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Sweatman Drugs in Pregnancy Flashcards

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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
can fetal liver metabolize drugs
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
26
placenta increases or decreased fetal exposure or toxicty
decreases exposures usually and decreaeses toxicity (placenta is kinda protective)
27
one bad thing placental metabolism does
may increase exposure to carcinogens--> benpyrene
28
use off-label for monring sickness and caused tertogenic effects in the 1950s in england
thalidomide
29
effect of thalidomide
phocomelia-seal limbs (weird stubby arms)
30
prenatal death in weeks
1 and 2
31
major morphologic abnormalitis
week 3-7
32
physiologic defects and minor morphologic defects seen in
week 8-term
33
single exposure to teratogen is unlikely to
produce adverse effects on the fetus | *expectant mother must take it on a more chronic basis, although not necessarily the entire pregnancy
34
to be a proven teratogen..must show (3)
>characteristic set of malformations >exert effects at a particular stage of fetal development >dose dependent incidence
35
what percentage of pregnancies are unplanned
50%
36
how many births have some sort of defect
4% | genetic or unidentified environmental factors
37
many women may go____days before they realize theya re pregnant
14--> giving time for toxic drug exposure during this critical phase of implantation and initial development
38
all candidate drugs must be tested in ____ _____. one ____ and one ____
two species one rodent one non-rodent
39
PERHAPS THE MODELS BEING INDICATED TO SHOW TOXICITY ARE OVERSENSITVE BECAUSE
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
6 MECHS OF RECOGNIZED TERATOGENICITY
``` >FOLATE ANTAGONISM >NEURAL CREST DISRUPTION >OXIDATIVE STRESS >ENDOCRINE DISRUPTION >VASCULAR DISRUPTION, >SPECIFIC RECEPTOR OR ENZYME MEDIATED EVENTS ```
41
folate antagonism also affects
DNA and RNA-protein synthesis
42
nuclear receptor targetting drugs such as______, can lead to up or down regulation of critical genes durining
Pax 3, cadherin, RAR, and RXR neural crest embryologic development
43
where a drug interrupts hormonal dependent organs development
agonists or antagonist will disrupt hromonally dependent organ development
44
drugs that cuase oxidative stress do so by
teratogen stimulate prostaglandins and lipoxygenases
45
fetal hypoxia and fetal damage can be insuduced by drugs that
interrupt adequate oxygenation of developing fetus thru placental obstruction or spasm
46
ace and arb's cause
permanent renal dysfunction in the developing fetla kidney
47
widespread fetal dysfunction from lack of cholesterol for membrane production induced by
statins
48
chronic NSAIDS in pregnancy-->teratogenic on the basis that
developing body needs PG's and lipoxygenases for proper development
49
conundrum with depressed mothers
depression itself has bad outcomes for the fetus, while the SSRI's cause ahrm to the fetus to
50
SSRI's and pregnancy complications
incr. SA risk and risk of pre-eclampsia
51
SSRI's have what unique side effect in the infants
persistane PAH
52
paint the pciture of what a SSRI's teratogenized baby would look like
preterm, long, low BW, SfGA, anencephaly, omphalocele, cardiac defects, unresponsive to pain, tremors, psychomotor abn, autism
53
class A indicates
adequate studies in pregnant women-->no defects in first trimester, no increase risk in 2nd or 3rd
54
class B indicates
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
class c indicates
animal studies=adverse, but no adequate studies in humans, or-no animal repro studies or human studies
56
class d
*maybe indicated if benefite>>>>risk and no other alternative evidence of human fetal risk, but benefits might be acceptable despite potential risk
57
class x indicates
studies in animals or humans DEMONSTRATE fetal abnormalities, report indicate evidence of fetal risk, risk >>>>>>benefit in pregnant women
58
limitation for pregnancy exposure registries
unles very veyr large they will be unable to detect increased risk especially for rare malformations
59
three tools useful in determining causality
1. registry 2. case-controlled (probably able to determine causality)-->some bis 2. retrospective cohort study-->recall bias, can reveal associated but not causality
60
describe body composition and drug distribution in the newborn-first year
less body fat-lipophillic drugs distribute worse | *more body water-better distribution of hydrophillic agents
61
plasma binding in the neonate exxagerated organ effect and greater potential distribution per dose
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
elimination in the neonate
immature kidney function compromises a major elimination foute for some drugs
63
skin of newborn
more easily perfused--> transdermal mroe sensitive route in the newborn
64
newborn and subcutaenous dosing
immature regulation of vascular perfusion lends to erradic absorption
65
liver/body wt for infants
larger liver/body weight in infants
66
enzyme profiles in infant
immature-->slower to break down/activate drug
67
brain/body wt ratio
larger in infants
68
blood brain barrier in infants
more permeable in infants
69
renal function in infants
immature
70
protein binding in infants
limited
71
absorption profiles in infants
slower GI | faster IM
72
neonatal changes in half life of drugs
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
calculate dosing based on weight ratio to adult
Adults dose x (weight in kg/70) | *however, more accurately based upon Surface Area
74
breastfeeding and risk of drug exposure
the benefits of breastfeeding outweigh the risk of exposure to therapeutic agents via human breast milk
75
which ones desevere SPECIAL consideration
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
caution is also advised for drugs with
unproven benefits, with long half lives that may lead to drug accumulation, or with known toxicity to the mother or infant
77
what types of drugs will be in breastmilk with greater concentrations
lipid soluble drugs drugs with pH greater than 7 (bases) *pH of breast milk is 7 (blood 7.4)
78
drugs that will not transfer into the breast milk as well
highly protein bound drugs
79
preferred drugs/timing during breast feeding
give dose after feeding | drugs with short half like preferred
80
time of greatest concern for drug in breast feeding
early post partum | *as the breast bud alveolar cells mature they transmit drug less and less
81
Drugs problematic in breast feeding: act in CNS: produce sedation/drowsiness/dependence
``` >Chloral Hydrate-drowsiness >Methadone-withdrawal >Diazepam-sedation >Heroine-narcotic dependence Lithium-avoid ```
82
antimicrobial problematic in breast feeding--causes grey baby syndrome
Chloramphenicol-Blood dyscrasia, bone Marrow Supress., grey baby *if given directly or via breast milk
83
Drugs problematic in breast feeding: supress thyroid function
>iodine-thyroid supression | >Propothiouracil-thyroid supressed
84
Name some major SSRI's the pediatrician should be extra vigilant of when mother taking
Citalopram, Fluoxetine, Lamotrigene, Nortriptyline, Venlafaxine *can exceed 10% of materanl plasmaconcentration in the infant
85
how long does it take for a functional spermatogonia to make a spermatozoon
64 days
86
paternal toxicity could cause
>mutation in the DNA or altered gene expression | >direct contact with the fetus via seminal fluid
87
paternal teratogens could lead to
early preganancy loss, still birth, preterm delivery, growth restriction
88
name some known paternal teratogens
``` heavy metals solvents pesticides anesthetic gases, hydrocarbons *workplace exposures ```
89
major drug classes represented for male teratogenicity
``` antivirals anticancer mab's retinoids DMARDS AED Androgen receptor antagonist ```

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