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Pathophys II > Hepatic part 2 > Flashcards

Hepatic part 2 Flashcards

1
Q

Excess bilirubin in the ECF is known as

A

jaundice

large quantities of unconjugated or conjugated bilirubin

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2
Q

Common causes of jaundice include:

A

increased destruction of RBCs- hemolytic jaundice

obstruction of bile ducts or damage to hepatocytes preventing bilirubin from being excreted- obstructive jaundice

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3
Q

The toxic form of bilirubin to hepatocytes is

A

conjugated form

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4
Q

In hemolytic jaundice, RBS are

A

hemolyzed rapidly

  • also have increased production of bilirubin by macrophages
  • increased unconjugated bilirubin- hepatocytes cannot process all of the bilirubin
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5
Q

When RBCs are hemolyzed rapidly in hemolytic jaundice, it results in an

A

increase in unconjugated bilirubin in the blood

-but also a secondary increase in conjugated (direct) bilirubin

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6
Q

In hemolytic jaundice, the excretory function of the liver

A

is not impaired

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7
Q

In hemolytic jaundice, the rate of formation of urobilinogen

A

in the intestines increases and urinary excretion increases

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8
Q

Obstructive jaundice can be due to

A

obstruction of the common bile duct (most common)

damage to hepatic cells

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9
Q

Obstruction of the common bile duct in obstructive jaundice can be due to

A

gallstone & malignancy

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10
Q

Damage to hepatic cells in obstructive jaundice can be a result of

A

hepatitis

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11
Q

Describe the formation of bilirubin in obstructive jaundice.

A

Unconjugated bilirubin enters the hepatocytes and is conjugated in the usual way

  • the rate of conjugated bilirubin formation is normal but it cannot pass from the liver into the intestines
  • the conjugated bilirubin enters the blood probably by rupture of the bile Canaliculi and direct emptying of bile into the lymph system
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12
Q

In obstructive jaundice, most of the bilirubin in the plasma exists in

A

the conjugated form

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13
Q

Describe the diagnostic differences between hemolytic & obstructive jaundice.

A

hemolytic jaundice- almost all bilirubin in the plasma is the unconjugated form (AKA free bilirubin)
obstructive jaundice- bilirubin in the plasma is in the conjugated form

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14
Q

In obstructive jaundice, when there is total obstruction of bile flow,

A

no conjugated bilirubin can reach the intestines to be converted to urobilinogen
no urobilinogen is reabsorbed into the blood and excreted by the kidney- test for urobilinogen in the urine is completely negative

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15
Q

Generally liver function tests are not

A

very sensitive or specific

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16
Q

Serum transaminase measurements reflect

A

hepatocellular integrity as apposed to liver function

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17
Q

Tests that measure the livers synthetic function include:

A

serum albumin
prothrombin time or INR
cholesterol
& pseudocholinesterase

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18
Q

Due to its large functional reserve, lab tests may be

A

NORMAL in the presence of cirhossis

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19
Q

In order to assess overall liver function,

A

we must take tests in total as no one tests reflects overall liver function

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20
Q

Liver abnormalities are typically divided into

A 
parenchymal disorders (hepatocellular dysfunction)
obstructive disorders (biliary excretion)
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21
Q

Normal total bilirubin is encompassing of

A

conjugated + unconjugated
is < 1.5 mg/dL
reflects the balance between production and biliary excretion

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22
Q

Jaundice is usually clinically evident when the total bilirubin is

A

> 3.0 mg/dL

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23
Q

A predominantly conjugated hyperbilirubinemia is associated with

A

an increased urobilinogen & may reflect: intrahepatic cholestasis, extrahepatic biliary obstruction
both of these may lead to hepatocellular dysfunction

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24
Q

_________ is toxic to cells

A

conjugated bilirubin; unconjugated is not

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25
Q

A primary unconjugated hyperbilirubinemia may be seen with

A

hemolysis, congenital, or acquired defects in bilirubin conjugation

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26
Q

Serum aminotransferases are enzymes released in the circulation as a result of

A

hepatocellular injury

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27
Q

Two commonly measured serum aminotransferases include

A 
aspartate aminotransferase (AST)
Alanine aminotransferase (ALT)
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28
Q

Aspartate aminotransferase is present in

A

many tissues in addition to the liver (non-specific)

heart, skeletal muscle, & kidneys

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29
Q

Alanine aminotransferase is present in

A

the liver (more specific than AST)

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30
Q

Normal AST & ALT levels are

A

below 35 to 45 IU/L

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31
Q

Mild elevations in AST & ALT are seen with

A

cholestasis or metastatic disease

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32
Q

Absolute levels of AST & ALT are

A

of value in acute liver disease- drug OD, ischemic injury, fulminant hepatitis
poorly correlate with the degree of hepatic injury in chronic liver disease

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33
Q

Serum alkaline phosphatase is produced in

A

the liver bone, small bowel, kidneys, and placenta and is excreted into the bile

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34
Q

Most of the circulating alkaline phosphate comes from

A

bone

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35
Q

In the presence of biliary obstruction, alkaline phosphate

A

(More of it) is synthesized and released into the circulation

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36
Q

Elevations up to 2x normal of serum alkaline phosphatase are associated with

A

hepatocellular injury or hepatic metastatic disease

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37
Q

Higher elevations of serum alkaline phosphatase are indicative of

A

intrahepatic cholestasis & biliary obstruction

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38
Q

Serum albumin half life is

A

long and therefore its value may initially be normal with acute liver disease

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39
Q

Serum albumin values <2.5 are generally indicative of

A

chronic liver disease, acute stress, & malnutrition

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40
Q

Hypoalbuminemia can also occur due to increase loss of albumin via the

A 
GI tract (enteropathy with protein loss)
in the urine (nephrotic syndrome)
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41
Q

Increased ammonia in the blood usually reflects

A

disruption of hepatic urea synthesis

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42
Q

Marked elevations of blood ammonia usually reflect

A

severe hepatocellular damage

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43
Q

A PT of > 3 to 4 seconds from control

A

is considered significant & corresponds to an INR of 1.5

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44
Q

PT measures the activity of

A

fibrinogen, Factor II (prothrombin), factor V, factor VII, & factor X

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45
Q

Factor VII has a _____ half-life therefore

A

short half-life; the PT is useful in evaluating hepatic synthetic function of patients with acute or chronic liver disease

46
Q

A prolonged PT usually reflects

A

severe liver disease because only 20-30% of normal factor activity is necessary for NL conjugation

47
Q

If the PT does not correct following IV administration of Vitamin K, then

A

severe liver disease is likely present (correct requires 24 hours)

48
Q

Hepatic blood flow is usually (w/ anesthetics)

A

decreased during general & regional anesthesia due to direct and indirect effects of:
anesthetic agents themselves, type of ventilation, & surgical procedure

49
Q

Describe the diagnostic features (include bilirubin, aminotransferase enzymes, alkaline phosphatase, prothrombin time, & albumin) for pre-hepatic liver dysfunction.

A 
Bilirubin- increased (unconjugated fraction)
aminotransferase enzymes- no change
alkaline phosphatase- no change
prothrombin time- no change
albumin- no change
50
Q

Causes of pre-hepatic liver dysfunction include:

A

hemolysis, hematoma, reabsorption, bilirubin overload from whole blood

51
Q

Describe the diagnostic features (include bilirubin, aminotransferase enzymes, alkaline phosphatase, prothrombin time, & albumin) for intrahepatic (parenchymal/hepatocellular) liver dysfunction.

A

Bilirubin- increased (conjugated fraction)
aminotransferase- markedly increased
alkaline phosphatase- no change to slightly increased
prothrombin time- prolonged
albumin- decreased

52
Q

Causes of intrahepatic liver dysfunction include:

A

viruses, drugs, sepsis, arterial hypoxemia, CHF, & cirrhosis

53
Q

Describe the diagnostic features (include bilirubin, aminotransferase enzymes, alkaline phosphatase, prothrombin time, & albumin) for post-hepatic (cholestasis) liver dysfunction

A

Bilirubin- increased (conjugated fraction)
aminotransferase- normal to slightly increased
alkaline phosphatase- markedly increased
prothrombin time- no change to prolonged
albumin- no change to decreased

54
Q

Causes of post-hepatic liver dysfunction include:

A

stones, cancer, & sepsis

55
Q

Describe the effect that volatile agents has on portal blood flow.

A

all volatile agents decrease portal blood flow

greatest with halothane/ least with isoflurane

56
Q

Spinal & epidural anesthesia decrease hepatic blood flow primarily by

A

decreasing blood pressure

57
Q

General anesthesia usually decreases hepatic blood flow by

A

decreasing blood pressure & CO & resulting SNS stimulation

58
Q

All anesthetic agents cause

A

indirectly decreased hepatic blood flow in proportion to any decrease in CO or MAP
-decrease in CO also reduces hepatic blood flow by reflex SNS stimulation and vasoconstriction of the arterial and venous sphlanchnic vasculature

59
Q

Describe the ventilatory effects on hepatic blood flow.

A

controlled PPV with high mean airway pressures decrease venous return & CO & compromise hepatic blood flow
PEEP accentuates these effects

60
Q

The most advantageous ventilation for maintaining hepatic blood flow is

A

spontaneous ventilation

61
Q

Hypoxemia will produce (in relation to hepatic blood flow)

A

increase SNS stimulation & decrease hepatic blood flow.

62
Q

Hypo & hypercapnea/acidosis & alkalosis have

A

variable effects on hepatic blood flow

63
Q

Drugs that decrease hepatic blood flow include

A

beta adrenergic blockers
alpha 1 adrenergic agonist
& vasopression

64
Q

This drug is though to increase hepatic blood flow:

A

low dose dopamine

65
Q

Surgical procedures on or near the liver can reduce hepatic blood flow most likely by:

A

SNS activation, local vascular reflexes, direct compression of vessels of hepatic circulation

66
Q

The endocrine stress response may be at least partially blunted by

A

regional anesthesia, deep general anesthesia, & pharmacological block of the SNS (esmolol & labetalol)

67
Q

Endocrine stress response secondary to fasting and surgical stress results in increased circulating levels of

A

catecholamines, glucagon, & cortisol

68
Q

Carbohydrates & protein stores are mobilized resulting in

A

hyperglycemia & negative nitrogen balance

69
Q

In terms of biliary tract function, all opioids can potentially cause

A

spasm of the sphincter of Oddi and increase biliary pressure

70
Q

The order of effect of opioids that cause spasm is

A

fentanyl/alfentanil (short-lived), morphine, meperidine, butorphanol, nalbuphine

71
Q

IV opioids can induce

A

biliary colic or result in false positive cholangiograms

-sphincter spasm may be less likely if the opioid is given slowly in small increments

72
Q

These drugs have been reported to relieve opioid induced sphincter spasm

A

naloxone & glucagon

73
Q

Mild postoperative liver dysfunction in healthy patients is not uncommon due to a combination of factors:

A

decreased hepatic blood flow
SNS stimulation
surgical procedures

74
Q

Surgical procedures in close proximity to the liver frequently result in

A

modest elevations in lactate dehydrogenase & transaminases regardless of the anesthetic agent or technique employed

75
Q

Postoperative elevation of liver function test are usually the result of

A

the procedure itself or underlying liver disease

76
Q

Persistent abnormalities in liver function test may be indicative of:

A

viral hepatitis (usually transfusion related), sepsis, idiosyncratic drug reaction, & surgical complications

77
Q

The most common cause of postoperative jaundice is

A

overproduction of bilirubin due to reabsorption of a large hematoma or RBC breakdown following transfusion

78
Q

Hepatitis has been associated with these volatile anesthetics:

A

methoxyflurane, enflurane, & isoflurane

79
Q

Hepatitis has not been associated with these volatile anesthetics:

A

sevoflurane, desflurane

80
Q

Potential mechanisms for halothane hepatitis include:

A

formation of hepatotoxic metabolites & immune hypersensitivty

81
Q

Risk factors associated with halothane hepatitis include:

A

middle age, obesity, female gender, repeated exposure particularly within 28 days- most important

82
Q

Halothane hepatitis is a diagnosis of

A

exclusion

hepatitis from all viral causes should be excluded

83
Q

Severity of halothane hepatitis can vary from

A

asymptomatic elevation of transaminases to fulminant hepatic necrosis

84
Q

The liver has a great functional

A

reserve capacity

85
Q

Clinical manifestations of hepatic disease are often

A

absent until extensive damage has occurred

86
Q

In patients with significant liver disease with little reserve, anesthesia & surgery can

A

precipitate further hepatic injury & overt failure

87
Q

Acute hepatitis is usually the result of

A

viral infection, drug reaction, exposure to a hepatotoxin

88
Q

Clinical manifestation of acute hepatitis depends on

A

severity of the inflammatory reaction

& amount of cellular necrosis

89
Q

In acute hepatitis, the severity of the inflammatory reaction may present as

A

asymptomatic elevations in serum transaminases

90
Q

In acute hepatitis, the amount of cellular necrosis can lead to ____ & presents as

A

acute fulminant hepatic failure; presents as rapid, massive necrosis of liver parenchyma and a decrease in liver size

91
Q

Acute hepatitis viral infections are most commonly due to

A

hepatitis A, B, or C viruses

92
Q

Hepatitis A is transmitted by the

A

oral-fecal route

93
Q

Hepatitis B & C are transmitted primarily

A

percutaneously and by contact with body fluids

94
Q

Other viruses that may cause hepatitis include

A

D, E, Epstein-Bar, herpes simplex, cytomegalovirus, & coxsackievirsus

95
Q

The hepatitis A form of viral hepatitis is (severity, recovery, & transmission)

A

least severe
most recover in weeks to months
transmission through fecal contamination

96
Q

The hepatitis E form of viral hepatitis is (severity, transmission)

A

similar to A in terms of severity (least severe & most recover in weeks to months)
occurs in 3rd world countries
transmission through fecal contamination

97
Q

The hepatitis D form of viral hepatitis does not

A

produce hepatitis by itself
only occurs as a co-infection with acute hepatitis B or super infection with chronic hepatitis B
severe infection in this setting
transmission through fecal contamination/body fluids

98
Q

Summarize the Hep B form of viral hepatitis

A

HBsAg (surface antigen part of the virus)
often anicteric- doesn’t produce jaundice
can lead to fulminant hepatic necrosis or chronic hepatitis
HBsAg disappears with recovery but disease can be diagnosed by presence of hepatitis B antibody
transmission through sexual contact/blood

99
Q

Summarize the Hep C form of viral hepatitis.

A

antibodies not present for long period- difficult to diagnose
subclinical nonicteric infection is common
rarely produces fulminant hepatic failure
a significant number of those who are chronically infected will develop cirrhosis or liver cancer- 20% develop cirrhosis/major cause of hepatocellular carcinoma
produces asymptomatic carriers
no effective vaccine currently available
transmission through blood

100
Q

Patients suffering from acute hepatitis often have a

A

prodromal illness for 1 to 2 weeks with: fatigue, malaise, low-grade fever, nausea and/or vomiting

101
Q

The prodromal period of acute hepatitis may or may not be followed by

A 
jaundice- typically lasts 2 to 12 weeks
complete recovery (evidenced by normal serum transaminases) usually takes 4 months
102
Q

Clinical course of acute hepatitis tends to be

A

complicated and prolonged with hepatitis B & C viruses

103
Q

Clinical manifestations from the causative agents overlap in acute hepatitis and therefore,

A

serological testing is necessary to determine the particular offending viral agent

104
Q

The clinical course of drug-induced hepatitis resembles

A

viral hepatitis which makes diagnosis difficult

105
Q

The most common cause of drug-induced acute hepatitis is

A

alcohol induced

106
Q

Chronic alcohol ingestion can result in fatty infiltration as a result of:

A

impaired fatty acid oxidation
increased uptake & esterification of fatty acids
diminished lipoprotein synthesis & secretion

107
Q

Acute drug-induced hepatitis results from

A

direct dose-dependent toxicity of a drug or a metabolite
idiosyncratic drug reaction
combination of the two

108
Q

The incidence of chronic active viral hepatitis is

A

approx. 3 to 10% following infection with the B virus

at least 50% following infection with the C virus

109
Q

A small percentage of patients with acute viral hepatitis become

A

asymptomatic infectious “carriers” of a hepatitis virus

110
Q

Infectious carriers of hepatitis pose a major health threat to OR personnel:

A

avoid direct contact with blood & secretions
immunization is highly effective against hepatitis B infection
no vaccine for hep C available and prior infection does not confer immunity upon re-exposure
post-exposure prophylaxis with hyperimmune globulin is effective for hep B but not for C

Pathophys II (43 decks)

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