be left alone
A

Solitary liver cysts

178
Q

Malignant liver tumors:

- metastases:primary ratio

A

20:1

179
Q

Most common cancer worldwide

A

Hepatocellular carcinoma (hepatoma)

180
Q

Risk factors for hepatocellular carcinoma

A

HepB (#1 cause worldwide), HepC, ETOH, hemochromatosis, alpha1-antitrypsin deficiency, primary sclerosing cholangitis, aflatoxins, hepatic adenoma, steroids, pesticides

181
Q

Not risk factors for hepatocellular carcinoma

A

Primary biliary cirrhosis, Wilson’s disease

182
Q

What have the best prognosis for malignant liver tumors?

A

Clear cell, lymphocyte infiltrative, and fibrolamellar types (adolescents and young adults)

183
Q

Correlates with tumor size in malignant liver tumors

A

AFP level

184
Q

5 year survival rate with resection in hepatocellular carcinoma

A

30%

185
Q

Why are few hepatic tumors resectable?

A

Secondary to cirrhosis, portohepatic involvement, or metastases

186
Q

Margins for resection in hepatocellular carcinoma

A

1 cm margins

187
Q

Where is tumor recurrence most likely after resection of hepatocellular carcinoma?

A

Tumor recurrence most likely in the liver after resection

188
Q

Risk factors: PVC, thorotrast, arsenic -> rapidly fatal

A

Hepatic sarcoma

189
Q

Management: Isolated colon carcinoma metastases to liver

A

Can resect if you leave enough liver for the patient to survive; 35% 5-year survival rate after resection for cure

190
Q

Primary liver tumors

A

Hypervascular

191
Q

Metastatic liver tumors

A

Hypovascualr

06 - absite (44 decks)

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