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PSYT 301 > Lecture 9: prenatal > Flashcards

Lecture 9: prenatal Flashcards

1
Q

what are the most common substances used by pregnant women?

A

alcohol and tobacco

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2
Q

what is the most common psychoactive substance taken by pregnant women?

A

cannabis

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3
Q

what are risk factors for substance use during pregnncy?

A
  • History of drug or alcohol related problems
  • Family history of substance use (genetic and
    environmental factors)
  • Frequent encounters with law enforcement
  • Having a partner who abuses substances
  • History of sexual abuse
  • Poverty and homelessness
  • Psychiatric illness (up to 60%)– anxiety,
    depression, PTSD
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4
Q

what is the possible drug effect on the fetus if the substance is taken within 20 days after fertilization, 3-8 weeks after fertilization, and in the2nd/3rd trimester?

A
  • within 20 days: all or nothing (death or no effect)
  • 3-8 weeks: maybe no effect, miscarriage, birth defect, increase risk of childhood cancer
  • 2nd/3rd trimester: changes in growth and function of normally formed organs and tissue, no birth defect
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5
Q

what is the placenta?

A

a temporary organ that develops during pregnancy that attaches to the wall of the uterus, where the umbilical cord arises from

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6
Q

what is the function of the placenta?

A
  • Provide oxygen and nutrients
  • Remove harmful waste product
  • Produce hormones
  • Pass immunity
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7
Q

how is the drug transferred to the baby?

A

via the placenta through the same path for oxygen and other nutrients

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8
Q

the ability of a drug to cross the placenta depends on what drug properties?

A
  • MW (<500-1000 Da)
  • lipid solubility
  • ionization/charge
  • protein binding
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9
Q

what placental properties affect the ability of a drug to cross the placenta?

A
  • surface area
  • thickness
  • pH of fetal and maternal blood
  • metabolism
  • uteroplacental blood flow
  • presence of transporters
  • concentration gradient across the placenta
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10
Q

what are the two main mechanism of fetal harm via drugs?

A
  • direct: to the fetus itself (i.e. the drug binds to fetus)
  • indirect: via the placenta, the mother’s physiological response to the drug, poor nutritional health (i.e. drug affect mother, which affects fetus)
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11
Q

what are the mechanisms of tobacco fetal harm?

A
  • Nicotine and CO2 increases, causing vasoconstriction of blood vessels and reduces oxygen levels to fetus.
  • Nicotine increases other chemicals that cause deregulation in normal fetal development (ex: catecholamines, cytotrophblast).
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12
Q

what are some obstetrical outcomes with tobacco use?

A
  • Spontaneous abortion
  • placenta abruption
  • Placenta Previa
  • Premature rupture of membranes
  • Uterine infections
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13
Q

what are some neonatal outcomes of tobacco use?

A
  • low birth weight
  • Fetal growth restriction
  • Increased risk of SIDS
  • Cleft Lip/Palate
  • Stillbirth
  • Premature births
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14
Q

what are some childhood outcomes of prenatal tobacco use?

A
  • SIDS
  • risk of asthma
  • congenital heart defects
  • diabetes
  • cognition
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15
Q

effect of tobacco on breast milk

A
  • nicotine readily absorbed, and can decrease supply
  • may cause: reduced appetite, diarrhea/vomiting, sleep issues, SIDS, increase HR/respiratory illness
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16
Q

mechanism of alcohol fetal harm

A
  • Damages cells by production of reactive oxygen species and oxygen radicals, which interact with DNA, protein, and lipids.
  • Ethanol and its metabolite, acetaldehyde are responsible for the biological effects.
  • Alcohol is metabolized by the liver but often the liver is underdeveloped in a fetus and it is unable to eliminate the alcohol. It is sent back to the mother as a waste product and therefore, there is increased exposure time until the waste is eliminated.
  • Prolonged exposure to fetus causes teratogenic effects, especially in 1st trimester.
17
Q

neonatal outcomes of alcohol use

A
  • FAS
  • withdrawal symptoms at birth
  • fetal death
  • decreased birth weight
18
Q

obstetrical complication of alcohol use

A
  • Intrauterine growth
    restriction
  • Increased risk of stillbirth
  • Increased risk of miscarriage
19
Q

what is fetal alcohol syndrome and its symptoms?

A

physical:
- inadequate growth
- birth defects of the face (thin upper lip, flat midface, underdeveloped jaw)
- microcephaly (small head)
cognitive:
- intellectual disability
- abnormal behavioural development
- increase risk of ADHD/ SUDs

20
Q

effect of alcohol on breastmilk

A
  • can cause decrease blood intake/sleep issues
  • need to wait until all alcohol metabolized before breastfeeding (newborns metabolize it half of our rate)
21
Q

what are the reported reasons for the increase use of cannabis in pregnant women?

A

anxiety, insomnia, morning sickness

22
Q

mechanism of cannabis fetal harm

A
  • Cannabinoids cross the placenta due to high lipophilicity and distribute into the fetal brain
  • CB1 and CB2 receptors are found as early as 14 weeks gestation- deregulation in the development of this intricate system might be associated with adverse outcomes.
  • long half-life so, low fetal clearance and measurable 15 mins after in fetal brain
23
Q

neonatal outcomes of cannabis use

A
  • Neonatal morbidity and death
  • Premature birth
  • Smaller head circumference
    -Neurobehavioural
    outcomes: ex: ASP
  • Congenital abnormalities; only correlations exist
24
Q

obstetrical complications of cannabis use

A
  • premature delivery
  • risk of miscarriage
  • IUGR
  • reduced blood flow to placenta
25
Q

effect of cannabis on breastmilk

A
  • THC and CBD accumulate in breast milk due to their lipophilic nature
  • not well studied but can: increase sedation/lethargy, reduce appetite, reduce maternal bonding
26
Q

mechanism of opioid fetal harm

A
  • cross readily the placenta
  • Infants born to opioid dependent mothers have “ passive dependency” but this supply is disrupted when the umbilical cord is cut, which can cause withdrawal symptoms in the baby
  • Repetitive patters of withdrawal reduces blood flow to placenta, lowers oxygen supply and interferes with fetal development
27
Q

neonatal outcomes of opioid use

A
  • pre-term birth
  • poor fetal growth
  • neonatal abstinence syndrome
28
Q

obstetrical outcomes of opioid use

A
  • placenta abruptions
  • infection
  • premature labor
  • premature rupture of membrane
  • miscarriage
  • postpartum hemorrhage
29
Q

what is neonatal abstinence syndrome?

A

a group of conditions that can occur when newborns withdraw from certain substances, including opioids, that they were exposed to before birth

30
Q

what symptoms are associated with neonatal abstinence syndrome

A

CNS: crying, high pitch screaming, skin irritation, tremor, seizures
GI: poor feeding, excessive sucking, loose/watery stool
autonomic: sweating, nasal stuffiness, sneezing, fever

31
Q

when do neonatal abstinence syndrome symptoms begin and how long do they last

A

bout 24 to 2 hours after birth and can last 3 days (for shorter half-life like hydrocodone) to 7 days (for longer half-life like methadone)

32
Q

mechanism of cocaine fetal harm

A
  • increase BP and HR
  • blood vessels narrow
  • so placental blood flow decreased
33
Q

neonatal outcome of cocaine use

A
  • low birth weight
  • low head circumference
  • may be abnormalities linked to decreased blood flow to placenta during critical periods
34
Q

obstetrical complication of cocaine use?

A
  • miscarriage
  • IUGR
  • hypertension
  • placental abruption
  • premature birth
35
Q

childhood outcomes linked with prenatal cocaine use

A
  • cardiovascular disorders, cleft palate, polydactyl, kidney issues
  • ADHD, oppositional defiant disorder, impaired memory, language issues
36
Q

mechanisms of fetal harm of amphetamines

A

Increases maternal heart rate and blood pressure, limiting oxygen to fetus

37
Q

neonatal outcomes of amphetamine use

A
  • risk of preterm birth
  • low birth weight
38
Q

obstetrical outcomes of amphetamine use

A
  • high BP
  • increased HR
  • reduced placental oxygen flow
39
Q
A

PSYT 301 (8 decks)

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