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Elsa AACN > Ch 21 Toxic exposure in utero > Flashcards

Ch 21 Toxic exposure in utero Flashcards

1
Q

Alcohol

A

teratogen that passes through the placental barrier and affects the developing fetus throughout gestation

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2
Q

fetal alcohol spectrum syndrome (FASD) is a diagnostic term T or F?

A

False, it’s not a diagnostic term, it’s an umbrella term

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3
Q

FASD describes

A

craniofacial
cardiovascular
skeletal
neurological deficits

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4
Q

FASD includes what syndromes

A

Fetal alcohol syndrome
Partial FAS (PFAS)
alcohol-related birth defects (ARBD)
alcohol-related neurodevelopmental disorder (ARND)

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5
Q

Leading cause of preventable ID

A

Fetal alcohol syndrome

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6
Q

Small amount of alcohol consumption is safe during pregnancy. T or F

A

False - no level of alcohol consumption is safe during pregnancy

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7
Q

prenatal alcohol exposure leads to alterations in

A

size and structure across brain regions

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8
Q

during 1st and 2nd trimester, prenatal alcohol consumption interferes with what?

A

migration, proliferation, organization of brain cells

results in varying craniofacial and brain malformations

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9
Q

during the 3rd trimester, prenatal alcohol consumption interferes with what?

A

damage to the cerebellum, hippocampus, prefrontal cortex

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10
Q

neurochemical effects of alcohol

A

increased turnover of norepinephrine and dopamine
decreased transmission of acetylcholine
increased transmission in GABA system
increased production of beta endorphin in the hypothalamus

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11
Q

Which part of the brain is affected in FASD?

A

white matter!!

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12
Q

Structural abnormalities in FASD

A

microcephaly
migrational anomalies
disproportionate reduction in gray and white matter volume (frontal, parietal, temporal)
white matter hypoplasia > gray matter hypoplasia

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13
Q

Diagnosis of FAS (4 criteria)

A

growth deficiency
craniofacial features
CNS dysfunction
prenatal alcohol exposure

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14
Q

FAS Criteria 1 - growth deficiency

A

below average height and or weight
small for gestational age
show growth deficiency as adolescents and adults

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15
Q

FAS Criteria 2 - craniofacial features

A 
short palpebral fissures (eye width decrease with increase prenatal alcohol)
flat midface
short upturned nose
smooth or long philtrum (ridges between lip and nose)
thin vermilion (upper lip thinner with more alcohol)
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16
Q

FAS Criteria 3 - CNS dysfunction

A 
microcephaly (2+ SD below the mean)
callosal agenesis
cerebellar hypoplasia
seizure
fine and gross motor problems
hearing loss
cognitive deficits (memory, EF, attention, LD)
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17
Q

FAS Criteria 4 - Prenatal Alcohol Exposure

A

confirmed ur unknown

no biochemical marker can confirm consumption

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18
Q

Alcohol-related birth defects (ARBD)

A 
congenital anomalies in
cardiac
skeletal
renal
ocular
auditory
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19
Q

alcohol related neurodevelopmental disorder (ARND)

A

A. CNS abnormalities such as structural brain abnormalities

B. behavior or cognitive abnormalities inconsistent with development

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20
Q

ND-PAE (neurodevelopmental disorder associated with prenatal alcohol exposure)

A

some exposure to alcohol

impaired neurocognitive fx, self regulation, adaptive fx

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21
Q

prevalence of FAS

A

10%

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22
Q

USA prevalence of FAS higher than Europe by

A

2x

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23
Q

FASD rates in USA

A

9/1000 births

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24
Q

Risk factors of FAS in USA

A 
Race and SES are confounded
higher maternal age
low education
low econ background
MH issues
social isolation
abuse hx
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25
Q

which racial group has the highest FAS rate

A

Black or native americans

10x more than whites or high SES

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26
Q

factors that determine severity of FAS

A 
quantity consumed 
pattern of exposure
timing of exposure
additional risk factors
- multiple drugs
- high maternal age
- maternal Health issues
- lower education, reduced access, nutrition, stress, abuse
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27
Q

quantity consumed definition

A

no consensus but 3 risk levels

  • high risk - BAC > 100mg/dL (average size woman drinking 6-8 beers in one sitting)
  • some risk - use less than high risk
  • unknown risk
  • no risk (no use)
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28
Q

pattern of exposure

A 
chronic consumption (4-5 drinks daily)
binge drinking (5 or more standard drinks)
9 or more a week
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29
Q

timing of exposure

A

drinking in 1st trimester - increases FASD by 12x
drinking in 1st and 2nd trimester - increases FASD by 61x
drinking in ALL trimester - increases FASD 65x

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30
Q

children with FAS have CNS damage, true or false

A

TRUE

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31
Q

FASD NP - IQ

A

great variability, IQ 20-120
more dysmorphic features = lower IQ
25% FAS and 10% ARND IQ <70

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32
Q

FASD NP LD

A

learning difficulties, reading and spelling and math
low school performance
school attendance

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33
Q

FASD NP Attention

A

60-95%ADHD
3-9x higher than normal kids
impaired visual sustained attention, auditory verbal attention

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34
Q

FASD NP processing speed

A

deficits on challenging tasks and complex

working memory deficits

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35
Q

FASD NP speech and language

A

oral motor function and speech production
naming
expressive and receptive language disorder
comprehension higher level
pragmatics

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36
Q

FASD visuospatial

A

deficits in local vs global analysis of visual stimuli

VS construction deficits (maybe due to motor deficits)

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37
Q

FASD Executive function

A

deficits many domains

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38
Q

FASD sensorimotor

A

delay motor development
deficits in fine motor (reduced cerebellar size)
tremor, weak grasp, poor eye hand coordination
balance
sensory integration

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39
Q

FASD emotion and personality

A 
restless, impulsive, disruptive, aggressive, delinquent
antisocial behaviors
juvenile delinquency
sleep disturbance
adaptive behavior
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40
Q

% of cases that get diagnosed with FASD

A

only 25% due to limited expertise

only 11% diagnosed by age 6

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41
Q

early intervention is important with diagnosis because it can..

A

mitigate development of secondary disability
have appropriate intervention, counseling
get support

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42
Q

comorbid dx with FASD

A

ADHD
CD
ODD
OCD

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43
Q

protective factors for FASD

A

early dx
services
stable home
protection from violence

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44
Q

how does cocaine affect the CNS in utero exposure?

A

effects on monoamine system
dopamine
exposure in early gestation affects neural proliferation and migration
exposure in late gestation affects neuronal maturation and synaptogenesis

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45
Q

brain abnormalities 2/2 cocaine exposure in utero?

A

abnormalities in frontocingulate cortex

anterior cingulate gyrus

46
Q

% of pregnant women worldwide using cocaine

A

0.5-3%

47
Q

consequences of maternal cocaine use on infants?

A 
Small head circumference 
low birth weight
Poor sleep cycle 
abnormal startle response 
abnormal brain stem evoked potential 
impulsivity 
emotional lability 
low frustration tolerance
48
Q

NP results for cocaine exposure in utero

A

Lower overall IQ
Deficits in academic achievement (parent education, SES)
Impairment in sustained and selective attention
Slow processing speed (due to poor attention regulation)
Language delay (esp expressive)
visual spatial deficits
working memory and executive function

49
Q

marijuana

A

psychoactive and medicinal use

50
Q

Predominant psychoactive constituent in marijuana

A

THC

51
Q

What pathway is associated with the rewarding property of cannabis

A

Meso cortical limbic dopamine system

52
Q

What changes are produced by THC use

A 
mood
perception
motor coordination
short-term and working memory
concentration
53
Q

Does THC cross the placenta during gestation?

A

yes
It is secreted in maternal milk during lactation
8x higher concentration in breast milk than in plasma

54
Q

Effects of prenatal cannabis exposure

A 
Fetal growth restriction in mild in late pregnancy
Low birth weight
Increased risk of stillbirth 
altered sleep patterns irritability 
excitability and arousal
55
Q

Infants exposed to cannabis in utero have increased risk of birth defects, true or false

A

false

56
Q

Heavy marijuana exposure effects

A

Delay in visual maturation and visual attentiveness
Heightened tremors
exaggerated startle and visual responses
poor habituation to novel stimuli
exaggerated moro reflex
athetoid movements
disinhibition in motor tests (like in narcotic withdrawal)

57
Q

Which is the third most used drug after alcohol and tobacco during pregnancy

A

Marijuana

58
Q

Percentage of pregnant women using marijuana during pregnancy

A

2-6%

59
Q

Heavy marijuana use has been associated with what changes in length of gestation

A

Reduction in length of gestation by one week

60
Q

Which gender is more vulnerable on testing after prenatal cannabis exposure

A

male

61
Q

Neuropsychological assessment results for prenatal cannabis exposure (PCE)

A

IQ unaffected
underachievement in reading, spelling math
problems with attention and concentration (could be confounded by alcohol use
hyperactivity, inattention, impulsivity
executives functions deficit, working memory
Visual spatial processing

sensorimotor - unaffected by age 1 but

  • decreased rate of visual habituation
  • increased tremor (4 day olds)

mood:
delinquent behavior in middle adolescence
depression
behavioral dysregulation

62
Q

Primary human exposure of methylmercury

A

eating contaminated fish (shark, tuna, swordfish)

shellfish

63
Q

Consumption of mercury can be done through what ways

A

Ingested
inhaled
absorbed through the skin

64
Q

Organs commonly affected in mercury exposure

A

Neurologic
gastrointestinal
renal systems

65
Q

How does methyl mercury gain access to brain tissues

A

By active transport into the endothelial cells in the blood brain barrier

Methylmercury destroys neurons and causes cerebral atrophy in both hemisphere

66
Q

Deadliest of the Mercury compounds

A

dimethylmercury

67
Q

What happens when exposed to dimethylmercury

A

It can cause acute mercury poisoning by permeating the skin, getting into the bloodstream, and depositing in the brain, kidneys and other organs

68
Q

Symptoms of exposure to dimethylmercury

A 
Paresthesia
deterioration in fine motor coordination
restriction of visual fields 
severe ataxia 
dementia
death
69
Q

which barrier can methylmercury cross

A

placenta barrier

blood brain barrier

70
Q

prenatal exposure to mercury results in

A 
atrophy of cerebral cortex and corpus callosum
dysmyelination of pyradmidal tract
ID
poor motor coordination
blindness
seizure
inability to speak
progressive cortical degenerative disease
cerebral palsy
sensory deficits
microcephaly
limf malformationlumb
71
Q

common exposure to mercury

A

fish consumption
vaccine
dental amalgams

72
Q

why do fetuses have greatest risk to mercury exposure?

A

because they can’t secrete it

73
Q

which brain structures are affected in infants or children when mother is exposed to mercury

A

occipital cortex

cerebellum

74
Q

Neuropsych assessment results in mercury exposure

A 
deficits in attention
motor skills
language
VS
memory
expressive language
overall IQ
reduction in activity level in boys
75
Q

Environmental toxicant - polychlorinated biphenyl (PCB))

A

used in transformers, adhesives, tapes, plastic and rubber products, oil based pain, electrical devices, carbonless copy paper

76
Q

primary human exposure of PCB

A

highly contaminated fish and sea mammals

77
Q

neuropathology of PCB

A

disruption of endocrine system
changes in thyroid hormone level in infants
decreased size of splenium of corpus callosum

78
Q

effects of PCB in utero exposure

A

low birth weight

delays in sensorimotor and cognitive abilities

79
Q

NP results of PCB

A

deficit in verbal ability

EF

80
Q

Inorganic lead exposure through what means

A

drinking water from lead pipes
imported candies, toys, cosmetics, pottery
paint chips and paint dust

81
Q

lead can pass through what barrier

A

blood brain barrier

82
Q

what happens after lead reaches CNS?

A

CNS -> interferes with neurulation, migration, synaptogenesis, neurotransmission

83
Q

what happens when lead reaches the fetus

A

crosses the placenta and accumulates in fetal organs

84
Q

how is the brain impacted by lead exposure

A 
decreased cerebral volume in:
frontal gray matter
ACC
prefrontal cortex
possible neuronal loss
85
Q

incidence rate of lead exposure up or down

A

declined sharply but high in low income areas, minority

86
Q

determinants of severity of lead exposure

A

ACTION LEVEL = blood lead level of 5 mg/dl or higher

87
Q

different lead levels and classification of deficits

A

<30 low lead level
>44 pharmacological intervention CHELATION Therapy
>80 can lead to lead encephalopathy

88
Q

signs of elevated lead level?

A 
headache
irritability
abdominal pain
vomiting
weight loss
attention problems
hyperactivity
learning problems
slowed speech
89
Q

NP results in lead exposure

A 
decline in IQ
decline in academic achievement
EXECUTIVE FUNCTION most affected
visual spatial skills
restless, impulsivity, inattentive, aggressive
ADHD ODD
antisocial behaviors
90
Q

% of lead that can be absorbed by children

A

50%

91
Q

% of lead that can be ingested by adults

A

10-15%

92
Q

more severe effects are seen when lead is exposed during what stage of development?

A

in utero and infancy (more severe than later childhood and adulthood)!

93
Q

What is chelation therapy

A

treatment for children whose blood lead level is >44
trap lead in the blood and remove it through urine
helps with reducing lead level but NOT reverse cog deficits

94
Q

in utero exposure to Nicotine and Tobacco results

A

reduced fetal oxygen supply
fetal undernourishment
vasoconstrictor effects on placenta and umbilical cord

95
Q

in utero exposure to amphetamine results in

A

motor deficits during infancy
EF deficits in childhood
poor emotional regulation

96
Q

in utero exposure to opiates results in

A 
decrease in neural plasticity 
increase in cell death
lower birth weight
motor deficits in infancy
deficits in EF and ADHD in childhood
97
Q

in utero exposure to pesticides results in

A

enzymes that regulate acetylcholine

98
Q

in utero exposure to air pollution results in

A

lower IQ
poorer academics
behavioral problems

99
Q

in utero exposure to antiepileptic meds in 1st trimester

A

major anatomical birth defects

100
Q

in utero exposure to antiepiletic meds in 3rd trimester

A

behavioral and cognitive deficits

101
Q

in utero exposure to valporic acide and polytherapy

A

verbal deficits

increased risk for adhd, ASD

102
Q

in utero exposure to Coumadin/blood thinner

A

developmental delay

dandy walker syndrome

103
Q

in utero exposure to accutane (acne meds)

A

birth defect

ID

104
Q

in utero exposure to SSRI

A

neonatal abstinence syndrome

-excessive crying, irritability, hyperactive reflex, seizure, increased muscle tone

105
Q

Acrodynia

A

affects young children exposed to mercury
misdiagnosed as measles, kawasaki disease
sx = irritability, photophobia, pink discoloration, edema of hands and feet, hair loss…

106
Q

reference dose

A

exposure without recognized adverse effects

107
Q

Lead NP

A

EF!!!

108
Q

Tobacco NP

A

Adhd

Externalizing

109
Q

Cocaine NP

A

Attention

110
Q

PCB potentiates by

A

Mercury!

111
Q

Alcohol

A

Affects parietal > temporal and occipital

Elsa AACN (35 decks)

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