Lourence M.

Patagoc block 1 SGD group 1

Module 2 GYNE case

HIRSUTISM AND VIRILIZATION

A 25-year-old G0 woman presents with complaints of increased hair growth on the face, particularly the upper lip, chin
and neck. Her menses started about age 13 and she has never had regular cycles. Her periods come every 2-4 months.
She saw a physician when she was 14 who stated that it was not uncommon to have irregular cycles initially and she has
not seen a physician since. She noted the onset of facial hair around the onset of menses and it has gradually worsened.
She has not noticed any recent increase in severity; however, she is seriously dating someone and is interested in getting
rid of this hair growth. Currently, she has been using a combination of shaving twice a week and electrolysis when she
can afford it. Her electrologist recommended this evaluation. She would like to be able to conceive in the near future
and wonders about her fertility.

Allergy and medications:

None

Ob-Gyn history:

G0. LMP: 2 months ago. Menarche: 13 years old. Cycle length: every 2-4 months. Duration: 7-10 days with heavy flow for
the first 3 days. No STD history. She has been sexually active and has used condoms for contraception. No prior pap
smear.

Past medical and surgical history:

None

Social history:

She smokes ½ p

ack of cigarettes per day for 8 years. Occasional alcohol. No street drugs. She works as a bus driver.

Family history:

A number of family members are obese. Mother has irregular cycles, obesity, diabetes, hypertension and similar facial
hair growth. Her father had some balding, obesity, hypertension and died of a heart attack at age 50. Her sister is obese,
has irregular cycles, similar facial hair growth and she has 2 children. Her 2 brothers are healthy, except for being
overweight.

VS: Ht: 5’3” Wt: 204 pounds, BP=120/80, Pulse=88, Respirations=18

Obese African-American woman in no apparent distress

Physical examination:

HEENT: NC/AT
Terminal hair is noted on the upper outer 1/3 of lip, few sparse hairs in the sideburn area and chin, neck with hair
recently shaved.

Neck: No thyromegaly palpable. Supple and no lymphadenopathy

Lungs: Clear to auscultation and percussion

CV: Nl S1 and S2. No murmurs

Chest: Few midline terminal hairs

Breasts: Few periareolar hairs. No palpable masses, discharge or nipple inversions.

Abdomen: NT, ND, obese, No hepatosplenomegaly and No striae. Terminal hair noted in a vertical band below the
umbilicus.

Extremities: Non-tender. No edema. DTRs: 2+/= bilaterally. Upper inner thighs with sparse terminal hair.

Pelvic exam:

-Normal external genitalia -Vagina: moist, pink with rugae -Cervix: Nullipara, non-tender, no lesions -Pap smear was
done -Uterus: anteflexed, anteverted, midline and normal size -Adnexae: no palpable masses and non-tender

-Rectal: peri-anal tuft of hair noted

-Ferriman-Gallwey Score: 10 (Normal <8)

Laboratory or studies:

-Urine hCG: negative

-Hgb: 11.0 Hct: 33.6

-Total Testosterone: 84 ng/dl (Normal range: 20-80)

-DHEA-S: 247 uG/dl (Normal range: 62-615 uG/dl)

-Prolactin: 15 ng/dL (Normal range <20)

-TSH: 2.6 uIU/mL (Normal range: 0.4-4.0)

-17-hydroxyprogesterone: 120 ng/dl (Normal range < 200)

-Fasting glucose: 86 (Normal: 60-110)

-Pap smear: Normal

-Endometrial biopsy with Pipelle: Hyperplasia without atypia

A. Recognize the normal variations and abnormalities in secondary sxual characteristics

 Thelarche (breast budding) developed at an average age of 11 years
 Pubarche - development of pubic hair
 Adrenarche - development of axillary hair

Abnormalities in secondary sexual characteristic

 No breast development by age 13 years (delayed puberty)

 Premature thelarche – occurs in 2 waves. Within the first 2 years and between 6 and 8.
 Premature Pubarche > increase androgen production in the adrenals.
 Premature Adrenarch> increase androgen production in the adrenals.
  Absence of menarche by age 14 years in the presence of hirsutism or history or exam suggestive of eating
disorder or excessive exercise or an outflow abnormality
 Absence of menarche by age 15 years.

In females, breasts are a manifestation of higher levels of estrogen; estrogen also widens the pelvis and increases the
amount of body fat in hips, thighs, buttocks, and breasts. Estrogen also induces growth of the uterus, proliferation of
the endometrium, and menses.

 Enlargement of breasts and erection of nipples.

 Growth of body hair, most prominently underarm and pubic hair
 Greater development of thigh muscles behind the femur, rather than in front of it (as is typical in mature males)
 Widening of hips; lower waist to hip ratio than adult males
 Elbows that hyperextend 5-8° more than male adults
 Face is more rounded, with softer features
 Smaller waist
 Upper arms approximately 2 cm longer, on average, for a given height
 Changed distribution in weight and fat; more subcutaneous fat and fat deposits, mainly around the buttocks, thighs,
and hips
 Labia minora, the inner lips of the vulva, may grow more prominent and undergo changes in color with the
increased stimulation related with higher levels of estrogen

Abnormalities in Secondary Sex Characteristics:

Correlated with HYPERANDROGENISM or androgen excess in women

 Skin Manifestations (e.g. Acne, hirsutism, alopecia)- understood via pilosebaceous unit (PSU) which is composed
of a sebaceous component and pilary component from which hair shaft arises; Abnormalities in sebaceous
components lead to ACNE; Abnormalities of the pilary unit lead to excessive growth (HIRSUTISM) or excessive
shedding (ALOPECIA)

 Virilization
- Relatively uncommon clinical finding; usually associated with markedly elevated levels ofcirculating
testosterone (> 2 ng/mL)
- Signs (Masculinizing)- temporal balding, clitoral hypertrophy, decreased breast size, dryness of the
vagina, and increased muscle mass.
 Are almost always AMENORRHEIC

B. Define hirsutism and virilization

1. Hirsutism, which is defined as androgen-dependent excessive male-patternhair growth, affects approximately

10% of women. Cutaneous manifestations commonly associated with hirsutism include acne and male-pattern
balding (androgenic alopecia). The presence of hirsutism without othersigns of virilization is associated with a
milder increase in androgenic activity.

2. Virilization refers to a condition in which androgen levels are sufficiently high to cause additional signs and
symptoms, such as deepening of the voice, breast atrophy, increased muscle bulk, clitoromegaly, and increased
libido. Virilization has a longer and mre gradual onset
C. Describe the pathophysiology and identify etiologies of hirsutism

Hirsutism is an androgen dependent disorder resulting from interaction between circulating androgen
levels and the increased sensitivity of the hair follicles or the hypersecretion of androgens. The skin can
 convert testosterone into a more potent dihydrotestosterone and binds to androgen receptors ot the
pilocebaceous follicles.

Dihydrotestosterone(DHT) is the androgen that acts on the hair follicle to produce terminal hair. This hormone
is derived from both the bloodstream and local conversion of a precursor, testosterone. The local production of
dihydrotestosterone is determined by 5- alpha-reductase activity in the skin. Differences in the activity of this
enzyme may explain why women with the same plasma levels of testosterone can have different degrees of
hirsutism.

ETIOLOGY OF HIRSUTISM

 Polycystic ovary syndrome. This most common cause of hirsutism is caused by an imbalance of sex hormones that
can result in irregular periods, obesity, infertility and sometimes multiple cysts on your ovaries.
 Cushing's syndrome. This occurs when your body is exposed to high levels of the hormone cortisol. It can develop
from your adrenal glands making too much cortisol or from taking medications such as prednisone over a long
period.
 Congenital adrenal hyperplasia. This inherited condition is characterized by abnormal production of steroid
hormones, including cortisol and androgen, by your adrenal glands.
 Tumors. Rarely, an androgen-secreting tumor in the ovaries or adrenal glands can cause hirsutism.
 Medications. Some medications can cause hirsutism. These include danazol, which is used to treat women with
endometriosis; systemic corticosteroids and fluoxetine (Prozac) for depression
 idiopathic

D. Describe the steps in evaluation and initial management options for hirsutism and virilization

Initial Management options:

1. elimination of specific cause

a. removal of ovarian or adrenal tumor

b. suppress excess androgen production
c. ilimination of the drugs that suspected to contribute to the abnormal hair growth
d. treatment of the cushings syndrome, thyroid disease, hyperprolactinemia
2. suppression of the androgen synthesis

A. Oral contraceptives reduces LH production

B. Spironolactone inhibits testosterone production
C. flutamide and cyproterone acetate, androgen blockers
D. Eflornithine hydrochloride 13.9% is an irreversible inhibitor of L-ornithine decarboxylase, which slows and
shrinks hair.

For the patient’s case PCOS secondary to obesity type II, she wants to conceive

 Weight reduction
 Ovulation induction
- Clominophine citrate
 Insulin sensitaion
- Meformin
- Metformin + clominophene citrate
2)EVALUATION
E. Describe how hirsutism and virilization are manifested in other medical disorders

Cushing Syndrome and Cushing Disease:

1. Cushing syndrome: An adrenal tumor produces ↑ levels of cortisol with clinical fi ndings—hirsutism,
menstrual irregularity, central obesity, moon face, buffalo hump, abdominal striae, weakness, and muscle
wasting. Exogenous or endogenous cortisol can be the cause. Confi rm diagnosis with dexamethasone
suppression test.
2. Cushing disease (pituitary disease)

is a subset of Cushing syndrome. A benign pituitary adenoma causes an ↑ in the secretion of adrenocorticotropic
hormone (ACTH) which results in ↑ cortisol levels. It accounts for 70% of Cushing syndromes. Virilization and
hirsutism are associated with this condition because the ACTH stimulates androgen production as well.

3. Paraneoplastic syndromes, in which tumors (usually small cell lung cancer) produce ectopic ACTH, also cause ↑
cortisol. These account for 15% of Cushing syndromes.

4.Adrenal tumors (adenoma or carcinoma) account for the remaining 15% of Cushing syndromes. In general,
adenomas produce only cortisol, so no hirsutism or virilization is present. Carcinomas, by contrast, often produce
androgens as well as cortisol, so they may present with signs of hirsutism and virilization. DHEA-S is markedly elevated,
and hirsutism and virilization has a rapid onset. Computed tomography (CT) or magnetic resonance imaging (MRI) can
confi rm the diagnosis.

Congenital Adrenal Hyperplasia (CAH)

Caused by a congenital defect in an enzyme that produces cortisol.

21-hydroxylase deficiency: The most common form of congenital adrenal hyperplasia. The condition has various levels
of severity. Affected individuals lack an enzyme crucial to cortisol and mineralocorticoid production. Therefore, the ↑
precursors of cortisol are shunted to androgen production. Elevated serum 17-hydroxyprogesterone is used as a marker
for establishing the diagnosis of 21-hydroxylase deficiency. In the severe form, affected females have ambiguous
genitalia at birth, along with severe salt wasting and cortisol insufficiency. Lateonset 21-hydroxylase deficiency resents
with varying degrees of virilization and hirsutism in females after puberty.

11β-hydroxylase deficiency: Associated with ↓ cortisol, but ↑ mineral corticoids and androgens. A typical patient
with this enzyme defi ciency has severe hypertension with virilization/hirsutism (which results in
pseudohermaphroditism of female babies). 11-deoxycortisol levels are high in 11β-hydroxylase deficiency.
MENOPAUSE

Discussions and questions:

A. What are the symptoms of menopause

1. Menstrual alteration
- Beginning at approximately 40 years of age, the number of a woman’s ovarian follicles diminishes,
and subtle changes occur in the frequency and length of menstrual cycles. A woman may note
shortening or lengthening of her cyclesHot flushes and vasomotor instability
- As a woman approaches menopause, the frequency of ovulation decreases from 13 to 14 times per
year to 11 to 12 times per year. With advancing reproductive age, ovulation frequency may decrease
to 3 to 4 times per year.
2. Hot flashes
- are recurrent, transient episodes of flushing, perspiration, and a sensation ranging from warmth to
intense heat on the upper body and face, sometimes followed by chills.
- The hot flush is the most common symptom of decreased estrogen production and is considered
one of the hallmark signs of perimenopause
3. Sleep disturbance
- Declining estradiol levels induce a change in a woman’s sleep cycle so that restful sleep becomes
difficult and for some, impossible. The latent phase of is lengthened; the actual period of sleep is
shortened
4. Vaginal dryness and genital tract atrophy
- With decreasing estrogen production, these tissues become atrophic, resulting in various symptoms.
The vaginal epithelium becomes thin and cervical secretions diminish.
5. Mood changes
6. Skin, hair, and nail changes
 7. Osteoporosis
- Estrogen receptors are present in osteoblasts, which suggests a permissive and perhaps even an
essential role for estrogen in bone formation. Therefore decrease estrogen=decrese bone formation
and repair
8. Cardiovascular disorders
- Total cholesterol increases, high-density lipoprotein (HDL) cholesterol decreases, and low-density
lipoprotein (LDL) cholesterol increases
B. How do you make the diagnosis of menopause
- Physical exam
C. What are the patient’s risk factors for osteoporosis
- Rarely exercise
- Smoker (2packs per day)
- Decrease estrogen
- Family history of osteoporosis
D. How do you diagnose and treat osteoporosis

Treatment:

 Hoemone therapy

- The most widely used contain a combination of conjugated equine estrogens and
medroxyprogesterone acetate in one tablet.

- Newer preparations include a combination of micronized estradiol and norethynodrel acetate or

ethinyl estradiol and norethindrone acetate.
- Transdermal preparations include a combination of micronized estradiol and norethindrone
acetate.
- Low-dose oral contraceptives may also be used to relieve the vasomotor symptoms of menopause.
 Alternative therapies for the shortterm treatment of common symptoms of menopause
• Soy and isoflavones may be helpful in the short-term (≤2 years) treatment of vasomotor
symptoms. Given the possibility that these compounds may interact with estrogen, these agents
should not be considered free of potential harm in women with estrogen-dependent cancers.
• St. John’s wort may be helpful in the short-term (≤2 years) treatment of mild to moderate
depression in women.
• Black cohosh may be helpful in the short-term (≤6 months) treatment of women with
vasomotor symptoms.
• Soy and isoflavone intake over prolonged periods may improve lipoprotein profiles and
protect against osteoporosis. Soy in foodstuffs may differ in biological activity from soy and
isoflavones in supplements.
E. What laboratory and diagnostic test would you order for this patient
 BRACA screening
Infertility

A 37-year-old female and her 37-year-old husband present with the complaint of a possible fertility problem. The couple
has been married for 2 years. The patient has a 4-year-old daughter from a previous relationship. The patient used birth
control pills until one-and-a- half-years-ago. The couple has been trying to conceive since then and report a high degree
of stress related to their lack of success.
The patient reports good health and no problems in conceiving her previous pregnancy or in the vaginal delivery of her
daughter. She reports that her periods were regular on the birth control pill, but have been irregular since she
discontinued taking them. She reports having periods every 5-7 weeks.
Past history is remarkable only for mild depression. Imipramine 150 mg qhs for the last 8 months is her only medication.
She works as a cashier, runs 12-24 miles each week for the last 2 years, and has no history of STDs, abnormal Paps,
smoking, alcohol or other drugs. She has had no surgery.
The patient’s partner also reports good health and reports no problems with erection, ejaculation or pain with
intercourse. He has had no prior urogenital infections or exposure to STDs. He has had unprotected sex prior to his
current relationship, but has not knowingly conceived. He has no medical problems or past surgery.
He works as a long-distance truck driver and is on the road 2-3 weeks each month. He smokes a pack of cigarettes a day
since age 18 and drinks 2-3 cans of beer 3-4 times a week when he’s not driving. He occasionally uses amphetamines to
stay awake while driving at night. The couple has vaginal intercourse 3-5 times per week when he is at home.
The patient is 5’9” and weighs 130 pounds. Breast exam reveals no tenderness or masses, but bilateral galactorrhea on
compression of the areola. Pelvic exam reveals normal genitalia, a well-estrogenized vaginal vault mucosa and cervical
mucus consistent with the proliferative phase. The uterus is anteflexed and normal in size without masses or
tenderness. Several tests were orderd.

A. Define infertility.
Infertility is defined as inability to achieve pregnancy after 12 months ofunprotected and frequent intercourse
within reproductive age (15-44)
B. List the causes of male and female infertility.
Causes of Female infertility
Ovulation disorders
 Polycystic ovary syndrome (PCOS)
 Hypothalamic dysfunction
 Premature ovarian failure.
 Too much prolactin
Damage to fallopian tubes (tubal infertility)

 Pelvic inflammatory disease,

 Previous surgery in the abdomen or pelvis-- adhesions
 Previous ectopic (tubal) pregnancy
 Pelvic tuberculosis
Uterine or cervical causes

 Benign polyps or tumors

 Endometriosis/ fibroid
 Uterine abnormalities present from birth
 Cervical stenosis
 Abnormal cervical mucus
 Infections
DES syndrome (DES, given to prevent miscarriage can result infertility)
Prior bilateral salpingectomy, total abdominal hysterectomy with bilateral salpingo-oophorectomy

Causes of male infertility: abnormal male reproductive tract or abnormal semen quality

C. Describe the evaluation and initial management of an infertile couple.

Fig:Diagnostic algorithm for the basic evaluation of the infertile couple. BBT, basal body temperature; EMB, endometrial
biopsy; FSH, follicle-stimulating hormone; HSG, hysterosalpingogram.(Chantilis SJ, Carr BR: Evaluation and treatment of
the infertile couple. In Quilligan EJ, Zuspan F [eds]: Current Therapy in Obstetrics and Gynecology. Philadelphia, WB
Saunders, pp. 83–90, 2000.)

Fig: Treatment algorithm for infertile couples with oligo-anovulation. Fig: Treatment algorithm for elevated cycle
day 3 FSH
D. Describe the psychosocial issues associated with infertility.

E. Describe management options for infertility.

Treatment for men

Men's options can include treatment for general sexual problems or lack of healthy sperm. Treatment may include:

 Altering lifestyle factors. Improving lifestyle and behavioral factors can improve chances for pregnancy, including
discontinuing select medications, reducing/eliminating harmful substances, improving frequency and timing of
intercourse, establishing regular exercise, and optimizing other factors that may otherwise impair fertility.
 Medications. Certain medications may improve a man's sperm count and likelihood for achieving a successful
pregnancy. These medicines may increase testicular function, including sperm production and quality.
 Surgery. In select conditions, surgery may be able to reverse a sperm blockage and restore fertility. In other cases,
surgically repairing a varicocele may improve overall chances for pregnancy.
 Sperm retrieval. These techniques obtain sperm when ejaculation is a problem or when no sperm are present in
the ejaculated fluid. They may also be used in cases where assisted reproductive techniques are planned and
sperm counts are low or otherwise abnormal.

Treatment for women

Although a woman may need just one or two therapies to restore fertility, it's possible that several different types of
treatment may be needed before she's able to conceive.

 Stimulating ovulation with fertility drugs. Fertility drugs are the main treatment for women who are infertile due
to ovulation disorders. These medications regulate or induce ovulation. Talk with your doctor about fertility drug
options — including the benefits and risks of each type.
 Intrauterine insemination (IUI). During IUI, healthy sperm are placed directly in the uterus around the time the
woman's ovary releases one or more eggs to be fertilized. Depending on the reasons for infertility, the timing of
IUI can be coordinated with your normal cycle or with fertility medications.
 Surgery to restore fertility. Uterine problems such as endometrial polyps, a uterine septum or intrauterine scar
tissue can be treated with hysteroscopic surgery

F. Describe ethical issues confronted by patients with infertility.

Higher-Order Multiple Births

Between 1997 and 2009, the use of IVF has increased 84 %, yet the number of embryos transferred and multiple
pregnancies, have decrease. However, several scholars believe that physicians should remain concerned with
multiple pregnancy rates due to the many risks to both infants and the mother, as well as the high medical costs
associated with delivery, neonatal care, and long-term complications of HOMB. Ethical issues surrounding
HOMB often revolve around the principle of parental responsibility, which posits that people should not be only
concerned with their own interests in reproducing, but also the welfare of the child. This can be applied to
potential or existing children; thus, an assessment of the resources available to the parent(s) for both obtaining
and caring for children enter into this equation. Manninen implicates various people and entities that should be
held ethically accountable for HOMB, which include the patient, clinic, media that glamorizes HOMB, and
insurance companies that do not cover certain fertility treatments and thus drive people to utilize fewer and
riskier attempts at assisted reproduction.
 Egg Banking

The health risk for women donating oocytes for somatic cell nuclear transfer (SCNT) has been an indirect
argument against embryonic stem cell research. One such risk is ovarian hyperstimulation syndrome (OHSS),
which some say women are not adequately warned about during the consent process. Others, however, have
argued that incidence rates of OHSS are not applicable to oocyte donors, especially if proper precautions are
taken. New developments may help to defuse this debt. First, new stimulation protocols, such as replacing
human chorionic gonadotrophin (hCG) with hLH or gonadotropin-releasing hormone (GnRH) for women who do
not have PCOS, has been suggested to reduce the risk of OHSS. Second, “spare” oocytes may soon be available,
negating the need to stimulate women solely for research purposes. With vitrification (ultrarapid freezing) and
improvements to slow-freezing methods, freezing oocytes is becoming more efficient. If oocytes, rather than
embryos, are frozen, this should deter ethical problems for both patients and policymakers who attribute a high
moral value to the embryo .With the creation of a limited number of embryos for each cycle, few will become
supernumerary. First, this will help lessen couple-level conflicts surrounding embryo disposition if a
disagreement arises (e.g., divorce), because the woman will be the sole decision maker regarding her oocytes.
Second, it is likely that when given a choice regarding the outcome of unused genetic materials (destruction,
donation for science, or donation for reproduction), many women will donate to science due to fewer ethical
and psychological ramifications Moreover, Mertes and Pennings contend that this new freezing method will
result in increased “social freezing,” where women bank their oocytes until a time when they are ready to
reproduce. The oocytes of women who have not found a partner by the time they reach the age limit could be
donated to science, as could the oocytes from “medical freezers.”This two-phased donation cycle of stimulation
and pickup, followed by donation, could avoid the ethical questions of donors being lured into taking
unnecessary risks for a study with uncertain benefit.

Psychosocial Distress and Counseling

During the past few years, more attention has been paid to the emotional distress associated with infertility and
the process of assisted reproduction, including greater attention to subgroups of infertile women

G. Identify the impact of genetic screening and testing on infertility associated treatments.
o It is estimated that genetics are a contributing factor in up to 10 percent of couples who experience infertility or
recurrent pregnancy loss, so it stands to reason that genetic testing has the potential to help many of those
couples in their quest to have a family.
o Genetic testing examines DNA, which has been called the “chemical database” that carries instructions for the
body’s functions and can reveal gene changes that may cause illness or disease, including infertility. Since both
men and women can have fertility issues, they can all benefit from genetic testing.
o Identifying a genetic cause for your infertility can help you make the right decision on how to proceed by
choosing the treatments that are most likely to help.
o Additionally, genetic testing is advised before you have children if you or your partner has a family history of a
genetic disorder, such as sickle cell anemia, Tay-Sachs disease or cystic fibrosis. Such testing can reveal if either
or both of you carry a copy of an altered gene that would put a child at risk of developing the disorder.
o Genetic abnormalities may affect sperm production or transport. Genetic testing is indicated in men with
azoospermia(no sperm) and severe oligospermia. The most common abnormalities identified include gene
mutations in the cystic fibrosis transmembraneconductase regulator (CFTR),somatic and sex chromosome
abnormalities, and micro-deletions of the Y chromosome. Men with mutations in one or both copies of the CFTR
gene often exhibit congenital bilateral absence of the vas deferens or other obstructive defects, and many have
no pulmonary symptoms. A karyotype may reveal abnormalities, such as Klinefeltersyndrome(47 XXY) or
chromosome inversions and translocations.
Special testing must be performed to search for Y chromosome microdeletions, because they are not detected
 by routine karyotype analysis; these microdeletions are associated with altered testicular development and
spermatogenesis.
o If a genetic condition is identified, genetic counseling is strongly recommended.

Discussion Questions:

1. What is the definition of infertility?

Inability to become pregnant despite 12 months of trying to conceive without using contraception. About 15% of
couples experience this problem.

2. What are the etiologies of infertility?

o Ovulatory dysfunction (around 20%) - anovulation

o Male factor (around 30%) – decreased sperm count, decreased motility or normal forms
o Tubal and pelvic (30%) – tubal damage due to pelvic infection, pelvic factor - endometriosis, pelvic adhesions
o Unexplained (10%)
o Unusual problems (10%)

3. What is the initial work-up for infertile couples and what tests would you add for this particular couple?
o Physical examination
o Medical history
o Semen analysis
o Check for ovulation – basal body temperature, ovulation prediction kits, luteal phase serum progesterone
o Hysterosalpingogram: check for normal uterus and open fallopian tubes
o Discussion about frequency and timing of intercourse
o For this couple specifically, TSH and prolactin
4. Studies were reviewed and showed a normal TSH, a prolactin of 60 ng/ml (normal range < 20 ng/ml) and a semen
analysis with 2cc of semen, 4 million sperm per ml, 30% normal forms and 20% motility. Basal body temperature chart
shows a monophasic temperature graph. What is the differential diagnosis at this point?
o Anovulation secondary to hyperprolactinemia from imipramine
o Oligospermia – repeat semen analysis once or twice to confirm the diagnosis

5. What is the appropriate management for both these diagnoses?

o For anovulation secondary to imipramine, the patient should taper her imipramine. If she was still anovulatory,
the patient could empirically use clomiphene citrate for ovulation induction

o For oligospermia, options include in vitro fertilization, artificial insemination with partner’s sperm, artificial
insemination with donor sperm, adoption.
DYSMENORRHEA

Clinical case

A 14-year-old female comes to your office complaining of severe dysmenorrhea (painful periods) for the past six months.
She began menstruating 10 months ago with her first two periods occurring about 2 months apart without pain or any
other symptoms. Since then, she menstruates every 28 days and also notices nausea, diarrhea and headaches during her
periods. The pain has gotten so bad for 3 days each month that she often misses school.

You speak to the patient without her mother and ask if she has ever been sexually active in any way. The patient denies
this activity and you believe her. She is a good student, is involved in sports and after school programs, and you think it is
unlikely that she is pretending to have dysmenorrhea to get out of school. She denies use of drugs or alcohol, and you
believe it is unlikely she is drug seeking. She says that she gets partial relief by using 3-4 Advil, two or three times a day
during her period.

The review of systems, past medical history and social history are noncontributory. The patient’s mother, but no other
relatives, has endometriosis

Physical exam:

The patient’s vital signs are normal and she id afebrile. Abdominal exam reveals no masses or organomegally, and no
tenderness or rebound. Because patient is virgin and you don’t want to induce undue pain, you defer the pelvic exam
anf do a rectal exam showing a normal size, nontentder uterus, which is mobile and anteflexed. There are no nodules on
the back of the uterus and there is no adnexal mass or tenderness.

Laboratory:

Urinalysis is negative for blood, nitrites and leukocytes

DISCUSSIONS AND QUESTIONS

1. Define dysmenorrheal and distinguish primary from secondary dymenorrhea

Dysmenorrhea is defined as painful menstruation that prevents a woman from performing normal activities. It
may also be accompanied by other symptoms, including diarrhea, nausea, vomiting, headache, and dizziness.

Primary Dysmenorrhea Secondary Dysmenorrhea

  Caused by an excess of prostaglandins,  clinically identifiable cause
leading to painful uterine muscle activity

2. Describe the pathophysiology and identify the itiologies of dysmenorrheal

Primary dysmenorrhea Secondary Dysmenorrhea

 Caused by excess prostaglandin F2  Secondary dysmenorrhea is caused by structural
produced in the endometrium. abnormalities or disease processes that occur
Prostaglandin production in the uterus outside the uterus, within the uterine wall, or
normally increases under the influence of within the uterine cavity
progesterone, reaching a peak at, or soon
after, the start of menstruation. With the
onset of menstruation, formed prostaglandins
are released from the shedding endometrium.
Prostaglandins are
- potent smooth-muscle stimulants that
cause intense uterine contractions,
resulting in intrauterine pressures that
can exceed 400 mm Hg and baseline
intrauterine pressures in excess of 80
mm Hg.
- Prostaglandin F2α also causes
contractions in smooth muscle
elsewhere in the body, resulting in
nausea, vomiting, and diarrhea.
- In addition to the increase in
prostaglandins from endometrial
shedding, necrosis of endometrial
cells provides increased substrate
arachidonic acid from cell walls for
prostaglandin synthesis.
- Prostaglandin E2 is also produced in
the uterus. Prostaglandin E2, a potent
vasodilator and inhibitor of platelet
aggregation, has been implicated as a
cause of primary menorrhagia

3. Discuss steps in the evaluation and management of dysmenorrheal

 History and PE
- Patient complains of midline, crampy lower abdominal pain
- Can be severe and involves the lower back and thighs
- Pain gradually resolves 12-72 hrs
- Does not occur on times other than menses and only in ovulatory cycles
 Primary dysmenorrhea

- Providing patient education and reassurance

- Individualized supportive therapy can be tailored to patient’s specific symptoms
 Non pharmacologic interventions
 Exercise
 Hot compress
 Behavioral interventions
 Medical interventions
 NSAIDS
 Combined contraceptives
 Progestin only formulations
 tocolytics
 MODULE 3 GYNE CASES

Lourence M. Patagoc block 1 SGD group 1

Uterine leiyomyoma

1. What are the likely causes of the mass

Leiomyomata are considered hormonally responsive, benign tumors, because estrogen may induce their
rapid growth in high-estrogen states, such as pregnancy
2. Describe the pathological changes
Bleeding is the most common presenting symptom in uterine fibroids. Although the kind of abnormal bleeding
may vary, the most common presentation includes the
 development of progressively heavier menstrual flow that lasts longer than the normal duration
(menorrhagia, defined as menstrual blood loss of >80 mL). This bleeding may result from significant
distortion of the endometrial cavity by the underlying tumor.
Three generally accepted but unproved mechanisms for increased bleeding include:
1. Alteration of normal myometrial contractile function in the small artery and arteriolar blood supply
underlying the endometrium
2. Inability of the overlying endometrium to respond to the normal estrogen/progesterone menstrual
phases, which contributes to efficient sloughing of the endometrium
 3. Pressure necrosis of the overlying endometrial bed, which exposes vascular surfaces that bleed in excess
of that normally found with endometrial sloughing

3. Discuss the appropriate management of women with fibroids

TREATMENT
Most patients with uterine myomas do not require (surgical or medical) treatment. Treatment is
generally first directed toward the symptoms caused by the myomas. If this approach fails (or there are other
indications present), surgical or other extirpative procedures may be considered.
For example,
 if a patient presents with menstrual aberrations that are attributable to the myomas, with bleeding that
is not heavy enough to cause her significant hygiene or lifestyle problems—and the bleeding is also not
contributing to iron-deficiency anemia—reassurance and observation may be all that are necessary.
 Further uterine growth may be assessed by repeat pelvic examinations or serial pelvic ultrasonography.
 An attempt may be made to minimize uterine bleeding by using intermittent progestin supplementation
and/or prostaglandin synthetase inhibitors, which decrease the amount of secondary dysmenorrhea and
amount of menstrual flow.
 If significant endometrial cavity distortion is caused by intramural or submucous myomas, hormonal
supplementation may be ineffective. If effective, this conservative approach can potentially be used until
the time of menopause.
Of the surgical options available, myomectomy is warranted in patients who desire to retain childbearing
potential or whose fertility is compromised by the myomas, creating significant intracavitary distortion
Although hysterectomy is commonly performed for uterine myomas, it should be considered as definitive
treatment only in symptomatic women who have completed childbearing. Indications should be specific and
well-documented.
In addition to surgery, pharmacologic inhibition of estrogen secretion has been used to treat fibroids. This is
particularly applicable in the perimenopausal years when women are more likely anovulatory, with relatively
more endogenous estrogen. Pharmacologic removal of the ovarian estrogen source can be achieved by
suppression of the hypothalamic-pituitary-ovarian axis through the use of gonadotropin-releasing hormone
agonists (GnRH analogs)
4. What are the indications for hysterectomy in women with fibroids
Ovarian Neoplasms

Clinical Case:

A 48y.o G3P3 woman comes to the office for a health maintenance exam. She has no concerns. She is in good health.
She had 3 normal vaginal deliveries and underwent a tubal ligation after the birth of her 3 rd child 15 years ago. She has
no history of abnormal Pap smears or STDs. Her cycles are regular and her LMP was 18 days ago. She is not taking any
medications. Her family history is significant for a maternal aunt who was diagnosed with ovarian cancer at age 60. On
examination, she has normal vital signs. Her heart, lungs and abdominal exams are normal. On pelvic examination, she
has a normal external genitalia, normal vagina and cervix. On bimanual exam, she has a slightly enlarged uterus and a
palpable right adnexal mass which is confirmed on the vagino-rectal exam.

Discussion Questions:
1. What is the next step in management of this patient?
 BRACA assessment
 Periodic surveillance with TVUS
 Prophylactic oophrectomy, salphingo-oophrectomy (since she underwent tubal ligation)
 biomarker evaluation CA-125 (>35 U/mL is increased )
2. How would you’re approach be different if the patient was postmenopausal at 62 yrs of age?
 3. You obtain an ultrasound which shows a 6 cm right complex ovarian cyst. What is your differential diagnosis?
- Gonadal stromal tumors
- Sertoli-Leydig cell tumors
- Germ cell tumors (teratomas)
- Serous/mucinous cystadenoma
- Endometiod tumors

4. What risk factors does this patient have for ovarian cancers?
Risk factors:
 Familial history - Answer
 Familial history of breast cancers
 Personal history of breast and ovarian cancers
 Genetic mutation of BRCA tumor suppressor gene on chromosome 17q
 1.5% - 5% ↑ risk with one first-degree relative with ovarian cancer
 7% - 12% ↑ risk with 2 or more relatives with ovarian cancer

 Related to frequent ovulation

 Late menopause
 Nulliparity
 Late childbearing
 Ovulation – inducing drugs
 Gonadotropin
 Clomiphene citrate
 hCG
 GnRH
 Diet high in animal fat (saturated fat)
 Most frequent in
 United States and Western Europe
 More frequent among White women
5. List physical exam elements which help support or rule out the diagnosis of ovarian cancer?
Rule In Rule Out
Slightly enlarged uterus Normal Vital Signs
Palpable right adnexal mass confirmed on the Normal PE
vagino-rectal exam Normal Pelvic Exam

6. Assuming the mass is persistent and you need to surgically explore the patient, describe the pre-operative, intra-
operative and post-operative management of this patient.
Postoperative Instructions: Pelvic Surgery

After you have had your pelvic surgery, there are a variety of steps that need to be taken to make sure that you recover
as fully and quickly as possible.

1. What you should eat: When you go home you will be eating a regular diet or what ever specific diet may be needed
for any medical condition that you have (high blood pressure, diabetes, etc.) It will take a while for your intestines to
completely recover, therefore we recommend that you : a) eat multiple small meals, b) avoid hot, spicy, and fatty
foods, c) east lots of fruits, vegetables, and high bulk foods. If there are any other special restrictions or guidelines, your
doctor will inform you prior to your discharge.
2. What you should drink: It is very important that you stay adequately hydrated after the surgery. Therefore, we
recommend that you drink at least 3 quarts of liquid a day. You should try to drink more in the early part of the day
(before the end of the afternoon) so that you don't have to get up to go to the bathroom at night.
3. What you should do: When you go home you will be walking around, probably without assistance. It is important
that you be as active as possible to avoid infections, blood clots, and slow intestinal recovery. Don't just sit in the chair
and watch TV!! You can climb steps, walk outside, go to Services, go shopping, etc. You cannot drive a car or lift
anything more than 25 pounds. If you were doing regular aerobic exercises, you should not restart them until your
doctor tells you that it is OK to do such. Most women can resume normal sexual relations in about 6 weeks after the
surgery.
4. Discharge Medications: You will be going home on some specific medications.
These include a pain medication, a stool softener, and any other medications that your physician feels may be needed.
Make sure that you re-read the instructions on the medication bottles and take them the way that they are prescribed.
You also should continue to take the medications that you were taking prior to being admitted to the hospital.
5. Return Visits: You will need to return to see your surgeon about one week to 10 days after your surgery. At that time,
you will have your incision checked, any questions that you may have will be answered, and you will be given
instructions as to what more you physically can do (like drive a car). We usually request that patients return again in
about 4 to 6 weeks after surgery for their final post-operative visit. This may be changed if there are any problems with
healing.
6. Returning to Work: How soon you can return to work will depend upon what type of surgery you had and how
quickly you recover. Most people who don't have a large abdominal incision can return to work about 2 weeks after
surgery. Women who have a large incision usually take about 4 weeks to recover before they are ready to go back to
work. Remember these are just general guidelines and your doctor will discuss the specifics with you when you return
for your post-operative visits.

What to expect after surgery

When you wake up from surgery, you will be in a recovery room near the operating theatre. Once you are fully
conscious, you will be taken back to your bed on the hospital ward.
Tubes and drips
You will have several tubes in place, which will be removed as you recover:
 a drip inserted into a vein in your arm (intravenous drip) will give you fluid, medicines and pain relief
 a small plastic tube (catheter) may be inserted into your bladder to collect urine in a bag
 a tube may be inserted down your nose into your stomach (nasogastric tube) to drain stomach fluid and prevent
vomiting
 tubes may be inserted in your abdomen to drain fluid from the site of the operation.
Pain
After an operation, it is common to feel some pain, but this can be controlled. For the first day or two, you may be given
pain medicine through a drip or via a local anaesthetic injection into the abdomen (a transverse abdominis plane or TAP
block) or spine (an epidural). Some patients have a patient-controlled analgesia (PCA) system. This machine allows you
to self-administer a measured dose of pain relief by pressing a button. Let your doctor or nurse know if you are in pain
so they can adjust the medicine. Managing your pain will help you to recover and move around more quickly.
Injections
It is common to have daily injections of a blood thinner to reduce the risk of blood clots. These injections may continue
for some time after the operation and while you're having chemotherapy. A nurse will show you how to give this
injection to yourself before you leave hospital.
Compression devices and stockings
Some women have to use compression devices or wear elastic stockings to keep the blood in their legs circulating. Once
you are moving around, compression devices will be removed so you can get out of bed, but you may still wear the
stockings for a couple of weeks.
Wound care
You can expect some light vaginal bleeding after the surgery, which should stop within two weeks. Your doctor will talk
to you about how to keep the wound clean once you go home to prevent it becoming infected.
Length of stay
You will probably stay in hospital for 4–7 days for a big operation, less for a laparoscopy or smaller operation.
Taking care of yourself at home after surgery
Your recovery time will depend on the type of surgery you had, your general health, and your support at home. Most
women are able to fully return to their usual activities after 4–8 weeks.
Rest
Take things easy and do only what is comfortable. You may like to try meditation or some relaxation techniques to
reduce tension.
Lifting
Avoid heavy lifting (more than 3–4 kg), hanging out the washing, or vacuuming for at least six weeks. Use a clothes horse
or dryer instead of hanging the washing on a line. If you have a partner or children, ask them to help around the house.
You can also check with a social worker if it's possible to get help at home.
Driving
You will most likely need to avoid driving for a few weeks after the surgery. Check with your car insurer for any
conditions regarding major surgery and driving.
Work
Depending on the nature of your work, you will probably need 4–6 weeks leave from work.
Bowel problems
You may have constipation following the surgery. It is important to avoid straining when passing a bowel motion, so you
may need to take laxatives.
Nutrition
To help your body recover from surgery, focus on eating a balanced diet (including proteins such as lean meats and
poultry, fish, eggs, milk, yoghurt, nuts, seeds and legumes/beans).
Sex
Sexual intercourse should be avoided for about six weeks after the operation to give your wounds time to heal. Ask your
doctor when you can resume sexual intercourse and explore other ways you and your partner can be intimate, such as
massage.
Exercise
Your health care team will probably encourage you to start walking the day after the surgery. Exercise has been shown
to help people manage some of the common side effects of treatment, speed up a return to usual activities and improve
overall quality of life. Start with a short walk and go a little further each day. Speak to your doctor if you would like to try
more vigorous exercise.
Bathing
Take showers instead of baths, and avoid swimming for 4–6 weeks after surgery.
Further treatment
Your doctor should have all the test results within two weeks of surgery. Further treatment will depend on the type of
ovarian cancer, the stage of the disease and the amount of any remaining cancer. If the cancer is advanced, it's more
likely to come back, so surgery will usually be followed by chemotherapy, and occasionally by targeted therapy.
Radiation therapy is not often recommended.

Pre-operative Preparation for Pelvic Surgery

After the decision has been made to proceed with pelvic surgery, there are a variety of steps that need to be
taken to make sure that you are completely prepared for the surgery:
1. Scheduling
2. Pre-operative testing: Every individual undergoing surgery needs some degree of assessment to make sure
that the surgery can be done as safely as possible. This assessment may include blood tests, imaging studies
(chest x-rays, CT scans, ultrasounds, etc.) and cardiograms (EKG). We try to have these done as soon as possible
after the decision to have surgery is made so that if there is anything that is abnormal it can be corrected. Special
tests that we recommend for you are:
3. Blood donation: The vast majority of women undergoing pelvic surgery never need a blood transfusion.
However, if your surgeon thinks that you have a 5% chance or more of needing a transfusion, he or she may
recommend that you donate a unit of your own blood, if possible. This will be arranged by the OR Coordinator.
4. Pre-operative Medicine or Anesthesia Consultation: Just like with pre-operative testing, there are some
women who need to be more intensively evaluated prior to the surgery to make sure that everything that can be
done is done before the operation to make the surgery as safe and successful as possible.
5. Bowel Preparation: Pelvic surgery is safer and easier if the lower intestine has been completely cleaned.
Therefore, your surgeon wants you to complete a bowel preparation prior to you having the surgery.
6. Medications you are taking: It is important that you continue to take the medications that you need to keep
you healthy. Therefore, on the morning of your surgery, please take the medications that your doctors have
prescribed but take them with the smallest amount of plain water needed to swallow them.
7. Fasting before Surgery: Beginning at midnight the night before surgery you should have absolutely nothing to
eat or drink except for the medications that your doctors have prescribed (see # 6 above).

The main preoperative concerns include the

anesthetic implications of chemotherapeutic agents, evaluation of organ system affliction by the
malignancy/metastasis, problems due to ascites, DVT (Deep Vein Thrombosis) prophylaxis and discussions
regarding options of perioperative pain management [10]. Pre-anesthetic evaluation must be
extensive and thorough.

Intra-operative care must focus on managing the hemodynamics during fluid/blood loss; maintaining
oxygenation, normothermia and normocarbia; supplementing analgesia with epidural
drugs; and preventing perioperative
metabolic/electrolyte derangements.

Endometrial Carcinoma

Clinical Case:

A 56y.o G0 presents to the clinic with complaints of intermittent vaginal bleeding. She went through the menopause 2
years ago and had no vaginal bleeding until 6 months ago when she had a 3 day episode of light bleeding. Since that
time, she has had another 3 such episodes. Past medical history is remarkable for well-controlled HPN, depression and
“borderline” diabetes for which the patient is on a diet to which she minimally adherent. She never used contraceptives
but was unable to become pregnant. She has had a laparoscopic cholecystectomy. She takes Lisinopril and Zoloft. Her
family history is non-contributory. On examination, she has normal vital signs, she weighs 247 pounds. Her heart, lungs
and abdominal exams are normal. On pelvic examination, she has normal external genitalia, normal vagina and cervix.
The bimanual exam is difficult secondary to the patient’s habitus, but the uterus feels slightly enlarged and no adnexal
masses are palpable.

Discussion Questions:
1. What is your differential diagnosis for this patient?
 Endometrial hyperplasia
 Endometrial polyp
 Endometrial carcinoma
  Endometriosis
 Cervical carcinoma
2. What is the etiology of endometrial cancer?
Endometrial carcinoma is typically a disease of postmenopausal women. Between 15% and 25% of
postmenopausal women with bleeding have endometrial cancer. A majority of cases are diagnosed while in
stage I (72%). Most primary endometrial carcinomas are adenocarcinomas because squamous epithelium
maycoexist with the glandular elements in an adenocarcinoma. In cases where the squamous element is benign
and makes up less than 10% of the histologic picture, the term adenoacanthomais used. Uncommonly, the
squamous element may appear malignant on histologic assessment and is then referred to as adenosquamous
carcinoma. Other descriptions, such as clear cell carcinoma and papillary serous adenocarcinoma,may be
applied, depending on the histologic architecture. All of these carcinomas are considered under the general
category of adenocarcinoma of the endometrium and are treated in a similar manner.

3. What risk factors does this patient have for endometrial cancer?
 Nulliparous (G0)
 Age (56 years old)
 Obesity (247 lbs)(BMI >30kg/m2)
 Diabetes

4. What factors are protective against endometrial cancer?

 Combination oral contraceptives protect against endometrial cancer, with most studies showing a
relative risk reduction to approximately 0.5. The protection begins after 1 year of use and lasts
approximately 15 years after discontinuation.
 Progestin therapy
 Multiparity
 Menopause before 49 years old

5. What are the next steps in diagnostic work up of this patient?

 Transvaginal Ultrasound
 Postmenopausal women with any vaginal bleeding should be evaluated with an office endometrial
sampling or a D&C.
 Pap smear
 Heteroscopy if the cause of abdominal bleedingis not clear from the tissue obrtained

6. You obtain an ultrasound which shows a 10 cm uterus and no adnexal masses. Endometrial biopsy reveals
complex hyperplasia with atypia. Are further diagnostic tests indicated?
 Controversy re: need for formal D&C in the OR
 15-40% of patients with diagnosis of endometrial hyperplasia have co-existing early stage endometrial
cancer
 Diagnosis/treatment is primarily surgical although medical management is used in exceptional cases

7. How would you manage this patient?

 Pre-operative work-up: Physical exam and CXR as staging is primarily surgical

 Intra-operative: Staging procedures include pelvic washings, TAH/BSO, lymph node dissection, except in
women with early stage disease (like this patient)
 In early stage disease (Stage1, Grade1) hysterectomy with BSO is sufficient
 Stage 1 – Limited to uterus
 Stage 2 – Tumor invades cervix but not beyond
 Stage 3 – Local or regional spread
  Stage 4 – Distant metastases
 Post-operative: Depends on stage of endometrial cancer, most common adjuvant therapy is radiation:
vaginal brachytherapy
 Non-surgical management is sometimes chosen by nulliparous women and by women with such major
co-morbidities that surgery is not an option
 Treatment with high dose progestin (provera, megace)
 Most respond but diligent follow-up essential given high recurrence

Cervical diseases and neoplasia

Discussion questions:
1. How many Pap smear should this patient have had given her age and clinical history. Discuss the guidelines
 ACOG recommendation for pap smear
- Start screening at 21 yrs old every 3 yrs until the age of 30
 PSCPC recommendation for pap smear

2. Which historical risk factors does this patient have for having cervical dysplasia or for having cervical dysplasia
progress to cervical cancer
 >1 sexual partner
 Smoking
  Infrequent or pap smear test

3. What is meant by the term “ high-grade scquamous intraepithelial lesion ”

An area of abnormal cells that forms on the surface of certain organs, such as the cervix, vagina, vulva,
anus, and esophagus. High-grade squamous intraepithelial lesions look somewhat to very abnormal when
looked at under a microscope. They are usually caused by chronic infection with certain types of human
papillomavirus (HPV) and are found when a Pap test or biopsy are done. If not treated, these abnormal cells may
become cancer and spread to nearby normal tissue. 
4. What would you recommend as the next step in the evaluation of this patient’s abnormal Pap smear
5. Would typing for the human papilloma virus aid in the management of this patient.
Yes. Because the rate of CIN 2 or CIN 3 is so high in adults with HSIL cytologic findings, immediate
treatment with the loop electrosurgical excision procedure is an acceptable management approach.
In women planning a future pregnancy, the risks of a LEEP procedure—which include preterm delivery,
premature rupture of membranes, and low-birthweight infants—should be taken into consideration.
The other management approach is colposcopic examination, followed by appropriate treatment and
follow-up.

6. From a reproductive health perspective , how would you council this particular patient about smoking
cessation.
 Smoking is associated with cervical intraepithelial neoplasia and invasive CC. Multiple factors seem to
intervene on cervical carcinogenesis related with tobacco, especially by direct local carcinogenic effect and local
immunosuppression. Smoking addition is also closely related with other confounding factors, like unfavorable
psychosocial events, systemic immunity, contraception, and nutrition, which got difficult epidemiologic
evaluation of smoking role on cervical carcinogenesis. Smoking habits should be taken in account.
Endometrial Carcinoma

Clinical Case:

A 56y.o G0 presents to the clinic with complaints of intermittent vaginal bleeding. She went through the menopause 2
years ago and had no vaginal bleeding until 6 months ago when she had a 3 day episode of light bleeding. Since that
time, she has had another 3 such episodes. Past medical history is remarkable for well-controlled HPN, depression and
“borderline” diabetes for which the patient is on a diet to which she minimally adherent. She never used contraceptives
but was unable to become pregnant. She has had a laparoscopic cholecystectomy. She takes Lisinopril and Zoloft. Her
family history is non-contributory. On examination, she has normal vital signs, she weighs 247 pounds. Her heart, lungs
and abdominal exams are normal. On pelvic examination, she has normal external genitalia, normal vagina and cervix.
The bimanual exam is difficult secondary to the patient’s habitus, but the uterus feels slightly enlarged and no adnexal
masses are palpable.

Discussion Questions:
8. What is your differential diagnosis for this patient?
 Endometrial hyperplasia
 Endometrial polyp
 Endometrial carcinoma
 Endometriosis
 Cervical carcinoma
9. What is the etiology of endometrial cancer?
Endometrial carcinoma is typically a disease of postmenopausal women. Between 15% and 25% of
postmenopausal women with bleeding have endometrial cancer. A majority of cases are diagnosed while in
stage I (72%). Most primary endometrial carcinomas are adenocarcinomas because squamous epithelium
maycoexist with the glandular elements in an adenocarcinoma. In cases where the squamous element is benign
and makes up less than 10% of the histologic picture, the term adenoacanthomais used. Uncommonly, the
squamous element may appear malignant on histologic assessment and is then referred to as adenosquamous
carcinoma. Other descriptions, such as clear cell carcinoma and papillary serous adenocarcinoma,may be
applied, depending on the histologic architecture. All of these carcinomas are considered under the general
category of adenocarcinoma of the endometrium and are treated in a similar manner.

10. What risk factors does this patient have for endometrial cancer?
 Nulliparous (G0)
 Age (56 years old)
 Obesity (247 lbs)(BMI >30kg/m2)
 Diabetes

11. What factors are protective against endometrial cancer?

 Combination oral contraceptives protect against endometrial cancer, with most studies showing a
relative risk reduction to approximately 0.5. The protection begins after 1 year of use and lasts
approximately 15 years after discontinuation.
 Progestin therapy
 Multiparity
 Menopause before 49 years old

12. What are the next steps in diagnostic work up of this patient?
 Transvaginal Ultrasound
  Postmenopausal women with any vaginal bleeding should be evaluated with an office endometrial
sampling or a D&C.
 Pap smear
 Heteroscopy if the cause of abdominal bleedingis not clear from the tissue obrtained

13. You obtain an ultrasound which shows a 10 cm uterus and no adnexal masses. Endometrial biopsy reveals
complex hyperplasia with atypia. Are further diagnostic tests indicated?
 Controversy re: need for formal D&C in the OR
 15-40% of patients with diagnosis of endometrial hyperplasia have co-existing early stage endometrial
cancer
 Diagnosis/treatment is primarily surgical although medical management is used in exceptional cases

14. How would you manage this patient?

 Pre-operative work-up: Physical exam and CXR as staging is primarily surgical

 Intra-operative: Staging procedures include pelvic washings, TAH/BSO, lymph node dissection, except in
women with early stage disease (like this patient)
 In early stage disease (Stage1, Grade1) hysterectomy with BSO is sufficient
 Stage 1 – Limited to uterus
 Stage 2 – Tumor invades cervix but not beyond
 Stage 3 – Local or regional spread
 Stage 4 – Distant metastases
 Post-operative: Depends on stage of endometrial cancer, most common adjuvant therapy is radiation:
vaginal brachytherapy
 Non-surgical management is sometimes chosen by nulliparous women and by women with such major
co-morbidities that surgery is not an option
 Treatment with high dose progestin (provera, megace)
 Most respond but diligent follow-up essential given high recurrence
Gestational Trophoblastic Neoplasia (GTD)

Clinical Case:

A 15-y.o primigravida presents for routine prenatal care. She is 14 weeks pregnant by LMP. She has some nausea but
otherwise feels well. The pregnancy to date has been unremarkable. She has support from her parents and the father of
the baby.

The uterus is enlarged, measuring 27 cm from the pubic symphysis. FHT are not auscultated by Doppler. She denies
vaginal bleeding or passage of tissue from vagina. Vaginal exam is unremarkable.

Routine prenatal labs were unremarkable. She is Rh(+). Quantitative β-hCG levels were markedly elevated at 112,320
µICU/mL. TSH was low and further thyroid testing revealed the patient to be mildly hyperthyroid.

U/S showed the uterus to be enlarged, with multiple internal echoes and a “snow storm” appearance. No fetus is noted.
U/S also showed enlarged multi-loculated ovarian cysts bilaterally. CXR was normal.

Discussion Questions:
1. What is the differential diagnosis?
 Poor dates, most likely if irregular menses
 Complete hydatidiform mole
 Partial hydatidiform mole
 Beckwith-Wiedemann syndrome
 Placental angiomatous formation
 Existing fetus

2. What additional evaluation is needed to confirm the diagnosis?

(1) CBC
(2) AST, ALT
(3) LDH
(4) Urinalysis
(5) Electrolytes
(6) Pt & ptt to check for:
(7) Chest x-ray anemia, electrolyte imbalance, DIC
(8) Blood type with antibody and preeclampsia, matastasis screening

3. What is the final diagnosis?

- Complete Hydatidiform mole. Because of the :
i) Lack of fetal tissues
ii) Gestational age of 14 wks
iii) Large for date uterus= 27 cm in a 14 wks AOG
iv) Hyperemesis
v) High levels of beta hcg >100,000 IU/L
vi) Mild Hyperthyroidism
vii) multiple internal echoes and a “snow storm” appearance

1. What is the epidemiology and clinical course of this condition?

Epidemiology:
- Highest incidence occurs among Asian women.(1 in 200 pregnancies)
- Incidence in United states is approximately 1 in 1500 pregnancies, with recurrence rate of 1%-2%.
- More common in older women -associated with low dietary carotene consumption and Vit. A def.
- Partial moles are associated with history of infertility And spontaneous abortion

Clinical presentation
- Painless first /second trimester vaginal bleeding -lack of fetal heart tones
- US: imaging confirms the diagnosis of molar pregnancy characterized by “snowstorm” appearance
- Absence of fetal parts(complete mole), fetus often present (partial mole)

Molar pregnancies may present with other signs and symptoms:

- Severe nausea, vomiting -marked elevated gestational hypertension
- Proteinuria -(rare)clinical hyperthyroidism
- Most of these findings can be attribute to high levels of hCG produced by abnormal pregnancy. -some
patients experience tachycardia -shortness of breath -bimanual pelvic exam reveals large adnexal
massas(theca lutein cysts)
2. What is your management plan?
Tx:
- Dilatation and curettage
- Hysterectomy
- Profilactic chemotherapy
 MODULE 3 OB CASES

MULTIFETAL GESTATION

DISCUSSION QUESTIONS

1. Discuss the etiology of multiple gestation

- Two or more fertilization events
 Single fertilization followed by a splitting of the zygote
 Fertilization of two eggs by 2 sperms
- Increase of maternal age
- Assisted Reproductive Technology
- Ovulation induction

2. Discuss the zygosity of twin gestation , understanding diagnosis and complications unique to each
 Twin gestations can be characterized as dizygotic (fraternal) or monozygotic (identical). Dizygotic twins
occur when two separate ova are fertilized by two separate sperm. Monozygotic twins result from the
division of the fertilized ovum after conception
 Chorionicity is when the monozygotic conceptus separates into twins
 Diamnionic/Dichorionic: If division of the conceptus occurs within 3 days of fertilization, each fetus
will be surrounded by an amnion and chorion
 Diamnionic/Monochorionic: If division occurs between the 4th and 8th day following fertilization,
the chorion has already begun to develop, whereas the amnion has not. Therefore, each fetus will
later be surrounded by an amnion, but a single chorion will surround both twins.
 Monoamnionic/Monochorionic: In 1% of monozygotic gestations, division occurs between days 9
and 12, after development of both the amnion and the chorion, and the twins will share a common
sac. Division thereafter is incomplete, resulting in the development of conjoined twins. The fetuses
may be fused in a number of ways, with the most common involving the chest and/or abdomen.
This rare condition is seen in approximately 1 in 70,000 deliveries. This condition is associated with a
mortality rate of up to 50%.

Twin–Twin Transfusion Syndrome

As development of a monochorionic gestation progresses, various vascular anastomoses between the
fetuses can develop that, in turn, can lead to a condition known as twin–twin transfusion syndrome.
In this circumstance, through arterial-venous anastomoses, there is net flow from one twin to another,
often with untoward pregnancy outcomes.

donor twin recipient twin

 can have:  can develop
- impaired growth - hypervolemia
- anemia - hypertension
 - Hypovolemia - Polycythemia
- other problems - Congestive heart
failure as a result of
this preferential
transfusion
Amniotic fluid  hypovolemia leads to decreased  hypervolemia which leads to an
dynamics urinary output and, possibly, a increase in urinary output and, in turn,
decrease in amniotic fluid volume to an increase in amniotic fluid
(oligohydramnios). volumes (hydramnios)


3. Duscuss antepartum , intrapartum and postpartum management and complications of twin gestation
a) Antepartum

b) Intrapartum
is largely determined by the presentation of the twins. In general, if the first (presenting) twin is
in the cephalic (vertex) presentation, labor is allowed to progress to vaginal delivery, whereas if the
presenting twin is in a position other than cephalic, cesarean delivery is often performed.
During labor,
 heart rate of both fetuses is monitored separately
 Approaches to the delivery of twins vary, depending on:
- gestational age or estimated fetal weight
- presentation of the twins
 - the experience of the attending physicians.
Regardless of the delivery plan, access to full obstetric, anesthetic, and pediatric services is
mandatory because cesarean delivery may be required on short notice. About 40% of all twin pairs enter
labor with both in the cephalic (vertex) presentation.
After delivery of the first twin, if the second fetusremains cephalic, vaginal delivery of the
second twin generally proceeds smoothly. With proper monitoring of the second twin, there is no
urgency in accomplishing the second delivery. If the second twin is presenting in any way other than
cephalic (40% of all twin deliveries), there are two primary manipulations that may affect vaginal
delivery. The first is external cephalic version. Using ultrasonographic visualization, the fetus is gently
guided into the cephalic presentation by abdominal massage and. The second maneuver is breech
extraction, in which the physician reaches a hand into the uterine cavity, grasps the lower extremities of
the fetus, and gently delivers the infant via breech delivery. Delivering the second twin via cesarean
delivery is another management option, but is usually reserved for inability to safely deliver vaginally.
The possibility of a prolapsed umbilical cord must always be borne in mind when delivery of twins is to
be accomplished. Twin gestations in which the first twin is in the breech presentation (20% of all twin
deliveries) are most often delivered via cesarean delivery. Some clinicians and their patients plan for
cesarean delivery unless both fetuses are in a cephalic presentation
c) Postpartum
The overdistended uterus may not contract normally, leading to uterine atony and postpartum
hemorrhage, therefore management of post partum hemorrhage is done.
 Uterotonic agents
- Oxytocin
- Ergot alkaloids
- Carboprost tromethamine
- Dinoprostone
- Misoprostol (not DFA approved )
 Benign bimanual uterine compression
 Balloon tamponade
d) complications of twin gestation
 spontaneous abortion
 congenital malformations
 low birthweight
 hypertension
 preterm birth
 long term infant development
Lourence M. Patagoc block 1 SGD group 1

1. What should every physician needs to know about hypertension in pregnancy?

 Classification of hypertensive disease in pregnancy

 Severity
 Gestational age
 Presence of preeclampsia

2. What other clinical features that you should ask in the history?

 presence of headache
 -presence of visual disturbances like scotomata
 -shortness of breath
 -family history of pre eclampsia
 -presence of chronic hypertension
 -BMI if high there is higher chance
 -platelet count (decrease in pre eclampsia)

3. What are the key points in the management for all types of hypertensive disorders of pregnancy? What is the initial
treatment guidelines?

MANAGEMENT
The goal of management of hypertension in pregnancy is to balance the management of both fetus and mother and to
optimize the outcome for each. Maternal blood pressure should be monitoredand the mother should be observed for
the sequelaeof the hypertensive disease. Intervention for maternal indicationsshould occur when the risk of permanent
disabilityor death for the mother without intervention outweighs therisks to the fetus caused by intervention. For the
fetus, thereshould be regular evaluation of fetal well-being and fetalgrowth, with intervention becoming necessary if the
intrauterineenvironment provides more risks to the fetus thandelivery with subsequent care in the newborn nursery.

4.
4. What is the emergent management?

1. Control of convulsions using an intravenously administered loading dose of magnesium sulfate that is followed by a
maintenance dose, usually intravenous, of magnesium sulfate.

2. Intermittent administration of an antihypertensive medication to lower blood pressure whenever it is considered

dangerously high.

3.Avoidance of diuretics unless pulmonary edema is obvious, limitation of intravenous fluid administration unless fluid
loss is excessive, and avoidance of hyperosmotic agents

4.Delivery of the fetus to resolve preeclampsia.

6. What is the specific treatment?

 Between 24-34 weeks, corticosteroid should be given to enhance fetal lung maturity
-Betamethasone= 12 mg IM every 24 hours for 2 doses
-Dexamethasone = 6 mg IM every 12 hours for 4 doses
 Labetalol = 10-20mg IV then 20-80 mg every 20 minutes, maximum of 300mg
 Hydralazine = 5 mg IV, then 5-10 mg every 20-40 minutes- once BP is controlled repeat every 3 hours
 Nifedipine = 10-20 mg orally, repeat in 30 minutes if needed, then 10-20 mg po every 2-6 hours
 Methyldopa = 0.5 -3 g/day in 2-3 divided doses
The goal of antihypertensive therapy is not to normalize BP, but to achieve a range of 140-150/90-100 mmHg- to
prevent repeated prolonged exposure of the patient to severe systolic HPN, with subsequent loss of cerebral
vasculature autoregulation.
 Magnesium Sulfate(MgSO4.7H2O USP)
 For women with eclampsia the administration of parenteral MgSO4 is recommended
  For women with severe preeclampsia, the administration of parenteral MgSO4 during expectant mgt. is
recommended
 For women with severe preeclampsia-give intrapartum, postpartum MgSO4-to prevent eclampsia
 For severe preeclampsia women undergoing cesarean delivery- the continued intraoperative administration of
parenteral MgSO4-to prevent eclampsia is recommended
 MgSO4 is the therapy of choice for eclampsia
 The IV route has few side effects
 MgSO4 is mostly excreted in the urine
Urine output should be closely monitored and if it becomes reduced below 20 ml/hour, the magnesium infusion
should be halted.
Bec magnesium is cleared exclusively by renal excretion, plasma magnesium concentration is excessive if the
glomerular filtration rate is decreased.
The ideal standard dose of MgSO4 can be safely administered without knowledge of renal function.
Renal function is thereafter estimated by measuring serum creatinine. And whenever it is 1.3mg/dl or higher,
only half of the maintenance dose is given.
 MgSO4 toxicitycan be assessed by clinical assessment of the maternal deep tendon reflexes(DTRs) and
respiratory rate (RR)
If there is loss of the DTRs and the respiratory rate falls below 12 cycles /minute, MgSO4 infusion should be
halted
Calcium gluconate 1 gram(10ml) over 10 minutes can be given if there is concern of MgSO4 toxicity.
 MgSO4 is the the drug of choice for the prevention of convulsions among patients with severe preeclampsia
who are managed expectantly.
These patients should receive MgSO4 for 24 hours during expectant management.
The dose depends on the patient’s body weight. Two grams per hour is given if the patient weighs >70 kg.
Patient’s weighing < 70 kg can receive 1 gram/hour infusion.
If BP is controlled adequately and fetal testing is reassuring, MgSO4 is discontinued after 24 hours.
MgSO4 is cleared by the kidneys 5 hours after the last dose.
MgSO4 is continued up to 24 hours postpartum

7) What are the indications for delivery?

For chronically hypertensive women who have complications such as fetal-growth restriction or superimposed
preeclampsia, the decision to deliver is made by clinical judgment. The route of delivery is dictated by obstetrical factors.
Certainly, most women with superimposed severe preeclampsia are better delivered even when there is a markedly
preterm pregnancy.These women are at increased risk for placental abruption, cerebral hemorrhage, and peripartum
heart failure.
For women with mild to moderate chronic hypertension who continue to have an uncomplicated pregnancy, there are
at least two options for timing of delivery. The first is delivery at term, that is, ≥ 39 completed weeks. Another option is
consideration for delivery at 38 to 39 weeks, that is, ≥37 completed weeks. A trial of labor induction is preferable, and
many of these women respond favorably and will be delivered vaginaL
8. how will you  monitor, follow up and dispose hypertensive  disorders of pregnancy?
9. How will you prognosticate Preeclampsia?

Preeclampsia is a self-limiting condition of pregnancy that usually resolves once the placenta has been delivered,
although it may persist for a few days post delivery. There are few long-term sequelae; however, there are some long-
term disease associations.

Disease course

The course of preeclampsia is altered by treatment, and the condition can be controlled easily in most patients, usually
within a few hours of starting treatment. Once controlled, the length of the disease depends on when delivery is
decided. After delivery, the condition normally settles within 2 to 4 days; however, some women have hypertensive
problems and proteinuria for some weeks after.

Recurrence

The overall risk of recurrence in subsequent pregnancies ranges from about 10% to 50%, depending on the severity of
preeclampsia, the gestation it occurred at, and subsequent interventions in the next pregnancy. Generally, in previous
severe or early onset (i.e., <30 weeks) preeclampsia, the risk of recurrence is 50%. In mild to moderate or late-onset
preeclampsia, the risk of recurrence is reduced to around 10%.
Long-term disease associations

Women with preeclampsia have an increased long-term risk of type 2 diabetes, cardiovascular disease, including
hypertension and stroke. There are no clear guidelines on the long-term follow-up of women who have had
preeclampsia. However, an evaluation of their risk for cardiovascular disease should include previous preeclampsia
alongside body mass index and other lifestyle factors.

Monitoring

After initial assessment and stabilization, monitoring needs to be at intervals dictated by the severity of the
condition. Blood pressure should be monitored regularly for rising levels, need for intervention, and response to
therapy; however, there is little guidance on how often this should be. A good guide is at least 4 times per day on a
ward, or continuously in an intensive care unit. Laboratory tests (i.e., complete blood count, liver function tests, renal
function) should be monitored at least twice weekly (daily if severity dictates). There is no strong evidence linking the
level of proteinuria with adverse outcome; therefore, once a diagnosis has been made, there is no benefit in repeating
urinalysis.

Fetal cardiotocography should be done no more than twice weekly, unless there is a cause for concern such as
vaginal bleeding, reduced fetal movements, or increased severity of disease, in which case it should be done daily, or
continuously if delivery is planned. Umbilical artery Doppler velocimetry and fetal ultrasound are recommended twice
weekly.

After delivery, continued maternal monitoring is required until the condition has improved. This can be done as
an outpatient if the condition allows. If the condition has not completely improved by 6 weeks, the diagnosis should be
reconsidered and a referral to the appropriate specialist for investigation instigated.

Patient Instructions

There is very little the patient can do once the condition has been diagnosed; however, the need for hospitalization and
early delivery should be explained. After delivery, there are various organizations that the patient may find useful.
Postpartun infection
1. What are the risk factors for post partum infection
 Route of delivery
- Vaginally 1-2%
- Cesarean 25 fold increase
 Membrane rupture 5-6%
 Prolonged labor 5-6%
 Multiple cervical exams 5-6%
 Chorioamnionitis 13%
2. List the microorganisms – etiology for puerperal sepsis

3. Identify prophylaxis that will decrease the likelihood of endometritis after c-section
 Antimicrobial profilaxis
- Single dose prophylaxis with a 2g dose amphicilin or 1st generation cephalosphorin
- For obese women, 3g dose of cefazolin
 - Extended-spectrum prophylaxis with single dose azithromycin after cesarean delivery
 Abdominal preoperative skin preaparation to prevent surgical sit infections
- Chlorhexidine alcohol
4. Discuss the sequelae of puerperal sepsis

- abscesses, or pockets of pus

- peritonitis, or an inflammation of the abdominal lining

- pelvic thrombophlebitis, or blood clots in the pelvic veins

- pulmonary embolism, a condition in which a blood clot blocks an artery in the lungs.

- sepsis or septic shock, a condition in which bacteria get into the bloodstream and cause

dangerous inflammation

Souces:
 Williams Obstetrics 25th edition
 Beckmann And Lings Obstetrics And Gynecology 8 th edition
 Comprehensive Gynecology 7th edition