Liver Flashcards
The posterior edge of the liver straddles what major vessel?
IVC
What lies posterior to the liver, major vessel?
IVC
The peritoneal duplications of the liver are referred to as ligaments, the diaphragmatic peritoneal duplication are referred to as what?
coronary ligaments (whose lateral margins on right and left side are the triangular ligaments)
This is a thin membrane of anterior liver surface, connecting to the diaphragm, abdominal wall and umbilicus;
falciform ligament
This runs along the inferior edge of the falciform ligament from the umbilicus to the umbilical fissure;
ligamentum teres
What’s the ligamentum teres?
obliterated umbilical vein
What structure used to be the obliterated umbilical vein?
ligamentum teres (runs along the inferior edge of falciform ligament)
On posterior surface of left liver we have the ligamentum venosum, what’s that?
obliterated sinus venosus
How does venous drainage of the liver occur?
thru R, L, and M hepatic veins–> empty into suprahepatic IVC
The liver is covered in peritoneum except in these specific areas:
gallbladder fossa
porta hepatis
on either side of IVC on posterior aspect of liver
What is the area on the posterior liver to the right of IVC called?
bare area of the liver
In the adult liver what does the obliterated umbilical vein and ductus venosus become?
left umbilical vein—> ligamentum teres, runs in the falciform ligament
ductus venosus–> ligmentem venosum
Fetal liver plays an important role in what?
hematopoiesis
What divides the liver into right and left lobes?
Cantlie’s line (portal fissure)
Where does Cantlie’s line run thru which divides the liver into right and left lobes;
runs from the GB to left side of IVC
What segment of liver seen posteriorly embracing IVC?
segment 1 (caudate lobe)
Caudate lobe is also known as which liver segment?
1
What are the segments of the right side of the liver?
5, 6, 7, 8
What are the segments of the left side of the liver?
left medial segments; IV A, IV B
left lateral segments; II, III
What secures the liver to the diaphragm?
right and left triangular ligaments
What ligaments of liver can we dissect in an avascular plane to mobilize it for resection?
falciform, triangular, coronary ligaments, round ligaments
The hapatoduodenal ligament is AKA?
porta hepatis
What does the porta hepatis contain?
portial triad; CBD, hepatic artery, portal vein
What’s the Pringle maneuver?
clamping of the hepatoduodenal ligament which contains the CBD, portal vein and hepatic artery
What do we find deep to the porta hepatis?
foramen of winslow–> entrance into the lesser sac
this will allow complete vascular inflow of liver by clamping the porta hepatis
THe liver is separated into right and left lobes by plane from GB fossa to IVC known as;
Cantlie’s line
This liver lobes lies to the left and anterior to the IVC:
segment 1; caudate lobe
What segments make up left side of liver:
left lateral segments: II, III
left medial segments: IVa, IVb
What segments make up left side of liver?
left lateral segments: II, III
left medial segments: IVa (cephalad), IVb
What are the segments of the right lobe of liver?
R-anterior lobe; V, VIII
R-posterior lobe; VI, VII
The liver has a dual blood supply consisting of what?
hepatic artery
portal vein
What % of blood delivered to liver by hepatic artery and portal vein?
portal vein delivers 75%
hepatic artery delivers 25%
Where does hepatic artery originate from?
celiac trunk–> splenic, left gastric, common hepatic
common hepatic–> gastroduodenal, hepatic artery proper
hepatic artery proper–> R + L hepatic arteries
In 76% of cases, the hepatic artery proper divides into right and left hepatic arteries, what are some anatomic variations we commonly see?
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%)
The cystic artery feeding the GB usually arises from what artery?
right hepatic artery
What forms the portal vein?
splenic vein + SMV
IMV joins into the splenic vein
What is normal portal vein pressure?
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
What are the main hepatic veins and what do they do?
R, M, L hepatic veins
drain blood to the suprahepatic IVC and right atrium
These two hepatic veins usually form a trunk before entering into the IVC together:
left and middle hepatic veins (95% of time)
What are the connections between the portal and systemic venous system?
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
Describe the formation and course of the portal vein?
SMV joins the splenic vein posterior to neck of pancreas
the IMV joins the splenic vein (most commonly)
Where does the portal vein lie in relation to CBD and hepatic artery?
it’s more posterior to both structures
How much O2 is delivered to liver via portal vein and hepatic artery ?
50/50
Where does the hepatic artery lie in the porta hepatis?
anterior to portal vein
left of the CBD
Calot’s triangle?
cystic duct
common hepatic duct
liver edge
Difference between an accessory vs replaced vessel?
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
Common locations of accessory cystic arteries?
can originate from proper hepatic artery
gastroduodenal artery
(can run anterior to bile duct)
Within the hepatoduodenal ligament where we have the portal triad, where does the CBD lie?
anteriorly and to the right
Anatomy of the CBD:
gives off the cystic duct to the GB
becomes the common hepatic duct
splits into right and left hepatic ducts
In what segments of the liver do we find the gallbladder residing?
IV B of left lobe
V of right lobe
The intra-pancreatic distal CBD joins with this pancreatic duct to empty into the second portion of the duodenum in the major papilla;
main pancreatic duct of Wrisung
What regulates bile flow and prevents reflux of duodenal contents into the biliary tree?
sphincter of oddi
This is a biliary reservoir that lies in segments IVB and IV of liver:
GB
What’s a normal CBD diamter?
6 mm
The GB is covered by a peritoneal layer except where?
in area adhered to the liver
Parts of the gallbladder?
body
fundus
infundibulum
neck
This part of GB AKA Hartmann’s pouch;
infundibulum (proximal to GB neck)
This is the part of the GB between the infundibulum (Hartmann’s pouch) and cystic duct:
GB neck
The first part of the cystic duct is tortuous and has mucosal duplications referred to as:
folds of Heister (regulate filling and emptying of the GB)
CBD blood supply found where?
at 3 and 9 oclock positions
Innervation of the liver?
PSNS–> left vagus–> anterior hepatic branch
right bagus–> posterior hepatic branch
SNS–> greater thoracic splanchnic nerves, celiac ganglia
Bilirubin is the breakdown product of?
normal heme catabolism
Describe bilirubin metabolism:
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)
What is bile made of?
bile salts
bile pigments
cholesterol
phospholipids
How much bile i secreted daily?
approx 1.5 L (80% secreted by hepatocytes into canaliculi)
What is enterohepatic circulation?
way to reabsorb bile acids
Aside from allowing us to reabsorb bile acids, what does enterohepatic circulation do?
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
Describe enterohepatic circulation;
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
Describe bilirubin metabolism:
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)
What’s kernicterus?
bilirubin is a toxic compound
causes neonatal encephalopathy and cochlear damage when unconjugated
it needs to be bound to albumin
What is bile made of?
water electrolytes bile pigments bile salts phospholipids cholesterol (lecithins)
Two fundamental roles of bile?
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
Bile is produced by hepatocytes and secreted into the gallbladder, where it?
is concentrated by GB (absorbs water and electrolytes)
upon food entry into duodenum, it is released
liver produces approx. 1 L of bile daily
Approx. 90-90% of bile salts are absorbed where?
terminal ileum via active transport
these re-absorbed bile salts transported back to the liver via portal circulation and re-used
Hepatocellular liver injury can usually be seen by elevations in what markers?
ALT/AST
AST–> can also be found in heart, muscle kidney
ALT–> specific to liver
In alcoholic liver dx, what ratio of AST/ALT ratio do we see?
2/1
How do we measure synthetic liver fxn?
check albumin levels (produces 10 g of albumin daily)
WHy is albumin not a good marker for acute liver injury?
has a half life of 15-20 days
Aside from albumin what other tests can we use to assess synthetic liver fxn?
PT/INR
assess clotting factors, which are exclusively made in the liver
Which clotting factor is not made in the liver?
factor 7
What is PT and INR?
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
What is cholestasis and how does indirect vs direct bilirubin help our differential?
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
SOme causes of unconjugated hyperbilirubinemia?
increased bilirubin production from hemolytic disordersor resorption of hematomas
defects in hepatic uptake or conjugation of bilirubin
Some causes of conjugated hyperbilirubinemia?
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)
Where do we see ALK phos mostly?
liver
bone
What does the half life of Alk phos being 7 days mean?
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
What factors make up the Child-Pugh classification system?
bilirubin PT ascites albumin encephalopathy
A; 5-6 points
B; 7-9 points
C; 10-15 points
How much blood goes to liver?
25% of CO (1500 cc/minute)
What is jaundice?
yellowing of skin, sclera, and mucus membranes with the pigment bilirubin
Hyperbilirubinemia is manifested as jaundice when bilirubin levels are what?
> 2.5- 3 g/dl
What’s prehepatic jaundice?
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
Intrahepatic causes of jaundice involve?
inherited disorders
toxins
viruses
What is Gilbert’s syndrome?
inherited disorder where we have reduced activity of enzyme glucuronyltransferase, thus we have decreased conjugation of bilirubin to glucuronide
Is Gilbert’s syndrome benign or malignant?
BENIGN
affects 4-7% of population
have reduced enzyme activity of glucuronyltransferase
decreased conjugation of bilirubin
This genetic liver disease cause transient mild increases in unconjugated hyperbilirubinemia and jaundice during levels of stress, fasting, or illness:
Gilbert’s syndrome
**episodes are usually self limited, no tx needed
This is a rare disease found in neonates, and can result in neurotoxic sequelae from bilirubin encephalopathy
Crigler-Najjar
inherited disorder in bilirubin conjugation
These two liver disorders that disrupt the excretion of conjugated bilirubin from the liver;
Dubin-Johnson syndrome
Rotor syndrome
This imaging modality is the gold standard to identify liver lesions:
intra-operative US
can identify 20-30% more lesions that pre-op imaging
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?
most liver tumors receive their blood supply from the hepatic artery
using contrast, these tumors light up well during the arterial phase
Difference in arterial vs venous/portal phase use of CT to evaluate the liver:
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)
How does an MRI work?
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
T1 and T2 in relation to MRIs?
T1–> tells us how quickly a tissue can get magnetized
T2–> tells us how quickly it loses magnetization
This entity occurs when the rate and extent of hepatocyte damage exceeds liver’s regenerative ability;
acute liver failure
How do we define acute liver failure?
hepatic encephalopathy within 26 weeks of acute liver injury in a pt without previous hx of liver dx or portal htn
MCC of death in pts with acute liver failure?
intracranial htn due to cerebral edema
sepsis
multisystem organ failure
Causes of ALF in East vs West?
East–> viral hepatitis
West–> drugs/toxins with acetaminophen being most common
Antidote for acetaminophen toxicity, which is a leading cause of ALF?
n-acetylcysteine
replenishes glutathione
How do we dose N-acetylcysteine for acetaminophen toxicity?
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
Liver transplantation has increase 5 year survival rates in pts with ALF from what to what?
< 20% to >70%
This is the result of sustained wound healing in in response to chronic liver injury:
cirrhosis
Causes of cirrhosis?
autoimmune drug induced cholestatic viral metabolic diseases
Liver biopsy of alcoholic cirrhosis shows?
hepatocyte necrosis
Mallory bodies
neutrophil infiltration
perivenular inflammation
MCC of chronic liver dx and most common frequent indication for liver transplant in the US:
Hep C
Autoimmune causes of cirrhosis?
primary sclerosing cholangitis
primary biliary cirrhosis
autoimmune hepatitis
This is a chronic cholestatic disease of the liver assc with Crohn’s dx and UC:
PSC
With this autoimmune cause of cirrhosis we see dilated bile ducts with a beaded appearance:
PSC
In auotimmune hepatitis, biopsy will show this classic finding:
plasma cells
MCC metabolic disorder causing cirrhosis?
hereditary hemochromatosis
WHat are the genetic disorders of liver cirrhosis?
hereditary hemochromatosis
A1-anti trypsin
Wilson’s disease
Spider angioma and palmar erythema are though to be a cause of what in cirrhotic pts?
alterations in sex hormone metabolism
When do we see asterixis in pts with cirrhosis?
when they have hepatic encephalopathy
What are the mortality rates for pts with specific Child-Pugh scores?
Class A; 10 % mortality risk
Class B: 30%
Class C; 75-80%
Five variables of the Child-Pugh score:
INR albumin encephalopathy bilirubin ascites
This is a linear regression model based on objective findings for liver dx:
MELD: model for end-stage liver dx
This has been validated and used as the sole method of liver transplant allocation in US:
MELD
What MELD scores and surgical risk do we use?
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
What is normal portal venous pressure?
5-10 mmHg
with this pressure, very little blood is shunted from portal venous system to systemic circulation
What happens when we see portal venous pressure exceed 10 mmHg?
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
Best evidence for portal htn is?
hepatic vein wedge pressure > 10 mmHg
How do we get formation of esophageal varices in portal htn?
collaterals between the coronary and short gastric veins to the azygous vein–> forms esophageal varices
Clinically significant portal HTN is apparent when hepatic venous pressure gradient is > than?
10 mmHg
Causes of portal HTN?
pre-hepatic
intra-hepatic
post-hepatic
Most common cause of portal HTN in the US?
intra-hepatic —> cirrhosis
*** most significant findings of portal htn due to cirrhosis is esopheageal varcies (supplied by left gastric vein)
What causes the visible collaterals we see in the umbilical abdominal region in cirrhotic pts?
recanulization of umbilical vein
Most common cause of pre-hepatic portal HTN?
portal vein thrombosis
50% of cases of portal HTN in kids are due to ?
portal vein thrombosis
What is left sided portal htn?
isolated splenic vein thrombosis (usually due to pancreatic inflammation or neoplasm)
Why is left sided portal HTN (isolated splenic vein thrombosis) important to recognize?
can be treated by splenectomy
MCC of portal HTN in US?
alcoholic cirrhosis
What are some causes of post-hepatic portal HTN?
budd-chiarri syndrome (hepatic vein thrombosis)
constrictive pericarditis
heart failure
This is the single most life-threatening complication of portal htn;
bleeding from esophageal varices
** responsible for deaths in 1/3 of all pts w/cirrhosis
Once control of bleeding from esophageal varices is established, when is the greatest risk of rebleeding?
greatest within first few days
Mainstay of non-operative treatment for bleeding esophageal varices?
endoscopic tx
*** bleeding controlled in > 85% of pts
*** this allows for nutritional optimization, improving hepatic function, resolution of ascites before definitive treatment
What pharmacotherapy do we use for bleeding due to esophageal varices?
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)
Major advantage of using the Blakemore tube for acute esophageal variceal bleeding is?
you see immediate cessation of bleeding in > 85% of pts
Treatment of choice for esophageal bleeding that doesn’t respond to endoscopic intervention and Blakemore ballooning?
TIPS
What are some surgical procedures for esophageal variceal bleeding if endoscopic tx, balloon tx or TIPS fail?
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%
AFter a pt has bled from varices, the likelihood of repeat bleeding is?
70%
Beta-blockers as pharmacotherapy for esophagea varices?
combo of beta-blocker + long acting nitrate has shown to be more effective than variceal ligation
TIPS frequently used as definitive treatment for pts who bleed from portal htn, what’s a limitation of TIPS?
up to 50% have shunt stenosis or thrombosis within 1 yr
Aside from shunt stenosis and thrombosis, pts that have TIPS also experience what?
encephalopathy
portal venous blood flow bypasses the liver, can’t detoxify stuff as much
Which pts benefit from TIPS?
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
Beta-blockers commonly used in esophageal variceal bleeding?
non-slective b-blocker; nadolol, propranolol
In pts w/variceal bleeding, each episode of bleeding assocaited w/ what % mortality?
20-30%
Preferred pharmacological agent for initial management of of acute variceal bleeding?
octreotide
Why shouldn’t the Blakemore balloon not be used for more than 36 hrs?
usually controls bleeding in 90% of pts
can cause tissue necrosis
TIPS is a connection from where to where?
metallic stent placed between an intrahepatic branch of portal vein + hepatic vein
High rate of thormbosis of TIPS is due to?
intimal hyperplasia of metallic stent
frequent dilations or restenting are needed
Hepatic encephalopathy occurs in what % of pts after TIPS?
25-30%
What is a distal spleno-renal shunt?
connection between distal splenic vein to renal vein
splenectomy also performed
(distal splenic vein larger diameter compared to proximal, less chance of thrombosis)
TIPS is what type of shunt?
non-selective shunt
so is a spleno-renal shunt
What’s a Warren shunt?
distal spleno-renal shunt
Whats the Sugiura procedure?
extensive devascularization of the stomach and distal esophagus
along w/transection of esophagus, splenectomy, truncal vagotomy, pyloroplasty
What is Budd Chiari syndrome?
obstruction of hepatic venous outflow
Some of the most common causes of Budd Chiari syndrome?
primary myeloprolierative disorders 30-50% of cases of BCS
