Ch 31 Liver Flashcards
____ separates medial and lateral segments of left lobe and carries remnants of _____
falciform ligament; umbilical vein
2 hepatic artery variants
- RHA off SMA (20%) behind pancreas, posterolateral to CBD
2. LHA off left gastric (20%) found in gastrohepatic ligament medially
_____ carries the obliterated umbilical vein to the undersurface of the liver
ligamentum teres//extends from falciform
________ line separates right and left lobes and extends from ____ to ____
Cantlie’s line or portal fissurel drawn from middle of gallbadder fossa to IVC
L liver segments
I, II, III, IV
R liver segments
V, VI, VII, VIII
Describe location of L segments
4 medial (in center of liver)
2 and 3 lateral with 2 above 3
1 behind 4
Describe location of R segments
5, 6, 7, 8 clockwise with 5 inferomedial/anterior to 6
*think of the liver as a mitered corner
___ segment is the caudate lobe
I
___ segment is the quadrate lobe
IV/Left medial
____ covers the liver
glisson’s capsule/peritoneum
_____ is a bare area not covered’ by glisson’s capsule
area on the posterior superior surface of liver
_____ are the extensions of the coronary ligament that connect the liver to the ____ and are made of
right and left triangular; diaphragm; peritoneum
the portal triad enters which segments?
IV and V
the gallbladder lies under which segments?
IV and V
_____are liver macrophages
Kupffer cells
the portal triad includes ____ (3) and runs in the _______
cbd (lateral)
portal vein (posterior)
PHA (medial)
hepatoduodenal ligament/porta hepatis
the _____ maneuver involves clamping the portal triad //caveat?
pringle maneuver
does not stop hepatic vein bleeding or IVC bleeding
You do the pringle maneuver and then mobilize the R lobe. You see a rush of blood.
Injury to a hepatic vein likely
You do the pringle maneuver and then mobilize the R lobe. You see a hematoma.
Injury to IVC likely –> pack the liver, sternotomy, Rummel tourniquet on IVC, repair vessel
Structures in foramen of winslow
anterior - portal triad
posterior - ivc
inferior - duodenum
superior - liver
what structures form the portal vein
smv and splenic vein (no valves) come together
imv enters the splenic vein
portal veins/volume of flow/which segments
2 in liver; 2/3 of hepatic blood flow
L - segments II, III, IV
R - V, VI, VII, VIII
What is the blood supply of the caudate?
separate right and left portal and arterial blood flow; drains directly into IVC with separate veins
Arterial and venous blood supply of the liver
R/L/MHA (mha branch of LHA)
R/L/MHV (mhv join LHV 80% before going to IVC/20% directly to IVC)
L - II,II, superior IV
M - inferior IV, V
R - VI, VII, VIII
Which vessel supplies most primary and secondary liver tumors
hepatic artery
_____ drains medial aspect of R lobe directly to IVC
accessory right hepatic veins (inferior phrenic veins also dump into IVC)
AlkPhos is normally released from the _____ membrane
canalicular
Nutrient uptake in the liver takes place in the ____ membrane
sinusoidal
___ is the usual source of energy for liver
ketones; glucose stored as glycogen/excess glucose converted to fat
where are vwf and factor VIII made?
vascular epithelium (not liver)
what is the only water soluble vitamin stored in liver
b12
most common problems with hepatic resection (2)
bile leak, bleeding
which hepatocytes are most susceptible to ischemia
central lobular (acinar zone III//by central veins)
maximum amt liver that can be safely resected
75%
Hgb downstream breakdown (3)
hgb, heme, biliverdin, bilirubin)
what improves water solubility of bilirubin and what molecule is implicated?
liver conjugation to glucoronic acid with glucoronyl transferase
Where does conjugated bilirubin go?
bile –> ileum –> bacterial breakdown in terminal ileum –> conversion to urobilinogen (colorless)–>
1/2 –> converted to stercobilin –> feces
1/2 –> absorped through PV –> circulation –> kidney releases in urine as (oxidized in circulation) urobilin (yellow) –> excess conjugated bilirubin turns urine cola dark (i.e. in biliary obstruction, cbili enters circulation and peed out)
Composition of bile
85% bile salts proteins lecithin (phospholipids) cholesterol bilirubin
_____ determines final bile composition/density
Na/K ATPase mediates reabsorption of water in gallbladder
Primary bile acids
cholic and chenodeoxycholic
Secondary bile acids
deoxycholic and lithocholic (dehydroxylated primary bile acids by bacteria in gut)
What improves the water solubility of bile salts?
conjugation to taurine and glycine
___ is the main biliary phospholipid
lecithin
Jaundice occurs at bilirubin > ___ and is first evident ___
2.5; under the tongue
Maximum bilirubin is ___ unless (3 conditions)
30; renal disease, hemolysis, bile duct-hepatic vein fistula
Causes of elevated unconjugated bilirubin
deficient/reduced hepatic uptake, deficiency in glucoronyl transferase, hemolysis/prehepatic
Causes of increased conjugated bilirubin
posthepatic biliary obstruction (stones, strictures, tumor), absence of gut bacteria (e.g. from abx)
What disease? abnormal conjugation; mild defect in glucoronyl transferase
Gilbert
What disease? inability to conjugate; severe deficiency of glucoronyl transferase, high unconjugated bilirubin, life threatening
Crigler-Najjar
What disease? immature glucoronyl transferase; high unconjugated bilirubin
physiologic jaundice of newborns
What disease? deficiency in storage; high conjugated bilirubin
Rotor’s
What disease? deficiency in secretion; high conjugated bilirubin
Dubin-Johnson (black liver)
bilirubin encephalopathy is also known as
kernicterus –> common in crigler najjar prior to bililamps
Which hepatitis can cause acute hepatitis
All of them
Which hepatitis can cause fulminant hepatic failure
B,D,E (rare with A and C)
which hepatitis can cause chronic hepatitis
B,C,D
which hepatitis can cause chronic hepatoma
B,C,D
Hepatitis - RNA or DNA?
RNA except for B (DNA)
most common hepatitis leading to transplant
C
____ leads to fulminant hepatic failure in ___ trimester of pregnancy
hepatitis E in 3rd trimester
Hep B ab progression
infected: anti-HBc-IgM elevated in first six months and then IgG; HBsAg present
vaccination: elevated anti-HBs; no HBsAg
recovery: elevated anti-HBc and anti-HBs; no HBsAg
Most common cause of liver failure
cirrhosis
Best indicator of synthetic function in patient with cirrhosis
prothrombin time (PT)
mortality rate in acute liver failure and main determinant
80%; course of encephalopathy
King’s College Criteria for acetominophen induced ALF
ph6.5, creat >3.4, grade III/IV encephalopathy
King’s College Criteria for non acetominophen induced ALF
INR>6.5
OR ANY 3 of:
age40, drug tox/undetermined etiology, jaundice >7days before encephalopathy, INR>3.5, bili >17
pathophys of hepatic encephalopathy
liver failure –> inability to metabolize –> buildup of ammonia, mercatanes and false nt’s
Differential for encephalopathy
liver, gi bleed, infection (SBP), electrolyte, drugs
Tx and functions of hepatic encephalopathy
- lactulose (titrate to 2-3 stools/day) - removes gut bacteria, acidifies colon (prevents NH3 uptake by converting to ammonium)
- limit protein intake (
Mechanism of cirrhosis
hepatocyte destruction –> fibrosis and scarring of liver –> increased hepatic pressure –> portal venous congestion –> lymphatic overload –> leakage of splanchnic and hepatic lymph into peritoneum –> ascites
Albumin replacement for paracentesis
1 g for every 100 cc removed
Tx of ascites
water restriction (1-1.5 L/day)
salt restriction (1-2g/day)
diuretics (spironolactone counterats hyperaldo seen in liver failure)
paracentesis
TIPS
prophylactic abx for sbp (norfloxacin if previous SBP or current UGI bleed)
heptorenal syndrome findings and tx
progressive renal failure (sign of end stage liver disease); same lab findings as prerenal azotemia
Tx: stop diuretics, give volume, no good therapy other than liver txp
Likely cause of postpartum liver failure with ascites -DX and Tx
hepatic vein thrombosis (has an infectious component)
Dx: SMA arteriogram with venous phase contrast
Tx: heparin and abx
Findings in SBP
fever, abdominal pain
PMN>250 in fluid, positive cultures
Causes of SBP
ecoli > pneumococci >streptococci
Concern for SBP but with multiple species
–> probably bowel perforation (SBP typically monoorganism)
Tx of SBP and response time
3rd gen cephalosporin –> response within 48 hours
How do esophageal varices bleed?
rupture
Tx of varices
tx: banding and sclerotherapy (95% effective)
temporize:
1. vasopressin (splanchnic artery constriction)
2. octreotide (reduce portal pressure)
prevent rebleed: propanolol
Concern with vasopressin for treating varices
hx of CAD should not receive NTG while on vasopressin
Tx of refractory variceal bleeding
TIPS
Framework and differential for portal hypertension
pre-sinusoidal: schisto, congenital hepatic fibrosis, portal vein thrombosis (50% of phtn in kids)
sinusoidal: cirrhosis
post sinusoidal obstruction: budd chiari, constrictive pericarditis, CHF
Normal portal vein pressure
_____ act like collaterals between portal vein and systemic azygous vein
coronary veins
major cause of portal htn in children
extrahepatic portal vein thrombosis; most common cause of massive hematemesis in children
Consequences of portal hypertension
esophageal varices, ascites, splenomegaly, hepatic encephalopathy
indications for TIPS
protracted bleeding, progression of coagulopathy, visceral hypoperfusion, refractory ascites
Complication of TIPS
development of encephalopathy
Describe TIPS
transjugular intrahepatic portosystemic shunt
catheter in hepatic vein via jugular vein.
needle passed through to a major portal vein branch, dilated with angioplasty and then stent
_____ shunts can worsen ascites but reduce _____.
Splenorenal; encephalopathy
Indication for splenorenal shunt
Child’s A with bleeding as only symptom –> this shunt is more durable; otherwise tips
Indication for TIPS
Child’s B or C with shunt indication
How does Child’s score correlate with mortality
only after open shunt placement
A: 2% mortality with shunt
B: 10% mortality with shunt
C: 50% mortality with shunt
Child’s A score
5-6
Child’s B score
7-9
Child’s C score
> 9
Child’s components
PT/INR, albumin, bilirubin, ascites, encephalopathy
“pour another beer at eleven”
Dx and Tx of budd chiari syndrome
occlusion of hepatic veins or ivc
dx: angiogram with venous phase, CT angio
tx: portocaval shunt (need to connect to IVC above obstruction)
Symptoms of budd-chiari
ruq pain, hsm, ascites, fulminant hepatic failure, muscle wasting, variceal bleeding
____ can lead to isolated gastric varices without elevation of pressure in rest of the portal system
splenic vein thrombosis
*these varices can bleed
Most common cause of splenic vein thrombosis
pancreatitis
Tx of splenic vein thrombosis
splenectomy if symptomatic
Amoebic abscess: labs, location, primary infection
increased WBC, LFTs with + serology for entamoeba histolyica usually single in right lobe; primary infection = amebic colitis
risk factors for amoebic abscess
travel to mexico (fecal/oral), etoh
____% of those with + entamoeba serology have infection
90
Amebic abscess: clinical features
jaundice, hepatomegaly, fever, chills, RUQ pain
Amoebas reach the liver via ____
portal veinydatid cyst
Culture finding in amoebic abscess
culture negative –.> protozoa only exist in peripheral rim
Dx of amoebic abscess
ct
Tx amoebic abscess
flagyl, aspiration only if refractory, surgery only if free rupture
Hydatid cyst caused by ___ and tends to be in ___ lobe
echinococcus; R
Dx of hydatid cyst
+ casoni skin test, + serology, CT
CT findings in hydatid cyst
ectocyst (calcified) and endocyst (double walled cyst)
Echnococcus carrier is ____ and transmitted to humans via _____
sheep; dogs
Tx of hydatid cyst
preop albendazole (2 weeks) then intra op alcohol injection to kill organisms, aspirate, then need to get cyst wall
Why not aspirate hydatid cyst percutaneously?
spillage of cyst contents will cause anaphylactic shock
What preop mgmt for hydatid cyst?
- 2 weeks preop albendazole
2. preop ERCP for jaudnice, increased lft, cholangitis to check for biliary communication
Primary infection in schisto and findings at primary site
sigmoid colon –> fine granulation tissue, petechaie, ulcers
Tx of schisto
praziquantel and control of variceal bleeding
Clinical findings in schisto
maculopapular rash, increased eosinophils
80% of liver abscesses
pyogenic
symptoms of pyogenic abscess
fever, chills, weight loss, ruq pain, increased lfts, increased wbc, sepsis
pyogenic abscess mortality
15% with sepsis
pyogenic abscess location
increased in r lobe
most common organism in pyogenic abscess
gnr - ecoli
etiology of pyogenic abscess
typically secondary to contiguous infection from biliary tract
also from bacteremia from other infections (appendicitis, diverticulitis)
Dx of pyogenic abscess
aspiration
Tx of pyogenic abscess
ct guided drainage and antibiotics; surgical drainage for unstable condition and continued signs of sepsis
4 benign liver tumors
adenomas, focal nodular hyperplasia, hemangiomas, solitary cysts
Risk factors for hepatic adenoma
women, steroid use, ocps
Symptoms of hepatic adenoma
80% symptomatic
20% risk of significant bleeding/rupture
symptoms: pain, hemodynamic instability (from rupture) palpable mass
Malignant potential of hepatic adenoma
possible transformation
Dx of hepatic adenoma
no kupffer cells in adenomas thus no uptake on sulfur colloid scan (cold); MRI shows hypervascular tumor
Tx of hepatic adenoma
asymptomatic: stop ocps, if regression no more therapy; if no regression, resection
symptomatic: tumor resection for bleeding and malignancy risk; embolization for multiple and unresectable
location of hepatic adenoma
R lobe preference
lab findings in hepatic adenoma
elevated lfts
focal nodular hyperplasia has a _____ sign that may look like cancer
central stellate star
malignancy risk of focal nodular hyperplasia
none and unlikely to rupture
Dx focal nodular hyperplasia
ct scan; has kupffer cells so will take up sulfur colloid on scan; mri/ct shows hypervascular tumor
Tx focal nodular hyperplasia
conservative therapy
Most common benign hepatic tumor
hemangioma
hemangioma rupture risk
low; more in women
Dx hemangioma
don’t biopsy –> rupture
MRI/CT show peripheral to central enhancement of hypervascular lesion
Tx hemangioma
conservative unless symptomatic, then surgery +/- preop embolization; steroids (possible XRT) for unresectable disease
Rare complications of hemangioma (2)
consumptive coagulopathy (kasabach merritt), CHF –> both typically in children
Solitary cysts are msot common in ____ location in ____ population and are unique because ____
R lobe; women; blue hue
Tx of solitary hepatic cysts
leave alone
Metastasis:primary ratio in liver tumor
20:1
Most common cancer worldwide
hcc
risk factors for hcc
hep B (#1), hepC, etoh, hemochromatosis, alpha1antitrypsin deficiency, psc, aflatoxin, hepatic adenoma, steroid, pesticide
primary hepatic diseases that are not risk factors for hcc
wilsons and pbc
3 types of hcc with best prognosis
clear cell, lymphocyte infiltrative, fibrolamellar (adolescents and young adults)
____ correlates with tumor size in hcc
afp level
hcc survival rate with resection
30% at 5 years
why can we not resect many hepatic tumors
cirrhosis; portohepatic involvement; metastases
margin for hcc
1 cm
tumor recurrence of hcc is most likely in ____ after resection
liver
risk factors hepatic sarcoma
pvc, thorotrast, arsenic –> rapidly fatal
management of colon CA mets to liver
resect if can leave sufficient liver
survival of colon CA met resection in liver
35% @ 5 years after resection
Vascularity of malignant liver tumors
primary = hyper met = hypo
Recess of liver from which accessory bile ducts (e.g. luschka) communicate with gallbladder
Rouviere’s Sulcus aka incisura hepatis dextra, Gans incisura
