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Reproductive > Sweatman Drugs in Pregnancy > Flashcards

Sweatman Drugs in Pregnancy Flashcards

1
Q

name some indications when we are directly giving the fetus drugs

A
  1. lung maturation-corticosteroids
  2. fetal arrhythmias-digoxin
  3. patent ductus arteriosus-NSAIDS promote closure
  4. anti HIV to prevent maternal infection of fetus
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2
Q

drugs that cross placenta

A

nearly all dude

  • short term and long term effects possible
  • effect depends on timing and duration of exposure and how that drug affects fetal growth
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3
Q

number of women who are pregnant and taking drugs is

A

declining

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4
Q

most common drugs given to pregnant women

A

antibiotics (10-14 days), antifungals, analgesics

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5
Q

opioid drugs of abuse

A

morphine, codeine, hydrocodone, naloxene, buprenorphine

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6
Q

stimulant drugs of abuse

A

amphetamines, cocaine, phencylidine, nicotine

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7
Q

depressant drugs of abuse

A

alcohol, barbiturates, cannabis, marijuana, hashish

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8
Q

hallucinogen drugs of abuse

A

LSD, psilocybin, mescaline, inhalants, nitirtes

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9
Q

major signs that alert of of dependency withdrawl of abused substance

A

autonomic hyper reactivity, irritability, excessive crying, poor feeding, and abnormal reflexes

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10
Q

rate of onset of symptoms from these abused substances depends on…

A

varies by drug from immediate to delayed. dependent on how much of the drug has accumulated in the CNS and the relative rate of release from the tissue (rate of decline)

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11
Q

duration of adversity

A

not short term–> weeks to months

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12
Q

how, in rare cases is the adversity counteracted…

A

by subjecting the infant to lower and tapering doses of the prescription drug

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13
Q

opiate receptors are located priminently in the

A

brain and enteric nervous system of the GI tract

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14
Q

in the CNS and opiate would be…

and thus, absence/withdrawal would lead to …..

A

sedating

CNS hyperreactivity and associated autonomic hyperactivity upon withdrawal

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15
Q

in the GI tract and opiate would be…thus, withdrawal would manifest as

A

consitpation—> withdrawal=diarrhea

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16
Q

neonatal narcotis abstienence syndrome varies with

A

opiate and time of exposure and exposure amount

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17
Q

if withdrawal symptoms are severe enough, and not responding to non-pharm (environemental measures) nor milder pharm support
what should you give

A

low, tapering doses of morphine or methadone

*phenobarbitol if first line agents not effective

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18
Q

fetus has an extra compartment for ciruclating drug that the mother does not have

A

amniotic fluid

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19
Q

placental involvement

A

can conduct some metabolic processed and therefore convert materials from maternal to fetal tissues

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20
Q

what determines the amount of drug that crosses the placenta

A

LIPID, MW, Ionization
>duration and timing (small duration less likely to cause harm)
>Maternal plasma protein binding
>Placental development and blood
>energy dependent drug trannys (pgp and MRP and BCRP)

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21
Q

rationale for heparin in pregnancy rather than warfarin

A

lower molecular weight

*dont wage WARFARin on baby keep the baby HEPPY

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22
Q

polymorphisms in energy dependent drug pumps can affect drug passage on an individual basis are present where

A
  1. placenta
  2. GI
  3. BBB
  4. Kidney
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23
Q

polymorphisms in ___, ____, _____ can determine fetal drug exposure on an individual basis (must be accounted for and different in everyone)

A

PGP, BCRP, MDR1

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24
Q

metabolic capabilities of placenta

A

hydroxylation, n-dealkylation, demethylation

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25
Q

can fetal liver metabolize drugs

A

yes, 40-60%, but not all the placental blood travels thru the fetal liver…there some metabolism takes place
*hepatic metabolism alters toxicity profile acting at the location of the fetus

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26
Q

placenta increases or decreased fetal exposure or toxicty

A

decreases exposures usually and decreaeses toxicity (placenta is kinda protective)

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27
Q

one bad thing placental metabolism does

A

may increase exposure to carcinogens–> benpyrene

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28
Q

use off-label for monring sickness and caused tertogenic effects in the 1950s in england

A

thalidomide

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29
Q

effect of thalidomide

A

phocomelia-seal limbs (weird stubby arms)

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30
Q

prenatal death in weeks

A

1 and 2

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31
Q

major morphologic abnormalitis

A

week 3-7

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32
Q

physiologic defects and minor morphologic defects seen in

A

week 8-term

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33
Q

single exposure to teratogen is unlikely to

A

produce adverse effects on the fetus

*expectant mother must take it on a more chronic basis, although not necessarily the entire pregnancy

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34
Q

to be a proven teratogen..must show (3)

A

> characteristic set of malformations
exert effects at a particular stage of fetal development
dose dependent incidence

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35
Q

what percentage of pregnancies are unplanned

A

50%

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36
Q

how many births have some sort of defect

A

4%

genetic or unidentified environmental factors

37
Q

many women may go____days before they realize theya re pregnant

A

14–> giving time for toxic drug exposure during this critical phase of implantation and initial development

38
Q

all candidate drugs must be tested in ____ _____. one ____ and one ____

A

two species
one rodent
one non-rodent

39
Q

PERHAPS THE MODELS BEING INDICATED TO SHOW TOXICITY ARE OVERSENSITVE BECAUSE

A

OF THE THOUSANDS OF DRUGS OUT THERE…600 HAVE BEEN SHOWN TO BE TOXIC IN ANIMAL MODELS…LESS THAN 10% OF WHICH ARE PROVEN HUMAN TERATOGEN/TOXIC

40
Q

6 MECHS OF RECOGNIZED TERATOGENICITY

A 
>FOLATE ANTAGONISM
>NEURAL CREST DISRUPTION
>OXIDATIVE STRESS 
>ENDOCRINE DISRUPTION
>VASCULAR DISRUPTION, >SPECIFIC RECEPTOR OR ENZYME MEDIATED EVENTS
41
Q

folate antagonism also affects

A

DNA and RNA-protein synthesis

42
Q

nuclear receptor targetting drugs such as______, can lead to up or down regulation of critical genes durining

A

Pax 3, cadherin, RAR, and RXR

neural crest embryologic development

43
Q

where a drug interrupts hormonal dependent organs development

A

agonists or antagonist will disrupt hromonally dependent organ development

44
Q

drugs that cuase oxidative stress do so by

A

teratogen stimulate prostaglandins and lipoxygenases

45
Q

fetal hypoxia and fetal damage can be insuduced by drugs that

A

interrupt adequate oxygenation of developing fetus thru placental obstruction or spasm

46
Q

ace and arb’s cause

A

permanent renal dysfunction in the developing fetla kidney

47
Q

widespread fetal dysfunction from lack of cholesterol for membrane production induced by

A

statins

48
Q

chronic NSAIDS in pregnancy–>teratogenic on the basis that

A

developing body needs PG’s and lipoxygenases for proper development

49
Q

conundrum with depressed mothers

A

depression itself has bad outcomes for the fetus, while the SSRI’s cause ahrm to the fetus to

50
Q

SSRI’s and pregnancy complications

A

incr. SA risk and risk of pre-eclampsia

51
Q

SSRI’s have what unique side effect in the infants

A

persistane PAH

52
Q

paint the pciture of what a SSRI’s teratogenized baby would look like

A

preterm, long, low BW, SfGA, anencephaly, omphalocele, cardiac defects, unresponsive to pain, tremors, psychomotor abn, autism

53
Q

class A indicates

A

adequate studies in pregnant women–>no defects in first trimester, no increase risk in 2nd or 3rd

54
Q

class B indicates

A

animal studies do not indicate risk, inadequate studies in humans,

or

animal studies show adverse effects and trials in pregnant women have been safe in first and no inc risk in 2nd or 3rd

55
Q

class c indicates

A

animal studies=adverse, but no adequate studies in humans, or-no animal repro studies or human studies

56
Q

class d

A

*maybe indicated if benefite»»risk and no other alternative
evidence of human fetal risk, but benefits might be acceptable despite potential risk

57
Q

class x indicates

A

studies in animals or humans DEMONSTRATE fetal abnormalities, report indicate evidence of fetal risk, risk&raquo_space;»»benefit in pregnant women

58
Q

limitation for pregnancy exposure registries

A

unles very veyr large they will be unable to detect increased risk especially for rare malformations

59
Q

three tools useful in determining causality

A
  1. registry
  2. case-controlled (probably able to determine causality)–>some bis
  3. retrospective cohort study–>recall bias, can reveal associated but not causality
60
Q

describe body composition and drug distribution in the newborn-first year

A

less body fat-lipophillic drugs distribute worse

*more body water-better distribution of hydrophillic agents

61
Q

plasma binding in the neonate

exxagerated organ effect and greater potential distribution per dose

A

reduced capacity for plasma ptoetin binding in the newborn
*for drugs tat are significantly protein bound this greatly increases the free fraction-especially if another drug is even more affinity for protein

62
Q

elimination in the neonate

A

immature kidney function compromises a major elimination foute for some drugs

63
Q

skin of newborn

A

more easily perfused–> transdermal mroe sensitive route in the newborn

64
Q

newborn and subcutaenous dosing

A

immature regulation of vascular perfusion lends to erradic absorption

65
Q

liver/body wt for infants

A

larger liver/body weight in infants

66
Q

enzyme profiles in infant

A

immature–>slower to break down/activate drug

67
Q

brain/body wt ratio

A

larger in infants

68
Q

blood brain barrier in infants

A

more permeable in infants

69
Q

renal function in infants

A

immature

70
Q

protein binding in infants

A

limited

71
Q

absorption profiles in infants

A

slower GI

faster IM

72
Q

neonatal changes in half life of drugs

A
  1. in general, all drugs have longer half lives than in the adult
  2. pehnytoin-dose adjustment may be necessary in an ongoing basis to account for continual organal maturation of the fetus
73
Q

calculate dosing based on weight ratio to adult

A

Adults dose x (weight in kg/70)

*however, more accurately based upon Surface Area

74
Q

breastfeeding and risk of drug exposure

A

the benefits of breastfeeding outweigh the risk of exposure to therapeutic agents via human breast milk

75
Q

which ones desevere SPECIAL consideration

A

tose that are CONCENTRATED in the human breast milk or those that result in clinically significant on the basis of relative infant dose or detectable serum concentrations

76
Q

caution is also advised for drugs with

A

unproven benefits, with long half lives that may lead to drug accumulation, or with known toxicity to the mother or infant

77
Q

what types of drugs will be in breastmilk with greater concentrations

A

lipid soluble drugs
drugs with pH greater than 7 (bases)
*pH of breast milk is 7 (blood 7.4)

78
Q

drugs that will not transfer into the breast milk as well

A

highly protein bound drugs

79
Q

preferred drugs/timing during breast feeding

A

give dose after feeding

drugs with short half like preferred

80
Q

time of greatest concern for drug in breast feeding

A

early post partum

*as the breast bud alveolar cells mature they transmit drug less and less

81
Q

Drugs problematic in breast feeding: act in CNS: produce sedation/drowsiness/dependence

A 
>Chloral Hydrate-drowsiness
>Methadone-withdrawal
>Diazepam-sedation
>Heroine-narcotic dependence
Lithium-avoid
82
Q

antimicrobial problematic in breast feeding–causes grey baby syndrome

A

Chloramphenicol-Blood dyscrasia, bone Marrow Supress., grey baby
*if given directly or via breast milk

83
Q

Drugs problematic in breast feeding: supress thyroid function

A

> iodine-thyroid supression

>Propothiouracil-thyroid supressed

84
Q

Name some major SSRI’s the pediatrician should be extra vigilant of when mother taking

A

Citalopram, Fluoxetine, Lamotrigene, Nortriptyline, Venlafaxine
*can exceed 10% of materanl plasmaconcentration in the infant

85
Q

how long does it take for a functional spermatogonia to make a spermatozoon

A

64 days

86
Q

paternal toxicity could cause

A

> mutation in the DNA or altered gene expression

>direct contact with the fetus via seminal fluid

87
Q

paternal teratogens could lead to

A

early preganancy loss, still birth, preterm delivery, growth restriction

88
Q

name some known paternal teratogens

A 
heavy metals
solvents
pesticides
anesthetic gases, hydrocarbons
*workplace exposures
89
Q

major drug classes represented for male teratogenicity

A 
antivirals
anticancer
mab's
retinoids
DMARDS
AED
Androgen receptor antagonist

Reproductive (9 decks)

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