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phys Flashcards

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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
what does a biophysical profile look at
fetal breathing, fetal tones, amniotic fluid levels, NST, and gross fetal movements (each is 2 points, want. above 6)
26
when should I screen for GBS
36 weeks if +: give prophylactic antibiotics during delivery - IV penicillin (2nd line is ampicillin, cephalosporins, clindamycin, vancomycin)
27
Complications of GBS
mom: chorioamnionitis, preterm labor, asymptomatic bacteriuria, cystits, pyelonephritis baby: early postpartum infection (meningitis, septic arthritis, osteomyelitis)
28
how does progesterone affect GnRH pulse frequency
negative feedback - slows the pulse frequency
29
functional hypothalamic amenorrhea
altered GnRH and gonadotropin secretion
30
Where are LH receptors expressed?
theca, granulosa, and luteal cells respond to both LH and hCG
31
where are FSH receptors expressed?
granulosa cells
32
FSH functions
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
LH stimulates
theca cells to produce andostenedione + testosterone Granulosa cells to produce progesterone Ovulation Development of corpus luteum
34
effects of estrogen
``` 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
effects of progesterone
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
inhibin A
present in luteal phase can be increased in preeclampsia and fetal down syndrome
37
inhibin B
seen in follicular phase low levels in early follicular phase can be suggestive of declining ovarian reserve tumor marker for granulosa cells
38
how does clomid work?
blocks estrogen negative feedback --> increase in FSH --> exaggerated follicular response
39
contraindications for estrogen
``` >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
andrenarche
increased secretion of adrenal androgens --> acne, adult type body odor, pubic + axillary hair
41
gonadarche
growth and maturation of gonads --> folliculogenesis and ovulation
42
pubarche
appearance of pubes
43
thelarche
appearance of boobies
44
menarache
onset of menses, usually 2-3 years after thelarche irregular and anovulatory cycles common after menarche for ~5 years
45
average onset of puberty for females
8-13 - biggest determinant is genetic other factors: nutrition, obesity, chronic illness, geography, endocrine-disrupting chemicals
46
delayed pubtery
absence of thelarche by 13, absence of menarche by 16
47
tanner stage 1
prepubertal boobs, no pigmented pubic hair
48
tanner stage 2
budding with larger areolae, small amount of coarse pigmented hair mostly along labia majora
49
tanner stage 3
enlargement of breast and areolae, spread of coarse pigmented hair over mons pubis
50
tanner stage 4
secondary mound of areolae, almost adult pattern pubes
51
tanner stage 5
mature contour boobs, adult pattern pubes
52
follicular threshold for menopase
1000
53
when does menopause usually occur
between 51-53 - genetics is big determinant
54
symptoms of menopause
hot flushes, night sweats, sleep disturbances, mood changes, short term memory loss, headaches, loss of libido, AUB
55
physical changes of menopause
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
what holds the ovaries in place?
ovarian ligament, broad ligament, and suspensory ligament *Ovarian artery, vein, and nerve plexus all pass through suspensory ligament
57
at what level does estrogen switch from negative feedback to positive feedback of FSH and LH
200pg/mL - this surge causes increase in FSH + LH --> allows primary oocyte to complete meiosis --> secondary oocyte
58
what happens in ovulation
follicle ruptures and secondary oocyte release into fallopian tube stops in metaphase of meiosis II until fertilization
59
where is progesterone coming from in luteal phase
granulosa cells respond to decreased LH by increasing activity of P450scc --> cholesterol --> pregnenolone --> progesterone
60
what does corpus luteum secrete
progresterone, inhibin A, estradiol (leads to FSH and LH suppression)
61
what causes bleeding during menses
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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