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Neonatal Pathophysiology > Glucose Metabolism > Flashcards

Glucose Metabolism Flashcards

1
Q

What is the primary fuel of the brain?

A

glucose; unlike the liver, skeletal muscle or cardiac muscle, the brain cannot store adequate amounts of glucose in the form of glycogen. it requires a steady supply of glucose to function normally.

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2
Q

How is glucose provided to the fetus?

A

fetal glucose is supplied along a concentration gradient by a carrier mediated transport system across the placenta–> it readily crosses the placenta

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3
Q

When do fetal stores of glucose first appear?

A

present by 9th wk GA

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4
Q

When is the majority of glucose stored but the fetus?

A

in the 3rd trimester, particularly in the last month

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5
Q

At term, how do the glucose stores of an infant compare to that of an adult?

A

infant stores are 3x > and adult

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6
Q

In preparation for delivery, what changes occur with glucose storage?

A

glucagon levels increase and insulin levels decrease

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7
Q

What is the definition of hypoglycemia?

A

the def and mgmt of hypoglycemia remains controversial an recommendations vary; measurement of serum glucose is the amount dissolved glucose in the blood stream

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8
Q

What is the most common metabolic problem in the newborn?

A

hypoglycemia

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9
Q

Why can’t hypoglycemia can’t be described by a single value?

A

bc it may be different bw babies due to their physiologic immaturity and their current pathophysiology

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10
Q

When do glucose levels reach their nadir?

A

30-90 min of age

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11
Q

What can be indicated by the presentation of asymptomatic hypoglycemia in the neonate?

A

other energy substrates such as lactate and ketone bodies are providing the adequate fuel for the brain

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12
Q

What happens to samples of blood left out at room temperature?

A

for every hour it is left out, it decreases the value by 13-18g/dL

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13
Q

Point of care testing utilizes what sample of blood?

A

whole blood; if you send a sample to the lab, it should be just a little higher than the value you get at the bedside

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14
Q

How do whole blood measurements of glucose compare to plasma values?

A

whole blood measurements are approximately 15% lower than plasma values

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15
Q

How do venous blood measurements of glucose compare to arterial values?

A

venous samples are approximately 10-15% lower than plasma values

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16
Q

What sample of blood is considered the “true level”?

A

plasma

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17
Q

What other factors can alter a glucose level?

A

elevated HCT will alter results

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18
Q

What stimulates the processes of glycogenolysis and gluconeogensis?

A

epinephrine, norepinephrine, growth hormone, cortisol and glucagon

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19
Q

What is the definition of glycogenolysis?

A

the initial process to convert glycogen into glucose

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20
Q

What is the definition of gluconeogenesis?

A

the initial glucose production method-break down CHO sources and convert them into glucose; not effective or efficient

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21
Q

What are prenatal and family history related risk factors for the postnatal development of hypoglycemia?

A

MOB c glucose alt; previous LGA babies, LGA, h/o previous stillbirths, HTN/PIH, h/o metabolic dz

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22
Q

What are birth history related risk factors for the postnatal development of hypoglycemia?

A

low APGARs, poor fetal tracing, signs of infix (PROM, maternal fever)

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23
Q

What are physical exam findings that increase the risk for the postnatal development of hypoglycemia?

A

SGA, LGA, IUGR, Beckwith-Wiedmann

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24
Q

What is universal screening for hypoglycemia?

A

screen every baby for hypoglycemia, AAP now suggests only screening the babies at high risk

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25
Q

What is included in the Beckwith-Wiedmann constellation?

A

known for profound and/or persistent hypoglycemia, physically typically LGA, protuberant tongue and abnormal umbilicus (may have an omphalocele)

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26
Q

What are the common causes of neonatal hypoglycemia?

A

1) inadequate substrate supply
2) abnormal endocrine fx
3) increased glucose utilization
4) iatrogenic causes

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27
Q

What percentage of hypoglycemia is r/t inadequate substrate supply?

A

15%

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28
Q

What infants are at the greatest risk for hypoglycemia secondary to inadequate substrate supply?

A

VLBW infant (<1250g), SGA, discordant twins

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29
Q

What are the mechanisms of inadequate substrate supply r/t hypoglycemia r/t pulmonary and neuro?

A

1) if they have a significant respiratory course, we know that hypoxia uses glucose as an energy source, depleting what glucose stores were present 2) babies with decreased glucose stores may also have high glucose brain utilization

30
Q

What percentage of infants have hypoglycemia secondary to abnormal endocrine function?

A

8%

31
Q

What infants are at increased risk for hypoglycemia secondary to abnormal endocrine function?

A

LGA, infants born to IDM, erythroblastosis fetalis

32
Q

Fetal glucose levels are what percentage of maternal values?

A

70-80%

33
Q

How does hyperinsulinemia occur in the infant of a IDM MOB?

A

the fetal pancreas will secrete insulin in response to glucose load and secretes levels appropriate to that environment. After delivery, with maternal glucose supply gone, the baby’s pancreas may not be able to back off for hours or days, creating a hypoglycemic environment

34
Q

What is erythroblastosis fetalis?

A

dz of hemolysis, the enzyme glutathione reductase is a by product of that hemolysis and it inactivates circulating insulin. As is inactivates insulin, it stimulates the pancreas to produce even more

35
Q

What infants are at increased risk for hypoglycemia secondary to increased glucose utilization?

A

babes that are stressed or sick, with increased energy needs and may rapidly deplete their glycogen stores; perinatal asphyxia, hypothermia, neonatal sepsis and polycythemia/ hyperviscosity

36
Q

What are some iatrogenic causes of hypoglycemia?

A

use of maternal drugs, erroneous placement of umbilical lines and administration of IV glucose to the mother during labor

37
Q

What maternal drugs are known to contribute to neonatal hypoglycemia?

A

tocolytics, terbutaline, ratidine, propanolo and oral hyperglycemic agents; cause MOB to become hyperglycemia and the baby will over secrete insulin

38
Q

What are the landmarks for umbilical line placement?

A

high lines: T6-T9; low lines: L3-4

39
Q

How does erroneous line placement contribute to hypoglycemia in the neonate?

A

if UAC is T11-12, this is about the location that the celiac artery is connected to the aorta. If the UAC is there then is infusing dextrose, it may be close enough to this artery that it directly stimulates the pancreas to secrete even more insulin

40
Q

How should hypoglycemia secondary to umbilical line placement be treated?

A

pull line into low lying position and within hours, hypoglycemia should be resolved

41
Q

Why are so many symptoms of hypoglycemia neurological?

A

since the brain needs glucose to fx, many manifestations of hypoglycemia are neurological in origin

42
Q

What are symptoms of hypoglycemia?

A

jitteriness/tremors, cyanosis, overt sz, apnea/irregular breathing, irritability/lethargy, hypothermia, weak and/or high pitched cry, poor feeding, eye rolling, sweating, cardiac failure, hypotonia, respiratory distress and pallor

43
Q

What pathologic states include hypoglycemia in its presentation?

A

sepsis, asphyxia, hypocalcemia, CNS lesions, CHD, polycythemia/hyperviscosity and metabolic abnormalities

44
Q

If a baby can be fed enterally, how should hypoglycemia be treated?

A

feed them, reassess glucose 15-30 min after the intervention

45
Q

If a baby cannot be fed enterally, how should hypoglycemia be treated?

A

D10 bolus 2-4cc/kg given over 1mL/min (minimum infusion rate) followed by continuous IVF

46
Q

What is the GIR of D10W at TF 80cc/kg/d?

A

5.5mg/kg/min

47
Q

What course of action should be taken if hypoglycemia persists after intervention?

A

increase GIR either by increasing the rate of infusion or the concentration of glucose in the IVF; monitor line position, insert central lines if D>12.5%, monitor insulin levels

48
Q

Why might insulin levels need to be drawn in an infant born to IDM MOB?

A

to document levels of hyperinsulinemia

49
Q

What is the effect of insulin on an infant’s respiratory function?

A

insulin tends to decrease surfactant production and quality and increase their cumulative risk for RDS (even if later GA)

50
Q

What is insulin?

A

a hormone that enables glucose to enter the cell by ∆ cell wall permeability ; the major blood glucose reducing hormone

51
Q

How does insulin levels affect brain utilization of glucose?

A

cerebral glucose utilization is NOT dependent on insulin

52
Q

When does insulin first appear in the fetus?

A

by 12wk GA

53
Q

How does hyper insulin affect growth?

A

insulin should work in synergy with growth hormone and is vital for growth. when the fetus has excessive insulin, then glucose, protein and fat synthesis is accelerated, leading to macrosomia

54
Q

What is the maximal glucose oxidative capacity and when is it exceeded?

A

do not want to exceed 16-18mg/kg/min; occurs when excess glucose is converted to fat leading to increased O2 consumption and increased CO2 production

55
Q

When should adjunct therapies be considered for the treatment of refractory hypoglycemia?

A

not until GIR is > 12mg/kg/min with no ∆ in glucose levels

56
Q

What is glucagon and how is it helpful in treating refractory hypoglycemia?

A

an agent that releases glycogen from hepatic stores. its helpful when the newborn has adequate stores and hyper insulin levels. It allow for a RAPID, TRANSIENT increase in glucose concentration- may be helpful in babe that IV access is difficult

57
Q

How is GIR calculated?

A

(%D x IVF rate)/ (6x wt in kg)

58
Q

At what levels is an infant considered hyperglycemic?

A

term infant >125mg/dL; preterm infant > 150mg/dL

59
Q

What are causes of hyperglycemia in the neonate?

A

inability to metabolize glucose, excess administration, medications, hyperosmolar formula, neonatal diabetes, sepsis, stress response (ex: asphyxia)

60
Q

In what population is hyperglycemia of greatest concern?

A

infants <1500g

61
Q

What medications are known to cause hyperglycemia?

A

dilantin,caffeine, theophylline and MOB on diazoxide

62
Q

What is diazoxide?

A

a non-diuretic thiazide, it suppresses pancreatic insulin release; some units use this as a first line therapy for refractory hypoglycemia

63
Q

How do steroids affect serum glucose levels?

A

steroids derease peripheral glucose utilization and increase gluconeogensis and enhances the infant’s response to glucagon

64
Q

What are s/s of hyperglycemia?

A

increase serum glucose levels, glycosuria (more than trace is concerning), osmotic diuresis with resultant dehydration and hyperosmolar state

65
Q

Why should hyperosmolar states be avoided?

A

a/w IVH

66
Q

How should hyperglycemia be treated?

A

adjust fluids/GIR, insulin gtt

67
Q

Why should IVF with <D5W be avoided in the treatment of hyperglycemia?

A

cannot take dextrose away entirely, if you need to lower a level re not giving adequate substrate for body fx

68
Q

What is the desired range of GIR?

A

5-8mg/kg/min

69
Q

What is the potential long term implications of prolonged, recurrent low blood glucose levels?

A

play a role in adverse neurologic sequelae

70
Q

Why are glucose related mistakes one of the most common causes of lawsuits for pediatricians?

A

lack of screening at risk groups, failure to confirm, poor documentation of intervention and symptoms s/p treatment

Neonatal Pathophysiology (17 decks)

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