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OBGyn > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

Define G, P (including TPAL) and ROM (A and S)

A
  • Gravida (G): total pregnancies
  • Parity (P): total deliveries

o T: term (> 37 wks)

o P: preterm (20-37 (less than 37.0 wks) )

o A: abortions/losses including miscarriages, ectopics, etc. (

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2
Q

Mean pregnancy is 40 wks (280 days) from when?

A
  • 1st day of LMP
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3
Q

Define term, preterm and post-term pregnancy

A
  • Term: 36th completed (37.0) - > 42.0

- Preterm: 42.0

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4
Q

Diagnosis of labor

A
  • Clinical diagnosis: regular painful contractions, progressive cervical effacement & dilation, bloody show
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5
Q

List phases of normal labor

A
  • 0: functional quiescence
  • 1: cervical softening
  • 2: activation
  • 3: labor (has stages, see separate card)
  • 4: puerperium or post-partum interval
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6
Q

Briefly define the phases of labor

A

0: Functional quiescence:
- Occurs via inhibition functions of progesterone, prostacyclin, relaxin
1: Cervical softening:
- Slow changes to extracellular collagen matrix
2: Activation:
- Myometrial changes (irritability and responsive via oxytocin and uterotonins)
- Fetal presenting part descends
- Cervical ripening via PGs, relaxin, estrogen, progesterone
- Progesterone withdrawal, CRH function?
3: Labor (see 3 stages on separate card):
- Influence of oxytocin, PGs and relaxin
4: Puerperium or postpartum interval:
- Myometrium = rigid and in state of constant contraction under oxytocin
- Uterine involution and cervical repair

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7
Q

List the stages of labor in terms of timing and events

A

** must know

  1. First: onset of labor -> full cervical dilation
    a. Latent: onset of labor -> change in slope of rate of cervical dilation (slow cervical change)
    b. Active: onset at ~4cm, period of most dilation occurs here
    a. Acceleration, phase of max slope, deceleration
    c. Descent: ~9-10 cm, usually coincides with second stage, not widely recognized, pushing happens
  2. Second: full cervical dilation -> delivery of infant
  3. Third: delivery of placenta
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8
Q

Define the mechanics of normal labor

A
  • Powers: forces generated by uterus
  • Passenger: fetus
  • Passage: bony and soft tissues of maternal pelvis
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9
Q

Define adequate uterine activity during labor

A
  • Defined by frequency, intensity and duration of a contraction
  • 3-5 contractions in 10 minutes
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10
Q

Define lie (of fetus)

A
  • Spatial relationship of fetal spine to maternal spine. Longitudinal lie = better.
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11
Q

Define presentation (of fetus)

A
  • Fetal part that directly overlies pelvic inlet
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12
Q

Define malpresentation of fetus

A
  • Any presentation of fetus that is not cephalic with occiput leading
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13
Q

Define position of fetus

A
  • Relationship between a fetal part and maternal pelvis. Described by three letters.
  • First and last = maternal pelvic quadrants toward which the fetal part points
  • Middle = fetal part
  • Eg. LOA: left occiput anterior (fetal occiput is at left anterior quadrant). Also OA and OP if oriented midline and not in one of the quadrants.
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14
Q

Define station of fetus

A
  • Relationship of fetal presenting part to maternal ischial spines in cm (-5 to +5). –ve value = above spines, 0 station at plane of spines, +ve value = below spines.
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15
Q

Define diagonal conjugate vs true (obstetric) conjugate

A
  • Diagonal: Measurement from sacral promontory to inferior aspect of pubic symphysis. Measured and used clinically.
  • True (obstetric): Measurement from sacral promontory to superior aspect of pubic symphysis. Not measured clinically.
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16
Q

Most common shape of female bony pelvis and has easiest / best prognosis for birth

A
  • Gynecoid (classic oval shape)

- Worst = android and platypelloid

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17
Q

What is the limiting factor in the midcavity of the pelvis for delivering baby?

A
  • Interspinous diameter (approx. > 10 cm)
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18
Q

Review progression of labor graph in L20

A

Review progression of labor graph in L20

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19
Q

Review progression of labor graph in L20

A
  • Hypotension
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20
Q

Absolute contraindications for neuraxial analgesia at delivery

A
  • Refractory maternal hypotension, maternal coagulopathy, thrombocytopenia, LMWH within 12 hours, untreated maternal bacteremia, skin infection over site of needle placement, increased ICP caused by a mass lesion
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21
Q

How long does second stage of labor take in a nulliparous woman? Multiparous?

A
  • Nulliparous: max 2 hr w/o epidural, 3 hr with epidural

- Multiparous: max 1 hr 2/o epidural, 2 hr with epidural

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22
Q

How long does delivery of placenta take? When is intervention needed?

A
  • Usually
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23
Q

Describe cardinal movements of fetus in labor

A
  • Engagement, descent, flexion, internal rotation, extension, external rotation, expulsion
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24
Q

Lab draws necessary with initial assessment in labor

A
  • CBC, blood type/Rh, antibody screen, check for HIV/hepB/syphilis if no prenatal labs done
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25
Q

Describe when monitoring of fetal heart rate should be done during L&D and how often?

A
  • First stage of labor (labor -> full cervical dilation): HR q 30 mins during and immediately after contraction taken for ~ 2 mins
  • Second stage of labor (full cervical dilation -> delivery): HR q 15 mins during and after a contraction for ~ 2 mins
  • Note: no evidence for routine use of electronic fetal monitoring
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26
Q

How often should cervical checks be done during L&D period?

A
  • Done during 1st stage of labor q 1-4 hours
  • Prior to analgesia, especially epidural
  • When patient feels urge to push
  • Note: don’t do too frequently as uncomfortable and to minimize infection risk
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27
Q

Describe when placenta is being delivered passively?

A
  • Lengthening of umbilical cord, gush of blood from vagina, change in shape of uterine fundus
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28
Q

Define abnormal patterns of labor disorders in latent phase

A
  • Protracted labor: nulliparous > 20 hrs, multiparous > 14 hrs
  • Arrest
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29
Q

Management of protracted labor and arrest in latent phase

A
  • Not much is happening in this phase and prolongation doesn’t correlate with adverse perinatal outcome
  • Do expectant mgmt. Not indication for c/s.
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30
Q

Define abnormal patterns of labor disorders in active phase

A
  • Protracted labor: lasting for a long time w/cervical dilation rate
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31
Q

Is protracted labor in active phase an indication for c/s?

A
  • No, unless maternal or fetal data aren’t reassuring

- This carries risk for secondary arrest and poor perinatal outcome (ie. blood loss, infection etc.)

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32
Q

What is the most common causes of protracted labor disorder (aka primary dysfunctional labor) in active phase? Define tx?

A
  • Nulliparous = inadequate uterine activity / hypocontractile uterine activity

o Tx = amniotomy (break water) and/or oxytocin

  • Multiparous = cephalopelvic disproportion

o Tx = C/S

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33
Q

Management of secondary arrest in active phase of labor?

A
  • Confirm adequate uterine contractions, exclude macrosomic fetus/small pelvis/malpresentation!*know, examine to verify dilation/presentation/position/station
  • Amniotomy
  • Augment labor with IV oxytocin: dose to point where contractions are q2-3 mins, lasting 60-90 seconds and IU pressures are 50-60 mmHg
  • Monitor fetal heart pattern and uterine contractions throughout augmentation
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34
Q

Risks of IV oxytocin to augment labor

A
  • Uterine hyperstimulation, water intoxication (similar to ADH and acts as anti-diuretic), hypotension if bolus, uterine rupture
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35
Q

Management of combined disorder of first stage labor

A
  • C/section
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36
Q

Define abnormal patterns of labor in second stage

A
  • Protraction of descent:
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37
Q

Management of protracted descent in second stage of labor

A
  • Expectant mgmt./watchful waiting if FHT reassuring/descent progressive and delivery imminent
  • Consider intervention if prolonged (we don’t need to know time) for example via episiotomy, operative vaginal delivery
  • Aggressive attempts to shorten this stage associated with increased perinatal/maternal morbidity
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38
Q

Management of arrested descent in second stage

A
  • Evaluate labor pattern, maternal and fetal well-being, cephalopelvic relationship, distended bladder, maternal effort, dense anesthesia?, soft-tissue resistance
  • Use clinical judgment to decide between operative delivery intervention (episiotomy) vs surgical vs expectant mgmt.
  • Adverse outcomes can be: hemorrhage, trauma, chorioamnionitis
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39
Q

Define intervention at third stage of labor

A
  • > 30 mins: IV oxytocin, cord traction, manual extraction using anesthesia and abx.
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40
Q

Define episiotomy

A
  • Incision into perineal body
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41
Q

When is episiotomy indicated?

A

When is episiotomy indicated?

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42
Q

Compare and contrast the types of episiotomies in terms of benefits and risks

A
  1. Midline: posterior fourchette towards rectum
    - Benefits: straight incision, reduction of second stage, reduction of trauma to pelvic floor muscles
    - Risks: increased blood loss if done too early, potential fetal injury, localized pain, increased incidence of 3rd/4th degree lacs associated with incontinence and prolapse
  2. Mediolateral: 45 degree angle incision from inferior portion of hymenal ring
    - Benefits: no increase in incidence of 3rd/4th degree angle lacs, less damage to anal sphincter/mucosa, procedure of choice in IBD patients
    - Risks: unsatisfactory cosmetically, inclusion cysts form within scar, greater blood loss
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43
Q

What are 3rd and 4th degree perineal lacerations?

A
  • 3rd degree: into anal sphincter

- 4th degree: into rectum

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44
Q

Risk factors for shoulder dystocia?

A
  • Fetal macrosomia, maternal diabetes, obesity, postdatism, prolonged deceleration phase of labor
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45
Q

Results of shoulder dystocia

A
  • Neonatal trauma (brachial plexus injury) and death, postpartum hemorrhage
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46
Q

Mgmt. of shoulder dystocia

A
  • Episiotomy, McRoberts Maneuver (knees to armits, which changes angle in pelvis and increases opening)
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47
Q

What is operative vaginal delivery?

A
  • Delivery in which operator uses forceps or vacuum device to extract fetus
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48
Q

Indications for operative vaginal delivery

A
  1. Maternal: exhaustion, inadequate expulsive efforts, lack of efforts, need to avoid expulsive efforts (depending on comorbidities)
  2. Fetal: non-reassuring fetal heart tracings, prolonged second stage
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49
Q

Define criteria for operative vaginal delivery

A
  1. Maternal: adequate analgesia, lithotomy position, bladder empty, adequate pelvimetry, consent
  2. Fetal: head first, known position, engaged in pelvis, station > = +2
  3. Uteroplacental: cervix fully dilated (2nd stage of labor), ruptured membranes, no placenta previa
  4. Other: experienced operator, capability to perform emergency c/s
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50
Q

Types of forceps delivery

A
  1. Outlet forceps
  2. Low forceps
  3. Midforceps
  4. High forceps
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51
Q

Risks for forceps assisted birth

A
  • Maternal: perineal injury, vaginal and cervical lacerations, postpartum hemorrhage
  • Fetal: IC hemorrhage, cephalic hematoma, facial/brachial palsy, injury to soft tissues of face/forehead, skull fx
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52
Q

Indications for c/s delivery

A
  • Maternal: obstructive benign and malignant tumors, large vulvar condyloma, abdominal cervical cerclage (stich in cervix), prior vaginal colporrhaphy (vaginal wall repair), prior classic c/s or full thickness myomectomy (vertical more likely to rupture), prior uterine rupture
  • Maternal-fetal: cephalopelvic disproportion, failure to progress/arrest, placental abruption, placental previa (over cervix), uterine dehiscence of prior uterine scar, maternal request (controversial), large pelvic mass
  • Fetal: non-reassuring fetal heart tracing, malpresentation, HSV active, ITP, major congenital anomalies, cord prolapse
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53
Q

Risks of c/s

A
  • Blood loss, infection, injury, thrombotic events/PE, risk of future c/s, maternal mortality (note: 10x greater than with vaginal births)
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54
Q

Current practice for delivery of breech

A
  • Usually delivered by c/s. Occasionally unavoidable to deliver vaginally.
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55
Q

Define menopause

A
  • Cessation of menses after significant decrease of ovarian E production. 12 consecutive months w/no menstrual bleeding!
  • Preceded by perimenopause (aka menopausal transition) where E production fluctuates unpredictably.
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56
Q

Mean age of menopause

A
  • 51 years
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57
Q

Risk factors for early and late menopause

A
  • Genetic predisposition. Not related to age of menarche
  • Early: tobacco users, vegetarians, malnourished with slight build, high altitudes
  • Late: etoh users
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58
Q

Describe endocrine changes that happen prior to and during menopause

A
  1. Ovarian follicles become resistant to FSH & LH which are increasing d/t no response = E falls (levels still present d/t peripheral conversion esp. by muscle and adipose).
  2. P production stops and PMS sx disappear.
  3. Androgen production decreases w/SHBG.
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59
Q

SSx of menopause

A
  1. Alteration of menstrual flow/oligomenorrhea leading up to lack of menses
  2. Change in mood / behavior: depression, anxiety, irritability, loss of libido
  3. Vasomotor instability: hot flash = cardinal sx. D/t changes in NTs and PGs causing SNS activation and regional dilation.
  4. Decrease in REM sleep
  5. Changes in short term memory
  6. Urogenital atrophy (loss of collagen, pH and lube): vaginal pruritus, dryness, dyspareunia, urinary frequency, urgency and nocturia
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60
Q

What is the #1 morbidity in menopausal women? What is the best way to assess this? What is the #1 mortality in this group?

A
  • # 1 morbidity = Osteoporosis. DEXA is best. Normal T 2.5 SD
  • # 1 mortality = CV dz.
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61
Q

Describe the long term sequelae of menopause. What are the risk factors for these?

A
  1. Osteoporosis = #1 morbidity in menopausal women (loss of balance between osteoclasts and blasts). Risk factors = Caucasian, Asian, slender body build, poor diet, etoh/tobacco use, sedentary lifestyle, meds
  2. CV dz = #2 mortality in menopausal women. Risk factors = HTN, DM, central obesity, tobacco use. How? E changes lipid profile that predispose to atherosclerosis.
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62
Q

Tx options for menopause

A
  1. W/o uterus: E (incl. SERMS)
  2. W/ uterus: E & P combined
  3. Other non-steroids: clonidine (adrenergic antagonist) for hot flashes, SSRI
  4. Other non-meds: adequate diet (1500 mg Ca w/800 mIU of vit D daily), weight loss, avoid caffeine/etoh/tobacco, weight bearing exercise, stress reduction techniques, acupuncture, natural remedies
    - Note: per ACOG, HRT should only be used for short term (
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63
Q

Risks of standard HRT tx for menopause

A
  • Endometrial hyperplasia (leading to CA), breast cancer (slight risk), stroke/MI (slight increased risk), VTE (2x increase in women at risk)
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64
Q

When in HRT tx contraindicated?

A
  • Breast cancer hx w/in 5 years, E dependent neoplasm, undiagnosed vaginal bleeding, thromboembolic dz, liver dz/dysfunction, known/suspected pregnancy, hypersensitivity to hormone tx
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65
Q

Side effects of E HRT

A
  • Vaginal bleeding, breast tenderness, mood changes, weight gain/water retention
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66
Q

Side effects of P HRT

A
  • Affective sx (? Psychological), weight gain
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67
Q

What is premature ovarian failure (POF)?

A
  • Menopause occurring spontaneously before 40. May be secondary to natural causes, chemo or surgery. R/o other endocrine abnormalities in these patients.
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68
Q

Define prenatal, antenatal, postnatal, perinatal

A
  • Waiting for Shaw and Olesen
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69
Q

Define antepartum, postpartum

A
  • Waiting for Shaw and Olesen
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70
Q

What is advanced maternal age?

A
  • > 35
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71
Q

Sx and PE findings for diagnosis of pregnancy

A
  • Sx: missed period(s), fatigue, N/V, breast tenderness, Quickening (perception of fetal movement)
  • PE: enlargement of uterus, Chadwick sign (bluish discoloration of vagina), Hegar sign (softening of cervix)
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72
Q

When does uterus emerge from pelvis in pregnancy, ie. when can it be palpated?

A
  • Emerges from pelvis at pubic symphysis at 12 weeks
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73
Q

When can pregnancy be diagnosed from urine test?

A
  • ~ 4 weeks following first day of LMP (around time of missed period/2 weeks from ovulation)
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74
Q

When are fetal heart tones (FHT) detectable in pregnancy?

A
  • Traditional fetoscope/auscultation methods: 18-20 weeks

- Doppler: ~ 12 weeks

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75
Q

Describe how fundal height corresponds to gestational age? During what gestational time frame does this correspond?

A
  • Fundal height in cm represents GA from time it exits pelvis ~ 12 wks (at superior pubic symphysis = 12 cm) to ~ 36 wks (+/- 2 weeks/2cm)
  • Eg. 2 cm from pubic symphysis to fundus = 12 + 2 = 14 weeks
  • 12 weeks at pubic symphysis
  • 20 weeks at umbilicus
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76
Q

Factors that are assessed at initial prenatal visit?

A
  • Nutrition/weight gain counseling, sexual activity, exercise, smoking, environment/work hazards, etoh, home meds, illicit drugs, domestic violence/sexual abuse, seat belt use
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77
Q

Define gestational age

A
  • # of weeks that have elapsed between 1st day of LMP (not presumed conception date) and date of delivery
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78
Q

How is EDD (estimated due date) calculated?

A
  1. Naegele rule: add 1 year + 7 days to first day of LMP – 3 months. Example: LMP 1st day = 5/10/2016. EDC = 5/10/2016 + 1 year = 5/10/2017 + 7 days = 5/17/2017 – 3 months = 2/17/2017
  2. US established
    a. Abdominal: pregnancy sac visualized at 5-6 weeks or BHCG 5-6 K
    b. TV: pregnancy sac 3-4 weeks or BHCG at 1-2 K
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79
Q

When can cardiac activity of embryo be seen via US?

A
  • BHCG > 4 K
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80
Q

Normal intervals of antenatal visits from 1st prenatal visit?

A
  • Normal pregnancy: q 4 weeks til 28 wks, q 2 weeks til 36 wks, q 1 week until delivery
  • High risk: more frequently
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81
Q

What is done at every antenatal visit before delivery?

A
  • BP, weight, OB findings (fundal height, FHT, UA, uterine palpation for fetal presentation at 3rd trimester)
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82
Q

Which labs are done at 1st prenatal visit?

A

**

  • ABO/Rh; CBC, TSH, hep C, rubella, HIV, hep B, VDRL, GC, chlamydia, pap (depending on previous results and age), glucose if BMI > 30, UA with culture and sensitivity
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83
Q

When is gestational diabetes screening done in pregnancy?

A

**

  • 24-28 wks gestation. Give 50 g glucose load and see how body handles it. If +ve, do glucose tolerance test with fasting.
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84
Q

When is GBS vaginal culture done in pregnancy?

A

**

  • 35-37 wks gestation. If +ve, give abx during delivery.
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85
Q

Lab test at postpartum day #1

A
  • Hbg
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86
Q

What is the 1st integrated screen done in pregnancy? When does it occur? What is being measured?

A
  • HCG and PAPP-A between 10 and 13 6/7.
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87
Q

What screening is done during 2nd TM pregnancy?

A

**

  • 2nd integrated screen (aka quad screen): HCG, Estriol, Inhibin-A and AFP. Done around 16-20 wks.
  • Also anatomy US
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88
Q

When is movement of fetus perceived in nulliparous women? Multiparous?

A
  • ~ 18-20 wks in nulliparous

- ~ 16 wks in multiparous

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89
Q

If 1st TM bleeding occurs, you should think? 2nd TM? 3rd TM?

A
  • 1st TM: Threatened abortion esp. if N/V if previously present wanes rapidly
  • 2nd TM: Threatened abortion if 20 wks, think: PTL, placental abruption, placenta previa, cervical insufficiency
  • 3rd TM: labor, PTL, PROM, PPROM
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90
Q

Diet in pregnancy

A
  • Caloric increase +/- 300-500 kcal / day
  • If normal BMI: gain ~ 30 lbs
  • Folic acid: 4 weeks preconception to 12 weeks gestation prevents NTDS. Take ~ 400 mcg per day. If hx of NTD, take 4 mg per day.
  • Moderate intake of soft cheese, uncooked lunchmeat d/t Listeria concern and fish. No uncooked fish.
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91
Q

Describe skin changes at pregnancy

A
  1. Moles/tags darken/grow
  2. PUPP: Pruritic urticarial papules of pregnancy; prurigo; pemphigoid gestationalis; erythema of palms (BVs dilate); telangiectasias
  3. Melasma
  4. Linea nigra
  5. Stria
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92
Q

What abdominal complaints are normal in pregnancy?

A
  • Diastasis recti, GERD, GB stones, hydronephrosis, urinary frequency/urgency, colon peristalsis decreases, NV
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93
Q

Normal thyroid changes in pregnancy?

A
  • Thyroid may increase, thyroid bruit d/t increased vascularity
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94
Q

Normal eye changes in pregnancy?

A
  • Change in power, increase tear production
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95
Q

Normal breast changes in pregnancy?

A
  • Lobularity, nodularity, Montgomery tubules, vascularization, mastitis risk increase
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96
Q

Normal ENT changes in pregnancy

A
  • Capillaries of nose/pharynx, Eustachian tubes engorged; hoarseness/voice deepening
  • Gingival hypertrophy
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97
Q

Normal respiratory changes in pregnancy?

A
  • Minute ventilation/TVolume/VC increase, functional residual capacity decrease, RR same, dyspnea common
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98
Q

Normal heart/CV changes in pregnancy?

A
  • BV increase by up to 50%, CO/HR/SV increase, position of heart shifted toward horizontal, systolic murmurs not uncommon over P area
  • SVR decreases
  • Peripheral vasodilation
  • Compression of IVC = hypotension when supine, dependent edema, varicosities of legs/vulva, hemorrhoids (esp. late pregnancy)
  • Increased risk of PE/DVT in pregnancy and postpartum *note: higher than BC risk
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99
Q

How early can Braxton-Hicks contractions begin?

A
  • 3 months.
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100
Q

Describe normal MSK findings during pregnancy

A
  • L-spine lordosis; cervical flexion increased, mobility / instability of SI and pubic symphysis, CTS d/t fluid retention
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101
Q

Normal neurologic complaints in pregnancy

A
  • Migraine headaches may be more common
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102
Q

Define Puerperium

A
  • Aka the post-natal period (first 6 weeks after delivery)
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103
Q

Common complications during Puerperium

A
  • Wound infections, wound separation (fascia intact vs dehiscence where fascia not intact), endomyometritis, UTI, postpartum hemorrhage (early = at time of delivery; delayed: up to 1 week); VTE, postpartum depression
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104
Q

Describe immediate postpartum assessment/things to check for

A
  • 5 Bs
  • Brain (depression), breast (breastfeeding), bladder, bleeding (lochia = foul-smelling vaginal dc after birth containing blood, mucus, uterine tissue), birth control
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105
Q

Define baby blues vs postpartum depression

A
  1. Baby blues (up to 70%): sadness, emotional instability within 1st week of delivery, resolving by 10 days postpartum
  2. Postpartum depression (up to 25%): onset within 4 weeks lasting up to 7 months, sx similar to “standard” depression
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106
Q

Predisposing risk factors for postpartum depression

A
  • Hormonal changes, stressful life events, hx of depression, family hx of depression
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107
Q

Recommendations for post-partum contraception

A
  • Pelvic rest x 6 weeks
    1. Give P. Avoid E initially if breastfeeding (can decrease quantity and quality)
    2. No combo until 3 wks postpartum d/t risk of VTE. After 6 weeks, risk of VTE decreases to that of non-pregnant state.
    3. IUD: inserted immediately, but lower expulsion if waiting until 6 weeks
    4. Barriers
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108
Q

Define gestational diabetes

A
  • Diagnosed (or recognize) in second or third TM of pregnancy that is not overt diabetes
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109
Q

White classification of gestational DM

A
  • Class A1 & A2
  • A1: fasting 105, 2Hr post-prandial >= 120, tx = oral medication or insulin
  • Note: class D -> H w/vascular dz. Class B -> H treated with insulin.
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110
Q

Most common medical complication in pregnancy

A
  • Diabetes. >90% d/t gestational diabetes.
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111
Q

Criteria for DM diagnosis

A
  1. FPG >=126 (fasting = no intake for 8 hours)

OR

  1. 2-hr plasma glucose >= 200 on 75 gm OGTT

OR

  1. HgA1C >= 6.5%

OR

  1. Random plasma glucose >= 200 mg/dl
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112
Q

When does screening for GDM take place? Describe strategy for diagnosis

A
  • 24-28 weeks GA. If certain risk factors, screen earlier (see next flash card). Two-step process per ACOG. There are 1-step strategies outside USA.
    1. 1 hr 50g non-fasting glucose challenge test (aka glucose load test): If > 135 (per ACOG) proceed to step 2.
    2. OGTT-100g: diagnosis of GDM if 2 or move values from threshold are met. Thresholds set by NDDG and Carpenter/Coustan groups. Should we remember.
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113
Q

Who should be screened for GDM earlier than the general population?

A
  • GDM in previous pregnancy, known impaired glucose tolerance (pre-DM, PCOS), BMI > 30, people > 35 (advanced maternal age)
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114
Q

Pathophysiology of GDM

A
  • Increased insulin resistance (~16-20 wks) = increased insulin secretion = adequate in 1st TM, but inadequate in later gestational age = inadequate secretion = hyperglycemia
  • Factors responsible for resistance = HPL (human placental lactogen), HPGH (human placental), P, cortisol, prolactin, FFAs, TNF alpha, leptin, resistin. These all increase.
  • Adiponectin a protein synthesized by adipocytes decreases throughout pregnancy. It is an endogenous insulin sensitizer.
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115
Q

Complications resulting from pregestational DM

A
  • HTN, preterm birth, macrosomia, stillbirth (note: GDM not at risk for this!!!), perinatal death, malformations
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116
Q

Neonatal complications of DM

A
  • Macrosomia, asymmetric growth = shoulder dystocia, fetal growth restrictions (generally with vascular involvements), surfactant deficiency (RDS), polycythemia and hyperviscosity (EPO synthesis), hypertrophic and congestive cardiomyopathy
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117
Q

Prevalence of impaired glucose tolerance in adolescent offspring of diabetic mothers.

A
  • 6 X increased risk for developing diabetes prior to insulin. This is in absence of genetic etiologies.
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118
Q

Are mothers with GDM at risk for developing overt diabetes?

A
  • Yes. At ~10 years, 70% of GDM become overt diabetics.
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119
Q

Talk to your diabetics prior to conception! Get glucose under control. Tx comorbidities.

A

Talk to your diabetics prior to conception! Get glucose under control. Tx comorbidities.

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120
Q

Rule of thumb for estimating glucose from HgA1c

A
  • 8% = 180 mg in preceding period. 1% change = 30 mg/dl
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121
Q

How to manage DM in pregnancy

A
  1. Diet/exercise cornerstones of therapy for pre-GDM and GDM
  2. Tight control with insulin
  3. If T2DM, maintain oral meds or discontinue and substitute with insulin per some experts. Do same for DGM. Oral 1st choice = glyburide. This is better from fetal side as minimal transplacental passage.
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122
Q

Target glucose levels in GDM

A
  • Fasting: 65-95

- 1 hour postprandial

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123
Q

Target glucose levels in pre-GDM

A
  • Fasting: 65-95

- 1 hour postprandial

124
Q

Management of GDM in postpartum period

A
  • Discontinue therapy
  • Do 75g 2-hour OGTT at 6-8 wks. If –ve, do this testing at least q3 years d/t risk for developing T2.
  • Do thyroid function tests (Why? Close association bw thyroid dysfunction and DM)
  • Lifetime risk of HTN and CV dz and metabolic syndrome increased. Check for these.
125
Q

Define preterm vs term

A
  • Preterm: = 37.0
126
Q

Define late and early preterm

A
  • Late: 34.0 to 36.6

- Early:

127
Q

Define early, full and post term

A
  • Early: 37.0 to 38.6
  • Full: 39.0 to 41.6
  • Post: >= 42.0
128
Q

Define SGA, AGA and LGA

A
  • Not same as pre-term, term

- SGA: 90th percentile

129
Q

Define LBW, VLBW and ELBW

A
  • LBW
130
Q

Most preterm births are during what timeframe?

A
  • Late preterm (34 to 36.6): ~ 75%.
131
Q

Infant death rates are highest in what gestational age delivery group?

A
  • ~80% in
132
Q

List immediate complications of prematurity

A
  • Pulmonary (RDS, bronchopulmonary dysplasia, apnea of prematurity)
  • CV (PDA, apnea/brady, hypotension)
  • GI (necrotizing enterocolitis, dysmotility, reflux, poor feeding, jaundice, hypoglycemia)
  • CNS (IVH, periventricular leukomalacia)
  • Visual (retinopathy of prematurity)
  • Skin (hypothermia, excess insensible water loss)
  • Immune/hematologic (infection-sepsis, meningitis, anemia of prematurity)
133
Q

Long term complications of prematurity

A
  • Risk inversely proportional to GA
  • Chronic lung dz, CP, retinopathy of prematurity (impaired vision, blindness), decreased cognition and academic difficulties, ADD, ? autism, GI disorder (secondary to necrotizing enterocolitis), death
134
Q

Etiologies that lead to preterm birth syndrome

A
  • Infection, multiple pregnancy, nulliparity, nutrition, genetics, environment toxins =
  • Intra-amniotic inflammation, fetal allergy, utero-placental ischemia, decidual hemorrhage, oxidative stress, stress, uterine-overdistention =
  • Uterine contractions, cervical ripening, PPROM, fetal damage
135
Q

Describe what effectively happens to P:E ratio at delivery

A
  • P withdrawal and E dominates. Specifically doesn’t happen in humans, but P receptor isoforms change. A responsible for pro-E effect, B responsible for quiescence of uterus. As labor progresses, predominance of A occurs with downregulation of B. Functionally, change in P:E effect with E effect predominating.
136
Q

Phenotypes of preterm birth. Which is most common?

A
  1. Spontaneous preterm labor (primary 85%, recurrent 15%)

2. PPROM (preterm premature ROMS)

137
Q

Risk factors for preterm birth. Which is biggest?

A
  • Biggest = prior preterm birth (has recurrence ranging from 15 to 50%)
  • Genetics (if patient was preterm, sib had preterm birth)
  • Race: non-hispanic blacks with double risk
  • Prior stillbirth
  • Education: risk decreases with increasing education
  • Maternal stress: RR 1.4
  • GU infections, peridontal infection/dz
138
Q

How many of preterm labors diagnosed are wrong?

A
  • 50%
139
Q

How is preterm labor diagnosed?

A
  • Sx: increase in pelvic pressure, persistent menstrual-like cramps, contractions particularly > 6 / hr, back pain, vaginal discharge
  • PE: cervix dilated > 3 cm, effaced > 75%
  • US: cervical length (in to ex os):
140
Q

How does cervical length correlate with preterm labor?

A
  • 1-5 mm: 95% chance of delivery in next 7 days.
141
Q

Utility of fetal fibronectin in preterm labor? Function?

A
  • Function: ? responsible for adhesion of fetal membranes to decidual. It is present in cervico-vaginal secretions until 22-24 weeks and after 34 weeks.
  • Utility: -ve predictive value. If –ve for FFN, likelihood of delivering in next 7 days is nearly 99.5 %. If +ve, can’t say she won’t deliver.
142
Q

Describe mgmt. protocol of preterm labor

A
  • CL 30 = discharge
  • CL 20-29 = do FFN. If –ve, likelihood of delivery low, so discharge. If contractions persist, consider 24 hour observation. If +ve, treat.
143
Q

What is a tocolytic?

A
  • Anti-uterine contraction medication
144
Q

Tocolytic (s) used for preterm labor. MOA? Which is preferred?

A
  • COX-2 inhibitor indomethacin. MOA – disruption of contraction and gap junction formation (uterine myocytes engage via gap junctions when labor occurs, otherwise disengaged)
  • Nifedipine (= PREFERRED if asked on test): CCB
  • Call to stop use of mag sulfate as tocolytic. Can be used prior to 32 weeks to protect small vessels in neonates brain (remember these infants are at risk for IVH: interventricular hemorrhage).
145
Q

SE of terbutaline as tocolytic

A
  • Terb + multiple gestations = maternal death and pulmonary edema in multiples.
146
Q

What is a previable PPROM?

A

-

147
Q

Does bed rest help for preterm labor?

A
  • Does not reduce
148
Q

What is the most common medical condition in pregnancy?

A
  • HTN. Worldwide 24% of stillbirths are d/t HTNsive disorders
149
Q

What happens to BP during the 1st trimester?

A
  • Decreases during 1st TM. Lowest BP point at 13-20 wks gestation.
  • NB: obtain BP readings early in pregnancy to identify chronic HTN and increase vigilance for detecting complications
150
Q

4 types of BP in pregnancy. Define

A
  1. Chronic HTN: BP >=140/90 ( 12 wks postpartum
  2. Gestational HTN: mild ( 160/110), no proteinuria, > 20 weeks gestation
  3. PE: new onset HTN (as 1) and proteinuria > 20 wks gestation
  4. PE superimposed on chronic HTN
151
Q

Is there increased fetal/maternal risk with chronic HTN (ie. diastolic

A
  • No increased risk
152
Q

Common obstetrical complications of severe chronic HTN

A
  1. Superimposed PE
  2. Premature birth (66%)
  3. IUGR (33%)
  4. Fetal demise (3x compared to gen pop; 50% if uncontrolled in 1st TM)
  5. Placental abruption
153
Q

Mgmt. of chronic HTN in pregnancy

A
  1. Lifestyle modification: smoking cessation, dietary changes, regular exercise, no etoh
  2. Start antihypertensives when BP > 160/110 OR continue pre-pregnancy tx if multiple meds required pre-pregnancy or evidence of organ dysfunction
154
Q

Signs and symptoms of development of PE superimposed on chronic HTN

A
  • Proteinuria, sudden BP increase when well controlled previously, HA, visual disturbances, upper abdominal discomfort
155
Q

Compare and contrast between mild and severe PE

A
  1. Mild: >140/90 on two occasions (6+hrs apart), proteinuria
  2. Severe (any of these): SBP > 160 or DBP > 110 on two occasions (4+hrs apart) while on bedrest, thrombocytopenia, impaired liver function, progressive renal insufficiency, pulmonary edema, new onset cerebral/visual (tunnel vision) disturbances
156
Q

Maternal risk factors for PE

A
  • Age 35
  • Black race (x2 higher than whites)
  • Family hx of PE
  • Nulliparity!!!
  • PE in previous pregnancy
  • Stress
  • Obesity, thrombophilias, antiphospholipid syndrome
157
Q

Define eclampsia

A
  • Appearance of seizures in a patient with PE. Note: 80% with elevated BP, 20% have DBP
158
Q

What is HELLP syndrome? Lab findings?

A
  • Variant of severe PE. Hemolysis, Elevated Liver enzymes, Low Platelet count
  • Labs: hemolysis (burr cells/schistocytes/other abnormal cells, LDH high, bilirubin), elevated liver function tests, low platelets
159
Q

Women not receiving prenatal care are 7x more likely to die from complications

A

Women not receiving prenatal care are 7x more likely to die from complications

160
Q

Mgmt. of PE

A
  • Delivery (of placenta) is ultimate cure (rapid improvement usually seen)
  • Goals: control HTN, prevent seizures
161
Q

Seizure mgmt. in PE/E

A
  • Prevent maternal injury, mag sulfate
162
Q

Indications for delivery in PE/E patients

A
  • Maternal: > 37 weeks, worsening labs, placental abruption, persistent HA or visual changes, persistent vomiting/epigastric pain, ECLAMPSIA
  • Fetal: severe IUGR, non-reassuring fetal surveillance, oligohydramnios
163
Q

When is risk of seizures greatest in postpartum patients with eclampsia?

A
  • First 24 hours
164
Q

Postpartum complications of PE and severe chronic HTN

A
  • Pulmonary edema, heart failure, hypertensive encephalopathy, renal failure
165
Q

Define IUGR

A
  • Fetal weight
166
Q

Asymmetric vs symmetric IUGR. Etiologies?

A
  • Asymmetric: fetal head circumference > abdominal circumference, aka head-sparing. Etiology: placental dysfunction.
  • Symmetric: proportionally small. Etiology: chromosomal abnormality, constitutionally small parents.
167
Q

Risk factors for IUGR

A
  • MATERNAL: Hx of IUGR, HTN, DM, elevated MSAFP, antiphospholipid syndrome, chronic medical illnesses, low maternal weight gain, twin gestation/multiples** (spacing issue), substance abuse, PE, preterm labor, abnormal placentation, vaginal bleeding, maternal anemia, maternal hypoxia, maternal hemoglobinopathies, drug ingestion
  • FETAL: infection (CMV, toxo, rubella), congenital malformations, chromosomal abnormalities
  • PLACENTAL: abruption, excessive fibrin (placental infarction), circumvallate (don’t need to know types), chrorioamniotis, placental cysts, chorioangioma
168
Q

How is IUGR screened? Diagnosed?

A
  • Screening: measure fundal height, elevated MSAFP (risk raised 5-10 x)
  • Diagnosis: sequential US for estimated fetal weight (EFW)
169
Q

Mgmt. of IUGR

A
  • Preterm ( 34 weeks): delivery
170
Q

Effects/risks of IUGR on fetus

A
  • Meconium aspiration, hypoglycemia, hyperbilirubinemia, seizures, sepsis, pulmonary hypoplasia (secondary to oligohydramnios), death
171
Q

Define alloimmunization

A
  • Aka isoimmunization. Immune response generated in an individual of one species by alloantigen from different individual of same species. Mom and fetus in case of RH disease
172
Q

Inheritance pattern of RH factor

A
  • AD
173
Q

What combination for RH disease matters between mother and baby?

A
  • RH-ve mother with RH+ve baby
174
Q

When RH antigen expressed by fetus?

A
  • 30 days GA
175
Q

Ig isotype responsible for causing pathology in RH disease?

A
  • IgG crosses placental and attaches to fetal RBCs
176
Q

Fetal complications from RH disease

A
  • Anemia and fetal hydrops (accumulation of fluid) if severe
177
Q

Does jaundice occur before delivery in fetus affected by RH disease?

A
  • No. There is processing of bilirubin (indirect to direct) by maternal liver.
178
Q

Causes of RBC transfer in pregnancy

A
  • Abortion/ectopic, partial molar, blighted ovum, antepartum bleeding, procedures (amnio, cordo, CVS), external version (turning baby), platelet transfusion, abdominal trauma, inadvertent transfusion of RH+ blood, postpartum RH+ baby
179
Q

When is screening for RH/ABO blood type done?

A
  • At 1st prenatal visit, 28 weeks, postpartum, antepartum bleeding
180
Q

Gold standard test for RH disease

A
  • Coombs
    1. Indirect (do on mother’s blood): mix RH+ cells with maternal serum, anti-RH+ abs adhere, wash and suspend in antihuman globulin (Coombs serum), RBCs coated with ab will agglutinate
    2. Direct (do on baby’s blood): mix infants RBCs with Coombs serum, if maternal ab present cells agglutinate
181
Q

If mother is +ve for RH antibody, describe mgmt.

A
  • Do serial antibody titers every 2-4 weeks
  • If titer >= 1:16, do amniocentesis or MCA dopplers and more frequent titers
  • When titers critical, there is significant risk for hydrops (Hgb
182
Q

Describe Lily curve zones

A
  • I: fetus low risk of severe fetal anemia
  • II: mild to moderate fetal hemolysis
  • III: severe anemia with high probability of death 7-10 days
183
Q

Function of MCA doppers

A
  • MCA = middle cerebral artery

- Measures velocity of blood flow. Anemic fetus preserves o2 delivery to brain by increasing flow.

184
Q

Tx of at risk fetuses with RH disease

A
  • Intravascular fetal transfusion

- Preterm birth

185
Q

Describe diagnosis of RH disease in infant

A
  • History of antibodies to RH, early jaundice
186
Q

Tx of RH disease in infant

A
  • Phototherapy, exchange or direct blood transfusion
187
Q

How is RH disease prevented?

A
  • RhoGAM, which is anti-D (RH) immunoglobulin.
188
Q

What is Kleihauer-Betke test?

A
  • Measures % of fetal RBCs in maternal circulation. How? Fetal RBCs contain Hgb F.
  • Fetal RBCs = (MBV x maternal Hct x % of fetal cells in KB) / newborn Hct. MBV = maternal blood volume (5L)
  • One dose of 300 mcg covers 30 ml fetal whole blood in maternal circulation or 15 ml of fetal cells.
189
Q

Dizygotic vs monozygotic twins

A
  • Di: two ova fertilized by two sperm

- Mono: division of fertilized ovum AFTER conception

190
Q

Least common monozygotic twin amnion/chorion configuration

A
  • Monoamniotic/monochorionic: one placenta, one amnion, one chorion
191
Q

How are multiple gestations diagnosed?

A
  • Size > Dates on exam

- US to determine chorionicity

192
Q

Risks/complications with multiple gestations

A
  • PRETERM LABOR AND DELIVERY
  • Anemia, operative delivery, discordant growth, hydramnios, PE, congenital anomalies, abnormal placentation and antepartum bleeds, postpartum hemorrhage secondary to atony or abruption, umbilical cord accidents/entanglement
193
Q

Is mortality/morbidity greater with monochorionic or dichorionic gestation?

A
  • Monochorionic
194
Q

What is twin-twin transfusion syndrome?

A
  • Monochorionic gestation where vascular anastomoses develop between fetuses
  • Donor twin: impaired growth, anemia, hypovolemia, oligohydramnios
  • Recipient twin: hypervolemia, HTN, polycythemia, CHF, polyhydramnios
195
Q

Relationship between birth weights and mean GA in multiple pregnancies.

A
  • Higher order = lower birth weights with mean GA decreased
196
Q

Type of delivery necessary for multiples

A
  • More common to have C/S. If attempting twin delivery by vaginal, have setup for c/s. This is known as double setup.
  • Need team for each infant.
197
Q

Types of female sexual dysfunctions. What are the etiologies? Which is most common?

A
  1. Sexual desire disorder (most common): situational (social, marital), meds, endocrine, abuse
  2. Sexual arousal disorder: meds (commonly SSRIs), medical conditions, distractions (family, children, work)
  3. Female orgasmic disorder: abuse or trauma, cultural, result of another sexual dysfunction
  4. Sexual pain disorder: dyspareunia/vaginismus, post-menopausal (lack of E) vaginal atrophy, scarring, endometriosis
198
Q

Workup/tx of sexual desire disorder

A
  • Not recommended to workup with T or other hormones
  • Careful hx taking
  • Try E for vaginal atrophy
  • Therapist
199
Q

Tx of arousal disorders

A
  • Some studies looking at T rx

- Clitoral therapy device

200
Q

Key to workup/mgmt. of sexual dysfunction

A
  • Detailed history
201
Q

Prevalence of and effects of sexual abuse

A
  • 1 in 5 women has experienced childhood sexual abuse. Most occurred more than once, family member and at home.
  • Effects: emotional reactions, symptoms of PTSD, distorted self-perception, physical effects (somatizations), sexual effects, interpersonal effects
202
Q

Things to remember in mgmt. of sexual abuse cases

A
  • Give pt control over disclosure
  • Consider postponing exam
  • Give positive messages
  • Thoroughly explain procedures
  • Inform before touching
  • Respect patient’s signal to stop
  • Patient may need to re-ground or re-group
203
Q

Define premenstrual syndrome

A
  • Cyclic recurrence of symptoms with luteal phase of menses with variable intensity and effect on daily life. Ceases shortly after menses.
204
Q

Diagnostic criteria for PMS

A
  • One of following affective and somatic sx during 5 days before menses in each three menstrual cycles. Sx relieved within 4 days of most menses without recurrence until at least cycle day 13.
    1. Affective: depression, angry outbursts, irritability, anxiety, confusion, social withdrawal
    2. Somatic: breast tenderness, abdominal bloating, headache, swelling of extremities
205
Q

What is premenstrual dysphoric disorder?

A
  • Severe PMS to interfere with function. Comparable to MDD.
206
Q

Describe mgmt. options for premenstrual disorder patients

A
  • Step 1: supportive – diet, exercise, Ca supplement, possible spironolactone, decaffeinate
  • Step 2: SSRIs (fluoxetine most studied) and anxiolytics for symptoms/cycles
207
Q

Describe elements normal female sexual response

A
  1. Excitement: deep breathing, increased HR, increase BP, warmth/erotic feelings, increased tension, generalized vasocongestion, skin flush, breast engorgement, nipple erection, engorgement of labia and clitoris, vaginal transudation, uterine tenting
  2. Plateau
  3. Orgasm: release of tension, myotonic contractions (generalized), contractions of perivaginal muscles and anal sphincter, uterine contractions
  4. Resolution
208
Q

Genetics screening vs diagnostic test

A
  • Screening: assess risk that x person will have a genetic dz, does not confirm or rule out presence of dz
  • Diagnostic: if screening pos, assess presence of absence of dz
209
Q

1st TM screening options

A
  • Two biochemical markers: HCG and PAPP-A
  • US: nuchal translucency. Can be used along for detection of aneuploidy. Discovery of major fetal organ abnormality OR finding of two or more minor malformations increases risk sufficiency to warrant genetic testing regardless of age of parental karyotype.
  • These assess for risk of trisomies 21, 18, 13
210
Q

Describe process if 1st TM screening +ve for aneuploidy?

A
  • Genetic counselling

- Diagnostic testing by amnio and CVS

211
Q

When is CVS done? Amniocentesis? Percutaneous umbilical blood sampling (PUBS)?

A
  • CVS: done as early as 10 weeks
  • Amniocentesis: at 15-20 weeks
  • PUBS: after 20 weeks
212
Q

Women presents to your office at the 2nd TM. She has been seen for 1st TM screening. She is requesting 2nd TM screening for aneuploidy. How do you proceed?

A
  • If having 1st screening, should NOT undergo 2nd TM serum screening in same pregnancy. Why? Picture can get muddy. What do you do if false pos or neg?
213
Q

When is 2nd TM screening done? What is tested?

A
  • 15-20 weeks

- Quadruple screen: MSAFP, HCG, unconjugated estriol and inhibin A. This is to check for DS, trisomy 18.

214
Q

What is integrated screening during pregnancy?

A
  • Combining results from 1st and 2nd TM screening and US to increase ability to detect DS and adjust woman’s age-related risk. Provides highest sensitivity with lowest false-pos rates.
  • Downside to this is having to wait to 2nd TM. Loose ability for termination. Anxiety.
215
Q

What cancers does BRCA 1&2 predispose one to?

A
  • Breast and ovarian
216
Q

Describe mgmt. if pos for BRCA 1&2?

A
  • Alter surveillance frequency (annual breast MRI in additional to annual mammogram)
  • OR risk-reduction surgery
217
Q

What cancers does HNPCC type A and B predispose one to?

A
  • Type A (Lynch I): colorectal and endometrial cancer

- Type B (Lynch II): all of type A + ovarian, gastric, pancreatic

218
Q

Most important initial step in identifying women at high risk for hereditary cancers?

A
  • Family history: cancers in 1st-degree relatives, cancers at young ages (
219
Q

Effect of diabetes on fetus. Most common?

A
  • Macrosomia (d/t insulin, a growth factor in utero)
  • Small for gestational age (more likely in long term diabetic)
  • Sacral agenesis, femoral hypoplasia, heart defect, cleft palate
  • Hypoglycemia = most common **
  • Hypocalcemia
  • Hypomagnesemia
  • Polycythemia
  • Hyperbilirubinemia
  • RDS
  • Hypertrophic cardiomyopathy
220
Q

Most common effect of diabetes on fetus. Cause? Sx?

A
  • Hypoglycemia
  • Cause: hyperinsulinism secondary to increased maternal glucose
  • Sx: poor feeding, poor tone, jitteriness, etc.
221
Q

Treatment of hypoglycemia in fetus born to diabetic

A
  • If symptomatic and
222
Q

Define prolonged ROM. What is risk?

A
  • ROM > 18 hours

- Greater risk for infection. Screen at 35-37 weeks.

223
Q

Sx of GBS infection of neonate

A
  • Poor temp control
  • RDS/Apnea/Hypoxemia
  • Poor color
  • Poor feeding
  • Excessive jaundice
  • Decreased tone
224
Q

Compare and contrast presentation of GBS in infant? Which is most common? Which has decreased in incidence? Which is increased incidence of meningitis?

A
  • Early onset (within 1st week): majority within 24 hours, decreased with use of intrapartum abx.
  • Late onset (1 week – 3 months): increased incidence of meningitis, incidence hasn’t decreased with abx use
225
Q

How to prevent GBS infection in infant?

A
  • GBS pos mothers should receive IV PCN or Ampicillin at least 4 hours prior to delivery!!!
  • If status unknown, give abx for PROM or maternal fever
226
Q

Tx of asymptomatic infants born to pos GBS mother?

A
  • Observe in hospital for ssx of illness. If maternal abx
227
Q

Describe workup and tx for neonate with fever in nursery. What is the concern in infant

A
  • If no source per history and exam and

-

228
Q

Greatest risk of AMA on infant

A
  • Genetic diseases: trisomy 21, 18, 13
229
Q

Common features of DS infant

A
  • Endocardial cushion defect and mental retardation **per Metts
  • Other = brachycephaly, inner epicanthal folds, upward palpebral fissures, mid face hypoplasia, small/low set ears, Brushfield spots, incurved 5th finger, wide space between 1st and 2nd toes, extra skin on neck nape, hypotonia, excessive protrusion of tongue
230
Q

Diagnosis of DS infant

A
  • Clinical findings, karyotype
231
Q

Tx of DS infant

A
  • Cardiology involvement, support groups, interprofessional team
232
Q

Define polyhydramnios per AFI. Define oligohydramnios

A
  • AFI = amniotic fluid index. > 25 = polyhydramnios

- Oligo = AFI

233
Q

Associations with polyhydramnios

A
  • Fetal GI abnormalities (specifically tracheo esophageal fistulas) **per Metts
  • Other = multiple gestation, maternal diabetes, anencephaly, hydrops, NTDs
234
Q

Presentation of polyhydramnios d/t GI abnormalities in fetus

A
  • Initial = poor feeding, excessive secretions, respiratory distress
235
Q

Most common TE fistula

A
  • Blind esophagus

- Trachea connected distally (near carina) to esophagus

236
Q

Diagnosis of TE fistula

A
  • Placement of orogastric tube = difficult

- X-ray = coiled esophagus

237
Q

Tx of TE fistula

A
  • Immediate surgical correction

- Search for VACTERL association

238
Q

What else may TE fistula be associated with?

A
  • VACTERL: vertebral defect, anal atresia, cardiac defects, TE fistula, renal anomalies and limb anomalies (eg. Radial atresia)
239
Q

Associations with oligohydramnios

A
  • Potter syndrome (fetal compression), fetal growth retardation, fetal GU abnormalities, pulmonary hypoplasia, positional deformities of fetus, flat face/beaked nose/low set ears
  • Other = chromosomal abnormalities, umbilical cord compression during labor
240
Q

Fetal etoh syndrome ssx

A
  • Mental retardation

- Thin upper lip and smooth philtrum**, short palpebral fissures, short nose with flat nasal bridge

241
Q

Effect of tobacco use on fetus

A
  • IUGR, heart defects, limb deficiencies

- Nicotine in general causes vasoconstriction of BVs = decrease in uterine blood flow

242
Q

Goal of antenatal testing

A
  • Prevent fetal death
243
Q

Does antepartum fetal surveillance improve perinatal outcome?

A
  • Not proven to improve outcome. Except in some populations.
244
Q

T/F. Single antepartum testing modalities are the most likely to yield reliable results.

A
  • False. Multiple modalities.
245
Q

What is fetal movement assessment? When used?

A
  • Kick counts assessed by mother

- No optimal protocol

246
Q

What is non-stress test?

A
  • HR of fetus will temporarily accelerate with fetal movement. Good indicator of normal fetal ANS function.
247
Q

What is biophysical profile?

A
  • Type of NST where fetal breathing, movement, fetal tone and amniotic fluid volume is measured
248
Q

What is umbilical artery Doppler velocimetry?

A
  • Doppler used to assess hemodynamic components of vascular impedance
249
Q

When is antepartum testing needed?

A
  • Pre-existing insulin-requiring diabetics, previous hx of IU fetal demise, post-date pregnancies, chronic HTN, decreased fetal movement
250
Q

2 parts of fetal monitoring

A
  • FHR monitoring

- Uterine activity monitoring

251
Q

Has fetal monitoring decreased frequency of CP in last 20 years?

A
  • No
252
Q

Is fetal monitoring diagnostic?

A
  • NO, screening
253
Q

How does fetal monitoring change between active phase and second phase of labor

A
  • Frequency increases. First stage: q 30 mins. Second stage: q 15 mins.
254
Q

Internal vs external fetal monitoring. When is each used?

A
  1. External: clinically undesirable or impossible to rupture membranes; US transducer/Doppler for FHR and tocodynamometer for uterine frequency and duration of contraction
  2. Internal: requires ruptured membranes/amniotomy, cervix needs to be dilated 1-2 cm before intrauterine pressure catheter (measures strength, duration and frequency) and fetal scalp electrode attached to scalp or buttock
255
Q

Normal uterine activity at labor

A
  • 5 ctx or less in 10 mins averaged over 30 minutes
256
Q

Define uterus that is tachysytolic

A
  • > 5 ctx in 10 mins averaged over 30 mins

- Most commonly d/t too much oxytocin

257
Q

What is the normal baseline fetal HR. Tachy? Brady?

A
  • Normal = 110-160. Tachy = > 160. Brady =
258
Q

T/F. Most consistent baseline fetal heart rate is measured between contractions.

A
  • True!!
259
Q

Does hypoxia lead to fetal tachy or brady?

A
  • Either
260
Q

Describe FHR variability. What does loss of the variability mean? What can cause this?

A
  • Normal FHR variability is one of best indicators of intact integration bw CNS and heart of fetus. By the time the fetus is 28 weeks GA or more, CNS should be mature to produce normal variability.
  • Loss = fetal hypoxia d/t fetal sleep state, CNS depressant drug, fetal tachy, anomalies of heart and CNS, prematurity
261
Q

Mechanisms by which uterine contractions can cause a decrease in FHR

A
  • Compression of: fetal head, umbilical cord, uterine myometrial vessels
262
Q

Define periodic HR changes. Non-periodic?

A
  • Periodic: When FHR changes are associated with contractions.
  • Non-periodic: FHR changes NOT associated with contractions.
263
Q

What are FHR accelerations? Decelerations?

A
  • Accelerations: transient increase in HR

- Decelerations: transient decrease in HR

264
Q

Define early decelerations of FHR. Cause?

A
  • Symmetrical gradual decrease and return of FHR with a contraction (aka MIRROR image of contraction). Note: nadir occurs at same time as peak of contraction. When contraction over, these are over. HR never falls below 100 bpm.
  • Cause: vagal stimulation from head compression, reassuring!! And not sign of fetal problems
265
Q

Define late decelerations of FHR. Cause?

A
  • Transitory decrease in HR
  • Cause: uteroplacental insufficiency (compromised blood flow to baby) and not enough o2 needed to withstand stress of labor.
266
Q

Define variable decelerations. Cause?

A
  • Visually abrupt decrease in FHR of 15 bpm or greater lasting 15 seconds or greater and
267
Q

Most common category of FHR tracing during labor

A
  • Variable deceleration
268
Q

How is variable deceleration FHR tracing corrected?

A
  • Changing maternal position to alleviate cord compression
269
Q

Define FHR tracing classification per NICHD 2008. Action?

A
  • Category I: normal, predictive strongly of normal acid base status, no action
  • Category II: indeterminate, not predictive of acid base status, surveillance w/ additional testing
  • Category III: abnormal, associated with abnormal fetal acid bases status, requires intervention expeditiously (o2 or resuscitation), if no resolution then deliver
270
Q

Components of intrauterine resuscitation

A
  1. Left lateral position or knee chest to alleviate cord compression w/variable decels
  2. Reduce or stop oxytocin
  3. Initiate tocolysis to decrease uterine activity and increase placental blood flow
  4. Increase IV fluid to increase maternal blood flow volume
  5. Give o2 @ 10-12 L to promote o2 delivery across placenta
  6. Internal monitor to verify external monitor readings
  7. Administer amnioinfusion to decrease pressure if cord compression causing variable decels.
271
Q

What does moderate FHR variable reliable predict?

A

**

  • Predicts absence of metabolic acidemia at time of observation. Minimal / absent variability alone doesn’t reliably predict presence of acidemia.
272
Q

T/F. Intrapartum interruption of fetal o2 does not result in neurologic injury.

A

**

  • True. Unless it progresses to significant metabolic acidema (umbilical artery pH 12 mmol/L)
273
Q

Define abortion

A
  • Loss of pregnancy prior to 20 weeks
274
Q

Threatened abortion
a. Define, presentation

b. Treatment

A

a. Vaginal bleeding within 1st 20 weeks of gestation not ending in spontaneous abortion. No cervical dilation or expulsion of POC (products of conception)
b. Pelvic rest, minimal to no intervention

275
Q

Inevitable abortion
a. Define, presentation

b. Treatment

A

a. Vaginal bleeding with cervical dilation but not expulsion of POC. Viable pregnancy unlikely.
b. Surgical (D&C), misoprostol (PG) to induce cervical dilation and uterine contractions, expectant

276
Q

Incomplete abortion
a. Define, presentation

b. Treatment

A

a. Vaginal bleeding with cervical dilation and partial expulsion of POC.
b. Surgical (D&C), misoprostol (PG) to induce cervical dilation and uterine contractions, expectant

277
Q

Complete abortion
a. Define, presentation

b. Treatment

A

a. Vaginal bleeding that is decreasing with all POC expelled with cervix closed
b. Follow quant weekly until 0, may need TV US to rule out retained POC

278
Q

Missed abortion
a. Define, presentation

b. Treatment

A

a. Fetal death with or without spotting, no cervical dilation, complete retention of POC. Often proceeds to spontaneous abortion in 1-3 weeks
b. Surgical (D&C), misoprostol (PG) to induce cervical dilation and uterine contractions, expectant

279
Q

Septic abortion
a. Define, presentation

b. Treatment

A

a. Threatened, inevitable or incomplete abortion with signs of uterine infection – elevated temp, leukocytosis, lower abdominal tenderness, CMT, foul-smelling discharge
b. Vaginal cultures, chem panel, blood cultures, CXR, coag studies. Surgical evacuation, IV abx, IV fluids.

280
Q

Causes for 1st TM pregnancy loss

A
  • Most common = chromosomal abnormality (accounting for over 50% of all SABs: spontaneous). Specifically autosomal trisomy most common.
  • Congenital anomaly
  • Septate uterus (no question on this)
281
Q

Risk factors for 1st TM pregnancy loss

A
  • Increasing maternal age, etoh/smoking/drugs, recurrent pregnancy loss (>= 3), extremes of weight
282
Q

How is pregnancy loss/abortion diagnosed?

A
  • Sx: vaginal bleeding, cramping
  • PE
  • Labs: decrease quant HCG, serum P 1500), fetal cardiac activity (usually seen when HCG > 13K)
283
Q

Define surgical techniques used in 1st TM abortion? 2nd semester?

A
  • 1st TM: D&C (dilation and curettage)

- 2nd TM: D&E (dilation and evacuation)

284
Q

When is PG such as misoprostol good for medical abortion?

A
  • Safe through 49 days of gestation
285
Q

Causes of recurrent pregnancy loss

A
  • Define as >=3 losses prior to 20 weeks excl. ectopic, molar and biochemical pregnancies
  • Genetic, anatomic (uterine malformations, fibroids), immunologic, thrombophilias, endocrine, infectious, environment (smoking, etoh, coffee), unexplained
286
Q

Abortion laws in IA

A
  • 1 parent must be notified
  • No waiting period
  • No mandatory US
287
Q

Normal blood loss with standard vaginal delivery? C/S?

A
  • SVD: 500 ml

- C/S: 1L

288
Q

Causes of 3rd TM bleeding

A
  • Placental abruption, placenta previa, vasa previa

- Non-uterus source: hemorrhoids, vulva, varicose veins, tears/lacerations, vagina, cervix, polyp, etc.

289
Q

What is placental abruption?

A
  • Premature separation of normally implanted placenta from uterus. Inspection shows retroplacental clot with depression of underlying placental tissue
290
Q

Clinical triad of placental abruption

A
  • **Painful uterine bleeding (3rd TM = hallmark), uterine hypertonus/hyperactivity, fetal distress/death
291
Q

Grading of placental abruption

A
  1. Slight vag bleeding, uterine irritability, maternal BP unaffected, fibrinogen nml, FHT nml
  2. Mild / moderate vag bleeding, uterus irritable/tetanic, maternal BP maintained, HR elevated, fibrinogen decreased, FHT shows distress
  3. Moderate / severe vag bleeding, uterus tetanic/painful, maternal hypotension, fetal death, fibrinogen
292
Q

Etiologies of placental abruption

A
  • Maternal HTN **know per Olesen, advanced parity, maternal smoking, poor nutrition, Cocaine use (classic for boards), chorioamnionitis, blunt abdominal trauma, rapid decompression of overdistended uterus, vascular abnormalities of placental bed, previous hx
293
Q

Describe mgmt. of placental abruption

A
  • Observation (grade 1), tocolysis (controversial), fetal monitoring continuously, urine output/fibrinogen/hct, delivery depending on findings, restore blood volume/coag status
294
Q

What is placenta previa?

A
  • Implantation of placenta over cervical os

- Three variations: total, partial, marginal. Partial = edge; marginal = part of edge

295
Q

Type of placenta previa that is most common and has the most serious maternal risk

A
  • Total
296
Q

What is the leading cause of third TM hemorrhage?

A
  • Placenta previa
297
Q

Classic presentation of placenta previa

A
  • Painless vaginal bleeding***, often stops bleeding, abdominal pain absent, FHT normal, coag defects rare
298
Q

Risk factors for placenta previa

A
  • Advanced maternal age, black and other minorities, previous c/s
299
Q

Mgmt. of placenta previa

A
  • Depends
  • Consider vaginal delivery for patients with marginal previa with minimal bleeding. Do double set-up.
  • Expectant mgmt.
300
Q

Define placental accreta, increta, percreta

A
  • Abnormal placentation
  • Accreta: attachment to myometrium
  • Increta: invades myometrium
  • Percreta: penetrates myometrium
301
Q

What is vasa previa? Presentation?

A
  • Fetal vessels transverse placental membranes and cover os

- Classic: SROM, laceration of fetal vessel, rapid fetal death

302
Q

What determines hemostasis after separation of placenta?

A
  • Dependent on contraction of myometrium to compress vessels. If post-partum hemorrhage occurs, attributed to myometrial dysfunction or retained placental fragments.
303
Q

Risk factors for postpartum hemorrhage

A
  • Myometrial dysfunction: overdistention of uterus (multiples, polyhydramnios, fetal macrosomia), oxytocin-stimulated labor, prolonged labor, rapid labor, uterine relaxants, amnionitis, history of PP hemorrhage, episiotomy eps mediolateral, operative delivery, Asian or Hispanic ethnicity
304
Q

How to prevent or minimize PP hemorrhage?

A
  • Before delivery: baseline HCT, blood type and screen, IV access, baseline coag studies and platelet count, identify risk factors
  • Delivery: avoid excess traction on umbilical cord, use vacuum or forceps, inspect placenta for complete removal, digital exploration of uterus, active mgmt. of 3rd stage of labor (oxytocin), visualize cervix and vagina, remove all clots in uterus/vagina
  • Recovery: closely observe for excessive bleeding, continue uterotonic agents, frequently palpate uterus with fundal massage, determine vital signs frequently
305
Q

Differences in degrees of perineal/vaginal lacerations

A
  • 1st degree: fourchette, vaginal mucosa and perineal skin
  • 2nd degree: muscles of perineal body, anal sphincter intact
  • 3rd degree: anal sphincter
  • 4th degree: extends through rectal mucosa
306
Q

Tx of vulvar hematoma

A
  • Volume support, I&D, close dead space, pressure dressing, indwelling cath
307
Q

Most dangerous postpartum hemorrhage

A
  • Retroperitoneal hematoma

OBGyn (2 decks)

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