OBGYN Flashcards

Question

Preterm labor (vs cervical insufficiency) 1. Risk factors 2. Assessing risk 3. Management 4. Tocolytics and side effects

Answer 1

Preterm labor - cervical change (2 cm dilated, 80% effaced) with contractions between 20 and 37 weeks *vs cervical insufficiency which is painless dilation 1. Risk factors - *hx of prior*, PPROM, multis, hx cervical cone biopsy, cocaine, trauma, pyelo, gonococcal cervicitis, uterine anomalies (bicornuate), placental abruption 2. 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 3. 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 4. 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)

Answer 2

PPROM - Preterm premature ROM prior to onset of labor at <37 weeks; prolonged if >18 hours 1. 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 2. 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 3. 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 4. 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

Answer 3

Congenital intrauterine infections (part of TORCHeS) 1. Parvovirus - fetal aplastic anemia (sinusoidal FHR), hydrops fetalis (excess fluid in 2+ fetal body cavities; caused by parvovirus), hydramnios - mgmt - intrauterine transfusion, delivery 2. 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 3. 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 4. 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

Answer 4

IUGR - birthweight <10th percentile for gestational age (small and sick) 1. 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 2. 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 3. 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 3. 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

Answer 5

Endomyometritis - infection of decidua, myometrium, and parametrial tissues due to ascension of polymicrobial bacteria from normal vaginal flora (MC is staph aureus and strep) 1. 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 2. Presentation - fever over 100.4F (MCC of fever in woman post C-section) usually on POD2 - uterine fundal tenderness - purulent foul-smelling lochia 3. 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

Answer 6

1. 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

Answer 7

2. 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

Answer 8

1. CBC - first visit, Hb up to 10.5 is normal, if lower --> could lead to preterm delivery; do trial of iron 2. Blood type and Screen (indirect coombs) - first visit, Ab screen may indicate isoimmunization --> hemolysis - Abs: Lewis (lives), Duffy (dies), Kell (kills) 3. 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) 4. 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 5. Rubella - first visit, if nonimmune --> give live attenuated vaccine postpartum 6. 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

Answer 9

1. 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) 2. Quad screen (MSAFP, hCG, Estriol, and Inhibin-A) - 16 to 20 weeks, can indicate trisomy or NTD --> confirm dates via U/S or amniocentesis 3. Screening U/S - 18 to 20 weeks to look for fetal abnormalities 4. GBS culture - 35 to 37 weeks; if (+) - penicillin during labor 5. TdaP vaccine - 28 to 36 weeks - killed vaccine so safe, results in passive transmission of IgG response 6. Chorionic villus sampling - 10 to 13 weeks; for definitive karyotype 7. Amniocentesis - 15 to 20 weeks; for definitive karyotype

Answer 10

Menopause - cessation of menses for 12 months; occurs after age 40, mean age is 51 1. 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 2. 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) 3. 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+

Answer 11

Ureteral injury 1. 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 2. 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 3. Mgmt - IV pyelogram to diagnose - abx and cysto to r/o kinked ureter - stenting, repair

Answer 12

Pelvic organ prolapse (POP) - due to defect of pelvic support; family history increases risks, so does age, obesity, chronic constipation 1. Enterocele - defect of pelvic support of uterus and cervix --> small bowel descends into vagina --> feeling of bulging mass in vagina 2. 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 3. Rectocele - defect of pelvic support of rectum --> constipation, difficulty pooping - posterior colporrhaphy, culdoplasty (since large cul-de-sac can lead to POP)

Answer 13

Urinary incontinence 1. 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 2. 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

Answer 14

3. 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 4. 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

Answer 15

Salpingitis - infection of fallopian tubes PID - infection of upper female genital tract - includes endometritis, salpingitis, TOA, and pelvic peritonitis 1. Diagnosis (clinical): - lower abdominal tenderness (due to peritoneal irritation of pelvis) - cervical motion tenderness (chandelier sign) and/or - adnexal tenderness 2. 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 3. 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) 4. 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

Answer 16

Chronic pelvic pain 1. Define - persistent pain in lower abdomen / pelvis for >6 months, causing significant effects on daily function, QOL 2. 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) 3. Evaluation - r/o pregnancy - GCC, UA/Ucx, CBC - pelvic US 4. Treatment - NSAIDs and/or OCPs for 3 month trial, then diagnostic laparoscopy

Answer 17

Vaginal infections - clinical, diagnosis, and treatment 1. 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 2. 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 3. 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

Answer 18

Syphilis - caused by bacteria Treponema pallidum 1. 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 2. 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 3. 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

Answer 19

4. 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

Answer 20

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 2. 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)

Answer 21

3. Urethral syndrome - recurrent episodes of urgency, dysuria caused by urethral inflammation A. Etiology - unknown, urine cxs negative B. Clinical - urgency, frequency, dysuria 4. 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)

Answer 22

Uterine leiomyomata (ie fibroids) - benign smooth muscle tumor surrounded by pseudocapsule 1. 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 2. 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 3. 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

Answer 23

1. 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 2. 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

Answer 24

3. 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) 4. 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)

Answer 25

5. 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 6. 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

Answer 26

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 1. 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

Answer 27

2. 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 3. 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 4. 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) 5. 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

Answer 28

Hyperprolactinemia - PRL > 20 ng /mL 1. 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) 2. Clinical - galactorrhea - white watery b/l breast discharge - oligomenorrhea or amenorrhea (high PRL --> increased dopa --> interrupts pulsatile GnRH --> inhibits FSH, LH --> decreased estradiol) 3. 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

Answer 29

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 2. 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 3. 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)

Answer 30

Hirsutism - MCC is PCOS 1. 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 2. 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

Answer 31

3. 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) 4. 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 5. 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

Answer 32

Puberty 1. Normal puberty stages - thelarche (breast bud by 13 yrs) --> adrenarche (axillary and pubic hair) --> growth spurt --> menarche (by 16 yrs) 2. 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

Answer 33

3. 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

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1. Amenorrhea - Primary - no menarche by age 16 with nl breast devlpt - Secondary - absence of menses > 6 mos in previously menstruating woman 2. 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 3. 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

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3. 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) 4. Mgmt - diagnose Asherman via hysterosalpingogram --> irregular filling defects - gold standard is hysteroscopy, operative hysteroscopy allows transection of adhesions

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Infertility - 1 year inability to conceive with unprotected sex 1. 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 2. Uterine disorder eg fibroids A. Clinical - recurrent pregnancy losses B. Dx - hysterosalpingogram C. Mgmt - hysteroscopy 3. Male factor A. Clinical - hernia, varicocele, mumps B. Dx - semen analysis C. Mgmt - repair, IVF 4. Tubal disorder A. Clinical - hx GCC, PID (Salpingitis) B. Dx - hysterosalpingogram C. Mgmt - laparoscopy, IVF 5. Peritoneal factor eg endometriosis A. Clinical - dysmenorrhea, dyspareunia, dyschezia B. Dx - laparoscopy C. Mgmt - laparoscopy for excision/ablation

Answer 37

Endometrial cancer - MC female genital tract malignancy 1. 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 2. 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 3. 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 4. 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

Answer 38

Cervical cancer - 2nd MC gyn malignancy 1. Risk factors - smoking, HIV, multiple sexual partners, STDs, low SES, HPV infection (16 and 18) 2. 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 3. 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 4. Mgmt - clinical staging - cervical biopsy when lesion is seen - early --> sx (radical hysterectomy) or radiation - late --> chemo (cisplatin) + radiation

Answer 39

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) 1. 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 2. 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)

Answer 40

3. 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 4. 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

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Vulvar disorders 1. 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) 2. 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) 3. 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

Answer 42

4. 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 5. 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) 6. 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)

Answer 43

Endometriosis - endometrial glands and stroma outside the uterus 1. 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) 3. 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 3. Intraop findings - adhesions, powder burn lesions, flesh colored / dark nodules, collections of chocolate fluid (endometrioma aka "chocolate cysts" --> homogenous cystic appearance on US) 4. 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

Answer 44

1. 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 2. 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

Answer 45

3. 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 3. Tx - respiratory and hemodynamic support (intubation, ventilation) - dx of exclusion after eclampsia, cardiomyopathy, PE

Answer 46

1. 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 2. 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) 3. 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)

Answer 47

4. 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 5. 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) 6. Complete abortion - pregnancy < 20 weeks where all POC have passed, cervix is closed, resolved cramping and bleeding - tx - follow hCG levels to zero

Answer 48

7. 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) 8. 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

Answer 49

Fetal heart rate monitoring 1. 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) 2. Variability - bw 6 - 25 bpm - decreased variability --> baby could be sleeping (do scalp stimulation to induce acceleration) or could be acidotic 3. Accelerations - normal! abrupt increase in FHR >15 bpm for >15 sec

Answer 50

4. 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

Answer 51

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

Answer 52

Hyperemesis gravidarum 1. Risk factors - prior hx, multis, mole 2. Clinical - severe, persistent vomiting with dehydration, hypotension, and >5% loss of prepregnancy weight 3. Lab values - ketonuria, hypochloremic hypokalemic MA, hemoconcentration 4. 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 5. Complication - Wernicke encephalopathy (AMS, nystagmus, gait ataxia) 2/2 thiamine deficiency --> hypoglycemia, elevated LFTs due to vomiting

OBGYN Flashcards

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