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Flashcards in OB/GYN Deck (101):

ACOG prenatal care

first visit: 8-10 weeks

every four weeks for next seven months (28 weeks)

Every 2 – 3 weeks until 36 weeks gestation.

Every week after 36 weeks gestation


QUAD screen

maternal blood screen -16-18 weeks

o AFP: alpha-fetoprotein is a protein that is produced by the fetus
• High levels of AFP = neural tube defect such as spina bifida or anencephaly. However, the most common reason for elevated AFP levels is inaccurate dating of the pregnancy.
• Low levels of AFP and abnormal levels of hCG and estriol may indicate that the developing baby has Trisomy 21(Down syndrome), Trisomy 18 (Edwards Syndrome) or another type of chromosome abnormality.
o hCG: human chorionic gonadotropin is a hormone produced within the placenta
o Estriol: estriol is an estrogen produced by both the fetus and the placenta
o Inhibin-A: inhibin-A is a protein produced by the placenta and ovaries


Trisomy 21:

• US may show increased nuchal translucency
• On quad screen
• Decreased=AFP, estriol
• Increased=b-HCG, inhibin A

• Flat facies, epicanthial folds (eyelid fold), duodenal atresia, congenital heart defects, increased risk of Alzheimers and leukemias


Trisomy 18:

• Aka Edward’ Syndrome, 1:8,000 pregnancies
• On quad screen
• Decreased=AFP, b-HCG, estriol
• Normal=inhibinA

• Severe mental retardation, rocker bottom feet, micrognathia, low set ears, clenched hands, prominent occiput

• 50% of babies die within the first week life


Trisomy 13:

• Aka Patau’s Syndrome. 1:15,000 pregnancies
• US may show increased nuchal translucency
• On screening
• Most often this is normal
• Sometimes b-HCG will be decreased
Severe mental retardation, rocker bottom feet, microcephaly, cleft lip, cleft palate, holoprosencephaly, polydactly
Median survival is 2.5 days


normal FHR

Bradycardia: Mean FHR < 110 BPM

Tachycardia: Mean FHR>160 BPM


types of variability in FHR

o Absent variability = Amplitude range undetectable
o Minimal = < 5 BPM
o Moderate = 6 to 25 BPM
o Marked = > 25 BPM

• **Persistently minimal or absent FHR variability appears to be the most significant intrapartum sign of fetal compromise. On the other hand the presence of good FHR variability may not always be predictive of a good outcome.

• Etiologies of decreased variability: Fetal metabolic acidosis, CNS depressants, fetal sleep cycles[10], congenital anomalies, prematurity, fetal tachycardia, preexisting neurologic abnormality, normal, betamethasone.\
• NOTE: absent variations = greatest indicator for bad!! – means placenta isn’t giving baby enough O2, and baby isn’t tolerating labor well (could be d/t metabolic acidosis, CNS depression, mother’s pain meds, sleep, prematurity)



• = abrupt increase in FHR above baseline with onset to peak of the acceleration less than < 30 seconds and less than 2 minutes in duration.
• Adequate accelerations are defined as:
o 15 BPM above baseline for > 15 seconds.
• Prolonged acceleration: Increase in heart rate lasts for 2 to 10 minutes
• The absence of accelerations for more than 80 minutes correlates with increased neonatal morbidity.
• Fetal scalp stimulation can be used to induce accelerations. There is about a 50% chance of acidosis in the fetus who fails to respond to stimulation in the presence of a nonreassuring pattern


gradual vs. abrupt deceleration

o Gradual decrease and return to baseline with time from onset of the deceleration to nadir >30 seconds.
o Abrupt decrease in FHR of > 15 beats per minute with onset of deceleration to nadir < 30 seconds.


early decleration

o Gradual decrease in FHR with onset of deceleration to nadir >30 seconds. The nadir occurs with the peak of a contraction

**think head contraction


late deceleration

o Gradual decrease in FHR with onset of deceleration to nadir >30 seconds. Onset of the decleration occurs after the beginning of the contraction, and the nadir of the contraction occurs after the peak of the contraction.

**uteroplacental insufficiency **
- excessive contractions, maternal hypotension, maternal hypoxemia

late deceleration with beat to beat variety:
- fetal hypoxia --> chemoreceptors to stimulate alpha receptors --> increased constriction of vessels --> HTN --> slowing of fetal heart rate

late decelerations w/ no variability: (should delivery baby soon if persists!)
- hypoxia --> lactic acidosis

Deliver baby if pH <7.2!!!


• Variable deceleration:

o Abrupt decrease in FHR of > 15 beats per minute measured from the most recently determined baseline rate. The onset of deceleration to nadir is less than 30 seconds. The deceleration lasts > 15 seconds and less than 2 minutes. A shoulder, if present, is not included as part of the deceleration.

** partial cord compression
- decreased O2 --> increased vessel constriction --> HTN --> decreased HR


• Recurrent decelerations ( variable, early, or late ):

Decelerations occur with > 50% of uterine contractions in any 20 minute segment.


• Prolonged deceleration

A decrease in FHR of > 15 beats per minute measured from the most recently determined baseline rate. The deceleration lasts >= 2 minutes but less than 10 minutes.
o Etiologies: Maternal hypotension, uterine hyperactivity, cord prolapse, cord compression, abruption, artifact (maternal heart rate) , maternal seizure.
o Although umbilical cord compression is often responsible for a prolonged deceleration a pelvic examination should be performed to rule out umbilical cord prolapse or rapid descent of the fetal head.



• early deceleration (onset before contraction) = head contraction (these are normal!)
• late deceleration (decrease in HR after contraction) = uteroplacental insufficiency – think hypoxia
• variable deceleration: think cord compression
• no variability = worrisome



• First-degree vaginal tears are the least severe, involving only the skin around the vaginal opening. Although the patient might experience some mild burning or stinging with urination, first-degrees tears aren't severely painful and heal on their own within a few weeks.
• Second-degree vaginal tears involve vaginal tissue and the perineal muscles — the muscles between the vagina and anus that help support the uterus, bladder and rectum. Second-degree tears typically require closure and heal within a few weeks.
• Third-degree vaginal tears involve the posterior vaginal tissues, perineal muscles AND the capsule of the anal sphincter.
• Fourth-degree vaginal tears are the most severe. They involve the perineal muscles and anal sphincter as well as the tissue lining the rectum. Fourth-degree tears require repair, sometimes in an operative setting.
o Complications such as fecal incontinence and painful intercourse are possible.


When to induce labor?

• risks are greater than that of induction
• At 41+ weeks
• Within 96 hrs of ruptured membranes at term
• For pre eclampsia at term
• For maternal diabetes at term


How to induce labor?

• For prolonged pregnancy first sweep/strip the membranes: separation of amniotic sac from wall of uterus
• For ruptured membranes:
o Oxytocin by IV infusion
o Although wait-and-see and vaginal PG’s are acceptable
• For all other patients (except those with a uterine scar)…
o Vaginal prostaglandins
o Regardless of the state of the cervix or the parity of the patient
o Amniotomy followed by oxytocin infusion 3 – 12 hours later is likely to be the most cost effective when the cervix is ripe


C sections

Vaginal birth after one lower segment C-sections:
• For spontaneous labor the risk of scar rupture is 1:200
• With oxytocin infusion the risk is 1:100
• With prostaglandins the risk is 1:40
• Maternal risk of death ~2 for every 10,000
• scar rupture
Risks of Caesarean birth:
• C sections: increased hospital stay, increased IC, increased eath (2-10x), bladder/ureter damage, future hysterectomy risk, increased thromboembolism, increased future placenta previa and stillbirth in next pregnancy
• no difference in postpartum hemorrhage, endometritis, genital tract injury, fecal incontinence, depression, back pain, dyspareunia
• vaginal birth: more likely to have perineal pain, urinary incontinence and uterovagianl prolapse with vaginal birth


when to consult during prolonged labor?

o a Nullipara whose delivery is not imminent after 2 hours
o And 1 hour in a previously parous patient
o Reassess all patients with an epidural who do not push within 1 hour after fully dilated



gravida, TPAL (term, premature, abortions, living children)
• Gravida means number of pregnancies (5)
• Parity means number of births/viable offsprings (4)



• testing?
o nitrazine test – blue means that vagina is alkaline – positive result!
o microscopic examination: amniotic fluid shows “ferning”

Premature Rupture of Membranes (PROM): Spontaneous rupture of membranes prior to onset of labor

Preterm PROM (PPROM): PROM before 37 weeks gestation

• About 1/3 of women with PPROM develop potentially serious intrauterine infections
• increased risk of: placental abruption, umbilical cord prolapse, pulmonary hypoplasia

Risk Factors:
• Genital tract infections ** most common cause **
• Previous PPROM
• Antepartum bleeding
• Cigarette smoking
• Mechanical Stress
• Most patients have no identifiable risk factors

• delivery of patients >34 weeks gestation
• tx: expeditious delivery!!!
• corticosteroids given to help fetal lung maturity: Betamethasone
• Give antibiotic prophylaxis
• maternal and fetal monitoring



• most commonly: ureaplasma urealyticum, gram – anaerobes, mycoplasma hominis, bacteriods bivius, gardnerella vaginalis Group B strep

Risk factors:
• prolonged labor
• prolonged membrane rupture
• multiple digital vaginal examinations (especially with ruptured membranes)
• nulliparity
• previous IAI
• meconium-stained amniotic fluid
• internal fetal or uterine monitoring
• presence of genital tract pathogens
• alcohol or tobacco

Clinical Presentation:
• Fever**
• Uterine tenderness
• Maternal tachycardia (>100/min)
• Fetal tachycardia (>160/min)
• Purulent or foul amniotic fluid
• Maternal leukocytosis (variously defined as white blood cell [WBC] count >12,000/mm3 or >15,000/mm)
o 70 to 90 percent of cases

How do diagnose?
• ***FEVER and
o Maternal leukocytosis (greater than 15,000 cells/mm3)
o Maternal tachycardia (greater than 100 beats/minute)
o Fetal tachycardia (greater than 160 beats/minute)
o Uterine tenderness
o Foul odor of the amniotic fluid

• standard treatment: ampicillin 2 g intravenously every six hours plus gentamicin 1.5 mg/kg every eight hours for patients with normal renal function
• other options: ampicillin-sublactam, ticarcillin-clavulanate, cefoxitin


uterine rupture

uncommon in developed countries

1/56 chance in resource poor areas!


Placenta Previa

placental tissue over or adjacent to the cervical os
• Suspected with painless antepartum bleeding after 20wks

• Total placenta previa- internal os completely covered
• Partial- internal os partially covered
• Marginal- Edge of placenta is at the margin of the internal os
• Low-lying placenta- placenta is implanted in the lower uterine segment does not reach the interal os, but is at close proximity
• Vasa Previa- fetal vessels present at cervical os

risk factors:
previous experience, previous Csection, multiparity, advanced maternal age, maternal smoking, cocaine

• male fetus, non-white race
• Asymptomatic previa: monitor placental position with ultrasound examination as an outpatient. Avoid strenuous exercise. Planned C-section for delivery
• Bleeding Previa: Potential emergency. Hospitalize for maternal and fetal monitoring. Emergency C-section if life threatening maternal hemorrhage. If stable patient can be monitored on an outpatient basis with continuous US examination.
• Vaginal delivery: May be attempted if the placental edge is >10mm from the internal os due to the lower risk of hemorrhage during labor.
• C-Section: Due to risk of hemorrhage from placental tear a C-section is the preferred method of delivery for patients who present with placenta previa.


Post partum hemorrhage:

• Blood Loss occurs in 4% of deliveries
o >500 ml vaginal delivery
o >1000ml during C-section
“ The Four T’s”: Tone, Trauma, Tissue, Thrombus
• Tone: (uterine atony) no contraction → spiral arterioles and decidual veins to continue to bleed
o this is the reason for 75% of PPH
o treatment: massage, pitocine/cytotec, methergine (caution for HTN) or hemabate (caution for asthma)
o predisposing factors: over distention of uterus, multiple gestations, polyhydramnios, prolonged labor, fetal macrosomia (increased birth weight), oxytotic augmentation of labor, multiparity (>5), precipitous labor (lasting <3 hours), chorioamnionitis, uterine leiomyomas
• Trauma: second most common cause of PPH
o d/t lacerations – esp. with the use of forceps/extractors
o uterine inversion: seen in 1 in 20,000 pregnancies – d/t improper management of third stage of labor (placenta fails to detach and uterus comes through the vagina)
• Tissue: uterus is unable to contract and involute around the retained placental tissue mass
o tx: manual removal after 30 minutes has passed to allow for spontaneous delivery, followed by D&C
• Thrombus:
o rare
o ITP: abnormal platelet fn
o amniotic fluid embolus- thromboplastin in amniotic fluid leaks into mothers vascular system → consumptive coagulopathy
o VW disease
o tx: coagulation studies



HTN after 20 weeks gestation w/ associated proteinuria and edema
o Leading cause of maternal and prenatal morbidity and mortality worldwide
o Increased 25% in US during last 20 years
o Risk factor for future Cardiovascular disease and Metabolic disorders
Risk factors:
o nulliparity, age >40, <18, family hx, chronic HTN, CRD, DM, black, woman too small


difft. criteria for preeclampsia

Criteria for ddx of Preeclampsia 1:
o Systolic blood pressure >140 mmHg or diastolic blood pressure >90 mmHg on two occasions at least 4 hours apart after 20 weeks of gestation in a previously normotensive patient
o If systolic blood pressure is >160 mmHg or diastolic blood pressure is 0.3 grams in a 24-hour urine specimen or protein (mg/dl)/creatinine (mg/dl) ratio >0.3
o Dipstick 1+ if a quantitative measurement is unavailable
Criteria for ddx of preeclampsia-2:
o new onset hypertension without proteinuria, the new onset of any of the following is diagnostic of preeclampsia:
o Platelet count 1.1mg/dL or doubling of serum creatinine in the absence of other renal disease
o Liver transaminases at least twice the normal concentrations
o Pulmonary edema
o Cerebral or visual symptoms
Criteria for ddx of preeclampsia-3: SEVERE preeclamptic disease
o CNS dysfunction: cerebral/visual distrubances, (h/a, altered mental status, vision changes)
o hepatic abnormality: severe RUQ or epigastric pain
o severe BP elevation >160 or >110 diastolic
Criteria for ddx of preeclampsia-4:
o Thrombocytopenia: 1.1)
o pulmonary edema
Criteria for mild preeclampsia:
o BP elevated on two occasions >140/90 – normotensive before 20 weeks
o >.3 g protein in urine sample or 3+ proteinuria
o no end organ damage


Early onset vs. Late onset preeclampsia:

o Early onset (34 weeks)
o Early-onset preeclampsia was significantly associated with a high risk for fetal death (adjusted odds ratio [AOR], 5.8), but late-onset preeclampsia was not (
o However, the AOR for perinatal death/severe neonatal morbidity was significant for both early-onset and late-onset
Preeclampsia indications for delivery:
o poor fetal heart status, ruptured membrane, uncontrollable BP, oligohydramnios (AFI 1.5, pulmonary edema,

***SOB or c/p w/ pulse ox <94%, h/a that is persistent/severe, RUQ tenderness, HELLP syndrome


clinical sx of preeclampsia

o Mild Preeclampsia- can have a milder HTN, Proteinuria, but may not have other SX
o Severe Preeclampsia- needs urgent delivery:
o Severe hypertension (SBP>160mmHg or DBP>110mmHg (2 occasions at least 4hrs. Apart or 1X if treated)
o Persistent and/or severe headache
o Visual abnormalities (scotomata, photopsia, photophobia, blurred vision, or temporary blindness)
o Upper abdominal or epigastric pain
o Nausea, vomiting
o Dyspnea, retrosternal chest pain
• Laboratory abnormalities:
• MAHA (Schistocytes, elevated bilirubin/LDH, or low serum haptoglobin levels U/L)
• Thrombocytopenia (1.1mg/dL)
• Elevated liver enzymes (twice the upper limit of normal)
• Meeting the criteria for:
• New onset HTN and either Proteinuria OR end organ dysfunction
• Post diagnosis evaluation includes-determination of severity and assesment of fetal well being

Symptoms of severe disease?
o Severe headache
o Blurred vision/other vision disturbances
o Upper abdominal pain (RUQ, epigastric)
o Nausea/vomiting
o SOB, chest pain
o Altered mental status
Maternal complications:
o placental abruption, ARF, cerebral hemorrhage, hepatic failure, PE, DIC, progression to eclampsia



HELLP: hemolysis, elevated liver enzymes, low platelet count
• Occurs <100,000
• Liver function test (especially AST)
• Peripheral smear w/schistocytes & bilirubin (Tennessee classification)
• If not all laboratory abnormalities are met = partial HELLP syndrome, which may progress to complete HELLP
• Only cure/effective treatment is delivery
• Antihypertensive as needed for HTN
• Platelet transfusion for actively bleeding patients or possible C-section
• daily ASA starting late 1st trimester
• w/l and increased exercise
• Early detection and treatment decreases risk of serious complications
• Risk correlates with increased severity of symptoms and lab abnormalities
• Death rate among babies born to mothers with HELLP depends on birth weight and organ development
o Many are born prematurely
• Recurrence rate 2-6%
o Partial HELLP = 24-27%
o Preeclampsia = 20-50% (higher recurrence if 2nd tri HELLP)



• One or more generalized convulsions or comma in the setting of preeclampsia and without another neurological condition
• 2-3% of women with severe preeclampsia
• Risk factors same as preeclampsia
• can occur antepartum, intrapartum and post partum
o post partum eclampsia is often missed: present with h/a, SOB, blurry vision
• tx: tx seizures, control BP, deliver fetus


Posterior Reversible encephalopathy syndrome (PRES)

= h/a, confusion, seizures, visual loss---see edema in the brain

• Cerebral edema, ischemia/hemorrhages in posterior hemispheres
• Changes seen on MRI/CT
• Findings are due to HTN causing: Vasospasm, Hypoperfusion, Cerebral edema or loss in autoregualtion, Hypoperfusion, Cerebral edema
• Risk Factors – Eclampsia, HTN (acute/severe). Immunosuppression
• Clinical Manifestations:
o HA, AMS, Visual disturbances, Seizures
• Treatment:
o Control HTN (no more than 25% in 6 hrs)
o Control Seizures (Eclampsia responds to MgS04 better than Phenytoin/Diazepam
o Decrease cytotoxic drug
o Manage comorbid conditions (sepsis, fluid overload, electrolyte abnormalities)
• Prognosis:
o Most recover within 2 weeks
o Not always reversible, can lead to neurological deficits
o Can cause death from cerebral edema, hemorrhage


Pre-Gestational Diabetes Mellitus

(Diabetic before pregnancy):
• Pre-existing type 1 or 2 diabetes in a pregnant woman (~4% in US)
• diabetic pt. who gets pregnant, need to evaluate eyes, kidneys, neuropathy, heart and HBA1C levels
Type I Diabetes:
• Caused by destruction of the beta cells of the pancreas, which leads to an absolute insulin deficiency
• Accounts for 5-10% of all diabetes
• 1% of diabetes in pregnancy
• have growth restricted babies and don’t have chubby babies
Type II Diabetes
• Most form of diabetes, accounting for 90-95% of cases (CDC, 2008)
• Characterized by insulin resistance and relative insulin deficiency
• Can be managed through lifestyle modification, diet, exercise and pharmacologically


Gestation Diabetes Mellitus (GDM

Diabetes during pregnancy
• Any degree of glucose intolerance with onset or first recognition during pregnancy (~7% in US)
• GDM is a condition in which a hormone (hPL) made by the placenta prevents the body from using insulin effectively. Glucose builds up in the blood instead of being absorbed by the cells.
o Not caused by a lack of insulin, but by other hormones causing insulin resistance!
• GDM is a risk factor for subsequent diabetes (50-70%)
• Pancreas cannot secrete enough insulin, which increases glucose, glucose crosses placenta and is stored as energy/fat by the fetus. It also results in fetus producing high amounts of insulin.
Epidemiology of GDM:
• Increasing maternal age and weight
• Previous GDM – if had LGA baby
• Previous macrosomic infant
• Family history of diabetes among first-degree relatives
• Ethnic background with a high prevalence of diabetes
• Hispanic, black, American indian, Asian/pacific islander


Risks of uncontrolled diabetes in pregnancy:

• diabetic can result in congenital malformations:
o heart anomalies, spina bifida, renal anomalies, situs inversus
• Pregnancies complicated by diabetes are at increased risk of perinatal morbidity and mortality.
For mothers w/ preexisting DM:
• Hypertension
• Preeclampsia (RR increased x4) – severe HTN, proteinuria, severe edema
• SAB (RR ~3)
• Worsening of diabetic complications – risk of developing type 2 DM
• If Vasculopathy is present, fetal growth restriction
• Ketoacidosis or Severe hypoglycemia
For Baby:
• Macrosomia (birth weight > 4kg)
• Hypoglycemia at birth
• Hyperbilirubinemia
• Low calcium and magnesium
• Respiratory distress syndrome – lungs don’t mature properly
• Polycythemia
• Hyperviscosity
• Increased risk for childhood and adult obesity
• Increased risk of type 2 diabetes later in life

Preterm labor complications:
• incidence of preterm birth is increased
• Vascular disease, hypertensive disorders and obesity contribute to the increased risk of preterm birth in women with diabetes.

Perinatal implications:
• increased risk of RDS!


Metabolic changes during pregnancy:

• During the first trimester, fasting blood glucose decreases because of insulin production, and sensitivity slightly increases
o in early pregnancy see decreased glucose, increased insulin secretion, and glycogen storage along with increased peripheral glucose utilization (d/t baby using up glucose)
o before 20 weeks see decreased maternal glucose, production of FFAs and ketones and continued insulin in response to elevated glucose
o towards end have risk of becoming hypoglycemic!
• By the end of the first trimester, insulin sensitivity decreases, with a responding increase in insulin production; this change creates the diabetogenic state of pregnancy. (d/t hPL)
o increase in hormones allows for ample glucose available to fetus
• increased hCS (hPL) → “diabetogenic” decreased glucose tolerance
• increased PRL → insulin resistance
• increased cortisol → hepatic glucose production
• Euglycemia is maintained in pregnancy because the pancreatic beta cells produce enough insulin to counteract increasing insulin resistance
• In pregnant women, hepatic glucose production is 1.3 times higher than it is in non-pregnant women

maternal hyperglycemia → fetal hyperglycemia → fetal nyperinsulinemia (Bcell hypertrophy/hyperplasia) → excessive fetal growth (macrosomia, increased need for C-sections, maternal HTN)


HcG levels

• normal – HCG should double every 48 hours
• abnormal – HCG can stay the same, decrease (miscariage), or increase minimally (preg. outside of uterus)


spontaneous abortion

Risk factors for spontaneous abortion:
• Age 20 to 30 years (9 to 17 percent), age 35 years (20 percent), age 40 years (40 percent), and age 45 years (80 percent)
• Previous spontaneous abortion
• prolonged time to conception/implantation interval
• smoking, EtOH, cocaine, NSAIDS, caffeine, low folate
• weight extremes: obesity or thin
• fever during pregnancy, celiac disease

Fetal etiology of spontaneous abortions:
• Chromosomal abnormalities**
o 50% of all spontaneous abortions
• Trisomy 16 is most common, almost always lethal
• Congenital abnormalities**
• Trauma


sx of spontaneous abortion

• Vaginal bleeding
• Pelvic pain
• Absence of fetal movement (rate, as usually before movement is perceived)
• Incidental finding on US/hand-held Doppler

Criteria for ddx?
• Ultrasound:
o A gestational sac >25mm in mean diameter that does not contain a yolk sac or embryo
o An embryo with a crown rump length (CRL) >7 mm that does not have cardiac activity
o After a pelvic ultrasound showed a gestational sac without a yolk sac, absence of an embryo with heartbeat in >2 weeks
o After a pelvic ultrasound showed a gestational sac with a yolk sac, absence of an embryo with a heartbeat in >11 days


Threatened abortion:

• Diagnostic criteria for spontaneous abortion are not met
• Vaginal bleeding has occurred and the cervical OS is closed
• First trimester bleeding may be associated with adverse outcomes later in pregnancy
o Prognosis is worse when the bleeding is heavy or extends into the second trimester
o Up to 50% will miscarry
• Tx: bed rest and expectant management


Inevitable abortion:

• Symptoms of vaginal bleeding, crampy pelvic pain, and dilated cervix
o Products of conception can often be felt or visualized through the internal cervical os
o No passage of fetal tissue per os
• Tx options:
o Medical abortion
• Usually with Misoprostol (one time dose of 800 mcg per vaginum, or 600 mcg sublingual)
• Surgical abortion
o D&C or D&E; Doxycycline 100mg Po for two doses 12 hours part on the day of the procedural to decrease risk of postabortal sepsis
• Expectant management: Majority of expulsions occur in the first two weeks after diagnosis


Incomplete abortion:

• Vaginal bleeding and/or pain are present, the cervix is dilated, and products of conception are found within the cervical canal on examination
• After 12 weeks , the membranes often rupture, and the fetus is passed, but significant amounts of placental tissue may be retained, leading to an incomplete abortion
• Tx options:
o Medical abortion - Usually with Misoprostol (one time dose of 800 mcg per vaginum, or 600 mcg sublingual)
• Surgical abortion - D&C or D&E; Doxycycline 100mg Po for two doses 12 hours part on the day of the procedural to decrease risk of postabortal sepsis
• Expectant management: but no one does this d/t increased infections - Usually Staph aureus or mixed infections


Completed Abortion:

• Products of conception are entirely out of the uterus and cervix
• Cervix is closed and the uterus is small and well contracted
• Vaginal bleeding and pain may be mild or may have resolved
• More common outcome than incomplete >12 weeks gestation
• Tx: examination of passed tissue to confirm products of conception, transvaginal US to visualize empty uterus, follow hCG levels until zero (should halve within 48-72) hours


Missed abortion:

• Patient with or without symptoms having a closed cervical OS
• Women may notice that symptoms associated with early pregnancy such as nausea, breast tenderness, etc. have abated and they do not “feel pregnant” anymore
• Tx options:
o Medical abortion
o Surgical abortion
o Expectant management: Majority of expulsions occur first two weeks after diagnosis


Ectopic Pregnancy

(abnormal pregnancy outside of uterus)
Risk factors:
• Previous Ectopic, may have been from previous PID
• PID: most common cause: ascending infection from gonorrhea or chlamydia à scarring in fallopian tubes (esp. worry about chlamydia b.c doesn’t present with sx in women)
• Assisted Reproductive Technology
• History of peritonitis (appendectomy, C-section w/ post partum endometritis à infection)
• Smoking (damages cilia, same as lungs)
• Previous Tubal Ligation
• Medical – Methotrexate –
o * Folic acid inhibitor – kills pregnancy (pregnancy may abort out tube and pt. may have pain) – may get postpartum bleeding d/t removal of hCG – must follow hCG in order to make sure that it works!
• Surgical – Removal of ectopic – reserved for pts. that com in w/ acute presentation, or worry about rupture – or done if pregnancy is in a worrisome location
o Removal of tube is now used, there is no difference in fertility rates, that tube is damaged
• both procedures reduce fertility in the long run


painless bleeding

think gestational trophoblastic disease


painful bleeding

think spontaneous abortion


Gestational Trophoblastic Disease:

• nausea and vomiting - d/t increased hCG
• uterus palpable, along with enlarged ovaries

Causes of Molar pregnancy:
• Genomic imprinting
• Paternal genes = Placental growth (xs paternal genes result in increased placental growth )
• Maternal genes = Fetal growth
• Excess paternal genes à excessive placental or trophoblastic growth
Complications/PE of Molar pregnancy?
• 1st trimester painless bleeding
• Uterine size >EGA (greater than date expected)
• Ovarian enlargement due to theca lutein cysts (complete mole) d/t high hCG
• Hyperemesis gravidarum (increased n/v)
• Early development of preeclampsia (before 20 weeks)
• Hyperthyroidism (hCG looks like TSH) – can see women in thyroid storm
• Hemorrhage (<500mL common)
Risk factors? extremes of age, diet deficient in folate/ Beta-carotene, incidence higher in Asian/latin American countries


Complete Mole:

• 46, XX
o Can have 46, XY if fertilized by two sperm
• All paternal chromosomes
• Haploid sperm fertilizes an “empty” ovum (w/o or inactivated maternal chromosomes)
• No fetal tissue
• see “snowstorm appearance” on US
• Excessive uterine size for gestational age d/t tumor or hemorrhage and retained clot
• assoc. w/ choriocarcinoma
• less common
• see trophoblast hyperplasia/atypia
• uterine size large for dates
• more dangerous
• theca lutein cysts present


Incomplete (Partial) Mole:

• 69, XXY
• Fertilization of ovum with haploid maternal chromosomes by two sperm
• Fetal tissue present; some fetal cardiac tones may be detected
• less ass. w/ choriocarcinoma
• more common
• less trophoblast hyperplasia/atypia seen
• uterine size small for dates
• less dangerous



• Dysmenorrhea- painful menses
• Amenorrhea-absence of three menstrual periods or no menstruation by age 15
• Oligomenorrhea-irregular menses with intervals > 35 days or 4-9 periods in a year
• Menorrhagia- heavy menstruation >80cc
• Metrorrhagia- bleeding in between periods
• Menometrorrhagia-heavy bleeding and bleeding in between menses
• Post- Menopausal Bleeding- bleeding after menopause
• Dyspareunia-Painful intercourse


tampon holds




• AVAF = antevertex (axis of vagina) anteflexed (tipped forward) – felt with abdominal hand
• RVRF = retroverted (axis of patient) retroflexed (tipped back) – felt more with vaginal hand
• axial = strait uterus – not folded over, may appear larger



- Complete Procidentia = uterine and vaginal prolapase
- D/t weaking of muscles (levator ani), fascia (Urogenital diaphragm), ligaments (uterosacral, cardinal ligaments)
- Risk factors:
• Postmenopausal women
• previous pregnancy and vaginal delivery
• Difficult delivery
• Obesity
- Treatment Options:
• Nothing
• Conservative Measures including Kegels, Weight Loss
• Estrogen Cream
• Pessary: plastic device that pushes up everything past pubic bone, take out for sexual intercourse
• Bladder Sling
• Colposacropexy
• Colpocleisis



Overactive bladder:
• Urgency, with or without urge incontinence, usually with frequency and nocturia
• In the absence of pathologic or metabolic conditions that might explain these symptoms
• Diagnosis: very common! is often overlooked and NOT treated
o patient history, symptom assessment
o physical examination
o urinalysis
o Initiation of noninvasive treatment does not require an extensive further workup
• must rule out infection, polydipsia, diabetes, drugs
OAB can lead to disabling conditions ---- must be diagnosed!!!
• OAB is significantly associated with the risk of hospitalization (30% Increased risk in women; 50% increased risk in men) and admission of elderly persons to nursing homes
• Urinary tract infections and skin irritation frequently occur
• 60% of patients with OAB have depression
o OAB may lead to depression or vice cersa – they share common neurogenic pathogenesis
• 19-42% sustain falls – often d/t trips to the bathroom.
o hip fractures assoc. w/ high rates of morbidity and mortality


stress incontinence

• occurs with sneeze, cough, laugh, jog, or do other things that put pressure on your bladder. It is the most common type of bladder control problem in women.
• d/t increased pressure on bladder, combined w/ improper urethral sphincter function along with weak pelvic mm. function
• Causes: genetic, child birth, old age
• 1/3 of women


urge incontinence

• happens when you have a strong need to urinate but can't reach the toilet in time.
• 1/3 of women


Causes of incontinence

• Delirium - addresses by toileting
• Infection – urinary exacerbates incontinence and causes frequency and urgency
• Atrophic urethritis and vaginitis – contribute to irritative symptoms
• Pharmaceuticals – anticholinergics = detrusor underactivity-may cause retention; cholinergics = detrusor overactivity – may cause frequency;α-agonist=outlet overactivity - may cause retention;α-blockers = outlet underactivity – may cause stress incontinence
• Psychological disorders – toileting
• Excessive urine production – or physiologic or pharmacologic nocturia
• Restricted mobility – toileting
• Stool impaction – retention
- need to evaluate DIAPPERS before making a ddx of stress, urgency, mixed or overflow incontinence


LGA baby

LGA baby >4000 grams!


estrogen implant

etonogestrel rod
more effective than permanent sterilization

* break through bleeding thats unpredictable
o irregularity and unpredictability
o ~20% amenorrhea in 1st year --- Increases to 30-40% after 1st year
• can use estrogen to manage bleeding

Other Side effects:
• Acne – b/c its purely progesterone, 17% reported acne
• weight gain – not a significant increase seen, though 12.7% of women did report weight gain
• not contraindicated in obese women or girls! no clinical data
• does not suppress estrogen, and doesn’t cause decreased bone mineral implant
• Bleeding irregularity is the most common reason for discontinuation
• Overall U.S. continuation rate: 75%-84%

Conraindications: very few
• SLE with anti-phospholipid antibodies
• Hepatocellular adenoma
• Discontinue if develops during use: Migraines with aura
• Unexplained vaginal bleeding suspicious for serious condition, before evaluation

Appropriate patients:
• Women desiring highly effective, confidential, “forgettable” contraception


copped IUD

Paragard: Copper T
o Use up to 10 years
o Heavier periods
o No hormonal side effects
o Mechanism:
• mass effects, copper alters uterine and tubal fluid hindering spermatozoa function and motility – inhibits fertilization (but NOT an abortifacient)
o NOTE: DO NOT USE with Wilson’s disease
SE of Copper IUD’s: menstrual changes
o increased menstrual flow – prob not best for younger women
o increased dysmenorrhea,


Mirena IUD

Mirena: Levonorgestrel releasing IUS
o Local Progestin
o Use up to 5 years
o Lighter periods - Irregular for 3-6 months
o Some systemic effects
o Mechanism:
• impairs sperm motility/function
• inhibits contraception – no fertilized ova – NOT an abortifacient
• thickens cervical mucus, causes atrophy of endometrium, impairs tubal motility
• usually doesn’t suppress ovulation
SE of Progestin IUDs: hormonal SE are rare – no weight gain!
• IUD’s should be used as first choice among young women – this is a SAFE form of BC
• 99% effective (more than sterilization!!)


risks for IUDs

• Insertion may be more difficult in nulliparous women
• Higher expulsion in adolescents – d/t fact that it might be too large
• May have higher rates of copper IUD removals due to bleeding and pain
• NOTE: IUD’s had bad rap in the 60’s b/c caused PID and STIS along with perforated uteri
• IUD and PID risk? there is no increased risk
• infertility? does NOT cause infertility
IUD candidates:
• not contraindicated for prior STI/PID
• IS contraindicated for current PID or cervicitis in past 3 mos
• adolescence are OK to use IUDs


injectable contraceptive?

Depot Medroxyprogesterone Acetate: Injectable contraceptive (DMPA)

• can be initiated at any time in cycle, but need to rule out pregnancy

• Highly effective: 96%
• Little compliance required
• Easily concealed
• No decreases in efficacy in overweight women

• Bleeding irregularities – this decreases progressively w/ reinjection – often pts. have amenorrhea after 1st year
• Delayed return of fertility
• **Weight gain – w/g is greater in adolescents who are overweight – 10lb w/g in obese teens
o relative CI for obese teens!!
• Decrease in bone mineral density – after stopping recovery of BMD is seen in 104 years

Contraindications: very few
• Similar to progestin implant
• Severe hypertension (>160/>100)
• Diabetes with vascular disease and / or > 20 years disease

Appropriate pt. population:
• Women desiring effective, confidential, method and who can return for injections
• Women who cannot use estrogen
• Tolerant of irregular bleeding
• Special populations - Sickle cell disease and Epilepsy
o results in decreased vivo sickling and improved hematoligic studies
o raises seizure threshold


Combined Hormonal Contraceptives:

• Safe for most young women
• Added benefit of regulation of menses
• “Typical-use” effectiveness ~ 92% (though perfect use is 99%)
• poor continuation rates among young adults
Side effects:
• break through bleeding, common cause for discontinuation
• acne: certain pills will actually improve acne! (desogestrel and LNG)
• History of a venous thromboembolism
• Known thrombogenic mutations – i.e. Factor V Leiden mutation
• Migraines with aura
• Hypertension, esp. if poorly controlled
• Lupus with antiphospholipid antibodies

Combined Oral Contraceptives:
• Weight and Combined hormonal contraceptives – there is no weight gain link!
• many options go beyond the standard 21-7 method, and can give 3 mos and 12 mos cycles
o advantages: decreased follicular activity and fewer bleeding days/breakthrough bleeding


Contraceptive Patch:

• Weekly transdermal patch - 20 mcg EE + 150 mcg norelgestromin daily
• Continuous delivery
• Less effective if body weight > 90 kg


The Vaginal Ring:

• 3 weeks with 1 week ring-free interval
• Lowest ethinyl estradiol dose (15 mcg EE, 120 mcg etonorgestrel daily) – estrogen is used to prevent break through bleeding
• Continuous dosing
• Use back-up method if out for > 3 hours


bacterial vaginosis

- no inflammation: no itching/inflammation
- overgrowth of gardnerella
- risk factors: sex activity, douching

Diagnosis: Gardnerella Vaginalis
• Diagnosis based on 3 or more Amsel criteria
o Homogenous white to gray discharge – milky discharge w/ fishy odor
o pH > 4.5
o (+) whiff test with KOH
o Clue cells on wet mount
• Gram stain is gold standard, rarely done
BV treatment:
• **Metronidazole = flagil (avoid alcohol)


Yeast infection: Candida Albicans

• KOH prep shows hyphae and spores
• see coattage cheese like discharge with lots of itching


Trichomonas Vaginalis:

• Bubbly discharge of vaginal fluid
• flagellated organisms seen on microscope



• 75% of sexually active adults will be infected sometime in their life
• More than 100 types of virus
• Latent infection:
o Accounts for most HPV
o No visible lesion
o Only diagnosed by DNA hybrid testing
o DNA testing performed in the evaluation of an abnormal pap smear
• Subclinical Infection
o Lesions visible only during colposcopy (looking at cervix through microscope)
o Frequently have an abnormal pap
• Clinical Infection:
o Visible “warty” growths called Condylomata Accuminata
o On vulva, vagina, cervix, urethra, perianal
HPV 6 and 11 = Genital warts = Condylomas: “Low Risk”
• 1 million new cases in U.S. yearly
• HPV infection usually clears spontaneously within 2 years
• tx: relives sx of pain and bleeding and cosmetic concerns
HPV 16 and 18 = Genital neoplasia : “High Risk”
• ASCUS – Atypical Squamous Cells of Undetermined Significance
• ASC – H - Atypical Squamous Cells favor high grade lesion
• AGUS – Atypical Glandular Cells of Undetermined Significance (endocervical cells)
• LSIL – Low Grade Squamous Intraepithelial Lesion
• HSIL – High Grade Squamous Intraepithelial Lesion
• Invasive Cancer
Risk factors:
• no recent pap, young age at first intercourse, increased number of partners, HIV
• smoking – damages the cilia


histology of HPV

• Cervical Intraepithelial Neoplasia
o CIN I - Mild Dysplasia (70% regress, 20% stay same, 10% progress)
o CIN II – Moderate Dysplasia (30% regress, 30% stay same, 30-40% progress)
o CIN III - Severe Dysplasia, Carcinoma in Situ (will go into invasive cancer)
• all need treatment
• Invasive Cancer – all need treatment!


tx of HPV

• Follow up Pap
• Destruction (cauterization, cryotherapy)
• Excision (loop, cone)
o indications for conization:
• Treatment for CIN II or III
• Endocervical disease on colposcopy
• Discrepancy between PAP and colposcopy
• Inadequate colposcopy
• Depth of invasion
• Hysterectomy
• Radical Hysterectomy (includes top third vagina parametrium and lymph nodes)


Endometrial Polyp:

** typoically present with abnormal bleeding

• Hyperplastic overgrowths of endometrial glands and stroma that project from the surface of the endometrium
• Common cause of perimenopausal and early postmenopausal uterine bleeding
• Generally benign, but malignancy highest in postmenopausal women
• Growth of polyps can be stimulated by estrogen therapy or tamoxifen


Uterine Leiomyoma:

" aka fibroids"
Most common type of benign tumor in females
• Leiomyosarcoma is malignant variant

o Asymptomatic
o Abnormal/painful menses
o Abdominal pain
- urinary frequency

NOTE: no mitoses seen

• Subtypes based on location: Pedunculated, Subserosal, Submucosal, Intramural

• Most common benign neoplasia of female genitals
• Smooth muscle and connective tissue growth with thin capsular covering
• Present usually with abnormal uterine bleeding or pelvic pain/pressure
• E/P sensitive (will stop growing during pregnancy and menopause)
o Tend to increase over time as they are stimulated by estrogen
• Rarely (1.5%) become leiomyosarcoma
• Complications: torsions and infertility
• Most common noncancerous tumors of women of childbearing age - 1/5 women greater than 30yo will have fibroids
o Leading cause of hyterectomy in the US



(endometrial tissue in uterine mm.)
• Triad=noncyclical pain, menorrhagia, enlarged uterus w/o adnexal tenderness
• Endometrial tissue growth within myometrium
• Tx: NSAIDs, OCPs, Progestins, ablation, hysterectomy

In adenomyosis, basal endometrium penetrates into hyperplastic myometrial fibers. Therefore, unlike functional layer, basal layer does not undergo typical cyclic changes with menstrual cycle


Postmenopausal Bleeding considerations:

• Bleeding may be a single episode of spotting or profuse bleeding for days or months
• Usually painless
• Pain present if cervix is stenotic, if bleeding is severe and rapid, or if infection, torsion, or extrusion of tumor is present
• Incidence - 4-11% of postmenopausal women
• Atrophic endometrium-59% - endometrium is so thin that it tears
• Endometrial polyps-12%
• Endometrial cancer-10%
• Endometrial hyperplasia-9.8%
• Hormonal effects-7%
• Cervical Cancer-<1%

Atrophic Endometrium:
• Hypoestrogen causes atrophy of the endometrium and vagina results in microerosions which is prone to light bleeding or spotting
• Classic vaginal findings: pale, dry vaginal epithelium that is smooth and shiny with loss of most rugation


Endometrial Hyperplasia:

• Proliferation of endometrial glands resulting in greater gland-to-stroma ratio than observed in normal endometrium
• Postmenopausal women should be estrogen deficient, so endometrial hyperplasia is abnormal and requires an explanation – shouldn’t be seen in these women
• Endogenous estrogen production from ovarian or adrenal tumors or exogenous estrogen therapy are possible causes
• Obese women have high levels of endogenous estrogen due to the conversion of androgens to estradiol, which occur in peripheral adipose tissue
• Classification
o Simple or complex hyperplasia without atypia – tx w/ progesterone
o Simple or complex hyperplasia with atypia – precancerous lesion

NOTE : strong relationship w/ endometrial carcinoma


uterine cancer

• Approx 5-10% of PMB is endometrial cancer
• Incidence increases with age
• Adenocarcinoma of the endometrium is the most common genital cancer in women over 45 years of age


• Thelarche

is the onset of female breast development.



• Pubarche is the appearance of sexual hair.



• Adrenarche is the onset of androgen-dependent body changes such as growth of axillary and pubic hair, body odor, and acne.



• Menarche is the onset of menstruation.


Tanner Stage –Breast:

• Stage 1: Prepubertal
• Stage 2: Breast bud stage with elevation of breast and papilla; enlargement of areola
• Stage 3: Further enlargement of breast and areola; no separation of their contour
• Stage 4: Areola and papilla form a secondary mound above level of breast
• Stage 5:Mature stage: projection of papilla only, related to recession of areola


Tanner Stage – Pubic Hair:

• Stage 1: Prepubertal (can see velus hair similar to abdominal wall)
• Stage 2: Sparse growth of long, slightly pigmented hair, straight or curled, at base of penis or along labia
• Stage 3: Darker, coarser and more curled hair, spreading sparsely over junction of pubes
• Stage 4: Hair adult in type, but covering smaller area than in adult; no spread to medial surface of thighs
• Stage 5: Adult in type and quantity, with horizontal distribution ("feminine")


primary amenorrhea

Failure to menstruate by age 16 (age 15 in US)

if pt. doesn't have secondary sexual characteristics then look at FSH and LH
- elevated FSH And LH = hypergonadotropic hypogonadism: premature ovarian failure or Turner's (45, XO)
- low FSH/LH: hypogonadotrpic hypogonadism

if patient does have secondary sex characteristics then perform U/S of uterus:
- if absent/abnormal: then 46XY (androgen insensitivity syndrome) or 46XX (Mullerian agenesis)
- if uterus present: the look for outflow obstruction (imperforate hymen)
- if no outflow obstruction then evaluate for secondary amenorrhea!!!


secondary amenorrhea

amenorrhoea = Absence of menstruation for >6 months

Secondary amenorrhea = pt. had period then stopped (need to know where you start and how to approach this patient) – want to think about thyroid disease, progesterone challenge, TSH levels and prolactin levels

First check TSH and PRL levels:

1. If both normal then do progestogen challenge test:
A. if bleed = normogonadotropic hypogonadism
B. if no bleeding then do estrogen/progesetogen challenge:
ii. no bleeding = outflow obstruction
iii. bleeding - check FSH And LH levels (if high= hypergonadotropic hypogonadism, if low think pituitary tumor or hypogonadotropic hypogonadism)

2. normal PRL, abnormal TSH = thyroid disease

3. Normal TSH, anbnormal PRL: consider prolactinoma


look at amenorrhea flow charts!

do it now!!!


causes of primary amenorrhea?

• Constitutional delay
• Chromosomal e.g. 45XO, 46XY (they are male OR have Turner Syndrome – short stature, webbed neck, amenorrhea, developmental difficulties )
• Pituitary tumour e.g craniopharyngioma
• Congenital adrenal hyperplasia ** most common cause **
• Genital tract anomaly
• (Plus all the causes of secondary amenorrhoea)
Clues to ddx:
• Constitutional delay – delayed secondary sexual characteristics
• Chromosomal e.g. 45XO, 46XY – think Turners Syndrome
• Pituitary tumour e.g craniopharyngioma – Visual field defect
• Congenital adrenal hyperplasia – Virilzation
• Genital tract anomaly- Imperforate hymen
Diagnostic Steps:
• Height, weight and BP
• Evaluate secondary sexual characteristics
• Look for signs of androgen excess- hirsuitism, acne
• Do visual field exam → pituitary tumor
• Chromosomes
• FSH, LH and E2
• Maybe HydroxyPROG, Androgens, PRL, TSH
• Maybe CT pituitary


causes of secondary amenorrhea?

Common Causes:
• Hypothalamic
o “Stress” – can cause hypothalamic dysfunction
o Weight loss/gain (Anorexia)
o Post Pill and Depo Provera
• PCO Syndrome (1:20 women)
• Premature Menopause
o Idiopathic
o Iatrogenic
o Resistant ovary syndrome – ovary doesn’t respond to FSH/LH
• Hyperprolactinaemia
o Physiological
o Pituitary adenoma
o Drug-induced
• Remember also pregnancy & progestins!
Uncommon causes:
• Kallman’s Syndrome – have loss of smell,
• Sheehan’s Syndrome – postpartum hemorrhage – infarct their pituitary
• Cushing’s Syndrome -
• Other Pituitary Tumors
• Post encephalitis/trauma
• Thyroid disease – both hyper and hypothyroid can cause abnormal menstruation
• Androgen-producing Tumors
• Asherman’s Syndrome – there is no endometrium – open uterus and put IUD in the uterine cavity
• Cervical stenosis – cervix is closed, there is no os for the blood to come out
Clinical evaluation:
• Life events
• Weight/Exercise history
• Pregnancy
• Drugs
• Galactorrhoea – pituitary adenoma
• Hot flushes – premature ovarian failure
• Headaches/Vision – pituitary adenoma
• Height/Weight BP
• 20 Sexual characteristics- Hirsutism/Virilisation
• Genital tract oestrogenisation
• Cervical stenosis
Primary tests:
• Androgens
• Ultrasound pelvis
• Visual fields
• Progesterone challenge test
Secondary tests:
• CT Pituitary
• Other pituitary hormones
• Dexamethasone suppression
• HydroxyPROG – thinking CAH
• Hysteroscopy or HSG – look inside uterus esp. if they have had prior issues
• Laparoscopy & ovarian biopsy



• Ectopic endometrium i.e. “internal menstruation” = endometrium outside of uterus, unknown how it gets there- could be blood born, or could just b d/t retrograde menstruation (which all women have)
• Requires laparoscopy +/- biopsy for diagnosis

Classic Triad:
• Dysmenorrhoea – painful menses
• Dyspareunia – most common site is utero-sacral ligament → painful sex
• Infertility
- abnormal bleeding, disordered cycles also common

ddx of endometriosis:
#1: careful hx
#2: rule out other causes of sx
* laparoscopy is gold std. but very invasive


management of endometriosis?

when problem infertility – need to make sure tubes are open and reduce tumor volume – use surgery
o laparoscopy: w/ cauterization of endometriosis is more effective than just looking – works great for pain as well and results in slightly improved fertility

when the problem is pain – use medical rx
o Progestins – use longer pills where pt. doesn’t have their period at all
• COC (best in continuous form) -
• Provera or Norethisterone
• The Mirena IUD
o Danazol & Gestrinone – like a GnRH agonist – don’t get feedback, putting pt. into menopause through inhibition of ovulation feedback loop
• less side effects than GnRH agonists
o GnRH agonists +/- Add Back Therapy – will develop hotflashes unless use “add back” therapy – use progesterones to stimulate some ovulatory type sx
• have lots of dyspareunia and bad side effects

when there is no problem – don’t have to treat it



= walled off endometriosis causing a chocolate cyst = filled with hemosiderin laden macrophages and blood w/in the cyst



After 12 months of regular sex without contraception...
• The age of the woman has a major influence

• A basal body temperature chart (BBT)
o Accurate body temperature measured once daily after >8 hours at rest
o Progesterone (released only after ovulation) raises BBT by 0.3 – 0.50C
o know that when progesterone is circulating, they have ovulated
• Serum Progesterone luteal phase of the cycle
o Preferably 7 days before menstruation
• LH surge in urine
o False positives can occur
• Endometrial biopsy 2nd half of the cycle
o Look for secretory changes on histology

Tests of tubal patency:
• Hysterosalpingogram- Passage of radio-opaque dye from the cervix with pressure and fluoroscopy or still images
• Laparoscopy with dye studies
o **The best test because it involves direct observation
o **And the only way of diagnosing endometriosis
o may be a form of tx b/c die may push the blockage out
• All of these tests have potential for therapy if there is minor tubal obstruction
o And diathermy of minimal endometriosis reduces “reproductive toxins”



Perimenopause – time leading up to menopause -0 the time when ovarian function and hormone production are declining but have not yet stopped
• if start HRT early, there may be a window where you can prevent the disease of menopause like dementia
• median onset = 47 years



a permanent cessation of the menstrual cycle
• Greek “meno” (month) and “pausis” (a pause)
• Defined as not having a period for 12 months
• average women reach menopause age 51

Menopause related changes:
• Vasomotor symptoms – hot flashes may continue for long time after
• Sleep quality1
• Mood changes2
• Urogenital symptoms – burning
• Sexual well-being3,4
• Skin changes5


post menopuase

: time in woman’s life after last period
• women live in this stage for longer time than ever before
• most women spend 1/3 to ½ of life in post menopause


hormonal changes during menopause?

Decreased estrogen results in….
• Well Established
o Vasomotor Symptoms – hot flashes
o Urogenital Disorders – prolapse, incontinence, dyspareunia
o CHD Risk Factor (Lipids) – decreased HDL → CV disease
o Skin Changes
• Association
o Cardiovascular Disease
o Bone Loss/Osteoporosis
Decreased Progesterone results in ….
• Irregular periods
• Premenstrual syndrome (PMS)
Decreased Androgens (produced by ovaries as well)
• Decrease in mood
• Diminished energy
• Impaired sexuality
• Muscle weakness
• Osteopenia


Risks and benefits of HT?

• Cardiac disease: no change
o HT does not increase CHD risk in women who initiate therapy close to the onset of menopause (within-5 years of last menses)
o HT does not prevent and may increase the risk of CHD in women who initiate therapy years after menopause

Venous Thromembolism: is an infrequent but well established risk of HT
o Risk increases approximately 2-fold with HT use
o Greatest risk occurs in the first year of use
o Absolute risk remains low in HT users due to the low baseline incidence of VTE in the general, non-hospitalized population – may just be because women have higher risk of VTE

coronary heart disease – this is the number one killer - reduced
o coronary artery disease: on initiation of HRT women had reduced risk of death
o age of initiation of HRT determines if CV risk is increased or not – if want to get the most benefit then need to start it early
o the people who use HT have decreased risk of CAD than women who don’t
o thus women who start HT closer to menopause tend to have reduced CAD!!!!

osteoporosis - reduced

breast cancer
o combination HT users have similar risk vs. nonusers – if women uses estrogen she is more likely to be node negative
o estrogen only HT has different or decreased risk in breast cancer

• dementia – HRT is helpful for this
o estrogen seems to protect against dementia when taking early in perimenopuase or in early menopause!

transdermal route/patch has less SE of VTE and is thus preferred

HT is best for women w/ moderate to severe menopausal sx!



= "hyperandrogenic anovulation"

hormone levels:
o hCG – is normal
o FSH/LH : LH>FSH: 3:1
o TSH normal
o PRL normal

U/S: shows string of pearls multiple immature follicles
o don’t have to get an U/S – can be a clinical ddx

Criteria for PCOS:
o oligoovulation
o excess androgen
o polycystic ovaries on US

clinical findings:
- anovulation
MMR and amenorrhea d/t increased tesosterone and increased androgens
- infertiliy
- acne: hyperandrogenism
- polycistic ovaries
- insulin resistance
- high cholesterol and premature atheroscloerosis

• abnormal bleeding
• infertility, secondary to anovulation
• increased risk of endometrial cancer – pt. is seeing more cancer
• increased CRP
• metabolic syndrome, increased CVD
• increased risk of type II DM, HTN, hyperlipidemia
• non alcoholic steatohepatitis
• obstructive sleep apnea

• the pt. has high levels of testosterone and androstenedione and really high levels of estrogen b/c they aren’t ovulating (keep making estrogen until finally endometrium sloughs off) – don’t make progesterone b/c don’t ovulate
• make more LH than they should – thus the ovaries get luteinized and don’t respond appropriately
• So they don’t menstruate

• contraceptions used for abnormal bleeding
• if don’t want contraception then treat them cyclically – given progesterone every few months to stimulate shedding
• if come in for hirsuitism – use OC’s, steroids, spironolactone
• pregnancy: make sure its PCOS, and induce ovulation through FSH or through clomiphene