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216 Cards in this Set

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Labial Fusion
associated with excess androgens, 21-hydroxylase deficiency (elevated 17alpha, urine 17-ketosteroid, low serum cortisol) leading to congential adrenal hyperplasia.
- ambiguous genitalia, hyperandrogenism, salt wasting, hypotension, hyperkalemia, and hypoglycemia.
- requires reconstructive surgery
Imperforate Hymen
Hymen is at the junction between the sinovaginal bulbs and UG sinus.
- Imperforate- no opening develops. obstruction of outflow tract of the reproductive system. Diagnosed w/ primary amenorrhea and cyclic pelvic pain. (can develop to persistent ab pain) Requires surgery

Microperforation- small opening
septate- midline hymen.
Tranverse Vaginal Septum
Occurs from improper canalization of the mullerian tubercle. At the junction between upper 3rd and lower 2/3rds.
- diagnosis made at puberty w primary amenorrhea.
- Thicker than the hymen, normal hymen will be proximal.
- Surgical Correction
Vaginal Atresia
UG sinus fails to contribute to the lower portion of the vagina. Absent lower vag is replaced by fibrous tissue.
- presents w/ amenorrhea, cyclic pelvic pain.
- no introitus and presence of vaginal bulge. Large hematocolpos. Surgical correction achieved w/ vaginal pull through.
Vaginal Agenesis
occurs in mayer-rokitansky-kuster-auser syndrome, testicular feminization.
Mayer-Rokitansky-Kuster-Hauser syndrome
Congenital absence or hypoplasia of the proximal vagina, cervix, uterus, and fallopian tubes. 10% of pts have normal uterus w/ functioning endometirum. There may or may not be a rudimentary pouch.
- Serial Dilation of peroneal body (years) , surgical neovag.
Blood behind the hymen
buildup of secretions
testicular feminization
46 xy peeps w/ insenstivity to testosterone
beginning of vag, undescended gonads.
Benign Gestational trophoblastic disease:
what makes up most of these?
hydatidiform moles
90% complete- no associated fetus.
10% incomplte- molor degeneration w abnl fetus
What are the types of malignant trophoblastic disesae?
invasive moles, choriocarcinoma, PSTTs.
What is the pathogenesis of a complete molar?
fertilization of an enucleate ovum. (all paternal chromosomes). 46XX

Complete mole-> trophoblastic proliferation and hydropic degeneration in absecnce of fetal parts. Higher malignant potential
What is the epidemiology of molar pregs?
1:1000 among white women.
Asians- 1:200
What are the risk factors for a molar pregnancy?
women under 20 or over 40. Low beta-carotene, folic acid in diet
prior miscarriages
What is the clinical manifestation of complete molar?
irregular or heavy vag bleeding during early pregs. Painless, or w/ contractions.
May also present w:
passage of molar pregs
Discrepency of uterine size and date
Bilateral theca lutein cysts
Trophoblastic PE

B-HCG-> N/V, irritability, dizziness, photophobia, nervousness, anorexia, tremors. (pre-eclapmsia prior to 22 wks is classic for molar)
What is the pex for molar pregs?
expulsion of molar clusters into vagina, or blood in cervical os. Theca lutein cytsts. No fetal heart tones,
How do you Dx a molar preg?
B-HcG are HIGH.
pelvic US.
What is the differential for a molar?
high B-HcG or enlarged placentas:
multiple gestation, erythroblastosis fetalis, intrauterine infecction, fibroids, threatened abortion, ectopic, normal preg
What is the Rx for molar?
immediate removal of uterine contents.
What is the follow up for molar pregs?
95% to 100% cure.
Serial B-hCG should be monitored weekly, then monthly for a year.
Pahtogenesis of partial mole?
normal ovum fertilized by two sperm. 69 XXY.
Focal hydropic villi and trophoblastic hyperplasia of the syncytial layer.
Incomplte moles often appear w/ a coexistent fetus w/ a triploid genotype.
Lower malig potential
clincial manifestation of a partial mole?
delayed menses, preg diagnosis. 90% present with miscarriage or missed abortions. much less severe symptoms.
Pex- normal but not fetal heart tones
Rx- immediate removal.
Follow up- B-HCG
why get surgery?
womens get them when they are of child-bearing age, regress in menopause.
surgery-> irrecgular bleeding, infertility, mass effect-> pelvic pain, pressure, urinary frequency or constipation.
What is the pathogenesis of fibroids?
monoclonal-> single muscle cell. Development from smooth muscle cells of the uterus.
Homonally responsive to estrogen. Grow quickly and to huge proportions in preggers.
menopause-> stop growing, may atrophy.
How are fibroids classified?
submucosal- beneath endometrium
intramural- in muscular wall of the uterus
subserosal- beneath the uterine serosa
What is a parasitic leiomyoma?
pedunculated fibroid that becomes attached to the pelvic viscera or omentum. Has it's won blood supply
How might fibroids cause pain?
outgrow blood supply and infarct
What are the risks for fibroids
AA, nonsmokers, peri-menopausal, obese.
How do fibroids present?
most asymptomatic
Abnl uterine bleeding is #1- submucosal imping on endometrial cavity. Bleeding occurs w increased heavy periods.

Can cause iron deficiency, anemia, weakness, dizziness

Pelvic pain only if vasc compromise is present (subseroud, pedunculated)

2ry dysmneorrhea w menses
pressure symps- pelvic pressure, fullness, heaviness.
constipation, urinary frequency, or urinary retention.
Increased infertility.
What is the DDx for a fibroid?
endometrial hyperplasia
endometiral cancer
exogenous uterine bleeding

ovarian cysts
ovarian neoplasm
tubo-ovarian abscess
How do you work up a fibroid?
pelvic ultrasound, hypoechogenic, MRI, HSG, saline sonograph, and hysteroscopy
How do you manage a fibroid?
rule out malignancy
monitor every 6 months
treat if symptomatic
medical Rx- depo, danazol, and GnRH
Uterine artery emoblization. (no if they want preggers)
Myomectomy (recur in 50% of patients)
what are theindications for myomectomy?
Abnl bleeding-> anemia
sever pelvic pain or scondary amenorrhea
size > 12 wks by gestation.
urinary frequency or retention
growth after menopause
rapid increase in size
What is the pathogenesis of endometriosis?
1) Halban theory- transported via the lymphatic system to various sites in the pelvis.
2) Meyer- multipotential cells in peritoneal tissue undergo metaplastic transformation into endometrial tissue
3) Sampson- retrograde menstruation-> intraabdominal implants
What are the most common sites for endometriosis?
ovary and pelvic peritoneum.
Ovary- cystic collection known as endometrioma.
also uterosacral ligaments, ant and post cul-de-sacs and the posterior uterus and broad ligaments.
What is the mechanism of symptoms for endometriosis?
disrupt normal tissue, form adhesions, and fibrosis, and sever inflamation.
epidemiology of endometriosis?
women of reproductive age
most common reason for hospitalization.
20% of women w/ chronic pelvic pain.
What are the risk factors for endometriosis?
1st degree relatives.
Lupus, other autoimmune disordres.
less often in black women
What is the clinical hx of endometriosis?
cyclic pelvic pain. dysmenorrhea, dyspareunia, abnl bleeding, and infertility.

Dysmenorrhea in 3rd decade, worsens w age; consider if w previous hx of not painful menses.

Dyspareunia w/ deep penetration that can aggravate endometriae lesions in cul-de-sac
how does endometriosis cause infertility?
exact mechanism is unclear, endometriosis thought to distort pelvic architecture, interfere w tubal mobility and cause tubal obstruction from dense adhesions
What is the pex for endometriosis?
subtle to non-existent. PEX during early menses w/ large implnts. Uterosacral nodularity, rectovaginal exam, or fixed retroverted uterus. ovary-> tender, fixed adnexal masss.
How do you Dx endometriosis?
direct visualization w laparoscopy or laparotomy. Peritoneal biopsy not necessary but is helpful in confirming the Dx of endometriosis.
Implants may appear rust colored.
What is the DDx for endometriosis?
PID, recurrent acute salpingitis, adenomyosis, fibroids, adhesions, hemorrhagic corpus luteum, ectopic preggs., ovarian neoplasm
What is the Rx for endometriosis?
Expectant management used in pts w/ minimal or noexistent symptoms.

NSAIDS, OCCs (Provera. (not seaking to conceive

Psudomenopause- Danocrine (androgen) or GnRH.

Conservative surgical therapy- ablation or excision of visible endometriosis during laparoscopy.

TAHBSO, LOA,a nd removal of endometriosis
What are SEs of using Danazol in Endometriosis?
acne, oily skin, weight gain, edema, hirsutism, deepened voice (effects of androgens)
What are the SEs of using GnRH for endometriosis?
headache, vasomotor flushing, sweating, atrophic vaginitis w/ Lupron.

Hot flashes, osteoporosis (use add back estrogen)
hat is endometrial proliferation?
normla part of themenstrual cycle that occurs during the follicular or estrogen-dominant phase of the cycle.
What is simple proliferation?
overabundance of histologically normal endometrium. Simple endometrial proliferation can advance to endometrial hyperplasia.
What is endometrial hyperplasia?
abnl proliferation of glandular and stromal ellements of the endometrium resulting in histologic alterations in its cellular architecture and/or cytologic atypia. focally develop in normal endometrium. Not automatically advance to carcinoma if left untreated but they can occur simultaneously w endometrial carcinoma.
what is simple vs. complex endometrail hyperplasia?
simple- abnl proliferation of stromal and glandular endometrial elements. <1% of lesions progress.

Complex- abnl proliferation of gland, w/o stromal elements. Glands are crowded in a back to back fashon and are varying shapes and sizes. No atypia. 3% progress
What is cytoloic atypia?
found in severe endometrial hyperplasia; large nucleai, lost polarity, increased nuclear-to-cytoplasmic ratios. Prominent nuclei, and irregular clumped chromatin.

atypical simple- cellular atypia and mitotic figures in addition to glandular crowding and complexity. Lesions progress to carcinoma in 8% of cases.

Atypical complex- 29% progress.
What are the risks for endometrial hyperplasia?
Late menopause, >55
Exogenous estrogen use w/o progesterone
Chronic anovulation
Diabetes mellitus
Tamoxifen use
(unopposed estrogen)
What is teh epidemiolgy of endometrial hyperplasia?
menopausal or perimenopausal women or shortly after menarche if ovulation is infrequent
What are the clinical manifestations of endometrial hyperplasia?
irregular bleeding. enlarged uterus.
growth of the myomerium in response to continuous estrogen.
Diagnostic eval- biopsy.
what is the Rx for endometrial hyperplasia?
progestin (depo; inhibi and reverse the endometrial hyperplasia. D&C, or hysterectomy
when do you experience morning sickness?
first week to 12-16 wks
what is the high of BHCG in pregnancy and when does it occur?
100,000 at 10 wks. decreases throughout the 2nd trimester., levels off at 20,000 to 30,000
how do you confirm a pregnancy?
at 5 wks by ultrasound showing a gestational sac at BHCG of 1500 to 2000. Fetal heart at 6wks or 5000-6000.
What is a pregancy called an embryo?
up to 8 wks (10 wks gestational)
afterwards is a fetus
delivery and 1 year is an infant
When is a delivery pre-term?
<37 wks
What is the definition of parity?
beyond 20 wks tha tled to an infant weighting more than 500mg.
How do you date a pregnancy?
Gestational age is from the LMP.
Developmental age is from fertilization.
Estimated date of delivery is to subtract 3 months and add 7 days.
what is the relationship between US and LMP in determining Gestational Age?
1st trimester, not off by more than 1 wk.
2 wks in 2nd
3 wks in 3rd
(done by crown-rump length in 1st half of 1st trimester)
When can you hear the fetal heart?
20 wks by nonelectric fetoscopy or at 10 wks by doppler.
when is fetal movemet felt by mom?
16 and 20 wks.
What CV changes occur in Preggers?
CO increases by 30-50%
Most during 1st trimester max at 20-24 wks.
SVR decreases-> drop in BP. SBP down 5-10, DBP down 10-15 (from increased progesterone)
What happens to pulm during preggesr?
Increase of 30-40% in tidal volume in pregs. Decrease in total lung capacity.
Increase in minute ventilation of 30-40%. Increase in PAO2, and PaO2. Decrease in PACO2, and PaCO2 to 30 from 40
dyspnea of pregs occurs in 60-70%.
What GI changes occur in preggers?
N/V in >70%.increased egen, progesterone and HcG. N/V should resovle by 14-16wks.

In pregs, prolonged gastric emptying and decreased GE sphincter tone.-> Ptyslism, spitting.

decreased colon motility-> increased water absorb and constipation.
What renal changes occur in preggers?
increase in size of kidneys and uretur. Increased pyelo. GFR increases by 50%. BUN and Cr decrease by 25%. Increase in renin-angiotension. Increased Na resorp. no increase of plasma Na
What are the heme changes in preggers
plasma volume increases by 50%.
RBC volume increases by 20-30%.
i.e. dcrease in Hct.
WBC increases to 10.5
WBC may increase to 20 in labor
decreased platelets.
hypercoaguable (increased VII-X) no change in clotting, bleeding times. increased thromboembolic events
What are the endocrine changes in preggers?
hyperestrogenic. Derived from circulating precursors from adrenals, converted by placenta. causes increase in Thyroid blinding globulin. hCG has thyroid stimulatiog properties (increase in T3 and T4) -> euthyroidPRL increase.
hCG doubles for every 48hrs
peak at 10-12 wks
What is hPL
Human placental lactogen i sproduced in placenta and is important for ensuring a constant nutrient supply to the fetus. hPL, known as human chorionic somatomammotropin.
lipolysis and increase in FFA floating around. increased insulin, and proteins.
Progesterone in pregs?
corpus luteum makes int in early pregs. Derived from LDL.
relatxes smooth muscle.
What are the musculoskeletal changes in preggers?
shift in posture, lower back strain.
What are the skin changes in preggers?
spider angiomata, palmar erythema.
hyperpigmentation of nipples, umbilicus, abdominal midline, perineum and face 2/2 to increased alpha-melanocyte-stimulationg hormone and the steroids.
Melasma, chloasma
What are teh nutrition increases?
to 2000, 2500 kcal per day. (300kcal per day)
protein, iron, folate, ca and others.
Protein goes to 70-75 from 60
Ca should be 1.5g/day.
Folate increase from .4-.8mg/day.
How much weight should be gained in pregs?
between 20 and 30 lbs. Obese should gain 15 and 20. thin should gain 25-35.
What are the basics of a prenatal OB visit?
BP, weight, U/A, uterus measurement, ascultation of fetal heart.

- bp drops during 1st and 2nd trimester, and rises after.
- large weight gain can be fluid overload
- fundal height should respond to gestational age.
- at 10-14 wks use doppler for heart tones
- U/A for protien dm, uti
- vaginal bleeding (miscarriage, ectopic), vaginal discharge (infection, cervical change) or leaking of fluid (ruptured fetal membranes), urinary symptoms.
- 20 wks, fetal movement, contractions (> 5 or 6 per hour is preterm labor).
What shoudl be done in the first-Trimester?
patients, nulliparous should be familiarized w preggers.
Hct, type and screen, RPR, rubella ab, hep b, gonorrhea, chlamydia, ppd, pap, UA, culture, VZV, HIV
What groups should be screened in high risk?
Gestational diabetic
HTN, Renal dz, other
Cardiac disease
Pregestational diabetic
AA- sickle cell
35 or older- prenatal genetics
Diabetes risk- glucose loading test
pregestational diabetic- sonogram date
HTN, Renal dz, pregestational diabetic, prior preeclampsia, renal transplant, SLE- 24 hr urine
pregestational diabetic, prior carciac disease- ECG
Graves- immunoglobulins
thyroid- TSH, free T4
SLE- anti-Rho, anti-La
What is key in teh 2nd-trimester visit? What labs?
most screenign is done. Alpha fetoprotein. triple screen
fetal heart tones, no more N/V. fetal movement. Screening US at 18-20wks (anatomic survey, amniotic fluid volume, placental location and gestational age.

Childbirth classes, tours of the labor floor.

may get amnio
what is significant about an elevated Afp?
neural tube defects
What is the triple screen?
B-HcG, estriol, MSAFP
What happens in the 3rd trimester visit?
27-29 wks, ordr Hct, RPR, glucose loading test, gonorrhea, chlamydia, CXR, PPD, Group B strep; examine cervix.

increase visits to 2-3 wks. every wk at 36 wks. Rh neg should receive RhoGAM at 28 wks.
Leopold's maneuvers at 32-34 wks.
what is looked at in labs of the 3rd trimester?
HCT below 32-33% Hgb of 11 are started on Fe and stool softeners. GLT > or equle to 140 is indication for glucose tolerance test.
What is the deal with back pain in preggers?
stretching helsp release endorphins. Gentle massage, heating pads, and tylenol for pain.
severe pain, requires muscle relaxants, narcotics
What is the deal with constipation in preggers?
elevated progesterone-> decreased motility. increased absorption of water from GI tract.
Solution: increase PO fluids, water. Stool softeners, bulking agents may help. Laxatives can be used. avoided in 3rd trimester.
What is the deal with contractions in preggers?
occasional irregular contractions occur several times per day. Dehydration cause increased contractions, and pts should be advised to drink many glasses of water and juice per day. Regular contractions as often as every 10-15 minutes is preterm labor.
What is teh deal with dehydration in preggers?
expanded intravasc space and 3rd spacing, difficult time maintaining volume. Increased fluids (may lead to contractions)
What is the deal with edema in preggers?
IVC and pelvic veins are copmressed by the utureus-> increased hydrostatic pressure in Lower extremities and eventually to edema in feet and ankles. Elevation of the lower extremities above the heart can ease this. Sleep on their sides.
What is the deal with GERD in preggers?
Relax LES, transit time in stomach increased frflux and nausea.
pts w reflux should be placed on antacids., eat mult small meals, no lying down. continued symps-> H2 blocker or PPI.
What is the deal with hemorrhoids in preggers?
topical anesthetics and steroids for pain. Prevent constipation.
Define infertility
inability to conceive after 12 months of frequent intercourse w/o contraception
Define fecundability
probability that a single cycle will result in preggers 25%
define fecundity
probability that a single cycle will resutl in a live birth.
What is capacitation?
Set of cellular changes sperm must undergo to fertilize

influx of intracellular calcium
destabilization of sperm membrane
What is the acrosomal reaction?
breakdown of the first block of the egg
What is the zona reaction?
rejection of additional sperm after the first one gets in.
what drives decreasing fertility in the U.S.?
decreased family size
improved contraception
later marriage
access to family planning
increased educational and professional opportunities
delayed child bearing
what are the male causes of infertility?
congenital GU defects
erectile dysfunction
What is needed to work up male infertility?
Semen analysis, endocrine blood tests
When should you draw LH, FSH?
day 3 of a cycle
What lifestyle changes can be made to help fertility?
weight loss
smoking cessation
drug use cessation
decrease caffeine
decrease in stress
What are Group I ovulatory disorders?
hypothalamic pituitary failure (kallmans)
can use comiphene
What are group II ovulatory disortders?
hypothalamic pituitary disfunction
what are group III ovulatory disorders?
ovarian failure
turners, older
what are the risks of assisted reproductive therapy?
ectopics, multiple gestation
ovarian hyperstimulation syndrome
genetic abnlties
what are the stresses of infertility?
expensive, cycles of hope and loss.
guilt, shame, embarassment
What is the infection rate of HIV to a baby w/o treatment?
What increases transmission from mother to child w/ HIV?
higher viral load
rupture of the membranes, events during labor and deliviery taht exposes fetus to maternal blood.
transmission occurs late in pregs, labora nd deliviery.
what decreases transmission of HIV?
Cesarean delivery lowers transmission rates by 2/3rds. w/o therapy.
AZT during the antepartum, intrapartum, and neonatal period reduces transmission by 2/3rds.
Transmission rates are less than 1% in an undetectable viral load.
HIV positive women should be on triple therapy. HAART in pregs to keep viral load down.
What is the risk of maternal HSV on teh fetus?
vertical transmission can occur. Cesarean is preferred if there are lesions.
acyclovir from 36 wks on.

1ry herpes infections are highre attack rate than 2ry. can be transmitted across the placenta. Antibody titers can be examined.

Late primary is most risky as there is no maternal abs.

HSV causes severe infections of skin, mouth.
sepsis, pneumonia, encephalitis.

IV acyclovir if suspected.
what is the risk of maternal VZV on teh fetus.
transplacental transmission.; can cause spontaneous abortions, teratogenic threat. Postnatal infection may range from chickpox, to fulminant dissemintaed infection.

Varicella zoster immune globulin may prevent transmission of the disease. Should receive w/in 72hrs of disease.
what is the risk of maternal parvovirus on the fetus?
erythema infectiosum. slapped cheek. resovles w/ minimal intervention.
1st trimester, abortion, later infections. can cause fetal hydrops.

look for IgM levels.
US 4-6wks after exposure
what is the risk of maternal CMV on the fetus?
subclinical or mild viral illness. Rarely will cause hepatitis or mononucleosis like syndrome.

can cause hepatomegaly, splenomegaly, thrombocytopenia, jaundice, cerebral calcifications, chorioretinitis, and interstitial pneumonitis. mortality rate ofup to 30%, may develop mental retardation, hearing loss, neuromuscular disorder.

no Rx or prophylaxis for the disease.
What is the risk of maternal rubella on the fetus?
maculopapular rash, arthritis, arthralgias, and a diffuse lymphadenopathy that lasts 2-4 days. can be transmitted to the fetus and cause congenital rubella infection. can cause deafness, cardiac abnlties, cataracts, and mental retard.

latent DM, throid, deafness, ocular, GH deficiency.
What is the risk of maternal GC infection on the fetus?
eye, oropharynx, external ear, anorectal mucosa. Disseminated, cause arthritis, and meningitis.
Rx is ceftriaxone, penicillin and probenecid.
what is the risk of maternal chlamydia infection on the fetus?
conjunctivitis, and some with pneumonia.
what is the risk of maternal Hep B on the fetus?
viral hepatitis caued by hep b dna virus can be aquired from sex, blood, transplacental.
mild hepatic dysfunction to fulminant lliver failure and death.
what is the risk of maternal syphilis on the fetus?
must be transplacental. latent syphilis is okay. 1ry or 2ry is more likely.
late abortion, stillborn infant, congenital infection

early have maculopapular rash, snuffles, hepatomegaly, splenomegaly, hemolysis, lymphadenopathy, and jaundice..

Dx is by IgM
How does maternal toxo affect the child?
a patient will develop fevers, malaise, lymphadenopahty and rash.
transmitted in 3rd trimester

kids will get fevers, seizures, chorioretinitis, hydro, microcephaly, hepatosplenomegaly, and jaundice.
what are the risks for an ectopic?
tubal scarring, decreased peristalsis of tube, IUD

prior ectopic pregnancy
previous tubal surgery
prior pelvic or abdominal surgery resulting in adhesions.
current use of exogenous hormones including progesterone or estrogen
DES-exposed pts w congenital abnlties
Congenital abnlties of fallopian tubes
Use of an IUD for birth control
What is the Hx givien by pts w/ ectopic
unilateral pelvic pain. vaginal bleeding

pex may shwo adnexal mass, tender, and uterus that is small for gestational age.
what are the signs of a ruptured ectopic?
hypotensive, unresponsive, peritoneal irrritation
what labs can be obtained for an ectopic?
bHCG, predictable manner, should cause doubleing, ectopic, does not double. may have a low hematocrit.

US can show a pregs thats IUP.
1500-2000, fetal heartbeat seen >5000
What is the treatment for ectopic?
stabalize w/ fluids
ex lap for removal.

unruptured ectopic shoudl be monitored for rupture. saproscoic resection.
MTX for treatment of the ectopic preganncy is sued at most institucionts.
complte abotion
Incomplete abortion
Inevitable abortion
threatened abortion
missed abortion
abortus- fetus lost before 20wks
complte- complte expusion of all products of conception
incomplete- partial expulsion of some but not all POC before 20 wks gestation
Inevitable abortion- no expulsion of products, bleeding and dilation of the cervix such athat a viable pregnancy is unlikely
threatened abortion- Intrauterine bleeding b4 20 wks w/o dilation of the cervix
missed- death of embrio, w/o expulsion
first trimester abortions?
what percentage of all abortions occur in 1st trimester?
how does a patient present?
60-80% of all abortions
early are at < 12 wks
associated w/ abnl chromosomes.
% may be higher because many abortions likely occur before implantation.

bleeding from the vagina. cramping, abdominal pain, decreased symptoms of pregnancy. PEX should include vital signs to rule out shock and febrile illness.
Pelvic exam can be performed to look for sources of bleeding other than uterine and for changes in the cervix suggestive of an inevitable abortion.
Lab tests: quant, CBC, blood type, antibody screen.
US can assess fetal viability and placentation.
what si the treatment for a first trimester abortion?
follow for recurrent bleeding and infection.
incomplted- D&C or prostas.
2nd trimester abotions.
infection, maternal uterine or cervical anatomic defects, maternal systemic disease, exposure to fetotoxic agents, and trauma. abnl chromosomes are not a frequent cause of late abortions. Late 2nd trimester abortions and periviable deliveries are also seen w PTL.
how is a 2nd trimester ab diagnosed?
bleeding from vagina, cramping, abdominal pain, decreased symptoms of pregnancy. occasionally patiens will note a lack of fetal movement in a previously active fetus.
what is the Rx fora 2nd trimester ab?
D&E for retained POC.
what are the risk factors for incompetent cervix?
Hx fo cervical surgery
Hx of cervical lacerations
uterine anomalies
what are complicatsion of cerclage placement?
rupture of membranes, PTL, and infection.
when is a prophylactic cerclage placed?
12-14 wks
what is a recurrent aborter?
what is the pathogenesis?
how is a Dx made?
3 or more consecutive SABs.

chromosomal abnlties, maternal systemic diseasse, maternal anatomic defects, and infection. (antiphospholipid antibody)

thyroid, DM, APA, hypercoag, and SLE, lupus anticoagulant, factor V leiden, and ANA.
what is the treatment for translocation?
for luteal phase defect?
APA syndrome?
cystic fibrosis screening?
autosomal recessive disorder
mutation of cl channels.
-> chronic lung disease, recurrent infections.
pancreatic insufficiency

needs homozygote
if mom's a carrier, test dad, if he's positive, fetus has 25%, so CVS or amniocentesis can be done. negative screen cannot rule out.
what are teh two mutations in cystic fibrosis?
sickle cell:
AR or AD?
who should be screened?
how are they screened?
Sickle cell is AR
Pts have hemolytic anemia, shortened life expectancy, and pain crises.
All african descent should be screened in pregs.
Hbg electrophoresis
AR or AD?
Who is most likely carrier?
what are some of the symptoms?
What can be seen on PEX?
Eastern European Jews, French Canadians
founder effect (small ancestral group)
Infants develop symps 3-10 months after birth
loss of alertness, excessive reaction to noise. Progressive neurologic degeneration w developmental delay.
Myoclonic and akinetic seizures.
PEX- cherry-red spot., pale macula
paralysis, blindness, dementia; die by 4y/o
what is the basis of tay-saches?
deficiency of hexoaminodase A, enzyme is responsible for degradation of Gm2 gangliosides.
What are teh obstetric complications of diabetes in pregs?
Postpartum hemorrhage
increased cesarean section.
what are the diabetic emergencies posible in pregs?
diabetic coma
what are teh vascular and end organ involvement problems in diabetes and pregs?
peripheral vasc
what ae the neurologic probs of diabetes in pregs?
what are the fetal complications of DM in pregs?
macrosomia- tramatic delivery, shoulder dystocia, Erb's palsy

Delayed organ maturity- pulmonar, hepatic, neurologic, Pit thyroid axis

congenital malformations
CV defects
neural tube
caudal regression syndrome
situs inversus
duplex renal ureter

IUGR- intrauterine death
what is white class A of dm in pregs?
abnormal Glucose at any age or of any duration treated by diet
what is white class B of DM in pregs?
onset of DM at 20 or older and less thaen 10 yrs.
what is white class C of DM in pregs
onset at 10-19y/o or duration of 10-19 yrs
what is white class D1-4 of DM in pregs?
D1- onset before age 10
D2- duration >20yrs
D3- calcification of vessels of leg
D4- benign retinopathy (microvascular disease)
D5- HTN, not preeclampsia
what is white class R of DM in pregs?
proliferative retinopathy or vitreous hemmorhage
what is white class F of DM in pregs?
nephropathy over 500 mg/day proteinuria
what is white class RF of DM in pregs?
proliferative retinopahty AND nephropathy
what is white class G of DM in pregs?
mult preg failures
what is white class H of DM in pregs?
evidence of ateriosclerotic heart disease
what is white class T for DM in pregs?
renal transplant
what is white class A1 in DM in pregs?
gestational diabetes w/ diet control
what is white class A2 in DM in pregs?
insuln-treated DM in pregs
what tests are performed at the first prenatal visit in DM and pregs?
routine blood type, abs, Rh
Hct, Hbg, pap, rubella, syphillis, UTI, hep b, HIV, chlamydia

asymptomatic bateruira
random Cr/Protein.
TSH, free T4
eye exam

blood gcose 4-8x qday
urine keones for gcose>200
urine protein dipstick; quantitative/trimester for poor renal function
serum cr- each trimester

First trimester US.
2nd prenatal visit?
when is it scheduled?
what should have been monitored in that time?
1 wk.
glucose, results form optho, labs should be back.
what are the components of the quad screen?
serum alpha fetal protein, estriol, and beta-HCG
downs syndrome?
what chromosome?
what risks?
what phenotype?
higher rate of miscarriages, still births.
short, facies, developmental delay, and retardation.
cardiac defects, duodenal atresia, stenosis, and short limbs.
Trisomy 18
how is it screened?
what is seen on screening?
not compatible with life beyond age 2
US is a good tool: clenched fists, overlapping digits, rocker bottom feet; VSD, tetralogy of Fallot, omphalocele, congenital diaphragmatic hernia, neural tube defects, choroid plexus cysts
Trisomy 13
85% will not live past age 1
holoprosencephaly; cleft lip and palate; cstic hygroma; single nostril or absent nose; omphalocele; cardiac anomalies including hypoplastic left heart; and limb anomalies (club foot, polydactyly ,and overlapping fingers.
when does the neural tube form?
22-23 days after conception.
ant neuropore closes by 25
posterior pore closes by 27
what is associated with NT defects?
folic acid
homo zygote for MTHFR gene (methyl tetrahydrofolate reductase)
Spina bifida-> lemon sign, banana sign.
what are the findings in tetrology of fallot?
VSD, overriding aorta, pulmonary stenosis, adn RVH.
what is potter's syndrome?
renal failure causeing anhydramnios, pulmonary hypoplasia and contractures in the fetus
what is the first trimester screen?
nuchal translucency
b-hCG and PAPP-A
what is the second trimester screen?
MSAFP, B-hcg, estradiol.
what is an echogenic cardiac focus signifcant for?
doubles the odds of Down's syndrome
what is looked for in for rupture of membranes?
what is fetal lie?
transverse vs. longitudinal
what is fetal presentation?
vertex or breech
what is the bishop score?
0- closed, 0-30% effaced, -3, firm, posterior

1- 1-2 dilationg, 40-50% effaced, -2, medium consistency, mid position

2- 3-4, 60-70%, -1, soft cervix, anterior position

3- <5cm, <80% effaced, <+1
what are the indications for induction?
bishop score of 5 or less = failed induction 50% of the time.
what is significant about decelarations of FHR?
Early decelerations begin and end at the same time as contractions., from increased vagal tone secondary to head compression during a contractoin

Variable decelerations- occur any time and tend to drop precipitously. From umbilical cord compression.

Late Decelerations- begin at the peak of a contraction and slowly return to baseline after the contraction has finished. Uteroplacental insufficiency
what type of decelerations are the worst?
late, may degrade into bradycardias
what is stage 1 of labor?
onset of labor until complte dilation of the cervix has occured. lasts 10-12 hrs.
consists of latent and active pahse.
latent phase goes til 3-4cm are doen.
active phase- 1cm/hr
what are the three P's of labor?
power, pasenger and pelvis
affect transit time.
cephalopelvic disproportion results.
what is stage 2 of labor?
cervix is dilated.
stage 2 ends w deliver.
prolonged if > 2hrs.
rare to be > than 30 min.

early and variable decels are common in this stage. If they resolve quickly, it helps.

repetitive late decels, bradycardias, adn loss of variability are all signs of nonreassuring fetal status. (should be given O2 and placed on Left side if this happens)
what is uterine hypertonus?
long contraction- may cause decels.
what is tachysystole?
more than 5 contractions in a 10 minute period.
what is the solution for uterine hypertonus/tachysystole causing decels?
terbutaline to relax the uterus.
what are maternal-fetal resons for cesarean?
cephalopelvic disproportion;
failed induction of labor
what are the maternal reasons for cesarean?
Disease: herpes, HIV (untreated), cervical cancer

uterine surgery: classic cesarean; myomectomy

prior uterine rupture

obstruction: fibroids, tumors
what are the fetal reasons for cesarean?
bradycardia, no FHR variability
scalp pH< 7.2

breech, transverse

mult gestations: nonvertex, >2

anomalies: hydrocephalus, osteogenesis imperfecta
what are placental reasons for cesarean?
placenta previa
abruptio placenta
what is the role of measurign pH of fetal scalp?
reassuring when > 7.25
what points towards success of trial of vag after cesarean?
prior vag
prior vag after cesarean
nonrecurring indication for prior c/s
labor at 3cm, >75% effaced
what points towards no success of vag after cesarean?
prior c/s for cephalopelvic disproportion
induction of labor
what increases the risk of uterine rupture in vag after cesarean?
more than 1 prior cesarean
prior classical cesarean
induction of labor
high amounts of oxytocin
time from last cesarean < 18 months.
uterine infection druing last cesarean
what decreases the risk of uterine rupture in vag after cesarean?
prior vag delivery
cicrumvallate placenta
membranes double back over the edge of the placenta, dense ring around periphery of placenta. variant of placental abruption, major cuase of 2nd trimester hemorrhage.
placenta previa
placenta develops over teh internal os. can be complte, partial or marginal.
placenta accreta
abnl adherence of part or all the placenta to the uterine wall. associated w placenta in normal locations, incidence increases in placenta previa
placenta increta
abnl placentatoin where the placenta invades the myomeetrium
placenta percreta
abnl placentation where placental invades myometrium and utereine serosa.
vasa previa
velamentous cord insertion causes fetal vessels to pass over the internal cervical os. seen w velamentous and succenturiate placenta
Velamentous placenta
occurs when the blood vessels insert between teh amnion and the chorion, away from the margin of the placenta. leaves the vessels largely unprotected and vulnerable to compression or injury
succcenturiate placenta
extra lobe of the placenta that is implanted at some distance away from the rest of the placenta. Fetal vessels may course between the two lobes. possibly over the cervix.
what are placental causes o fanepartum bleeding?
placenta previa, placental abruption, vasa previa
what are the maternal causes of antepartum bleeding?
uterine rupture
what are the fetal causes of antepartum bleeding?
fetal vessel rupture
what are cervical causes of antepartum bleeding?
cervicitis, polyps, cervical ca
what are vaginal/vulvar causes of antepartum bleeding
lacerations, varices, cancer
what are some non-obstetric causes of ante-partum bleedign?
hemorrhioids, congenital bleeding disorder, abdominal trauma, pelvic trauma, hematuria.
what are the fetal complications associated w/ placenta previa?
preterm delivery and its complications
preterm premature rupture of membranes
Intrauterine growth restriction
vasa previa
congenital abnlties.
what is the presentation of placenta previa?
painless vaginal bleeding. after 28 wks of gestation. (accreta is asymptomatic)
what is the treatment for a placenta previa?
pelvic rest, modified bed rest.
- unstoppable labor, fetal distress, and life-threatening hemorrhage are all indications for immediate cesarean delivery.

70% have rebleed, will need delivery before wk 36.

amnio for fetal lung maturity, and delivery by c-section.

1. stabalize the patient- hospitalized, fetal monitoring, IV access.
what are risks for placenta previa?
prior cesarean
uterine scarring.
mult gestations,
mult parity
what are some predisposing factors for placental abruption?
previous placental abruption
avanced maternal age
uterine distension
multiple pregancy
vascular deficiency
collagen vascular disease
cocaine use
cigarete smoking
alcohol use
circumvallate placenta
short umbilical cord
what are some of the precipitation factors for placental abruption?
external/internal version
abdominal trauma
sudden uterine voulme loss
delivery of first twin
rupture of membranes
preterm premature rupture of membrates.
what is the presentation of placental abruption?
3rd trimester bleeding w severe abdominal pain, strong contractions.
what is the pex of placental abruption?
firm tender uterus, vaginal bleeding. TOco w small contractions.