REI CREOG Review Embryology & Anatomy

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
D

Which of the following is associated with DES exposure?
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 27yo G3P0030 is undergoing recurrent SAB evaluation. A pelvic US reveals the following. What is the treatment recommendation? Expectant management Strassman metroplasty Hysteroscopic resection Jones Metroplasty 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?
Fibroids Polyp Asherman’s Septum 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
53yo on Tamoxifen complains of postmenopausal bleeding. What is the diagnosis Fibroid Polyp Asherman’s Septum 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 Oxytocin GnRH Dopamine D 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

Vasiliki A. Moragianni, MD, MS
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: 6 spontaneous abortions 2 spontaneous abortions 3 spontaneous abortions, each separated by a healthy term infant 1 spontaneous abortion, 2 term infants (1 with unbalanced translocation) 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

The most appropriate next diagnostic test for this pt is:
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: T3 concentration Repeat TSH concentration TRH stimulation test Pituitary MRI Thyroid u/s Q. 78 Normal values: Prolactin: 0-17 ng/mL TSH: U/mL Free T4: ng/dL

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)

Decrease in bone-specific serum alkaline phosphatase
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: Decrease in bone-specific serum alkaline phosphatase Increase in urinary hydroxyproline Decrease in urinary N-telopeptide Increase in urinary deoxypyridinoline 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!

The best next step in mgmt is to obtain: A Pituitary stimulation test
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 Pituitary stimulation test Insulinlike growth factor (IGF)-1 level Growth hormone (GH) level An X-ray of her wrist 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

24-hr urinary free cortisol excretion test
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: 24-hr urinary free cortisol excretion test High-dose decamethasone (8mg) suppression test Overnight dexamethasone (1mg) suppression test Plasma ACTH concentration 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 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

HE I G HT ■ ■ ■ ■ ■ ■ ■ WE I G HT ■ ■ ■ ■ ■

11β-hydroxysteroid dehydrogenase deficiency
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: Hyperprolactinemia 11β-hydroxysteroid dehydrogenase deficiency Impaired insulin sensitivity 5α-reductase deficiency 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

The most appropriate initial management is: Observation only
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: Observation only Bone age X-ray of the hand only MRI of head only 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 (thelarche) Pubic Hair (adrenarche) Menses (menarche) AA 8.87 yo 8.78 yo 12.16 yo White 9.96 yo 10.51 yo 12.88 yo

Appropriate initial management for this patient is: Thyroxine Calcium
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: Thyroxine Calcium Recombinant human growth hormone 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

The most appropriate next step in mgmt is:
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: Bone age imaging of hand and wrist Observation and follow-up in 6 months GnRH challenge test MRI of head Q. 75

The most appropriate next step in mgmt is: Observation for 6 months
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: Observation for 6 months GnRH challenge test Pelvic u/s MRI of head Q. 39

Premature thelarche, < 2 y/o
If isolated, OBSERVE! d/t  in gonadotropins during infancy 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 High Normal Pelvic u/s Bone age imaging > 2 years difference GnRH challenge test (rarely >250 pg/mL in adult ovulatory menstrual cycle) Pelvic u/s: r/o ovarian neoplasm Granulosa cell (#1) Sertoli-Leydig (rare) Mean dx: 4yo Sx: precocity, ascites, abdominal pain

GnRH Challenge Test GnRH Challenge Test FSH > LH LH > FSH
Isolated premature thelarche True precocious puberty FSH > LH LH > FSH Brain MRI

Combination estrogen and progestin OCP Progestin-only OCP
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: Combination estrogen and progestin OCP Progestin-only OCP Intermittent injection of progestin, depot medroxyprogesterone acetate Progestin-releasing IUD 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

Menstrual history and sx BBT chart
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: Serum FSH Serum lH Serum estradiol Menstrual history and sx 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

Based on these findings the most likely dx is:
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: Mixed gonadal dysgenesis Congenital adrenal hyperplasia (CAH) Androgen insensitivity 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

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

(A) laparoscopy for repeat coagulation of endo
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

(A) tissue plasminogen activator (TPA) (B) nifedipine (Procardia)
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

(A) ethinyl estradiol and norgestrel (B) mestranol (C) desogestrel
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

(A) in vitro fertilization with the partner’s sperm
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

(C) selective serotonin reuptake inhibitor
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%)

(B) alendronate (Fosamax) (C) oral estrogen-progestin therapy
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 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:

(B) irrigation of the cyst cavity
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

(B) exudative salpingitis (C) caseating cervicitis (D) oophoritis
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

(A) continue the clomiphene citrate (B) combined oral contraceptives
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

(A) discontinue thiazide (B) add bisphosphonate
11. A 35yo African-American woman undergoes a DEXA scan. Her T score at the hip is 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

(A) polychlorinated biphenyl hydrocarbons (PCBs) (B) lead
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

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

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

REI CREOG Review Embryology & Anatomy

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