OBGYN Flashcards
Define 3 stages of labor
Labor - cervical changes and regular uterine contractions (firm, every 2-3 min, last up to 60 sec, nl intensity > 40 mm Hg and nl sum total of >200 montevideo units in 10 min interval)
1st stage - onset until full cervical dilation
A. latent - cervix effaces (thins) until dilation of 6 cm
- can be up to 20 hours in nulli, 14 hrs in multip
* if prolonged - NOT an indication for C-section, give pitocin
B. active - more rapid dilation until 10 cm; 1.2 cm/hr in nulli, 1.5 cm/hr in multip
* arrest of active phase if ROM with no progress for 4 hours (w ctx) or 6 hrs (w/out ctx) –> amniotomy, then C-section
2nd stage - 10 cm to delivery of baby
- 3 hours - nulli w epidural
- 2 hours - nulli w/out epi
- 2 hours - multip w epidural
- 1 hour - multip w/out epi
- MCC of arrested second stage is fetal malposition (optimal is occiput anterior); manage with operative vaginal delivery (forceps / vacuum)
3rd stage - delivery until placenta is delivered
- less than 30 min (if longer, try manual extraction)
- bloody show, uterus becomes firm and globular and rises in abdomen, and umbilical cord lengthens
Fetal heart rate monitoring - categories
Fetal heart rate monitoring
Category I - reassuring –> normal baseline and variability, no late or variable decelerations, reactive (2 accelerations of 15+ bpm that last for 15 seconds over a 20 min period)
Category II - represents majority; concerning but not ominous eg tachycardia w/out decelerations
- if minimal variability (non-reactive) - scalp stimulation should induce an acceleration (indicates normal umbilical cord pH >7.2)
- if nonreassuring - fetal scalp electrode to directly measure FHR
Category III - ominous - indicates hypoxia or acidosis e.g. absent baseline variability + recurrent late or variable decelerations, or sinusoidal HR pattern (indicates fetal anemia), or prolonged bradycardia
*indication for C-section if intrauterine resuscitation maneuvers do not work
When to do C-section
Cardinal movements of labor
NO trial of labor with:
- active herpes
- prior classical C-section with vertical incision
- prior abdominal myomectomy with uterine cavity entry
- placenta previa
- vasa previa
- HIV with viral load >1000
- transverse lie / breech presentation
Cardinal movements of labor - engagement, descent, flexion, internal rotation, extension, external rotation
Fetal orientation
- Lie
- Presentation
- Posture / attitude
- Position
Fetal orientation - can do Leopold maneuvers or U/S to determine
- Lie - transverse, longitudinal, or oblique
- Presentation
A. Long - cephalic (compound, face, brow, vertex, ideal) or breech (complete, frank, footlong)
B. Transverse - shoulder presents –> C-section
C. Incomplete - leg coming out - Posture / attitude - fetus folds so back is convex, arms crossed, necks flexed
- Position - relationship of fetus to R or L side
- Vertex - occiput anterior e.g. ROA, OA, LOA ideal, malposition is OT or OP
- Face - chin –> must be mentum anterior for NSVD
- Breech - sacrum
*mentum posterior of cephalic face presentation –> will NOT deliver vaginally
Bishop score - components
Bishop score - >8 –> cervix favorable for spontaneous and induced labor
- Dilation - how open the internal os of the cervix is
- 10 cm is fully dilated - Effacement - length of the cervix from internal to external os (normal is ~4 cm)
- 2 cm is 50% effaced
- as thin as lower uterine segment is 100% effacted - Station - relation of fetal head to ischial spines of pelvis
- level of pelvic outlet is +3 station - Consistency of cervix - firm, medium soft
- Position of cervix - posterior, middle, anterior
* labor - cervix goes to soft and anterior
Differential and workup for anemia in pregnancy
- Microcytic
- Macrocytic
- Normocytic
Anemia in pregnancy - Hb < 11 in 1st and 3rd trimesters, 10.5 g/dL in 2nd trimester (<12 in nonpregnant women)
- Microcytic
A. iron deficiency - therapeutic trial of iron, recheck Hb in 3 weeks
- then evaluation iron stores, Hb electrophoresis
B. Hemoglobinopathies - do Hb electrophoresis
- B thalassemia minor - elevated HbA2 and HbF–> prophylactic folate
- A thalassemia - trait is normal eletrophoresis, ferritin; can have HbH or HbBart’s
- sickle cell trait (50% HbS) vs disease (almost 99% HbS)
- Macrocytic - vitamin B12 and folate deficiency –> MCC is folate
- Normocytic
A. G6PD deficiency - triggered by nitrofurantoin, sulfa drugs –> jaundice, fatigue, bilirubinuria
B. HELLP - hemolysis, elevated liver enzymes, low platelets
C. Consider bone marrow process (leukemia) if other cell lines eg WBC, platelets also decreased
- do bone marrow bx
D. Anemia of pregnancy - increased demands for iron due to fetus need and expanded maternal blood volume (increase in plasma»_space; increase in RBC)
Uterine inversion
- Risk factors
- Etiology
- What to do if it happens
Uterine inversion - need to deliver placenta within 30 min in 3rd stage of labor
- Risk factors - placenta implanted in fundus, placenta accreta
- Etiology - massive hemorrhage bc uterine atony –> myometrial fibers do not exert tourniquet on spiral arteries –> placental bed pours out blood
- What to do if it happens - fluid resuscitation
- reduce the uterus
- if initial attempt is unsuccessful, use relaxation agents (halothane, terbutaline, mag sulfate) then try again to reduce the uterus
- then give uterotonic agents (e.g. oxytocin) to prevent it from coming out again
- if unsuccessful, laparotomy
Shoulder dystocia
- Risk factors
- Management
- Complications
Shoulder dystocia - impaction of anterior shoulder behind symphysis pubis
*cannot be predicted or prevented in majority of cases
- Risk factors - prior shoulder dystocia, fetal macrosomia, maternal gestational diabetes, maternal obesity, prolonged 2nd stage labor
- “turtle sign” - head retracts towards perineum - Mgmt - need to deliver < 5 min to avoid compression of umbilical cord
A. Maneuvers
- McRoberts (flex maternal thighs to straighten the sacrum and rotate symphysis pubis)
- apply suprapubic pressure (move fetal shoulder from AP to oblique plane)
B. Episiotomy
C. Fracturing fetal clavicle
D. Put infants head back in pelvis and C-section - Neonatal complications - 90% cases have none
- fractured clavicle or humerus (decreased Moro, intact biceps/grasp reflexes); hypoxia
- Erb palsy (C5-C6) –> Affects deltoid, infraspinatus –> arm internally rotated, pronated “waiter’s tip sign”; most spontaneously recover
- Klumke Palsy (C8-T1) –> “claw hand” with absent grasp (intact Moro/biceps reflexes), Horner’s syndrome
- maternal complication - PPH, vaginal lacerations
Umbilical cord prolapse
- Risk factors
- Management
- Neonatal complications
*DDx for fetal bradycardia
Umbilical cord prolapse - cord protrudes through cervical os
- Risk factors - unengaged fetal head (-3, -2, -1 station), footlong breech, transverse fetal lie
* engagement - largest diameter of fetal head has negotiated pelvic inlet (0 station)
* do not do AROM with unengaged presentation - Management -
- digital exam for cord through cervical os (pulsating)
- elevate the presenting part (trendelenberg)
- immediate C-section - Neonatal complications - sustained fetal bradycardia post AROM (<110 bpm for >10 min) –> take maternal pulse first to differentiate fetal pulse from mom’s
- improve maternal 02 (100% face mask)
- place patient on side to move uterus from great vessels –> improve blood return
- IVF bolus
- stop oxytocin
*DDx for fetal brady –> cord prolapse, uterine rupture, uterine hyperstimulation 2/2 misoprostol
Uterine atony
- Risk factors
- Management
- DDx
Uterine atony - myometrium does not contract to cut off uterine spiral arteries supplying placental bed “boggy uterus” –> MCC of early PPH (>500 cc blood loss in NSVD and >1000 cc in C-section)
*can exsanguinate in 10-15 min!
- Risk factors
- magnesium sulfate (for preeclampsia)
- rapid OR prolonged labor/delivery
- prolonged oxytocin stimulation (hyponatermia, hypotension, tachysystole)
- chorioamnionitis
- high parity
- uterine overdistension (macrosomia, multis, hydramnios) - Management
- ABCs
- palpate uterine fundus –> if boggy –> oxytocin and bimanual massage
- uterotonic agents –> rectal misoprostol / Cytotec, ergot alkaloid eg Methergine (c/i in HTN), prostaglandin F2ef eg carboprost / Hemabate (c/i in asthma)
- if bleeding continues –> large bore IVs, foleys, blood; Bakri balloon, OR for embolization/ligation of uterine arteries or compression stitches (B-lynch) or hysterectomy - DDx - if there is PPH but uterus is firm –> Suspect laceration to genital tract
Postpartum hemorrhage - causes
- Early
- Late
PPH
- Early PPH - <24 hours
- MCC is uterine atony
- genital tract laceration
- uterine inversion
- placenta accreta, increta, percreta (can do MRI to dx)
- retained placenta
- coagulopathy - Late - >24 hours
- subinvolution of placental state (~2 weeks PP) –> eschar falls off and leads to bleeding; give uterotonic agent
- uterine atony 2/2 retained products conception –> uterine cramping bleeding –> D and C
- infection eg endometritis - uterine fundal tenderness, fever, foul smelling lochia
Serum screening in pregnancy - first and second trimester
- DDx elevated msAFP
- DDx decreased msAFP
- Serum levels associated with:
A. Trisomy 21
B. Trisomy 18
C. Trisomy 13 - Mgmt
Serum screening: >2 MOM are considered elevated
- first trimester in weeks 11 - 14: PAPPA, bhCG, nuchal translucency
- second trimester screening in weeks 15-20:
- — triple screen - msAFP, estriol, bHCG
- — quad screen - msAFP, estriol, bHCG, inhibin A
- DDx elevated msAFP - underestimating gestational age (MCC), multis, defects of skin, abd wall, or neural tube; olighydramnios, cystic hygroma, decreased maternal weight, fetal demise
- DDx decreased msAFP - overestimation of gestational age (MCC), trisomies, molar pregnancy, increased maternal weight
- Serum levels associated with:
A. Trisomy 21 - ↓ PAPPA, ↑ bhCG, ↑ Inhibin A, ↓ AFP, ↓ estriol
B. Trisomy 18 - ↓ PAPPA, ↓ bhCG, ↓ Inhibin A, ↓ AFP, ↓ estriol
C. Trisomy 13 (holoprosencephaly, cleft lip, polydacyly, club foot) - results are variable and not generally reported - Mgmt - do U/S to determine correct gestational age, look for multis or NT defects, exclude fetal demise
Twins
- Monozygotic - timing of division and chorion/amnion
- Dizygotic
- Maternal complication
- Neonatal complications
Twins
1. Monozygotic - timing of division and amnion (innermost placenta), chorion (outer membrane)
A. first 72 hours ie 3 days (morula) –> dichorionic / diamniotic
B. Days 4-8 (blastocyst) –> monochorionic / diamniotic
C. Days 8-12 (implanted) –> monochorionic / monoamniotic
D. After day 13 –> conjoined twins
- Dizygotic - fertilization of two eggs by two sperms
- incidence ↑ with maternal age, fertility tx
- dichorionic / diamniotic - Maternal complication - preeclampsia, GDM, anemia, DVT, PPH, and C-section more common
- Neonatal complications - preterm delivery, stillbirth, placenta previa
- twin-twin transfusion syndrome (TTTS - one twin has polyhydramnios, polycythemia and other has IUGR, oligohydramnios –> need laser ablation)
HSV infections
- Primary infection
- Nonprimary first episode infection
- Recurrent infection
- Mgmt in pregnant women with HSV
- Neonatal herpes
HSV infections - HSV1 (labialis) and 2 (genitals) –> dx via PCR
- Primary infection - no HSV Ab
- clinical: asx, local sx (burning, herpetic lesions), systemic sx (malaise, fever, n/v), can have urinary retention 2/2 lumbosacral neuropathy
- lesions last ~ 2 weeks - Nonprimary first episode infection - first infection HSV2 in pt who has IgG HSV1
- milder sx and less duration than primary - Recurrent infection - no systemic sx, lesions last ~9 days, usually with decreasing recurrence over time
- can also have asymptomatic viral shedding - Mgmt in pregnant women with HSV - offer oral acyclovir at 36 wks for pt with first episode or recurrence
- no lesions or prodromal sx –> NSVD
- lesions or burning/itching/tingling –> offer C-section - Neonatal herpes - encephalitis, herpetic lesions of eyes/skin/mucosa, or asx
- transmission MC due to asx viral shedding during primary or nonprimary first episode at term (mother has no HSV hx)
Antepartum bleeding Risk factors, clinical presentation, and mgmt for: 1. Placenta previa 2. Placental abruption 3. Vasa previa
Antepartum bleeding - vaginal bleeding post 20 weeks gestation
- Placenta previa - placenta < 2 cm from cervical os
A. Risk factors - multis, prior C-section, prior D and C, prior previa
- previa increases risk of placenta accreta
B. Clinical - postcoital spotting, painless vaginal bleeding
C. Mgmt - if preterm, pelvic rest and repeat TVUS at term; if there is still previa at term –> pelvic rest, C-section @ 34-37 weeks - Placental abruption - placenta detaches from uterus
A. Risk factors - HTN, prior abruption, short cord, trauma (eg MVA), cocaine use, submucosal leiomyomata, hydramnios, smoking, PPROM
B. Clinical - painful vaginal bleeding, Couvelaire uterus (bleed into myometrium), firm tender uterus
- blood clot adherent to placenta, can lead to coagulopathy (DIC) 2/2 hypofibrinogenemia
C. Mgmt - clinical diagnosis, US to r/o previa
- C-section, unless there is fetal demise –> vaginal delivery - Vasa previa - umbilical vessels cross internal os in front of fetal presenting part
A. Risk factors - velamentous cord insertion, placenta with accessory lobes, IVF babies, or multis
B. Clinical - sinusoidal FHR (due to fetal anemia) –> fetus can exsanguinate on ROM (abrupt sustained fetal bradycardia)
C. Mgmt -
- diagnose via color Doppler US (middle cerebral artery peak systolic velocity)
- Apt test for fetal nucleated RBCs (determine fetal vs maternal hemorrhage)
- C-section prior to ROM (~35 weeks gestation)
Ectopic pregnancy
- Risk factors
- Clinical
- Mgmt
Ectopic pregnancy - embryo implants not in uterine lining, MC in fallopian tube ampulla
- Risk factors - prior ectopic, IVF, IUD, prior tubal sx (adhesions), PID, endometriosis, DES-exposed, smoking
- Clinical - triad: amenorrhea, unilateral pelvic or lower abdominal pain, irregular vaginal bleeding
- palpable tender adnexal mass
- bHCG does not increase appropriately (2x) after 48 hrs
- if ruptured - hypotensive, tachycardic, peritoneal, fever - Mgmt - do US (need bHCG > 2000 to visualize IUP)
A. If unruptured – methotrexate
B. If ruptured (erodes through tissue –> hemorrhage from exposed vessels) – pelvic US, stabilize (ABCs), and OR for ex lap to coagulate bleeding and resect ectopic
C. if stable and r/o ectopic – can follow bHCG (should double every 48 hrs)
Spontaneous abortion
- Risk factors
- Clinical
- Mgmt
Spontaneous abortion i.e. miscarriage - pregnancy that ends prior to 20 weeks gestation
- can be complete, incomplete (partial expulsion), inevitable (no expulsion but bleeding), threatened (normal but bleeding), or missed (no expulsion and not bleeding)
- Risk factors -
- first trimester - due to abnormal chromosomes (most commonly autosomal trisomies due to failures in maternal gametogenesis)
- second trimester - due to infection, anatomic defects, exposure to teratogens, trauma - Clinical - vaginal bleeding, cramping, abdominal pain, decreased symptoms of pregnancy
- Mgmt - give Rhogam if mom is Rh (-), use Kleihauer - Betke test to see how many fetal nucleated RBCs are to dose the rhogam
- threatened (normal pregnancy with bleeding) - pelvic rest
- incomplete, inevitable, missed - medical (misoprostol) or surgical (D and C or Dand E or inducing labor with pitocin and PGEs)
* need to r/o preterm labor and incompetent cervix in second trimester since they can lead to abortions
for patients w recurrent abortions –> check AP Ab (tx - aspirin + heparin), SLE, thyroid, DM, karyotypes
Incompetent cervix (cervical insufficiency)
- Risk factors
- Clinical
- Mgmt
Cervical incompetence - painless dilation and effacement of the cervix, MC in 2nd trimester
*preterm labor is d,e with ctx
- Risk factors - surgery e.g. D and C, LEEP, conization; uterine anomalies, DES exposure, hx of cervical lacerations with vaginal delivery
- Clinical - lower abdominal cramping or contractions
- vaginal bleeding –> amniotic sac bulging through cervix –> exposure to vaginal flora –> fever / infection, vaginal discharge, ROM
* “funneled lower uterine segment” on U/S - Mgmt - do TVUS to look at cervix
- normal cervix and no hx PTL –> routine prenatal care
- short cervix (<2.5 cm) and no hx PTL –> vaginal progesterone
- normal cervix and hx PTL –> serial TVUS (q2wks) until 24 wks
- short cervix (<2 cm) and hx PTL –> cerclage at 12-14 weeks, serial TVUS (q2 wks) until 24 wks
* give betamethasone from 24 - 37 weeks
DDx for abdominal pain in pregnancy
A. Timing
B. Clinical
C. Mgmt
DDx for abdominal pain in pregnancy:
- Appendicitis - any time, in RUQ (NOT RLQ), tx is surgery regardless of gestational age + abx
- Cholecystitis - after 1st trim, RUQ dx via U/S, tx is surgery
- Ovarian torsion - ~14 weeks or after delivery, acute onset n/v and colicky pain, see complex adnexal mass w/out Doppler flow on US
- tx - lap detorsion, cystectomy, or oophorectomy if necrosis - Ectopic - in 1st trim, u/l pelvic pain and spotting, track bHCG (<2x ↑ in 48 hrs), tx is methotrexate or sx
- Ruptured corpus luteum (secretes E and P to maximize endometrial implantation) - in 1st trim, sudden onset lower abdominal pain + peritoneal signs
- U/S and laparoscopy show hemoperitoneum (pelvic free fluid)
- tx - hemostasis, cystectomy; need progesterone supplement if excised before 10 weeks gestation
* more common in bleeding d/o (vW, heparin) - Placental abruption - in 2nd and 3rd trims, crampy midline uterine tenderness and vaginal bleeding; tx - delivery
DDx for pruritus in pregnancy - clinical, mgmt
- ICO
- PUPPP
DDx for pruritus in pregnancy
- Intrahepatic cholestasis of pregnancy (ICP) - generalized mild pruritus without lesions, worse at night
A. Clinical - in 3rd trimester, clinical dx of exclusion
- extremities (palms and soles)»_space; trunk
- normal labs initially but after several days of symptoms –> v high LFTs, ALP, Tbili - need to r/o viral hepatitis
- increased risk fetal demise with higher bile acid levels
B. Mgmt - 1st line is antihistamines, topical emollients, then ursodeoxycholic acid, delivery once fetal maturity achieved - Pruritic urticarial papules and plaques of pregnancy (PUPPP)
A. Clinical - pruritus and erythematous papules, begins on abdomen and spreads to thighs
- no lab abnormalities
B. Mgmt - topical steroids and antihistamines
- no adverse fetal/maternal outcomes
DDx for pruritus in pregnancy - clinical, mgmt
- Pemphigoid gestationis
- Acute fatty liver of pregnancy
- Pemphigoid gestationis - pruritus followed by extensive patches of cutaneous erythema and then vesicles / bullae
A. Clinical - in 2nd trimester, autoimmune (IgG)
- limbs»_space; trunk
B. Mgmt - oral corticosteroids - AFLP - microvesicular steatosis
A. Clinical - RUQ pain, persistent nausea / vomiting, anorexia, progressive jaundice
- develops over weeks late in third trimester
- increased LFTs, Bili, clotting times
- decreased glucose, cholesterol, albumin, fibrinogen
- can lead to fulminant liver failure (hepatic encephalopathy)
B. Mgmt - delivery! high fetal mortality
Hypertensive diseases of pregnancy - define, clinical, mgmt
- Gestational HTN
- Chronic HTN
- Superimposed preeclampsia
Hypertensive diseases of pregnancy - risk for maternal PPH, GDMA, placental abruption; for fetal IUGR, PTL, oligohydramnios
- Gestational HTN - HTN w/out proteinuria at >20 weeks for at least 4 hours
- risk for IUGR, placental abruption
- deliver at 37 weeks - Chronic HTN - BP of 140/90 before pregnancy or <20 weeks, persisting more than 12 weeks postpartum
- antiHTN
- deliver 38-39 weeks - Superimposed preeclampsia - patient with chronic HTN that develops preeclampsia - new onset uncontrollable HTN, new onset proteinuria, or severe features
Hypertensive diseases of pregnancy - define, clinical, mgmt
- Eclampsia
- HELLP
- PRES
- Eclampsia - preeclampsia + seizures
- most commonly occur in 3rd trimester just prior to delivery, labor, or 24 hrs postpartum
- seizures can cause posterior shoulder dislocation, death due to intracerebral hemorrhage
- tx - delivery via c-section
- give mag sulfate and monitor for side effects at >8 (1st sign is hyporeflexia, also pulm edema, somnolence, muscle paralysis) –> give calcium gluconate to counteract
- give IV labetalol to control HTN
* can get hypermagnesemia with renal insufficiency (lower dose with higher Cr - so monitor urine output) - HELLP - microangiopathic hemolytic anemia, elevated LFTs, low platelets; affects up to 1/5 women with preeclampsia
- n/v, RUQ pain (due to liver capsule distension)
- LFTs up to 1000s, patelets <100K
- due to abnormal placentation –> systemic inflammation –> activates coagulation / complement cascades
- tx - delivery, mag sulfate, antiHTNs - PRES - posterior reversible encephalopathy syndrome
- headache, seizures, visual disturbances
- dx via clinical and MRI (Vasogenic edema 2/2 breakdown of BBB)
- tx - antiHTN, antiepileptics, ICU dispo
Hypertensive diseases of pregnancy
Preeclampsia A. Pathophys B. Definition - severe features C. Risk factors D. Mgmt i. Stable ii. Severe features iii. HTN emergency
Preeclampsia
A. Pathophys - to arterial vasospasm and endothelial damage –> hypoxemia, ↑ SVR, ↓ intravascular volume 2/2 third spacing, ↓ oncotic pressure
- typically presents in late third trimester
B. Definition - HTN >140/90 measured 2x 6 hours apart AND 1 of the following:
- new onset proteinuria (>300 mg over 24 hours or urine protein:cr >0.3) at 20+ weeks gestation
OR severe features:
- thrombocytopenia (plt <100K)
- ↑ LFTs (2x nl) or persistent RUQ pain
- AKI (Cr > 1 .1)
- pulmonary edema (sudden onset DOE, crackles, hypoxia)
- new onset visual or cerebral disturbance (headache, hyperreflexia)
C. Risk factors - nulliparity, young or old, black, prior preeclampsia or family hx, chronic HTN or CKD, antiphospholipid syndrome, DM, multis
*obesity is risk factor for gestational HTN and PEC
D. Mgmt
i. Stable, uncomplicated - expectant mgmt (dont need antiHTN), deliver at 37 weeks
ii. Severe features -
<34 weeks - mag sulfate, corticosteroids (betamethasone) over 24 hrs, assess status
>34 weeks - mag sulfate and deliver
iii. HTN emergency (SP>160 or DP>110 for 15+min) or severe features - give IV labetelol, IV hydralazine (if bradycardic and HTN), or oral nifedipine to lower BP and avoid stroke; improve oxygenation
*alpha methyldopa used to treat chronic HTN (slower onset)
Preterm labor (vs cervical insufficiency)
- Risk factors
- Assessing risk
- Management
- Tocolytics and side effects
Preterm labor - cervical change (2 cm dilated, 80% effaced) with contractions between 20 and 37 weeks
*vs cervical insufficiency which is painless dilation
- Risk factors - hx of prior, PPROM, multis, hx cervical cone biopsy, cocaine, trauma, pyelo, gonococcal cervicitis, uterine anomalies (bicornuate), placental abruption
- Assessing risk
- fetal fibronectin (after 20 weeks) - if negative, no delivery in the next week
- TVUS to look at cervical length measurement - <25 mm = increased risk - Management - if no c/i –> pts at >34 weeks can be managed expectantly
- steroids (betamethasone) for <34 weeks –> tocolytics, which extend gestation by 48 hrs so you can give 2 doses steroids
- 17OHprogesterone from 16 to 36 weeks in high risk women with prior PTL
- penicillin if GBS (+)
- mag sulfate (Ca2+ competitive antagonist, membrane stabilizer) for fetal neuroprotection for <32 weeks –> hyporeflexia, flushing, HA, diplopia, respiratory depression - Tocolytics - decreased Ca2+ –> fewer uterine smooth muscle contractions
A. ritodrine, terbutaline (B2 agonists) - smooth muscle relaxation but can cause anxiety, hyperglycemia, hypokalemia, hypotension tachycardia, pulm edema; c/i in diabetes and terbutaline dangerous if given >48 hrs
B. nifedipine (CCB) - headache, flushing, dizziness; c/i at > 34 weeks bc risk of maternal hypotension
C. indomethacin (NSAID blocks PGE -> decreased Ca) - c/i >34 weeks bc it closes DA and can cause fetal renal failure (–> oligohydramnios –> cord compression –> FHR variable decels)
PPROM
- Diagnosis tests for ROM
- Risk factors
- Management - based on GA (34 wks)
- Complication - chorioamnionitis
PPROM - Preterm premature ROM prior to onset of labor at <37 weeks; prolonged if >18 hours
- Diagnosis - gush of fluid from vagina with constant leakage
- pooling of amniotic fluid on speculum exam
- positive nitrazine test (alkaline changes of vaginal fluid)
- positive fern test (cervical mucus ferns under microscope)
- US shows oligohydramnios (single deepest pocket < 2 cm)
- Amnisure - tests placental alpha macrogolobulin 1
- tampon test - seeing if dye injected in amniotic fluid leaks into vagina - Risk factors - primary risk factor is genital tract infection (eg BV)
- also prior PPROM, smoking, conization, multis, hydramnios, placental abruption
- can lead to olighydramnios –> cord compression –> variable decels on FHR - Management - depends on gestational age
A. <34 weeks -
- no signs of infection –> abx, steroids, observe
- signs of infections –> abx, steroids, Mag (if <32), and deliver
B. > 34 weeks - delivery esp with fetal lung maturity (phosphatidyl glycerol in vaginal fluid)
- abx - ampicillin, erythromycin to prolong latency period
- Chorioamnionitis –> maternal fever and 1+: fetal or maternal tachycardia, maternal WBC, uterine fundal tenderness, and/or malodorous vaginal discharge
- baby can be septic (pale, lethargic, high temp)
- tx - IV amp and gent and induce labor regardless of gestational age
Congenital intrauterine infections incl presentation, treatment:
- Parvovirus
- CMV
- Toxo
- Rubella
Congenital intrauterine infections (part of TORCHeS)
- Parvovirus - fetal aplastic anemia (sinusoidal FHR), hydrops fetalis (excess fluid in 2+ fetal body cavities; caused by parvovirus), hydramnios
- mgmt - intrauterine transfusion, delivery - CMV - DNA virus, 90% of congenital CMV is asymptomatic but it is the MC congenital infection in the USA, MCC of retardation and deafness due to viral infection
- hydrops fetalis in first trimester
- microcephaly, periventricular calcifications, sensorineural hearing loss, chorioretinitis, seizures, blueberry muffin rash
- no treatment - prevent! frequent handwashing - Toxoplasma - CNS protozoa
- triad (hydrocephalus, intracranial calcifications, chorioretinitis) + ventriculomegaly, IUGR, deafness
- use PCR to diagnose (not serology)
- prevent with pyrimethamine, sulfadiazine
- transmitted via undercooked meats or oocytes from feces of cats - Rubella - triad (sensorineural deafness, cataracts, cardiac defects eg patent DA) + microcephaly, purpura / blueberry muffin rash, IUGR, jaundice
- immunize, live attenuated vaccine (give postpartum)
- increased transmission in 1st trimester
IUGR
1. Risk factors
- Etiology
A. Asymmetric
B. Symmetric - Presentation at birth
- Mgmt
IUGR - birthweight <10th percentile for gestational age (small and sick)
- Risk factors -
A. maternal - smoking/cocaine, HTN, cardiac/renal/pulm dz, anemia
B. uterine/placenta - abruption, previa, infection
C. fetal - Multis, aneuploidy, congenital syndromes, structural abnormalities, infection - Etiology
A. asymmetric (abdominal circ and femur length are low, head circ normal) –> later insults eg HTN, maternal malnutrition, Factor V leiden mutation
B. symmetric - all are low –> early insults eg chromosomal abnormalities, congenital infection - Presentation - loose peeling skin, wide anterior fontanel, thin umbilical cord
- high morbidity e.g. NRDS, necrotizing enterocolitis, meconium aspiration syndrome (respiratory distress), hypothermia
- IUGR babies at risk for developing DMII, obesity, COPD, CVD, stroke as an adult - Mgmt - twice weekly NSTs / AFI or weekly BPPs
- reversed end diastolic doppler flow from umbilical artery –> associated with stillbirth w/in 48 hrs
- steroids if <34 weeks, mag sulfate if <32 weeks
- at birth –> send placenta for histopathology, neonatal urine tox screen
Postpartum Endomyometritis
- Risk factors
- Presentation
- Mgmt
Endomyometritis - infection of decidua, myometrium, and parametrial tissues due to ascension of polymicrobial bacteria from normal vaginal flora (MC is staph aureus and strep)
- Risk factors - C-section (MC), chorioamnionitis, GBS, numerous vaginal exams, operative vaginal delivery, long labor, low SES, multis, young maternal age, chlamydia, manual extraction of placenta
- Presentation - fever over 100.4F (MCC of fever in woman post C-section) usually on POD2
- uterine fundal tenderness
- purulent foul-smelling lochia - Mgmt - IV gentamicin and clindamycin until pt afebrile >24 hours; add amp if GBS infection, infection persists
- if fever does not improve after 2-3 days –> do CT to r/o abscess, infected hematoma, or septic pelvic thrombophlebitis
- if fever is due to wound infection –> open wound
Diabetes in pregnancy 1. Pregestational diabetes A. Fetal risks B. Maternal risks C. Mgmt
- Pregestational diabetes - hyperglycemia existing prior to pregnancy; accounts for 10% diabetes in pregnancy
A. Fetal risks - congenital anomalies (cardiac, skeletal, NTD), growth restriction (IUGR), fetal macrosomia (less likely), miscarriage, prematurity
B. Maternal risks - diabetic retinopathy, worsening nephropathy (if already existing), and HTN –> preeclampsia
C. Mgmt - target <105 fasting glucose
- glycemic control during labor to avoid neonatal hypoglycemia after birth
- C-section if big baby to avoid shoulder dystocia
Diabetes in pregnancy 2. Gestational diabetes A. Screening B. Risk factors C. Fetal risks D. Maternal risks E. Mgmt
- Gestational diabetes - hyperglycemia caused by insulin resistance during pregnancy due to increased levels of human placental lactogen
- GDMA1 - controlled with diet; GDMA2 - controlled with insulin
A. Screening - from 24 to 28 weeks Glucola test
(high risk do ASAP) –> 50g glucose and assess after 1-hour –> abnormal >140
*high risk (prior GDM, FHx, or BMI > 30) - do Glucola ASAP
- then 100g GTT and assessing every hour for 3 hours, 2 abnormals needed
B. Risk factors - age > 25, obesity, prior macrosomic infant
C. Fetal risks:
i. anatomic - macrosomia (>4000 g), congenital abnormalities (NTD, cardiac), shoulder dystocia
ii. endocrine - increased insulin –> decreased surfactant –> NRDS, neonatal hypoglycemia
- polycythemia, hyperbilirubinemia, hypocalcemia
iii. polyhydramnios
D. Maternal risks - preeclampsia, risk of C-section, PTL, UTIs
E. Mgmt - diet, insulin or glyburide; goal is fasting glucose <105
- breast-feeding
- 75g GTT at 6- 8 weeks postpartum; should be <126 fasting
Prenatal labs - when they should occur, abnormal findings, ramifications, and mgmt:
- CBC
- Blood type and screen
- Rh factor
- HIV
- Rubella
- STD screening
- CBC - first visit, Hb up to 10.5 is normal, if lower –> could lead to preterm delivery; do trial of iron
- Blood type and Screen (indirect coombs) - first visit, Ab screen may indicate isoimmunization –> hemolysis
- Abs: Lewis (lives), Duffy (dies), Kell (kills) - Rh factor - first visit, if negative and indirect Coombs shows no isoimmunization–> Give RhoGAM at 28 weeks (to prevent alloimmunization ie anti-Rh Ab titers); if baby is Rh (+) –> give after delivery
- check Rh status in subsequent pregnancies via indirect Coombs (to see if there are Rh+ Ab that can harm baby) - HIV - first visit, if positive –> confirm ELISA with Western blot, then HAART with IV ZDV in labor, neonatal HIV testing at 24 hrs, and no breastfeeding
- Rubella - first visit, if nonimmune –> give live attenuated vaccine postpartum
- STD screening - first visit
A. RPR or VRDL - for syphilis; need to confirm positive test with FTA-ABS; treat with penicillin, if allergic - desensitize then give penicillin
B. NAAT is gold standard for GCC, treat pt + partner
- gonorrhea –> conjunctivitis (up to 5 days after), blindness, preterm labor; if (+) –> IM ceftriaxone + azithromycin
- chlamydia –> conjuncitivitis (up to 2 weeks after birth), blindness, pneumonia; if (+) –> give azithromycin PO
Prenatal testing - when they should occur, abnormal findings, ramifications, and mgmt:
- Nuchal translucency
- Quad screen
- Screening U/S
- GBS culture
- TdaP vaccine
- Chorionic villus sampling
- Amniocentesis
- Nuchal translucency - 11 to 13 weeks, can indicate trisomy –> karyotype, f/u US
- also PAPPA, bHCG –> first-trimester combined test
- also offer cell free DNA screen after 10 weeks (most sensitive for Down syndrome, confirm via karyotyping - CVS or amnio) - Quad screen (MSAFP, hCG, Estriol, and Inhibin-A) - 16 to 20 weeks, can indicate trisomy or NTD –> confirm dates via U/S or amniocentesis
- Screening U/S - 18 to 20 weeks to look for fetal abnormalities
- GBS culture - 35 to 37 weeks; if (+) - penicillin during labor
- TdaP vaccine - 28 to 36 weeks - killed vaccine so safe, results in passive transmission of IgG response
- Chorionic villus sampling - 10 to 13 weeks; for definitive karyotype
- Amniocentesis - 15 to 20 weeks; for definitive karyotype
Menopause
- Pathophysiology
- Clinical incl perimenopause
- Mgmt
Menopause - cessation of menses for 12 months; occurs after age 40, mean age is 51
- Pathophysiology - follicular atresia due to decreased ovarian reserve –> decreased AMH, then inhibin B, then estradiol
* ovaries stop making estrogen, but still make androgens
- persistently elevated LH, FSH - Clinical - sx due to low estrogen levels:
- perimenopause - oligomenorrhea (infrequent)
- vasomotor symptoms (hot flushes)
- vaginal and vulvar atrophy
- bone loss –> osteoporosis fracture (MC compression fracture at thoracic spine) - Mgmt
A. Hot flushes, sleep disturbances, other vasomotor sx - if woman has uterus and is <60 yo –> HRT (progestin + estrogen) *do for as little time as possible bc of risk of endometrial, breast cancers, PE, stroke, heart disease, which are all c/i (these people are given SSRIs instead)
- if woman is s/p hysterectomy –> just estrogen replacement
- clonidine or gabapentin
B. Irregular menses - progestin or low dose OCP
C. Bone loss - bisphosphonates or raloxifene (SERM, VTE is c/i); DEXA screening at 65+
Ureteral injury
- Most common locations
- Clinical
- Mgmt
Ureteral injury
- Most common locations - MC is cardinal ligament (attachent of cervix to pelvic walls), contains uterine arteries and ureter traverses just below (“water under the bridge”)
- other locations - pelvic brim, UVJ - Clinical -
- ureteral ligation: vague flank/ abdominal pain, n/v, fever post op esp after lap hysterectomies –> risk of hydronephrosis, pyuria, hematuria
- bladder perforation - gross hematuria, pain, suprapubic tenderness
- urine leak can cause sepsis, abscess, pyelo - Mgmt - IV pyelogram to diagnose
- abx and cysto to r/o kinked ureter
- stenting, repair
Pelvic organ prolapse - types, clinical, and mgmt
Pelvic organ prolapse (POP) - due to defect of pelvic support; family history increases risks, so does age, obesity, chronic constipation
- Enterocele - defect of pelvic support of uterus and cervix –> small bowel descends into vagina –> feeling of bulging mass in vagina
- Cystocele - defect of pelvic support of anterior vagina, hypermobile urethra –> stress urinary incontinence with valsalva (cough, sneeze), difficulty voiding
- Q-tip placed in urethra and angle moves with valsalva –> >30 degrees implies urethral hypermobility
- kegels, pessaries, mesh support or fixation - Rectocele - defect of pelvic support of rectum –> constipation, difficulty pooping
- posterior colporrhaphy, culdoplasty (since large cul-de-sac can lead to POP)
Urinary incontinence - for each type, describe mechanism, clinical, diagnosis, and treatment
- Stress
- Urge
Urinary incontinence
- Stress (ie outlet incompetence)
A. Mechanism - bladder neck falls out of normal position –> increased intrabdominal pressure transmits to bladder and exceeds outlet (sphincter) resistance –> leakage
- due to intrinsic sphincter dysfunction (“drain pipe urethra”), loss of pelvic support in multips, urethrocele / cystocele
- can also be due to fibroids
B. Clinical - painless and immediate leakage of urine with valsalva (coughing, sneezing)
C. Diagnosis - loss of bladder angle, hypermobile urethra (>30degree on qtip test)
D. Mgmt - kegels, pessaries, urethropexy (sling or fixation) to return urethra back to position; urethral bulking - Urge
A. Mechanism - hyperactive / unstable detrusor muscle –> overactive bladder
B. Clinical - leak with urge to void ASAP, delayed leakage after coughing
C. Diagnosis - cytometric examination
D. Mgmt - antimuscarinics eg oxybutynin
Urinary incontinence - for each type, describe mechanism, clinical, diagnosis, and treatment
- Overflow
- Fistula
- Overflow
A. Mechanism - outlet obstruction or detrusor underactivity –> overdistended hypotonic bladder –> incomplete emptying
B. Clinical - dribbling, inability to void
- diabetes, spinal cord injury, or postpartum (2/2 epidural or perineal swelling)
C. Diagnosis - increased postvoid residual (>100 - 150 mL or >1/3 instilled volume)
D. Mgmt - intermittent self-cath to avoid detrusor muscle damage 2/2 wall ischemia - Fistula
A. Mechanism - communication bw bladder or ureter and vagina
B. Clinical - constant leakage after labor or sx
C. Diagnosis - dye into bladder showed vaginal discoloration
D. Mgmt - surgical repair
Salpingitis (ie PID) 1. Diagnosis 2. Etiology 3. Clinical A. Presentation B. Complications C. TOA 4. Mgmt incl meds, when to hospitalize
Salpingitis - infection of fallopian tubes
PID - infection of upper female genital tract - includes endometritis, salpingitis, TOA, and pelvic peritonitis
- Diagnosis (clinical):
- lower abdominal tenderness (due to peritoneal irritation of pelvis)
- cervical motion tenderness (chandelier sign)
and/or
- adnexal tenderness - Etiology - ascending infection often during menses
- polymicrobial, due to gonorrhea, chlamydia (MCC) –> dx via NAAT (bc no organisms on microscopy)
- IUD, nulliparity, STIs increase risk for PID - Clinical
A. Presentation - dyspareunia, fever, postcoital spotting
- cervicitis (friable cervix with purulent d/c), urethritis
B. Complications
- fallopian tubes can become damaged –> tubal occlusion –> chronic pelvic pain, infertility, ectopic pregnancy
- Fitz-Hugh-Curtis - perihepatitis (RUQ pain)
- gonorrhea (sx worse during/after menses) can also cause septic arthritis, painful pustules, pharyngitis
C. TOA = PID + adnexal mass / fullness, fever, WBC, abdominal pain
- complex multiloculated adnexal mass with internal debris on U/S –> needs IV clinda/gent/amp, rupture is sx emergency (U/S drainage or laparoscopy) - Mgmt - pelvic US to r/o TOA
- speculum exam - hyperemic friable cervix, mucopurulent exudative discharge (do wet mount to r/o vaginitis)
- GCC test; laparoscopy is gold standard for diagnosis
- treatment - azithromycin or doxy 100 BID for 14 days + ceftriaxone 250 IM (for patient and partner)
- hospitalize if pregnant, unresponsive to tx after 48 hrs, peritoneal signs, TOA
Chronic pelvic pain
- Define
- DDx and clinical clues
- Evaluation
- Treatment
Chronic pelvic pain
1. Define - persistent pain in lower abdomen / pelvis for >6 months, causing significant effects on daily function, QOL
- DDx and clinical clues - 30% idiopathic, 30% endometriosis, 20% pelvic adhesions or PID and remaining 20% variety causes
A. GI - bloating, diarrhea/constipation –> IBS, IBD, diverticulitis, hernia
B. Psych - depression, PTSD, anxiety
C. Neuro - burning, radiating –> nerve entrapment, fibromyalgia (trigger points)
D. GYN
- excessive vaginal bleeding (fibroids, adenomyosis)
- dyspareunia, dyschezia (endometriosis)
- hx PID, gyn sx (adhesions)
- cyclic pain s/p BSO (residual ovarian syndrome)
- Evaluation - r/o pregnancy
- GCC, UA/Ucx, CBC
- pelvic US - Treatment - NSAIDs and/or OCPs for 3 month trial, then diagnostic laparoscopy
Vaginal infections - clinical, diagnosis, and treatment
- Bacterial vaginosis
- Trichomonas vaginitis
- Candida vulvovaginitis
Vaginal infections - clinical, diagnosis, and treatment
- Bacterial vaginosis - overgrowth of anaerobic bacteria which replaces normal lactobacilli, due to Gardnerella
A. Clinical - fishy odor with KOH, gray-white discharge
B. Diagnosis - positive whiff test, pH > 4.5, Clue cells on wet mount (epithelial cells coated with bacteria)
C. Tx - oral or vaginal metronidazole - 500 mg BID for 7 days - Trichomonas vaginitis - protozoan that can also inhabit the urethra or Skene’s glands
A. Clinical - frothy, green discharge, strawberry red cervix
B. Diagnosis - pH > 4.5, mobile trichomonads on wet mount
C. Tx - oral metronidazole, treat partner too - Candida vulvovaginitis - increased risk in DM2, OCP use, Abx use, pregnancy (increased estrogen state)
A. Clinical - cottage cheese discharge, vulvar/vaginal itching and burning –> erythema, swelling, excoriations
B. Diagnosis - pH =< 4.5, pseudohyphae, hyphae, and budding yeast on KOH prep
C. Tx - oral fluconazole, intravaginal imidazole or nystatin
Syphilis
1. Diagnosis
2. Clinical A. Primary B. Secondary C. Latent D. Tertiary E. Congenital
- Treatment
Syphilis - caused by bacteria Treponema pallidum
- Diagnosis -
- nontreponemal tests - VDRL, RPR; nonspecific, titers fall with tx, sometimes not positive with primary syphilis
- specific serologic tests - FTA-ABS; remain positive for life after infection
- darkfield microscopy biopsy
- also assess for HSV via PCR or viral culture or serology –> painFUL ulcers - Clinical
A. Primary - shallow, painless, nonexudative genital chancre with indurated edges
B. Secondary - systemic lymphadenopathy, maculopapular “copper penny” rash on palms and soles, condyloma lata (painless flat papules) on genitals
C. Latent - can be early (<1 year) or late (>1 year)
D. Tertiary - tabes dorsalis, aortic aneurysms / aortitis, Argyll Robertson pupil, ataxia and + Romberg
E. Congenital - saddle nose, mulberry molars, saber shins, VIII deafness - Treatment
A. Early disease (1, 2, early latent) - one dose IM benzathine penicillin
B. Late disease (late latent, 3) - 3 doses IM benzathine penicillin; neurosyphilis requires IV penicillin
*Vs condyloma acuminata caused by HPV 6 and 11 – treat with imiquimod, trichloroacetic acid
4. Compare to other causes of ulcers - clinical presentation, tx A. HSV B. Chancroid C. Lymphogranuloma venereum D. Granuloma inguinale
- Other ulcers
A. HSV - genital is HSV2
- primary episode is systemic (fever, malalise) and local, vs just local (syphilis)
- vulvar burning and paresthesias, then small, superficial groups of painful ulcers on a red base
- tx - oral acyclovir
B. Chancroid - due to H. ducreyi
- painful ulcer of vulva with ragged edges on necrotic base + tender lymphadenopathy
- school of fish on Gram stain
- tx - oral azithromycin or IM ceftriaxone
C. LV - C. trachomatis L1-L3
- primary - painless papule or shallow ulceration
- secondary - unilateraly painful inguinal LAD –> buboes (enlarged tender nodes) and groove sign (separation of lymph nodes by inguinal ligament)
- tx - doxy or erythromycin
D. Granuloma inguinale - K. ulomatis
- Donovan intracellular inclusion bodies in macrophages
- large painless beefy red ulcers w/out LAD
- tx - doxy or TMP-SMX
Urinary tract infection
For each type - etiology, clinical, and tx
1. Cystitis
2. Urethritis
UTI
1. Cystitis - bacterial infection of bladder with >100K CFUs in midstream (non-contaminated) specimen
A. Etiology - infection due to bacteria from GI tract / rectum (NOT STI)
- MCC is E. coli
- also Klebsiella, Pseudomonas, Enterobacter, Proteus, GBS, Staph saprophyticus
B. Clinical - urgency, frequency, dysuria with no fever or flank pain
- hematuria, hesitancy –> hemorrhagic cystitis or kidney stones
C. Tx - do UA/Ucx and sensitivity; 3 days of TMP-SMX unless resistance (cipro BID for 3 days)
*recurrent UTIs can be treated prophylactically with Bactrim
- Urethritis
A. Etiology - STI –> Chlamydia trachomatis; also Neisseria, Trichomonas
B. Clinical - urethral discharge, dysuria
C. Tx - urethral swabbing for cultures, NAAT;
- doxy (for chlamydia) or azithro in pregnant pts
- IM ceftriaxone (for neisseria)
Urinary tract infection
For each type - etiology, clinical, and tx
3. Urethral syndrome
4. Pyelonephritis
- Urethral syndrome - recurrent episodes of urgency, dysuria caused by urethral inflammation
A. Etiology - unknown, urine cxs negative
B. Clinical - urgency, frequency, dysuria - Pyelonephritis
A. Etiology - starts off as lower UTI
B. Clinical - fever/chills, n/v, CVA tenderness
C. Tx -
i. nonpregnant - oral TMP-SMX or fluoroquinolone for 14 days
ii. pregnant, immunocompromised - hospitalize and give IV amp/gentamicin, ceftriaxone, or zosyn; then suppressive therapy with macrobid for remainder of therapy
*treat pregnant pts with asymptomatic bacteriuria –> 25% chance of developing pyelo (MCC sepsis in pregnancy)
Uterine leiomyomata (ie fibroids)
- Subtypes
- Clinical - compare to endometrial polyps
- Mgmt
Uterine leiomyomata (ie fibroids) - benign smooth muscle tumor surrounded by pseudocapsule
- Subtypes
- submucosal - on endometrium, protrudes into uterine cavity; associated with recurrent abortion
- intramural - MC, in uterine muscle
- subserosal - on serosa outside of uterus
- can be pedunculated or prolapsed - Clinical - most common symptom is menorrhagia (heavy bleeding) –> anemia
- PE - firm, irregular, midline, nontender mass that moves with the cervix
- pelvic pain due to carneous degeneration (2/2 rapid growth) or vascular compromise of a pedunculated one
- contractions due to prolapsed fibroid
- rapid growth (esp after menopause) and hx of pelvic radiation – could be leiomyosarcoma instead
* endometrial polyps - also in uterus, but lead to metrorrhagia (intermenstrual spotting) w/out uterine enlargement
* differentiate from adenomyosis w pelvic MRI - Mgmt - asymptomatic –> no tx; dx via pelvic US
A. Medical
- NSAIDs, progestin therapy (Mirena, OCPs, Depo provera)
- GnRH agonist (Leuprolide) therapy –> shrinks size, used preop bc it is reversible; postmenopausal sx
- f/u 6 mos to monitor size/growth
B. Surgical for symptomatic fibroids
i. myomectomy (if future pregnancy desired AND fibroids caused complications in past pregnancies) - risk of uterine rupture during labor
ii. hysterectomy (MCC of hysterectomy in the US)
iii. uterine artery ligation
Contraception For each form - mechanisms, benefits, risks/ contraindications: 1. Barrier 2. Combined hormonal -- what does estrogen do vs progesterone
- Barrier - condoms, diaphragms
A. Mechanism - mechanical obstruction
B. Benefits - also provides protection against STIs
C. Risks - need to use each time, lack of spontaneity, allergies to material - Combined hormonal (Estrogen and progestin) - OCPs, patch, vaginal ring
A. Mechanism
i. estrogen - inhibits FSH and LH to inhibit ovulation; supports lining to prevent breakthrough bleeding
ii. progesterone - inhibits LH to inhibit ovulation; thickens cervical mucus to inhibit sperm; thins endometrium
B. Benefits - good for pts with dysmenorrhea, IDA, endometriosis, ovarian cysts, acne; decreased risk endometrial/ovarian cancer and benign breast disease
C. Risks - VTE, strokes in pts with migraines with aura, and MI in women over 35 who are heavy smokers; increased risk breast cancer, gallstones
- OCPs can cause or worsen HTN
D. C/i - prior thromboembolic event or CVA, smoking over age of 35, liver tumors, uncontrolled HTN, breast/ endometrial ca, migraines with aura, diabetic retinopathy/nephropathy/PVD
Contraception
For each form - mechanisms, benefits, risks/ contraindications:
3. Injectable
4. Implant
- Injectable - depot medroxyprogesterone acetate (Depo provera) –> progestin only; every 3 months
A. Mechanism - inhibits ovulation (inhibits LH surge), thickens cervical mucus to inhibit sperm, thins endometrium
B. Benefits - pts with IDA, breastfeeding, sickle cell, epilepsy, cysts, endometriosis, dysmenorrhea
C. Risks / contraindications - causes osteopenia (reversible), weight gain, depression
- takes while for ovulation to be restored (10 months) - Implant - etonorgestrel implant in arm (Nexplanon) –> progestin only
A. Mechanism - inhibits ovulation, thickens cervical mucus to inhibit sperm, thins endometrium
B. Benefits - lasts 3 years, for pts breastfeeding, with IDA, cysts, endometriosis, dysmenorrhea
C. Risks - irregular vaginal bleeding
D. C/i - liver tumors, breast ca, hx VTEs/PE/MI (similar to OCPs bc its systemic progesterone)
Contraception
For each form - mechanisms, benefits, risks/ contraindications:
5. IUD - levonorgestrel
6. IUD - copper
- IUD - levonorgestrel (Mirena)
A. Mechanism - thickens cervical mucus to inhibit sperm, thins endometrium to prevent implantation; does NOT inhibit ovulation
B. Benefits - long-term, reversible; decreased bleeding, breastfeeding
C. Risks / contraindications - current STI, PID, malignant gestational trophoblastic disease, breast / cervical / endometrial ca (but NOT ovarian cancer), uterine fibroids or abnormalities distorting uterine cavity - IUD - copper
A. Mechanism - inhibits sperm viability and migration, damages ovum; does NOT inhibit ovulation
B. Benefits - long-term, reversible; most effective emergency contraceptive (up to 5 days post)
C. Risks / contraindications - Wilson disease, current STI or PID, cervical / endometrial ca, uterine fibroids or abnormalities distorting uterine cavity
- increased risk heavy periods, cramping
Breast masses
Treatment algorithm based on age (> 30)
Clinical, diagnosis, treatment
1. Fibrocystic changes
Palpable breast mass: triple test is clinical exam, imaging, and biopsy
A. 30 or older - mammo +/- US –> core biopsy if suspicious for malignancy
–> simply cyst - FNA; excise and send for cytology if bloody, mass persists, or fluid reaccumulates
–> palpable solid mass - core needle biopsy
–> nonpalpable solid mass - wire-guided excisional bx
B. younger than 30 - US +/- mammo
- -> simple cyst - same as for >30 yo pts
- -> complex cyst / palpable solid mass –> FNA; if not enough tissue obtained, or mass is large/suspicious, then excisional biopsy
- Fibrocystic changes - most common benign breast condition
- exaggerated response to ovarian hormones –> mass size increases before menses
A. Clinical - multiple, irregular lumps –> diffuse breast nodularity bilaterally
- cyclic, painful, engorged breasts before menstruation, sometimes green discharge
- more common in premenopausal
B. Diagnosis - FNA or core needle biopsy
C. Tx - decrease caffeine and chocolate; NSAIDs, OCPs, oral progestin, danazol (weak antiestrogen), vit E and B6
Breast masses - clinical, diagnosis, treatment
- Fibroadenoma
- Intraductal papilloma
- Breast cancer
- Fat necrosis
- Fibroadenoma - benign smooth muscle tumor
- MCC breast mass in women <25
A. Clinical - firm, nontender, rubbery, mobile mass on upper outer quadrant
B. Diagnosis - FNA for cytology (BUT only one that does not require tissue diagnosis) to r/o cystosarcoma phyllodes (large low-grade malignancy –> wide local excision)
C. Tx - if small and not growing –> careful observation
- if large –> excisional biopsy - Intraductal papilloma
A. Clinical - benign and solitary –> MCC unilateral serosanguineous nipple discharge with absence of mass
B. Diagnosis - core needle biopsy, physical exam
C. Tx - ductogram, excision of involved ducts - Breast cancer - invasive ductal carcinoma (MC), invasive lobular, Paget (adenocarcinoma), inflammatory (aggressive)
A. Clinical - irregular, fixed mass with LAD
- Paget is eczematous painful changes, inflammatory is peau d’orange, painful edematous red breasts
- risk factors - AGE, HRT, nulliparity, alcohol consumption, early menarche / late menopause, FHx, white
B. Diagnosis - mammo, biopsy, stage via TNM system
C. Tx - BCT (lumpectomy with radiation) and SNLB
- ER (+) - tamoxifen (SERM –> hot flushes, VTE, endometrial hyperplasia) - Fat necrosis - similar to breast cancer (dimpling, mixed mass) but US shows hyperechoic mass and biopsy shows fat globules and foamy histiocytes
- excisional bx to r/o cancer
Hyperprolactinemia
- Causes
- Clinical
- Mgmt
Hyperprolactinemia - PRL > 20 ng /mL
- Causes
- drugs eg OCPs, antHTN, TCAs, antipsychotics
- hypothyroidism (TRH elevates TSH and PRL)
- pituitary adenoma
- empty sella syndrome
- acromegaly
- renal disease / failure
- chest surgery or trauma (implants, T2 dermatome herpes) - Clinical
- galactorrhea - white watery b/l breast discharge
- oligomenorrhea or amenorrhea (high PRL –> increased dopa –> interrupts pulsatile GnRH –> inhibits FSH, LH –> decreased estradiol) - Mgmt - obtain PRL levels after fasting and no breast stimulation for 24 hrs, get TSH and MRIbrain
- anterior pituitary adenoma – bromocriptine, cabergoline (dopamine agonist) if symptomatic (bitemporal hemianopsia, headache) or transphenoidal resection
- hypothyroidism - levothyroxine
- hyperPRL but nl E2 –> periodic progestin withdrawal
PCOS
- Diagnosis
- Clinical
- Mgmt
PCOS
1. Diagnosis - 2 out of 3:
- oligmenorrhea / amenorrhea (2/2 anovulation)
- hyperandrogenism –> increased testosterone (secreted by ovary) and DHEA-S (secreted by adrenals), not otherwise explained by hyperPRL,Cushing, thyroid, CAH, etc.
- evidence of multiple ovarian cysts “string of pearls” on TVUS
also high GnRH, increased LH:FSH ratio also seen often (not always) –> no LH surge –> anovulation
- Clinical - onset in menarche of androgen excess (acne, hirsutism, temporal balding), chronic menstrual irregularities
- obesity – insulin resistance –> low SHBG –> high testosterone
- at risk for DM, endometrial / ovarian cancers, hyperlipidemia, cardiovascular disease - Mgmt - weight loss via diet and exercise
- will bleed in response to progestin challenge
- OCPs to regulate menstrual cycles
- to induce ovulation –> clomiphene citrate (BMI < 30) or letrozole aromatase inhibitor (BMI > 30)
Hirsutism - clinical presentation, diagnosis, and treatment of:
- Cushing syndrome
- Adrenal tumor
Hirsutism - MCC is PCOS
- Cushing syndrome - increased cortisol
A. Clinical - buffalo hump, violaceous striae, HTN, central obesity, osteoporosis, amenorrhea
B. Diagnosis
- high ACTH - dexamethasone suppression test –> Cushing disease (ACTH pituitary adenoma) vs ectopic ACTH secretion
- low ACTH - adrenal tumor vs exogenous corticosteroids
C. Tx - surgical - Adrenal tumor
A. Clinical - rapid onset virilism (clitoromegaly, male balding, acne, voice deepening); abdominal mass
B. Diagnosis - increased DHEA-S (produced by adrenals)
C. Tx - surgical
Hirsutism - clinical presentation, diagnosis, and treatment of: 3. CAH 4. Sertoli-Leydig tumor 5. Aromatase deficiency vs 5AR deficiency
- Congenital adrenal hyperplasia (CAH)
- MCC is 21OH deficiency –> Decreased cortisol, aldosterone but increased sex hormones
A. Clinical -
- at birth - hypotension, ambiguous genitalia and salt wasting
- at puberty - precocious puberty in men and virilization in women
B. Diagnosis - elevated morning fasting 17hydroxyprogesterone, increased renin / low BP, high K+
C. Tx - replace cortisol, aldosterone; antiandrogens (spironolactone, OCPs) - Sertoli-Leydig tumor - androgen-secreting ovarian tumor
A. Clinical - rapid onset hirsutism, virilization, adnexal mass
B. Diagnosis - elevated testosterone level
C. Tx - surgical
*estrogen counterpart is granulosa cell tumor –> precious puberty in girls - Aromatase deficiency - cannot convert androgens to estrogens
A. Clinical - masculinization of XX infants –> normal internal genitalia but ambiguous external genitalia, external virilization (clitoromegaly)
- osteoporosis, delayed puberty
- maternal virilization during pregnancy
B. Diagnosis - high levels of FSH, LH, testosterone, androstenedione but undetectable estrogen levels
C. 5alphareductase deficiency (AR) - cannot convert testosterone to DHT –> feminization of XY infants until virilization at puberty; increased testosterone, LH, estrogen
Puberty
1. Normal puberty stages
Definition, causes, and mgmt of:
2. Precocious puberty
Puberty
- Normal puberty stages
- thelarche (breast bud by 13 yrs) –> adrenarche (axillary and pubic hair) –> growth spurt –> menarche (by 16 yrs) - Precocious puberty - developing secondary sexual characteristics in girls <8 and boys <9
- MCC is idiopathic (central cause), dx of exclusion
A. Central cause - early maturation of HPG axis
- e.g. brain tumors, hydrocephalus, idiopathic - normal FSH, LH
- treat with GnRH agonists eg leuprolide
B. Peripheral cause - excess secretion of sex hormones
- e.g. granulosa cell tumor, CAH, McCune-Albright (menses before thelarche/adrenarche), adrenal tumor - low FSH, LH
- does not respond to GnRH agonists, need to block production based on cause
- –> CAH - glucocorticoids
- –> ovarian cysts - regress spontaneously
- –> ovarian, testicular, adrenal tumors - surgery
*hypothyroidism causes delayed bone age, all other causes cause precocious puberty with accelerated bone age
Puberty
Definition, causes, and mgmt of:
3. Delayed puberty
- Delayed puberty - lack of secondary sexual characteristics by 14 years
A. Hypergonadotropic hypogonadism - high FSH, low estrogen
i. Causes
- MCC is gonadal dysgenesis e.g. Turner syndrome (streak ovaries do not produce estrogen) - short, webbed neck, shield chest; Klinefelter (XXY)
- CAH eg 17hydroxylase deficiency
- gonadotropin resistance - Leydig cell hypoplasia, FSH insensitivity
- also acquired causes eg orchitis, premature ovarian failure, chemo/radiation
ii. Mgmt - unopposed estrogen until breasts are formed, then progestins (via OCPs)
B. Hypogonadotropic hypogonadism - low FSH, low estrogen
i. Causes
- primary eg Kallman syndrome
- secondary:
- —- hypothalamic dysfunction due to eating disorders, chronic illness, stress
- —- primary hypothyroidism, Cushing, craniopharyngioma
ii. Mgmt - MRI to r/o tumor, then same estrogen / hormone replacement therapy
- – GnRH agonist for Kallman syndrome
Amenorrhea
- Primary vs secondary
- Differentiate the 2 MCC of primary
- Other causes of primary amenorrhea
- Amenorrhea
- Primary - no menarche by age 16 with nl breast devlpt
- Secondary - absence of menses > 6 mos in previously menstruating woman - Primary amenorrhea - absent uterus, upper vagina –> blind vaginal pouch
A. Mullerian agenesis (Mayer-Rokitansky-Kuster-Hauser syndrome) - congenital absence of devlpt of uterus, cervix and fallopian tubes in 46,XX female
- normal breasts bc of ovaries (gonads develop due to lack of SRY gene)
- normal testosterone, normal pubic hair
- pts usually also have urinary tract / renal abnormality
B. Androgen insensitivity - receptor defect in which 46,XY individuals are phenotypically female with nl breast devlpt
- functional testes that secrete AMH –> Mullerian ducts regress; and also testosterone (but no response since no receptors) –> so Wolffian ducts degenerate, no male sex characteristics (voice deepening, pubic hair)
- urogenital sinus defaults to external female genitalia (instead of penis/scrotum), testosterone peripherally converted to estrogen (–> breasts)
- high testosterone, LH, estrogen
- need gonadectomy (removal of testes) after puberty due to risk of developing malignancy
- Other causes of primary:
- Turner 45,X - amenorrhea with streak ovaries, delayed breast devlpt, normal uterus and vagina; estrogen and GH therapy to prevent osteoporosis, promote devlpt of sec sex characteristics
- transverse vaginal septum - no canalization of vagina bw Mullerian top 1/3 and urogenital lower 2/3
- imperforate hymen - cyclic pelvic pain
Amenorrhea
- Workup of secondary and DDx
- Mgmt
- Workup of secondary amenorrhea:
A. pregnancy test (MCC secondary amenorrhea)
B. PRL, TSH levels –> hypothyroid, hyperPRL
C. progestin challenge test –> if bleeding, probably PCOS (increased estrogen) or immature HPO axis
–> if not bleeding –>
D. estradiol, FSH, LH levels –> if normal E2, probably outflow tract problem (cervical stenosis, Asherman syndrome ie intrauterine adhesions that damage decidua basalis layer)
Ei. if low estradiol, high FSH/LH –> premature ovarian failure or Turner syndrome
Eii. if low estradiol, low FSH/LH –> hypothalamic (weight loss, stress), or pituitary (Sheehan, irradiation) - Mgmt
- diagnose Asherman via hysterosalpingogram –> irregular filling defects
- gold standard is hysteroscopy, operative hysteroscopy allows transection of adhesions
Infertility For each cause - clinical presentation, diagnosis, and mgmt: 1. Ovulatory dysfunction 2. Uterine disorder 3. Male factor 4. Tubal disorder 5. Peritoneal factor
Infertility - 1 year inability to conceive with unprotected sex
- Ovulatory dysfunction eg PCOS, hypothalamic disturbances, premature ovarian failure
A. Clinical - irregular menses, obesity
B. Dx - basal body temperature chart (biphasic is nl), LH surge urine test kit
C. Mgmt - clomiphene citrate - Uterine disorder eg fibroids
A. Clinical - recurrent pregnancy losses
B. Dx - hysterosalpingogram
C. Mgmt - hysteroscopy - Male factor
A. Clinical - hernia, varicocele, mumps
B. Dx - semen analysis
C. Mgmt - repair, IVF - Tubal disorder
A. Clinical - hx GCC, PID (Salpingitis)
B. Dx - hysterosalpingogram
C. Mgmt - laparoscopy, IVF - Peritoneal factor eg endometriosis
A. Clinical - dysmenorrhea, dyspareunia, dyschezia
B. Dx - laparoscopy
C. Mgmt - laparoscopy for excision/ablation
Endometrial cancer
- Risk factors
- Type I vs Type II
- Endometrial biopsy indications
- Mgmt
Endometrial cancer - MC female genital tract malignancy
- Risk factors
- estrogen exposure w/out progesterone –> early menarche / late menopause, anovulation, nulliparity, obesity, PCOS
- older age, hx infertility
- HTN, DM2 (independent risk factors)
- Lynch syndrome (colon, endometrial, colon ca)
- complex atypical endometrial hyperplasia - Type I - estrogen dependent, in early menopausal patient, lower grade, adenocarcinoma; precursor is hyperplasia; in women with classic risk factors
Type II - aggressive, papillary serous or clear cell; in thin, late menopausal women with regular menses - EMB indications (can also do TVUS for endometrial stripe, nl is <11 mm –> thickened in postmenopausal but can be normal in premenopausal)
- >45 – AUB or postmenopausal bleeding
- <45 – AUB + estrogen (obesity, anovulation) or Lynch
- > 35 with atypical glandular cells on pap smear - Mgmt -
- for low-grade cancer - can do high dose progestin therapy with endometrial sampling so woman can have kids; afterwards –> surgery
- hysteroscopy for surgical staging –> TAHBSO
Cervical cancer
- Risk factors
- Clinical presentation
- Screening
- Mgmt
Cervical cancer - 2nd MC gyn malignancy
- Risk factors - smoking, HIV, multiple sexual partners, STDs, low SES, HPV infection (16 and 18)
- Clinical presentation - abnormal vaginal bleeding eg postcoital spotting
- arises in squamocolumnar junction (transition zone) of cervix –> MC type is squamous cell carcinoma
- can lead to hydronephrosis bc it spreads through cardinal ligaments towards pelvic sidewalls –> MCC death is uremia 2/2 b/l ureteral obstruction - Screening –> colposcopy and bx if abnormal
* if pap is ASCUS, do HPV typing first, then colpo if + or repeat cotesting in 3 yrs if -
* if pap is HSIL –> can do immediate LEEP
- paps w/out HPV co-testing every 3 yrs starting at 21
- paps w HPV co-testing every 5 yrs starting at 30
- no more pap tests if no abnormal history + 3 consecutive negatives starting at 65 - Mgmt - clinical staging
- cervical biopsy when lesion is seen
- early –> sx (radical hysterectomy) or radiation
- late –> chemo (cisplatin) + radiation
Ovarian tumors - types, clinical presentation, and mgmt of:
- Germ cell tumors
- Epithelial tumors
Ovarian cancer risk factors: unopposed estrogen exposure (PCOS, obesity, endometriosis), more ovulatory cycles (age, infertility), and genetics (BRCA 1/2, Lynch)
* decreased risk with breastfeeding, OCPs (anovulation)
- Germ cell tumors
A. Types - benign cystic teratoma (MC), struma ovarii, choriocarcinoma, dysgerminoma (hCG, LDH), endodermal sinus tumor (yolk sac - AFP)
B. Clinical - in young women 20-30 years, can cause torsion
C. Mgmt - use US to diagnose (eg teratoma is a complex cystic structure - hyperechoic nodules and calcifications); treat via cystectomy or u/l oophorectomy - Epithelial tumors
A. Types - serous (MC, usually b/l), mucinous (u/l, grows v large and can lead to pseudomxyomaperitonei –> recurrent SBO), endometrioid, brenner (transitional cell), clear cell
B. Clinical - primarily in postmenopausal or BRCA 1/2 mutations
- adnexal mass, SBO, pleural effusion, ascites (SOB, abdominal distension), pelvic pain
C. Mgmt - CA-125 biomarker level (in postmenopausal pt) + pelvic US
- exlap for cancer resection, staging, debulking, possible hysterectomy + BSO
*do NOT do biopsy (could spread cancerous cells)
- postop chemo (taxane, cisplatin)
* Ovarian cancer - 3rd MC gyn malignancy but leading cause of death (MCC is cachexia due to small bowel mets)
Ovarian tumors - types, clinical presentation, and mgmt
- Sex cord stromal tumors
- When to observe vs operate
- Sex cord stromal tumors - functional neoplasms in either ovaries or testicles
A. Types - granulosa cell (MC), Sertoli-Leydig, thecoma, fibroma
B. Clinical - depends on type (precocious puberty, virilization)
C. Mgmt - solid on U/S - General mgmt
A. In prepubertal –> operate if >2 cm
B. In reproductive age –> observe if <5 cm (probably physiologic cyst eg follicular, corpus luteal) and operate if >7 cm
C. In menopausal, operate if >5 cm
*functional ovarian cyst - result of normal ovulation; U/S shows unilocular simple cyst
Vulvar disorders Clinical presentation and mgmt of: 1. Lichen sclerosis 2. Lichen planus 3. Atrophic vaginitis
Vulvar disorders
- Lichen sclerosis - inflammatory skin condition of vulva only
A. Clinical - epithelial thinning (Cigarette paper quality), white plaques, hyperkeratosis, resorption of clitoris, labial fusion
- seen in postmenopausal women
B. Mgmt - vulvar biopsy (increased risk squamous cell carcinoma), corticosteroids (clobetasol) - Lichen planus - inflammatory skin condition
A. Clinical - affects skin, oral cavity, vulva, vagina –> lacy, reticulated rash (purple papules with white striae); chronic burning and itching; can cause vaginal adhesions
B. Mgmt - corticosteroids (clobetasol) - Atrophic vaginitis - postmenopausal genitourinary syndrome –> loss of vaginal wall elasticity f
A. Clinical - vaginal bleeding, dyspareunia
- also urinary sx eg UTIs, urgency, frequency, and incontinence
- sparse pubic hair, loss of rugae, fissures; elevated vaginal pH > 5, narrowed introitus
B. mgmt - vaginal estrogen, UA/UCx to dx concurrent infection
Vulvar disorders
- Lichen simplex chronicus
- Bartholin gland abscess
- Vulvar cancer
- Lichen simplex chronicus
A. Clinical - itch/scratch cycle –> thickened skin with excoriations
B. Mgmt - give diphenydramine so they sleep through night and don’t scratch - Bartholin gland abscess
A. Clinical - polymicrobial (incl anaerobic), not due to STIs
- painful masses at 5 or 7oclock
B. Mgmt - Word balloon catheter in gland, marsupialization (fixation of cyst wall to vulva) - Vulvar cancer
A. Clinical - most common squamous cell carcinoma, spreads to ipsilateral inguinal lymph nodes
B. Mgmt - radical vulvectomy
Also vulvar psoriasis (salmon plaques with silver scales)
Endometriosis
- Clinical
- Physical exam findings - compare to adenomyosis
- Intraop findings
- Treatment
Endometriosis - endometrial glands and stroma outside the uterus
- Clinical - hallmark is cyclical pelvic pain beginning 1-2 weeks pre, peaking 1-2 days pre-menses, subsiding at onset of menses
- 3D’s = dysmenorrhea, dyspareunia, dyschezia
- or asymptomatic, or progression to chronic pelvic pain
- cause of infertility (2/2 adhesions, inflammation) - PE - fixed, immobile uterus, can be tilted laterally due to adhesions
* adenomyosis (MC in older multips)- endometrial tissue in myometrium –> soft, boggy, globular and uniformly enlarged uterus; dysmenorrhea and heavy menstrual bleeding –> tx - Mirena, hysterectomy - Intraop findings - adhesions, powder burn lesions, flesh colored / dark nodules, collections of chocolate fluid (endometrioma aka “chocolate cysts” –> homogenous cystic appearance on US)
- Treatment:
A. asymptomatic - observe, no treatment indicated
B. symptomatic
i. medical
- NSAIDs, OCPs
- leuprolide (GnRH agonist, temporary action) or danazol (androgen derivative) –> inhibit LH and FSH surges –> suppress estrogen stimulation of ectopic endometrial glands
*clomiphene if trying to conceive
ii. surgical
- laparoscopy and excision of implants / ablation
- TAH / BSO
Risk factors, presentation, and mgmt of:
- Intrauterine fetal demise
- Uterine rupture
- Intrauterine fetal demise (IUFD) at > 20 weeks and before onset of labor
A. Risk factors - obesity, HTN, DM2, smoking, drug use
B. Clinical - Diagnosis via absence of fetal cardiac activity on US (FHR nonstress test / Doppler can be false negative)
- or nonviable fetuses with FHR (anencephaly, b/l renal agenesis, acardia, holoprosencephaly)
C. Mgmt -
- <24 weeks –> D and E
- >24 weeks –> induce vaginal delivery
- fetal autopsy and placental evaluation
- maternal testing for antiphospholipids and fetomaternal hemorrhage - Uterine rupture
A. Risk factors - weakened uterine wall –> prior uterine surgery (C-section, myomectomy), congenital uterine anomalies, fetal macrosomia / multis, trauma
B. Clinical factors - sudden excruciating abdominal pain, vaginal bleeding, abdominally palpable fetal parts
- maternal hypotension and tachycardia (2/2 hemorrhage)
- loss of fetal station (pathognomonic), cessation of contractions
- abnormal FHR –> persistent variable decelerations
C. Mgmt - laparotomy and delivery through rupture site; rupture repair or hysterectomy
Risk factors, presentation, and mgmt of:
3. Amniotic fluid embolism
- Amniotic fluid embolism - amniotic fluid enters maternal circulation through placental insertion site, cesarean incision site, endocervical veins –> inflammatory response with vasospasm
A. Risk factors - advanced maternal age, gravida >5, C-section, placenta previa, placental abruption, preeclampsia
B. Clinical - cardiogenic shock, DIC (purpuric rash, bleeding from IV lines), hypoxemic respiratory failure, seizures, coma
- Tx - respiratory and hemodynamic support (intubation, ventilation)
- dx of exclusion after eclampsia, cardiomyopathy, PE
Spontaneous abortions For each type, describe clinical presentation and treatment: 1. Threatened abortion 2. Inevitable abortion 3. Incomplete abortion
- Threatened abortion - <20 weeks with vaginal spotting / bleeding but NO cervical dilation or passage of tissue, due to:
A. Viable intrauterine pregnancy (50%)
B. Spontaneous abortion (35%)
C. Ectopic pregnancy (15%)
- if stable, f/u hCG level in 48 hrs
- abnl hCG rise (<66%) –> D and C –> miscarriage (chorionic villi on path) or ectopic (no villi, give IM methotrexate)
- give RhoGAM if Rh (-), or can lead to hydrops later on - Inevitable abortion - pregnancy < 20 weeks with uterine cramping, bleeding, and cervical dilation (open os) but NO passage of tissue yet
* differentiate from incompetent cervix (painless cervical dilation)
- tx - expectant mgmt, medical (vaginal misoprostol), or surgical (D and C) - Incomplete abortion - pregnancy < 20 weeks with cramping, bleeding, and cervical dilation (open os) AND passage of some tissue but also retained tissue
- tx - expectant mgmt, medical (vaginal misoprostol), or surgical (D and C)
Spontaneous abortions For each type, describe clinical presentation and treatment: 4. Septic abortion 5. Missed abortion 6. Complete abortion
- Septic abortion - retained POC from missed or incomplete abortion, or elective abortion
- f/c, heavy bleeding, malodorous vaginal d/c, dilated cervix and boggy tender uterus
- broad-spectrum abx (gent and clinda) then curettage after 4 hours - Missed abortion - pregnancy < 20 weeks with fetal demise but no sx (no cramping, bleeding)
- tx - expectant mgmt, medical (vaginal misoprostol), or surgical (D and C) - Complete abortion - pregnancy < 20 weeks where all POC have passed, cervix is closed, resolved cramping and bleeding
- tx - follow hCG levels to zero
Spontaneous abortions
For each type, describe clinical presentation and treatment:
7. Molar pregnancy (hydatidiform mole)
8. Choriocarcinoma
- Molar pregnancy - trophoblastic placental tissue without fetus; increased risk among asians, multiple miscarriages, <20 or >40, prior moles
- Complete mole - XX or XY (enucleated egg + sperm), no fetal parts, increased risk GTD
- Partial mole - XXX, XXY, or XYY (egg + 2 sperm), fetal parts
A. Clinical - vaginal bleeding, absence of FHR, size greater than dates, early preeclampsia at <20 weeks
- hyperemesis, hyperthyroidism
- v high beta hCG (>100,000) –> hyperstimulation of ovaries –> theca lutein cyts (b/l multilocular ovarian cysts that resolve)
- Diagnosis - U/S shows snowstorm pattern
B. Tx - D and C, monitor hCG weekly until undetectable and then 6 months post for choriocarcinoma (so give contraception for 6 mos)
- Choriocarcinoma - metastatic form of gestational trophoblastic neoplasia (no chorionic villi present)
- diagnose via + bHCG (NO biopsies bv lesions vascular)
A. Clinical - postpartum woman with enlarged uterus, irregular vaginal bleeding
- pulmonary symptoms, and multiple infiltrates on CXR (lungs MC site of mets)
B. Tx - methotrexate or hysterectomy
Fetal heart rate monitoring
1. Normal heart rate
A. Tachy
B. Brady
- Variability
- Accelerations
Fetal heart rate monitoring
- Normal - baseline (avg HR in 10 min window) is 110 - 160 bpm with accelerations and variability
A. Tachy –> due to chorioamnionitis (maternal fever), hyperthyroid
B. Brady - FHR <110 for >10 minutes –> due to preuterine (maternal hypoxia 2/2 epidural, seizure, PE, AFE), uteroplacental (placental previa or abruption), or postplacental (cord prolapse, vasa previa) - Variability - bw 6 - 25 bpm
- decreased variability –> baby could be sleeping (do scalp stimulation to induce acceleration) or could be acidotic - Accelerations - normal! abrupt increase in FHR >15 bpm for >15 sec
Fetal heart rate monitoring
4. Decelerations - etiologies and interventions A. Early B. Late C. Variable D. Prolonged
- Decelerations - abrupt decrease in FHR <15 bpm for 15 sec - 2 min (prolonged decel = 2-10 min)
A. Early - when ctx begins and recovers when ends –> physiological, benign (2/2 vagal tone from fetal head compression)
B. Late - begin at peak of ctx –> due to fetal hypoxia (uteroplacental insufficiency 2/2 chronic HTN, postterm)
- recurrent late –> due to fetal acidemia
- move mom to LLD, give 02 and IVF, d/c pitocin
C. Variable - abrupt in decline and resolution (<30 sec from onset to nadir) –> due to cord compression, cord prolapse, or oligohydramnios
- if persistent (with >50% ctx) –> maternal repositioning to LLD, then amnioinfusion for repetitive variable decels to decrease risk C-section
D. Prolonged decels
- tachysystole (>5 ctx in 10 min) –> stop pitocin, give B2 agonist tocolytic e.g. terbutaline or nitroglycerin
- hypotension 2/2 epidural –> give IVF bolus or ephedrine
- rapid cervical dilation –> positional changes (place in LLD left lateral decubitus to avoid compression of IVC)
- umbilical cord prolapse –> C-section
- placental abruption –> support BP, C-section
- uterine rupture –> C-section
External cephalic version - indications
external cephalic version - manual conversion of fetus from breech to vertex
- do if >37 weeks, no c/I to vaginal delivery (placenta previa, herpes, prior classical C-section) or to ECV (waters broken, abnormal FHR, oligohydramnios, multis)
- if ECV fails –> C-section by 39 weeks
*if presentation is breech at labor (eg waters have broken) –> do C-section
internal podalic version - breech extraction of malpresenting second twin, preferable to C-section
Hyperemesis gravidarum
- Risk factors
- Clinical
- Lab values
- Treatment esp compared to morning sickness
- Complication
Hyperemesis gravidarum
- Risk factors - prior hx, multis, mole
- Clinical - severe, persistent vomiting with dehydration, hypotension, and >5% loss of prepregnancy weight
- Lab values - ketonuria, hypochloremic hypokalemic MA, hemoconcentration
- Treatment - fluids (NS w 5% dextrose), antiemetics, admission to hospital, corticosteroids if tx unresponsive
vs morning sickness - vitamin B6, doxylamine, ginger; resolves by week 16 - Complication - Wernicke encephalopathy (AMS, nystagmus, gait ataxia) 2/2 thiamine deficiency –> hypoglycemia, elevated LFTs due to vomiting
