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Appendix > Liver > Flashcards

Liver Flashcards

1
Q

The posterior edge of the liver straddles what major vessel?

A

IVC

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2
Q

What lies posterior to the liver, major vessel?

A

IVC

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3
Q

The peritoneal duplications of the liver are referred to as ligaments, the diaphragmatic peritoneal duplication are referred to as what?

A

coronary ligaments (whose lateral margins on right and left side are the triangular ligaments)

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4
Q

This is a thin membrane of anterior liver surface, connecting to the diaphragm, abdominal wall and umbilicus;

A

falciform ligament

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5
Q

This runs along the inferior edge of the falciform ligament from the umbilicus to the umbilical fissure;

A

ligamentum teres

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6
Q

What’s the ligamentum teres?

A

obliterated umbilical vein

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7
Q

What structure used to be the obliterated umbilical vein?

A

ligamentum teres (runs along the inferior edge of falciform ligament)

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8
Q

On posterior surface of left liver we have the ligamentum venosum, what’s that?

A

obliterated sinus venosus

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9
Q

How does venous drainage of the liver occur?

A

thru R, L, and M hepatic veins–> empty into suprahepatic IVC

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10
Q

The liver is covered in peritoneum except in these specific areas:

A

gallbladder fossa
porta hepatis
on either side of IVC on posterior aspect of liver

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11
Q

What is the area on the posterior liver to the right of IVC called?

A

bare area of the liver

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12
Q

In the adult liver what does the obliterated umbilical vein and ductus venosus become?

A

left umbilical vein—> ligamentum teres, runs in the falciform ligament

ductus venosus–> ligmentem venosum

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13
Q

Fetal liver plays an important role in what?

A

hematopoiesis

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14
Q

What divides the liver into right and left lobes?

A

Cantlie’s line (portal fissure)

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15
Q

Where does Cantlie’s line run thru which divides the liver into right and left lobes;

A

runs from the GB to left side of IVC

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16
Q

What segment of liver seen posteriorly embracing IVC?

A

segment 1 (caudate lobe)

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17
Q

Caudate lobe is also known as which liver segment?

A

1

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18
Q

What are the segments of the right side of the liver?

A

5, 6, 7, 8

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19
Q

What are the segments of the left side of the liver?

A

left medial segments; IV A, IV B

left lateral segments; II, III

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20
Q

What secures the liver to the diaphragm?

A

right and left triangular ligaments

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21
Q

What ligaments of liver can we dissect in an avascular plane to mobilize it for resection?

A

falciform, triangular, coronary ligaments, round ligaments

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22
Q

The hapatoduodenal ligament is AKA?

A

porta hepatis

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23
Q

What does the porta hepatis contain?

A

portial triad; CBD, hepatic artery, portal vein

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24
Q

What’s the Pringle maneuver?

A

clamping of the hepatoduodenal ligament which contains the CBD, portal vein and hepatic artery

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25
Q

What do we find deep to the porta hepatis?

A

foramen of winslow–> entrance into the lesser sac

this will allow complete vascular inflow of liver by clamping the porta hepatis

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26
Q

THe liver is separated into right and left lobes by plane from GB fossa to IVC known as;

A

Cantlie’s line

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27
Q

This liver lobes lies to the left and anterior to the IVC:

A

segment 1; caudate lobe

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28
Q

What segments make up left side of liver:

A

left lateral segments: II, III

left medial segments: IVa, IVb

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29
Q

What segments make up left side of liver?

A

left lateral segments: II, III

left medial segments: IVa (cephalad), IVb

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30
Q

What are the segments of the right lobe of liver?

A

R-anterior lobe; V, VIII

R-posterior lobe; VI, VII

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31
Q

The liver has a dual blood supply consisting of what?

A

hepatic artery

portal vein

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32
Q

What % of blood delivered to liver by hepatic artery and portal vein?

A

portal vein delivers 75%

hepatic artery delivers 25%

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33
Q

Where does hepatic artery originate from?

A

celiac trunk–> splenic, left gastric, common hepatic

common hepatic–> gastroduodenal, hepatic artery proper

hepatic artery proper–> R + L hepatic arteries

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34
Q

In 76% of cases, the hepatic artery proper divides into right and left hepatic arteries, what are some anatomic variations we commonly see?

A

Replaced right hepatic artery from SMA (10-15%)

Replaced left hepatic artery from Left Gastric A (3-10%)

replaced r and l hepatic arteries (1-2%)

completely replaced common hepatic artery off of SMA (1-2%)

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35
Q

The cystic artery feeding the GB usually arises from what artery?

A

right hepatic artery

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36
Q

What forms the portal vein?

A

splenic vein + SMV

IMV joins into the splenic vein

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37
Q

What is normal portal vein pressure?

A

in a pt with normal physiology its 3-5 mmHg

in a pt with portal htn, portal vein pressure can be 20-30 mmHg because portal vein is valveless

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38
Q

What are the main hepatic veins and what do they do?

A

R, M, L hepatic veins

drain blood to the suprahepatic IVC and right atrium

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39
Q

These two hepatic veins usually form a trunk before entering into the IVC together:

A

left and middle hepatic veins (95% of time)

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40
Q

What are the connections between the portal and systemic venous system?

A

submucosal veins of proximal stomach and esophagus (via short gastric and left gastric veins)

umbilical and abdominal wall veins, recanalize via flow thru the umbilical vein in ligamentem teres and produce caput medusae

superior hemorrhoidal plexus receives portal flow from IMV and can form hemorrhoids

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41
Q

Describe the formation and course of the portal vein?

A

SMV joins the splenic vein posterior to neck of pancreas

the IMV joins the splenic vein (most commonly)

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42
Q

Where does the portal vein lie in relation to CBD and hepatic artery?

A

it’s more posterior to both structures

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43
Q

How much O2 is delivered to liver via portal vein and hepatic artery ?

A

50/50

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44
Q

Where does the hepatic artery lie in the porta hepatis?

A

anterior to portal vein

left of the CBD

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45
Q

Calot’s triangle?

A

cystic duct

common hepatic duct

liver edge

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46
Q

Difference between an accessory vs replaced vessel?

A

accessory; aberrant origin of a branch that is in addition to the normal branching pattern

replaced; aberrant origin of a branch that substitutes for the lack of a normal branch

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47
Q

Common locations of accessory cystic arteries?

A

can originate from proper hepatic artery
gastroduodenal artery

(can run anterior to bile duct)

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48
Q

Within the hepatoduodenal ligament where we have the portal triad, where does the CBD lie?

A

anteriorly and to the right

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49
Q

Anatomy of the CBD:

A

gives off the cystic duct to the GB

becomes the common hepatic duct

splits into right and left hepatic ducts

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50
Q

In what segments of the liver do we find the gallbladder residing?

A

IV B of left lobe

V of right lobe

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51
Q

The intra-pancreatic distal CBD joins with this pancreatic duct to empty into the second portion of the duodenum in the major papilla;

A

main pancreatic duct of Wrisung

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52
Q

What regulates bile flow and prevents reflux of duodenal contents into the biliary tree?

A

sphincter of oddi

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53
Q

This is a biliary reservoir that lies in segments IVB and IV of liver:

A

GB

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54
Q

What’s a normal CBD diamter?

A

6 mm

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55
Q

The GB is covered by a peritoneal layer except where?

A

in area adhered to the liver

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56
Q

Parts of the gallbladder?

A

body
fundus
infundibulum
neck

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57
Q

This part of GB AKA Hartmann’s pouch;

A

infundibulum (proximal to GB neck)

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58
Q

This is the part of the GB between the infundibulum (Hartmann’s pouch) and cystic duct:

A

GB neck

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59
Q

The first part of the cystic duct is tortuous and has mucosal duplications referred to as:

A

folds of Heister (regulate filling and emptying of the GB)

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60
Q

CBD blood supply found where?

A

at 3 and 9 oclock positions

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61
Q

Innervation of the liver?

A

PSNS–> left vagus–> anterior hepatic branch

right bagus–> posterior hepatic branch

SNS–> greater thoracic splanchnic nerves, celiac ganglia

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62
Q

Bilirubin is the breakdown product of?

A

normal heme catabolism

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63
Q

Describe bilirubin metabolism:

A

heme catabolism–> produces bilirubin
carried by albumin to the liver

in the liver conjugated by glucuronyl transferase to make it water soluble

majority of conjugated bilirubin excreted as waste in the intestine (intestinal mucosa is impermeable to conjugated bilirubin)

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64
Q

What is bile made of?

A

bile salts
bile pigments
cholesterol
phospholipids

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65
Q

How much bile i secreted daily?

A

approx 1.5 L (80% secreted by hepatocytes into canaliculi)

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66
Q

What is enterohepatic circulation?

A

way to reabsorb bile acids

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67
Q

Aside from allowing us to reabsorb bile acids, what does enterohepatic circulation do?

A

circulation of bile is the major way body gets rid of excess cholesterol

b/c cholesterol is consumed during production of bile salts and is excreted in feces

bile salts also play a role in absorption of ADEK vitamins

68
Q

Describe enterohepatic circulation;

A

bile salts made in liver (cholix acid + chenodeoxycholic acid)

these bile salts get conjugated to taurine and glycine in the liver

these conjugated bile acids then get secreted in the gut

gut bacteria secondarily conjugate them; become deoxycholic and lithocholic acid

bile acids then get reabsorbed passively in jejunum and actively in ileum and re-enter portal venous sytem

90% get reabsorbed by hepatocytes

69
Q

Describe bilirubin metabolism:

A

senscent RBCs break down–> release hem

heme–> biliverdin (by heme oxygenase)
biliverdin–> bilirubin (biliverdin reducatse)
circulating bilirubin bound to albumin –> sent to liver

inside hepatocytes bilirubin conjugated to glucuronic acid

conjugated bilirubin then secreted with bile into GI
in the GI, bilirubin deconjugated by gut bacteria into urobilinogen

small % of urobilinogens excreted in urine and feces (yellow and brown color of stool)

70
Q

What’s kernicterus?

A

bilirubin is a toxic compound
causes neonatal encephalopathy and cochlear damage when unconjugated

it needs to be bound to albumin

71
Q

What is bile made of?

A 
water
electrolytes
bile pigments
bile salts
phospholipids
cholesterol (lecithins)
72
Q

Two fundamental roles of bile?

A

help in digestion and absorption of lipids, ADEK vitamins

help to eliminate waste products like bilirubin + cholesterol by incorporation into bile and excretion in fees

73
Q

Bile is produced by hepatocytes and secreted into the gallbladder, where it?

A

is concentrated by GB (absorbs water and electrolytes)

upon food entry into duodenum, it is released

liver produces approx. 1 L of bile daily

74
Q

Approx. 90-90% of bile salts are absorbed where?

A

terminal ileum via active transport

these re-absorbed bile salts transported back to the liver via portal circulation and re-used

75
Q

Hepatocellular liver injury can usually be seen by elevations in what markers?

A

ALT/AST

AST–> can also be found in heart, muscle kidney
ALT–> specific to liver

76
Q

In alcoholic liver dx, what ratio of AST/ALT ratio do we see?

A

2/1

77
Q

How do we measure synthetic liver fxn?

A

check albumin levels (produces 10 g of albumin daily)

78
Q

WHy is albumin not a good marker for acute liver injury?

A

has a half life of 15-20 days

79
Q

Aside from albumin what other tests can we use to assess synthetic liver fxn?

A

PT/INR

assess clotting factors, which are exclusively made in the liver

80
Q

Which clotting factor is not made in the liver?

A

factor 7

81
Q

What is PT and INR?

A

PT measures the conversion time it takes to go from prothrombin to thrombin

to standardize the PT among laboratories the INR was developed, it;s the ratio of patients PT to control PT

82
Q

What is cholestasis and how does indirect vs direct bilirubin help our differential?

A

cholestasis is when bile flow from liver to duodenum is impaired (causes can be intra-hepatic vs extra-hepatic)

elevated indirect bilirubin (unconjugated)–> usually signifies intrahepatic cholestasis

elevated direct bilirubin (conjugated)–> signifies extrahepatic cholestasis

83
Q

SOme causes of unconjugated hyperbilirubinemia?

A

increased bilirubin production from hemolytic disordersor resorption of hematomas

defects in hepatic uptake or conjugation of bilirubin

84
Q

Some causes of conjugated hyperbilirubinemia?

A

can be seen in inherited disorders of extrahepatic excretion

or seen in extrahepatic obstruction

(conjugated bilirubin that can’t be excreted in accumulated in hepatocytes, which leads to secretion into systemic circulation)

85
Q

Where do we see ALK phos mostly?

A

liver

bone

86
Q

What does the half life of Alk phos being 7 days mean?

A

in cases of biliary obstruction, ALK phos levels can be elevated

it can take 7 days for levels to normalize even after resolution of the biliary obstruction

87
Q

What factors make up the Child-Pugh classification system?

A 
bilirubin
PT
ascites
albumin
encephalopathy

A; 5-6 points
B; 7-9 points
C; 10-15 points

88
Q

How much blood goes to liver?

A

25% of CO (1500 cc/minute)

89
Q

What is jaundice?

A

yellowing of skin, sclera, and mucus membranes with the pigment bilirubin

90
Q

Hyperbilirubinemia is manifested as jaundice when bilirubin levels are what?

A

> 2.5- 3 g/dl

91
Q

What’s prehepatic jaundice?

A

hyperbilirubinemia as a result of a process that interferes with conjugation of bilirubin in the hepatocytes

usually due to excess heme production–> overwhelms liver’s conjugation apparatus

  • ** acquired genetic hemoglobinopathies
  • ** poor nutritional status, no albumin to carry bilirubin to the liver as seen in burn pts
92
Q

Intrahepatic causes of jaundice involve?

A

inherited disorders
toxins
viruses

93
Q

What is Gilbert’s syndrome?

A

inherited disorder where we have reduced activity of enzyme glucuronyltransferase, thus we have decreased conjugation of bilirubin to glucuronide

94
Q

Is Gilbert’s syndrome benign or malignant?

A

BENIGN

affects 4-7% of population

have reduced enzyme activity of glucuronyltransferase

decreased conjugation of bilirubin

95
Q

This genetic liver disease cause transient mild increases in unconjugated hyperbilirubinemia and jaundice during levels of stress, fasting, or illness:

A

Gilbert’s syndrome

**episodes are usually self limited, no tx needed

96
Q

This is a rare disease found in neonates, and can result in neurotoxic sequelae from bilirubin encephalopathy

A

Crigler-Najjar

inherited disorder in bilirubin conjugation

97
Q

These two liver disorders that disrupt the excretion of conjugated bilirubin from the liver;

A

Dubin-Johnson syndrome

Rotor syndrome

98
Q

This imaging modality is the gold standard to identify liver lesions:

A

intra-operative US

can identify 20-30% more lesions that pre-op imaging

99
Q

THe liver has a dual blood supply, 75% from portal vein and 25% from hepatic artery, how does this help us see liver tumors on CT imaging?

A

most liver tumors receive their blood supply from the hepatic artery

using contrast, these tumors light up well during the arterial phase

100
Q

Difference in arterial vs venous/portal phase use of CT to evaluate the liver:

A

arterial phase usually seen in 20-30 seconds after IV contrast given —> good for tumors

venous/portal phase usually seen 60-70 seconds after IV contrast –> good for normal liver parenchyma (most of liver receives most of blood supply from portal vein)

101
Q

How does an MRI work?

A

creates a powerful magnetic field that aligns the H atoms in the body

radio waves are used to alter the alignment of this magnetization

different tissues absorb and release radio waves at different rates—> creates a picture

102
Q

T1 and T2 in relation to MRIs?

A

T1–> tells us how quickly a tissue can get magnetized

T2–> tells us how quickly it loses magnetization

103
Q

This entity occurs when the rate and extent of hepatocyte damage exceeds liver’s regenerative ability;

A

acute liver failure

104
Q

How do we define acute liver failure?

A

hepatic encephalopathy within 26 weeks of acute liver injury in a pt without previous hx of liver dx or portal htn

105
Q

MCC of death in pts with acute liver failure?

A

intracranial htn due to cerebral edema

sepsis

multisystem organ failure

106
Q

Causes of ALF in East vs West?

A

East–> viral hepatitis

West–> drugs/toxins with acetaminophen being most common

107
Q

Antidote for acetaminophen toxicity, which is a leading cause of ALF?

A

n-acetylcysteine

replenishes glutathione

108
Q

How do we dose N-acetylcysteine for acetaminophen toxicity?

A

PO 140 mg/kg initial dose then 70 mg/kg every 4 hrs for 17 doses

IV 140 mg/kg loading dosethen 50 mg/kg every 4 hrs for 12 doses

109
Q

Liver transplantation has increase 5 year survival rates in pts with ALF from what to what?

A

< 20% to >70%

110
Q

This is the result of sustained wound healing in in response to chronic liver injury:

A

cirrhosis

111
Q

Causes of cirrhosis?

A 
autoimmune
drug induced
cholestatic
viral
metabolic diseases
112
Q

Liver biopsy of alcoholic cirrhosis shows?

A

hepatocyte necrosis
Mallory bodies
neutrophil infiltration
perivenular inflammation

113
Q

MCC of chronic liver dx and most common frequent indication for liver transplant in the US:

A

Hep C

114
Q

Autoimmune causes of cirrhosis?

A

primary sclerosing cholangitis
primary biliary cirrhosis
autoimmune hepatitis

115
Q

This is a chronic cholestatic disease of the liver assc with Crohn’s dx and UC:

A

PSC

116
Q

With this autoimmune cause of cirrhosis we see dilated bile ducts with a beaded appearance:

A

PSC

117
Q

In auotimmune hepatitis, biopsy will show this classic finding:

A

plasma cells

118
Q

MCC metabolic disorder causing cirrhosis?

A

hereditary hemochromatosis

119
Q

WHat are the genetic disorders of liver cirrhosis?

A

hereditary hemochromatosis
A1-anti trypsin
Wilson’s disease

120
Q

Spider angioma and palmar erythema are though to be a cause of what in cirrhotic pts?

A

alterations in sex hormone metabolism

121
Q

When do we see asterixis in pts with cirrhosis?

A

when they have hepatic encephalopathy

122
Q

What are the mortality rates for pts with specific Child-Pugh scores?

A

Class A; 10 % mortality risk
Class B: 30%
Class C; 75-80%

123
Q

Five variables of the Child-Pugh score:

A 
INR
albumin
encephalopathy
bilirubin 
ascites
124
Q

This is a linear regression model based on objective findings for liver dx:

A

MELD: model for end-stage liver dx

125
Q

This has been validated and used as the sole method of liver transplant allocation in US:

A

MELD

126
Q

What MELD scores and surgical risk do we use?

A

pts with MELDs less than 10; safe to proceed w/surg

pts w/ MELD 10-15; surgery w/caution

pts w/ MELD >15; should not undergo elective procedures

127
Q

What is normal portal venous pressure?

A

5-10 mmHg

with this pressure, very little blood is shunted from portal venous system to systemic circulation

128
Q

What happens when we see portal venous pressure exceed 10 mmHg?

A

as portal venous pressure increase
collaterals between the venous and systemic circulation will dilate
large amount of blood is shunted around the liver to the systemic circulation

129
Q

Best evidence for portal htn is?

A

hepatic vein wedge pressure > 10 mmHg

130
Q

How do we get formation of esophageal varices in portal htn?

A

collaterals between the coronary and short gastric veins to the azygous vein–> forms esophageal varices

131
Q

Clinically significant portal HTN is apparent when hepatic venous pressure gradient is > than?

A

10 mmHg

132
Q

Causes of portal HTN?

A

pre-hepatic
intra-hepatic
post-hepatic

133
Q

Most common cause of portal HTN in the US?

A

intra-hepatic —> cirrhosis

*** most significant findings of portal htn due to cirrhosis is esopheageal varcies (supplied by left gastric vein)

134
Q

What causes the visible collaterals we see in the umbilical abdominal region in cirrhotic pts?

A

recanulization of umbilical vein

135
Q

Most common cause of pre-hepatic portal HTN?

A

portal vein thrombosis

136
Q

50% of cases of portal HTN in kids are due to ?

A

portal vein thrombosis

137
Q

What is left sided portal htn?

A

isolated splenic vein thrombosis (usually due to pancreatic inflammation or neoplasm)

138
Q

Why is left sided portal HTN (isolated splenic vein thrombosis) important to recognize?

A

can be treated by splenectomy

139
Q

MCC of portal HTN in US?

A

alcoholic cirrhosis

140
Q

What are some causes of post-hepatic portal HTN?

A

budd-chiarri syndrome (hepatic vein thrombosis)
constrictive pericarditis
heart failure

141
Q

This is the single most life-threatening complication of portal htn;

A

bleeding from esophageal varices

** responsible for deaths in 1/3 of all pts w/cirrhosis

142
Q

Once control of bleeding from esophageal varices is established, when is the greatest risk of rebleeding?

A

greatest within first few days

143
Q

Mainstay of non-operative treatment for bleeding esophageal varices?

A

endoscopic tx

*** bleeding controlled in > 85% of pts

*** this allows for nutritional optimization, improving hepatic function, resolution of ascites before definitive treatment

144
Q

What pharmacotherapy do we use for bleeding due to esophageal varices?

A

initiate abx
somatostatin/ocreotide

in severe cases of bleeding, vasopressin can be used to constrict mesenteric blood flow (nitroglycerin should be given simultaneously to avoid other systemic effects)

145
Q

Major advantage of using the Blakemore tube for acute esophageal variceal bleeding is?

A

you see immediate cessation of bleeding in > 85% of pts

146
Q

Treatment of choice for esophageal bleeding that doesn’t respond to endoscopic intervention and Blakemore ballooning?

A

TIPS

147
Q

What are some surgical procedures for esophageal variceal bleeding if endoscopic tx, balloon tx or TIPS fail?

A

esophageal transection w/stapling device

can do a portocaval shunt

can do a distal spleno-renal shunt

***regardless, in emergency surgery operative mortality is 25%

148
Q

AFter a pt has bled from varices, the likelihood of repeat bleeding is?

A

70%

149
Q

Beta-blockers as pharmacotherapy for esophagea varices?

A

combo of beta-blocker + long acting nitrate has shown to be more effective than variceal ligation

150
Q

TIPS frequently used as definitive treatment for pts who bleed from portal htn, what’s a limitation of TIPS?

A

up to 50% have shunt stenosis or thrombosis within 1 yr

151
Q

Aside from shunt stenosis and thrombosis, pts that have TIPS also experience what?

A

encephalopathy

portal venous blood flow bypasses the liver, can’t detoxify stuff as much

152
Q

Which pts benefit from TIPS?

A

pt’s who need short term treatment of bleeding esophageal varices who will eventually get a transplant

it’s a segway to a transplant

also pts who have advanced liver function decompensation who won’t live long enough for TIPS to malfunction

153
Q

Beta-blockers commonly used in esophageal variceal bleeding?

A

non-slective b-blocker; nadolol, propranolol

154
Q

In pts w/variceal bleeding, each episode of bleeding assocaited w/ what % mortality?

A

20-30%

155
Q

Preferred pharmacological agent for initial management of of acute variceal bleeding?

A

octreotide

156
Q

Why shouldn’t the Blakemore balloon not be used for more than 36 hrs?

A

usually controls bleeding in 90% of pts

can cause tissue necrosis

157
Q

TIPS is a connection from where to where?

A

metallic stent placed between an intrahepatic branch of portal vein + hepatic vein

158
Q

High rate of thormbosis of TIPS is due to?

A

intimal hyperplasia of metallic stent

frequent dilations or restenting are needed

159
Q

Hepatic encephalopathy occurs in what % of pts after TIPS?

A

25-30%

160
Q

What is a distal spleno-renal shunt?

A

connection between distal splenic vein to renal vein

splenectomy also performed

(distal splenic vein larger diameter compared to proximal, less chance of thrombosis)

161
Q

TIPS is what type of shunt?

A

non-selective shunt

so is a spleno-renal shunt

162
Q

What’s a Warren shunt?

A

distal spleno-renal shunt

163
Q

Whats the Sugiura procedure?

A

extensive devascularization of the stomach and distal esophagus

along w/transection of esophagus, splenectomy, truncal vagotomy, pyloroplasty

164
Q

What is Budd Chiari syndrome?

A

obstruction of hepatic venous outflow

165
Q

Some of the most common causes of Budd Chiari syndrome?

A

primary myeloprolierative disorders 30-50% of cases of BCS

Appendix (39 decks)

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