Chronic Week 11

In what situations would suppressing ovulation be useful to Tx underlying causes of chronic pelvic pain? How do you accomplish this?

Accomplished via: Gonadotropin-releasing hormone agonists: cause a central downregulation of the ovarian hormones (downregulation of GnRH receptors) Can Tx: 1. Endometriosis 2. Relieve IBS Sx 3. Relieve Intersitial cystitis Sx 4. Pelvic congestion syndrome Sx (in which engorged pelvic blood vessels are purported to cause pelvic aching and pain)

Endometriosis: Tx?

Hormonal medications are for pain ADD: NSAIDs subcutaneous depot medroxyprogesterone acetate (DMPA) or implants, suppresses gonadotropin release and, in turn, ovarian steroidogenesis; it also directly affects the uterine endometrium and endometrial implants oral medroxyprogesterone is an option for women who are trying to become pregnant insofar as it does not offer a reliable contraceptive effect.

Menopause: S/S and complications (part 1)? Why do these occur?

Hot flashes (flushing, perspiration, and sensation ranging from warmth to intense heat on upper body/face)=first Sx and sign of vasomotor instability-->sometimes followed by chills and diaphoresis Hallmark of perimenopause (lasts ~3 minutes). Vaginal dryness: epithelium, cervix, endocervix, endometrium, myometrium, uroepithelium (atrophy without estrogen). Atrophic vaginitis (itching/burning). endometrium also becomes atrophic, sometimes resulting in postmenopausal spotting.

Vulvar cancer: S/S?

If metastasis to the lymph nodes

Lichen planus: Prev? Define? S/S? Tx? Gross morph? Histo findings?

Inflammatory response--huge inflammatory infilatrate on Bx

Menopause: S/S and complications (part 2)?

Irritiable due to lack of sleep. Also, difficultty with concentration and interpersonal relationships.

Vaginal Cancer: Tx?

Left=less aggressive cancer Right=more aggressive cancer Chemo/radiation only if metastasis

How to do the assessment for dysmenorrhea?

Looking for causes of secondary dysmenorrhea--if physical exam is normal, this points you in direction of primary dysmenorrhea

Psoriasis: Prev? Dx? Management?

Management: send to derm

IBS: mechanism? Risk factors?

Mechanism: Unknown: Thought to be related to altered bowel motility, visceral hypersensitivity, psychosocial factors (especially stress), an imbalance of neurotransmitters (especially serotonin), and infection (often indolent or subclinical). Risk factors: Hx of childhood sexual or physical abuse is highly correlated with the severity of symptoms experienced by those with IBS

Define menopause and perimenopause?

Menopause: permanent cessation of menses after significant decrease of ovarian estrogen production. This is evidenced by 12 consecutive months with no menstrual bleeding. The time period during which the changes of menopause occur is called the climacteric. Perimenopause: period before menopause, that is, the transition from the reproductive to the nonreproductive years during which ovarian estrogen production may fluctuate unpredictably.

Vulvar cancer: SCC: Prev? Comes from what kind of cells? Risk factors? Demo? Precancerous lesions? Causes? Next steps?

More common from HPV Next step: PET/CT: to see if invaded the lymph node Demo: women over the age of 65

Secondary dysmenorrhea: Causes?

Most common: 1. endometriosis (the presence of endometrial glands and stroma outside of the uterus) 2. adenomyosis (the presence of ectopic endometrial tissue within the myometrium) 3. adhesions 4. pelvic inflammatory disease (PID) 5. leiomyomata (uterine fibroids)

Vulvar cancer: Dx?

Next step: PET/CT: to see if invaded the lymph node

Vulvar cancer: Tx?

Nodal dissection Can do minimally invasive strategy if VIN or minimally invasive cancer (less than 1 mm). If not, must do more invasive surgery (will see a mass on gross morph)

Precancerous grades for vagina? Risk factor?

ONLY HPV related. Grades are VaIN 1, 2, and 3. Just like cervix and vulva. Vulva is the only one that has non-HPV group though. Very rare to be primary!

Bartholin cyst: Dx? Tx?

Opening cyst to create a pouch=Marsupialization

Primary dysmenorrhea: S/S?

Pain diffusely located in the lower abdomen and suprapubic area, with radiation around or through to the back. Pain is described as "coming and going" or similar to labor. Moderate to severe: N/V, diarrhea ADD: pale and diaphoretic

Secondary dysmenorrhea: Describe the pain pattern?

Pain often lasts longer than the menstrual period. It may start before menstrual bleeding begins, become worse during menstruation, then persist after menstruation ends.

Vaginal cancer: squamous cell carcinoma: Risk factors? Associated conditions? Demo? Precanceroius lesions? Comes from what kind of cells?

Prev: most common Almost always a metastasis from other location, mainly cervix. Precancerous lesions: intraepithelial neoplasia are very rare. Categories are VaIN 1, VaIN 2, and VaIN 3

IBS: Prevalence of chronic pelvic pain? Diagnosis? Subcategories?

Prevalence of chronic pelvic pain: 50-80% Rome III criteria=diagnosis: 1. Symptoms of recurrent abdominal pain or discomfort and a marked change in bowel habit for at least 6 months, with symptoms experienced on at least 3 days of at least 3 months Two or more of the following must apply: (1) pain is relieved by a bowel movement (2) onset of pain is related to a change in frequency of stool (3) onset of pain is related to a change in the appearance of stool Subcategories: pain, diarrhea, constipation, or alternating constipation and diarrhea

Pelvic Inflammatory Disease (PID): Prevalence of chronic pelvic pain? Mechanism?

Prevalence: 18-35% have chronic pelvic pain Mechanism: Not exactly known; may involve chronic inflammation, adhesive disease, and the coexistence of psychosocial factors.

When is the highest prevalence of primary dysmenorrhea seen? Secondary dysmenorrhea?

Primary: Late teens-early 20s Secondary: More common as women age

Menopause: Tx and prognosis?

Progestins prevent endometrial hyperplasia and cancer effect of unopposed estrogens-->do not give progestins to hysterectomy patient's because they no longer have an endometrium and thus are not at risk for cancer Hormone replacement therapy can Tx many Sx. The administration of continuous unopposed estrogens (17Beta-estradiol) can result in endometrial hyperplasia and an increased risk of endometrial adenocarcinoma. Therefore, it is essential to administer a progestin in conjunction with estrogens in women who have not undergone hysterectomy. (progestins=medroxyprogesterone acetate, norethindrone, or micronized progesterone)

Lichen simplex chronicus: Physio? Demo? Complications? S/S? Dx? Tx? Prognosis?

Prognosis: excellent if you can remove offending irritant Irritation caused by unknown irritants/chemical exposures

What role does estrogen play in postmenopausal women?

Promotes endometrial proliferation and can lead to endometrial hyperplasia and carcinoma. Obese menopausal women have higher risk of endometrial hyperplasia and carcinoma (make more estrogen (estrone) than slender women). Although slender women, tend to have higher odds of Sx.

What are the contraindications to hormonal therapy in menopausal women?

Prospective studies using low-dose HT in women with a prior history of limited lesion breast cancer demonstrate unacceptable risk; HT is not recommended in these patients. Similar studies in women with prior treated limited-lesion, low-risk endometrial cancer have been completed and show no increased risk of recurrence for estrogen users. As with all clinical decisions, a careful risk-benefit analysis should be performed taking into account patient goals.

Vulvar cancer: most common presenting S/S?

Pruritis

Is dyspareunia considered a sign of primary or secondary dysmenorrhea?

Secondary

Vulvar cancers: Prev? Demo? Dx? Location? Spreads how? Most common types? Associated diseases/risk factors?

Some repeat information here Spreads mainly to lymph nodes 20% are aged 50 and under Associated: Smoking

Vaginal cancer: S/S?

Spread to lymph nodes: Lower 2/3 of vagina=Inguinal Upper 1/3 of vagina=Iliac lymph nodes

Compare hormones levels in premenopausal, postmenopausal, and postoophorectomy?

Testosterone declines, but remains high in postmenopausal women compared to women who have their ovaries removed Estrone (E1): predominant estrogen produced in postmenopasual women. Direct concentrations are related to amount of adipose tissue

Lichen sclerosis: Bx findings?

The upper dermis exhibits homogenization of collagen, limited movement. May crack and bleed

Endometriosis: Dx?

Two of the following features on Bx: • Endometrial epithelium • Endometrial glands • Endometrial stroma • Hemosiderin-laden macrophages US can detect endometriomas CA-125 will be elevated (not reliable for Dx)

Tx for secondary dysmenorrhea?

Underlying cause, if not possible symptomatic therapy in the form of analgesics or modification of the menstrual cycle may be effective.

Lichen sclerosis: Complications? S/S? Dx? Tx? Complications?

Unknown why there is increase chances of squamous cell carcinoma and differentiated VIN S/S: white epithelial areas, termed "onion skin" Complications: can progress to vulvar cancer DIAGNOSIS MADE VIA Bx.

Vaginal Cancer: Dx (part 1)

Upper 1/3 of posterior vaginal wall is most common location CT/MRI can be done to look for metastasis

Female anatomy review?

Uterus is posterior to bladder and anterior to rectum Round ligaments: atnerior body wall and uterus attachment Support laterally via the meometrium and cardinal ligaments. Wall of uterus: 1. Perimetrium: lining continous with lining of peritoneal cavity 2. Myometrium: smooth muscle that helps push baby out 3. Endometrium: Mucosal layer that undergoes monthly cyclic changes

Vulvar cancer: Paget Disease: Gross morph? S/S? Complicatoins? Dx? Tx?

Vulvectomy if things are getting bad

Secondary dysmenorrhea: definition?

caused by structural abnormalities or disease processes that occur outside the uterus, within the uterine wall, or within the uterine cavity

What are the risks of hormone therapy?

combination of conjugated equine estrogens and continuous low-dose medroxyprogesterone acetate resulted in an increased risk of heart attack, stroke, thromboembolic disease, and breast cancer, with a reduced risk of colorectal cancer and hip fractures. One arm of the study reviewed the same outcomes in women taking unopposed estrogen and found that these women had no increased risk of cardiac events and a trend toward decrease in breast cancer compared to women on combined therapy. Therefore, Tx via hormonal therapy should be only be used for Tx of symptoms and revisited frequently

Vulvar cancer: melanomas: arise how? Gross morph? Tx? Prognosis? Dx/Bx?

nevi=moles

Define chronic pelvic pain?

noncyclic pain lasting for more than 6 months that localizes to the anatomic pelvis, anterior abdominal wall at or below the umbilicus, the lumbosacral back, or the buttocks and is of sufficient severity to cause functional disability or lead to medical care.

Physical exam findings for a chief complaint of chronic pelvic pain?

1. Assess using the patient's Hx as a guide 2. If severe tenderness during the exam, you can avoid the assessments that the patient cannot handle 3. Carnett sign or tensing of the abdominal wall while raising the legs or chin in the supine position can help identify myofascial pain, which should increase with these maneuvers involving the rectus muscles. Visceral pain will decrease/remain unchanged by these maneuvers. 4. Examine for muscle spasm pain induced by the obturator internus muscle (abduct and internally rotate leg against pressure) 5. Examine for muscle spasm pain induced by the levator ani muscle (tighten pelvic floor as if to stop urine or Kegel exercise).

Primary dysmenorrhea: home remedies to help with symptom relief?

1. Assume the fetal position 2. Using a heating pad 3. Using a hot water bottle

Endometriosis: pathophysio?

1. Cells that make up the endometrium implant themselves in other parts of the body-mainly the fallopian tubes, ovaries, and uterine ligaments (other places are the perimetrium, rectovaginal septum, recto-uterine pouch (pouch of Douglas), uterosacral ligaments, the round ligament, and the colon (sigmoid)/bladder (ureters). Rarely, surgical scars, umbilicus, and places like lungs, and brain. 2. Once there, they proliferate and form masses of endometrial tissue. They also have same secretion and participate in the menstruation cycle the same because they have estrogen receptors. 3. Two key differences between the implanted cells and normal endometrial cells: a. High levels of aromatase meaning they produce their own estrogen b. Release pro-inflammatory factors leading to inflamattion, scarring, and adhesions which bind to organs and differing structures c. Both (a) and (b) promote new blood vessel growth.

DDx for secondary dysmenorrhea with presentations?

1. Complaints of heavy menstrual flow combined with pain suggest uterine changes such as adenomyosis, leiomyomata, or polyps. 2. Pelvic heaviness or a change in abdominal contour should raise the possibility of large leiomyomata or intra-abdominal neoplasia. 3. Fever, chills, and malaise suggest infection. 4. A coexisting complaint of infertility may suggest endometriosis or chronic PID or its sequelae.

Which contraceptives can be used to Tx primary dysmenorrhea in patient's that do not want children?

1. Depot medroxyprogesterone acetate (Depo Provera) 2. Longacting implantable progesterone contraceptives (Nexplanon) 3. Progesterone intrauterine delivery systems (Mirena)

Describe the pathways of getting vulvar cancer SCC?

1. HPV (convential type) happens in younger women 2. Nothing to do with HPV. Happens in older women.

Describe the management of intersitial cystitis?

1. Intravesical agents 2. Oral agents aimed at decreasing inflammation and pain signals (antihistamines, tricyclic antidepressants) 3. caffeine, alcohol, artificial sweeteners, and acidic foods should be eliminated (dietary modifications) 4. Dimethyl sulfoxide is the only drug approved for direct bladder instillation to treat interstitial cystitis, although many physicians treat with a combination of anti-inflammatory and analgesic medications 5. pentosan polysulfate sodium, a glycosaminoglycan analog that may help reestablish the disrupted mucosa of the bladder.

What are secondary therapies (second line) Tx of menopause Sx?

1. Lifestyle changes: eating a healthy diet that is less than 30% fat and rich in calcium, getting regular exercise, maintaining a healthy weight, avoiding smoking, limiting alcohol and caffeine intake, and getting regular health care. 2. lowering the temperature of the room, utilizing bedsheets that wick away moisture and heat and avoid triggers. 3. Progesterone (depot medroxyprogesterone acetate) 4. SSRI 5. SNRI 6. Gabapentin and clonidine Things that have some or questionable evidence: 7. Phytoestrogens 8. Acupuncture 9. Black cohosh 10. Exercise

Causes of primary ovarian insuff. (menopause before 40)?

1. Long arm of X chromosome decides reproductive life 2. Autoantibodies against ovarian endocrine tissues 3. Smoking: metabolize E2 primarily to 2-hydroxyestradiol. The 2- hydroxylated estrogens are termed catecholestrogens because of their structural similarity to catecholamines. The catecholestrogens act as antiestrogens and block estrogen action. 4. Alkylating cancer chemo: Hasten follicular atresia 5. Hysterectomy

Common infections that may cause secondary dysmenorrhea?

1. Neisseria gonorrhoeae 2. Chlamydia trachomatis

Tx of primary dysmenorrhea?

1. Non-pharm: application of heat, exercise, psychotherapy, reassurance 2. NSAIDs (prostaglandin synthase inhibitors (COX)): Ibuprofen, naproxen, and mefenamic acid 3. Combined oral contraceptives to induce anovulation and pain relief: stabilize estrogen and progesterone levels, with a resultant decrease in endometrial prostaglandins and spontaneous uterine activity. Desirable in patient's that do not want children currently either 4. (last resort): Presacral neurectomy: involves surgical disruption of the "presacral nerves," the superior hypogastric plexus, which is found in the retroperitoneal tissue from the fourth lumbar vertebra to the hollow over the sacrum. May damage surrounding vascular structures and long-term sequalae like chronic constipation

What aspects of the Hx should you evaluate in a patient with chronic pelvic pain?

1. OLD-CARTS 2. SMASH-FMS 3. Menstrual and sexual history 4. Associated symptoms 5. Proactive and palliative factors 6. Home status 7. Work status 8. Sleep distirubances and other signs of depression 9. Physical/sexual abuse->If yes, screen for current physical/sexual abuse

List the conditions that increase the risk of chronic pelvic pain?

1. PID 2. IBS 3. Intersitial cystitis 4. Endometriosis 5. Adhesions

How should of management of IBS be handeled?

1. Refer to GI 2. Food diary to ID/eliminate foods assocaited with Sx 3. Limiting caffeine, EtOH, fatty foods, acidic foods and gas producing veggies 4. Lactose or wheat gluten intolerance may be identified by the diary 5. If constipation is a major symptom, the consumption of 20 to 30 g of fiber or the use of osmotic laxatives such as lactulose is often useful. 6. If diarrhea is a major symptom, diarrhea is a major symptom, antidiarrheals can be useful 7. Gas pain and cramping may be treated with antispasmodics such as dicyclomine and hyoscyamine.

What are the physical exam findings of adhesions/inflammation?

1. Restricted motion 2. Thickening and tenderness of adnexal structures

What are the 5 main theories as to why endometrial cells migrate outside of the endometrial layer of the uterus in endometriosis?

1. Retrograde mensuration theory (Sampson): During menstruation, some blood carrying endometrial cells will flow backwards into the fallopian tubes into nearby tissue. The fallopian tubes could even be patent and the endometrial cells could go to abdominal structures 2. Dysfunctional immune system: B and T cells do not respond to endometrial implants and do not inhibit their growth 3. Metaplastic theory: Cells of peritoneum become metaplastic and become endometrial tissue (would explain endometriosis in hysterectomy pt's) 4. Benign metastases theory: endometrial cells metastasize to other parts of body 5. Extrauterine stem cell theory: stem cells from bone marrow transform into endothelial cells and travel to distant areas of the body

Follow-up for dysmenorrhea?

1. Should be carefully monitored for success of therapy 2. Should be assessed for possibility of complications of therapy 3. Patients on oral contraceptives for the first time should be asked to return for follow-up after 2 months and again after 6 months. 4. Once successful therapy is established, routine periodic health maintenance visits should continue.

Follow-up for chronic pelvic pain?

1. Should be carefully monitored for success of therapy 2. Should be assessed for possiblity of compolications of therapy 3. Should be encouraged to return for follow-up on a periodic basis, rather than only when pain is present, thus avoiding reinforcing pain behavior as a means to an end.

What factors can bring about earlier onset menopause?

1. Smoking 2. Undernourished

Vulvar cancer: subtypes?

1. Squamous cell carcinoma (most common) 2. Melanomas 3. Adenocarcinomas 4. Paget Disease

Name some adjuvant therapies for chronic pelvic pain?

1. transcutaneous electrical nerve stimulation 2. biofeedback 3. Nerve blocks 4. Laser ablation of the uterosacral ligaments 5. Presacral neurectomy 6. Psychotherapy

How long is the menstrual cycle? How is it regulated?

28 days; cyclic 1. 1st 2 weeks: Estradiol inhibits production of FSH 2. 2nd 2 weeks: Progesterone inhibits production of LH **also inhibit the hypothalamus

Lichen sclerosis: Physio? Location? Demo?

50s-60s

What physical exam findings will you have for a leiomyomata?

A pelvic examination may reveal asymmetry or irregular enlargement of the uterus; irregular contontour of the uterus and rubbery solid consistency of the fibroids

Diagnosis of primary ovarian insuff. (menopause before 40)?

FSH>30-40 on two sperate occasions

Explain the details of menstruation and how it relates to menopause?

Follicle ruptures and releases primary oocyte down the fallopian tube 1. Hypothalamus: secretes GnRH that travels to the pituitary gland 2. Pituitary gland: Release FSH and LH in response to GnRH 3. LH/FSH make theca cells release Androstenedione (sex hormone precursor) 4. Androstenedione travels to the granulosa cell where it is turned into estrogen and progesterone 5. LH/FSH also stimulate a couple of follicles until one becomes the dominant follicle and ruptures; the others that were stimulated die off 6. Over time follicles keep dying off. The remaining ones become less and less sensitive to LH/FSH. 7. This leads to perimenopause where there are fewer functional follicles and you get missed/irregular periods. Without mature follicles you get a drop in estrogen and progesterone with their negative feedback on pituitary and hypothalamus-->burst of GnRH and FSH/LH 8. Finally this process continues until menopause. Without mature follicles you get a drop in estrogen and progesterone with their negative feedback on pituitary and hypothalamus-->burst of GnRH and FSH/LH

Endometriosis: S/S?

ADD: very variable (includes asymptomatic) and exam may be normal on pelvic. ADD: restricted motion of uterus, retroflexed position ADD: rare rectal bleeding or hematuria ADD: uterosacral nodularity (not always present) Ovarian endometriomas may be tender, palpable, and freely mobile in the pelvis, or adhered to the posterior leaf of the broad ligament, the lateral pelvic wall, or the posterior cul-de-sac

Vulvar cancer: Adenocarcinomas: Develop from what kind of cells?

Glandular cells like Bartholin cells

Bartholin cyst: pathophysio? Demo? Causes? Complications?

Bartholin glands lie underneath vestibule

Vaginal Cancer: Dx (part 2) Bx findings?

Can distinguish types and precancerous lesions >2/3 of epithelial cells involved=VAIN 3 as does carcinoma in situ and invasive cancer

Primary dysmenorrhea: pathogenesis?

Caused by excess prostaglandin F2alpha (PGF2alpha) produced in endometrium: 1. Prostaglandin production in endometrium increases under influence of progesterone, reaching a peak at or soon after mensturation. With onset of menstruation, formed prostaglandins are released from the shedding endometrium. 2. Necrosis of endometrial cells provides increased substrate arachidonic acid from cell walls for prostaglandin synthesis. 3. Prostaglandins are potent smooth muscle stimulants that cause intense uterine contractions, resulting in intrauterine pressures that can exceed 400 mm Hg and baseline intrauterine pressures in excess of 80 mm Hg (normal baseline is about 20 mm Hg). 4. PGF2α also causes contractions in smooth muscle elsewhere in the body, resulting in nausea, vomiting, and diarrhea 5. prostaglandin E2 (PGE2) is also produced in the uterus. PGE2, a potent vasodilator and inhibitor of platelet aggregation, has been implicated as a cause of primary menorrhagia.

What physical exam findings will you have for adenomyosis?

Causes a tender symmetrically enlarged, "boggy" uterus. Supported when other causes cannot be found. Definitively needs a Bx of a hysterectomy specimen

Lichen simplex chronicus: gross morph? Bx findings?

Chronic inflammation found underneath

Describe the cycles of the menstrual cycle?

Corpus luteum makes progesterone in second phase

Menopause: S/S (part 3) from book?

Declining E2 levels: restful sleep becomes difficult or impossible. Trouble falling/staying asleep. ADD: memory loss, depression, apathy, and "crying spells." ADD: skin thinning (more susceptible to abrasion/trauma), nails become thinner

Intersitial cystitis: defn? S/S? Etiology? Diagnosis?

Defn and S/S: chronic inflammatory condition of the bladder that is often characterized by pelvic pain, urinary urgency and frequency, and dyspareunia. Etiology: disruption of the glycosaminoglycan layer that normally coats the mucosa of the bladder Diagnosis: 1. The interstitial cystitis symptom index predicts the diagnosis of interstitial cystitis and may be used to help determine whether cystoscopy is indicated. 2. Further evaluation can be done with bladder distention with water or intravesical potassium sensitivity testing

Endometriosis: complications?

Endometrioma=on ovary-->increase risk of cancer ADD: Torsion

Endometrium: basic defn?

Endometriosis=endometrial cells growing outside of the uterus' endometrium