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CREOG Review_ Anatomy _ Embryology

VIEWS: 81 PAGES: 112

									  REI CREOG Review
Embryology & Anatomy
       Ben Lannon
   Session 1: 11/13/09
    The rate of ovarian follicular atresia is
             greatest between:
•   A. conception and 10 weeks EGA
•   B. 10 wks and 20 wks EGA
•   C. 20 wks and term
•   D. birth and menarche
•   E. menarche and menopause
              C. 20 wks and term

•   20 wks 6-7 million oocytes
•   Birth 1-2 million
•   Puberty 200,000
•   Fertile 500
    Which of the following is associated
     with 11B-hydroxylase deficiency
•   A. Imperforate hymen
•   B. Bicornuate uterus
•   C. Didelphic uterus
•   D. Vaginal agenesis
•   E. Labial fusion
              E. Labial fusion
• Reproductive tract anomolies are not typically
  associated with steroidogenic enzyme defects
• Ambiguous genitalia (labial fusion) is result of
  hyperandrogenism – think CAH
• 11B-hydrox def – causes elevated
  mineralocorticoids (HTN) and
  hyperandrogenism
    The primitive germ cells in the fetus
            originate from the:
•   A. Yolk Sac
•   B. Allontois
•   C. Mesonephros
•   D. Metanephros
•   E. Undifferentiated gonad
                               A. Yolk Sac




Germ cells migrate from the yolk sac to the gonadal ridge where they begin differentiation
    At what stage due oocytes arrest at
                   birth:
•   A. Metaphase 2
•   B. Mitosis
•   C. Prophase 1
•   D. Anaphase
•   E. Prophase 2
               C. Prophase 1


Prophase I




Metaphase II
         In the absence of AMH, the
         metanephric duct will form
•   A. fallopian tube
•   B. Vas deferens
•   C. ureter
•   D. cloaca
•   E. epididymis
                  C. ureter
• Metanephros forms kidney and duct forms
  ureter and collecting system
• In absence of AMH, paramesonephric
  (Mullerian) duct forms the fallopian tube,
  uterus, upper vagina
    In an XX fetus exposed to 5HT the
       mesonephric duct will form:
•   A.   Epididymis
•   B.   Vas deferens
•   C.   Fallopian tube
•   D.   Bladder trigone
•   E.   Seminal vesicle
            D. Bladder trigone
• Another sneaky one
• Testosterone is the differentiating factor for
  internal genitalia – not 5HT which is critical for
  external genitalia
• The mesonephric (Wolfian) duct in males and
  females forms part of the bladder trigone. The
  remainder regresses in absence of Testosterone
• A,B, and E are all derivatives of the mesonephric
  duct in males
    Absence of SRY leads to which of the
        following findings in an XY
•   A. CAUV
•   B. Labial fusion
•   C. Ambiguous genitalia
•   D. Streak gonads
•   E. Undescended testicle
             D. Streak gonads
• SRY is the sex determining region on the Y
  chromosome and serves as one of the primary
  testis determining factor
• Absence/mutation of SRY (Swyer syndrome) leads
  to XY female with streak gonad. (Something
  unknown factor makes a full ovary)
• Without testes
  – No AMH – so normal female internal,
  – No T so absent male internal,
  – No T to DHT so normal female external
Label the following structures
                         E



                         F
          A

          B
                     C


                 D
Which of the following is associated
       with DES exposure?
 A            B          C




 D           E           F
                       A.
•   T shaped uterus is most common with DES
•   B is arcuate
•   C is bicornuate
•   D is bicornuate
•   E is didelphys
•   F is vaginal septum
     A 27yo G3P0030 is undergoing recurrent SAB
 evaluation. A pelvic US reveals the following. What is
           the treatment recommendation?


A. Expectant management
B. Strassman metroplasty
C. Hysteroscopic resection
D. Jones Metroplasty
E. NSAIDs
      C. Hysteroscopic resection
• This is a uterine septum – with this size and in
  setting of RSAB would favor treatment
• Strassman is a wedge resection for bicornuate
  or didelphys
• Jones is an abdominal wedge resection, not
  considered first line
• Tomkins is an abdominal procedure in which
  the horns are divided and reconnected
  without removal of a wedge
        27yo G2P2 with secondary
     amenorrhea. What is the diagnosis?

A.   Fibroids
B.   Polyp
C.   Asherman’s
D.   Septum
E.   Air bubbles
              C. Asherman’s
• This is an HSG revealing uterine adhesions
• The presentation would argue against other
  diagnosis
• Polyps and fibroids have a more rounded or
  discrete appearance
• Can get air bubbles but usually isolated and
  they move
         53yo on Tamoxifen complains of
      postmenopausal bleeding. What is the
                   diagnosis

A.   Fibroid
B.   Polyp
C.   Asherman’s
D.   Septum
E.   Foreign body
                  B. Polyp
• This is a sonohysterogram of a polyp
• Again the case gives you some hint
• A fibroid will have a density of myometrium
  typically on US
Match the hormone with its origin

FSH
Prolactin               D
Oxytocin
GnRH
Dopamine          E
                            C

              A
                                B
                 Pituitary anatomy




Anterior – FSH, LH, ACTH, PRL
Posterior - ADH, Oxytocin
Hypothal – GnRH, DA
What is the primary support structure
            of the breast
•   A. Poupart’s ligament
•   B. Cooper’s ligaments
•   C. Dermal papilla
•   D. Pectoralis Fascia
•   E. Adipose
         B. Cooper’s ligaments
• Coopers ligaments
• With edema or invasion the tension on these
  ligaments resulting in skin retraction give the
  “peau d’orange” appearance to the breast
    Which of the following are a primary
        blood supply to the breast?
•   A. Thoracic aorta
•   B. Subclavian artery
•   C. Axillary artery
•   D. All of the above
•   E. None of the above
           D. All of the above
• All three provide arterial supply
• The lymphatic drainage follows with drainage
  to the axilla, subclavian and thoracic nodes
Genetics & Physiology
 Vasiliki A. Moragianni, MD, MS
Five couples come in for evaluation of RPL.
Of the following pregnancy histories, the couple most
  likely to have parental balanced chromosome
  translocation as the cause of their loss(es) has:

A.6 spontaneous abortions
B.2 spontaneous abortions
C.3 spontaneous abortions, each separated by a
  healthy term infant
D.1 spontaneous abortion, 2 term infants (1 with
  unbalanced translocation)
E.1 term infant followed by 3 spontaneous abortions

                                                   Q. 46
     Chromosomal abnl - RPL
• MYTHS:
  – large # of SAb
  – consecutive SAb
  – no liveborns
  – normal baby r/o chromosomal abnl

• #1 chromosomal abnl: TRANSLOCATION (balanced
  > Robertsonian)  mixed pregnancy outcome,
  includes newborn with anomalies
           Translocations




BALANCED              ROBERTSONIAN
Segregation of balanced
reciprocal translocation
Segregation of Robertsonian
       translocation
33yo woman comes in for evaluation of primary
infertility. Good health, nl menses, nl FSH + LH.
Prolactin: 31 ng/mL, TSH: 4 U/mL, free T4: 1.1
ng/dL.
The most appropriate next diagnostic test for this pt is:

A.T3 concentration                        Normal values:
B.Repeat TSH concentration                Prolactin: 0-17 ng/mL

C.TRH stimulation test                    TSH: 0.3-3 U/mL

D.Pituitary MRI                           Free T4: 0.9-2.3 ng/dL

E.Thyroid u/s


                                                           Q. 78
       Subclinical hypothyroidism
• 10-20%; mildly  TSH (>2.5), nl free T4
• Repeat TSH to r/o:
   –   Recovery from nonthyroidal illness
   –   Large pulse of TSH secretion, late in evening
   –   Assay variability
   –   Adrenal insufficiency
   –   Rx (metoclopramide, domperidone)
   –   TSH-secreting pituitary adenomas
• T3 levels not useful b/c usually wnl
• TRH stimulation test: not useful with 3rd generation TSH
  assays, use for untreated central hypothyroidism
• Pituitary gland tumors  MRI
• Nodular / cystic thyroid  thyroid u/s (>=2mm nodules)
65yo has had amenorrhea for 10 years, not taking
hormone therapy. DEXA scan reveals decreases in
lumbar and hip bone densities with T-scores of -2.7
and -2.4, respectively. You prescribe calcium, vitamin
D, and a bisphosphonate and check bone biomarkers
after 3 months.
The test result that would most likely represent
evidence of compliance and drug efficacy is:

A.Decrease in bone-specific serum alkaline
phosphatase
B.Increase in urinary hydroxyproline
C.Decrease in urinary N-telopeptide
D.Increase in urinary deoxypyridinoline
E.Decrease in serum osteocalcin

                                                   Q. 15
          Dx of osteoporosis
• T-score: compared to young controls
    • +1 to -1: nl
    • -1 to -2.5: osteopenia
    • -2.5 or lower: osteoporosis


• Z-score: compared to your age + BMI
    • Higher than -2.5: nl
                   Bone markers
• NOT for dx!
• Used to assess response to tx
• 1. N-telopeptide ***
   – Bone-specific, direct product of osteoclastic proteolysis
   – Low levels in urine = bone stabilization + tx compliance
• 2. Alk Phos
   – >95%: liver cells, osteoblasts
   – Dx of liver and metabolic bone dz
• 3. Deoxypyridinoline
   – Bone-specific, should be stable in compliant pt
• 4. Pyridinoline, hydroxyproline: not bone-specific
• 5. Osteocalcin
   – Correlates with bone formation, highly variable!
15yo p/w primary amenorrhea. No FHx of
developmental anomalies or delayed puberty. On PE:
173cm (5’8’’), arm span is 178cm (5’10’’) and weight
56.9kg (127lb). Tanner I breasts, + fine axillary hair,
Tanner II pubic hair, virginal introitus with small cx,
uterus non-palpable. Labs show nl TSH and prolactin,
while FSH and estradiol are low. Nl sense of smell.
The best next step in mgmt is to obtain:

A.A Pituitary stimulation test
B.Insulinlike growth factor (IGF)-1 level
C.Growth hormone (GH) level
D.An X-ray of her wrist
E.Karyotype

                                                    Q. 109
Hypogonadotropic Hypogonadism
• Failure of GnRH neuronal migration (+/- anosmia)
 GnRH
 LH, FSH  no follicular development (Delayed puberty,
   primary amenorrhea)
 estradiol  inappropriate development of E-target tissues:
   breast, uterus, adipose tissue, bone (delayed epiphyseal
   closure  arm span > overall hgt &  bone age)
(lack of LH, FSH response to GnRH b/c pituitary not
   adequately exposed to endogenous GnRH)
• Nl ACTH, GH, IGF-1  nl development of pubic / axillary
   hair
• Nl karyotype, ovarian reserve
Pt p/w 6-month h/o amenorrhea, 9.1kg
(20lb) weight gain, fatigue, and occasional
headaches.
Based on this presentation, the best
screening test for her condition is:

A.24-hr urinary free cortisol excretion test
B.High-dose decamethasone (8mg)
suppression test
C.Overnight dexamethasone (1mg)
suppression test
D.Plasma ACTH concentration
E.4:00pm serum cortisol concentration

                                           Q. 19
        Cushing’s syndrome
• DDx of  cortisol:
  – CRH-secreting hypothalamic tumors
  – Cushing’s disease = Cushing’s syndrome d/t
    pituitary tumor
  – Adrenal gland hyperplasia/CA
  – ACTH-secreting tumors (lungs)
            Hypothalamus: CRH


            Pituitary:   ACTH (corticotropin)


            Adrenals:    Cortisol
                     Dx of  cortisol
– 24-hr urinary free cortisol excretion test ***
     • Nl: <100g/day, Cushing’s: >250g/day
     • >100g/day with obesity, depression, alcoholism, chronic stress so check x 3
– Overnight dexamethasone suppression test (for screening, not as sensitive)
     • 1mg of dexa PO btwn 23:00 + MN
     • Check 08:00 plasma cortisol
          – Nl: <5g/dL, Cushing’s: >10g/dL
          – Abnl values with obesity, depression, alcoholism, chronic stress
– Low-dose dexamethasone suppression test
     • 2mg of dexa (0.5mg PO QID) x 2days
     • Nl: <5g/dL, Cushing’s: >10g/dL
– High-dose dexamethasone suppression test (not for screening!)
     • 2mg of dexa PO QID x 2days
     • Pituitary ACTH-secreting tumors: >50% suppresion of cortisol
     • Adrenal tumors: no suppression
– Plasma ACTH levels (highly variable)
     • High: no adrenal tumors
     • Undetectable: adrenal tumors  CT of adrenals
     • Nl/: pituitary tumors, ectopic ACTH  give CRH IV
          – Pituitary ACTH-secreting tumors: high ACTH
          – Extrapituitary ACTH-secreting tumors: rarely respond
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7yo white girl p/w pubic hair growth, oily skin, and
body odor. No signs of masculinization. BP: 90/60.
Her growth chart is shown here.
The most likely pathophysiologic process responsible
for these signs is:

A.Hyperprolactinemia
B.11β-hydroxysteroid dehydrogenase deficiency
C.Impaired insulin sensitivity
D.5α-reductase deficiency
E.Adrenal tumor
                                                 Q. 59
       Premature adrenarche
• Pubic hair in girls < 8yo
• Insulin resistance > > > CAH
  – High BMI
  – Hyperandrogenism (acne, body odor, oily skin)
  – Acanthosis nigricans
  – Labs: abnl lipid panel, hyperandrogenism,
    insulin resistance, fasting glc/insulin<7 (adults:
    <4),  IGF-1,  IGF-1/IGF binding protein ratio,
     leptin
7.5yo AA girl p/w precocious puberty. Pubic hair at
6yrs 11mths, breast budding 1 month ago. Excellent
health, no other sx. Exam: Tanner III pubic hair,
Tanner II breasts. Longitudinal growth has increased
from 55th to 60th percentile. Her growth velocity chart
demonstrates she has moved from 4-cm to 5.5-cm
growth per year.
The most appropriate initial management is:

A.Observation only
B.Bone age X-ray of the hand only
C.MRI of head only
D.ACTH challenge test
                                                      Q. 9
          Precocious puberty
• Traditionally - secondary sexual development
  < 8yo
• Currently - Evaluate if:
  – Secondary sexual characteristics < 6yo (AA)
  – Secondary sexual characteristics < 7yo (White)
  in the absence of other CNS/behavioral findings.
       Race       Breast    Pubic Hair    Menses
               (thelarche) (adrenarche) (menarche)
        AA      8.87 yo      8.78 yo     12.16 yo

       White    9.96 yo     10.51 yo     12.88 yo
13yo p/w “lack of sexual development”. PMHx and
FHx: unremarkable. VS: nl. PE: hgt 142cm (56in),
Tanner I breast and pubic hair, webbed neck, high-
arched palate, broad chest, small uterus, nl cx,
nonpalpable ovaries. Bone age: 11.2 yrs. Labs: FSH
41mIU/mL, LH 24mIU/mL, estradiol <10pg/mL,
karyotype: 45,X.
Appropriate initial management for this patient is:

A.Thyroxine
B.Calcium
C.Recombinant human growth hormone
D.Medroxyprogesterone acetate
                                                 Q. 33
                  Turner’s syndrome
• Once karyotype confirms Turner’s (gonadal dysgenesis):
    – IV pyelogram or renal u/s (r/o renal anomalies – horseshoe kidney)
    – Echo or MRI (r/o coarctation of aorta, bicuspid aortic valves  risk of SBE, aortic
      dilation/dissection/rupture)
    – Hearing exam, if h/o multiple ear infections
    – TFT, thyroid Ab (r/o autoimmune thyroiditis, Graves’ dz)
    – Fasting glc (r/o insulin resistance, DM)
    – Fasting lipids
    – Bone density test (r/o osteoporosis, scoliosis)
• Initial tx:
    – Augmentation of stature:
         GH
         • FDA-approved
         • es final hgt by 5-10cm
         • The earlier the better
         • Until growth rate <2cm/yr or bone age >15yrs
         Low-dose estrogen
         • AFTER GH!
         • Use periodic progesterone or switch to OCPs
    – Correction of somatic anomalies
    – Counseling
20 month-old p/w premature breast development.
Tanner II-III breast development, absent pubic hair,
prepubertal genitalia. She is in the 65th percentile for
height and weight.
The most appropriate next step in mgmt is:

A.Bone age imaging of hand and wrist
B.Observation and follow-up in 6 months
C.GnRH challenge test
D.MRI of head
                                                     Q. 75
4yo p/w precocious thelarche associated with serum
estradiol level of 382 pg/mL. Tanner III breast
development and Tanner I pubic hair. Longitudinal
growth in the 75th percentile, an increase from the 50th
percentile of the previous years.
The most appropriate next step in mgmt is:

A.Observation for 6 months
B.GnRH challenge test
C.Pelvic u/s
D.MRI of head
                                                    Q. 39
  Premature thelarche, < 2 y/o
• If isolated, OBSERVE!
• d/t  in gonadotropins during infancy (peak
  @ 2yo)
  – Boys: LH > FSH, testosterone made in low
    adult male range until fetal Leydig cells
    disappear
  – Girls: FSH > LH, minimal estrogen elevation
• Resolves by 2-4 y/o with suppression of
  arcuate nucleus
  Premature thelarche, > 2 y/o
              Check estradiol levels       (rarely >250 pg/mL in adult ovulatory menstrual cycle)




       High                              Normal




    Pelvic u/s                    Bone age imaging


Pelvic u/s:
r/o ovarian neoplasm
                                                    > 2 years difference
Granulosa cell (#1)
Sertoli-Leydig (rare)
Mean age @ dx: 4yo
Sx: precocity, ascites, abdominal pain                               -GnRH challenge test
                                                                     -Pelvic u/s
    GnRH Challenge Test
            GnRH
         Challenge Test

  Isolated               True
premature             precocious
 thelarche              puberty


FSH > LH              LH > FSH



                                   Brain MRI
41yo with sx of irregular vaginal bleeding, hot flushes
and dyspareunia is concerned about her risk for an
unplanned pregnancy. She smokes 15 cigarettes qd
and has h/o depression. She is self-conscious about
her weight and is following a low-fat diet.
The most convenient contraceptive method with the
lowest failure rate for this woman is the:

A.Combination estrogen and progestin OCP
B.Progestin-only OCP
C.Intermittent injection of progestin, depot
medroxyprogesterone acetate
D.Progestin-releasing IUD
E.Use of a diaphragm
                                                    Q. 23
         Contraception in the
        menopausal transition
• Non-smoker: low-dose OCP
• Smoker:
  – barrier method
    • Diaphragm with spermicide: 16% failure rate within
      1st year of use
  – progestin-only
    • OCP: 8% failure rate
    • Depo: 3% failure rate, depression, weight gain
    • IUD: 0.1% failure rate, change in menstrual pattern
46yo p/w 9-month h/o irregular mestrual periods with
unpredictable onset. She has noticed associated
periodic hot flushes with profuse perspiration, which
have caused her to awaken from sleep. Pelvic exam
demonstrates a normal uterine size, without palpable
adnexal masses.
The most appropriate way to diagnose the
menopausal transition in this patient is:

A.Serum FSH
B.Serum lH
C.Serum estradiol
D.Menstrual history and sx
E.BBT chart
                                                  Q. 38
      Menopausal transition
• Early menopausal transition: when regular
  menstrual cycles become > 7 days
  different from normal cycle interval
• Late menopausal transition: 2 or more
  skipped cycles and at least 1 interval of
  amenorrhea of 60 days or more
• Menopausal transition completed: 1 full
  year after last period
• Duration: 2-6 years
• Labs: highly variable
Newborn term infant evaluated for ambiguous
genitalia. Brief physical exam: no palpable mass in
labioscrotal folds. Infant has phallic structure and
evidence of internal müllerian structures.
Based on these findings the most likely dx is:

A.Mixed gonadal dysgenesis
B.Congenital adrenal hyperplasia (CAH)
C.Androgen insensitivity
D.Male pseudohermaphroditism

                                                       Q. 96
                    CAH
• AR disorder; defect in pathway that
  converts cholesterol to cortisol
• # 1 cause: 21-hydroxylase deficiency
  – Ambiguous genitalia (newborn female)
  – Progressive virilization (both sexes)
• Palpation of gonads
• Karyotype (~4wks but SRY gene result in
  1 day)
• Hormones ( 17-OH-P = dx of classic
  CAH)
• Electrolytes (salt-wasting)
         Ambiguous genitalia
• Palpation of gonads in inguinal /
  labioscrotal folds
  – NO: likely dx of female pseudohermaphrodite
     • Abnl fetal adrenal gland
     • Elevated maternal androgens
       (ovary/adrenal/exogenous)
     • Excess placental androgens (sulfatase deficiency)
        – Declared sex: female!
  – YES: likely dx of male pseudohermaphrodite
     • Defective androgen action / biosynthesis
     • Androgen insensitivity
     • 5-reductase deficiency
        – Declared sex: ???
        – Remove gonads!
Pharmacology & Pathology

        Laura Smith
 1. A 48yo G1P0 underwent simple mastectomy 5 years
     ago secondary to stage 1 breast Ca. She recently
completed 4 years of tamoxifen therapy for prevention of
contralateral Ca. She has been amenorrheic for 6 months
 and is having occasional night sweats. She is interested
     in knowing whether she should consider taking
    raloxifene (Evista) to further decrease her risk of
 recurrent breast cancer and to reduce her vasomotor sx.
  You advise her that at this time, the clinical indication
               for taking raloxifene is for:
•   (A) cardiovascular disease
•   (B) endometrial hyperplasia
•   (C) recurrent breast cancer
•   (D) osteoporosis
•   (E) vasomotor symptoms
 1. A 48yo G1P0 underwent simple mastectomy 5 years
     ago secondary to stage 1 breast Ca. She recently
completed 4 years of tamoxifen therapy for prevention of
contralateral Ca. She has been amenorrheic for 6 months
 and is having occasional night sweats. She is interested
     in knowing whether she should consider taking
    raloxifene (Evista) to further decrease her risk of
 recurrent breast cancer and to reduce her vasomotor sx.
  You advise her that at this time, the clinical indication
               for taking raloxifene is for:
•   (A) cardiovascular disease
•   (B) endometrial hyperplasia
•   (C) recurrent breast cancer
•   (D) osteoporosis
•   (E) vasomotor symptoms
 SERMS and breast cancer (Prolog p. 8)
• Raloxifene increases BMD at spine, hip,
  wrist 1-3% over 3 years
• Raloxifene may offer protection against
  some types of breast cancer, but not
  currently FDA approved for that indication
• Raloxifene increases hot flashes  not
  helpful to Rx vasomotor sx
• Raloxifene does not appear to have any
  adverse effects on the endometrium, but
  does not treat hyperplasia
 2. A 33yo G0 with regular menses presents with 1 year
h/o infertility. A recent workup, including HSG, semen
  analysis, and PNL was normal. She and her husband
       have been timing intercourse appropriately.
 Laparoscopy was performed 2 years ago for suspected
appendicitis showing minimal endometriosis, which was
    ablated. The next step in the management of this
                  patient’s infertility is:

•   (A) laparoscopy for repeat coagulation of endo
•   (B) GnRH agonist for 3 months
•   (C) empiric clomiphene citrate with IUI
•   (D) expectant mgmt and stress reduction
•   (E) IVF
 2. A 33yo G0 with regular menses presents with 1 year
h/o infertility. A recent workup, including HSG, semen
  analysis, and PNL was normal. She and her husband
       have been timing intercourse appropriately.
 Laparoscopy was performed 2 years ago for suspected
appendicitis showing minimal endometriosis, which was
    ablated. The next step in the management of this
                  patient’s infertility is:

•   (A) laparoscopy for repeat coagulation of endo
•   (B) GnRH agonist for 3 months
•   (C) empiric clomiphene citrate with IUI
•   (D) expectant mgmt and stress reduction
•   (E) IVF
  Minimal endometriosis and infertility
            (prolog p.10)
• Unclear why minimal endo causes infertility
• women with minimal endo do have
  decreased monthly fecundity (est. 4-5%)
  with no treatment
• study: l/s vs. no in women with endo and
  infertility -- no difference in preg 1 year
  after surgery (20% vs. 22%)
• medical suppression of endo only delays
  treatment of infertility
3. Your patient’s spouse is a 45yo male with a history of
oligospermia who goes to the ER with chest pains. He is
   presently taking L-carnitine (Proxeed) and sildenafil
citrate (Viagra) to help improve sperm quality as well as
  duration of erection and sexual response during timed
 intercourse. The medication which would most likely
  precipitate chest pains in the presence of sildenafil or
other erection-enhancing drugs, such as tadalafil (Cialis)
                 or vardenafil (Levitra) is:
•   (A) tissue plasminogen activator (TPA)
•   (B) nifedipine (Procardia)
•   (C) sublingual nitroglycerine
•   (D) lidocaine
•   (E) cimetidine (Tagamet)
3. Your patient’s spouse is a 45yo male with a history of
oligospermia who goes to the ER with chest pains. He is
   presently taking L-carnitine (Proxeed) and sildenafil
citrate (Viagra) to help improve sperm quality as well as
  duration of erection and sexual response during timed
 intercourse. The medication which would most likely
  precipitate chest pains in the presence of sildenafil or
other erection-enhancing drugs, such as tadalafil (Cialis)
                 or vardenafil (Levitra) is:
•   (A) tissue plasminogen activator (TPA)
•   (B) nifedipine (Procardia)
•   (C) sublingual nitroglycerine
•   (D) lidocaine
•   (E) cimetidine (Tagamet)
 Treatment for impotence (prolog p. 11)
• up to 82% on viagra have improved erections
  compared to 24% on placebo
• during sexual stimulation, NO that is released into
  corpus cavernosusm is responsible for physiologic
  mech of erection
• viagra enhances the effect of NO by inhibiting
  phosphodiesterase type 5  increased cGMP in
  corpus cavernosum  smooth musc relaxation 
  inflow of blood to area
• with the effect of vasodilation and venous pooling,
  there is potential for increased cardiac risk if take
  nitrates = contraindicated b/c risk MI / arrhythmia
• Tagamet may prolong the T1/2
       4. A 29yo comes to your office with a history of
    unprotected intercourse within the past 24 hours. She
     requests emergency contraception therapy. The oral
    steroid hormone treatment that would provide her best
            option for emergency contraception is:

•    (A) ethinyl estradiol and norgestrel
•    (B) mestranol
•    (C) desogestrel
•    (D) levonorgestrel
•    (E) norgestimate
       4. A 29yo comes to your office with a history of
    unprotected intercourse within the past 24 hours. She
     requests emergency contraception therapy. The oral
    steroid hormone treatment that would provide her best
            option for emergency contraception is:

•    (A) ethinyl estradiol and norgestrel
•    (B) mestranol
•    (C) desogestrel
•    (D) levonorgestrel
•    (E) norgestimate
Emergency contraception (prolog p. 15)
Emergency contraception (prolog p. 15)

• Crude pregnancy rate 1.1% (11/976)
  levonorgestrel vs. 3.2% (31/979)
  combination OC group
• levonorgestrel estimated to prevent 85% of
  pregnancies vs. 57% combined OC
• mechanism: delayed ovulation and
  prevention of fertilization
5. A 33yo G0 who is HIV negative requests information
 on how to eliminate her risk of becoming HIV positive
   when conceiving with sperm from her HIV positive
   partner. They currently use condoms for all acts of
sexual intercourse. You inform her that the only way to
                  eliminate her risk is:
• (A) in vitro fertilization with the partner’s sperm
• (B) not to use her partner’s sperm
• (C) intrauterine insemination with her partner’s
  sperm
• (D) high-dose antiretroviral therapy for her partner
• (E) use of antiretroviral therapy by the patient
5. A 33yo G0 who is HIV negative requests information
 on how to eliminate her risk of becoming HIV positive
   when conceiving with sperm from her HIV positive
   partner. They currently use condoms for all acts of
sexual intercourse. You inform her that the only way to
                  eliminate her risk is:
• (A) in vitro fertilization with the partner’s sperm
• (B) not to use her partner’s sperm
• (C) intrauterine insemination with her partner’s
  sperm
• (D) high-dose antiretroviral therapy for her partner
• (E) use of antiretroviral therapy by the patient
Reproduction in individuals with AIDS (prolog p. 17)
  • Decreasing the male partner’s viral load to
    undetectable can potentially reduce the risk of
    sexual transmission
  • A specific technique of sperm washing using a
    combination of Percoll gradient and swim-up
    technique for IUI has been developed to decrease
    viral load in the semen and reduce risk of HIV
    infection
  • in a study of 350 women, there were no
    seroconversions using this technique
  • IVF will not limit risk of transmission unless the
    sperm are prepared in this way
    6. A 42yo G1P1 presents with severe hot flashes, trouble
 sleeping, fatigue, severe headaches, and increasing irritability
 for the past 2 months. One year ago, she received a diagnosis
  of breast Ca and was treated with WLE and chemo. One LN
  was positive, and the tumor was ER and PR negative. After
    multiple courses of chemo, her menstrual cycles became
irregular. Her PE is unremarkable. Lab results showed normal
 TSH, elevated FSH, and low E2 levels. Her CBC was WNL.
      The most appropriate next step in her management is:
  •   (A) clonidine
  •   (B) progesterone
  •   (C) selective serotonin reuptake inhibitor
  •   (D) conjugated equine estrogen
  •   (E) black cohash
    6. A 42yo G1P1 presents with severe hot flashes, trouble
 sleeping, fatigue, severe headaches, and increasing irritability
 for the past 2 months. One year ago, she received a diagnosis
  of breast Ca and was treated with WLE and chemo. One LN
  was positive, and the tumor was ER and PR negative. After
    multiple courses of chemo, her menstrual cycles became
irregular. Her PE is unremarkable. Lab results showed normal
 TSH, elevated FSH, and low E2 levels. Her CBC was WNL.
      The most appropriate next step in her management is:
  •   (A) clonidine
  •   (B) progesterone
  •   (C) selective serotonin reuptake inhibitor
  •   (D) conjugated equine estrogen
  •   (E) black cohash
Alternative therapies for treatment of hot
          flashes (prolog p. 24)
• Progestins contraindicated in h/o BrCa b/c
  reported proliferative stimulatory effects
• Estrogens not a great idea
• clonidine can reduce hot flashes by 30%
  with onset after 1 wk Rx
• Effexor and paxil can reduce by 50%
• black cohash similar to placebo (20-40%)
   7. A 65yo comes in for annual. She has vaginal dryness and
burning during and after intercourse. PE shows pale, pink, thinned
vulva and absent rugae of vaginal mucosa. The remainder of PE is
 normal. She had normal mammo and pap 1 yr ago. A cholesterol
  profile this year showed total chol 236mg/dL, HDL 35mg/dL,
 VLDL 45mg/dL, LDL 156mg/dL, and TG 278 mg/dL. Her TSH
was 3.3 and T4 was 9.8. DEXA showed T -1.2 at spine and -1.3 at
      hip. She takes MVI, 1500 Ca2+, and 800IU vit D QD.

                    The most approp mgmt is:
  •   (A) vaginal lubricant
  •   (B) alendronate (Fosamax)
  •   (C) oral estrogen-progestin therapy
  •   (D) raloxifine hydrochloride (Evista)
  •   (E) low-dose vaginal estrogen
   7. A 65yo comes in for annual. She has vaginal dryness and
burning during and after intercourse. PE shows pale, pink, thinned
vulva and absent rugae of vaginal mucosa. The remainder of PE is
 normal. She had normal mammo and pap 1 yr ago. A cholesterol
  profile this year showed total chol 236mg/dL, HDL 35mg/dL,
 VLDL 45mg/dL, LDL 156mg/dL, and TG 278 mg/dL. Her TSH
was 3.3 and T4 was 9.8. DEXA showed T -1.2 at spine and -1.3 at
      hip. She takes MVI, 1500 Ca2+, and 800IU vit D QD.

                    The most approp mgmt is:
  •   (A) vaginal lubricant
  •   (B) alendronate (Fosamax)
  •   (C) oral estrogen-progestin therapy
  •   (D) raloxifine hydrochloride (Evista)
  •   (E) low-dose vaginal estrogen
  SERMS in osteoporosis (prolog p.39)
• Local vag estrogen will not appreciably
  increase systemic estrogen, but do provide
  suitable local response
• BMD shows mild osteopenia - Rx
  recommended if T< -2.0 without risk factors
  or T < -1.5 with risk factors
• ACOG recommends oral estrogen be
  limited to use for vasomotor sx and as an
  alternative Rx for osteoporosis
 8. A 32yo G0 seeks consultation because of a 1 year h/o
    progressively worsening pelvic pain. She refuses
    therapy with GnRH agonist. Pelvic exam reveals
fullness in the right adnexa, a retroverted uterus, and cul-
    de-sac tenderness, particularly when palpating the
 uterosacral ligaments. An U/S is done and the findings
 are shown below. The best treatment for the patient is:
 8. A 32yo G0 seeks consultation because of a 1 year h/o
    progressively worsening pelvic pain. She refuses
    therapy with GnRH agonist. Pelvic exam reveals
fullness in the right adnexa, a retroverted uterus, and cul-
    de-sac tenderness, particularly when palpating the
 uterosacral ligaments. An U/S is done and the findings
 are shown below. The best treatment for the patient is:


•   (A) oophorectomy
•   (B) irrigation of the cyst cavity
•   (C) evacuation and cautery of the cyst
•   (D) excision of the endometrioma
 8. A 32yo G0 seeks consultation because of a 1 year h/o
    progressively worsening pelvic pain. She refuses
    therapy with GnRH agonist. Pelvic exam reveals
fullness in the right adnexa, a retroverted uterus, and cul-
    de-sac tenderness, particularly when palpating the
 uterosacral ligaments. An U/S is done and the findings
 are shown below. The best treatment for the patient is:


•   (A) oophorectomy
•   (B) irrigation of the cyst cavity
•   (C) evacuation and cautery of the cyst
•   (D) excision of the endometrioma
 9. A 29yo G0 who recently immigrated from Asia to the US
     undergoes a late luteal phase endometrial biopsy for
     infertility and amenorrhea. The biopsy results show
  lymphocytic infiltration, epithelioid tubercles, and several
 giant cells (Fig 1). She has a history of oligomenorrhea, and
   her HSG is shown (Fig 2). The most frequent concurrent
        disease process in a patient with this presentation is:




Fig 1



                                     Fig 2
9. A 29yo G0 who recently immigrated from Asia to the
US undergoes a late luteal phase endometrial biopsy for
  infertility and amenorrhea. The biopsy results show
   lymphocytic infiltration, epithelioid tubercles, and
     several giant cells (Fig 1). She has a history of
  oligomenorrhea, and her HSG is shown (Fig 2). The
  most frequent concurrent disease process in a patient
                 with this presentation is:
•   (A) pleuritis
•   (B) exudative salpingitis
•   (C) caseating cervicitis
•   (D) oophoritis
•   (E) myometritis
9. A 29yo G0 who recently immigrated from Asia to the
US undergoes a late luteal phase endometrial biopsy for
  infertility and amenorrhea. The biopsy results show
   lymphocytic infiltration, epithelioid tubercles, and
     several giant cells (Fig 1). She has a history of
  oligomenorrhea, and her HSG is shown (Fig 2). The
  most frequent concurrent disease process in a patient
                 with this presentation is:
•   (A) pleuritis
•   (B) exudative salpingitis
•   (C) caseating cervicitis
•   (D) oophoritis
•   (E) myometritis
 Diagnosis of amenorrhea (prolog p.51)
• TB  characteristic HSG with “stiff” ampullary
  tubal segments and endo bx with nonnecrotizing
  granuloma with Langerhans cells
• genital TB usually secondary to pulm TB,
  spreading hematogenously
• the fallopian tube forms a favorable nidus for
  bacilli, and once enlarges it develops an exudative
  salpingitis but remains fairly free of adhesions, it
  becomes saturated with caseous material, and
  releases a purulent exudate
• TB endometritis on bx generally indicates TB
  salpingitis is also present
10. A 28yo G0 with primary infertility has been treated with
  clomiphene citrate for superovulation the past 2 months.
   She presents on day 3 of her menstrual cycle with right
lower quadrant pain and the ultrasound taken at that time is
    shown below. The most appropriate management is:

                      7.2cm
10. A 28yo G0 with primary infertility has been treated with
  clomiphene citrate for superovulation the past 2 months.
   She presents on day 3 of her menstrual cycle with right
lower quadrant pain and the ultrasound taken at that time is
    shown below. The most appropriate management is:

 •   (A) continue the clomiphene citrate
 •   (B) combined oral contraceptives
 •   (C) ovarian cystectomy
 •   (D) expectant management
 •   (E) transvaginal cyst aspiration
10. A 28yo G0 with primary infertility has been treated with
  clomiphene citrate for superovulation the past 2 months.
   She presents on day 3 of her menstrual cycle with right
lower quadrant pain and the ultrasound taken at that time is
    shown below. The most appropriate management is:

 •   (A) continue the clomiphene citrate
 •   (B) combined oral contraceptives
 •   (C) ovarian cystectomy
 •   (D) expectant management
 •   (E) transvaginal cyst aspiration
     Ovarian cyst management during
     ovulation induction (prolog p.54)
• D/dx follicular cyst vs. corpus luteum
• randomized controlled trials have shown that
  functional cysts are not affected by OCPs
  (complete resolution 76% over 1 cycle w/ OCP vs.
  72% observe group)
• All persistent cysts disappeared after a 2nd cycle
  without treatment
• no studies to date have observed TV drainage
  during ovulation induction
     11. A 35yo African-American woman undergoes a
     DEXA scan. Her T score at the hip is - 2.8. She has
    eumenorrhea and a h/o SLE. Her medications include
     daily prednisone (20mg) for immunosuppression, a
    thiazide and ace inhibitor for HTN, and Coumadin as
     prophylaxis. She also takes supplemental vit D and
     Ca2+. At this time, it would be most appropriate to:

•   (A) discontinue thiazide
•   (B) add bisphosphonate
•   (C) change Coumadin to heparin
•   (D) add raloxifene
•   (E) add calcitonin
     11. A 35yo African-American woman undergoes a
     DEXA scan. Her T score at the hip is - 2.8. She has
    eumenorrhea and a h/o SLE. Her medications include
     daily prednisone (20mg) for immunosuppression, a
    thiazide and ace inhibitor for HTN, and Coumadin as
     prophylaxis. She also takes supplemental vit D and
     Ca2+. At this time, it would be most appropriate to:

•   (A) discontinue thiazide
•   (B) add bisphosphonate
•   (C) change Coumadin to heparin
•   (D) add raloxifene
•   (E) add calcitonin
   Glucocorticoid induced osteoporosis
              (prolog p.60)
• If received prednisone > 2.5mg daily for as short
  as 3 mo are at increased risk osteoporosis
• glucorticoids lead to osteoporosis by: direct
  impairment of osteoblast / osteoclast fxn,
  enhanced effect of PTH, increased renal elim of
  Ca2+
• currently, risenodronate and alendronate are the
  only bisphosphonates approved by FDA for
  treament of glucocorticoid-induced osteoporosis
• stopping thiazide may reduce Ca2+ loss from
  urine, but not as good as bisphosphonate
 12. A tobacco farmer is concerned that his occupation
         may be contributing to his documented
  oligoasthenospermia (reduced sperm count with low
  motility). He admits to occasional use of marijuana.
 The factor that is most likely to be responsible for his
           increased risk of asthenospermia is:

• (A) polychlorinated biphenyl hydrocarbons
  (PCBs)
• (B) lead
• (C) tetrahydrocannabinol
• (D) ionizing radiation
• (E) nicotine
 12. A tobacco farmer is concerned that his occupation
         may be contributing to his documented
  oligoasthenospermia (reduced sperm count with low
  motility). He admits to occasional use of marijuana.
 The factor that is most likely to be responsible for his
           increased risk of asthenospermia is:

• (A) polychlorinated biphenyl hydrocarbons
  (PCBs)
• (B) lead
• (C) tetrahydrocannabinol
• (D) ionizing radiation
• (E) nicotine
Environmental toxicity and sperm counts
            (prolog p.76)
• PCBs are halogenated, lipophilic, aromatic
  hydrocarbons with known estrogenic effects
• PCBs are components of insectisides
• it has been demonstrated that the total motile
  sperm counts in infertile men are inversely
  proportional to the concentrations of estrogenlike
  substances in the environment
• THC may affect sperm, but is not specific to farm
• heavy metals assoc with low fert rates
• smoking affects sperm count, motility, but gloves
  13. A 36yo G0 and her husband come in for consultation
  regarding the best method for them to achieve pregnancy.
 The husband has undergone 2 Sas, which have documented
sperm concentrations of 1-2million/mL, motility 10-15%, and
morphology 10-15%. His urologist had documented a small,
    nonpalpable varicocoele on U/S. The woman has an
 ovulatory menstrual history and no hx suspicious for pelvic
  adhesions. The most cost-effective means of achieving a
                 pregnancy in this couple is:
 •   (A) varicocoele repair for the husband
 •   (B) clomiphene citrate for the husband
 •   (C) IVF with ICSI
 •   (D) donor insemination
 •   (E) IUI with the husband’s sperm
  13. A 36yo G0 and her husband come in for consultation
  regarding the best method for them to achieve pregnancy.
 The husband has undergone 2 Sas, which have documented
sperm concentrations of 1-2million/mL, motility 10-15%, and
morphology 10-15%. His urologist had documented a small,
    nonpalpable varicocoele on U/S. The woman has an
 ovulatory menstrual history and no hx suspicious for pelvic
  adhesions. The most cost-effective means of achieving a
                 pregnancy in this couple is:
 •   (A) varicocoele repair for the husband
 •   (B) clomiphene citrate for the husband
 •   (C) IVF with ICSI
 •   (D) donor insemination
 •   (E) IUI with the husband’s sperm
    Males with oligospermia and ART
              (prolog p.77)
• The absolute effect of varicocoele on male fertility
  remains controversial and recently there has been a
  consensus re: the lack of impact of subclinical
  varicocoele on fertility
• varicocoele repair may improve motility, but it is
  unlikely to improve sperm count appreciably
• clomid thought to improve semen parameters by
  increasing FSH, LH, and potentially improve quality,
  but unlikely to help dramatically here
• donor sperm costs several hundred $ per insemination
• if count < 10 million and motility 10-15%, IUI very
  poor prognosis
 15. A 52yo comes to your office to discuss options re: her HRT
   in view of the results of the WHI. The patient had her LMP
approx 5 years ago and has been taking combination HRT for the
 past 2 years for treatment of vasomotor sx. The patient believes
      that this regimen has helped control her hot flushes and
   insomnia. She is concerned that remaining on the HRT may
  increase her risk for breast cancer, although she has no family
           history of the disease. You counsel her that:
• (A) combination HRT does not increase her risk of breast cancer
• (B) the progestin protects her from developing cancer
• (C) only medroxyprogesterone acetate is associated with an
  increased risk of breast cancer
• (D) only conjugated estrogen is associated with an increased risk
  of breast cancer
• (E) there appears to be some increased risk of breast cancer with
  any combination HRT
 15. A 52yo comes to your office to discuss options re: her HRT
   in view of the results of the WHI. The patient had her LMP
approx 5 years ago and has been taking combination HRT for the
 past 2 years for treatment of vasomotor sx. The patient believes
      that this regimen has helped control her hot flushes and
   insomnia. She is concerned that remaining on the HRT may
  increase her risk for breast cancer, although she has no family
           history of the disease. You counsel her that:
• (A) combination HRT does not increase her risk of breast cancer
• (B) the progestin protects her from developing cancer
• (C) only medroxyprogesterone acetate is associated with an
  increased risk of breast cancer
• (D) only conjugated estrogen is associated with an increased risk
  of breast cancer
• (E) there appears to be some increased risk of breast cancer with
  any combination HRT
   Hormone therapy and risk of breast
        cancer (prolog p.83)
• WHI E+P  increased invasive breast
  cancer
• WHI E alone  reduced risk of BrCa but
  not statistically significant
• Million women study: E+P  RR 2 breast
  cancer over 2.6 years f/u
• Million women study: E alone  RR 1.3
  breast cancer over 2.6 years f/u
• rec taper off HRT over 1-3 months

								
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