Prenatal Flashcards

1
Q

Why is it important to talk about SUD and pregnancy?

A

1) Increased concerns for mother and baby
2) Increased stigma
3) Chronic and relapsing nature of SUD

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2
Q

What are the most common substances used by pregnant women?

A

1) Tobacco
2) Alcohol

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3
Q

What is the most common psychoactive drug used by pregnant women?

A

Cannabis

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4
Q

T or F: Substances used during pregnancy vary by race and ethnicity.

A

True.

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5
Q

List some risk factors for SUD during pregnancy.

A

1) History of drug/alcohol related problems
2) Family history of SUD (genetic and environmental factors)
3) Frequent encounters with law enforcement
4) Having a partner who abuses substances
5) History of sexual abuse
6) Poverty and homelessness
7) Other psychiatric illnesses

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6
Q

Read slides 4-8.

A

go queenie

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7
Q

T or F: Teratogenic effects are mostly seen in the first trimester.

A

True.

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8
Q

T or F: Neurodevelopment occurs mainly in the first trimester.

A

False.
Limb formation mainly occurs in the first trimester. Neurodevelopment mainly occurs in the second and third trimesters.

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9
Q

What are the possible drug effects during the following time frames:
1) Within 20 days after fertilization
2) 3-8 weeks after fertilization
3) Second and third trimesters

A

1) All or nothing
2) Vulnerability to birth defects
3) Changes in growth and function of normally formed organs and tissue

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10
Q

How are drugs transferred from mother to fetus?

A

Via the placenta.
→ same route used to provide O2 and nutrients

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11
Q

What is the placenta?

A

The placenta is 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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12
Q

List the functions of the placenta.

A

1) Provide O2 and nutrients
2) Remove harmful waste products
3) Produce hormones
4) Pass immunity

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13
Q

List some placental properties that might affect drug transfer across the placenta.

A

1) Surface area
2) Thickness
3) pH of maternal and fetal blood
4) Metabolism
5) Uteroplacental blood flow
6) Presence of placental drug transporters
7) Concentration gradient across placenta

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14
Q

List some drug properties that might affect drug transfer across the placenta.

A

1) Molecular weight
2) Lipid solubility
3) Ionization/charge
4) Protein binding

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15
Q

Explain how each drug property might increase transfer across the placenta.

A

Increased transfer:

1) Low molecular weight (<1000 daltons)
2) High lipid solubility
3) Low ionization / uncharged
4) Low protein binding (free)

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16
Q

T or F: Drugs are most likely to pass into breast-milk with the same physiochemical properties that allow them to transfer across the placenta.

A

True.

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17
Q

List the direct/indirect mechanisms of fetal harm.

A

1) Direct: To the fetus itself (eg. teratogen)
2) Indirect: via the placenta
3) Indirect: via the mother’s physiological response
4) Indirect: poor nutritional health secondary to substance use

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18
Q

Tobacco: Mechanisms of fetal harm

A

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

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19
Q

Tobacco: Obstetrical complications

A

1) Spontaneous abortion
2) Placenta abruption
3) Placenta previa
4) Premature rupture of membranes
5) Uterine infections

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20
Q

Tobacco: Neonatal outcomes

A

1) Low birth weight
2) Fetal growth restriction
3) Increased SIDS risk
4) Cleft palate/lip
5) Stillbirth
6) Premature birth

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21
Q

Tobacco: Childhood outcomes

A

1) SIDS
2) Increased asthma risk
3) Increased CHD risk
4) Increased diabetes risk
5) Declined cognition

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22
Q

Tobacco: Breast milk

A

Nicotine is readily absorbed in breast milk.

It may cause:
1) SIDS (!!)
2) Reduced appetite
3) Diarrhea
4) Vomiting
5) Sleep disturbance
6) Decreased milk supply
7) Increased heart rate
8) Respiratory problems
9) Increased risk of obesity and thyroid problems

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23
Q

Tobacco: Breast milk recommendation

A

Recommendation is to AVOID using tobacco during
pregnancy.

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24
Q

Tobacco: Harm reduction strategies

A

1) Smoke 30 min before feeding
2) Change clothing often
3) Smoke outside
4) Use vape

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25
Q

Alcohol: Mechanisms of fetal harm

A

1) Damages cells by production of reactive oxygen species and oxygen radicals, which interact with DNA, protein, and lipids.
2) Ethanol and its metabolite, acetaldehyde are responsible for the biological effects.
3) Alcohol is metabolized by the liver but often the liver is underdeveloped in a fetus and it is unable to eliminate the alcohol.

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26
Q

Alcohol: Obstetrical outcomes

A

1) Intrauterine growth restriction
2) Increased risk of stillbirth
3) Increased risk of miscarriage

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27
Q

Alcohol: Neonatal outcomes

A

1) Fetal Alcohol Syndrome (FAS)
2) Withdrawal symptoms at birth
3) Fetal death
4) Reduced birth weight

28
Q

What are the consequences of FAS?

A

Physical:
1) Inadequate growth
2) Facial deformation
3) Microcephaly

Cognitive:
1) Intellectual disability
2) Abnormal behavioural development
3) Increased risk of ADHD and antisocial behaviour

29
Q

Alcohol: Childhood outcomes

A

Increased risk of:

1) Poor growth
2) Attention deficits
3) Delinquent/criminal behaviour
4) SUD
5) Impaired cognition
6) Language and communication disabilities

30
Q

T or F: Newborns metabolize alcohol at the same rates as adults.

A

False.
Newborns metabolize alcohol at approximately half the rate of adults.

31
Q

T or F: “Pumping and dumping” is an effective strategy when breast feeding.

A

False.
“Pumping and Dumping” does not work! Dumping does not speed up metabolism.

32
Q

Alcohol: Breast milk

A

May cause:

1) Decrease in milk intake
2) Interference with sleep-wake cycles

33
Q

Alcohol: Breast milk recommendation

A

Avoid while breastfeeding, or consume AFTER breastfeeding.

34
Q

Alcohol: Harm reduction strategies

A

For breastfeeding:
1) 1 drink → wait 2 hours
2) 2 drinks → wait 4 hours

35
Q

T or F: The endocannabinoid system development only occurs in the third trimester.

A

False.
From the start, the fetus begins the development of their endocannabinoid system.

36
Q

Cannabis: Mechanisms of fetal harm

A

1) Cannabinoids cross the placenta due to high lipophilicity and distribute into the fetal brain.
2) 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.
3) Cannabis has a long half-life, leading to low fetal clearance.

37
Q

Cannabis: Obstetrical outcomes

A

1) Premature delivery
2) Risk of miscarriage
3) Intrauterine growth restriction
4) Reduced blood flow to placenta

38
Q

Cannabis: Neonatal outcomes

A

1) Neonatal morbidity
2) Premature birth
3) Smaller head circumference
4) Neurobehavioural deficits
5) Congenital abnormalities

39
Q

Cannabis: Breast milk

A

THC and CBD accumulate in breast milk due to their lipophilic nature.
Some effects possibly include:
1) Increased sedation and lethargy
2) Reduced appetite
3) Reduced maternal bonding

40
Q

Cannabis: Breast milk recommendation

A

Given lack of evidence for negative association, breast- feeding while using cannabis is discouraged.

41
Q

Opioids: Mechanisms of fetal harm

A

1) Opioids have low molecular weight, low protein binding, and high lipid solubility which allows them to readily cross the placenta.
2) 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.
3) Repetitive patterns of withdrawal reduces blood flow to placenta, lowers oxygen supply and interferes with fetal development.

42
Q

Opioids: Obstetrical outcomes

A

1) Placenta abruption
2) Intrauterine infection
3) Preeclampsia
4) Premature labour and delivery
5) Premature rupture of membranes
6) Miscarriage
7) Postpartum hemorrhage

43
Q

Opioids: Neonatal outcomes

A

1) Neonatal abstinence syndrome (NAS) !!
2) Premature birth
3) Low birth weight
4) Poor fetal growth

44
Q

Define: NAS

A

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

45
Q

List symptoms of NAS.

A

1) CNS
→ Inconsolable crying, high pitch crying, skin irritation, hyperactive reflexes, tremor, seizures
2) GI
→ Poor feeding, excessive sucking, feeding intolerance, loose or watery stools
3) Autonomic
→ Sweating, nasal stuffiness, sneezing, fever, tachypnea

46
Q

When do signs of NAS typically begin?

A

Signs of withdrawal usually begin within 24- 72 hours after birth (but vary depending on the opioid they were exposed to in utero).

47
Q

How does NAS affect preterm infants?

A

Preterm infants have a later onset and less severe symptoms, likely because of developmental immaturity of the nervous system or reduced total drug exposure in shortened gestations.

48
Q

T or F: The length and extent of withdrawal symptoms is shorter for hydrocodone compared to methadone.

A

True.

49
Q

Opioids: Childhood outcomes

A

Emerging association between fetal exposure to opioids and adverse neurocognitive and behavioural deficits, increasing the risk of:

1) Lower IQ
2) Intellectual difficulties
3) Behavioural problems in school
4) Poor language development
5) Hyperactivity

50
Q

Opioids: Breast milk

A

Present in breast milk, some are safer than others.
Neonatal toxicity has been found:
1) CNS depression
2) Lethargy
3) Reduced clearance in baby
4) Reduced appetite

51
Q

Opioids: Harm reduction strategies

A

Short acting opioids may be safe for short periods of time only (except for Codeine).

52
Q

Cocaine: Mechanisms of fetal harm

A

1) Cocaine is lipophilic, crosses the placenta and exposes fetus to 89% of the cocaine a mother uses.
2) Increased blood pressure
3) Increased heartbeat
4) Narrowing of blood vessels
5) Decreased blood flow to placenta
6) Suppression of mother’s appetite

53
Q

T or F: The effects of cocaine are the same with all administration routes.

A

False.
→ Fastest onset of action: Smoking - IV - Intranasal
→ Longest duration of effect: Intranasal - IV - Smoking

54
Q

Cocaine: Obstetrical outcomes

A

1) Miscarriage
2) Intrauterine growth restriction
3) Hypertension
4) Placental abruption
5) Spontaneous abortion
6) Premature birth
7) Cardiovascular cocaine toxicity

55
Q

Cocaine: Neonatal outcomes

A

1) Low birth weight
2) Low head circumference
3) Possible abnormalities linked with reduced blood flow during critical periods of development

56
Q

Cocaine: Childhood outcomes

A

1) Physical abnormalities
→ CVD, cleft palate, polydactyl, kidney malformatio
2) Neurodevelopmental issues
→ impaired adolescent function, impaired perceptual reasoning, ADHD, impaired memory, impaired executive function, language issues

57
Q

Amphetamines: Mechanisms of fetal harm

A

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

58
Q

Amphetamines: Obstetrical outcomes

A

1) High BP
2) Increased heart rate
3) Reduced O2 flow to placenta

59
Q

Amphetamines: Neonatal outcomes

A

1) Premature birth
2) Low birth weight
3) No congenital defects

60
Q

T or F: Long Term effects related to amphetamine use are unknown.

A

True.

61
Q

Amphetamines: Breast milk

A

Found in breast milk at concentrations 2.8 to 7.5 times maternal plasma. Not recommended.

62
Q

Adverse outcomes secondary to substance exposure in utero depend on…

A

1) Ingested substance
2) Duration of exposure
3) Ingested amount

63
Q

Read slides 55-58.

A

fini!!!

64
Q
A
65
Q
A
65
Q
A
66
Q
A