BIO 116 OBGYN Study Guide- Luther College/BIO 116 OBGYN Study Guide- Luther College/BIO 116 OBGYN Study Guide- Luther College/BIO 116 OBGYN Study Guide- Luther College/BIO 116 OBGYN Study Guide- Luther College/BIO 116 OBGYN Study Guide- Luther College
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OBGYN EOR Study Guide
Menstruation (15%)
1) Amenorrhea (See Prof. Brown’s notes)
a. Primary Amenorrhea
i. Failure of menarche onset by age 15 years (in the presence of secondary sex
characteristics) or age 13 years (in the absence of secondary sex characteristics)
ii. Workup:
1. hCG & FSH = most important!
2. TSH & prolactin also usually ordered initially
3. Karyotype testing done if increased FSH & little breast development
b. Secondary Amenorrhea
i. Absence of menses for > 3 months in a pt with previously normal menstruation
ii. Etiologies:
1. Pregnancy = MC cause!
2. Hypothalamic Dysfunction – Functional Hypothalamic Amenorrhea (FHA)
a. Puberty delay (s/a in athletes, illness or anorexia)
b. Female athlete triad: hypothalamic amenorrhea, eating disorder & OP
(d/t loss of bone production by estrogen)
c. FHA can cause primary or secondary amenorrhea!
3. Pituitary Dysfunction – prolactinoma or pituitary infarct (Sheehan syndrome)
a. Assoc. with decreased FSH, LH & estrogen
4. Ovarian Dysfunction – PCOS, Turner Syndrome, Premature Ovarian Failure
(follicular failure or follicular resistance to FSH/LH)
a. Decreased estrogen & increased FSH & LH
b. May have sx of estrogen deficiency (similar to menopause)
5. Uterine dysfunction: Asherman’s syndrome
a. Acquired endometrial scarring secondary to postpartum hemorrhage,
after D&C or endometrial infection
b. Pelvic US absence of normal uterine stripe
c. Do hysteroscopy!
iii. Workup:
1. Beta-hCG = best initial test!
2. If negative, order serum prolactin, FSH, LH, TSH & estrogen
3. Testosterone measured if evidence of hirsutism or hyperandrogenism
Uterus Present Uterus Absent
Breasts Outflow obstruction – transverse vaginal Mullerian agenesis (46 XX), Androgen
Present septum, imperforate hymen insensitivity (46 XY)
Breasts Elevated FSH/LH = Ovarian causes Rare, usually caused by a defect in
Absent Premature Ovarian Failure (46XX) testosterone synthesis. Presents like a
Gonadal dysgenesis (s/a Turners) phenotypic immature girl w/ primary
Normal/Low FSH/LH = Hypothalamus- amenorrhea (will often have intraabdominal
Pituitary Failure testes)
Puberty delay (athletes, illness,
anorexia)
2) Dysfunctional Uterine Bleeding (aka AUB)
a. Unexplained abnormal bleeding in a nonpregnant woman in regards to quantity, schedule or
duration
b. Anovulatory (90%) – ovaries produce estrogen but no ovulation = no corpus luteum
formation
i. Unopposed estrogen (from no progesterone) leads to endometrial growth &
unpredictable shedding
c. S/S: abnormal bleeding w/ relatively normal PE
d. Dx:
i. No specific test – w/u as indicated may include:
, 1. Beta-hCG to r/o pregnancy
2. Hgb & Hct
3. Additional tests depending on etiology
ii. Endometrial biopsy to r/o endometrial carcinoma should be done in all women > 35
y/o with obesity, HTN or DM and all pts with postmenopausal bleeding
e. Management:
i. Acute Hemorrhage – IV HD estrogen or HD OCPs
ii. Chronic – Estrogen/progestin contraceptives = 1st line!
1. Progesterone if estrogen is CI
2. Levonorgeserel-releasing IUD
3. NSAIDs in pts unwilling or unable to be tx with hormonal therapy
4. Surgery – if not responsive to medical tx
a. Hysterectomy = definitive management
b. Endometrial ablation in pts who do not want a hysterectomy
3) Dysmenorrhea
a. Painful menstruation that affects normal activities
b. Primary: d/t increased prostaglandins (not d/t pelvic pathology)
i. Prostaglandins cause increased uterine wall contractions
ii. Usually starts 1-2 years after menarche onset in teenagers
c. Secondary: d/t pelvic or uterus pathology (s/a endometriosis, PID, adenomyosis &
leiomyomas)
d. S/S: recurrent, crampy midline lower abdominal or pelvic pain 1-2 days before or at the
onset of menses, gradually diminishes over 12-72 hours
i. Pain may radiate to lower back & thighs & may be assoc. with HA, N/V
ii. PE: normal if primary dysmenorrhea
e. Dx: clinical, labs & imaging should be done if pelvic disease suspected
f. Management:
i. Supportive therapy – heat compresses, vit B & E started 2 days prior to and for 3
days into menses, exercise
ii. NSAIDs or hormonal therapy = 1st line medical management
1. NSAIDs started prior to pain onset & given x2-3 days
2. Hormonal therapy: estrogen/progestin contraceptive pills or progestin only
iii. Laparoscopy - indicated if unresponsive to x3 cycles of initial therapy to r/o
secondary causes
1. MC causes of secondary in younger pts are PID & endometriosis
4) Menopause
a. Cessation of menses > 1 year d/t loss of ovarian function, leading to decreased estrogen &
progesterone production
b. Avg age in the US = 50-52 years, premature if < 40 years
c. S/S:
i. Estrogen deficiency menstrual cycle alterations, vasomotor instability (including
hot flashes (MC perimenopausal symptom)), sleep disturbances, mood changes,
skin/nail/hair changes, increased CV events, HLD, OP, dyspareunia, vaginal atrophy &
urinary incontinence
d. PE: decreased bone density, dry & thin skin w/ decreased elasticity, vaginal atrophy w/ thin
mucosa, decrease in breast size
e. Dx:
i. FSH assay = most sensitive initial test (increased serum FSH > 30 IU/mL)
ii. Increased LH & decreased estrogen
iii. Androstenedione levels don’t change
iv. Estrone is the predominant estrogen after menopause
f. Complications: loss of estrogen’s protective effects leads to OP, HLD & increased CV risk
g. Management:
i. Hormone replacement therapy – risks vs. benefits must be considered (see below)
1. Estrogen only if no uterus
2. Estrogen + Progestin if uterus still present
nd
ii. 2 line = SSRIs (Paroxetine) or Gabapentin
, h. Vulvovaginal Atrophy:
i. Seen in hypoestrogenic states (s/a menopause, postpartum lactation, progesterone-
only or LD OCPs)
ii. S/S: vaginal dryness, dyspareunia, vaginal inflammation, infection & recurrent UTIs w/
increased pH (loss of lactobacilli which normally converts glucose to lactic acid)
iii. Management:
1. Vaginal moisturizers: improves sx but no effect on atrophy
2. Topical vaginal estrogens: safest, most effective medical tx
a. Cream, vaginal ring, vaginal troches
b. ADRs: vaginal bleeding, breast pain, nausea, thromboembolism (CVA,
DVT/PE), endometrial cancer
c. Less risk compared to PO estrogen
d. Estrogens increase hepatic production of coagulation factors
3. Ospemifene: SERM that is an estrogen agonist in the vagina & bone and an
estrogen antagonist in the breast & uterus
i. HRT
i. Indications:
1. Healthy woman < 60 y/o for menopause symptom relief (vasomotor sx, mood
changes, vaginal atrophy
2. Decreases OP risk
ii. Risks:
1. DVT or PE
2. Endometrial cancer (estrogen only)
3. BC risk with estrogen-progestin therapy (controversial)
iii. Contraindications:
1. Women w/ increased risk of CVD
j. Tamoxifen
i. MOA: SERM – estrogen antagonist in the breast but estrogen agonist in the
endometrium, bone, liver & coagulation system
ii. Indications:
1. Adjuvant tx in estrogen & progesterone receptor-positive BC, BC prevention &
OP prevention in postmenopausal women
iii. ADRs: increased risk of endometrial cancer, VTE, hot flashes (induces menopause),
ocular toxicity
k. Raloxifene
i. MOA: SERM – estrogen agonist in bone but estrogen antagonist in endometrium &
breast
ii. Indications:
1. BC prevention in high risk women & OP prevention in postmenopausal women
iii. ADRs: weight gain, VTEs (less than Tamoxifen), hot flashes (induces menopause)
5) Normal Physiology
a. Phase 1: Follicular (Proliferative)
i. Days 1-12
ii. Estrogen predominates –
1. Pulsatile GnRH from the hypothalamus increased FSH & LH from the
pituitary gland to stimulate the ovaries
2. Ovaries:
a. Increased FSH follicle & egg maturation in the ovary
b. Increased LH stimulates maturing follicle to produce estrogen
3. Endometrium (Uterus):
a. Estrogen “builds up” the endometrium (proliferative)
4. Causes negative feedback in HPO system –
a. Increasing levels of estrogen inhibits hypothalamic GnRH release as
well as pituitary release of LH & FSH (so no new follicles start maturing)
, b. Ovulation
i. Days 12-14
ii. Increased estrogen
being released from
the mature follicle
switches from
negative to positive
feedback on GnRH
mutual increases in
estrogen, FSH & LH
iii. Sudden LH surge
causes ovulation (egg
release)
c. Phase 2: Luteal (Secretory)
i. Days 14-28
ii. Progesterone
predominates –
1. LH surge also
causes the
ruptured
follicle to
become the
corpus luteum
a.
Secretes
progesterone & estrogen to maintain the endometrial lining
b. Estrogen & progesterone switches back to negative feedback
iii. If pregnancy occurs:
1. The blastocyst (maturing zygote) keeps the corpus luteum functional
(secreting estrogen & progesterone, which keeps the endometrium from
sloughing & prepares it for implantation)
d. Menstruation (during 1st days of Follicular Phase)
i. If the egg is not fertilized, the corpus luteum soon deteriorates (causing a fall in
progesterone & estrogen levels)
1. Endometrium is no longer maintained & sloughs off menstruation
2. Negative feedback on GnRH subsides, causing increased pulsatile GnRH
secretion
a. This leads to increased FSH & LH, which starts the follicle maturation
process all over again
6) PMDD (see below)
7) PMS
a. PMS = cluster of physical, behavioral & mood changes w/ cyclical occurrence during the
luteal phase of the menstrual cycle
b. PMDD = severe PMS w/ functional impairment where anger, irritability & internal tension are
prominent (DSM V diagnostic criteria)
c. S/S:
i. Physical: abdominal bloating & fatigue (MC), breast swelling or pain, weight gain, HA,
changes in bowel habits, muscle or joint pain
ii. Emotional: irritability (MC), tension, depression, anxiety, hostility, libido changes
iii. Behavioral: food cravings, poor concentration, noise sensitivity, loss of motor senses
d. Dx:
i. Sx occurring 1-2 weeks before menses (luteal phase), relieved w/in 2-3 days of the
onset of menses + at least 7 symptom free days during the follicular phase
ii. Pt should record a diary of sx for >2 cycles
e. Management:
i. Lifestyle Mods – stress reduction & exercise most beneficial; caffeine, ETOH, cigarette
& salt reduction; NSAIDs, Vit B6 & E
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