Leiomyomata are what
Localized proliferation of smooth muscle cells surrounded by a pseudocapsule of compressed muscle fibers.
Highest prevalence of leiomyomata what age
Fifth decade
1/2 of black women
1/4 white women
Clinically apparent in 25-50% of women, but studies suggest that the prevalence may be as high as 80%
More conservative options than hysterectomy for leiomyomata
Myomectomy
Uterine curettage
Operative hysteroscopy
Uterine artery embolization
Leiomyoma, hormone responsiveness
Estrogen --> grows... esp in high estrogen conditions such as pregnancy.
Menopause thus causes cessation of umor growth, and some atrophy.
How does estrogen trigger growth of myomas
Estrogen increases progesterone receptors, which then triggers increased growth.
Leiomyomata arise from what
Single cells --> in many cases the cell is smooth muscle from the vasculature in origin.
Leiomyosarcoma, suspicion should be high in what context
Rapidy enlarging uterine mass, PMB, unusual vaginal discharge, and pelvic pain in a postmenopausal patient.
Enlarging uterine mass in a PM patient should be evaluatled with considerably more concern than the premenopausal patient.
Composition of leiomyosarcomas
More heterolgous, mixed... contains other sarcomatous tissue elements not necessarily found only in the uterus...
Most common presentation of leiomyomata
Development of progressively heavier menstrual flows that last longer than normal duration... menorrhagia (defined as blood loss >80ml)
Mech of bleeding in leiomyomata
1. Alt of normal myometrial contractile function in the small artery and arteriolar blood supply underling the endometrium.
2. Inability of overling endometrium to respond normally to hormones
3. Pressure necrosis with exposure of underlying vasculature.
Besides bleeding, another common symptom for LM
"Pelvic pressure" or the sensation of pelvic fullness... these may attaina massive size and are most easily palpable on bimanual.... lumpy bumpy or cobblestone sensation....
Large LM may lead to compression of ureters...
LM may also cause secondary dysmenorrhea. Occasionally torsion of pedunculated --> acute pain.
Labor like pain with LM
Dull intermitteint low midline cramping when a pedunculated myoma progressively prolapses through the internal os of the cervix...
How to diagnose fibroids
Endometrial sampling --> irregularities of the uterine cavity, often the diagnosis is incidental to path assessment
Abdominopelvic exam ---> can feel midline irregularly countered mobile pelvic mass --> say in date weeks
Pelvic US -> but diagnosis is clinical --> may be acoustic shadowing, areas of distorted endometrial stripe
CT/MRI for large ones
Hysteroscopy, hysterosalpingography, saline infusion US
Uterine sounding as a part of endometrial biopsy. (biopsy is good to rule out other things)
Surgery if diagnosis is unclear
Medical treatment for myomata
Progestin supplementation intermittent. Decreaes the amount of menstrual flow and 2/ dysmenorrhea.
Indications for a myomectomy
Rapidly enlarging pelvic masss
Persistent bleeding
Pain or pressure
Enlargement of an asymptomatic myoma to more than 8 cm in a women who has not completed childbearing
Actions before hysterectomy for myomata
Confirm no cervical or endometrial malig
Surgical risk from anemia
Eliminate anovulation and otehr causes of weird bleeding.
GnRH analogs for myomata?
CAn reduce fibroid size by as much as 40% to 60%, but generally limited to six months of treatment. Commonly used before a planned hysterectomy to reduce blood loss as well as difficulty of the procedure.
Danazol has been less effective.
What is involved in UAE
Bilateral uterine artery cannulation
Injection of polyvinyl alchol particles, which cause acute infarction of target myomata.
Bleeding,pressure, and pain relieved in >85% of patients.
Complications of UAE
Postembolization pain in 10-15% of patients
Delayed infection
Passage of necrotic fibroids up to 30 days after procedure.
Newest approach for leiomyomata
MRI guided focused US which raise temp in myomas by 70 deg cel. Coagulative necrosis. Minimal pain, appears to improve quality of life...
Myoma size that starts to impede with labor, and complications
>3 cm
Preterm labor, placental abruption, pelvic pain, cesarean delivery... Myomas can grow a lot during pregnancy, and can cause pain due to red or carneous degeneration as they outgrow their blood supply.
When should myomectomy be used in pregnancy
Only when myoma is pedunculated with a clear stalk
Patients typically pretreated wth B-adrenergic tocolytics
Vag birth after this is controversial, sig risk of uterine rupture.
Risk factors for pelvic support defects
Genetic predisposition
Parity
Menopause
Advancing age
Pelvic surgery
Connective tissue d/o
Elevation of intraabdominal pressure --> obesity, or chronic constipation, or heavy lifting
Atrophic changes due to loss of estrogen
Prolapse may be so severe as to cause what
Hydronephrosis or hydroureter, due to insertion of hte urter into the trigone, thus kinking the trigone
What may mimic a cystourethrocele (pelvic support defect)?
Urethral diverticulum
Skene gland abscess
Women at high risk for prolapse complications and who no longer desire sexual intercourse
Colpocleisis --> complete obliteration of the vaginal lumen.
Prolapsed but no incontinence, what should be discussed at the time of surgery
Some women may develop incontinence AFTER the surgery...
What happens in stress incontinence
Normal phys allows increased ab pressure to be transmitted along entire urethra. In patients with stress incontinence, pressure is only on bladder and its neck, thus it descends
How to eval urinary incontinence
PE --> pelvic
Direct obs of urine loss
Measurement of postvoid residual
Urine culture
U/A
Urodynamic testing
Cystourethroscopy (in prep for surgery)
Urodynamic testing, single channel
Patient voids, and the volume is recorded. Urinary cath is then placed and the post void residual is recorded. Bladder filled in retrograde fashion. PAtient is asked to note when she first feels fullness/diesre to void, and when she can no longer hold urine
First - 100-150 cc
Second - 250 cc
Third - 500-600 cc
Urodynamic testing, multichanel
Transducer to measure intraabdominal pressure.. allows assesment of entire pelvic floor. Uninhibited bladder contraction can be clearly documented.
What explains 20% asymptomatic bacteriuria in PM women
Estrogen deficiency causes a decrease in urethral resistance to infection, which contributes to ascending contamination.
Organisms assoc with structural abnormalities of urinary tract, indwelling catheters, renal calculi
Proteus
Pseudomonas
Klebsiella
Enterococcus
GBS, fungal stuff in people with indwelling catheters.
When is a culture used in the mgmt of UTI
Lower - usually when treatment fails
Upper - at time of diagnosis
Problem with Dipstick tests
False negatives are common, so if symptoms are there, a urine culture or U/A should be performed.
Duration of therapy for UTIs
As low as three days is effective, of BActrim, Trimethoprim, Cipro, Levo, and Gati
Mgmt of recurrent UTIs
Assess for risk factors:
- frequent sex
- long term spermicide
- diaphragm use
- new sex partner
- young age at first uti
- maternal history of uti
Who should be treated for asymptomatic bacteriuria
All pregnant women
Urologic procedures
Catheter acquired bacteriuria persistent for 48 hours.
Thats it!!
Why does FSH begin to rise many years before the advnce of actual menopause
As reproductive age grinds on, remaining oocytes become increasingly resistant to FSH
FSH in menopause
>30 mIU/mL
FSH in prime reproduct years - 6-10
Perimenopause - 14-24
Childhood - <4
Postmenopausal ovary, what is going on
Theca cell islands produce androgens in response to LH.... Postmenopausal testosterone concentrations are higher by 2/3 in women with intact ovariies
What estrogen is considered extragonadal
Estrone. Concentration is related directly to body weight, because androstenedione is converted to estrone in fatty tissue.
Obese vs thin menopausal tradeoff
Obese - higher risk of endometrial cancer
Thin - higher rate of hot flashes
What is considered perimenopause
Late 30s early 40s, when the concentration of FSH begins to increase from normal cyclic ranges (6-10) to perimenopausl 14-24.... During this period, women begin to experience ssx of decreasing estrogen levels.
What is the first physical sign of decreasing ovarian function
Hot flush, a sx of vasomotor instability
Hot flushes differential diagnosis
Menopause
Thyroid disease
Epilepsy
Infection
Hodgkin lymphoma
Alcohol/use of certaind rugs.
Bone density decline in perimenopausal vs postmenopausal
0.5% vs 1-2% per year
Loss is more in trabecular vs cortical bone.
Chromosomal aberrations behind premature menopause
Partial deletion of long arm of one X chrom --> premature ovarian failure.... thus Turner syndrome.
What is Savage Syndrome
aka Gonadotropin resistant Ovary Syndrome. Adequate number of ovarian follicles yet these follicles are resistant to FSH and LH. Exogenous estrogen helps... because estrogen stimulates FSH receptors in ovarian follicles.
Hysterectomy with ovarian preservation.... menopause effects
Go into menopause 3-5 years earlier than other people.
WHI revealed what cancer effects of HRT
Increased risk of MI, stroke, VTE, and breast cancer
Decreased risk of colorectal cancer and hip fractures
Definite CI to HRT
Undiagnosed abnormal genital bleeding
Known or suspected estrogen-dependent neoplasia, except in appropriately selected patients
ACtive DVT, PE, or history
Active stroke or MI
Liver dysfunction or disease
Known or suspected pregnancy
HSN to HRT
Problems with Dong quai or red clover
Interaction with drugs, esp by potentiating the effects of warfarin.
Non estrogen treatment of hot flushes
SSRIs (venlafazine, paroxetine, and fluoxetine)
Gabapentin
Cetirizine
Progesterone (off label!)
PAtient has history of weird vaginal bleeding, you want to start HRT. What hsould be documented
Normal endometrium by tissue diagosis
Pelvic US with an endometrial strip of <4mm
Colles fracture
Fracture of the distal radius in the forearm with dorsal (posterior) displacement of the wrist and hand.
Most common reason why women will stop HRT
VAginal bleeding - irregular bleeding occurs within the first six months.
When who are amenorrheic for a time are often disturbed by the resumption of any vaginal bleeding/spotting and find it intolerable.
Incidence of multiple gestations inthe US
3%
1/90 twinning, slightly higher in blacks than in whites.
Incidence is increasing with age and the use of assisted reproductive techniques. Weirdly enough this includes monozygotic twins
Diamnionic / Dichorionic, when is the split
Within 3 days of fertilization. Each fetus surrounded by own amnion and chorion
Division day for monoamnio/dichorio
4-8 days post fertilization... Chorion has already started developing, whereas the amnion has not....
Conjoined twins, where conjoined, how often, and mortality rate
Chest or abdomen most commonly
1/70000 deliveries
Mortality rate of >50%
Multifetal vs singleton pregnancies.... morbidity
3-4x that of a singleton pregnancy, mostly from preterm labor.
Average age of delivery of twins
37 weeks
Triplets - 33 weeks
Quadruplets - 29 weeks
With each additional fetus, GA at delivery is decreased by approx 4 weeks.
Morbidities of multifetal gestation
Preterm - biggest
IUGR
Hydramnios - 10%
Preeclampsia
Congenital anomalies
PPH
Abruptio placenta
Umbilical cord accidents
Cord abnormalities in twins
Single umbilical artery in 3-4% of twins, compared to 0.5-1% of singletons.
Twin-twin transfusionsyndrome
Seen in monochorionic
Donor twin - impaired growth, anemia, hypovolemia, and other problems incl oligohydramnios
Recipient twin - Hypervolemia, HTN, polycythemia, CHF as a result of this preferential transfusion
Percent of twins with IGUR, and admission to NICU
IUGR - 14-25%
PICU - 25%
Risk of CP gets higher as well
When should twins be suspected
When uterine size is large for calculated gestational age. >4 cm or more ...
>4 cm beyond gestational age in fundal size
Inaccurate dates
Multiple gestation
Hydramnios
GEstational trophoblastic disease
Pelvic tumor
What percent of twins diagnosed in first trimester result in delivery of viable twins
50%... other 50% result in single fetus because of intrauterine demise and ultimate resorption of one embryo/fetus --> vanishing twin syndrome.
Management of twin gestation, what should be done in midtrimester
Cervical exams to detect early effacement and dilation q1-2 weeks.
Transvag U/S for cervical legnth
What is discordant growth in multifetal gestation
15-25% reduction in estimated fetal weight of the smallest fetus vs the largest. Perform U/S more frequently in this case.
TWin presentation during delivery
40% vertex vertex (aka cephalic cephalic)
40% A: vertex, B: anything else --> eexternal cephalic version using US, or breech extraction (aka internal podalic version)
20% first twin is in breech, C-section....
Late follicular phase, what happens
Peak estradiol oconcetratiosn from the dominant follicle reverse and instead have a postivie feedback effect on the pituitary which stimulates the mdicycle surge of LH that is necessary for ovulation.
What leads to cessation of menstruation
Rising estrogen levels in the early follicular phase --> induces endometrial healingand leads to cessation off menstruation
What becomes the dominant follicle
The follicle with the most granulosa cells thus the most FSH receptors. The other follicles undergo atresia
Oocyte arrests in what phase
Meiosis of primary follicle completes after LH surge. The oocyte then arrests in metaphase of meiosis II until fertilization
What is luteinization
Coversion of follicle to producing progesterone post ovulation. Progesterone has negative feedback on pituitary secretion of FSH and LH, and thus both hormones are suppressed in the luteal phase.
Corpus luteum also produces estradiol at the same time asprogesterone, but less than progesterone.
hCG does what early on
Sustains the corpus luteum for antoehr 6-7 weeks. After which, the placenta produces the progesterone.
Cervical mucus changes
Estrogen - Large quantities of thin clearwatery mucus - Spinnbarkeit
Progesterone - thicker, decreased mcuus --> mucus plug.
When is Adrenarche, approximately
6-8 yo. Involves the increased production of androgens, occurring in the adrenals.
Obesity and pubertal onset
Mild to moderate obesity results in earlier puberty, whereas thinness results in later puberty. Much of the ethnic differences can be attributed to that
Abnormalities of puberty
Precocious
Primary amenorrhea
Delayed sexual maturation
Incomplete sexual maturation
Initial eval for pubertal problems
FSH and LH, which can help distinguish a hypothalamic pituitary problem from a gonadal problem
Idiopathic precocious puberty, what happens
Arcuate nucleus of the hypothalamus is triggered early. This also results in short stature in adulthood 2/2 premature closure of the epiphyseal plates.
What is McCune-Albright syndrome
aka Polyostotic fibrous dysplasia.
Multiple bone fractures
Cafe-au-lait spots
Precocious pubrety, which can be the first sign.
Thought to arise from defect in the cellular regulation with a mutation in the alpha subunit of the G protein which stimulates cAMP formation, which causes tissues to function autonomously. E.g. ovary produces estrogen without need for FSH.
Late onset CAH
Tedne to present in adolescence, in this disorder, cortisol and aldosterone is not produced as much as androgens. This results in precocious adrenarche. Appears somewhat like PCOS
Pathognomonic finding in 21 hydroxylase deficiency
Elevated 17 hydroxyprogesterone level. You can also measure renin to determine mineralocorticoid deficiency.
Goals of treatment for precocious puberty
Arrest and diminishment of sexual maturation until normal pubertal age
Maximize adult height.
Peripheral causes of precocious puberty
Exogenous steroid administration
Primary hypothyroidism
Ovarian tumors --> Granulosa or theca cell, lipoid cell, gonadoblastoma, cystadenoma, germ cell
Simple ovarian cyst
McCune-albright syndrome
Delayed puberty
2/ sex characteristics not by age 13
No evidence of menarche by age 15-16
When menses have not begun 5 years post thelarche.
Delayed puberty + elevated FSH
Gonadal dysgenesis e.g. Turner syndrome. Hypergonadotropic hypogonadism
Delayed puberty + FSH + LH <10
Constitutional physiologic delay
Kallman syndrome
Anorexia / Extreme exercise
Pituitary tumors / Pituitary dysorders
HyperPRL
Druguse
Most common cause of delayed puberty
Turner syndrome. Streak gonads with absence of gonadal follicles
Treatment for Turner syndrome
Estrogen administration at normal initiation of puberty.
GH before that to maximize adult height
Progestins once Tanner Stage IV has been reached, because progestin therapy can prevnet breast from devloping completely thus, resulting in an abnormal contour - tubular breast
Hypogonadotropic hypogonadism
Most commonly due to constitutional delay with concurrent delay of boen maturation with resulting short stature.
Kallmann syndrome
Olfactory tracts are hypoplastic
Arcuate does nnotsecrete GnRH.
Young women with Kallmann syndrome have little or no sense of smell and do not have breast development.
Can be treated with GnRH pulsatile!! Everythign is pretty normal. Ovulation can be triggered through exogenous gonadotropin, and progesterone can be given in the luteal phase to allow implantation of the embryo.
Most common tumor associated with delayed puberty
Craniopharyngioma. Develosp in the pituitary stalk with suprasellar extension from nests of epithelium derived from Rathke pouch. Radiologic hallmark is the appearance of a suprasellar calcified cyst
Most common cause of primary amenorrhea in women with normal breast development
Mullerian agenesis or Mayer rokitansky kuster hauser syndrome. Congential absence of the vagina, and usually an absence of the tuerus and fallopina tubes. Ovarian fucntion is normal... so that's why there is normal seconday sex characteristics.
May also have renal weridness, skeletal anolies.
Sporadic in expression!!
Imperforate hymen, how does this present
Pain in the area of the uterus
Bulging, blueish appearing vagnial introitus
Most common gynecologic abnormalities in reproductive aged women
Amenorrhea
Abnormal uterine bleeding (ovulatory or anovulatory)
In amenorrhea, what test can be used to determien if the patient has adequate estrogen and competent endometrium, and also a good outflow tract
Progesterone challenge test
Treatment of heavy abnormal uterine bleeding
Acute - High dose estrogen and progestin therapy
Long term - Intermittent progestin treatment or oral contraceptives. Uterine bleeding that does not respond to medical therapy often is managed usrgically with endometrial ablation or hysterectomy. But you need to r/o endometrial carcinoma first.
What three androgens may be looked at in diagnosing hirsutism and virilization
Dehydroepiandrosterone (DHEA) (Sulfate is longer lasting, produced principally by the adrenals)
Androstenedione
Testosterone
Most potent androgen
Dihydrotestosterone (DHT), which is produced from testosterone by the local action of 5alpha-reductase
Why is estrogen and testosterone prety well connected
Estrogen stimulates liver production of SHBG, which binds up free testosterone, and thus less is available for physiologic actions.
Diagnostic criteria of PCOS
Oligoovulation or anovulation usually marked by irregular menstrual cycles
Hyperandrogenism clinical or biochem evidence
Polycystic appearing ovaries on Ultrasound
Hormone concentrations in women with PCOS
LH:FSH ratio increased
Estrone > estradiol
Androstenedione at upper limits of normal or increased
Testosterone at upper limit of normal, or slightly increased
Cholesterol in PCOS
Metabolic syndrome (Syndrome X)
Elevated triglcyeride levels
Low HDL
Elevated LDL
Hyperthecosis
More severe form of PCOS. May be so great that testosterone concentratin reaches virilization capacity. Temporal balding, clitoral enlargement, deepening of the voice, and limbgirdle remodeling.
Hyperthecosis!!! Refractory to OCPs commonly
What tumors cna cause hirsutism and virilization
Sertoli-Leydig cell tumors
Uncommonly:
- Gynandroblastoma
- Lipid (lipoid) cell tumors
- hilar cell tumors
Sertoli-Leydig cell tumors
<0.4% of ovarian neoplasms
Ages 20-40
Unilateral 95%
may reach 7-10 cm in size.
Sertoli Leydig cell tumor onset
Rapid onset of acne, hirsutism, amenorrhea, and virilization. Defeminization and then masculiization. May occur over 6 months or less
Hilar cell tumors, who gets them
Overgrowth of mature hilar cells or from ovarian mesenchyme and are typically found in postmenopausal women. hilar cells ar ehomolog sof itnerstitial or leydig cells of the tests.
hilar cell tumors histo
Pathognomonic Reinke albuminoid crystals. Grossly, always small, unilateral, and benign.
CAH (21h def) manifestations at puberty if it doesnt present until then
Adrenarche precedes thelarche
Pubic hair growth before onset of breast development
Diagnosis of 21h deficiency can be made how
Increased 17-OH progesterone in plasma during follicular phase. If les severe, may only come out with ACTH stim test.
Clinical features of 11beta hydroxylase deficiency
Increased androgen production, Mild hypertension, and mild hirsutism.
Androgen secreting adrenal adenomas
DHEA-S > 6 mg/ml. Diagnose via CT or MRI scan of adrenal glands.
Constitutional hirsutism, possible root cause?
Greater activityof 5alpha-reductase.
Treatment: Spironolactone can do it. Androgen blocker that also inhibits testosterone production by the ovary, reduces 5alpha-reductase activity.
Androgen blockers
Spironolactone
Flutamide
Cyproterone acetate
Finasteride (inhibits 5alpha-reductase)
Also should take OCPs because these are teratogenic. OCPs also increase production of SHBG...
Drugs with possible virilization qualities
Danazol - attenuated androgen used for endometriosis. Voice changes may be irreversible.
Progestin only oral contraceptives - some are more androgenic then others.
What dominate the luteal phase of the menstrual cycle
Progesterone --> thickens cervical mucus, increasesa basal body temp by about 0.6 degrees F.
When does ovulation occur according to LH kits
Approx 24 hours after urinary evidence of hte LH surge.
Testing for women center first around what
Ovulation or anovulation
Then --> PCOS, or thyroid disorders, or PRL
Lab testint for ovulatory dysfunction
bHCG
TSH
PRL
total testosterone
Dehydroepiandosterone sulfate
FSH
LH
Estradiol
Treatment centers around any of these
Potential uterine abnormalities
Leiomyomata
Endometrial polyps
Intrauterine adhesions
Congenital anomalies - septate, bicornuate, unicornuate, or didelphyic uterus
Obstructive azoospermia, possibly treatment
Percutaneous epididymal sperm aspiration PESA
Microsurgical epididymal sperm aspiration MESA
Gonadotropin therapy requires frequent monitoring with what
Transvaginal US
Serum estradiol measurements...
Then HCG is administered to trigger ovulation.
IUI, what sperm concentration is necesary
1 million must be present, as pregnancy is rarely achieved with lower results. Good for mild male infertility
Success rates of IVF depend upon what
Etiology of infertility and the age of the female partner. As high as 40-50% and as low as 2%...
Counseling of patients with IVF
Risk of multiple gestation
Ethical issues surroudnign multifetal pregnancy reduction
Adoption
FSH in exercise induced hypothalamic amenorrhea
Normal usually. But still treated with LH and FSH if behavioral modification does not work.
What is a good test for ovarian reserve
Clomiphene challenge test. Clomiphene is given days 5-9 of menstraul cycle, FSH is checked on day 3 and 10.
Cycles that vary in length, best way to get pregnant from having sex once?
Use an ovulation predictor kit.
Normal and predictable sequence of sexual maturation
Thelarche
Adrenarche
Growth spurt
Menarche
Age 10 to age 12.7
Three known critical elements for secondary sexual characteristics
Adequate body weight
Sleep
Optic exposure to sunlight
Noonan syndrome
Characteristic facies
Learnign disabilitites
Delayed menarche
Forehead is wide and face taper to chin,
Chest is broad, widely spaced
Absent uterus, vagina ends in a blind pouch, but present ovaries. Amenstrual
Mullerian agenesis --> renal ultrasound to look for kidney abnormalities which go hand in hand with this diagnosis sometimes (25-35% of patients)
Rokitansky-Kuster-Hauser syndrome
Vaginal and uterine agenesis, is not suspected in this case due to the normal pelvic exam findings. Aka mullerian agenesis. Ovaries are there!!
Kallman syndrome treatment
Pulsatile GnRH. Defect is all the way up in the arcuate nucleus where pulsatile GnRH is created.
Post pill amenorrhea
History of irregular cycles prior to pill use may increase the risk of amenorrhea upon discontinuation. Sometimes referred to as post pill amenorrhea.
Lifestyle interventions helpful in PMS and PMDD
Aerobic exercise
Calcium carbonate and mag supplementation
Pharm agents in PMS
NSAIDs --> esp in dysmenorrhea, breast pain, and leg edema. Not useful in treating other aspects of PMS.
Spironolactone decreases bloating but no other symptoms.
Danazol
GnRH agonists
OCPs
SSRIs
PMDD treatment
Ovulation suppression doe snot seem to help patients wtih PMDD
SSRIs do help --> gold standard of treatment.
The ONLY OCP --> Drospirenone and Ethinyl Estradiol.
Oophorectomy is a last resort.
Risk factors for PMS
FHx
Vit B6, calc, mag deficiencies
Age --> 30s
Prev anxiety, depression, or other mental health issues --> PMDD
Hirsutism in a teenager with normal testosterone levels
Consider CAH --> get a 17-hydroxyprogesterone level
Treatment of idiopathic hirsutism
OCPs --> establish regular mensese, and lower ovarian androgen production. They also increased SHBG which binds up more free testosterone.
Postpartum hair loss?
High estrogen levels in pregnancy can increase the synchrony of hair growth. This can result in significant apparent hair loss post partum
Virilization symptoms
Frontal hair thinning
Oily skin or acne
Deepening of the voice
Clitoral enlargement
Menstrual irregularities
Increased muscle strength
What is hyperthecosis
More severe form of PCOS --> assoc with virilization due to the high androstenedione production and testosterone levels.
Mechanism for progesterone controlling of irregular bleeding
Irregular bleeding is due to proliferative endometrium from unopposed stimulation by estrogen. Progestins inhibit further endometrial growth, thus converting proliferative ot secretory endometrium.
Next step after endometrial biopsy for intermenstrual bleeding
Look for structural abnormalities with a pelvic ultrasound
ACOG routine screening
25yo and younger - chlamydia
All sexually active adolescents for chlamydial infection
Women with developmental disabilities
HIV screening for all women who are or evenr have been sexually active
ACOG screening based on risk factors
Multople sexual partners, sexual partner with multiple contacts
ASymptomatic women aged 26 yo and older at risk --> GC and chlamydia
C. trach, what is this
Gram neg obligate intracellular bacterium
Most frequently reported infectious disease in the states
Chlamydia treatment
Azithromycin
Doxycycline
Alternatives:
Erythromycin base, erythromycin ehtylsuccinate, ofloxacin, levofloxacin
Who gets a test of cure
Suspected nonadherence
Reinfection?
3-4 weeks after treatment
All women with chlmaydia infection should be retested 3 months after treatment.
Chlamydia treatment sex recomendations
Abstain until treatment is complete, and all partners are tested.
N. gonorrhea compliucations
Increased transmission of HIV
PID
Bartholin abscesses -> I&D may be appropriate
Testing for gonorrhea of the pharynx or rectum
Culture, no other tests are availableor FDA approved.
Antibiotics for GC
Ceftriaxone
CEfixime
Cipro --> quinoline resistance on the rise.
If Chlamydia is r/o via NAAT, no need to treat
Other nonGC&C organisms for PID
Mycoplasma
STreptococcus
STaphylococcus
Haemophilus
E. coli
Bacteroides
Pepto
Clostridium
Actinomycyes
Greatest risk factors for PID
Prior PID
Adolescence
Multiple sex partners
Not using condoms
Infection with any caustive organisms
PID DDx
Ectopic
Septic incomplete abortions
Acute appendicitis
Diverticular abscesses
ADenexal torsion
PID may be minor in presentation!! Just some vaginal bleeding or discharge.
Clinical criteria for acute salpingitis
All three:
- Abdominal tenderness w/ or w/o rebound
- Adnexal tenderness
- Cervical motion tenderness
PLUS:
1 or more:
- Gram stain fo endoervix postiive fo rGNID
- Temp >38
- WBC >10
- Pus
- Pelvic abscess on bimanual exam or sonogram
But empiric therapy for of age women who present with just one of the major criteria, and one or more of the others.
Perihepatitis more with what
Chlamydial rather than GC.. Inflammation leading to localized fibrosis and scarring of the anterior surface of the liver.
TOA presentation
Acutely ill: high fever, tachycardia, severe pelvic and abdominal pain, nausea and vomtiing
First episode HSV infections
3-7 days after exposure. Systemic symptoms along with lots of lesions. Usually resolvesin about 1 week. May be complicated by bladder involvement, or later on by aseptic meningitis.
Recurrent are milder and shorter in duration, and may just present as fissuresor vulvar irritation. HSV1 less likely to recur.
Viral culture spec and sens
Highly specific, not very sensitive(25% false negative rates). Replaced by PCR
Antibody tests, 22 days until seroconversion.
Patient applied products for condyloma acuminatum
Podophyllin
Imiquimod, should not be administered in pregnancy
Why C-delivery for condyloma acuminatum
More because of vaginal lacs than risk of transmissio, which can result in laryngeal papillomata
Chancre of syphilis appearance
Firm, punched out appearance and rolled edges. Small and painless. MAy be missed during routine. Adenopathy may or may not be present. Serology typically negative at this stage.
When does secondary syphilis happen
Four to 8 weeks after chancre. SKin rash taht often appears as rough, red or brown lesions on the palms of hte hands and soles of the feet
Other stuff: LAD< fever, headache, weight loss fatigue, muscle aches, etc.
Moist areas of the body get condyloma lata.
This resolves in about 2-6 weeks, enteris latent phase.
Transmissin during tertiary syphlis
Transmissin unlikely except through blood or placental transfer. Gummas --> 1-10 years fater ifneciton
Treponemal test positive, then treated, what happens to the test
Is never negative
VDRL will decrease....
LGV presentation
Inguinal or femoral LAD with vaginal transmission
Anal bleeding, purulent anal discharge, constipation, anal spasms with anal transmission.
Self limited genetial or rectal vesicle or paule sometimes forms at site of bacterial entry.
LGV complication
Systemc infection, if untreated may cause secondary infection of rectal or anal lesiosns, which may lead to abscesses or fistulas.
Klebsiella granulomatis
RAre in US
Endemic in PApau New Guinea, central australia, iindia, western Africa.
Lesions are vascular and bleed easily. Granuloma inguinale
Chancroid occurs in what pattern
Discrete outbreaks. 10% are also diagnosed with HSV or T. pallidum, and it is also a cofactor for HIV transmission.