OB exam 3

  1. What are the risk factors for cervical cancer?
    • STDS (HPV 16, 18/ HIV)
    • low socioec status
    • >1 sexual partner
    • immunosuppression
    • tobacco
    • hx of previous cervical dz
    • DES exposure
  2. What is the most common presenting symptom of cervical CA?

    What are other presenting symptoms of cervical CA?
    • MC: post coital bleeding and AUB (including post menopausal)
    • Other: persistent vaginal discharge/pelvic pain/leg swelling/urinary sxs (late findings)
  3. What is the workup for cervical CA?
    • H&P (signs/symptoms)
    • colpo referral for visible cervical lesions
    • rectal exam for staging re local invasion
    • imaging for local & distant dz
  4. What is stage I cervical dz confined to? What are the subclasses of stage I?
    • confined to cervix
    • A= microscopic; B= clinical dz
  5. What is the most common gynecologic malignancy in the US?
    endometrial CA
  6. What are the risk factors for endometrial CA?
    • UNOPPOSED ESTROGEN! (anovulatory cycles)
    • obesity
    • affluent
    • white
    • low parity
    • post meno (esp if on estrogen replacement w/o progestin)
    • type 2 DM
    • women w/ lynch syndrome (familial nonpolyposis colorectal CA)
  7. What is the workup for endometrial CA?
    • endometrial biopsy (EMB): positive is CA, negative has 90% dx accuracy
    • TVUS: for post meno pts as INITIAL dx test (not sufficient in eval of pre meno pts)
  8. How are post meno pts managed based on TVUS endometrial stripe results?
    • </=4 mm stripe: initial tx with HRT
    • >4 mm stripe: reqs EMB +/- D&C
  9. What are the 2 main types of cervical CA influenced by HPV infection?
    • squamous cell (more prevalent-80%)
    • adenocarcinoma
  10. What HPV strains are responsible for 70% of all cervical CA?
    HPV 16, 18
  11. What EMB method uses minimal/no dilation, little/no anesthesia, and is 1/10th of the cost of D&C?
    Pipelle method
  12. How is an EMB result of hyperplasia without atypia managed?
    • progesterone tx
    • EMB q 3-6 months
  13. How is an EMB result of hyperplasia with atypia managed?
    • hysterectomy
    • if refused use progesterone, then EMB q3 months is recommended
  14. What are the indications for doing a D&C for cervical CA?
    • unable to tolerate EMB
    • benign EMB w/ continued AUB
    • non-dx EMB in hormone replacement (HR) pt
    • insufficient tissue on EMB
    • severe cervical stenosis
    • if laparoscopy is also req'd
  15. What is the second most common gyncologic malignancy? At what age does the risk increase?
    • ovarian CA (overall risk is 1 in 70 in a lifetime)
    • 40-60 yrs have increased risk (median age @ dx is 61 yrs)
  16. What is the most common cause of gyn cancer deaths?
    ovarian CA
  17. What are the risk factors for developing ovarian CA?
    • low/no parity
    • breast/colon CA
    • tobacco
    • + family hx
  18. What are some things that are protective again ovarian CA?
    • multiparity
    • OCP use
    • hx of breastfeeding
    • take birth control pills, have a baby, breastfeed, take pills again, have more kids and breastfeed those, get your tubes tied and don't smoke= best chances against it per Col Cunningham ;)
  19. How are pts with familial ovarian CA syndrome (BRCA-1, 2) managed?
    • freq pelvic exams
    • TVUS
    • CA 125 serum markers
  20. What are some useful screening tests for ovarian CA?
    there aren't any
  21. What is the most common physical finding during H&P with ovarian CA?

    What are the late symptoms of ovarian CA?
    • MC: pelvic mass/ascites
    • Late: anorexia, early satiety, wt loss, constipation, freq UTIs in meno pt
  22. What test should be performed for a complex cystic mass?
  23. What test for ovarian CA is most useful in following CA tx, and may be of value in post meno pts in combo w/ clinical evaluation or US?
    serum marker CA-125
  24. A sustained elevation of serum marker CA-125 >65u/ml is 75% predictive of malignancy in what situation?
    in post meno pelvic mass
  25. What is the most common type of vulvar CA?
    squamous cell carcinoma (SCC)
  26. What is the second most common type of vulvar CA?
    malignant melanoma (ANY pigmented lesion of the vulva warrants biopsy!!)
  27. What are the two hypotheses proposed as the cause of vulvar CA from SCC?
    • young: HPV (16, 18, 33)/VIN/smoking
    • older (avg 65 yrs): chronic inflammation/lichen sclerosis
  28. If you notice during an examination that the pt has a pigmented lesion on the vulva that looks like a nevus what should you do?
    • BIOPSY!!
    • any pigmented lesion should be checked for malignant melanoma
  29. What are the 3 types of gestational trophoblastic disease (GTD)?
    • benign hydatidiform mole (noninvasive)
    • persistent/invasive mole
    • choriocarcinoma (frankly malignant)
    • **majority have benign course**
  30. What are the risk factors for GTD?
    • age >35 or <20
    • hx of previous GTN
  31. Which type of hydatidiform mole has no identifiable fetal features, generalized hydatidiform swelling of villi, diffuse trophoblastic hyperplasia, is diploid paternal, and produces typical hCG levels of >100K (nl preg peaks @ <100K)?
    complete hydatidiform mole
  32. Which type of hydatidiform mole has identifiable fetal features (triploidy stigmata), focal swelling of chorionic villi, focal trophoblastic hyperplasia, is triploid (2/3 paternal), and may allow detection of FHT?
    partial hydatidiform mole
  33. What are the clinical presentation features seen with GTN (complete hydatidiform moles)?
    • vaginal bleed
    • increased uterine size
    • pre-eclampsia
    • hyperemesis
    • hyperthyroid
    • trophoblast emboli
    • theca-lutein cyst
    • elevated hCG (>100k)
    • absent FHT
  34. What are the clinical presentation features seen with GTN (partial hydatidiform moles)?
    • vaginal bleed
    • increased uterine size
    • pre-eclampsia
    • elevated hCG
    • absent FHT
  35. What is the diagnostic approach and pathognomic finding for a complete mole?
    • US shows "snowstorm"
    • do CBC to exclude anemia
  36. What is the diagnostic approach and pathognomic finding for a partial mole?
    • detected after tissue exam of SAB
    • US, shows focal placental cysts/gestational sac +/- fetus
  37. What is the usual approach for treating a molar pregnancy?
    suction curettage (confirms dx, relieves sxs, prevents complications)
  38. What is the required post evacuation monitoring for molar pregnancy?

    What is the tx if levels persist?
    • weekly until 3 consecutive normals
    • monthly for 6 months after 3 normals
    • persistent levels get chemotherapy
  39. Occurs in up to 20% of complete molar pregnancies vs 3-4% of partial moles, invades the myometrium, is diagnosed by persistent HCG levels following evac of a molar pregnancy, is rarely associated with metastasis and requires a hysterectomy as treatment.
    persistent/invasive mole
  40. They are highly anaplastic with no chorionic villi, cause necrosis and hemorrhage, are rapidly invasive and can lead to hematogenous metastases (vagina & lungs=common; CNS, GI/liver, kidney=other sites).
    • choriocarcinoma (tx with chemo)
    • **50% have a preceding molar pregnancy, 50% have preceding SAB/induced AB/ectoptic/normal pregnancy**
  41. What are the follow up recommendations for GTN disease?
    • b-HCG monthly x 1 year (up to 5yrs w/ mets)
    • contraception for 6-12 months
    • future pregnancy presents increased risk of subsequent GTN (esp if >40 yrs), but there are no increased risks of OB complications once pregnant
  42. What conditions cause vaginitis resulting in vaginal discharge (leukorrhea)?
    • BV
    • vulvovaginal candidiasis (VVC)
    • trichomoniasis
    • other (atrophic, FB)
  43. What conditions cause cervicitis/urethritis resulting in vaginal discharge (leukorrhea)?
    • chlamydia
    • gonorrhea
  44. What is considered normal vaginal pH?
  45. What can upset the balance of normal vaginal microflora?
    • abx
    • douching
    • intro of semen
    • FB (tampons, diaphragms)
    • hypoestrogenized (atrophic) from menopause, pregnancy, hormonal contraception (high progesterone to estrogen)
  46. What is the most common cause of vaginal discharge (leukorrhea)?
  47. Polymicrobial vaginal infection involving loss of lactobacilli and overgrowth of anaerobes, produces a profuse, milky d/c with a fish odor (esp after sex).
  48. Dx of BV requires 3 out of what 4 criteria (Amsel's)?
    • homogenous d/c
    • pH >4.5 (turns nitrazine paper blue)
    • + "whiff" test (10% KOH to vag secretions=fishy smell)
    • clue cells on wet prep (nl saline)
  49. What vaginal condition is associated with adverse pregnancy outcomes of PROM, preterm delivery, intraamniotic infection and postpartum endometritis?
    • BV
    • **tx ALL symptomatic preggos, screen asx preggos at high risk for preterm delivery**
  50. What is the second most common cause of vaginitis?
    vulvovaginal candidiasis (VVC)
  51. Condition that presents with vaginal burning, irritation, post voiding dysuria, odorless thick white "cottage cheese" d/c.
  52. How is VVC diagnosed?
    • observed vulvovaginal erythema
    • pH <4.5
    • budding yeast, pseudohyphae on KOH
    • cx (if recurrent sxs suggest yeast infix but there not no findings on KOH)
  53. What is the definition of recurrent VVC?
    >4 episodes in 1 year
  54. What are the risk factors for recurrent VVC?
    • OCPs
    • diaphragm
    • DM
    • abx
    • pregnancy
    • immunosuppression
    • tight clothing
    • **consider cx for candida glabrata which is resistant to "azoles"**
  55. What is the third most common cause of vaginal d/c?
  56. Vaginal condition diagnosed by presence of frothy green-yellow d/c with "musty" odor, dyspareunia, dysuria, strawberry cervix, pH >4.5, and a positive wet prep.
  57. What is the treatment for BV?
    • metronidazole 500mg bid x 7 days OR
    • topical metronidazole cream 5gm/d X 5 days OR
    • topical clindamycin cream 5gm/d x 7 days
  58. What is the treatment for vaginal yeast infections (VVC)?
    • fluconazole 150mg po (single dose) OR
    • topical "azole" creams (only regimen approved for pregnancy)
  59. What is the treatment for recurrent VVC?
    • longer duration therapy for each episode (7-14 days vaginal tx, repeat fluconazole dose q3 days X 3 doses) AND
    • maintenance regime (weekly fluconazole x 6 months, twice weekly topical azole creams)
  60. What is the treatment for trichomoniasis?
    • metronidazole 2g po in single dose
  61. Most common cause of vaginal irritation after menopause resulting in vulvar irritation, clear/yellow/blood tinged d/c, urinary sxs.
    atrophic vaginitis
  62. Diagnosed by presentation of friable vaginal epithelium, loss of vaginal rugae, pale color, and pap smear changes.
    atrophic vaginitis
  63. How is atrophic vaginitis treated?
    • topical estrogen cream/suppository/ring
    • PO estrogen
    • tx any concomitant infection
  64. Most prevalent STI causing life long infection, 70% transmission through saliva/direct contact from asymptomatic viral shedding, causes painful vesicles/ulcers and fever, HA, malaise & LAD with primary infection.
    herpes simplex (HSV 1 & 2)
  65. What is the treatment for herpes simplex?
    • acyclovir
    • famciclovir
    • valacyclovir
  66. An intracellular bacteria causing asymptomatic disease in 70% of women and urethritis and cervicitis in 30%.
    chlamydia trachomatis
  67. What are the treatment steps for chlamydia?
    • azithromycin 1g po x 1 OR
    • doxycycline 100mg bid x 7 days
    • Tx all sexual contacts
    • test for other STIs
    • abstinence for 7 days on abc
    • no test of cure needed unless pregnant
    • rescreen in 3-4 months
  68. Also known as the "clap", is asymptomatic in most women but causes urethritis and cervicitis when it IS symptomatic.
    neisseria gonorrhea
  69. How is gonorrhea treated?
    • ceftriaxone IM or cefixime PO
    • NO quinolones in Ca, HI, Pacific rim or during pregnancy
    • tx for chlamydia as well
    • tx all sexual contacts
    • abstinence for 7 days on abc
    • rescreen in 3-4 months
  70. Bacterial spirochete transmitted by direct contact/transplacental resulting in a painless chancre.
    treponema pallidum (syphilis)
  71. How is syphilis treated?
    • PCN 2.4 million units IM
    • ONLY proven rx modality
    • pts allergic to PCN should be desensitized
  72. How does secondary syphilis present?
    • LAD
    • exanthem
    • condyloma lata
    • **1/3 of cases present with 2nd syphilis**
  73. Transmitted by contact, inanimate objects, birth canal to larynx causing a latent infection in the majority of pts, clinically presents with condyloma accuminatum.
    HPV 6, 11 (genital warts)
  74. How are genital warts diagnosed?
    • clinically (acetic acid application)
    • biopsy if there is no response to tx
  75. What is the treatment for genital warts (HPV)?
    • podophyllin or TCA (provider applied)
    • podofilox or imiquimod (pt applied--not for preggo)
    • surgical (LN2, excision, electrocautery, laser, intralesional interferon)
  76. What is the most common cause for upper genital tract inflammation/infection?
    ascending lower tract infections
  77. What are the most common organisms that cause PID?
    • chlamydia trachomatis
    • neisseria gonorrhea
    • BV microflora (anaerobes)
    • genital mycoplasmas (m. hominis, u. urealyticum, m. genitalium)
  78. What conditions can occur as sequelae from PID?
    • infertility
    • ectopic pregnancy
    • preterm birth
  79. What is the minimum criteria that is diagnostic for PID?
    uterine/adnexal or CMT in sexually active young women/women with risk factors
  80. What are more specific diagnostic criteria than the minimum required for PID?
    • oral temp 101F
    • mucopurulent cervical/vaginal discharge
    • WBCs on saline prep
    • elevated CRP
    • lab diagnosis of C. trachomatis/ N. gonorrhea
  81. What are the most specific diagnostic criteria for PID?
    • US
    • MRI
    • laparoscopic/endometrial biopsy
  82. What is the outpatient treatment for PID?
    • ceftriaxone 250mg IM (OR cefotetan IV) PLUS
    • doxycycline 100mg bid for 2 weeks
    • +/- metronidazole 500mg bid for 2 weeks if trich or recent instrumentation
  83. PID complication occuring in 10%, can rupture leading to peritonitis &/or sepsis, and is distinguished from endometritis/salpingitis by presence of a tender inflammatory adnexal mass (use US, CT, MRI or laparoscopy if in doubt).
    tubo-ovarian abscess (TOA)
  84. How is a tubo-ovarian abscess treated?
    • broad spectrum IV abx
    • surgical if no improvement in 24-48 hours
  85. Caused by preformed toxin from staph aureus, associated with super absorbent tampons, has <3% mortality and tx is NOT for the initial syndrome but to decrease recurrence.
    toxic shock syndrome
  86. What is the classic triad for TSS?
    • fever
    • diffuse macular rash
    • HoTN
  87. What is the average age for menopause ("THE last menstrual period") to occur? At what age is menopause "premature"?
    • 51 yrs
    • <40 yrs
  88. What can cause "premature" menopause (<40 yrs old)?
    • abnl karyotype (turner's XO)
    • autoimmune disorders
    • iatrogenic (surgery--BSO, chemo, radiation--XRT)
  89. If there are no eggs in the ovaries, there will be no physiologic response to what?
    gonadotropins (FSH/LH)
  90. What are the defined stages (STRAW) of menopause?
    • Transition: stage -2 (variable cycle length-->7d), stage -1 (>/= 2 missed cycles + amenorrhea >/= 60 days)
    • Menopause: 12 month amenorrhea after FMP
    • Post menopause: stage +1 (1st 5 yrs after menopause), stage +2 (from stage +1 till death)
  91. How is irregular ovulation managed with waxing and waning ovary function in perimenopause?
    contraception is requited until amenorrhea x 1 yr
  92. Why is there fluctuating hormone production during perimenopause?
    • waxing & waning ovary function
    • estrogen/progesterone ultimately cease
    • ovary still produces small amounts of androgens during menopause
  93. Leads to irregular menses and increased estrogen effects (relatively unopposed) exacerbated by obesity that can cause endometrial hyperplasia or CA during perimenopause.
    • anovulatory cycles
    • **ultimately no more eggs=no more ovarian estrogen!**
  94. How is menopause diagnosed?
    • no menses x 1 yr
    • FSH level not necessary since it varies throughout perimenopause
  95. Explain menopausal estrogen production.
    • adrenals: androstenedione precursor is converted to estrone in peripheral fat
    • women may have continued large amount depute lack of ovary estradiol: leads to increased risk of endometrial & breast CA
  96. What are the consequences of estrogen loss?
    • vasomotor sxs/mood sxs
    • vulvovaginal atrophy
    • osteoporosis
    • increased risk of CAD/CVA
    • increased risk of colon CA
  97. What are the treatment options for vasomotor symptoms of menopause?
    • lifestyle
    • HRT
    • time (1-5 yrs)
    • SSRIs/SNRIs
  98. What are the indications for HRT/ERT in menopause?
    • vasomotor sxs
    • vulvovaginal atrophy
    • osteoporosis (in women that also have vasomotor sxs)
  99. What are the CIs for HRT/ERT?
    • pregnancy
    • AUB
    • estrogen sensitive CA
    • thrombosis or CVA
    • liver disease
  100. What did the WHI determine as being the most effective tx for vasomotor sxs during menopause? What were the overall conclusions?
    • HRT
    • decreased risk for osteoporotic fractures and colon CA
    • increased risk for CAD, CVA, blood clots, breast CA
  101. What does ACOG say in regards to HRT and long term rx in asymptomatic menopause patients?
    • HRT: smallest does for shortest time (preferably <4 years)
    • long term in asx pt: stop by tapering (helps decrease rebound sxs)
  102. What are the meds used as alternatives to HRT in menopause therapy?
    • SSRIs: effexor, paxil, prozac, zoloft
    • gabapentin (neurontin)
    • clinidine (catapres)
  103. How are the vulvovaginal sxs of dyspareunia, atrophic vaginitis, and urinary sxs of frequency/dysuria, incontinence and UTIs due to a lack of estrogen during menopause (vaginal atrophy w/ alkaline pH) treated?
    • vaginal estrogen as cream/suppository/ring (BEST!)
    • oral estrogen/transdermal estrogen
  104. Deterioration of trabecular bone tissue leading to decreased bone mass, fragility and increased fracture risk.
  105. What is the definition of osteoporosis according to the WHO?
    bone mineral density >2.5 SD below the mean
  106. What is the definition of osteopenia according to the WHO?
    bone mineral density >1.0 but <2.5 SD below the mean
  107. What are the clinical risk factors for osteoporotic fractures (independent of BMD)?
    • advancing age
    • previous hx of fragility fracture as adult
    • hx of fragility fracture in 1st degree relative
    • low body weight
    • current smoking
    • glucocorticoid therapy
    • excessive use of alcohol
    • RA
  108. How is screening for osteoporosis done and who gets screened?
    • DEXA (measures hip & spine)
    • post meno women <65 w/ 1 or more risk factors besides menopause; ALL 65 yr olds
  109. What are the T and Z scores used in DEXA when diagnosing osteoporosis?
    • T-score: compares BMD to that of a "normal" young adult
    • Z-score: compares BMD with the same age and weight
  110. What are the ways in which osteoporosis can be prevented?
    • nutrition: Ca 1000-1500 po/day, vit D 800 IU po/day
    • wt bearing exercise (promotes balance): 20-30 mins 3x/wk, high intensity not helpful
    • avoid: tobacco & ETOH
  111. What are some fracture prevention strategies for menopausal women?
    • reduce risk of falls: vision assessment, lighting, clean well marked stairs and floors, footwear, hip pads
    • tx osteoporosis with pharmalogic agents in menopausal women with a T-score of: >-2.5 SD/ -2.0 to -2.5 SD plus 1 addition risk factor for fracture
  112. Drug for osteoporosis that is an agonist at the bone and antagonist at the breast/endometrium, worsens vasomotor sxs, but prevents vertebral fractures.
    selective estrogen receptor modulators (SERM) such as raloxifene
  113. Osteoporosis treatment of choice, indicated for osteoporosis prevention (osteopenia + risk factor).
  114. What are the CIs to using bisphosphonates for osteoporosis?
    • esophageal dysmotility
    • inability to be upright x 30mins
    • hypersensitivity
    • hypocalcemia
  115. What are the complications that can come from using bisphosphonates?
    • erosive esophagitis
    • jaw osteonecrosis
  116. What are the second line therapies for osteoporosis?
    • PTH: stimulates osteoblasts and osteoclasts (autoinjector)
    • calcitonin: inhibits osteoclasts, indicated for osteoporosis fx pain (nasal spray)
  117. How is tx for osteoporosis monitored?
    • repeat DEXA q2 years
    • get bone metabolism markers @ 6 months (serum CTX, urinary NTX)
    • **~15% of women continue to lose BMD despite tx**
  118. What are the different protrusions/pelvic organ prolapse (POP) types via the vagina and what are they called?
    • urinary bladder: cystocele
    • rectum: rectocele
    • bowel: enterocele
    • uterus: procidentia
  119. What are the etiologies for pelvic organ prolapse?
    • erect, bipedal posture
    • congenital/developmental
    • pregnancy, labor & delivery
    • increased intra abd pressure
    • atrophy
    • iatrogenic
    • whites>blacks/asians
    • increased parity
    • obesity
  120. What are the s/s of pelvic organ prolapse?
    • "fullness"
    • urinary frequency, urgency, incontinence, retention w/ cystocele, constipation (splint w/ rectocele)
    • exacerbated by posture & duration of day
    • relieved by supine position
  121. How is pelvic organ prolapse diagnosed?
    • H&P: inspect vaginal walls w/ single blade speculum (lithotomy position/standing)
    • rectovaginal exam: distinguishes rectocele from enterocele
  122. What is the management for pelvic organ prolapse?
    • correct underlying issues with...
    • estrogen: post meno w/ signs of atrophy
    • kegel's: mild incontinence
    • pessaries
    • surgery
  123. What are the different types of incontinence?
    • stress
    • urge
    • overflow (incomplete emptying)
    • functional (mixed)
  124. What are the transient etiologies for incontinence (DIAPPERS)?
    • D: delirium/dementia
    • I: infection
    • A: atrophic vaginitis/urethritis
    • P: psych disorders
    • P: pharmacologic agents
    • E: endocrine disease
    • R: restricted mobility
    • S: stool impaction
  125. Incontinence characterized by urine loss with cough, laugh/sneeze, "dribble", and is d/t pelvic floor or urethral weakness (change in urethral angle) from surgery/hypoestrogenic state/aging.
    stress urinary incontinence (SUI)
  126. Incontinence characterized by urinary urgency, large volume loss, and is d/t detrusor instability.
    urge incontinence
  127. Incontinence characterized by symptoms to SUI and urge but is d/t over distention from impaired detrusor contractility, and/or bladder outlet restriction from prior surgery or injury.
    incomplete bladder emptying (overflow)
  128. What meds should be avoided in overflow incontinence?
    • Ca blockers
    • a-adrenergic agonists
  129. What is the "workup" for incontinence?
    • med review
    • PE/cough with full bladder
    • UA & UC
    • post void residual (PVR) in HR pts: new incontinence after surgery, neuro dx (parkinson's, spinal cord injury, etc), failed med therapy, recurrent UTI
    • previous urinary retention
  130. Incontinence characterized by the combination of urge and stress, and is the MOST COMMON type in women.
    mixed incontinence
  131. What are the treatments for incontinence?
    • tx transient causes (DIAPPERS)
    • scheduled voids (bladder training): starts @ 2 hr intervals then works up
    • kegel's (pelvic muscle exercise): 3 sets of 8-12 contraction for 6-8 seconds 3-4 times/wk, for 15-20 wks
    • meds
    • surgery
  132. What specific tx is used for urge incontinence?
    • timed voids
    • anti-cholingerics
  133. What specific tx is used for stress incontinence?
    • PMEs/pessary
    • peri urethral collagen injections
    • surgery
    • topical estrogen if atrophic (not oral)
    • duloxetine
    • AVOID: a-antagonists
  134. What specific tx is used for overflow incontinence?
    • surgery
    • intermittent cath
    • AVOID: a-agonists, anti-cholinergics, and Ca blockers
  135. Define infertility and it's two types.
    • failure of couple to conceive within 12 month w/ regular coitus and no contraception
    • types are primary (never had a baby) and secondary (had at least one baby)
  136. The probability of achieving a live birth in a single menstrual cycle.
  137. The probability of conception.
    • fecundability
    • 20% per cycle; 50% per 3 months; 85% per year
  138. What are the main causes for infertility?
    • anovulation
    • abnl spermatogenesis
    • anatomic defects of the female genital tract
  139. Sperm take ___ days to generate + time in the _______ to gain mobility which leads to a general time frame of ______ for spermatogenesis.
    • 73
    • epididymis
    • 3 months
  140. How long should a pt abstain before performing a semen analysis?
    at least 2 days
  141. How many semen specimens are evaluated if the 1st analysis is normal? If it is abnormal?
    • at least 2 a few weeks apart
    • at least 3 a few weeks apart
  142. What components of semen are assessed when doing a workup for infertility? What are the WHO accepted 5th percentile criteria for these components?
    • amount: >1.5CC
    • concentration: >15 million/ml
    • motility: >40%
    • morphology: >4% nl
    • progressive motility: at least 32%
    • total sperm: 39 million/ejaculate
    • vitality: at least 58% live
  143. What are the luteal phase symptoms/PMS symptoms present (looking for ovulation)?
    • heaviness of breasts
    • decreased vaginal secretions
    • abd bloating
    • mild peripheral edema
  144. What tests are used to look for ovulation when working up infertility?
    • basal body temp: pts must do each AM, looks for 0.4F increase on 2 consecutive days
    • endometrial biopsy: in late luteal phase
    • serum progesterone: >3ng/ml during luteal phase means 80% chance ovulation
    • urinary ovulation detection kit: measures changes in urinary LH
  145. If a pt has a hx of irregular menstrual cycles suggesting anovulation, what tests should you order?
    • TSH
    • prolactin
    • FSH
    • total testosterone
    • DHEA-S
  146. When working up a female for infertility how are tubal patency, uterine and peritoneal issues detected/assessed?
    • US
    • HSG
    • hysteroscope
    • laparoscope
  147. What is the basic management for infertility?
    • establish a calendar
    • confirm regular ovulation
    • coitus every other day in ovulation window
    • document hx, examine, culture, assess semen
    • refer if regular ovulation, normal sperm
  148. What female anatomic defects are being looked for when performing an US, HSG, hysteroscope or laparoscope while doing an infertility workup?
    • congenital/other anatomic deformity
    • scarred tube (2nd to PID/endometriosis)
    • endometriosis
    • leiomyomata
  149. Vellus (fine & short) hair, lanugo (fine & long hair) that are normal genetic variants NOT due to androgens.
    hypertrichosis-nonsexual hair
  150. Terminal (thick) hair in a male distribution on a female due to androgens.
  151. Acne, libido, voice, strength, clitoromegaly, strength, male pattern baldness due to androgens.
  152. Steroid hormone that causes "maleness" produced from the adrenal gland and has weak potency.
    dehydroepiandrostenedione (DHEA)
  153. Steroid hormone that causes "maleness" produced from the adrenal gland & ovary and has weak potency.
  154. Steroid hormone that causes "maleness" produced from the adrenal gland, ovary & adipose tissue and is potent.
  155. Steroid hormone that causes "maleness" produced at the hair follicles/genital skin and is the most potent.
    dihydrotestosterone (DHT)
  156. What controls adrenal androgen production?
    ACTH stimulation from pituitary
  157. What controls ovarian androgen production in the granulosa/theca cells?
    LH from pituitary
  158. The peripheral conversion of testosterone that occurs in adipocytes depends on what?
    magnitude of androstenedione production from adrenals/ovaries
  159. Where does the peripheral conversion of DHT occur?
    hair follicles/genital skin
  160. What percentage of circulating androgens are bound to SHBG? Albumin? What percentage is free (bioactive)?
    • 80% (SHBG)
    • 20% (albumin)
    • 1-2% (free)
  161. What increases and decreases SHBG levels?
    • estrogens (increase)
    • androgens & insulin (decrease)
  162. What are the adrenal causes of hyperandrogenism?
    • neoplasm
    • Cushing's
    • congenital adrenal hyperplasia (CAH)
  163. What are the ovarian causes of hyperandrogenism?
    • neoplasm
    • PCOS (increased androgen & estrogen levels)
  164. Severe form of PCOS in which pts suffer from temporal balding, clitoral enlargement, deepening of voice, and remodeling of the limb-shoulder girdle (virilization).
  165. Subgroup of PCOS characterized by hyperandrogenism, insulin resistance, and acanthosis nigricans.
  166. What are the most common clinical presentations of PCOS?
    • hirsutism
    • AUB
    • polycystic ovaries
    • infertility
    • obesity (suspect insulin resistance)
  167. How is PCOS clinically diagnosed?
    • hyperandrogenism (clinical signs/lab evidence)
    • chronic oligo/anovulation
    • rule out other dx
  168. What is the workup for hirsutism to rule out a neoplasm?
    • serum total testosterone (>150ng/dl)
    • DHEA-S (>800mcg/dl)
    • look for rapid onset of sxs, virilization (20% have nl labs)
    • pelvic US/CT scan
  169. How do you look for a functional disorder when doing a workup for hirsutism?
    • PCOS: oligo/amenorrhea, hirsutism, acne, obesity, mild elevations in DHEA-S/testosterone
    • CAH/Cushing's: consider in pts with regular menstrual cycles, get serum 17 hydroxyprogesterone @ 0800/ACTH stimulation test, 24 hr urine free cortisol level/dexamethasone suppression test
  170. How is anovulation with PCOS addressed/treated?
    • fertility drugs (those desiring pregnancy)
    • OCPs
    • cyclic progestins
  171. What must be addressed with PCOS treatment?
    • anovulation
    • hirsutism
    • insulin resistance (wt loss, DM screen)
    • dyslipidemia (screen & tx)
  172. How is hirsutism in PCOS treated?
    • antiandrogenic agents
    • cosmetic treatments (for present hair growth, includes shaving, depilatory creams, electrolysis, laser)
  173. What are the antiandrogenic agents used to treat hirsutism and how long must they be used to get an effect?
    • androgen receptor blockers: spironolactone, flutamide
    • 5-alpha reductase inhibitors: finasteride (proscar, propecia)
    • require 6-12 months for effect
  174. What are the phases of sexual response?
    • desire (libido)
    • excitement (arousal)
    • orgasm (climax)
  175. Phase of sexuality referred to as an "appetite" usually accompanied by fantasy, is modulated by testosterone-->excited by dopamine-->suppressed by serotonin.
    desire (libido)
  176. What are some disorders of the desire phase of sexuality?
    • hypoactivity (65% of sexuality issues)
    • aversion
  177. Phase of sexuality characterized by a reflex of T11-L2, S2-4 that is modulated by parasympathetics, is enhanced by estrogen, and causes extragenital effects.
    excitement (arousal)
  178. What is the most common cause of a disorder of the excitement phase of sexuality?
    lack of estrogen
  179. What are the genital effects of estrogen during the excitement phase of sexuality?
    • labial fullness
    • clitoral enlargement
  180. What are the extragenital effects of the excitement phase of sexuality?
    • HR, BP, muscle tension
    • breast size, areolar engorgement, nipple erection
    • "sex flush" (75%)
  181. Phase of sexuality characterized by a reflex of T11-L2, S3-4 that is modulated by sympathetics, and optimized by clitoral input (afferent concentration).
    • orgasmic phase
    • **masturbation usually leads to increased rate & intensity**
  182. What are the sexual dysfunction pain disorders?
    • dyspareunia
    • vaginismus
  183. What is the general management for sexuality dysfunction?
    • dx & tx organic path
    • facilitate autonomy
    • refer when necessary
    • **PLISSIT= permission, limited info, specific suggestion, intensive therapy**
  184. When should domestic violence be suspected?
    • injury to torso, face/genitals
    • defensive injuries (abd & breast in pregnant women)
    • bilateral injuries, unexplained/inconsistent with hx
    • delay to ER or multiple ER visits
    • psychological symptoms
    • partner reluctant to leave room
  185. What is the incidence of sexual assault among women and who are the perpetrators?
    • 20% of women <21 yrs; 41% of all women
    • 75% of perps know the victim (husband, boyfriend, father)
  186. Any sexual act without consent by use of or threat of force, or with a victim who has the inability to give consent (date rape drug/statutory rape).
    "sexual assault"
  187. Generally a violent sexual act which may/may not stem from desire (control/power is more often the intent).
  188. How should a PE be done for a victim of sexual assault?
    • SANE (sexual assault nurse examiner) if available
    • checklist eval (institutional, rape kit)
    • consent for exam
    • chaperone
    • law enforcement notification (judicial authority, NOT in exam!)
  189. What are the components of a SEALED and STERILE rape kit?
    • microscopic slides
    • saline
    • swabs
    • tubes
    • specimen containers
    • comb
    • nail scraper
    • pap setup, including forms (not for dysplasia, but for sperm)
  190. How is a rape kit used during examination?
    • pt disrobes on white sheet
    • use wood's lamp to detect semen
    • use saline, pap, & gram stain for sperm
    • get samples for STDs (GC/chlamydia, BV, trich, candidiasis, HIV, hep B syphilis)
    • blood & ETOH tox screen
  191. What is the treatment for a victim of sexual assault/rape?
    • STD proph: GC, chlamydia, trich, HBIG/Hep B vaccine if not vaccinated, HIV (male on male, high prevalence of dz in population, multiple assailants, anal rape, bleeding)
    • emergency contraception: plan B, anti-emetic
  192. What does the care after sexual assault consist of?
    • referral for mental health/counseling
    • follow up: 1 wk w/ prophylaxis to review labs/repeat testing if sxs develop; 2 weeks & repeat GC/chlamydia & trich; syphilis repeat @ 6 weeks, HIV repeat 6, 12 & 24 wks
    • ensure safe place to go, transportation, resource info
  193. What are the phases of rape trauma syndrome?
    • acute/disorganization
    • intergration/resolution
  194. Phase of the rape trauma syndrome that lasts hours to days, is characterized by distortion/paralysis of victim's coping mechanisms with complete loss of emotional control or calm.
    • acute/disorganization phase
    • **signs include generalized pain, HA, chronic pelvic pain, eating/sleeping disturbances, vaginal sxs, emotional sxs (anxiety, depression)**
  195. Phase of the rape trauma syndrome that occurs months to years after the event, is characterized by flashbacks, nightmares, phobias and gynecological or menstrual complaints.
    integration/resolution phase
  196. What is the prevalence of PTSD in rape victims? How is PTSD be mitigated?
    • 50%
    • acute crisis counseling
  197. What are the criteria for PTSD?
    • persistence of sxs for at least one month
    • exposure to trauma
    • re-experiencing of trauma
    • persistent avoidance of the trauma
    • increased arousal
    • causes life dysfunction
  198. Amenorrhea characterized by no menses by age 16 in the presence of normal secondary sexual characteristics OR no menses by age 13 in the absence of secondary sexual characteristics OR no menses within 2 years of thelarche.
    primary amenorrhea
  199. Amenorrhea characterized by the absence of menses for at least 6 months in women who were previously menstruating.
    secondary amenorrhea
  200. What can cause primary amenorrhea in a pt with secondary sexual characteristics present?
    • imperforate hymen
    • transverse vaginal septum
    • cervical agenesis
    • mullerian agenesis
  201. What can cause primary amenorrhea in a pt with absent secondary sexual characteristics and high FSH levels?
    • gonadal agenesis
    • gonadal dysgenesis
    • ovarian resistance syndrome
    • galactosemia
    • **Turner's syndrome**
  202. What can cause primary amenorrhea in a pt with absent secondary sexual characteristics and low FSH levels?
    • GnRH deficiency
    • constitutional delay of puberty
    • CNS neoplasm/mass
    • stress
    • hyperprolactinemia
    • **Kallman's syndrome (if anosmic)**
  203. What can cause primary amenorrhea in a pt with secondary sexual characteristics but arrested puberty?
    • hypothalamic-pituitary
    • premature ovarian failure
  204. What can cause primary amenorrhea in a pt with neg breast development and positive pubic/axillary hair growth?
    complete androgen insensitivity ("T-fem")
  205. What is the pathogenesis for functional (non-pathologic) amenorrhea?
    • abnl GnRH secretion causing low gonadotropin levels, absent surges, etc (non-ovulatory)
    • FSH is usually in low/normal range
  206. What are the contributing factors to developing functional (non pathologica) amenorrhea?
    • stress, eating disorders, excessive exercise
    • wt loss or wt <10% IBW
    • celiac disease
  207. What is the most common cause of secondary amenorrhea?
  208. What is the second most common cause of amenorrhea?
    anovulatory cycles
  209. When evaluating secondary amenorrhea and the pregnancy test, TSH, and prolactin level labs are negative (normal) what is the next step?
    progesterone challenge test
  210. When evaluating a pt for secondary amenorrhea and the progesterone challenge test causes withdrawal bleeding, what are the causes?
    • anovulatory cycles
    • PCOS
  211. When evaluating a pt for secondary amenorrhea and the progesterone
    challenge test does not cause withdrawal bleeding, what is the next step?
    estrogen/progestin challenge test
  212. When evaluating a pt for secondary amenorrhea and the estrogen/progestin challenge test causes withdrawal bleeding and the FSH level is >40, what are the causes?
    • menopausal ovarian failure
    • premature ovarian failure
  213. When evaluating a pt for secondary amenorrhea and the estrogen/progestin
    challenge test causes withdrawal bleeding and the FSH level is <5, what are the causes?
    • stress (eating disorder/chronic illness)
    • CNS tumor/cranial radiation
    • Sheehan's syndrome
  214. When evaluating a pt for secondary amenorrhea and the estrogen/progestin
    challenge test does not cause withdrawal bleeding, what are the causes?
    • outflow obstruction
    • asherman's syndrome
  215. Excessive (>80ml)/prolonged (>7 days) regular bleeding.
  216. Irregular bleeding.
  217. Bleeding that occurs at intervals of <24 days.
  218. Heavy irregular bleeding.
  219. Bleeding that occurs at intervals >35 days.
  220. What is the most common gyn presenting complaint?
  221. What are the organic causes for AUB?
    • pregnancy
    • tumor (fibroids, polyps, adenomyosis, endometrial CA)
    • inflammation (cervical, uterine infx)
    • abnl clotting (von Willebrand's)
    • disorders of hepatic metabolism (advanced liver dz=reduced clotting factors)
    • IUD
    • meds (ASA, coumadin, exog estrogen)
  222. Termed "DUB", results from anovulation d/t factors affecting HPO axis or systemic diseases, is NOT associated with organic pathology and is a diagnosis of exclusion.
    AUB from endocrine causes
  223. What is the most common etiology of secondary amenorrhea after pregnancy is ruled out?
    anovulatory cycles
  224. Characterized by lots of estrogen with no corpus luteum (no progesterone) leading to an "unopposed estrogen" state, and is more common at extremes of age.
    anovulatory cycles
  225. What is the age stratification for the DDX of AUB?
    • Pre-pubertal: bleeding defects
    • Peri-menarchal: 5-7 yrs after menarche, immature HPO axis
    • Reproductive age: less cycle variability ages 20-40 yrs
    • Peri-menopausal: declining ovarian fnx (fibroids, polyps, endometrial CA)
    • Pay attention to AUB in post-menopausal pts!
  226. What is the workup for AUB?
    • ensure it is a uterine bleed
    • rule out organic causes
    • H&P
    • labs (hcg, TSH, prolactin, coags, pap)
    • studies (US, EMB)
  227. What is the medical therapy used to treat mild AUB?
    • observation
    • expectant management
  228. What is the medical therapy used to treat moderate AUB?
    • cyclic estrogens plus progestin (HRT)
    • OCPs
  229. What is the medical therapy used to treat severe AUB?
    • high dose estrogen (premarin 25mg IV)
    • D&C (ToC in unstable pts)
  230. What is the medical treatment for a pt with AUB who is hemodynamically stable but going through >1 pad/hr?
    premarin 2.5mg qid till bleed subsides then add provera 10mg/day for last 10 days of cycle
  231. What is the medical treatment for a pt with AUB who is hemodynamically stable and going through <1 pad/hr?
    • cascading OCPs¬†
    • 5 pills day1, 4 on day 2, 3 on day 3, etc
    • **should have w/d bleed when stopped, may need anti-emetics**
  232. What is the medication used to treat younger patients with AUB?
    progestin only pills (provera 10-20mg bid x 5-10 days)
  233. Which patients are candidates for surgical management of AUB?
    • those w/ underlying organic cause
    • those who fail medical therapy
  234. What surgical treatments for AUB should be considered in patient who have completed child-bearing desires?
    • endometrial ablation (75% effective)
    • hysterectomy (TAH/TVH)
  235. Condition caused by ectopic estrogen dependent tissue that is common in women in their 30s who are typically nulliparous and/or infertile.
  236. What is the classic symptoms triad for endometriosis?
    • dysmenorrhea
    • dyspareunia
    • dyschezia
    • **NOTE: many pts may have infertility as their only sxs!**
  237. What are the signs of endometriosis?
    • tender adnexal mass (endometriomas "chocolate cysts")
    • retroverted uterus
    • rectovaginal septum nodules
    • sharp firm "barb" on uterosacral ligament
  238. What is the definitive diagnostic test for endometriosis?
    biopsy via laparoscopy
  239. How are pts with suspected endometriosis having mild to moderate pain treated?
    • NSAIDs
    • empiric OCPs/progestins
  240. What is the next step in evaluating pts with suspected endometriosis who are having moderate to severe pain?
    laparoscopic diagnosis
  241. After laparoscopic diagnosis of endometriosis in a pt with moderate to severe pain what should you do?
    surgical excision and ablation of lesions
  242. What is the medical therapy for pts with endometriosis who have had surgical excision and/or ablation of the lesions?
    • immediate postsurgical therapy with...
    • danazol
    • OCPs
    • GnRH agonists (depo-lupron)/progestins
  243. How are pts with endometriosis who have been treated surgically but have recurrence without intractable pain managed?
    medical therapy for 6-9 months
  244. How are pts with endometriosis who have treated surgically but have recurrence with intractable pain and child bearing is not factor managed?
    hysterectomy, oophorectomy
  245. What is the next step in evaluating pts suspected of having endometriosis with infertility?
    laparoscopic diagnoses
  246. What is the management for a pt with infertility and laparoscopic diagnosed endometriosis?
    • surgical excision and ablation of lesions
    • invitro fertilization/superovulation therapy
  247. What is the hallmark for diagnosing PMS/PMDD?
    regular ovulation
  248. What is the epidemiology of PMS/PMDD?
    • 70% women have some sxs
    • 30-40% w/ reg cycles have PMS
    • 3-8% of PMS pts have PMDD
  249. What are the general criteria for the diagnosis of PMS/PMDD?
    • sxs during luteal phase
    • sxs free interval of at least 7 days in 1st half of cycle for >/=2 cycles
  250. What are the top physical and behavioral symptoms of PMS/PMDD?
    • physical: fatigue & bloating
    • behavior: labile mood
  251. What is the UCSD criteria COPE for PMS/PMDD?
    <40 days 3-9 + >42 last 7 days
  252. What is the prevailing theory for the etiology of PMS/PMDD?
    abnormal neurotransmitter response to luteal hormone changes (serotonin likely involved)
  253. What are the efficacious treatments for PMS/PMDD?
    • SRIs: fluoxetine 20-40mg/day (best response)/sertraline, paroxetine, citalopram/either continuous or luteal phase therapy
    • anovulatory agents: GnRH agonists (leuprolide) with "add-back"/danazol
  254. What treatments are NOT efficacious for PMS/PMDD management?
    • progestin only OCPs
    • conventional use of OCPs
    • evening primrose oil
    • gingko biloba
    • essential fatty acids
    • TCAs/lithium
  255. Dysmenorrhea that starts w/i 6-12 months menarche, is related to uterine ischemia/contraction, has increased prostaglandin levels, starts w/i 48-72 hrs of menses.
    primary dysmenorrhea (during ovulatory cycles)
  256. What is the preferred tx for primary dysmenorrhea?
    • NSAIDs
    • OCPs
  257. Dysmenorrhea in older pts that is related to underlying pathology (endometriosis, fibroids, adeonmyosis, ovarian cysts), has less well defined prostaglandin role, is not limited to menses and usually comes with other assoc. sxs like dyspareunia, infertility or AUB.
    secondary dysmenorrhea
  258. What is the sequence of pubertal milestones?
    thelarche (8.9/10 yrs)>pubarche (8.8/10.5 yrs)>menarche
  259. Define precocious puberty.
    appearance of 2nd female sex characteristics prior to age 8 (2.5-3 SD below mean age of puberty onset--10.8yrs)
  260. What are the 3 classifications of precocious puberty?
    • gonadotropin dependent PP
    • gonadotropin independent PP
    • incomplete PP
  261. Considered to be central or "true" PP caused by early maturation of the HPO axis with 80% of cases being idiopathic while the rest are d/t CNS lesions, is isosexual (phenotype=genotype), has a usual sequence of development with pubertal levels of FSH/LH and increased FSH/LH with GnRH.
    gonadotropin dependent PP
  262. How is gonadotropin dependent PP treated?
  263. Considered to be pseudo/peripheral PP caused by excess secretion of sex steroids most commonly d/t functional ovarian cysts, is either iso or contra-sexual (virilization), FSH/LH are suppressed and don't respond to GnRH, and can also be caused by CAH or adrenal tumors.
    gonadotropin independent PP
  264. PP that is usually a normal variant causing early development of secondary sexual characteristics.
    • incomplete PP
    • **check bone age: no therapy req'd if there is no accelerated growth**
  265. Define delayed puberty.
    lack of thelarche by age 12 (>95th percentile)
  266. What is the most common type of delayed puberty?
    constitutional delay
  267. What testing should you start with when evaluating delayed puberty and what to the results mean?
    • FSH/LH levels
    • elevated levels: primary hypogonadism
    • low or normal levels: secondary hypogonadism
  268. What is the most common presentation in vulvar disease?
  269. What are the "white lesions" (dystrophies) that cause vulvar itching/dz?
    • lichen sclerosis
    • squamous hyperplasia
  270. Most common vulvar dystrophy in menopausal women d/t autoimmune inflammation in the dermis with sxs of pruritus, irritation, and dyspareunia.
    lichen sclerosis
  271. What is the tx for lichen sclerosis?
    topical fluorinated corticosteroids (clobetasol 0.05%)
  272. Non-neoplastic morphologic alteration of vulvar skin related to chronic irritation d/t prolonged itch/scratch cycle that can be mixed with lichen sclerosis but the major difference being that it can resolve with treatment.
    squamous cell hyperplasia (lichen simplex chronicus)
  273. What is the tx for squamous cell hyperplasia (lichen simplex chronicus)?
    fluorinated topical steroids (clobetasol 0.05%)
  274. What are the vulvar dermatoses aka "red lesions"?
    • atopic & contact derm
    • psoriasis
    • vestibulitis
    • lichen planus
  275. Pts with this vulvar condition should have an underlying allergy hx and familial predisposition, it often begins in childhood.
    atopic derm (endogenous)
  276. What is the tx for vulvar atopic derm?
    low potency steroids
  277. Vulvar condition in which a trigger induces an immune response leading to skin damage (allergic) or in which the trigger itself directly damages the skin (irritant).
    contact derm (exogenous)
  278. Condition characterized by adherent silver scales but in skin folds are more red with a fine scale (inverse), is d/t an autoimmune process and is incited in the vulva by trauma (koebnerization).
  279. What is the tx for vulvar psoriasis?
    • emollients, steroids
    • dovenex after it is controlled
  280. Purple pruritic polygonal papules and plaques d/t an autoimmune disorder of T-cells which can involve the vagina and gingiva (VVG syndrome) which is very resistant to tx.
    lichen planus
  281. What is the tx for lichen planus?
    clobetasol bid
  282. Condition to be suspected in new onset of insertional dyspareunia (3-4mo) as well as with tampon insertion and/or bathing, and is diagnosed with a light touch cotton applicator in the right area + redness.
    localized provoked vulvodynia
  283. What is the tx for localized provoked vulvodynia?
    • symptomatic tx...
    • neuropathic pain meds: gabapentin, tricyclics
    • topical lidocaine
  284. Vulvar irritative condition that occurs in skin folds d/t maceration from friction that leads to a yeast infection, and is diagnosed clinically.
  285. What is the tx for intertrigo?
    • clear infection
    • try to modify underlying friction
    • Nystatin, Clotrimazole
    • consider predisposing factors (HIV, DM, steroids, incontinence, occlusive clothing, obesity)
  286. Vulvar irritative condition d/t corynebacterium spp (red under Wood's lamp) or irritative causes (ddx candida).
  287. What is the tx for erythrasma?
    • erythromycin x 14 days if widespread
    • clindamycin 1% 2-3 x/day for 1 wk if local
  288. Vulvar "honey-crusted" lesions d/t staph aureus or GABHS.
  289. What is the tx for impetigo?
    • dicloxicillin/cephalexin
    • mupirocin topical
    • hydrogen peroxide cream
  290. This vulvar condition is transmitted through direct contact and presents with pruritus, excoriations, and lymphadenopathy on gross exam.
    pthirus pubis "crabs" (pubic lice)
  291. What is the tx for pubic lice?
    • permethrin
    • pyrethrins
    • lindane (not in gravid/infant)
    • household contacts/linens
  292. This vulvar condition is transmitted through direct contact and presents with pruritus, dermatitis, is found in intertriginous areas including the glans and is diagnosed with an oil scrape gross examination.
    sarcoptes scabei (scabies/itch mite)
  293. What is the tx for scabies?
    • permethrin
    • lindane
    • ivermectin po repeat 2 wk
    • household contacts/linens
  294. Common condition in reproductive age women and is concerning for CA in women >40 yrs, occurs in a duct and causes NO PAIN.
    bartholin's cyst
  295. How is a bartholin cyst treated?
    • I&D alone is discouraged
    • word cath for BOTH cyst & abscess
    • marsupialization if word cath failed
  296. How is a bartholin's abscess treated?
    • I&D for immediate relief followed by word cath
    • abc only if its recurrent or high risk for complicated infection (preggo, cellulitis, systemic infection, immunosuppressed)
    • get culture d/t MRSA prevalence
  297. What are the causes for cervical stenosis?
    • tx for CIN (LEEP/CKC)
    • congenital
    • spontaneously occurs in hypoestrogenic women
  298. What is the tx for cervical stenosis?
    • cervical dilators
    • vaginal estrogen x 4 wks in hypoestrogenic women
  299. What are the implications of severe cervical stenosis?
    • impeded flow can cause uterine distention (hematometra)
    • impeded access for dx/tx
    • increased risk for cervical related dystocia
    • increased risk of infection from retained products (esp in post meno pts)
    • <2mm assoc with retrograde flow (5mm is sufficient for flow)
  300. Exists when the columnar epithelium is exposed to the vaginal milieu by eversion of the endocervix, is observed during high estrogen states (adolescence/preggo/OCP use), can increase vaginal secretions (physio d/c) and requires no treatment.
  301. Columnar cells become "trapped" beneath squamous cells during metaplasia and continue to secrete mucus resulting in discrete cysts that are usually asymptomatic and require no treatment.
    nabothian cysts
  302. When should nabothian cysts be treated and how is it treated?
    • if symptomatic (pain/fullness in vagina)
    • refer for electrocautery/excision
  303. These masses usually arise from the endocervical canal during the reproductive years, and are typically <3cm in size.
    cervical polyps
  304. When should cervical polyps be treated and how are they treated?
    • tx if large/symptomatic
    • if small and pedunculated: grasp @ base with forceps and twist
    • if sessile: remove with biopsy forceps & cauterize the base
    • **despite low malignancy potential ALL polyps should be sent to path**
  305. What are the 3 estrogen dependent uterine fibroids?
    • leiomyomata "fibroids"
    • adenomyosis
    • endometrial hyperplasia
  306. Most common pelvic tumor in women, is an estrogen dependent smooth muscle tumor with low intrinsic malignant potential, and is the most common indication for hysterectomy.
    leiomyomata uteri ("fibroids")
  307. What are the 3 types of leiomyomata uteri?
    • intramural
    • submucosal
    • subserosal
  308. What are the symptoms of leiomyomata uteri?
    • bleeding
    • mass effect (pelvic pressure)
    • pelvic pain
    • infertility
    • can be asymptomatic
  309. What diagnostic procedure is preferred and highly sensitive for leiomyomata uteri? What can delineate between fibroids and adenomyosis?
    • ultrasound
    • MRI (excellent but $$$)
  310. How leiomyomata uteri "fibroids" managed?
    • observation
    • hormones (mirena)
    • GnRH agonist (mostly pre-op)
    • myolysis (laparoscopic thermal coag
    • hysterectomy
    • uterine artery embolization
    • MRI-directed focused US
  311. What are the indications for surgical intervention in pts with a uterine leiomyoma (fibroid)?
    • AUB causing anemia
    • severe pelvic pain/secondary dysmenorrhea
    • inability to eval adnexa (fibroid >/= 12 wks gestational size)
    • urinary tract sxs (freq/retention)
    • growth of myoma following menopause
    • infertility
    • rapid increase in size
  312. Endometrial glands & stroma embedded w/i the muscular uterine wall, pts present w/ heavy AUB/dysmenorrhea (parous women 40-50 yrs), classic tx is hysterectomy (do TVUS/MRI for dx).
  313. Most common in post menopausal women, AUB is the most common presentation, is characterized by the overgrowth of endometrial lining in the proliferative phase and occurs as a result of anovulation.
    endometrial hyperplasia
  314. What is the gold standard for dx of endometrial hyperplasia?
    • EMB
    • **can use TVUS for postmenopausal pts**
  315. What is the WHO classification of hyperplasia?
    • glandular/stromal architecture: simple/complex
    • nuclear atypia: absent/present
  316. What are the criteria for women who should undergo eval for endometrial hyperplasia/endometrial CA?
    • > 40yrs with AUB
    • < 40 its with AUB & risk factors
    • failure to respond to medical tx of AUB
    • women with uterus in situ getting unopposed estrogen therapy
    • presence of atypical glandular cells on cervical cytology
    • presence of endometrial cells on cervical cytology in a woman >/= 40 yrs
    • women with hereditary nonpolyposis colorectal CA
  317. What is accepted as the equivalent first diagnostic step in postemenopausal women for endometrial hyperplasia?
    TVUS (<4mm thick stripe=low risk of CA)
  318. What is the most common symptom of endometrial polyps?
  319. Can be follicular or lutein, hemorrhagic (may be either of 1st two), or numerous theca lutein cysts assoc with molar pregnancy/choriocarcinoma.
    functional ovarian cysts
  320. An ovarian cyst is considered "function" when it it is how big?
  321. How are functional cysts diagnosed?
    • bimanual
    • US
  322. What are the most common benign neoplasms as a group?
  323. What is the most common epithelial benign ovarian neoplasm? What is the largest?
    • MC: serous cystadeoma
    • largest: mucinous cystadenoma
  324. What are the stromal benign neoplasms?
    • granulosa theca cell: estrogen production
    • sertoli leydig cell: testosterone production
    • ovarian fibroma: no hormones
  325. What is the single most common ovarian neoplasm arising from the germ cell?
    • benign cystic teratoma (dermoid cyst)
    • **risk of torsion**
  326. What symptoms of an ovarian mass are more indicative of a malignant process?
    • weight loss
    • ascites
  327. What are the general symptoms of ovarian masses?
    • most are asx (unless torsion/rupture)
    • slow increase abd girth
    • pressure on surround organs leading to constipation/UTIs
  328. US showing a unilocular ovarian mass is ______ vs a ________ mass.
    • reassuring
    • multilocular/solid
  329. What are the types of surgical tx for ovarian masses?
    • cystectomy
    • unilateral salpingo-oophorectomy
    • TAH/BSO if suspicion of malignancy
  330. What is recognized the THE prime etiologic factor in the development of cervical dysplasia?
  331. What HPV types produce high grade CIN and low grade CIN/genital warts?
    • high: 16, 18, 31, 33, 35
    • low/warts: 6, 11
  332. What are the risk factors for persistent HPV leading to possible progressive to cervical CA?
    • multiple sex partners (>2)
    • early onset of sexual activity (<20)
    • high risk partner
    • hx of STDs
    • cigarette smoking (4x)
    • immunosuppression (HIV, SLE, transplants)
    • age
  333. What are the types of HPV vaccines and which types to they protect against?
    • quadravalent (gardasil): 16, 18 & 6, 11
    • bivalent (cervarix): 16, 18 only
  334. How is the HPV vaccine given?
    • 3 injections over 6 months
    • for 9-26 yrs (target 11-12 yrs)
    • encourage for women with prior HPV exposure/abnl pap
  335. What is the spectrum of CIN?
    normal-->ASC (atypical squamous cells)-->CIN I (mild dysplasia)-->CIN II (mod)-->CIN III (sev)-->carcinoma in situ
  336. Preinvasive phase of cervical cancer.
    cervical intraepithelial neoplasia (CIN)
  337. What does the pap smear need to sample?
    • both endocervical canal & ectocervix (T-zone)
    • **screen ALL women >30 for HPV in addition to pap with HPV HR DNA**
  338. When should screening for cervical CA be initiated, discontinued and how freq should women be screened according to ACS/ASCCP/ASCP?
    • initiate: 21yrs regardless
    • discontinue: 65yrs (3 consec. neg cytology results/ 2 consec. neg co-tests within prev 10 yrs with most recent being within last 5 yrs & no hx of CIN 2 or greater in last 20 yrs))
    • frequency: cyto q3 yrs (21-29yo), co-test q5 yrs (>30yo)
  339. When should screening for cervical CA be initiated, discontinued and how freq should women be screened according to USPSTF?
    • initiate: 21yrs regardless
    • discontinue: 65yrs (3 consec. neg cytology results/ 2 consec. neg co-tests within prev 10 yrs with most recent being within last 5 yrs)
    • frequency: cyto q3 yrs (21-29yo), cyto q3 yrs (>30yo) OR co-test q5 yrs (>30yo)
  340. When should screening for cervical CA be initiated, discontinued and how freq should women be screened according to ACOG?
    • initiate: 21yrs regardless
    • discontinue: 65yrs (3 consec. neg cytology results/ 2 consec. neg co-tests within prev 10 yrs with most recent being within last 5 yrs)
    • frequency: cyto q3 yrs (21-29yo), cyto q3 yrs (>30yo) OR co-test q5 yrs (>30yo) preferred
  341. What does the Bethesda 2001 reporting template consist of?
    • description of specimen type: conventional/liquid
    • description of adequacy: sat, unsat, rejected, endocervical cells not present
    • general category (opt): neg/epithelial cell abnormality
    • interpreation/result: neg for intraepithelial lesion/malignancy, organisms, reactive changes, atrophy
    • Description of ancillary testing: HPV, auto pap
    • Educational notes (opt)
  342. What are the different squamous epithelial cell abnormalities as described with pap interpretation/results?
    • ASC (atypical squamous cells): ASCUS (unknown significance), ASCH (can't r/o HSIL)
    • LSIL: HPV, mild dysplasia, CIN I
    • HSIL: mod/sev dysplasia, CIN II/III, CIS
    • SCC: squamous cell carcinoma
  343. What are the different glandular epithelial cell abnormalities as described with pap interpretation/results?
    • ACG (atypical glandular cells)...
    • favor neoplastic
    • AIS (adenocarcinoma in situ)
    • adenocarcinoma
  344. How is ASCUS treated in pregnant women?
    • same as non pregnant except...
    • no ECC/EMB
    • may defer colpo till 6 wks postpartum
    • biopsy only suspected high grade lesions
  345. How is ASCUS-H treated in pregnant women?
    • same as non pregnant
    • DO NOT defer colpo until postpartum
  346. What is the general workup of an abnormal pap?
    • colpo is "diagnostic"
    • if colpo exam is unsatisfactory (entire T-zone can't be seen) then do a LEEP (loop electrosurgical excision procedure) or CKC (cold knife cone)
  347. How is colposcopy performed?
    • cleanse cervix with 3% acetic acid: causes CIN areas to turn white ("acetowhite")
    • green filter accentuates vascular changes: CIN lesions often accompanied by abnl vascular architecture
    • biopsies are taken of acetowhite + ECC performed
  348. What are some treatment options for cervical dysplasia?
    • LLETZ (large loop excision of T-zone)
    • laser
    • cryosurgery
    • electrocoagulation
    • cervical conization (CKC/LEEP)
Card Set
OB exam 3
OB exam 3