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ABSITE > Fiser Chapter 31. LIVER > Flashcards

Fiser Chapter 31. LIVER Flashcards

1
Q

Right hepatic artery variant

A

Off SMA: courses behind pancreas, posterolateral to CBD

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2
Q

Left hepatic artery variant

A

Off L gastric artery: in gastrohepatic ligament medially

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3
Q

Falciform ligament

A

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

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4
Q

Ligamentem teres

A

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

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5
Q

Cantlie’s line separating right and left liver

A

Middle of gallbladder fossa to IVC (aka portal fissure)

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6
Q

Couinaud’s segments

A

1-4 clockwise starting with caudate

5-8 clockwise (5 is inferior medial)

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7
Q

Glisson’s capsule

A

Peritoneum that vocers liver

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8
Q

Bare area

A

Posterior-superior surface not covered by Glisson’s capsule

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9
Q

Triangular ligaments

A

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

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10
Q

Where does portal triad enter

A

Segments IV and V

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11
Q

Where does the gallbladder lie

A

Under segments IV and V

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12
Q

Kupffer cells

A

Liver macrophages

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13
Q

Portal triad

A

CBD (lateral), PV (posterior), proper hepatic artery (medial)

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14
Q

Pringle maneuver

A

Clamp porta hepatic, will not stop HV bleeding

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15
Q

Entrance to lesser sac

A

Foramen of windslow (anterior is portal triad, posterior is IVC, inferior is duo, superior is liver)

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16
Q

What forms PV?

A

SMV joining splenic vein

IMV enters splenic vein

There are two portal veins in liver, and they may 2/3 of hepatic blood flow. Left goes to segments 2-4, right goes to 5-8.

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17
Q

Arterieal blood supply of liver

A

R, M, and L hepatic arteries (follow hepatic vein system)

Middle most commonly a branch off left hepatic

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18
Q

Most primary and secondary liver tumors are supplied by what blood flow?

A

Hepatic artery

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19
Q

Hepatic veins

A

R, M, L

R: 6-8
M: 5 and inferior 4
L: 2, 3, and superior 4

Middle HV comes into LHV before going into IVC in 80%, in remaining goes directly into IVC

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20
Q

Accessory R hepatic veins

A

Drain medial aspect of R lobe directly to IVC

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21
Q

Inferior phrenic veins

A

Drain directly into IVC

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22
Q

Caudate lobe blood flow

A

Receives separate R and L portal and arterial blood flow

Drains directly into IVC via separate hepatic veins

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23
Q

Where is alkaline phosphatase normal located?

A

Canalicular membrane

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24
Q

Where does nutrient uptake occur?

A

Sinusoidal membrane

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25
Q

Usual enrgy source for liver

A

Ketones

Glucose is converted to glycogen and stored

Excess glucose converted to fat

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26
Q

Where is urea synthesized

A

Liver

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27
Q

Where is vWF and factor 8 synthesized?

A

Endothelium

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28
Q

What does liver store?

A

Fat-soluble vitamins and B12

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29
Q

Most common problems with hepatic resection

A

Bleeding and Bile leak

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30
Q

Hepatocytes most sensitive to ischemia

A

Central lobular (acinar zone III)

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31
Q

How much of a normal liver can be resected?

A

75%

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32
Q

Bilirubin synthesis

A

Hgb -> heme -> biliverdin -> bilirubin

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33
Q

What does bilirubin do?

A

Conjugated to glucuronic acid with glucuronyl transferse in the liver, which improves bili’s water solubility

Conjugated bili is actively secreted into bile

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34
Q

Breakdown of conjugated bilirubin by bacteria in TI

A

Free bili reabsorbed andconverted to urobilinogen, and eventually released in urine as urobilin. Excess urobilinogen turns urine dark like cola

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35
Q

Bile contains what?

A

85% bile salts; proteins; phospholipids (lecithin); cholesterol; bilirubin

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36
Q

What determines the final bile composition?

A

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

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37
Q

What is used to make bile salts/acids?

A

Cholesterol

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38
Q

What happens to bile salts?

A

There are conjugated to taurine or glycine (improves water solubility)

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39
Q

Primary and secondary bile acids (salts)

A

Primary: cholic and chenodeoxycholic acid

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

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40
Q

Main biliary phospholipid

A

Lecithin

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41
Q

What does bile do?

A

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

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42
Q

At what level does jaundice occur?

A

Tbili > 2.5

First evident under tongue

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43
Q

Maximum bilirubin

A

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

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44
Q

Elevated unconjugated versus conjugated bilirubin

A

Unconjugated: prehepatic causes (hemolysis); hepatic deficiencies or uptake or conjugation

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

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45
Q

Gilbert’s disease

A

Abnromal conjugation; mild defect in glucuronyl transferase

46
Q

Crigler-Najjar disease

A

Inability to conjugate; sevre deficiency of glucuronyl transferase; high unconjugated bilirubin causing life threatening disease

47
Q

Physiologic jaundice of newborn

A

Immature glucuronyl transferase; high unconjugated bilirubin

48
Q

Roto’s syndrome

A

Deficiency in storage ability; high conjugated bilirubin

49
Q

Dubin-Johnson syndrome

A

Deficiency in secretion ability; high conjugated bilirubin

50
Q

What viral hepatitis can cause fulminant hepatic failure?

A

B, D, E

Very rare with A and C

51
Q

What viruses can cause chronic hepatitis and hepatoma?

A

B, C, D

52
Q

MOst common virus leading to OLT and HCC

A

HCV

53
Q

Cofactor for HBV

A

D (worsens prognosis)

54
Q

Virus with fulminant hepatic failure in pregnancy

A

E, most often in 3rd timester

55
Q

Most common cause of liver failure

A

Cirrhosis (palpable liver, jaundice, ascites)

56
Q

Best indicator of synthetic function in cirrhosis

A

PT

57
Q

Acute liver failure (fulminant hepatic failure) mortality

A

80%

Outcome determines by course of encephalopathy

Consider urgent liver txp if King’s College criteria met

58
Q

King’s College Criteria of Poor Prognostic Indicators

A

Tylenol-ALF:

  • If pH < 7.3, OR
  • INR > 6.5, Cr > 3.4, Grade 3/4 HE

Non-Tylenol ALF:

  • INR > 6.5, OR 3 of:
  • Age < 10 or > 40, drug toxicity or undetermined etiology, jaundice > 7 days before encephalopathy, INR > 3.5, bilirubin > 17
59
Q

HE

A

Liver failure -> inability to metabolize -> buildup of ammonia, mercanatanes, false neurotransmitters

Causes other than liver failure: GIB, SBP, electrolytes, drugs

60
Q

HE treatment

A

May need to embolize shunts or other major collaterals

Lactulose: cathartic that gets rid of bacteria and acidifies colon (preventing NH3 uptake by converting it to ammonium), titrate to 2-3 stools/day

Limit protein intake (<70 g/day)

Branched-chain aa’s (metabolized by skeletal muscle, may be of some value)

No abx unless for specific infection

Neomycin (gets rid of ammonia producing bacteria from gut), rifaximin?

61
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

62
Q

Paracentesis for ascites

A

Replace with albumin

63
Q

Ascites

A

From hepatic/splanchnic lymph

Tx: water restriction (1-1.5 L/day), decrease NaCl (1-2g/day), diuretics (spironolactone counteracts hyperaldosteronism seen with liver failure), paracentesis, TIPS, prophylactic abx to prevent SBOP (norfloxacin; used if previous SBP or current UGIB)

64
Q

Aldosterone in liver failure

A

Elevated due to impaired hepatic metabolism and GFR

65
Q

HRS

A

Progressive renal failure, same lab findings as prerenal azotemia, usually a sign of ESLD

Tx: Stop diuretics, give volume, no good tx other than OLT

66
Q

Neurologic changes in liver failure

A

Asterixis; sign that liver failure is progressing

67
Q

Postpartum liver failure with ascites

A

From HVT; has an infectious component

Dx: SMA arteriogram with venous phase contrast

Tx: Heparin and antibiotic

68
Q

Fever, abd pain, PMNs >250 in fluid, positive cultures

A

SBP

69
Q

MCC organisms in SBP

A

E coli

Pneumococcus

Streptococcus

If polymicrobial, worry about bowel perf

70
Q

SBP risk factors

A

Prior SBP

UGIB (variceal hemorrhage)

Low-protein ascites

71
Q

SBP tx

A

3rd gen cephalosporins; usually respond within 48 hr

72
Q

Esophageal varices

A

Bleed by rupture

Tx: Banding and sclerotherapy (95% effective); vasopressin (splanchnic artery constriction) and ocreotide (decrease portal pressure by decreasing blood flow) can be used to temporize; patients with history of CAD should receive NTG while on vasopression; Sengstaken-Blakemore esophageal tube (has a balloon used to control variceal bleeding; risk of esophageal rupture so hardly used anymore); propranolol may help prevent re-bleeding but no good role acutely; can get later strictures from sclerotherapy usually easily managed with dilatation; TIPS for refractory variceal bleeding

73
Q

Portal HTN: pre-sinusoidal, sinusoidal, and post-sinusoidal

A

Pre-sinusoidal obstruction: schistosomiasis, congenital hepatic fibrosis, PVT (50% of portal HTN in children)

Sinusoidal: cirrhosis

Post-sinusoidal obstruction: Budd-Chiari syndrome (HVT), constrictive pericarditis, CHF

74
Q

Normal portal vein pressure

A

<12mmHg

75
Q

Coronary veins in portal HTN

A

Act as collaterals between PV and systemic venous system of lower esophagus (azygous vein)

76
Q

Portal HTN consequences

A

Esophageal variceal hemorrhage

Ascites

Splenomegaly

HE

77
Q

Portal HTN tx

A

Shunts to decompress portal system: TIPS, splenorenal

78
Q

TIPS uses

A

protracted bleeding, progression of coagulopathy, visceral hypoperfusion, or refractory ascites

allows antegrade flow

complication: HE

79
Q

Splenorenal shunt

A

Low rate of HE

Need to ligate L adrenal vein, L gonadal vein, IMV, coronary vein, and pancreatic branches of splenic vein

80
Q

Splenoreal shunt uses

A

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

Contraindicated in patients with refractory ascites, as splenorenal shunts can WORSEN ascites

81
Q

Child’s B or C with need for shunt

A

TIPS

82
Q

Child’s A that has just bleeding

A

Consider splenorenal shunt (more durable), otherwise TIPS

83
Q

Mortality after open shunt placement

A

CTP correlates

84
Q

Child-Pugh Scoring

A

BEIAA

Bilirubin
Encephalopathy
INR
Albumin
Ascites

Child’s A: 2% mortality with shunt
Child’s B: 10%
Child’s C: 50%

85
Q

Portal HTN in children

A

Usually caused by extra-hepatic PVT

Most common cause of massive hematemesis in children

86
Q

Budd-Chiari syndrome

A

Hepatic vein or IVC occlusion

Dx: Angiogram with venous phase, CT angiogram; liver biopsy shows sinusoidal dilatation, congestion, centrilobular congestion

Tx: Pora-caval shunt (needs to connect to the IVC above obstruction)

87
Q

RUQ pain, hepatosplenomegaly, ascites, fulminant hepatic failure, muscle wasting, variceal bleeding

A

Budd-Chiari syndrome

88
Q

Isolated gastric varices without elevated pressure in rest of portal system

A

Splenic vein thrombosis.

These gastric varices can bleed

Most often caused by pancreatitis

Tx: Splenectomy if symptomatic

89
Q

Diagnosis and treatment of amebic abscess

A

Serology and imaging (culture may be sterile, protozoa exist only in peripheral rim)

Tx: flagyl; aspiration only if refractory; surgery only if free rupture

Starts with amebic colitis, reaches R liver by PV

90
Q

Dx and Tx of hydatid cyst (echinococcus)

A

Positive serology and Casoni skin test

CT showing ectocyst (calcified) and endocyst (double walled); do NOT aspirate (anaphylaxis)

Tx: albendazole x2 weeks, then surgical removal (intraop inject cyst with EtOH to kill organisms then aspirate out) and remove entire wall without spilling contents; preop ERCP if jaundice, transaminitis, or cholangitis to check for communication with biliary system

91
Q

Maculopapular rash and eosinophilia with liver abscess

A

Schistosomiasis

Primary infection in sigmoid

Fine granulation tissue, petechiae, ulcers; can cause variceal bleeding

Tx: Praziquantel and control of variceal bleeding

92
Q

MCC liver abscess

A

Pyogenic (bacterial are 80%

93
Q

Fever, chills, weight loss, RUQ pain, high LFTs, high WBC, sepsis, R liver lobe abscess

A

Pyogenic abscess

15% mortality with sepsis

94
Q

MCC pyogenic abscess

A

E coli
Secondary to contiguous infection from biliary tract

Can occur following bacteremia from other infections (diverticulitis and appendicitis)

95
Q

Dx and Tx of pyogenic abscess

A

Aspiration

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

96
Q

Women with OCPs or steroid use, has R liver mass

A

Hepatic adenoma

20% risk rupture and bleed

5% malignant potential

97
Q

CT or MRI with hypervascular tumor

A

No uptake of sulfur colloid (cold): adenoma (no Kupffer cells)

Uptake of sulfure colloid: FNH

98
Q

Tx of hepatic adenoma

A

Asymptomatic: stop OCPs, if still no regression then need resection

Symptomat: resect for bleeding and malignancy risk; embolization if multiple and unresectable

99
Q

Central stellate scar in liver mass

A

Focal nodular hyperplasia

No malignancy risk, very rare rupture

100
Q

Tx of FNH

A

Conservative, no resection

101
Q

MCC benign hepatic tumor

A

Hemangioma: rupture is rare (but avoid biopsy due to risk of hemorrhage), more common in women, most asymptomatic

102
Q

MRI or CT with peripheral to central enhancement of a hypervascular lesion

A

Hemangioma

103
Q

Tx of hemangioma

A

Conservative

If symptomatic: surgery +/- preop embolization; steroids (possible XRT) for unresectable disease

104
Q

Liver mass with CHF or a consumptive coagulopathy

A

Kasabach-Merritt syndrome (coagulopathy with hemangioma); usually seen in children

105
Q

Solitary liver cysts

A

Congenital; women; right lobe; walls have blue hue; rare complications, leave alone

106
Q

Malignant liver tumors

A

20x more likely to be mets

Primary are hypervascular, metastatic are hypovascular

107
Q

Most common cancer worldwide

A

HCC

108
Q

Risk factors for HCC

A

HepB, HepC, EtOH, hemochromatosis, alpha-1 antitrypsin def, PSC, aflatoxins, hepatic adenoma, steroids, pesticides

(PBC and Wilson’s are NOT risk factors)

109
Q

HCC types with best prognosis

A

clear cell

lymphocyte infiltrative

fibrolamellar (young people)

110
Q

Risk factors for hepatic sarcoma

A

PVC, thorotrast, arsenic -> rapidly fatal

111
Q

Survival after CRC liver met resection

A

35% at 5 years

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