Menstruation
Normal physiology
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The main players in the female reproductive cycle are the pituitary, ovaries, and the uterus. Their activities are closely coordinated
each month. Each month one or other ovary releases a single egg in an event called ovulation.
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It is brought about by a series of complex interactions between the pituitary gland, uterus, and the ovaries. The pituitary gland is
under the control by a small section/ layer of the brain known as the hypothalamus.
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A new menstrual cycle begins when the nerve cells of the hypothalamus secrete a hormone called gonadotropin-releasing
hormone GnRH into the network of blood vessels that surround the pituitary gland. Stimulated by pulses of gonadotropin
releasing cells, the pituitary gland secretes another hormone called follicle-stimulating hormone or FSH.
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FSH travels in the bloodstream reaching the ovaries where it stimulates the formation and growth of an ovarian follicle on one or
other ovary the follicle consist of an egg and number of surrounding cells that secrete estrogen hormones and fluid. FSH helps the
egg to mature and prepare it for release.
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As the follicle matures the hypothalamus increases secretion of a GNRH. This in turn stimulates the pituitary to secrete a second
hormone which acts on the ovary this is luteinizing hormone or LH.
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Toward the middle of the cycle there is a sudden increase in blood level of LH (after 2-3 days of high estradiol it is released) this
acts as the trigger for ovulation. Within minutes of its release it is guided by suction by the fringed opening by the outer end of the
fallopian tube starting on its 5-6 day journey to the uterus via the Fallopian tube.
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After the follicle ruptures it is converted into a yellow body known as the corpus luteum. Cells of the corpus luteum secrete a
hormone called progesterone, which brings about important changes in the lining of the uterus. Preparing it for possible
pregnancy. In fact the lining of the uterus known as the endometrium undergoes changes in response to hormone levels during the
cycle.
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In the first half of the cycle known as the follicular phase the developing follicle secretes increasing amounts of estrogen hormone,
which encourages regeneration of the endometrium. After ovulation there are important changes in the endometrium aimed at
making it suitable to receive a fertilized egg. These changes are brought about by a secretion of progesterone from the corpus
luteum.
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The secretion of progesterone is maintained for several days but if the egg is not fertilized in that time the corpus luteum whither,
and falling levels of progesterone and estrogen trigger the shedding of the uterine lining as the menstrual flow. The cycle then
starts again, but if the egg is fertilized no menstruation occurs as a corpus luteum continues to function secreting progesterone
during the first three months of pregnancy. There after, numerous changes occur to support the developing embryo.
Treatment- Progesterone is the most important hormone for implantation. It stops proliferation/ prevents hyperplasia (anti-mitotic). It
also causes the glands in the lining of the endometrium to secrete mucus.
Etc.
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Duration of menstruation ranges 2-7 days. Average is 4 days (4+/-2 days).
Cycle is 28 days +/- 7 days
21 days= Polymenorrhea. <21 days then the cycles tend to be anovular and are associated with dysfunctional uterine bleeding
35 days= Oligomenorrhea
Mean blood loss is 40ml+/- 20ml. blood loss >80 ml (menorrhagia/ hyper menorrhea) per cycle is abnormal and frequently
produces anemia.
Average loss of Fe in menses is 13 mg.
Dysfunctional uterine bleeding (DUB)
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Etiology-A sub category of abnormal uterine bleeding. AUB is organic in origin (commonly fibroid tumors, uterine polyps, or
systemic disease) or a problem that is hormonal in origin (known as DUB). DUB is irregular uterine bleeding that occurs in the
absence of a recognizable pelvic pathology, general medical disease, or pregnancy (organic etiology). DUB reflects a disruption in
the normal cyclic pattern of ovulatory hormonal stimulation to the endometrial lining. Bleeding is unpredictable and can be light,
heavy, prolonged, frequent or random.
o
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DUB most commonly occurs when the ovaries do not release an egg. The changes in hormone levels cause your period to
be later or earlier and sometimes heavier than normal. Anovulatory >ovulatory and polycystic ovarian syndrome is the
most common etiology for anovulatory. Ovulatory although less common is a functionality of progesterone withdrawal.
Signs/ Symptoms Bleeding/ spotting from vagina between periods
 Periods that occur less than 28 days apart (MC) or more than 35 days apart
 Time between periods changes each month
 Heavier bleeding (passing clots, soaking through sanitary pad or tampon every hour for 2-3 hr in a row/10 a day
 Bleeding lasts for more days than normal or for more than 7 days
 Others caused from variation in hormones (hirsutism, hot flashes, mood swings, tenderness and dryness of the vagina)
Labs/procedures- besides pelvic and Pap smear.
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CBC
Serum/urine pregnancy test- rule out pregnancy first!
Blood clotting profile-PT/PTT
Hormone tests- FSH, LH, androgen levels, prolactin, progesterone
Pregnancy test
Thyroid function tests-TSH, free T3/T4, thyroid antibody
Possibly (Biopsy-cancer, pre-cancer, or infection), Hysteroscopy, transvaginal Ultrasound
Treatment- If close to first period and young then not treated unless very severe such as excessive blood loss/anemia. The goal of tx
however is to control the menstrual cycle
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Birth control pills or progesterone only pills
Intrauterine device that releases the hormone progestin
Ibuprofen or naproxen taken just before the period starts
Iron supplements for women with anemia
If continue to want children may give meds to stimulate ovulation. If pt no longer wants children may consider
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Endometrial ablation or resection to remove the lining of the uterus (preoperative endometrial biopsy to rule out cancer should be
done prior to)
Hysterectomy (absolute cure)
Dilatation and curettage to remove polyps and diagnose certain conditions.
Complications-infertility, severe anemia, increased risk of endometrial cancer
Amenorrhea- The absence of menstruation (monthly period).
Primary- when a women has not yet started her monthly periods
and she has gone through other normal changes that occur during
puberty and is older than 15. Primary and secondary are same but differ in time.
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Etiology Most girls begin menstruating between ages of 9 and 18, with an average of 12. Primary amenorrhea typically occurs
when a girl is older than 15, if she has gone through other normal changes that occur during pregnancy. Primary amenorrhea may
even occur with or without other signs of puberty.
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Poorly formed genital organs-Narrow or blockage of cervix, imperforate hymen, missing uterus or vagina, vaginal septum.
Hormonal problems-changes occur to brain where hormones are controlled to manage the menstrual cycle. The ovaries
are not working properly .
Any above problem may be due to- anorexia, chronic illness (CF/ heart dz), genital disorders, infections that occur in the
womb or after birth, other birth defects, poor nutrition, tumors.
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Blood test/labs-estradiol, FSH, LH, prolactin, TSH, T3, and T4. Others: 17 hydroxyprogesterone, chromosome analysis, head
CT/MRI scan, pelvic ultrasound, serum progesterone.
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Treatment-Depends on the cause of the missing period. Primary amenorrhea caused by birth defects may require medications
(hormones) surgery, or both.
o If the amenorrhea is caused by a tumor in the brain (pituitary tumor)
 Meds can shrink tumor
 Surgery to remove it
 Radiation therapy is last resort.
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If systemic dz, tx may resolve amenorrhea
If amenorrhea is due to anorexia or excessive exercise, with proper return to weight and less exercise menorrhea will
return to normal.
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If menstruation can not be obtained, medicines can sometimes create a menstrual-like situation (pseudomenstruation).
Can help against osteoporosis as well.
Estrogen/ progesterone combinations are the mainstay of tx for hormonal imbalance. CMDT has a whole list of them.
SecondarySecondary amenorrhea occurs when a woman who has been having normal menstrual cycles stops getting her periods for 6 or more
months.
Women who are pregnant, breastfeeding, or in menopause are not considered to have secondary amenorrhea.
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Etiology
Women who are taking birth control pills or who receive hormone shots such as Depo-Provera may not have any monthly
bleeding. When they stop taking these hormones, their periods may not return for more than 6 months.
You are more likely to have amenorrhea if you:
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Are obese
Exercise too much and for long periods of time
Have very low body fat (less than 15% - 17%)
Have severe anxiety or emotional distress
Lose a lot of weight suddenly (such as with strict or extreme diets or after gastric bypass)
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Other etiology:
 Brain (pituitary) tumors
 Chemotherapy drugs for cancer
 Drugs used to treat schizo or psychosis
 Overactive thyroid
 PCOS
 Reduced function of the ovaries
Procedures such as a dilation and curettage can lead to scar tissue formation that may cause a woman to stop menstruating. This is
called Ashermans syndrome. Scarring may also be caused by some severe pelvic infections.
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Signs/ Symptoms
In addition to having no menstrual periods, other symptoms can include:
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Breast size changes
Weight gain/loss
Discharge from the breast (galactorrhea) or change in breast size
Increased hair growth in a "male" pattern (hirsutism) and acne
Vaginal dryness
Voice changes
If amenorrhea is caused by a pituitary tumor, there may be other symptoms related to the tumor, such as vision loss and headache.
Exams and Tests
A physical exam and pelvic exam must be done to check for pregnancy. A pregnancy test will be done.
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Blood tests may be done to check hormone levels, including:
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Estradiol level
(FSH level)
(LH level)
Prolactin level
Serum hormone levels such as testosterone levels
Thyroid stimulating hormone (TSH)
Other tests that may be performed include:
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CT scan or MRI scan of the head to look for tumors
Biopsy of the lining of the uterus
Genetic testing
Ultrasound of the pelvis or hysterosonogram
Treatment
Treatment depends on the cause of the amenorrhea. Normal monthly periods usually return after the condition is treated.
A lack of menstrual period due to obesity, vigorous exercise, or weight loss may respond to a change in exercise routine or weight
control.
Dysmenorrhea
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Primary dysmenorrhea- associated with menstrual cycles in the absence of pathologic findings. Begins 1-2 after menarche onset.
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Signs/ symptoms-Primary dysmenorrhea is low, midline, wave-like, cramping pelvic pain that radiates to the back or
inner thighs. Cramps may last a few days and are associated with nausea, diarrhea, headache, and flushing. The pain is
caused by uterine vasoconstriction, anoxia, and sustained contractions mediated by prostaglandins.
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TX- NSAIDS (Ibuprofen, ketoprofen, mefenamic acid, naproxen). Should start medication 1-2 days before expected menses.
Symptom suppression is easily obtained through the use of oral contraceptives, depot-medroxyprogesterone acetate, or
the levonorgestrel releasing IUD.
 Continuous use of oral contraceptives can be used to suppress menstruation completely. If women do not wish to
use hormonal contraceptives, they may use other therapies such as local heat, thiamine 100mg/d orally, Vit E 200
units/d orally for 2 days prior and first 3 days of menses, or the use of a TENS unit.
Secondary dysmenorrhea- menstrual pain for which an organic cause exists. Often associated with endometriosis or uterine
fibroids. Usually begins way after menarche in the 3-4th decade of life. Hx/ PE may also suggest PID, adenomyosis, myoma, IUD
use, cervical stenosis with obstruction, or blind uterine horn (rare).
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DX-Obtain cervical cultures to rule out infection. Pelvic imaging can detect fibroids submucosal myomas, or adenomyosis,
Cervical stenosis may result from induced abortion. Laprascopy can be used to dx endometriosis or other abnormalities
not visualized by imaging.
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TX- NSAIDs and oral contraceptives may give relief, particularly in endometriosis. Danazol and GnRH agonists are
effective in the treatment of endometriosis, although use is limited by cost or side effects. Adenomyosis may respond to the
same effective hormonal tx as endometriosis, levonogestrol releasing intrauterine system, or uterine artery embolization,
but hysterectomy remains the definitive tx of choice if the women is at the completion of childbearing.
Premenstrual syndrome (premenstrual tension)
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Definition-A recurrent variable cluster of troublesome physical and emotional symptoms that develop 7-14 days before the onset
of menses and subside when menstruation occurs. Occurs in 50% of those premenstrual women ages 25-40 and are severe in
some cases.
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Signs/Symptoms-bloating, breast pain, ankle swelling, sense of increased weight, skin disorders, irritability, aggressiveness,
depression, inability to concentrate, libido change, lethargy, and food changes. If mood or emotional symptoms predominate on
top of physical symptoms it is termed premenstrual dysphoric disorder PMDD. The pathogenesis of PMS/PMDD is still uncertain.
Current tx is empiric.
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TX- Support for both the patients’ emotional and physical distress. Includes:
 Careful eval of pt
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Pt keeping a daily diary of symptoms to rule out if its depression or other emotional problems
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Advise lifestyle habits: increased aerobic exercise and proper nutritional diet.
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When physical symptoms predominate, spironolactone 100mg orally daily during the luteal phase, is effective for reduction
of bloating and breast tenderness. Oral contraceptive or injectable progestin depot medroxyprogesterone acetate will
decrease breast pain and cramping. NSAIDs will reduce a number of symptoms.
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When mood disorders predominate, several serotonin reuptake inhibitors (fluoxetine 20mg orally) have been shown to be
effective in relieving tension, irritability, and dysphoria.
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When the above regimens are not effective, ovarian function can be suppressed with high dose progestin (20-30mg oral
medroxyprogesterone acetate or 150 mg depot medroxyprogesterone every 3 months or GnRH agonist with add back therapy
such as conjugated equine estrogen 0.625 orally daily with medroxyprogesterone acetate, 2.5-5mg orally.
Menopausal syndrome- Cessation of menses due to aging or to bilateral oophorectomy. Elevation of FSH and LH levels. Hot
flushes and night sweats. Decreased vaginal lubrication; thinned vaginal mucosa with or without dyspareunia.
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Etiology- The term menopause denotes the final cessation of menstruation, either as a normal part of aging or as the result of
surgical removal of both ovaries. It denotes a 1-3 year period during which a woman adjusts to a diminishing and then absent
menstrual flow and the physiologic changes that may be associated-hot flushes, night sweats, and vaginal dryness. The average
age at menopause is 51. Premature menopause is defined as ovarian failure and menstrual cessation before age 40.
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Signs and symptoms Cessation of menstruation-Menstrual cycles generally become irregular as menopause approaches. Anovular cycles occur
more often. Menstrual flow usually diminishes in amount owing to decreased estrogen secretion, resulting in less abundant
endothelial growth. Cycles become longer with missed periods. When no bleeding has occurred for 1 year, the menopausal
transition can be said to have occurred. Any bleeding after this time warrants investigation by endometrial curettage or
aspiration to rule out endometrial cancer.
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Hot flushes- Occur as a result of the decrease in ovarian hormones. Flushes can begin before the cessation of menses. They
typically persist for 2-3 years and are more severe in women who undergo surgical menopause. Occurring at night, they often
cause sweating and insomnia and result in fatigue on the following day.
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Vaginal atrophy-With decreased estrogen secretion thinning of the vaginal mucosa and decreased vaginal lubrication occur
and may lead to dyspareunia. On PE there is a pale, smooth vaginal mucosa and a small cervix and uterus. The ovaries are not
normally palpable after menopause.
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Osteoporosis- May occur as a late sequelae of menopause.
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Labs- Serum FSH and LH levels are elevated.
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Treatment
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Natural menopause- Education and support from health providers, midlife discussion groups, and reading material will help
most women having difficulty adjusting to menopause.
o Vasomotor response-For women with moderate to severe vasomotor symptoms, estrogen or estrogen/preogestin
regimens are the most effective approach to symptom relief. If the patient has had a hysterectomy, a progestin need
not be used.
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Vaginal atrophy- Due to a lack of estrogen. Vaginal suppositories, patches, rings or pills work well.
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Osteoporosis-Women should ingest at least 800mg of calcium daily throughout life. In addition 1200 mg of elemental
calcium should be taken as a supplement at the time of the menopause and thereafter; calcium supplements should be
taken with meals to increase to increase their absorption. Vit D 800 IU/d is necessary to enhance the calcium
absorption and maintain bone mass.
Risk of hormone therapy- Coronary heart events, increased risk of cognitive decline, strokes, thromboembolic disease,
gallstones, breast cancer along with increased mortality of it.
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Women who have been receiving long term estrogen/progestin hormonal replacement therapy in the absence of
complications should be encouraged to stop, especially if they do not have menopausal symptoms.
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The risks appear to be lower in women starting therapy at the time of menopause and higher in previously untreated
women starting therapy long after menopause. Therapy should be individualized as the risk-benefit profile varies with age
and individual risk factors.
Surgical menopause- Abrupt hormonal decrease resulting from oophorectomy generally results in severe vasomotor
symptoms and rapid onset of dyspareunia and osteoporosis unless treated. If not contraindicated, estrogen replacement is
generally started immediately after surgery. Conjugated estrogen or estrogen sulfate at 1.25mg orally or estradiol at 2 mg
orally given for 25 days of each month. After age 45-50 years this dose can be tapered to 0.625 mg of conjugated estrogens or
equivalent.
Contraception
Oral contraceptive –MC primary method used in women, # 2 is female sterilization and #3 is condom use.
1. Combined- The primary mode of action is suppression of ovulation. Pills can be initially started on the first day of the menstrual
cycle or any day during the cycle. But on any other day during the cycle a back up method should be used. If an active pill is missed
and no intercourse has taken place in past 5 days, should take two pills immediately and a backup method should be used for 7
days. If intercourse occurred in the previous 5 days, emergency contraception should be used immediately, and the pills restarted
the following day. The Estrogen/ progesterone combination prevents ovulation by interrupting the feedback loop of sex hormone
production. This decreases the amount of endometrial proliferation and thickens cervical mucous. The most important effect is to
prevent ovulation by suppression of hypothalamic gonadotropin releasing factors (prevents pituitary secretion of FSH and LH).
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Benefits- Lighter menses, reduced anemia, dysmennorhea unlikely, functioning ovarian cysts, ovarian and endometrial
cancer, salpingitis and ectopic pregnancy are all less likely. Acne is usually improved. The frequency of developing myomas is
lower. There is a beneficial effect on bone mass. The predictability of menstrual cycles is favorable as well.
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Monophasic- A constant dose of Estrogen (ethanyl estradiol or mestranol) is given with a constant dose of progesterone,
which aims for a less risk of breakthrough bleeding.
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Triphasic- developed to minimize the amount of progesterone dose often combined with variable estrogen dose (more risk
for breakthrough bleeding).
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Contraindications- at increased risk for myocardial infarction, thromboembolic diseae, cerebrovascular disease in those
taking estrogen dose 50mcg or grater. Non-estrogen contraceptive is warranted in increased hypercoagulable disease
states(DVT, MI, stroke).
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Adverse effects- Contraceptives may worsen depression, cause hypertension with extended use, elude to severe headaches,
and impair the quantity and quality of breast milk. Nausea and vomiting may occur during the first few months of pill use.
Weight gain may occur as well. Fatigue and decreased libido can occur as well as chloasma (tan or dark brown skin
discoloration).
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Drug-drug interactions- Rifampin is the only antibiotic proven to decrease serum ethinyl estradiol and progestrin levels in
women taking oral contraceptives (including Ortho Evra and Nuva Ring) a nonhormonal contraceptive method is
recommended in these women. In spite of other anecdotal reports of oral contraceptive failure, other antibiotics have not been
proven to affect the pharmacokinetics of ethinyl estradiol. For women taking ABX other than rifampin with oral contraception,
back-up contraception is not required.
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Anticonvulsants-including phenytoin, carbamazepine, barbituates, primidone, topiramate, or oxcarbazepine should
not use hormonal contraception (with the exception of depo-medroxyprogesterone acetate.
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Antiretroviral-especially ritonavir may significantly reduce the efficacy of combined oral contraceptives.
Contraceptives may also increase the toxicity of the retroviral.
2. Transdermal/ Mucosal methods- The patch and ring avoid hepatic first pass effect. Wathc for increased risk of
thromboembolism since the lower overall dos 15-20mcg of ethinyl estradiol has higher systemic absorption these ways.
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Ortho Evra- Patch that delivers 20mcg of ethinyl estradiol and 150 mcg of norelgestromin daily
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Nuva Ring- delivers 15 mcg ethinyl estradiol and 120mcg of etonogestrel daily.
3. Progesterone only methods Mini-pill-Noreyhindrone. Safe to use during lactation. Does not reliably suppress ovulation but promote cervical mucous
thickness and decrease in endometrial proliferation to help prevent implantation. Less effective than combination.
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Injectable- Depo-provera-depo Sub-Q provera 104 (Depo-Medroxyprogesterone Acetate). Dosed every 90 days. Usually
amenorrhea 20% risk for spotting as well. Usually results in a longer interval to resumption of normal fertility >90% in 2
years, 50% in 6-12 months. Bone density loss- likely reversible.
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Implantable- Nexplanon/ Implanon (etonogestrel) 68mg used long term up to 3 years. Subcutaneous placement and removalA newer rod vinyl polymer compared to the usual silicone.
4. Intra Uterine Device (IUD)-Implantable chemical eluting device that prevents pregnancy by prevention of fertilization (acts as a
spermicidal, disrupts the intra-uterine lining, thickening of cervical mucous, and inhibition of ovulation). There is an increased risk
for PID if pt develops STD. There is also an increased risk of ectopic pregnancy if pregnancy occurs. No decrease in fertility after
removal.
 Mirena- Levonogestrel releasing IUD- Low doses of progesterone with some systemic absorptiom. Decreases menstrual
bleeding nad lasts up to 5 years.
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Paragard copper device- causes uterus to release leukocytes and prostaglandins which are spermicidal and make the uterine
lining inhospitable. Associated with increased menstrual bleeding but is hormone free and effective up to 10 years.
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Contraindications- Pregnancy, acute PID, postpartum endometriosis or infected abortion in the past 3 months, noted or
suspected uterine or cervical malignancy, genital bleeding of unknown origin.
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Complications- Increased PID risk leading to infertility if infection occurs, risk of perforation during insertion, wilson’s dz,
copper allergy.
5. Barrier methods- perfect use is important for good efficacy.
 Diaphragm- latex flecible dome placed over cervix used with spermicidal jelly
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Cervical cap- smaller tighter fitting latex dome
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Sponge impregnated with nonoxynol-9 spermicide- single use. Failure rates re similar to the cap but ok for repeated use up to
24 hrs. There are issues with timing, failure rates, and risk for toxic shock; no STD protection.
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Male condoms- perfect use with spermicide close to 95%. No spermicide with animal skin condoms.. Male condoms are cheap
and affordable, protct from many sexually transmitted infections making them most used barrier device.
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Female condoms- not widely available and more difficult to use.
6. Sterilization Femaleo Tubal ligation- excision to interrupt passage of egg through the fallopian tubes to the uterus
o Essure-steel/nickel coil, trans cervical placement into tubes, use backup method x 3 months and confirm tubal
blockage via hysterosalpingogram. Permanent with some success at reversal. There is some risk for ectopic pregnancy
and the essure may be done without general anesthesia. Essure is a highly effective method of contraception without
any long term hormone exposure/ drug interaction potential.
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Maleo Vasectomy-surgical ligation/ excision of the vas deferens. 1-3 month back up method to ensure no residual sperm.
Contraceptive based on awareness of fertile periods
Calendar/ Rhythm method- reliable if regular and predictable menstruation. It requires periods of abstinence. There is perfect use
with effectiveness comparable to barrier methods.
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Symptothermal method- daily measurement of basal body temperature. A slight decrease indicates ovulation.
Emergency contraception-to prevent pregnancy after unprotected intercourse within 72 hours. Plan B. Next choice- Levonogestrel.
Works by inhibiting or delaying ovulation, disruption of endometrial lining. If menses is delayed by 3 weeks or more assume pregnancy.
Use barrier method or abstinence until end of cycle. IUD insertion within 5 days of unprotected sex results in effective contraception. RU
486(mifepristone) usually is used as abortive therapy.
Endometriosis-The aberrant growth of endometrial tissues outside the lining of the uterus. Most commonly found in the
dependent parts of the pelvis (ie. Fallopian tubes, ovaries or the tissue lining your pelvis-perimetrium or peritoneum). However, it can
appear anywhere within the abdominal cavity.9-10% of women. MC in high achieving “type A”, nulliparous women.30-40% of infertile
women will have endometriosis. Some pt’s have severe dz where the endometriosis and adhesions grow like KUDZU.
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Hypothesis-The cause of endometriosis remains unknown. Retrograde menstruation (most widely accepted)-menstrual blood
containing endometrial cells flows back through the fallopian tubes, takes root and grows outside the endometrium. Lymphatics
and vascular metastasis- the bloodstream is responsible for carrying endometrial cells to other sites in the body. Genetic
predisposition-familial distribution. Iatrogenic dissemination-during surgery endometrial tissue contaminates portions of the
abdomen.
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Pathophysiology-ectopic endometrial tissue responds to normal hormonal stimulation (but more unpredictably). The
endometrial cells respond to estrogen and progesterone w/ proliferation and secretion. During menstruation, the ectopic tissue
bleeds, which causes inflammation of the surrounding tissues. The inflammation causes fibrosis, leading to adhesions and produce
pain and infertility.
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Signs & symptoms-pelvic pain (dysmenorrhea) pain normally begins 2-7 days before menses peaks and may increase in severity
until menstrual flow slackens. Severity of pain is NOT indicative of extent of dz. Abnormal uterine bleeding, and infertility
(main three) others- dyspareunia, rectal pain w/ bleeding (colonic), suprapubic pain and hematuria (bladder).
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PE- Pelvic examination-difficult to ID and palpate endometrial tissue but secondary cysts may be located. May also note uterine
retroversion w/ decreased uterine mobility. Cervical motion tenderness and/ or adnexal mass or tenderness. Most women w/
endo have a normal pelvic US. Transvaginal US-does not obtain the dx however it can identify cystic structures, CT/MRI of limited
value as well. Laparoscopy-The only definitive way to dx endometriosis is via laparoscopy or laparotomy. Direct visualization of
endometrial tissue confirms the dx; bx help as well.
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Management and TX of endometriosis-2 main goals of tx-Improvement of pain, to promote fertility.
o Medical management-can help decrease pain but may not increase likelihood of pregnancy. Most therapies are designed to
inhibit ovulation over 4-9 months and lower the hormone levels thus preventing cyclic stimulation of endometionic
implants and inducing atrophy.
 Pain meds-Ibuprofen/ NSAID’s
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Hormonal therapy-An androgen, such as danazol (danocrine) to help suppress menstruation by inhibiting
LH/FSH. Oral/ injectable contraception (for those w/ minimal or mild sx’s). Gonadotropin releasing
hormone(GnRH) Agonists (seems counterintuitive since they overstimulate LH and FSH receptors of the anterior
pituitary. But over stimulation leads to a down regulation of these receptors, resulting in a decrease in LH/FSH
secretion- Leuprolide acetate 3.75mg IM (Lupron) once monthly for up to 6 months(one option).
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Surgical-effective in both reducing pain and promoting fertility.conservative surgery( LAP exporation)removal of implanted endometrial tissue, scar tissue, and adhesions. (total hysterectomy- including both
ovaries(TAH w/ BSO) definitive tx option for those w/ severe pain and no longer desire childbearing.
Uterine Fibroids-AKA fibromyomas, leiomyomas, or myomas.The most common benign neoplasm of the female genital tract.
Benign growths that occur on the uterus- develop from the uterine myometrium and lead to a round, firm, and often multiple uterine
tumor composed of smooth muscle and connective tissue.
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S&S- Asymptomatic to significantly symptomatic, heavy prolonged/ irregular menstrual bleeding (anemia), dyspareunia,
infertility, pelvic pain or pressure, urinary incontinence, Acute ABD/pelvic pain-out grows the available blood supply or ruptures.
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Etiology-Genetic alterations-many fibroids contain alterations in genes that code for uterine muscle cells. Hormonal-excess in
estrogen and progesterone. Additional substances-insulin like growth factor may be related to fibroid growth.
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DX-MC found during routine pelvic exam- irregularly shaped uterus or masses, always check serum pregnancy.
Transabd/transvaginal US-confirms the dx and determine location and size of fibroids. Hysterosonography-TVUS w/ saline to
expand the uterine cavity. Hysteroscopy-Easily performed during an office visit to visualize the walls of the uterus and fallopian
tubes.
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Management/Tx- Identification, awareness, and watchful waiting.
 GnRH Analogs-Depo leuprolide 3.75 mg IM once monthly can be used preoperatively for 3-4 months to induce reversible
hypogonadism, which temporarily reduces the size of myoma, suppresses further growth, and reduces surrounding
vascularity prior to surgical intervention. GnRH agonist rapidly suppresses pituitary gonadotropin release, which leads to a
profound hypoestrogenemia, and a 50% reduction in uterine volume.

Oral/ injectable contraception-typical hormonal changes shrinks fibroid tissue.

Surgical-Myomectomy-removal of fibroids more commonly indicated for pt’s of childbearing years. Hysterectomy.
Ovarian cyst-Usually a fluid filled sac on an ovarian structure. Common in reproductive years. Often related to ovulation. Usually
unilateral. Most cysts resolve spontaneously over the next few menstrual cycles.

Follicular cysts-mature follicle that fails to rupture

Corpus luteum cyst-result from bleeding into center of corpus luteum.

Theca-lutein cysts-associated w/ elevated levels of chorionic gonadotropin. (ie. Choriocarcinoma, clomiphene therapy,
hydatiform mole or rarely w/ normal pregnancy.
S&S-may be asymptomatic, change in menstrual cycle, pelvic pain, dyspareunia, abnormal vaginal bleeding. Possible adnexal mass on
bimanual exam. BEWARE!-that a ruptured cyst w/ bleeding can present as an acute abdomen w/ decreased systolic bp.
Workup/TX for ovarian cysts-Check b-HCG for pregos, Pelvic US for acute processes. If adnexal mass (cystic structure) has not resolved
in 6-8 weeks, then evaluate for malignancy via laparoscopic cystectomy. CT abdomen/ pelvis to look for metastasis or possible primary
lesion.
Urinary Incontinence
Prevalence increases with age. More
Consequences of UI



Social isolation
Depression
Rash/ decubitus ulcer
Falls/ fractures
debilitated the greater the likelihood of incontinence.



Infections
Increased likelihood of
admission
Caregiver stress
Bladder physiology-Age related changes





Decreased bladder capacity
Increased involuntary bladder contractions
Increased post void residual
Increased nocturia
Gender-related change
Neurology of Urination



Parasympathetic tone (cholinergic) causes detrusor constriction and bladder emptying. Pelvic nerves S2-S4.
Sympathetic tone (adrenergic) facilitates storage of urine. Beta-adrenergic receptors in detrusor, alpha adrenergic in the internal
sphincter. Hypogastric nerve Tll-L2
Somatic (voluntary control) via the pudendal nerve
Continence requirements
Mobility, Manual dexterity, cognitive ability to want to go to the bathroom, motivation to stay dry, Balance and coordination (muscles and
nerves): Bladder smooth muscle and urethral sphincter mechanisms, Sympathetic & parasympathetic nervous systems.
#’s to remember
Abnormal PVR>200, normal void 80% of bladder volume, Capacity 300-600ml, First urge 150cc, normal urine velocity 20-25ml/sec,
empty bladder within 20 seconds. PVR should be less than 50 cc.
Reversible causes (transient)-DIAPPERS
Delirium (transition inhibition), Infection, atrophic vaginitis, pharmacy, psychological, excess urine output, restricted activity (functional
incompetence), stool impaction.
Serious causes of incontinence
Lesions of the brain and spinal cord, cancer of the bladder or prostate, bladder stones, hydronephrosis.
Established causes

Urge incontinence (Detrusor overactive)-medical hx (leakage w/out stress maneuvers or urinary retention, preceded by intense
urge to urinate), Little PVR increased contraction on refilling.

Overflow incontinenceo Detrusor underactive- Least common. Strain to void, low output, incomplete emptying, nocturia.Causes: LMN problem/
damage, autonomic neuropathy, medications, or fibrosis of detrusor, remember meds, increased PVR.
o
Outlet obstructive-mechanical obstruction-prostate, urethral stricture, cystocele. Symptoms: hesitancy, frequency,
increased PVR.

Stress incontinence (outlet incompetence)-F>M. secondary to pelvic floor laxity or urethral sphincter dysfunction. Primary cause
(males): radical prostatectomy. Symptoms: dribble, aggravated by increased intra-abdominal pressure. Normal PVR.

Mixed incontinence-Characteristics of urgency and stress incontinence.
Evaluation
HX-Sx’s, bladder or voiding diary, fluid intake, Meds, use of pads or protective devices, previous tx’s, expectations

PE-rectal and pelvic exams.
TX general principles-DX-reversible cause? Remember: mixed incontinence, management of comorbidities. Consider social history.
Incontinence tx’s
Behavioral approacheso For cognitive intact-Pelvic floor exercises (kiegel), bladder training, Biofeedback, electrical stimulation.
o For cognitively impaired-Habit training, timed voiding, prompted voiding, improved toilet access, manage fluid and diet,
proper undergarments.

Pharmacological approaches
o Anticholinergics/ Antimuscarinics agents: Promote bladder relaxation, decrease urgency with behavioral therapy.







Oxybutinin- Ditropan
Tolterodine- Detrol
Fesoterodine
Trospium-Sanctura
Solifenacin- Vesicare
Darifenacin- Enablex
o
Alpha adrenergic agonists-Mechanism: relax smooth muscle, decrease urine flow resistance.
 Selective a1 agents (Prazosin, Alfuzosin-uroxactral)
 Long acting a1 agents (terazosin-hytrin, doxazosin-cardura)
 Long-acting a1a subtype selective agents (tamsulosin-flomax)
o
o
o
Estrogens: little/ no evidence to support use.
Serotoninergic/ norepinephrine drugs
5-alpha-reductase inhibitors
 Finasteride- proscar
 Dutasteride- 34vodart
Specific tx’s:
o Detrusor overactive- bedside commode, bladder training, (Oxybutinin, imipramine, dicyclomine, propantheline,
estrogen)
o Detrusor underactive- intermittent catheterization, Bethanacol (weak evidence), Foley catheter.
TX strategies



Urge-bladder training, meds, surgery, sacral nerve stimulation.
Stress:-kegel’s and bladder training, meds, surgical procedures
Overflow-intermittent, indwelling, or supra pubic catheter
Misc-pessaries, vaginal cones, periurethral injections, biofeedback, compression devices.


Indications for chronic indwelling catheter in long-term care-urinary retention, short term care, palliative care, patient
preference
Referral to urology-uncertain dx, tx failure, hematuria w/out infection, comorbidities.
Domestic violence- Intimate partner violence

Intimate partner violence is a pattern of abusive behavior by a person who is in some type of intimate relationship with the victim.

The abuse can be physical sexual or emotional and can include economic deprivation. IPV is common but is often not diagnosed in
part because patience try to hide the abuse.

Rates are higher when measured an emergency departments.

Risk factors for abuse include being young, being pregnant, being single, divorced, or separated, alcohol or drug abuse in the
victim or the partner, smoking, and being poor.
Evaluation

Clinicians must be alert to clues that suggested abuse including an explanation of the injuries that do not fit with what is being
seen. These may include frequent visits to the emergency department and somatic complaints such as chronic headache,
abdominal pain, and fatigue.

The patient may be vague about some of her symptoms and May avoid Eye contact. It is critical that the patient has the
opportunity to speak with the clinician alone.

Physical examination often reveals injuries in the central area of the body. As with any situation of expected abuse bruises that are
in various stages of healing may be an important clue. Post dramatic stress disorder, depression anxiety, and alcohol or others
substance-abuse can develop in victims. Somatization is also very common.

Several instruments have been developed to screen for IPV. These include HITS, (hurt insult threatens screen) tool, the woman
abuse screening tool, the partner violence screen, and abuse assessment screen, and the woman's experience with battering scale.

Inclusion of one question in the context of the medical history," Have you ever been hit, kicked, punched her otherwise hurt by
someone within the past year? If so b whom?" Has shown to increase identification of IPV. Women preferred written
questionnaires over face-to-face interview.

Screening for IPV has been advocated by many experts, although no evidence has improved outcomes. The USPSTF has concluded
that there is insufficient evidence to recommend for or against universal screening for IPV, since there is currently no evidence
that screening improves outcomes. However, clinician should remain on High alert for clues to IPV among patients.
Interventions for IPV
Interventions can include encouraging the woman to leave the abusive situation, ensuring that she has a safe place to go, and
counseling so that she can adequately assess her risk of danger and create a plan for safety.
When to refer
Victims should be referred to social services so that they can provide information on local resources. In general, mandatory
reporting of IPV or suspicion of it in adult women who are competent is not required in most states. However, mandatory
reporting by physicians is required in California, Colorado, Kentucky, Mississippi, Ohio, and Rhode Island.
Sexual assault- Women neither secretly want to be raped nor do they expect, encourage, or enjoy rape. Rape is always a terrifying
experience in which most victims fear for their lives. The rapist is usually a hostile man who uses sexual intercourse to terrorize and
humiliate a woman. Knowledge of state laws and collection of evidence requirements are essential for clinicians evaluating possible rape
victims.
General considerations



It is essential that persons treating rape victims recognize the nonconsensual and violent nature of the crime.
95% of rape victims are women and penetration may be vaginal, anal, or oral by the penis hand, or a foreign object.
The assailant may be unknown to the victim or more frequently, may be an acquaintance or even the spouse.
Rape represents an expression of anger, power, and sexuality on the part of the rapist. Consequently, all victims suffer some
psychological aftermath( anxiety disorder, PTSD etc.). Some even acquire sexually transmitted diseases or become pregnant.
Rape trauma syndrome- 2 principle phases

Immediate/acute- Shaking, sobbing, and restless activity lasts a few days to a few weeks. Pt experiences shame, guilt, or anger.

Late/chronic- develop weeks to months later. The lifestyle and work patterns of the individual may change. Sleep disorders or
phobias often develop.
General office procedures
Secure written consent. If police are to be notified, do so, and obtain advice on the preservation and transfer of evidence.

Obtain and record the history in the patients own words. Note the details of the assault and whether the pt is calm, agitated or
confused. Also record whether the patient came directly to the hospital or whether she bathed or changed her clothing.

Have the pt disrobe while standing on a white sheet. Hair, dirt, and leaves, underclothing, and any torn or stained clothing should
be kept as evidence.

Examine the pt, noting any traumatized areas that should be photographed.

Perform a pelvic exam and appropriate laboratory tests as needed (STI’s/Pregnancy etc.).

Transfer clearly labeled evidence directly to the clinical pathologist in charge or to the responsible laboratory technician in the
presence of witnesses so that the rules of evidence will not be breached.
Treatment-

Give analgesics or sedatives if indicated. Give emergent contraception and available antibiotics to prevent against STD’s. Due to
psychological manifestations it is important for the patient along with family and friends have a source of ongoing counseling and
psychological support.

All women who seek care for sexual assault should be referred to a facility that has expertise in the management of victims of
sexual assault and is capable of performing expert forensic examination, if required.
Infertility
A couple is said to be infertile if pregnancy does not result after 1 year of normal sexual activity without contraception.
Initial testing- During the initial interview, the clinician can present an overview of infertility and discuss a plan of study. Separate
private consultations are then conducted, allowing appraisal of psychosexual adjustment without embarrassment or criticism. Pertinent
details must be obtained (prior pregnancies/ STD’s). Pay particular attention to cigarette, alcohol, and recreational drug use in male
fertility. Prescription meds may impair male motility. Scrotal hyperthermia can cause this as well. The gynecologic history should include
menstrual pattern, the use and types of contraceptives, douching, libido, sex techniques, frequency and success of coitus, and correlation
of intercourse with the time of ovulation. General physical and genital examinations are performed on the female partner and a basic lab
panel is obtained. Note that luteal phase serum progesterone above 3ng/ml establishes ovulation. A semen analysis to rule out a male
factor for infertility should be completed. Semen should be examined within 1-2 hours after collection. If the sperm count is abnormal,
further evaluation includes physical examination of the male partner and a search for exposure to environmental and workplace toxins,
alcohol or drug abuse.
Further testing
Intracytoplasmic sperm injection is the treatment option available for sperm deficiencies except for azoospermia(absence of
sperm).

Screening pelvic ultrasound and hysterosalpingography to identify uterine cavity or tubal anomalies should be performed.

Absent or infrequent ovulation requires additional laboratory evaluation.
o Elevated FSH and LH levels indicate ovarian failure causing premature menopause.
o
o
o
Elevated LH levels in the presence of normal FSH levels confirms the presence of polycystic ovaries.
Elevation of prolactin levels suggest a pituitary adenoma.
A markedly elevated FSH on the 3rd day of menses suggests inadequate ovarian reserve. In addition a Clomiphene Citrate
challenge test with measurement of FSH on day 10 after administration from day 5-9 should be completed to determine if
diminished ovarian reserve indicates a need for donor eggs.

Ultrasound monitoring of folliculogenesis may reveal the occurrence of unruptured luteinized follicles.

If all the above testing is normal, the patient is diagnosed with unexplained fertility.
Treatment-Fertility may be restored by treatment of endocrine abnormalities; particularly hypothyroidism or hyperthyroidism ABX tx of
cervicitis may be of value. Microsurgical relief of tubal obstruction due to salpingitis or tubal ligation will reestablish fertility in a number
of cases.

Induction of ovulationo Clomiphene citrate- Stimulates gonadotropin release, especially LH. Consequently plasma estrone and estradiol also rise,
reflecting ovarian follicle maturation. If estradiol rises sufficiently, an LH surge occurs to trigger ovulation. After a normal
period one should give 50 mg of clomiphene orally daily for 5 days. If ovulation does not occur, the dosage is increased to
100 mg daily for five days. If ovulation still does not occur repeat with 150mg then 200mg. Add 10,000 units of chorionic
gonadotropin 7 days after clomiphene.
o
Letrozole- aromatase inhibitor, appears to be as effective as clomiphene for ovulation inductionnin women with PCOS.
Dose 5-7.5 mg daily starting day 3 of menstrual cycle.
o
Bromocriptine- used only if PRL levels are elevated and there is no withdrawal bleeding following progesterone
administration. Initial dose is 2.5 mg orally once daily increased to two or three times daily in increments of 1.25 mg. the
drug is discontinued once pregnancy has occurred.
o
Human menopausal gonadotropin (hMG) or recombinant FSH- indicated in cases of hypogonadotropism and most
other types of anovulation resistant to clomiphene treatment. Refer to infertility specialist.
o
Artificial insemination in Azoospermia- If azoospermia is present, artificial insemination by a donor usually results in
pregnancy, assuming female function is normal. Frozen sperm is currently preferable to fresh (frozen can be held pending
cultures and blood tests).
o
Assisted reproductive technologies-These techniques are complex and require a highly organized team of specialists. All
of the procedures involve ovarian stimulation to produce multiple oocytes, oocyte retrieval and handling oocytes outside
the body. With IVF, the eggs are fertilized in vitro and the embryos transferred to the uterine fundus. In the event of a
multiple gestation pregnancy, a couple may consider selective reduction to avoid the medical issues related to multiple
births. This issue should be discussed with the couple before embryo transfer.
OBGYN
PREGNANCY COMPLICATIONS
Abortion




Spontaneous Abortion: Any loss of fetus < 20 weeks. Occurs in 10-25% of all
pregnancies. (However this is underestimated and it is probably 2/3
miscarry)
1st trimester abortion most likely CHROMOSOMAL and most are evident by
the 12th week.
2nd trimester abortion most likely due to STRUCTURAL cause (Incompetent
Cervix)
Types of Spontaneous Abortions
o Complete: Complete expulsion of products of conception (POC), NO
GESTATIONAL SAC in uterus, OS is CLOSED
o Incomplete: Partial expulsion of POC, some tissue is passed with
blood, OS is OPEN
Inevitable: NO EXPULSION of sac, but there is usually bleeding and
the OS is OPEN.
o Threatened: Vaginal bleeding before 20 weeks, NO tissue is passed,
OS is closed.
o Missed abortion: Retention of the POC, usually no VB, may have
brownish discharge. NO fetal heart tones, sac is irregular, lacunae
from degenerating villi
TX of spontaneous abortion:
o Based on pt preference and diagnosis.
o Complete: Send placenta for pathology report
o Incomplete, blighted ovum, inevitable, missed: Expectant(let patient
miscarry on their own and POC will usually pass); D&C or
Misoprostol. Make sure to monitor for fever or prolonged VB
 Make sure to give Rh neg mothers RhoGAM if there is any
bleeding
o Threatened: Expectant management and pelvic precautions. 50/50
chance of viability
o

2nd trimester abortions
o Present with painless dilation and effacement of Cx
o Fetal membranes bulge & exposed to vaginal flora, trauma Infection
& vaginal discharge common
o Inc. Cx estimated to cause 15% of all 2nd trimester losses
Risk factors of Inc. Cervix:
o
o
o
o
o
Hx of cervical surgery (cone Bx/LEEP or dilation of cervix)
Hx of cervical lacerations with vaginal delivery
Uterine anomalies
Hx of DES exposure (now rare)
Family history of Incompetent cx
TX:
o
o
o
o
o
o
o
o

If pre-viable (<23-24wk) elective TOP or expectant management with
bed rest & pelvic rest
May be a candidate for “rescue cerclage”
Consider cerclage at 13-14 wks in future pregnancies
McDonald Cerclage (@ cervico-vaginal junction most common)
Shirodkar (higher up and buried)
Abdominal (with history of prior failed cerclage)
If dx unclear based on hx, may follow with serial TVUS to assess
cervix q 1-2 wk from 16-24 wk
Placement of cerclage only if clinically indicated
Recurrent Abortions
o Unknown cause in up to 50% of PTs. 3 or more SAb or 2 or more SAb
for women over 35.
Causes: (M/C SLE, Hypothyroidism, or DM)
o
o
o
o
o
Genetic Abnormalities (usually parental; 70% karyotype
abnormality)
Hormonal and Metabolic Disorders
 Thyroid
 DM
 Luteal Phase Defect (corpus luteum doesn’t make
enough Progesterone. Give IVF patient progesterone
until 10wks
Uterine Anomalies – more common in 2nd trimester
 Incompetent cervix
 Asherman’s Syndrome (uterine synechiae)
 Fibroids
Infectious CausesLike if they have a previous septic abortion
(sporadic not recurrent abortions)
Environmental
o
o
 Smoking, ETOH, Organic Solvents
Thrombophilias
 Factor V Leiden, Prothrombin G20210A mutation
 Protein C, s and antithrombin III deficiency
Autoimmune Disorders
 Antiphospholipid antibody syndrome – associated
with SLE and other AI diseases. Suspect if any
thrombotic event or recurrent abortions.
 Thyroid antibodies (anti-thyroglobulin, thyroid
peroxidase antibodies)
 Antinuclear Antibodies (ANA)
 Alloimmune Disorders (NK cells) (placenta is
semiallogenic tissue so may be attacked by maternal
NK cells)
**2/3 of subsequent pregnancies will be normal; most causes of recurrent abortions
are not identifiable and TX depends on etiology

Obstetric
Hemorrhage


Induced Abortion – termination of pregnancy before viability intentionally,
whether for medical purposes or personal decision.
o Approximately ½ of pregnancies are unintentional
o Medical Abortifacients are used up to 9 weeks usually consisting of
Mifepristone (antiprogesterone Ru-486) + Misoprostol (Cytotec
prostaglandin).
o Surgical: up to 15 weeks you use Manual Vacuum Aspiration (MVA)
and after 15 weeks it is completed by D&C
Leading cause of maternal death
3rd trimester bleeding occurs in 3-4% of pregnancies may be obstetric or
non-obstetric



Major causes of antepartum hemorrhage include:
o Placenta previa (20%)
o Placental abruption (30%)
o Uterine Rupture
Placenta Previa: Abnormal implantation of placenta over the internal cervical
os
o Signs/Symptoms: Sudden profuse PAINLESS bleeding usually after
28 wks as the lower uterine segment thins and disrupts attachment
o Risks: Prior C/S, Uterine surgery, Multiparity, Multiple gestation,
Smoking, Hx of placenta previa
 Complete: Covers the os
 Partial: Covers portion of the os
 Marginal: At the edge of the os
 Low lying: Implanted on lower uterine segment
o Fetal Complications: Preterm, PROM, IUGR, Vasa Previa, congenital
abnormalities
o Accreta: Abnormal invasion into the uterine wall (5-15% of the time).
Usually asymp unless it invades the bladder or bowel
 Accreta: superficial attachment & invasion
 Increta: invades myometrium
 Percreta: penetrates myometrium to uterine serosa
o Dx: U/S, vaginal exam is CI, speculum exam to assess bleeding
o Tx: Stabilize the PT and if acute hemorrhage  C/S
 Admit, Non Stress Test, 2 large bore IVs
 Labs: cbc, type & cross, DIC panel, Kleihauer-Betke if Rh –
 Prepare for bleeding and PTD (MgSO4 and steroids)
 Consider amnio for Fetal lung maturity if < 37 and consider
C/S
Placental Abruption: Premature separation of a normally implanted placenta
from the uterine wall. 50% before labor and after 30 wks
o Signs/Symptoms: Sudden PAINFUL bleeding with uterine pain and
contractions, with 50% showing fetal distress
o Risks: HTN, Prior abruption, Advanced maternal age, Multiparity, DM,

Ectopic
pregnancy




Connective tissue dz, Cocaine/smoking, short cord/Circumvallate
placenta, trauma, PROM, ROM w/ polyhydraminos
 30% of 3rd trimester VB; Risk increases in future pregnancy
o Dx: bleeding, firm uterus; Tocometer (frequent or tetanic
contractions); FHR non reassuring due to hypoxia
o Tx: Stabilize the PT and deliver if hemorrhaging or non reassuring
FHR
 Admit, Non Stress Test, 2 large bore IVs
 Labs: cbc, type & cross, DIC panel, Kleihauer-Betke if Rh –
 Prepare for bleeding and PTD (MgSO4 and steroids)
 Consider tocolysis and steroid if <34 wks
 Consider amnio for Fetal lung maturity if < 37 and consider
C/S
 Vaginal delivery is preferred as long as bleeding is controlled
and no abnormal FHR.
Uterine Rupture
o Signs/Symptoms: Sudden onset of intense abdominal pain +/- vaginal
bleeding.
o Risks: Prior uterine surgery, excessive Pitocin, Grand Multiparity,
Marked uterine distention, Abnormal fetal lie, Large fetus, External
version, Trauma
 Potential OB catastrophe, most occur during labor and 90%
associated w/ prior uterine scar
o Tx: Stabilize the PT immediate laparotomy and delivery of fetus
 Discourage future pregnancies
 No future Trial of Labor (must have C/S)
 Deliver future pregnancy by C/S consider amniocentesis @36
wks for Fetal Lung Maturity
Pregnancy implants outside the uterine cavitypositive hGC
Incidence in 1:100 pregnancies
No bleeding, just severe pain, just one side with palpation
Risks:
o Hx of STD/PID
o
o
o
o
o
o
o
*****Prior ectopic ***** (25%-->Underlying tubal disease, often post
STD)
Previous tubal surgery
Prior pelvic or abdominal surgery
Endometriosis
IVF
Antiretroviral therapy
DES exposed with congenital anomalies
Use of IUD for birth control: Almost no chance of getting pregnant
with IUD; if they do, then the risk of that pregnancy being ectopic is
higher.
o
Unilateral pelvic/abdominal pain +/- vaginal bleeding
o
o
adnexal mass, tender; uterus SGA; +/- VB; +/- peritoneal Sx
Shock with rupture
o

Hx

PE
 DX
LABS: bhCG levels lower than expectedQuantitative bhCG is best lab to get
Inappropriate rise
 > 66% in 48 hr &
 At least double in 72hr
 But 15 % of inappropriately rising bhCG can be
normal pregnancy
 Use the same lab
o +/- anemia and  WBC
o Progesterone level
 <5 ng/ml: ectopic or nonviable pregnancy
 >25 ng/ml: 97% with normal IUP
US: 20-30 % NO sonographic abnormality
o
o
Adnexal mass or gest sac, fluid in pelvis, no IUP with yolk sac are
classic findings
•
•
•
Pseudosac often confused with IUP
o Seen in 10-20% of ectopics, decidual cast
Small risk of IUP + ectopic with ART = heterotopic pregnancy
Should see IUP if bhCG 1,500-2,000 and FHR should be seen if beta > 5,000
mIU/mL
Surgical TX:
• Laparoscopic surgery
• Salpingostomy – hole in tube
• Salpingectomy –resect tube
• Fimbrial expression – “milking out of the tube”
• Exploratory laparotomy – if unstable
Medical TX:
•
•
•
•
Methotrexate inhibits rapidly growing cellsMild side effects
Single IM dose 50mg/sq meter
Resolution of ectopic in ~70-95% of cases
Tubal patency rates by HSG ~70-85% after MTX
Criteria for Methotrexate Rx:
o Hemodynamically stable
o No evidence of rupture
o Ectopic< 3-4 cm in diameter
o No contraindication to MTX
o Compliant with f/up
o No cardiac activity
o Bhcg < 15,000
*After treatment, risk of persistent ectopic
o
o
After laparatomy 3-5% of cases
After LSC range 3-20% (avg. 5-15%)
o Follow weekly bhCG until negative
*After 1 ectopic:
o
o
Gestational
diabetes







Recurrent ectopic risk 20-25%
Infertility risk 25-30%
Diabetes in Pregnancy
Priscilla White Classification: not used as much anymore
o A1 diet controlled GDM (gestational diabetes mellitus)
o A2 GDM controlled with insulin; polyhydramnios, macrosomia, prior
stillbirth
o B DM onset > 20 yo; duration < 10y
o C onset 10-19 yo; duration < 20 y
o D juvenile onset dur > 20 y
o F nephropathy
o R retinopathy
o M cardiomyopathy
o T renal transplant
Etiology : impairment in carbohydrate metabolism that manifests during
pregnancy ; 50% in subsequent preg ; many get DM later in life.
Risk Factors: >25 yo, obesity, family history, high risk ethnicity, prev infant
>4000 g, prev. stillborn, prev. polyhydramnios, recurrent Ab
Associated with: 4x more pre eclampsia, 2x more S Abs, inc. infection,
polyhydraminos, macrosmia, c/s, pp hemorrhage, fetal death
Risk of Fetal anomalies: Transpostion of the great vessels, sacral agenesis,
macrosomia, still birth
DX: O’Sullivan Oral Glucose Challenge Test “Glucola” (50 g glucose) @28
o > 140 then need 3 hr OGTT.
o 100g 3hr OGTT (need 2/4): fasting 95, 1hr 180, 2 hr 155, 3 hr 140
Management: ADA 1800 – 2200 kcal/d diet; glucose checks, insulin if necessary,
deliver @ 38-40 w oral glucose tolerance test after delivery in six weeks to



screen for Post Partum DM (OGTT fasting >126, 2hr >200)
o Diet: Carbohydrate restriction (35-40% of daily caloric intake)
o Exercise: Regular exercise has been shown to improve glycemic control in
women with GDM.
o Self-monitoring of blood glucose
o Oral agents such as Metformin or Glyburide
o Addition of insulin therapy to achieve and maintain euglycemia when diet
and exercise fail
Antepartum care:
o U/S in first trimester to confirm gestational age
o U/S at 18-20 weeks for fetal anatomy assessment
o Maternal glycemic control by self-monitoring and of fetal growth and
development by ultrasound are essential during evaluation
o @ 30-32 w US q 4w (look for IUGR, polyhydramnios), kick counts, Non
stress test (NST), Biophysical profiles (BPP) – Make sure to monitor fetal
growth
Consider delivery at 38 weeks if macrosomia or poorly controlled DM and
consider C/S if fetus is >4250-4500g
Watch for neonatal hypoglycemia after delivery
Overt (Pregestational DM)









Initial assessment ideally done prior to conception try to achieve normal HgA1c
before conception
Assessment of other end-organ damage
Comprehensive eye examination
Renal function
Thyroid studies (T1DM)
ECG (older than 30 yo or DM more than 5 years)
Urinalysis and Culture (TOC if Tx)Asymptomatic bacteruria 3X more common
Begin prenatal vitamins with additional folate
U/S in first trimester to confirm gestational age


Pregnancy
induced
hypertension





U/S at 18-20 weeks for fetal anatomy assessment
Maternal glycemic control by self-monitoring and of fetal growth and
development by ultrasound are essential during evaluation
Common medical condition that affects 20-30% of populationSustained BP >
140/90
Second leading cause of maternal mortality in the United States
Complicates 5-8% of all pregnancies
Associated with Intrauterine Growth Restriction (IUGR)
Classification
1. Chronic hypertension (CHTN)
2. Preeclampsia-Eclampsia
3. Preclampsia super imposed on CHTN
Gestational hypertension
History of Hypertension prior to pregnancy or recognized during first half of
pregnancy
o Hypertension evident before 20 weeks gestation
o Does not worsen appreciably during pregnancy
o High blood pressure lasts longer than 12 weeks postpartum
Complete Comprehensive History and Physical
Exclude underlying disorders
Laboratory
 CBC, CMP
 UA and Culture
o 24 hour urine (baseline)
o Urinary catecholamines (pheochromocytoma)
Diagnostic Tests
 EKG (LVH)
 Fetal ultrasound early (confirm date and anatomy) then q 4 weeks for
growth assessment
o





TX:
 Avoid alcohol and tobacco
 Consider dietary sodium restriction
 Avoid rigorous activity
 Medications
o Required if BP is sustained at or above 160/105 Threshold if no endorgan involvement
o 140/90 as threshold if evidence of renal involvement
o Target goal: 130-150 / 80-100 mmHg
 Methyldopa (Aldomet) – initiation
o Previously used as a first line agent in pregnancy by many clinicians.
 Labetalol (Never use Atenolol)
o BB that is safe during pregnancy and crosses the placental boarder in
very small amounts.
 Nifedipine (Procardia)
o CCB that is safe in pregnancy.
 ACEI contraindicated in all trimesters

Sustained BP > 150 / 100
o Initiate medications
o Frequent prenatal visits (q2-4wk)
o Effectiveness of medications
o Proteinuria monitoring
o Fetal monitoring (32 wks)
o Early delivery (39 wks)
1. Preeclampsia - 2-8% of all pregnancies (250,000/yr)
2. Preeclampsia and eclampsia account for 10-15% of maternal deaths
worldwide
3. Hypertension - 17.6% of maternal deaths in the U.S.
Preeclampsia/
eclampsia







The cause of preeclampsia remains unknown
ETIOLOGY: vasospasm; inc. thromboxane; inadequate trophoblast invasion of
spiral arteries; immune mediated maternal reaction
Recurrence of pre eclampsia in subsequent pregnancy is 25 – 33%
Risks: First pregnancy or new partner, Multifetal gestation, Hx of PIH, CHTN,
Medical Dz: pregestational DM, vascular or autoimmune dz, nephropathy, APLS,
Obesity, AMA >35 or too young < 20yo, African American ethnicity
Prolongation of gestation, even in severe preeclampsia, offers the best option for
improving neonatal outcome with an acceptable level of maternal risk
Ambulatory management of preeclampsia (no severe features) is acceptable with
some caveats
Magnesium sulfate should be used for seizure prophylaxis in cases of severe
preeclampsia and/or impending eclampsia
Types
A. Mild Preeclampsia:
o BP > 140/90mmHg [ or >30/15 ]
o Proteinuria: >300mg/24 hr or > 1-2+ on dipstick
o Non-dependent edema
B. Severe Preeclampsia: (some findings)
o
o
o
o
o
o
o
o
o
Proteinuria: > 5gm/24 hr or > 3-4+ on dip
Cvascular: BP > 160/110mmHg
Neuro: HA, visual changes (blurry, scotomata)
Pulmonary: Edema
Renal: ARF with rising creatinine or oliguria (<400ml/24hr or < 30ml/hr)
GI: RUQ pain, elevated LFTs
Heme; hemolytic anemia, platelets < 100K, DIC
Fetal: IUGR, abnormal umbilical artery dopplers
HELLP SYNDROME:
o
o
o
o
o
o
~10% of pts with severe PIH will develop HELLP syndrome
~80% of pts develop HELLP after diagnosis with PIH
Stillbirth (10-15%), Neonatal death (20-25%), Proteinuria
Hemolysis – uric acid, LDH & total bilirubin
Elevated LFTs - AST, ALT
Low Platelets < 100K +/- DIC
C. Eclampsia: Seizure
o Presence of new-onset grand mal seizures in woman with PIH
o Other etiologies for seizures include: AVM, ruptured aneurysm, idiopathic …
more likely to be diagnosis when eclampsia occurs after 48-72 hrs
postpartum
Fetal Complications: IUGR, prematurity, dec blood flow to placenta; abruption/fetal
distress, oligohydramnios



Prematurity related complications
Acute Uteroplacental insufficiency (UPI)
o Placental infarcts and/or abruption
o Intrapartum fetal distress
o Stillbirth (in severe cases)
Chronic UPI
o Asymmetric & symmetric IUGR
o Oligohydramnios
Management – Delivery is the cure (if need to deliver stabilize and give
betamethasone for 48hrs then deliver)

Bed rest










Fetal surveillance
Laboratory testing
Antihypertensives (if BP >160/110)
o Hydralazine: 5-10mg dose iv q 15-20mins until desired response achieved
o Labetalol: 20mg iv bolus dose followed by 40mg if not effective w/in 10min
 80mg q 10mins to max total dose of 220mg
Timing of delivery (34wks severe; 37 mild) Delivery at >37wk if worsening PIH
Mode of delivery (want vaginal b/c they won’t tolerate blood loss very well)
Anesthesia (No epidural b/c drop BP)
Goal is to prevent eclampsia
With severe HELLP/eclampsia deliver as soon as possible
Consider expectant management for 48hr to let steroids  Fetal Lung Maturity
then deliver
Use of Magnesium Sulfate
 Antenatal surveillance and close f/up usually outpatient or in-house
 Start MgSO4
o 4gm load – 2gm/hr maintenance  continue 12-24 hrs postpartum
 Preterm expectant management:
o Bed rest
o Betamethasone if < 34 wks
Post-partum management




CBC with platelets
Serum creatinine and BUN
24 hour urine for protein
Baseline transaminases
Optional – LDH, uric acid
Gestational
trophoblastic
disease
 Hydatidiform MolePartial Mole or Complete Mole
 Invasive Mole
 Gestational Choriocarcinoma
 Placental Site Trophoblastic Tumor
*Hydatidiform moles


90% of molar pregnancies are benign
o Complete (classic): molar degeneration with no associated fetus
o Incomplete (Partial): molar degeneration with an abnormal fetus
Complete Mole: Result from fertilization of an empty egg
o All chromosomes are paternal; Most common pattern 46,XX
o Sperm penetration with duplication
o Trophoblastic proliferation with hydropic degeneration
o Higher malignant potential than partial moles- 20%
o Quant bhCG extremely high (>100,000mIU/mL)
o Incidence: 1:1000 pregnancies
 Highest rate: Asians in the Far East 1:200
 Lowest rate: Black women in U.S.
Risks:
o
o
o
Age less than 20 or greater than 40
Higher in areas with diet deficient in b-carotene and folic acid
Higher incidence among women with Hx of prior SAbs or GTD
Pelvic US:
o
o
o
“snowstorm” pattern due to swelling of villi
No fetus in uterus
+/- Theca Lutein ovarian cysts
o
Immediate evacuation
TX:
o
o
o
o
F/U:
D&E  by suction curettage
IV pitocin to minimize blood loss
Consider hysterectomy if completed childbearing
3-5% develop recurrent Dz even after hysterectomy
95-100% cure rate15-25% persistent disease
Serial bhCG weekly until 3 consecutive negatives then monthly for 1
yr
o Contraception during follow-up
Incomplete: Normal egg fertilized by 2 sperm
o Triploid karyotype (2 sets from father); M/C 69,XXX (80%)
o Focal hydropic villi and trophoblastic hyperplasia of syncitial layer
coexist with fetus
o Almost always benign
o 90% present with incomplete or missed Ab
o Usually dx later and less severe than complete mole
o Physical Exam can be normal and Dx by US
TX:
o
o

o
o
o
Immediate evacuation of uterine contents
Follow up weekly bhCG until neg x 3 then monthly for 1 yr
Contraception during follow up
Good Prognostic Factors
o
o
o
o
o
o
Age < 40
Post mole
< 4 mo from antecedent pregnancy
Bhcg < 40,000
No brain or liver mets
No prior chemotherapy
Sensitive to chemotherapy
 Methotrexate or Actinomycin D
 Good prognosis GTD: single agent
 Poor prognosis GTD: multi-agent
Choriocarcinoma
o Malignant necrotizing tumor; 25% after molar pregnancy; 50% after
normal term pregnancy; 25% after SAb, EAb or ectopic
o Often metastatic: Lungs, vagina, brain, & liver
o Rare in US 1:20,000 pregnancies:  incidence in Asia
o Often presents with Sx of metastatic disease
TX:
o

o Same as for invasive moles; Follow up: same as for others
Placental Site Trophoblastic Tumors (PSTTs)
o Extremely rare; Arise from any type of pregnancy
o Absence of villi and proliferation of cytotrophoblasts
o Spread by invasion into myometrium & blood vessels
o Usually present with VB & persistent + bhCG
o Not sensitive to chemo
**Hydatidiform moles generally benign; Invasive moles usually don’t metastasize

**GTD treated with chemo except PSTT
POSTPARTUM CARE
Postpartum
hemorrhage



Leading cause of perinatal maternal death.
> 500ml following vaginal delivery; > 1000ml following C/S
Etiology:
o Uterine Atony - the inability of the uterus to contract and may lead to
continuous bleeding. Retained placental tissue and infection may contribute
to uterine atony. Uterine atony is the most common cause of postpartum
hemorrhage
o Trauma - trauma from the delivery may tear tissue and vessels leading to

Endometritis/

Chorioamnioni
tis

significant postpartum bleeding
o Retained Placenta
o Coagulopathy
Management (stages from California Maternity Quality Care Collaborative)
o Stage 0: normal - treated with fundal massage and oxytocin.
o Stage 1: more than normal bleeding
o Establish large-bore intravenous access, assemble personnel
o Increase oxytocin, consider use of methergine, perform fundal
massage
o Prepare 2 units of packed red cells.
o Stage 2: bleeding continues
o Check coagulation status, assemble response team, move to OR
o Place intrauterine balloon, administer
additional uterotonics(misoprostol, carboprost tromethamine)
o Consider: uterine artery embolization, dilatation and curettage,
and laparotomy with uterine compression stitches or hysterectomy.
o Stage 3: bleeding continues
o Activate massive transfusion protocol, mobilize additional personnel,
o Recheck laboratory tests, perform laparotomy, consider
hysterectomy.
Chorioamnionitis
o Def: infection of amniotic fluid
o Requires delivery; increased risk with inc. length of rupture of membranes
o S/S: fever > 38 c, inc WBC, tachycardia, uterus tender, foul discharge; signs of
maternal fever or fetal/maternal tachycardia
o TX: Ampicillin and Gentamycin, add Clindamycin if c/s, DELIVERY
o Most common cause of neonatal sepsis
Endometritis
o Risk factors: compromised abortions, medical instrumentation, retention of
placental fragmentprolonged labor, PROM, more c/s than vag delivery
o Organisms: polymicrobial  anerobes/aerobes like E Coli/Group B
Strep/Bacteroides
Perineal
laceration/epis
iotomy care
o S/S: uterine tenderness, foul discharge
o TX: gentamycin and clindamycin (continue until 24-48 h afebrile)
1. First degree laceration: Skin only
2. Second degree lacerations: Skin + Mucosa
3. Third degree lacerations: Skin+ mucosa+ perineal body + anal sphincter
4. Fourth degree lacerations: 3rd + rectal mucosa
The perineal body, located between the vagina and the rectum, is formed
predominantly by the bulbocavernosus and transverse perineal muscles (Figure 1).
The puborectalis muscle and the external anal sphincter contribute additional
muscle fibers.
The internal anal sphincter provides most of the resting anal tone that is essential for
maintaining continence. Laceration of this sphincter is associated with anal
incontinence.
Surgical Principles
Obstetric perineal lacerations are classified as first to fourth degree, depending on
their depth. A rectal examination is helpful in determining the extent of injury and
ensuring that a third- or fourth-degree laceration is not overlooked.
Repair of the perineum requires good lighting and visualization, proper surgical
instruments and suture material, and adequate analgesia. Compared with surgical
repair using catgut or chromic suture, repair using 3-0 polyglactin 910 (Vicryl)
suture results in decreased wound dehiscence and less postpartum perineal pain.
Local anesthesia can be used for repair of most perineal lacerations. However,
general or regional anesthesia may be necessary
Severe perineal lacerations involving the anal sphincter complex pose a surgical
challenge. There is a 20 to 50 percent incidence of anal incontinence or rectal
urgency after repair of third-degree obstetric perineal lacerations. These DON’T
require immediate repair so an inexperienced physician can delay the procedure for
a few hours until appropriate support staff are available.
With severe perineal lacerations irrigate copiously to improve visualization and
reduce the incidence of wound infection. Because these lacerations are contaminated
by stool, a single dose of a second- or third-generation cephalosporin may be given
intravenously before the procedure is started.
Repair of Second-Degree Perineal Lacerations
Repair of a second-degree laceration requires approximation of the vaginal tissues,
muscles of the perineal body, and perineal skin. The steps in the procedure are as
follows:
Second-degree perineal laceration.
The apex of the vaginal laceration is identified. For lacerations extending deep into
the vagina, a Gelpi or Deaver retractor facilitates visualization.
An anchoring suture is placed 1 cm above the apex of the laceration, and the vaginal
mucosa and underlying rectovaginal fascia are closed using a running unlocked 3-0
polyglactin 910 suture. If the apex is too far into the vagina to be seen, the anchoring
suture is placed at the most distally visible area of laceration, and traction is applied
on the suture to bring the apex into view. The running suture CAN BE LOCKED FOR
HEMOSTASIS, if needed.
The sutures must include the rectovaginal fascia (Figure 4), which provides support
to the posterior vagina. The running suture is carried to the hymenal ring and tied
proximal to the ring, completing closure of the vaginal mucosa and rectovaginal
fascia.
The muscles of the perineal body are identified on each side of the perineal
laceration (Figure 5). The ends of the transverse perineal muscles are
reapproximated with one or two transverse interrupted 3-0 polyglactin 910
sutures (Figure 6)
2nd degree perineal laceration
Repair of transverse perineal muscles
A single interrupted 3-0 polyglactin 910 suture is then placed through the
bulbocavernosus muscle(Figure 7). The torn ends of the bulbocavernosus muscle are
frequently retracted posteriorly and superiorly. Use of a large needle facilitates
proper suture placement.
Repair of bulbocavernosus muscle
If the laceration has separated the rectovaginal fascia from the perineal body, the
fascia is reattached to the perineal body with two vertical interrupted 3-0
polyglactin 910 sutures (Figure 8)
Reattachment of rectovaginal septum to muscles
of perineal body.
When the perineal muscles are repaired anatomically as described above, the
overlying skin is usually well approximated, and skin sutures generally are not
required. Skin sutures have been shown to increase the incidence of perineal pain at
three months after delivery.15 [Evidence level B, uncontrolled trial] If the skin
requires suturing, running subcuticular sutures have been shown to be superior to
interrupted transcutaneous sutures.16 The 4-0 polyglactin 910 sutures should start
at the posterior apex of the skin laceration and should be placed approximately 3
mm from the edge of the skin.
An alternative approach to repair of the perineal body muscles is a running suture
that is continued from the vaginal mucosa repair and brought underneath the
hymenal ring. However, we prefer the interrupted approach because it facilitates a
more anatomic repair, allowing reapproximation of the bulbocavernosus muscle and
reattachment of the vaginal septum with minimal use of sutures.
Repair of Fourth-Degree Perineal Lacerations
Repair of a fourth-degree laceration requires approximation of the rectal mucosa,
internal anal sphincter, and external anal sphincter (Figure 9)
.Fourth-degree perineal laceration.
A Gelpi retractor is used to separate the vaginal sidewalls to permit visualization of
the rectal mucosa and anal sphincters. The apex of the rectal mucosa is identified,
and the mucosa is approximated using closely spaced interrupted or running 4-0
polyglactin 910 sutures (Figure 10). Traditional recommendations emphasize that
sutures should not penetrate the complete thickness of the mucosa into the anal
canal, to avoid promoting fistula formation. The sutures are continued to the anal
verge (i.e., onto the perineal skin).
Repair of rectal mucosa.
The internal anal sphincter is identified as a glistening, white, fibrous structure
between the rectal mucosa and the external anal sphincter (Figure 11). The
sphincter may be retracted laterally, and placement of Allis clamps on the muscle
ends facilitates repair. The internal anal sphincter is closed with continuous 2-0
polyglactin 910 sutures.
sphincter.
Internal sphincter and external anal
The external anal sphincter appears as a band of skeletal muscle with a fibrous
capsule. Traditionally, an end-to-end technique is used to bring the ends of the
sphincter together at each quadrant (12, 3, 6, and 9 o'clock) using interrupted
sutures placed through the capsule and muscle (Figure 12). Allis clamps are placed
on each end of the external anal sphincter. We use 2-0 polydioxanone sulfate (PDS),
a delayed absorbable monofilament suture, to allow the sphincter ends adequate
time to scar together. Recent evidence suggests that end-to-end repairs have poorer
anatomic and functional outcomes than was previously believed.
End-to-end technique repair external sphincter.
An alternative technique is overlapping repair of the external anal sphincter.
Colorectal surgeons prefer to use this method when they repair the sphincter remote
from delivery.14,17 The overlapping technique brings together the ends of the
sphincter with mattress sutures (Figure 13) and results in a larger surface area of
tissue contact between the two torn ends. Dissection of the external anal sphincter
from the surrounding tissue with Metzenbaum scissors may be required to achieve
adequate length for the overlapping of the muscles. The suture is passed from top to
bottom through the superior and inferior flaps, then from bottom to top through the
inferior and superior flaps. The proximal end of the superior flap overlies the distal
portion of the inferior flap. Two more sutures are placed in the same manner. After
all three sutures are placed, they are each tied snugly, but without strangulation.
When tied, the knots are on the top of the overlapped sphincter ends. Care must be
taken to incorporate the muscle capsule in the closure.
Overlapping technique repair external
sphincter.
Postpartum Care
Sitz baths and an analgesic such as ibuprofen. If a woman has excessive pain in the
days after a repair, she should be examined immediately because pain is a frequent
sign of infection in the perineal area. After repair of a third- or fourth-degree
laceration, we include several weeks of therapy with a stool softener, such as
docusate sodium (Colace), to minimize the potential for repair breakdown from
straining during defecation.
Prevention
The incidence of severe perineal trauma can be decreased by minimizing the use of
episiotomy and operative vaginal delivery. A Cochrane review demonstrated that
liberal use of episiotomy does not reduce the incidence of anal sphincter lacerations
and is associated with increased perineal trauma.
Episiotomy:

Indications:
o There is a serious risk to the mother of second- or third-degree tearing
o In cases where a natural delivery is adversely affected, but a Caesarean
section is not indicated
o "Natural" tearing will cause an increased risk of maternal disease being
vertically transmitted
o The baby is very large
o When perineal muscles are excessively rigid
o When instrumental delivery is indicated
o When a woman has undergone FGM (female genital mutilation), indicating
the need for an anterior and or mediolateral episiotomy
o Prolonged late decelerations or fetal bradycardia during active pushing
o The baby's shoulders are stuck (shoulder dystocia), or a bony association
(Note that the episiotomy does not directly resolve this problem, but it is


Normal
physiology
changes of
puerperium



indicated to allow the operator more room to perform maneuvers to free
shoulders from the pelvis)
Types:
o Medio-lateral: The incision is made downward and outward from midpoint
of fourchette either to right or left. It is directed diagonally in straight line
which runs about 2.5 cm away from the anus (midpoint between anus
and ischial tuberosity).
o Median: The incision commences from centre of the fourchette and extends
on posterior side along midline for 2.5 cm.
o Lateral: The incision starts from about 1 cm away from the centre of
fourchette and extends laterally. Drawback include chance of injury
to Bartholin's duct; thus some practitioners have totally condemned it.
o J-shaped: The incision begins in the centre of the fourchette and is directed
posteriorly along midline for about 1.5 cm and then directed downwards and
outwards along 5 or 7 o'clock position to avoid the anal sphincter. This is
also not done widely
Episiotomy has been shown to not be as effective and has led to more tears.
Perineal lacerations are also increased with use of forceps rather than vacuum
delivery.
Puerperium is the period following childbirth which the body tissues, specially
the pelvic organs revert back to the pre-pregnant state both anatomically and
physiologically.
o Involution is the process whereby the reproductive organs return to their
nonpregnant state.
Duration: puerperium begins as soon as the placenta is expelled and lasts for
approximately 6 weeks
o The period is arbitrarily divided into – Immediate- within 24 hours; Earlyupto 7 days; Remote- upto 6 weeks.
Uterus becomes firm and retracted and measures about 20 X 12 X 7.5 cm and
weighs about 1000 g
o At the end of the first week, it weighs 500g








o By the 6 weeks, it weighs approx. 50g.
Cervix contracts slowly. External os will be two fingers wide for a few days but
by the end of first week, narrow down to admit the tip of finger only.
o It never returns back to the nulliparous state, usually remains slightly open
and appear slitlike or stellate
Muscles - there is a reduction of the myometrial cell size. Withdrawal of estrogen
and progesterone lead to increase in the activity of the uterine collagenase and
the release of the proteolytic enzyme.
Blood vessels - The arteries are constricted by contraction of its wall and
thickening of the intima followed by thrombosis. New blood vessels grow inside
thrombi. There is also degeneration of the elastic tissues.
Endometrium - The superficial layer becomes necrotic and is sloughed. The basal
layer adjacent to the myometrium remains intact and is the source of new
endometrium.
o By the 10th day: Regeneration of the epithelium is completed.
o By the day 16: the endometrium is restored.
o At about 6 weeks: the endometrium of placental site is restored
Placental site involution - Complete extrusion of the placental site takes up to 6
weeks.
o When this process is defective, late-onset puerperal hemorrhage may occur.
o Size of placental site immediately after delivery is approx. the size of the
palm, but it rapidly decreases thereafter.
Vagina takes a long time(4-8 weeks) to involute. It regains its tone but never to
the virginal state.
o The mucosa remains delicate for the first few weeks
o Rugae partially reappear at third week.
o The introitus remains permanently larger than the virginal state.
Abdominal Wall as a result of ruptured elastic fibers in the skin and prolonged
distension caused by the pregnant uterus, remains soft and flaccid for several
weeks
Lochia - the vaginal discharge beginning the first night during puerperium.
o The discharge originates from the uterine body, cervix and vagina.
o Odor and reaction: it has an offensive fishy smell and is alkaline at first then
acid towards the end.
Color – red for 1-4 days; the color is yellowish or pink or pale brownish days
5-9; white days 10-15 days.
o Duration: may extend up to 3 weeks.
o 1. Persistence of red lochia means subinvolution
o 2. Offensive lochia means infection
o 3. In severe infection with septicaemia, lochia is scanty and not offensive
Insulinaze causes the diabetogenic effects of pregnancy to be reversed.
Estrogen and progesterone levels decrease. The estrogen levels in nonlactating
women begin to increase by 2 weeks after birth.
Lactating and non-lactating women differ in the time of the first ovulation.
o In women who breast feed, prolactin levels remain elevated into the sixth
week after birth.
o Prolactin levels decline in nonlactating women, reaching the prepregnant
range by third week.
Menstruation: If the woman does not breast fed her baby, the menstruation
returns by 6th week following delivery in about 40% and by 12th week in 80%
of cases.
Ovulation: In non-lactating mothers, may occur as early as 4 weeks and in
lactating mothers about 10 weeks after delivery.
o A women who is exclusively breastfeeding, the contraceptive protection is
about 98% up to 6 months postpartum. Thus, lactation provides a natural
method of contraception.
o Non-lactating mother should use contraceptive measures after 3 weeks and
the lactating mothers after 3 months of delivery.
Urinary system - Because of relative insensitivity to the raised intravesical
pressure due to trauma sustained to the nerve plexus during delivery, the
bladder may be overdistended without any desire to pass urine.
Blood and fluid changes - Diuresis b/t second and fifth day after birth, as well as
blood loss at birth, reduce the added volume accumulated during pregnancy and
it returns to normal by first or second week after birth.
The white blood cell count sometimes reaches 30,000/L, with the increase
predominantly due to granulocytes. Normally, during the first few postpartum
o














days, hemoglobin concentration and hematocrit fluctuate moderately.
Cardiac Output: Remains elevated for 24 to 48 hrs postpartum and declines to
nonpregnant values by 10 days.
The GI system - Digestion and absorption begin to be active again soon after
birth, but passage of stool through the bowel may be slow because of the still
present effect of relaxin on the bowel. Bowel evacuation may be difficult because
of the pain of episiotomy sutures or hemorrhoids.
Weight loss - Rapid diuresis and diaphoresis during 2nd to 5th days after birth
result in weight loss of 5 lb (2 to 4kg), in addition to approx. 12 lb (5.8 kg) lost at
birth. Lochia flow- 2-3 lb(1kg) loss
o Total weight loss- 19 lb
Integumentary system - Stretch marks in women’s abdomen still appear
reddened and may be even more prominent than pregnancy. Excessive pigment
on face and neck (Chloasma) and on abdomen (Linea nigra) barely detectable in
6 weeks time.
o Diastasis recti (Overstretching and separation of the abdominal
musculature) if present, the area will be slightly indented.
o Abdominal wall and ligaments require 6 weeks time to return to normal
Lactation - midway through pregnancy, she begins secreting colostrum, a thin,
watery, prelactation secretion, which continues the first 2 postpartum days. On
the third day, her breasts become full and feel tense (primary engorgement) or
tender as milk forms within breast ducts.
o When breast milk forms, the milk ducts become distended. The nipple
secretion changes from the clear colostrum to bluish white which is typical
color of breast milk.
Vital sign changes
o Temperature – may have a slight increase in temperature during the first 24
hours after birth. Occasionally, when breasts fill with milk on the third or
fourth postpartum day, temperature rises for a period of hours from
increased vascular activity.
o Pulse - after initial tachycardia associated with labor and delivery, a
bradycardia often develops in the early puerperium. During the postpartal
period it is usually slower than normal (60 and 70 bpm). As diuresis
o
diminishes blood volume and causes blood pressure to fall, the pulse rate
increases and returns to normal in 1 weeks.
Blood pressure - Systolic and diastolic blood pressures remain unchanged
from late pregnancy values until about 12 weeks post partum, after which
they increase. Within 2 weeks post partum, systemic vascular resistance
increases by 30%
Condition
Definition
Pathophysiolog
y
Physical Exam
Findings
Carcinoma of
the lining of
the uterus
Unopposed
estrogen (from
HRT or
peripheral fat
stores)
stimulates
proliferation of
the
endometrium,
leading to
hyperplasia and
eventually
neoplasia.
m/c Postmenopausal
bleeding
Work Up/Diagnose
Treatment 1st
line
Treatment 2nd
line
GYNECOLOGY
Neoplasms
Endometrial
cancer
Second most
common
gynecological
malignancy
Risk Factors:
Obesity, HTN
advancing
age, PCOS,
early
menarche,
late
menopause,
nulliparity,
oligomennorh
ea, long-term
high-dose
menopausal
Abnormal bleeding
50-70 yos
Obstruction of cervix
with pus or blood
(pyometra/hematomet
ra)
Pelvic or Lower
abdominal pain or
pressure (late in
disease)
Frequent urination
(from compression)
*HNPCC (Lynch
Syndrome)**
Serum HCG
Pap smear – atypical
endometrial cells
(frequently negative)
Vaginal ultrasound –
thickened endometrium
Diagnostic –
endocervical/endometri
al sampling via
hysteroscopy, D&C, or
office Pipelle biopsy
Staging of tissue and
regional nodes.
75% are
adenocarcinoma
Determine extent by
CXR, IV urography,
cystography,
Total
hysterectomy
with bilateral
salpingooophorectomy
Sampling of
peritoneal
material and
lymph node
resection with
irradiation if
positive for
tumor
Chemotherapy
Radiation
Palliatiation for
advanced disease
with large doses
of progestins
Ovarian
neoplasms
estrogen or
tamoxifen use
sigmoidoscopy, and
MRI.
FHx of Colon
or Gyn Cancer
75% confined in uterus
corpus at initial dx.
Malignant
tumor of the
ovary
3rd most
common gyn
cancer,
leading cause
of death from
reprod. tract
cancer
Risk Factors:
Increasing
age,
nulliparity,
birth of child
>40 yo, BRCA
Increased risk
with BRCA 1/2
genes. (breast
cancer)
Asymptomatic
Serum HCG
Mild nonspecific GI
symptoms (pain and
prolonged bloating)
Frequently detected on
routine pelvic exam
Ascites
Abdominal mass
Transperitoneal
dissemination when
metastasis
Transvaginal U/S
(benign/malignant
mass)
CT abdomen /pelvis (to
see other structures)
Genetic testing to rule
out BRCA if mass
confirmed.
Cancer markers –
CA125 greater than 35
units increases risk of
malignant tumor
Surgical removal
and staging of
tumor +/unilateral
oophorectomy
Early stage –
abdominal
hysterectomy
Advanced –
tumor removal +
chemo
Selective
lymphadenectom
y
Cervical
Dysplasia
AKA
intraepithelial
dysplasia
Dysplasia of
the cervix
CIN 1 – mild
dysplasia, pap
result of LSIL
CIN II –
moderate
dysplasia, pap
result of HSIL
HPV causes
cellular
abnormalities
within the
transformation
zone of the
cervix.
Asymptomatic
Cervical lesions may
be present
Pap smear (screening
for women ages 2165)or within 3 yrs of
sexual act.
ASC-US – low risk of
invasive Ca
Repeat PAP at 6 and 12
months
Reflex HPV test
CIN III –
severe
dysplasia or
carcinoma in
situ, pap
result HSIL
If either of above
abnormal – colposcopy
LSIL, HSIL – colposcopy
and biopsy
AGC – colposcopy with
endocervical and
endometrial evaluation
AIS, adenocarcinoma in
situ– may require
excisional procedures
Cervical
carcinoma
HPV causes high
grade cellular
Metorrhagia
Pap smear is the
screening test. 3 yrs
Based on degree
of CIN
Cauterization or
cryosurgery for
small
noninvasive
lesions
CO2 laser for
large visible
lesions
LOOP excision
for entirely
clearly visible
lesions
Conization
(removal of
entire
transformation
zone) for severe
dysplasia of CIS
Guardasil
vaccine for 9-
IB1-may be
candidate for
changes that
eventually lead
to dysplasia that
results in cancer.
Postcoital spotting
Can be
considered a
sexually
transmitted
disease.
Bloody, purulent,
odorous, nonpruritic
discharge
Highly
associated with
HPV types 16
and 18.
Leg-edema from
hepatic obstruction
80% squamous
20% glandular
Can also be a
mixture.
Smoking is a risk
factor.
Cervical ulceration or
tumor
Bladder/rectal fistulas
in late stages
Abnormal bimanual
exam
after onset of sexual
activity or at 21 yo
Colposcopy
26 yo . Will not
treat existing
infection.
Punch Biopsy
Endocervical curettage
AISadenoCarcinom
a in situ:
Complete
childbearing –
total
hysterectomy
Incomplete child
bearing – cervical
conization or
ablation of lesion
with laser or
cryotherapy
Invasive
carcinoma:
HIV is a risk
factor.
IA1-simple
extrafascial
hysterectomy
Low dietary
vitamin A may
IA2, IB1, and IIAradiation and
fertility sparing
surgery:
Radical
trachelectomy
and lymph node
dissection with
preservation of
the uterus and
ovaries
be associated.
chemo +/radical
hysterectomy
IB2, IIB, III, and
IV-radiation +
cisplatin-based
chemo
Breast cancer
Most breast
tumors are
estrogen
sensitive=
fertilizer to
grow
Carcinoma of
the breast
Histologic types
of breast cancer:
Risk factors:
Infiltrating
ductal carcinoma
the m/c* (8090%)(lining of
milk ducts)
Delayed
childbearing
or never
giving birth.
Family hx
BRCA1/2
Early
menarche or
late
menopause
Endometrial
cancer
Invasive lobular
(6-8%)(glands
that make milk)
Noninvasive (46%)-only in
breast lobules
Inflammatory
(<3%)- most
malignant form.
Red.swollen
Early findings:
Chemotherapy
Radiotherapy
Breast asymmetry
Mammography –
calcifications are
earliest findings
Radiation
Dimpling
U/S
SurgeryMasectomy or
Partial
mastectomy
Reconstructive
surgery
Discharge from nipple
MRI
Single, nontender, firm
to hard mass with illdefined margins
PET scanning
Abnormal
mammogram
TNM staging
No palpable mass
Late findings:
Skin/nipple retraction
Axillary
FNA, core, open biopsy
Cytologic evaluation of
discharge
Mastectomy with
sentinel node
biopsy for
noninvasive
Mastectomy with
axillary
dissection for
invasive
Preventative
treatment in
women with risk
factors includes
prophylactic
mastectomy,
oophorectomy, or
tamoxifen.
Other SERMs and
aromatase
inhibitors have
also been found
to prevent breast
cancer.
Develops in
1/8 women
Most common
cancer in
women
Paget (1%)- skin
of nipple and
areola
Rare (<1%)
lymphadenopathy
Breast enlargement,
redness, edema, pain
Fixation of mass to
chest wall or skin
Weight loss
Bone/back pain
Jaundice
Peau de orange
Vaginal
neoplasms
Vaginal
intraepithelial
neoplasia
(VAIN)
Characterized by
a loss of
epithelial cell
maturation
Associated with
HPV high risk
genotypes
Most lesions are
asymptomatic
Abnormal pap smear is
often first sign
Vulvar warts
Colposcopic
examination with a
directed biopsy
May apply Lugol’s
iodine to identify
borders of a lesion
VAIN I – no
treatment
Surgical excision
or CO2 laser
ablation for VAIN
II and III
Carcinoma in situ
– partial or
complete
removal or
vagina and
hysterectomy
Topical 5FU for
multifocal VAIN
Imiquimod for
high grade VAIN
per several small
studies
with
reconstruction
Vulvar
neoplasms
Slow growing,
squamous
lesions
May be asymptomatic
Vulvar colposcopy
Pruritus/irritation
Post menopausal
women, Strongly
associated with
HPV (16/18/31)
and smoking
Hx of genital warts
**Biopsy to diagnose
vulvar intraepithelial
neoplasia (VIN)
Multi sex
partners, prior
cervical cancer
Slight bloody
discharge
Lesions on labia
minora appear
leukoplakic, ulcerative,
papular, macular,
cauliflower and
ulcerated in late
lesions
Treat any
predisposing or
irritative causes
(lichen sclerosis)
CT/MRI to rule out
lymphadenopathy and
to stage if bx is positive
Clobetasol
proprionate
0.5% BID x 2-3
weeks
Invasive
carcinoma
warrants local
wide excision and
inguinal
lymphadenectom
y, and possible
chemo or
radiation
High grade VIN –
topical chemo,
laser ablation,
excision,
vulvectomy
INFECTIONS
(VAGINA)
Trichomoniasis
Flagellated
protozoan
infection by
Trichomonas
Vaginalis
Sexually transmitted
infection
Symptoms- vaginal
discharge (yellowgreen), irritation,
pruritus, dysuria
½ asymptomatic
Wet mount:
-Flagellated
protozoans on
wet prep
-Large # of
Metronidazole(Flagy Resistant
l) 2g single dose
infection
requires higher
Metronidazole
dose of flagyl
500mg BID x 7d
or may
(alt)
consider
Treat part
and avoid
intercours
until both
partners a
cured
Bacterial
vaginosis
Bacterial infection
of the vagina most
commonly
associated with
Gardenerlla
vaginalis,
Bacteroides sp.,
Peptostreptococcu
s sp, and G.
mobiluncus
Can be linked to
presence of STDs,
multiple sex
partners, IUDs, and
douching
Signs- discharge,
odor, edema,
erythema, or none
WBCs
“Strawberry
cervix”
erythematous,
punctuate lesions
on ectocervix
Pap Smear
(used less
commonly)
Avoid EtOH while
taking flagyl
Vaginal discharge
(milky and
adherent to walls
of vagina), oder
(fishy)
Amsel
Criteria:
Metronidazole(Flagy No EtOH w/
l) PO 500mg BID
Flagyl
x7d
Refrain from
-Gel at bed time x5
intercourse or
nights
use condoms
until cured
Clindamycin PO
300mg BID x7d
No Doushing
Itching and
irritation
Can be
asymptomatic
-pH 5.0-7.0
-Elevated
Vaginal pH >
4.5
-Positive amine
odor with +
whiff test (10%
KOH mixed)
-Clue cells on
wet mount
-Gray,
homogenous
vaginal
discharge
If allergic- must
desensitize d/t
Flagyl being only TX
-Cream at bed time
x7 nights
tinidazole
Consider
screening
female
partners
Can be
associated
PID, postinfections
gyn proce
Atrophic
vaginitis
Irritation of the
vagina
Decreased estrogen
especially in
postmenopausal
women
Presents ~ 4 yrs
after menopause
Dyspareunia
Vaginal dryness,
soreness, itching,
dyspareunia,
occasional
spotting/discharge
(thin, scant, and
yellow-pink)
Wet Prep:
Erythrocytes
Increased PMN
neutrophils
Small round
epithelial cells
Topical vaginal
estrogen
Oral estrogen
**No estro
for pts wit
of cancer o
reproduct
organ
Recurrent
infections can
be suppressed
with PO drugs.
If persiste
infections
consider C
-Creams, pessaries,
tablets and estradiol
vaginal rings all
effective
Loss of normal
vaginal rugae
Virginal mucosa
becomes
attenuated, pale,
and almost
transparent
Vagina becomes
shorter in length
and loses elasticity
Candidiasis
Fungal or yeast
infection
Most common agent
is Candida albicans
More common in
women with
Symptoms-Pruritis, vaginal
leukorrhea,
external dysuria,
Wet Prephyphae
KOH Prephyphae and
Azoles > Nystatin
oVarious forms- pt’s
preference OTC
diabetes, preg,
young at 1st
intercourse, IUD
users, recent abx,
chronic steroids,
immunocompromise
d
dyspareunia
Exacerbation with
coitus or prior to
menses (alkaline
pH)
budding yeast
w/ - whiff test
Ph <4.5
Creams, lotions,
sprays, vag. Tablets,
suppositories,
coated tampons
Treatment lasts
from 1-7 days
depending on if it is
simple/complicated
Signs- vulvar
erythema and
edema, vaginal
erythema,
discharge (cottage
cheese-like)
Azoles not as good
with C. glabrata
organism
Fluconazole
INFECTIONS
(CERVIX)
Gonorrhea
Cervical infection
by Neisseria
gonorrhoeae, a
gram-negative
diplococcus
Sexually transmitted
Presentationyellow-green
vaginal discharge,
erythematous,
edema or easily
friable cervix.
abnormal
menstrual
bleeding, anorectal
discomfort
Endocervical
Culture- Gold
standardkidney bean
diplococcic in
PMN
Molecular
probe assay –
high sensitivity
and specificity
Ceftriaxone
(Roecephin) 250 mg
IM x1 dose
(gonorrhea) +
Azithromycin 1gm
PO x1dose or
Doxycycline 100mg
BID x7d (chlamydia)
Always cotreat for
Cefixime
(Suprax) 400mg
PO x1 dose +
Azithromycin
1gm PO x1dose
or Doxycycline
100mg BID x7d
Ophthalmia
Neonatorum
-1% silver
PID if left
untreated
Sterility
Dysuria in absence
of bacteruria in
sexual active
females
Nucleic Acid
amplification
testing
Chlamydia
Disseminated
disease: Ceftriaxone
1g IM or IV q24h x
7d
Disseminated
gonococci infection
(DGI)
nitrate,
erythromycin
or tetracycline
ophthalmic
solution
-skin lesions
-Start as
papules/pustules
-Can be
hemorrhagic
Arthritis,
pericarditis,
endocarditis,
meningitis (all rare
to see)
Chlamydia
C trachomatis
Most common STD
in women < 25 yo
Symptoms, PE
findings and
immediate lab
findings are
nonspecific
Nucleic acid
amplification
tests (NAATs)
(80-95%
sensitivity)
Endocervical
infections are
PCR
Azithromycin 1g PO
x1dose and
Doxycycline 100 mg
PO BID x7d
Ofloxacin
300mg PO BID
x7d
Levofloxacin
500mg PO
daily x7d
Infertility
usually
asymptomatic, if
present are
nonspecific
New or increased
vaginal discharge,
intermenstrual
bleeding, lower
abdominal pain,
pain during
intercourse
Strand
displacement
amplification
Transcriptionmediated
amplification
Pregnant :
Azithromycin 1g PO
x1dose
Amoxicillin 500mg
PO TID x7d
Direct
fluorescent
antibody (7085%
sensitivity)
Herpes simplex
Definition
Pathophysiolo
gy
Physical Exam
Findings
Workup/Diagno
sis
Treatment 1st
line
HSV1- mostly
oral/labial
Present with
multiple painful
Cell culture
First Episode:
PCR (test of
Acyclovir 400mg
Erythromycin
ethylsuccinate
800mg PO
4xdaily x7d
Pregnant:
Erythromycin
May have
Tissue culture
concomitant
urethral infections- (70-85%
sensitivity)
can present w/
painful urination,
urinary frequency
or both
Condition
Erythromycin
base 500mg PO
4xdaily x7d
Treatment
2nd line
Prognosis
lesionssalivary
transmission
HSV2- most
genital/anal
lesions- genital
transmission
DNA Virusmigrates to
neurons In
latent state
Reactivation
can be
triggered:
fever, sunlight,
stress
vesicular or
ulcerative
lesions on
genitals
Fever, HA,
malaise
Prodrome of
skin
irritation/burri
ng followed by
painful vesicles
on
erythematous
base (Dew
Drops on Rose
Petal)
Usually go
away on own in
7 days
choice for CNS
infection)
Serologically
PO TID x 5d
Acyclovir 200mg
PO 5xdaily for 710d
Famciclovir
250mg PO TID
x7-10d
Valacyclovir 1g
PO BID x7-10d
Suppressive
Therapy:
Valacyclovir
500mg PO daily
Acyclovir 400mg
PO BID
Famciclovir
250mg PO BID
Valacyclovir 1g
PO daily
Pregnancy:
Use Acyclovir
Human
papilloma -virus
6,11 cause
mostly
genital
warts
16,18
cause
mostly
cervical
dysplasia
and
Cervical CA
HPV causes
atypical cell
changes that
can result in
warts and
dysplasia
Flat, popular or
pedunculated
growths
Gray or flesh
colored
Verrucous
lesions on any
genital mucosal
surface
(internal or
external)
PAP smear for
dysplasia
HPV DNA
serological test
Colposcopy
Tissue Biopsy
Warts:
Dysplasia:
Provider
Administered:
Watchful
waiting/repea
t testing
Cryotherapy,
laser ablation,
surgical excision
Ablation
Excision
Trichloracetic
acid/bichloraceti
c acid
High risk
forms can
lead to
dysplastic
changes
that may
evolve
into
cancer.
Pt Applied:
Perianal lesions
Imiquimod 5%
cream, interferon
(Preg Cat C)
Lesions
may/may not
cause
discomfortitching, pain,
fullness
Topical tx for 46wk
INFECTIONS
(other)
Pelvic
Inflammatory
Disease
Bacterial
infection of
the
reproducti
Neisseria
gonorrhoeae
and Chlamydia
trachomatis are
Characterized
by cervical
motion
tenderness
BhCG to r/o
pregnancy/ectopi
c
Posterior
colpotomy to
drain abscess
Transabdominal
Ceftriaxone
(Roecepin)
250mg IM +
Doxycycline
May lead
to chronic
pelvic
pain,
ve tract
common
causes of PID.
(CMT) uterine
or adenxal pain
Begin as
endocervical
infection and
ascend to
endometrium
and fallopian
tubes.
Lower abd pain
Has also been
known to
involve other
anaerobic
bacteria from
the vaginal
tract.
Syphilis
Complex
disease
caused by
the
spirochete
Trepenom
a Pallidum
Sexually
transmitted
through skin or
mucosal
contact.
General signs:
Rash, patchy
Purulent
cervical
discharge
ESR
drainage under
laparoscopic
C-reactive protein guidance to drain
pelvic abscesses
CBC- elevated
WBC
Ultrasound
Chills and fever
Cervical Cultures
Dyspareunia
Pelvic exam
Menstrual
disturbances
CMT
100mg BID
x14d
May add
metronidazole
500mg BID
x14 days to
cover
BV/trichomon
as
tubal/pelv
ic
scarring,
infertility,
and
ectopic
pregnancy
Ultrasound
(transvaginal)
Endometrial
biopsy
Primary:
chancre(painles
s ulcer filled w/
spirochetes),
inguinal
lymphadenopat
hy
Darkfield
microscopy with
visable
treponemal
bodies
Primary/Seconda
ry:
NAATs
Benzathine
Penicillin G 2.4
million units IM
x1dose
Secondary:
maculopapular
rash on palms
Nontreponemal
Tests:
Doxycycline
100mg PO BID
Curable,
but will
progress
to
secondary
or tertiary
if left
untreated.
Must treat
all
alopecia,
genital lesions,
fever, weight
loss, anorexia,
myalgia,
lymphadeno.,
nephritis, and
hepatitis
and soles,
condylomata
lata, swollen
glands,
systemic
symptoms
Tertiary: multi
organs, CVA,
dementia,
neuromotor,
gummatous,
cardiovascular
symptoms,
gummatous
RPR
x7d
VDRL
+ titers need to be Latent of
confirmed with
unknown
Treponemal test
duration/Tertiar
y Syphilis:
TreponemalFTA-ABS or the
Benzathine
TP-PPA Specific
penicillin G
Tests
2.4million units
IM once weekly
for 3 wk
Doxycycline
100mg PO BID
x28d
Neurosyphilis:
Aqueous Pen G
18-24milllion
units IV daily
given 2-4million
units q4hrs cont.
for 10-14 days
partners.
Can cause
congenital
diseases.
Chancroid
sexually
transmitte
d genital
ulcer
disease
caused by
Haemophil
us ducreyi,
a small,
fastidious,
gramnegative
rod
H. ducreyi
enters skin
through
microabrasions
that occur
during
intercourse.
Erythematous
papulebecom
es pustule
becomes
saucer-shaped
ragged ulcer
circumscribed
by
inflammatory
wheal
Based on
symptoms and
negative testing
for other
ulcerative disease
such as syphilis
and HSV
Tender
Azithromycin 1g
PO x1dose
Ceftriaxone
250mg IM x1dose
Ciprofloxacin
500mg PO BID
x3d (non preg,
non-lactating
patient)
Fluctuant
lymph node
should be
needle
aspirated or
I&D through
normal
adjacent skin
to prevent
fistula
formation
Curable,
but can
reoccur
with
reexposur
e.
Aspirate
buboes – may
not be
Excellent
if
recognize
Erythromycin
base 500mg PO
TID x7d
Heavy, foul
discharge that
is contagious
Usually have >1
ulcer, confined
to genital
region
Painful inguinal
adenitis (less
common in
women)
Lymphogranulo
ma venereum
a systemic
sexually
transmitte
C. trachomatis
invades and
proliferates in
Primary Stage:
Small genital
papule or ulcer
Done based on
clinical suspicion
and ruling out
Doxycycline
100mg PO BID
x21d
d disease
caused by
L1, L2, and
L3
serovars
(subtypes)
of
Chlamydia
trachomati
s
lymphoid
tissue.
3-30 days after
exposure and
heals in ~ 1wk
other diagnosis
Involves
theglans or
shaft of penis,
urethra, vulva,
or vagina,
anus/rectum,
or perineum
and adjacent
skin
CT- makes sure
that inflammation
is localized to a
region and not
diffuse as in
lymphoma
Painless lesion,
can clear before
noticed by
patient
Secondary
Stage:
Weeks to
month later
becomes
systemic and
involves
extension to
Erythromycin
base 500mg PO
4xdaily x21days
(pregnancy drug
of choice)
completely
healed by
completion of
ABX
d and
treated.
Buboes
and
fistulas
may
persist
and
require
aspiration
and
drainage.
Buboes
may result
in
scarring.
lymph nodes
(usually
unilateral)
“Groove sign” delineation of
nodes by
inguinal
ligament
Tenderness and
inflammation of
lymph nodes
Bubo- abscess
formation
within lymph
node
Fever, chills,
night sweats,
HA, malaise,
myalgias
Leukocytosis