Pelvic and Ovarian disorders Flashcards Preview

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Flashcards in Pelvic and Ovarian disorders Deck (64)
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1
Q

What is chronic pelvic pain?

A
  • pain of at least 6 months duration that occurs below the umbillicus
  • significantly impacts a woman’s daily fxning and relationships
  • episodic-cyclic, recurrent pain that is interspersed with pain-free intervals
  • continuous non-cyclic pain
  • frustrates both pt and her clinician
  • many times etiology not found or tx of presumed etiology fails: pain becomes the illness
2
Q

How common is it to have no obvious pathology in chronic pelvic pain? Procedures used in these pts?

A
  • 1/3 have no obvious pelvic pathology
  • comprises of up to 10% of outpt gyn visits
  • accounts for 40% of GYN laparoscopies
  • accounts for 20% of hysterectomies
  • approx 70,000 hysterectomies are performed annually due to chronic pelvic pain
3
Q

Differential of chronic pelvic pain?

A
- 6 major sources:
gyn
GI
urological
psych
musculoskeletal
neuor
- complete hx of pt's pain and good ROS
4
Q

Etiologies of chronic pelvic pain?

A

episodic:
- dyspareunia
- midcycle pelvic pain (mittelschmerz)
- dysmenorrhea

continuous:

  • endometriosis (mostly cyclic pain)
  • adenomyosis
  • chronic salpingitis (PID)
  • adhesions
  • loss of pelvic support
5
Q

MC gyn etiologies of chronic pelvic pain?

A
  • endometriosis is MC (1/3 CPP)
  • PID 30% of women with PID develop CPP
  • dysmenorrhea
  • adenomyosis
  • adhesions
  • ovarian cysts
  • ovarian cancer
6
Q

RFs for CPP?

A
  • hx of sexual abuse or trauma
  • previous pelvic surgery
  • hx of PID
  • endometriosis
  • personal or family hx of depression
  • hx of other chronic pain syndromes
  • hx of alcohol or drug abuse
  • sexual dysfxn
7
Q

Hx of pt with CPP?

A
  • pain duration greater than 6 mo
  • incomplete relief by most previous tx, including surgery and non-narcotic analgesics
  • significantly impaired fxning at home or work
  • signs of depression such as early morning awakening, wt loss, and anorexia
  • pain out of proportion to pathology
  • hx of childhood abuse, rape or other sexual trauma
  • hx of sexual abuse
  • current sexual dysfxn
  • previous consultation with one or more health care providers and dissatisfaction with their management of her condition
8
Q

PE of pt with CPP?

A
  • systematic PE of abdominal, pelvic and rectal areas focusing on location and intensity of pain
  • attempt to reproduce the pain
  • note general appearance, demeanor, and gait..may suggest severity of pain and possible neuromusc. etiology
  • if a fever: acute process
  • if vomiting: acute process
  • inspect and note any well healed scars
  • palpate scars for incisional hernias
  • palpate for femoral and inguinal hernias
  • palpate for any unsuspected masses
9
Q

What are abdominal sxs of a more acute process of pelvic pain?

A
  • rebound tenderness (peritoneal irritation)
  • increased abdominal pain on palpation with tension of rectus muscles
  • straight leg raise:
    decreases - pelvic origin
    increases - abdominal wall or myofascial origin
10
Q

What may be seen on speculum and bimanual/rectum exam in pt with CPP?

A

speculum: cervicitis - source of parametrial irritation
bimanual/rectal:
-tender pelvic or adnexal mass, abnormal bleeding, tender uterine fundus, cervical motion tenderness - then think acute process such as PID, ectopic pregnancy, or ruptured ovarian cyst
-non-mobility of uterus - presence of pelvic adhesions
- existence of adnexal mass, fullness, tenderness
- cul-de-sac nodularities = endometriosis
- ID any areas that reproduce deep dyspareunia
- palpate the coccyx, both internally and externally (rectal exam)

11
Q

Dx tests for CPP?

A
  • should be selected discriminately as indicated by findings of H&P
  • avoid unecessary and repetitive dx testing
  • serum HCG
  • UA
  • wet prep/KOH
  • cervical cultures/GC and chlamydia
  • CBC with diff
  • ESR
    -stool guaiac if + then do GI w/u
  • US to ID pelvic masses
  • dx laparascopy may ID:
    acute or chronic salpingitis, ectopic pregnancy, hydrosalpinc, endometriosis, ovarian tumors and cysts, torsion, appendicitis, adhesions
12
Q

Tx of CPP?

A
  • tx underlying cause
  • psychosocial interventions
  • meds:
    avoid long term narcotic use
    NSAIDs
    antidepressants
    OCPs
  • surgical interventions: dx and therapeutic laparoscopy
    hysterectomy
13
Q

Alt interventions for CPP?

A
  • biofeedback
  • stress management techniques
  • self-hypnosis
  • relaxation therapy
  • transcutaneous nerve stimulation (TNS)
  • trigger pt injections
  • spinal anesthesia
  • nerve blocks
14
Q

What is PID?

A
  • clinical syndrome assoc with ascending spread of microorganisms from vagina or cervix to endometrium, fallopian tubes, ovaries, and contiguous structures
  • comprises of spectrum of inflammatory disorders including any combo of: endometritis, salpingitis, turbo-ovarian abscess, and pelvic peritonitis
15
Q

PID: incidence and prevalence?

A
  • occurs in approx 1 mill US women annually
  • annual cost approx: $2 bill
  • hospitalizations for acute PID steadily declined from approx 70,000 cases/yr in 1998 to 38,000 cases/yr in 2010
  • outpt visits for PID also have declined primarily due to aggressive pop. based chlamydia screening and tx programs nationwide
16
Q

RFs for PID?

A
  • young age at onset of sexual activity
  • new, multiple or sx partners
  • unprotected sexual intercourse
  • hx of PID
  • gonorrhea or chlamydia or a hx of gonorrhea or chlamydia
  • current vaginal douching
  • insertion of IUD (w/in fist 3 wks)
  • bacterial vaginosis
  • sex during menses
17
Q

Etiology of PID microbiology?

A
  • most cases are polymicrobial
  • MC pathogens:
    N. gonorrhoeae - recovered from cervix in 30-40% of women with PID
    C. trachomatis - recovered from cervix in 20-40% of women with PID
  • overgrowth of microorganisms that comprise vaginal flora: streptococci, staph, enterobacteriacea, anerobes, gardenella vaginalis, strep. agalactiae
18
Q

Pathway of ascendant infection to PID?

A

go from cervicitis to endometritis to salpingitis/oophoritis/tubo-ovarian abscess to peritonitis

19
Q

Complications of PID?

A
  • approx 10-20% of women with a single episode of PID will experience sequela including:
    ectopic preg.
    infertility
    tubo-ovarian abscess
    chronic pelvic pain
    fitz-hugh-curtis syndrome (perihepatitis)
  • tubal infertility occurs in 50% of women after 3 episodes of PID
20
Q

What is the minimum criteria for dx of PID?

A
  • uterine/adnexal tenderness or

- cervical motion tenderness (Positive chandelier sign)

21
Q

Additional criteria to increase specificity of dx of PID?

A
  • temp over 101F
  • abnormal cervical or vaginal mucopurulent d/c (positive swab test)
  • presence of WBCs on saline wet prep
  • elevated ESR
  • elevated CRP
  • gonorrhea or chlamydia test positive
22
Q

More specific criteria for dx PID?

A
  • transvaginal US
  • pelvic CT or MRI
  • laparoscopy
  • endometrial bx
23
Q

PID tx considerations?

A
  • tx should be instituted as early as possible to prevent long term sequelae
  • need to tx sexual partners if +GC/chlamydia
  • educate pt to avoid sexual activity until she and partner complete tx
  • need close f/u to ensure cure
24
Q

Tx for PID?

A

Regimens must provide coverage for N. gonorrhpeae, C. trachomatis, anaerobes, gram - bacteria and streptococci
- outpt first line:
ceftriaxone 250 mg IM single dose, and azithro 1 g PO once wkly x 2 wks
or
ceftriaxone and doxy 100 mg orally bid for 14 days
or
cefoxitin 2 g IM in single dose and probenecid 1 g orally in single dose and doxy 100 mg orally 2x a day for 14 days
- any of the above regimens with or w/o
metronidazole 500 mg orally bid for 14 days

25
Q

F/U care for pt with PID?

A
  • pts should demonstrate substantial improvement w/in 72 hrs
  • pts who don’t improve usually reqr hospitalization, additional dx tests, and surgical intervention
  • some experts recommend rescreening for C. trachomatis and N. gonorrhoeae 4-6 wks after completion of therapy in women with documented infection with these pathogens
26
Q

PID criteria for hospitaliziaton?

A
  • inability to exclude surgical emergencies
  • pregnancy
  • non-response to oral therapy
  • inability to tolerate an outpt oral regimen
  • severe illness, looks septic, N/V, high fever or tubo-ovarian abscess
  • HIV infection w/ low CD4 count
27
Q

Parenteral regimens for PID?

A
  • A:
    cefotetan 2 g IV q 12 hrs, or
    cefoxitin 2 g IV q 6 hrs
    plus doxy 100 mg orally or IV q 12 hrs
  • B:
    clindamycin 900 mg IV q 8 hrs plus gentamicin loading dose IV or IM followed by maintenance dose q 8 hrs, single gentamicin dosing may be used
  • continue either of these regimens for at least 24 hrs after substantial clinical improvement then complete a total of 14 days therapy with:
    doxy 100 mg PO bid with regimen A or
    doxy or clindamycin (450 mg PO qid) if using regimen B
28
Q

Screening - for prevention of PID?

A
  • to reduce incidence of PID, screen and tx for chlamydia
  • annual chlamydia screening is recommended for:
    sexually active women 25 and under and sexually active women who are older than 25 at high risk
  • screen pregnant women in 1st trimester
29
Q

Tx of partners with PID?

A
  • male sex partners of women with PID should be examined and tx if they had sexual contact with pt during 60 days preceding the pt’s onset of sxs
  • male partners of women who have PID caused by C. trachomatis or N. gonorrhoeae are oftne asx
  • sex partners should be tx empirically with regimens effective against both C. trachomatis and N. gonorrhoeae, regardless of apparent etiology of PID or pathogens isolated from infected woman
30
Q

Reporting PID cases?

A
  • report cases of PID to local STI program in states where reporting is mandated
  • gonorrhea and chlamydia are reportable in all states
31
Q

Pt counseling and education of PID?

A
  • nature of infection
  • transmission
  • risk reduction:
    assess pt’s behavioral- change potential, discuss prevention strategies, develop individualized risk-reduction plans
32
Q

PCOS is MC cause of what?

A
  • of androgen excess and hirutism in women

- most common hormonal disorder among women of reproductive age (6-8% in US approx 5 mill)

33
Q

Typical sxs of PCOS? Highly assoc with?

A
  • oligomenorrhea or amenorrhea, anovulation, obesity, acne, hirsutism and infertility
  • highly assoc with insulin resistance (many pts have impaired glucose tolerance or frank DM2)
34
Q

Dx of PCOS? What is the criteria?

A
  • dx: no single definitive test for PCOS b/c no exact cause of condition has been est. (this is a syndrome)
  • rotterdam criteria: a dx of PCOS can be made with 2 out of the 3 following features (once related disorders have been excluded):
  • oligomenorrhea (light or infrequent flow) or anovulation
  • clinic and/or biochemical signs of hyperadrenogenism (acne and hirsutism)
  • polycystic ovaries in US
35
Q

PCOS possible etiologies?

A

likely multiple systems are affected:

  • defect in HPA: causing release of excessive LH by anterior pituitary which cause increased androgen production in ovary making local concentrations of androgens elevated thus inhibiting ovulation
  • defects in ovaries: which cause androgen overproduction (testosterone, androstenedione, DHEAS, DHA, 17 hydroxyprogesterone and estrone)
  • defect in insulin sensitivity: leads to insulin resistance and compensatory hyperinsulinemia - increased insulin levels, can stimulate androgen production by stromal cells of the ovary
  • genetic factors: contribute
36
Q

Signs of PCOS? What could help restore regular fxn of ovulation and menses?

A
  • acanthosis nigricans can be present in these pts b/c of elevated insulin levels
  • fasting blood sugar to fasting insulin ratio should be greater than 4.5 in normal pt - anything below that is considered insulin resistnat
  • 70% of women with PCOS have insulin resistance - results in elevated blood glucose level, insulin stimulates storage of glucose in liver and muscle cells as glycogen
  • once max amt of glycogen has been reached, insulin next converts excess glucose to fat
  • as little as 10% of wt reduction can be effective in restoring regular ovulation and menses
37
Q

US findings of PCOS?

A
  • multiple follicles around periphery of ovary (this is a finding not the cause - 25% of normal women can have this finding, and not all PCOS pts will have cystic ovaries)
  • US isn’t necessary to make dx
38
Q

Lab tests for PCOS?

A
  • testosterone
  • androstenedione
  • DHEAS
  • 17 hydroxyprogesterone
  • prolactin
  • TSH
  • HCG
  • fasting blood sugar
  • fasting insulin level
  • LH/FSH
39
Q

Why should we tx PCOS?

A
  • decrease risk of endometrial hyperplasia and cancer, possible decrease risk of breast CA, decrease all sequela that occurs with DM
  • pt satisfaction
40
Q

What factors go into deciding on what therapy is right for pt with PCOS?

A
  • how much hirsutism does pt have?
  • does pt desire to become pregnant
  • how willing is pt to exercise and reduce her wt?
41
Q

Therapeutic options for PCOS?

A
  • diet and exercise: wt loss of 7-10% can regulate periods of a woman with PCOS
  • OCPs: these suppress LH and therefore suppress circulating androgens. Also regulates periods
  • spironolactone: act as antiandrogen (helps with hirsutism in conjunction with OCPs) - binds with androgen receptors and blocks the effects of dihydrotestosterone as well (preg D, monitor for hyperkalemia, may be tumorigenic)
  • metformin - heps with insulin resistance and wt loss
  • clomiphene (clomid): those trying to get pregnant and are still anovulatroy after diet, exercise, and metformin have been tried - binds estrogen receptors in hypothalamus to create state of hypoestrogenicity, thereby causing an enhanced GnRH release followed by increase secretion of gonadotropins which induces ovulation
42
Q

Key to eval ovarian disease?

A
  • with excellent hx and physical
  • ovaries shouldn’t be palpable in premenarchal group, nor should they be palpable in postmenopausal group
  • ovary is palpable less frequently in reproductive age women taking OCPs
  • older the woman the more likely tumor is malignant vs. benign
43
Q

What are ovarian cysts? Sxs?

A
  • not a neoplasm, but arises as a result of normal ovarian physiology
  • ovarian cysts are fluid filled sacs that develop in or on the ovary
  • they occur commonly in women of all ages
  • some women have pelvic pain or pressure, while others have no sxs
44
Q

What is a follicular cyst?PE findings?

A
  • if an ovarian follicle fails to rupture during maturation, ovulation doesn’t occur, and a follicular cyst may defelop, these may be sx or asx
  • clinically significant if large enough to cause pain or if it persists beyond the menstrual interval
  • PE characteristics: mobile, cystic, adnexal mass
45
Q

Management of follicular cysts?

A
  • usually spontaneously resolves
  • management: reeval in 6-8 wks to ensure the cyst has resolved. May order transvaginal US as needed on a case by case basis
  • OCP may be given to suppress gonadotoin stimulation of cyst
  • Rupture of follicular cyst may produce transient acute pelvic pain
46
Q

What is a corpeus luteum cyst? Presentation?

A
  • enlarged corpus luteum, which often continues to produce progesterone for longer than standard 12 days
  • often presentation is of dull lower quadrant pain along with a missed menstrual period: (gets confused with pregnancy - so rule this out with test)
  • PE findings: same as follicular cyst - mobile, cystic, adnexal mass
  • cyst may rupture and hemorrhage with blood causing pain
47
Q

Management for corpus luteum cyst?

A
  • may reevaluate this pt to make sure cyst has resolved
  • pts may benefit from cyclic OCP therapy
  • may use tranvaginal US on a case by case basis
48
Q

What should you do after palpating a mass on ovaries?

A
  • f/u - some cysts can persist for some time and may benefit from a laparoscopy
49
Q

Other names for follicular cyst and corpus luteum cyst?

A
  • fxnl ovarian cyst

- physiologic cyst

50
Q

Diff benign neoplasms of the ovaries?

A
  • benign epithelial cell tumors
  • benign germ cell tumors ( can create benign cystic teratoma aka dermoid cyst)
    80% of these occur during reproductive years, often produce tumor markers such as HCG or AFP
  • benign stromal cell tumors: common one of these is called sertoli-leydig cell tumor
51
Q

Benign vs malignant tumors of the ovaries? Do they need surgery?

A
  • benign tumors are more common than malignant tumors in all age groups
  • chance for malignancy goes up with age
  • warrant surgical tx b.c of potential for transformation to malignancy
  • surgical tx may be conservative for benign tumors, especially if future pregnancy is desired
52
Q

Main RF of malignant ovarian tumors? When are these discovered?

A
  • increasing age dramatically increases risk that ovarian enlargement is malignant
  • 1st time many are discovered is at time of routine pelvic exam
  • Aging women should still have physical and bimanual exam annually (even if they don’t have to have a pap)
53
Q

Numbers of ovarian cancer in US? How common is it? Mortality?

A
  • 20,000 cases anually in US
  • incidence increases with age: 1.4/100,000 under 40, 38/100,000 over 60
  • rarely sx in early stages of disease
  • late dx and early mets usually signify a poor prognosis and low survival rate
  • 5th MC of all cancers in women
  • mortality rate is higher than that of any other gyn cancer (presents in late stage)
54
Q

When does ovarian cancer most commonly present? What gene has been found to be assoc with ovarian cancer?
What has protective effect?

A
  • rarely sx in early stages
  • presents MC in 50s, and 60s
  • BRCA1 gene has been found to be assoc with ovarian cancers in approx 5% of cases
  • suppression of ovulation tends to have a protective effect: use of OCPs for 5 yrs decreased lifetime risk of ovarian cancer in half
55
Q

RFs for ovarian cancer?

A
  • aging (esp 45-60)
  • postmenopause
  • periods of prolonged ovulation w/o pregnancy
  • having a 1st degree relative with ovarian, colon or breast cancer
  • BRCA1 and BRCA2 gene mutation
56
Q

Is there screening for ovarian cancer?

A
  • no effective method of mass screening has yet been developed
  • routine US and CA-125 but neither is recommended for routine screening, it is really expensive and has poor sensitivity and reliabilty
  • annual bimanual exam is recommended by ACOG
57
Q

What pts should be followed up with further eval if palpable ovary or mass found?

A
  • any postmenopausal pt with palpable ovary or mass should be refered on for further eval
58
Q

MC type of ovarian malignant neoplasms?

A
  • 90% of ovarian malignancies are of epithelial cell type

- but still can arise from germ cell, and stromal neoplasms

59
Q

What is ovarian torsion?

A
  • complete or partial rotation of ovary on ints ligamentous supports: the ovary typically rotates around both the infundibulopelvic ligament and the utero-ovarian ligament
  • often resulting in imepedance of its blood supply
  • the fallopian tube often twists along with the ovary; when this occurs it is referred to as an adnexal torsion
60
Q

Causes of ovarian torsion?

A
  • rare event, reported with both normal and pathologic fallopian tubes
  • secondary to ovarian mass in approx 50-60% of pts (another reason why we follow up on masses and one of main reasons that benign ovarian tumors are removed)
  • R more often than L (3:2): possibly b/c the right utero-ovarian ligament is longer than the left and/or that the presence of sigmoid colon in left side may help prevent torsion
61
Q

Presentation of ovarian torsion?

A
  • abrupt onset of acute, severe, unilateral, lower abdominal and pelvic pain often assoc with N/V. Often the severe pain will come on suddenly with a change of position (can be confused with appendicitis)
  • a unilateral, extremely tender adnexal mass is found in more than 90% of pts
  • many pts have noted intermittent previous episodes of similar pain for several days to several weeks
62
Q

Dx and Tx of ovarian torsion?

A
  • color flow doppler US can help
  • with early dx, pts often managed with conservative surgery: if necrosis developing, unilateral salpingooopherectomy is TOC
63
Q

Severe complications of PID?

A
  • peritonitis, sepsis, and infertility
64
Q

What can happen to ovarian cysts if they become too large?

A
  • esp follicular cysts - if they become larger than 5 cm they are at high risk of becoming torsed and need a laparoscopy
  • always f/u on ovarian mass!