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Reproductive > Sweaty's Drugs: Neonatal, HRT > Flashcards

Sweaty's Drugs: Neonatal, HRT Flashcards

1
Q

general signs of drug withdrawal in infant

A

onset: varies depending on amount of drug accumulated and rate of release from tissue
lasts: weeks to months
signs: autonomic hyperactivity, irritable, excessive crying, poor feeding, abnormal reflexes
Tx: may have to re-expose and taper down

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2
Q

signs of opiate withdrawal in infant

A

CNS hyperactivity: tremor/ seizure, irritable, increased wakefulness, crying, hyperactive reflexes, frequent yawn/sneeze
autonomic hyperactivity: sweat, nasal stuffiness, mottling, fever
GI tract: diarrhea, poor feeding
CAN mimic other diseases

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3
Q

Determinants for drugs to cross placenta

A
  1. lipid solubility
  2. ionization
  3. Mol. Wt less than 600
  4. duration/timing of drug MOST important
  5. maternal plasma protein drug binding
  6. placental development and blood flow
  7. energy dependent transporters (consider polymorphisms)
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4
Q

effects of placental drug metabolism

A

can increase/decrease fetal exposure

can also get SOME metabolism in fetal liver (only some blood goes straight to liver and liver is immature)

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5
Q

requirements for teratogen designation

A
  1. characteristic set of malformations
  2. exert effects at a particular stage of fetal development
  3. show dose dependent incidence
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6
Q

What 2 species are candidate drugs required to be tested in?
Whys 2?

A

one rodent: usually rats
one non-rodent: usually rabbit
better chance of identifying teratogens: may be oversensitive

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7
Q

Mechanisms that contribute to teratogenity

A
  1. folate antagonism
  2. neural crest disruption
  3. endocrine disruption
  4. oxidative stress
  5. vascular disruption
  6. specific receptor or enzyme mediated events
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8
Q

SSRI in pregnancy

A

depression and SSRI can have adverse effects on fetus and pregnancy
SSRI effect in fetus: pulmonary artery HTN, others

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9
Q 
Pregnancy Category
A
B
C
D
X
A

risk benefit relationship
A: studies in PREGNANT WOMEN have not demonstrated risk in pregnancy
B: ANIMAL studies have not demonstrated risk; no adequate human reproduction study
C: ANIMAL studies have shown adverse effect on fetus OR no animal/human reproduction studies
D: evidence of fetal risk, but potential benefits may be acceptable despite risk in some circumstances
X: human or animal studies demonstrate fetal abnormalities, risk clearly outweighs benefit

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10
Q

Differences in infant drug metabolism (compared to adult)

  1. metabolic capacity
  2. body composition: fat, TBW
  3. plasma binding capacity
  4. renal function
  5. GI absorption
  6. IM absorption
  7. liver and brain/body weight ratio
  8. enzymes
  9. BBB permeability
  10. general trends
A
  1. poor
  2. less fat, more total body water
  3. lower: increases free drug in highly bound drugs
  4. immature: can alter elimination
  5. slower
  6. faster
  7. larger liver and brain to body weight ratio
  8. immature
  9. BBB more permeable
  10. longer T1/2, change in pharmacokinetics as neonate ages (over days rather than weeks or months)
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11
Q

How are drugs adjusted for children?

A

based on weight although surface area would be more accurate

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12
Q
  1. What drugs will concentrate in breast milk?
  2. Drugs less likely to be transferred?
  3. Drugs/methods preferred when breastfeeding?
A
  1. concentrate: BASIC, LIPID soluble
  2. less transferred: high protein bound drugs
  3. short T1/2 drugs, dose after feeding, most cautious early-post partum
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13
Q

Groups of drugs that are problematic in breast feeding

A
  1. CNS acting drugs: sedation, infant dependence
  2. thyroid suppressors
  3. chloramphenical: blood dyscrasia, bone marrow suppression
  4. antidepressants: not sure of effect but lots passes to baby
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14
Q

mechanisms of paternal teratogenicity

major drug classes?

A
  1. mutation in DNA or altered gene expression
  2. direct contact with fetus
    drug classes: antivirals, anticancer, traditional and mAb, retinoids
    unexpected: androgen receptor antagonist, DMARD, anti epileptic
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15
Q

TOXNET

A

website to find drug toxicity in utero and through breast milk

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16
Q

LACTMED

A

part of TOXNET for breast milk

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17
Q

Which menopausal signs will improve over time without treatment?
Which will not improve without treatment?

A

vasomotor: improve without Tx (may take years)
vaginal dryness: does not improve without Tx
undetermined: sleep and mood problems

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18
Q

CEE (conjugated equine estrogens) alone for HRT: Risks vs. Benefits

A

more balanced than CEE plus MPA

decreased risk: breast CA

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19
Q

CEE plus MPA (medroxyprogesterone acetate) for HRT: Risks vs. Benefits

A

increased risk: CHD, breast CA, stroke, PE, gallbladder disease, dementia, urinary incontinence
decreased risk: hip fracture, DM, vasomotor symptoms

20
Q

Although most risks of HRT dissipate after Tx is discontinued, what risk remains?

A

breast CA

21
Q

When is HRT appropriate?

A

moderate to severe menopausal symptoms in EARLY menopause (not for chronic disease prevention)

22
Q

HRT: vaginal estrogen

A

genitourinary symptoms without vasomotor symptoms

23
Q

CI for estrogen

A
  1. undiagnosed abnormal genital bleeding
  2. breast CA, estrogen dependent CA
  3. DVT, PE, stroke, MI
  4. liver dysfunction
  5. allergic to preparation
  6. pregnancy
24
Q

Caution with estrogen

A
  1. dementia
  2. gallbladder disease
  3. hypertriglyceridemia
  4. prior cholestatic jaundice
  5. hypothyroid
  6. fluid retention plus cardiac or renal dysfunctionn
  7. hypocalcemia
  8. prior endometriosis
  9. hepatic hemangiomas
25
Q

Who gets HRT according to 10 yr CHD risk?

  1. less than 5 years since LMP
  2. 6-10 yrs
  3. greater than 10 yrs
A
  1. low risk: oral; mod. risk: transdermal
  2. very low: oral; low to mod.: transdermal
  3. AVOID
    also AVOID in anyone that is high risk for developing CHD
26
Q

non-pharm Tx of vasomotor symptoms in menopause

A

cognitive behavioral therapy

other with caution: weight loss, stress reduction, soy isoflavones, stellate ganglion block

27
Q

paroxetine

A

non-hormonal: antidepressant

Tx: vasomotor Sx (only FDA approved non hormonal)

28
Q

fluoxetine

A

non-hormonal: antidepressant

Tx: vasomotor Sx (off label)

29
Q

escitalopram

A

non-hormonal: antidepressant

Tx: vasomotor Sx (off label)

30
Q

venlafaxine

A

non-hormonal: antidepressant
Tx: vasomotor Sx (off label)
AE: also anorexia, dry mouth, vomiting

31
Q

clonidine

A

non-hormonal
MOA: lowers peripheral vascular reactivity, raises sweating threshold
Tx: vasomotor Sx (off label)
AE: dry mouth, insomnia, drowsy

32
Q

gabapentin

A

non-hormonal
MOA for VMS: unclear
Tx: vasomotor Sx (off label)
AE: dizzy, unsteady, drowsy

33
Q

MOA and AE for antidepressants used for vasomotor Sx

A

MOA for VMS: unknown

AE: nausea, headache, insomnia, sex dysfunction

34
Q

17 B estradiol

A

oral, transdermal, vaginal estrogen

35
Q

ethinyl estradiol

A

oral estrogen

36
Q

conjugated estrogen

A

oral estrogen

37
Q

medroxyprogesterone acetate

A

oral progestogen

38
Q

norethindrone acetate

A

oral, transdermal progestogen

39
Q

drospirenone

A

oral progestogen

40
Q

micronized progesterone

A

oral progestogen

41
Q

levonorgestril

A

transdermal progestogen

42
Q

What is the MOST effective therapy for both VMS and Urogenital atrophy in menopause?

A

estrogen +/- progestogen

AE: breast tenderness, uterine bleeding, N/V, headache, weight change, rash, pruritus, cholecystitis

43
Q

Why is transdermal estrogen preferred?

A

avoid first pass metabolism that promotes prothrombotic hemostatic changes in factor IX, protein C resistance, tPA activator
less weight gain
oral increases: coagulation effects, CRP, fibrolytic markers, worse effect on triglycerides
both benefit: lipid profile (oral more so)

44
Q

bazedoxifene

A

estrogen and SERM combo
agonist is some tissues, antagonist in others
use: menopause (reduces endometrial over growth)

45
Q

What happens when HRT is stopped?

A

bone reposition accelerates, vulvovaginal atrophy recurs

half have VMS return

Reproductive (12 decks)

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