phys Flashcards
how does glucose move from mom to baby
facilitated diffusion
passive diffusion into placenta
oxygen, carbon dioxide, creatinine, urea, bilirubin, water, and drugs
facilitated diffusion into placenta
glucose and lactate
active transport into placenta
amino acids, peptides, hormones, vitamins, FA, inorganic ionos
pinocytosis into placenta
proteins, lipids, antibodies (IgG)
first trimester increased risk for down syndrome
NT (nuchal translucency) > 4mm
PAPP-A (serum pregnancy associated plasma protein A) decreased
free beta hCG increased
first trimester risk for trisomy 18
NT (nuchal translucency) increased
PAPP-A (serum pregnancy associated plasma protein A) decreased
free beta hCG decreases
first trimester risk for trisomy 13
NT (nuchal translucency) increased (not as much as down syndrome)
PAPP-A (serum pregnancy associated plasma protein A) decreased
free beta hCG decreased
when can you do chorionic villus sampling
~10-13 weeks in women with increased risk of chromosomal abnormalities
women with increased risk of chromosomal abnormalities
prior child with chromosomal abnormality > 35 abnormal 1st or 2nd trimester screening abnormal nuchal translucency prior pregnancy losses
cons to chorionic villus sampling
increased risk of spontaneous abortion (1:200-1:300)
increased infection
potential fluid leak
what does triple screening measure
alpha-feroprotein, unconjugated estriol, and beta-hCG
when to do 2nd trimester screening
15-18 weeks
quadruple screening
alpha-fetoprotein, unconjugated estriol, beta-hCG, and inhibin A
2nd trimester increased risk for down syndrome
decreased AFP and estriol
increased beta-hCG and inhibin A
2nd trimester increased risk for trisomy 18
decreased AFP, estriol, and beta hCG
no change in inhibin A
2nd trimester increased risk for trisomy 13
all levels unchanged
what is trisomy 18 called
edwards syndrome
what is trisomy 13 called
patau syndrome
high AFP on screening test
open neural tube defects - spina bifida (OR multiple gestations)
when to do amniocentesis
between weeks 15-18 (+ fetal karyotyping)
gold standard chromosomal abnormality tests
chorionic villus sampling + amniocentesis
when should I test for gestational diabetes?
between 24-28 weeks
when should I give RhoGAM (anti-D Rh immunoglobulin) to unsensitizied women
28 weeks gestation
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)
when should I screen for GBS
36 weeks
if +: give prophylactic antibiotics during delivery - IV penicillin (2nd line is ampicillin, cephalosporins, clindamycin, vancomycin)
Complications of GBS
mom: chorioamnionitis, preterm labor, asymptomatic bacteriuria, cystits, pyelonephritis
baby: early postpartum infection (meningitis, septic arthritis, osteomyelitis)
how does progesterone affect GnRH pulse frequency
negative feedback - slows the pulse frequency
functional hypothalamic amenorrhea
altered GnRH and gonadotropin secretion
Where are LH receptors expressed?
theca, granulosa, and luteal cells
respond to both LH and hCG
where are FSH receptors expressed?
granulosa cells
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
LH stimulates
theca cells to produce andostenedione + testosterone
Granulosa cells to produce progesterone
Ovulation
Development of corpus luteum
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
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
inhibin A
present in luteal phase
can be increased in preeclampsia and fetal down syndrome
inhibin B
seen in follicular phase
low levels in early follicular phase can be suggestive of declining ovarian reserve
tumor marker for granulosa cells
how does clomid work?
blocks estrogen negative feedback –> increase in FSH –> exaggerated follicular response
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
andrenarche
increased secretion of adrenal androgens –> acne, adult type body odor, pubic + axillary hair
gonadarche
growth and maturation of gonads –> folliculogenesis and ovulation
pubarche
appearance of pubes
thelarche
appearance of boobies
menarache
onset of menses, usually 2-3 years after thelarche
irregular and anovulatory cycles common after menarche for ~5 years
average onset of puberty for females
8-13 - biggest determinant is genetic
other factors: nutrition, obesity, chronic illness, geography, endocrine-disrupting chemicals
delayed pubtery
absence of thelarche by 13, absence of menarche by 16
tanner stage 1
prepubertal boobs, no pigmented pubic hair
tanner stage 2
budding with larger areolae, small amount of coarse pigmented hair mostly along labia majora
tanner stage 3
enlargement of breast and areolae, spread of coarse pigmented hair over mons pubis
tanner stage 4
secondary mound of areolae, almost adult pattern pubes
tanner stage 5
mature contour boobs, adult pattern pubes
follicular threshold for menopase
1000
when does menopause usually occur
between 51-53 - genetics is big determinant
symptoms of menopause
hot flushes, night sweats, sleep disturbances, mood changes, short term memory loss, headaches, loss of libido, AUB
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
what holds the ovaries in place?
ovarian ligament, broad ligament, and suspensory ligament
*Ovarian artery, vein, and nerve plexus all pass through suspensory ligament
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
what happens in ovulation
follicle ruptures and secondary oocyte release into fallopian tube
stops in metaphase of meiosis II until fertilization
where is progesterone coming from in luteal phase
granulosa cells respond to decreased LH by increasing activity of P450scc –> cholesterol –> pregnenolone –> progesterone
what does corpus luteum secrete
progresterone, inhibin A, estradiol (leads to FSH and LH suppression)
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
