week 9- gyn 2 Flashcards

1
Q

• What are 4 types of abnormal menstruation?

A

o Amenorrhea
o Dysfunctional uterine bleeding (DUB)
o Dysmenorrhea (primary or secondary)
o Premenstrual syndrome (PMS)

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2
Q

• What is amenorrhea? 2 types? 2 etios?

A

o pathological absence of menstruation
o usu dt endocrine dysfxn → anovulation
o or dt genital anatomic AbN (ovulatory amenorrhea)
o Primary: no menarche by 16, > 2yrs after the onset of puberty or if no signs of puberty by 14
o Secondary: menses cease  3 - 6 mos, not pregnant, lactating, or menopausal
o Etio: anovulatory, ovulatory

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3
Q

• What is anovulatory amenorrhea?

A

o Both ovulation & menses are absent
o Mc, dt functional causes
o HPA intact, ovaries functional, gonadotropin secretion is  → mild E deficiency
o Causes: hypothalamic, pituitary, ovarian, other endocrine dos, some genetic dos
o Hypothalamic causes: multifactorial, mb unknown factors
o Endocrine causes: altered level free testosterone, androgens, or E dt: Lack of SHBG (chronic Lv dos, obesity, PCOS, DM), Excessive extraglandular prod of E (obesity), Ovarian or adrenal androgen excess, PCOS

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4
Q

• What is ovulatory amenorrhea? 2 types?

A

o Less common
o Dt anatomical genital AbN, normal hormonal function
o Ovarian fxn normal, external genitalia & secondary sex characteristics dev normally
o Acquired uterine abn: Acquired endometrial lesions (Asherman’s syndrome, endometrial TB), Obstructive fibroids and polyps
o Congenital genital abn: Cervical stenosis (rare), Imperforate hymen, Male pseudohermaphroditism (rare), Transverse vaginal septum (rare), Vaginal and uterine aplasia (rare)

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5
Q

• What could cause hypothalamin dysfxn w anovulatory amenorrhea? Pituitary dysfxn? *=chronic

A

o H: Anorexia nervosa, Excessive exercise, Hypothalamic chronic anovulation, Kallmann’s syndrome (rare), Prader-Willi syndrome (rare), Psychogenic factors (severe stress), Tumors (hamartomas, gliomas), Weight loss (acute), Undernutrition (chronic)
o P: Galactorrhea* (hyperprolactinemia), Benign pituitary adenoma, Hypopituitarism* (dt Sheehan’s syndrome, head trauma, tumor), Isolated gonadotropin deficiency, Panhypopituitarism, Pituitary tumors* (Forbes-Albright syndrome), Antipsychotic drugs (olanzapine)

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6
Q

• What could cause ovarian failure/dysfx with anovulatory amenorrhea? Other endocrine? Genetic dos? *=chronic

A

o Ov: AI, Chemo and pelvic irradiation, Congenital thymic aplasia, Galactosemia, Gonadal dysgenesis (very rare), Metabolic dos (Addisons dz, DM), Viral infx (mumps)
o Other: Congenital or adult-onset adrenal virilism, Cushing’s, Drug-induced virilization (antidepressants), Hyperthyroid, Hypothyroid, Obesity, PCOS*, Tumors producing androgens, estrogens, or hCG

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7
Q

• How do you diagnose amenorrhea?

A

o Eval girls w No signs of puberty by 14, If no menarche by 16,  2 yrs since onset of puberty
o Women of reproductive age: if 2nd amenorrhea (3-4% of women), (+) preg test, Missed menses  3 mos, < 9 menses/yr (avg 46 d), Sudden change in menstrual pattern

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8
Q

• How do you take hx for amenorrhea?

A

o Menstrual hx very important: have they ever had a menses before?
o Possibility of pregnancy
o Risk factors:
o Genetic cause of primary: abn growth and dev, FHx genetic defects
o Hypothalamic: wt change, Dietary deficiencies, Excess exercise, Enviro stress
o asherman’s: Hx D & C, endometritis, obstetric hx, uterine surgery, meds that can cause virilism or galactorrhea (antidepressants cause drug-induced virilization, antipsychotics, phenothiazines, certain anti-hypertensives, opioids)
o endocrine d/os

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9
Q

• what are ssx of endocrine dos that can cause amenorrhea?

A

o Thyroid: fatigue, cold/heat intolerance, constipation, dry/moist skin,  conc, myxedema, palpitations, nervousness, tremor, insomnia/hypersomnia
o Virilization – hirsutism, temporal balding, deepening voice,  mm mass, clitoral enlargement,  in previously normally dev 2nd sex characteristics ( breast size, vaginal atrophy); consider true hermaphroditism, pseudohermaphroditism, gonadal dysgenesis, PCOS, virilizing ovarian or adrenal tumor, Cushings, adrenal virilism, genetic do
o estrogen deficiency: hot flashes, vaginal dryness, sleep disturbances, fractures, ↓ libido
o Obesity in hirsute women: prob PCOS
o Cushngs: Moon facies, truncal obesity, abd striae, thin extremities
o Assess 2nd sex characteristics using Tanner method
o Assess for nipple d/c & galactorrhea – prob hyperprolactinemia

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10
Q

• What do you look for on PE for amenorrhea cc? red flags?

A

o Vitals, ht & wt BMI, waist circumference
o Thyroid: enlargement, tenderness, nodularity
o Breast exam: nipple d/c
o Anatomic genital d/o’s
o Ambiguous genitals – virilization, true hermaphroditism, male or female pseudohermaphroditism
o Fused labia or clitoromegaly: exposure to androgens in 1st tri, congenital adrenal virilism, true hermaphroditism, drug-induced virilization.
o In girls not yet sexually active: external genital exam only; only do speculum/bimanual exam if other assessment does not reveal cause
o Absent cervix & uterus, ext genitalia is N, 2nd sex characteristics are not fully dev: androgen insensitivity syndrome
o Reproductive age women 2nd amenorrhea: Vitals (hypothermia, bradycardia, hypertension), BMI, waist:hip ratio, Thyroid exam, DTR’s, skin, abdominal, Pelvic exam
o RF: Delayed puberty (r/o genetic do), Virilization (PCOS, Cushing’s, androgen secreting tumor), Visual field defects (prolactinoma)

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11
Q

• What labs are done for amenorrhea?

A

o Preg test
o Thyroid study: FFT (free T3, free T4, TSH), prolactin. TSH > 3.5 =hypo. Thryroid dz common, hypo ↑ prolactin levels in 40% of women (dt ↑TRH, TSH)
o Prolactin: ↑ (>20 ng/mL) w/o thyroid dz mb pituitary tumor [microadenoma (10mm)] → MRI
o FSH & estradiol: > 30 suggests POF, retest in 1 mo before making dx. ↓FSH & estradiol indicate hypothalamic anovulation/amenorrhea
o Free testosterone, DHEAS,
FSH/LH: Mild  of either suggest PCOS. FSH/LH normal ratio 3:1, in PCOS will be 1:3.If LH or FSH 200 ng/dL mb ovarian/adrenal tumor
o DHEA  500 g/dL mb adrenal tumor, adult-onset adrenal virilism
o Metabolic: CMP (systemic dos), CBC (anemia), ESR, celiac panel
o Bone age: for primary amenorrhea only

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12
Q

• What is work-up of labs are normal with primary amenorrhea?

A

o TVUS → normal uterus = hypothalamic anovulation
o If TVUS → uterus absent = Rokitansky syndrome
o If TVUS → uterus enlarged = imperforate hymen
o Karyotype testing if genetic defect is suspected

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13
Q

• How can you determine if there’s an E deficiency with amenorrhea?

A

o Progenertone challenge: Provera 5-10 mg po qd x 5 days OR Micronized progesterone 100-200+/day x 5 days; see if it induces a period
o Bleeding: she has E, but anovulation
o No bleed: no E, or some obstruction with outfow
o Many gyn expterts think doesn’t have consistent results, not necessary if run FSH and estradiol
o isn’t as dependable so most don’t use it routinely.

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14
Q

• What is the mc cause of primary amenorrhea?

A

o Physiologic/constitutional delay of puberty
o Functional hypothalamic chronic anovulation (excessive exercise, eating dos, stress)
o Delayed growth may accompany these sxs

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15
Q

• what are mc causes 2nd amenorrhea?

A

o Pregnancy - #1, Breast feeding
o PCOS, Obesity,
o Thyroid dysfx, Pituitary dysfx (hyperprolactinemia), Hypothalamic dysfx (excessive exercise, eating dos, stress), Ovarian failure/ insufficiency
o Use/Abuse drugs (OCP, anti-depressants/psychotics, Depo-Provera)
o Remaining etiologies far less common

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16
Q

• What is chronic anovulatory syndrome?

A

o seen w anorexia, weight loss, low protein intake, exercise with body fat levels below 10%, chronic illness, hypothalamic anovulation, hyperprolactinemia, hypopituitism, pituitary tumors, Cushings, hypo/hyperthyroid, obesity, PCOS, tumors that produce hormones and mb psychogenic.

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17
Q

• What drugs could cause hyperprolactinemia with amenorrhea? Other possible finding?

A

o Affect DA (Anti-HTN, Anti-psychotics (2nd gen or conventional)
o Cocaine, Estrogens, GI Drugs, Hallucinogens, Opioids, TCAs
o Mb also galactorrhea

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18
Q

• What drugs could cause drug-induced virilization w amenorrhea?

A

o Hormones and certain other drugs that affect the balance of estrogenic and androgenic effects

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19
Q

• How can body habitus indicate causes of amenorrhea?

A

o ↑BMI (>30): virilization, extrogen excess, PCOS
o ↓BMI (<18.5): chronic do, dieting, eating do; Functional hypothalamic anovulation dt anorexia nervosa, starvation, bulimia w freq vomit; ssx: Hypothermia, bradycardia, hypotension, Reduced gag reflex, palatal lesions, subconjunctival hemorrhages
o Short stature: turner’s; Primary amenorrhea, webbed neck, widely spaced nipples

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20
Q

• What skin abnormalities could help dx cause of amenorrhea? Other possible findings

A

o Warm, mosit: hyperthyroid; aslo tachycardia, tremor
o Course, thick, loss eyebrow hair: hypothyroid; Bradycardia, delayed DTRs, weight gain, constipation
o Acne: virilization, Androgen excess dt PCOS, androgen-secreting tumor, Cushing’s, adrenal virilism, drugs
o Striae: cushings; Moon faces, buffalo hump, truncal obesity, thin extremities, virilization, HTN
o Acanthosis nigricans: PCOS; obesity, virilization
o Vitiligo/hyperpigmented palm: addison’s; orthostatic hypotension

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21
Q

• What are some general findings suggesting estrogenic or androgenic abn, w amenorrhea?

A

o sxs of E def: hot flashes, night sweats, vag dryness, atrophy; dt Premature ovarian failure/primary ovarian insufficiency; risk factors: oophorectomy, chemo, pelvic irradiation
o hirsutism w virulism, 1st amenorrhea: Androgen excess dt PCOS, androgen-secreting tumor, Cushing’s, adrenal virilism, drugs; OR dt hermaphroditism, pseudohermaphroditism, gonadal dysgenesis, genetic d/o
o H,V w enlarged ovaries: Androgen excess dt 17-hydroxylase deficiency, PCOS, or androgen-secreting ovarian tumor

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22
Q

• What are some breast and genital abn seen w amenorrhea? Possible cause and other findings?

A

o Galactorrhea: hyperprolactinemia, pituitary tumor; Nocturnal HA, visual field defects
o Absent/incomplete dev breasts (& 2nd sex charact): normal adrenarche (1st anov amen dt isolated ovarian failure); absent adrenarche (1st anov amen dt HP dysfx); no adrenarche & impaired smell (kallmann syndrome)
o Delay brest dev and 2nd sex: constitutional delay of growth and puberty; FHx delayed menarche
o Normal dev, 1st amen: genital outflow obstruction; Cyclic abdominal pain, bulging vagina, uterine distension
o Ambiguous genitals: True hermaphroditism, Pseudohermaphroditism, Virilization
o Fused labia, clitoral enlargement at birth: Androgen exposure in 1st tri, mb congenital adrenal virilism, true hermaphroditism, drug-induced virilization
o Clitoral enlargement after birth: Androgen-secreting tumor (usu ovarian), Adrenal virilism, anabolic steroids; virilization
o Norm ext gen, incomplete dev 2nd sex (st breast, min pubic hair): Androgen insensitivity syndrome; Apparent absence of cx and uterus
o Ovarian enlargement (BL): Premature ovarian failure dt AI oophoritis (Sxs of E def); virilization (dt PCOS, 17-hydroxylase def)

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23
Q

• What lesion could indicate cause of amenorrhea?

A

o Pelvic mass (UL) → pelvic tumors, pelvic pain

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24
Q

• What is dysfunctional uterine bleeding?

A

o no clinical or US evidence of structural AbN, inflammation, CA, systemic do, preg/complication, OCPs, certain drugs (dx of exclusion)
o >50% cases > 45; in puberty (20% of cases); =common periods in life when anovulation occurs
o PCOS also common cause of anovulation.
o 90% are anovulatory, 10% ovulatory

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25
Q

• What is pathophysiology of an/ovulatory DUB?

A

o A: w/o progesterone secretion from corpus luteum → excessive proliferation of endometrium, eventually outgrows blood supply; sloughs and bleeds incompletely, irregularly, st profusely or long time. if repeatedly, endometrium → hyperplastic, mb dysplasia
o O: progesterone secretion is prolonged → irregular shedding of endometrium, dt ↓ E (near threshold for bleeding like during menses). Obese: can occur if ↑E → amenorrhea alt w irregular or prolonged bleeding

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26
Q

• What are ssx of DUB?

A

o Polymenorrhea: menses < 21 d
o Menorrhagia: > 7 d or > 80 ml
o Metrorrhagia: occur frequently & irregularly between menses
o Anov DUB: unpredictable times, patterns, no cyclic changes in BBT
o Ovu DUB: excessive bleeding w menses; usu sxs of ovulation (breast tenderness, midcycle cramping, change in BBT, st dysmenorrhea)

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27
Q

• What labs are done for DUB?

A

o Preg
o CBC & ferritin
o r/o coag dos in adolescents w DUB & anemia or hospitalized for bleeding
o LFTs
o Thyroid panel (FFT) & prolactin
o Serum/salivary PG, d 21, serum < 3 ng/mL = anovulation
o Serum/salivary T & DHEAS, r/o PCOS
o Pap if no test in >1 yr
o GC/CT if suspect PID, endometritis, cervicitis

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28
Q

• What imaging/procedures are done for DUB?

A

o TVUS: r/o structural AbN: >35 or unopposed prolonged E in younger, Risk factors for endometrial CA, Bleeding continues despite empiric hormonal tx
o EMB: R/O hyperplasia: >35 or unopposed E, obese, PCOS, DM, HTN, endometrial thickness > 4 mm, inconclusive TVUS findings
o Hysterectomy: if findings of adenomatous hyperplasia

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29
Q

• How is DUB diagnosed?

A

o If all clinically indicated tests are normal

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30
Q

• What is dysmenorrhrea? Ssx? Etio?

A

o uterine pain assoc w menses either primary (MC) or secondary (dt pelvic abn)
o w menses or precede by 1-3 d, peak 24 hrs after onset, subside after 2-3 d
o sharp, or cramping, throbbing, dull, constant ache
o may radiate to the legs
o H/A, N/D/V, constipation, ↓BP, urinary freq. S/t endometrial clots or casts

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31
Q

• What is primary dysmenorrhea?

A

o Begins adolescence, no underlying gyn structural do, st improves w age and preg
o Occurs in ovulatory cycles
o RFs for severe sxs: early menarche, long or heavy periods, smoking, FHx
o MOA: ↓ P→ lysosome breakdown → enzymes → ↑ PGs in uterus (endometrium/menstrual fluid) → ↑ uterine contractions & ischemia
o Factors: menstrual tissue thru os, narrow os, Malpositioned uterus, ↓exercise, Anxiety about menses

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32
Q

• What is 2nd dysmenorrhea?

A

o begin in adulthood, underlying pelvic AbN causes pain wi menstruation
o MC causes: Endometriosis (mc), Adenomyosis, Fibroids
o Other: Congenital malformations, Ovarian cysts and tumors, PID, Pelvic congestion, Copper IUD, Narrow os dt conization, cryotherapy, or LEEP; Pedunculated submucosal fibroid or endometrial polyp thru cervix

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33
Q

• What should you ask on hx for dysmenorrhea? PE? Red flags?

A

o Usu hx
o degree of disruption of daily life and presence of pelvic pain unrelated to menses
o Effect of contraceptives on pain: Paragard IUD ↑, OCP’s & Mirena IUD ↓
o Identify known causes such as endometriosis, adenomyosis or fibroids
o PE: pelvic exam
o RFs: New or sudden-onset pain, Unremitting pain, Fever, Vaginal d/c

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34
Q

• What is work-up for dysmenorrhea?

A

o Preg
o TVUS
o If suspect PID: cx culture or urine GC/CT
o If inconclusive and sxs persist, sonohysterogram (SIS) or hysterosalpingogram (HSG)
o →MRI
o →Hysteroscopy or laparoscopy

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35
Q

• What is tx for dysmenorrhea?

A

o Tons of ND treatments
o Anti-PG drugs (ASA, ibuprofen), caffeine, painkillers
o Low dose OCP
o Local heat, exercise

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36
Q

• What is PMS (premenstrual syndrome)? Etio?

A

o sxs in 2nd ½ of cycle (7-10 d before menses), relieved w flow onset
o Related to AbN responses to fluctuations of E and P
o Fluid retaining effects of E, P, aldosterone, ADH
o changes in CHO metabolism in luteal phase, and adrenal production of corticosteroids
o Possible hypoglycemia, hyperprolactinemia
o Possible serotonin connection

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37
Q

• What are ssx of PMS and PMDD?

A

o Intensity of sxs vary from pt to pt & from cycle to cycle
o Sxs last a few hrs to  10 d
o as many as 200 diff sxs assoc, MC >30, in some starts after childbirth
o common: wt gain, bloating, breast swelling and pain, H/A, fatigue, lethargy, anxiety, anger, irritability, depression, insomnia, salt/sugar cravings, emotional lability, pelvic heaviness/ pressure, backache
o less: dermatitis, acne, migraine/HA, vertigo, asthma, exacerbation of mental illness, paresthesias of extremities, N/V/D, constipation, syncope, palpitations, Changes in appetite
o generally very regular, rarely have severe cramping

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38
Q

• what is PMDD (premenstrual dysphoric do)?

A

o Severe PMS sxs
o marked depressed mood, anxiety, irritability, emotional liability
o mb Suicidal thoughts
o Interest in daily activities is greatly decreased
o severe enough to interfere w routine daily activities or overall fxn

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39
Q

• how are PMS and PMDD diagnosed?

A

o Both: PMS diary for 2-3 months
o PMDD: sx pattern for most of past yr, severe enough to interfere w daily activities and fxn
o >5 of following sxs for most of wk before menses, at least 1 of first 4:
o Feeling sad, hopeless, self-depreciation
o tense (on edge) feeling or anxiety
o Emotional liability w freq tearfulness
o Irritability or anger, ↑ interpersonal conflicts
o Loss of interest in daily activities →withdrawal
o ↓ concentration
o Fatigue, lethargy
o Changes in eating habits, including binging
o Insomnia or hypersomnia
o Feelings of being overwhelmed or out of control
o Physical sxs assoc w PMS

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40
Q

• What is ddx of PMS/PMDD? Labs? Tx?

A

o Ddx: Thyroid dz, Other hormonal dos, Affective dos
o Labs: No specific
o Tx: individual; diet, lifestyle, counseling, supplements (Mg, B vits, Ca, others), drugs (SSRI’s, OCPs)

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41
Q

• What is PCOS?

A

o Aka Hyperandrogenic Chronic Anovulation
o 5-10% of women
o Mb or no ovarian pathology: mb enlarged w 2-9mm follicular cysts w atretic cells
o Presents w anovulation & androgen excess
o Etio unclear: many metabolic AbN (hyperinsulinemia/glucose issues, lipid AbN, obesity, metabolic syndrome,  E & T,  P, AbN FSH:LH ratio [1:3 instead of normal 3:1])
o ** can’t process insulin in liver and muscles dt probable genetic susceptibility that causes hyperinsulinemia, all other factors are considered downstream

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42
Q

• What are ssx of PCOS?

A

o Usu start w menarche & worsen w time
o Irregular menses: oligomenorrhea, polymenorrhea, amenorrhea
o Hirsutism, acne, temporal balding
o Acanthosis nigricans
o Mild to severe obesity
o Mb enlarged ovaries/cystic ovaries
o Dx: signs of anovulation & hyperandrogenism
o Untx, serious: CVD, DM II, metabolic syndrome, endometrial CA, mb BR CA (due to ↑ E and T, hyperinsulinemia, ↓ P)

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43
Q

• What is work-up for PCOS?

A
o	Preg
o	Salivary or serum E, P, T, DHEA, cortisol
o	Serum FSH/LH
o	Thyroid studies (FFT) and Abs
o	Prolactin
o	FG, GITT (insulin) & lipids
o	TVUS: string of pearls ovary
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44
Q

• How is PCOS diagnosed?

A

o Suspect if at least 2 typical sxs
o 2/3:
o Ovulatory dysfunction causing menstrual irregularity
o Clinical or biochemical evidence of hyperandrogenism
o >10 follicles per ovary on TVUS, usu in periphery, like string of pearls
o →serum cortisol to exclude Cushings
o → fasting serum 17-hydroxyprogesterone to exclude adrenal virilism

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45
Q

• What is tx for PCOS?

A

o Lots of ND treatments
o Conventional: OCPs, Metformin (also on our formulary)
o Prevent major sequelae of dz: CVD, Endometrial CA, DM II, Metabolic Syndrome, breast CA

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46
Q

• What is premature ovarian failure? Etio? Ssx?

A

o Aka Premature Menopause/Primary Ovarian Insufficiency
o ovaries don’t make enough E despite ↑ gonadotropins (esp FSH), < 40
o etio: AI, Congenital thymic aplasia, Galactosemia, Gonadal dysgenesis (Y chromosome  risk of ovarian CA)
o Physical and environmental factors: Chemotherapy & pelvic irradiation, smoking, Viral infxns (mumps)
o Ssx: Amenorrhea or irregular blding, E deficiency (osteoporosis (fractures), atrophic vaginitis,  libido

47
Q

• What is work-up for premature ovarian failure?

A

o Preg test
o Serum FSH
o estradiol: if FSH > 20-30 IU/mL & E < 20 pg/mL repeat in 1 mo to confirm
o Further testing is to look for cause
o Karyotype if < 35 w confirmed ovarian failure

48
Q

• What is menopause? perimenopause

A

o physiologic (1 yr) or iatrogenic cessation of menses due to  ovarian fxn
o avg 51, range 45-55
o Perimenopause: the yrs before & 1 yr after LMP
o Initially ↑ freq of menses followed by ↓(oligomenorrhea)=hallmark; Conception still possible

49
Q

• What happens to the ovaries in menopause? Effect on hormones?

A

o ↓ # follicles, ↓ response to FSH & LH → initially short follicular phase, ↓ovulations, ↓ P
o → follicles do not respond
o → ↓ E2 & inhibin, → ↑ LH & FSH
o ↑ E1 (peripheral conversion from androgens)
o ↑T: from ovary stroma and adrenal gland

50
Q

• What is premature menopause? Iatrogenic menopause?

A

o dt noniatrogenic ovarian failure <40
o Contributory fxs: Smoking, Living in high altitude, Undernutrition
o Iatrogenic: oophorectomy, chemotherapy, pelvic irradiation, impairing ovarian bld supply

51
Q

• What is the hallmark ssx of menopause? Cause of other sxs?

A

o * Changes in menses bleeding patterns: first more freq, then longer apart, eventual stop
o usu begin in 40’s
o daily E fluctuations ~1 yr before menopause & cause sxs, 6 mos – 10 yrs, range none-severe

52
Q

• describe the hot flashes and sweating sxs of menopause?

A

o Common, dt vasomotor instability, 75-85%
o > 1 yr in most, > 5 yrs in 50%
o Dt ↓ E, ↑LH,FSH
o Triggers: smoking, hot beverages, foods w nitrites/sulfites, spicy foods, ETOH, caffeine
o Sudden feeling of extreme heat, flushed skin, esp head & neck
o 30 sec – 5 min
o Wake at night, mb drenching sweat, or clamminess/chills
o May mask hypo/hyperthyroidism

53
Q

• What are other common ssx with menopause?

A

o Vaginal dryness, atrophy, dyspareunia, dysuria
o Psych: nervousness, irritability, depression & anxiety (esp w hx), poor conc, memory loss
o night sweats, fatigue, insomnia
o Light-headed, palpitations, numbness, tingling
o Atrophic changes: urinary frequency, incontinence
o GI: N/D/C
o m/s: back pain, arthralgias, myalgias, cold hands & feet
o lack libido
o Physiologic changes are many: ↑ rate of bone loss, lipid profile change, mb ↑ glucose

54
Q

• What are some health problems assoc w menopause?

A

o Osteoporosis: Dt ↓ E → ↑ bone resorption by osteoclasts; most in 1st 2 yrs after ↓E
o CVD: ↑ chol, LDL, TGs, ↓ HDL, HTN, ↑ FG
o Breast CA: ↑ risk w each decade

55
Q

• How is menopause managed and diagnosed?

A

o cessation of menses > 50, hx irregular menses, no other AbN findings → no dx testing necessary
o FSH consistent ↑ predicts menopause
o Screening for osteoporosis, CVD, breast CA

56
Q

• How is osteoporosis dx/managed in PM women?

A

o Screening: Pm w risk factors for osteoporosis & all > 65 for bone loss (DEXA (dual x-ray absorptiometry at hip & lumbar vertebrae)
o BMD: in T-scores (# SDs from young adult mean BMD); N= -1; Osteopenia = –1- -2.5; Osteoporosis = < -2.5
o Tx is mandatory if dx
o Evaluate for possible pathology & check for thyroid & adrenal dysfxn/pathology
o FFT – Free T3, Free T4, TSH, ASI (adrenal stress index – cortisol x 4, DHEA, anti-gliadin Ab, SIgA)

57
Q

• What are general risk factors for osteoporosis/osteopenia?

A
o	Alcohol > 7 oz per week
o	Amenorrhea > 6 months
o	Caucasian or Asian 
o	Certain dz like hyperthyroid
o	Smoking
o	RA
o	FMHx (esp maternal hip fracture)
o	Female 
o	Lack of adequate calcium and Vitamin D (look at GI absorption)
o	Menopause, esp premature
o	Previous fracture
o	Sedentary lifestyle
o	steroids or anti-seizure drugs 
o	Wt less than 127 lbs or BMI < 21
58
Q

• How is CVD dx/monitored in PM women? Breast CA?

A

o Lipid panel, glucose/insulin
o BP, BMI, waist circumference
o inflammatory and CVD markers if ↑ risk w (+) above findings: hsCRP, fibrinogen, homocysteine, Lp(a), Boston Heart Panel
o CA: mammogram yearly starting at 40-50

59
Q

• How is menopause “treated”?

A

o It’s a natural process
o HRT= last resort
o hot flashes, insomnia, mood changes: Regular exercise; Stress reduction & relaxation techniques; Soy, black cohosh, other botanicals; Vit E; Acupuncture; 5HTP, GABA
o Vaginal dryness, atrophy, dyspareunia: OTC vaginal lubricants; Lactobacillus suppositories, Vit E; Local estriol cream

60
Q

• What are the infections of the genital tract?

A

o Vaginitis: bacterial, candida, atrophic/inflammatory, trichomonas, cytolytic
o PID: gonorrhea, chlamydia, cervicitis

61
Q

• What is vaginitis?

A

o Infx/non infla of vaginal mucosa, st vulva
o Infx mc; or flora imbalance
o Normally (reproductive), Lactobacillus is predominant constituent of normal vaginal flora, keeps vaginal pH at 3.5-4.5, prevent overgrowth
o ↑E maintain vaginal wall thickness, ↑ local defenses
o Common gyn do; vulvitis if affects vulva alone; vulva + vagina = vulvovaginitis

62
Q

• What are predisposing factors to vaginal bacterial pathogens?

A
o	abx (↓ lactobacilli)
o	Alkaline vaginal pH dt menstrual blood, semen, ↓ in lactobacilli
o	Poor hygiene
o	Freq douching
o	Preg
o	DM
o	HIV
63
Q

• What are ssx of vaginitis?

A

o Abn vag d/c (mc, w or w/o vulvar irritation)
o Irritation, tenderness
o Pruritis
o Erythema
o Mb Dysuria or dyspareunia
o d/c watery/bloody mb from uterine, ovarian, vulvar, vaginal CA, DES related tumors

64
Q

• What is abn vag d/c?

A
o	Offensive odor
o	W pruritis or irritation 
o	burning, pain, or blood in d/c
o	amount of d/c distressing 
o	must be distinguished from normal: Common w ↑E, First 2 weeks of life, first few mos before menarche; Milky white/mucoid, odorless, non-irritating
65
Q

• what can cause vaginitis in kids?

A

o Infx suu involves GI tract flora
o 2-6: poor perineal hygiene (wiping back to front), not washing hands after BM, touching in response to pruritis
o Chem in bubble baths, soaps can cause inflammation
o Foreign bodies: mb non-specific, w bloody d/c
o *candida, strep, staph, pinworms, E.Coli

66
Q

• What causes vaginitis in Reproductive Age Women?

A

o Usu infx (mb lactobacillus imbalance); mc: trichomonas vaginitis (STI), Bacterial Vaginosis (BV), Candida
o Things that  pH: menstrual blood, semen, tight non-porous underclothing, poor hygiene, douching, diaphragm/spermicide use
o Foreign bodies (forgotten tampons)
o Inflammatory vaginitis (non-infx) is uncommon

67
Q

• What can cause vaginitis in Pm women? Any age?

A

o Usu atrophic or inflame, mb overlapping BV or candida
o ↓E → vag thinning   lactobacillus   vag pH
o Poor hygiene (incontinent or bed-ridden)
o Any: entero-genital Fistulas; Pelvic radiation or tumors
o Hygiene sprays, perfumes, laundry soaps, bleaches, menstrual pads, fabric softeners, fabric dyes, synthetic fibers, bathwater additives, toilet tissue, spermicides, vag lubes/creams, latex condoms, vag contraceptive rings or diaphragms

68
Q

• What are some causes of vag pruritis and d/c, w findings, in children?

A
o	Poor perineal hygiene: Pruritis, vulvovaginal erythema, vag odor, dysuria. No d/c
o	Chemical irritation (soaps, bubble bath): Vulvovaginal erythema, soreness, often recurrent and accompanied by pruritis and dysuria
o	Foreign bodies (toilet paper): Vag d/c, usu foul odor and vag spotting
o	Infx (candida, pinworm, Staph/strep): Pruritis, vag d/c, vulvar erythema, swelling; often dysuria, Worsening of pruritis at night (pinworms), Sig erythema, vulvar edema w d/c (strep or staph)
o	Sex abuse: Vulvovaginal soreness, bloody or malodorous vag d/c; Often vague/non-specific complaints, fatigue, abd pain, or behavior changes
69
Q

• What are some causes of vag pruritis and d/c, w findings, in women of reproductive age?

A

o Bacterial Vaginosis: Malodorous (fishy), thin, gray vag d/c, pruritis, irritation; Erythema and edema uncommon; Clue cells on wet prep; Vag pH > 4.5
o Candida: Vulvar and vag irritation, edema, pruritis; D/c like cottage cheese on vag wall; St worse after vag penetration, before menses; St recent abx use, hx of DM
o Trichomonal: Yellow-green, frothy vag d/c, soreness, erythema, edema of vulva and vag; dysuria, dyspareunia; punctate, red “strawberry” spots on cervix or vag walls; Mild CMT; pH > 4.5
o Foreign bodies (forgotten tampon, cervical cap): Extremely malodorous, profuse vag d/c, vag erythema, dysuria, dyspareunia; Object mb visible during exam

70
Q

• What are some causes of vag pruritis and d/c, w findings, in Pm women?

A
o	Atrophic (inflammatory) Vaginitis: Dyspareunia, scant d/c, thin and dry vaginal tissue; ↑ Ns, parabasal cells and cocci; ↓ bacilli on microscopic 
o	Chemical vulvitis dt irritation from urine or feces: Diffuse redness. Risk factors: incontinence, restriction to bed rest
71
Q

• What are some causes of vag pruritis and d/c, w findings, for all ages?

A
o	Hypersensitivity rxns: Vulvovaginal erythema, edema, pruritis, vag d/c; Hx recent sprays/perfume, bath water additives, topical tx candida infx, fabric softeners, bleach or laundry soaps
o	Inflammatory (pelvic radiation, oophorectomy, chemo): Purulent vag d/c, dyspareunia, dysuria, irritation; pruritus, erythema, burning pain, mild bleeding; Thin, dry vag tissue
o	Enteric fistulas (complication of delivery, pelvic surgery, IBD): Malodorous vag d/c w passage of feces from vag; Direct visualization or palpation of fistula in lower vag
72
Q

• What hx Qs would you ask for vaginitis cc?

A

o Amount of d/c, color, consistency, odor, irritation (when it occurs in relation to cycle, intercourse, vag penetration)
o Pruritus, burning, pain
o Duration, intensity
o Urinary freq, burning, pain (urethritis)
o Self-tx, douching
o OB/gyn/menstrual hx
o Pregnancies, birth control use: OCPs, IUDs, condoms, diaphragm, spermicide, vag ring
o Vag creams, lubes
o Sex habits, orientation, practices w men, women, both
o hygiene: including changes in laundry products, sprays, perfumes
o Does male sex partner have urethral d/c, pruritis, penile lesions, post-coital irritation? Female partner as well
o Recurrent sxs
o Txs tried and response to tx
o Has she seen another physician for this and had any workup?

73
Q

• What Qs do you ask about PMHx for vaginitis cc?

A

o Recurrent abx, hypothyroid, DM, HIV, immunosuppressive dos (risk candida)
o Crohn’s, GU/GI CA, pelvic/rectal surgery, lacerations during delivery (fistulas)
o Unprotected or multiple sex partners (STIs)

74
Q

• What ROS do you ask about vaginitis cc? Red flags?

A

o ROS: Fever, chills, abd or suprapubic pain, polyuria, polydipsia
o RF: Trichomonal vaginitis in children (sex abuse)
o Fecal d/c (fistula, even if not seen)

75
Q

• What PE done for vaginitis? Labs?

A

o Palpate inguinal LNs
o Examine external genitalia, vag mucosa, glands, urethra, cervix for erythema, edema, excoriation & lesions, amount of d/c, color & odor
o Bimanual: assess for CMT, adnexal, uterine tenderness
o vagpH
o Labs: Wet prep, culture, vag pH; DNA culture for BV, Candida, Trichomonas in chronic conditions

76
Q

• What is ddx of vaginitis?

A

o Infx: (BV, Candida, Trichomonas, Cytolytic, Beta-hemolytic strep)
o Atrophic vaginitis (loss of lubrication)
o UTI
o Allergy and irritation
o Malignancy higher in the tract
o Psychological factors: abuse, rape, loss of libido, trauma
o Dermatological: lichen sclerosus, lichen simplex chronicus
o Systemic dzs
o Paget’s disease (looks like Candida)

77
Q

• What is Bacterial vaginosis (BV)?

A

o Mc infx vaginitis
o Dt ↓ lactobacillus → ↑ anaerobic bacteria (10-100x)
o Anaerobic pathogens: Prevotella, peptostreptococcus, gardnerella vaginalis, mobiluncus, mycoplasma hominis

78
Q

• What are risk factors for BV?

A
o	IUDs
o	↓vitamin D
o	Poor nutrition
o	Douching
o	No condom use
o	Anal sex before vag intercourse/sex/penetration
o	Sex w uncircumcised male
o	Spermicides
o	New male partner
o	↑ #sexual partners
o	Smoking
o	Non-white ethnicity
79
Q

• What are assoc risks with BV?

A
o	PID, HPV
o	Post-abortion and post-partum endometritis
o	Post-hysterectomy vag cuff infx
o	Chorioamnionitis
o	Pre-mature rupture of membranes (PROM)
o	Pre-term labor & pre-term birth
80
Q

• What are ssx of BV?

A

o Mild, often asx
o malodorous Vag d/c (fishy odor), gray, thin, profuse
o Odor stronger after menses and intercourse ( ↑ pH)
o Pruritus and irritation
o Erythema and edema are uncommon

81
Q

• How is BV diagnosed? Ddx?

A

o 3-4 of Amsel’s criteria: gray d/c, vag pH >4.5, fishy odor, clue cells on wet prep (KOH test, pleomorphic rods)
o usu < 50 WBs (if higher likely concomitant infx:trich., GC, CT, need additional testing)
o DDX: Trichomonas vaginitis

82
Q

• What is candida vaginitis? Risks factors?

A
o	Mc cause fungal vaginitis, usu abincans
o	abx or corticosteroids
o	pregnancy
o	constrictive undergarments
o	immunocompromised
o	IUD, OCPs, vag ring
o	DM, HIV
83
Q

• What are ssx of candida vaginitis?

A

o Thick white cottage cheese like vag d/c on vag wall
o Vaginal or vulvar pruritus, burning or irritation; mb worse from vag penetration
o Dyspareunia
o Worse week before menses
o Erythema, edema, excoriation, st fissures at introitus

84
Q

• How is candida vaginitis diagnosed?

A

o Wet prep: budding yeast, pseudohyphae, st mycelia
o If no buds or pseudohyphae = different Candida strain (not Albicans) = mc Glabrata
o yeast on wet-prep only 30%
o normal Vag pH ( test for add’l infx
o If chronic low-grade sxs consider DNA culture for candida to specify type

85
Q

• What is ddx for candida vaginitis?

A
o	contact irritant or allergic vulvitis
o	chem irritation
o	vulvodynia
o	Paget’s dz
o	Cytolytic vaginosis
86
Q

• What is Atrophic/Inflammatory Vaginitis? Risk factors?

A

o vag inflam w/o usu causes of infx vaginitis
o risk: ↓ E dt menopause or premature ovarian failure or insufficiency
o Genital atrophy predisposes to inflam vaginitis and increases risk of recurrence
o Possible AI

87
Q

• What are ssx of atrophic vaginitis?

A

o Clear or purulent vag d/c
o Dyspareunia, dysuria (sxs like UTI),vag irritation
o Vag pruritus, erythema, burning, pain, minor bleeding
o Thin and dry vag mucosa

88
Q

• How is atrophic vaginitis dx? Ddx?

A

o pH >6
o wet prep: ↑WBCs, ↓ lactobacillus, parabasal cells
o May have ↑cocci (streptococci overgrowth)
o DDX: erosive lichen planus

89
Q

• What is Trichomonas vaginitis? Ssx? Dx? Ddx?

A

o Dt trichomod protozoa; STI
o Ssx: copious yellow/green frothy d/c, soreness of vulva and perineum, dyspareunia, dysuria, edema of labia, vaginal walls and cervix surface may have punctate red (strawberry) spots, urethritis and possibly cystitis
o dx: pH > 5.5; Wet Prep: ↑ WBCs, flagellated trichomod, mb incidental on PAP
o ddx: BV, atrophic vaginitis

90
Q

• what is cytolytic vaginosis? Ssx? Dx?

A

o Overgrowth of lactobacillus strain
o ssx: Burning, pruritus, rawness, vulvovaginitis, dyspareunia, erythematous & excoriated tissue
o dx: pH N or ≤ 3.5; wet prep: some WBCs, ↑ rods, false/atypical clue cells

91
Q

• what is PID? Etio?

A

o infx of upper genital tract: cervix, uterus, fallopian tubes, ovaries
o (poly)microorganisms ascend from vag/cx into endometrium, fallopian tubes (MC)
o If severe, spread to ovaries, peritoneum
o MC: Neisseria Gonorrhea (GC) and Chlamydia trachomatis (CT)
o Other: anaerobic and aerobic bacteria, like BV pathogens
o < 35: usu dt STIs
o > 35: usu overgrowth of anaerobic/aerobic bacteria in vagina that ascend

92
Q

• What are risk factors for PID?

A

o Hx STIs, PID
o IUD in > 35
o Single, young, Nulliparous, ↑ #sex partners, or new
o Alcohol use
o Low socioeconomic status
o Non-white ethnicity
o Adolescents: w older sex partners, hx CPS involvement, attempted suicide

93
Q

• What are ssx of PID?

A
o	Mild-severe or absent
o	LQ pain: radiates to back/sacrum
o	Fever, N/V
o	Cx d/c, AUB, Dysuria
o	Onset common during or after menses
o	Acute salpingitis: U/BL LQ pain; early- mild or asx; late- CMT, guarding, rebound tenderness; mb pain UQ
o	IGC more acute/severe than CT
94
Q

• What PE is done for PID?

A

o Inguinal LA w tenderness
o Fever >= 101 F
o ↑ HR
o Speculum: Cx red, erythematous, easily friable; Mucopurulent d/c, yellow green, from os
o Bimanual: CMT, Guarding, rebound tenderness, Skene’s glands enlarged, tender (GC or CT), Uterine and adnexal (U/BL) tenderness

95
Q

• How is PID diagnosed?

A

o Wet prep: > 10 WBCs/hpf
o CBC: ↑WBC
o ↑ESR, >15 mm/hr
o If al above (-) probably exclude endometritis/PID
o TVUS if too painful to be assessed
o r/o ectopic pregnancy
o PCR, culture or DNA probe for GC/CT, or Aptima test on urine

96
Q

• What are complications of PID?

A

o Fitz-Hugh-Curtis syndrome (perihepatitis RUQ pain, dt acute GC or CT salpingitis); PID mb chronic w intermittent exacerbations
o Tubo-ovarian abscesses (in 15% w Salpingitis): severe sxs if rupture, septic shock, w acute or chronic PID, esp w late/incomplete tx; Pain, fever, peritoneal signs
o Hydrosalpinx: usu asx, chronic pelvic pressure/pain, deep dyspareunia
o Peritonitis (surgical emergency)
o Adhesions & tubal scarring
o Infertility
o Adnexal torsion
o Tubal scarring and adhesions →Chronic pelvic pain, menstrual irregularities, infertility, ↑risk ect preg
o menstrual irregularities

97
Q

• what is tx for PID?

A

o Any women with risk of PID and either CMT, uterine or adnexal pain
o MUST be treated with 2 or 3 abx depending on histo (SAVE THE TUBES!!!)
o ?? 36 hrs of onset of initial sxs ↑ likelihood of infertility
o If no response to abx within 42-72 hrs, TVUS ASAP
o still uncertain →laparoscopy

98
Q

• what is ddx for PID?

A
o	Endometriosis
o	Appendicitis
o	Ectopic pregnancy
o	Bowel dos
o	Septic abortion
o	UTI
o	Complicated ovarian cyst
99
Q

• What is a gonorrhea infx? Ssx?

A
o	Neisseria gonorrhea; (-) intracellular diplococcus, infx vagina, urethra, rectum, pharynx 
o	M & F carriers
o	Sxs begin 7-21 d after exposure
o	Acute green/yellow mucopurulent cx d/c
o	Mb urinary sxs, d/c
o	Mb inflamed Bartholin and Skene’s glands 
o	Red cervix, local glands inflamed
o	Pelvic pain and fever
100
Q

• What are labs for gonorrhea?

A

o ↑ pH
o ↑ WBCs (> 100/hpf) on wet prep
o  ESR and WBC
o Most serious complication is PID in women
o Culture or DNA to confirm, Aptima (urine), liquid pap
o 7-10 d inc period when they are infectious
o Reportable disease

101
Q

• What is a chlamydia infx? Ssx? Sequelae?

A

o Infx of urethra and cervix w Chlamydia trachomatis
o Usu no external d/c; most asx (up to 70%)
o may mimic GC infx, more urethritis sxs, outcome mb same as GC
o Sequelae: bartholinitis, bartholin gland cysts, damage to fallopian tubes, PID

102
Q

• What are labs for chlamydia?

A

o ↑ pH
o Wet prep: ↑ WBCs > 100/hpf
o fluorescent Ab or DNA, Aptima (urine), liquid pap
o reportable disease

103
Q

• what is cervicitis? Ssx?

A

o inflam cervix
o endocervical junction esp vulnerable to infx
o aside from STDs, Staph, strep and E coli are common infections
o may be a major problem during labor
o Ssx: red congested friable cervix, mb ulceration, pus; may look like ectopy

104
Q

• What is endometriosis? Incidence?

A

o Noncancerous, implants like endometrial tissue outside uterine cavity
o Mc peritoneal & serosal surfaces: broad ligs, posterior cul-de-sac, uterosacral ligs, ovaries
o Less: surfaces of S/L I, ureters, bladder, vagina, cx, surgical scars, pleura, pericardium
o 10-15% menstruating women, 25-44; 20-50% infertile women
o Avg dx 27

105
Q

• What are some hypotheses to etio of endometriosis?

A

o Coelomic metaplasia
o Embryonic rests theory (mullerian remnants)
o E dominance (Defective formation & metabolism)
o Environmental: PCBs mimic estrogens, from meat, fish, eggs, milk
o Candida overgrowth in GI tract
o Genetics
o Lymphatic/vascular problems
o Immune system, dysfxn
o Menstruation Preconditioning Hypothesis: ↑endometrial and junctional zone blood flow during late secretory phase
o Metaplasia, of endometrium

106
Q

• How does endometriosis cause sxs (pathogenesis)?

A

o Bleeding from implants initiates inflammation  fibrin deposition  adhesion formation  scarring, distorts peritoneal surfaces of organs and pelvic anatomy

107
Q

• What is the staging for endometriosis?

A

o Stage I, Minimal: a few superficial implants
o Stage II, Mild: more, slightly deeper implants
o Stage III, Moderate: many deep implants, small endometriomas on ovaries, some filmy adhesions
o Stage IV, Severe: many deep implants, large endometriomas on ovary, many dense adhesions, st rectum adheres to uterus

108
Q

• What are risk ractors for endometriosis?

A
o	Shorter menstrual cycles, < 27 d
o	Longer bleeding, 8+ d 
o	Mullerian duct defects
o	Early menarche
o	FHx
o	Nulliparity
o	1+ alcoholic drinks per week 
o	Never used OCPs 
o	Use of tampons 
o	High fat diet
o	↑ serum E
o	IUD
o	Natural red color hair
o	Dioxin: P receptor polymorphism, ↓ immune system, deter implantation 
o	Stress: NE →vasoconstriction, hypoxia → ROS, ↑IL-6, IL-8 TNFa 
o	P receptor polymorphism
109
Q

• What are factors that ↓ risk for endometriosis?

A

o Exercise, esp if begun before 15, > 7h/wk or both
o Cigarette Smoking → ↑ SHBG (sex hormone binding globulin)
o Multiparous
o Low dose OCP

110
Q

• What are ssx of endometriosis?

A
o	Severity not affected by staging
o	*Generally pain & infertility MC
o	Pelvic pain: dysmenorrhea (esp after several yrs of pain free menses), deep dyspareunia
o	Pelvic mass: endometriomas
o	Dyschezia: esp during menses
o	Dysuria, suprapubic pain
o	Infertility
111
Q

• What is incidence of infertility w endometriosis?

A

o 25-50% infertile women have endometriosis
o Esp severe endometriosis and distorted pelvic anatomy: impair mechanisms of ovum pick up and tubal transport
o W minimal endometriosis and normal pelvic anatomy, dt:
o ↑incidence of luteinized un-ruptured ovarian follicle syndrome (trapped oocyte)
o ↑ peritoneal PG production or M0 activity (→ occyte phagocytosis)
o Non-receptive endometrium (luteal phase dysfunction or other abn); P polymorphism

112
Q

• What PE is done for endometriosis?

A

o External pelvic: rare, st vulvar lesions
o Speculum: st vag lesions in posterior fornix or cx
o Bimanual: mb normal or retroverted or fixed uterus, enlarged, tender ovaries, fixed ovarian masses, induration in cul-de-sac, nodularity of uterosacral ligs
o RVE: thickened rectovaginal septum, re-check cul-de-sac & ligs

113
Q

• How is endoemtriosis diagnosed?

A

o only by bx during laparoscopy or laparotomy
o TVUS, CT, MRI, IV urography, barium enema: not dx, mb identify extent of dz, monitor progress
o Serum Ca 125 (>35 units/mL) & antiendometrial Ab: not dx, may help monitor dz

114
Q

• How is endometriosis treated?

A

o Generally ND treatments 1st depending pts desires; lots
o Sx tx for pain; Ex: Mirena
o More definitive tx based on age, sxs, desire to preserve fertility & extent of do
o Allopathic: drugs suppress ovarian fxn, growth, activity of endometriotic implants, conservative surgical resection of endometriotic tissue