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259 Cards in this Set

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Describe the hormonal sequence of events leading to ovulation and the formation of the corpus luteum:
Name 3 causes of anovulation:
- Central
Inhibition of GnRH pulsatile secretion
(Due to excess CRH in stress response)
Elevated prolactin
Immature GnRH pulsatility
- Abnormal signals
Estrogen levels don’t cycle normally e.g. extraglandular estrogen production
- Local ovarian responses
Elevated local testosterone
Local tumor
Name 4 signs in the presentation of anovulation:
Amenorrhea
Hirsutism (from excess testosterone)
Dysfunctional Uterine Bleeding
Infertility
Name 3 causes of anovulation:
- Gyn cancer
- Endometrial hyperplasia
- Polycystic ovarian syndrome
Describe the process through which overproduction of androgens in the theca cells can inhibit ovulation:
Appearance of PCOS on an ultrasound:
Ultrasound shows lots of little follicles and hypertrophic stroma.
Overactivation of what enzyme in ovarian theca cells contributes to PCOS?
17-a-hydroxylase
What common chronic disease is associated with PCOS regardless of weight and why?
Diabetes;
Insulin resistance results in compensatory hyperinsulinemia, which stimulates ovarian androgen production in an ovary genetically predisposed to PCOS.
What is another name for polycystic ovary syndrome?
Stein-Leventhal syndrome
Describe the appearance of the ovaries in a patient with PCOS:
Ovaries are twice the normal size, are gray white and studded with subcortical cysts.
The cysts themselves are lined with granulosa cells with a hypertrophic and hyperplastic luteinized theca interna. (Theca interna cells express receptors for luteinizing hormone (LH) to produce androstenedione, which via a few steps, gives the granulosa the precursor for estrogen manufacturing) There is a conspicuous absence of any corpus luteum.
What levels of androgens, LH, FSH and estrogen would you expect to see in a patient with PCOS?
- High androgens (from overproduction and increased LH)
- High estrogen (from increased peripheral conversion in fat)
- Low FSH (inhibited by estrogen)
- High LH (positive feedback from increased testosterone)

* So, increased production of androgens increases LH, which in turn increases production of androgens....
Describe the rather circular connection between insulin resistance and increased androgen production in the ovaries:
- IR is seen in 30% of lean and 75% of obese patients with PCOS
- Hyperinsulinemia is most marked in obesity
- Hyperinsulinemia directly and indirectly stimulates ovarian and adrenal secretion of androgens and lowers SHBG levels
- Increased androgens in the ovary cause follicular atresia leading to anovulation , irregular menses, and infertility
- Anovulation increases risk for endometrial cancer
- Increased androgens in the periphery cause hirsutism, acne, weight gain…and more insulin resistance!
Flowchart detailing the mechanism of hyperinsulinemia leading to increased androgen production:
Name 3 symptoms that may be required in order to diagnose PCOS:
- Hyperandrogenism*
- Oligomenorrhea or amenorrhea*
- Polycystic ovaries on ultrasound

* Required for diagnosis by the NIH
Name 3 risk factors for development of PCOS:
1. Premature adrenarche (hallmark sign)
2. Family history
3. History of weight gain in perimenarchal period
Clinical presentations of PCOS:
- Menstrual disorders
- Infertility/pregnancy complications
- Hirsutism
- Severe acne
- Androgenic alopecia
- Insulin resistance/associated complications (metabolic syndrome, obesity, type II diabetes, CV disease)
- Endometrial disease
- Mood disturbances/depression
What skin condition might be seen on a patient with PCOS?
Acanthosis nigricans
What chronic disease should you screen for in a patient with PCOS?
Diabetes
Lab tests to run to rule out differential diagnosis of disorders other than PCOS:
If when evaluating a patient for PCOS the androgen levels come back normal, what would getting a FSH level be usefule for?
Obtain an FSH if evaluating primary amenorrhea or prolonged secondary amenorrhea in absence of androgen excess
- Will be elevated in premature ovarian failure or ovarian agenesis
- LH/FSH ratios are not valuable for diagnosing or managing PCOS
- Up to 40% of women with PCOS have a normal LH/FSH ratio
What is the most common cause of anovulatory infertility?
PCOS
What percentage of women of childbearing age are effected by PCOS?
5-10%
The effect of obesity of the ovaries and the endometrium:
What are 5 criteria for diagnosis of metabolic syndrome (often seen with PCOS)?
Elevated BP (130/85)
Increased waist circumference (35 inches)
Elevated fasting glucose (100 mg/dL)
Reduced HDL (50 mg/dL)
Elevated Triglycerides (150 mg/dL)
Treatment goals for patients with PCOS:
- Reduce risk of diabetes and metabolic syndrome
- Correct abnormal bleeding
and reduce risk of endometrial cancer
- Correct symptoms of hyperandrogenism;
reduce acne and hirsutism
- Improve acanthosis nigricans
What one intervention can reduce multiple symptoms of PCOS?
Weight loss
Why are oral contraceptives used to treat PCOS?
- Suppresses LH and ovarian androgen secretion
- Inhibits androgen binding
- Increases SHBG
- Reduces acne/hirsutism
- Progesterone prevents endometrial hyperplasia and reduces endometrial cancer risk
*The estrogens in birth control pills are given at a very high dose; this is why the pill will increase SHBG and the endogenous increase in estrogens normally seen in PCOS would not.
Why would Yasmin be a good choice of OC for PCOS patients?
- Contains drospirenone, a progesterone with spironolactone- like properties
- Associated with weight loss and improved acne and decreased hirsutism compared to desogestrel OC
- Associated with decreased androgen production from the adrenal glands by inhibition of ACTH
Why would metformin be a good choice of medication to treat PCOS?
- In skeletal and adipose tissue, insulin resistance leads to a decreased glucose uptake and increased lipolysis,
- The ovary, adrenal, liver, and skin remain insulin sensitive leading to anovulation and increased androgen production
- Decreases fasting insulin levels
- Decreases LH and free testosterone
- Improve glucose tolerance
- Decrease IR lowering androgen levels and improve lipids
- Restore normal menses and fertility
- Weight loss or stabilization
What are some potential disadvantages of metformin?
- GI disturbance in 1/3 of patients
- Generalized feeling of malaise
- Decreased absorption of Vit B12
- Lactic acid build up

* Not as effective in teenagers for weight loss; first line in teens is OC.
What 3 drugs may be used to reduce hirsutism?
Spironolactone, Flutamide and Finasteride (all antiandrogens)
* These drugs are teratogens and are contraindicated in pregnancy; may result in incomplete virilization of a male fetus
What two drugs may be used to treat acanthosis nigricans?
LacHydrin lotion and RetinA
What two drugs may be used to induce ovulation in patients with PCOS?
1. Clomiphene (with or without metformin)
2. Exogenous gonadotropins
Define amenorrhea, oligomenorrhea, menorrhagia, polymenorrhea and metrorrhagia:
- Amenorrhea: no menses for 6 months
- Primary amenorrhea: Never menstruated
- Secondary amenorrhea: Menstruated in past then stopped
- Oligomenorrhea: menses every 35 days -6 months
- Menorrhagia (hypermenorrhea): prolonged (>7 days) or heavy (>80 cc) of uterine bleeding occurring at regular intervals
- Polymenorrhea: bleeding occuring more often then every 21 days
- Metrorrhagia: irregular menstrual bleeding
H-P-O-U axis for diagnosing cause of amenorrhea:
- Hypothalamus
Disorders affecting GnRh pulsatility
- Pituitary
Disorders affecting FSH,LH, TSH
Adenomas
- Ovary
PCOS
Ovarian failure
- Uterus
Anomalies of outflow (imperforate hymen, transverse septum)
Absence of uterus (Müllerian agenesis, also known as Rokitanski-Kuster-Hauser-Meyer)
In determining the reason for amenorrhea, why is determining the presence or absence of breasts and/or a uterus helpful?
- In patients presenting with primary amenorrhea, the presence of breasts indicate the presence of estrogens
- In patients with primary amenorrhea, the presence of a uterus implies the absence of testes, and indicates that there is a hormonal reason for amenorrhea.
A 17 year old girl presents with primary amenorrhea. She has no breast development and has a normal vagina and uterus. Her FSH is 80 mIU/mL. Which of the following diagnosis would be most likely?
1. Androgen insensitivity
2. Gonadal dysgenesis
3. Mullerian agenesis
4. PCOS
Gonadal dysgenesis
A 16 year old presents with primary amenorrhea. She has breast development but no uterus. She has normal pubic hair. Her FSH is 4. Her serum testosterone is 30 pg/dL. Her probable diagnosis is:
1. Androgen insensitivity
2. Gonadal dysgenesis
3. Müllerian agenesis
4. PCOS
Mullerian agenesis
An 18 year old girl presents with primary amenorrhea. She has breasts but no uterus. She has sparse pubic hair. Her serum testosterone is 400 pg/mL. What is her probable diagnosis?
1. Androgen insensitivity
2. Gonadal dysgenesis
3. Müllerian agenesis
4. PCOS
Androgen insensitivity
A 15 year old has minimal breast development, has a uterus, and has not menstruated. Her FSH is 2 mIU/mL. Which of the following is the most likely cause of her amenorrhea?
1. Anorexia
2. Obesity
3. Turner syndrome
4. Müllerian agenesis
Anorexia
A 17 year old had adrenarche and thelarche at age 9, has had 3 menses per year since then. She has a BMI of 39.5. She has acathosis nigricans and significant acne. Which of the following lab tests would be most useful?
1. FSH
2. Free T4
3. 2 hour GTT
4. Estradiol
2 hour GTT
A 25 year-old patient reports she had regular menses until 1 year ago at which time they became less frequent and stopped altogether 6 months ago. She has noticed some spontaneous leakage of milk from her breasts. She wants to conceive. Which medication would you prescribe?
1. Tamoxifen
2. Letrazole
3. Cabergoline
4. Oral contraceptives
Cabergoline
Chart detailing gynecological causes of abnormal bleeding:
Effects of elevated progesterone and estrogen on abnormal bleeding:
What STI causing intracellular parasite may be a cause of abnormal uterine bleeding?
C. trachomatis
Non-gynecological causes of abnormal uterine bleeding:
A 46 year-old obese woman presents with increasingly heavy frequent menses. On exam you feel an enlarged, irregular uterus. Her last pap test was 6 months ago and normal. Her Hgb is 8 mg/dL. Which 2 studies would you do next?
1. FSH, MRI
2. Prolactin, Ultrasound
3. Pap test, MRI
4. Endometrial biopsy and ultrasound
Endometrial biopsy and ultrasound
A 12 year old girl presents to the emergency room, pale and dizzy. She has been bleeding heavily for 4 days. This is her first menses. Which of the following tests should you order?
1. 17α-hydroxy-progesterone
2. Von Willebrands Panel
3. Protein C and S levels
4. FSH
Von Willebrand panel
A 32 year-old presents with previously normal menses and complaints of persistent irregular bleeding and bleeding after intercourse for 2 months. Her last pap test was 4 years ago. She is sexually active and on oral contraceptives. Where do you predict the problem lies?
1. Hypothalamus
2. Pituitary
3. Ovary
4. Uterus
Uterus
A 40 year-old woman presents with irregular heavy menses. She has diabetes and hypertension. She had a normal TSH and FSH, pap test and ultrasound. An endometrial biopsy showed simple hyperplasia without atypia. Which therapy would be best next step?
1. Levonorgestrel IUD
2. Oral contraceptives
3. Hysterectomy
4. GnRH agonist
Levonorgestrel IUD
Histology of acute cervicitis:
Histology of chronic cervicitis:
Metaplasia is present; because there is a squamous covering above endocervical tissue - should be endocervical tissue throughout.
Histology of inflammatory lesions of the endocervix:
When the ducts get blocked this causes the gland to dilate.
Identifying infections in a Pap Smear:
Reparative vs radiation changes in cells on Pap test:
Atrophy and atrophic vaginitis on a Pap smear:
HPV vaccine recommendations:
Other malignancies of the vulvar region:
- Malignant melanoma of Vulvar region
Malignancy of melanocytes similar to those seen elsewhere in skin (refer to S-5 content)
Often presents with poor prognosis as discovered late in vertical growth phase
Differential diagnosis includes Paget and squamous Ca
- Paget disease of vulva
- Vaginal adenocarcinoma: DES exposure
- Embryonal rhabdomyosarcoma (sarcoma botryoides): uncommon vaginal tumor in children
Vulvar Paget's Disease:
Vaginal Clear Cell Carcinoma:
Embryonal Rhabdomyosarcoma:
Lower genital SLM test your knowledge slide:
Pregnancy termination options based on gestational age:
Efficacy of abortion options:
- Both surgical and medication abortion are highly effective in achieving complete abortion.
MVA at < 6 weeks is 99% effective (Edwards and Creinin), the same rate at < 10 weeks.
- At later gestational ages, medication abortion is less effective:
With oral misoprostol: effective through 7 weeks’ gestation (91%–97% at < 49 days’ gestation; 88% at < 63 days’ gestation)
With vaginal misoprostol: effective through 9 weeks’ gestation (98% at < 49 days’ and at < 63 days’ gestation)
Formation of the blastocyst:
Invasive nature of trophoblasts:
Definitions of gestational trophoblastic disease and neoplasia:
- Gestational trophoblastic disease:
Pregnancy-related trophoblastic proliferative abnormalities
Derived from Placental Trophoblasts
Includes:
Hydatiform moles (Molar pregnancies)
Complete mole
Partial mole
- Malignant Gestational Trophoblastic Neoplasia (GTN)
Refers to lesions that have ability to invade locally or cause distant metastases
Includes:
Invasive moles
Gestational choriocarcinoma
Placental site tumors
Name 2 risk factors for hydatiform moles:
- Age less than 15 or greater than 45
7.5 X higher risk in women over 40
- Previous molar pregnancy
Risk of repeat molar pregnancy is 1%
Formation of a complete hydatiform mole:
What kind of villi and fetal tissue would you find in a complete mole?
What kind of cysts would you find in the ovaries of a woman with a complete mole?
How is a partial hydatiform mole formed?
- Forms when 2 (haploid) sperm fertilize a single (haploid) egg
- Triploid karyotype (69XXY, 69XYY, 69XXX)
What kind of villi and fetal tissue would you expect to find in a partial mole?
Clinical presentation of a molar pregnancy:
- Uterine bleeding, usually in the second trimester (12-16 weeks)
- Enlarged uterus for gestational age, often softer than normal
- Absence of fetal activity felt by mother. (This is usually felt at 17-20 weeks but can be slightly earlier in women who have had previous pregnancies).
- Hyperemesis gravidarum (nausea and vomiting)
Due to elevated hCG
- Hyperthyroidism (2% of complete moles)
Elevated plasma thyroxine levels due to thyrotropin –like effects of hCG
- New onset of gestational hypertension
Rare in early gestation(before 20 weeks), if present, consider mole
Evaluation of a possible molar pregnancy:
- Take a full history and review of symptoms. Be sure to get date of last menses.
- Physical exam
Vital signs
Look for hypotension (volume loss from bleeding or vomiting) or hypertension (pre-eclampsia)
Evaluate for tachycardia (volume loss from heavy bleeding or thyrotoxicosis)
Dyspnea or tachypnea (pulmonary edema)
- Physical exam
Gentle speculum exam to evaluate source of bleeding and quantify amount of active bleeding
Bimanual exam to evaluate uterine size
Useful lab tests to evaluate a molar pregnancy:
Laboratory studies:
- Complete blood count (CBC)
- Blood type and Rh (type and screen, consider type and cross match to have blood ready for surgery)
- Serum quantitative hCG
Can be useful for diagnosis
Is needed for follow-up evaluation
May have implications for prognosis
- Clotting function studies
- Renal and liver function tests
- Chest X-ray
Evaluate for pulmonary edema and metastases
What might a high Hcg level tell you about a pregnancy?
Hcg peaks around 9-10 weeks because that is when placenta takes over production from corpus luteum.
Appearance of a mole on ultrasound:
What is the treatment for a hydatiform mole?
Suction curettage
Why is it important to follow Hcg levels after treatment of a molar pregnancy?
- Follow serial quantitative hCG levels until zero for 6 months
- Ideally obtain levels every 1-2 weeks until zero, then every 1-2 months for 6-12 months
- Provide adequate contraception while monitoring levels
- This is important as invasive mole or choriocarinoma (malignant gestational neoplasia(GTN)) follows 15-20% of complete moles and is detected by the hCGs
Only 5% of partial moles will develop postmolar malignant GTN
What are the 3 types of gestational trophoblastic neoplasia?
Invasive mole (most common)
Choriocarcinoma
Placental site trophoblastic tumor
Characteristics of an invasive mole:
What is the treatment for an invasive mole?
Characteristics of a choriocarcinoma:
- Def’n: Carcinoma of the chorionic epithelium
- Pathology
Cytotrophblasts and syncytiotrophoblasts
No chorionic villi
- Hemorrhage
- Behaves like a sarcoma-invades aggressively and spreads hematogenously
Detection of a choriocarcinoma:
- Choriocacinoma can occur after any type of pregnancy:
50% occur after molar pregnancy
25% occur after an apparently normal pregnancy
25% occur after an abortion
- Detected by persistently elevated hCG levels or abnormal bleeding
Gestational choriocarcinoma:
Placental Site Tumor:
Will not respond to chemotherapy.
Difference is that invasive mole comes after molar pregnancy, while placental site tumor comes after normal pregnancy.
Comparison of complete vs. partial moles:
Comparison of invasive mole, choriocarcinoma and placental site tumor:
Characteristics of Lichen Sclerosis:
- Benign epithelial disorder that can occur at any age (mean age of onset in fifth to sixth decade)

- Chronic condition

- Autoimmune process or possible genetic link (see increased rates of alopecia, vitiligo, hypothyroidism, thyrotoxicosis, pernicious anemia)
Images of early and late Lichen Sclerosis:
Histology of Lichen Sclerosis:
Of the following options, the one most recommended for the treatment of lichen sclerosus is?
1. Topical estrogen
2. Topical testosterone
3. Topical progesterone
4. Oral steroids
5. Topical steroids
Topical steroids (Clobetasol cream/ointment)
The risk of vulvar cancer in women with lichen sclerosus is?
1. Similar to women without LS (<0.1%)
2. 4-5%
3. 10-15%
4. 25%
5. 50%
4-5%
How does Lichen Sclerosis progress to Vulvar Cancer?
- Vulvar LS is a chronic inflammatory process ass'd with scarring and as such can give rise to carcinoma (this process has been well documented). As a chronic inflammatory scarring dermatosis, vulvar LS could act as a both an initiator and promotor of carcinogenesis.
- Not usually HPV mediated
- Simplex vulvar intraepithelial neoplasia (VIN) is a precursor lesion to vulvar cancer.
What are the 2 types of VIN?
Comparison of warty and simplex VIN:
How are the 2 types of VIN named?
The warty type is just called VIN.
The simplex type is called differentiated VIN.
Which type (warty or simplex) of VIN has a higher chance of progressing to cancer?
Simplex
Vaginal Cancer:
A small proportion of adenocarcinomas are clear cell carcinomas arising in women exposed to DES in utero. The highest incidence of clear cell carcinoma arises in young women in their late teens and early 20s.
Lichen simplex chronicus:
Histology of lichen simplex chronicus:
What is the treatment for lichen simplex chronicus?
Topical medium strength steroids PLUS Fluconazole for prophylaxis of candida.
Bartholin Cyst:
What is the best treatment for a Bartholin cyst?
Insertion of a "Word" catheter to allow for drainage of the cyst.
Comparison of the cytology of LSIL, HSIL and SCCa:
As cells become more abnormal they:
become smaller than normal basal cells
Have an increased N/C ratio: Dense, opaque chromatin with a small rim of cytoplasm
Clump together in sheets with poorly defined borders
Low grade changes detected on colposcopy:
High grade changes detected on colposcopy:
How does application of acetic acid visualize abnormal cervical cell?
When acetic acid is applied, it dehydrates the cells --> light cannot penetrate the dehydrated cells with overlapping enlarged nuclei (enlarged because they are abnormal cells!!)
A 22 year old G1P1 presents with LSIL. How would you manage her?
1. Repeat cervical cytology in one year
2. Repeat cervical cytology in six months
3. Perform colposcopy
4. Perform HR HPV test and manage based on test
Perform colposcopy
Treatment algorithm of LSIL:
1. Normal
2. CIN 1
3. CIN 3
4. Carcinoma
CIN1

Management of CIN1 in a young woman = watch and wait
A 32yo G3P2 presents for her annual exam. Her last Pap was negative 3 years ago. Her cervix looks grossly normal. Her Pap test returns abnormal. Possible management options include:
A. Colposcopy
B. HPV DNA testing
C. Excisional procedure
D. Cryosurgery
Colposcopy and/or excisional procedure
Treatment algorithm for HSIL:
1. Normal
2. CIN 1
3. CIN 2 or 3
4. Carcinoma
CIN 2 or 3
What is the definition of infertility?
The inability to conceive after 1 year of unprotected sex.
What is the definition of fecundability?
- The probability of achieving a a pregnancy within one menstrual cycle
- 25% in normal couples
What is considered a "normal" sperm sample?
2 cc
20 million sperm/cc
50% motility
40% morphology
Reasons for male infertility:
Varicocele
Idiopathic
Gonadal Failure
Hypogonadal hypogonadism
Obstructive anomalies
Retrograde Ejaculation
Spinal Cord Injury
Environment
Hysterosalpinogram:
A dye is inserted into the uterus and allowed to flow out of the fallopian tubes; used to assess patency of the tubes in an infertility workup.
What is Asherman syndrome and how does it relate to infertility?
Asherman's is when the basal layer of endometrium has been scraped away by too many D&C's so that there is no longer any proliferation and nothing for the egg to implant in.
How can basal body temperature tracking be used to predict ovulation?
Right after ovulation there is a temperature spike of about 0.5 – 1 degree.
The spike in temperature comes from an increase in progesterone; not LH!!!!!
How do ovulation prediction kits work?
- Measures the secretion of LH
LH surge early in the morning
- 90% accurate
- Highest fecundity is on the day of the positive LH surge
What is the average age of menopause?
51
When do the first oocytes appear in a female fetus?
- Meiosis occurs such that the first oocytes appear at ~15 weeks in the female fetus
- Primordial follicles appear at ~20 weeks
- Follicular growth and oocyte atresia begins soon after the appearance of the primordial follicles
- Decrease in oocyte number begins then and continues until menopause
What are the 3 types of menopause?
Describe what happens to Inhibin, FSH and LH levels during the transition to menopause:
Stages of reproductive aging:
What is the definition of spontaneous (normal) menopause?
Occurs after 12 consecutive months of amenorrhea for which no other obvious pathologic or physiologic cause exists
Characteristics of premature ovarian failure:
Q)An appropriate concern to discuss with a women newly diagnosed with primary ovarian insufficiency is:

A) Contraception
B) Cost
C) Cancer
D) Removal of the ovaries
Contraception; because ovarian insufficiency can reverse itself suddenly
Hormone and syptom changes during the progression of menopause:
What causes hot flashes to occur during menopause?
A decline in estrogen. Replacing the estrogen alleviates hot flashes.
What kind of effect can a decrease in estrogen cause on mood and memory?
In the perimenopausal period, mood disorders are more pronounced (may be related to distressing symptoms/insomnia).
Short term memory problems improve with replacement estrogen and early use of HRT in the first decade decrease chances of developing Alzheimer's
What do osteoclasts do?
Break down bone to increase serum calcium (resorption)
What do osteoblasts do?
Build up bone
What is a Dexa scan?
A scan to determine bone density
What are some of the effects of decreased estrogen on the urogenital tract?
- With decreased estrogen, epithelium becomes pale, thin, less elastic, and dry; vaginal pH increases
- Loss of collagen, adiposity
- Dryness, irritation, painful intercourse, discharge
What are some alternative treatments for symptoms of menopause?
What is the difference between hypoactive sexual desire and sexual aversion disorder?
- Hypoactive sexual desire: Persistence or recurring deficiency or absence of thoughts or fantasies or receptivity to sexual activity that causes personal distress.
- Sexual aversion disorder: Persistent or recurring phobic aversion and avoidance of sexual contact, which causes personal distress. It is often due to trauma or sexual abuse.
Important questions to ask when evaluating a woman with low sexual desire:
- “When did you notice a change in your sexual desire?”
- “Does anything appear to improve your sexual desire or make it worse?”
- “How is this problem affecting you? Are you concerned about or bothered by it?”
- “Have you seen anyone else about this problem? If so, what was suggested? What steps were taken?”
Relationships between gynecological and breast conditions and low libido:
Are laboratory tests useful in diagnosis of hypoactive sexual desire disorder?
- A diagnosis of hypoactive sexual desire disorder is established by its symptoms and circumstances; there are no specific laboratory tests recommended for assessing HSDD.
Assessment of total testosterone may be supportive but is not consistently indicative of HSDD.
Sex hormone–binding globulin (SHBG) and the free androgen index are rarely helpful and should not be ordered.
Medications that can effect desire and arousal:
- Medications that can cause disorders of desire
Psychoactive meds: Antipsychotics, barbituates, Benzodiazepines, SSRIs, Lithium, TCAs
Cardiovascular meds: Anti-lipid meds, beta blockers, clonidine, digoxin, aldactone
Others: H2 blockers, indocin
Hormonal meds: OCs. GnRH agonists/antagonists
- Medications that can cause disorders of arousal
Anticholinergics
Antihistamines (can dry out mucous membranes)
Antihypertensives
Psychoactive meds as above
How do oral contraceptives decrease libido?
Lower free testosterone levels*
Serotonin effects
Direct progesterone effects

*An increase in estrogen from the OC's causes and increase in SHBG; SHBG binds up testosterone --> decreased libido
How can decreased libido caused by OC's be treated?
- Consider using more androgenic progesterone (levonorgestrel), e.g. LoOvral
- Reduce estrogen dose (30 mcg to 20mcg)
- Try progesterone only pill
- Discuss vaginal dryness and recommend lubricant
- Cycle off for a month and keep diary to be sure it is a pill effect.
When is testosterone treatment of decreased libido recommended?
- Recommended in oophorectomized women and postmenopausal women who have not responded to estrogen therapy alone
- 5-35% of patients can have side effects of , lower HDL, acne, hirsutism, clitoromegaly, voice deepening
- Therapeutic options:
Estratest or Estratest HS
Methyltestosterone 1.25 to 2.5 mg daily
Micronized oral testosterone 5 mg bid
Topical testosterone proprionate 2% daily
Injectables
- Check liver enzymes and lipid levels q 6-12 months
Female pelvic floor muscles:
What part of the nervous system is the female orgasm regulated by?
The involuntary or autonomic nervous system
What are the 4 different classifications of anorgasmia?
- Primary : Orgasm has never been achieved
- Secondary: Orgasm has been achieved in the past
- Absolute: Orgasm impossible in all situations
- Situational: Orgasm impossible only in certain situations
Medical causes of anorgasmia:
Medications that cause anorgasmia:
Methyldopa (Aldomet)
Amphetamines and related anorexic drugs
Antipsychotics
Benzodiazepines
Selective serotonin reuptake inhibitors
Narcotics
Trazadone (Desyrel)
Tricyclic antidepressants
Examination of the patient with Dyspareunia:
What is the difference between active and passive immunity?
- Active:
Type associated with
common vaccines
Slow - stimulates
immune response
Induces memory
- Passive:
Rapid - antibody from another host
Temporary- antibody is gradually lost due to breakdown, no memory
What type of Ig is transferred across the placenta? What type is transferred via breast milk?
IgG goes across the placenta; IgA via breast milk
How is maternal IgG transferred across the placenta?
How does maternal IgA enter breast milk?
Immunoglobulin levels in infancy and childhood:
Sites of hematopoisis during fetal development:
Which part of the immune system are functional or non-functional in neonates?
What test is used to detect anti-Rh antibodies in a mother's serum and how does it work?
What is Rhogam used for and how does it work?
Rhogam = an anti-D gamma globulin fraction of pooled human plasma. It mops up Rh+ fetal RBC's in maternal circulation.
In cases of recurrent abortion, when would anti-phospholipid antibody syndrome be suspected?
- One or more unexplained deaths of a morphologically normal fetus at or beyond the 10th week of gestation.
- One or more premature births of a morphologically normal neonate before the 34th week of gestation because of eclampsia, pre-eclampsia or placental insufficiency
- Three or more unexplained consecutive spontaneous abortions before the 10th week of gestation

**Frequently associated with other autoimmune diseases associated with high levels of pro-inflammatory cytokines such as thyroid autoimmunity, SLE, and Sjogren’s syndrome.
If the fetus is considered an allograft, why doesn't the maternal immune system reject it?
Possibilities:
- Trophoblast does not contain MHC antigens
- Uterine decidua is an immunologically privileged site (like brain, eye, testis)

*Maintenance of fetus as allograft is due in part to suppression of anti-fetal immune response by regulatory T cells, and anti-inflammatory cytokines
What evidence exists for the suppression of the maternal immune system as an explanation for non-rejection of the fetal allograft?
What are the definitions of early pregnancy failure?
PTD= preterm delivery. These women are also at risk for low birth weight infants.
KNOW THIS SLIDE!!
What is an anembryonic pregnancy?
Ultrasound appearance of an embryonic demise:
What is the most common cause of spontaneous abortion?
Genetic abnormalities

- Overall most common cause
- Up to 50-70% of all spontaneous abortions
- Most common abnormalities
Autosomal trisomies (64%)
Polyploidy (9%), Monosomy 45,X (7%)
*Advanced maternal age increases risk of trisomy
What is the most common trisomy associated with first trimester loss?
Trisomy 16
What is the most common chromosome abnormality associated with first trimester loss?
Monosomy X
What is the association of congenital Mullerian abnormalities and spontaneous abortion?
- 1 in 200 to 1 in 500 women
- 20-30% of women with pregnancy loss
- Mechanisms:
Reduced uterine capacity
Cervical incompetence
Impaired implantation
Types of congenital Mullerian abnormalities:
How is DES exposure connected to early spontaneous abortion?
What is the connection between uterine fibroids and early spontaneous abortion?
Loss of a pregnancy in which trimester is associated with cervical incompetency?
Second trimester
What kind of inherited maternal disorder MAY be associated with recurrent fetal loss, although studies have failed to find a connection?
Thrombophilias
What two kinds of acquired thrombophilia are associated with recurrent spontaneous abortion?
What kind of fluctuation in hCG levels would you expect to see in an ectopic pregnancy or a spontaneous abortion?
Counseling guidelines for spontaneous abortion:
Recurrent losses: 3% chance that one partner is a symptomless carrier of a genetically balanced chromosomal translocation.
For women with recurrent losses and evidence of antiphospholipid antibodies, therapy may be reasonable. Current data support the use of unfractionated heparin and aspirin.
What are some risk factors for ectopic pregnancy?
Ectopic pregnancy locations:
Because the tube lacks a submucosal layer, the fertilized ovum promptly burrows through the epithelium, and the zygote comes to lie near or within the muscularis. The rapidly proliferating trophoblast may invade the subjacent muscularis, however, half of ampullary ectopic pregnancies stay within the tubal lumen with preservation of the muscularis layer in 85 percent (Senterman and associates, 1988). The embryo or fetus in an ectopic prengnancy is often absent or stunted.
How does infection with C.trachomatis versus N.gonorrhoeae lead to tubal scarring and ectopic pregnancy?
Acute chlamydial infection causes inflammation. Despite negative cultures, persistent chlamydial antigens can trigger a delayed hypersensitivity reaction with continued scarring. Whereas endotoxin-producing Neisseria gonorrhoea causes virulent pelvic inflammation with rapid clinical onset, chlamydial inflammatory response is indolent and peaks at 7 to 14 days.
What physical exam findings would you expect with a ruputured versus non-ruptured ectopic pregnancy?
If ruptured:
Shock (e.g., hypotension, tachycardia)
Rebound tenderness
Surgical emergency

If not ruptured:
Bleeding (usually intermittent, light, either bright or dark red, rarely exceeds normal flow). This is due to hCG levels not increasing like they should; leading to shedding of the endometrium.
Crampy abdominal and/or pelvic pain (unilateral or diffuse, ranges from mild to debilitating)
Diagnosis of an ectopic pregnancy:
What are the 3 medical treatment options for ectopic pregnancy?
1. Observation
2. Medical
3. Surgical
Surgical management of ectopic pregnancy:
Medical management of an ectopic pregnancy:
What is the MOA of methotrexate treatment for ectopic pregnancy?
- MTX competitively and irreversibly inhibits DHFR
- Folic acid required for thymidine synthesis (and DNA synthesis)
-Folic acid needed for purine base synthesis
- MTX cytotoxic during S-phase; greatest affinity for rapidly dividing cells
What is the effect of ectopic pregnancy on future fertility?
Changes in uterine size and blood flow during pregnancy:
Pertinence: Laceration of the uterine arteries can result in massive hemorrhage in a short period of time
What type of growth does the uterus undergo during pregnancy?
- Hyperplasia (increase in cell number) in first 2-3 months
- Hypertrophy (increase in cell size) during remainder
What type of changes do the cervix, vagina and ovaries undergo during pregnancy?
- Cervix
Increased vascularity (Chadwick sign)
Mucous plug
- Vagina
Thickened secretions
Increased vascularity
Increased capillary pressure from uterus obstructs venous return (edema, varicosities)
- Ovary
Ovulation suppressed, corpus luteum supports early pregnancy
Follicle/oocyte atresia continues
What effect does pregnancy have on the size and position of the heart?
- Uterus expands, displaces GI contents superiorly.
- Diaphragm is elevated, leading to restriction of lung volume and left axis deviation of the heart
- Apex found lateral to mid-clavicular line, in 4th rather than 5th intercostal space
- Will see mild myocardial hypertrophy during pregnancy. This structural change is consistent with the effects of chronic strain on the heart.
Anatomic changes in the heart during pregnancy:
Cardiac output changes during pregnancy:
Cardiac output is a function of the maternal heart rate and stroke volume, both of which increase during pregnancy and contribute to the overall rise in CO observed in pregnancy. Initial increases in heart occur occur by 5 weeks’ gestation and continues until it peaks at 32 weeks of gestation (at this point, maternal HR is 17% greater than the pregravid state). Stroke volume begins to rise by 8 weeks and reaches max at 20 weeks (this represents a 20-30% increase in stroke volume over the nonpregnant state).
Organs that get increased blood flow during pregnancy:
What kind of blood pressure changes occur during pregnancy?
- Systolic and diastolic blood pressure decline slightly during 2nd trimester:
Systolic BP declines 5-10 mm Hg, diastolic 10-15 mm Hg
Usually seen from 12-26 wks, with slow return to pre-pregnancy levels by 36 wks
- Decreases in BP occur from compression of inferior vena cava:
Most marked in late pregnancy, supine position
Decreases cardiac output, leading to fall in BP
How does progesterone lead to decreased systemic vascular resistance during pregnancy?
Progesterone hyperpolarizes the cell membrane, depressing membrane electrical potential.
Smooth muscle relaxation leads to increased capacitance → intravascular volume expansion → increased venous return → increased cardiac output
Normal heart changes in pregnancy that mimic disease:
What increases more during pregnancy, plasma volume or RBC mass?
Plasma volume increases the most; RBC mass increases as well, but not as much --> dilutional anemia
How much iron supplementation is needed per day during pregnancy?
- Iron requirement in pregnancy is 1,000 mg
200 mg excreted, 300 mg transferred to fetus and 500 mg needed for mom
- Mother needs to absorb 3.5mg/day of iron (during second half of pregnancy, needs can reach 6-7mg/day)
- Non-anemic pregnant women who do not supplement have significant decreases in hemoglobin, serum iron, serum ferritin and serum iron-binding capacity by term
- Purpose of supplementation is to maintain maternal iron levels
- Fetus receives its iron through active transport, primarily during the last trimester. Adequate iron transport to the fetus is maintained despite severe maternal iron deficiency. There is no correlation between maternal and fetal hemoglobin concentrations.
How does the WBC count and immune function change during pregnancy?
- Total blood leukocyte counts:
Increase to 5,000-12,200/mm3 in last trimester and in labor, can rise to 25,000/mm3
- Increases usually secondary to an increase in number of polymorphonuclear cells
- Altered Immune Function:
Fetus is semi-allograft; for pregnancy to be successful, immune response must be adapted
- Major change: shift from cell-mediated immune response to humoral or antibody-mediated immunity
- Lessens maternal cytotoxic potential against fetal antigens

(Increase in PMNs may be the result of elevated estrogen and cortisol levels in pregnancy)

(As result of shift to antibody-mediated immunity, one does see an increased susceptibility to intracellular pathogens (such as CMV, malaria) in pregnant women)
What kind of coagulation changes occur during pregnancy?
What type of pulmonary changes occur in pregnancy?
- Mechanical:
Changes in thoracic cage
Level of diaphragm rises
Consumption:
Increase in oxygen demands
Hormonal:
Progesterone stimulates ventilation, increases sensitivity of respiratory centers to CO2
How do ventilation requirements change during pregnancy?
Tidal volume: volume of air inspired and expired with each breath
Minute ventilation: volume inspired or expired in one minute

Pertinence: A normal pregnant woman has a compensated respiratory alkalosis and a diminished pulmonary reserve.
What type of renal changes occur during pregnancy?
- Increase in kidney size and weight
- Ureteral dilatation (Right > Left)
- Hypotonia (↑progesterone)
- Compression by gravid uterus
- Dextrorotation of uterus impacts right ureter
- Enlarged ovarian vein may compress ureters
- Bladder becomes intra-abdominal organ

*Pertinence: Pregnant women are more prone to pyelonephritis and bladder rupture during abdominal trauma.
What kind of changes in renal FUNCTION occur during pregnancy?
- 75% increase in renal blood flow by 16w
- 50% increase in glomerular filtration rate (GFR) by end of first trimester
- Increased GFR presents greater amount of solutes to kidneys:
24h creatinine clearance increases
BUN and serum creatinine decrease
May see glycosuria due to change in resorptive capability of proximal tubules
24h urine protein remains unchanged
What type of body water changes occur during pregnancy?
Total body water due to following: (1) additional 3.5 L results from the water content of the fetus, placenta and amniotic fluid; (2) maternal blood volume expansion of 1.5 L; (3) plasma volume expansion of 1.3L and (4) expansion of RBCs equal to 0.4 L. Remainder due to extravascular fluid, intracellular fluid in uterus and breasts and expanded adipose tissue.
What kind of GI changes occur during pregnancy?
- Decreased motility
Smooth muscle changes from influence of progesterone, though recent studies suggest the etiology may be estrogen
Decreased motilin production
Prolonged emptying and transit time
- Decreased esophageal sphincter tone
Increased symptoms of heartburn/GERD
- Constipation
Increased transit time increases absorption of water from colon, leading to constipation
- Small and Large Bowel
Moved upward and laterally
- Appendix
Displaced superiorly in right flank area
- Gallbladder
Distended, hypotonic (progesterone effect)
Emptying time slowed and often incomplete
Biliary cholesterol saturation increased, and chenodeoxycholic acid levels decreased
Change in composition of bile fluid → formation of cholesterol crystals, and with incomplete emptying, gallstone formation enhanced
What type of liver changes occur during pregnancy?
- Serum alkaline phosphatase activity doubles
Secondary to increased placental alkaline phosphatase isoenzymes
- A decrease in the albumin/globulin ratio occurs normally in pregnancy
Decreased colloidal pressures favors edema
What type of pituitary gland changes occur during pregnancy?
- Enlarges 135% during pregnancy
- 10-fold increase in maternal plasma prolactin level
- Estrogen stimulates increase in thyrotropin-releasing hormone production
- Primary function of increased prolactin is to ensure lactation.
What kind of changes occur in the thyroid gland during pregnancy?
The increase in thyroid function may resemble hyperthyroidism, with tachycardia, palpitations, excessive perspiration, and emotional instability. However, true hyperthyroidism occurs in only 0.08% of pregnancies.
What kind of adrenal function/output changes occur during pregnancy?
- Due to increased production of corticosteroid-binding globulin, serum cortisol increases to 2-3x non-pregnant levels
- Diurnal variation maintained
- Free cortisol increases, and it is only free cortisol which is metabolically active. Free cortisol increases as result of increased CRH and ACTH.
- Aldosterone increases (recall: compensates for natriuretic effect of progesterone)
What type of changes occur in the metabolism during pregnancy?
Changes in glucose and insulin during pregnancy:
What is responsible for the pigment changes seen in pregnant women?
Increased levels of:
Estrogen
Progesterone
Melanocyte Stimulating Hormone (by placenta)
What 3 types of pigment changes can occur during pregnancy?
- Melasma- mask of pregnancy
Blotchy, brownish pigment over forehead and malar eminences
- Darkening of areolae, axilla, and genitals
- Linea nigra
Dark line that appears down the midline of abdomen
Normal placental structure:
What type of immune cells help trophoblasts burrow into the endometrium?
Natural killer cells
Normal placental implantation:
What two types of trophoblasts are there in the placenta?
- Trophoblasts (Greek: trephein: to feed, blastos: germinator) the fetal cells that invade the maternal tissues and are the interface between maternal and fetal cells
- Villous Trophoblasts- cover the villi which contain the fetal vessels. These cells contact maternal blood
- Extravillous Trophoblasts- anchor the placenta to the maternal surface and invade maternal tissues
Components of villi and extravillous structures:
- Villous structure
Cytotrophoblasts- germinal cells on maternal surface
Syncytiotrophoblasts- secretory cells on maternal surface
-Fetal vessels
Connective tissue
- Extravillous trophoblasts- invade to inner 1/3 myometrium
Interstitial
Endovascular
What is the function of the extravillous trophoblasts?
What are the functions of the chorion and the amnion?
What role does the surfactant secreted by fetal lungs play in induction of labor?
The surfactant secreted by the fetal lungs signal the chorion to produce prostaglandins.
So…when the fetal lungs are mature, labor becomes more likely
Histology of the placenta:
What hormones do cytotrophoblasts secrete?
Hypothalamic Analogues: GnRH
Somatostatin
GHRH
CRF
TRF
Dopamine
What kinds of hormomes do the synctiocytotrophoblasts secrete?
Pituitary Analogues:
hPL
oxytocin
placental variant GH
What placental cells make hCG?
What is the function of hCG?
Progesterone in pregnancy:
- Placenta has limited ability to synthesize cholesterol from acetate
- Maternal LDL cholesterol is the principal precursor of progesterone biosynthesis in pregnancy
- Progesterone (P4) most prevalent and secreted by corpus luteum, placenta, and adrenal gland
- P4 prepares endometrium for implantation and maintains pregnancy by increasing secretory activity of uterine lining and by inhibiting motility of myometrium
- P4 develops the alveoli of the mammary gland
- High levels of P4 inhibit estrus and ovulatory surge of LH
Progesterone has numerous functions during pregnancy:
Numerous actions:
- Suppresses uterine contractions
- Stimulates uterine growth
- Suppresses LH and FSH
- Stimulates development of alveolar tissue of the mammary gland
- Prevents lactation until after birth
- Strengthens pelvic walls in preparation for labor
- Slows motility of GI tract
- Increases pulmonary function
- Induces depression, sleep disorganization
- Inhibits T cell-mediated responses
Other medical uses for progesterone:
- Progesterone supplementation in pregnancy has been shown to decrease the incidence of preterm birth in certain senerios
- High-dose progestogen-only contraceptives, such as injectable Depo Provera, inhibit follicular development and prevent ovulation as their primary mechanism of action
- Progesterone is used in patients with chronic pulmonary disease to improve respiratory function
Hormone levels changes during pregnancy:
Where is most DHEA-S (estrogen precursor) made during pregnancy?
- Corpus luteum is main source during first few weeks, then the placenta takes over
- Estrogens = estradiol, estrone, and estriol
- Major precursor of estrogens is DHEA-S
- Fetal adrenal glands are quantitatively the most important source of placental estrogen precursors in human
Estrogen is made from DHEA-S in the placenta by 4 enzymes:
This all occurs in the syncytiotrophoblast
Estrogen functions in pregnancy:
Endometrial growth during pregnancy
Inhibition of prolactin secretion
Growth of mammary ducts
Enlargement of and increased blood supply to uterus
Softening of symphysis pubis and pelvic ligaments
Regulates bone density in fetus

*Estrogen decreases prolactin production in pregnancy to prevent lacation in pregnancy. Combination birth control pills can be used as birth control after delivery, but are known to decrease milk production, so are not the best choice in women who wish to breast feed.
Functions of human placental lactogen during pregnancy:
- Maternal lipolysis (leads to increased FFAs, thus providing energy source to mother/fetus). In vitro studies show hPL also inhibits leptin secretion.
- Diabetogenic or anti-insulin action (increased maternal insulin levels, provides source of amino acids to fetus)
- Potent angiogenic role; may play role in formation of fetal vasculature
What is the connection between human placental lactogen and gestational diabetes?
Other fetal/placental hormones:
- Placental growth hormone: nearly identical to GH, involved in insulin resistance/lipolysis
- Relaxin: acts to stabilize myometrium in early pregnancy
- Hypothalamic-Like Releasing Hormones
- GnRH: regulates trophoblast hCG production
- CRH: role in labor initiation
- Leptin: made also by adipocytes
Important role in fetal development/growth
Levels correlate positively with fetal birth weight
Why is an increase in lipids considered normal during pregnancy?
Cholesterol is physiologically increased in pregnancy. Lipid lowering agents are not used in pregnancy as no benefit has been demonstrated, and they may inhibit adrenal and gonadal endocrine function in the fetus
What are E3 levels useful for measuring during pregnancy?
Estriol (E3) is produced by the placenta working with precursors from the fetal liver. Maternal Urinary Estriol levels were used to determine fetal well being and a sudden decline in urine Estriol was used to predict fetal compromise in the 1960s and 1970s. E3 levels in the maternal circulation are a key part of estimating the risk of Trisomy 21 and Trisomy 13 in the fetus. For both these karyotypic abnormalities, the E3 levels are low.
Abnormal implantation types:
Definitions of types of abnormal implantation:
- Placenta accreta- an abnormal placental implantation in which the anchoring villi attach to the surface of the myometrium, rather than being contained by decidual cells. This results in a placenta that is abnormally adherent to the uterus
- Placenta increta- when the anchoring villi attach deep within the myometrium
- Placenta percreta- when the anchoring villi invade through the uterine serosa and potentially into surrounding organs
2 factors that may contribute to abnormal implantation:
- Trophoblasts might not respond to the signals to limit invasion
- The maternal immune system may fail to block invasion
- Areas in which the endometrium has been damaged allows contact with tissue that cannot limit trophoblast invasion
Uterine operative procedures
D&Cs, Myomectomies
Correction of congenital uterine abnormalities
Endometrial ablation
Previous cesarean section

* Women who have four or more cesareans have a risk as high as 67% for a placenta accreta
In what trimester would you see bleeding due to placenta acreta?
Third trimester
Treatment of placenta accreta:
Planned surgical delivery
Blood products available
Placement of catheters in iliac arteries for embolization of pelvic vessels in vascular operating room with delayed hysterectomy after placental involution is noted

*At birth, the uterine arteries are enlarged and prone to tear; this is why you want to wait a few weeks for the arteries to regress before performing further surgery.
List 6 causes of 3rd trimester bleeding:
Placenta previa
Placental abruption
Vasa previa
Cervical change
Trauma/laceration
DIC
Placenta Previa:
Rarely a cause of exsanguinating maternal hemorrhage unless instrumentation or digital exam is performed. Most common maternal morbity is necessity for operative delivery and its associated risks of bleeding ,anesthetic and postop complications.
Placental migration:
Risk factors for placenta previa:
- Maternal age > 35 years
- Smoking
- Increased parity
- Previous previa
- Previous cesarean delivery—linear increase. 4 or more, risk is 10%
- Instrumentation or surgical procedure: inability of placenta to migrate
Why is bleeding associated with placental attachment close to the cervix?
Associated with the development of the lower uterine segment in the third trimester
Placental attachment is disrupted as the lower uterine segment thins
Uterus in unable to contract adequately to stop the flow from the open vessels

*Anytime the placenta is within 2 cm of the cervix (because there are no uterine muscles within 2 cm of the cervix) there is a risk of bleeding because the lack of muscle means there is nothing to “clamp” down on the arteries in the placenta and prevent bleeding.
Diagnosis and management of placenta previa:
- Classical clinical presentation is painless bleeding in late 2nd or 3rd trimester
- Diagnosed on ultrasound
Transabdominal has higher
false positive rate
Transvaginal ultrasound
more accurate, and safe

- Delivery by cesarean section
Timing dependent on:
Gestational age of fetus
Amount of bleeding
Fetal condition
Characteristics of placental abruption:
- Premature separation of the normally implanted placenta
- Occurs in approximately 1 in 120 births
- Accounts for 15% of perinatal mortality
- Uterine bleeding
- Uterine hypertonicity and/or hyperactivity
- Fetal distress and/or death
Placental abruption symptoms:
- Pain
Varies from mild cramping to severe pain
- Back pain—think posterior abruption
- Bleeding
May not reflect true amount of blood loss
- Trauma
Other risk factors (smoking, drugs)
Placental abruption findings on exam:
- Signs of circulatory instability
Maternal tachycardia
Maternal hypotension
Cap refill is slow, low urine output, altered mentation
Shock if >30% blood loss
- Maternal abdomen
Fundal height will show distension from clot
Location of tenderness
Tetanic contractions
Vasa Previa:
Velamentous Insertion of the umbilical cord - Normally, blood vessels run from the placenta via the umbilical cord to the baby. Velamentous insertion means that these veins travel across the amniotic membranes before they come together into the umbilical cord. Velamentous insertion happens in 1-2% of all pregnancies. The figures beneath show Velamentous insertion of Nathan's cord. Notice how the vessels run across the membranes. This is a delicate arrangement, but doesn't necessarily pose any threat (or symptoms, for that matter) during pregnancy.
Alternations in fetal heart rate and diagnosis of vasa previa:
- Initial fetal tachycardia—fetus attempts to compensate for acute blood loss (HR > 160 bpm)
- Bradycardia (HR < 110 bpm)
- Intermittent decelerations

- Have a high index of suspicion in patients who present with painless bleeding
- Must make diagnosis rapidly and institute definitive therapy and delivery
- Fetal mortality reported to be greater than 50%