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obgyn > phys > Flashcards

phys Flashcards

1
Q

how does glucose move from mom to baby

A

facilitated diffusion

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2
Q

passive diffusion into placenta

A

oxygen, carbon dioxide, creatinine, urea, bilirubin, water, and drugs

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3
Q

facilitated diffusion into placenta

A

glucose and lactate

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4
Q

active transport into placenta

A

amino acids, peptides, hormones, vitamins, FA, inorganic ionos

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5
Q

pinocytosis into placenta

A

proteins, lipids, antibodies (IgG)

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6
Q

first trimester increased risk for down syndrome

A

NT (nuchal translucency) > 4mm
PAPP-A (serum pregnancy associated plasma protein A) decreased
free beta hCG increased

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7
Q

first trimester risk for trisomy 18

A

NT (nuchal translucency) increased
PAPP-A (serum pregnancy associated plasma protein A) decreased
free beta hCG decreases

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8
Q

first trimester risk for trisomy 13

A

NT (nuchal translucency) increased (not as much as down syndrome)
PAPP-A (serum pregnancy associated plasma protein A) decreased
free beta hCG decreased

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9
Q

when can you do chorionic villus sampling

A

~10-13 weeks in women with increased risk of chromosomal abnormalities

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10
Q

women with increased risk of chromosomal abnormalities

A 
prior child with chromosomal abnormality
> 35
abnormal 1st or 2nd trimester screening 
abnormal nuchal translucency 
prior pregnancy losses
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11
Q

cons to chorionic villus sampling

A

increased risk of spontaneous abortion (1:200-1:300)
increased infection
potential fluid leak

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12
Q

what does triple screening measure

A

alpha-feroprotein, unconjugated estriol, and beta-hCG

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13
Q

when to do 2nd trimester screening

A

15-18 weeks

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14
Q

quadruple screening

A

alpha-fetoprotein, unconjugated estriol, beta-hCG, and inhibin A

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15
Q

2nd trimester increased risk for down syndrome

A

decreased AFP and estriol

increased beta-hCG and inhibin A

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16
Q

2nd trimester increased risk for trisomy 18

A

decreased AFP, estriol, and beta hCG

no change in inhibin A

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17
Q

2nd trimester increased risk for trisomy 13

A

all levels unchanged

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18
Q

what is trisomy 18 called

A

edwards syndrome

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19
Q

what is trisomy 13 called

A

patau syndrome

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20
Q

high AFP on screening test

A

open neural tube defects - spina bifida (OR multiple gestations)

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21
Q

when to do amniocentesis

A

between weeks 15-18 (+ fetal karyotyping)

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22
Q

gold standard chromosomal abnormality tests

A

chorionic villus sampling + amniocentesis

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23
Q

when should I test for gestational diabetes?

A

between 24-28 weeks

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24
Q

when should I give RhoGAM (anti-D Rh immunoglobulin) to unsensitizied women

A

28 weeks gestation

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25
Q

what does a biophysical profile look at

A

fetal breathing, fetal tones, amniotic fluid levels, NST, and gross fetal movements (each is 2 points, want. above 6)

26
Q

when should I screen for GBS

A

36 weeks

if +: give prophylactic antibiotics during delivery - IV penicillin (2nd line is ampicillin, cephalosporins, clindamycin, vancomycin)

27
Q

Complications of GBS

A

mom: chorioamnionitis, preterm labor, asymptomatic bacteriuria, cystits, pyelonephritis
baby: early postpartum infection (meningitis, septic arthritis, osteomyelitis)

28
Q

how does progesterone affect GnRH pulse frequency

A

negative feedback - slows the pulse frequency

29
Q

functional hypothalamic amenorrhea

A

altered GnRH and gonadotropin secretion

30
Q

Where are LH receptors expressed?

A

theca, granulosa, and luteal cells

respond to both LH and hCG

31
Q

where are FSH receptors expressed?

A

granulosa cells

32
Q

FSH functions

A

acts on granulosa cells to help convert androstenedione and testoosterone into estrogens

stimulates secretion of inhibin B (negative feedback to pituitary)

increases granulosa cell number –> follicular growth

increases LH receptor expression –> ovulatory capacity

33
Q

LH stimulates

A

theca cells to produce andostenedione + testosterone
Granulosa cells to produce progesterone
Ovulation
Development of corpus luteum

34
Q

effects of estrogen

A 
endometrial proliferation
skeletal homeostasis
neuroprotective
maintenance of collagen
breast development
feedback to HPO axis (negative at low concentrations, positive at high)
vasodilation
protective against atherosclerotic plaque formation 
adipose tissue regulation
increased production of coag factors
35
Q

effects of progesterone

A

inhibits endometrial proliferation and promotes decidualization
facilities implantation
stimulates uterine growth
suppresses myometrial contraction
decreases maternal immne/inflammatory response
promotes breast development for lactation

36
Q

inhibin A

A

present in luteal phase

can be increased in preeclampsia and fetal down syndrome

37
Q

inhibin B

A

seen in follicular phase
low levels in early follicular phase can be suggestive of declining ovarian reserve

tumor marker for granulosa cells

38
Q

how does clomid work?

A

blocks estrogen negative feedback –> increase in FSH –> exaggerated follicular response

39
Q

contraindications for estrogen

A 
>35 + smoker of >15 cigs/day
HTN
Current or hx of VTE
Known ischemic heart disease
Complicated valvular heart disease 
Current breast cancer
Decompensated cirrhosis
Migraine with aura
Hepatocellular adenoma or malignant hepatoma 
Long standing DM or DM complications
Multiple risk factors for arterial CVD
40
Q

andrenarche

A

increased secretion of adrenal androgens –> acne, adult type body odor, pubic + axillary hair

41
Q

gonadarche

A

growth and maturation of gonads –> folliculogenesis and ovulation

42
Q

pubarche

A

appearance of pubes

43
Q

thelarche

A

appearance of boobies

44
Q

menarache

A

onset of menses, usually 2-3 years after thelarche

irregular and anovulatory cycles common after menarche for ~5 years

45
Q

average onset of puberty for females

A

8-13 - biggest determinant is genetic

other factors: nutrition, obesity, chronic illness, geography, endocrine-disrupting chemicals

46
Q

delayed pubtery

A

absence of thelarche by 13, absence of menarche by 16

47
Q

tanner stage 1

A

prepubertal boobs, no pigmented pubic hair

48
Q

tanner stage 2

A

budding with larger areolae, small amount of coarse pigmented hair mostly along labia majora

49
Q

tanner stage 3

A

enlargement of breast and areolae, spread of coarse pigmented hair over mons pubis

50
Q

tanner stage 4

A

secondary mound of areolae, almost adult pattern pubes

51
Q

tanner stage 5

A

mature contour boobs, adult pattern pubes

52
Q

follicular threshold for menopase

A

1000

53
Q

when does menopause usually occur

A

between 51-53 - genetics is big determinant

54
Q

symptoms of menopause

A

hot flushes, night sweats, sleep disturbances, mood changes, short term memory loss, headaches, loss of libido, AUB

55
Q

physical changes of menopause

A

atrophy of vaginal epithelium, increased vaginal pH, decreased vaginal secretions, decreased circulation to vagina and uterus, pelvic relaxation, urinary dysfunction, CVD risk increased, osteoporosis, collagen loss

56
Q

what holds the ovaries in place?

A

ovarian ligament, broad ligament, and suspensory ligament

*Ovarian artery, vein, and nerve plexus all pass through suspensory ligament

57
Q

at what level does estrogen switch from negative feedback to positive feedback of FSH and LH

A

200pg/mL - this surge causes increase in FSH + LH –> allows primary oocyte to complete meiosis –> secondary oocyte

58
Q

what happens in ovulation

A

follicle ruptures and secondary oocyte release into fallopian tube

stops in metaphase of meiosis II until fertilization

59
Q

where is progesterone coming from in luteal phase

A

granulosa cells respond to decreased LH by increasing activity of P450scc –> cholesterol –> pregnenolone –> progesterone

60
Q

what does corpus luteum secrete

A

progresterone, inhibin A, estradiol (leads to FSH and LH suppression)

61
Q

what causes bleeding during menses

A

fall in estrogen and progesterone when corpus luteum regresses, release of prostaglandins –> rhythmic vasodilation and constriction of spiral arteries –> bye bye functionalis layer

obgyn (14 decks)

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