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152 Cards in this Set

  • Front
  • Back
Stages of Adolescence
Early: age 11-14 elementary and middle
Middle: age 15-17 high school
Late: age 17- 21 college or employed
Early Stage of Adolescence
Concerns with physical changes, normality
Exaggeration of physical complaints
Self-centeredness, feelings of being “center stage”
Strong sense of invulnerability, omnipotence
Middle Stage of Adolescence
High school
Puberty almost complete
Testing/showing off “new body”
Strong independence; independence conflicts
Shift of attachments from adults to PEERS
Late Stage of Adolescence (college)
Post high school to early 20’s
Adult functional role achieved or approaching
Position in family seen as an adult not child
Independent decisions, actions
Realizations of limitations, vulnerability
Obtaining History
Interview (HEADSS-“Is Very Good”
Home, Education, Activities, Drugs, Sexuality, Suicide, Internet, Violence, Gangs
Data on Sexual Activity
Nearly half of American high school students report sexual activity before graduation

15 million identified STI’s annually in US, 25% in adolescents

4% of females reported initiating sexual activity before age 13 (possible abuse)
Age of First Pelvic Exam
Within 3 years after initiation of sexual activity
Annually in sexually active adolescents

21 for pap smear
Relaxation Techniques for Pelvic Exam
Deep rhymthic breathing-relaxes pelvic muscles and distracts patient
Progressive muscle relaxation-alternate tensing and releasing of major muscle groups
Guided imagery-using mental imagery to visualize a pleasant memory of favorite activity
Speculum Exam
Place one finger inside the vaginal
Gently push on pubococcgygeal muscle as you insert the speculum
Direct speculum in downward direction 45 degrees
The Cervix Inspection
Adolescents have darker, more erythematous area surrounding the cervical os
Cervical ectopy – columnar epithelial cells will appear as a red concentric ring surrounding the os
SMR Females
Breast Examination and Pelvic exams, education
21, with pap smear
Adol IMZ
Primary Dysmenorrhea
Menstrual pain without pathology
-Within 1-2 years of menarche
After ovulatory cycles

-Myometrial contractions induced by prostaglandins
originates in secretory endometrium

-Begins a few hours prior to or just after onset of menses and lasts 48-72 hours.
Primary Dysmenorrhea S/S
Pain (usually colicky)
Suprapubic cramping (intense, labor-like)
Radiating pain (anterior thigh, lumbo-sacral)
Systemic symptoms
Prostaglandin release into systemic circulation

Mild uterine tenderness on exam
During menses

N/V/D-prostaglandin release
Headache
Syncopal episodes (rare)
VS, Pelvic exam: normal
Mild suprapubic tenderness

Systemic symptoms
Prostaglandin release into systemic circulation

Mild uterine tenderness on exam
During menses
Confirm Dx of Primary Dysmenorrhea
Rule out other pathology
NL pelvic exam
NL vital signs
Not pregnant
No acute/chronic abdominal pain
No chronic pelvic disorders (non-cyclic)
adhesions, salpingo-oophoritis, cancer
No GI, GU, Neurologic problems
Primary Tx of Primary Dysmenorrhea
Prostaglandin inhibitors
Ponstel (Mefenamic Acid) 500mg Stat, 250mg q6

Ibuprofen 400mg q4-6

Naproxen sodium 550mg Stat, 275mg q8
80% effective
take prior to or at onset of pain
every 6-8 hours
prevents re-formation of prostaglandin byproducts
Take with food

Try NSAID’s x4-6 months
change after 2-4 cycles if no relief

OCP’s
90% of women have at least some relief of symptoms

If nothing helps
REFER : will probably need laparoscopy.
Education of Primary Dysmenorrhea
-Medication compliance

-Exercise
Very helpful - especially when pain is worst! (endorphins) 1st thing to do

-Heating pads/warm baths
-Relaxation
-Good diet
-Follow-up
% of Dysmenorrhea: 2 types
50%
Rule of 4s
. Rule of 4s: 4 days before period starts-load up Cox receptors with ibuprofen, 400mg q4h (before period begins)
Secondary Dysmenorrhea
Menstrual pain with PATHOLOGY

Imperforate hymen (blood backs up)
Transverse vaginal septum
Cervical stenosis
Uterine anomalies
Endometrial polyps
Adenomyosis
Uterine leiomyomas (Fibroids)
-Endometriosis
-IUD
-Atypical problems
chronic ectopic: ectopic pregnancy doesn’t go away, keeps producing low levels of HCG, always 10 ex.
chronic functional cyst

-Differential: GI, GU, Neuro, GYN
Adhesions, infection
Secondary Dysmenorrhea S/S
Pain frequently begins 1-2 weeks PRIOR to menses and PERSISTS until after menses stops

NSAIDS/OCP’s not as helpful
Endometriosis
Presence of endometrial tissue outside the uterus
Endometriosis Sites
-Often includes glands & stroma
-Most frequent sites of implantation
pelvic viscera & peritoneum
-Extra-pelvic sites
intestines (Colon and Rectum)
ureteral
lungs
umbilicus
Endometriosis Retrograde menstruation
Lying down for the rest of our life. Retrograde menstruation, flows outside to tubes and peritoneal cavity. Every woman has potential for endometriosis. Immune system goes in and cleans up.
Endometriosis Etiology
Estrogen dependent
Ectopic transplantation of endometrial tissue (retrograde menses)
Host immune system factors
changes in immune response
antibody formation
Genetic Component of Endometriosis
7x’s greater risk if mother/sister effected
75% incidence in homozygotic twins
Endometriosis Incidence and Symptoms
Up to 7% of menstruating women
Postmenopausal women on HRT
Associated Symptoms
dysmenorrhea
pelvic pain (wide range)
infertility
dyspareunia
Pain: abdominal, back
GI and GU problems
Endometriosis Evaluation
History & PE
many women asymptomatic
w/ normal exam
Exam abnormalities (if present)
uterosacral/cul-de-sac nodularity
ovarian enlargement/mass
rectovaginal septal swelling and pain
uterus fixed and non-mobile
CA 125 elevated in mod/severe disease (careful!)
Diagnosis of Endometriosis

Endometriosis Management
-Dx: Laparascopy

-Surgery
laser ablation
hysterectomy w/ oophrectomy

-Continuous OCP’s
-Depo Provera 104mg SQ
FDA approved for pain management

-GNRh Agonists (Lupron)
-Danazol
Common Causes of Vaginitis
Vulvovaginal candidiasis
Bacterial vaginosis
Trichomoniasis
Dual infections
Vaginal Atrophy
Physiologic Discharge

Normal vaginal flora ?
and functions?
lactobacilli

Colonize the vaginal epithelium
Maintain normal ph at 3.8 to 4.4
Quantity and quality vary in same woman in cycles
Factors that influence physiologic discharge
-Age
Prepubertal
Reproductive
Post-menopausal

-Local Factors
Menstruation
Post partum
Malignancy
Semen
Personal habits and hygiene


-Hormones
The pill
Cyclical hormonal changes
Pregnancy
Pathological vaginal discharge
Candidiasis and bacterial vaginosis– most common
50% of BV is asymptomatic
Questions to ask women who complain of vaginal discharge
-Discharge
Onset
Duration
Amount
Color
Blood staining
Consistency
Odor
Previous episodes
Associated s/s of Vaginal discharge
Associated symptoms
Itching
Soreness
Dysuria
Intermenstrual or post-coital bleeding
Lower abdominal pain
Pelvic pain
Dyspareunia –superficial and deep
Physical examination should include
-Complete pelvic exam
To determine source of discharge (cervical or vaginal)
Check for foreign bodies (sometimes the white mouse gets lost)

-Gross evaluation of the discharge for consistency

-Adherence of discharge to the vaginal wall or cervix

-Wet mount preparation
Saline – clue cells, WBC and Trichomoniasis
KOH – for yeast
Amine testing=+fishy odor
Less Common Infectious Causes of Vaginitis
Streptococcoal infections
Cytolytic vaginosis/vaginal lactobacillosis
Recurrent herpes simplex
Genital warts
Cervicitis
Noninfectious Causes of Vaginitis
Contact dermatitis
Erosive lichen planus
Diabetic vulvodynia
Lichen sclerosis
Vulvar hyperplasia
Other dermatologic conditions
Carcinoma
Vulvovaginal Candidiasis
A fungal infection
Usually caused by Candida albicans, but can be caused by other yeast forms
75% of all women report at least 1 episode of VVC, and 40-45% will have 2 or more occurrences
About 10% of women will have recurrent/complicated VVC
Precipitating factors of VVC
Immunocompromised
Diabetics or high sugar intake
Recent antibiotic use
Douching
Diaphragm/cervical cap users
Spermacide users
Chronic conditions or poor diet
Pregnancy
Clinical Presentation and Diagnosis
Pruritus and erythema in vulvovaginal area
White discharge, may be “cheesy” or “curd like” in consistency
Diagnosed via pH<4.5 (Normal pH)
10% KOH prep will show peudohyphae, yeast spores
Can culture for a yeast species, if recurrent
Common Intravaginal VVC Treatments
"Azoles"

Miconazole 2% (5g) qHS X 7 days
Miconazole 100 mg vag supp, 1qHS X 7 days
Butaconazole 2% (5g) qHS X 3 days, or single dose (OTC)
Clotrimazole 1% (5g) X 7-14 days
Clotrimazole 100 mg vag tab qHS X 7 days
Intravaginal Treatments of VVC
Clotrimazole 100 mg vag tab, 2 tabs X 3 days
Clotrimazole 500 mg vag tab X 1 dose
Clotrimazole 1% Vaginal Cream, 1 applicatorful into vaginal hs x 7 days
Tioconazole 6.5% ointment vag X 1 dose
Terconazole 0.4% (5g) qHS X 7 days
Oral Regimen for VVC
Fluconazole (Diflucan) 150 mg po X 1 dose
Helpful VVC Measures
2% Hydrocortisone cream for pruritis
Loose fitting clothing, + cotton underwear
Treat before menses and before antibiotic rx in selected patients
Decrease sugary foods
Acijel (0.921% glacial acetic acid) or “boric acid” suppositories
Bacterial Vaginosis

Characterization?
Most frequent causes?
-Caused by replacement of normal vaginal flora with anaerobic micoorganisms
-Characterized by vaginal discharge, vulvar itching and irritation, and vaginal odor
-Most frequent causes:
Gardnerella vaginalis
Mycoplasma
BV associations
Associated with new sexual partner and frequent change of sexual partners (Ask about internet partners)
Reduced rate in monogamous relationships, can also occur in virginal women
Increased incidence in women who douch (upset the flora)
Can also be associated with concurrent STI commonly Trichomonas
Dx of BV

3 out 4 to Dx
Requires 3 out of 4:

Homogenous, white, noninflammatory D/C coating the walls of the vagina
Vaginal pH of >4.5
Fishy odor (+Whiff/Amine test)
Clue cells on microscopic exam
Dx adjuncts of BV
DNA probe for high levels of G.vaginalis (Affirm VPIII- Manuf. By Becton Dickinson, Sparks, MD)
Fem Exam Card, which detects  pH and trimethylamine. This has proven effective in combat operations.
BV Tx First Line
First Line:
-Metronidazole gel 0.75% (5g), 1 app. Vag QHS X 5 days (antiparasitic)

-Metronidazole 500 mg po BID X 7 days (NO ALCOHOL for three days prior to or after treatment)

-Clindamycin Cream 2% (100 MG / 5 g), 1 app Intravaginally x1 or QHS x 7 days
In pregnancy
In pregnancy Oral metronidazole preferred over gel and clindamycin.
BV Treatments During Pregnancy
Metronidazole 250 TID X 7 days
Clindamycin 300mg BID X 7 days
If woman at high risk for preterm delivery, consider follow-up evaluation 1 month after completion of therapy
Trichomoniasis Background
-Results from infection with Trichomonas vaginalis, a flagellated protozoan
-3-5 million women infected annually
-Comprises 15% of STI clinic visits
-Non-sexual transmission rare, but possible
Trichomoniasis S/S
Malodorous yellow vaginal D/C
Vaginal soreness
Vulvar itching
Dyspareunia ,dysuria
10% may have abdominal symptoms
Asymptomatic infection is not uncommon
Incubation 5-10 days, range 1-28 days
Dx Trichomoniasis
-Copious, thin, homgenous pools of yellow or green D/C
-D/C may be frothy, since this is an anaerobe
-May be confused with candidiasis or mucopurulent cervicitis
-Wiping the cervix clean to see if D/C is oozing from the cervix may be helpful
-Abdominal and bimanual exams may show mild lower quadrant discomfort, but focal tenderness, guarding or masses should not be detected

pH>4.5
Positive amine test
Wet prep demonstrates protozoa in only 60% of women
Pear-shaped with undulating flagella
Increased WBCs

"Strawbery Cervix"
Tx Trichomoniasis
Metronidazole 2 g po X 1 dose
Treat the partner !!!!!!!!

Alternative Regimen:
Metronidazole 500 mg BID X 7 days

Treat systemetically. can be in the bladder
Trichomoniasis in Pregnancy
-Trichomoniasis associated with:
PROM
Preterm delivery
Low birth weight

-Metronidazole 2 gm in 1 dose (Class B drug)

-Treat the partner !!!!!!!
Causes of Recurrent and Persistent Vaginitis
Reappearance of trichomoniasis (Partner not treated)
Sexually transmitted diseases of the cervix (GC, Chlamydia, Syphilis)
Atrophic vaginitis
Irritant or allergic contact dermatitis
PID Definition
“Acute infection of the upper genital tract in women involving any or all of the uterus, oviducts, and ovaries.”
What is the Cardinal Rule for PID
Any woman of reproductive age who presents with abdominal pain has an ECTOPIC PREGNANCY until proven otherwise!!!!!!!!!!!
PID Epidemiology
Community acquired infection initiated by a sexually transmitted agent.
Accounts for approximately 2.5 million outpatient visits annually
Accounts for approximately 200,000 hospitalizations per year.
Clinical Evaluation of PID
Lower abdominal pain is the cardinal presenting symptom in women with PID, although the character of the pain may be quite subtle.

Abnormal uterine bleeding occurs in about one – third or more of patients with PID.

New vaginal discharge, urethritis, proctitis, fever, and chills can be associated signs.
Risk factors of PID
Age less than 35 years
Non barrier contraception
New, multiple, or symptomatic partners
Previous episode of PID
Oral contraceptives
African – American ethnicity (higher reported incidence)
Physical Exam of PID
Only about 50% of patients have fever

Diffuse lower quadrant abdominal tenderness which may or may not be symmetrical

Purulent endocervical discharge and / or acute cervical motion tenderness and adnexal tenderness by bimanual examination is highly suggestive of PID

Rectovaginal examination should reveal the uterine adnexal tenderness


Rebound tenderness and decreased bowel sounds are common

Right upper quadrant tenderness does not exclude PID (10% have perihepatitis)
Dx of PID
The index of suspicion should be high, especially in adolescent women

CDC minimum criteria for empiric treatment: lower abdominal tenderness, adnexal tenderness, cervical motion tenderness

CDC minor determinants (signs that may increase the suspicion of PID: Fever > 101 degrees F, Vaginal discharge, Documented STD, Increased Sed Rate (ESR), C-Reactive protein, Systemic signs (pt looks sick), Dyspareunia
When to Use Empiric Tx in PID
Pregnancy test is negative

The examination suggests PID

Demographics (risk factors) are consistent with PID
Lab Eval of PID
Pregnancy test !!!!!
Microscopic exam of vaginal discharge
Complete Blood Count (CBC)
Test for Gonorrhea and Chlamydia
Urinalysis
Fecal Occult Blood
C-reactive protein (optional)
Gram stain is only useful if it stains positive for Gram negative intracellular diplococci (Gonorrhea)
Dx Tool of PID
Ultrasound

Should be reserved for the acutely ill patient with PID in whom a pelvic abscess is suspected
Recommendations for PID
Maintain a low threshold of suspicion for the diagnosis of PID

Sexually active young women with lower abdominal pain, adnexal and cervical motion tenderness should receive empiric treatment

If clinical findings suggest PID then initiate empiric treatment
Differential Dx of PID
Ectopic Pregnancy !!!!!!!!!!!!!!!!!!!!!
Appendicitis
Hemorrhagic ovarian cyst
Ovarian torsion
Endometriosis
Urinary tract infection
Irritable Bowel Syndrome
Gastroenteritis
Cholecystitis
Nephrolithiasis
Somatization (Don’t be afraid to ask about rape, incest, sexual abuse, domestic violence)
Tx of PID
Gonorrhea and Chlamydia are the most common initiators of PID
Treatment coverage should also include Streptococcus Group A and B, Gram negative enteric bacilli (E. coli, Klebsiella, and Proteus), and anaerobes

(“2 inch no man’s land, rectum & vag”)
Inpatient PID Tx
Recommended Parenteral Regimen A Cefotetan 2 g IV every 12 hours OR Cefoxitin 2 g IV every 6 hours  PLUS Doxycycline 100 mg orally or IV every 12 hours

Recommmended Parenteral Regimen B : Clindamycin 900 mg IV every 8 hours  PLUS Gentamicin loading dose IV or IM (2 mg/kg of body weight), followed by a maintenance dose (1.5 mg/kg) every 8 hours. Single daily dosing may be substituted.
Outpatient PID Tx
Recommended Oral Regimen Ceftriaxone 250 mg IM in a single dose    PLUS Doxycycline 100 mg orally twice a day for 14 days    WITH OR WITHOUT Metronidazole 500 mg orally twice a day for 14 days


Cefoxitin 2 g IM in a single dose and Probenecid, 1 g orally administered concurrently in a single dose    PLUS Doxycycline 100 mg orally twice a day for 14 days    WITH OR WITHOUT Metronidazole 500 mg orally twice a day for 14 days

Other parenteral third-generation cephalosporin (e.g., ceftizoxime or cefotaxime)    PLUS Doxycycline 100 mg orally twice a day for 14 days    WITH OR WITHOUT Metronidazole 500 mg orally twice a day for 14 days
If parenteral cephalosporin therapy is not feasible, use of what is feasible?
If parenteral cephalosporin therapy is not feasible, use of fluoroquinolones (levofloxacin 500 mg orally once daily or ofloxacin 400 mg twice daily for 14 days) with or without metronidazole (500 mg orally twice daily for 14 days) may be considered if the community prevalence and individual risk for gonorrhea is low
PID other considerations/tests
Women with PID should also have serology testing for HIV, Hepatitis B & C, and Syphilis
Provisional STD Statistics 2009 As of 26 Sep 2009
Chlamydia: 816,901
Gonorrhea: 194,369
Syphilis (Primary & Secondary): 9,544
STD: Biological Factors
Gender – females at greater risk
Preexisting STDs including HIV
Lack of conspicuous signs and symptoms
Long lag time for symptom presentation
Women infected more than men
Other factors: circumcision, douching, oral contraceptives, IUD’s
STD: Social Factors
Poverty
Inadequate access to health care
Substance abuse
Lack of education
Sexual abuse and violence
Secrecy
STD: REPORTABLE
Syphilis
Gonorrhea
AIDS
Chlamydia
Chancroid
Other STDS (Varies by State)
Reporting may be provider and/or lab based
STD: HX
History of Present Illness: onset, duration, timing of symptoms
Gyn Hx: Previous STD, Lesions, Treatment
Sexual HX: Practices, Number of partners, New partner, Partner symptoms
Medications: Contraceptives, OTC’s
Review of Systems
The Five P's
Partners
Prevention of Pregnancy
Protection from STD’s
Practices
Past History of STD’s
STD Workup
Cardinal Rule: ANY woman of reproductive age with a complaint of abdominal / pelvic pain has an ectopic pregnancy until proven otherwise!!
Always test for other STDs
DNA probe (Nucleic Acid Amplification Tests) Gonnorhea and Chlamydia
Cultures
RPR
HIV
HBSAg
Wet mount
Chlamydia Background
#1 STD in USA
15-28% of Sexually Active Adol
Chlamydia Manifestations & Serious Sequelae
Clinical Manifestations
Cervicitis-MOST COMMON IN FEMALES
pharyngitis
Bartholinitis-bartholin’s gland
Proctitis-male or female
Endometritis-can head towards PID
Urethritis-can head towards PID

PID-scarring in the tube, sperm goes anywhere but
ECTOPIC PREGNANCY
INFERTILITY
Chlamydia Risk Factors
young age (15 – 21 highest prevalence)
multiple sex partners
non-white race
low Socioeconomic status
cervical eversion-show columnar
OCP’s
New partner
Unprotected sex
Chlamydia S/S
asymptomatic
abnormal vaginal discharge
postcoital or intermenstrual spotting/bleeding
dysuria, frequency-urethritis d/t chlamydia infection
dyspareunia
pelvic / abdominal pain

Signs*
General-usually wnl
Elevated temp
Abdominal – usually wnl
RUQ pain
Pelvic-r/t PID
CERVIX (+swab test): may be friable with mucopurulent discharge
FUNDUS: may be tender if endometritis present
ADNEXAE: may be tender; mass may be present
Chlamydia Dx
DIAGNOSIS*
Nucleic Acid Amplified Tests (NAATs) are the most sensitive test for endocervical and male urethral swab specimens
Sensitivity: 80 – 100%
Specificity: near 100%
Chlamydia Tx
RECOMMENDED REGIMENS
Azithromycin 1 GM po x 1 dose, OR
Doxycycline 100mg po bid x 7 days
ALTERNATIVE REGIMENS
Erythromycin base 500 mg po qid for 7 days
Erythromycin ethylsuccinate 800 mg po qid for 7 days
Ofloxacin 300 mg po bid for 7 days
Levofloxacin 500 mg po qd for 7 days

FOLLOW-UP: except in pregnancy (retest 3-4 weeks after completing therapy) test of cure is not indicated
Chlamydia Sexual Partners
Management of Sexual Partners:
Partners should be referred for evaluation, testing, and treatment.
All partners with sexual contact 60 days prior to onset of symptoms should be evaluated
The most recent sexual partner should be evaluated even if contact > 60 days

Treated before next intercourse
Abx Contraindicated in Pregnancy with Chlamydia
Doxycycline (Tetracylcines), Ofloxacin, and Levofloxacin (Quinolones) are CONTRAINDICATED in pregnancy
Recommended Regimens for pregnant women
Azithromycin 1 gm po in a single dose (macrolide) OR
Amoxicillin 500mg po tid x 7 days (penicillin)
Gonorrhea Facts
“Clap, Drip, Dose, Gleet, Whites”
ORGANISM - Neisseria gonorrhoeae
300,000 new cases in USA each year
May not be symptoms in women until PID
Incubation: 1 – 14 days
20 – 40% co-infected with Chlamydia

Males have “drippy” discharge
Extremely painful to urinate (finger impressions in the side of the urinal)
Gonorrhea Transmission
Sexual
Typical is Men to Women or Men to Men
80-90% transmission from male to female with a single act of intercourse
Gonorrhea Sites of Infection
Endocervix - primary site in women
Urethra – primary site in men. Usual site in hysterectomized pt
Skene’s and Bartholin’s
Rectum – women and men
Pharynx –women and men
Gonorrhea Serious Sequelae
PID - 15-20%
INFERTILITY
ECTOPIC PREGNANCY
DISSEMINATED GONOCOCCAL INFECTION (DGI)
Gonorrhea S/S
SYMPTOMS
asymptomatic
vulvar pruritis, irritation, labial edema
abnormal vaginal discharge
abnormal vaginal bleeding
Other: dysuria, urgency/ frequency, dyspareunia, dysmenorrhea

SIGNS
GENERAL
temperature may be increased
ENT
pharyngeal injection, cervical nodes
SKIN
volar aspects of arms, hands, fingers
EXTREMITIES
joint tenderness, swelling, erythema, effusion
ABDOMEN
usually WNL; tender if PID
PELVIC
EXTERNAL GENITALIA - erythema, edema, excoriation
VAGINA - abnormal discharge, blood, pus
CERVIX - purulent/mucopurulent discharge; friable
UTERUS - tender if PID
ADNEXIA - tender, mass if PID
Gonorrhea Dx
GRAM STAIN: high specificity and high sensitivity (polymorphonuclear leukocytes with Gram negative, intracellular diplococci in symptomatic males)
Nucleic Acid Amplified Tests (DNA / RNA) tests both GC
Can be co-infected with Chlamydia
Tx for Uncomplicated Gonorrhea of Cervix, Urethra and Rectum
Recommended Regimens (Cephalosporins Only)
Ceftriaxone 125 mg IM in a single dose    OR Cefixime 400 mg orally in a single dose or 400 mg by suspension (200 mg/5ml)    PLUS TREATMENT FOR CHLAMYDIA IF CHLAMYDIAL INFECTION IS NOT RULED OUT
Tx for Gonorrhea and Chlamydia
Treatment for Chlamydia if concurrent infection not ruled out: Gonorrhea regimen PLUS
Azithromycin 1 gram po in a single dose, OR
Doxycycline 100mg po bid x 7 days
Tx for Gonorrhea Partner
Sex partners with sexual contact 60 days prior to onset of symptoms should be evaluated and treated for Gonorrhea and Chlamydia
Most recent sexual partner should be treated even if sexual contact was over 60 days prior to onset of symptoms
Tx for Gonorrhea Pregnancy
NO Quinolones, tetracyclines
Use recommended or alternate cephalosporin
If cephalosporin intolerant, then Spectinomycin 2 gm single dose IM
Either Azithromycin or Amoxicillin is recommended for treatment of presumptive Chlamydia
STDs Characterized by LESIONS
GENITAL HERPES* most prevalent
SYPHILIS
CHANCROID
Frequency varies by geographic location and patient population
All three are associated with an increased risk for HIV infection
-ULCERS
GENITAL HERPES
CHANCROID
SYPHILLIS
GRANULOMA INGUINALE
LYMPHOGRANULOMA VENEREUM
-WARTS
HPV (condyloma)

Diagnosis based only on HPI, PMH, and PE is often inaccurate
Serology testing should be done on all patients with genital lesions
Genetic Ulcer Test
Darkfield examination or direct immunofluorescense test for Treponema pallidum
Culture or antigen test for HSV, and
Culture for Haemophilus ducreyi (where chancroid is prevalent)

HIV testing!
Genital herpes
Recurrent, incurable viral disease; latent in the spinal root ganglia
Serotypes: HSV-1 and HSV-2
HSV-2 diagnosed in at least 45million USA
Genital Herpes Transmission
Mucosal contact with HSV-infected secretions
Asymptomatic viral shedding
Human reservoir
Hormone Therapy

What is Rate? Relative Risk?
Rate:
Number of events per number of individuals per time interval:
44 events in 10,000 people per year
Relative Risk (Ratio)

Rate of disease in exposed group divided by rate of disease in unexposed group.
Risk of DVT
2.0

Annual rate of DVT in postmenopausal women
Oral ET: 22/10,000
No ET: 11/10,000

Risk for DVT in women using ET twice that of non ET users
How do you Interpret Relative Risk?
RR <1.0: exposure appears to Decrease risk
RR 0.50 = 50% Decrease risk for exposed group
RR 0.3 = 70% Decrease risk for exposed group
RR >1.0: exposure appears to Increase risk
RR 1.2 = 20% Increase risk for exposed group
RR 2.0 = risk is doubled for exposed group
RR = 1.0 exposure/non-exposure = risk
What is Absolute Risk and why should you use it with your patients?
More clinically useful than RR in explaining risk to patients
Addresses number of new cases
Quantifies the impact on Public Health

Difference between incidence rates in exposed and unexposed groups (risk difference)
Absolute Risk Example
22/10,000 - 11/10,000=11/1000

For every 10,000 ET users
11 additional cases of DVT per year of ET use
Difference between Rare and Very Rare
1998 CIOMS risk levels:
RARE: < or = 10/10,000/year
VERY RARE: < or = 1/10,000/year
Menopause Background: Longevity and Population Expansion
Longevity
1/3 of lifetime postmenopausal
Population expansion
By 2020: 45 million American women >50
Why is the Nachtigall study significant?
First randomized controlled trial in postmenopausal women
1965-1987 = 22 years
84 matched pairs (chronically hospitalized)
Wide array of clinical endpoints
MI, CA, Thromboembolism, Gall Bladder etc.
First 10 years
Placebo or CEE 2.5mg & MPA 10mg
Next 12 years
CEE  to 0.625mg patients free to stop or switch
Nachtigall Results?
Higher incidence Gall Bladder disease

No difference: MI, Uterine CA, Thrombophlebitis

Lower incidence of Breast CA
0 cases in HRT group (N=116)
6 cases in placebo group
What is the Coronoary Drug Project?
The first E2 Clinical Trial
Question:
Is estrogen cardioprotective in men?
Men given 2.5 or 5 mg/day of CEE

Stopped prematurely
Early excess VTE & Heart Disease

What did it tell us?
E2 in high doses is NOT good for men…
What is the HERS I and HERS II Study?
Heart & Estrogen-Progesterone Replacement Study
What were the HERS I results?
Treatment group had more CHD events in the first year, and fewer years 3-5.

Probable that prothrombotic/arrhythmic/ ischemic effects in first year counterbalanced lipid improvements
What was the HERS II study? and its results?
Confirm trend toward improvements in cardiovascular profile in treatment group

No Improvement!

Estrogen in women with documented heart disease is Not Good! No Benefits even after 6 years
If no evidence of heart disease with smoking, obese, on bcp..not a good idea to start estrogen. Although she has a hx of hormone use with bcp.
What is the Bottom Line of the WAVE, ERA and WELL HART Studies?
WAVE: Women’s Angiographic Vitamin & Estrogen
ERA: Estrogen Replacement and Atherosclerosis
WELL-HART Women's Estrogen/Progestin & Lipid Lowering Hormone Atherosclerosis Regression
Bottom line: No change in progression or outcomes of CVD
WHI clinical endpoints?
CHD (Non-fatal MI & Death)
Invasive Breast Cancer
Global Index: Balance of risk/benefit
2 primary outcomes +
Stroke
Pulmonary Embolism
Endometrial Cancer
Colorectal Cancer
Hip Fracture
Death due to other causes

WHI: told us there are a difference between combine and estrogen only, and difference with Women’s Age. The earlier, the more benefit.
WHI CEE only findings?
12 more women with stroke.
44 in CEE vs. 32 in placebo group.
? Increase in clots
6 fewer women with hip fractures.
Possibly 7 fewer breast cancers
Bottom line:
CEE should not be used to prevent chronic disease overall and heart disease in particular
WHI CEE vs CEE/MPA findings?
Similarities
Increased stroke and decreased fractures similar to CEE/MPA

Differences
CEE did not increase breast cancers or decrease colorectal cancers

Possible explanations:
Different health factors for women with hysterectomy
MPA changes disease risks and benefits
Findings of Rossouw etal (2007) - 2ndary Analysis if WHI?
Effect of age & yrs since menopause
Primary endpoints: CHD & Stroke
Age groups:
50-59
60-69
70-79
Years since menopause
<10
10-19
>10
Findings of Rossouw etal (2007) - 2ndary Analysis if WHI? (continued)
50-59 yrs: overall  in mortality
<10 yrs, CHD reduced (not significant)
CHD risk  in ET vs HT (not significant)
If <10 yrs since menopause
No differences in total mortality or CHD
If >20 years, HT  CHD risk
Stroke risk  across all categories
Findings of Hsia (2006) & Manson (2007)?
ET between 50 & 59 significantly reduced coronary artery plaque & prevalence of subclinical coronary artery disease
Consistent with observational studies
ET may be protective in younger women
What is NAMS Position Statement?
“The benefit-risk ratio for menopausal hormone therapy (HT) is favorable for women beginning HT close to menopause but decreases in older women and with time since menopause in previously untreated women”
NAMS 2010 Summary?
Absolute risks for use of HT are low,
-particularly for the women on ET only
-considerable safety for 0.625 mg/day of oral CE.

Risks rare except for stroke

Absolute risk or benefit small for women
<50
At low risk of CHD, stroke, osteoporosis, breast cancer, or colon cancer,

Type of hormones , administration routes and timing of doses have distinct beneficial and adverse effects (po vs cream)
Risk Factors related to hormone therapy?
Risk factors related to
Baseline disease risks
Current age & age at menopause
Time since menopause
Cause of menopause
Prior hormone use
Types, routes, and doses of HT
Emerging medical conditions
Hormone Therapy Terminology
ET: Estrogen therapy
EPT: Combined estrogen-progestogen
HT: Hormone therapy (ET + EPT)
Progestogen: Progesterone & Progestin
Systemic therapy: HT resulting in serum levels high enough to produce clinically significant effects:
Local therapy: Vaginal ET therapy that does not result in clinically significant effects.
Terminology:
Spontaneous/Natural Menopause
Induced Menopause
Perimenopause/menopause transition
Spontaneous/natural menopause:
The final menstrual period (FMP), confirmed after 12 consecutive months of amenorrhea with no obvious pathologic cause
Induced menopause:
Permanent cessation of menstruation after bilateral oophorectomy (ie, surgical menopause) or iatrogenic ablation of ovarian function (eg, by chemotherapy or pelvic radiation therapy)
Perimenopause/menopause transition:
Span of time when menstrual cycle and endocrine changes occur a few years before and 12 months after the FMP resulting from natural menopause
Terminology
Premature menopause
Early menopause
Premature ovarian failure
Early post menopause
Premature menopause:
Menopause reached at or under age 40, whether natural or induced
Early menopause:
Natural or induced menopause that occurs well before the average age of natural menopause (51 y), at or under age 45
Premature ovarian failure:
Ovarian insufficiency experienced under age 40, leading to permanent or transient amenorrhea
Early postmenopause:
The time period within 5 years after the 1FMP resulting from natural or induced menopause
What is the Primary indication for HT?

What are vasomotor symptoms?
Primary indication for HT = moderate to severe vasomotor symptoms

ET (w/ or w/o progestogen) most effective treatment for menopausal vasomotor symptoms & side effects
Hot flashes & night sweats
Diminished sleep quality, irritability & lower QOL

Systemic products all approved for this indication
How bout Vaginal symptoms?

Local or Systemic?
ET most effective treatment for mod-severe vulvar & vaginal symptoms
Dryness, dyspareunia, atrophic vaginitis

Many systemic products & all
vaginal products approved for this indication

If ONLY vaginal c/o – consider local treatment only
What are the effects of HT on Sexual Function?
Vaginal sx relief (local or systemic HT) can improve sexual function
Local E2 may  blood flow & sensation

1 oral product approved for treatment of pain with intercourse

HT not recommended as sole treatment for other sexual problems
e.g. decreased libido
Effects of HT on Urinary Health?
Urge: Local ET may help (vaginal atrophy)

Overactive bladder: Benefit unclear

Stress UI:
-Unclear about local
-Systemic HT can provoke
Change in uterine volume or periurethral collagen
Local HT may help with recurrent UTI
Proliferative effect on urethra & bladder epithelia
Restores pH and vaginal flora
No drugs FDA approved
What are the BMI changes and HT?
Peak BMI between 50 and 59
-Changes in exercise & diet patterns
-Decreased metabolic rate
Menopausal hormonal changes may add to this tendency for weight gain.

No statistically significant differences between women on HT vs off HT
HT and Osteoporosis
HT  fracture risk even in women w/o osteoporosis

Extended HT use an option for women with osteoporosis or osteopenia
Prevents further bone loss and fracture if other treatments not useful/tolerable
Optimal initiation time: immediately post menopause
Benefits dissipate rapidly after stopping
HT and CHD
Timing of initiation
Observational studies: younger women (2-3 years postmenopause)
RCTs: older women 63-64 years old (>10 years post menopause)
When age matched, RCTs = Observational results
HT may reduce CHD risk if initiated at younger age (recently postmenopausal)

Duration of HT use
Observational studies: longer use =  risk for CHD and related mortality
Short term: HT associated with increase in CHD risk in older women
Coronary artery calcium may be the reason…HT may slow the development of CA calcium.
HT and Stroke
HT NOT effective in
dec risk of recurrent stroke in women with established cardiovascular disease (CVD)
Preventing a first stroke
NOT recommended as stroke prevention
HT may INC rate of 1st stroke
particularly in women over age 60

Stroke not INC in 50 to 59 in overall WHI analysis
BUT stroke risk nearly doubled in ET group >10 years post menopause.
Why? Possibly due to
Relatively few events
Difficulty in accurately timing onset of menopause in the ET group.
HT and VTE
All studies show  risk with oral HT
WHI
Effect emerges early (1-2 years),  with time
Excess risk lower in women <60 years
7/10,000/year EPT; 4/10,000/year ET (“Rare”)
BMI >30, risk 3 fold higher
Prior history of VTE or factor V Leiden at INC risk on HT
Lower doses and transdermal route may decrease risk (no RCT data)
Bottom Line: Cardiac
HT NOT recommended as sole or primary indication for coronary protection: irrespective of age
HT does not seem to INC risk for CHD events in women 50-59 or initiated w/in 10 years of menopause
HT initiation in early postmenopause may DEC CHD risk
HT and Diabetes
RCT suggests that HT DEC new onset Type II DM
WHI
Women on HT 21% reduction in DM (15/10,000/year)
? Mechanism
Lower weight gain, DEC insulin resistance
No evidence for recommending HT as sole or primary indication for prevention of DM in peri or postmenopausal women

Women who have Type II
Transdermal ET may be better
Trigylceride levels don’t increase with transdermal
BP changes only reported with oral ET, not with transdermal delivery methods
HT and Endometrial Cancer
USE PROGESTOGEN IF INTACT UTERUS

Unopposed systemic ET:  risk dose & duration related
Risk persists after discontinuation
3 years = 5 fold risk
10 years = 10 fold risk
Early bleeding to early diagnosis; minimal impact on life expectancy
HT and Breast Cancer
Hormones  breast cell proliferation, pain & density on mammogram
Br Ca  with EPT use >3-5 years
Rare (4 to 6/10,000/year)
? If sequential vs continuous is worse
Br Ca not  with ET use
6 fewer cases/10,000/year (not statistically significant)
Decrease seen across all age groups
50-59, 60-69, 70-79
ET use <5 years little impact on risk
HT and Mood/Depression
Progestogens may worsen mood
History of PMS/PMDD/Clinical depression
RCT’s in depressed peri/post menopausal women
HT antidepressant effect (2 studies)
HT no effect 5-10 years post (1 study)
Controversial: does ET augment SSRI?
Evidence does not support HT use to treat depression
HT and Cognitive decline/Dementia
No association between age at menopause & AD
Case/control study bilateral oophorectomy before menopause associated with dementia & risk increased with younger age at oophorectomy
HT and Premature Menopause
Distinctly different population
Limited data but possibly:
 risk breast cancer,  risk for CHD
Earlier onset osteoporosis
HT may be more protective
Don’t extrapolate WHI data to these women
No trial data, but risks potentially smaller & benefits possibly greater
HT and Total Mortality
WHI = to observational studies
DEC total mortality if HT initiated soon after menopause
total mortality DEC 30%; statistically significant if ET/EPT data combined
Not associated with DEC mortality if initiated >60
Prescribing HRT: Estrogens
Primary indication: vasomotor instability
Secondary: vaginal symptoms
NOT considered cardioprotective
E2 receptors are everywhere
Endometrium Breast, Brain, Vagina, Skin
SERM: turns OFF some, ON others
VAGINAL ET: Not SYSTEMICALLY absorbed
Prescribing HRT: Progestogens
Primary indication: DEC endometrial cancer risk
INTACT UTERUS, using systemic ET needs adequate progestogen
NO UTERUS: No progestogen
Vaginal ET: No progestogen
Vasomotor symptoms may improve more if E + P
WHI results comprehensive
Compared with the placebo, estrogen plus progestin resulted in:

* Increased risk of heart attack
* Increased risk of stroke
* Increased risk of blood clots
* Increased risk of breast cancer
* Reduced risk of colorectal cancer
* Fewer fractures
* No protection against mild cognitive impairment and increased risk of dementia (study included only women 65 and older)

Compared with the placebo, estrogen alone resulted in:

* No difference in risk for heart attack
* Increased risk of stroke
* Increased risk of blood clots
* Uncertain effect for breast cancer
* No difference in risk for colorectal cancer
* Reduced risk of fracture

(Findings about memory and cognitive function are not yet available.)