Professional Documents
Culture Documents
Gyne
Gyne
1
Page
**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
2
-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
3
+Deep
.endometriosis
Page
.adenomyosis
.leiomyomata/fibroids
.PID
.hydrosalpinx
.TOA
.uterine retroversion
.ovarian cyst
-Complications :
Page
.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
5
*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
6
**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 :
7
+Estrogen Dependent Diseases (estrogen receptor ER + progesterone receptor PR + androgen receptor AR) :
.breast cancer
.endometrial cancer
.endometriosis
.adenomyosis
*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
8
*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
9
11
Page
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)
*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)
12
-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
**Disorders Of Menstruation
+Hypomenorrhea (bleeding that is decreased in amount)
Page
*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
+Kallmann Syndrome
.primary amenorrhea
Page
+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
.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)
**Infertility
-Is defined as inability to achieve pregnancy after 12 months of unprotected and frequent intercourse
17
+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
*Male Factors
-Causes :
.varicocele
.idiopathic
.obstruction
.cryptorchidism
.immunological
-Investigations :
.semen analysis and culture
.post-coital (Huhner) test (rarely done)
*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)
*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
**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
*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
**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)
.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
*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
**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
-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
.post-coital spotting
.mild pruritus
Page
-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
*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
.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
+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
.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
*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)
.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)
.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)
Page
+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)
.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)
+Spread
.M.C is direct extension
.lymphatic spread to pelvic and para-aortic nodes
.hematogenous spread (usually to lungs, liver)
-Includes :
.labia majora
Page
.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
40
.crohn's disease
.fixed drug eruptions
Page
-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
*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
41
.inclusion cysts
.endometriosis
.gartner`s duct cysts
Page
+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
+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
43
Page