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liver section Flashcards

1
Q

where is bile produced and stored

A

produced by hepatocytes and stored in gallbladderr

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2
Q

what drains bile into bile duct

A

canaliculi

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3
Q

bile ducts converge to form

A

hepatic duct

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4
Q

what two ducts join the common hepatic duct before it empties into the gallbladde

A

the cystic duct and the pancreatic duct

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5
Q

sphincter of oddi role

A

controls flow of bile released from common hepatic duct

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6
Q

contraction of sphincter of oddi increases

A

biliary pressure

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7
Q

3 key functions of bile

A
  1. absorption of fat soluble vitamins (DAKE)
  2. excretory pathway for bilirubin and products of metabolism
  3. alkalization of duodenum
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8
Q

where is cholecystokinin produced

A

duodenum

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9
Q

lymph and proteins drain into

A

space of disse (between hepatocyte and sinusoid)

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10
Q

how much CO does the liver receive

A

~30% (1500mL/min)

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11
Q

is flow through the portal vein auto regulated

A

no

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12
Q

what does increased splanchnic vascular resistance do to portal vein blood flow

A

reduces portal vein blood flow

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13
Q

normal portal vein pressure

A

7-10mmHg

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14
Q

portal vein pressure diagnostic for portal HTN

A

> 20-30mmHg

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15
Q

normal pressure in sinusoids

A

0mmHg

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16
Q

pressure in sinusoids diagnostic for portal HTN

A

> 5mmHg

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17
Q

how does the hepatic arterial buffer respond when theres a reduction of portal vein blood flow

A

washout of vasodilators such as adenosine, increase BF through hepartic artery

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18
Q

hepatic artery perfusion pressure=

A

MAP-hepatic vein pressured

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19
Q

preoperative factors that reduce liver BF (5)

A
  1. increased splanchnic vascular resistance (SNS, stimulation, pain, hypoxia)
  2. things that increase CVP (PPV, excessive hydration, CHF)
  3. some beta blockers (propranolol reduces CO and increases splanchnic vascular resistance)
  4. intraabdominal surgical procedures
  5. laparoscopic surgery (pneumoperitoneum)
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20
Q

what do hepatocytes produce (3)

A

thrombopoeitin
alpha 1 acid glycoprotein
factor 7

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21
Q

why is PT an early indicator of synthetic liver dysfunction

A

factor 7 has the shortest t1/2 of all procoagulant proteins

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22
Q

what does the liver not produce?

A

factors 3 (produced by vascular endothelial cells) and 4 (calcium comes from diet)
vWF (endothelial cells and megakaryocytes)

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23
Q

liver produces all plasma proteins except for

A

immunoglobulins (gamma globulins)

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24
Q

albumin is a reservoir for

A

acidic drugs

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25
Q

alpha 1 acid glycoprotein is a reservoir for

A

basic dugs

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26
Q

what does impaired plasma protein synthesis do to vascular oncotic pressure

A

reduces vascular oncotic pressure

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27
Q

what happens to pseudocholinesterase production with liver failure

A

reduced, so increased DOA of succ and possibly DOA of esters.

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28
Q

during hyperglycemia, how does the liver respond?

A

releases insulin from pancreatic beta cells. glycogenesis

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29
Q

during hypoglycemia, how does the liver respond?

A

release of glucagon from pancreatic alpha cells, epi from adrenal medulla. glycogenolysis and gluconeogenesis.

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30
Q

what is the amino acid deamination process

A

allows body to convert proteins to carbs and fats. some are utilized in krebs cycle to produce ATP.
-produces large quantity of ammonia. liver converts this to urea, which is eliminated by kidney

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31
Q

role of lipids in the liver (3)

A

-energy storage in the form of triglycerides
-energy release by beta oxidation of fatty acids
-synthesis of cholesterol, phospholipids, lipoproteins

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32
Q

life cycle of an erythrocyte

A

120 days

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33
Q

what are old RBCs broken down by

A

reticuloendothelial cells in spleen

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34
Q

precursors of unconjugated bilirubin

A

hemoglobin->heme

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35
Q

is unconjugated bilirubin hydrophilic or lipophilic

A

lipophilic

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36
Q

how is unconjugated bilirubin transported to the liver

A

bound to albumin

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37
Q

what does liver conjugate bilirubin with to increase water solubility

A

glucoronic acid

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38
Q

metabolism of conjugated bilirubin

A

excreted into bile, metabolized by intestinal bacteria, eliminated in stool

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39
Q

liver function tests to assess synthetic function

A

PT (sensitive for acute injury) and albumin (not sensitive for acute injury(

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40
Q

liver function tests that assess hepatocellular injurry

A

AST (10-40 units/L)
ALT (10-50 units/L)
-marked elevation of both suggests hepatitis
-AST/ALT ratio >2 suggests cirrhosis or alcoholic liver disease

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41
Q

liver function tests that assess hepatic clearance

A

bilirubin (0-11 units/L)
- confounding factors: hemolysis or hematoma reabsorption

42
Q

liver function test that assess biliary duct obstruction

A

alkaline phosphatase (45-115 units/L)
y glutamyl transpeptidase (0-30 units/L)
5 nucleotides (0-11 units/L)
-AP is not very specific

43
Q

most specific indicator of biliary duct obstruction

A

5 nucleotidase

44
Q

pre hepatic liver disease
bilirubin
aminotransferase (AST and ALT)
prothrombin time
albumin
alkaline phosphatase
y glutamyl transpeptidase
5 nucleotidase
causes

A

bilirubin (increased in conjugated)
aminotransferase (AST and ALT) 0
prothrombin time 0
albumin 0
alkaline phosphatase 0
y glutamyl transpeptidase 0
5 nucleotidase 0

45
Q

pre hepatic lier disease causes

A

hemolysis
hematoma reabsorption

46
Q

hepatocellular injury/ liver disease
bilirubin
aminotransferase (AST and ALT)
prothrombin time
albumin
alkaline phosphatase
y glutamyl transpeptidase
5 nucleotidase

A

bilirubin increased conjugated
aminotransferase (AST and ALT) increased
prothrombin time increased
albumin not changed for acute injury, decreased for chronic injury
alkaline phosphatase 0 or increased
y glutamyl transpeptidase 0
5 nucleotidase 0

47
Q

causes of hepatocellularr injury

A

cirrhosis
alcohol abuse
durgs
viral infection
sepsis
hypoxemia

48
Q

after the liver (cholestatic) liver injury
bilirubin
aminotransferase (AST and ALT)
prothrombin time
albumin
alkaline phosphatase
y glutamyl transpeptidase
5 nucleotidase

A

bilirubin increased conjugated
aminotransferase (AST and ALT) 0 or increased during late disease
prothrombin time 0 or increased during late disease
albumin 0 or decreased during late disease
alkaline phosphatase increased
y glutamyl transpeptidase increased
5 nucleotidase increased

49
Q

causes of cholestatic liver injury

A

biliary tract obstruction
sepsis

50
Q

most common form of viral hepatitis

A

hepatitis A

51
Q

which forms of hepatitis can cause cirrhosis

A

hepatitis B and C

52
Q

how can halothane produce hepatitis

A

metabolized to inorganic fluoride ions and trifluoroacetic acid (TFA). can produce immune mediated response leading to hepatitis

53
Q

hepatitis A
transmission route
prophylaxis after exposure
serum markers
does it cause cirrhosis and hepatocellular carcinoma

A

transmission route: oral fecal
prophylaxis after exposure: pooled gamma globulin, hep A vaccine
serum markers: IgM (early) IgG (late)
does it cause cirrhosis and hepatocellular carcinoma: no

54
Q

hepatitis B
transmission route
prophylaxis after exposure
serum markers
does it cause cirrhosis and hepatocellular carcinoma

A

transmission route: percutaneous, sexual contact
prophylaxis after exposure: hep B immunoglobulin, hep B vaccine
serum markers: HBsAg, anti HBcAg
does it cause cirrhosis and hepatocellular carcinoma: yes

55
Q

hepatitis C
transmission route
prophylaxis after exposure
serum markers
does it cause cirrhosis and hepatocellular carcinoma

A

transmission route: percutaneous
prophylaxis after exposure: interferon and ribavirin
serum markers: Anti HCV (1.5-9 months)
does it cause cirrhosis and hepatocellular carcinoma: yes in up to 75%

56
Q

hepatitis D (co infection with type B)
transmission route
prophylaxis after exposure
serum markers

A

transmission route: percutaneous
prophylaxis after exposure: unclear
serum markers: anti HDV (late)

57
Q

most common cause of acute liver failure in US

A

aceta overdose

58
Q

toxic metabolite of acetaminophen

A

n acetyl p benzoquinoneimine (NAPQI)

59
Q

chronic hepatitis diagnosis

A

hepatic inflammation that exceeds 6 months. increased liver enzymes and bilirubin, histologic evidence of liver inflamamtion
- PT is prolonged and albumin is decreased

60
Q

s/sx of chronic hepatitis

A

jaundice, fatigue, thrombocytopenia, glomerulonephritis, neuropathy, arthritis, myocarditis

61
Q

ways to maintain hepatic BF during anesthesia

A

-use iso or sevo but avoid halothane
-avoid PEEP
-ensurer normocapnia
-administer liberal IVF
-regional is ok if no coat defects

62
Q

hepatic drugs that should be avoided due to inhibiting CYP450 (4)

A

-aceta
-halothane
-amio
-abx (PCN, tetracycline, sulfonamides)

63
Q

what does alcohol potentiate the effect of

A

GABA, so increased effect of benzos
also inhibits NMDA receptors

64
Q

how does ETOH cause an aspiration risk

A

impairs pharyngeal reflexes
assume acutely intoxicated patient has full stomach

65
Q

s/sx of withdrawal begin at ____ hours and peaks at _______ hours

A

begin 6-8h after BAC is back to normal and peaks at 24-36 hours

66
Q

early s/sx alcohol withdrawal syndrome

A

tremors, disordered perception (hallucinations, nightmares)

67
Q

late s/sx alcohol withdrawal syndeome

A

increased SNS activity (tachycardia, HTN, dysrhythmias), n/v, insomnia, confusion, agitation

68
Q

treatment of alcohol withdrawal syndrome

A

alcohol, beta blockers, alpha 2 agonists

69
Q

disulfiram

A

treatment for alcoholics in recovery. hepatotoxic, inhibits beta hydroxylate (NE synthesis) -> HoTN

70
Q

etiologies of cirrhosis

A
  • non alcoholic fatty liver disease (most common cause of liver disease)
  • alcohol abuse
  • alpha 1 antitrypsin deficiency
  • biliary obstruction
  • chronic hepatitis
    -right sided heart failure (increased hepatic vascular resistance)
  • hemochromatosis (iron overload)
  • wilsons disease
71
Q

MELD score

A

predicts 90 day mortality in patients with ESLD
- low risk <10
- intermediate risk 10-15
- high risk >15

72
Q

modified child pugh score

A

examines five factors of hepatic function: albumin, bilirubin, ascites, encephalopathy
-class A (5-6 points) 10% risk of periop mortality
-class B (7-9) 30% risk of periop mortality
-class C (10-15 points) 80% risk of periop mortality

73
Q

which child pugh scores are ok to proceed with surgery after optimization

A

classes A and B

74
Q

ESLD manifestations: CV

A

hyper dynamic circulation
portal HTN
ascites

75
Q

how does ESLD hyper dynamic circulation present

A

portosystemic shunt and vasodilator release, decreased SVR and BP-> increased CO
increased RAAS activation, increased BV)
decreased peripheral blood flow -> increased SVO2
decreased response to vasopressors
diastolic dysfunction

76
Q

how does ESLD portal hypertension present

A

increased hepatic vascular resistance, increase back pressure to proximal organs
esophageal varices -> bleeding
splenomegaly -> thrombocytopenia

77
Q

how does ESLD ascites present

A

decreased oncotic pressure, decreased protein binding, increased Vd, drainage-> HoTN

78
Q

pulmonary effects of ESLD include

A

restrictive defect (ascites and perfusion decreases compliance and atelectasis)
respiratory alkalosis (hypoxemia-> compensatory hyperventilation)
hepatopulmonary syndrome (pulmonary vasodilation -> intrapulmonary shunt (R to L) -> hypoxemia)
portopulmonary HTN (PAP >25mmHg in the setting of portal HTN)

79
Q

how ESLD affects CNS

A

hepatic encephalopathy r/t decreased hepatic clearance, increased ammonia, cerebral edema, increased ICP, increased ammonia treated with lactulose, abx, and decreased protein intake
-bleeding-> blood reabsorption -> increrase in nitrogen load-> increase in ammonia

80
Q

how ESLD affects ANS

A

increased SNS, increased RAAS, ANS reflex dysfunction

81
Q

how ESLD affects renal

A

renal hypoperfusion (decreased GFR, RAAS, Na/H2O retention)
hepatorenal syndrome (decreased GFR, renal failure)

82
Q

how ESLD effects hematologic status

A

anemia (decreased CaO2 d/t hemorrhage, folic acid deficiency, hemolysis, bone marrow depression.
reduced factor production (decreased procoagulants and anticoagulants, bleeding or clot risk.
thrombocytopenia- decreased thrombopoeitin and bone marrow depression decreases platelet production
splenomegaly increases platelet consumption

83
Q

what is the TIPS procedure

A

transjugular intrahepatic portosystemic shunt. bypasses portion of hepatic circulation by shunting blood from portal vein (hepatic inflow vessel) to hepatic vein (hepatic outflow vessel). this reduces portal pressure and minimizes back pressure on splanchnic organs. reduces likelihood of bleeding from esophageal varies and reduces volume of ascites.

84
Q

most common indication of liver trransplant

A

hepatitis C

85
Q

if the patient suffers from hepatic encephalopathy, avoid

A

anxiolytic premedication

86
Q

three phases of liver transplantation

A
  1. pre an hepatic phase
  2. an hepatic phase
  3. neohepatic phase
87
Q

preanhepatic phase time course and surgical objectives

A

begins with surgical incision, ends with cross clamping of portal vein, hepatic artery, and IVC
objectives: surgical incision, mobilization of liver structures and vascular structures, isolation of bile duct

88
Q

an hepatic phase time course and surgical objectives

A

begins with removal of native liver and ends with implantation of donor liver
objectives: removal of sick liver, implantation of donor liver (allograft)

89
Q

neohepatic phase time course and surgical objectives

A

begins with reperfusion of donor liver and ends with biliary anastomosis (for transport to ICU)
objectives: reperfusion of donor liver
anastomosis of hepatic artery and biliary structures

90
Q

HGB, platelet, fibrinogen, TEG goals during pre an hepatic phase

A

HGB >7g/dL
platelets >40,000
fibrinogen >100
TEG >45

91
Q

an hepatic phase: bicaval clamp and special considerations

A

clamps applied to IVC (above and below liver). full obstruction of IVC flow)
-significant preload reduction (HoTN, tachycardia)
aggressive fluid administration to combat HoTN can lead to volume overload when clamps are released

92
Q

anhepatic phase: piggyback technique and special considerations

A

side clamping of IVC. partial obstruction to IVC flow
- allows for some amount of BF
-less preload reduction when compared to bicaval clamping
-reduced OR and warm ischemic times
-fewer blood products required

93
Q

an hepatic phase venovenous bypass and special considerations

A

sites of cannulation (outflow: femoral vein and portal vein)
(return to body: axillary vein: blood returns to IVC- heart)
-piggyback technique has reduced the need for VVB.
-associated with less hemodynamic instability, blood loss, and prevention of portal and splanchnic congestion. higher complication rate though.

94
Q

neo hepatic phase key complications include

A

hyperkalemia (highest risk in neo hepatic phase, give CaCl or bicarb), hypocalcemia, cytokine release, lactic acidosis, embolic debris, hypovolemia, systemic HoTN, pHTN, cardiac arrest.
-avoid elevated CVP as this will cause graft complications
-

95
Q

most important consideration during neohepaticc phase

A

post reperfusion syndrome (PRS). defined as systemic HoTN more than 30% below baseline for at least one minute during first 5 minutes of reperfusion of donor liver

96
Q

s/sx of poorly functioning graft post:

A

hemodynamic instability and lack of bile output (if the implant is taking, the patient should start to stabilize in neo hepatic phase)

97
Q

obstruction of cystic duct s/sx (4)

A

gallbladder distention, edema, risk of perforation, jaundice

98
Q

obstruction of common bile duct s/sx (4)

A

cholecystitis, jaundice, pancreatitis, peritonitis

99
Q

s/sx of gall stones

A

leukocytosis, fever, RUQ pain, worse with inspiration (murphys sign)

100
Q

biliary pathology includes

A

increase alkaline phosphatase, conjugated bilirubin, amylase, y glutamyl transpeptidate, 5- nucleotidase

101
Q

surgical tx for choledocholithiasis (stones in common bile duct)

A

ERCP

102
Q

drugs that relax sphincter of oddi

A

glucagon, naloxone, NTG. glycopyrrolate and atropine may help as well

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