Textbooks: Essentials of Ob/Gyn, Ob/Gyn Secrets, First Aid for Ob/Gyn Clerkship
--- 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
--- Procedures: NEJM Videos In Clinical Medicine: http://www.nejm.org/multimedia/videosinclinicalmedicine --- 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. --- 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.
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)
--- 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.
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.
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.
--- Kaplan Videos (2001) – Gynecology with Dr. Manuel Penalver, MD
---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 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.
---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.
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.
---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. ---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.
---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.
---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.
* 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.
---Vulvar Cancer
* Vulva: cancer etiology is HPV.
* Most common symptom is pruritus (itchiness).
* Histology is squamous cell cancer. Second most common is melanoma. * Mortality commonly caused by metastatic disease.
* Pre-cancer is dysplasia/carcinoma in situ.
* 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.
---Vaginal Cancer
* Vagina: cancer etiology is HPV.
* Most common symptom is bloody vaginal discharge. * Histology is squamous cell cancer.
* Mortality commonly caused by metastatic disease. * Pre-cancer is dysplasia/carcinoma in situ.
* 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.
---Fallopian Tube Cancer
* Fallopian Tube: cancer etiology is unknown.
* Most common symptom is clear serous vaginal discharge. * Histology is adenocarcinoma.
* Mortality commonly caused by metastatic disease.
* 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.
---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 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. ---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. ---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.
---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.
---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.
* 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.
---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.
* 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.
---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.
---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.
---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.
---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.
---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.
---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.
---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.
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
