Study Notes Obstetrics Gynecology

Study Notes – Obstetrics & Gynecology James Lamberg 28Jul2010
Textbooks: Essentials of Ob/Gyn, Ob/Gyn Secrets, First Aid for Ob/Gyn Clerkship
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Common Problems in Obstetrics & Gynecology
Pregnancy: Prenatal and Antepartum Care, Normal Labor and Delivery patterns, Caesarian Section, Postpartum
hemorrhage, Postpartum infection
Complications: Diabetes Mellitus, UTI, Pre-term labor, Third trimester bleeding, Hypertension, pre-eclampsia and
eclampsia, Multiple Gestations, Premature Rupture of Membranes, Post-term pregnancy
Gynecology: Abnormal and Dysfunctional Uterine Bleeding, Vaginal Infections, Pelvic Masses, Endometriosis,
Benign and Malignant Breast Disease, Contraceptive counseling, Hormonal Replacement, Cervical Dysplasia and
Cancer
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Procedures: NEJM Videos In Clinical Medicine: http://www.nejm.org/multimedia/videosinclinicalmedicine
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Pelvic Exam Tips From Gynecologists
Sexual abuse during childhood is not uncommon and a pelvic exam can bring back memories and emotions, even if
the patient has forgotten the abuse. The patient may be sensitive to the subtle nuances in physician’s words or facial
expression. The demeanor of the physician is extremely important in establishing and maintaining rapport.
Always obtain consent prior to a pelvic exam. Always have a second medical professional present for the exam and
one medical provider should be female.
If the patient is getting a pelvic exam for a non-routine visit (e.g. Pap screen), always explain why it is needed.
A good starter phrase prior to the pelvic exam is “If anything I do is uncomfortable, please let me know.”
Use neutral language during the exam. Say the exam looked “healthy” or “normal.” Do not say works like good or
great as these could be construed as references to the patient’s genitalia.
Connotation matters. Say “let your legs gently fall wide apart,” not “spread your legs.”
Show you care about the patient’s comfort during the exam. Place the warmed speculum against the patient’s leg
and ask if the temperature is good.
Telling a patient to “relax” is patronizing and basically impossible during a pelvic exam. A better method to help
relax the pubococcygeal muscles is ask the patient to push their bottom into the table like they are sinking into sand.
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How To Succeed – First Aid For The Obstetrics & Gynecology Clerkship (Stead, Stead, & Kaufman)
Be On Time: Most OB/GYN teams begin rounding between 6am and 7am. Give yourself at least 10 minutes per
patient for pre-rounding to learn about events that occurred overnight or lab/imaging results.
Dress In A Professional Manner: Regardless of what the attending wears. A short white coat should be worn over
your professional dress clothes unless it is discouraged (e.g. pediatrics).
Act In A Pleasant Manner: The medical rotation is often difficult, stressful, and tiring. Smooth out your experience
by being nice to be around. Smile a lot and learn everyone’s name. Don’t be afraid to ask how your resident’s
weekend was. If you do not understand or disagree with a treatment plan or diagnosis, do not “challenge.” Instead,
say “I’m sorry, I don’t quite understand, could you please explain...” Show kindness and compassion toward your
patients. Never participate in callous talk about patients.
Take Responsibility: Know everything there is to know about your patients: their history, test results, details about
their medical problem, and prognosis. Keep your intern or resident informed of new developments that they might
not be aware of, and ask them for any updates you might not be aware of. Assist the team in developing a plan;
speak to radiology, consultants, and family. Never give bad news to patients or family members without the
assistance of your supervising resident or attending.
Respect Patient’s Rights:
1) All patients have the right to have their personal medical information kept private. This means do not discuss the
patient’s information with family members without that patient’s consent, and do not discuss any patient in
hallways, elevators, or cafeterias.
2) All patients have the right to refuse treatment. This means they can refuse treatment by a specific individual (you,
the medical student) or of a specific type (no nasogastric tube). Patients can even refuse life-saving treatment. The
only exceptions to this rule are if the patient is deemed to not have the capacity to make decisions or understand
situations, in which case a health care proxy should be sought, or if the patient is suicidal or homicidal.
3) All patients should be informed of the right to seek advanced directives on admission. Often, this is done by the
admissions staff, in a booklet. If your patient is chronically ill or has a life-threatening illness, address the subject of
advanced directives with the assistance of your attending.
More Tips: Volunteer, be a team player, be honest, and keep patient information handy.
DO NOT DISTRIBUTE -1-

Present In An Organized Manner: “This is a [age]-year-old female with a history of [major history such as
abdominal surgery, pertinent OB/GYN history] who presented on [date] with [major symptoms, such as pelvic pain,
fever], and was found to have [working diagnosis]. [Tests done] showed [results]. Yesterday the patient [state
important changes, new plan, new tests, new medications]. This morning the patient feels [state the patient’s words],
and the physical exam is significant for [state major findings]. Plan is [state plan].”
Terminology: G (gravidity) 3 = total number of pregnancies, including normal and abnormal intrauterine
pregnancies, abortions, ectopic pregnancies, and hydatidiform moles (Remember, if patient was pregnant with twins,
G = 1.) P (parity) 3 = number of deliveries > 500 grams or ≥ 24 weeks’ gestation, stillborn (dead) or alive
(Remember, if patient was pregnant with twins, P = 1.)
Ab (abortion) 0 = number of pregnancies that terminate < 24th gestational week or in which the fetus weighs < 500
grams LC (living children) 3 = number of successful pregnancy outcomes (Remember, if patient was pregnant with
twins, LC = 2.)
TPAL: Or use the “TPAL” system if it is used at your medical school:
T = number of term deliveries (3) P = number of preterm deliveries (0) A = number of abortions (0) L = number of
living children (3)
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Top 100 Secrets – Ob/Gyn Secrets (3rd, Bader)
1) The ulcer of syphilis is usually single and painless, while the ulcer of herpes is more often multiple and painful.
2) Trichomoniasis and candidiasis are diagnosed by visualizing the organisms on microscopy of vaginal discharge;
bacterial vaginosis is diagnosed by the "whiff test" and the appearance of "clue cells".
3) PID is often a polymicrobial infection but generally begins with infection with N. gonorrhoeae or C. trachomatis.
4) Midcycle surge of luteinizing hormone (LH) predicts impending ovulation.
5) In females, the order of puberty is thelarche, pubarche, maximum growth velocity, and menarche.
6) The three most common causes of primary amenorrhea are gonadal dysgenesis, müllerian agenesis, and androgen
insensitivity.
7) The most common cause of secondary amenorrhea is pregnancy.
8) The two syndromes that are characterized by breast development and the absence of a uterus, androgen
insensitivity and müllerian agenesis, can be differentiated by a karyotype.
9) Premenstrual syndrome (PMS) is defined as the emotional and physical symptoms that occur at the same time
prior to the menstrual cycle each month.
10) Fibroids are estrogen-sensitive, fibromuscular benign tumors that are thought to originate from a monoclonal
cell line.
11) There are no diagnostic criteria for polycystic ovarian syndrome (PCOS), but common findings include
increased LH:FSH ratio, decreased fasting glucose:insulin ratio, polycystic ovaries on ultrasound, hirsutism, and
obesity.
12) Endometriosis, or endometrial tissue outside the uterus, causes pelvic pain, dyspareunia, and infertility.
13) Adenomyosis, or endometrial tissue in the myometrium, causes menorrhagia and dysmenorrhea.
14) All pelvic pain is not gynecologic in origin.
15) Ovarian failure is normal at menopause (average 51 years old) and premature at > 40 years; it requires work-up
in women < 30 years old.
16) Risks of ovulation induction include multiple gestation and ovarian hyperstimulation.
17) Initial evaluation of an infertile couple should include basal body temperature chart to assess ovulation, semen
analysis, hysterosalpingogram to check tubal patency, then postcoital test to evaluate cervical mucus.
18) In vitro fertilization (IVF), a procedure used to overcome tubal or male factor infertility, requires ovarian
hyperstimulation with injectable gonadotropins, egg retrieval, fertilization, and embryo transfer.
19) Stress incontinence is loss of urine due to increased intra-abdominal pressure, and urge incontinence is due to
detrusor instability.
20) Stress incontinence can be due to urethral hypermobility or, less commonly, intrinsic sphincter deficiency.
21) 15-20% of clinically recognized pregnancies end in miscarriage, but this risk is decreased to 6-8% once
embryonic cardiac activity is seen.
22) The most common type of chromosomal abnormality in miscarriages is autosomal trisomies, but the single most
common karyotype is monosomy X.
23) Legalization of abortion has significantly reduced the number of women hospitalized with complications of
abortions.
24) Patients with ectopic pregnancies usually present with abdominal pain and abnormal vaginal bleeding.
25) In a normal pregnancy, beta-hCG levels approximately double every 48 hours.

26) Combination oral contraceptives (OCPs) work primarily by inhibiting ovulation through suppression of LH and
FSH.
27) OCPs decrease the risk of ovarian and endometrial cancers.
28) The phases of the sexual response cycle are excitement, plateau, orgasm, and resolution.
29) Vaginismus is often associated with a history of sexual abuse or trauma.
30) Symptoms of menopause include irregular then absent menses, hot flashes, and vaginal atrophy or dryness.
31) Vulvar cancer is predominantly squamous cell and spreads via lymphatics to superficial inguinal nodes.
32) Paget's disease of the vulva may be associated with underlying adenocarcinoma; therefore, local excision is
recommended.
33) Human papillomavirus (HPV) can trigger genital dysplasia and is linked to invasive cervical cancers.
34) The incidence of cervical cancer is decreasing secondary to regular screening with Pap smears.
35) Cervical cancer is staged clinically with exam under anesthesia, cystoscopy, and proctoscopy.
36) Important risk factors for endometrial cancer include obesity, anovulation, and tamoxifen use.
37) The most common presenting symptom of endometrial cancer is abnormal uterine bleeding, especially
postmenopausal bleeding.
38) Sex cord and germ cell tumors are usually diagnosed early and are highly curable, while epithelial ovarian
cancer presents late in the disease.
39) Meigs syndrome mimics advanced-stage ovarian cancer but actually involves benign ovarian fibroma associated
with ascites and pleural effusion.
40) The highest risk for serious injury or death is when or after an abused woman leaves her abuser.
41) The incidence of domestic violence increases during pregnancy and postpartum.
42) A woman with a history of a child with a neural tube defect needs 4 mg of folic acid prenatally, but those
without such a history need only 400 mcg.
43) Advanced maternal age is associated with increased chromosomal abnormalities, increased first-trimester losses,
and increased risk of most obstetric complications.
44) An increase in plasma volume that is greater than the increase in red blood cell mass causes the dilutional
physiologic anemia of pregnancy.
45) Pregnancy is a hypercoagulable state due to increased clotting factors and venous stasis.
46) To decrease group B streptococcal neonatal sepsis, the CDC recommends maternal screening for the bacteria via
vaginal and rectal cultures in the late third trimester and prophylaxis with antibiotics in labor for those who test
positive.
47) The nonfasting 1-hour, 50-gm glucose tolerance test is used to screen for gestational diabetes, and the fasting 3-
hour, 100-gm glucose tolerance test confirms the diagnosis.
48) The recommended weight gain in pregnancy is 25-35 pounds for normal weight women.
49) Nausea and vomiting of pregnancy typically begin around the fourth to the seventh week and end by the twelfth
week.
50) There is no method proven to prevent preeclampsia, and the only cure is delivery.
51) Magnesium sulfate is given to preeclamptic women during labor and for 24 hours after delivery to prevent
seizures.
52) If a woman has a history of gestational diabetes, her lifetime risk of developing type 2 diabetes is 36%.
53) To decrease the malformation risk in patients with insulin-dependent diabetes mellitus (IDDM), good glycemic
control should be achieved prior to conception.
54) Circulating T4 and T3 increase in pregnancy secondary to increased thyroid-binding globulin, but free levels are
unchanged.
55) The risk of congenital anomalies is 2-3 times higher than baseline in women on anticonvulsants, but the risk is
increased above baseline even in women with epilepsy not on medications.
56) Cardiac output increases in pregnancy, first by increased stroke volume, then by increased heart rate.
57) Women with cardiac valvular disease and ventricular septal defects should receive subacute bacterial
endocarditis prophylaxis at the time of vaginal delivery.
58) Treatment of asthma in pregnancy is essentially the same as in nonpregnant women.
59) Pulmonary embolism is the leading cause of maternal mortality in the U.S.
60) During pregnancy, increased renal plasma flow and increased glomerular filtration rate lead to decreased serum
BUN and creatinine.
61) Pregnancy increases the risk of pyelonephritis due to anatomic changes, changes in urine content, and increased
progesterone affecting ureteral motility.
62) Maternal parvovirus infection can lead to fetal anemia, hydrops, and even IUFD.

63) Women with active HSV at the time of delivery should undergo cesarean section to prevent neonatal
transmission.
64) Possible fetal effects of lupus include congenital heart block and neonatal lupus.
65) There is no safe level of alcohol consumption in pregnancy; the best advice is not to drink alcohol at all.
66) Placental abruption and stillbirth occur in 8% of pregnant cocaine users.
67) Lithium, a common treatment for bipolar disorder, has been associated with cardiac malformations, especially
Ebstein's anomaly, but the extent of the risk is unclear.
68) Postpartum blues occur in 50-80% of women, depression in 8-15%, and psychosis in 1-2/1000.
69) Special considerations for general anesthesia in the pregnant woman include aspiration risk, physiologic
respiratory changes, IVC compression by gravid uterus, and hypercoagulability.
70) Initial evaluation of a pregnant trauma patient is the same as in the nonpregnant woman; stabilize the mother
before evaluating the fetus.
71) Perimortem cesarean section should be done after 4 minutes of CPR in a pregnant woman.
72) Preterm labor and delivery are much more common in multiple gestations; in fact, mean gestational length for
twins is 35 weeks; for triplets, 33 weeks; and for quadruplets, 31 weeks.
73) Twin-to-twin transfusion syndrome of monozygotic pregnancies occurs due to a placental vascular anastomosis
between the fetuses.
74) Fetal hemolytic disease can occur if the mother produces antibodies against fetal red blood cell antigens.
75) Rhogam, which is anti-D immunoglobulin, is given to Rh-negative women at 28 weeks, at other times when
fetomaternal hemorrhage may occur, and postpartum if the newborn is Rh-positive.
76) The baseline risk of congenital anomalies is 2-3%.
77) The most common autosomal disorders are trisomy 21 in live births, trisomy 18 in stillbirths, and trisomy 16 in
first-trimester losses.
78) The discriminatory zone is the β-hCG level at which an intrauterine pregnancy should be seen on ultrasound.
79) Gestational dating is done using the crown-rump length in the first trimester and biparietal diameter, head
circumference, femur length, and abdominal circumference in the second and third trimesters.
80) Although intrauterine growth restriction (IUGR) is defined as estimated fetal weight less than the tenth
percentile, most adverse perinatal outcomes occur at less than the fifth percentile.
81) Fetal urine is the major source of amniotic fluid production while fetal swallowing is the major mode of
resorption.
82) The majority of cases of polyhydramnios are idiopathic followed by maternal diabetes.
83) HCG is made by the syncytiotrophoblast to maintain the corpus luteum's production of progesterone.
84) Abnormal placental development may occur over the internal cervical os (previa), attached to the myometrium
(accreta), into the myometrium (increta), or through the myometrium (percreta).
85) Placenta previa classically presents as painless third-trimester vaginal bleeding, but placental abruption presents
as painful third-trimester vaginal bleeding.
86) Even after two consecutive mid-trimester losses due to premature cervical dilation, women have a 70-75%
chance of carrying the next pregnancy to term.
87) Cervical cerclage is indicated for treatment of cervical incompetence, but its benefit is still controversial.
88) Premature rupture of membranes (PROM) is confirmed by pooling, positive nitrazine test, and ferning of vaginal
fluid.
89) External cephalic version is a technique where one or two people attempt to maneuver a fetus from breech to
cephalic presentation.
90) Non-stress tests assess fetal heart rate baseline, variability, and accelerations and are part of antepartum fetal
surveillance to detect fetuses at risk secondary to uteroplacental insufficiency, but non-stress tests cannot predict
sudden events.
91) Intrapartum fetal heart rate monitoring has decreased the number of intrapartum fetal deaths, but it has increased
the number of cesarean sections without changing the rate of long-term neurologic sequelae or cerebral palsy.
92) Decelerations are characterized based on timing with contractions: early (head compression), late (uteroplacental
insufficiency), and variable (cord compression).
93) The stages of labor are stage one (onset of contractions to complete dilation), stage two (complete dilation to
delivery of fetus), and stage three (delivery of fetus to delivery of placenta).
94) The cardinal movements of labor are engagement, descent, flexion, internal rotation, extension, external
rotation, and expulsion.
95) The most common complication of cesarean section is infection, namely endometritis.

96) The main complication of vaginal birth after cesarean section (VBAC) is uterine rupture, and the level of risk
depends on the type of previous uterine incision.
97) As in the adult, neonatal resuscitation utilizes the ABCs (airway, breathing, and circulation).
98) Postpartum hemorrhage is loosely defined as blood loss greater than 500mL for a vaginal delivery and 1000mL
for a cesarean section.
99) The most common cause of postpartum hemorrhage is uterine atony.
100) The most common cause of postpartum fever is endometritis, and the greatest risk factor for this infection is
cesarean section.
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Kaplan Videos (2001) – Gynecology with Dr. Manuel Penalver, MD
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Oncology Overview
* Distal to proximal: vulva, vagina, cervix, endometrium, fallopian tubes, ovaries. Avoid using the term uterine
cancer. The uterus includes the cervix (lower part of uterus), endometrium (inner lining of the uterus).
* Vulvar cancer includes anything between the pubic symphysis to the anus including the introitus.
* Perineum (or perineal body) is defined between the vagina and the anus. Cancer of the clitoris or labia majora is
considered vulvar cancer. Cancer in the area of the perineum is also vulvar cancer.
* What is the most common gynecological cancer in the U.S.? Answer is endometrial cancer. It use to be cervical
cancer, prior to Papanicolaou smear development in about 1950. Every country that uses Pap smear with cytology
has been able to demonstrate a decrease in the incidence of cervical cancer.
* Etiology of cervical cancer is human papilloma virus (HPV). Thus, cervical cancer is technically a sexually
transmitted disease (STD) like gonorrhea or syphilis. HPV gives pre-cancer of the cervix then eventually gives you
cancer of the cervix. Pre-cancer described as dysplasias and carcinoma in situ.
* Significant difference between pre-cancer and cancer is invasion of the basement membrane. Characteristic of pre-
cancer is there is a lack of invasion of basement membrane.
* Basement membrane separates the epithelium from the stroma (connective tissue). There is no access to
lymphatics or blood vessels in the epithelium, thus no chance of metastasizing. Cancer has mortality because it
spreads to other organs. By detecting pre-cancer, you are curing the patient.
* It takes about 8-10 years to progress from pre-cancer phase to real cancer phase.
* The incidence of pre-cancer has risen drastically since 1950. Why? Because we do Pap smears now and have a
way of detecting pre-cancer. Incidence of invasive cervical carcinoma has decreased as mentioned.
* What is the most common cancer in women? Breast cancer. Most common gynecological is endometrial cancer.
* The gynecological cancer with the highest mortality is ovarian cancer. Ovarian cancer is very silent and spreads by
peritoneal seeding (or exfoliation), where cancer cells fall off the surface of the ovary and spread into the abdomen.
Ovarian cancer is usually diagnosed by family practitioner, internal medicine physician, gastroenterologist, not
primarily by the gynecologist. Cancer cells will develop on the omentum or bowel. Presenting signs include
abdominal distension or ascites. At this point, we are at stage III disease. Most other gynecologic cancers are found
at stage I or II, because they give early symptoms (e.g. bleeding after intercourse, post-menopausal bleeding).
* Ascites could be from the liver, kidney, or heart, but in a female patient consider ovary in the differential.
* Which cancer has the highest mortality in women? Answer is lung cancer.
* Incidents is highest with breast cancer, then lung cancer, then colon cancer.
* Mortality is highest with lung cancer, then breast cancer, then colon cancer.
* Cause of mortality in patients with ovarian cancer is bowel obstruction.
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Cervical Cancer Overview
* Cervix: cancer etiology is HPV.
* Most common symptom is post-coital bleeding.
* Histology is squamous cell cancer 85%. Adenocarcinoma seen in 15%.
* Mortality commonly caused by renal failure.
* Cervical cancer is the only cancer that has good screening, via Pap smear.
* Pre-cancer is dysplasia/carcinoma in situ.
* Genital warts (condyloma accuminata) is caused by HPV. Genital warts are benign and can be treated with
excision, podophyllin, laser removal. There are over 75 subtypes of HPV and those that cause genital warts (6, 11)
are not the same ones that cause cervical cancer (16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 66, 68, and 73). Types
16 and 18 account for about 70% of cervical cancer. HPV quadrivalent vaccine covers 6, 11, 16, 18.
* Pap smear screening recommendation is at age 18 or onset of sexual intercourse. Do three yearly Pap screenings, if

those are negative then you can Pap smear every other year.
* So why do we start screening non-sexually active women at age 18? Most cervical cancer arises from the
ectocervix (what you see with speculum). Endocervical carcinoma is adenocarcinoma, not HPV related.
* Ureters is very close to ureters. So growing cervical cancer obstructs ureters, leading to renal failure.
* For screening to be recommended to the general population, it has to be cost-effective. You need to decreased
disease incidence, decreased disease mortality, or find earlier disease lesions.
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Endometrial Cancer
* Endometrium: cancer etiology is estrogen.
* Most common symptom is post-menopausal bleeding.
* Histology is adenocarcinoma.
* Mortality commonly caused by metastatic disease.
* Pre-cancer is hyperplasia from estogen.
* Divide a woman’s life into 3 parts: pre-menarche prior to menarche (about age 12) and post-menopausal (about
age 52). In between is reproductive part of life, between 12 and 52, ovaries are functional.
* Every 28 days there is a full cycle. Two weeks before ovulation, the follicle is secreting estrogen. Ovulation cause
the formation of the corpus luteum that secretes progesterone. Ovulation is roughly day 14, always 2 weeks prior to
menstruation.
* In a woman’s life, when does most endometrial cancer occur? Answer is post-menopausal, when the ovaries are
not producing estrogen. But why? The characteristic of endometrial cancer patient is that she is obese. In adipose
tissue, androgens are converted into estrogen. It is unusual to see a thin patient with endometrial cancer.
* Why doesn’t every woman develop endometrial cancer when they are exposed to estrogen from the follicle every
month for 40 years? Progesterone from the corpus luteum is a protector.
* 32yo patient with endometrial cancer. What is unusual? Her age, in the reproductive age group. This patient has
polycystic ovarian (PCO) disease (Stein-Leventhal syndrome) until proven otherwise. The characteristic of
polycystic ovaries is anovulation, so there is unopposed estrogen.
* Estrogen increases “youthfulness.” There was a movement of “youthfulness forever” 1940-1950s where estrogen
only was given, endometrial cancer went up.
* Most ovarian cancer originates from the outer layer, epithelial cancer. Ovarian cancer can arise from the eggs,
germ cell cancers. The point is cells surrounding the eggs, stromal cells. These can be masculinizing, like sertoli
leydig cell tumors secreting testosterone (facial hair, cliteromegaly, baldness). They can be feminizing, like
granulosa theca, high incidence of concomitant endometrial cancer because they secrete estrogen.
* Post-menopausal bleeding is endometrial cancer until proven otherwise. Next step is endometrial sampling.
Answer is not Pap smear. Endometrial sampling can be done in the office at times. If cervix is stenotic, go to
operating room to do a dilatation and curettage (D&C). Canal is dilated with progressively larger metal rods then a
curette is inserted (like a spoon) to sample the endometrium.
* What percent of post-menopausal bleeders are endometrial cancer? Maybe 10-15%. Other 85% are atrophy. Most
common cause of post-menopausal bleeding is atrophy of the vagina/endometrium. Treat that with estrogen.
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Post-Menopausal Hormone Replacement Therapy (HRT)
* A post-menopausal woman comes to your office complaining of hot-flashes, sweats, dyspareunia (due to dry
vagina), mood changes. “My family tells me that I’m in a bad mood.” Aside from these post-menopausal quality of
life changes, there are important medical risks. These include coronary artery disease (KEEPS study) and
osteoporosis. To treat these patients, we give hormone replacement therapy (HRT). So we give estrogen. However,
we must also give progesterone to decrease the risk of developing endometrial cancer.
* Premarin (estrogen) derived from pregnant mare urine. From day 1 to day 25, give estrogen 0.625mg PO daily.
From day 15 to 25, give progesterone (e.g. Provera/medroxyprogesterone) 10mg PO daily. From day 25 to day 30,
tell the patient they will bleed (menses). Anytime you give the uterus estrogen and progesterone, you get menses.
* Only time you give estrogen only is if patient had hysterectomy (e.g. fibroid uterus). Then do Premarin 0.625mg
PO daily for the entire month, without taking a break. There is no need to protect the uterus.
* HRT used to treat hot flashes, sweats, dyspareunia, mood changes, decreases colon cancer risk, decreases
Alzheimer risk, decreases CAD risk, decreases osteoporosis. So big advantages to HRT. Why only about 20-25% of
post-menopausal women on HRT? There is an association with estrogen replacement therapy (ERT) and breast
cancer. No prospective randomized study had proven this in the early 2000s, now studies going both ways. All the
prior data was from retrospective studies. 2002 WHI study created a stir and many patients stopped taking HRT
without consulting their physician. In the end, HRT is not all good or all bad; there are risks and benefits.

* Number one cause of mortality to women in this country is heart disease. When does heart disease occur? Post-
menopausal, where there is less estrogen. Patient has a much higher chance of dying from heart disease than from
breast cancer. So weigh the benefits of HRT (less heart disease) with the risks (more breast cancer). Let the patient
decide. No point in arguing because the data is not completely accurate. Routine mammography should be done
routinely as well, with baseline at 35-40yo. Between 40-50yo, every two years. After 50yo, every year.
* Is there an ideal selective estrogen? We want all benefits and no breast cancer association. A selective estrogen
receptor modulator (SERM) can act as estrogen in certain body tissues. Example is tamoxifen for breast cancer or
raloxifene for osteoporosis and reducing invasive breast cancer risk. Tamoxifen and raloxifene are not ideal yet
because they do not decrease hot flashes.
* Number one reason why post-menopausal woman sees gynecologist is due to hot flashes and sweats. SERMs
cannot treat hot flashes and they increase venous thrombosis and embolism.
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Oral Contraceptive Pills (OCPs)
* Women taking estrogen during reproductive ages is usually for contraception (birth control pills, BCPs). After
menopause, estrogen is for menopausal symptoms (estrogen replacement therapy).
* How do birth control pills prevent pregnancy. Axis: Hypothalamus to pituitary (GnRH), pituitary to ovary (FSH,
LH), ovary to endometrium (steroids estrogen and progesterone). BCPs inhibit the axis, so no ovulation. The amount
of estrogen needed to inhibit the axis is much higher than that to reduce post-menopausal symptoms. Dosage is at
least 8-10 times more in contraceptives than in post-menopause symptoms.
* Woman starting on BPCs, tell them increase risk of DVT, increase risk of PE, increase risk of MI, increase risk of
stroke. This is only significant if the patient is > 35yo and smokes. >35yo is alright as long as she does not smoke.
* So a 55yo woman presents asking for ERT. She’s a smoker. Is ERT contraindicated? No, >35yo and smoker is the
risk category for birth control pills. The ERT dose is 10x lower. Smoking, although bad, is a separate issue.
* Dominant hormone of BCPs is progesterone.
* BCP benefits: contraception, best way to regulate menses, decreased ovarian cysts (inhibition of axis slows down
ovary), decreased breast cysts, decreased endometrial cancer, decreased ovarian cancer.
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Ovarian Cancer
* Ovary: cancer etiology is ovulation.
* Most common symptom is ascites or abdominal distension.
* Histology is epithelial most commonly. Germ cell cancers from eggs. Stromal cell cancers from cells around eggs.
Epithelial cancers are serous cystadenocarcinoma, mucinous cystadenocarcinoma, endometrioid, Brenner. Germ cell
cancers are dysgerminoma, endodermal sinus tumor, teratomas, choriocarcinoma. Stromal cell cancers are stromal
leydig (masculinizing) and granulosa theca (secrete estrogen).
* Mortality commonly caused by bowel obstruction.
* Pre-cancer is borderline cancer of the ovary (aka low malignant potential).
* Studies have shown that even if you screen for ovarian cancer (e.g. CA-125, post-menopausal ultrasound), you
still pick up disease at stage III. So this does not change mortality.
* Post-menopausal women get epithelial cancers, most common is serous cystadenocarcinoma.
* Teenagers get germ-cell cancers, most common is dysgerminoma.
* Between ages 12 and 52, for 40 years, the woman ovulates every month on day 14. It is thought that the trauma on
the epithelial layer every month is what causes ovarian cancer. So why doesn’t every woman develop ovarian
cancer? There are protective mechanisms. The most protective is pregnancy, because the woman does not ovulate
for 9 months. The woman who gets ovarian carcinoma is the nullipara. Birth control pills are also protective because
you do not ovulate. The longer you are on the pill, the more protection you have.
* Clomiphene or human menopausal gonadotropin (Pergonal) make a woman ovulate. So anovulation can be treated
with these; but there is data that associated ovulatory drugs with the development of ovarian cancer.
* Ovarian cancer spreads by seeding the omental cavity, irritating the omentum and bowel, leading to fluid
formation in the form of abdominal distension.
* Meig syndrome is ascites, pleural effusion (usually right-sided), and benign ovarian tumor (fibroma).
* Tumor marker of epithelial cancers is CA-125.
* Dysgerminoma tumor marker is lactate dehydrogenase (LDH). Endodermal sinus tumor marker is alpha
fetoprotein (aFP). Choriocarcinoma tumor marker is human chorionic gonadotropin (hCG); so a positive home
pregnancy test could be due choriocarcinoma.
* Dysgerminoma is similar to seminoma in male, so it responds well to radiation therapy.

* Most germ cell cancers present at stage I (versus ovarian cancer at stage III). A baby is suppose to grow rapidly
over 9 months, thus germ cell cancers grow rapidly and hurt rapidly.
* Epithelial-type ovarian cancers are treated with debulking surgery, taking out uterus, taking out ovary, bowel
resection. This is a very aggressive operation. TAH-BSO: total abdominal hysterectomy, bilateral salpingo-
oophorectomy. Omentectomy will be done too. Plus/minus bowel resection depending on metastasis. Debulking also
known as cytoreductive surgery. Then six courses of carboplatinum (carboplatin) and paclitaxel (taxol). Follow
tumor marker CA-125.
* Germ cell type ovarian cancers are treated with unilateral oophorectomy, uterus and other ovary stays, get some
chemotherapy. Be less aggressive so they can have families.
* Most important distinguishing characteristic of borderline cancer of the ovary is that it is not invasive.
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Vulvar Cancer
* Vulva: cancer etiology is HPV.
* Most common symptom is pruritus (itchiness).
* Histology is squamous cell cancer. Second most common is melanoma.
* All external gynecological cancers are HPV etiology.
* HPV leads to pre-cancer (dysplasia, carcinoma in situ) for 8-10 years leading to squamous cell carcinoma.
* You have to examine a patient with vulvar itchiness and any vulvar lesion must be biopsied. Don’t think that it
looks benign, biopsy.
* Depth of invasion is the most important prognostic factor for melanoma anywhere in the body. The only safe
depth is less than 0.76mm, not even a mm. Once the basement membrane is invaded, it tends to metastasize. Clark
level is histology-based, Breslow levels are depth-based.
* Black vulvar lesion think melanoma.
* Red vulvar lesion with icing think Paget disease of the vulva. Most of the time, Paget disease is intra-epithelial. So
it has not invaded and thus no access to lymphatics or vessels.
* To treat invasive vulvar cancer, you have to remove the vulva. This can lead to sexual dysfunction. Vulvar cancer
can go to inguinal lymph nodes, so post-op lymphedema of the legs to pain with walking and exercising. So there is
significant morbidity to the treatment of vulvar cancer.
* What is the initial treatment of Paget disease of the vulva? Answer is wide excision. If pathologist says it is
invasive, then you do the vulvectomy with lymph node removal.
* 30% of patients with red vulvar lesion (“red flag” of Paget disease) will develop cancer elsewhere. Elsewhere
could be breast, GI tract, and female genitalia.
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Vaginal Cancer
* Vagina: cancer etiology is HPV.
* Most common symptom is bloody vaginal discharge.
* Histology is squamous cell cancer.
* Mucoid discharge with blood is more suggestive of vaginal cancer.
* Patient is referred to you and has adenocarcinoma of the vagina. This should not happen. Why? This is DES
exposure until proven otherwise. DES is diethylstilbestrol, metastatic to the vagina from the endometrium or cervix.
In 1940-1950s, DES was commonly used in high-risk pregnancy to prevent miscarriage and other problems. DES
was stopped when they discovered later on that the daughter developed clear cell adenocarcinoma of the vagina or
the cervix.
* DES can also give structural abnormalities, of the uterus for example. Normal uterus is pear-shaped. DES
exposure causes higher incidence of T-shaped uterus, leading to higher rate of miscarriages and higher rate of
ectopic pregnancy. DES exposure causes higher incidence of hypoplastic cervix (small), so higher rate of
incompetent cervix that cannot hold a pregnancy. DES exposure causes higher incidence of adenosis, where the
lining of the vagina is columnar instead of squamous.
* Miscarriages in the first trimester are usually chromosomal. Miscarriages in the second trimester are usually
anatomical, such as T-shaped uterus.
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Fallopian Tube Cancer

* Fallopian Tube: cancer etiology is unknown.
* Most common symptom is clear serous vaginal discharge.
* Histology is adenocarcinoma.
* As a side note, there are three cost-effective screening tests for women. They are Pap smear, mammogram, and
colon endoscopy. Pap at age 18 or first sexual encounter. Mammogram annually at age 40. Stool guaiac annually at
age 40 and colonoscopy every 3-5 years starting at age 50. Update (2009 by ACOG): Pap smears every other year
starting at age 21 regardless of sexual activity. After age 30 and with 3 consecutive normal Pap smears, do them
every three years. Normal meaning no CIN II, no CIN III, no DES exposure, no immunocompromised, no HIV. Do
breast exams every three years starting at age 20 and mammograms routinely starting at age 40.
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Cervical Pre-Cancer Treatment
* Only difference between severe dysplasia and carcinoma in situ is how much of the epithelium is involved. Lower
third involved is severe dysplasia. If entire lower epithelium involved it is carcinoma in situ. Abnormality with HPV
starts at upper third near the basement membrane (with nuclei nearby). Next third is moderate dysplasia.
Histologically, the lower third of the epithelium is near the basement membrane (where the dysplasia starts).
Anatomically, the lower third (most distal) is the furthest from the basement membrane (where dysplasia is
considered most severe).
* CIN stands for cervical intraepithelial neoplasia.
* CIN I is mild dysplasia. CIN II is moderate dysplasia. CIN III is severe or carcinoma in situ.
* Bethesda classification uses SIL (squamous intraepithelial lesion). Low grade is LG SIL, similar to CIN I. High
grade is HG SIL, similar to CIN II-III.
* 32yo patient has moderate dysplasia of the cervix. This is pre-cancer. Moderate dysplasia could be CIN III or HG
SIL. Next step is colposcopy.
* Colposcopy is a magnification (10-12x) of the cervix. Acetic acid is used to visualize the lesions better.
* If the colposcopy lesion looks like tiles, call it mosaicism. A bunch of dots is called punctuation. A white patch is
called white epithelium. The most aggressive is abnormal blood vessels, seen in invasive cancers.
* 32yo patient has moderate dysplasia of the cervix. Next step is colposcopy. Always do an ectocervical biopsy and
an endocervical curettage (ECC).
* Describe colposcopy lesions using a clock configuration. Such as mosaicism from 2-6’o-clock.
* Say ectocervical biopsy comes back as moderate dysplasia and ECC is normal. This is pre-cancer. Next step is to
destroy the epithelium. You can destroy with heat (laser), cold (cryo), removal (wide excision). If you don’t want
the wide excision to bleed, you can do a LEEP, laser electrosurgical excision procedure. This is like a long pencil
with a loop on the end. The loop has cautery, so the heat burns and reduces bleeding. Do not do a hysterectomy; yes
this will cure the patient, but it is completely unnecessary. Cure with heat/cold/LEEP is 97%.
* Follow patient with Paps every 3 months for 2 years after one of these treatments. If it recurs, treat again.
* 32yo patient has moderate dysplasia on Pap. Say cytology is moderate dysplasia, colposcopy 2-6’o-clock
mosaicism that extends into canal. Ectocervical biopsy is moderate dysplasia and ECC is moderate dysplasia. What
is the next step? Cone biopsy. In 3-5% the cone gives an incompetent cervix (miscarriage during 2nd trimester).
These patients need a cerclage (e.g. McDonald or Shirodkar), which are sutures around the cervix.
* Indications for cone biopsy are positive ECC, unsatisfactory/inadequate colposcopy, discrepancy between
cytology and histology (e.g. Pap says severe dysplasia and biopsy is mild dysplasia, meaning you probably biopsied
the wrong place), and diagnosis of micro-invasive cervical cancer. Cone biopsy is the only way to diagnose micro-
invasive cervical cancer.
* 32yo patient with Pap showing carcinoma in situ. Next step is colposcopy. Ectocervical biopsy is micro-invasive,
ECC is normal. Micro-invasive means invasive less than 3mm past basement membrane. Next step must be cone
biopsy, not punch biopsy, not cryo.
* 32yo patient with Pap showing severe dysplasia. She is 16 weeks pregnant. What do we do? Next step is
colposcopy with acetic acid. Do not do the ECC because you can disrupt the pregnancy. So just do the ectocervical
biopsy, and it shows severe dysplasia. Treat this patient after the baby is born. If you do laser, cryo, or wide-excision
and the patient miscarries, you better have a good lawyer. It takes 8-10 years for full cancer formation. Treat patient
about 2 months after birth to let the uterus cool off because of all the vascularity that grows during pregnancy.
* 32yo patient with Pap showing HPV positive. So, we are even before pre-cancer. We know this is HPV by seeing
koilocytosis (halo around nucleus), so cytologist says HPV. What is the next step here? Repeat Pap in 3-6 months.
* 32yo patient with Pap showing ASCUS (atypical squamous cells of undetermined significance). This falls into the

HPV area; most common cause of ASCUS is likely HPV infection without koilocytosis. What is the next step?
Answer is repeat Pap in 3-6 months.
* ASCUS commonly caused by HPV, could also be due to atrophy or inflammation.
* With classical Pap, cells are placed on a slide and they can clump up, resulting in loss of clarity. Traditional Pap
smear sensitivity is 51%.
* Liquid based cytology (e.g. ThinPrep) is done like a normal Pap but spatula and brush are placed into liquid
solution and cells rubbed off. Then the prep is centrifuged so the cells present in a thin layer instead of clumping up.
Sensitivity with liquid based cytology is about 80%. So liquid based cytology is better than classical Pap.
* If Pap comes back with HPV, we can do HPV DNA typing. They can tell you types 6, 11, or 16, 18, 31, etc. So if
the Pap comes back HPV and we get types 6, 11, we can say there is no problem and come back next year. If we get
types like 16, 18, 31, 33, 35, we should do a colposcopy with biopsy.
* So if the Pap comes back HPV, repeat Pap in 3-6 months. If they give you the type, decide based on cancer risk.
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Vulvar & Vaginal Pre-Cancer Treatment
* 67yo woman presents with vulvar pruritus. Exam shows a 1.5cm white lesion at the base of the left labia majora
near the perineum. Next step is vulvar biopsy. Biopsy shows carcinoma in situ of the vulva. Treatment is wide
excision, or laser therapy, or cryo therapy. This is pre-cancer because it has not invaded the basement membrane. So
we can treat locally. Answer is not vulvectomy with groin lymphadenectomy (treatment for invasive).
* 62yo woman shows a 2cm white lesion in left vaginal wall on speculum exam. Next step is biopsy, shows severe
dysplasia of vagina. This is pre-cancer, so next step is wide excision or laser or cryo. Do not remove the vagina.
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Endometrial Pre-Cancer Treatment
* Etiology of endometrial cancer is estrogen, pre-cancer stage is hyperplasia (cystic then adenomatous then
atypical), progresses to adenocarcinoma. It takes about 8-10 years to progress to cancer.
* All hyperplasias are treated with progesterone except atypical hyperplasia. For atypical, do hysterectomy.
* With hysterectomy in atypical hyperplasia, 10-15% of the time you find cancer. You cannot get a full sample
when you sample the uterus, so you may be missing the cancer.
* Causes of menometrorrhagia (heavy bleeding between periods) include hormone imbalance, endometriosis,
uterine fibroids, and cancer.
* 42yo with 6-month history of menometrorrhagia. Endometrial sampling is done in the office and shows
adenomatous hyperplasia of endometrium. Treatment is oral progesterone.
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Ovarian Pre-Cancer Treatment
* 32yo with 6cm complex right adnexal mass. Patient is taken to exploratory laparotomy (e-lap) and a right
salpingo-oophorectomy is performed. Take out the bad side and send for frozen section (to get immediate pathology
report). Pathology comes back as borderline ovarian cancer, also known as low malignant potential ovarian cancer.
No next step because this patient has been treated and cured.
* If this were an invasive cancer, we would have done a debulking procedure with 6-months of platinum chemo.
* Be very conservative with pre-cancer patients and be aggressive with cancer patient.
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Gestational Trophoblastic Disease (GTD)
* Gestational means pregnant, trophoblastic refers to placenta.
* Hydatidiform mole (molar pregnancy), patient got pregnant and instead of a baby growing there is a placental
tumor growing. Most common symptom is vaginal bleeding.
* Common signs are anemia due to vaginal bleeding, greatly elevated hCG, hyperemesis gravidarum (HG).
* HG causes hypovolemia, hypotension, electrolyte imbalances, tachycardia, ketones in urine. Morning sickness is
physiology. HG is pathologic.
* When is hCG highest in a pregnancy? During the first trimester. Morning sickness decreases after first trimester
because hCG has decreased.
* With molar pregnancy, there is a size-date discrepancy. At 12 weeks we are at symphysis pubis, at 20 weeks we
are at the umbilicus level. Patient may say my last period was 7 weeks ago and on exam you find the uterus above
the symphysis pubis.
* Hypertension late in pregnancy is suspect for pre-eclampsia. Hypertension before 20 weeks is suspect for
hydatidiform mole.
* Patient can have adnexal masses, called theca-lutein cysts. Ovaries become large due to hCG stimulation.
* There will be no fetal heart tones because there is no baby.
DO NOT DISTRIBUTE - 10 -
* Patient may have hyperthyroidism. TSH and hCG have similar biochemical structures. When hCG is very high, it
actually stimulates the thyroid because the biochemical structures are similar.
* Summary of molar signs: anemia, vaginal bleeding, hyperthyroidism, hypertension, hyperemesis.
* Next step in management is diagnosis via sonogram. Looking for bunch of grapes ("cluster of grapes" or
"honeycombed uterus" or "snow-storm" or “snow-flake” pattern).
* Treatment of hydatidiform mole is a suction curettage of the uterus. Answer is not D&C. One of the characteristics
of moles is that the uterus is very large and thus the walls are thin. With a D&C curette, you can perforate the uterus.
Suction will make the uterus smaller and the walls thicker, then you can do curettage.
* Follow the patient with weekly beta hCG levels. Characteristically will see hCG drop steadily over 10-12 weeks,
in 80% of cases. In 20% of cases, the hCG will start to go up and patient is developing persistent GTD also known
as choriocarcinoma. Treat choriocarcinoma with chemotherapy. Treat mole originally with suction curettage.
* About 1:1200 U.S. pregnancies results in a hydatidiform mole. Frequency can reach 1:60 in some Asian countries.
* After suction curettage, keep the patient on medical contraception for 1 year. If the hCG starts to go up from the
pregnancy, we don’t know if it’s due to pregnancy or choriocarcinoma.
* Say the patient develops choriocarcinoma based on hCG. Now we have to determine where the disease is. Next
step is a CT scan of the brain, a CT scan of the thorax, and a CT scan of the abdomen/pelvis. With persistent GTD,
classification is either non-metastatic or metastatic. Metastatic categories are good and poor prognosis.
* Poor prognosis means there is liver or brain metastasis, hCG is > 40,000, pregnancy > 4 months, or follows a
normal pregnancy.
* Anytime you are exposed to pregnancy tissue in your body, you can develop choriocarcinoma. 50% of
choriocarcinoma are from moles, 25% from ectopics or miscarriages, 25% from normal pregnancy.
* Non-metastatic or good prognosis metastatic choriocarcinoma treated with methotrexate or actinomycin D.
* For poor prognosis metastatic choriocarcinoma, give MAC therapy. MAC is methotrexate, actinomycin D, and
cyclophosphamide.
* Say you are suspicious of a mole and the sonogram shows a mole and a baby. This is a partial (incomplete) mole.
Treatment of a partial mole is a suction curettage and follow beta hCG on weekly basis. These babies are
chromosomally abnormal.
* Normally you have 23 chromosomes in egg and 23 chromosomes in the sperm leading to a zygote with 46
chromosomes. In a complete mole, the egg is empty. So the zygote combination is an X sperm only. This sperm
duplicates, giving 46XX. All the chromosomal material is paternal. Why not 46YY? It is not known why, but nearly
all complete moles are 46XX. In a partial mole, the egg is normal but two X sperms get inside (dispermy). This
results in 69XXX, triploidy.
* The babies are chromosomally abnormal, which is why you recommend a suction and curettage. If the mother
wants to keep the baby, you cannot do the procedure. You have to explain to the mother that partial or complete
moles do not live past 24 weeks. They will always abort prior to 24 weeks. You would not want this to be a
miscarriage in the middle of the night with massive blood loss. Recommend the suction curettage.
* Follow up for moles is birth control pills for a year and beta hCG testing every week.
* Molar pregnancies are seen at the extremes of age. Ideally pregnancy should occur from 20-35 years of age. Moles
are seen before the age of 20 or after the age of 35.
* Choriocarcinoma occurs in 20% of complete moles and 10% of partial moles.
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Cervical Cancer
* 32yo patient presents with post coital bleeding. On speculum exam, you see an exophytic lesion coming out of the
cervix. What is the next appropriate step? Answer is not Pap smear, not colposcopy, these are for pre-cancer. In this
case, the patient has post-coital bleeding and a lesion, so answer is punch biopsy of the lesion. Biopsy returns as
invasive squamous cell cancer of the cervix.
* What is the next step when you have pathology of invasive cervical cancer? Answer is metastatic work-up. You
want to know if this cancer is localized to the pelvis or metastasized elsewhere. If cancer is localized, we can do
surgery or radiation. If metastasized, we should use chemotherapy.
* Metastatic cancer for all gynecologic cancers involves looking anterior (bladder), posterior (rectum), and lateral
(ureters). So do cystoscopy, sigmoidoscopy, intravenous pyelogram (IVP), chest x-ray, and pelvic examination.
Again, do not get the diagnosis and take the patient to the O.R. Do a metastatic workup.
* If cancer is limited to the cervix, it is stage I. If it extends to upper vagina, stage IIA. If it extends to lower vagina,
stage IIIA. If it extends into the parametrium (cardinal ligament), stage IIB. If it extends to the pelvic wall, stage
IIIB. So “A”s go down the vagina and “B”s go lateral.
* If IVP is abnormal, what stage is this? Answer is stage IIIB. To effect the ureters, it has to extend to the side walls.
* Stage IVA is bladder or rectum involvement. Stage IVB is metastatic disease.

* 32yo patient presents with post-coital bleeding. Biopsy of exophytic lesion on speculum exam of cervix comes
back as SCC of cervix. You perform a metastatic workup (cystoscopy, IVP, chest x-ray PA/lateral, pelvic exam,
sigmoidoscopy). Pelvic exam shows extension into the upper vagina and into the parametrium. What stage is this?
IIA or IIB? Go with the highest, stage IIB.
* All gynecological cancers are surgically staged (pathology report) except the cervix. Cervix is clinically staged.
* 32yo with SCC of cervix. Pelvic exam shows entire cervix is covered with cancer. This is stage I disease.
* Surgery is performed for stages I and IIA only. Stage IIB and higher, do radiation and chemotherapy. Most active
drug for cervical cancer is cisplatin (cis-platinum).
* 32yo with SCC of cervix. Stage I disease. Treatment is radical hysterectomy. This takes the top of the vagina, the
cervix, part of the cardinal ligaments (parametrium), uterus. If the patient had uterine fibroids, we would do a simple
hysterectomy (total or sub-total). Sub-total (supra-cervical) saves the cervix, not performed often. Total ends at the
top of the vagina (radical takes a larger portion of the vagina). Hysterectomy does not include the ovaries.
* Hysterectomy can be done via abdominal or vaginal. Radical vaginal hysterectomy is a Schauta operation.
* Hysterectomy is done +/- BSO (bilateral salpingo-oophorectomy). Recommendation is to remove the ovaries only
if the patient is over the age of 45. You can only do what the patient wants, so give the recommendation and let the
patient decide.
* With cancer surgery, always remove pelvic lymph nodes and para-aortic nodes. With fibroid uterus, no need to
remove lymph nodes.
* 32yo with SCC at stage I. Do radical hysterectomy with pelvic and para-aortic node dissection. Pathology report
will say good prognosis or poor prognosis. Poor prognosis factors are positive nodes poor tumor differentiation, size
larger than 4cm. If there are poor prognostic factors, add adjuvant therapy. Adjuvant therapy is radiation therapy and
chemotherapy.
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Endometrial Cancer
* 62yo patient presents with post menopausal bleeding. Next step is endometrial sampling in the office. If there is
stenosis, do a D&C in the operating room. Endometrial sample comes back adenocarcinoma of the endometrium.
What is the next step? Answer is no surgery. Answer is to do a metastatic workup.
* For endometrial cancer, we do a simple hysterectomy (save parametrium). The margins are the myometrium, so
the uterus’ own wall holds the cancer. Surgical treatment is total abdominal hysterectomy (TAH) with BSO, pelvic
node and para-aortic node dissection.
* You have to take out the ovaries for endometrial cancer. You don’t have to for cervical cancer; suggested to
remove them after the age 45. Two reasons for ovarian removal in endometrial cancer are because the cancer is fed
by estrogen and the cancer metastasizes to the ovaries.
* Poor prognostic factors for endometrial cancer are positive nodes, myometrium involvement, poor differentiation.
Add adjuvant therapy of radiation and chemotherapy.
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Ovarian Cancer
* 62yo patient referred to you because of abdominal distention and ascites. On pelvic exam, you find an 8cm left
adnexal mass. This is ovarian cancer until proven otherwise.
* Meig syndrome is a benign condition that can present like this. Meig’s is adnexal mass, ascites, and right pleural
effusion. This is caused by a ovarian fibroma; a benign enlargement of the ovary.
* In the 62yo patient, you do an exploratory laparotomy. Most common stage you find ovarian cancer in is stage III.
Next step is debulking surgery (TAH, BSO, omentectomy, +/- bowel resection) and follow with 6 courses of
paclitaxel and carboplatin (carbo-platinum).
* Follow tumor marker CA-125.
* 16yo with left adnexal mass. In surgery you find a dysgerminoma (pathology report). Next step is left salpino-
oophorectomy but do not remove the uterus. Give chemotherapy. All germ cell tumors need chemotherapy.
* When you hear ovarian cancer, they are usually talking about epithelial cancer. If exam question is a teenager,
they are looking for germ cell tumor with conservative management.
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Vulvar Cancer
* 62yo with vulvar pruritus. On vulva you see a lesion. Next step is biopsy. Biopsy shows invasive SCC of vulva.
Answer is not laser or wide excision. Answer is metastatic workup. Answer then is vulvectomy with dissection of
groin lymph nodes.
* Morbidity associated with this surgery is sexual dysfunction and lymphedema of the lower extremities.
Lymphedema is like breast cancer patient who gets upper extremity edema after mastectomy.
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Benign Gynecology: Post-Partum Hemorrhage (PPH)
* Ovarian arteries arise from the aorta. Ovarian vein on left drains to left renal, right drains to IVC (same as testes).
* Ovarian vessels travel in the infundibulopelvic (IP) ligament, also known as suspensory ligament of the ovary.
* Uterine arteries arise from the internal iliac artery (hypogastric arteries). Uterine veins drain into the internal iliac
veins (hypogastric veins). When using a tenaculum on the cervix, avoid the 9-o’clock and 3-o’clock positions
because this is normally where the uterine arteries runs.
* Bifurcation of the aorta into the common iliacs occurs at about level L4, corresponding to the umbilicus.
* In post partum hemorrhage (PPH) is commonly caused by uterine atony. The uterus does not contract well. This
can occur in twins, hydramnios, or multiparity. Treatment includes massaging the uterus to cause contraction.
Medications include oxytocin (first), methylergometrine (second), or prostaglandin (last).
* If the medications do not work for post partum hemorrhage, do exploratory laparotomy. Do a bilateral uterine
artery ligation. Internal iliacs are the main supply of blood to the pelvic viscera (bladder, uterus, rectum).
* The aorta branches to common iliacs, common iliacs branch into internal iliacs (into the pelvis) and external iliacs
(outside the pelvis). After the inguinal ligament, the external iliacs are called the femoral arteries.
* Uterine arteries come off the internal iliac arteries. Tie off both of the uterine arteries. The pelvis is known for
extensive collateral circulation, so no big worry about the patient not being able to have kids in the future.
* If ligation of the uterine arteries does not work, you have to do bilateral hypogastric artery ligation, ligating both
of the internal iliac arteries. You do not need to worry about necrosis of the bladder or rectum because there is a lot
of collateral circulation. This just reduces the pressure in the pelvis.
* Treatment for post partum hemorrhage is massage, then medication, then uterine artery ligation, then internal iliac
artery (hypogastric) ligation, and finally hysterectomy as last resort.
* There have been cases of surgeons ligating the external iliac arteries instead of the internal iliac arteries. This
would lead to ischemia and possibly amputation of the lower extremities.
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Benign Gynecology: Endometriosis
* Ligament going backward from the vagina and uterus is the uterosacral ligaments, going on each side of the
rectum to the sacrum. These can be palpated by recto-vaginal examination.
* Endometriosis is endometrium (inner lining of the uterus) outside of the uterus. No one really knows what causes
endometriosis but the most common theory is retrograde menstruation, also called Sampson theory. Most common
site of endometriosis is the ovary, instead of menstruation going through vagina it goes retrograde into ovaries.
* In endometriosis, there is bleeding every month. If the bleeding is into the ovary, it causes an endometrioma (e.g.
chocolate cyst due to brownish color).
* Second most common site of endometriosis is the endometrium falling out the fimbriated end into the cul du sac
(pouch of Douglas). The ligament there is the uterosacral ligament. So patient may have tenderness and nodularity
of the uterosacral ligament on reco-vaginal. Patient may complain of pain with bowel movements only when they
are menstruating (dysmenorrhea).
* Patient complains of dysmenorrhea due to bleeding in their belly. Patient will have dyspareunia because the blood
in the cul du sac causes fibrosis of the rectum to the vagina. Patient will also have infertility.
* Endometriosis triad is dyspareunia, dysmenorrhea, and infertility.
* Typical pelvic examination is nodularity and tenderness of the uterosacral ligaments.
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Benign Gynecology: Pelvic Relaxation
* Cervix dilates to 10cm for delivery of baby, which is basically the wall to wall. So what happens to the supporting
cardinal ligaments? The ligaments relax, causing uterine prolapse. Cardinal ligaments originate from the pelvic
sidewall, they are fascia so they are strong. As the ligaments approach the pelvic organs, they split into anterior and
posterior to sandwich the vagina. As baby passes through this area, the fascia anteriorly tears (cystocele) and
possibly posteriorly (rectocele).
* Most common etiology of pelvic relaxation is child birth. Symptoms include vaginal pressure/fullness sensation
and low back pain. Components are uterine prolapse, cystocele, and rectocele.
* Degrees of pelvic relaxation: organ at level of introitus is second degree, past introitus (hanging outside) is third
degree, above the introitus (inside vagina) is first degree.
* Treatment is a vaginal hysterectomy to take care of uterine prolapse. Also do an anterior and posterior vaginal
repair (colporrhaphy) to fix the cystocele and rectocele.
* Always ask if patient has control of their urine. A pessary is a non-surgical option. The pessary is inserted to hold
up the prolapse and is held in place by pelvic floor musculature.
* If the urinary sphincter has dropped down in a cystocele, urinary incontinence is more likely (urinary stress
incontinence). When the patient laughs or coughs, intra-abdominal pressure is placed on the bladder but cannot
reach the sphincter because the sphincter is dropped. If a large portion of the bladder had dropped in a cystocele but
not the sphincter, the intra-abdominal pressure would reach the sphincter and prevent incontinence.
* Patients may be embarrassed socially and embarrassed to discuss the urinary incontinence with their doctor. It is
important to know about this because during surgery they get their urethra attached to the pubic symphysis. This is a
Marshall-Marchetti-Krantz (MMK) procedure. Another option is the Burch procedure. The idea behind any of these
surgeries is to bring the sphincter back into the original position so it receives intra-abdominal pressure.
* Most common type of incontinence is stress incontinences. Next is neurogenic incontinence, urge incontinence,
“nervous bladder,” or unstable bladder, or detrusor dyssynergia.
* Urge incontinence is treated medically with medication. Stress incontinence is treated with surgery. If you treat
neurogenic (urge) incontinence, you may make the bladder more active thus worsening symptoms.
* Medications for urge incontinence are anti-spasmodics (oxybutynin) and anti-cholinergics (propantheline).
* Symptoms of neurogenic incontinence are loss of urine with sitting or sleeping. Other symptoms are urge and
urinary frequency. Symptoms of stress incontinence are loss of urine with laughing or coughing.
* Pelvic exam is helpful in differentiating, because a prolapse suggests stress incontinence. A Q-Tip test is done by
putting a cotton tipped swab in the urethra (after injecting some lubrication) and asking the patient to cough. If the
swab rotates more than 30-degrees, this suggests stress incontinence.
* Do pressure studies to differentiate between stress and urge incontinence. Bladders hold about 250mL until you
feel bladder pressure sensation. In urge (neurogenic) incontinence, patient will have pressure spikes even with low
volumes of urine. So on a normal P vs. V graph, you see flat-line low pressure until 250mL then pressure increases.
With urge incontinence, you see pressure spikes at various volumes even below 250mL. With stress incontinence,
you see a normal pressure curve.
* Stress incontinence treated with MMK or Burch procedure. If patient is not good surgical candidate, you can treat
medically with a pessary. Pessary is silicone or plastic object (e.g. donut shaped, dice shaped). They are not ideal
because they can get infected and are associated with foul odor. Kegal exercises may be used as well, where patient
learns to contract levator ani and pubococcygeal muscles to help keep organs in place.
* Urge incontinence treated with medical therapy, anti-spasmodic oxybutynin or anti-cholinergic propantheline.
* Big muscle of the pelvic floor is the levator ani. Pelvic roof is the pelvic diaphragm. The muscle below the levator
ani is the urogenital diaphragm. The urogenital diaphragm is made of 3 muscles, bulbocavernosus (just lateral to
introitus), ischialcavernosus (more lateral), and superficial transverse perineal muscles (running transverse). These
three muscles make a triangle on each side, they are components of the urogenital diaphragm.
* Episiotomy is an incision created during childbirth to aid in delivery and prevent a skin tear. There is a midline
and a mediolateral episiotomy. First degree episiotomy is vagina only, second degree is vagina plus part of perineal
body, third degree is vagina plus perineal body including anal muscle sphincter, fourth degree is vagina down
through anal mucosa. Ideal episiotomy is second degree. A third degree can cause fecal incontinence. A fourth
degree can cause a rectovaginal fistula.
* Both types of episiotomy procedures cut the bulbocavernosus and superficial transverse perineal muscles.
* Most common cause of rectovaginal fistula is fourth degree obstetrical laceration.
* Advantage of mediolateral is that you avoid the sphincter and the anus (prevent third and fourth degree).
Disadvantage of mediolateral is that it is harder for patient to heal, more painful, and higher blood loss.
* Patients with vesicovaginal fistula (bladder to vagina) have leakage of urine through the vagina because it
bypasses the urinary sphincter. Most common cause of a vesiovaginal fistula is traumatic hysterectomy.
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Benign Gynecology: Adnexal Masses
* Only time an adnexal mass can be normal is during reproductive age group. In menopause, where ovaries do not
work anymore, they should be atrophic. Before puberty, the ovaries do not work.
* 62yo with adnexal mass. Patient has ovarian cancer (e.g. epithelial tumor) until proven otherwise. Patient is
headed to the operating room after metastatic workup.
* 8yo with adnexal mass. Patient has ovarian cancer (e.g. germ cell tumor) until proven otherwise. Patient is headed
to the operating room after metastatic workup.
* Follicle secretes estrogen. Ovulation causes the corpus luteum, which secretes progesterone. These structures can
be filled with fluid and are called physiological cysts.
* 32yo with adnexal mass. Patient has physiological cyst. Patient should not go to the operating room, these cysts
dissolve by themselves in a couple of months.

* 62yo with 6cm left adnexal mass. What is the next most appropriate step? Answer is sonogram (at all age groups).
Ultrasound shows 6cm complex mass. This lady has ovarian cancer until proven otherwise. This patient should go
for exploratory laparotomy, debulking surgery, and six courses of carboplatinum and paclitaxel.
* 32yo with 6cm left adnexal mass. What is the next step? Answer is sonogram. What is the most likely etiology?
Answer is physiologic cyst. Ultrasound shows simple cyst. Next step is see patient again in 2 months. If you want to
speed up cyst resolution, give birth control pills because they inhibit the axis.
* Say ultrasound on 32yo comes back complex cyst. What is the most common complex adnexal mass in the
reproductive age group? Answer is dermoid cyst (teratoma). Teratoma has endoderm, mesoderm, ectoderm.
Dominant layer is the ectoderm, thus they are given the term dermoid cyst (mostly skin, hair, sebaceous material).
* Say patient missed a period and has a complex adnexal mass, think ectopic pregnancy.
* Say patient complains of dysmenorrhea, dyspareunia, infertility, think endometrioma (chocolate cyst).
* Say patient has fever, leukocytosis, adnexal mass, think tubo-ovarian abscess (pelvic inflammatory disease, PID).
* Say patient has severe sudden onset of pain, think ovarian torsion.
* Very last thing to think about (uncommon) in a patient of reproductive age with ovarian mass is ovarian cancer.
* 32yo 6cm left adnexal mass. Sonogram shows 6cm simple cyst. Next step is have patient return to office in 2
months. Offer birth control pills to speed resolution by relaxing the over-stimulated ovary.
* 32yo 6cm left adnexal mass. Sonogram shows 6cm complex cyst. Think teratoma. Next step is ovarian cystectomy
and send to pathology. Leave both ovaries in. Why not take out the ovary on the side of the dermoid cyst? Because
dermoid cysts can be bilateral in 10-15% of patients. If you take out the ovary at age 32, you may find another
dermoid on the other side a year later. So you would be putting the patient into menopause at age 34.
* Surgery for teratoma can be laparoscopic or via laparotomy, depends on surgeon’s comfort level.
* 32yo with complex adnexal mass and missed period. Think ectopic pregnancy. Most common etiology of ectopic
pregnancy is PID from chlamydia or gonorrhea (GC). These patients get salpingitis and egg gets stuck in the
ampulla of the tube (most common location).
* Common symptoms of ectopic pregnancy are amenorrhea, lower abdominal pain, and vaginal spotting.
* Ectopic pregnancy treated by salpingectomy (remove tube), salpingostomy (open tube and remove ectopic),
methotrexate (MTX). In salpingostomy, you don’t even need to sew tube back together, it heals itself. Treatment of
choice is a salpingostomy. Only do salpingectomy if tube has ruptured.
* Ectopic pregnancies occur in 1% of pregnancies. After one ectopic, rate is 15% (increases 15x). After
salpingectomy, rate of recurrence is 15%. After salpingostomy, rate of recurrence is 15%. So no increase in
recurrence with the surgery. What increases with salpingostomy is subsequent successful pregnancies.
* Methotrexate requires criteria: mass < 3.5cm by sonogram, hCG < 6000, no fetal heart tones, and no folate
replacement. MTX dissolves the ectopic pregnancy by acting as an anti-folate. Folate is required for the pregnancy
to grow. If the ectopic is too advanced, the MTX will not work, thus the criteria.
* It would be nice to treat all ectopic pregnancies with methotrexate because there is no need for surgery. However,
there are criteria that need to be met (mass < 3.5cm, hCG < 6000, no heart tones, no folate replacement).
* 32yo with 6cm complex cyst. Patient has severe sudden onset of pain. Think torsion of the ovary. Treatment for
torsion is to un-twist it. The ovary can revitalize (picks up color) or it stays necrotic/dark. Do not remove the ovary
initially, attempt un-twist for revitalization (wait up to a half hour, maybe wait 20 minutes). If it revitalizes, do a
cystectomy. If it stays necrotic, do a salpingo-oophorectomy.
* Germ cell tumors usually present in stage I, do unilateral salpingo-oophorectomy, conservative therapy. This is the
only time to be conservative with ovarian carcinoma.
* For dermoid tumors, do an ovarian cystectomy, not an oophorectomy unless the cyst takes over the entire ovary.
There is bilaterality in dermoid cysts so you want to ensure the patient can still have children.
* 25yo pregnant with simple cysts. Answer is physiologic cyst.
* 25yo pregnant with complex cyst. Answer is dermoid cyst.
* Patient sleeping and wakes up with pain, or patient sitting at computer and suddenly bends over in pain, think
ovarian torsion. Ligament that brings blood supply to ovary is suspensory or infundibulopelvic (IP) ligament. The
weight of the cyst causes the ovary to cyst. A small percentage of torsions occur in normal ovaries.
* Sampson theory says endometriosis is retrograde menstruation. How do you explain endometriosis in the lungs
liver, or skin then? Nobody knows.
* Treatment of endometriosis involves inactivating the endometrium. Going back to axis: hypothalamus and
pituitary release GNRH to pituitary, which releases gonadotropins FSH and LH to ovary, which releases estrogen
and progesterone to the endometrium. So inhibit the axis, such as via birth control pills. Steroids inhibit the axis
also, so we can treat endometriosis with medroxyprogesterone (Provera). We can treat with testosterone
danazol/danocrine. Patient will complain about testosterone side-effects like hirsutism.

* Best way to inhibit axis is a GNRH analog. Wait, doesn’t GNRH stimulate the pituitary? Yes, but in a pulsatile
fashion. If you give a GNRH analog in a constant fashion, it inhibits the pituitary. The pituitary gets tired out, which
down-regulates the pituitary gland.
* With leuprolide, patient can go about 3-6 months before symptoms. Inhibiting the axis like this will make the
patient menopausal, so this 32yo will feel like she is 52yo. She will complain of sweats, hot flashes, dyspareunia
(due to dry vagina), mood changes.
* Treatment of endometriosis is thus 3-6 months of leuprolide then either attempt pregnancy (9 months or so of no
menstruation, progesterone dominates pregnancy) or do birth control pills (more moderate treatment).
* Diagnosis of endometriosis has to be made via laparoscopy. Suspect endometriosis because of amenorrhea,
dyspareunia, dysmenorrhea, pelvic exam feeling nodularity and tenderness of uterosacral ligaments. On
laparoscopy, you see “powder burns” (bluish discoloration of endometrium) and/or endometriomas.
* Patient has lower abdominal pain and fever about a week after menses. This is typical of PID.
* Acute PID is characterized by cervicitis (cervical motion tenderness, CMT) and salpingitis (adnexal tenderness on
examination). This is commonly caused by GC and chlamydia. Recommendations for treatment of acute PID are
cephalosporin plus tetracycline. Example is ceftriaxone IM and vibramycin oral x 10 days (or doxycycline).
* Current treatment (2009) for GC and chlamydia is ceftriaxone IM and oral azithromycin x 1 dose.
* One of the functions of the tube is to prevent ascending infections from the vaginal flora, protecting the ovary.
With acute PID multiple times (GC and chlamydia), the vaginal organisms can reach the ovaries. Chronic PID is not
GC and chlamydia, it is the vaginal flora.
* Vaginal flora has aerobic bacteria (penicillin like ampicillin and gentamycin) and anaerobes (clindamycin or
metronidazole). So an example treatment regimen would be ampicillin, gentamycin, and clindamycin x 72hours.
* Hallmark of chronic PID is tubo-ovarian abscess. Most lethal anaerobe is bacteroides fragilis.
* If no improvement within 72 hours of treatment, must drain abscess. You do not want the abscess to rupture. If the
tubo-ovarian abscess ruptures, mortality can be as high as 20-25%.
* How do we drain the abscess? Laparatomy with drainage is one option. Most common option is percutaneous
drainage with interventional radiology (using ultrasound). Another option is colpotomy if the abscess falls into the
cul du sac, which can be felt on vaginal exam as fullness.
* Acute PID can cause ectopic pregnancy, tubo-ovarian abscess, infertility (due to blockage), and chronic pelvic
pain (due to adhesions).
* 32yo 6cm left adnexal mass. Sonogram shows simple cyst. You see the patient in 2 months and the cyst is still
there. Next step is surgical evaluation, either laparoscopy or laparotomy. Surgically evaluate a persistent cyst.
* 32yo 8cm left adnexal mass, sonogram shows simple cyst. Physiologic cysts do not get larger than 7cm. Next step
is surgical evaluation, not waiting for 2 months. 7cm is the diameter of a tennis ball.
* 32yo 6cm left adnexal mass, sonogram shows simple cyst. You tell the patient she has a physiological cyst. She
tells you she has been on the pill for 6 months. If patient has been on BCPs for more than 2 months, they should not
have an ovarian cyst. Next step is surgical evaluation, not waiting for 2 months.
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Benign Gynecology: Vaginitis
* 32yo complaining of vaginal discharge. What is the next best step? Answer is not treatment. Do not jump from
vaginal discharge directly to metronidazole or nystatin. You have to make the diagnosis first.
* 32yo complaining of vaginal discharge. Next best step is speculum exam and microscopic evaluation of the
vaginal discharge. Most common vaginitis are candida, bacterial vaginosis (BV), and trichomonas. BV was
originally hemophilus, then gardnerella. BV is diverse and includes Gardnerella vaginalis, Mobiluncus, Bacteroides,
and Mycoplasma.
* Candida is a sticky vaginal discharge, the only one that adheres to lateral vaginal walls. Microscopic exam will
show pseudohyphae (strands). KOH used to destroy epithelial cells and leave hyphae. Maintains normal vaginal pH
of 4. Treatment is an antifungal, such as miconazole or nystatin.
* BV is fishy odor (whiff test, more pronounced with KOH). Microscopic exam will show clue cells (lots of dots).
Will have a basic vaginal pH, about 5. Treatment is metronidazole.
* Trichomonas is frothy, has air bubbles in discharge. Microscopic exam will show flagellated organisms. Will have
a basic vaginal pH, about 6. Treatment is metronidazole.
* If patient is put on metronidazole, remind them not to drink alcohol as it leads to a disulfiram-like reaction.
* Say patient is in first trimester of pregnancy and has monilial vaginitis (yeast infection). You can use anti-fungals.
* Say patient is in first trimester of pregnancy with BV or trich. Do not use metronidazole. Option is vaginal
douches or clindamycin vaginally.
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Benign Gynecology: Abnormal Vaginal Bleeding
* 62yo with vaginal bleeding. Think endometrial carcinoma until proven otherwise. Most appropriate next step is
endometrial sampling in the office. Answer is not Pap smear. Most common cause of post menopausal bleeding is
atrophy. 10-15% is due to cancer, but you don’t know so you have to sample. Atrophy treated with estrogen and
progesterone. If cervix is stenosed, do D&C in operating room.
* From day 1 to day 25, give estrogen. From day 15 to 25, give progesterone. From day 25 to day 30, tell the patient
they will bleed (menses). What if patient is on progesterone and estrogen and has bleeding on day 14? This is not
normal, do endometrial sampling.
* 8yo with vaginal bleeding. Most common cause is foreign body, like a piece of tissue paper stuck in the vagina.
Think about traumatic (e.g. sexual abuse), cancer (e.g. sarcoma botryoides, “grapes”), or precocious puberty. What
is the most appropriate next step? Answer is exam under sedation. Do not put a speculum into an 8yo girl. Must
obtain appropriate consent.
* Precocious puberty is a diagnosis of exclusion. Puberty is a 3-4 year period. Generally, breast development at age
9, axillary and pubic hair at age 10, growth spurt at age 11, menarche at age 12. Puberty is maturation of the axis.
Puberty leads to secondary sexual characteristics. Primary sexual characteristics you are born with (clitoris, vulva,
uterus), they are chromosomally determined and distinguish boy from girl. Secondary sexual characteristic are
determined by exposure to hormones (specifically estrogen).
* Precocious puberty, worry about ovary, pituitary, and adrenal secretion of estrogen. Do CT scan of brain
(pituitary), CT scan of abdomen and pelvis (granulosa thecal tumor of ovary or adrenal tumor secreting estrogen).
* Most common cause of precocious puberty is idiopathic.
* Epiphyseal plates fuse after menses, so girls grow very little after menses. Patient will not reach their maximal
height, so you treat precocious puberty even if it is idiopathic.
* Treat by turning off the axis, leuprolide. Leuprolide is a GnRH analog. You can treat this patient for a long time,
they will not get hot flashes and sweats. So, treatment can go up to 2-3 years. This patient is not use to full estrogen.
A reproductive aged woman is use to estrogen, so you take away the axis and get symptoms quicker.
* Usually the bone age is ahead of the chronological age in precocious puberty, so maintain on therapy until the two
start to match up again.
* 32yo with abnormal bleeding, 6 months of menometrorrhagia. First step is rule out pregnancy (beta hCG). Next
step is anatomical causes, fibroids, adenomyosis (endometriosis in the myometrium), and polyps. Fibroids is large
and bumpy. Adenomyosis is large but smooth, like a balloon, boggy. If patient is not pregnant, last step is say
dysfunctional uterine bleeding (DUB), which is basically a hormonal imbalance.
* Mnemonic for abnormal bleeding in reproductive age group: PAD. Pregnancy, Anatomical causes, DUB.
* Anatomical causes investigated by pelvic exam, endometrial sampling, hysteroscopy, sonogram.
* 32yo with abnormal bleeding, 6 months of menometrorrhagia. You rule out pregnancy and anatomical causes. So
patient has dysfunctional uterine bleeding (DUB), a hormonal imbalance.
* Endometrium proliferates for 2 weeks due to estrogen. Ovulation and corpus luteum releases progesterone, which
stops the proliferation. Most common cause of DUB is anovulation, no egg released. With anovulation, entire month
is estrogen, so endometrium proliferates the entire month. Patient has estrogen breakthrough bleeding.
* Most common cause of anovulation is stress and anxiety because they affect the axis.
* 32yo with breakthrough bleeding. Beta hCG is negative. Sonogram, pelvic exam, and endometrial sampling are
negative. Tell patient she has DUB. Most likely cause is not ovulating and say that most common cause of that is
stress and anxiety. Talk to the patient, she will likely share what is happening (e.g. divorce, family death, illness).
* Treatment is medroxyprogesterone 10mg oral between days 14 and 25. So you are giving the patient what she
does not have. You could also give birth control pills, as they contain estrogen and progesterone. BCPs are easier to
manage. Usually treat patient for 3-6 months and then they start ovulating again.
* PCO, polycystic ovaries (Stein Leventhal Syndrome) is a genetic problem, inherited. The problem with PCO is
anovulation. DUB is a temporary problem, PCO is a chronic problem. Patient with PCO will not ovulate from age
12 to 52. Characteristics of PCO include anemia due to irregular bleeding, higher incidence of endometrial cancer
because no progesterone exposure, and infertility due to anovulation.
* PCO patient who bleeds to the point of anemia can be put on BCPs to regulate. BCPs also reduce the risk of
endometrial cancer. If the PCO patient wants to become pregnant, she can be given clomiphene or human
menopausal gonadotropin (Pergonal).
* Most common cause of hirsutism in women is PCO. One follicle ovulates each month. The follicles that do not
ovulate are called atretic follicles and they secrete testosterone. After ovulation, there is no more atresia so
testosterone decreases. So ovulatory patient has a testosterone peak around day 14. PCO patient never ovulates, so
constantly undergoing atresia and thus a sustained elevation of testosterone. Treat hirsutism with BCPs, slows down
FSH and LH so follicular stimulation and atresia will be decreased, thus less testosterone production. BCPs also
cause the liver to increase sex hormone binding globulin production, so less free testosterone.
* To diagnose PCO, look at LH to FSH ratio. Normal LH:FSH ratio is 1.5:1. Cause of ovulation is LH surge. PCO
patient cannot ovulate so will have a high LH, attempting to ovulate. PCO LH:FSH ratio is 3:1, doubled.
* 32yo with 6 months of menometrorrhagia. Beta hCG is negative. Exam shows 16 week size fibroid uterus
(leiomyoma). At menopause, fibroids regress on their own because they need estrogen to grow. Thus, fibroids are
generally benign. So to treat leiomyoma, there must be indications.
* Fibroids outside the uterus are subserosal fibroids, fibroids inside the muscle are intramural fibroids, and fibroids
impinging on the endometrium are submucosal fibroids. If fibroid has a finger projection, it is a pedunculated
fibroid. The pedunculated fibroids can break off from the uterus and are then called parasitic fibroids, and can get
their blood supply from the omentum, or liver, or bowel.
* Indications for treating fibroids are anemia, pain (due to degeneration, outgrowing blood supply), visceral
obstruction (difficulty urinating, difficulty defecating, ureter blockage), infertility due to fallopian tube blockage, or
fibroids that grow after menopause.
* Degenerations are hyaline, calcific, and carneous (seen in pregnancy) or red because it looks like red meat.
* A fibroid that grows after menopause may not be a leiomyoma, it may be a leiomyosarcoma.
* Treatment for fibroids (with indication) is myomectomy if the patient wants a family. If the patient is at
menopause or does not want a family, hysterectomy is the treatment. With a myomectomy, the fibroids may recur.
Leuprolide inhibits the axis thus it will shrink the fibroids. You can only take leuprolide for about 6 months. Once
you stop the leuprolide, the fibroids grow back.
* Leuprolide can be used in conjunction with surgical therapy. Toss in the drug to a myomectomy, so the fibroid is
shrunk and you decrease the estimated blood loss (EBL). With leuprolide, you could change an abdominal
hysterectomy to a vaginal hysterectomy because the uterus is smaller and now can come through vagina.
* 32yo with 6 months of menometrorrhagia and positive beta hCG. Possibilities are threatened abortion, incomplete
abortion (miscarriage), ectopic pregnancy, and molar pregnancy. With threatened abortion, os is closed.
* With an incomplete abortion, the cervical os will be open. Next step then is D&C. If you overdo a D&C for an
incomplete abortion, you can get Asherman syndrome. Asherman syndrome is adhesions, called synechiae. Treat
Asherman by giving estrogen because it stimulates the endometrium and do a hysteroscopic lysis of adhesions.
* Biggest worry here is ectopic pregnancy because it can rupture and cause death.
* 32yo with 6 months of menometrorrhagia and positive beta hCG. Speculum exam shows a closed os. Next step is
a vaginal sonogram. There is a 2 week advantage of the vaginal sonogram, picking up the pregnancy at 4 weeks
versus about 6 weeks by abdominal sonogram. Vaginal sonogram will see the pregnancy at 1500 beta hCG whereas
the abdominal sonogram needs 6500 beta hCG. This two weeks is important because an ectopic could rupture during
that period.
* Say vaginal sonogram comes back intrauterine pregnancy (IUP). Patient probably has threatened abortion. Next
step is bed rest.
* Say vaginal sonogram comes back as a molar pregnancy (snow storm). Next step is suction curettage and follow
beta hCG on a weekly basis, give BCPs for one year.
* Say vaginal sonogram detects an ectopic pregnancy. Next step is salpingostomy or salpingectomy if ruptured. Or,
methotrexate if indications are met.
* Say vaginal sonogram comes back no IUP, no ectopic. Next step is quantitative beta hCG. Before we had a
qualitative beta hCG (pregnant or not pregnant). If hCG is over 1500, we expect to see an IUP. Say hCG comes back
as 1800. This patient has an ectopic pregnancy, should go for laparoscopy. Say hCG comes back as 1100. It might
be too early, so repeat in 48 hours and expect hCG to be 2200 (doubles every 48 hours).
* What is hCG is 1100 and comes back as 1800 two days later? It should have doubled, but didn’t. So next step is
laparoscopy.
* Missed abortion without bleeding will present as a decreasing hCG with a uterus that is not growing. The baby is
dead in this situation. Missed abortions usually do not bleed.
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Benign Gynecology: Amenorrhea
* 32yo with six months of amenorrhea. Most common cause of amenorrhea is beta hCG. So next step is check for
pregnancy via beta hCG. Test comes back negative. Next step is evaluate the thyroid. Hypothyroidism is not
uncommon in women, much more common in women than men. Thyroid evaluation via TSH.
* In hypothyroidism, TRH is high and TSH is high. Elevated TRH cause the pituitary to secrete prolactin. Prolactin
goes back and inhibits GnRH, which causes amenorrhea. The axis is effected, which effects bleeding. So
hypothyroid can cause too little bleeding or too much bleeding. The axis is what regulates normal menstruation.
* Stress and anxiety affect the axis at the hypothalamus, causing DUB. Can they cause amenorrhea? Yes.
* 32yo with six months of amenorrhea, beta hCG negative, TSH is elevated. Next step is give synthroid. Within 2-3
months, patient should be menstruating normally. Mechanism is regulation of TRH and thus normal secretion of
prolactin (and no abnormal GnRH inhibition).
* Sheehan syndrome is postpartum necrosis of the pituitary from hemorrhage, blood pressure decreases too much
and pituitary necrosis. Patient has trouble breast feeding or does not get menstruation back after pregnancy.
Diagnosis is made by giving patient TRH and seeing no production of prolactin.
* 32yo with six months of amenorrhea, beta hCG negative, TSH is normal. Next step is get serum prolactin. You are
trying to rule out a pituitary tumor. So on first visit of amenorrhea, get hCG, TSH, prolactin.
* Patient may forget to tell you (or be embarrassed to tell you) they are taking psychiatric medications, such as
antipsychotics or antidepressants. These medications have an anti-dopaminergic effect. Dopamine inhibits prolactin.
Thus, patients on these medications will have increased prolactin section, which inhibits GnRH.
* Treat pituitary tumor patients with bromocriptine, a dopamine agonist. This lower prolactin.
* 32yo with six months of amenorrhea, beta hCG negative, TSH is normal, prolactin is normal, patient not on
medications. What are the causes now? Hypothalamic causes include stress and anxiety, anorexia nervosa, or
excessive exercise (e.g. long distance runners). It isn’t easy to treat the excessive exercise patients because they get
hooked on endorphins, especially in running with “runners high.” Pituitary causes include tumor (adenoma).
Ovarian causes include menopause (only pathologic before age 40) and resistant ovary syndrome (Savage
syndrome). Endometrial causes include Asherman syndrome.
* Menopause is diagnosed by elevated FSH and LH.
* Menopause differentiated from Savage syndrome by ultrasound. No follicles in menopause.
* To assess for ovarian problem, look at FSH and LH (high values). To assess for endometrial problem, look at
estrogen and progesterone, give them to patient and they will not bleed if there is a problem. To assess for pituitary
problem, do an MRI or a CT scan, if scanning not an option pick prolactin. GnRH is pulsatile so drawing this value
will be worthless, could be at a peak, could be at a trough.
* Start at the bottom of the axis and work your way up to the top. Patient has amenorrhea. So initially look at
endometrium, give patient progesterone and see if they bleed or do not bleed. If she bleeds, then she was missing
progesterone (anovulatory, most common cause is stress and anxiety). If the patient does not bleed on progesterone,
give estrogen and progesterone together. If she does not bleed, this is Asherman syndrome. If she bleeds on estrogen
and progesterone, she was missing both, so problem is above in the axis.
* Patient bleeds only when given both estrogen and progesterone. Now check ovary via FSH and LH. If they are
high, it is either menopause of resistant ovary syndrome. If no follicle on ultrasound, menopause, give estrogen and
progesterone. If there is follicle on ultrasound with high FSH and LH, this is Savage syndrome, treatment is
estrogen. If FSH and LH are low, problem is above in the axis.
* Differentiate pituitary from the hypothalamus with MRI. If MRI abnormal, pituitary problem. If MRI normal,
problem is in the hypothalamus.
* 32yo with 6 months of amenorrhea. Next step is check beta HCG, TSH, prolactin/medications. These are normal,
so not look at the axis.
* 16yo brought in by her mother because she has not gotten her period (primary amenorrhea). By age 16, 99% of
women will menstruate. Do not let them go past age 16 for waiting. With secondary amenorrhea, we focus only on
the axis. In primary amenorrhea, we focus on both the axis and the anatomy (e.g. Mullerian agenesis aka Mayer-
Rokitansky-Küster-Hauser syndrome, MRKH).
* Two mullerian ducts fuse to create the tubes, uterus, cervix, and upper vagina. Lower vagina comes from the
urogenital sinus. Patient with mullerian agenesis will develop secondary sexual characteristics because the ovaries
are still present, not part of the mullerian ducts. Short vagina will have to be surgically elongated for satisfactory
intercourse.
* 16yo with amenorrhea. Assess axis by exam, breast development, axillary hair, pubic hair, normal growth for her
age. If these are present, the axis is likely working. Be careful when examining anatomy on a 16yo, next best step
may be ultrasound to look for a uterus. When there is uterus problems, may be problems with kidneys and ureters so
order an IVP.
* In primary amenorrhea, assess axis via secondary sex characteristics (breasts) and assess anatomy via ultrasound
(uterus presence).
* Amenorrhea with breast positive and uterus positive: imperforate hymen, vaginal septum, anorexia nervosa,
excessive exercise, pregnancy.
* Amenorrhea with breast positive and uterus negative: mullerian agenesis (treat by surgically elongating vagina and
order an IVP), testicular feminization (androgen insensitivity syndrome, testes secrete estrogen to make breasts and
mullerian inhibiting factor to block uterus, treat by removing testes to prevent cancer, surgically elongating vagina,
and ordering an IVP).
* Amenorrhea with breast negative and uterus positive: if FSH/LH low high then Turner syndrome (do karyotype
next, treat with progesterone and estrogen, or BPCs), if FSH/LH are low then do an MRI or CT scan (abnormal MRI
means pituitary like craniopharyngioma, normal MRI is hypothalamus like stress, anxiety, weight loss, Kallman
syndrome).
* Amenorrhea with breast negative and uterus negative: very rare, enzymatic problem, less than 0.1% of primary
amenorrhea.
* Use testosterone to differentiate mullerian agenesis (normal level) from testicular feminization (high level). Also
differentiate by karyotype as mullerian agenesis is XX and testicular feminization is XY.
* XX gives you ovaries. In Turner syndrome (45XO), patient has streak gonads and no real ovaries. Characteristics
of Turner syndrome are webbed neck, short stature, heart defects, shield chest (broad chest). Once you see high FSH
and LH in breast negative uterus positive, next best test is a karyotype looking for 45XO.
* Kallman syndrome causes primary amenorrhea, defect in brain so they do not product GnRH, patient as anosmia
as this defects is near olfactory center.
* Puberty is a 3-4 year period with beast development (9yo), axillary and pubic hair (10yO), growth spurt (11yo),
and menarche (12yo). Worry about 16yo with amenorrhea. Worry about 14yo with no secondary sexual
characteristics, think about axis problem so order FSH and LH.
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Benign Gynecology: Infertility
* Definition of infertility is one year of unprotected “frequent” intercourse and no pregnancy. It occurs in about 10-
15% of couples in the country. 60% of the problem is the female, 40% is the male.
* 32yo presents with one year of unprotected intercourse and no success at pregnancy. Next step is the evaluation of
the male factor by semen analysis (refer to urologist or endocrinologist). Say semen analysis is normal. Next step
now is evaluation of the female factor by looking at the ovary, tubes, and cervix.
* For low male sperm count, one can do an intrauterine insemination (IUI). You place a catheter into the vagina and
uterus and inject the semen. Another option is ICSI.
* ICSI is intracytoplasmic sperm injection. Sperm is injected into egg in the laboratory then place in the uterus, so
this is a form of in vitro fertilization (IVF).
* Evaluate female factor by looking at ovary (not ovulating), tubes (tubal blockage), or cervix (mucus problem).
Sperm antibodies is very rare.
* Test mucus of the cervix. Mucus is hard initially, soft around day 14, and hard toward the end of a cycle.
Softening of the mucus is called spinnbarkeit. Tell patient to have sex in the morning then visit within 4-6 hours.
Place speculum in vagina and swab mucus from the endocervix. Place mucus on a glass slide then place another
glass slide on top. Then separate the slides, the mucus should be stringy/stick for at least 6cm without breaking. This
tells you the mucus is soft. If the mucus breaks when you barely move the slides apart, this is firm “hostile” mucus.
You already know the semen analysis is normal, so when you look at mucus here you should be able to see sperm
from the intercourse that morning. If you do not see sperm, it means the mucus is not allowing penetration. Mucus
should have ferning when seen under microscope, it will look like the leafs of fern trees which means the mucus has
been exposed to estrogen.
* Middleschmertz is pain in the middle, where a women can feel a unilateral sensation of ovulation.
* When you look at ferning for premature rupture of the membranes, the amniotic fluid contains estrogen. So the
swab you do will show ferning on a slide.
* Treatment of mucus problem is intrauterine insemination (IUI) or give patient estrogen in the first half of the cycle
to soften the mucus.
* 32yo presents with one year of infertility. Sperm analysis is normal, mucus testing is normal. Next step is assess
ovulation. Basal body temperature (BBT), progesterone raises temperature by one degree at day 14, and at day 25
the temperature starts to decline. Early indication of pregnancy is the temperature stays elevated (progesterone).
Another test for ovulation is endometrial biopsy. If biopsy is on second half of cycle and returns secretory, you
know she is ovulating. Another test is day 22 serum progesterone, when the progesterone is the highest. Ovulatory
patient will have regular cycles, anovulatory patient will have irregular cycles. Another test is LH surge, a urine strip
to measure LH looking for surge around day 14. Once positive, you know ovulation will occur in 24-48 hours.
* Treat anovulatory patient with clomiphene or human menopausal gonadotropin to help with ovulation.
Clomiphene is almost identical to estrogen biochemically, it fits into estrogen receptor at pituitary. Pituitary
recognizes that this molecule is not estrogen, so the pituitary thinks there is low estrogen. Thus, pituitary pumps out
a bunch of FSH and LH. Human menopausal gonadotropin is FSH and LH given to the patient. Menopausal women
secrete lots of FSH and LH in their urine, which is where we get the medication from.
* Multiple gestation rate is 10% for clomiphene and 20% for human menopausal gonadotropin. Twins are high risk
pregnancies, pre-eclampsia, placenta previa, congenital anomalies. Thus, clomiphene is the first choice. Another
reason to use clomiphene first is there is lower risk of ovarian hyperstimulation syndrome, which makes the patient
look as though they have ovarian cancer with big ovaries, abdominal distension, hypovolemia, tachycardia, ascites.
* 32yo presents with one year of infertility. Normal sperm analysis, normal mucus, normal ovulation. Next step is to
look for a tubal factor. Most common cause of tubal blockage is pelvic inflammatory disease (PID). Diagnosis is via
hysterosalpingogram (HSG). Abnormal HSG treatment is surgery (tuboplasty, remove part that is obstructed) or in
vitro fertilization (IVF). To do IVF, give patient human menopausal gonadotropin then on day 14 place a needle
through the vagina (under sedation) to uterus and aspirate eggs. Then mix eggs with sperm in laboratory to create
zygotes. Zygotes places back in uterus, four are used because less than four results in low pregnancy rate and more
than four increases multiple gestations. Success of IVF is about 60%, but IVF can be expensive which is why
tuboplasty is still an option.
* 32yo presents with one year of infertility. Normal sperm analysis, normal mucus (good spinnbarkeit), normal
ovulation, normal tubes. So now we’ve tested the male and the common causes for the female. Last step in infertility
workup is laparoscopy. In about 20-25% of patients with normal findings there will be endometriosis. Sometimes
endometriosis is asymptomatic. So you do the laparoscopy and find powder burns. Treatment is to inactivate
endometrium by inhibiting axis.
* 32yo with infertility, male and female tests are normal, laparoscopy is normal. This is diagnosed as unexplained
infertility. 50% will get pregnant in 4-5 years in unexplained infertility. The problem with that is female age can lead
to chromosomal abnormalities and other complications. So telling a 36yo to wait 4-5 years may not be acceptable to
the patient. One additional option is to recommend adoption.
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Benign Gynecology: Masculinization Syndromes
* Divide masculinization syndromes into hirsutism (facial/trunk hair) and virilization (hirsutism with baldness, voice
changes, skeletal muscle mass, cliteromegaly).
* Most common cause of hirsutism if polycystic ovaries (PCO). Most common cause of virilization is tumor, such as
from the adrenal or the ovary (sertoli leydig cell tumors).
* 32yo presents with facial hair growth for 6 months. History is important, ask if this runs in the family. Ask about
onset, PCO will have onset young, tumor will have adult onset. Order a serum testosterone and serum DHEAS
(dehydroepiandrosterone sulfate). Testosterone implies ovarian source, DHEAS implies adrenal source. Order an
abdominal pelvic CT scan to see ovaries and adrenals.
* 32yo patient with hirsutism, high testosterone, normal DHEAS. CT scan shows bilaterally enlarged ovaries.
Answer is PCO. Diagnose via LH:FSH ratio of 3:1 (increased from normal of 1.5:1). Treatment is BCPs to inhibit
the axis, decrease FSH, decrease atresia, therefore decease testosterone production. BCPs also increase sex hormone
binding globulin so less testosterone around. Treatment also includes spironolactone, a diuretic that competes with
testosterone at the hair follicle receptor.
* 32yo patient with virilization, high testosterone, normal DHEAS, CT shows enlarged right ovary. Answer is
ovarian tumor (sertoli leydig cell tumor). Treatment is right salpingo-oophorectomy.
* 32yo patient with virilization, normal testosterone, high DHEAS, CT shows enlarged right adrenal mass. Answer
is adrenal tumor. Treatment is surgery.
* 32yo patient with hirsutism, normal testosterone, high DHEAS. CT is normal in the abdominal and pelvic region.
Answer is congenital adrenal hyperplasia, 21-hydroxalase deficiency. Diagnosis via 17-hydroxy progesterone.
Treatment is with steroids. This is late onset congenital adrenal hyperplasia. Treatment prevents further hair growth.
Hair that has formed should be removed, such as plucking or laser removal.
* 32yo patient with hirsutism, normal testosterone, normal DHEAS. CT is normal. Answer is familial hirsutism. 5-
alpha reductase creates dihydrotestosterone (DHT) from testosterone. These patients have an increased 5-alpha
reductase level.
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Breast Discharge
* 32yo presents with breast discharge. What is the next most appropriate step? Answer is microscopic evaluation of
the discharge. If galactorrhea (fat globules), worry about pituitary tumor. May be mastitis (infectious, WBCs), may
be bloody (intraductal papilloma), cancer cells (mitotic figures).
* Discharge contains fat globules. Diagnosis is galactorrhea. With galactorrhea, we know prolactin is high. Confirm
with serum prolactin as next step. Say prolactin is elevated. If pregnancy within a year, this is normal. Concerned
about pituitary tumor. Next step is brain MRI and serum TSH (hypothyroidism). Ask in history about recent
pregnancy and medication use (antidepressants, antipsychotics, methyldopa) because of anti-dopaminergic effect. If
it is pregnancy or medication related, give bromocriptine (dopamine agonist). Pituitary tumors divided into micro <
1cm (treated with bromocriptine) and macro > 1cm (treated surgically).
* Ask about recent thoracic surgery, recent herpes zoster of the chest. When a baby is breast feeding, there is
feedback from the breast to inhibit the axis. Breastfeeding inhibits the axis, so prolactin increases. Sometimes a
thoracic scar or a scar from herpes zoster can stimulate the same nerve endings, inhibiting the axis, and increasing
prolactin. Treatment is bromocriptine.
* Breastfeeding inhibits the axis, thus inhibits FSH and LH, so no ovulation (gives contraception).
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Breast Masses
* Breast self exam and physician breast exams should be done 10-14 days after menses. During menses, the breasts
are hormonally stimulated and get nodular and cystic. Thus fall positives.
* Mammography signs to worry about are calcifications and irregular borders. A smoothly demarcated boarder is
likely benign. Do a baseline mammography between age 30-40. Age 40-50 every two years, after 50 every year.
There is controversy between ages 40-50 for mammography screening.
* Ultrasound is not a better test because it does not pick up micro-calcifications. Useful for cystic versus solid.
* 32yo patient with palpable left breast mass. What is the next step in management? Answer is needle aspiration. If
it is clear and disappears, just follow patient. If it persists, then mass excision is needed, refer to surgery.
* 32yo patient with positive routine mammography, unable to feel mass. Next step is stereotactic biopsy under
computer localization. If that isn’t an option, needle localization under ultrasound.
* Fibrocystic disease occurs in 50% of reproductive aged women. Also known as fibrocystic change (FCC) or
mammary dysplasia. This is a benign condition. It is characterized by nodularity and tenderness in both breasts. The
tenderness decreases when menses begins. 2-3% of patients with fibrocystic disease have hyperplasia, which may be
pre-cancerous. Suspect when there is a dominant mass. In that case, do needle aspiration. In general though,
fibrocystic disease is not precancerous and is benign, requiring no therapy.
* Fibrocystic change is diffuse nodularity in the upper outer quadrants, which is where most breast tissue exists.
There is no dominant mass in normal fibrocystic change. There is no treatment for fibrocystic change, but it can be
decreased by reducing caffeine (chocolate, soda). BCPs improve fibrocystic disease. Fibrocystic disease disappears
after menopause.
* 25yo with a well circumscribed rubbery 2cm left breast mass. This is fibroadenoma. This is not cancerous, but is
associated with cystosarcoma phyllodes. Fibroadenomas are not precancerous. Resect if the patient is symptomatic.
Next step after you feel the mass is needle aspiration to get the diagnosis of fibroadenoma. Tell the patient the
results and let them make the decision. If non-painful, recommend no treatment. If the patient has pain with running,
sleep, etc. recommend excision.
* Most common cancer in women is breast cancer, then lung, then colon. Mortality is highest with lung, then breast,
then colon.
* Tumor suppressor genes for the breast are BRCA1 and BRCA2. Cancer develops with alteration in these genes.
Two ways to get alterations, sporadic and hereditary. About 5% is familial and 95% is sporadic. Worry about
familial when it is early onset, prior to age 50. Think about familial cancer if two or more first degree relatives, such
as mother, sister, and patient.
* If patient says “my mom had breast cancer, am I at risk?” Answer is no, not more than the general population. You
need two or more first degree relatives. You can offer BRCA1/BRCA2 testing. If it is positive, options are more
frequent mammography, tamoxifen, and mastectomies (aggressive therapy). Tamoxifen can increase endometrial
cancer. Example: patient on tamoxifen with vaginal bleeding, next step in management is endometrial sampling.
* With a BRCA1/BRCA2 mutation, there is a 30-40% chance of developing cancer.
* 65-70% of breast cancer is intraductal carcinoma. Most breast cancers are detected by the patient on self
examination. Doubling time of breast cancer is 100 days, about 3.5 months. A lesion has to be 2cm for a clinician to
palpate. If the lesion is 1cm, it has been there for 8 years already; so it is suggested that there is no localized breast
cancer. By the time the lesion is detected, it has already spread. This is why breast cancer is treated with surgery and
adjuvant therapy (tamoxifen and chemotherapy). Surgery only may possibly be used for lesions <1cm.
* A modified radical mastectomy spares the pectoralis muscle in the chest. A lumpectomy takes out about 1-2cm
around the cancer margins, and is combined with axillary lymph node dissection. Additional to lumpectomy and
axillary lymphadenectomy, add radiation therapy. If the patient is post-menopausal, most common adjuvant therapy
is tamoxifen. Most common adjuvant therapy given to pre-menopause patient is cytotoxic chemotherapy. There is
too much estrogen in the pre-menopausal group to use tamoxifen effectively.

* Most common protocol for post-menopausal breast cancer patients who are estrogen receptor negative (ER neg) is
CMF, cyclophosphamide, methotrexate, 5-FU.
* In reproductive age group, surgery with radiation, adjuvant with CMF. If estrogen receptor positive, CMF plus
tamoxifen.
* Most common sites of metastasis for breast cancer are lung, liver, and bone.
* No increase or decrease in survival with lumpectomy + node dissection versus mastectomy. Reason for less
aggressive surgery is quality of life issues.
* Lactation does not lower the risk of breast cancer. Lactation inhibits the axis so the thought was that estrogen
would be reduced. Although some controversy, general agreement is lactation does not reduce breast cancer.
* 36yo patient with breast cancer, will she benefit from bilateral salpingo-oophorectomy? Only recommend this in
metastatic breast cancer with positive estrogen receptor (ER+). Prophylactic BSO not recommended otherwise.
* Lobular carcinoma is associated with bilaterallity.
* If a patient has breast cancer, can she get pregnant after treatment? Yes. Dominant hormone of pregnancy is
progesterone (not estrogen). Pregnancy will not make breast cancer worse.
* Can you breast feed if you have breast cancer? Answer is yes, from the opposite breast.
* What is the most important prognostic factor for breast cancer? Answer is status of axillary lymph nodes.
* Mammography is more accurate post-menopausal patient because the breast is less dense.
* Most common site of metastasis for ovarian cancer? Peritoneal cavity.
* Most common site of metastasis for endometrial cancer? Vaginal cuff (vagina).
* Can patients with breast cancer be on birth control pills? Yes. Dominant hormone of BCPs is progesterone.
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Kaplan Videos (2001) – Obstetrics with Dr. Elmar Sakala, MD, MA, MPH, FACOG
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Human Genetics: Diagnostic Procedures
* 37yo G5 P0 Ab4 comes for prenatal care at 7 weeks gestation. She has experienced 4 previous spontaneous first
trimester abortions. She is concerned regarding the likelihood of her next pregnancy being successful.
* Maternal age >= 35 is the highest risk for chromosomal anomalies. This is considered advanced maternal age
(AMA). Most common indication for genetic counseling is AMA.
* Risk of Down at age 20 is 1:1600. Risk of Down at age 35 is 1:365. Risk at Down at age 45 is 3%.
* What is the most common trisomy seen? Trisomy 21. At meiosis, normally a polar body splits. In non-disjunction,
it does not split. Thus we have 2 of a particular chromosome in the egg. Thus we get a total of 3 (with the sperm)
chromosomes. Sometimes called “sticky chromosomes.”
* Indications for genetic counseling are advanced maternal age, multiple fetal losses, previous child with death (fetal
death, neonatal death, aneuploidy), pregnancy losses (stillborn), family history (genetic diseases), abnormal prenatal
screening, parental aneuploidy.
* Aneuploidy is something other than 46XX or 46XY chromosomes.
* Ask patients if they have had babies die before birth or after birth. Ask if there is a history of mental retardation in
the family. Ask if there is any history of birth defects. That covers most of them, so if that is negative the patient
likely does not require genetic counseling.
* If patient meets indications, must offer genetic counseling.
* Gravida is number of pregnancies ever, para is number of pregnancies that went to 20 weeks or more.
* 24yo G2 P1 at 11 weeks gestation comes to the office. Her previous baby has trisomy 21. She is concerned that
this fetus may have this condition. She inquires about possible diagnostic testing for this pregnancy. Testing to offer
is ultrasound, CVS (chorionic villus sampling), PUBS (percutaneous umbilical blood sampling), amniocentesis,
fetoscopy. All this testing is elective.
* Always think about ultrasound as an option for the next step. What is the next step if the uterus is enlarged? What
is the next step if the mother hasn’t felt the baby move? If the uterus is too small or large for their gestation, if you
are not sure about the presentation, if you are not sure of the number of babies.
* Ultrasound is non-invasive imaging of intrauterine contents. You can first see a gestational sac in the uterus at
about 5 weeks. No adverse outcomes have been seen with ultrasounds. However, there is no indication for routine
ultrasound. The test is only done if there is an indication to do it.
* CVS (chorionic villus sampling) is invasive, aspiration of placental tissue precursors. This is done between 9-12
weeks gestation. Pregnancies are lost at about 0.7% from CVS.
* Amnio (amniocentesis) is invasive, aspiration of amniotic fluid with living fetal cells (amniocytes). We can
measure amniotic aFP, acethylcholinesterase for neural tube defect, cultures, PCR, and more. This is typically done
at 15 weeks or greater. If we do it earlier, there is not enough fluid so we could lose the pregnancy. Pregnancies are
lost at about 0.5% from amniocentesis. Make sure the reason you are doing the test is higher than the loss rate, if the
procedure is more hazardous than the condition you are looking for then do not do the test.
* At age 35, likelihood of finding something on amniocentesis is 1:200 (0.5%), which is why age 35 was chosen.
* PUBS (percutaneous umbilical blood sample), aspiration of fetal blood, two umbilical arteries and a larger
umbilical vein (vein is target for aspiration). This is done after 20 weeks so vein is large enough. Pregnancies are
lost at about 1-2% from PUBS.
* Fetoscopy is looking at fetus from within the amniotic sac. The reason to do this is fiberoptic visualization of the
fetus and then biopsy. Biopsy commonly of fetal skin, looking for ichthyosis (fish like skin). This is done at 18-20
weeks. Pregnancies are lost at about 3-5% from fetoscopy. This is usually done in specialized centers.
* Ultrasound shows cystic hygroma, fluid-filled sac that result from a blockage in the lymphatic system. Cause is
Turner syndrome. Web-shaped neck is due to collapsed cystic hygroma.
* Ultrasound turtle sign is the scrotum and head of penis, used to say fetus is a boy. Hamburger sign for a girl.
* What is the most common adverse effect of obstetrical ultrasound? None.
* When do you do ultrasound for anomaly screening? Answer is 18-20 weeks. Before 18 weeks the structures are
too small. After 20 weeks there is calcification. The accuracy of ultrasound for dating is +/- 7 days.
* Optimal gestational age for sonogram for pregnancy dating is 8-12 weeks (+/- 5 days).
* Sensitivity and specificity of sonogram for anomaly screening is highly variable. Depends on size of mother,
experience of the sonographer, abdominal wall scaring if previous surgery. Do not tell the patient their baby is
normal from ultrasound. Say the likelihood is low of abnormalities.
* CVS can be done transcervically or transabdominally. Placenta came from zygote, so you expect chromosomes of
placenta to be the same as the fetus.
* CVS optimal gestational age is 9-12 weeks. Follow-up testing required for CVS is triple-marker (or quad-marker)
screen and ultrasound. Pregnancy loss with CVS is 0.7%. Advantages to performing CVS are finding problems
earlier in gestational age than amniocentesis. If the patient is going to terminate the pregnancy, the risks are lower
and the emotional attachment is lower.
* CVS done for things with a high recurrence rate, like autosomal recessive with 25% chance of getting disease.
* Optimal gestational age for performing amniocentesis (under ultrasound guidance) is 15-20 weeks for genetic
studies looking at AFP and amniocytes. Age for isoimmunization is > 24 weeks, looking at amniotic fluid bilirubin.
For fetal lung maturity, do amnio at > 34 weeks, looking for L/S (lecithin/sphingomyelin of 2 for mature) and
phosphatidylglycerol (PG). Lecithin also called phosphatidylcholine (PC). Pregnancy loss rate is 0.5%.
* PUBS done via transabdominal needle aspiration. Optimal gestational age > 20 weeks. Purpose is for fetal
karyotyping, IgM, blood typing, IUT (intrauterine transfusion). Pregnancy loss rate is 1-2%.
* Fetoscopy for biopsy, could do a liver biopsy then enzyme studies for autosomal recessive enzyme disorders.
Optimal gestation age 18-20 weeks. Pregnancy loss rate 3-5%.
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Human Genetics: Chromosomal Aberrations
* Aneuploidy is numeric chromosomal abnormality other than 46XY or 46XX. Most common kind of aneuploidy is
trisomy. When looking at a karyotype, the top is large autosomes and will not have a trisomy as the pregnancy
would terminate because of the amount of genetic material. Next line is medium autosomes, rare to see aneuploidy
here either. Look at the last line, the smaller autosomes. Look at 13, 18, 21, and sex chromosomes.
* Trisomy is presence of a single extra chromosome. Most common specific trisomy is 21 (Down syndrome), 50%
of cases of trisomy.
* Monosomy is an absence of a single chromosome. Most common specific monosomy is X (Turner syndrome),
98% of Turner syndrome patients never make it to term, they spontaneously abort. In Turner syndrome, the X that is
deleted is the paternal X.
* Polyploidy is the presence of an extra chromosome set (23). Most common type of polyploidy is triploidy
(69XXY). Obstetrical complication with 69XXY is incomplete mole.
* Structural alteration is deletion, gaining, rearranging of chromosomal material. Example is cri du chat syndrome,
is partial deletion of chromosome 5.
* Mosaicism is two or more distinct cell lines. Examples are 45X/46XX, 45X/46XY, 45X/46XY/47XXY,
45X/46XX/47XXY for Turner mosaic. Patient may look like Turner syndrome, but may have follicles in ovary.
* What is the effect of mosaicism on ovarian follicles? Answer is premature ovarian failure, gonadal malignancy. If
patient has menopause before age 40, do a karyotype. If the karyotype is mosaic, worry about gonadoblastoma.
* Reciprocal translocation is breakage and reunion of non-homologous chromosomes.
* Robertsonian translocation is centric fusion of acrocentric chromosomes. We lose a chromosome as far as

chromosome number, but the actual material is all present.
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Human Genetics: Pregnancy Loss
* Spontaneous abortion (miscarriage) in 15-20% of pregnancies.
* Turner syndrome (45XO). Ultrasound will show an early nuchal skin fold (first trimester), cystic hygroma later on
(turning into webbed-neck). Fetus has short stature, normal IQ, primary amenorrhea because no follicles to produce
estrogen.
* Kleinfelter syndrome (47XXY). Ultrasound not diagnostic, seldom diagnosed until puberty. This makes a good
point, just because the ultrasound shows no abnormality does not mean the baby is normal, so do not tell the mother
that their baby is normal. Fetus is tall, decreased IQ, testicular atrophy, infertility, gynecomastia, central obesity.
* Many dwarfism syndromes do not develop until late 2nd trimester or even third trimester. So 18-20 week
ultrasound would not be diagnostic for dwarfism.
* Down syndrome (47XX+21 or 47XY+21). Ultrasound will show shortened femur, shortened humerus,
intracardiac echogenic focus, enlargement of the ventricles, echogenic bowel, pyelectasis. Fetus is short, mental
retardation, heart disease specifically endocardial cushion defects.
* Edward syndrome (47XX+18 or 47XY+18). XAFP is extended AFP, includes AFP, estriol, beta hCG. All serum
markers are low with trisomy 18. Fetus has profound mental retardation, survival 40% after one year.
* Patau syndrome (47XX+13 or 47XY+13). Rare, profound mental retardation, high mortality rate.
* What is the most common cause of spontaneous abortion (miscarriage)? Answer is aneuploidy.
* 25% of IVF embryos have abnormal karyotype.
* It is suggested that every living person has over a dozen lethal recessive chromosomes, which is why society
prohibits couples who are close genetically from getting together because of increased chromosomal complications
with the offspring.
* The most common type of aneuploidy in spontaneous abortions is autosomal trisomy.
* The most common single aneuploidy in single abortions is Turner syndrome.
* Turner syndrome (45X) from Mother, father’s X is lost. No secondary sexual characteristics. Breasts in a female
are an endogenous assay for estrogen, thus not enough estrogen in Turner syndrome. There are no follicles in the
ovary to stimulate. Patients have a web neck. Triad is primary amenorrhea, web neck, streak gonads.
* Kleinfelter syndrome (47XXY) 1:2000, tall, long arm span, small gonads , centripetal adiposity. Triad is
gynecomastia, testicular atrophy, azoospermia.
* Down syndrome (trisomy 21) 1:700. Fluorescent in situ hybridization (FISH) can give a rapid (24hours) result via
amniocytes for trisomy. Then do complete karyotype to confirm diagnosis. Triad is short stature, mental retardation,
encocardial cushion cardiac defects. Most Down syndrome occurs between ages 20-30 because more babies are born
during those time periods. So even though the age-specific rate increases as you get older, more Down babies are
born before age 35. Do not limit screening to women over age 35 or you’ll miss most Down cases. Most common
cause of Down syndrome is non-disjunction. Hispanics have a higher rate of Down syndrome.
* Optimal time for pregnancy, physiologically, is age 18-24 taking all things into account.
* 47XYY (“super male”) initially identified in prison populations. Then they did the same study on medical students
and found the same ratio. So this is likely not related to violent behavior.
* Edward syndrome (trisomy 18), risk factor is AMA.
* Patau syndrome (trisomy 18) has low-set ears and sloping forehead, most do not survive.
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Human Genetics: Mendelian Genetics
* 23yo black primigravida is 12 weeks gestation. She has been diagnosed with sickle cell trait (AS). Her husband
and father of the baby is also AS. What is the risk of her baby having sickle cell disease (SS)?
* Autosomal dominant (AD) is equally found in male and female, no sex predominance. It does not skip
generations. It is typically an anatomic disorders, such as achondroplastic dwarfism. There are no carrier states,
either you have the disease or you do not have the disease.
* Autosomal recessive (AR) also no sex predominance. It does skip generations, a classic finding. Parents may both
be carriers then the disease shows up in the child. These are typically enzyme disorders. Carrier states are frequent.
* X-linked recessive (XR) has no male to male transmission because father gives son the Y chromosome. Only
males are affected. These tend to be enzyme disorders. Only females can be carriers (homozygous females could be
affected).
* X-linked dominant (XD) is rare because they are often lethal. Because this is dominant it is equal in males and
females, does not skip generations. Females survive but males do not.
* Pedigree: squares are males, circles are females, filled means affected, X means unaffected but heterozygous,
double lines between means consanguineous.
* In the past, royalty was required to marry royalty. After generations, autosomal recessive traits started coming out.
Example is hemophilia in Queen Victoria (European royalty in the 19th and 20th centuries).
* Autosomal dominant triad is transmitted by both genders, all generations affected, no carrier states.
* Most common abnormality with AD traits is anatomic.
* Autosomal dominant traits include achondroplasia, Marfan syndrome, polycystic kidneys (children, more fatal).
* Autosomal recessive triad is transmitted by both genders, often skips generations, has male and female carriers.
* Most common abnormality with AR traits is enzymatic.
* Autosomal recessive traits include cystic fibrosis (CF), sickle cell, Tay Sachs, phenylketonuria (PKU), congenital
adrenal hyperplasia (CAH).
* Cystic fibrosis is the most common genetic disorder in Caucasian populations.
* With autosomal dominant normal father and heterozygous mother, 2:4 (50%) will be normal, 2:4 (50%) will be
carriers, none will have the disease.
* With autosomal dominant both parents carriers, 1:4 (25%) will be normal, 2:4 (50%) will be carriers, 1:4 (25%)
will have the disease.
* With autosomal recessive homozygous mother normal father, 50% will have the disease and 50% will be normal.
* X-linked recessive triad is no male-to-male transmission, expressed only in males, only female carriers.
* X-linked recessive traits include hemophilia A, testicular feminization (androgen insensitivity), Duchenne
muscular dystrophy (DMD).
* With X-linked recessive normal father and carrier mother, unaffected female, unaffected male, affected male,
carrier female. So 50% chance of boy being affected or normal, 50% chance of girl being carrier or normal.
* With X-linked recessive affected father and carrier mother, 50% chance of boy being affected or normal, 50%
chance of girl being carrier or affected.
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Human Genetics: Multifactorial (Polygenetic) Inheritance
* What is the most common cause of birth defects? Answer is multifactorial, environmental and genetic.
* 32yo woman with corrected tetralogy of Fallot is pregnant at 18 weeks with a male fetus. She inquires as to the
chance what her son has congenital heart disease. Answer is 2-3%.
* 70% of birth defects are multifactorial. 1% are cytogenetic. 15% are Mendelian (AD, AR, etc).
* What is the overall recurrence rate of polygenic defects? Answer is 2-3%.
* Examples of polygenic birth defects are neural tube defect (NTD), congenital heart defect (CHD), cleft lip/palate.
* When do neural tube defects develop, what are the post-conception days? Answer is days 26-28, 3-4 weeks after
conception. This is 5-6 weeks after the last menstrual period. The average patient presents to prenatal care at about
12 weeks. So to prevent neural tube defects, it has to occur before the patient even visits the clinician. We can
decrease this by recommending folic acid at 400mcg/day (0.4mg), highest risk for NTD are women with previous
history, women with type I or type II diabetes, women on anticonvulsants (decreased folate absorption). The U.S.
Food and Drug Administration (FDA) requires that all manufacturers of breads and pastas include folic acid. So the
average woman will get about 150mcg/day in the food they eat.
* 50% of neural tube defects are anencephalic. Diagnosis this on ultrasound by seeing no cranium above the orbits.
The other 50% are spina bifida.
* What is the most common gender affected by pyloric stenosis? Answer is males.
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Human Genetics: Embryology
* Week 1 goes from ovulation to implantation. Sperms enter the egg, one of the largest cells in the body. It is about
the size of the period at the end of this sentence, you can actually see it.
* First half of the first week begins with ovulation, fertilization occurs typically in the distal tube (12-24 hours). By
the time the zygote reaches the proximal tube, it is a ball of cells called a morula. Any one of the morula cells is
totipotential, stem cells. Morula enters uterus about day 3, in the middle of the first week.
* Second half of the first week the morula turns into a sphere of cells that has an inner mass. This is the blastula.
This will implant on the surface of the uterus at the end of the first week.
* Week 1 first half is intratubal phase and second half is intrauterine phase. Zygote, morula (middle of week),
blastula. During the first week, the cells have not fused and have no blood supply, so there is no risk of teratogenesis
from the mother’s bloodstream.
* What is the post-conceptional period when the morula develops? Answer is week 1, first half.
* What is the post-conceptional period when the blastula develops? Answer is week 1, second half.
* Week 2 is the development of the bi-laminar germ disc. Mnemonic is week 2 for bi.
* Bilaminar germ disc is epiblast and hypoblast surrounded by trophoblast that invades into endometrium, day 9.
The trophoblast is trying to reach the maternal sinuses (blood).
* Trophoblast invades the sinuses by day 12. This is the first time the pregnancy test becomes positive. Beta hCG
from the syncitiotrophoblast can now get into maternal circulation. So when the first pregnancy test comes back
positive, the pregnancy has to be at least 2 conceptional weeks (or 4 menstrual weeks).
* No organs have developed at day 13, there aren’t even the three germ layers.
* At day 13, a groove develops called the primitive streak.
* What is the post-conceptional week when gastrulation occurs? Answer is week 2.
* What is the post-conceptional week when beta hCG becomes positive? Answer is week 2.
* Week 3 is the development of the trilaminar germ disk. Mnemonic is week 3 for tri.
* Trilaminar germ disc requires the primitive streak. These are ectoderm, mesoderm, endoderm.
* What is the most common post-conceptional weeks for teratogenesis? Answer is weeks 3-8.
* Weeks 4-8 are the formation of the major organ systems.
* Ectoderm organ systems are nervous (central and peripheral), seeing, hearing, integumentary.
* Mesoderm organ systems are muscles, cartilage, cardiovascular, urinary, genital.
* Endoderm organ systems are gastrointestinal and respiratory tract lining.
* Paramesoneprhic (Mullerian) duct gives rise to ovaduct, corpus of uterus, cervix, proximal vagina. So with
Mullerian agenesis, patient will have ovaries and a short vagina.
* There is no estrogen needed for female external genitalia development from the indifferent stage. To get male
external genitalia, androgens are needed. Everyone will become female unless there is a stimulus to become male.
Default development is female.
* What hormone is needed for forming female external genitalia? Answer is none.
* What hormone is needed for suppressing female external genitalia? Answer is Mullerian inhibiting factor (MIF).
* Mesonephric (Wolffian) duct. What is the hormone needed for forming male external genitalia? Answer is
dihydro-testosterone (DHT).
* What is the hormone needed for suppressing male external genitalia? Answer is none.
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Human Genetics: Teratology
* 36yo woman underwent a barium enema for rectal bleeding on February 1 with estimated radiation dose of 4 rads.
Her LMP was January 1 and she has 35 day cycles. She was not using any contraception. A urine pregnancy test was
positive on March 15. She inquires regarding the risk to her fetus of teratogenic injury. When did she conceive?
Answer is January 21 (35 minus 14). How many days post-conception was the barium enema? Answer is 10 days,
this is week 2 with bilaminar germ disc. What is the chance that she will have a fetus born with defects because of
this procedure? Answer is zero. If the exposure was enough to injure the embryo, it will die. Else it will be intact.
* Studies were done on Nagasaki and Hiroshima taking the distance from the atomic blast into account with
pregnant women. They could estimate the radiation dosage for the pregnant women. Less than 10 rads is minimal
risk and less than 5 rads is basically no risk. Exposure of most diagnostic studies is less than 10 rads and most of
those are less than 5 rads. Medical x-rays do not increase the number of babies born with birth defects.
* If you have one full CT scan covering the abdomen and pelvis over the course of a scan, then the fetus may
receive between 1.2 and 3 rad. If you actually receive two scans, an abdominal scan that covered the area of the
uterus plus a separate pelvis CT scan, then the fetus may receive between 2.4 and 6 rad. There is no concern for fetal
birth defects below 15 rad.
* According to the American College of Radiology, no single diagnostic x-ray has a radiation dose significant
enough to cause adverse affects in a developing embryo or fetus. In general, CT scans are not recommended during
pregnancy unless the benefits of the CT scan clearly outweigh the potential risk.
* Thalidomide was used during pregnancy and was an excellent anti-emetic. It was widely used in Europe in
particular. There is a narrow window of time after conception where thalidomide leads to birth defects, thus it is no
longer used in pregnancy (contraindicated).
* Trimesters are 0-13, 14-26, 27-birth. Division point are 14 and 27 weeks.
* What is the effect of teratogenic agents from conception to the end of the 2nd week? Answer is the embryo will
either survive intact or it will die.
* What is the effect of teratogenic agents from post-conception weeks 3 to 8? Answer is greatest risk of defects.
* What is the effect of teratogens after post-conception week 9? Answer is low, more problems in organ hypertrophy
and hyperplasia (not in organ formation).
* Women with overt diabetes have the same birth defect rates if they have their blood sugars controlled. Thus, it is
very important for clinicians to monitor and manage diabetes. This should start pre-conception.
* When you use a pregnancy wheel, it assumes a 28 day cycle and ovulation occurring on day 14. The pre-ovulatory
part is the part that changes with short or long cycles.
* Infectious agents include bacterial (chlamydia, gonorrhea), viral (rubella, CMV, HSV), spirochete (syphilis), and
protozoa (toxoplasmosis).
* With ionizing radiation, the risk is dose related. What is the threshold of ionizing radiation for teratogenesis to
occur? Answer is 5 rads. The gradient starts here. Threshold means you can be exposed up to that point before it has
an effect, and from thereon it become dose related.
* Chest x-ray is on the magnitude of 1/10th of a rad. Average is 1/300 of a rad (0.015 rads).
* Chemotherapy effects are mostly during first trimester, after that the effects are minimal.
* What is the safe level of alcohol a mother can drink? Answer is zero. Fetal alcohol syndrome, midface hypoplasia,
microcephaly, mental retardation, intrauterine growth restriction (IUGR).
* What is the safe level of cigarettes a mother can smoke? Answer is zero. There is no syndrome, but there is
associated IUGR, prematurity. Prematurity rate would be reduced by 1/3 if pregnant women stopped smoking.
* Cocaine causes abruptio placenta (serious risk), prematurity, intraventricular hemorrhage (IVH), IUGR.
* Marijuana causes prematurity, no associated syndrome.
* FDA categories of drugs are A (no risk), B (no evidence of risk), C (risk cannot be ruled out), D (risk), X
(contraindicated in pregnancy).
* Drugs under category A: acetaminophen, thyroxine, folate.
* Most medications used in pregnancy are B and C.
* Drugs under category B: penicillins, cephalosporins, methyldopa. These are safe but no one is going to do the
studies to put them into category A.
* Category C means there is risk at very high doses in animals. At normal doses, the benefit has to outweigh the risk.
* Drugs under category C: codeine, steroids, beta-blockers.
* Drugs under category D: anticonvulsants.
* Drugs under category X: isotretinoin, warfarin, ergot.
* What is the most common physical finding with in-utero exposure to alcohol? Answer is midface hypoplasia, long
philtrum.
* What is the most common physical finding with in-utero exposure to diethylstilbestrol (DES)? This use to be
given to women who were spotting/bleeding in first trimester to prevent miscarriage. Answer is Mullerian anomalies
in women, vaginal clear cell adenocarcinoma. The cohort of these women may have passed through reproductive
years now, so not likely to see clear cell adenocarcinoma from DES exposure anymore.
* What is the most common physical finding with in-utero exposure to phenytoin? Answer is craniofacial
dysmorphism, mental retardation, microcephaly, nail hypoplasia.
* What is the most common physical finding with in-utero exposure to isotretinoin? Answer is small ears (microtia),
CNS anomalies, cardiac anomalies. The manufacturer now require the patient to sign a document saying they will
use a form of contraception while using the drug.
* What is the most common physical finding with in-utero exposure to lithium? Answer is Ebstein anomaly (right
heart defect with tricuspid valve displaced toward apex).
* What is the most common physical finding with in-utero exposure to streptomycin? VIII nerve damage (hearing).
* What is the most common physical finding with in-utero exposure to tetracycline? Discolored teeth (yellow).
* What is the most common physical finding with in-utero exposure to thalidomide? Phocomelia (limb hypoplasia).
* Thalidomide is now being used for leprosy and multiple myeloma.
* What is the most common physical finding with in-utero exposure to trimethadione? Answer is facial
dysmorphism. Many of the anticonvulsants cause facial dysmorphism.
* What is the most common physical finding with in-utero exposure to valproic acid? Neural tube defect, almost
always spina bifida (where normal is 50% spina bifida and 50% anencephaly).
* What is the most common physical finding with in-utero exposure to warfarin? Stippled epiphyses and optic
atrophy. Warfarin exposure is an issue at any point during the pregnancy.
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Physiology of Pregnancy: Overview
* Pregnant women have different laboratory values than normal population. Complaints of pregnancy may be
related to normal physiology.
* Pregnancy hormone, beta hCG. There is an alpha subunit that is like FSH, LH, TSH. Beta subunit is unique.
* Beta hCG comes from syncytiotrophoblast. You cannot be pregnant (even ectopic) with no trophoblastic material.
* When does beta hCG peak and when does it stabilize? Peaks at 9-10 weeks, levels off at about 20-22 weeks.
* What is the purpose of hCG in pregnancy? Answer is to maintain the corpus luteum, production of progesterone
until 8-10 weeks.
* Most common cause of excessively high beta hCG is twins and mole.
* Normal doubling time of beta hCG is 48 hours (about 2-3 days some say).
* Most common cause of too low beta hCG is ectopic and miscarriage.
* Human placental lactogen (hPL) is similar to growth hormone and prolactin. What is the main effect of hPL?
Answer is hPL antagonizes insulin. Gestational diabetes is related to hPL.
* What is the gestational age when we diagnosed gestational diabetes? After 20 weeks. Why? The placenta produces
hPL and the amount of hPL is proportional to the size of the placenta. Until 20 weeks, there is not enough hPL
present to produce antagonism of the insulin.
* What is the common cause of too low hPL levels? Answer is miscarriage and IUGR.
* What is the most common site of non-pregnant progesterone production? Answer is corpus luteum. When
pregnant, the site is the placenta. If deficient in progesterone, you know patient is not pregnant and is anovulatory.
The corpus luteum will not continue to make progesterone indefinitely, it needs a signal of pregnancy, beta hCG. So
beta hCG maintains the corpus luteum production of progesterone until the placenta can take over (8-10 weeks).
* When do you stop giving an IVF patient progesterone? Answer is at 10 weeks, placenta takes over then.
* What is the purpose of progesterone in early pregnancy? Answer is secretory endometrium favorable for
implantation. Late in pregnancy, progesterone stabilizes the myometrium to prevent premature labor.
* Estrogen as estrone (E1), estradiol (E2), and estriol (E3).
* What is the most common estrogen in the reproductive years? Answer is estradiol, produced by granulosa cells in
the follicle. Aromatase enzyme converts androgen to estrogen within the granuloma cell.
* What is the most common estrogen in pregnancy? Answer is estriol, produced by the placenta from fetal adrenal
steroids (90%) and is converted from DHEAS.
* Most common estrogen after menopause is estrone, produced by adipose from adrenal steroids. Obese women tend
to have less hot flashes, less osteoporosis, but increased risk of breast cancer.
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Physiology of Pregnancy: Physiologic Changes
* Striae gravidarum (stretch marks). Spider angiomata, palmar erythema, Chadwick sign all from increased
vascularity. Chadwick sign is blue hue to cervix. Linea nigra and chloasma (facies) from increased pigmentation.
* People will say they have the perfect cure and try to sell you oils/lotion to prevent stretch marks. The truth is none
of these really work. Stretch marks are likely genetic.
* Pregnant woman will always have a warm hand (palmar erythema).
* Systolic blood pressure decreased in pregnancy. Diastolic blood pressure decreases even more. This occur even by
the end of the first trimester. Blood pressure never goes higher in pregnancy than it did before pregnancy. High
blood pressure is never normal in pregnancy.
* Central venous pressure (CVP) does not change with pregnancy.
* Femoral venous pressure increases, lower part of the body. This almost triples by the end of pregnancy. If a
woman has a predisposition to varicose veins or hemorrhoids, they can get pretty bad.
* Plasma volume in pregnancy increases even more than RBC volume. There is a direct relationship between the
size of the baby and the expansion of plasma volume. Cardiac output corresponds. A mid-systolic diamond-shaped
murmur in pregnancy is benign, or even good. It implies the blood volume has expanded; if it hadn’t expanded,
there may not be room for the baby.
* Peripheral vascular resistance (PVR=BP/CO), BP decreases, CO increased, so PVR decreases significantly. You
want to enhance perfusion to the fetal-placental unit.
* Cardiac output (CO=HR*SV), HR increases, SV increases, so CO increases significantly.
* What trimester is a women with heart disease going to have the most problems? Answer is first trimester.
* Cardiac output depends on maternal position. The inferior vena cava (IVC) can get compressed when the mother is
on her back, so position her rolled slightly to the left. For surgery, use a wedge under the right hip.
* Mother pregnant with twins is undergoing an ultrasound and starts to feel dizzy. This is supine hypotensive
syndrome (inferior vena cava syndrome). Turn patient to their left side.
* Cardiac output varies with the stage of labor. About 5L/min normally, goes up with labor. Stage I of labor the
output goes up more, patient is anxious and/or in pain (heart rate goes up). If patient has heart disease, give epidural
anesthetic, reassure. Stage I of labor, patient is pushing/working so heart rate goes up. If patient has heart disease, let
their own contractions work, don’t have the patient push, then deliver with forceps or vacuum. Greatest stress on the
heart is immediately post-partum, when the placenta comes out.
* Watch for postpartum heart failure from autotransfusion of uteroplacental blood rapidly into the peripheral
circulation, this occurs within 5 minutes. We normally take a couple of hours to transfuse a unit of blood. So there is
increased vascular volume.
* Only normal heart murmur in pregnancy is mid-systolic diamond-shaped crescendo-decrescendo ejection murmur.
This murmur is due to increased cardiac volume passing through the aortic and pulmonary valve. Diastolic murmurs
are never normal.
* Heart moves toward left in pregnancy, left axis deviation. ECG should show LAD. Point of maximal impulse
(PMI) will go up and to the left. This is normal in pregnancy.
* RBC mass increases in pregnancy, but not as much as plasma volume. Hemoglobin and hematocrit will go down,
but this is not anemia. Anemia is decrease in oxygen carrying capacity. This is dilutional in pregnancy. At what
point is H&H the lowest? About 28-30 weeks, which is why we check H&H at that point. Non-pregnant hemoglobin
should be > 12, and > 10 in pregnancy.
* WBC count increases by 15,000 in pregnancy and 25,000 in labor. This is normal. So a pregnant patient with right
lower quadrant pain and high WBC may be just normal round ligament pain.
* Sedimentation rate (sed rate) increases. All plasma proteins increase except albumin, including gamma-globulins.
sed rate determined by gamma-globulins.
* Platelet count is typically unchanged in pregnancy, remains within normal range.
* Coagulation factors VII, VIII, IX, X increase. With decreased venous flow, this is a setup for deep venous
thrombosis (DVT). Fibrinogen is a plasma protein so it increases.
* Prothrombin time (pro time, PT) and partial thromboplastin time (PTT) do not change.
* GI tract smooth muscle wall tone decreases, likely due to progesterone smooth muscle relaxation effect. Motility
slows down. GI tract residual volume increases. GI tract emptying time goes down. This is a setup for reflux
esophagitis (GERD), cholelithiasis, and constipation.
* Most common cause of epigastric pain in pregnancy is reflux esophagitis. Worry about severe pre-eclampsia with
epigastric pain.
* Tidal volume increases in pregnancy. Minute ventilation (MV=RR*TV), respiratory rate is mostly unchanged and
tidal volume increases, so minute ventilation increases. Residual volume decrease.
* What happens to pCO2 if minute ventilation increases? pCO2 will decrease due to hyperventilation. Normal pCO2
in pregnancy is 30-35 (normal is 40).
* What happens to pH if pCO2 goes down? pH will increase. Normal pH in pregnancy is 7.45 (normal is 7.4).
* What happens to urine pH if blood pH increases? Urine pH will go up, body trying to kick out the pH. What
protects against UTIs is an acidic urine, so there are more UTIs in pregnancy with more alkaline urine.
* Kidney enlarge in length and width in pregnancy. This takes a couple of months to regress after pregnancy. The
increased perfusion increases the kidney size, increased thyroid size, increased anterior pituitary size.
* Renal pelvis volume increases. Ureteral volume increases, can increase in capacity by up to 200mL of urine. The
increase is more pronounced on the right side. Pyelonephritis occurs 90% of the time on the right side in pregnancy.
* Renal plasma flow increases. Glomerular filtration rate (GFR) increases. Creatinine clearance increases. Blood
urea nitrogen (BUN) decreases, wastes in blood decreases. Serum creatinine decreases. Serum uric acid decreases.
* Non-pregnant BUN upper limit of 15-20, in pregnancy it is 10. A BUN of 15 in pregnancy is an issue. Non-
pregnant serum creatinine is 1-1.5, in pregnancy it is 0.5. Normal (non-pregnant) kidney results imply kidney
disease or a complication of pregnancy like pre-eclampsia.
* Glucose in the urine increases in pregnancy. This is normal. Some feel it is a waste of time to do urine “short dips”
in the clinic looking for glucose. Short dip is glucose and protein. Long dip includes nitrites, LE, pH, and more.
* Protein in the urine does not change in pregnancy. If there is an increase, think about renal disease or an affect on
the kidney like pre-eclampsia.
* Pituitary blood supply increases to the anterior pituitary, increased risk of hypotension (Sheehan syndrome).
* Adrenal glands increase in size in pregnancy. Cortisol production increases 2-3x.
* Thyroid gland size increases. TRH and TSH do not change. Thyroid binding globulin increase. All transfer
binding proteins increase in pregnancy, like sex hormone binding globulin, gamma globulins, beta globulins. So,
total T3 will increase and total T4 will increase. Free T3 (active hormone) is unchanged. Free T4 is unchanged. Free
thyroxine index (FTI) will not change in pregnancy.
* Fetal hemoglobin dissociation curve shifts to the left. Hemoglobin F (fetal) hangs onto oxygen at a greater
concentration even when oxygen is low. PO2 is low in fetus, like 30-40 from umbilical vein, basically living on
Mount Everest, baby does fine because of shift to left of dissociation curve.
* Highest PO2 in the fetus is in the umbilical vein just prior to reaching the fetal vena cava.
* Foramen ovale allows oxygenated blood from RA to get to LA of fetal heart.
* Asymmetric IUGR is where the head is normal but abdomen is small. Head is spared because brain gets
oxygenated blood in fetal circulation almost first.

* Ductus arteriosus bypasses lungs as gas exchange does not occur there. This stays open until birth. Medication to
close this is indomethacin, so this should not be given prior to birth but can be given to help close the ductus
arteriosus after birth.
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Antenatal Care: Fetal Testing & Pregnancy Duration
* Presumptive signs of pregnancy are unrelated to the uterus or fetus, amenorrhea, breast tenderness, nausea and
vomiting, skin pigmentation, striae.
* Probably signs of pregnancy are related to the uterus or fetus, increased uterus size, maternal feels uterine
contractions, Hagar sign (softening of the junction of the corpus of the uterus and cervix), beta hCG elevation.
* Pseudocyesis is false pregnancy, patient “feels” baby movement and contractions but is not actually pregnant.
* Definitive signs of pregnancy are to heart fetal heart tone (FHT), sonogram of fetus, x-ray of fetus (avoid if
possible), external examiner who feels the baby move.
* Mother may say she felt the baby move in the waiting room but clinician finds fetal death on sonogram with skin
sloughing (death not recent). So maternal report is not a definitive sign.
* What is the duration of pregnancy using conception dating? Answer is 266 days or 38 weeks (ideally).
* What is the duration of pregnancy using menstrual dating? Answer is 280 days or 40 weeks from LMP, assuming
a 28 day cycle.
* Method of calculating due date with Naegele’s rule uses the 28 day cycle. LMP – 3 months + 7 days.
* Basal body temperature increases due to thermogenic effect of progesterone, one way of dating.
* Pregnancy dating can be done via menstrual history. Most frequently occurring cycle is 28 days, but this is about
10-15% of the curve. A normal menstrual cycle is 21 to 35 days (28 +/- 7).
* Secretory phase is constant, after ovulation, 14 days. Proliferative phase, before ovulation, is variable.
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Antenatal Care: Clinical Landmarks & Ultrasound Dating
* What is the earliest that you can hear fetal heart tones with a Doppler stethoscope? Answer is 10-12 weeks.
* The earliest you can heart with a fetoscope (rarely used anymore) is 18-20 weeks.
* Quickening (mother’s perception of the baby’s movement) occurs at 16-18 weeks for a multigravida and 18-20
weeks for a primigravida. Initially feels like gas bubbles, primigravida may write off movements as gas.
* After 20 weeks, the fundus should measure in 20cm the number of gestational weeks. At 12 weeks, fundus is at
the pubic symphysis. At 20 weeks, at the umbilicus. At 16 weeks, midway between umbilicus and pubic symphysis.
* Variation is +/- 3cm when measuring.
* Ultrasound dating uses four landmarks, the biparietal diameter (BPD), head circumference (HC), abdominal
circumference (AC) at umbilicus, and femur length (FL).
* What is the accuracy of ultrasound as a function of gestational age? At 12 weeks, it is +/- 5 days. At 12-18 weeks,
it is +/- 7 days, at 18-24 days it is +/- 10 days. The further along the more spread there is in dating.
* Use the earliest ultrasound for dating. Any subsequent ultrasound will say if there is appropriate growth or
inappropriate growth. Do not change the due date with new ultrasounds, it is just appropriate or inappropriate
growth (accelerated or decelerated growth).
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Antenatal Care: First Prenatal Visit
* Again, parity is number of pregnancies that last 20 weeks or more. Gravida is confirmed pregnancies.
* Parturient is a women in labor. Puerpera is a woman who has just given birth.
* Abortion is pregnancy loss prior to 20 weeks. Antepartum death is fetal loss between 20 weeks and labor.
* In order for a pregnancy to be reported in the United States as part of the perinatal statistics, it has to go beyond 20
weeks. In some countries, it is 24 weeks or other dates. So you cannot compare international statistics.
* Intrapartum death is fetal death from the onset of labor until birth. Perinatal death includes antepartum and
intrapartum plus 28 days after birth. Neonatal death is a death between birth and first 28 days. Infant death rate is
death between birth and first year of life. Maternal death is a woman who died during pregnancy or within 90 days
of giving birth. Maternal death can be indirect (e.g. car accident) or direct (e.g. seizure from pre-eclampsia).
* Fertility rate is the number of live births per 1000 women aged 15-44.
* Birth rate is the number of live births per total 1000 population. 4million births in the U.S. Pyelonephritis occurs in
2% of women, so there are 80,000 per year.
* Maternal mortality rate is the number of maternal deaths per 100,000 live births. Rate is about 8 per 100,000.
* Perinatal mortality in the United States is about 8 per 1000.
* Infant mortality rate is combining neonatal and first year of life.
* Highest maternal death rate in the country is in the southeast, poverty-related. Lowest in the Midwest.
* How many women die from pregnancy and childbirth every day round the world? Answer is 1650 per day, so
more than one every minute. Most occur in Asia and Pacific, Sub-Saharan Africa.
* Most common cause of maternal death is thromboembolism.
* First question to ask when a patient comes on the first prenatal visit: is she pregnant. Urine beta hCG as accurate
as serum beta hCG. Urine is qualitative (yes or no), serum can be qualitative or quantitative (actual value). So to
determine if a patient is pregnant order a qualitative urine beta hCG.
* Hearing fetal heart tones is helpful, but she needs to be 10-12 weeks along.
* After confirming pregnancy, next question is what is her gestational age. Best time to determine this is on the first
prenatal visit. Later on memories will fade, “I can’t remember when my last period was.”
* Crown rump length (CRL) is accurate within 5 days during first trimester, then within 7 days after first trimester.
* There is a clear relationship between educational level and preterm birth. Young women have a higher rate.
* Ask about marital status and what type of social support the patient has. Abuse and domestic violence increases in
pregnancy. Determine if the patient is low risk or high risk, deserving special attention.
* Ask about obstetrical history and how far the pregnancies went. Ask about obstetrical complications. Ask what
type of delivery the patient had, vaginal delivery with induction, spontaneous vaginal delivery, cesarean section,
shoulder dystocia, fetal fractures, were forceps used. What were the outcomes of the pregnancies.
* Ask specifically about medical complications, like diabetes (2-3% will develop this). Hypertension is common.
Most common heart disease is acquired heart disease. Rheumatic heart disease causes mostly mitral stenosis.
* Women who are hypothyroid are usually anovulatory. Seizure disorder is common (1% of patients). Most
common anemia in pregnancy is iron deficiency.
* Ask about inherited disease such as sickle cell. Ask about mental retardation. Ask about perinatal death.
* Ask about lifestyle, alcohol, tobacco (adolescents in particular), street drugs, nutritional evaluation.
* Ask about medications, specifically anticonvulsants, warfarin, isotretinoin. If patient has a metallic heart valve and
is on warfarin, they can be switched to heparin during the pregnancy.
* If patient is low risk, follow-up visit schedule is every month up until 30 weeks, then every 2-3 weeks until 36
weeks, then every week after that. Why weekly after 36 weeks? We are looking for preterm and pre-eclampsia.
* First visit labs include CBC looking for anemia, urinalysis and culture/sensitivity looking for UTI, TB skin test if
she is at risk, sickle cell screening if she is at risk, Pap smear looking for cervical dysplasia, cervical cultures looking
for chlamydia and gonorrhea.
* First visit labs for fetus are atypical antibody test (AAT) indirect Coombs test, diabetes mellitus screen,
VDRL/RPR for syphilis, HepB surface antigen, and HIV if consent is obtained.
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Antenatal Care: Return Visit
* Ask about maternal well-being. Get a blood pressure, hypertension is 140/90 or greater, that is the point that
outcome changes. Check for weight gain, after 20 weeks there should be one pound per week. Pattern is important.
* Fetal well-being assessed by seeing if fetus is moving. Fetus goes through sleep-wake cycles of 40 minutes.
Before you say the baby is not moving, wait an hour and then see. A vibroacoustic device can be used as well to
wake up the baby. Moms only feel about half of the fetal movements.
* Normal fetal heart rate is between 110 and 160. Check fundal growth by measurement. Number of weeks gestation
should equal the fundal height in centimeters after 20 weeks.
* Ask about danger signs. Ask about vaginal fluid leakage, concerned about premature rupture of the membranes
mostly in 2nd and 3rd trimester. Women can experience urinary incontinence and feel wetness on their underwear
and perineum. Ask about vaginal bleeding, bleeding is never normal. In first trimester, bleeding may imply
spontaneous abortion (SAB). In second and third trimester, bleeding may imply abruptio placenta or placenta previa.
* You have to ask these questions specifically. Do not say “is everything going okay?”
* Ask about nausea and vomiting. In the first trimester, hyperemesis is common. In the later part of the pregnancy,
one of the serious complications is pyelonephritis, which can comes with fever, nausea, and vomiting.
* Ask about pain with urination. This implies acute cystitis or pyelonephritis.
* If the fetus is not moving, it could be hypoxia. If not hypoxia, it could be sedation such as from street drugs.
* Ask about cramping, could be preterm contractions or preterm labor. Important difference is dilation of the cervix.
With preterm contractions there is no dilation of the cervix. With preterm labor there is dilation and effacement.
* Ask about facial and hand edema. Lower extremity edema is common in pregnancy because of decreased femoral
venous pressure in the lower body, decreased albumin with decreased oncotic pressure. Edema of the face and hands
should make you think about pre-eclampsia.
* Ask about epigastric pain. Most common cause is reflux esophagitis. But, it could be pre-eclampsia. Protein in
urine and hypertension are seen with pre-eclampsia, so epigastric pain then would be likely reflux.
* Most common cause of headache in non-pregnant women is muscle contraction headaches. Most common cause
of headaches in pregnancy is muscle contraction also. A new onset of headaches or headaches that do not go away,
think about pre-eclampsia. Rule out pre-eclampsia with blood pressure and urine protein.
* Visual changes, specifically scotoma (light flashes) may imply pre-eclampsia. Lens changes do occur normally.
* At 15-20 weeks, offer patient the triple (or quad) marker screen of estriol, aFP, and beta hCG. Tell them it could
show defects such as Down and spinal cord problems, but would need confirmation with amniocentesis.
* At 28 weeks, get H&H for anemia, 1-hour glucose tolerance test with 50g glucose load, atypical antibody test if
she is RH negative to determine if she is isoimmunized and needs RhoGAM.
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Antenatal Care: Normal Pregnancy Events
* First trimester is up to 13 weeks. Most common normal symptoms are nausea, vomiting, fatigue, breast tenderness,
and polyuria.
* If she has bleeding in first trimester, most common outcome is successful pregnancy.
* How much weight gain is ideal during first trimester? Answer is 5-8 pounds.
* Most common pregnancy complication in first trimester is spontaneously abortion. About 15% of known
pregnancies abort, 25% or so will have bleeding with half aborting and half continuing.
* Second trimester 13-25 weeks is often when patient feels the best. Normal symptoms are feelings of well-being,
round ligament pain. Diagnose round ligament pain with normal peritoneal signs, normal bowel sounds, but pain
contralateral to uterus movement (stretching of the round ligament possibly), this is benign.
* Braxton-Hicks contractions are long-duration, low-intensity lasting sometimes from 4-6 minutes. May start as
early as 14-15 weeks. They are not effective in changing cervical dilation, painless.
* Most common gestational age of quickening with primigravidas? Answer is 18-20 weeks.
* Most common gestational age of quickening with multigravidas? Answer is 16-18 weeks.
* Rate of maternal weight gain in second trimester is about a pound per week.
* Most common pregnancy complications in the second trimester are incompetent cervix, premature rupture of the
membranes (PROM), and preterm labor (PTL). Alveoli develop in the lung at about 24 weeks, so prior to 24 weeks
respiratory exchange occurs in the terminal bronchioles, so survival cannot really occur earlier than that.
* Third trimester (26-40 weeks), most common symptoms are decreased libido, lower back pain, leg pain, polyuria,
Braxton-Hicks contractions.
* Lightening is engagement, fetus descends down into pelvis, “baby drops”, pressure is taken off the diaphragm,
easier for patient to breath, more pelvic pressure.
* Bloody show is vaginal bloody endocervical mucus from pre-labor cervical dilation. The mucus plug from the
cervix is released as the cervix dilates and sometimes there is capillary bleeding from the columnar epithelium.
* Rate of maternal weight gain in the third trimester is about one pound per week.
* Most common third trimester pregnancy complications are PROM, PTL, PIH (pregnancy induced hypertension),
UTI, anemia, GDM (gestational diabetes mellitus, hPL is at a higher level).
* Ideal body weight is 100lbs for first 5ft of mother, then add or subtract 5lbs for each inch taller or shorter.
* Ideal weight gain is a function of pre-pregnancy weight. The larger the woman, the less the weight gain allowed.
Women who are underweight need to gain more, over 30lbs. Overweight women need to gain less, maybe 10lbs.
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Antenatal Care: Initial Prenatal Laboratory Tests
* 21yo G1 P0 presents for her 1st prenatal visit at 11 weeks, which is confirmed by sonogram. She has no risk
factors. What laboratory tests should be ordered?
* Lower limits of hemoglobin in pregnancy is 10g/dL.
* Lower limits of mean corpuscle volume (MCV) in pregnancy is 80mcg/m^3.
* The lab will likely give you non-pregnant ranges for these labs. So, you have to know the pregnancy values.
* Lower limits of platelet count in pregnancy? 100,000/mm^3.
* Upper limits of WBC in pregnancy? 16,000/mm^3.
* Prenatal screening test for rubella susceptibility is IgG antibody titer. 85% are positive, mostly because of MMR
immunizations. If rubella susceptible, she is at risk for developing rubella during pregnancy and this is only harmful
if it is a primary infection. Avoid people with known rubella and give inactivated virus vaccine after delivery.
* Most common prenatal screening test for HepB is the hepatitis B surface antigen.
* Initial prenatal labs include type, Rh, and antibody screen. The prenatal screening test for isoimmunization is an
indirect Coombs test, also called atypical antibody test (AAT).
* Direct Coombs test is used for identifying the blood type. Want AAT (indirect Coombs) to be negative.
* STD screening includes cervical cultures for chlamydia and GC, syphilis test via VDRL or RPR, diagnose syphilis
after positive VDRL/RPR with MHA-TP or FTA-ABS (FTA absorbed).
* 8% of pregnant women will have asymptomatic bacteriuria. 30% will develop pyelonephritis if not treated.
* Most common screening test for renal disease is urinalysis.
* Most common definitive test for asymptomatic bacteriuria is urine culture. A urine dipstick showing nitrite and
leukocyte esterase is not helpful in screening renal disease because it does not show casts or crystals.
* Screening for tuberculosis is skin Mantoux test, possibly QuantiFERON gold assay if available. If positive TB
skin test, next step is CXR. If QuantiFERON positive, diagnosis is determined. Only screen TB if risk factors.
* If positive skin test and negative CXR, management is INH & B6 for 6 months, not harmful in pregnancy.
* If positive skin test and positive CXR, sputum cultures then triple treatment.
* HIV screening (with consent) is ELISA antibody test. If positive, definitive test is Western Blot test. False positive
Western Blot test is 1 in 10,000. If patient asks you “do you think the HIV test could be an error?” Most likely no.
* Primary prevention is immunization and modification of risk factors.
* Major benefit of CBC is for mother. Anemic mother has no effect on the fetus due to active transport of iron
across the placenta.
* Rubella IgG antibody is for immunization. If patient is susceptible, immunize them post-partum.
* Hepatitis B surface antigen carrier, there is no risk to her, but there is risk to the fetus. We know to immunize the
baby post-partum with hepatitis B immunoglobulin and hepatitis vaccine.
* Hepatitis B and HPV are currently the only STDs that can be prevented by immunization.
* Blood type and Rh are to identify if the mother is a candidate for RhoGAM. If she is Rh negative, give RhoGAM.
* Atypical antibody test is an assessment of the risk of hemolytic disease to the newborn. There is no effect to the
mother, she is antigen negative. If fetus is antigen positive they could cross over.
* Cervical cultures benefit the mother and the fetus. Most common infection of the newborn with chlamydia or
gonorrhea is in the eyes or ears.
* When syphilis is diagnosed in pregnancy, it is usually latent. No hazards from latent syphilis. Risk to fetus exists
because spirochetes can cross the placenta and infect the fetus. Must treat mother and use an antibiotic that crosses
placenta to treat the fetus. Treatment is penicillin.
* Urine screening is to treat the mother to prevent pyelonephritis, patient could end up in ICU on vent with sepsis.
* TB skin test is primarily for the mother’s benefit.
* HIV primarily benefits the fetus. If mother has high CD4 and low viral titer, do you treat? No. Fetus is at 30% risk
of vertical transmission. So if mom is HIV positive, put her on AZT.
* Diabetic screening is to benefit the fetus. Gestational diabetes is not hazardous to the mother. Fetus may get
macrosomia, hypoglycemia, hypercalcemia, polycythemia.
* Sickle cell screen is to treat the mother. Many times if the mother has sickle cell disease, the baby doesn’t, has just
sickle cell trait.
* Triple marker screen is optional anomaly screening. Ultrasound is also anomaly screening.
* HepB transmission risk to fetus if surface antigen positive is 10%. If HepB e-antigen positive, risk is 80%.
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Antenatal Care: Mid-Trimester Laboratory Tests
* 23yo G2 P1 Ab1 is seen at 16 weeks gestation. Her previous pregnancy resulted in an anencephalic fetus that did
not survive. She took 4mg of folate preconception prior to this pregnancy but wants to know if this fetus is affected.
* All patients are offered a triple marker screen. If it is positive, they can undergo genetic counseling with a
professional that carries at least a master’s degree. They go through the risks of the therapy options.
* Many of the tests are gestational age specific, so we do an ultrasound to determine gestational age.
* Next test to be offered after a triple marker positive is amniocentesis. Under specific conditions, she may undergo
chorionic villus sampling (CVS).
* Criteria for prenatal diagnosis of abnormality include AMA, previous pregnancy complications, mental retardation
in family, genetic disorders in family.
* aFP high, estriol normal, hCG normal: neural tube defect.
* Estriol low, aFP low, hCG high: Down syndrome.
* aFP low, estriol low, hCG low: trisomy 18.
* Triple marker screen is not definitive. A negative triple marker screen does not exclude, but risk is low.
* If aFP is high, estriol and hCG is normal, what is the most likely explanation? Answer is dating error. Percentage
of newborns with birth defects is 1%. Percent of women with dating errors may be 10-20%. High aFP could be due
to multiple gestations. What we care about though is neural tube defects (spina bifida and anencephaly) and gastric
wall defects (gastroschisis and omphalocele). Placental bleeding can cause elevated aFP also.
* How do you know a high aFP is dating error? Answer for next step in management is ultrasound. This will
identify dates, twins, and anomalies.
* Next step in management now is amniocentesis, looking for amniotic fluid aFP, which is much more specific.
Acetylcholine esterase in amniocentesis is only elevated if neural tube defects. Since we are already doing
amniocentesis, do a karyotype with the fluid. A closed neural tube defect would not have elevated acetylcholine
esterase.
* If low estriol and aFP, high hCG, what is the most likely explanation? Answer is dating error. Concern is for
Down syndrome. Next step in management is ultrasound looking for dates. If no dates error, then amniocentesis
looking for mainly karyotype.
* If low estriol, aFP, and hCG, what is the concern? Trisomy 18. Dating error most common. So, next step in
management is genetic counseling and ultrasound looking for dates. After that, amniocentesis.
* CVS is done if there is a high aneuploidy risk. CVS done at 9-10 weeks up until 12 weeks.
* What is the major serum glycoprotein of the embryo? Answer is alpha-feto protein.
* Normal aFP changes in the fetus, amniotic fluid, and maternal serum are fetus and amniotic fluid rises and falls,
maternal serum rises until 30 weeks. Gestational dating is thus important for aFP analysis.
* True causes of abnormally high maternal serum aFP are neural tube defect, ventral wall defect, twins, placental
bleeding, and fetal renal disease (can give very high levels).
* Alpha-feto protein units are multiple of the means (MOMs).
* Maternal screening test for neural tube defects is aFP.
* Gestational ages for maternal serum aFP is 15-20 weeks.
* Most common cause of an abnormally high aFP is dating error.
* Next step in management with a high aFP is obstetrical ultrasound.
* What is the next step in management of a high aFP that corrects with sonogram dating? If 15-20 weeks, repeat the
test. What if aFP is persistently elevated even with dating? Answer is amniocentesis.
* What pregnancy complications are associated with unexplained increased maternal serum aFP with normal
amniotic fluid aFP? Answer is IUGR, stillbirth, pregnancy-induced hypertension.
* What is the next step in management of a low aFP that corrects with sonogram dating? If 15-20 weeks, repeat the
test. What if aFP is persistently low even with dating? Answer is amniocentesis.
* With only aFP, you pick up about 20% of Downs cases. With triple marker, you pick up about 60% of Downs.
* Triple marker screen for trisomy 18 has all three values low. If dates do not correct, do amniocentesis.
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Antenatal Care: Third-Trimester Laboratory Tests
* 33yo G4 P3 is at 25 weeks. Height is 63” and weight is 250lbs. She has gained 30lbs thus far in pregnancy. With
her last pregnancy, she gained 50lbs, was diagnosed with gestational diabetes (GDM), and delivered a 4300g female
neonate by cesarean section. She wants to know if she has GDM this pregnancy. Patient’s ideal body weight is
115lbs, ideal weight gain is less than 20 lbs.
* Mid-trimester labs are diabetes screen, CBC, and atypical antibody.
* Criteria for screening for GDM are all gravidas 24-28 weeks, universal screening.
* Higher risk in AMA, overweight, previous macrosomic baby, Hispanic women.
* Most common screening test for GDM is 1-hr 50g oral glucose tolerance test (OGTT).
* Criteria for a positive screening test for GDM is ≥ 140mg/dL on OGTT. 15% will have a positive screen.
* What is the follow up for a positive GDM test is 3-hr 100g OGTT in fasting state (8-12h of fasting), blood drawn
at 1h, 2h, and 3h after she drinks the glucose beverage.
* Diagnosis if fasting glucose >125mg/dL is overt diabetes. If patient shows up for the 3hr OGTT and has a blood
sugar > 125, she should not get anything to drink because you already have the diagnosis.
* What is criteria for 3hr 100g OGTT? Two abnormal values, FBS ≥ 95, 1hr ≥ 180, 2hr ≥ 155, 3hr ≥ 140.
* Maternal CBC should be drawn 24-28 weeks because maternal hemoglobin is lowest then.
* Iron deficiency is 8x more common in women than men due to menstrual periods and pregnancy. Men store about
1.5g of iron in their marrow, average woman has 500mg stored.
* With iron deficiency, there will be absent iron stores in the marrow. First thing to do is get peripheral hemoglobin
back up. Iron stores do not replace until hemoglobin goes up. So give iron for 3-6 months after peripheral
hemoglobin is replaced.
* AAT in Rh negative moms is repeated at 24-28 weeks because she could get isoimmunized before 28 weeks, then
we would not need to give RhoGAM.
* Rh negative mother who delivers Rh positive baby without getting RhoGAM has a 15% chance of
isoimmunizatation. If we give her Rh immune globulin before 28 weeks, risk of getting isoimmunized is 0.2%,
where it would be 2% without RhoGAM. Risk still is not zero, even with Rh immune globulin. If she has atypical
antibodies, there is no point in giving Rh immune globulin because she is already creating them.
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Antenatal Care: Antenatal Fetal Testing
* 37yo multipara with systemic lupus erythematosus is at 31 weeks. She has chronic HTN being controlled with
methyl-Dopa. She comes to the office stating her fetus is not moving as much as it used to.
* What are the main indications for antenatal fetal testing? #1 indication is decreased fetal movement. Also diabetes,
post-dates (more than 2 weeks past), chronic hypertension, IUGR.
* Most common test is non-stress test (NST). Think of accelerations. NST looks at contractions and fetal heart rate.
An acceleration is an elevation of fetal heart rate by 15bpm for 15 seconds. An NST with accelerations is called a
reactive NST (2 or more accelerations in 20 minutes). Interpretation is very good, baby is doing well, repeat weekly.
* Say NST is non-reactive, meaning less than 2 accelerations in 20 minutes. 80% of the time, this is false non-
reactive meaning baby is doing fine. Common false negative is sleeping baby.
* Next step in management with non-reactive NST? Wake up baby, vibroacoustic stimulation. The device sound is
80dB and it shakes. Place device on uterus near the head, buzz for 2 seconds. Look for accelerations. If reactive after
vibroacoustic stimulation, this is good. Management is repeat weekly.
* Say NST is non-reactive even with vibroacoustic stimulation. Next step in management is biophysical profile
(BPP). There are 5 components to the BPP, similar to APGAR score.
* BPP 5 components: non-stress test reactive is 2pts, amniotic fluid on ultrasound, fetal breathing movements
(abdomen and chest move paradoxically), gross body movements (turning and flexing of spine), and tone (extremity
extension and flexion, even just a finger movement).
* APGAR score is color, heart rate, respirations, grimace, and tone. Most important component is tone, implies
motor strip of brain is perfused. What is the likelihood of a pink baby with HR < 50? Not likely, they are not
independent factors.
* NST + amniotic fluid index (AFI) sometimes called modified biophysical profile. The NST and AFI are as good a
predictor as all of the BPP components put together. Reactive NST implies movement, not independent factors.
* Complete BPP maximal score is 10. Score of 8+ is reassuring. Score of 0 or 2 is ominous; perinatal mortality is
about 70% in this case. Get the kid out regardless of gestational age. Score of 4 or 6 is worrisome; if ≥ 36 weeks,
deliver the baby. The last organ system to mature is the lungs, developed at 34-36 weeks. If < 36 weeks (premature),
we do a CST (Contraction Stress Test).
* CST: think absence of late decelerations. Want to see ≥ 3 uterine contractions within 10 minutes. Start oxytocin
infusion with a nurse present to get contractions going (time intensive, cost intensive).
* Negative CST is no late decelerations with contractions ≥ 3x in 10 minutes. Interpretation is reassuring.
* What is the basis of CST? With contractions, intravillous blood flow in placenta decreases. Intrauterine pressure of
40mmHg or greater decreases intravillous blood flow. So fetus during that time is basically holding its breath. A
healthy fetus can handle that 40-45 interval just fine. A stressed fetus will have a decreased heart rate.
* A positive CST is troublesome and management is prompt delivery. So positive CST would be a contraction with
a fetal HR deceleration immediately following. Other worrisome signs on fetal heart rate tracing are flat heart rate
(non-variable), tachycardia, and non-reactive (no accelerations).
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Antenatal Care: Perinatal Infections
* Perinatal infections seropositive percentage in pregnant women: varicella 90%, rubella 85%, herpes simplex 50%,
cytomegalovirus 50%, toxoplasmosis 40%. Just because you have positive IgG titers doesn’t mean you have a recent
infection, you need IgM titers for that.
* Most common ways of HIV transmission are IV drug use, sexual, perinatal.
* Residual effect of HIV primary infection is lifelong latency.
* Most common cause of death with HIV/AIDS infection is opportunistic disease: TB, PCP, toxo, CMV,
coccidioides mycosis.
* Most common rout of HIV vertical transmission is during vaginal deliver. Can be transplacental and via breast
feeding, but mostly vertical transmission. Rate without AZT is 30%, with AZT is 10%, cesarean decreases more.
* AZT is zidovudine. Transmission rate of HIV is 95% for blood transfusion, 30% for delivery, 1% for needle
sharing, 0.5% for accidental needle stick.
* Most common result of neonatal HIV test when mom is HIV positive: baby is HIV positive, could be active
infection or passive antibodies across placenta so put baby on zidovudine.
* Start HIV positive mother on zidovudine at 14 weeks. Offer a C-section for delivery.
* Criteria for multidrug treatment with HIV positive mother is low CD4 count or high RNA viral load.
* 34yo multigravida presents for prenatal care in the 2nd trimester. She admits to past substance abuse but states she
has been clean for 6 months. With her 2nd pregnancy she delivered a 34week male neonate who died on DOL (day
of life) #1. At delivery, the baby was swollen with skin lesions. The placenta was large. She was treated but does not
remember details. Prenatal panel now shows positive VDRL.
* Route of syphilis vertical transmission is primarily transplacental, where STD transmission is mucocutaneous.
* Vertical transmission rate with primary and secondary syphilis is 60%. Tertiary rate is unknown.
* What are the early clinical findings with congenital syphilis? Non-immune hydrops, anemia, macerated skin, low
platelets. Normal ratio of fetus to placenta is 5:1. Syphilis ratio is maybe 2:1, so big placenta.
* A live macerated hydroptic fetus, think congenital syphilis. Thrombocytopenia also.
* Late congenital syphilis signs include Hutchinson (notched) teeth, mulberry molars (cusp dwarfing), saber shins,
saddle nose, 8th nerve deafness. Seen early in child’s life.
* Classic lesion of primary syphilis is the chancre. These have a rolled edge. Painless rolled-edge genital ulcer.
* Common false positive cause of VDRL/RPR is lupus, autoimmune diseases, parasitic diseases, viral diseases.
* Lab findings with primary syphilis are negative serology with positive darkfield microscopy. Not enough time for
the antibodies to develop, thus negative serology. Darkfield microscopy needed because they are so thin.
* What is the classic lesion of secondary syphilis (treponema pallidum)? Condylomata lata.
* Lab findings with secondary syphilis are positive serology and darkfield microscopy.
* Follow-up test with positive serology are FTA-ABS or MHA-TP, treponema specific tests.
* Most definitive diagnosis in syphilis is positive FTA-ABS or positive MHA-TP.
* Unique skin lesion of secondary syphilis is macrolupapular skin rash, “money spots.”
* Classic lesion of tertiary syphilis is gumma, cold abscess anywhere in the body.
* Mode of delivery with maternal syphilis is vaginal delivery. Treatment is benzathine penicillin because it crosses
the placenta. If penicillin allergy, still benzathine penicillin and give oral desensitization. Serology titers should
decreases in 4-6 months. Erythromycin can treat the mother but will not treat the fetus.
* Desensitization starts with small dose then doubles, increasing concentration to useful level at 14 doses.
* 29yo multigravida is found on routine prenatal lab testing to be positive for HBsAg. She is an ICU nurse. She
received 2 units of PRBCs two years ago after experiencing postpartum hemorrhage with her last pregnancy. Rates
of hepatitis B are very high in Southeast Asia.
* What is the most common mode of hepatitis B transmission? Body fluids. Most common ways of HepB
transmission are sexual, IV drug use, perinatal.
* Symptoms of HBV infection are usually none. Risk of transplacental HBV infection is low, mostly during third
trimester. Greatest risk is during vaginal delivery, vertical transmission.
* Likelihood of vertical transmission is 10% with surface antigen positive, 80% with e-antigen positive.
* What is the comparative likelihood of chronic hepatitis with HBV infection? Answer is 10% with adults (90%
carriers), 80% with neonates. 40% of hepatitis B is from perinatal transmission.
* Follow-up testing for mother with positive hepatitis B surface antigen? Complete hepatitis panel, liver enzymes,
and bilirubin. Normally liver enzymes are unchanged in pregnancy.
* Preferred route of baby delivery when mom is HBsAg positive? Vaginal delivery. Avoid scalp electrodes/needles.
Passive immunization can be given to the baby with immune globulin, then give active immunization.
* Lamivudine for HepB, Ribavirin/interferon for HepC.
* Term SGA neonate has hydrocephalus, intracranial calcifications, and chorioretinitis. Congenital toxoplasmosis.
* Term SGA neonate with deftness, aortic coarctation, and cataracts. Congenital rubella.
* Woman is seen at 17 weeks gestation. Her rubella status is non-immune. Antepartum management is education.
Intrapartum management is vaginal delivery. Postpartum management is maternal vaccine.
* A woman received a rubella immunization 6 weeks ago but now has a positive pregnancy test, what is the
management? Conservative, no abortion indicated. No syndrome within 3 months.
* 18yo G1 P0 with past history of recurrent herpes presents at 39 weeks with SROM (spontaneous rupture of the
membrane) for 20 hours. She has regular contraction but no genital lesions. Management? Vaginal delivery.
* 21yo G2 P1 presents at 18 weeks with fever, diffuse genital vesicular lesions and inguinal nodes. Management?
Acyclovir for primary herpes. Lesions should be painful.
* 21yo G2 P1 presents at 18 weeks, afebrile, painless vulvar ulcerative lesion, painless inguinal nodes. Best
diagnosis? Answer is primary syphilis.
* 32yo G5 P4 has positive VDRL on her first trimester prenatal laboratory screen. Management? FTA-ABS.
* 22yo G3 P0 presents in active labor with ruptured membranes, positive VDRL that was not followed or treated, is
now afebrile with no genital lesions. Management? Give penicillin presumptively, vaginal delivery.
* 20yo G2 P1 at 17 weeks is HBsAg positive, liver enzymes normal. Management? Antepartum management is
conservative, intrapartum management is vaginal delivery, postpartum is HepB Ig and hepatitis vaccine.
* 20yo G2 P1 at 17 weeks is HIV positive. Antepartum AZT, intrapartum AZT with offer cesarean section,
postpartum AZT for neonate.
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Antenatal Care: Pregnancy Bleeding
* Mother comes in with third trimester bleeding. What is the first question? Answer is what are the vital signs.
* Say BP is 50 over nothing, tachycardia (unstable). Management? Stabilize mother, large bore IV with NS or LR,
type and cross, Foley placement to monitor urine output, and deliver the baby.
* If mother is unstable, management is stabilize mother and deliver the baby.
* Causes of destabilization include abruptio placenta, placenta previa, rupture of the uterus.
* Evidence of unstable baby are bradycardia (< 110), tachycardia (> 160), severe variable decelerations, any late
decelerations. Next step in management is deliver regardless of gestational age.
* Unstable baby with stable mother: abruptio placenta, placenta previa, vasa previa.
* Where is the placenta implanted? Assess by ultrasound. Normal implantation is lateral, fundal, but not in lower
segment. Mom is stable, baby is stable, next step in management is placental location via ultrasound.
* Do not perform a digital cervical exam until you know where the placenta is (e.g. risk is placenta previa).
* Most common cause of third trimester bleeding is abruptio placenta, typically painful bleeding (mom’s blood).
* A concealed abruptio is bleeding between placental and uterine wall, harder to diagnose, rarer than overt.
* Abruptio placenta management varies by gestational age, contractions, and cervical dilation.
* Pre-term patient with no labor and abruptio placenta (bleeding and pain). Mother and baby are stable. Ultrasound
shows placenta is not low, patient now stops bleeding. Management is observation.
* Multigravida, mother stable, baby stable, bleeding, 9cm dilated. Management is deliver.
* Next most common cause of third trimester bleeding is placenta previa, painless bleeding, low segment
implantation that occurs at term 0.5% of the time.
* Marginal and partial placenta previa is maternal bleeding. If early in pregnancy, lower part may atrophy and upper
part may hypertrophy, making it seem like the placenta is moving away and patient could deliver vaginally.
* Central placenta previa should be managed by C-section.
* Vasa previa is painless bleeding, diagnosed when fetal vessels cross the cervix. Example is a main placenta and an
accessory lobe with a vessel connecting the two across the cervix. If the membranes rupture and the vessel tears, this
will be a loss of fetal blood (versus maternal blood). Say mother bleeds 300mL, no problem. Fetus blood volume is
about 100mL per kg. Say we have a 3kg fetus, blood volume is 300mL total.
* Triad for vasa previa is amniotomy (ruptured membranes), vaginal bleeding, fetal bradycardia. Management is
crash cesarean delivery, do not wait around.
* Management of uterine rupture is immediate cesarean delivery.
* Most common cervical causes of late trimester bleeding are erosion, polyps, carcinoma.
* Most common vaginal causes of late trimester bleeding are varicosities, lacerations.
* Most common placental causes of late trimester bleeding are abruptio (1%), placenta previa (0.5%), vasa previa.
* Initial assessment of late trimester bleeding are mom’s vital signs, fetal heart rate, and uterine contractions.
* Initial investigation for later trimester bleeding are CBC, DIC labs (platelet, PT, PTT, d-dimer, fibrinogen,
peripheral smear), type and cross, sonogram.
* Initial management of late trimester bleeding is LR with large bore IV, Foley catheter, type and cross.
* 32yo multigravida at 31weeks gestation is admitted to labor and delivery after a MVA. She complains of sudden
onset of moderate vaginal bleeding for the past hour. She has intense, constant, uterine pain and frequent
contractions. Fetal heart rate is 145/min and regular. On inspection, the perineum is grossly bloody.
* Painful late trimester bleeding, think abruptio placenta. Placental location is usually normal.
* Most common obstetrical cause of DIC is abruptio placenta.
* Risk factors for abruption are previous abruption, hypertension, maternal trauma, cocaine, PROM.
* Most common complications of abruptio placenta are shock, ATN (acute tubular necrosis), and DIC.
* Couvelaire (bruised) uterus. This is a severe abruption where blood has dissected between the myometrial fibers, it
will have bruises all over. This could be seen on exploratory laparoscopy.
* 34yo multigravida at 31weeks comes to birthing unit stating she woke up in the middle of the night in a pool of
blood. No pain or contractions occurred. Inspection of the uterus shows the fetus appears transverse lie. Fetal heart
tones are regularly at 145/min. On inspection, her perineum is grossly bloody.
* Fetus in transverse lie, think placenta previa.
* Placental villi can go through myometrial wall into the bladder, placenta percreta.
* Placenta previa: painless late trimester bleeding.
* At 16 weeks, 20% have placenta previa. At 40 weeks, 0.5% are placenta previa.
* Mechanism of placental migration with placenta previa is differential atrophy (LUS) and hypertrophy (upper).
* Pathophysiology of bleeding with placenta previa is avulsion of villi with LUS (lower uterine segment) stretching.
* Risk factors for abruptio placenta are previous abruptio placenta, multiple pregnancy, multiparity, AMA.
* Management of placenta previa: if maternal jeopardy, emergency section. If preterm and stable mom/fetus,
conservative in the hospital (observation). If margin of placenta is 2cm or more from os, vaginal delivery possible. If
over os, section at term.
* Complication of placenta previa is placenta accreta hemorrhage. Placenta usually invades through the site of a
previous uterine incision, most incisions made in the lower segment. If previous cesarean section and placenta
previa, 15% chance of placenta accreta. With two previous C-sections, risk is 30%.
* 21yo G1 at 38weeks is admitted to L&D at 6cm dilation with contractions every 3 minutes. AROM performed
resulting in sudden onset of bright red vaginal bleeding. The EFM tracing which has showed FHR of 135/min with
accels now shows bradycardia at 70/min. Mom’s vital signs are stable.
* Characteristic of bleeding with vasa previa is painless bleeding. Placental location is usually normal.
Pathophysiology is bleeding from fetal vessels that transverse the membranes.
* Cause of vasa previa is velamentous cord insertion or accessory placental lobe.
* Triad of vasa previa: ROM, painless vaginal bleeding, fetal bradycardia.
* Risk factors for vasa previa are velamentous cord insertion, accessory placental lobe, multiple gestation.
* Management of vasa previa is immediate C-section. Complication is fetal death from hypovolemia.
* 27yo G2 P1 on L&D for eval of UCs (uterine contractions) at 34weeks. Previous delivery was emergency CS at
32weeks due to hemorrhage from placenta previa. A classical uterine incision was used due to LUS varicosities.
Suddenly, patient has abdominal pain, profuse vaginal bleeding, fetal bradycardia, inability to pickup UCs.
* Characteristic of bleeding with uterine rupture is painful. Placental location is normal. Pathophysiology is
complete laceration of uterine wall. Types of rupture are complete (peritoneum open, fetus in abdomen), incomplete
(peritoneum intact). Key is loss of uterine contractions.
* Triad for uterine rupture: late trimester painful bleeding, loss of fetal heart tracing, inability to identify UCs.
* Risk factors for uterine rupture are classical uterine incision, myomectomy scar, excessive oxytocin (particularly
on a multigravida), grand multiparity, and marked uterine distension.
* Management of uterine rupture is emergency C-section with uterine repair or hysterectomy.
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Obstetrical Complications: First Trimester Bleeding
* 40yo woman G3 P1 Ab1 at 9 weeks comes to the office complaining of vag bleeding. A urine pregnancy test was
positive 3 weeks ago. She initially experienced breast tenderness, however it has now resolved. She denies passage
of any tissue vaginally.
* Next step is look at cervix to make sure there is not a polyp or similar cause.
* First step is look at obstetrical sonogram, is it normal? Abdominal ultrasound is dependent on size of patient,
vaginal ultrasound has a shorter focal length, doesn’t matter if patient weights 100lbs or 400lbs.
* An intrauterine gestational sac is the first thing you will see. Within the sac you will see a fetal pole. There should
be a yolk sac (4-5mm), normal up until 8-9 weeks gestation, and there should be cardiac motion.
* Gestational sac will appear round and smooth with a nearly empty inside. On one edge you may see the yolk sac.
* First trimester bleeding with normal ultrasound, internal cervical os is closed? Answer is threatened abortion.
Management is observation. There is no evidence that any medication changes outcome.
* First trimester bleeding with abnormal ultrasound, internal cervical os is closed (ring forceps meet resistance)?
Answer is missed abortion. This is an empty sac or dead fetus. Management is a scheduled D&C, or observation.
Best option is D&C, else bleeding/cramping over time and possible hemorrhage outside of the hospital setting.
* First trimester bleeding, ultrasound abnormal, internal os is open (ring forceps enter canal without resistance)?
Answer is inevitable abortion. Management is an emergency D&C.
* First trimester bleeding with abnormal ultrasound, internal os open, products of conception in uterus? Answer is
incomplete abortion. Management is an emergency D&C.
* First trimester bleeding, ultrasound abnormal, internal os is open, uterus is empty by ultrasound? Answer is a
completed abortion. Management is observation, serial beta hCGs if you think there could be an ectopic.
* First trimester bleeding, severe nausea/vomiting, hypertension, proteinuria? Answer is molar pregnancy.
Ultrasound would show a snowstorm pattern. Management is D&C with serial beta hCG tests weekly.
* Anytime with first trimester bleeding, also consider tubal pregnancy.
* Most common cause of early pregnancy wasting? Answer is aneuploidy.
* Most common fetal aneuploidy in first trimester losses? Answer is Turner syndrome (45X).
* An uncommon maternal cause of recurrent first trimester losses? Anticardiolipin antibody syndrome.
* Diagnostic modalities in assessing first trimester bleeding are speculum exam and obstetrical sonogram.
* First trimester bleeding, normal pregnancy on ultrasound, internal os closed: threatened abortion.
* First trimester bleeding, nonviable pregnancy on ultrasound, internal os closed: missed abortion.
* First trimester bleeding, no products of conception passed vaginally, internal os dilated: inevitable abortion.
* First trimester bleeding, retained products of conception, internal os dilated: incomplete abortion.
* First trimester bleeding slowed, no products of conception on ultrasound, internal os dilated: completed abortion.
* Important lab test to perform after first trimester D&C? Answer is blood Rh status, possible RhoGAM.
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Obstetrical Complications: Fetal Demise
* 28yo multigravida at 33 weeks comes to the office stating she has not felt her baby move for 24 hours. A previous
18 week sonogram showed a single fetus with grossly normal anatomy. You are unable to find FHT with a Doppler
stethoscope.
* Signs of fetal demise include absence of uterine growth, uterus small for dates (less than 20 weeks). After 20
weeks, absent fetal movement is the clinical finding.
* Diagnosis of fetal demise is made by ultrasound, not fetal Doppler stethoscope. The sonogram must show no
cardiac motion for the definitive diagnosis.
* Demise diagnosed, what is the next step? Determine if DIC is present. Do PT, PTT, fibrinogen, d-dimer, platelets.
* DIC is release of tissue thromboplastin from the deteriorating fetal tissue, which gets into the maternal circulation
and sets off the coagulation cascade. This is rare until 2-3 weeks after fetal demise. If it is present, this is a fetal
emergency so delivery the fetus. If vaginal delivery, give prostaglandin E2 to induce labor. If less than 20 weeks and
no autopsy needed, do a D&E. Do not do a C-section for a dead fetus.
* Fetal demise, DIC no present, what is the next step? Is the mother psychologically ready for delivery?
* So you’re doing the fetal ultrasound, scanning and describing what you see. There is the head, here are the feet,
there is the spinal cord. When you get to the heart and see no movement, you’ll probably stop talking. The mother
will be watching you and likely say, “Is everything okay?” Do not lie but do not break the news immediately. Say,
“No, I don’t like what I’m seeing.” Don’t say the baby is dead. You are trying to determine if the mother is
psychologically ready for this news. Let the mother talk. If they say they haven’t felt movement then maybe you can
approach the subject. If they say, “Oh I’m sure everything is okay” then you say “I should see heart movement” and
mother comes back with “Well I’m sure everything is okay,” then you know she is not ready to hear the news. If she
does not seem ready, next step could be to ask her to come back tomorrow for another look. She will either do this
and take the time to think about the baby, or she may say “The baby is dead isn’t it?” then you have to say “Yes.”
* If patient request observation and is not psychologically ready, then do weekly DIC panels.
* Fetal demise confirmed, no DIC present, mother psychologically ready. Next step is determine if an autopsy is
needed. Autopsy is to look for a syndrome that could predict if it will recur again in future pregnancies. If autopsy is
needed (fetal anomalies seen), do an induction of labor with PGE2. If less than 20 weeks, D&E is an option.
* D&C involves minor dilation and curettage early in pregnancy. Now the fetus is too large so we have to do a
D&E, where the cervix is dilated more, you reach in and pull a leg off, pull an arm off, make sure to get the head,
don’t forget the pelvis, you don’t want to leave anything in. You don’t want the patient to see a head after straining
on the toilet the next day, it could be psychologically destructive to the mother.
* Most common cause of early fetal demise? Idiopathic (>50%). Do work-up: autopsy, x-ray, karyotype.
* Others: lupus anticoagulant (LA), anticardiolipin antibody (ACA), antiphospholipid antibody (APLA).
* Kleihauer-Betke test looks to see if the fetus bled into the mother to become hypovolemia and died. So you look at
a peripheral smear of the mother for fetal cells. The dark staining larger cells are fetal cells.
* Definition of fetal demise is pregnancy that went to ≥ 20 weeks up to birth. Prior to 20 weeks it is called a
spontaneous abortion.
* Complications of fetal death are DIC and grief resolution.
* You may ask mother after fetal demise if she wants an autopsy. Mother may say “Oh the baby has suffered
enough, leave it alone.” Then she comes back 6 months later asking if we know why the baby died. So the optimal
time to know this is when an autopsy is needed. Explain why the autopsy is needed and it could help her with future
pregnancies.
* A prolonged retention early in pregnancy can lead to fetus papyraceous, where the mother or a twin absorbs the
fetal material.
* Even more rare is lithopedion, where fetal remains become calcified like a stone, “stone baby”. This most often
occurs with an abdominal pregnancy and when the fetus is too large to be reabsorbed.
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Obstetrical Complications: Multiple Gestation

* 21yo primigravida at 15 weeks gestation is seen for a routine visit. Four week sago, her uterus was appropriate for
size and dates. Today, her uterine fundus is palpable at the umbilicus. So this is large for dates.
* If you see two heads on ultrasound, it should be clear this is twins.
* Multiple gestation complications: cerebral palsy, spastic quadriplegia, blindness, deftness, even death.
* Each additional fetus, you subtract 4 weeks. One fetus, 40 weeks. Twins, 36 weeks mean gestational age. Triplets,
32 weeks mean gestational age.
* This is a preventable cause of prematurity. We hear about the good outcomes. But so many are permanently
injured because of prematurity.
* In the U.S., we have 2.5x more twins than expected, 1.4x more triplets than expected, 125x more quadruplets than
expected, and 1500x more supra-multiples than expected. This is because of infertility with embryo transfer,
ovulation induction.
* Definitive diagnosis of multiple gestation is done by ultrasound.
* Clinical suggestions of multiple pregnancy is fundus large for dates and maternal serum aFP is abnormally high.
* All twins are at risk for: increased C-section rate (50%), increased premature labor (50%), anemia of the mother
(2-3x higher), and pregnancy induced hypertension (2-3x higher).
* If the genders are different, you know the twins are dizygotic (fraternal twins), came from two eggs. These are
always dichorionic and diamniotic. This is the lowest risk twins.
* How many placentas are there? If two, we know this is dichorionic and diamniotic. If they are monozygotic with
two placentas, cleavage occurred between 0 and 3 days (up to the stage of the morula). These are low risk.
* Say we see one placenta. How determine if there is a dividing septum between the two twins. If there is a septum,
they are monochorionic, diamniotic. These always must be monozygotic. Cleavage occurred between 4-8 days in the
blastocyst stage. This is moderate risk. If they are sharing a placenta, they are at risk for twin-twin transfusion
syndrome (TTTS). Diagnosis is by seeing differences in estimated fetal weight and amniotic fluid. The smaller twin
tends to do better when it is born. Sometimes called oligo-poly syndrome (oligohydramnios-polyhydramnios).
* To determine twin-twin transfusion, take placenta and inject milk into one of the umbilical veins. If it is a
dichorionic fused placenta, the milk will turn vessels white up until the middle. If there is TTTS, the milk will go all
the way through.
* Say one placenta and no dividing septum. This is monochorionic and monoamniotic. These have to be
monozygotic. The split here was days 9-12, after implantation occurred, bilaminar germ disc present. These are the
highest risk of twins. They are at risk for TTTS and umbilical cord entanglement. Conjoined twins can only occur in
this case, monochorionic and monoamniotic. Split for conjoined twins occurs after day 12.
* Di Di 0 to 3 days, Mono Di 4-8 days, Mono Mono 9-12, Conjoined after day 12.
* If both twins are cephalic (head down), vaginal delivery. If first is non-cephalic (either breach or transverse lie), do
C-section. If first is cephalic and second is breach, it is up to the doctor. Some will delivery and many will section.
* Most common zygosity of twin pregnancy? 2/3 are dizygous.
* Twins of different genders? Dizygotic twins.
* Twins of same gender with two placentas? Could be either dizygotic or monozygotic.
* Risk factors for twin pregnancy: race, geography, family history, ovulation induction.
* Most common risk of multiple pregnancy with ovulation induction? Clomiphene 10%, human menopausal
gonadotropin (HMG) 30%.
* Vanishing twin syndrome can occur, so if you see two sacs on the first ultrasound do not say it is twins yet. Follow
until there is development. One twin is lost early.
* Medical complications of twin pregnancy: iron deficiency anemia, folate anemia, pre-eclampsia.
* OB complications of twin pregnancy: preterm labor, malpresentation, C-section, post-partum hemorrhage.
* TTTS occurs only in monochorionic. In mono-mono, must rule out conjoined twins.
* Umbilical cord entanglement occurs, think mono-mono twins.
* Clinical findings with twin pregnancy: hyperemesis, increased beta hCG, fundus large for dates.
* Antepartum management is iron and folate to prevent anemia, monitor BP to detect pre-eclampsia, pre-term labor
education to prevent preterm delivery, serial ultrasounds to detect TTTS.
* Superfecundation is rare in humans. Example would be two children born to a mother and her husband, both
parents blood types are O, one child is O and the other is AB. So mother slept with another guy close to the date she
slept with her husband. Generally when conception occurs there is no more ovulation. There could have been dual
ovulation so sperm from one partner penetrated one egg and sperm from the other partner penetrated the other egg.
* Acardiac and acephalic twins can rarely occur.
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Obstetrical Complications: Isoimmunization
* 32yo G2 P1 was seen for her first prenatal visit at 12 weeks Her prenatal labs reveal a blood type of O positive.
AAT (indirect Coombs) is positive. She has been married to the same husband for 10 years and states he is the father
of both her pregnancies. She did not receive Rh immune globulin during her last pregnancy.
* Isoimmunization is when a woman produces antibodies directed against foreign RBC surface antigens, often those
of her fetus. So this can occur from her fetus or from a transfusion with mismatched blood.
* Isoimmunization leads to fetal hydrops. Baby is anemic, placenta is huge, fetus is huge/swollen.
* Questions to ask: is mother antigen (Rh) negative? Is dad antigen positive? Is AAT positive? So you’re wondering
if the mother is negative Rh, dad is positive, and if there are antibodies present to the fetus. Next question, are the
antibodies present associated with hemolytic disease of the newborn (HDN)?
* Kell kills, Duffy dies, Lewis lives. Anti-Kell causes HDN, anti-Duffy causes HDN. No problem with anti-Lewis.
* If there are antibodies associated with hemolytic disease, the titer must be > 1:8. If < 1:8, no risk.
* Risk: mother antigen negative, dad antigen positive, AAT (indirect Coombs) positive, antibodies associated with
HDN (Kell, Duffy), and the titer must be over 1:8.
* So we’ve determined that there is a risk of HDN and the titer is high. Next question is to determine if the fetus is
anemic. The most common test for this is amniocentesis looking for amniotic fluid bilirubin. This is an indirect
measurement of hemolysis. The breakdown product of hemoglobin is bilirubin. Another option is PUBS and look
directly at fetal hematocrit.
* If fetal anemia is severe, we need to intervene. To make this determination via amniocentesis, the bilirubin must
be within Liley zone 3. Send bilirubin down for optical density scanning at 450nm. That value is then plotted on a
Liley graph, with x-axis being the weeks gestation. Zone 3 is high anemia risk.
* If using PUBS, intervene if fetal hematocrit is < 25%. Normal fetal hematocrit is about 40%.
* Fetal anemia intervention: if preterm (< 34 weeks) risk of prematurity is greater than risk of intervention, so we do
an intrauterine transfusion (IUT), intravascular or intraperitoneal. If 34+ weeks, delivery the baby.
* Most common method of meternal isoimmunization is feto-maternal bleed.
* Most common RBC Rh antigen is big “D.” There is C, c, E, e, no d.
* Screening test for maternal isoimmunization is atypical antibody test (AAT), indirect Coombs test.
* Neonatal outcomes with HDN vary from mild jaundice to erythroblastosis fetalis.
* Risk factors for isoimmunization are amniocentesis, ectopic pregnancy, D&C, abruptio placenta, placenta previa.
So all of these are indications for Rh immune globulin (RhoGAM).
* Effect of ABO incompatibility on risk of maternal isoimmunization? Protects against it. ABO incompatibility
means mother is O and baby is A. So mother has naturally occurring anti-A and anti-B. The blood cells will be
hemolyzed inside the mother before the mother’s lymphocytes can react and get turned on.
* Management of atypical antibody test if positive? Answer is identify if it is associated with HDN, so type.
* Management of atypical antibody that is associated with HDN? Answer is determine if FOB (father of baby) is
antigen positive or negative. Geneticists say 10% of the time the man who the woman says is the father of the baby
is not the father. Even if the mother knows, she may not tell.
* Management with FOB antigen positive and titer is > 1:8? Type fetal RBC antigen. If titer < 1:8, repeat monthly.
Father could be homozygous or heterozygous for the antigen, so need fetal RBC antigen with high titer.
* Is the fetus anemic? Amnio for bilirubin, PUBS for fetal Hct, or ultrasound for hydrops.
* If titer is > 1:8 and cannot type RBC antigen, do amniocentesis for amniotic fluid bilirubin (change in optical
density, ∆OD450) or a PUBS for fetal hematocrit.
* Management of amniotic fluid bilirubin if Liley zone I or II? Answer is repeat amnio in 1, 2, or 3 weeks.
* Management if PUBS hematocrit is > 25? Repeat PUBS.
* Management if Liley zone III or Hct < 25%? Answer is intervention, IUT if < 34 weeks, delivery if > 34 weeks.
* What is the mechanism of action of Rh immune globulin (RhoGAM)? Passive IgG antibodies lyse anti-D RBCs
before maternal lymphocytes are stimulated.
* When do you give RhoGAM? At 28 weeks to Rh negative mothers.
* Volume of fetal RBCs neutralized by 300mcg of RhoGAM? Answer is 15mL of RBCs, 30mL of blood.
* How do you assess how many vials of RhoGAM you need? Answer is Kleihauer-Betke test. You can count the
number of fetal RBCs in a high power field then extrapolate to determine mL of fetal RBCs.
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Obstetrical Complications: Premature Rupture of the Membranes (PROM)
* 22yo primigravida at 23 weeks gestation comes to birthing unit stating that two hours ago she had a gush of fluid
from her vagina. She denies vaginal bleeding or uterine contractions. Her perineum appears moist to gross
inspection. On exam her temperature is 102F.

* PROM is membrane rupture before labor onset, term or preterm.
* AROM is artificial rupture of the membranes, done with an amniotic hook (AmniHook). The end of the tiny hook
is sharp enough to cause bleeding if dragged across skin.
* Risk factor for PROM is ascending infection from lower genital tract. Women who smoke cigarettes have a higher
rate of PROM.
* Most common presentation for PROM is sudden gush of clear vaginal fluid. Ultrasound shows oligohydramnios.
* A patient coming in saying my panties are all wet is not very convincing, may just be urinary incontinence. A
women standing at the checkout counter who suddenly gets soaked in water and creates a pool on the floor is more
convincing for PROM.
* Diagnosis of PROM is by speculum exam for pooling (of fluid at posterior fornix), nitrazine (pH increased, turns
paper blue), and ferning (see fern-pattern as it dries on glass slide).
* Do not just take fluid from the perineum area. It could be urinary incontinence with alkaline urine.
* Management of suspected PROM at any gestational age is speculum exam.
* Method of diagnosing chorioamnionitis (infection)? Clinically: confirmed ROM, maternal fever, no URI or UTI.
* Management of PROM with uterine contractions? Do not do tocolysis (do not stop the contractions).
* Management of PROM with chorioamnionitis? Infection is with normal genital flora (anaerobes, aerobes, Gram
positives, Gram negatives). Answer is IV antibiotics and prompt delivery, culture done to determine if group B strep
exists. Antibiotics should be broad spectrum.
* Management of uncomplicated PROM is triage according to gestational age. Early in the pregnancy, the risk is
high. Toward the end of pregnancy, there is less risk. So the closer we are to term, the more likely we are to get the
baby out. The further from term we are, the more conservative we are because we’re thinking about complications
like respiratory distress syndrome, patent ductus arteriosus, grade III/IV intraventricular hemorrhage, necrotizing
enterocolitis.
* Function of pulmonary surfactant is to prevent alveolar collapse between inspirations. Most common fetal
pulmonary surfactant is lecithin (PC, phosphatidylcholine), second is phosphatidylglycerol (PG).
* What is the test for pulmonary maturity? Answer is lecithin/sphingomyelin ratio (L/S ratio). Maturity is when the
ratio is 2 or more. Pulmonary surfactant maturity occurs at 34-36 weeks.
* Management of uncomplicated PROM but pre-viable (< 24 weeks)? Answer is induce labor if she wishes or send
her home on bed rest. Viability is very low.
* Management of uncomplicated PROM preterm viable (25-35 weeks)? Answer is in-hospital management. We can
do bed rest, give steroids to induce fetal lung maturity, cultures for GBS, give prophylactic antibiotics.
* Uncomplicated PROM > 36 weeks? Answer is delivery.
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Obstetrical Complications: Preterm Labor (PTL)
* 24yo G2 P1 at 28 weeks by dates comes to the birthing unit complaining of regular contractions every 7-10
minutes. She is a smoker with chronic HTN. She has had no prenatal care. Fundal height is 35cm. Her last
pregnancy ended with spontaneous vaginal delivery at 30 weeks gestation.
* Fundal height at 35cm for 28 weeks could be incorrect dates or twins; twins has 50% preterm rate.
* Most common cause of perinatal morbidity and mortality? Answer is preterm delivery.
* Preterm labor diagnosis: 20-36 weeks, 3 UCs in 30 minutes, cervical change (most important factor).
* Most of the patients we treat with topolytic agents (e.g. magnesium sulfate) are not in labor to begin with. If her
cervix is long (effacement), closed, and posterior, likely not labor.
* Pregnancy 20-36 weeks, 3+ UCs in 30 minutes, dilated > 2cm or changing: preterm labor.
* Pregnancy 20-36 weeks, 3+ UCs in 30 minutes, dilated < 2cm without change: preterm contractions.
* Risk factors for preterm birth are twins (50%), uterine anomaly (50%), previous preterm delivery (25%). Minor
risk factors are PROM, smoking, short cervix.
* Most common symptoms of preterm labor are lower abdominal pressure, back pain, vaginal discharge.
* Obstetric contraindications to preterm labor tocolysis are severe abruption, PROM, chorioamnionitis.
* Fetal contraindications to preterm labor tocolysis are lethal anomaly (e.g. anencephaly, renal agenesis, trisomy
13), fetal demise, fetal jeopardy (severe late decelerations).
* Maternal contraindications to preterm labor tocolysis are eclampsia, severe pregnancy induced hypertension,
advanced dilation.
* In a patient who is actually in preterm labor, what percent will not have obstetric, fetal, or maternal complications?
Answer is 5%, only 5 of 100 will not have contraindications.
* So some say that many of the patients we treat are not in preterm labor and many of those who are in preterm labor
should not be treated.

* Tocolytic agents are MgSO4 (competes with calcium), beta-agonist (blocks B2 receptors), calcium channel
blockers (decrease intracellular calcium), prostaglandin synthesis inhibitors (decrease PG).
* Beta-agonists include ritodrine and terbutaline (off-label).
* Calcium channel blockers include nifedipine.
* PG inhibitors include indomethacin.
* Magnesium toxicity triad: preterm tocolysis, respiratory depression, muscle weakness.
* Treatment for magnesium overdose is calcium gluconate.
* Calcium channel blocker (nifedipine) toxicity triad: preterm labor tocolysis, tachycardia and hypotension,
myocardial depression.
* Beta agonist (ritodrine, terbutaline) toxicity triad: preterm tocolysis, hypokalemia, hyperglycemia.
* PG inhibitor (indomethacin) toxicity triad: preterm labor tocolysis, oligohydramnios, PDA closure in-utero.
* Sequence of tocolytic management is confirm preterm labor, rule out contraindications, initiate IV hydration, start
magnesium sulfate tocolysis, obtain cervical/urine cultures then IV penicillin G (GBS), administer IM
betamethasone if < 34 weeks to stimulate type II pneumocytes to produce surfactant and mature the lungs.
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Obstetrical Complications: Post Dates Pregnancy
* 21yo G1 at 42 weeks by dates comes to the outpatient prenatal clinic. She has been seen for prenatal care since 12
weeks, confirmed by an early ultrasound. She states that fetal movements have decreased. Fundal height is 42cm.
Cervix is long, closed, posterior. NST is reactive but amniotic fluid is only 4cm (AFI should be > 8cm, so this is
oligohydramnios).
* Postdates pregnancy is post-conception ≥ 40 weeks or ≥ 280 days, post-LMN ≥ 42 weeks or ≥ 294 days.
* Most common cause of post-dates pregnancy is idiopathic.
* Effect of post-dates pregnancy on perinatal mortality is increased 2-3x mortality and morbidity. Reasons for this
are macrosomia and dysmaturity.
* If placental function maintained (75%), macrosomia syndrome due to more nutrition and more substrates.
* Macrosomia implies difficult delivery, forceps, vacuum, shoulder dystocia, birth trauma, C-section.
* If placenta function decreases (25%), dysmaturity syndrome due to inadequate oxygenation and substrates.
* Dysmaturity implies placental insufficiency, acidosis (baby gasps meconium), oxygen deprivation, C-section.
* Factors affecting management of post-dates pregnancy are confidence in the dates and cervix favorability.
* Management of post-date pregnancy when dates are sure and cervix is favorable: induction of labor, IV oxytocin
and AROM with amniotic hook.
* Management of post-dates pregnancy when dates are sure and cervix is unfavorable (long, closed, posterior, firm):
PGE2 induction (aggressive) or NST and AFIs allowing her to go into labor on her own (conservative).
* Management of post-dates pregnancy when dates are unsure: NST, AFI, await labor.
* Meconium is the bowel movement that the fetus has first, made up of thick sticky stuff, swallowed cells from the
amniotic fluid, from desquamation of cells from the GI tract, swallowed hair.
* Management of meconium if patient in labor: amnioinfusion, infuse saline into amniotic sac, dilutes meconium.
* Management of meconium if head delivered: DeLee suction nose and pharynx immediately.
* Management of meconium once body delivered: visualize vocal cords with laryngoscope, suction meconium.
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Medical Complications: Hypertension
* Top medical risk factors in pregnancy: pregnancy related hypertension, diabetes, anemia.
* Criteria for hypertension are blood pressure sustained over 140/90. A single BP of 150/96 is not hypertension, this
is high blood pressure. Have patient rest on their left side and retake in 15 minutes. Generally don’t diagnose
hypertension in pregnancy unless it lasts more than 6 hours.
* Non-sustained elevation of blood pressure, no proteinuria: transient hypertension, conservative outpatient
management, no risk to fetus.
* If hypertension existed prior to pregnancy or less than 20 weeks gestation with no proteinuria: chronic
hypertension. Patient could have kidney damage with long standing hypertension. Management is conservative
outpatient, medication of choice is alpha methyl-dopa.
* Patient has chronic hypertension, now her BP rises, proteinuria increases: chronic hypertension and superimposed
pre-eclampsia, high mortality risk. Management is magnesium sulfate to prevent eclamptic seizures and deliver.
* Patient has sustained hypertension, proteinuria, unexplained seizures: eclampsia. Management of eclampsia is
magnesium sulfate and deliver. If patient tolerates MgSO4, can give oxytocin and vaginal delivery. Else section.
* Sustained BP elevation, no chronic HTN, no seizures, ask is there maternal or fetal jeopardy? Criteria is BP
160/110 or higher, protein over 5g on 24h urine, new onset worsening headache, scotomata (visual changes),
epigastric pain that isn’t relieved by antacids, DIC, liver function test abnormal, oliguria. These are criteria for
severe pre-eclampsia. Management is magnesium sulfate and deliver.
* Sustained BP elevation, no chronic HTN, no seizures, no maternal/fetal jeopardy signs: mild pre-eclampsia.
Management depends on gestational age, if ≥ 36 weeks then MgSO4 and deliver, if < 36 weeks then hospitalize and
conservative management.
* HELLP syndrome: Hemolysis, elevated liver enzymes, low platelets. Management is MgSO4 and deliver.
* Number one risk factor for pre-eclampsia is primipara.
* 19yo G1 is seen in the outpatient prenatal clinic for routine visit. She is 32 weeks confirmed by a first trimester
sonogram. She has no complaints. She denies headache, epigastric pain, or visual disturbances. She has gained 2lbs
since her last visit 2 weeks ago. Her BP is 155/95, but 10 minutes later it is 125/72, which is her usual BP. She has
only trace pedal edema. A urine dipstick is negative. This is transient hypertension.
* 21yo G1 seen in outpatient clinic at 32 weeks confirmed by first trimester ultrasound. Has swelling in her hands
and feet, no epigastric pain or visual changes. She has gained 10lbs over 2 weeks. BP is 155/95 twice. Her fingers
appear swollen, 3+ pedal edema, spot urine dipstick is 2+ protein. This is mild pre-eclampsia.
* Risk factors for pre-eclampsia are primipara, twins, molar pregnancy, diabetes, age extremes, chronic HTN.
* Pathophysiology of mild pre-eclampsia is diffuse vasospasm, resulting in capillary injury.
* Mild pre-eclampsia symptoms are very few, except related to weight gain and mild edema. >300mg/day protein.
* Pre-eclampsia causes renal changes, on renal biopsy you see glomerular endotheliosis.
* Mechanism of pre-eclampsia is probably vasoactive prostaglandins, increased thromboxane (vasoconstrictor),
decreased prostacyclin (vasodilator).
* 21yo G1 at 32 weeks confirmed by first trimester sonogram. For 24 hours, she has had severe occipital headache,
mid-epigastric pain not relieved by acetaminophen. She sees light flashes and spots. She has gained 10lbs in 2
weeks. BP is 165/115. She has 3+ pedal edema and her fingers are swollen. Fundal height is 29cm. FHT are regular
at 145/min. Urine shows 4+ protein. This is severe pre-eclampsia.
* Degree of hypertension for severe pre-eclampsia is BP ≥ 160/110 sustained.
* Degree of proteinuria for severe pre-eclampsia is 3-4+ on dipstick, ≥5g on 24h urine.
* Symptoms of pre-eclampsia are headache, epigastric pain, visual disturbances. Likely related to vasospasm
resulting in edema.
* Findings in severe pre-eclampsia are severe hemoconcentration (BUN, creatinine, uric acid), DIC, elevated LFTs,
pulmonary edema, oliguria, cyanosis.
* Schistocyte “helmet” cell is seen in DIC.
* Risk factors for severe pre-eclampsia are same as mild pre-eclampsia plus small vessel disease, lupus.
* Management of severe pre-eclampsia is MgSO4, induce labor if mother stable, lower BP to diastolic 90-
100mmHg (with hydralazine or labetalol) but not lower to maintain placental infusion.
* If 26-34 weeks gestation and BP brought down to < 160/110 with labetalol or hydralazine, then intensive
monitoring of mother and fetus in the ICU, continuous IV MgSO4.
* 21yo G1 is brought to the ED after a generalized tonic-clonic seizure at 32 weeks. The seizure was precluded with
a severe headache. She lost control of her bowels and bladder. She has gained 10lbs in 2 weeks. On exam she is
unresponsive in a post-ictal state. BP is 185/115 and a spot urine dipstick shows 4+ protein. This is eclampsia.
* Defining symptoms of eclampsia is seizure.
* Management of eclampsia is stop convulsions with MgSO4, prompt delivery.
* 35yo multigravida seen for her first prenatal visit. She is 12 weeks with a BP of 155/95. Chronic HTN was
diagnosed 5 years ago for which she takes oral nifedipine. Urine dipstick is 2+ protein. Recent 24h urine shows 1.2g
of protein and Cr Cl of 85mL/min. Serum creatinine is 1.2mg/dL. She denies headache or visual changes. This is
chronic hypertension.
* Risk factors for chronic hypertension are idiopathic, obesity, age, family history, DM, SLE.
* BP 140/90 to 170/109 and no end-organ damage is good prognosis.
* High BP with Cr > 1.4, retinopathy, LVH, are poorer prognosis.
* Uncontrolled hypertension 210/130, chronic HTN with pre-eclampsia is worse prognosis.
* Antihypertensives never to be used with pregnancy (contraindicated) are ACE inhibitor (fetal renal failure) and
diuretics (decreased plasma volume).
* Management of chronic hypertension is to discontinue hypertensive medications if diastolic pressure below 100
(BP drops with pregnancy), serial ultrasounds looking for IUGR, serial NST/AFI, serial BP and urine protein, and
induce labor at term.
* If superimposed pre-eclampsia, give MgSO4, induce labor, and lower BP using hydralazine or labetalol.
* 32yo multigravida at 32 weeks, routine prenatal visit BP is 160/105. Previous BPs were normal. Pre-eclampsia
workup shows increased total bilirubin, LDH, ALT, AST and platelet count of 85,000. She has no headache or
visual changes. This is HELLP syndrome.
* Hemolysis, elevated liver enzymes, low platelets: HELLP syndrome.
* Management of HELLP syndrome is MgSO4, induce labor, lower BP (if hypertension), maternal steroids can help
normalize laboratory values and improve recovery.
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Medical Complications: Cardiac Disease
* 30yo multigravida with a childhood history of rheumatic fever has an echocardiography diagnosing mitral
stenosis. She is now 20 weeks with no symptoms at rest but mild dyspnea with activity. Exam reveals a pansystolic
murmur. She is NYHA class II (dyspnea on exertion).
* Coronary heart disease is rare in pregnancy, the problem is hypoxia.
* Rheumatic heart disease is the most common, the problem is inadequate diastolic flow.
* Most common rheumatic heart disease is mitral stenosis, inadequate diastolic filling, issue when area is < 1cm^2.
* Normal pregnancy: plasma volume increases 50%, heart rate increases 15%, stroke volume increase 25%,
peripheral vascular resistance decreases by 30%.
* When you increase HR in pregnancy, systolic time remains the same because it takes the same amount of time for
the heart to contract. Thus, diastole is shortened.
* Factors worsening mitral stenosis are increased heart rate and increased blood volume (normal changes seen in
pregnancy).
* Most common congenital heart disease in pregnancy are ASD and VSD.
* Most common cyanotic congenital heart disease in pregnancy is tetralogy of Fallot.
* Maternal mortality is < 1% in ASD, VSD, corrected tetralogy of Fallot.
* Maternal mortality is 5-15% in uncorrected tetralogy of Fallot and Marfan syndrome with normal aorta.
* Maternal mortality is 25-50% with Eisenmenger and Marfan syndrome with abnormal aorta.
* Eisenmenger syndrome is pulmonary hypertension and bi-directional cardiac shunt. Normally the pulmonary
vascular resistance is less than the change in pressures between the left and right ventricles, so the heart operates as
it should. Peripheral vascular resistance in pregnancy drops below pulmonary vascular resistance, so blood takes
path of least resistance going directly from right heart to left heart bypassing the lungs, unoxygenated blood goes out
into the body, maternal mortality is the next.
* Marfan syndrome if aorta is dilated > 40mm (tension on vessel wall is related to the square of the radius), risk is
aortic dissection leading to possible maternal death.
* Peri-partum cardiomyopathy is idiopathic and usually occurs in the later part of pregnancy, bi-ventricular heart
failure leading to possible maternal death. Management is ICU care, intubation, supportive cardiac care.
* Bi-directional intracardiac shunt: think Eisenmenger syndrome.
* Dilated aortic root > 40mm: think Marfan syndrome.
* New York Heart Association (NYHA) heart failure class I is no symptoms at rest, no symptoms with activity.
* NYHA class II is no symptoms at rest and mild symptoms with activity, usually do well, do not need invasive
monitoring during labor (no arterial line, no pulmonary catheter).
* NYHA class III is no symptoms at rest and marked symptoms with activity. NYHA class IV is symptoms at rest.
* NYHA III/IV require intensive monitoring during labor.
* Management of cardiac disease in pregnancy are to minimize tachycardia (left lateral rest, avoid activity, avoid
anemia) and minimize increased vascular volume (left lateral rest, 2g sodium diet, diuretics as need).
* Minimizing tachycardia in labor: left lateral rest, reassurance, sedation, epidural, no pushing, elective forceps.
* Minimizing intravascular volume in labor: left lateral rest, monitor volume, possible arterial line or PA catheter.
* To minimize intravascular volume post-partum, watch for intravascular overload from sudden emptying of uterine
venous sinuses after placental delivery.
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Medical Complications: Thyroid Disorders
* 23yo G1 at 30 weeks. She lost 4lbs over 2 months. She states her heart “is racing” and pulse is 135/min. She has a
noticeable tremor when arms are held out straight and eyes appear prominent. She has frequent contractions.
* Thyroid gland increases in size in pregnancy, plasma iodine concentration decreases, but total T3 and T4 increase
due to increased thyroid binding globulin. Free T3 and T4 are unchanged in pregnancy.
* Uncontrolled hyperthyroidism is associated with poor outcome. Controlled hyperthyroidism has normal outcome.
Thyroid storm is life threatening for both mother and fetus.
* Most common type of hyperthyroidism in pregnancy is Graves disease.
* Pathophysiology of Graves diseases is associated with long acting thyroid stimulator (thyroid stimulating
immunoglobulin), an IgG antibody that stimulates the thyroid.
* Diagnosis of Graves disease is with high T4, low TSH, high LATS.
* Medication of choice with Graves is propylthiouracil (PTU) because it crosses the placenta less.
* Only do surgery with Graves in pregnancy if medications do not work.
* In pregnancy, never use radioactive I131 because it can destroy the fetal thyroid.
* If woman is hypothyroid, she is usually infertile because she is anovulatory, so not commonly seen in pregnancy.
* Risk of hypothyroidism in pregnancy is increased spontaneous abortion rate.
* Normal pregnancy if hypothyroidism is treated with thyroid replacement.
* Diagnosis of hypothyroidism is via high TSH.
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Medical Complications: Seizure Disorders
* Seizures tend to be unchanged in seizures, 75% of time. Those that get worse are patients who have more severe
epilepsy and have trouble controlling their seizures.
* Pregnancy usually drops seizure medication levels, unsure why.
* Pregnancy complications with seizure disorders are pregnancy induced hypertension, preterm delivery, IUGR, and
increased C-section rates.
* Seizure disorders associated with a 2-3x increase in fetal malformation, cerebral palsy, and mental retardation. The
malformation rate is related to medications (not the seizure disorder).
* Many of the seizure mediations are category D or C, but you have to use what is available to control seizures.
* Management of epilepsy is adding folate supplementation (4mg/day) because many of the anti-epileptic
medications decrease folate absorption. Folic acid is water soluble so you won’t get toxic levels.
* Do anomaly screening with triple marker screen and sonography.
* Use monotherapy for seizures if possible. If mother on 2 medications, birth defect risk increases.
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Medical Complications: Diabetes
* 32yo Hispanic multigravida is 29 weeks, her 1hr 50g OGTT is 175mg/dL. She is 60” tall and weighs 200lbs. Her
pregnancy weight gain has been 30lbs. Her previous babies weighed 3800 and 4200 grams.
* Screen all patients for diabetes at 24-28 weeks with 1 hour oral glucose tolerance test. Normal value is < 140.
* 15% of screened patients with have an abnormal 1h OGTT (≥ 140mg/dL).
* If 1h OGTT is ≥ 140, next step is fasting 3h 100g OGTT. Abnormal 3h OGTT is abnormal if two or more value
are high. One high value is impaired glucose tolerance. 2+ values is gestational diabetes (GDM). Patient likely has
no symptoms, it is a chemical diagnosis, just a laboratory test.
* If patient has GDM, educate them about ADA diet which is calorie spread throughout the day, encourage complex
rather than simple carbohydrates. Most important next step is to monitor home glucose values via blood sugars.
* Target range for home glucose values are fasting < 90, 1h < 140 (after eating), 2h < 120.
* If values are consistently outside of the target range, management is insulin.
* Fetal demise risk factors: previous fetal death, hypertension, macrosomia (baby outgrows placenta’s ability to
supply nutrients), and if patient is on insulin.
* If fetal demise risk factors, do NSTs and AFIs starting at 32 weeks.
* Say patient has GDM, home glucose in target range, no fetal demise risk factors. What problems can we expect in
labor? Macrosomia (shoulder dystocia, arrest of descent), insulin given if needed.
* If she has dystonia or arrest of labor, do cesarean section. Suprapubic pressure used for shoulder dystocia.
* Problem with shoulder dystocia is the anterior shoulder gets impacted behind the symphysis pubis. Suprapubic
pressure can be applied with hip external rotation and hyperflexion (McRoberts maneuver). If that does not work, try
corkscrew maneuver to twist fetus so that the shoulders go from anterior/posterior to oblique position. If that does
not work, deliver the posterior arm by reaching in and bringing it out (can be tough, could fracture bones), then
rotate the baby so the anterior shoulder is the posterior shoulder.
* Post-partum management is determine if glucose intolerance has persisted, do a fasting blood sugar. Criteria for
DM is > 126mg/dL after fast, done twice. If > 126mg/dL, overt diabetes. Generally, the insulin resistance from the
human placental lactogen (hPL) reverses post-partum.
* Diabetes in pregnancy can be GDM (insulin resistance diagnosed in pregnancy), type 1 DM (ketosis prone), and
type 2 DM (ketosis resistant).
* White classification of diabetes in pregnancy is more historic than useful. A1 is GDM not requiring insulin and A2
is GDM that requires insulin. This is not used like it was in the past.
* Oral hypoglycemics should be avoided because they cause fetal hypoglycemia.
* Rule of 15s: 15% of 1h OGTT will be positive, 15% of 3h OGTT will be positive (2.25% overall GDM). 15% of
GDM patients will require insulin.
* Overt diabetes antepartum: get hemoglobin A1c, 24h urine for kidney status, dilated fundoscopic exam for retinal
status, and home glucose monitoring 4-6x/day.
* Anomaly prevention with overt diabetes done by euglycemia and folate (4mg/day). Most common DM fetal tube
anomalies are neural tube defects, congenital heart defects, and sacral agenesis (200x more common with DM).
Sacral agenesis also known as caudal regression syndrome.
* Anomaly screening in overt diabetics includes 18 week triple-marker screen, 20 week targeted sonogram, 24 week
fetal echocardiogram (if elevated HgA1c).
* Target gestational age for delivery with DM is 40 weeks. Avoid going past 40 weeks.
* Labor complications with DM are arrest of 1st and 2nd stage of labor, shoulder dystocia.
* Post-partum hemorrhage is a complication of GDM, bigger uterus, does not contract as well.
* After the placenta is out, hPL rapidly leaves circulation, so turn down the insulin after delivery of the placenta.
* GDM neonates can get hypoglycemia due to hyperinsulinemia from high prenatal glucose, hypocalcemia due to
immature parathyroid gland, polycythemia due to increased erythropoietin from intrauterine hypoxia,
hyperbilirubinemia due to immature liver and excessive RBC breakdown from polycythemia, and respiratory
distress syndrome due to immature surfactant.
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Medical Complications: Anemia
* 18yo G3 P2 had prenatal labs drawn at 18 week. The CBC showed hemoglobin 9.5g/dL, hematocrit 28%, MCV
75, RDW 17. Her first child was delivered two years ago with her second child being born a year ago.
* MCV lower limit is 80 in pregnancy, RDW should be < 14. This is iron deficiency anemia.
* Hemoglobin < 10g/dL is anemia in pregnancy. Determine if the problem is heme (iron deficiency, folate
deficiency) or globin (sickle cell, thalassemia).
* MCV < 80, RDW increased: iron deficiency anemia, most common in pregnancy. Risks factors are bleeding
(nose, GI, vaginal) and serial pregnancies. Treatment is ferrous sulfate 325mg daily. Any ferrous salt will work.
* MCV > 100, RDW increased: folate deficiency anemia or B12 deficiency anemia. Most likely diagnosis is folate
deficiency because prolonged B12 deficiency causes infertility. Body has 3 months of stores of folate. Risk factors
are any hemolytic process and epilepsy (decreased folate absorption with anticonvulsants). Treatment is folic acid
1mg daily. With severe hemolytic process like sickle cell, patient may need 4mg daily.
* Hemoglobin anemias determined by hemoglobin electrophoresis.
* Sickle cell is autosomal recessive, abnormal hemoglobin. Trait is heterozygous, disease is homozygous. Risk is
African American or Mediterranean background. Management of sickle cell is to avoid hypoxia as decreased
oxygen tension causes cells to sickle. Patient will need extra folate because of the hemolysis processes.
* Decreased production of normal hemoglobin are thalassemias. Thalassemias are autosomal recessive with alpha
and beta versions. Risk is South East Asian. Treatment is supportive (no treatment).
* In iron deficiency anemia, after you give iron the first lab parameter to increase is reticulocyte count.
* In folate deficiency anemia, after you give folate the first lab parameter to increase is reticulocyte count.
* Anemia with multiple gestation: iron deficiency, folate deficiency.
* Anemia with seizure disorder: folate deficiency.
* Anemia with African descent: sickle cell.
* Anemia with South East Asian descent: thalassemia.
* 25yo African American multigravida is found to have anemia. What is the most likely diagnosis? Answer is iron
deficiency. Iron deficiency is the most common overall (including African Americans).
* Hypersegmented neutrophils seen on peripheral smear: folate deficiency.
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Medical Complications: Urinary Tract Infection (UTI)
* 23yo G1 at 31 weeks complains of flank pain, nausea and vomiting, and shaking chills for 12 hours. She has sickle
cell trait. On exam, temp is 103F. Pulse is 125, respirations are 30. Her skin is grossly diaphoretic and she has
exquisite CVA (costovertebral angle) tenderness. EFM shows a baseline heart rate of 170/min with reactivity. UC
are every 10 minutes.
* What is the only obstetrical complication that is increased with sickle cell trait? Urinary tract infection.
* Asymptomatic bacteriuria occurs in 8% of pregnancies. No symptoms, which is why you do screening tests.
Diagnosis with positive urine cultures/sensitivity. Most common organism is E. coli (Gram negative enteric).
Untreated, 30% will develop pyelonephritis. Treatment is single agent oral outpatient antibiotic, such as
nitrofurantoin which is concentrated in the urine (no systemic effect). If you gave ampicillin or a cephalosporin,
you’ll also be giving the woman a vaginal yeast infection.

* Acute cystitis occurs in 1% of pregnancies. Symptoms include urgency, frequency, and burning. Laboratory
findings are positive UA and culture/sensitivity. Management is outpatient oral antibiotic, nitrofurantoin.
* Acute pyelonephritis occurs in 1-2% of pregnancies, a serious complication of pregnancy. Symptoms are systemic,
high fever, CVA tenderness, positive UA and culture. 15-20% of these patients get bacteremia (sepsis). Can develop
adult respiratory distress syndrome (ARDS) due to release of toxins from bacteria, injuring the capillaries in the
lungs. Pre-term labor can also occur.
* “Lipstick Sign” when patient shows up saying they are in severe pain but wearing make-up, probably not that sick.
Negative “Lipstick Sign” if patient arrives looking like she just rolled out of bed, suggest they are not faking.
* If patient looks stable (positive lipstick sign) and pyelo, IV antibiotic like cephalosporin or ampicillin.
* If patient looks septic (negative lipstick sign) and pyelo, IV gentamycin and ampicillin.
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Intrapartum Events: Labor
* In order for labor to take place, cervix must go from thick rigid structure to a thin floppy one (“from nose to lip”).
* Most of the cervix is collagen, not smooth muscle. Physiology of cervical softening is breakage of disulfide
linkages and increased fluid into collagen.
* Effacement is the length of the cervix. Cervix at full effacement can be “paper thin.”
* Pelvic inlet greatest dimension is transverse, shortest dimension is anterior/posterior. So the head of the baby
should turn transversely to get through inlet. Mid-pelvis shortest dimension is transverse, longest is
anterior/posterior (90-degree change from inlet). So head of the baby must rotate here, neck flexion (chin to chest),
then extension under the symphysis pubis.
* Cardinal movements of labor are engagement, descent, flexion, internal rotation, extension, external rotation,
expulsion.
* Deliver anterior shoulder by bringing the head down, delivery the posterior shoulder by bringing the head up.
* Ritgen maneuver involves applying upward pressure from the coccygeal region to extend the head during actual
delivery, this protects the musculature of the perineum.
* Initial three events of labor take place almost simultaneously: engagement, descent, flexion.
* Final two events of labor take place together also: external rotation, expulsion.
* First stage of labor is onset of regular contractions until complete cervical dilation (or 10cm). Latent phase of stage
1 goes from onset of contractions to beginning of cervical dilation. Active phase of stage 1 goes through cervical
dilation acceleration until complete dilation.
* Second stage of labor is from complete dilation to delivery of baby.
* Third stage of labor is from delivery of baby to delivery of placenta.
* Mechanism of third stage of labor is separation of the placenta. It is dependent on uterine contractions to shear the
anchoring villi from their attachment to the decidual bed of the endometrium.
* Abnormal labor occurs when the duration of any stage of phase of labor is prolonged.
* 20yo G1 at 39 weeks is being observed in the maternity unit. She states she has been having regular UCs for 24
hours but cervical dilation remains at 1-2cm. Vital sings are stable. EFM tracing is reassuring regarding fetal status.
This is prolonged latent phase.
* Diagnosis of prolonged latent phase is cervical dilation < 3cm, time > 20 hours if primigravida, time > 14 hours if
she has had multiple babies.
* Say patient arrives at labor and delivery because her water broke. She has no contractions and no cervical dilation.
Once oxytocin is started, it could be up to 20 hours of latent phase prior to delivery.
* Most common cause of prolonged latent phase is injudicious analgesia. Example would be giving an epidural to a
patient who is 1cm dilated, contractions will slow. Other causes are hypotonic contractions, hypertonic contractions
with short duration.
* Management of prolonged latent phase is therapeutic rest and sedation, avoid a C-section in latent phase.
* 20yo G1 at 39 weeks has progressed in labor to 8cm cervical dilation but has not changed for 3 hours. Vital signs
are stable. EFM tracing is reassuring regarding fetal status. This is prolonged (arrested) active phase.
* Diagnosis of prolonged active phase is cervical dilation ≥ 3cm with either inadequate cervical change or no
cervical change. Inadequate cervical change is < 1.2cm/hour for primigravida or < 1.5cm/hour for multigravida. No
cervical change occurs for 2 hours or more.
* Causes of prolonged active phase are PPP: passenger (size or orientation of baby), pelvis, powers (uterine
contractions). The only one you can change is the UCs, so determine contraction quality.
* Good contraction quality is UCs coming every 2-3 minutes, lasting 45-60 seconds, 50mmHg or greater.
* If hypotonic UCs, give IV oxytocin. If adequate UCs present, do C-section.
* 20yo G1 at 39 weeks has progressed in labor to 10cm dilation and has been pushing for 3 hours without descent of
the head past +2 station. Vital signs are stable. EFM tracing is reassuring regarding fetal status. This is prolonged
second stage of labor.
* Diagnosis is failure to delivery fetus after complete dilation for 2 hours without an epidural or for 3 hours with an
epidural. Efforts not as strong with epidural.
* Causes of prolonged second stage are PPP: passenger (size or orientation of baby), pelvis, powers (uterine
contractions). The only one you can change is the UCs, so determine contraction quality.
* If hypotonic UCs, give IV oxytocin. If adequate UCs present, do C-section.
* If head has engaged, consider forceps or vacuum extraction.
* 20yo G1 at 39 weeks underwent a spontaneous vaginal delivery 40 minutes ago of a healthy 3500g daughter.
However, the placenta has still not delivered. Vital signs are stable. This is prolonged third stage.
* Third stage labor should not last more than 30 minutes.
* Most common cause of prolonged third stage of labor is inadequate uterine contractions.
* Treatment is IV oxytocin to cause contractions. If this does not work, do manual removal which of course is
uncomfortable for the patient. If manual removal does not work, think about placenta accreta, placenta increta,
placenta percreta.
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Intrapartum Events: Obstetrical Complications
* 34yo multigravida with a known uterine septum comes to the maternity unit at 34 weeks gestation with regular
UCs. She had a previous C-section at 37 weeks for breech. Exam shows footling breech. Cervix is 6cm with bulging
membranes. As you are examining the membranes suddenly rupture and a loop of umbilical cord protrudes through
the cervix between the fetal extremities. This is prolapsed umbilical cord.
* If baby is breech, consider a uterine anomaly. If baby is transverse lie, consider placenta previa.
* Occult prolapse cannot be seen on exam. The cord is next to the head so with each contraction the cord is
compressed. Fetal monitor will show variable decelerations.
* Partial prolapse can be felt. Complete prolapse can be seen.
* Most common cause of prolapse umbilical cord is rupture of membrane with unengaged head. Do not rupture
membranes with an unengaged head.
* Management of prolapsed cord is elevate fetal head, mother in trendelenburg, emergency C-section.
* Do not hold onto the cord because the vessels could go into spasm.
* 20yo G1 at 39 weeks was pushing in the 2nd stage of labor for 90 minutes and has delivered the fetal head.
However, in spite of vigorous pushing efforts by the mother and moderate traction on the fetal head, you are unable
to deliver the anterior shoulder. Since delivery of the fetal head, 30 seconds has passed. The FHR is now 70/min.
This is shoulder dystocia and can be a nightmare.
* Most common risk factor for shoulder dystocia is maternal diabetes.
* First two steps in management of shoulder dystocia are suprapubic pressure and flexion of maternal thighs.
* Final two steps in management of shoulder dystocia are corkscrew maneuver and delivery posterior arm.
* Shoulder dystocia triad: 2nd stage of labor, head has delivered, no further delivery of body.
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Intrapartum Events: Intrauterine Orientation
* Most common lie of the fetus is longitudinal. Most common presentation of the fetus is cephalic. Lie is fetal axis
in regard to maternal axis. Presentation is part of fetus that overlies the pelvic inlet.
* Vertex is not the same as cephalic. Cephalic means the head is at the pelvic inlet. Vertex means cephalic and the
head is flexed. If you do not know if the head is flexed, the proper term is cephalic presentation. Face presentation
would be cephalic with head extended.
* Breech is bottom at inlet. Frank breech is thighs flexed and knees extended. Complete breech is thighs and knees
both flexed. Footling (single or double) is breech with feet first. The problem with footling is the feet and body will
make it though, but there will not be enough cervical dilation for the head to deliver.
* The only breech that is considered reasonable for vaginal delivery is frank breech as the cervix would have to
dilate enough o fit the entire bottom. This is also called unstable breech because extension of a leg or both legs make
it a footling breech.
* The most common position of the fetal head in early labor and at delivery is LOT, OA. Position is location and
rotation of the head in relation to the mother’s bony pelvis. Left occiput transverse (LOT) in early labor and occiput
anterior (OA) at delivery.
* Most common attitude of the fetal head is vertex. Attitude is flexion and extension of the fetal head. Vertex is
flexed with chin against chest. Military is mid-line. Brow presentation is mild extension, face presentation is full
fetal head extension. Molding of the head after delivery is related to intrauterine attitude.
* Failure to progress in labor may be due to OP (occiput posterior) or transverse arrest.
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Intrapartum Events: Fetal Heart Rate Monitoring
* What are the criteria for an abnormal electronic fetal heart tracing (EFT)? Next, is there a non-hypoxic
explanation? Does intrauterine resuscitation correct the abnormality? If post-resuscitation tracing is confusing,
consider doing a fetal scalp pH. If baby is in trouble, expedite delivery. Once baby delivered, get a cord umbilical
artery pH to confirm acidosis.
* Criteria for abnormal fetal heart tracing are tachycardia (> 160) or bradycardia (< 110), decreased variability,
severe variable decelerations or any late decelerations.
* Variability is normal interplay between the sympathetic and parasympathetic nervous systems.
* Early decelerations are when deceleration occurs at the same time of the uterine contraction. This is due to head
compression, not to worry.
* Variable decelerations are rapid drops and rapid returns in FHR not related to uterine contractions. A severe
variable deceleration lasts 60+ seconds and drops 60 beats or more. This is caused by umbilical cord compression.
* Late decelerations are caused by uteroplacental insufficiency. The decelerations occur slightly after the uterine
contraction. This is non-reassuring.
* Non-hypoxic explanation are drugs (beta blockers, local anesthetics, beta agonists, parasympatholytic, MgSO4),
baby sleeping, premature baby, arrhythmia due to congenital heart block (lupus), maternal fever. If non-hypoxic
explanations, then conservative management.
* Say we have an abnormal tracing and no non-hypoxic causes. Next step is resuscitation. Treatment is stop
oxytocin, give terbutaline (decrease contractions to increase intravillous blood flow), mask O2 to mother, IV bolus
to mother (e.g. 500mL), change maternal position to left lateral. If these help, then conservative management.
* If intrauterine resuscitation does not work, do a pH. Say pH > 7.2, this is reassuring and conservative management.
If pH is < 7.2, worrisome, indication for delivery.
* Say we need to expedite delivery. In first stage, C-section. In second stage, forceps, vacuum extractor, or C-
section.
* After delivery, if umbilical cord pH > 7.2 then the baby was alright, this is “false distress.” If pH is < 7.2, this is
true distress.
* Most common fetal outcome with a non-reassuring FHR tracing? Normal well-oxygenated fetus.
* Cerebral palsy generally originates in the second trimester, prior to labor.
* Mechanism of fetal heart rate accelerations is fetal movement, sympathetic nervous stimulation.
* In labor, scalp stimulation of the fetus with FHR accelerations is reassuring.
* Fetal blood capillary pH done when membranes ruptures and cervix dilated. Place cone against fetal head, clear
amniotic fluid (alkaline pH), use special instrument to make a measured incision in scalp, fresh blood added to
heparinized tube. These are not commonly done. Normal pH is ≥ 7.20.
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Intrapartum Events: Operative Obstetrics
* Forceps are placed on the fetal head over the malar prominences. They should fit smoothly without pressure
points. They are a second class lever so they work by compression. If properly placed, they should not cause trauma.
* Kielland forceps used for rotation. Piper forceps used to deliver after-coming head of a breech presentation.
Simpson forceps are the classic ones used for delivery.
* Original forceps were the Chamberlain, named after a French physician in 1800s. At that time obstetrics was a
trade secret, done under a sheet for modesty. They delivered babies of women that no one else could deliver. The
secret got passed along from one generation to the next, makes you wonder how many women died unnecessarily
because of obstructed labor. Finally, one of the Chamberlain’s sold a single forceps to the Dutch Obstetrical Society.
* With forceps, pull straight out. Do not use a “fishtail” technique where you twist from side to side.
* Most common indication for use of obstetric forceps is prolonged second stage of labor.
* Vacuum extraction is done with a soft silastic cup connected to a handheld pump. Squeezing pumps and creates a
vacuum. As the mother pushes you pull to augment the traction. Cup of vacuum places on baby occiput.
* The problem comes when you pull too hard and the cup pops off. The sudden decompression is bad. You can get
sub-galeal hemorrhage and other issues.
* Vacuum used by following the pelvic curve, so you are using a lifting (toward ceiling) motion was the baby
delivers.
* Most common maternal complication of vacuum extraction is vaginal mucosal entrapment. If you’re not careful,
you can suck in the vaginal tissue and as you pull you get large lacerations. So before you pull, check with your
finger all the way around.

* Neonatal complications of vacuum extraction includes cephalohematoma and jaundice as blood breaks down.
* Cesarean section (C-section) can be done with three type of incision. The most common is the low segment
transverse. Advantages are less blood loss, fewer adhesions, and a vaginal birth after C-section is alright.
Disadvantages are risk of bladder injury because you have to take the bladder down, the lower uterine segment must
be formed (not formed wide enough earlier in pregnancy), and the fetus must be in longitudinal lie.
* Low vertical C-section gives much less room to remove the baby, so much less common.
* Classic C-section done vertically through top part of uterus. Advantages are delivery of any kind of fetus
regardless of orientation or gestational age and no need to move the bladder. Disadvantages are increased blood loss,
increased adhesions, vaginal birth would be unsafe in future due to risk of uterine rupture.
* Rate of uterine rupture with labor after classical C-section is 5%. But, 50% of those babies will die.
* Most common indication for primary C-section is cephalo-pelvic disproportion (CPD). CPD is sorta a garbage
term. In reality, 50% of women getting C-section for CPD could have a successful vaginal delivery the next
pregnancy with a larger baby. This really means failure to follow a normal labor curve, arrest in the active phase.
* Most common fetal malpresentation resulting in C-section is breech. This is the second most common cause for C-
section.
* Third most common indication for C-section is non-reassuring fetal monitor strip.
* External cephalic version is an attempt to rotate the baby prior to labor by manipulating the abdomen from the
outside. Pulling down on the head and lifting up on the butt is called a forward roll. A backwards roll can be
attempted.
* External version is about 65% successful and has a lot of variable, such as size of mother, placental location,
amount of amniotic fluid.
* External version is typically performed at 37 weeks gestation.
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Intrapartum Events: Incompetent Cervix
* 32yo G1 at 18 weeks comes to maternity unit complaining of pelvic pressure and thick vaginal mucus discharge.
She denies any UCs. On exam, membranes are bulging into the vagina and no cervix can be palpated. Fetal feet can
be felt through the membranes. Two years ago she underwent cervical conization (cone biopsy) for cervical CIN.
* Classic history is painless dilation of the cervix prior to viability resulting in delivery of a baby that is unable to
survive.
* Diagnosis is done by history of painless cervical dilation, no good diagnostic test.
* Management of incompetent cervix is cerclage, which stitches the cervix into a purse-string fashion around the
cervix. This is done for the next pregnancy once there is confirmation of a normal fetus, usually 12-14 weeks.
* Cervical cerclage taken out around 36 weeks, snip the stitch, remove, and she can go into labor. Do not wait until
she goes into labor because that could avulse the stitch out.
* Example of a bad outcome would be light anesthesia during placement of cervical cerclage stitches, the patient
could move causing the suture needle to rupture the membranes and thus terminate the pregnancy.
* Incompetent cervix: painless early pregnancy cervical dilation.
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Intrapartum Events: Obstetric Anesthesia
* Pain scores hourly in labor related to cervical dilation. Early in labor (1cm dilated), not much pain. Once dilation
gets > 2cm, pain increases greatly.
* Nerve roots involved in the pain of the first stage of labor are T10 to T12.
* T10 to T12 are nerve roots involved in uterine contractions and cervical dilation.
* Nerve roots involved in the pain of the second stage of labor are S2 to S4.
* S2 to S4 are nerve roots involved in the perineum.
* Stage one medications that can be used include narcotics. Usually narcotics given in stage 1 active phase (not
latent). You want to make sure things are progressing, so 4cm or more dilation. If you give in the latent phase, you
can end up with a prolonged latent phase.
* Giving narcotics too close to delivery can cause neonatal depression. We would like to allow at least an hour
between the last narcotic dose and delivery.
* Management of narcotic induced neonatal depression is with naloxone.
* Paracervical block is injection into the Frankenhauser ganglion on either side of the cervix to prevent the pain of
cervical dilation, using a local anesthetic.
* Most concerning side effect of a paracervical blood is build-up of local anesthetic and diffusion into fetus, causing
bradycardia. Classically you would watch the FHR on the monitor strip after giving the block and then see a
dropping deceleration. Treatment for this is tincture of time, local anesthetic will dilute and heart rate will rise. This
is not the time to do an emergency C-section.
* Pudendal block is injection of local anesthetic around the pudendal nerve with the needle transversing through the
vagina. The location of the pudendal nerve is not visualized, you assume it runs near the sacrospinous ligament. You
feel for the ischial spine, place needle, aspirate to ensure no vessel puncture, then inject at that point and again 1cm
over.
* Pudendal block usually done for second stage of labor.
* Epidural block done by placing needle millimeter-by-millimeter through ligamentum flavum until epigastric space
is reached. There will be loss of resistance once this space is reached. If you go too far, you will puncture the dura
(wet tap). Puncturing the dura causes a spinal headache.
* Once epidural space found, a single dose of anesthetic can be given or a catheter can be thread for continuous
infusion.
* Most common side-effect of epidural and spinal block is decreased blood pressure and sympathetic blockade.
Blocking the sympathetic nerves causes the vessels to open and drop BP, so adequately hydrate the patient.
* Management of hypotension from epidural or spinal block is ephedrine (vasospasm), patient in left lateral position,
give IV hydration to increase intravascular volume.
* Ensure patient has some dilation prior to giving narcotics or a spinal/epidural block. Else you can arrest labor.
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Postpartum Issues: Normal Changes
* Puerperium is time between delivery and the return to baseline physiologic function of the mother.
* Changes in the color of lochia after delivery are rubra (red), serosa (pink), and alba (white). Lochia is the shedding
off of the endometrial lining of pregnancy. It should not be bright red bleeding. It should be dark red initially (lochia
rubra), then pinkish after a few days (lochia serosa), then replaced with a whitish discharge (lochia alba).
* Physiology of stopping normal postpartum bleeding is via uterine contractions.
* Most common upper limits of post-partum bladder residual volume is 250mL. Up to 50mL in normal population.
More than 250mL is urinary retention, which can often occur after an epidural anesthetic.
* Pathophysiology of normal post-partum constipation is via decreased GI motility, pain, fluid mobilization. By the
time a pregnant women has finished the post-partum period she has lost 10L of fluid from her body.
* Management of post-partum constipation is stool softeners, not a bowel wall stimulant.
* Pathophysiology of normal post-partum hemorrhoids is via prolonged second stage pushing.
* Management of post-partum hemorrhoids is sitz bath, a warm water bath to sit perineum in and enhance
mobilization of blood flow to carry away the swelling.
* 1900g 31 week male in NICU on post-partum day #1, mom shows no interest in the baby. This is impaired
maternal bonding. A good question to ask the mother is “What is your baby’s name?” You expect the mother to
smile and say the name. If mother says, “I don’t know” or “I don’t care” this suggests problems with bonding and
needs to be followed up by social work.
* Risk factors for impaired maternal bonding are decreased neonatal contact and decreased social support.
* After delivery, let mother hold the baby even for a few seconds. Before baby goes to NICU, have mother hold the
baby again. This gets the initiation process going and can help reduce the risk of impaired maternal bonding.
* Spontaneous vaginal delivery of a term normal baby, post-partum day #1, mom cares for baby but is crying often.
This is post-partum blues, about 17% of the time.
* Management of post-partum blues is reassurance and encouragement.
* Post-partum day #21 after a term normal baby from spontaneous vaginal delivery, mom does not get out of bed
and does not care for herself or the baby. This is post-partum depression.
* Management of post-partum depression is anti-depressants, outpatient counseling is usually adequate.
* Post-partum day #21 after a term normal baby from spontaneous vaginal delivery, mom is showing bizarre
behavior and hallucinations. This is post-partum psychosis.
* Management of post-partum psychosis usually involves hospitalization and anti-psychotic medications. Patients
with post-partum psychosis are at high risk for recurrence after future pregnancies.
* Uterus normally is about 50 grams, right after birth it is about 1000 grams.
* Lochia comes from endometrial lining other than where the placenta is. It is shedding of the decidua superficial.
* Placental bleeding comes from the placental site, which is why you need uterine contraction to prevent
hemorrhage.
* Normal blood loss is 500mL for vaginal delivery, 1000mL for C-section, 1500mL for cesarean + hysterectomy.
* Estradiol levels rapidly decline after delivery. This causes engorgement of the breast. If there is no drop in
estradiol, there is impaired breast feeding.
* Do not put a patient who wants to breast feed on oral contraceptive pills because estrogen can prevent adequate
milk production.
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Postpartum Issues: Contraceptive Planning
* What is the length of time that post-partum lactation is associated with anovulation? 3 months if breast feeding, 3
weeks if not breast feeding.
* For post-partum vaginal contraceptive diaphragm fitting, wait 6 weeks for vaginal involution.
* For post-partum IUD placement, wait 6 weeks. There is a 20% expulsion rate if IUD is place right after delivery.
* Most common time post-partum for starting combination OCPs? Answer is 3 weeks if patient not breast feeding.
One reason is clotting factors still elevated so there is increased thrombosis risk.
* Most common time post-partum for starting progesterone-only methods? Answer is at any time.
* When do you give post-partum Rh immune globulin? Within 72 hours of delivery.
* 26yo G3 now P3 complains of lower abdominal pain 6 hours after spontaneous vaginal delivery with a midline
episiotomy. This is normal, just uterine contractions. Management is analgesics.
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Postpartum Issues: Hemorrhage
* Called about a patient who is bleeding heavily. First step is get IV access and open it wide with isotonic fluids.
* First step is feel for the uterus. If you cannot feel the uterus, this is uterine inversion (rare).
* Treatment of uterine inversion is elevate the vaginal fornices and give oxytocin to cause contractions. Then push
uterus back up if possible and stabilize uterus from above, surgically if needed.
* Signs of third stage of labor are lengthening of umbilical cord, gush of blood, and uterine balling (globular,
firming, uterus rises in the abdomen).
* Bleeding with a boggy (“feels like dough”) uterus is uterine atony, the most common cause of post-partum
hemorrhage (50%).
* Management of atonic uterus is by uterine massage, smooth muscle responds to tactile stimulation. Then give
medications, oxytocin first, then methylergometrine or ergot, then prostaglandin (carbaprost, 15 methyl F2 alpha,
injectable).
* Management compression (bimanual) of the uterus to reduce hemorrhage during uterine atony involve “punching”
the uterus up through the vagina with one hand and pushing down on the abdomen with the other hand.
* Bleeding with firm palpable fundus. Think about incomplete placenta, retained placenta. Examine the placenta
after delivery, both the maternal and fetal side. The maternal side has cotyledons, leaf-like chunks. If you see a
cotyledon missing, think that it might still be in the mother. Observe the placenta fetal vessels to see that they
terminate prior to the edge of the membrane. If you see the vessels extending over, this may imply an accessory lobe
to the placenta.
* With retained placental pieces, do manual removal or curettage. If there is retained placenta, think about placenta
accreta, placenta increta, placenta percreta. This is abnormal trophoblastic invasion.
* Bleeding with normal uterus and placenta is intact. Think about undiagnosed tears of the perineum, vagina, cervix.
This is the second most common, 20% of post-partum bleeding.
* Risk factors for post-partum lacerations are uncontrolled delivery (baby comes flying out), forceps delivery.
* Risk factors for uterine atony are a tired uterus (oxytocin going for hours), infected uterus (chorioamnionitis),
overdistended uterus (twins, macrosomia).
* Post-partum bleeding, uterus feels firm, placenta intact, no lacerations. You see diffuse oozing from the IV site
and some petechia on the skin. Think DIC (rare). Most common obstetrical cause of DIC is abruptio placenta. Other
causes include amniotic fluid embolus and prolonged retention of a dead fetus.
* Management of DIC is supportive care. Remove the products of conception (POC). Move patient to ICU. Give
blood products if she needs them.
* Post-partum bleeding, uterus feels firm, placenta intact, no lacerations, no DIC. This is unexplained hemorrhage
(rare). This is surgical management, start ligating vessels and consider a hysterectomy if uncontrolled. Ligating the
uterine artery on both sides is safe because of collateral circulation. If that does not work, think about ligating the
internal iliac vessels. Do not start messing around in the retroperitoneum unless you know what you are doing else
you’ll get big time bleeding.
* Post-partum hemorrhage, just delivered twins, uterus feels like dough: uterine atony.
* Most common cause of excessive post-partum bleeding is atonic uterus. Risk factors are rapid or protracted uterus.
* Medications that can cause atony are magnesium sulfate and halogenated general anesthetics (e.g. halothane).
* Management of uterine atony is massage and uterotonics (oxytocin, ergot, methylergometrine, carbaprost).
* Post-partum hemorrhage, uncontrolled vaginal delivery, uterus feels firm: perineal laceration.
* Management of post-partum lacerations is surgical repair.

* Post-partum hemorrhage, placental vessels extend over membrane edge, uterus feels firm: retained placenta.
* Management of retained placenta is manual removal.
* Post-partum hemorrhage, abruption placenta, blood oozing from IV site: DIC.
* Post-partum hemorrhage, beefy bleeding vaginal mass, cannot feel uterus: inverted uterus.
* Management of uterine inversion is uterine replacement and oxytocin.
* Management of unexplained post-partum hemorrhage is surgical, ligation of uterine vessels, then internal iliac
vessels, and finally hysterectomy.
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Postpartum Issues: Fever
* Ignaz Semmelweis was a Hungarian obstetrician who lived in Vienna in 1800s. At that time they had a midwife
delivery service and a medical delivery service. He found that 1-2% of women delivered by midwives died of post-
partum infection, and 20% of women delivered by the medical team died. This was before they knew about bacteria
and sepsis. The medical team would do autopsies of the women who died the night before then come in without
washing their hands and examine women in labor. So they were inoculating the women in labor. One doctor was
doing an autopsy, the knife slipped and he cut himself. That doctor got a fever and died. The autopsy on him looked
exactly like the women who had died from childbirth fever. He insisted that the residents and physicians start
washing their hands in chlorinated lime and immediately the death rate dropped. He wrote up the article but was a
bit weird and it wasn’t published prior to his death in an insane asylum.
* Day 0 post-partum fever. Are there crackles in the lungs? Atelectasis, no need for CXR. Treat atelectasis with
ambulation and pulmonary exercises (deep breaths). This is more likely in C-section.
* Day 1-2 post-partum fever. Dysuria? Urinary tract infection, pyelonephritis. Get urinalysis and culture. Treat with
single agent IV antibiotics. Risk is highest in patient with multiple catheterizations in labor, multiple vaginal exams,
and with indwelling catheter (C-section).
* Day 2-3 post-partum fever. Tender uterus? Endometritis, no need for cultures because you know what will grow.
Treat with broad-spectrum, IV gentamycin (Gram negatives) and clindamycin (Gram positives and anaerobes).
There should not be peritonitis. More commonly seen in C-section patients.
* Day 4-5 post-partum fever. Wound purulence? Culture wound drainage, wound infection. Treat wound infection
by opening wound to clear pus, saline soak packs in wound, start antibiotics.
* Day 5-6 post-partum fever. Pelvic mass? Pelvic abscess, do ultrasound or CT scan. Patient has spiking fevers, on
double or triple antibiotics, wound looks good, uterus not tender. Treatment is percutaneous drainage.
* Fever, no atelectasis, no UTI, uterus nontender, wound clean, no abscess found. Patient continues to have picket-
fence fever (undulating up and down over time). This is septic pelvic thrombophlebitis, a diagnosis of exclusion.
Patient may feel fine. Treatment is heparin to increase PTT by 1.5-2x baseline. Fever should drop in 24-48 hours.
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Study Notes Obstetrics Gynecology

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What are some common problems encountered in obstetrics and gynecology?

What are some common problems encountered in obstetrics and gynecology?

What are some procedures discussed in the notes?

What are some procedures discussed in the notes?

Study Notes – Obstetrics & Gynecology James Lamberg 28Jul2010

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Fallopian Tube Cancer

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* Stage IVA is bladder or rectum involvement. Stage IVB is metastatic disease.

dissolve by themselves in a couple of months.

danazol/danocrine. Patient will complain about testosterone side-effects like hirsutism.

too much estrogen in the pre-menopausal group to use tamoxifen effectively.

* Robertsonian translocation is centric fusion of acrocentric chromosomes. We lose a chromosome as far as

oxygenated blood in fetal circulation almost first.

Obstetrical Complications: Multiple Gestation

inspection. On exam her temperature is 102F.

should not be treated.

you’ll also be giving the woman a vaginal yeast infection.

finger all the way around.

* Management of post-partum lacerations is surgical repair.

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