Gynecology

By Dr.Mohammad Z. abu sheikha@

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**Dilatation And Curettage (D&C)
.dilation of cervix with dilation of increasing diameter
.anesthesia (general or local)
-Indications :
.diagnostic (rarely done without hysteroscopy) (abnormal uterine bleeding AUB / dysfunctional uterine bleeding DUB)
.therapeutic (removal of retained products of conception following abortion / termination of pregnancy in 1st trimester /
removal of small uterine polyps or pedunculated submucosal fibroids)
-Complications :
.bleeding
.infection
.perforation of uterus
.stenosis and laceration of cervix (cervical laceration-stenosis) - incompetent cervix – extremely rare
.asherman's syndrome

**Laparoscopy
-Used to view pelvic / abdominal contents through small incisions
-Indications :
.diagnostic (evaluation of infertility, pelvic pain, pelvic masses, congenital anomalies, hemoperitoneum and endometriosis)
.therapeutic (tubal ligation, lysis of adhesions, excision of ectopic pregnancy, excision/ablation of endometriosis, retrieval of
lost IUDs, cystectomy, salpingo—oophorectomy and hysterectomy, myomectomy)
-Contraindications :
.bowel obstruction
.large hemoperitoneum
.clinically unstable Pt.
.inability to maintain pneumoperitoneum
.multiple previous abdominal surgeries
-Complications :
.general anesthetic
.insufflation of the preperitoneal abdominal wall
.injury to vascular structures (aorta, inferior epigastric vessels)
.injury to viscous (bowel, bladder, ureters)
.may need to convert to laparotomy
.infection

**Hysteroscopy
-Indications :
.diagnostic (detection of uterine anomalies or pathology – infertility work-up, AUB, DUB)
.therapeutic (removal of uterine polyps, fibroids, adhesions, septums)
-Complications :
.suspected pregnancy
.perforation of uterus
.laceration of cervix
.bleeding
.infection
.absorption of excess distension medium, fluid overload, hyponatremia
.air emboli
.anaphylactic shock

**Hysterectomy
-Indications :
.uterine fibroids
.endometriosis, adenomyosis
.uterine prolapse
.pelvic pain
.AUB
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.cancer (endometrium, ovaries, fallopian tubes, cervical)

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-Complications :
.general anesthetic
.bleeding
.infection
.injury to other organs (ureter, bladder, rectum)
.loss of ovarian function (if ovaries removed, iatrogenic menopause)

**Pelvic Pain
+Acute
-Gynecological
.adnexal (mittelschmerz, ruptured, ovarian cyst, ruptured ectopic pregnancy, hemorrhage into cyst/neoplasm, ovarian/tubal
torsion)
.uterine (fibroid)
.infectious (acute PID, endometriosis)
-Non-gynecological
.GI (appendicitis, mesenteric adenitis, diverticulitis, IBD)
.GU (UTI, cystitis, pyelonephritis, renal colic)
-Pregnancy
.labor
.ectopic pregnancy
.spontaneous abortion
.placental abruption
+Chronic (intermittent or constant pain of >6 months duration)
-Gynecological
.chronic PID
.endometriosis
.adenomyosis
.adhesion
.dysmenorrhea
.ovarian cyst
.pelvic congestion syndrome
.ovarian remnant syndrome
.fibroid (rare)
.uterine prolapse (rare)
-Non-gynecological
.IBS, IBD
.constipation
.obstruction
.diverticulitis
.hernia formation
.sexual/physical/psychological abuse
.depression
.anxiety
.somatization

**Dyspareunia
+Introital
.vaginismus
.rigid/intact hymen
.Bartholin`s or Skene`s gland infection
.lichen sclerosis
.vulvovaginitis (atrophic hypoestrogen, chemical, infectious – chlamydia, trichomoniasis)
+Midvaginal
.urethritis
.short vagina
.trigonitis
.congenital abnormality of the vagina
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+Deep
.endometriosis
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.adenomyosis
.leiomyomata/fibroids
.PID
.hydrosalpinx
.TOA
.uterine retroversion
.ovarian cyst

**Pelvic Inflammatory Disease PID

-PID is a nonspecific term for a spectrum of upper genital tract (above cervix), including :
.endometrium
.fallopian tube
.ovaries
.pelvic peritoneum
.contiguous structures
-Signs & Symptoms :
.2/3 of cases are asymptomatic or mild symptoms
.fever >38 and chills
.lower abdominal – pelvic pain
.cervical – adnexal tenderness
.nausea, vomiting
.dysuria
.abnormal discharge (cervical or vaginal)
.abnormal uterine bleeding
.dyspareunia
.palpable mass
-Causative Organisms :
.M.C initial organisms are (Chlamydia and Gonorrhea) / Secondary bacterial include (Anaerobes and Gram-negative organisms)
.C.trachomatis
.E.coli, staphylococcus, streptococcus, enterococcus, bacteroides, peptostreptococcus, H.influenzae, G.vaginalis
.actinomyces israelii (Gram-positive, non acid-fast anaerobe)
.TB, CMV, U.urealyticum
-Risk Factors :
.female sexual activity in adolescence (M.C)
.multiple partners
.PID is increased in the month after insertion of an IUD
.age <30yrs
.vaginal douching
.invasive gynecologic procedures (D&C, endometrial biopsy)
-Diagnosis :
+Must Have :
.lower abdominal pain
.cervical motion tenderness
.adnexal tenderness
+Plus One Or More Of :
.temperature >38
.mucopurulent cervical discharge
.positive culture for N.gonorrhoeae, C.trachomatis, E.coli, or other vaginal flora
.cul-de-sac fluid, pelvic abscess or inflammatory mass on U/S or bimanual
.leukocytosis
.elevated ESR or CRP
-Investigations :
.beta-hCG (must rule out ectopic pregnancy), CBC, blood cultures if suspect septicemia
.cervical cultures for N.gonorrhoeae, C.trachomatis
.endometrial biopsy
.ultrasound (may be normal, free fluid in cul-de-sac, pelvic or tubo-ovarian abscess)
+Laparoscopy (gold standard) for definitive diagnosis
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-Complications :
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.infertility
.fitz-hugh-curtis syndrome
.abscesses
.chronic pelvic pain
.ectopic pregnancy
.peritonitis
.intestinal obstruction
.disseminated infection (sepsis, endocarditis, arthritis, meningitis)
.adhesion formation
.bacteremia
-Treatment :
.FOXY-DOXY (cefoxitin + doxycycline)

*Cervicitis
-Starts with invasion of endocervical glands with chlamydia and gonorrhea
-Signs & Symptoms :
.mucopurulent cervical discharge (M.C finding)
.friable cervix may be noted
.No pelvic tenderness is noted
.the Pt. is afebrile
+Cervical cultures will be positive, but symptoms are usually absent (no symptoms except vaginal discharge)
-Investigative Findings :
.diagnosis section for chlamydia
.WBC and ESR are normal
-Management :
.cefixime and azithromycin

*Acute Salpingo-Oophoritis
-The pathogenic organisms ascend through the uterus, causing an endometritis / the bacteria enter the oviduct where acute
salpingo-oophoritis develops
-Signs & Symptoms :
.bilateral lower abdominal - pelvic pain
.onset may be gradual to sudden, often after menses (after menstrual period)
.nausea, vomiting
.mucopurulent cervical discharge
.cervical-motion tenderness
.fever
.tachycardia
.abdominal tenderness
.peritoneal signs
-Investigative Findings :
.WBC and ESR are both elevated
.laparoscopy will show erythematous, edematous, purulent oviducts
.cervical cultures will be positive for chlamydia or gonorrhea
-Differential Diagnosis :
.adnexal torsion
.ectopic pregnancy
.endometriosis
.appendicitis
.diverticulitis
.CD, UC
.tubal pregnancy
.pyelonephritis
.ruptured ovarian cyst
-Diagnosis (Criteria) :
.sexually active young woman
.pelvic or lower abdominal pain
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.tenderness (cervical motion or uterine or adnexal)

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.oral temperature (>38.3)

.abnormal cervical or vaginal mucopurulent discharge
.presence of WBC on vaginal fluid saline microscopy
.elevated erythrocyte sedimentation rate ESR
.positive lab findings of cervical N.gonorrhea or C.trachomatis
.endometrial biopsy showing endometritis (Most specific criteria)
.MRI or vaginal sonography showing abnormal adnexa
.lab. abnormalities consistent with PID
-Management :
.ceftriaxone IM (outpatient antibiotics) / cefotetan IV (inpatient antibiotics), doxycycline + metronidazole

*Tubo-Ovarian Abscess TOA

-Is the accumulation of pus in the adnexa forming an inflammatory mass involving the oviducts, ovaries, uterus or omentum
-Signs & Symptoms :
.the Pt. look septic
.lower abdominal – pelvic – back - rectal pain (severe pain)
.pain with bowel movements
.nausea, vomiting
.high fever
.tachycardia
.septic shock with hypotension
.peritoneal signs
.guarding and rigidity
.bilateral adnexal masses may be palpated
-Investigative Findings :
.cervical culture are positive for chlamydia or gonorrhea
.blood cultures may be positive for gram-negative bacteria and anaerobic organisms such as (bacteroides fragilis)
.WBC and ESR elevated
.sonography or CT scan show bilateral complex pelvic masses
-Differential Diagnosis :
.septic abortion
.diverticular
.appendiceal abscess
.adnexal torsion
-Management :
.clindamycin IV and gentamicin

*Chronic PID
-Signs & Symptoms :
.chronic bilateral abdominal-pelvic pain
.history of infertility
.dyspareunia
.ectopic pregnancy
.abnormal vaginal bleeding
.bilateral adnexal tenderness
.cervical-motion tenderness
.nausea, vomiting (are absent)
.mucopurulent cervical discharge (is absent)
.fever and tachycardia (are absent)
-Investigative Findings :
.cervical cultures are negative
.WBC and ESR are normal
.sonography may show bilateral cystic pelvic masses with hydrosalpinx
-Diagnosis :
.laparoscopic visualization of pelvic adhesions
-Management :
.analgesics (for mild pain in outpatient) / If the ovaries are removed, estrogen replacement therapy is indicated
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+About Tuberculosis Of The Genital Tract :

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.most commonly affects the fallopian tubes

.it is transmitted by hematogenous spread
.can causes infertility and amenorrhea
.NOT predisposes to endometrial carcinoma

**Endometriosis
-Is a benign condition in which endometrial tissue (glands and stroma) are seen outside the uterus (uterine cavity) –
endometrial tissue (this is NOT a premalignant condition)
-It may be found in myometrium (rare outside the pelvis) / Present as secondary dysmenorrhea
+M.C site is Ovaries (Lt. Ovary) (chocolate cyst) - 2nd M.C site is the cul-de-sac (characteristic uterosacral ligament nodularity
and tenderness appreciated by rectovaginal examination). Menstruation into the cul-de-sac (creates fibrosis and adhesions of
bowel to the pelvic organs, which accounts for dyspareunia) / Other sites (ligament, bladder, lung, brain)
-Usually in reproductive age women – premenopausal women (mean age at presentation 25-30yrs) and regresses after
menopause (incidence 10-15% - family history)
-Progressive disease / It is estrogen dependent disease
-58% of infertile women have endomentriosis / 30-50% of women with endometriosis are infertile / 30-50% of women with this
disease have a miscarriage (It may cause infertility)
-Signs & Symptoms :
.may be asymptomatic
.chronic pelvic pain
.bowel and bladder symptoms (painful bowel movements-dyschezia, dysuria, hematuria, diarrhea, constipation, hematochezia)
.tender nodularity of uterine ligaments and cul-de-sac felt on rectovaginal exam
.fixed retroversion of uterus
.firm, fixed adnexal mass (endometrioma)
.back - abdominal pain
.dysmenorrhea, menorrhagia (principle feature), dysuria (mensturation pain)
.infertility - period type is congestive type / may cause ovarian cysts
.risk for ectopic pregnancy
.menstrual symptoms (secondary dysmenorrhea, sacral backache with menses, deep dyspareunia - painful intercourse) (NOT
amenorrhea)
.early menarche (before age 11yrs)
.long mensturation cycle
.shortness cycle <27 days
-Risk Factors :
.family history
.obstructive anomalies of the genital tract
.nulliparity
.age >25yrs
-Theories for causation of endometriosis :
.coelomic metaplasia
.retrograde menstruation
.immunologic deficiency
.lymphatic spread of endometrial fragment
-Examination :
.pelvic tenderness
.fixed, retroverted uterus (is caused by cul-de-sac adhesions)
.uterosacral ligament nodularity
.enlarged adnexa
-Investigative Findings :
.WBC and erythrocyte sedimentation rate ESR are normal
.CA-125 elevated
.sonogram will show an endometrioma (chocolate cysts on the ovaries)
.laparoscopy will show (mulberry spots, endometrioma, powder-burn, peritoneal ‘pockets’)
-Diagnosis :
.laparoscopy (appear as powder burn – white scarring – chocolate cyst)
.imaging (TVU, MRI, CT)
-Management :
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.medical (NSAIDs, OCP, progestin, GnRH-leuprolide, danazol)

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.surgical (laparoscopic; Hysterectomy with bilateral salpingo-oophorectomy) (Treatment of choice)

**Adenomyosis
-The presence of ectopic glandular tissue found in muscle (endometrial glands are located at uterus muscle)
+The benign invasion of endometrium into the myometrium
+Is most prevelent in women of late reproductive age 35-50yrs / 90% of cases occur in multiparous women / They have a high
incidence of early miscarriage
-Types :
.diffuse (diffuse uterine enlargement)
.focal (adenomyoma)
-Signs & Symptoms :
.35% of cases are symptomatic
.menorrhagia (M.C), secondary dysmenorrhea, pelvic discomfort, metrorrhagia
.dyspareunia, dyschezia
.subfertility
.uterus-enlarged <14cm (no associated adnexal)
.halban sign (tender, softened uterus on premenstrual bimanual exam)
-Investigations :
.MRI (Best) or ultrasound
.endometrial sampling to rule out other pathology
-Treatment :
.iron supplements as necessary
.NSAIDs
.OCP
.progesterone
.GnRH
.UAE
.Hysterectomy

+Estrogen Dependent Diseases (estrogen receptor ER + progesterone receptor PR + androgen receptor AR) :
.breast cancer
.endometrial cancer
.endometriosis
.adenomyosis

**Benign Diseases Of The Uterus And Cervix

-May be classified in terms of the tissue of origin :
.the myometrium (uterine fibroids)
.the uterine cervix
.the endometrium

*Fibroids (Leiomyoma)
-Benign smooth muscle tumor (arise from smooth muscle)
+M.C benign tumor of female pelvis
+M.C tumor of the uterine corpus
+M.C pelvic mass in (post)menopausal women
+M.C uterine neoplasm
+M.C indication for hysterectomy
+Diagnosed in approximately 40-50% of reproductive age women >35yrs
+Leiomyoma grow in childbearing age, pregnancy and regress in menopause
-Types :
.intramural (within myometrial muscle) (M.C)
.submucosal
.subserosal
-Changes :
.cystic
.hyaline
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.calcified (womb stone)

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.sarcomatous (NOT complication)

-Signs & Symptoms :
.asymptomatic (may be during pregnancy)
.abnormal bleeding (menorrhagia – M.C type of bleeding encountered with fibroids) (dysmenorrhea, post-menopausal
bleeding, antepartum hemorrhage) (NOT amenorrhea)
.pelvic pain (fibroid degeneration, fibroid torsion)
.pressure on bladder or rectum
.abdominal enlargement
.infertility rarely (or recurrent pregnancy loss)
.pregnancy complications (may be asymptomatic during pregnancy, potential enlargement and increased pain, obstructed
labour, difficult C-section)
-Risk Factors :
.non-smoker
.HTN
.multiparity
.perimenopause
.african women
+smoking, OCP, progesterone (decreased risk of leiomyoma)
-Complications :
.red-degeneration (M.C during pregnancy)
.fatty-degeneration (NOT changes)
.hyaline-degeneration
.excessive uterine bleeding
.abdominal enlargement
.micturition
-Investigations :
.bimanual exam (uterus asymmetrically enlarged)
.CBC (anemia)
.ultrasound
.sonohysterogram (useful for differentiating endometrial polyps from submucosal fibroids)
.endometrial biopsy to rule out uterine cancer for abnormal uterine bleeding (especially if age >40yrs)
-Treatment :
.myomectomy (Best)
.MRI (for distinguish fibroid from adenomyoma)

*The Uterine Cervix

-Cervical Ectropion
.is a condition in which the central (endocervical) columnar epithelium protrudes out through the external os of the cervix and
onto the vaginal portion of the cervix, undergoes squamous metaplasia, and transforms to stratified squamous epithelium
.this is benign condition which looks like a ‘raw’ area on the cervix
.an ectropion commonly develops under the influence of the three Ps (puberty, pill, pregnancy)
.a persistent cervical ectropion (being a ‘weaker’ columnar epithelium) undergoes metaplasia to a ‘stronger’ squamous
epithelium. This transmission zone undergoes dyskaryosis and possible malignant change due to HPV infection
-Cervical Stenosis
.is usually an iatrogenic phenomena caused by a surgical event
.treatment of pre-malignant disease of the cervix using cone biopsy or loop diathermy can cause cervical stenosis
.the ensuing hematometra (blood collected within uterus) causes cyclical dysmenorrhea with no associated menstrual bleeding
.treatment is by surgical dilation of the cervix with hysteroscopic

*Endometrium
-The uterine endometrium comprises glands and stroma with a complex architecture, including blood vessels and nerves
-Disorders of the endometrium give rise to abnormal uterine bleeding (post-menopausal bleeding PMB, intermenstrual
bleeding IMP, heavy menstrual bleeding HMB, bleeding of endometrial origin BEO)
-Endometrial Polyps :
.are discrete outgrowths of endometrium
.benign growth of endometrial gland (but removal is necessary to exclude the remote possibility of malignancy)
.they may cause intermenstrual bleeding
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.they may be single or multiple

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.M.C in women over the of 40yrs and pre-menopausal

.endometrial polyps diagnosed by ultrasound or hysteroscopy (for removal)
.with increasing age, the most common abnormality is endometrial hyperplasia
.polyps can also be caused by tamoxifen (treatment for breast cancer)
-Endometrial Hyperplasia
.hyperplasia or proliferation of endometrial tissue
.usually occur in menopausal women or peri-menopausal
.types (simple hyperplasia, complex hyperplasia, atypical simple hyperplasia, atypical complex hyperplasia)
.symptoms (abnormal uterine bleeding, post-menopausal bleeding)
.risk factors (increased pressure to estrogen, chronic anovulation, PCOS, obesity, nulliparity, late menopause >55yrs, DM, HTN,
tamoxifen, granulosa-theca-cell-tumor)
.diagnosis (pelvic ultrasound ‘thick end’, biopsy ‘BEST’)

**Polycystic Ovarian Syndrome PCOS (Stein-Leventhal syndrome / Chronic ovarian androgenism)

-Is a condition of chronic anovulation with resultant infertility
-Signs & Symptoms :
.anovulation
.irregular vaginal bleeding (oligomenorrhea, secondary amenorrhea) (NOT menorrhagia)
.obesity
.hirsutism
.infertility
.virilization
.acne
.acanthosis nigricans (in both lean and obese Pts.)
.bilaterally enlarged, smooth, mobile ovaries will be palpated on pelvic examination
.trouble getting pregnant
.patches of thick, darker, velvety skin
.show dense thickening of the capsula
-Associated Conditions :
.type 2 diabetes (insulin resistance – family history of diabetes)
.obesity
.obstructive sleep apnea
.heart disease
.mood disorders
.endometrial cancer (PCOS increased risk of endometrial cancer, hyperplasia / NO risk for ovarian cancer)
.ovarian cyst
.hyperprolactinemia
.adrenal hyperplasia
.hypothyroidism
-Complications :
.may undergo torsion
.may undergo rupture
.may undergo hemorrhage
.may undergo malignant changes
-Lab Tests :
.testosterone level is elevated
.LH to FSH ratio is elevated (3:1)
.sex hormone binding globulin SHBG is decreased
.androgen is elevated
.estrogen is elevated
.prolactin, 17-hydroxyprogesterone, DHEA-S (elevated), TSH, free T4, androstenedione
+Goal of investigations is to identify hyperandrogenism or chronic anovulation and rule out specific pituitary or adrenal disease
as the cause
-Diagnosis :
.it is confirmed with an LH to FSH ratio (3:1) (absence of LH / low or normal FSH)
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.pelvic ultrasound (polycystic ovaries on U/S ‘string of pearls’)

.oligomenorrhea / irregular menses for 7 months
.tests for insulin resistance or glucose tolerance (fasting glucose : insulin ratio <4.5) (75g OGTT – particularly if obese)
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-Management :
.wedge resection (is the treatment of choice)
.laparotomy and cystectomy
.decreased weight
.clomiphene citrate (in case of infertility to induction of ovulation)
.progesterone
.OCP monthly or cyclic provera to prevent endometrial hyperplasia due to unopposed estrogen (OCP in case of hirsutism)
.oral hypoglycemic (metformin)
+PCOS increased risk of endometrial cancer, hyperplasia / NO risk for ovarian cancer
+HA-IR-AN syndrome :
.HA (HyperAndrogenism)
.IR (Insulin Resistance)
.AN (Acanthosis Nigricans)

By Dr.Mohammad Z. abu sheikha@

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 Menstrual Abnormalities
-Menstrual Cycle Hormones :
.FSH (stimulates the growth of granulosa cells and induces the aromatase enzyme that converts androgens to estrogens)
.LH (stimulates the production of androgens by the theca cells)
.Estrogen (is produced in the granulosa cells in response to even low FSH concentrations, and stimulates proliferative changes
in the endometrium)
.Androgens (include androstenedione and testosterone)
.Progesterone (is produced by the corpus luteum and stimulates secretory changes in the endometrium)

**Premenarchal Vaginal Bleeding

-Is bleeding that occurs before menarche. The average age at menarche is 12yrs
-Differential Diagnosis and Etiology (Causes include) :
.ingestion of estrogen medication
.foreign body that irritates the vaginal lining (M.C.C)
.cancer of the vagina or of the cervix (sarcoma botryoides)
.tumor of the pituitary or adrenal gland (ovarian tumor)
.sexual abuse
.idiopathic precocious puberty
-Diagnosis :
.pelvic examination
.CT scan or MRI scan of the pituitary, abdomen and pelvis
+The scans are looking for evidence of a pituitary, ovarian or adrenal tumors, which may cause early estrogen production

**Abnormal Vaginal Bleeding

*Pregnancy
-In a Pt. Who has abnormal bleeding during the reproductive age group, pregnancy or a complication must first be considered
-Complications of early pregnancy that are associated with bleeding, include :
.incomplete abortion
.threatened abortion
.ectopic pregnancy
.hydatidiform mole
-Diagnosis :
.urine or serum beta-hCG test (to confirm pregnancy)
.vaginal ultrasound (if pregnancy is identified)

*Anatomic Lesion
-If the pregnancy test is negative, then an anatomic cause of vaginal bleeding should be considered
-The classic history is that of unpredictable bleeding (without cramping) occurring between normal, predictable menstrual
periods (with cramping)
-Factors (anatomic) Can Cause Bleeding :
.vaginal lesions (lacerations, varicosities or tumors)
.cervical lesions (polyps, cervicitis or tumors)
.endometrial lesions (submucous leiomyomas, polyps, hyperplasia or cancer)
.myometrial lesions (adenomyosis)
-Diagnosis (a number of tests can be used to for anatomic diagnosis) :
.lower genital tract (pelvic and speculum exam)
.upper genital tract (saline sonogram, endometrial biopsy, hysteroscopy)

*Inherited Coagulopathy
-Especially in the adolescent age group, have coagulopathies
-Review of systems may be positive foor other bleeding symptoms including (epistaxis, gingival bleeding, ecchymosis)
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+Von Willebrand disease (is the M.C hereditary coagulation abnormality)

+Coagulopathies can be due to (vessel wall disorders, platelet disorders, coagulation disorders, fibrinolytic disorders)
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-Diagnosis :
.positive family history
.lab tests (CBC with platelet count, PT and PTT)
.the best test screening test for Von Willebrand disease if a vWF antigen

*Dysfunctional Uterine Bleeding DUB

-If the pregnancy test is negative, there are NO anatomic causes for bleeding and coagulopathy is ruled out, then the diagnosis
of hormonal imbalance should be considered (Diagnosis by exclusion) (Abnormal menstrual pattern)
-Anovulation results in unopposed estrogen (estrogen without progesterone). With unopposed estrogen, there is continuous
stimulation of the endometrium with no secretory phase
+There is no organic disease in the uterus / It may cause menorrhagia and prolonged period / NOT malignant
+M.C.C of heavy bleeding in adolescent girls is DUB
+Vaginal bleeding in the newborn female infant is (Estrogen withdrawal) (if presented to your clinic with vaginal bleeding, the
most appropriate action to do is reassure the parents)
-Causes Of Anovulation :
+M.C.C of DUB is anovulation
.hypothyroidism (M.C.C) – diagnosed by a low TSH and treated with thyroid replacement
.hyperprolactinemia – diagnosed by a serum prolactin test (An elevated prolactin inhibits GnRH by increasing dopamine)
+Polycystic ovary (associated with DUB)
-Diagnosis :
.history of irregular, unpredictable bleeding
.bleeding without cramping since there is no PG release to cause myometrial contractions
.cervical mucus will be clear, thin, watery reflecting the estrogen dominant environment
.basal-body temperature BBT chart will not show a mid cycle temperature rise due to the absence of the thermogenic effect of
progesterone
.endometrial biopsy will show a proliferative endometrium
-Management :
.progestin (cyclic MPA, OCP, progestin intrauterine system LNG-IUS) (Progesterone – drugs commonly used for DUB)
.NSAIDs
.tranexamic acid (lysteda)
.endometrial ablation (removal of body tissue)
.hysterectomy (removal of uterus)

*Abnormal Uterine Bleeding AUB

-Gynecological :
.menorrhagia (hormone imbalance, fibroids/leiomyoma, uterine polyps, adenomyosis, copper IUD)
.metrorrhagia/menometrorrhagia (trauma, sexual abuse, foreign body, infection “endometriosis, cervicitis, vaginitis, STIs”,
benign growths “uterine, cervical, vaginal”, pregnancy-related, weight loss, exercise, stress, PCOS, DUB)
-Non-gynecological :
.endocrine (hyper/hypothyroidism, adrenal insufficiency, insulin resistance PCOS, prolactinoma)
.blood dyscrasias (vWD, platelet abnormalities ITP, leukemia, hematologic malignancy)
.renal failure (impaired estrogen, excretion)
.drugs (anticoagulants, danazol, OCP, HRT, steroids, spironolactone, chemotherapy, neuroleptics)
.hepatic disease (decreased coagulation factors, impaired estrogen, metabolism)
-Investigations :
.CBC, serum ferritin
.hCG
.coagulation profile (to rule out vWD)
.FSH, LH
.serum androgens (especially free testosterone)
.Pap test
.pelvic ultrasound
.endometrial biopsy
.D&C (not for treatment; diagnosis only)
+DUB (abnormal bleeding not attributable to organic (anatomic/systemic) disease. DUB is a diagnosis of exclusion. Anovulatory
AUB often used synonymously with DUB
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**Disorders Of Menstruation
+Hypomenorrhea (bleeding that is decreased in amount)
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+Polymenorrhea (bleeding occuring at intervals <21days)

+Menorrhagia/Hypermenorrhea (bleeding at regular intervals that is prolonged in duration (>7days) or excessive in amount
(>80cc per menstrual cycle)
+Metrorrhagia (bleeding at irregular intervals, particularly between expected menstrual periods)
+Menometrorrhagia (excessive bleeding at usual time of menstrual periods and at other irregular intervals)
+Postmenopausal bleeding (any bleeding that presents >1yr after menopause; endometrial cancer until proven otherwise)

*Amenorrhea
+Primary Amenorrhea
-Amenorrhea (absence of menstural bleeding)
-Primary Amenorrhea
.no menses by age 14 in absence of secondary sexual development; OR
.no menses by age 16 with secondary sexual development
.family history of delayed puberty, absent puberty
-Causes :
+Anatomic
.vaginal agenesis MRKH (mullerian agenesis – NO uterus, NO upper vagina, chromosome 46xx, ovarian seen)
.septum
.imperforate hymen
.mullerian agenesis
+Hormonal
.complete androgen insensitivity
.gonadal dysgenesis (Turner syndrome)
.hypothalamic-pituitary insufficiency
.pituitary tumor
.testiculat feminization syndrome (androgen insensitivity syndrome)
-Diagnosis (primary amenorrhea is diagnosed with absence of menses) :
.age 14 without secondary sexual development
.age 16 with secondary sexual development
-Investigations :
.chromosomal analysis (necessary)
.karyotype
.ultrasound
.hormonal proliferative (FSH, prolactin, testosterone)
.thyroid function
.DIC

+Mullerian Agenesis (46xx)

.primary amenorrhea
.(+) breasts / (-) uterus
.(+) pubic and axillary hair
.testosterone levels are normal / idiopathic absence of the mullerian duct derivatives (fallopian tubes, uterus, cervix, upper
vagina)
+Androgen Insensitivity (46xy – with lack of androgen receptor function)
.primary amenorrhea
.(+) breasts / (-) uterus
.(-) pubic and axillary hair
+Gondal Dysgenesis (Turner syndrome 45x – is caused by the lack of one X chromosome)
.primary amenorrhea
.(-) breasts / (+) uterus
.elevation of FSH levels
+Hypothalamic-Pituitary Failure
.primary amenorrhea
.(-) breast / (+) uterus
.decreased of FSH levels
14

+Kallmann Syndrome
.primary amenorrhea
Page

.(-) breasts / (+) uterus

.anosmia
+Breasts present, Uterus present :
.imperforate hymen
.vaginal septum
.anorexia nervosa
.excessive exercise
.possible pregnancy before first menses
.history and physical examination will identify the majority of specific diagnosis
+Breasts present, Uterus absent :
.mullerian agenesis (Rokitansky-Kuster-Hauser syndrome)
.complete androgen insensitivity (testicular feminization)
.testosterone levels and karyotype help make the diagnosis
+Breasts absent, Uterus present :
.gonadal dysgenesis (Turner syndrome)
.hypothalamic-Pituitary failure
.FSH level and karyotype help make the diagnosis

+Secondary Amenorrhea
-NO menses for 3 months if previously regular menses or 6 months if previously irregular menses in women, who have
previously normal menstruation
-Pathophysiology :
.there are multiple etiologies for secondary amenorrhea, which can be classified by alterations in FSH and LH levels. They
include (hypogonadotropic; hypothalamic or pituitary dysfunction) (hypergonadotropic; ovarian follicular failure)
(eugonadotropic; pregnancy, anovulation, uterine or outflow tract pathology)
+May be due to thyrotoxicosis and anorexia nervosa
-Causes :
.pregnancy – the first step is a beta-hCG to diagnose pregnancy (M.C.C of secondary amenorrhea)
.anovulation (if no corpus luteum is present to produce progesterone. Anovulation is associated with unopposed estrogen
stimulation of the endometrium)
.breast feeding
.early menopause
.pituitary tumor
.asherman syndrome – cervical stones (secondary to – intrauterine surgery, intrauterine adhesion, infection, DIC, endometritis,
myomectomy)
.ovarian failure (decreased estrogen, increased FSH over 40moL)
+M.C pelvic mass associated with amenorrhea in a reproductive age is pregnancy
+The Causes Of Anovulation :
.PCOS
.hypothyroidism
.pituitary adenoma
.hyperprolactenemia
.medication (antidepressants’)
.estrogen deficiency
+The Causes Of Hypoestrogenic States :
.absence of functional ovarian follicles
.hypothalamic pituitary insufficiency
.outflow tract obstruction
+Anovulatory Bleeding (Physiology) :
.irregular, unpredictable vaginal bleeding
.13yrs old adolescent
.normal height and weight
+Anovulatory Bleeding (Chronic) :
.irregular, unpredictable vaginal bleeding
.33yrs old women
.obese, hypertensive
-Management :
15

.pregnancy test (the first step in management of secondary amenorrhea is to obtain a qualitative beta-hCG test to rule out
pregnancy)
Page
.thyrotropin (TSH) level (if the beta-hCG test is negative, hypothyroidism should be ruled out TSH level. The elevated
thyrotropin-releasing hormone TRH in primary hypothyroidism can lead to an elevated prolactin. If hypothyroidism is found,
treatment is thyroid replacement)
.prolactin level (elevated prolactin)
+Medications (an elevated prolactin level may be secondary to antipsychotic medication or antidepressants, which have an anti
dopamine side effect)
+Tumor (a pituitary tumor should be ruled out with CT scan or MRI of the brain / If a pituitary tumor is found and is <1cm in,
treat medically with bromocriptine-parlodel / If >1cm in, treated surgically)
+Idiopathic (if the cause of elevated prolactin is idiopathic, treatment is medical with bromocriptine)
+Progesterone Challenge Test PCT (If the beta-hCG is negative, and TSH and prolactin levels are normal, administer either a
single IM dose of progesterone or 7 days of oral medroxyprogesterone acetate MPA)
.Positive PCT (any degree of withdrawal bleeding is diagnostic of anovulation)
.Negative PCT (absence of withdrawal bleeding is caused by either inadequate estrogen priming of the endometrium or outflow
tract obstruction)
+Estrogen-Progesterone Challenge Test EPCT (If the PCT is negative, administer 21 days of oral estrogen followed by 7 days of
MPA)
.Positive EPCT (any degree of withdrawal bleeding is diagnostic of inadequate estrogen. An FSH level will help identify the
etiology) (Elevated FSH suggests ovarian failure / Low FSH suggests hypothalamic-pituitary insufficiency)
.Negative EPCT (absence if withdrawal bleeding is diagnostic of either an outflow tract obstruction or endometrial scarring,
asherman syndrome)
+Asherman syndrome (is the result of extensive uterine curettage and infection-produced adhesions. It is treated by
hysteroscopic adhesion lysis followed by estrogen stimulation of endometrium) (secondary to – intrauterine surgery,
intrauterine adhesion, infection, DIC, endometritis, myomectomy)

*Dysmenorrhea
+It is painful menstruation
+Primary is Spasmodic / Secondary is Congestive
+Membranous dysmenorrhea is most uncommon

+Primary Dysmenorrhea
-Idiopathic / Usually occur <20yrs (young age)
+Primary Dysmenorrhea at the time of menstruation is caused by uterine hypercontractility due to prostaglandin release
-Features :
.menstrual pain in absence of organic disease
.begins 6 months-2yrs after menarche (once ovulatory cycles established)
-Signs & Symptoms :
.refers to recurrent
.crampy lower abdominal – lower back pain
.labia and inner thighs beginning hours before onset of bleeding and persisting for hours or days (48-72hrs) (The pain may
radiate from lower abdomen to the inner aspects of the thighs)
.colic pain (occurs with the onset of menstruation)
.nausea, vomiting and diarrhea, that occurs during menstruation in the absence of pelvic pathology (painful menstruation in the
presence of pelvic pathology)
.pain start at 1st-2nd day of menses
.the pain may radiate from lower abdomen to the inner aspects of the thighs
-Findings :
.the symptoms typically begin several hours prior to the onset of menstruation and continue for 1 to 3 days
.onset of pain generally does not occur until ovulatory menstrual cycles are established (always associated with ovulation)
.symptoms appear to be caused by excess production of endometrial prostaglandin F2a (resulting from the spiral arteriolar
constriction and necrosis that follow progesterone withdrawal as the corpus luteum involutes) (Primary dysmenorrhea at the
time of menstruation is caused by - Uterine hypercontractility due to prostaglandins release)
-Diagnosis (Associated) :
.dyspareunia
.abnormal bleeding
.infertility
16

+The Prostaglandins Causes :

.dysrhythmic uterine contractions
Page

.hypercontractility
.increased uterine muscle tone
.leading to uterine ischemia
.the effect of the prostaglandins on the gastrointestinal smooth muscle also can account for nausea, vomiting and diarrhea
-Management :
.NSAIDs, prostaglandins synthetase inhibitors (1st choice in treatment)
.combination estrogen-progesterone steroid agents (oral contraceptives pills OCP) (2nd choice)

+Secondary Dysmenorrhea
-Types :
.congestive
.acquired
-Signs & Symptoms :
.dyspareunia
.abnormal bleeding
.infertility
.pain start at 1-2wks before menses, a relieved by menses
-Causes (Of Acquired) :
.endometriosis
.adenomyosis
.uterine polyps
.uterine anomalies
.leiomyoma
.intrauterine synechiae
.ovarian cysts
.cervical stenosis
.imperforate hymen, transverse vaginal septum
.PID
.IUD – copper
.foreign body
+Dysmenorrhea secondary to organic disorder (Endometriosis, Fibroid, PID)

++Comparison Of Anovulatory And Ovulatory Abnormal Uterine Bleeding

+Anovulatory
-Unpredictable endometrial bleeding of variable flow and duration; sex steroids are produced but not cyclically, resulting in
irregular bleeding (incidence 90%)
-Causes :
.PCOS
.thyroid dysfunction
.elevated prolactin levels
.rare estrogen-producing tumors
.stress
.weight loss
.exercise
.liver and kidney disease
+Ovulatory
-Typically cyclic, but heavy or prolonged (incidence 10%)
-Causes :
.anatomic or physical lesion (polyp, fibroid, adenomyosis, neoplasm, foreign body)
.hemostatic defect
.infection
.trauma
.local disturbances in prostaglandins (endomyometrial vasodilatory prostaglandins, decreased vasoconstrictive prostaglandin)

**Infertility
-Is defined as inability to achieve pregnancy after 12 months of unprotected and frequent intercourse
17

+Primary infertility (infertility in the context of no prior pregnancies)

+Secondary infertility (infertility in the context of a prior conception)
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+15% of couples in the reproductive age is unable to conceive after one year of coitus without contraception
*Female Factors
-Causes :
.hypothalamic (hypothalamic amenorrhea)
.pituitary (prolactinoma, hypopituitarism)
.ovarian (PCOS, premature ovarian failure, luteal phase defect – poor follicle production, premature corpus luteum failure,
failed uterine lining response to progesterone)
.systemic disease (thyroid, cushings syndrome, renal/hepatic failure)
.congenital (turners syndrome, gonadal dysgenesis or gonadotropin deficiency)
.stress, poor nutrition, excessive exercise (even with presence of menstruation)
.tubal factors (PID, adhesion – previous surgery, peritonitis, endometriosis / ligation, occlusion – previous ectopic pregnancy)
.uterine factors (congenital anomalies – bicornuate uterus, uterine septum / intrauterine adhesions – asherman's syndrome /
infection – endometritis, pelvic TB / fibroids, polyps / endometrial ablation)
.cervical factors (acidic cervical mucus, anti-sperm antibodies, structural defects)
.endometriosis
.multiple factors
.unknown factors
-Investigations :
(ovulatory)
.day 3 (FSH, LH, TSH, PRL + DHEA, free testosterone)
.day 21-23 (serum progesterone to confirm ovulation)
.initial basal body temperature
.postcoital test
+When Should Investigations Begin ?
.<35yrs (after 1yr of regular unprotected intercourse)
.35-40yrs (after >6 months)
.>40yrs (immediately)
-Earlier of :
.history of PID
.history of infertility in previous relationship
.prior pelvic surgery
.chemotherapy/radiation in either partner
.recurrent pregnancy loss
.moderate severe endometriosis
-Treatment :
+Education
.timing of intercourse in relation to ovulation – from 2 days prior to 2 days following presumed ovulation, every other day
+Medical
.ovulation induction (clomiphene citrate, human menopausal gonadotropin, followed by beta-hCG for stimulation of ovum
release, bromocriptine – dopamine agonist-if elevated prolactin, dexamethasone for hyperandrogenism, luteal phase
progesterone supplementation for luteal phase defect)
+Surgical
.tuboplasty
.lysis of adhesions
.artificial insemination
.sperm washing
.IVF
.intrafallopian transfer
.GIFT
.ZIFT
.TET
.ICSI
.IUI
.oocyte or sperm donors
.IVM
18

+Induction of ovulation may be achieved by giving Clomiphene Citrate

+M.C major side effect of ovulation induction is (ovarian hyperstimulation)
Page
+Clomiphene Citrate Is Contraindicated in :
.endometrial hyperplasia
.post pill amenorrhea
.polycystic ovary (Stein-Leventhal syndrome)
.infrequent ovulation
+Complications Of Ovulation Inducers :
.multiple pregnancy
.ectopic pregnancy
.hypotension
.ascites
+Possible Indications Of Ovulation :
.increased plasma levels of progesterone in the second half of the cycle
.increased basal temperature in the second half of the cycle
.change in the cervical mucus
.mid cycle abdominal pain
+Ovulation Can Be Diagnosed By The :
.measuring day 14 serum progesterone
.observing a rise in basal body temperature in the second half of the menstrual cycle
.study of cervical mucus
.endometrial biopsy
+Tests To Detect Ovulation :
.basal body temperature
.endometrial biopsy
.progesterone level
.vaginal wall cytology

*Male Factors
-Causes :
.varicocele
.idiopathic
.obstruction
.cryptorchidism
.immunological
-Investigations :
.semen analysis and culture
.post-coital (Huhner) test (rarely done)

+Initial Noninvasive Tests

1.Semen Analysis
-The 1st step in the infertility evaluation is a semen analysis, which should be obtained after 2-3 days of abstinence and
examined within 2h (Must be obtained after 48-72 hours of abstinence)
+Normal Values :
.volume >2ml (2-5cc)
.pH 7.2-7.8
.sperm density-count >20 million/ml
.sperm motility >50%
.sperm morphology >30-50%
.consent >15*10(6) /ml
.WBC <1*106 (liquefaction in 30min)
.antisperm antibody negative
.absence of pyospermia, hyperviscosity, agglutination
+If values are abnormal, repeat the semen analysis in 4-6wks because semen quality varies with time
-Minimally Abnormal (if sperm density is mild to moderately lower than normal)
.intrauterine insemination may be used
19

.washed sperm are directly injected into the uterine cavity

+Idiopathic oligozoospermia is the M.C.C or M.C factor (male infertility)
Page

-Severely Abnormal (if sperm analysis shows severe abnormalities)

.intracytoplasmic sperm injection may be used in conjunction with in vitro fertilization
.embryo transfer
-NO Viable Sperm
.with azoospermia or failed ICSI, artificial insemination by donor AID may be used
+Causes Azoospermia :
.blockage of the ducts
.klinefelter syndrome
.orchitis due to mumps
.trauma to spermatic cord
.male sterilization (vasectomy)
+Causes Of Abnormal Spermatogenesis :
.drugs
.varicocele
.genetic abnormalities
.cryptorchidism
.sauna, hot bath
.febrile-illness
.prolonged sitting
+COLD environment, swimming (NOT)
2.Anovulation
-Causes Of Infertility :
.serum progesterone level will be low
.history of irregular, unpredictable menstrual bleeding
.hypothyroidism or hyperprolactinemia

*Unexplained Infertility
-This diagnosis is reserved for couples in which the semen analysis is normal, ovulation is confirmed, and patent oviducts are
noted (approximately 60% of Pts. with unexplained infertility will achieve a spontaneous pregnancy within the next 3 years)
-Management :
.control ovarian hyperstimulation COH with clomiphene
.intrauterine insemination IUI
.the fecundity rates for 6 months are comparable with IVF

**Sexual Dysfunction
-Causes :
.intrapsychic, Pts. experiences, value system
.relationship / interpersonal issues
.physical / organic
-Classification :
.lack of desire (60-70% of women)
.lack of arousal
.anorgasmia (primary anorgasmia – never before achieved orgasm under any circumstances) (secondary anorgasmia – was able
to achieve orgasms before bout now unable)
.dyspareunia (painful intercourse, superficial or deep)
+Causes Of Dyspareunia :
.vaginismus
.vulvodynia
.vaginal atrophy
.vulvar vestibulitis (associated with history of frequent yeast infections)
.PID

**Menopause
-Is a retrospective diagnosis and is defined as 12 months of amenorrhea (cessation of menses for 12 months after last period) –
Median age 50-52yrs, smokers experience menopause up to 2yrs earlier
+Occurrence of last spontaneous menstrual period, resulting from loss of ovarian function (loss of response to gonadotropins)
20

-Types :
.physiological (average age 51yrs – follicular atresia)
Page

.premature ovarian failure (before age 49 – autoimmune disorder, infection, turner's syndrome)
.iatrogenic (surgical, radiation, chemotherapy)
-Associated With :
.elevation of gonadotropins (FSH and LH >35iU/L BUT FSH > LH) (Both FSH and LH are elevated)
.elevation of androgen
.elevation of androstenedione
.inhibit estrogen (estrogen deficiency) (the quantity of estrogens present increase by obesity)
.decreased levels of estradiol (later)
+Combined estrogen and progesterone therapy is best (Withdrawal bleeding following combined therapy is NOT an indication
for curettage)
.the breast tend to decrease in size
.the uterus atrophies
.the vaginal mucosa becomes thin
.the pH of the vagina rises
.irritability, headache, vasomotor instability, bachache, hot flushes, palpitation, sweating
.insomnia, osteoporosis, loss of libido
+Associated With Estrogen Deficiency :
.vasomotor instability (hot flushes/flashes, night sweats, sleep disturbances, nausea, palpitations)
.urogenital atrophy involving vagina, urethra, bladder (dyspareunia, vaginal itching dryness, bleeding, urgency, incontinence)
.skeletal (osteoporosis, joint and muscle pain, back pain) (osteoporosis is the single most important hazard associated with
menopause)
.skin and soft tissue (decreased breast size, skin thinning/loss of elasticity)
.psychological (mood disturbance, irritability, fatigue, decreased libido, memory loss)
+Premature Menopause (occurs age 30-40 and is mostly idiopathic, but can also occur after radiation therapy or surgical
oophorectomy-ovariectomy)

+Premature Ovarian Failure

-Occur age <30 and may be associated with autoimmune disease or Y chromosome mosaicism
+Y chromosome mosaic (hot flashes, sweats / age 25yrs / elevation of FSH level)
-Symptoms (the lack of estrogen is responsible for the majority of menopausal symptoms and signs) :
.amenorrhea (M.C is secondary amenorrhea)
.hot flashes (sweating and sensation of heat) (obese women are less likely to undergo hot flashes)
.reproductive tract (low estrogen leads to decreased vaginal lubrication, increased vaginal pH, increased vaginal infections)
.urinary tract (low estrogen leads to increased urgency, frequency, nocturia, urge-incontinence)
.psychic (low estrogen leads to mood alteration, emotional lability, sleep disorders, depression, insomnia)
.cardiovascular disease (M.C.C of mortality in post-menopausal women, with prevalence rising rapidly after menopause)
.osteoporosis
.decreased breast volume
.increased facial hair growth
+Smoking and low-weight (decreased the age of menopause)
+Obese women; have-less symptoms of menopause
-Management :
.hormonal replacement the estrogen HRT
+Increased risk of breast cancer with HRT use

*Osteoporosis
+The M.C bone type of osteoporosis is trabecular bone
+The M.C anatomic site is in the vertebral bodies, leading to crush fractures, kyphosis and decreased height. Hip and wrist
fractures are the next most frequent sites)
-Diagnosis :
.the M.C method of assessing bone density is with a DEXA scan (dual-energy x-ray absorptiometry)
.the M.C method of assessing calcium loss is 24h urine hydroxyproline or NTX (N-telopeptide, bone breakdown product)
-Risk Factors :
.positive family history (M.C risk factor)
.thin women
.white female
.steroid use
21

.low calcium intake

.sedentary lifestyle
Page

.smoking and alcohol

-Management :
.lifestyle (calcium and Vit D intake, weight-bearing exercise, elimination of cigarettes and alcohol)
.medications (bisphosphonates ‘alendronate, risedronate’, estrogen replacement, SERMs ‘raloxifene’)
+To treat osteoporosis (1000-1500mg calcium daily, 800-1000 Vit D, weight-bearing exercise, quit smoking / bisphosphonates /
selective estrogen receptor modifiers SERMs – raloxifene)

*Hormone Replacement Therapy HRT

-Primary indication is treatment of menopausal symptoms (vasomotor instability) (HRT components – estrogen + progestin)
-Benefits (both hormone therapy HT – estrogen therapy ET) :
.decreased osteoporotic fractures
.lower rates of colorectal cancer - colon cancer
-Risk Factors :
.increased risk of (DVT, hyperplasia, endometrial - breast cancer, gallbladder stones) (heart disease, breast cancer – NOT
increased in the ET group-with estrogen only / NO elevated heart risks if used immediately after menopause or with estrogen-
alone)
.decreased risk of (osteoporosis)
-Contraindications :
+Absolute
.personal history of an estrogen-sensitive cancer (breast or endometrium)
.active liver disease (acute liver disease)
.active thrombosis (DVT / thromboembolic disease)
.unexplained vaginal bleeding (undiagnosed)
+Relative
.uncontrolled hypertension
.uterine fibroids and endometriosis
.familial hyperlipidemias
.family history of estrogen-dependent cancer
.migraine headache
.chronic thrombophlebitis
.DM with vascular disease
.fibrocystic disease of the breasts
-Side Effects Of HRT :
.abnormal uterine bleeding
.mastodynia – breast tenderness
.edema, bloating, heartburn, nausea
.mood changes (progesterone)
.can be worse in progesterone phase of combined therapy
-Modalities (estrogen can be administered by oral, transdermal, vaginal, parenteral routes) (M.C current regimen is current
regimen is oral estrogen and progestin given continuously)
+In Pts. with contraindications to estrogen-replacement therapy, SERMs can be used (like tamoxifen, raloxifene)
+Keep doses low (0.3mg premarin) and duration of treatment short (<5yrs)

**Hirsutism
-Is excessive male-pattern hair growth in a woman on (the upper lip, chin, chest, abdomen, back, proximal extremitis)
-Virilization is excessive male-pattern hair growth in a woman plus other masculinizing signs such as (clitorimegaly, baldness,
lowering of voice, increasing muscle mass, loss of female body contours)
-Lab Tests (to identify elevated free androgens) :
.dehydroepiandrosterone sulfate DHEAS (is produced only in the adrenal glands. A markedly elevated DHEAS is consistent with
an adrenal tumor)
.17-OH progesterone (it is elevated in late-onset congenital adrenal hyperplasia CAH, with 21-hydroxylase deficiency)
.testosterone (is produced by both the ovary and the adrenal glands. A mildly elevated level is suggestive of PCOS. A markedly
elevated level is consistent with an ovarian tumor)

*Adrenal Tumor
22

-History :
.typically the onset has been rapid without positive family history
-Examination :
Page

.physical examination will show evidence of virilization

.pelvic examination is unremarkable
-Lab Tests :
.DHEAS level is markedly elevated
-Imaging :
.CT or MRI scan will show an abdominal-flank mass
-Management :
.surgical removal of tumor

*Ovarian Tumor
-History :
.typically the onset has been rapid without positive family history
-Examination :
.physical examination will show evidence of virilization
.an adnexal mass will be palpated on pelvic examination
-Lab Tests :
.testosterone level is markedly elevated
-Imaging :
.pelvic ultrasound will show an adnexal mass
-Management :
.surgical removal of the mass, usually either a Sertoli-Leydig cell tumor or hilus cell tumor

*Congenital Adrenal Hyperplasia (21-Hydroxylase Deficiency)

-History :
.typically the onset has been gradual in the second or early third decade of life and is associated with menstrual irregularities
and anovulation
.precocious puberty with short stature is common
.family history may be positive
.late-onset CAH is one of the most common autosomal recessive genetic disorders
-Examination :
.physical examination will show evidence of hirsutism without virilization
.pelvic examination is unremarkable
-Lab Tests :
.serum 17-OH progesterone level is markedly elevated
-Management :
.treatment is medical with continuous corticosteroid replacement

**Precocious Puberty
-Diagnosis :
.criteria for diagnosis include development of female secondary sexual characteristics accelerated growth before age 8 in girls
and age 9 in boys (is more common in girls than boys)
-Normal Pubertal Landmarks :
.thelarche (breast development at age 9-10) (the M.C initial change)
.this is followed by adrenarche (pubic and axillary hair at age 10-11)
.maximal growth rate occurs age 11 and 12
.finally, the last change is menarche (onset of menses at age 12-13)
-Management :
.idiopathic (GnRH agonist)
.CNS lesions (medical or surgical treatment)
.ovarian tumor (surgical excision)
.McCune-Albright or polyostotic fibrous dysplasia (aromatase inhibitors)

**The Female Breast

-Anatomy
.there are 15-20 lobes in each breast
23

.80-85% of normal breast tissue is fat during the reproductive years

.in the nonpregnant, nonlactating breast, the alveoli are small / During pregnancy, the alveoli enlarge
Page

.ligaments called Cooper`s Ligaments, with keep the breasts in their characteristic shape and position, support breast tissue. In
the elderly or during pregnancy, these ligaments become loose or stretched, respectively, and the breasts sag
-Hormones
.estrogen, released from the ovarian follicle, promotes the growth ducts
.progesterone, released from the corpus luteum, stimulates the development of milk producing alveolar cells
.prolactin, released from the anterior pituitary gland, stimulates milk production
.oxytocin, released from the posterior pituitary in response to suckling, causes milk ejection from the lactating breast
-Lactation
.the first secretion of the mammary gland after delivery is colostrum. It contains more protein and less fat than subsequent
milk, and contain IgA antibodies that impart some passive immunity to the infant (Most of the time it takes 1-3 days after
delivery for milk production to reach appreciable levels

**Benign Breast Disorders

*Cystic Breast Mass
-Diagnosis :
.cyst aspiration and fine-needle aspiration
-Management :
.preaspiration mammography should be obtained

*Fibrocystic Breast Changes

-Diagnosis :
.cyclic premenstrual mastalgia (is associated with fibrocystic changes of the breast)
.palpable mass
.fine-needle aspiration can easily distinguish whether a mass is solid or cystic

*Breast Fibroadenoma
-Diagnosis :
.M.C breast tumors found in adolescence and young women
.clinically (discrete, smoothly contoured, rubbery, nontender, freely movable masses)
.fibroadenomas arise from the epithelium and stroma of the terminal duct lobular unit, most frequently in the upper outer
quadrant of the breast
.an association of fibroadenomas with the development of breast cancer has not been wall established. Any associated
increases in breast cancer risk depends on the presence of proliferative changes in the fibroadenoma itself or in the
surrounding breast, and on a family history of breast carcinoma
.cysts and fibroadenomas may be indistinguishable on palpation, ultrasound examination easily distinguishes cystic from solid
lesions. On fine-needle aspiration, cysts typically collapse

*Bloody Nipple Discharge

-Diagnosis :
.a bloody nipple discharge usually results from an intraductal papilloma. The treatment is total excision of the duct and
papilloma through a circumareolar incision

**Breast Cancer
-Prognostic Factors :
.lymph node status (to determining cancer staging and treatment options / Axillary lymph node status is the most important
factor in the prognosis of Pts. with breast cancer. As the number of positive axillary lymph nodes increases, survival rate
decreases and relapse rate increases)
.tumor size (the most significant factor)
.receptor status (it is standard practice to determine both estrogen and progesterone receptor status at the time of diagnosis
for definitive surgical therapy)
.DNA ploidy status
-Breast Cancer Risk Factors :
.BRCA 1 or 2 gene mutation (RR15)
.ductal or lobular CIS (RR15)
.atypical hyperplasia (RR4)
24

.breast irradiation age <20 (RR3)

.positive family history (RR3)
Page
*Infiltrating Ductal Carcinoma
-M.C breast malignancy
-Most are unilateral and start as atypical ductal hyperplasia in situ DCIS
-Over time the tumor will become a stony hard mass as it increases in size and undergoes a fibrotic response

*Infiltrating Lobular Carcinoma

-2nd M.C breast malignancy
-Most are unilateral and start as lobular carcinoma in situ LCIS
-The prognosis is better with lobular than with ductal carcinoma

*Inflammatory Breast Cancer

-Uncommon breast malignancy
-Usually, there is no single lump or tumor. It is characterized by rapid growth with early metastasis
-The breast becomes erythematous, swollen and warm to examination. The edematous skin of the breast appears pitted, like
the skin of an orange, giving the classic peau d`orange appearance

*Paget Disease Of The Breast/Nipple

-Uncommon breast malignancy with a better prognosis than infiltrating ductal carcinoma
-The lesion is pruritic and appears red and scaly often located in the nipple spreading to the areola
-The skin appearance can mimic dermatitis like eczema or psoriasis
-The nipple may become inverted and discharge may occur
-It is almost always associated with DCIS or infiltrating ductal carcinoma

+Sentinel Node Biopsy SLN

.is the first lymph nodes to which cancer cells are likely to spread from the primary tumor
.cancer cells may appear in the sentinel node before spreading to other lymph nodes
.a biopsy of the dye stained node is performed to determine the extent or stage of cancer
.the potential for side effects is lower (SLN biopsy)

**Gestational Trophoblastic Disease / Neoplasia (GTD/GTN)

-GTN or molar pregnancy, is an abnormal proliferation of placental tissue involving both the cytotrophoblast and/or
syncytiotrophoblast. It can be benign or malignant
-Malignant GTN can be characterized as either localized or metastatic
-Pregnancy <20 wks / HTN and proteinuria / NO fetal heart tones FHT, vaginal passage of vesicles
+Commoner in women of blood group A married to blood O men (Group AB women have the worst prognosis)
-Signs & Symptoms :
.bleeding prior to 16wks gestation and passage of vesicles from the vagina (M.C)
.hypertension
.hyperthyroidism
.hyperemesis gravidarum
.aggravated morning sickness
.no fetal heart tones appreciated
.commoner in older gravida and
.fundus larger than dates (M.C) (uterine size is larger than dates)
.bilateral cystic enlargements of the ovary (theca-lutein cysts) (bilateral ovarian cysts)
+The M.C site of distant metastasis is the Lungs
-Risk Factors :
.increased prevalence geographically (is M.C in taiwan and the philippines)
.maternal age extremes (<20yrs old, >35yrs old)
.folate deficiency
-Complications :
.complicated by ovarian cyst
.hemorrhage
.sepsis
25

.perforation of the uterus

.choriocarcinoma
Page

-Diagnosis :
.ultrasound ‘snowstorm’
.sonogram ‘homogenous intrauterine echoes without a gestational sac or fetal parts’
-Management :
.suction, curettage regardless of the size of the uterus (syction-evacuation of the uterus is BEST treatment)
.baseline quantitative beta-hCG titer
.CXR (to rule out lung metastasis)
.suction D&C to evacuate the uterine contents
.place the Pt. On effective contraception OCP
-Classification :
++Benign GTN (is the classic hydatidiform mole ‘H-mole’)
+complete mole
.is the M.C benign GTN
.it results from fertilization of an empty egg with a single X sperm resulting in paternally derived (androgenetic) normal 46XX
karyotype
.NO fetus, umbilical cord or amniotic fluid is seen
.the uterus is filled with grape-like vesicle composed of edematous avascular villi
.progression to malignancy is 20%
+Incomplete mole
.is less common benign GTN
.it results from fertilization of a normal egg with tow sperm resulting in triploidy 69XXY karyotype
.a fetus, umbilical cord and amniotic fluid is seen wich results ultimately in fetal demise
.progression to pregnancy is 10%
+Complete (Benign)
.empty egg
.paternal X`s only
.46XX (diploid)
.fetal absent
.20% (malignancy)
.NO chemotherapy (serial beta-hCG titers / follow-up 1yr on OCP)
+Incomplete (Benign)
.normal egg
.maternal and paternal X`s
.69XXY (triploid)
.fetus nonviable
.10% (malignancy)
.NO chemotherapy (serial beta-hCG titers (-) / follow-up 1yr on OCP)
++Malignant GTN (is the gestational trophoblastic tumor GTT which can develop om 3 categories)
.Non-metastatic disease (is localized only to the uterus)
.Good prognosis metastatic disease (has distant metastasis with the most common location being the pelvis or lung)
.Poor prognosis metastatic disease (has distant metastasis with the most common location being the brain or the liver. Other
poor prognosis factors are serum beta-hCG levels >40.000, >4 months from the antecedent pregnancy)
+Non metastatic (Malignant GTN)
.uterus only
.100% cure
.single-agent chemotherapy / 1yr follow-up on OCP after beta-hCG (-)
+Good prognosis (Malignant GTN)
.pelvis or lung (metastasis)
.>95% cure
.single-agent chemotherapy / 1yr follow-up on OCP after beta-hCG (-)
+Poor prognosis (Malignant GTN)
.brain or liver (metastasis)
.65% cure
.multiple agent chemotherapy
.5yr follow-up on OCP
26
Page
**Gynecological Infections
*Physiologic Discharge
.clear, white, flocculent odourless discharge (pH 3.8-4.2)
.smear contains epithelial cells (Lactobacilli)
.increase with increased estrogen states (pregnancy, OCP, mid-cycle, PCOS, premenarchal)
.if increased in premenopausal / postmenopausal woman, consider investigation for other effects of excess estrogen
(endometrial cancer)

*Vulvovaginitis
-Inflammation or infection of the vulva and vagina. It’s a common condition that affects women and girls of all ages, and it has a
variety of causes. Other names for this condition are vulvitis and vaginitis
-Signs & Symptoms :
.irritation of the genital area
.genital itching
.inflammation, specifically around the labia and perineal areas
.foul odor that’s typically quite strong
.increased vaginal discharge
.discomfort when urinating, including a burning sensation
-Causes :
.Candida albicans (M.C.C)
.bacteria (Streptococcus, Gardnerella, Staphylococcus)
.Viruses (simplex and human papillomavirus HPV)
.Parasites (Pinworms, scabies, lice)
.STI (trichomonas vaginitis, Chlamydia, gonorrhea)
.Chemicals (soap, bubble bath, feminine spray, perfume, vaginal contraceptives)
+Commonly requires treatment with systemic antibiotic
+M.C skin disease affecting the vulva is (Contact dermatitis)

1.Prepubertal Vulvovaginitis
-Signs & Symptoms :
.irritation, pruritus
.discharge
.vulvar erythema
.vaginal bleeding (specifically due to Group A Streptococci and Shigella)
-Causes :
.non-specific vulvovaginitis (M.C gynecological problem in prepubertal girls – in cheldren)
.sexual abuse
.infections (respiratory, enteric, systemic, sexually acquired, STIs)
.foreign body (toilet paper is M.C) (treated by irrigation of vagina with saline – may require local anesthesia or an exam under
anesthesia)
.candida (if using diapers)
.polyps, tumor (ovarian malignancy)
.vulvar skin disease (lichen sclerosis, condyloma acuminata) (lichen sclerosis – diagnosed by area of white patches and thinning
of skin / treated by topical steroid creams)
.trauma (injury, sexual abuse)
.endocrine abnormalities (specific to vaginal bleeding)
.blood dyscrasia (specific to vaginal bleeding)
.pinwprms (diagnosed by cellophane tape test / treated by empirical with mebendazole)
-Investigations :
.vaginal swab for culture

2.Postmenopausal Vaginitis / Atrophic Vaginitis

-Signs & Symptoms :
.dyspareunia
27

.post-coital spotting
.mild pruritus
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-Investigations :
.atrophy is usually a visual diagnosis (thinning of tissues, erythema, petechiae, bleeding points, dryness on speculum exam)
.rule out malignancy (especially endometrial cancer)
-Treatment :
.local estrogen replacement
.oral or transdermal hormone replacement therapy
.good hygiene

+Infectious Vulvovaginitis (Organisms)

-Candidiasis (Moniliasis) (caused by yeast) – Discharge (blood stained, whitish, cottage cheese) – Trans. (immunosuppressed
host ‘DM, AIDS’ / recent antibiotic use / includes estrogen levels) (associated with vulvar pruritus) (Pts. partner may ned
treatment)
.candida albicans
.candida glabrata
.candida tropicalis
-Bacterial Vaginosis (BV) – Discharge (gray, thin, diffuse) – Trans. (replacement of vaginal Lactobacillus with organisms above)
.gardnerella vaginalis
.mycoplasma hominis
.anaerobes (prevotella, mobiluncus, bacteroides)
-Trichomoniasis – Discharge (profuse cream frothy, yellow-green, malodorous, diffuse) – Trans. (sexually transmitted)
.flagellated protozoan
-Gardnerella Vaginalis – Bad smelling, frothy and irritative vaginal discharge, wet smear showed ‘clue cells’

*Pruritus Vulvae
-Is itchiness of the vulva
-Causes :
.vaginal infections
.vulvitis
.HPV (human papilloma virus), gonorrhea, monilial infection
.anal incontinence
.Bowen's disease
.dietary irritants (caffeine, tomatoes, and peanuts)
.psychological problem
.DM
.personal hygiene products
+The most effective treatment of vulvar pruritus associated with atrophic vulvitis is (topical estrogen therapy)
+M.C.C of vaginal itching during ptrgnancy is (Vaginal moniliasis) (Risk Factors for monilial infection – combined oral
contraceptive pills, DM, pregnancy, Pts. on broad spectrum antibiotics)
+The Following Might Increase Vaginal Discharge During Pregnancy :
.bacterial vaginitis
.trichomonas vaginalis
.ccandida vaginitis
.physiological

*Sexually Transmitted Diseases (STIs)

-Are infections that are commonly spread by sex, especially vaginal intercourse, anal sex and oral sex. Most STIs initially do not
cause symptoms
-Signs & Symptoms :
.vaginal discharge
.penile discharge
.ulcers on or around the genitals
.pelvic pain
-Include :
.Chancroid (Haemophilus ducreyi)
.Chlamydia (Chlamydia trachomatis)
.Gonorrhea (Neisseria gonorrhoeae)
28

.Granuloma inguinale or (Klebsiella granulomatis)

.Lymphogranuloma venereum
.Granuloma inguinale
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.Mycoplasma genitalium
.Mycoplasma hominis
.Syphilis (Treponema pallidum)
.Ureaplasma infection
.Candidiasis (yeast infection)
.Viral hepatitis
.Herpes simplex (Herpes simplex virus 1, 2)
.Herpes hominis (type 2)
.HIV
.HPV (Human Papillomavirus)
.CMV (cytomegalovirus)
.Crab louse
.Scabies (Sarcoptes scabiei)
.Trichomoniasis (Trichomonas vaginalis)
.Condyloma infections (condyloma acuminatum)
-Risk Factors :
.history of previous STI
.contact with infected person
.sexually active individual age <25yrs
.multiple partners
.new partner in last 3 months
.not using barrier protection
.screen involvement (homelessness, drug use)

+Chlamydia
.is caused by Chlamydia trachomatis
.it is the M.C bacterial STD in women
.associated with N.gonorrhea
.it is known as acute PID (salpingo-oophoritis)
.diagnosed by cervical culture or (NAAT) (nucleic acid amplification test) / urine and vaginal test (more effective than cervical
culture)
.treatment (doxycycline or azithromycin in a single dose and may be used in pregnancy)
.symptoms (asymptomatic in 80% of cases, muco-purulent endocervical discharge, urethral syndrome “dysuria, frequency,
pyuria, no bacteria’, pelvic pain, post-coital bleeding or intermenstrual bleeding, symptomatic sexual partner)
.complications (acute salpingitis, PID, Fitz-Hugh-Curtis syndrome – liver capsule infection / arthritis, conjunctivitis, urethritis
‘reactive arthritis – male predominance, HLA-B27’, infertility, ectopic pregnancy, chronic pelvic pain, perinatal infection
‘conjunctivitis, pneumonia’)
+Gonorrhea
.is caused by Neisseria gonorrhoeae, a Gram-negative diplococcus
.the long-term arise from pelvic adhesion, causing chronic pain and infertility
.it is known as acute pelvic inflammatory disease (acute PID) / systemic infection can occur
.symptoms same as with chlamydia (lower genital tract infection may lead only to vulvovaginal discharge, itching, burning with
dysuria or rectal discomfort) / (upper genital tract infection leads to bilateral abdominal-pelvic pain)
.disseminated gonorrhea is characterized by dermatitis, polyarthralgia, tenosynovitis
.diagnosed by (NAAT) (Gram stain shows Gram-negative intracellular diplococci / cervical, rectal and throat culture)
.treatment (single dose of ceftriaxone IM or cefixime or ciprofloxacin) (if pregnant – cephalosporin regimen or spectinomycin
IM)
.Gonorrhea may affect (fallopian tubes, urethra, cervix, bartholin gland)
.Neisseria gonorrhea culture during pregnancy, the highest positive culture is got from (Urethra)
+Human Papillomavirus HPV
.M.C viral STI
.HPV types 6 and 11 are classically associated with anogenital warts / condylomata acuminata
.HPV type 16 and 18 are the most oncogenic (associated with cervical HSIL)
.types 16, 18, 31, 33, 35, 36, 45 (associated with increased incidence of cervical and vulvar intraepithelial hyperplasia and
carcinoma)
29

.symptoms (asymptomatic, only detected by DNA hybridization tests, hyperkeratotic verrucous or flat, macular lesions, vulvar
edema)
.investigations (Pap test, biopsy of lesions att colposcopy, detection of HPV DNA subtype using nucleic acid probes not routinely
Page

done but can be done in presence of abnormal Pap test)

+Herpes Simplex Virus Of Vulva HSV
.HSV 1 (10%) (disease above the belt – Oral) / HSV 2 (90%) (disease below the belt – Genital)
.symptoms (asymptomatic, initial symptoms present 2-21 days following contact, prodromal symptoms ‘pruritus, burning,
tingling’, multiple-painful-shallow ulcerations with small vesicles appear 7-10 days after initial infection, inguinal
lymphadenopathy, malaise and fever with first infection, dysuria and urinary retention if urethral mucosa affected, recurrent
infections ‘less severe, shorter in duration especially with HSV1)
.investigations (viral culture preferred in Pts. with ulcer present, HSV DNA PCR)
.treatment (acyclovir or famciclovir or valacyclovir)
+Syphilis
.is caused by Treponema pallidum
.primary syphilis (3-4wks after exposure, painless chancre or vulva-vagina or cervix, painless inguinal lymphadenopathy,
serological tests usually negative, local infection only)
.secondary syphilis (can resolve spontaneously, 2-6 months after initial infection, nonspecific symptoms ‘anorexia, headache,
diffuse lymphadenopathy’, maculopapular, condylomata lata, serological tests usually positive)
.latent syphilis (no clinical manifestations; detected by serology only)
.tertiary syphilis (may involve any organ system, neurological ‘tabes dorsalis, general paresis’, cardiovascular ‘aortic aneurysm,
dilated aortic root’, vulvar gumma)
.congenital syphilis (may cause fetal anomalies, stillbirths or neonatal death)
.investigations (aspirate of ulcer serum or node, darkfield microscopy ‘most specific test’, VDRL-RPR ‘)
.treatment (primary, secondary, latent of <1yr duration – benzathine penicillin / latent >1yr duration – benzathine penicillin /
neurosyphilis – IV penicillin)
+Condyloma Acuminatum
.is caused by the human papilloma virus HPV
.it is the M.C overall STD in women – M.C viral STD
+Chancroid
.is caused by (Haemophilus ducreyi, a Gram-negative bacterium)
.it is cofactor for HIV transmission
+Lymphogranuloma Venereum LGV
.is caused by the L serotype of Chlamydia trachomatis
+Granuloma Inguinale (Donovanosis)
.is caused by Calymmatobacterium granulomatis, a Gram-negative intracellular bacterium

+With Ulcers :
.chancroid (ragged, soft edge inflamed)
.granuloma inguinale (beefy red, donovan bodies)
.genital herpes
.LGV (groove sign)
.syphilis (rolled, hard edge)
+Painful Ulcers :
.chancroid
.genital herpes
+No Ulcers :
.chlamydia
.HPV
.gonorrhea
.hepatitis B
.HIV

*Toxic Shock Syndrome

-Multiple organ system failure due to S. Aureus exotoxin
-Signs & Symptoms :
.sudden high fever
.sore throat, headache, diarrhea
.erythroderma
30

.signs of multisystem organ failure

.refractory hypotension
Page

.exfoliation of palmar and plantar surfaces of the hands and feet 1-2 wks after onset of illness
-Risk Factors :
.tampon use
.diaphragm, cervical cap or sponge use (prolonged use >24hrs)
.wound infections
.postpartum infections
-Treatment :
.penicillinase-resistant antibiotics, cloxacillin
.steroid use

*Surgical Infections
+Post-Operative Infections in Gynecological Surgery
(Pelvic Cellulitis)
.common post hysterectomy, affects vaginal vault
.erythema, induration, tenderness, discharge involving vaginal cuff
.treat if fever and leukocytosis with broad spectrum antibiotics, clindamycin and gentamicin
.can result in intra-abdominal and pelvic abscess

**Urogynecology
*Pelvic Relaxation / Prolapse
-Protrusion of pelvic organs into or out of the vagina
-Types :
.uterine prolapse (protrusion of cervix and uterus into vagina – groin, back pain, feeling of heaviness, pressure in the pelvis,
ulceration, bleeding, urinary incontinence)
.vault prolapse (protrusion of apex of vaginal vault into vagina, post-hysterectomy)
.cystocele (protrusion of bladder into the anterio vaginal wall – urgency, nocturia, stress incontinence, incomplete bladder
emptying)
.rectocele (protrusion of rectum into posterior vaginal wall – straining/digitation to evacuate stool, constipation)
.enterocele (prolapse of small bowel in upper posterior vaginal wall – similar to hernia repair)
-Signs & Symptoms :
.feeling like you are sitting on a ball
.vaginal bleeding
.vaginal discharge
.backache
.problems with sexual intercourse
.seeing the uterus or cervix coming out from the vagina
.pulling or heavy feeling in pelvis (heaviness in the vagina)
.constipation
.recurrent bladder infections
-Causes :
.relaxation, weakness, or defect in the cardinal and uterosacral ligaments wich normally maintain the uterus in an anteflexed
position and prevent if from descending through the urogenital diaphragm
-Risk Factors :
.vaginal childbirth
.aging
.decreased estrogen (post-menopause)
.following pelvic surgery
.increased intra-abdominal pressure (obesity, chronic cough, constipation, ascites, heavy lifting)
.congenital (rarely)
.ethnicity
.collagen disorders
-Treatment (for pelvic relaxation/prolapse and urinary incontinence) :
.kegel exercises
.local vaginal estrogen therapy
.vaginal pessary
31

+Uterine prolapse :
.Grade 0 - Normal position
Page

.Grade 1 - descent into vagina not reaching introitus

.Grade 2 - descent up to the introitus
.Grade 3 - descent outside the introitus
.Grade 4 - Procidentia

*Urinary Incontinence / Stress Urinary Incontinence (SUI)

-Stress Incontinence - involuntary loss of urine with increased intra-abdominal pressure (coughing, laughing, sneezing, walking,
running)
+Stress incontinence can worsen during the week before the menstrual period. At that time, lowered estrogen levels may lead
to lower muscular pressure around the urethra, increasing chances of leakage. The incidence of stress incontinence increases
following menopause, similarly because of lowered estrogen levels
-Risk Factors :
.pelvic prolapse
.pelvic surgery
.vaginal delivery
.hypoestrogenic state (post-menopause)
.multi parous
.age
.smoking
.neurological / pulmonary disease
-Diagnosis :
.multichannel urodynamics (the gold standard diagnostic test)
-Treatment (for pelvic relaxation/prolapse and urinary incontinence) :
.kegel exercises
.local vaginal estrogen therapy
.vaginal pessary
.anterior colporrhaphy
.colposuspension
+Surgical (tension-free vaginal tape TVT / tension-free obturator tape TOT, prosthetic / fascial slings or retropubic bladder
suspension – Burch or Marshall-Marchetti-Krantz procedures)
+Long term antibiotic therapy will NOT improve it

*Urge Incontinence
-Urine loss associated with an abrupt, sudden urge to void, overactive bladder
-Signs & Symptoms :
.frequency
.urgency
.nocturia
.leakage
+Rule out Neurological causes of urge incontinence (multiple sclerosis, slipped disc, DM)
-Causes :
.idiopathic (90%)
.detrusor muscle overactivity (detrusor instability)

By Dr.Mohammad Z. abu sheikha@

32
Page
 Gynecological Oncology
**Disease Of The Ovary
-Signs & Symptoms :
.most women with epithelial ovarian cancer present with advanced stage disease since often ‘asymptomatic’ until disseminated
disease
.vague abdominal symptoms (nausea, bloating, dyspepsia, anorexia, early satiety)
.increased abdominal girth (from ascites or tumor itself)
.urinary frequency
.constipation
.fluid wave (signs of ascites)
.postmenopausal bleeding (irregular menses if pre-menopausal) (rare)
-Risk Factors for epithelial ovarian cancer :
.nulliparity
.OCP
.breast feeding, tubal ligation
.hysterectomy
.family history
.increasing age (>40yrs)
.late menopause
.delayed child-bearing
.race (caucasian)
-Investigations :
.women with suspected ovarian cancer based on history, physical, or investigations (bimanual examination – solid, irregular or
fixed pelvic mass is suggestive of ovarian cancer)
.blood work (CA-125, CBC, liver function tests, electrolytes, creatinine)
.radiology (ultrasound, CT-scan for abdomen and pelvis)
.bone scan or PET scan NOT indicated
.no effective method of mass screening
.routine CA-125 level measurements or ultrasound NOT recommended
.familial ovarian cancer (>1 first degree relative affected BRCA-1 mutation)
.other cancers (endometrial, breast, colon)
.BRCA-1 or BRCA-2 mutation (may recommend prophylactic bilateral oophorectomy after age 35 or when child-bearing is
completed)

*Benign Ovarian Tumors

.most are asymptomatic
.usually enlarge slowly
.may rupture or undergo torsion, causing pain (pain associated with torsion of an adnexal mass)
.peritoneal irritation (may result from an infarcted tumor – rare)
-Benign Ovarian Tumors :
.functional (follicular cyst, corpus-luteum cyst, theca-lutein cyst, luteoma of pregnancy, endometrioma, polycystic ovaries)
.inflammatory (tubo-ovarian abscess, endometrioma)
.benign germ cell tumors (benign teratoma)
.epithelial (serous cystadenoma, mucinous cystadenoma, brenner tumor)
.sex cord stromal (fibroma, thecoma)
+Most benign ovarian tumors will be diagnosed by the presence of a pelvic/abdominal mass by symptoms (pain or pressure on
the bowel or bladder) or incidentally on ultrasound
-The Differential Diagnosis Of A Pelvic Mass :
.tumors of uterus
.fallopian tube
.urinary tract – bowel
.pregnancy (M.C.C of pelvic mass in the reproductive years)
33

.complex mass (M.C complex adnexal mass in young women is a dermoid cyst or benign cystic teratoma)
.other diagnosis (endometrioma, tubo-ovarian abscess, ovarian cancer)
Page

-Common Investigations :
.ultrasound scan (transvaginal or abdominal)
.CT scan
.MRI
.pregnancy test (to exclude pregnancy)
+Androblastoma (tumor can cause hirsutism)

+Functional Ovaria Cysts

-M.C.C of a simple cystic mass in the reproductive age years is a physiologic cyst (luteal or follicular cyst)
-Pelvic mass in reproductive years / beta-hCG (-) / ultrasound (fluid-filled, ovarian simple cyst)
-Include :
.follicular cyst
.corpus luteum cyst
.theca-lutein cyst
.luteoma of pregnancy
.endometrioma
.polycystic ovaries
-The risk of developing functional cysts is reduced by the use of the OCP
-Diagnosis is made when the cyst measures more than 3 cm (normal ovulatory follicles measure up-to 2.5cm)
-Treatment (if asymptomatic – observed and repeat ultrasound / if symptomatic – laparoscopic cystectomy)
+Follicular Cyst
.folicle fails to rupture during ovulation
.usually asymptomatic
.usually asymptomati and may rupture, bleed, tort, infarct
.causing pain + signs of peritoneal irritation
.U/S (4-8cm mass, unilocular, lined with granulosa cells)
+Corpus luteal Cysts
.corpus luteum fails to regress after 14 days, becoming cystic or hemorrhagic
.more likely to cause pain than follicular cyst and may delay onset of next period
.U/S (10-15cm and firmer than follicular cysts)
+Theca-lutein Cysts
.due to atretic folicies stimulated bu abnormal beta-hCG levels
.are associated with molar pregnancy, ovulation induction with clomiphene
.treatment (conservative, cyst will regress as beta-hCG levels fall)
+Luteoma Of Pregnancy
.usually bilateral
.due to prolonged elevation of beta-hCG
.associated with multiple pregnancy
.treatment (conservative, regresses postpartum)

+Inflammatory Ovarian Cyst

-This is usually associated with PID
+M.C in young women
+The inflammatory mass may involve the tube, ovary and bowel and can be noted as a mass or an abscess (the tubo-ovarian
mass can develop from other infective causes, for example appendicitis or diverticular disease)
+Diagnosis is based on that for PID, inflammatory markers
-Treatment :
.antibiotics
.surgical drainage or excision
+Pts. may present with endometriosis, often known as ‘chocolate cyst’ / they can reach 10 cm in size and have a characteristic
‘ground glass’ appearance on ultrasound

+Benign Germ Cell Tumors

.Germ cell tumors should be suspected if a young woman presents with a large solid ovarian mass which may be rapidly
growing and present in young women, they are often caused by fertility-preserving surgery and/or chemotherapy
.single most common ovarian germ cell neoplasm (childhood neoplastic ovarian masses most commonly from Germ cells)
34

.dermoid cysts are a combination of all tissue types (mesenchymal, epithelial and stroma)
.10%-20% bilateral / 20% occur outside of reproductive yrs
.U/S (smooth-walled, unilocular, ma show calcification wich is pathognomonic)
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.treatment (laparoscopic cystectomy)

+Dermoid cyst is commonest ovarian tumor associated with pregnancy
+Any mature tissue type may be present and often hair, muscle, cartilage, bone or teeth may be noted
+CXR (all Pts. should have it to exclude pulmonary metastases), MRI, CT scan
+M.C neoplastic ovarian masses in postmenopausal women originate from germ cells
+M.C ovarian tumors in young women
+M.C form of benign germ cell tumors is the mature dermoid cyst (cystic teratoma – dermoid cysts)
+Dermoid cysts (commonest cysts defected during pregnancy) / are malignant in less than 5% of cases
+M.C complication of large cystic teratoma during the first trimester is (Torsion)

+Epithelial Tumors
.most frequent diagnosed type of ovarian cancer
.benign epithelial tumors with age
.types (serous cystadenoma – are unilocular / mucinous cystadenomas – large multiloculated cysts and are bilateral)
+M.C malignant tumors of the ovary is epithelial tumors
+M.C epithelial tumors are serous cystadenomas
+M.C in peri-menopausal women
+Brenner tumors (are often small tumors found incidentally within the ovary. They may secrete estrogen)

+Sex Cord Stromal Tumors

.benign estrogen-secreting tumors (a significant percentage of these tumors present with manifestations of their hormone
production) (present with endocrine effects)
.may arise from increased estrogen production (granulosa, theca or sertoli cell) or androgen (sertoli leydig or steroid cell), that
causing precocious puberty, abnormal menstrual bleeding and an increased risk of uterine cancer)
.ovarian fibromas, granulosa cell tumors are the M.C sex cord stromal tumors (granulosa cell tumors may present as a large
pelvic mass or with pain due to torsion/hemorrhage)
.they are solid ovarian tumors composed of stromal cells
.they are present in older women often with torsion due to the heaviness of the ovary / They often present post-menopause
with manifestations of excess estrogen production such as post-menopausal bleeding (the peak incidence is around the
menopause)
+Pts. may present with Meigs syndrome (pleural effusion, ascites, ovarian fibroma)

+Other ovarian cysts (fimbrial cysts, paratubal cysts)

+Other uncommon (cysts of morgagni)
+Tumor Markers Used In Ovarian Carcinoma :
.Ca 125 (epithelial ovarian cancer- serous)
.Ca 19-9 (epithelial ovarian cancer – mucinous)
.inhibin (granulosa cell tumors)
.androgens (sertoli-leydig)
.LDH (dysgerminoma)
.beta-hCG (choriocarcinoma)
.AFP (yolk sack, teratoma)
.AFP + beta-hCG (embryonal cell)
+Causes Of Elevated CA-125 :
.age influences reliability of test as a tumor marker
.in early stage ovarian cancer and uterus
.pancreas, stomach, colon, rectum cancers
.benign ovarian neoplasm, endometriosis, pregnancy, fibroids, PID
.cirrhosis, pancreatitis, renal failure

*Malignant Ovarian Tumors

.in women >50yrs, more than 50% of ovarian tumors are malignant
.4th leading cause of cancer death
.65% epithelial; 35% non-epithelial
.5-10% of epithelial ovarian cancers are related to hereditary predisposition
35

.the first line of treatment for ovarian cancer is surgery

.bilateral / asymptomatic mass / more common post menopause / have a good prognosis after treatment
.ovarian cancer is the 2nd M.C gynaecological malignancy and the major cause of death from a gynecological cancer
Page

+Mean age of presentation is 64yrs / Ovarian cancer is rare in young women

+Ovarian cancers are derived from the ovarian epithelium
+Epithelial ovarian cancer is due to malignant transformation of the ovarian epithelium
-Risk Factors :
.nulliparity
.intrauterine device
.endometriosis
.cigarette smoking (mucinous tumors)
.obesity
+Decreased risk of ovarian cancer (multiparity, OCP, tubal ligation, hysterectomy, pregnancy)
+Genetic factors in ovarian cancer (BRCA1 ‘breast ovarian cancer syndrome’, BRCA2, HNPCC-lynch syndrome ‘is hereditary non-
polyposis colorectal cancer’ and is associated with endometrial cancer)
-Treatment (gentic testing for BRCA1 and BRCA2) (prophylactic – bilateral salpingo-oophorectomy)
-Classification Of Ovarian Cancer :
.primary ovarian tumors can originate from the epithelium, the connective tissue of the ovary (sex cord stromal) or the germ
cells
.the ovary is a common site for metastatic tumors (krukenberg tumors)
.common sites (colon, stomach, breast)
.epithelial tumors of the ovary can be benign, malignant or borderline
.the majority of borderline tumors are serous, mucinous borderline tumors may arise from the large bowel (appendix) and can
be associated with pseudomyxoma peritonei
-Classifications Of Malignant Ovarian Tumors :
.epithelial ovarian tumors (serous, mucinous, endometrioid, clear cell)
.sex cord stromal (granulosa cell, sertoli-leydig, gynandroblastoma)
.germ cell tumors (dysgerminoma, endodermal sinus, teratoma, choriocarcinoma)
.metastatic (krukenberg tumors) (the primar lesion of Krukenberg ovarian tumor is commonly in stomach)
+Malignant Germ-Cell Tumors (usually children and young women <30yrs)
.dysgerminoma (LDH, 10% bilateral)
.immature teratoma (NO tumor marker identified)
.yolk sac tumor (produces AFP, unilateral)
.embryonal (produces AFP and beta-hCG)
.carcinoma(Rare)
.choriocarcinoma(produces beta-hCG)

*Epithelial Ovarian Cancer EOC

+May be benign, malignant or borderline
-Types :
.serous (M.C ovarian tumor, 50% of all ovarian cancers, 75% of epithelial tumors, 70% benign) (25% bilateral)
.mucinous (85% benign, 20% of epithelial tumors) (complicated by Pseudomyxoma peritoneii)
.endometrioid (20% of epithelia ovarian cancer, high malignant potential)
.cleat cell (<1% of epithelial ovarian cancer, high malignant potential)
.brenner tumor (<1% of epithelial ovarian cancer, majority benign)
-Signs & Symptoms :
.persistent pelvic and abdominal pain
.increased abdominal size/persistent bloating
.difficulty eating and feeling full quickly
.change in bowel habit
.urinary symptoms
.backache
.irregular bleeding and fatigue
-Examination And Investigations :
.pelvic and abdominal examination may reveal a fixed, hard mass arising from the pelvis
.ascites (presence of it, a diagnosis of ovarian cancer is highly likely)
.chest examination and chest X-ray (to assess pleural fluid)
.examination of the neck and groin (for enlarged nodes)
.full blood count, urea, electrolytes
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.liver function tests

.any suspected pelvic tumor should have measurement of tumor markers (Ca 125 is the M.C and elevated in 80% of EOC)
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.ultrasound (most useful non invasive test of a suspected malignancy), CT scan, MRI, barium enema, colonoscopy
-Differential Diagnosis :
.non-EOC ovarian cancer
.tubo-ovarian abscess
.endometriosis or fibroids
-Management :
.surgery (a total abdominal hysterectomy and bilateral salpingo-oophorectomy)
.chemotherapy (combination of a platinum compound with paclitaxel) (if a Pt. unfit or unwilling to have surgery, chemotherapy
can be given as primary treatment)

+Primary Peritoneal Carcinoma PPC

.arises from the peritoneal lining
.this tumor type is histologically indistinct from serous ovarian carcinoma
.criteria for diagnosis, includes (normal sized ovaries, more extra-ovarian disease, mainly serous histology, low volume
peritoneal disease)
+Fallopian Tube Carcinoma
.is a rare cancer
.the clinical diagnosis, investigation and treatment of fallopian tube cancer is the same as for EOC

**Malignant Disease Of The Uterus

-Endometrial cancer is now the M.C gynecological malignancy worldwide and the 4th M.C female cancer after breast, colon and
lung
+The M.C type of cancer affecting the uterus is adenocarcinoma
+The mean age of diagnosis is 54 (can be diagnosed in women throughout their reproductive life – Majority are diagnosed in
early stage due to detection of symptoms) (endometrial carcinoma is M.C in >60yrs)
-Types :
.endometrioid adenocarcinoma (estrogen dependent, occur in younger women and have a good prognosis)
.serous papillary carcinoma – serous, clear cell carcinomas (non-estrogen dependent, occur in elderly women and have a much
poor prognosis)
+Clinical features of Type 1 (postmenopausal bleeding in majority, abnormal uterine bleeding in majority of affected pre-
menopausal women ‘menorrhagia, intermenstrual bleeding’)
+Clinical features of Type 2 (may not present with bleeding in early stage, more likely to present with advanced stage disease
with symptoms like ovarian cancer ‘bloating, bowel dysfunction, pelvic pressure’)
+Malignancy can arise from the stroma or myometrium (sarcoma)
-Signs & Symptoms :
.abnormal vaginal bleeding (M.C)
.postmenopausal bleeding PMB or irregular vaginal bleeding (90% of Pts. present with this symptoms)
+In advanced cancer, Pts. may present with evidence of fistula, bony metastases, altered liver function or respiratory symptoms
+Very rarely, endometrial cancer can be diagnosed by the presence of abnormal glandular cytology at the time of a cervical
smear
+An endometrial thickness of 5mm or more is considered abnormal in a postmenopausal woman with vaginal bleeding
-Risk Factors :
+Type 1
.advanced age
.PCOS
.use of hormone replacement therapy HRT (unbalanced HRT) - anovulation
.cancer (ovarian, breast, colon)
.obesity / DM
.high circulating levels of estrogen
.diabetes
.nulliparous
.low parity
.adenomatous hyperplasia (Estrogen drugs can cause endometrial hyperplasia) (M.C symptoms of endometrial hyperplasia is
vaginal bleeding)
.late menopause >52 yrs
.unopposed estrogen therapy (excess estrogen)
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.estrogen-producing ovarian tumors (granulosa cell tumors)

.tamoxifen therapy (SERMs) (used to prevent recurrent breast cancer by blocking estrogen receptors in the breast)
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.family history of colorectal or ovarian cancer

.HNPCC (hereditary non-polyposis colorectal cancer) / Lynch 2 syndrome
+Type 2
.not estrogen related (possibly tamoxifen)
+Carcinoma of the uterus is the M.C gynecological malignancy / The majority of cancers present with stage 1 disease, overall
five-year survival is 80% / Hyperestrogenic states and obesity play a major etiological role
+The M.C genetic link is with hereditary non-polyposis colorectal cancer syndrome (HNPCC)
+HNPCC (is associated with colorectal, ovarian, endometrial and urothelial tumors)
+OCP or progesterone only pill and smoking (anti-estrogen effects of tobacco) reduces the incidence of endometrial cancer
-Daignosis :
.blood may be noted arising from the cervix
.bimanual examination (enlarged uterus)
.ultrasound
.endometrial biopsy (Best)
.hysteroscopy + D&C
.transvaginal ultrasound scans TVS
.MRI
+The best preoperative test to look for metastases is CXR
-Management :
.surgery (stage 1 disease, surgery is the M.C treatment for endometrial cancer) (The standard surgery is total hysterectomy,
bilateral salpingo-oophorectomy BSO) (Hysterectomy is the primary mode of treatment for endometrial carcinoma)
.post-operative radiotherapy

+Spread
.M.C is direct extension
.lymphatic spread to pelvic and para-aortic nodes
.hematogenous spread (usually to lungs, liver)

*Sarcomas Of The Uterus (Uterine Sarcoma)

-These are rare tumors
+Arise from stromal components (endometrial stroma, mesenchymal or myometrial tissues) and behave more aggressively and
are associated with poorer prognosis than endometrial carcinoma
-Signs & Symptoms :
.bleeding (vaginal bleeding is M.C symptom)
.abdominal distension
.foul smelling vaginal discharge
.pelvic pressure
-Types :
+Carcinosarcoma (mixed mullerian mesodermal tumor)
.M.C type of uterine sarcoma
.both epithelioid and sarcomatoid malignant elements are present
+Leiomyosarcoma
.when occurs, often coexists with benign leiomyoma (fibroids)
.leiomyosarcoma arise within a fibroid (sarcomatous degeneration)
.average age of presentation is 55 yrs but may present in pre-menopause
.often diagnosed postoperatively after uterus removed for presumed fibroids
.treatment (hysterectomy / BSO / chemotherapy may be used if tumor has spread beyond uterus)
+Endometrial stromal sarcomas ESS
.ESS typically occur in perimenopausal women between 45-50yrs and presenting with irregular bleeding (ABNORMAL UTERINE
BLEEDING) and a soft, enlarged uterus
.diagnosed by histology of endometrial biopsy or D&C
.treatment (hysterectomy / BSO) (always remove ovaries as ovarian hormones may stimulate growth)

**Premalignant And Malignant Disease Of The Cervix

*Benign Cervical Lesions
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.nabothian cyst / inclusion cyst (no treatment required)

.endocervical polyps (treatment is polypectomy)
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+M.C benign neoplasm of the cervix and endocervix is Polyps

*Malignant Cervical Lesions
.majority are squamous carcinoma (95%), adenocarcinoma increasing (5%), rare subtypes include small cell, adenosquamous
.average age (53yrs old)
-Signs & Symptoms :
.post-coital bleeding (pain during intercourse) (1st sign)
.in the early stages of the disease there are no symptoms
.squamous cell carcinoma SCC (95%)
.adenocarcinoma (5%)
.vaginal discharge (initially watery, becoming brown or red)
.bleeding (post-coital, postmenopausal, irregular bleeding, intermenstrual)
.pelvic or back pain
.bladder / bowel symptoms
.friable, raised, reddened or ulcerated area visible on cervix
-Causes :
.at birth, vagina is lined with squamous epithelium; columnar epithelium lines only the endocervix and the central area of a
ectocervix (original squamocolumnar junction) (the lining of cervical erosion is Columnar epithelium)
.during puberty, estrogen stimulates (ectopy)
.the exposing it to the acidic pH of the vagina, leading to metaplasia (change of exposed epithelium from squamous to
columnar)
.the transformation zone TZ is the area located between the original and the current squamocolumnar junction
.the majority of dysplasias and cancers arise in the TZ of the cervix
.must have active metaplasia in presence of inducing agent HPV to get dysplasia
.metastasis occurs late
-Risk Factors :
.HPV infection (high risk of neoplasia associated with types 16,18) (low risk of neoplasia associated with types 6, 11)
.smoking
.high risk behaviours (risk factors for HPV infection, include; multiple partners, other STIs-HSV-trichomonas, early age first
intercourse, high risk male partner)
+In case of cervical carcinoma in old woman, the treatment of choice is Hysterectomy
+Papanicolay (Pap) smear is recommended for cervical cancer screening
+Pap smear and follow up is best management of asymptomatic cervical erosion in pregnant Pt.

*Premalignant Disease Of The Cervix

-Human papillomavirus HPV infection leads to premalignant change in the cervical epithelium (cervical intraepithelial neoplasia
CIN) (Cervical cancer and CIN is caused by HPV infection)
-Causes :
.human papilloma virus HPV (is a sexually transmitted infection spread by skin-to-skin contact during intercourse – condoms fo
not protect from infections)
.smoking
+HPVs are a large family of over 100 different virus types (types 6 and 11 cause vaginal warts) (types 16, 18, 31 and 33 have
oncogenic, cancer-causing properties)
+Colposcopy is used for both diagnosis and treatment)

*Malignant Disease Of The Cervix

-Most cervical cancers, are frable, vascular masses on the cervix and are likely to produce a number of complaints (post-coital
bleeding, intermenstrual bleeding, post-menopausal bleeding, blood stained vaginal discharge)
-Signs & Symptoms :
.pain (malignant infiltration of the spinal cord)
.incontinence (due to vesicovaginal fistula)
.anemia (chronic vaginal bleeding)
.renal failure (from ureteric blockage)

**Conditions Affecting The Vagina And Vulva

-The vulva is term used to describe the external female genitalia – The sexual organs
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-Includes :
.labia majora
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.labia minor
.clitoris
.fourchette
-The labia minora and majora are covered with keratinized, pigmented, squamous epithelium
-The normal vulva vestibule is covered with non-keratinized, non-pigmented squamous epithelium and is devoid of skin adnexa
-Investigations :
.keyes punch biopsy
-Differential Diagnosis Of Vulvar Complaints :
+Vulvar pruritus
.infections (candidiasis, trichomonas vaginalis)
.skin conditions (lichen sclerosis, eczema, VIN)
.contact dermatitis
+Vulvar pain
.infections (candidiasis)
.skin conditions (lichen sclerosus, eczema, VIN)
.vulvodynia
+Superficial Dyspareunia
.skin conditions (lichen sclerosis, eczema, VIN)
.vulvodynia
.vulvar fissures
.skin bridges of the vulva
+Microbiological swabs may be indicated to exclude infection as a cause of vulvar symptoms (candida an trichomonas vaginalis
can cause vulvar itching, herpes simplex may cause vulvar ulcers)

*Benign Conditions
+Lichen Sclerosis
-Is a destructive inflammatory skin condition which affects mainly the anogenital area of women
-Many Pts. have other autoimmune conditions, such as (thyroid disease, pernicious anemia)
-This lead to a fragility and white ‘parchment paper’ appearance of the skin and loss of vulval anatomy
-Signs & Symptoms :
.itching
.soreness of the vulva (scratching)
.splitting of the skin
.superficial dyspareunia
.on examination of the skin (whitening, fissuring and loss of anatomy)
-Diagnosis :
.biopsy
-Management :
.combination of good skin care and strong steroid ointments (Dermovate)
+Lichen Sclerosis is associated with vulval cancer, but is not a cause
(Many women with vulval cancer have lichen sclerosis at the time of diagnosis and it is estimated that there is a low risk of
cancer developing in a women with lichen sclerosis)
+Vulvodynia
-Describes a group of women with vulvar discomfort, most often described as a burning pain, occurring in the absence of skin
disease or infection, it is akin to a neuropathic pain syndrome
-Some Pts. have a spectrum of disease. Some Pts. have continuous burning, some have sexual pain only and some have both.
The cause is not known
-Clinical examination is normal, although some Pt. Have touch sensitivity – So called allodynia
+Genital Herpes Simplex
-M.C.C of reported vulval ulceration / Two types (1-2) are responsible for both oral and genital ulceration with increasing
numbers of genital infections being caused by type 1 (primary or secondary infection)
-Typical history of therapeutic illness is (irritation or paraesthesia at the site of the lesions, appearance of painful papules) (The
ulcers are often multiple, shallow-based, flat and small)
-Causes Of Vulvar Ulcers :
.trauma
.behcet's syndrome
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.crohn's disease
.fixed drug eruptions
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-Management :
.antiviral agents – acyclovir 200 mg orally (in the acute phase)
.suppression therapy should be considered with long-term acyclovir (in recurrent herpes)
+Benign Cysts Of The Vulva
-Bartholin's cyst is the M.C type of cyst and develops in the region of the Bartholin`s gland

*Vulval Intraepithelial Neoplasia VIN

-Is a premalignant skin condition which is increasing in incidence
-VIN associated with human papilloma viruses HPV or lichen sclerosis
-HPV associated VIN can occur in pre-menopausal women and lichen sclerosis-associated HPV in older, often post-menopausal
women
-The clinical presentation is variable with either pain and/or pruritus (the vaginal area can also be affected – called vaginal
intraepithelial neoplasia VAIN)
-Biopsy is essential for diagnosis
-Treated by surgical excision of the area

*Vulvar Cancer
-Is uncommon cancers / Most vulvar cancers are squamous cell cancers of the skin
+The etiologic agent for vulvar vancer is Unknown
+A blue swelling on the vulva is most likely due to Varicosity
-M.C sites are the labia majora and clitoris (tumors may be uni- or multifocal)
-Vulvar cancer spreads regionally to the groin nodes (inguinal and femoral)
-These are skin tumors of the vulva and are divided into :
.HPV associated (usually younger Pts.)
.non-HPV (usually older Pts.)
.cancer associated with VIN and lichen sclerosis
-Signs & Symptoms :
.pruritus (M.C symptom in elderly woman)
.lump (noticed when washing)
.vulval pain (some tumors are ulcerating)
.postmenopausal bleeding (some tumors bleed on touch)
.most tumors are small on examination
.cauliflower-type growth
.ulcerate and may produce a subtle skin thickening
-Investigations :
.biopsy (is essential for diagnosis)
.CXR (is useful to exclude obvious lung metastases)
-Management :
.surgery (excision of the primary site and removal of the groin lymph nodes)

*Vaginal Disease
-This is a rare cancer
+The M.C histopathological finding in primary carcinoma of the vagina is Squamous cell carcinoma
-The main vaginal problem is infection – Bacterial (bacterial vaginosis), Fungal (candida albicans), Protozoal (trichomonas
vaginalis)
-Infections can produce vaginal inflammation and discharge
-The cause remains unknown, although the risk factors are likely to be similar to cervical cancer
-The disease frequently presents at an advanced stage in the absence of symptoms with early disease. When the disease
becomes symptomatic vaginal bleeding and discharge are the presenting features
-The diagnosis is with a vaginal biopsy / Surgery is rarely an option as the disease is advanced and radiotherapy and
chemotherapy are usually first-line treatments
-Disease progression is usually local and, in the advanced stages of the disease. Pts. may develop symptoms that are difficult to
palliate, such as rectovaginal and vesicovaginal fistula
+Benign Vaginal Lesions
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.inclusion cysts
.endometriosis
.gartner`s duct cysts
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.urethral diverticulum (can lead to recurrent urethral infection, dyspareunia)

+Malignant Vaginal Lesions
.risk factors (associated with HPV infection, increased incidence in Pts. with prior history of cervical and vulvar cancer)
+Squamous Cell Carcinoma SCC
.80-90% of vaginal cancer
.M.C site is upper 1/3 of posterior wall of vagina
.clinical features (asymptomatic, painless discharge and bleeding, vaginal discharge, foul-smelling, vaginal bleeding especially
during/post-coitus, urinary and/or rectal symptoms)
.treatment (hysterectomy/upper vaginectomy/chemoradiation therapy)

+Adenocarcinoma
.most are metastatic, usually from the cervix, endometrium, ovary or colon
.2 types (non-DES, DES syndrome)
.management as for SCC
+Diethylstilbestrol (DES) syndrome
.DES exposure associated with malformations of upper vagina, cervix and interior of uterus, cervical collar and pseudopolyps of
cervix
+Fallopian Tube
.least common site for carcinoma of female reproductive system
.usually adenocarcinoma
.clinical features (watery vaginal discharge, pelvic pain, vaginal bleeding)
.most Pts. present with a pelvic mass

+Postmenopausal Bleeding
-Can only occur 6 months after the cessation of menses
-Causes Of PMB :
.polyps
.endometrial atrophy (because of lower estrogen levels), atrophic vaginitis
.endometrial hyperplasia (obesity)
.endometrial cancer (uterine cancer), cervical cancer, ovarian tumor
.hormone therapy (estrogen therapy)
.infection of the uterine or cervix
.urinary lesions
.GI lesions
.prolapse of the uterus
.certain medications such as (blood thinners)
+Is managed primarily by D&C

+Physiologic processes that are estrogen dependent in women include :

.menses
.vaginal cornification
.appearance of axillary hair
.production of cervical mucus

+Structures are included in the term vulva :

.clitoris
.urethral orifice
.labia minora
.bartholin’s glands
+The nerve supply to the vulva is derived from :
.the pudendal nerve
.the ileo-inguinal nerve
.the genito-femoral nerve
.the posterior cutaneous nerve to the thigh

+The lining epithelium of the vagina is (Stratified squamous epithelium)

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+The uterine artery is a branch of (Internal iliac artery)

+The best support to the uterus is by (Cardinal ligament)
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+The round ligament of the uterus terminates in (Upper portion of labium majus)
+The left ovarian vein empties in (Left renal vein)
+The most inner part of a mature Graafian follicle is (Zona pellucida)
+Maximal number of germ cells in the ovary occurs at (22 weeks of intrauterine life)
+Ovarian failure causes atrophic changes in :
.uterus
.vagina
.bone
.rectum

Dr.Mohammad Z. Abu sheikha@

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