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Peds Anesthesia Boards > Gastroenterology > Flashcards

Gastroenterology Flashcards

1
Q

At birth, the fetal supply of glucose is abruptly interrupted. How do neonates meet their glucose needs?

A

1) glucose intake (feeding)
2) gluconeogenesis
3) glycogenolysis

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2
Q

How does the liver of term infants compare to the adult in terms of glycogen stores?

A

The term infant has a greater store of glycogen than the adult. Preterm infants have less glycogen stores and are predisposed to hypoglycemia.

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3
Q

When is gluconeogenesis active in the fetal liver?

A

Gluconeogensis is NOT active in the fetal liver but hepatic enzymes that are involved such as glucose-6-phosphatase undergo rapid development after birth.

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4
Q

What are normal glucose levels for a neonate?

A

40 - 60 mg/dL

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5
Q

Below what glucose level defines hypoglycemia in a neonate?

A

Below 40 mg/dL

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6
Q

What infusion rate of glucose in terms of mg/kg/min maintains normoglycemia in both full-term and pre-term infants?

A

4 to 7 mg/kg/min

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7
Q

What are symptoms of hypoglycemia in a neonate?

A

Nonspecific symptoms such as jitteriness, cyanosis, apnea, lethargy, seizures and hypotonia

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8
Q

What are three common causes of hypoglycemia in neonates?

A

1) hypoxemia
2) sepsis
3) high levels of circulating insulin

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9
Q

What is Phase I liver biotransformation?

A

oxidation-reduction and hydrolysis performed by cytochrome p450 enzymes

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10
Q

What is Phase II liver biotransformation?

A

conjugation with glucoronic acid, glycine, acetate, or sulfate to form a more water soluble conjugate. Decreasing the lipid solubility facilitates excretion

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11
Q

What is Phase III liver biotransformation?

A

Transport from liver

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12
Q

How does the neonatal capacity for the various phases of liver metabolism compare to that of the adult or more mature child?

A

Neonates have a reduced capacity for Phase I and 2 reactions.

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13
Q

Which CYP family is responsible for approximately 50% of all drug metabolism?

A

CYP3A

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14
Q

Which CYP is present in utero but is negligibly expressed one week after birth?

A

CYP3A7

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15
Q

Describe the expression of CYP3A4 in the fetus, neonate and infant.

A

CYP3A4 levels are very low during fetal life but reach 50% of adult levels by 6 months of age.

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16
Q

Which CYP has a multitude of polymorphisms that are of particular relevance in the metabolis of psychotropic and anesthetic drugs?

A

CYP2D6

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17
Q

What enzyme is associated with Phase II biotransformation in the liver?

A

UGT (aka, uridine-5-diphosphate-glucoronyltransferase)

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18
Q

How does glucoronidation activity in the neonate/infant compare to that of the adult?

A

Glucoronidation is a Phase II biotransformation process in the liver facilitated by UGTs. UGT levels are low in neonates and infants, thus glucoronidation is not fully active. At 3 months of age UGT levels are 25% that of adults. This places infants at risk for toxic drug accumulation.

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19
Q

What phase of liver biotransformation is responsible for the metabolism of many opioids?

A

Phase II - Conjugation. The responsible enzyme is UGT.

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20
Q

What liver enzyme metabolizes acetaminophen?

A

UGT1A6 (phase II conjugation)

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21
Q

What liver enzyme metabolizes naproxen?

A

UGT1A6 (phase II conjugation)

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22
Q

Describe the expression of UGT1A6 in neonates and infants are compared to adult levels.

A

UGT1A6 has 10% of adult expression in the fetus and only 50% of adult activity by 6 months of age.

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23
Q

What liver enzyme metabolizes naloxone?

A

UGT2B7

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24
Q

What liver enzyme metabolizes codeine?

A

UGT2B7

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25
Q

What liver enzyme metabolizes lorazepam?

A

UGT2B7

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26
Q

Describe the expression of UGT2B7 in neonates and infants are compared to adult levels.

A

Fetal activity approaches 10% - 20% of adult levels with a rapid increase to adult levels by 2 months of age.

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27
Q

Where do fetal circulating coagulation factors come from?

A

They are made by the fetus because they inefficiently cross the placenta.

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28
Q

How do plasma concentrations of vitamin K derived factors in the fetus compare to the adult?

A

They are about 50% lower than adult levels.

29
Q

How do the concentrations of fibrinogen, factor V, and factor VIII compare to those of adults?

A

They are similar (i.e., about the same).

30
Q

What type of cell is responsible for producing the factors that affect PT?

A

Hepatocytes synthesize factors 1 (fibrinogen), II (prothrombin), V, VII, IX, and X and abnormal production of these factors is reflected in a prolonged PT. PT mostly reflects availability of factor VII.

31
Q

How do neonatal thrombin levels compare to those of adults?

A

Neonatal thrombin levels are about 50% those of adults.

32
Q

What coagulation study reflects the amount of generated thrombin?

A

aPTT

33
Q

How do infections or asphyxia affect coagulation in the newborn?

A

In the newborn, both of these can cause DIC.

34
Q

How might rapid infusion of FFP affect neonatal blood pressure?

A

Because FFP contains high concentrations of histamine and citrate, rapid infusion can cause histamine-related hypotension as well as hypotension from citrate toxicity (i.e., hypocalcemia)

35
Q

What is the primary parent source of bilirubin?

A

Hemoglobin (but cytochromes, catalases and myoglobin also contribute as they also contain heme)

36
Q

Would you expect a neonate who suffered significant hemolysis in utero to be jaundiced?

A

No because the normal placenta efficiently clears bilirubin.

37
Q

Would you expect a neonate who suffered significant hemolysis at birth to be jaundiced?

A

Yes.

38
Q

When should neonatal jaundice be considered abnormal?

A

It is abnormal if any of the following conditions are true:

1) present in the first 36 hours of life
2) persists beyond 10 days of life
3) is greater than 12 mg/dL and the direct (conjugated) bilirubin is greater than 2mg/dL or more than 30% of the total bilirubin concentration

39
Q

What type of bilirubin is responsible for the physiologic jaundice of the newborn?

A

Indirect (unconjugated) bilirubin

40
Q

What is the predominant feature of kernicterus?

A

Neuronal necrosis which occurs mostly in the basal ganglia, brainstem, oculomotor nuclei, and cochlear nuclei.

41
Q

What type of bilirubin contributes to the hyperbilirubinemia of sepsis?

A

Direct (conjugated) bilirubin

42
Q

What is the “anti-insulin effect of anesthesia?”

A

It is the inhibition of glucose uptake by hepatocytes caused by anesthetics. Halothane has the greatest impact on serum glucose with iso and sevo having lesser effects.

43
Q

What is the effect of 1 to 2 MAC of an inhalational anesthetic on glucose uptake by hepatocytes?

A

Glucose uptake is INHIBITED by up to 50%!

44
Q

Why are glucose-containing IV fluids no longer recommended for most healthy children undergoing elective surgery?

A

Because the combination of anti-insulin effect of anesthesia and the stress from surgery or trauma increase the serum glucose concentration.

45
Q

How do inhaled anesthetics affect protein synthesis?

A

Halothane and enflurane block protein synthesis in a dose dependent manner.
Halothane, sevoflurane, and enflurane inhibit protein synthesis and secretion.

46
Q

What sort of normal changes are expected in serum aminotransferase concentrations and bilirubin levels in the postoperative period?

A

Increases in serum aminotransferase concentrations and bilirubin up to two times the upper limit of normal occur commonly in the postoperative period and are typically self-limited and inconsequential.

47
Q

What LFT changes would you expect with hepatocellular injury?

A

Predominantly increased ALT and AST levels

48
Q

What LFT changes would you expect with cholestatic hepatotoxicity?

A

increases in alkaline phosphatase, GGT, and bilirubin

49
Q

Is perioperative mortality greater in those with acute hepatitis or those with chronic liver disease?

A

Those with acute hepatitis.

50
Q

When would you expect the development of parenteral nutrition-associated liver disease to occur?

A

After 60 days of parenteral nutrition use

51
Q

How does exposure to TPN affect perioperative glucose control?

A

Those exposed to TPN are at increased risk of perioperative glucose derangements and frequent perioperative glucose monitoring with adjustment of dextrose infusion is standard of care.

52
Q

When does a child with biliary atresia typically present to the hospital?

A

1 - 6 weeks of age

53
Q

What abnormalities are associated with biliary atresia?

A 
In 10 - 15% of those patients:
Absent IVC
intestinal malrotation
Polysplenia
Preduodenal portal vein
54
Q

What is another name for the Kasai procedure?

A

Hepatic portoenterostomy

55
Q

At what age is the Kasai procedure most successful?

A

The success rate is 80% in those operated on before 2 months of age and 50% in those operated on before 4 months of age

56
Q

What percentage of patients who have undergone a Kasai procedure go on to becoming liver transplant candidates?

A

80%

57
Q

What volatile agent is preferred for a Kasai procedure?

A

Isoflurane anesthesia maintains better hepatic blood flow and oxygen supply.

58
Q

What is adriamycin?

A

Adriamycin is an anthrcycline chemotherapeutic agent that causes a dosage-dependent irreversible cardiomyopathy.

59
Q

What causes the vast majority of death in fulminant hepatic failure?

A

Increased ICP with cerebral herniation is responsible for 80% of death in fulminant hepatic failure.

60
Q

Cerebral perfusion pressure should be maintained above what value?

A

Greater than 50 mmHg

61
Q

Define portopulmonary hypertension.

A

Portal hypertension with pulmonary systolic pressure > 25 mmHg with normal PCWP.

62
Q

Where is vWF produced?

A

The endothelium

63
Q

All factor levels are decreased in liver disease except for which factor(s)?

A

Fibrinogen and Factor VIII

64
Q

What are the primary etiologies of liver disease that require liver transplantion in children?

A

Biliary atresia (50% of infantile transplants)
Cholestatic liver disease (e.g. TPN cholestasis)
Liver failure 2/2 toxins or tumors
Metabolic diseases

65
Q

What are the notable differences in patients with metabolic diseases presenting for liver transplantation as compared to other patients?

A

Metabolic disease patients generally do NOT have liver dysfunction (i.e., no coagulopathy, no cirrhosis, no collateral vessels) and may be susceptible to metabolic crises.

66
Q

What is the pathophysiology of maple syrup urine disease?

A

Leucine accumulation as a result of metabolic error for branched-chain amino acids (leucine, isoleucine, valine).

67
Q

What is the normal action of Alpha-1 Antitrypsin?

A

A1AT inhibits neutrophil protease in setting of inflammation, this when A1AT levels are low there is excessive tissue injury during inflammation.

68
Q

What are the anesthetic concerns during the anhepatic phase of liver transplantation?

A 
Hypothermia
Hypoglycemia
Hypocalcemia/Citrate toxicity
Metabolic Acidosis
Loss of venous return
Decreased renal perfusion due to renal venous obstruction
69
Q

What does the term “physiologic GERD” in the pediatric population refer to?

A

GERD that is 2/2 immature lower esophageal sphincter mechanism that generally resolves by 15 months of age.

Peds Anesthesia Boards (5 decks)

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