CHAPTER 31- LIVER.txt

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CHAPTER 31- LIVER.txt
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  1. What are the hepatic artery variants?
    1) Right hepatic artery off superior mesenteric artery (#1 hepatic artery variant; 20%) courses behind pancreas, posterolateral to common bile duct.

    2) Left hepatic artery off left gastric artery (20%)- found in gastrohepatic ligament medially

    3) Common hepatic artery- most common variant is off SMA (2%)
  2. Describe the falciform ligament:
    separates the medial and lateral segments of the left lobe; attaches liver to anterior abdominal wall; extends to umbilicus and carries remnant of the umbilical vein.
  3. Describe Ligamentum teres
    carries the obliterated umbilical vein to the undersurface of the liver; extends from the falciform ligament
  4. What line separates the left and right lobes of the liver?
    Line drawn from the middle of the gallbladder fossa to IVC (portal fissue or cantalies line) separates the right and left lobes
  5. Describe the segments of the liver
  6. What is Glisson's capsule:
    peritoneum that covers liver
  7. What is the bare area?
    area on the posterior-superior surface of the liver not covered by Glisson's capsule
  8. What are the triangular ligaments-
    lateral and medial extensions of the coronary ligament on the posterior surface of the liver; made up of peritoneum.
  9. Where does the portal triad enter the liver (what segments)?
    IV and V
  10. Where does the gallbladder lie (under which segments)?
    IV and V
  11. What are kupffer cells?
    Liver macrophages
  12. What is the hepatoduodenal ligament-
    where bile duct, portal vein and hepatic artery meet (portal trial)
  13. What is the portal triad?
    • 1. Portal vein posteriorly
    • 2. Common bile duct laterally
    • 3. Hepatic artery medially
  14. What is the pringle maneuver
    porta hepatis clamping; will not stop hepatic vein bleeding.
  15. What is the foramen of winslow?
    • Anterior- portal triad
    • Posterior- IVC
    • Inferior- duodenum
    • Superior- liver
  16. Portal Vein:
    • 1) Forms from superior mesenteric vein joining splenic vein (no valves)
    • 2) Inferior mesenteric vein- enters splenic vein
    • 3) Portal veins- 2 in liver, 2/3 of hepatic blood flow:
    • Left- 2, 3, 4
    • Right- 5, 6, 7, 8
  17. Hepatic artery supply:
    • Right
    • Left
    • Middle (middle hepatic artery MC a branch off the left hepatic artery)

    (follows hepatic vein system)
  18. What supplies most primary and secondary tumors with blood?
    Most primary and secondary tumors of the liver are supplied by the hepatic artery
  19. What are the hepatic veins, what do they supply?
    3 hepatic veins:

    • Left- II, III, and superior IV
    • Middle- IV and V
    • Right- VI, VII, VIII
  20. What is a variation of the middle hepatic vein?
    Middle hepatic vein joins left hepatic vein in 80% before going into IVC; over 20% go directly into IVC.
  21. What do the accessory right hepatic veins drain?
    drain medial aspect of right lobe directly into IVC
  22. Where do inferior phrenic veins drain to?
    directly to IVC
  23. What is the blood supply of the caudate lobe?
    receives separate right and left portal and arterial blood flow; drains directly into IVC via separate hepatic veins.
  24. Where is alkaline phosphatase normally located?
    Canalicular membrane
  25. Where does nutrient uptake occur?
    sinusoidal membrane
  26. Ketones:
    usual energy source for liver

    glucose is converted to glycogen and stored

    excess glucose converted to fat
  27. Where is urea synthesized?
    liver
  28. What is not made in the liver?
    • 1. vWF
    • 2. factor VIII

    made in endothelium
  29. What kinds of vitamins does the liver store?
    fat soluble vitamins
  30. What is the only water soluble vitamin that gets stored in the liver?
    B12
  31. What are the most common problems with hepatic resection?
    bleeding and bile leak
  32. Which hepatocytes are most sensitive to ischemia?
    central lobular (acinar zone III)
  33. How much of the liver can be safetly resected?
    75%
  34. Bilirubin:
    • 1) Breakdown product of hemoglobin (Hgb->heme->biliverdin-> bilirubin)
    • 2) Conjugated to glucuronic acid (glucuronyl transferase) in the liver--> improves water solubility
    • 3) Cojugated bilirubin actively secreted into bile
    • 4) Urobilinogen
    • - breakdown of bilirubin by bacteria in the terminal ileum
    • - is reabsorbed in the blood, and released in the urine
    • - excess urobilinogen turns urine dark like cola
  35. Bile:
    • 1) contains
    • 1- bile salts (85%)
    • 2- proteins
    • 3- phospholipids (lecithin)
    • 4- cholesterol
    • 5- bilirubin

    2) Final bile composition determined by active (Na/K ATPase) reabsorption of water in gallbladder

    3) Cholesterol- used to make bile acids

    • 4) Bile acids conjugated to taurine or glycine (improves water solubility)
    • - Primary bile acids- cholic and chenodeoxycholic
    • - Secondary bile acids- deoxycholic and lithocholic (dehydroxylated primary bile acids by bacteria in gut)

    • 5) Lecithin
    • - main biliary phospholipid; solubilizes cholesterol and emulsifies fats in the intestine
  36. Jaundice
    • 1) occurs when bilirubin >2.5; 1st evident under the tounge
    • 2) maximum bilirubin is 30 unless patient has underlying:
    • - renal disease
    • - hemolysis
    • - bile duct-hepatic vein fistula

    3) Unconjugated bilirubin- prehepatic causes (hemolysis); hepatic deficiencies of uptake or conjugation

    4) Conjugated bilirubin- secretion defects into bile ducts; excretion defects into GI tract (stones, stricture, tumor)
  37. Describe each of these syndromes:
    1) Gilbert's disease
    2) Crigler-Najjar disease
    3) Physiologic Jaundice of the newborn
    4) Rotor's syndrome
    5) Dubin-Johnson syndrome
    1) Gilbert's disease- abnormal uptake- mildly high unconjugated bilirubin

    2) Crigler-Najjar disease- inability to conjugate; deficiency of glucuronyl transferase; high unconjugated bilirubin--> life-threatening disease

    3) Physiologic Jaundice of the newborn- immature glucuronyl transferase; high unconjugated bilirubin

    4) Rotor's syndrome- deficiency in storage ability; high conjugated bilirubin

    5) Dubin-Johnson syndrome- deficiency in secretion ability; high conjugated bilirubin
  38. Viral Hepatitis:
    1) all hepatitis viral agents can cause acute hepatitis and fulminant hepatic failure

    2) Hepatitis B, C, D can cause chronic hepatitis and hepatoma

    3) Hepatitis A (RNA)- serious consequences uncommon

    • 4) Hepatitis B (DNA)
    • - Infection IgM antibody dominates 1st 6 months
    • * Anti-HBc rises 10-12 wks after infection
    • * Anti-HBe rises 12-14 wks after infection
    • * Anti-HBs rises 14-16 wks after infection
    • - Anti HBc IgM is elevated in the first 6 months; then IgG takes over
    • - Vaccination- have increased anti-HBs antibodies only
    • - Increased anti-HBc and increased anti-HBs antibodies and no HBs antigens --> patient had infection with recovery and subsequent immunity

    5) Hepatitis C (RNA)- can have long incubation period; currently most common viral hepatitis leading to liver TXP

    6) Hepatitis D (RNA)- cofactor for hepatitis B

    7) Hepatitis E (RNA)- fulminant hepatic failure in pregnancy, most often in 3rd trimester
  39. Whats the most common cause of liver failure?
    cirrhosis
  40. Whats the best indicator of synthetic function in patient with cirrhosis?
    Prothrombin time (PT)
  41. Whats the mortality rate of acute fulminant hepatic failure?
    • 80%
    • - outcome determined by the course of encephalopathy
  42. Hepatic encephalopathy
    • 1) Liver failure leads to inability to metabolize
    • Build up of:
    • 1- ammonia
    • 2- mercatanes
    • 3- methane thiols
    • 4- false neurotransmitters

    • 2) Cases other than liver failure for encephalopathy-
    • 1- GI bleedings
    • 2- infection (SBP)
    • 3- electrolyte imbalances
    • 4- drugs

    3) May need to embolize previous therapeutic shunts or embolize other major collaterals

    • 4) Tx: lactulose- 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/day
    • 1-limit protein intake (70g/day)
    • 2-branched chain amino acids- metabolized by skeletal muscle, may be of some value
    • 3- no antibiotics unless for specific infection
    • 4-neomycin may help
    • 5- dopamine receptor agonists (L-dopa and bromocriptine) may help
    • 6-tap ascites to rule out SBP
    • 7-guaiac stools and place NGT to r/o bleed

    5) Cirrhosis mechanism- hepatocyte destruction->fibrosis and scarring of liver-> inc hepatic pressure-> portal venous congestion-> lymphatic overload->leakage of splanchnic and hepatic lymph into peritoneum-> ascities

    6) paracentesis for ascities- replace w/albumin (1g for every 100cc removed)

    • 7) Ascities- from hepatic and splanchnic lymph
    • Tx:
    • 1- decrease NaCl
    • 2- diuretics (spironolactone counteracts hyperaldosteronism often seen with liver failure)
    • 3- paracentesis
    • 4- TIPS
    • 5- peritoneovenous shunts (Denver, LeVeen shunt-> complications include DIC)
    • 6- prophylactic abx to prevent spontaneous bacterial peritonitis (cipro 750mg/wk)
    • 7- water restriction

    8) Increased aldosterone- secondary to impaired hepatic metabolism and impaired GFR

    9) Hepatorenal syndrome- same appearance as prerenal azotemia

    10) Neurological changes- asterixes; sign that liver failure is progressing

    11) Peritoneovenous shunts (Denver, LeVeen)- shunt ascities into venous system; can get DIC complications

    • 12) Postpartum liver failure with ascities- hepatic vein thrombosis
    • Dx: SMA arteriogram with venous phase contrast
  43. Spontaneous bacterial peritonitis:
    • 1) Symptoms
    • 1- Fever
    • 2- abdominal pain
    • 3-PMNs >250 in fluid
    • 4- positive cultures

    • 2) Bugs
    • 1- E.Coli (#1)
    • 2-pneumococci
    • 3- streptococci

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

    • 4) Risk Factors
    • 1- prior SBP
    • 2- variceal hemorrhage
    • 3- low-protein ascites
    • 4- nephrotic syndrome
    • 5- SLE in children

    5) Tx: 3rd generation cephalosporins; patients usually respond within 48hrs
  44. Esophageal Varices
    1) Bleed by rupture

    • 2) Tx:
    • 1-sclerotherapy (90% effective at treating)
    • 2-vassopressin (splanchnic artery constriction)
    • 3-octreotide (decreased portal pressure by decreasing blood flow)
    • 4- Patients with CAD should receive nitroglycerin while on vasopressin
    • 5- Sengstaken-Blakemore (S-B) tube- used to control variceal bleeding, risk of rupture of the esophagus (hardly used anymore)
    • 6- correct coags/blood transfusion

    3) Propranolol- may help prevent rebleeding; no good role acutely

    4) Can get later strictures from sclerotherapy; usually easily managed with dilatation

    5) TIPS needed for refractory variceal bleeding

    6) bleeding varices have 33% mortality rate with 1st episode

    7) 50% will rebleed; 50% mortality with each subsequent bleeding episode
  45. Veins of Sappey
    drain portal blood through the bare areas of the diaphragm and through the paraumbilical vein collaterals to the umbilicus.
  46. Veins of Retzius
    form in the retroperitoneum and shunt portal blood from the bowel and other organs to the vena cava.
  47. Portal Hypertension
    • 1. Presinusoidal obstruction-
    • 1- schistosomiasis
    • 2- congenital hepatic fibrosis
    • 3- portal vein thrombosis
    • (50% of portal HTN in children)

    • 2. Sinusoidal obstruction
    • -cirrhosis

    • 3. Postsinusoidal obstruction
    • 1- Budd-Chiari syndome (hepatic vein occlusive disease)
    • 2- constrictive pericarditis
    • 3- CHF

    • Normal portal vein pressure < 12mmHg
  48. Coronary Veins
    act as collaterals between the portal vein and the systemic venous system of the lower esophagus
  49. What does portal HTN lead to:
    • 1. esophageal variceal hemorrhage
    • 2. ascites
    • 3. splenomegaly
    • 4. hepatic encephalopathy
  50. What can shunts do?
    shunts can decompress portal system
  51. TIPS
    • used for:
    • 1. protracted bleeding
    • 2. progression of coagulopathy
    • 3. visceral hypoperfusion
    • 4. refractory ascites

    • *allows antegrade flow
    • *Risk- development of encephalopathy

    TIPS (Transjugular intrahepatic portosystemic shunt)- a catheter is passed into the hepatic vein via the jugular vein. A needle, inserted through the catheter is passed from the hepatic vein through the liver tissue into a major portal vein branch. This is followed by the placement of a guidewire and withdrawal of the needle. The liver tract is dilated with an angioplasty ballon catheter and the tract is kept open after deployment of an expandable metal stent.
  52. Splenorenal shunt
    1. low rate of encephalopathy

    • 2. Need to ligate:
    • 1- left adrenal vein
    • 2- left gonadal vein
    • 3- inferior mesenteric vein
    • 4- coronary vein
    • 5- pancreatic branches of splenic vein

    • * Used only for Child's A cirrhotics who present just with bleeds (rarely used anymore)
    • * Contraindicated in patients with refractory ascites as splenorenal shunts can worsen ascities
    • * Child's B or C with indications for shunt --> TIPS
    • * Child's A that just has bleeding as symptom- consider splenorenal shunt (more durable); otherwise TIPS
    • * Child's class correlates with mortality after shunt
  53. Distal splenorenal Warren Shunt
    The splenic vein is diveded near its junction with the superior mesenteric vein.

    The distal end of the splenic vein is anastomosed to the renal vein.

    Varices are selectively decompressed through the stomach and short gastric veins into the splenic vein and then into the vena cava through the renal vein.

    Portal hypertension is maintained in the portal and superior mesenteric veins to provide enough pressure to drive portal blood through the diseased liver.
  54. Portal HTN in children:
    1. Usually caused by extrahepatic thrombosis of the portal vein

    2. Most common cause of massive hematemesis in children
  55. Budd-Chiari Syndrome
    • 1. occlusion of hepatic veins and IVC
    • 2. RUQ pain, hepatosplenomegaly, ascites, fulminant hepatic failure, muscle wasting, variceal bleeding
    • 3. Dx: angio, CT scan; liver biopsy shows sinusoidal dilatation, congestion, centrilobular congestion
    • 4. Tx: portacaval shunt (needs to connect to the IVC above the obstruction)
  56. Splenic Vein Thrombosis
    • 1. can lead to isolated gastric varices without elevation of pressure in the rest of the portal system
    • 2. These gastric varices can bleed
    • 3. Splenic vein thrombosis is most often caused by pancreatitis
    • 4. Tx: splenectomy
  57. Amebic abscesses:
    • 1. increased LFTs; increased in right lobe of liver, usually single
    • 2. primary infection occurs in the colon--> amebic colitis
    • 3. Risk factors: travel to mexico, EtOH, fecal oral transmission
    • 4. Positive serology for Entamoeba histolytica- 90% have infection
    • 5. Symptoms: fever, chills, RUQ pain, inc WBC, jaundice, hepatomegaly
    • 6. Reaches liver via portal vein
    • 7. Cultures of the abscess often sterile--> protozoa exist only in peripheral rim
    • 8. Most do not require aspiration (anchovy paste)
    • 9. Can usually diagnose based on CT characteristics
    • 10. Tx: flagyl; aspiration if refractory or contaminated; surgery only for free rupture
  58. Echinococcus Abscess:
    • 1. forms cyst (hydatid cyst)
    • 2. positive casoni skin test, positive indirect hemagglutination
    • 3. sheep- carriers; dogs- human exposure. Increased in right lobe of the liver
    • 4. Do not aspirate --> can leak out and cause anaphylactic shock
    • 5. Abdominal CT shows ectocyst (calcified) and endocyst
    • 6. Preop ERCP for jaundice, increased LFTs, or colangitis to check for communication with the biliary system
    • 7. Tx: preop albendazole, surgical removal (may want to inject cyst with alcohol at time of removal to kill organism; need to get all of cyst wall
  59. Schistosomiasis abscess:
    • 1. maculopapular rash, increased eosinophils
    • 2. sigmoid colon- fine granulation tissue, petechiae, ulcers
    • 3. Can cause variceal bleeding
    • 4. Tx: praziquantel and control of variceal bleeding
  60. Pyogenic abscess:
    • 1. accounts for 80% of all abscesses
    • 2. symptoms: fever, chills, weight loss, RUQ pain, increased LFTs, increased WBCs, sepsis
    • 3. Increased in right lobe; 15% mortality with sepsis
    • 4. GNRs- #1 organism (E.coli)
    • 5. Commonly secondary to contiguous infection from biliary tract
    • 6. Can occur following bacteremia from other types of infection (diverticulitis, appendicitis)
    • 7. Dx: aspiration
    • 8. CT-guided drainage and antibiotics; surgical drainage for unstable condition and continued signs of sepsis
    • 9. May need surgery for biliary obstruction or multiple abscesses
  61. Name the benign liver tumors:
    • 1. Hepatic adenomas:
    • 1- women, steroid use, OCPs, type I collagen storage diseases
    • 2- 80% are symptomatic; 10-20% risk of significant bleeding (rupture)
    • 3- can become malignant
    • 4- more common in right lobe
    • 5- Symptoms: pain, increased LFTs, dec BP (from rupture), palpable mass
    • 6- Dx: no kupffer cells in adenomas, thus no uptake on sulfur colloid scan (cold)
    • - MRI demonstrates a hypervascular tumor
    • - has peripheral blood supply
    • 7. Tx:
    • Asymptomatic- stop OCPs, if regression, no further therapy is needed; if no regression, patient needs resection of the tumor
    • Symptomatic- tumor resection for bleeding and malignancy risk; embolization of multiple and unresectable
    • 2. Focal Nodular hyperplasia
    • 1- has central stellate scar that may look like cancer
    • 2- No malignancy risk; very unlikely to rupture
    • 3-Dx: abdominal CT; has kupffer cells, so will take up sulfur colloid on liver scan
    • 4- MRI/CT scan demonstrates a hypervascular tumor
    • 5- Tx- convervative therapy


    • 3. Hemangiomas
    • 1- most common benign hepatic tumor
    • 2- rupture rare; most asymptomatic; more common in women
    • 3- avoid biopsy--> risk of hemorrhage
    • 4- Dx: MRI and CT show peripheral to central enhancement
    • - appears as hypervascular lesion on CT scan/MRI
    • 5- Tx: conservative unless symptomatic, then surgery +/- embolization; XRT and steroids for unresectable disease
    • 6- rare complications of hemangioma- consumptive coagulopathy (Kasabach-Merritt syndrome) and CHF
    • - these complications are usually seen in children

    • 4. Solitary Cysts
    • 1- congenital; women, right lobe
    • 2- resection needed if bleeding or infected (cannot be treated percutaneously
    • 3- complications from these cysts are rare; most can be left alone
    • 4- Walls have a characteristic blue hue
  62. Hepatic Adenomas:
    • Hepatic adenomas:
    • 1- women, steroid use, OCPs, type I collagen storage diseases
    • 2- 80% are symptomatic; 10-20% risk of significant bleeding (rupture)
    • 3- can become malignant
    • 4- more common in right lobe
    • 5- Symptoms: pain, increased LFTs, dec BP (from rupture), palpable mas
    • 6- Dx: no kupffer cells in adenomas, thus no uptake on sulfur colloid scan (cold)
    • - MRI demonstrates a hypervascular tumor
    • - has peripheral blood supply
    • 7. Tx:
    • Asymptomatic- stop OCPs, if regression, no further therapy is needed; if no regression, patient needs resection of the tumor
    • Symptomatic- tumor resection for bleeding and malignancy risk; embolization of multiple and unresectable
  63. Focal Nodular hyperplasia
    • Focal Nodular hyperplasia:
    • 1- has central stellate scar that may look like cancer
    • 2- No malignancy risk; very unlikely to rupture
    • 3-Dx: abdominal CT; has kupffer cells, so will take up sulfur colloid on liver scan
    • 4- MRI/CT scan demonstrates a hypervascular tumor
    • 5- Tx- convervative therapy
  64. Hemangiomas:
    • Hemangiomas:
    • 1- most common benign hepatic tumor
    • 2- rupture rare; most asymptomatic; more common in women
    • 3- avoid biopsy--> risk of hemorrhage
    • 4- Dx: MRI and CT show peripheral to central enhancement - appears as hypervascular lesion on CT scan/MRI
    • 5- Tx: conservative unless symptomatic, then surgery +/- embolization; XRT and steroids for unresectable disease
    • 6- rare complicatoins of hemangioma- consumptive coagulopathy (Kasabach-Merritt syndrome) and CHF
    • - these complications are usually seen in children
  65. Solitary Cysts:
    • Solitary Cysts:
    • 1- congenital; women, right lobe
    • 2- resection needed if bleeding or infected (cannot be treated percutaneously
    • 3- complications from these cysts are rare; most can be left alone
    • 4- Walls have a characteristic blue hue
  66. Malignant Liver Tumors
    -Metastases:primary ratio 20:1

    • 1. Heptatocellular Ca
    • 1- most common cancer worldwide
    • 2- Risk factors:
    • 1-HBV (#1 cause worldwide)
    • 2-HCV
    • 3- EtOH
    • 4- hemochromatosis
    • 5- alpha-1-antitrypsin deficiency
    • 6- primary sclerosing cholangitis
    • 7- aflatoxins
    • 8-hepatic adenoma
    • 9-steroids
    • 10-pesticides

    • 3- Not risk factors:
    • primary biliary cirrhosis, wilsons's disease

    4- clear cell, lymphocyte infiltrative, and fibrolamellar types (adolescents and young adults) have the best prognosis

    • 5- AFP level correlates with tumor size
    • 6- 30% 5-yr survival rate with resection
    • 7- few hepatic tumors are resectable secondary to cirrhosis, portohepatic involvement, or metastases
    • 8- need 1cm margins
    • 9- tumor recurrence most likely in the liver after resection

    • 2. Hepatic Sarcoma
    • - Risk factors- PVC, thorotrast, arsenic--> rapidly fatal

    • 3. Cholangiosarcoma
    • 1) risk factors-
    • 1- clonorchiasis infection
    • 2- ulcerative colitis
    • 3- hemochromatosis
    • 4- primary sclerosing cholangitis
    • 5- choledochal cysts

    • 2) Intrahepatic associated with worse survival than extrahepatic
    • 3) Tumor size and satellite nodules correlate with outcome


    • ----------------------------------------------------------------------------------
    • - colon Ca metastases- can resect if you leave enough liver for the patient to survive
    • - 20% survival rate

    Metastatic and primary tumors of the liver are suppplied by the hepatic arteries

    Primary liver tumors- hypervascular

    • Metastatic liver tumors- hypovascular

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