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Repro/Endo flashcards > Repro > Flashcards

Repro Flashcards

1
Q

Epidemiology of Preeclampsia

A 
Increased incidence with:
- multiple gestations
- Chronic HTN
- Previous history of preeclampsia
- Renal disease
- DM
Prior to 20 weeks, preeclampsia pathognomonic for molar pregnancy
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2
Q

Pathophysiology of preeclampsia

A

Abberation in normal interaction between fetal allograft and maternal tissue
Vascular Changes: normal migration of trophoblast into uterus with spiral arterioles causes uteroplacental arteral bed into low resistance, high flow system
Preeclampsia= defective vascular changes–> decreased blood supply, fibrotic vascular changes, endothelial injury
- see vasospasm, coagulation system activation, abnormal hemostasis–> endothelial injury, increased platelet activation, platelet consumption–> decreased intravascular volume

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3
Q

Renal system changes in preeclampsia

A

Renal: nL= increased renal plasma flow, GFR

Preeclampsia = vasospasm, capillary endothelial swelling–> reduced GFR, increased uric acid, creatinine

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4
Q

Hemodynamic changes in preeclampsia

A 
Normal= Prostacyclin, thromboxane A2 increased in pregnancy (PGI > TXA)
- PGI allows for vasodilation, inhibits platelet aggregation
Preeclampsia= TXA>PGI
Capillary leak (proteinuria, edema)
NO reduced (less vasodilation)
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5
Q

Hepatic system changes in preeclampsia

A

Transaminase elevations in about 10% cases

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6
Q

Hematologic changes in preeclampsia

A

Thrombocytopenia

Severe= decreased fibrinogen, increased PT, PTT (seen in DIC)

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7
Q

Severe preeclampsia

A 
BP >= 160/110
Proteinuria= 5 g/24 hour urine or dip +3 to +4
Oliguria
Cerebral/visual disturbances (could be close to developing eclampsia)
Epigastric pain (HELLP)
Pulmonary edema
Impaired liver function
Thrombocytopenia

Treatment: delivery if maternal complications of abNL fetal testing
32 weeks: deliver

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8
Q

HELLP sydrome

A

Hemolysis, Elevated Liver enzymes, Low Platelets
2-12% cases of preeclampsia (severe)
DIC, periportal liver necrosis, hemorrhage, coma, nephrogenic diabetes insipidus, subcapsular liver hemotoma
May see NO HTN, proteinuria
Present with RUQ/epigastric pain, N/V

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9
Q

Maternal Complications of Preeclampsia

A 
Death
CVA
DIC
Placental abruption- 5%
renal failure
Subcapsular liver hematoma/rupture
Pulmonary edema
Eclampsia
Liver failure
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10
Q

Fetal complications of Preeclampsia

A 
Death- 10%
Prematurity
RDS (respiratory distress syndrome)
IVH (intraventricular hemorrhage)
Retinopathy
Necrotizing enterocolitis
BPD (bronchopulmonary dysplasia)
IUGR (intrauterine growth restriction)- 18%
Fetal asphyxiation
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11
Q

Treatment of preeclampsia

A

Only cure= delivery
Mild preeclampsia: deliver if >= 36 weeks
Severe preeclampsia: deliver if >= 32 weeks
Magnesium sulfate= best agent for treatment of eclampsia seizures, prophylaxis in preeclampsia

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12
Q

Mild preeclampsia

A

HTN: 120-140/70-90
Proteinuria= 300 mg/24 hours or 0.1 g/L spot
Deliver greater than 36 weeks
delivery

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13
Q

Magnesium sulfate

A

anticonvulsant, more efficacious than dilantin
Slows NM conduction, depresses CNS irritability
Renal excretion
Toxic levels= somnolence, respiratory difficulty, cardiac arrest

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14
Q

Eclampsia

A

Convulsions unrelated to other condutions, + evidence of preeclampsia
2-4% of preeclampsia patients
Headache, visual symptoms, RUQ/epigastric pain
Short-lived convulsions (60-75 seconds)

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15
Q

Recurrence rates of preeclampsia

A

25% in second pregnancy
severe preeclampsia–> 65% recurrence
HELLP recurrence low
Prevention: low dose aspirin (10-20% reduction in recurrence), calcium

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16
Q

Low risk HPV types

A

Associated with warts
6, 11
40, 42, 43, 44, 53, 54, 61, 72, 73, 84

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17
Q

High risk HPV types

A

Associated with cervical cancers (at least found in any case of cervical cancer), other cancers of genital tract
16, 18, 45
31, 33, 35, 39, 51, 52, 56, 58, 59, 68, 82

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18
Q

HPV and cervical cancer

A

HPV 16 found in 50% of cervical cancers, most commonly identified in HSIL
HPV 18= squamous carcinoma, adenocarcinoma, cervical adenocarcinoma in situ
* HPV clearance: 50% by 6 months, 66% at 12 moths, 80% at 2 years- only when integrated into genome can lesion progress from LSIL to HSIL or carcinoma

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19
Q

ASCUS (pap smear)

A

Atypical squamous cells of undetermined significance

  • 5-7% chance of biopsy confirmed CIN 2/3, but only 0.1% chance of invasive carcinoma (therefore need follow-up hr-HPV DNA testing)
  • ASCUS pap with positive HPV DNA has 30% incidence of high-grade lesion on colposcopy
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20
Q

ASC-H (pap smear)

A

Atypical squamous cells, cannot exclude high grade lesion

* colposcopy reading shows 25% to have severe pre-cancerous changes

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21
Q

AGC (pap smear)

A

Atypical glandular cells

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22
Q

AIS (pap smear)

A

Adenocarcinoma in situ

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23
Q

Possible high risk HPV

A

22, 66, 73

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24
Q

Detection of HPV

A

Liquid-based pap: can use residual material to detect high risk HPV DNA via:
Hybrid capture 2
Cervista
PCR

  • only recommended for women >30, performed every 3 years (or 6 years with pap smear)
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25
Q

Hybrid capture 2 HPV detection

A

Detection of 13 high-risk types of HPV DNA in cervical specimens
Nucleic acid hybridization assay with signal amplification
Qualitative detection using microplate chemiluminescence
* See which strands light up to indicate a high risk HPV strain present in sample

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26
Q

Cervista HPV detection

A

Screens for 14 types of HPV strains

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27
Q

Indications for using high-risk HPV DNA testing

A
  1. Women over age 20 with ASCUS results (unclear significance of pap smear)
    - If negative for hr-HPV, no need to perform culposcopy
    - If patient < 20 years, perform repeat cytology in 12 months
  2. Post-treatment surveillance of women with CIN 2/3
    * Failure of surgical excision 1-25%: need to perform to ensure no persisting cancer cells
  3. Adjunct to pap test in primary cancer screening in women over 30 (not recommended for women <30 because HPV so prevalent but most cases handled by immune system)
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28
Q

Management of CIN (cervical intraepithelial lesions)

A
  1. ASCUS: 20 years: hrHPV, if +, colposcopy
  2. LSIL: < 20 years: reperform cytology in 12 months
    > 20 years: colposcopy
  3. HSIL: 70% chance of CIN2-3
    1% risk of invasive cancer
    Colposcopy for diagnosis followed by excision
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29
Q

Recommendations for HPV screening

A

< 21 years: no screening
21-29 years: cytology alone every 3 years
30-65 years: HPV and cytology every 5 years (preferred), cytology every 3 years (acceptable)
>65 years: no screening follwing adequate negative prior screening
After hysterectomy: no screening (if no history HSIL)
HPV vaccinated: continue to follow screening recommendations for age group
High risk women need to be screened more frequently (high risk= HIV, organ transplant, exposure to DES)

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30
Q

Fertilization to implantation timeline

A

30 hrs: 2 cell organism
3rd day: 12-32 cell solid morula (totipotent)
- Arrives in uterus
6th day: Hollow blastocyst (250 cells) implants into uterus

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31
Q

Implantation to 12 weeks LMP timeline

A

6-9 days post fertilization= implantation
- inner layer= ecto, endo, mesoderm (fetus)
- outer layer= trophoblast (placenta, fetal membranes)
4 weeks: 6 mm embryo, 1,000,000s cells
5 weeks: human appearance (extremities, cerebral hemispheres)
6 weeks: heartbeat
12 weeks: external genitalia, fetus excretes urine

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32
Q

Spontaneous abortion

A

15% of known pregnancies (25-35% all pregnancies)
50% due to chromosomal abnormalities
80% in first trimester

Risk factors= toxicity (smoking, drugs, alcohol), medical illness (DM, HTN, thyroid), age (>35 for women, 50 for men), infection, uterine abnormalities

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33
Q

Missed abortion

A

Closed cervix
Fetus dead but still in uterus

Management=

  • Expectant (wait for body to expel)
  • Medical (prostaglandin–> contractions)
  • Surgical (EVA, MVA)
  • expectant and medical managment have a higher risk of hemorrhage
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34
Q

Threatened abortion

A

Close cervix
Uterine bleeding/passage of tissue before 20 weeks
25% of all pregnancies
50% of threatened pregnancies result in viable infants (but have higher incidence of prematurity, lower birth weight)

Managment:

  • Expectant (not much done except avoiding sex)
  • Monitor: serial beta-hCG (is it ectopic or molar pregnancy causing bleeding?), ultrasound, pelvic rest (not bed rest)
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35
Q

Complete abortion

A

Closed cervix
History of uterine bleeding, cramping (all products of conception passed)

Managment:

  • Expectant
  • Medical (uterotonics= methergine, misoprostol)
  • Surgical (EVA, MVA)
  • risk of another miscarriage goes up, but most women go on to have a healthy pregnancy
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36
Q

Incomplete abortion

A

Open cervix
Uterine bleeding, cramping, passage of some products of conception <20 weeks

Managment:

  • Expectant, medical, surgical
  • highest risk of post-partum hemorrhage
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37
Q

Recurrent abortion

A

At least 3 pregnancies lost before 20 weeks

ID and treat possible underlying causes:

  • Uncontrolled DM
  • Uterine synechiae (scarring), defects
  • antiphopholipid antibody syndrome (autoimmune disease)
  • Chromosomal abnormalities
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38
Q

Molar pregnancy

A 
Complete= 46 XX (2 sperm, empty egg)- no fetal formation
Incomplete= 69 XXY (2 sperm + 1 egg)- chromosomally abnormal fetus

Symptoms= patient “pregnant” but sick (vaginal bleeding, nausea/vomiting, increased BP; disproportionately enlarged uterus, tachycardia, tachypnea, snowstorm ultrasound

Managment: surgical (evacuation) + post-op monitoring of beta-hCG to prevent gestational trophoblastic neoplasia

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39
Q

Diagnosis of ectopic pregnancy

A

Risk factors= prior ectopic pregnancy, tubal surgery, history of PID, in utero DES exposure, cigarette smoking

Symptoms= vaginal bleeding/amenorrhea, pelvic pain, adnexal mass, 50% asymptomatic

Tests= ultrasound (empty uterus), beta hCG monitoring (will not rise appropriately), low serum progesterone

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40
Q

Management of ectopic pregnancy

A

Medical= methotrexate 50 mg/m2 IM
Patient MUST be: hemodynamically stable, can return for follow-up, no contraindications for methotrexate, unruptured, mass < 3.5 cm, no fetal heart activity, beta hCG <15,000

Contraindications to medical managment= breast feeding, immune compromised, abnormal liver/kidney function, sensitivity

Surgical= laproscopic salpingostomy (remove tissue) or salpingectomy (remove tube) or laparotomy

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41
Q

Ovarian torsion

A

Twisting of ovary on blood supply
Unilateral pelvic pain (waxes and wanes until excrutiating), adnexal mass

Risk factors= ovarian cysts, < 30 years old

Treatment: surgical (laproscopy, laparotomy), oophorectomy common

42
Q

Tubo-ovarian abscess (TOA)

A

Forms at end of tube, enveloping ovary

Symptoms= fever, vaginal discharge, pelvic pain
Diagnosis= cervical motion tenderness, adnexal tenderness, increased WBCs, fever, pus, palpable mass, fluid in pelvis
* confirmed by ultrasound, or finding fluid in pelvis (gold standard diagnosis)

Risks= STD infections
Treatment= surgical, drainage +/- removal of tube/ovary; surgical antibiotics
43
Q

Abruptio Placenta

A

Premature separation of placenta

  • 3rd trimester bleeding with fetal distress
  • Risk factors= cigarette smoking, HTN, abdominal trauma, illicit drug use
  • Treatment= c-section, hemodynamic support
44
Q

Non-reassuring fetal testing (NRFT)

A

Fetal HR monitored to assess acid/base status or oxygenation of tissues
Symptoms= late decelerations, prolonged bradycardia
Causes= prematurity, abruption, uteroplacental insufficiency, umbilical cord compression, infection, congenital anomalies

45
Q

Placenta previa

A

Placenta implants at base of uterus (near cervix) instead of fundus

  • Painless bright red bleeding in 3rd trimester
  • Risk factors= previous c-section, multiparity
  • Diagnosis= ultrasound
  • Treatment= tocolysis, expectant, c-section (induce labor)
    • AVOID digital exam
46
Q

Shoulder dystocia

A

Delivery of fetal head with failure to deliver shoulder
Risk factors= fetal macrosomia (big baby), gestational diabetes (big baby), rapid labor
Treatment= McRobert’s, episiotomy, suprapubic pressure, deliver posterior arm, Wood’s corkscrew, Zavenelli maneuver (push baby back in, c-section)

47
Q

Pre-term labor

A
  • Contractions, cervical changes < 37 weeks estimated gestational age
    Risk factors- previous pre-term labor, multiple pregnancies, infection, low SES, AA race, drugs, smoking, preterm rupture of membranes, macrosomia/ polyhydramnios
Treatment= underlying conditions, bedrest, tocolysis, betamethasone (increase lung maturity)
Tocolytics= magnesium sulfate, terbutaline, procardia (decrease contractions)
48
Q

Pre-eclampsia

A

HTN and proteinuria

  • HTN >140/90 after 20 weeks gestation (2+ measurements)
    • Severe HTN >160/110
  • Proteinuria= 300 mg protein in 24 hours or 0.1 g/L on spot speciment
    • Severe proteinuria= 5g/24 hour period or dip +3 to +4 + oliguria

*20% of women with chronic HTN develop pre-eclampsia

49
Q

Risk factors for endometrial cancers

A

Caused by estrogen stimulation, which increases with:
Age, obesity, late menopause (hyper-estrogenic state), high fat diet, DM, HTN, genetics, tamoxifen use (estrogen receptor stimulation in uterus vs supression in breast tissue)

50
Q

Protective factors against endometrial cancers

A

Pregnancy (50% reduction with first pregnancy)
Use of progesterone (OCP)
Tobacco smoking

51
Q

Genetic endometrial cancer

A

HNPCC (Lynch syndrome)

  • DNA mismatch repair gene mutations
  • Lifetime risk of developing endometrial cancer= 50%, ovarian= 10%
  • Associated with colon cancer, endometrial cancer at young age
  • 2% endometrial cancers due to Lynch syndrome
52
Q

Symptoms of ovarian cancer

A

Bloating
Pelvic/abdominal pain
Trouble eating/feeling full quickly
Feeling the need to urinate urgently/often
Other: fatigue, upset stomach/heartburn, back pain, pain during sex, constipation, menstrual changes

*Symptoms persisting for more than two weeks warrant prompt medical attention

53
Q

Stages of ovarian cancer

A

1: ovaries
2: pelvis
3: upper abdominal disease/lymphatic invasion
4: spread elsewhere outside abdominal cavity

54
Q

Ovarian cancer risk factors

A 
Women with ovaries
Long ovulation history
Unexplained infertility
Nuliparity
Family history of breast/ovarian cancer 
- 90% sporadic, 10% genetic
-- 7% BRCA (40% risk if carrying BRCA1, 20% for BRCA2)
-- 9% for lynch syndrome
Diet
Estrogen replacement therapy?
Talcum powder?
55
Q

Protective factors against ovarian cancer

A 
Increased parity (decreased ovulations), breast feeding
Later onset of menses, earlier menopause
OCP use
Tubal ligation
Hysterectomy
56
Q

Significant family history for ovarian cancer

A
  • 2 first degree relatives with breast/ovarian cancer (1 must be < 30 years
  • 1 relative with bilateral breast cancer < 40 years
  • 1 male relative with breast cancer
57
Q

Screening for ovarian cancer

A

Individual has family or personal history of estrogen-related cancer (breast cancer)

  • Annual vaginal exam for women 18 and above
  • Annual rectovaginal exam for women age 35 and above
  • Transvaginal sonography
  • Blood test (CA-125 gene): associated with many cancers, diseases, pregnancy, mid-menstrual cycle (therefore only when mass in pelvis- don’t screen asymptomatic patient)
  • Strategies for Risk reduction in BRCA patients: screening (no reduction in mortality), chemoprevention (but don’t want to enhance breast cancer risk), surgery (must remove ovaries AND tubes)
58
Q

BRCA risks for cancer

A

BRCA 1: remove everything once woman is no longer bearing children
BRCA2: can wait until post-menopausal stage to perform surgery as risk only increases post-menopause

59
Q

Cervical cancer risk factors

A 
Early onset of sexual activity
Multiple sex partners
High risk partner
History of STDs
Smoking
Immunosuppression (HIV, transplant)
60
Q

Symptoms of cervical cancer

A

Blood tinged watery discharge
Post-coital bleeding
Painless intermittent spotting

61
Q

Staging of endometrial and ovarian cancer

A 
Chest x-ray
Exploratory laparotomy
Peritoneal washing for cytology
Total abdominal hysterectomy
Bilateral salpingo-oophorectomy
Bilateral pelvic, paraaortic lymph node dissection
Omentectomy
  • Endometrial cancer: 80% diagnosed at stage 1 due to bleeding
  • Ovarian: 70% diagnosed at Stage 3, 15% at stage 4
62
Q

Pelvic prolapse

A

Loss of pelvic floor muscle support causing herniation of viscera into vagina. Can be caused by:

  • Vaginal delivery
  • Constipation
  • Co-morbid medical conditions (obesity)
  • Heavy lifting
  • Surgery
63
Q

Pelvic Anterior compartment prolapse

A

Cystocele= central or parvaginal defect

64
Q

Pelvic mid-compartment prolapse

A

Uterine prolapse, vaginal prolapse, vaginal vault prolapse, enterocele

65
Q

Pelvic posterior compartment prolapse

A

Enterocele, rectocele

66
Q

Treatments for pelvic organ prolapse

A

Non surgical= pessary (uses bony pelvis/muscles for support)

Surgical= attach suture material/grafts to bony pelvis to restore anatomy/function

67
Q

Stress urinary incontinence

A

Etiologies= childbirth, radical surgery, trauma, chronically increased intraabdominal pressure

Scenarios:
1. Lack of support in pelvic floor + abnormal pressure transmission + malposition of urethra–> urine loss

  1. Denervation of urethra–> lack of tone–> urine loss
  2. Damage to venous plexus and submucosal collagen/elastin–> loss of tone to urethral mucosa–> urine loss
  3. Damage to mucosa due to hypoestrogenism/radiation–> no coaptation–> urine loss

Treatments: keigel exercises, providing lost support, restablishing coaptation of mucosa

68
Q

Urge incontinence

A

People learn to control micturation reflex over time by suppressing detrusor muscle contraction and enhancing urethral sphincter control.

In urge incontinence, there’s a denervation of detrusor muscle inhibitory reflex–> disruption of normal voiding

Etiologies= suprapontine lesions (frontal lobe disease, Parkinsonism), pontine lesions (MS, encephalitis), spinal cord lesions (trauma, myelitis), subsacral lesions (spina bifida, cauda equina injury, small fiber neuropathy)

Treatment= Retrain neural pathways, block muscarinic receptors at detrusor muscle (Botox injection–> direct m. paralysis or anticholinergics)

69
Q

Overflow incontinence

A

Complete denervation of bladder with loss of detrusor function–> inability to contract/expel urine–> overflow

Etiologies= end-stage DM, denervation due to surgery, medications causing muscarinic receptor blockade

Treatment= self-catheterization

70
Q

PCOS

A 
Polycystic ovary syndrome
Diagnostic criteria (needs 2/3)
- oligo or anovulation
- hyperandrogenism
- polycystic ovaries

Seen with obesity, multiple ovarian cysts, insulin resistance

71
Q

Aging and infertility

A

Successful pregnancy declines 3.5%/year after 30 (Diminished ovarian reserve) as number and quality of eggs declines
- Spontaneous abortion increases with age; women >40 years have 75% risk of spontaneous risk of abortion

*FSH level testing on day 3 >15mIU/mL–> lower probability of pregnancy

72
Q

Ovulatory disorders causing infertility

A
  1. PCOS
  2. Hypothalamic dysfunction (stress, weight change, excess exercise, anorexia)
  3. Hypothalamic/pituitary lesions (tumors, trauma, CVA, surgery)
  4. Endocrine disorders: hyperprolactinemia, thyroid abnormalities
  5. Ovarian lesions: menopause, infections, tumors
  6. Inadequate luteal phase (corpus luteum fails to secrete adequate progesterone–> change in blastocyst implantation, survival)
73
Q

Endometriosis and fertility

A

Can cause fibrosis, adhesions–> tubal function impairment, decreased ovarian access
May also increase prostaglandins/ macrophages in peritoneal fluid

*No test for endometriosis: must biopsy or directly visualize tissue

74
Q

Male disorders causing infertility

A 
Testicular diseases (mumps orchitis)
Prostatitis
Epididymitis
Endocrine disorders
Severe medical disorders, drugs
Trauma, surgery
Congenital abnormalities, varicocele (?)

*35% of infertility in couples due to single defect with male

75
Q

Tests to determine fertility

A 
Urinary LH kit
Basal Body Temperature change at ovulation
Endometrial biopsy
Serum progesterone (above 3ng/mL= ovulation; 15-25 at days 18-22)
Semen analysis (number, MOTILITY, morphology of sperm)
76
Q

Clomiphene citrate

A

Synthetic nonsteroidal estrogen (like DES) that blocks hypothalamus estrogen receptors–> “low estrogen”–> increased GnRH pulse amplitude/frequency–> increased FSH/LH–> ovulation!

ONLY effective in patients with intact hypothalamic-pituitar-ovarian axis
*50-70% pregnancy success, only 5% risk of twin gestation

77
Q

hCG for infertility

A

Does not requiring functioning hypothalamus/pituitary: causes dominant follicle to release egg, stimulates progesterone release from corpus luteum
* Expensive, difficult to administer, hyperstimulates ovaries/multiple gestation risk increased BUT pregnancy rate 60-70%

78
Q

hMG for infertility

A

Human menopausal gonadotropin= urinary product (LH and FSH components) from post-menopausal women. VERY potent, given in injection and causes follicle growth/maturation. MUST be given with hCG to induce ovulation
* Expensive, difficult to administer, hyperstimulates ovaries/multiple gestation risk increased BUT pregnancy rate 60-70%

79
Q

FSH for infertility

A

Stimulates ovarian follicle growth in women without ovarian failure. Must be given with hCG
* Expensive, difficult to administer, hyperstimulates ovaries/multiple gestation risk increased BUT pregnancy rate 60-70%

80
Q

GnRH antagonist administration in infertility

A

Block action of endogenous GnRH/suppresses pituitary LH/FSH to ensure pituitary exposed to constant GnRH, and allows hMG to be sole source of follicle stimulation

81
Q

In vitro fertilization (IVF)

A

Woman’s ovaries hyperstimulated with gonadotropins + as many eggs as possible aspirated from ovaries under ultrasound guidance. Fertilization in petri dish, incubated to blastocyst, injected into uterus–> implantation. 50-60% success/cycle ($10,000 per cycle)

82
Q

Endometrial cancer types and prognosis

A

Type 1= 80% of endometrial cancers, related to unopposed estrogen, seen in more caucasian women, stage I/II. Favorable prognosis

Type 2= 20% of endometrial cancers, unrelated to estrogen exposure. Equal incidences among races. More likely Stage III/IV (less differentiated, non-endometrial appearing tissue). Unfavorable outcomes

83
Q

Premature menopause

A

Ovarian failure before age 35:could be due to genetics (X-chromosome mosaicism), autoimmune (anti-ovarian antibodies), idiopathic

84
Q

Hormonal changes in menopause

A

Estrogen: greatly decreased
FSH: greatly increased (Inhibin decreased)
LH: moderately increased
Testosterone: moderately decreased

85
Q

Changes to urogenital tract in menopause

A

Vaginal muscosal atrophy (atrophic vaginitis): dryness, dyspareunia, pruritis

Urothelial atrophy: cystitis, urethritis, urinary frequency, incontinence

86
Q

Non-menopausal causes of vasomotor symptoms

A 
Hyperthyroidism
Pheochromocytoma
Carcinoid (Leukemia, pancreatic)
Psychosomatic/stress disorders
Drugs, alcohol
87
Q

Hormone Replacement Therapy benefits

A

Estrogen:

  • neuronal growth, synaptic proliferation (mental health benefits)
  • Decreases CAD risk in women in peri- to post-menopausal years by 50% (not protective with pre-existing CAD)
    • Improved lipid profile, anti-atherosclerotic, augmentation of vasodilation/anti-platelet aggregation factors, antioxidant
  • Prevents osteoporosis
  • Prevents vaginal/urothelial atrophy
  • Prevents colon cancer
  • Relieves vasomotor symptoms
  • Prevents tooth loss (?)
88
Q

Adverse effects of estrogen therapy

A
  • Endometrial stimulation: vaginal bleeding, endometrial hyperplasia, carcinoma (add progesterone)
  • Venous thrombosis
  • Breast stimulation (increased risk of cancer after 4-5 years of use)
  • Ovarian cancer
  • Coronary risks with established CAD
89
Q

Contraindications to hormone replacement therapy

A
  • Current or past history of breast/ endometrial cancer
  • Unexplained vaginal bleeding
  • Pregnancy
  • Chronic/acute liver disease
  • Active venous thrombosis/ thromboembolic disease
90
Q

Non-hormonal treatment of vasomotor symptoms (hot flashes)

A
  • Clonidine (anti-hypertensive)
  • SSRIs
  • Herbal estrogens, vitamin E
91
Q

Non-estrogen treatment of Osteoporosis

A
  • SERMs (selective estrogen receptor modulator
  • Bisphosphonates
  • Calcitonin
  • Calcium, Vit D, weight-bearing exercise, smoking cessation
92
Q

Estrogen effect on bone

A

75% of bone loss in first 15 years after menopause due to decreased estrogen

  • Estrogen affects intestinal absorption of calcium
  • Modulates bone remodeling through antiresorptive effect
93
Q

Post-menopausal osteoporosis clinical effects

A

Hip fractures, vertebral fractures, back pain, decreased height, kyphosis

  • 50% of women over 65 have vertebral compression fractures
  • 15% of caucasian women will have hip fracture (300,000 per year in US, 15-20% die within 3 months of fracture)
94
Q

Yolk sac germ cell tumor

A

Ovarian cancer type: endodermal sinus

  • Highly malignant
  • Seen in women < 30 years
  • See Schiller-Duval body
  • Monitor alpha-fetoprotein
  • Chemosensitive
95
Q

Choriocarcinoma

A

Ovarian germ cell carcinoma

  • mimics chorionic villi epithelium of placenta
  • Seen in prepubertal girls
  • Monitor with beta-hCG
96
Q

Dysgerminoma

A

Ovarian germ cell carcinoma

  • Similar to testicular seminoma, poorer prognosis
  • 15% bilateral
97
Q

Embryonal carcinoma

A

Ovarian germ cell tumor:

Rarely pure germ cell tumor, usually mixed tumor cells

98
Q

Sertoli-Leydig sex cord ovarian tumor

A

Androgen-secreting tumor

  • low malignancy potential
  • ressembles embryonal testis
  • increased androgens–> virilization
99
Q

Metastatic ovarian tumors

A

3% ovarian tumors metastasize. Commonly metastasize to:

- breast, lower GI, endometrium, stomach

100
Q

Krukenberg tumor

A

metastatic tumor with signet ring features, usually from stomach (metastasizes to ovaries)

101
Q

BRCA and ovarian cancer

A

2-3% chance of ovarian cancer in general population
BRCA1= 35-60% chance by 70 years
BRCA2= 10-27% chance
Diagnosed 10 years earlier than general population
Recommendation: prophylactic salpingo-oophorectomy at 35 (post-reproductive)

Repro/Endo flashcards (6 decks)

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