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Contributors
Ayah M Boudal, medical student 2008
Development and Congenital Abnormalities of the Reproductive System, The anatomy of
female genital tract, Ovulation, Fertilization, Implantation and the Placenta.
Badr Rajb, medical student 2008
The menstrual cycle.
Dalal Al-Omar, medical student 2008
Miscarriage (Abortion), Pap smear.
Elham Algethami, medical student 2008
Renal disease in pregnancy.
Faisal Al-Gaows, medical student 2008
Infertility.
Jameel Khalid Rasheedi (Dr.JKR), medical student 2008
Amenorrhea.
Mohammad Bokhary, medical student 2008
Normal Labor, Diabetes Mellitus during Pregnancy.
Nedaa bhkali, medical student 2008
Development and Congenital Abnormalities of the Reproductive System, The anatomy of
female genital tract, Ovulation, Fertilization, Implantation and the Placenta.
Roa'a Mursi, medical student 2008
Premature Rupture of Membranes, Preterm Labour (PTL).
Salman Jan, medical student 2008
Ob/Gyne Instruments, Gestational Trophoblastic Disease-GTD.
Sameerah Albugami, medical student 2008
Bleeding in 3
rd
Trimester (Antepartum Hemorrhage).
Wafaa Al-Ahmadi, medical student 2008
Abnormal Labor & Delivery, Intrauterine Fetal Death (IUFD), Intrauterine Growth Restriction
(IUGR),Pelvic Mass, Pelvic pain, Ovarian cancer, Cervical cancer, Induction & augmentation of
labour, Postpartum Hemorrhage (PPH).
Design and production:
Jameel Khalid Rasheedi (Dr.JKR)
Suheab Abdulhamaid Maghrabi
With participate of
Iman Hani
C o n t e n ts
G Y N E C O L O G Y
The anatomy of female genital tract .1
Development and Congenital Abnormalities of the Reproductive System ..8
The menstrual cycle.12
-Premenstrual Syndrome (PMS).16
Pelvic Mass...17
Pelvic pain24
Amenorrhea .29
Infertility ..37
Ovarian cancer..41
Cervical cancer.46
Gestational Trophoblastic Disease-GTD.51
O B S T E T R I C S
Ovulation, Fertilization, Implantation and the Placenta..57
Diabetes Mellitus during Pregnancy....67
Renal disease in pregnancy...72
Bleeding in 3rd Trimester (Antepartum Hemorrhage).. ... 75
- Placenta previa 75
- Abruptio placenta 76
- Vasa previa..80
Miscarriage (Abortion) 81
Intrauterine Fetal Death (IUFD).83
Intrauterine Growth Restriction (IUGR)86
Normal Labor & Dystocia91
Induction & augmentation of labour96
Abnormal Labor & Delivery .100
- Labor Dystocia.100
- Malpresentation...102
-- breech: . .102
--- External cephalic version (ECV) ..102
-- Transverse (shoulder presentation) or oblique ...103
-- Other malpresentation103
- Intrapartum complications:..104
-- Shoulder dystocia104
-- Cord prolapsed 105
-- Other congenital neurological birth injuries 105
-- Intracranial hemorrhage ..105
Preterm Labour (PTL)106
Premature Rupture of Membranes.111
Postpartum Hemorrhage (PPH)115
Pap smear118
Ob/Gyne Instruments121
The anatomy of Female Genital Tract
Prepared by: Ayah M. Boudal ,and Nedaa bhkali
Source: Tareg arab sheets
The perineum is the inferior boundary of floor of the pelvis .
Bounded : Levator ani (superior)
Skin of thighs (inferior)
Extends : Symphyisis pubis and inferior borders of pubic bones (anteriorly)
Limited by ischial tuberosities , sacrotuberous ligaments and coccyx (posteriorly)
- The superficial and deep transverse perineal muscles cross the pelvic outlet between
the ischial tuberosies , and oin at the perineal body.
- They divide the outlet into urogenital triangle anteriorly and anal triangle posteriorly .
Urogenital triangle :
- Anterior to the anal triangle
- Bounded by the symphyisis and pubic rami .
Anal triangle :
- Posterior to the urogenital triangle
- Bounded by the ischial tuberosities , sacrotuberous ligaments and coccyx
The perineal body lies between the anal canal and the lower third of the vagina .
Urogenital diaphragm : pierced by the following structures :
- Vagina - Internal pudendal vessels
- Urethra - Dorsal nerve of clitoris - Artery of bulb
Inferior surface : Crura of clitoris Superficial
Perineal muscles
Vestibular bulbs
Bartholin glands
The transverse perineal muscles (profunda and superficialis ) form the perineal body. This is important
because often it is cut to facilitate birth.
Types of pelvis :
1- Gynecoid : t.d > ap.d , round inlet, classical female pelvis 60%
2- Android : typical male < 30%
3- Anthropoid : < 20% ap >> t.d (oval)
4- Platy pelloid : 3% ap<< t.d (oval)
Nerves of the pelvis :
Branches of the sacral plexus, which lies on the posterior pelvis wall in front of piriformis muscle.
- Branches to the pelvic muscles, viscera, perineum :
Pudendal nerve (S2,S3,S4) : external anal sphincter, mucous membrane of lower half anal
canal , perianal skin, clitoris , labii majora and minora .
Nerves to piriformis
Pelvic splanchnic nerves (S2,S3,S4) : sacral part parasymp
system
Perforating cutaneous nerve : supplies skin of lower medial
buttocks
- Branches to lower limb via greater sciatic foramen :
Sciac nerve (L4,L5,S1,S2,S3)
Superior gluteal nerve : gluteus medius , minimus and
fasciae lata
Inferior gluteal nerve : supplies gluteus maximus
Nerve to quadrates femoris
Nerve to obturator internus muscle
Posterior cutaneous nerve of the thigh
Blood supply of the pelvic organs :
Ovarian , internal iliac , and superior rectal arteries and veins
Lymphatic drainage :
Vulva and lower vagina : iguino-femoral lymph nodes to the external iliac nodes
Cervix : (Via the cardinal ligaments) pelvic nodes to the common iliac and para-aortic nodes
Endometrium : Via the broad ligament to pelvic and para-aortic chains
Ovaries: Via the infundibulo-pelvic ligaments to pelvic and aortic nodes
- Known as the vulva or pudenda
- Innervated by pudendal nerve
- Anterior to the vulva,innervations by ilioinguinal and genitofemoral nerves
Consists:
Mons pubis (target of testosterone, site of pubic hair )
Labii (majora) rich blood supply , hairy
Labia (minora) , posterior folds attach inferior surface clitoris , ant form prepuce , hairless
Clitoris (in front of urethra , consists glands,body,crura)
Bartholin`s gland (columnar epithelium) . Cyst forms if duct blocked
Furchette (where the minora attach ). Posterior portion of the vestibule above the perineal
body. Dimple in fossa implies no prev. pregnancy
Urethra
Paraurethral glands
Hymen-single opening , cryptiform,linear,imperforated
Corniculae myritiformes : hymen tags after birth
- Extends from hymenal ring to the fornices around the cervix
- Non keratinised stratified sq. epithelium
- Blood is supplied by the vaginal artery from the internal iliac
artery
- No mucous glands or hair follicles
- Adenosis occurs if exposure (gestational) to DES
- Inner circular and outer longitudinal muscle coats
- 8 cm in length adult
- Immediate proximity of posterior fornix to the pouch of
Douglas
- The pH of the vagina is 4.5 and is due to Doderlein`s bacillus,
which breaks down glycogen to lactic acid
- Surrounded by 3 layers : - visceral peritoneum
- Myometrium
- Endometrium
- Normally anteverted and antiflexed
- Blood is supplied via the uterine artery from the internal iliac artery
- Cervix and uterine corpus , joined by the isthmus
- Isthmus is where the endocervical epithelium changed to the endometrial lining
- Endometrial lining varies from 2-10 mm thick
- Isthmus is lower uterine segment in pregnancy
- 2-3 cm length (cervix)
- At the external cervical os, the squamous epithelium changed to simple columnar (squamocolumner
junction)
- Four paired sets of ligaments are attached :
- Round ligaments : extending between the labium majus and the anterior aspect of the uterus (in
front of the Fallopian tube)
- Uterosacral ligaments : condensation of endopelvic fascia , which
insert into the posterior-inferior portion of the uterus at the level of the isthmus.
The round ligament in IN
FRONT of the broad ligament
- Cardinal ligaments : extending from the pelvic fascia on the lateral walls and inserting into the
lateral portion of the cervix and vagina.
- Pubocervical ligaments : passing around the anterior of the bladder to the posterior aspect of
the symphysis pubis.
* For support the UTEROSACRAL ligaments and CARDINAL ligaments are the most important in preventing
prolapsed.
- Four peritoneal folds :
1-Vesicouterine fold (anterior), from the isthmus to the bladder
2-Rectouterine fold (post), from the posterior wall of the uterus to the rectum
* The pouch of Douglas lies between the two folds
3-Broad ligaments (laterally, paired), from the side of the uterus to the lateral wall of the pelvis.
4-The mesosalpinx is the fold containing the fallopian tube
- 10 cm in length
- Enclosed in the medial 4/5ths of the superior aspect of the broad ligament
- Segments : - interstitial
- Isthmus
- Ampullary (most common site of ectopic pregnancy)
- Fimbriated portion
- Ciliated columnar epithelium
- Uterine and ovarian arteries supply blood
- 3 by 2 by 2 cm
- The only intrabdominal structure not covered by peritoneum
- Located on the superior surface of the broad ligament, suspended between the ovarian ligament
(medially) and the suspensory ligament (laterally and superiorly)
- Found in the ovarian fossa of Waldeyer), which is lateral to the pelvic walls , anterior to the ureter
and hypogasteric vessels and posterior to the external iliac vessels
- Blood supply : long ovarian arteries from the abdominal aorta , below the renal arteries
- Veins : right ovary drains to the inferior VC , the left ovary drains to the left renal vein
- 25-30 cm from renal pelvis to the bladder
- Cross under the ovarian vessels , in front of the bifurcation of the
common iliac artery
- Located in the true pelvis, anterior to the hypogastric vessels , on
the side of the cervix and beneath the uterine artery (remember
: water under the bridge ).
- It run close to the internal vaginal fornix and passes to the
trigone of the bladder.
**Please refer to OB/GYN recall for more illustrations
Development and Congenital Abnormalities of the
Reproductive System
Prepared by: Ayah M Boudal & Nedaa bhkali
Source: Tarek Arab sheets
Embryological development of the ovary
Thickening of the peritoneal epithelium on the ventro-medial surface of urogenital ridge
occurs,thus a genital ridge is formed , parallel to mesonephric ridge.
5
th
week, sex cord formed
The primitive gonad is of multiple origin ( coelomic epithelium of the genital ridge , the
underlying mesoderm and primitive germ cells)
3 weeks gestation , primordial germ cells appear mixed with other cells in the endoderm
of the yolk sac wall of the primitive hindgut
At 8 weeks, it is contained in the undierenated urogenital ridge. Proliferaon results in
formation of oogonia that are incorporated into sex cords.
First evidence of follicles is seen at 20 weeks, granulose cells (coelomic epithelium) and
theca cells (mesenchymal origin) are evident . There are 200,000 follicles present at 20
wks and 300,000 present at 7 yrs of age.
Regression of primary sex chords results in formation of the rete ovarii.
The paramesonephric (Mullerian) ducts are the source of the:
Upper vagina
Uterus
Fallopian tubes
Absence of a Y chromosome results in regression of the mesonephric system and development of the
paramesonephric .
M ducts develop at 2-4 wks at the genital ridge, terminate caudally by opening into urogenital
sinus , and open cranially at a point to become tubium osteum
At 6 weeks gestaon . a groove forms in the coelomic epithelium of the paired urogenital ridges.
The two ducts fuse at the urogenital septum , forming the uterovaginal primordium . The distal
point of fusion in known as Muller`s tubercle .
Dissoluon of the septum between the 2 ducts leads to a single uterine fundus.
Degeneraon of mesonephric ducts from 10-16 weeks.
Derivatives:
Adjacent mesenchyme gives the : Myometrium & endometrium
Paramesonephric duct gives the : Glandular epithelium of fallopian tubes,uterus,cervix
At 12-20
th
weeks, vaginal plate formation takes place from the endoderm of the
urogenital sinus (controversial).
Prior to week 7 , same appearance of male and female genitalia
Elongation of the genital tubercle into a phallus takes place in males
In female , differentiation of the urogenital membrane (ectoderm and endoderm) into
genital folds laterally (give rise to labia majora) and urogenital folds medially (give rise to
labia minora and prepuce of clitoris ) occures.
By week 12, the female genitals are evident
The hymen is perforated at birth time
Abnormal development of the ovaries
Uncommon
Duplication or absence of ovarian tissue may occur
Turner`s syndrome (45 XO) is associated with lack of gonadal development , thus streaked
primitive ovaries in this condition.
Anomalies of paramesonephric ducts and urogenital sinus
Anomalies of fallopian tubes , uterus , cervix , and vagina are uncommon and are caused by
teratogenesis , genetic inheritance and multifactorial expression.
Agenesis (lack of development)
Hypoplasia ( incomplete development)
Atresia ( incomplete canalization)
Completely separate development
Variations of extent and level of fusion
Fallopian tubes :
Aplasia or atraemia of the distal ampullary segment occurs , most commonly unilateral.
Complete duplication is rare , but distal duplication and accessory ostia are common.
Cervix and uterine fundus :
In Mullerian agenesis , complete lack of development of paramesonephric system occurs. Usually ,
incomplete development of the fallopian tubes is associated with absence of uterus , cervix and most
of the vagina.
Mullerian agenesis occurs in women who are normal karyotypic and phenotypic females.
More commonly include :
Imperforate hymen
Longitudinal and transverse vaginal septum
Vaginal atresia
Double vagina
Absence
Imperforate : least severe abnormality
Occurs at the site of vaginal plate formation.
Blocks menses
Transverse vaginal septum similar but allows menses because of a sinus or tract
Usually discovered on examination after intercourse impeded.
Atresia: Upper vagina and cervix affected if cranially
placed , uterine fundus +tubes unaffected
Double vagina : Midline longitudinal septum is present thus deformity. Associated with double
cervix
Agenesis : Most extreme vaginal
abnormality
The uterus is usually absent
Partial unilateral development of para mesonephric ducts : absence of ipsilateral kidney
Uterus didelphys , one of 2 vaginas exisng as blind pouch : renal agenesis on the side of
pouch
Mullerian agenesis : pelvic kidney, horseshoe shaped kidney , duplication of collecting system
Sexual ID in case of ambiguous genitalia :
Female pseudohermaphroditism :
Due to masculinisation in-utero, the infant presents with ambiguous genitalia
Enlargement of clitoris is the most conspicuous abnormality
Internal genital development is normal
Male pseudohermaphroditism :
If 46 XY, tescular feminizaon syndrome can result in development of external genitalia
like those of a female (X linked recessive disorder).
The disorder is not recognized until failure of menarche at puberty
Testes are undescended
External genitalia normal on exam , but scanty pubic hair
True hermaphroditism :
Rare
Dual development of testes and ovaries
Usually 46 XX
The Menstrual Cycle
Prepared by: Badr Rajb (edited by Wafaa Al-Ahmadi)
Source: Obstetrics & Gynecology AT Glance + Tarek Arabs sheet
Definition
Menstrual refers to cyclic uterine bleeding experienced by most women of reproductive age.
Normal menstruation
Menarche before 16 years (average age at 12 years).
Menopause aer 40 years.
Menstruaon not more than 7 days (52 days).
Blood loss not more than 80 ml/day.
Cycle length 21-40 days (302).
No intermenstrual bleeding.
Hormonal changes of the menstrual cycle cause ovulation & induce changes that prepare tha
endometrium for implantation, should conception occur. Further changes are manifested in the cervix,
vagina, & breast.
For menstruation to occur, the hypothalamus-pituitary-ovarian axis must be intact.
Ovarian changes
Theres monthly increase in FSH which stimulates the growth of primordial follicles. One develops,
& ovulaon takes place on day 14 on the surge of LH.
Theres 3 phases of ovarian changes:
Follicular phase:
- Granulosa cells proliferate, with fluid filled spaces forming the antrum of the primary follicle.
Changes occur resulting in the formation of the vesicular follicle & finally the mature Graafian
follicle.
- The oocyte is enlarged, & surrounded by the zona pellucida & cumulus oophorus.
- Granulosa cell have FSH receptors that respond to FSH to produce E2.
- Theca cells (interna) are vascular & have LH receptors, producing androgens which stimulate
granulosa cells to secrete E2.
- High level of E2 cause ve feedback on LH & FSH.
- At mid-cyclic feedback is +ve on LH, thus a surge in LH concentration occurs, with subsequent
ovulation.
LH stimulate theca interna cells which secrete androgens ----- FSH + androgens stimulate granulosa cells
--------- producon of E2.
Ovulatory phase:
- The distended follicle ruptures, & the ovum is released into the peritoneal cavity the ovum is
surrounded by the zona pellucida & corona radiata.
- Swept into uterine tubes by fluid flow, caused by the beating cilia in fimbriae.
- The follicles enlarge, but if theres failure to ovulate, they degenerate into atretic follicles.
Luteal phase:
- Ruptured follicle fills with blood, forming corpus haemorrhagicum.
- Granulosa cells, theca cells, clotted blood replaced by lipid cells (luteal cells), thus the corpus
luteum is formed.
- Corpus luteum secretes E2 & progesterone.
- High E2 & progesterone impose ve feedback on LH & FSH.
- If pregnancy occurs, the corpus luteum changes to that of pregnancy, & no more cycles occur. If
pregnancy take place, the corpus luteum degenerates.
- An increase in FSH & LH take place in preparation for the next cycle.
Uterine changes
There are 3 phases:
Proliferative phase (pre-ovulatory):
- Takes place during follicular phase of ovarian cycle.
- High E2 causes rapid growth of the endometrium, epithelium, uterine glands. The glands are
NON-SECRETORY.
- Increased uterine blood flow.
- Increased contraction & excitability of the myometrium.
Secretory phase (post ovulation):
- Coincides with the luteal phase of ovarian cycle.
- Developed corpus luteum secretes predominantly progesterone, & estrogen in small amounts.
- Further changes in the endometrium, increased blood flow, edematous.
- Endometrial glands enlarge, coil, & become SECRETORY (glycogen, sugars, & amino acids).
- Deposition of the fats & glycogen in endometrial cells take place.
- Arteries prominent & coiled.
Menstrual phase:
- Occurs only if fertilization & implantation dont occur.
- If no implantation, no hCG is produced & therefore the corpus luteum regresses with a sharp
decrease in E2 & progesterone level.
- Reduction of endometrial tissue, & ischemia followed by necrotic foci giving subsequent spotty
hemorrhages which are manifest as menstrual blood flow.
- Menstruam (blood, tissue debris & ovum), accumulate in the uterine cavity, & is expelled by
uterine contractions.
- Blood containes brinolyc enzymes, & usually does not coagulate, thus it ows for 3-5 days.
Changes in the uterine cervix
a) Follicular phase increased E2: Mucus thin & alkaline.
b) Luteal phase increased progesterone: Mucous thick, tenacious, cellular.
Changes in vagina
a) Follicular phase increased E2: vaginal epithelium cornied.
b) Luteal phase increased progesterone: epithelial proliferation with leucocytes.
Cyclic changes in breast
a) Follicular phase increased E2: proliferaon of mammary ducts.
b) Luteal phase increased progesterone: growth of lobules & alveoli, swelling of breast &
tenderness.
Day 1 4: menstruation.
Day 5 13: proliferative phase.
Day 14 28: luteal/secretory phase.
Control of ovarian hormones:
Gonadotrophins (FSH. LH):
FSH from the anterior pituitary stimulate the growth of ovarian follicles.
FSH & LH are needed for final maturation of follicles.
LH surge at mid cycle causes ovulation & corpus luteum formation.
LH smulate secreon of E2 & progesterone from the corpus luteum.
Hypothalamic components:
Hypothalamus secrete GnRH in episodic bursts (60-120 mins) to smulate anterior pituitary to
secrete FSH & LH.
GnRH administration in continuous infusion results in down regulation of the receptors, & LH
secretion decreased to zero level.
GnRH administration episodically stimulates LH.
GnRH incresase GnRH decrease
Late follicular phase (due to +ve feedback of E2,
causes LH surge).
Secretory phase (because of progesterone)
At end of the cycle (due to ve feedback of E2 &
progesterone.
Negave feedback of E2 & progesterone
Feedback effects:
- Moderate levels of E2 inhibit both FSH & LH during early part of the cycle. Inhibin also inhibits
FSH.
- Rise of E2 36-48hrs before ovulaon causes +ve feedback on LH (LH surge). Ovulaon occurs 9 hrs
after LH peak.
- FSH peaks at mid cycle despite small rise in inhibin.
- During luteal phase LH & FSH are low because of elevated E2, progesterone & inhibin.
Control of the cycle:
- Prostaglandins causes regression of corpus luteum 3-4 days before menses.
- E2 & progesterone start to decrease, FSH & LH start to increase.
- New follicles develop under the effect of FSH & LH to ovulation & formation of corpus luteum.
- Rise E2, progesterone & inhibin with decrease both FSH & LH before luteolysis.
Clinical points:
Hormonal assays:
- To determine if ovulation occurred:
- Serum progesterone > 10 nmol/l indicate ovulaon has occurred.
- Blood should be drawn in the mid-luteal phase (day 21).
- The results can only be interpreted if a menstrual period occurs 7 days aer sampling.
PMS:
- These are clinical psychological, behavioral & physical symptoms starting at the luteal phase &
ending during menstruation.
- 95% women suer from it.
- Unknown etiology.
Clinical features:
- Tension.
- Breast pain.
- GIT upset.
- Depression.
- Loss of control
- Irritability.
- Aggression.
- Insomnia.
Pelvic Mass
Prepared by: Wafaa Al-Ahmadi
Source: On call obstetrics & gynecology + Toronto Notes 2008 + Approach to the Patient with a Pelvic
Mass (ptt) done by Lloyd D. Holm, D.O. (Associate Professor Department of Obstetrics and Gynecology
university o Nebraska medical center) + BPL management of pelvic mass - Done by group B 2008
The adnexa comprise the fallopian tubes, ovaries, & round ligaments.
Pelvic mass commonly arise from the adnexa & refered as adnexal mass.
Pelvic mass also can arise from the uterus as well as from organs other than reproductive
organs such as bladder & GI tract.
Differential diagnosis of an adnexal mass is vast & depend on the patients age.
Adnexal masses are uncommon in the premenarchal & post-menopausal patients, &
when they are encountered, malignancy should be suspected.
In contrast adnexal masses are commonly found in women in the reproductive age range
because the frequency of functional or physiological cysts (this cysts result from the
process of ovulation & usually resolve spontaneously.
Pressure/fullness
Pelvic pain
Abdominal pain
Abdominal distention
Dyspareunia
Vaginal bleeding
Urinary frequency
GI symptoms
Nausea.
Dyspepsia.
Obstipation (sever or complete constipation).
Painful bowel movement.
Differential diagnosis of pelvic mass
Gynecological:
Ovarian:
Functional cysts (always benign):
Corpus luteum cyst:
It could be discovered incidentally by obstetric
examination or annual examination.
Are approximately 4 cm in diameter & result from hemorrhage in the corpus luteum 2 or 3
days after ovulation? Because these cysts may rupture & result in intra-abdominal bleeding,
they can mimic tubal pregnancies. Rupture usually occurs late in the menstrual cycle & is
associated with acute abdominal pain, which usually lasts less than 24 hrs but may be present
for up to 1 week.
Follicular cyst:
The most common cystic masses found in the ovary. They result from either failure of the
mature follicle to ovulate or failure to an immature follicle to resorb or undergo atrasia. Most
follicular cysts are asymptomatic & range in size from several millimeters to 8 cm cysts.
Theca lutein cyst:
Developed from overstimulation of the ovaries by hCG. They are encountered in patients with
molar pregnancies & in those who undergone ovulation induction for infertility.
Hemorrhagic cyst
Polycystic ovary
Endometrioma:
It could develop in patients with endometriosis involving the ovaries.
These cysts are filled with old blood that has the appearance of chocolate,
& therefore, endometriomas are also called chocolate cysts.
Tube-ovarian abscess
Luteoma of pregnancy
Benign neoplasms:
Dermoid cyst most common
Malignant neoplasns:
Epithelial cell most common > 40 years
Germ cell most common < 20 years
Metastasis (e.g. Krukenberg tumor from gastric cancer)
Tubal:
Ectopic pregnancy.
Paratubal cysts:
Paratubale cyst are found adjacent to the fallopian tubes. They are predominantly
cystic & are asymptomatic unless they undergo torsion. Paratubal cysts found at the
fimbriated ends of the tube are also referred to as hydatid cysts of Morgagni.
Pyosalpinx/hydrosalpinx.
Primary fallopian tube neoplasms.
Uterine:
Intrauterine pregnancy
Adenomyosis of the uterus
Fibroid
Endometrial cancer
Leiomyosarcoma
leiomyomata
Imperforated hymen
Hematometra/pyometra
Congenital anomaly of the uterus:
Bicornuate uterus.
Rudimentary uterine horn.
Didelphic uterus.
Non-gynecological causes:
Gastrointestinal:
Appendiceal abscess
Diverticular abscess
Diverticulosis, diverticulitis
Carcinoma of the rectum/colon
Genitourinary:
Distended bladder (urinary retention).
Pelvic kidney.
Carcinoma of bladder.
Miscellaneous mass:
Abdominal wall abscess, seroma, or hematoma.
Retroperitoneal neoplasm.
Evaluation of pelvic mass
History:
Important historical points:
If the patient is pre-menarchal or post-menopausal?
Adnexal masses are most likely to be malignant in those patients, compared with
women in the reproductive age group.
Last menstrual period
Women who have missed menstrual period should have intrauterine & ectopic
pregnancy ruled out
Relation of the mass with menses
History of the mass;
o Duration (chronic pelvic mass include leiomyomata, hydrosalpinges, &
endometriomas).
o How it had been discovered
o Any changing in the mass ( increase, decrease or the same size).
o Does the patient have a Hx of weight loss & vague abdominal symptoms such as
anorexia, dyspepsia, distention, nausea, & dull pain or discomfort these
symptoms can be caused by ovarian malignancy.
o Other associated symptoms change in bowel habits, any gastrointestinal
bleeding, haematuria, dysuria, change in urine color.
Examination:
General:
Wt loss
Anemia
Jaundice
Lymphadenopathy
Breasts
Auscultation of heart + lungs
Effusion.
Abdomen:
Masses (all characteristics of the mass).
Distention from the mass or hemorrhage.
Ascites may be associated with ovarian malignancy.
Pelvic:
Masses (also with all characteristic of mass).
External genitalia & vagina: vaginal bleeding in ectopic pregnancy, intrauterine
pregnancy, uterine fibroids, or sarcoma.
Cervix: cervical motion tenderness may be present with PID or tubo-ovarian adcsess.
Uterus: enlargement with or without tenderness in leiomyomata, sarcoma, or
intrauterine pregnancy.
Adenxa: mass may be palpable, either unilateral or bilateral, with or without
tenderness. Fixed & nonmobile adenxa is suggestive of endometrioma, PID, or ovarian
malignancy.
PR.
Important signs you have to look for
In Ectopic pregnancy, ovarian torsion, cyst rupture, bleeding hemorrhagic cyst or pelvic abscess:
toxic looking,
fever
severe lower abdominal tenderness
muscle rigidity
peritonitis
Abscess ruptures :
abdominal distension
shock and tachycardia
PCOS :
obesity (centripetal)
hirsutism
acne
Investigations
CBC with differential:
A CBC with differential should be obtained to help with the diagnosis of masses associated
with PID, such as pyosalpinx or tubo-ovarian abscess.
It can also detect anemia in those patient with intra-peritoneal bleeding from any source.
Rapid urinary pregnancy test:
A pregnancy test should be obtained in all patient of reproductive age to rule out either
intrauterine or ectopic pregnancy.
Serum cancer antigen:
Cancer angen 125 (CA-125) is a tumor marker for ovarian epithelial cancers.
Unfortunately, CA-125 is non-specific & is also elevated in adenocarcinoma of the uterus
& colon, endometriosis, PID, IBD, pregnancy, & hepatitis.
Serum human chorionic gonadotropin (hCG) & alpha-fetoprotein (AFP):
Serum hCG & AFP are tumor markers in germ cell tumors of the ovaries. These tumors
make up nearly 20% of all ovarian neoplasms, & most occur in young women.
Ultrasound examination:
U/S examination will confirm the presence of a pelvic mass & furthermore will provide
information concerning the size, bilaterality, origin, & consistency of the mass, whether
cystic solid, or complex.
Ultrasonography is a method of choice in the radiological evaluation of an ovarian mass.
Computed tomography (CT):
CT scan can sometimes supplement the information obtained by U/S examination. CT
scan of the pelvis should be performed with contrast to opacify & therefore delineate the
bowel.
A CT scan in especially helpful in the evaluation of masses in the pelvic side wall.
A CT scan is also helpful in staging pelvic malignancies, detecting peritoneal implants, &
delineating pelvic abscess during drainage procedure.
Magnetic resonance imaging (MRI):
MRI provides soft-tissue contrast resolution that is superior to that obtained by U/S
examination or CT scan. It specially helpful in the assessment of conditions that result in
uterine enlargement such as congenital anomalies of the uterus, leiomyomata, &
adenomyosis, MRI can provide information on the size, number, & location of
leiomyomata.
Management
Ectopic pregnancy:
Goal of treatment: be conservative.
Surgical: (laparoscopy)
Linear salpingostomy if tube salvageable.
Salpingectomy if tube damaged or ectopic is ipsilateral recurrence.
May require lapratomy
Medical:
Methotrexate 50 mg/m
2
body surface area; given in a single IM dose
Follow beta-hCG levels weekly until beta-hCG is non-detectable.
Fallopian tube neoplasms:
Staging and treatment is similar to ovarian cancer.
Tubo-ovarian abscess:
Hospitalization
Adequate hydration
Analgesics
I.V antibiotic ( clindamycin, aminoglycoside )
Ultrasound guided aspiration
Endometrioma:
OCP, progestin, symptomatic relief of pain, gonadotropin releasing hormone agonist (6
month unless combined with add back estrogen +/- progestin
Endometrioms larger than 2 cm are best treated surgically
PCOS:
Weight reduction
OCP
Spironolactone for hirsutism
Progestin
Insuline sensitizing agent
Clomiphene citrate (for women who wanna get pregnant)
Surgical Rx ovarian drilling with laser or diathermy, laser hair removal
Ovarian Cancer Management
Guidelines for staging come from the International Federation of Gynecology and
Obstetrics (FIGO). Stages include:
Stage I (Growth limited to the ovaries, and subdivided into Stage IA, IB, and IC,
depending on the number of ovaries involved, presence or absence of ascites,
tumor cells on the external surface of the ovaries or in peritoneal washings)
Stage II (Growth beyond the ovaries, but limited to the pelvis. Stage II is further
subdivided into IIA, IIB, and IIC, depending on the specific areas of extension,
presence of ascites, and tumor cells in peritoneal washings)
Stage III (Growth out of the pelvis, but still within the epithelial surfaces of the
abdominal cavity. This is subdivided into IIIA, IIIB, and IIIC, depending on the
location of the growth and its size.)
Stage IV (Distant metastases outside the confines of the abdominal cavity or
within the liver parenchyma).
Surgical treatment options include local excision, TAH/BSO, and such debulking
procedures as omentectomy and bowel resection.
Early ovarian cancer might optimally be treated with TAH/BSO, but instead, a simple
oophorectomy is performed to preserve the woman's childbearing capacity.
Leiomyomas
Most pt dont require treatment
Medical:
GnRH-a up to 6 months, shrink broid and improve symotoms
Surgical:
Hystrectomy: most common indication
Liomyomectomy: preserve fertility
Uterine artery embolization: reduce menstrual flow
Adenomyosis:
No effective medical treatment
Hysterectomy is curative.
Pelvic Pain
Prepared by: Wafaa Al-Ahmadi
Sources: Obstetrics & Gynecology Recall + Obstetrics & Gynecology On Call + Obstetrics & Gynecology
At Glance + Tareq Arabs sheet
It could be either acute or chronic pelvic pain
Acute pelvic pain:
Acute pelvic pain requires aggressive management because of the possibilities that a life-
threatening condition exists.
Gynecological causes:
Ectopic pregnancy:
o In all reproductive-age women, the first priority in evaluating acute pelvic pain is to
rule out the possibility of ruptured ectopic pregnancy.
o Tubal rupture can lead to hemoperitoneum & shock.
Acute pelvic inflammatory disease (PID):
Is an ascending bacterial infection that usually present with high fever, acute pelvic pain, &
evidence of cervical emotion tenderness in sexually active women.
Rupture of ovarian cyst:
Intra-abdominal rupture of a follicular cyst, corpus luteum, or endometrioma, is the
common cause of acute pelvic pain the may be so acute & sever as to cause syncope. The
condition is usually self limiting with limited intra-peritoneal bleeding.
Adnexal torsion:
Is seen most commonly in adolescent or reproductive-age women. By twisting on its
vascular pedicle, any adnexal mass (ovarian dermoid, hydatid of Moegagni) can cause
acute, sever pain by suddenly compromising its blood supply. The pain will frequently wax
& wane with associated nausea & vomiting.
Threatened, inevitable, or incomplete abortions are generally accompanied by midline
pelvic pain, usually of crampy, intermittent nature.
Degeneration of fibroid or ovarian tumors: May cause, localized, acute, sharp, or aching
pain.
Hemorrhage into the cyst/neoplasm.
Torsion of pedunculated fibroid.
Endometritis.
Labour.
Placenta abruption.
Non-gynecological:
Gastrointestinal causes:
Appendicitis: is the most common acute surgical condition of the abdomen, occurring in all
age groups. Classically, the pain is initially diffused & centered in the umbilical area but
after several hours, localizes to the right lower quadrant (McBurreys point). It is often
accompanied by low grade fever, anorexia, & leukocytosis.
Diverticulitis: occurs most commonly in older women. It is characterized by left-sided
pelvic pain, bloody diarrhea, fever, & leukocytosis.
Mesenteric lymphadenitis: most often follows an upper respiratory infection in young
girls. The pain is usually more diffuse & less sever than in appendicitis.
IBD
Genitourinary causes:
UTI: cystitis, pyelonephritis, renal calculi) can cause acute or referred suprapubic pain,
pressure, and/or dysuria.
Chronic pelvic pain:
It is refer to unrelieved pain that has continued to be a major, disabling condition for at least 6
months.
Gynecological causes:
Dysmenorrhea: is the most common cause of chronic pelvic pain. It is defined as a cyclic
uterine pain occurring before or during menses. The pain is located in the lower abdomen & is
frequently described as a painful, crampy sensation that often accompanied by nausea,
vomiting, headache, swelling, sweating, fatigue, & lightheadedness.
Primary dysmenorrhea: is not associated with pelvic pathology, and is thought to be due
to excessive prostaglandin production by the uterus.
Secondary dysmenorrhea: usually it is due to acquired conditions (e.g. endometriosis).
Endometriosis: the presence & growth of endometrial glands & stroma in locations outside
the endometrial cavity of the uterus. Endometriosis most often involves the ovaries, the cul-
desac, the uterosacral ligaments, the rectosigmoid, & the posterior cervix. The classical
symptoms of endometriosis include dysmenorrhea, dyspareunia, dyschezia, & infertility. The
pain range from dysmenorrhea to sever, intractable, continuous pain which may be disabling.
The severity of the pain need not correlate with the degree of pelvic pathology.
Adenomyosis: the presence & growth of endometrial glands & stroma in the uterine
myometrium at a depth of 2.5 mm from the basal layer of the endometrium. It is a common
condion (usually found in women 35 to 50 years old) & most women are asymptomac, but
some patient may have dysmenorrhea & menorrhagia. An enlarged, boggy uterus, that is
mildly tender on palpation is characteristic.
Fibroids: are the most common (benign) tumor found in the females pelvis. They may cause
pain either by putting pressure on the adjacent organs or by undergoing degeneration.
Retained ovarian syndrome: is characterized by recurrent adnexal pain after hysterectomy.
Genital prolapse: may lead to complaint of heaviness, pressure, a dropping sensation, or
pelvic aching.
Chronic PID: characterized by continued pelvic pain, usually as a result of hydrosalpinx,
tubo-ovarian cyst, or pelvic adhesions.
Pelvic congestion syndrome: syndrome caused by pelvic varicosities that result in pelvic pain
or heaviness that is worse during the premenstrual period, after prolonged standing, & after
intercourse.
Non-gynecological causes:
Gastrointestinal:
IBS.
IBD.
GI neoplasm.
Constipation.
Partial bowel obstruction.
Diverticulitis.
Genitourinary:
Urinary retention.
Urethral syndrome.
Interstitial cystitis.
Others:
Referred pain (as in disk herniation).
Hernia formation.
Sexual/physical/psychological abuse.
Depression/anxiety/somatization.
Important points in the history:
Pain analysis (character, radiation, quality, intensity, & location of the pain)?
Temporal aspect (typical pattern, throughout the day/week/month, cyclicity, duration).
Her LMP: if the pt missed her menstrual period, either intra-uterine or ectopic pregnancy
should be suspected.
Relation of the pain to menstrual cycle & menorrhagia, abnormal bleeding (pain is correlate
with menses is suggestive of endometriosis, adenomyosis, primary dysmenorrheal).
Is the pain exacerbated by bowel movements, urination, sexual intercourse, physical activity
suggestive of endometriosis.
Is the pain associated with abnormal vaginal bleeding? suggestive of leiomyomata or
adenomyosis, if the patient is pregnant, tubal pregnancy or spontaneous abortion should be
ruled out.
Previous episodes.
Degree at which the pain disrupts daily activity.
Events that happened concurrent with pain onset (IUD, Rape, lifting heavy objects).
Pain medications.
Symptoms of stress/depression.
Recent changes in the bowel habits/urinary changes.
Recent onset of symptoms of GIT/GUT problems.
Gynecological Hx:
o Infertility Hx of infertility is consistent with endometriosis or pelvic adhesions from
prior PID.
o PID pelvic adhesions or hydrosalpnix.
o Past gonococcal/chlamydial infection.
o Endometriosis.
o Time of the last pelvic exam.
o Past abortions.
o OCP use.
o Sexual Hx (dyspareunia, frequency, effect of pain).
Past Hx:
o All past surgical procedures.
o Musculoskeletal disease.
o History of past sexual abuse, physical, emotional.
Physical examination:
Pelvic exam with attempt to reproduce & localize pain:
Endometriosis will yield a fixed retroverted uterus with tenderness uterosacral nodularity.
Chronic salpingitis may be suggested by bilateral, tender, irregular enlarged adnexae.
Prolapsed may present with pain/back pressure.
Abdominal wall examined for evidence of myofascial trigger points:
o Iliogypogastric T12, L1.
o Ilioinguinal T12, L1.
o Genitofemoral L1, L2.
Palpate for tenderness.
Patient straight leg raises or partial sit-up.
Pts still tender injected with marcain, & chronic abdominal wall pain confirmed if pain decrease
50% & outlasts duraon of marcaine.
Investigations:
CBC with differential: will help to diagnose infection. Sever anemia is suggestive of bleeding from
a ruptured tubal pregnancy or from hemorrhagic ovarian cyst.
ESR.
Beta hCG.
Urinanalysis.
Occult blood.
Liver function test.
Pelvic U/S will detect pelvic masses such as uterine leiomyomata & adnexal masses as well as
abdominal masses. Ultrasonography will not detect pelvic adhesions or pelvic endometriosis.
Diagnostic laparoscopy as last resort.
IF INDICATED GIT X-ray, endoscopy, cystoscopy, IVP, Lumbosacral X-ray, CT scan, MRI,
orthopedic consultation.
Treatment:
Conservative.
Medical treatment:
o OCP/GnRH agonists may relive pain in those with mid-cyclic, premenstrual, menstruation
exacerbated pain, ovarian pathology (peri-ovarian adhesions/recurrence functional
cysts).`
o NSAIDs.
o TCAs
The following are potential options:
o Unilateral adnexectomy for unilateral pain.
o TAH.
o Pre-sacral neurectomy.
o Uterosacral nerve ablation.
o Uterine suspension.
o Lysis of adhesions.
Full psychosomatic evaluation prior to surgery.
Anesthesia:
85% of patients have abdominal wall trigger points that respond to biweekly injections local
anesthetic.
AMENORRHEA
Prepared by: Jameel Khalid Rasheedi (Dr.JKR)
Sources: Toronto Notes 2008 + Kaplan USMLE 2008 + Ob/Gyn at Glance + Gynecology Illustrated +
Essentials of Ob/Gyn (Hacker) + National Medical Series + First Aid for Ob/Gyn
Amenorrhea is the absence or cessaon of menstruaon for 6 months or longer and can be Primary or
Secondary
PRIMARY: is the absence of menses at age 14 years without development of secondary
sexual characteristics or at age 16 years regardless of secondary sexual characteristic
development. ((menses have never occurred))
SECONDARY: is the cessaon of menses for 6 months or a three-cycle interval in women
who have been menstruating regularly.
According to . . .
Site of lesion Hormonal state
HYPOTHALAMIC : FSH/LH levels
1-Congenital lack of GnRH e.g. Kallmans syndrome.
2-Pituitary stalk compression: Tumors, granulomas,
irradiation, infiltrative disorder.
3-Decrease GnRH release: Stress, anorexia,
hyperprolactinemia, severe weight loss, extreme
exercise due to catecholamine & endorphin.
PITUITARY : FSH/LH levels
1-Hypopituitarism duo to Sheehans syndrome
(Simmond disease) : Pituitary infarction from
hypotension during postpartum hemorrhage.
2-Primary Hypopituitarism.
3-Tumors: adenoma, Craniopharyngioma, prolactin-
secreting tumors.
4-Hemosiderosis: Iron deposition in pituitary that
impairs its function.
OVARIAN : FSH/LH levels
1-Menopause.
2-Premature ovarian failure.
3-Savages syndrome: Ovarian resistance to FSH/LH
4-Enzyme defects: commonly 17-hydroxylase.
5-Gonadal dysgenesis : Turners syndrome 45X
6-Chronic anovulation: Polycystic ovary syndrome
PCOS, ovarian/adrenal tumor.
7-Radiation, chemotherapy.
HYPERGONADOTROOIC :
1-Turners syndrome 45X.
2-Premature ovarian failure.
3-Gonadal dysgenesis: XYgenotype, Swyer syndrome
4-Gonadal agenesis.
5-Resistant ovary syndrome (Savages syndrome).
6-Galactosemia: an autosomal recessive deficiency
in galactose-1-phosphate uridyltransferase (toxic
effect of galactose metabolites led to oogonia.
7-Enzyme deficiencies: a- 17-hydroxylase (prevent
synthesis of sex steroid) have ovaries but not
functioning, present with absent 2ndry sexual cha. ,
HTN, hypokalemia and progesterone level.
b- aromataze enzyme.
HYPOGONADOTROPIC :
1-Anorexia (amenorrhea, bradycardia, dry skin,
hypothermia, lanugo hair).
2-Exercise.
3-Stress increased corticotropin-releasing
hormone decreased GnRH pulsatile secretion and
thus decreased secretion of FSH and LH.
3-Congenital lack of GnRH e.g. Kallmans syndrome.
4-Postpill: amenorrhea may occure 6 or more
months after patient stop taking OCP.
5-Medication: Birth control pills, phenothiazine
derivatives, reserpine.
6-Pituitary diseases: sella turcica, Pituitary tumors
Craniopharyngioma, Adenomas.
UTERINE : normal FSH/LH
1-Congenital mullerian (uterine/vaginal) agenesis
(Mayer-RokitanskyKuster-Hause syndrome)
2-Imperforate hymen
3-Transverse vaginal septum
4-Cervical stenosis
5-Intrauterine adhesions :Asherman's syndrome
6-Congenital absence of uterus.
7-Androgen insensitivity syndrome (Testicular
Feminization)(XY)
ENDOCRINE :
1-Hyperprolactinemia.
2-Hyper/hypothyroidism.
3-Hyperandrogenism : PCOS, ovarian/adrenal
tumor, testosterone injections.
4-Cushing's disease.
EUGONADOTROPIC :
1-Disorders of androgen excess: polycystic ovary
syndrome.
2-Disorders of the outflow tract or uterus:
-Mullerian agenesis (Mayer-RokitanskyKuster-
Hause syndrome)
-Androgen insensitivity syndrome (Testicular
Feminization)(XY)
-Intrauterine adhesions :Asherman syndrome
-Infection: Tuberculosis and schistosomiasis
may cause intrauterine scarring and adhesions.
Physiologic causes: Pregnancy, Lactation, Menopause, Prepubertal.
Primary Amenorrhea
Is the absence of menses at age 14 years without development of secondary sexual characteriscs
or at age 16 years regardless of secondary sexual characteristic development. ((menses has never
occurred)) .
Prevalence: 1-2% of girls.
The two main categories of etiology, ANATOMICAL: Imperforate hymen, vaginal septum/agenesis, or
mullerian agenesis. HORMONAL: Androgen insensitivity syndrome, Gonadal dysgenesis(Turner Syndrome),
or hypothalamic-pituitary insufficiency.
Clinical Approach Based on Findings Regarding Breasts and Uterus.
By physical examination determine wither breasts are present or
not and by an ultrasound for uterus
A- Breasts present, uterus present: Differential diagnosis includes an imperforate hymen, a
vaginal septum, vaginal agenesis, anorexia nervosa, excessive exercise.
If non is the cause, then the workup should proceed as if for secondary amenorrhea.
* Imperforate Hymen & Transverse Vaginal Septum: three degrees are recognized
-Clinical features: Primary amenorrhea, pelvic pain of increasing severity, urinary
retention in longstanding case due to pressure of distended vagina.
- Examination: Palpable pelvic mass, bulging vaginal hymen but no lower vaginal bulging
in Transverse Vaginal Septum , MRI here is the diagnostic method of choice.
- Pregnancy must be excluded.
- Treatment: Surgical.
B- Breasts present, uterus absent : Differential diagnosis is Mullerian agenesis (Rokitansky-
Kuster-Hauser syndrome) and complete androgen insensitivity (testicular feminization).
* Testosterone levels and karyotype help make the diagnosis.
Mullerian agenesis : " Mayer-Rukitamisky-Kuster-Houser-Syndrom "
- Genetically normal females (46,xx).
- Absence of the Mullerian duct derivatives: fallopian tubes,
uterus, cervix, and upper vagina.
- Breasts are an endogenous assay of
ESTROGEN.
- Pubic & axillary hair are an endogenous
assay of ANDROGEN.
- When diagnose amenorrhea, always role
out PREGNANCY first.
_____________
*Gynecology illustrated
- Mullerian ducts do not give rise
to the ovaries.
- Mullerian Agenesis Triad:
1. Primary amenorrhea
2. (+) breasts but (-) uterus
3. (+) pubic and axillary hair
- Patients develop secondary sexual characteristics because ovarian function is intact.
- Normal pubic and axillary hair is present.
- Testosterone levels are normal female.
- One third of cases associated with congenital renal abnormality, ( intravenous pyelogram, US )
- 12% have skeletal lesion.
- Management: surgical neovagina.(Frank method : dilation of
vaginal pouch, or McIndoe vaginoplasty: using skin graft ), no hormones.
Androgen insensitivity :
- Genetically male (46,xy), with complete lack of androgen receptor function No respond to the
high levels of androgens internal Wolffian duct structures atrophy.
- With testicular Mullerian inhibitory factor present, the Mullerian duct derivatives involute.
- Without body recognition of dihydrotestosterone, external genitalia differentiate in a female
direction.
- Patients function psychologically and physically as females and are brought up as girls.
- Female secondary sexual characteristics (breast) are present because the testes do secrete
estrogens without competition from androgens & peripheral conversion of androgen.
- No (or scanty) pubic or axillary hair is noted due to Androgen insensitivity.
- Testosterone levels are normal male.
- At puberty, when primary amenorrhea is noted, the diagnosis is made.
- Management: 1- Testes removed at the age of 20 because the higher
temperatures associated with the intraabdominal position of the testes
lead to testicular cancer.
2- Estrogen replacement.
3- surgical neovagina.
C- Breasts absent, uterus present: Differential diagnosis is gonadal dysgenesis (Turner
syndrome) and hypothalamic-pituitary failure.
* FSH level and karyotype help make the diagnosis.
Gonadal failure (Hypergonadotropic Hypogonadism):
- Turner syndrome (45,x) is caused by the lack of one X chromosome, which is essential for
presence of normal ovarian follicles.
- Incidence 1/2500
- These patients develop streak gonads.
- Short status, webbed neck, cubitus vulgas, infantile genitalia, coarctation of aorta.
- No estrogen duo to absence of ovarian follicles.
- FSH levels are elevated because of lack of estrogen feedback to the hypothalamus and pituitary.
- No secondary sexual characteristics are noted.
- Other karyotype include: 46XX(pure gonadal dysgenesis), mosaicism, 47XXX, 46XY gonadal
dysgenesis (Swyer syndrome), Congenital adrenal hyperplasia (17-hydroxylase).
- Management: Estrogen and progesterone replacement for development of the secondary sexual
characteristics and prevent osteoporosis.
- Third commonest cause of
primary amenorrhea.
*Why testes removed at age of
20 ys not before?
- Cancer is rare to occure
before that.
- To allow full breast & puberty
development and linear
growth.
Second most common cause of
primary amenorrhea
Turner syndrome is the Single most common
cause of primary amenorrhea, accounting for
>50% of gonadal failure paents.
Hypothalamic-pituitary failure (Hypogonadotropic Hypogonadism):
- No secondary sexual characteristic but uterus present by ultrasound.
- FSH levels will be low.
A - HYPOTHALAMUS: stress, anxiety, anorexia nervosa, excessive exercise, tumors, TB,
sarcoidosis, congenital (KALLMAN's SYNDROME) :
- Insufficient GnRH production and also anosmia & color blindness.
- X- linked, male > female.
- The defect is in the area of the brain that produces GnRH, but it's also close to
the olfactory center.
- CNS imaging will rule out a brain tumor, MRI hypodevelopment of
olfactory sulci.
B- PITUITARY: Congenital ( empty sella turcica , atrophy ), adenoma, tumors ( prolactin
secreting & non-prolactin secreting ), exposure to chemical.
- Management: Estrogen and progesterone replacement for development of the secondary
sexual characteristics and prevent osteoporosis.
Breasts present, uterus absent Mullerian Agenesis (46,xx) Androgen Insensitivity (46.xY)
Cause of Uterus absent? Idiopathic MIF
Estrogen source Ovaries Testes
Pubic hair Present Absent
Testosterone level Female Male
Breasts absent, uterus present Gonadal Dysgenesis (4S.x) HPAxis Failure (46,xx)
FSH
Why No estrogen
No ovarian follicles
Follicles not stimulated
Ovaries?
"Streak"
Normal
Diagnostic test - CNS imaging
Breast Uterus
( - ) ( + ) 1
st
common(Gonadal failure, Hypothalamic-pituitary failure)
( + ) ( + ) Rare (same workup as 2
nd
amenorrhea)
( + ) ( - ) Common(Mullerian agenesis, androgen insensitivity)
( - ) ( - ) Very Rare , almost always 46,XY
Secondary Amenorrhea
Is the cessaon of menses for 6 months or a three-cycle interval in women who have been
menstruating regularly.
Prevalence: 4-5% of women (excluding pregnancy)
Can be classified by alterations in FSH and LH levels into:
-Hypogonadotropic (hypothalamic or pituitary dysfunction)
-Hypergonadotropic (ovarian follicular failure)
-Eugonadotropic (pregnancy, anovulation, uterine or outflow tract pathology)
Anovulation:
- No corpus luteum is present to produce progesterone No progesterone-withdrawal bleeding.
- Anovulation is associated with unopposed estrogen stimulation of the endometrium.
-Polycystic ovary syndrome -Hypothyroidism TRH stimulate prolactin production.
-Medications (e.g., antipsychotics, antidepressants).
- Hypothalamic dysfunction:
-Tumor -TB -Sarcoidosis -Drugs: OCP(post pill amenorrhea)
-Stress -Exercise -Anxiety -Anorexia nervosa
- Pituitary:
- Adenoma -Craniopharyngioma -Prolactin-secreting tumors.
- Sheehans syndrome - Iatrogenic hyperprolactinaemia
- Ovaries:
-Premature ovarian failure: Loss of all ovarian follicles with cessation of menstruation
prior to age 40.
- elevated FSH
-Causes: intrinsic ovarian defect, genetic mosaicism, autoimmune(MG),
chemotherapy, radiation, infection(mumps).
- Savage syndrome (resistant ovary syndrome): a condition in which although follicles
are seen in the ovary by sonogram, they do not respond to gonadotropins.
Estrogen Deficiency: priming the endometrium will be atrophic with no proliferative changes taking place.
Causes of hypoestrogenic states: -absence of functional ovarian follicles.
-hypothalamic-pituitary insufficiency.
Outflow Tract Obstruction: - Asherman's syndrome: intrauterine synechiae(adhesion) that interfere with
normal endometrial growth and shedding.
Causes: - Extensive uterine curettage.
- Infection-produced adhesions.(TB)
1- Pregnancy Test: The first step in management of secondary amenorrhea is B-hCG test to rule out
pregnancy. If negative . . .
2-Thyrotropin (TSH) Level: hypothyroidism should be ruled out. If positive treatment is thyroid
replacement. If negative . . .
3- Prolactin Level:
-Medications. An elevated prolactin level secondary to antipsychotic or antidepressants, which
have an anti-dopamine side effect (hypothalamic prolactin-inhibiting factor is dopamine).
- Pregnancy is the most common cause of
secondary amenorrhea.
- When diagnose amenorrhea, always role out
PREGNANCY first.
-Tumor. A pituitary tumor should be ruled out with a CT scan or MRI of the brain.
-Tumor is < 1 cm treated medically with bromocriptine (Parlodel), a dopamine agonist.
-Tumor is > 1 cm usually treated surgically.
-Idiopathic. treatment is also medical with bromocriptine.
*Quinagolide: is a dopamine agonist tolerated better than bromocriptine, given daily.
*Cabergoline: is a dopamine agonist with long half life, given weekly.
*Radiotherapy: reserved to patients fail with medical and surgical therapy.
If the B- hCG is negative, and the TSH and prolactin levels are normal . . .
4- Progesterone Challenge Test (PCT) "provera test" : administer either a single 1M dose of progesterone
or 7 days of oral medroxyprogesterone acetate (MPA).
Positive PCT: - Any degree of withdrawal bleeding is diagnostic of anovulation.
- Cyclic MPA is required to prevent endometrial hyperplasia.
- Clomiphene ovulation induction if pregnancy is desired.
Negative PCT: - Absence of withdrawal bleeding is caused by
- inadequate estrogen priming of the endometrium .
- outflow tract obstruction.
If the PCT is negative . . .
5- Estrogen-Progesterone Challenge Test (EPCT): 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.
An elevated FSH: suggests ovarian failure or Savage
A low FSH : - suggests hypothalamic-pituitary insufficiency.
- Order a CNS imaging study to rule out a brain tumor.
- CNS lesion empty sell syndrome, Sheehan syndrome.
- No CNS lesion Hypothalamic dysfunction
-Treatment: - estrogen-replacement therapy to prevent osteoporosis and estrogen-deficiency
morbidity.
- Cyclic progestins are also required to prevent endometrial hyperplasia.
Negative EPCT: - Absence of withdrawal bleeding is diagnostic of an outflow tract obstruction or
endometrial scarring (e.g., Asherman syndrome).
- A hysterosalpingogram (HSG) to identify where the lesion is.
- Asherman syndrome is treated by : - Hysteroscopic adhesion lysis.
- Estrogen stimulation of the endometrium.
- An inflatable stent is then placed into the uterine cavity to
prevent re-adhesion of the uterine walls.
_____________
*OB/GYN At a Glance
Infertility
Prepared by : Faisal Al-Gaows
Sources: Toronto notes2008 + Ob/gyn at glance
Fertility: the capacity to conceive and produce offspring.
Fecundity: the probability to conceiving during a single monthly cycle.
The fecundity of normal couple is 20% - 25% with cumulave 85% 90% chance of
pregnancy in 12 months
Infertility: Failure to conceive after one year of regular unprotected intercourse.
Primary infertility: no prior pregnancies
Secondary infertility: previous conception.
10-15% of couples
normally 75% of couples achieve pregnancy within 6 months, 85% within 1 year, 90% within
2 years
must investigate both members of couple
- Fecundity in women peak s at 25 years .Thereafter fertility rate declines.
- Other factors includes: cigarette smoking ,illicit drug use and occupational and
environmental exposures.
Ovary
Tube
Cervix
Endometrium
Male
Ovulatory dysfuncon (15-20/0)
Hypothalamic (hypothalamic amenorrhea)
Pituitary
Prolactinoma
Hypopituitarism
Ovarian
Pcas
Premature ovarian failure
Luteal phase defect (poor follicle production, premature corpus luteurn failure,
failed uterine lining response to progesterone) poorly understood
Systemic diseases (thyroid, Cushing's syndrome, renal/hepatic failure)
Congenital (Turner syndrome, gonadal dysgenesis, or gonadotropin deficiency)
Stress, poor nutrition, excessive exercise (even in absence of amenorrhea)
Outflow tract abnormality:
Tubal factors (20-30%)
PID
adhesions (previous surgery, peritonitis, endometriosis)
ligation/occlusion (e.g. previous ectopic)
Uterine factors (<5%)
Congenital anomalies (e.g. prenatal DES exposure), bicornuate uterus, uterine septum
Intrauterine adhesions (e.g. Asherman's syndrome)
Infection (endometritis, pelvic TB)
Fibroids/polyps (particularly intrauterine)
Endometrial ablation
Cervical factors (5%)
Hostile or acidic cervical mucous
Anti-sperm antibodies
Structural defects (cone biopsies, laser, or cryotherapy)
Endometriosis
Mulple factors (30%)
unknown factors (10-15%)
Ovulatory
Day 3 FSH, LH, TSH, PRL +/- DHEA, free testosterone (if hirsute)
Day 21-23 serum progesterone
initiate basal body temperature monitoring (biphasic pattern)
postcoital test - evaluate mucus for clarity, pH, spinnoarkeit (rarel~' done)
Tubal factors
HSG (can be therapeutic - opens fallopian tube)
SHG
Laparoscopy with dye insufflation
Peritoneal /uterine factors
HSG/SHG, hysteroscopy
Other
karyotype
Education - ming of intercourse in relaon to ovulaon (from 2 days prior to 2 days following
presumed ovulation), every other day
Medical
Ovulation induction
Clomiphene citrate (Clomid) - ovulation induction via increased pituitary gonadotropins
Human menopausaf gonadotropin [HMG (PergonaFM)]
Urofollitropin (FSH [Metrodin])
Followed by -hCG for stimulation of ovum release
May add
bromocriptine (dopamine agonist) if increased prolactin
dexametnasone for women with hyperandrogenism
(pCaS, adult onset congenital adrenal hyperplasia), metfonnin (PCaS)
luteal phase progesterone supplementation tor luteal phase defect
Surgical/procedural
Tuboplasty
Lysis of adhesions
Artificial insemination
Sperm washing
IVF (in vitro fertilization)
Intrafallopian transfers:
GIFT (gamete intrafallopian transfer)
immediate transfer with sperm after oocyte retrieval
ZIFT (zygote intrafallopian transfer) - transfer aer 24 hour culture of oocyte and sperm
TET (tubal embryo transfer) - transfer aer >24 hour culture
lCSI (intracytoplasmic sperm injection)
lUl (intrauterine insemination)
Oocyte or sperm donors
NM (in vitro maturation)
When should investigations begin?
<35 years: aer 1year of trying to conceive
-35-40 years: aer >6 months
>40 years: immediately
Earlier if:
- History of PID
- History of infertility in previous relationship
- Prior pelvic surgery.
- Chemotherapy/radiation in either partner
- Recurrent pregnancy loss
- Moderate & severe endometriosis
varicocele (>40%)
cryptorchidism (-8%)
idiopathic (>20%)
immunologic (-3%)
obstruction (-15%)
semen analysis and culture
post-coital (Huhner) test
Ovarian Cancer
Prepared by: Wafaa Al-Ahmadi
Sources: Toronto Notes 2008 + Obstetrics & Gynecology At Glance + Obstetrics & Gynecology Recall
Ultrasound characteristics of benign vs. malignant ovarian tumors:
Benign Malignant
< 8-10 cm in diameter >10 cm in diameter
unilateral Bilateral
Cystic Solid elements (internal papillary structures/mural
nodules)
Uniloculated Mutiloculated
Thin septations Thick septations
No ascites Ascites
Epidemiology
Life me risk 1.4% (1/70).
In women > 50 years, more than 50% of ovarian tumor are malignant.
4th leading cause of cancer death in women.
56% epithelial; 35% non-epithelial.
5-10 % of epithelial ovarian cancers have hereditary predisposion.
Risk factors
Nulliparity.
Early menarche/late menopause.
Age
Family history
Race Caucasian
Protective factors
OPC possibly because of ovulation suppression.
Pregnancy/breastfeeding.
Tubal ligation.
Hysterectomy.
Clinical features
Usually asymptomatic until disseminated.
Most present as stage III disease (advanced).
Early:
Post menopausal bleeding; irregular menses if pre-menopausal (rare).
Vague abdominal symptoms (nausea, bloating, dyspepsia, anorexia, early satiety).
Late (due to mass effect):
Increased abdominal girth from ascites or tumor itself.
Urinary frequency.
Constipation.
Fluid wave.
Lower malignant potential tumor:
Often called borderline tumors.
About 15% of all epithelial type ovarian tumors.
Tumor cells display malignant characteristics histologically, but no invasion is identified.
Treated with surgery.
No proven benefits of chemotherapy.
Slow growing, excellent prognosis.
5 years survival > 99%.
Pregnancy, OCP, & breast feeding are found to be protective.
Stages of ovarian cancer
Epithelia
ovarian tumor
87-90%
Metastatic
ovarian cancer
4-8%
Sex cord
stromal
5-7%
Germ cell tumor
5-7\%
Classification
of ovarian
cancer
Prognosis: (5 years survival)
Stage I: 75-95%
Stage II: 45-65%
Stage III: 20-40%
Stage IV: 10-15%
Classification of ovarian cancer
Epithelial ovarian cancer:
Origin
Arise from coelomic epithelium (i.e. the mesothelium).
This epithelium also give rise to peritoneum & the paramesonephric (mllerian duct), which
explains the histologic similarities between lesions of ovarian, peritoneum, & urogenital tract.
Types:
Serous (50-70%)
o 20-30 bilateral
Mucinous (10-15%)
o Rarely complicated by pseudomyxoma peritonei.
o Implants seed abdominal cavity & produce large quantities of mucous.
Endometroid
Undifferentiated
Clear cell
Age: the median age at diagnosis is 61 years.
Hereditary factors:
5-10% of ovarian cancer paent have a hereditary cancer syndrome (most commonly familial
breast ovarian cancer). Germline mutaon in the BRCA 1 or BRCA 2 gene account for the majority
of cases.
Germ cell tumors:
Origin:
Derived from primitive germ cells of the embryonic gonad.
The vast majority of germ cell tumors occur in young women.
Types:
Dysgerminomas:
o Are the most common type (50%).
o The median age at diagnosis is 17 years.
o Lactate dehydrogenase may be a useful tumor marker.
o Overall long-term survival is 85%.
Endodermal sinus tumors:
o Are the second most common type.
o Have elevated serum alpha-fetoprotein (AFP) levels.
o Median age at diagnosis is 19 years.
Embryonal carcinomas.
Choriocarcinoma.
Immature teratomas.
Sex cord stromal:
Origin:
Gonadal/stromal origin.
Have low grade malignancies & recurrence are very uncommon.
May occur at any age.
Types:
Granulose cell tumors:
o Are the most common type (70%).
o 95% are stage at diagnosis & unilateral.
o Estrogen producing feminization effects (precocious puberty, menorrhagia, post-
menopausal bleeding).
Sertoli-leyding tumors:
o Are rare & frequently presented with signs of hyperandrognism as its an androgen producing
tumor virilizating effects ( hirsutism, deep voice, recession of front hairline).
Metastatic ovarian cancer:
From GI tract, breast, endometrium, lymphoma.
Investigations
Bimanual examination.
Solid, irregular, fixed pelvic mass is suggestive of ovarian cancer.
Blood work: CA 125 for baseline, CBC, LFT, electrolytes, creanine.
Radiology: CXR, abdo-pelvic U/S, transvaginal U/S; CT or US to asses urinary tract.
Bone scan NOT indicated.
Try to rule out primary:
Occult blood: if positive endoscopy barium enema.
If gastric symptoms: gastroscopy upper GI series.
If abnormal vaginal bleeding: PAP smear & endometrial biopsy to rule out concurrent
endometrial or cervical cancer.
Mammogram.
Treatment
For epithelial ovarian tumors:
Primary therapy:
Complete surgical staging (peritoneal cytoplogicaly, abdominal exploration, total abdominal
hysterectomy (TAH), bilateral salpingo-oophorectomy (BSO), biopsy or smear of the diaphragm,
omentectomy, select pelvic & para-aortic lymphadenectomy) maximal tumor cytoreduction are
the cornerstone of primary treatment. The goal of the surgery is definitive diagnosis, accurate
staging, & removal of all gross disease.
Adjuvant therapy:
Platinum-based chemotherapy is generally recommended for all stage 1c & higher cases. Six cycle
of carboplatin & paclitaxel (Taxol
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Ob/Gyne Instruments
Used to visualize the cervix and vagina in cases of
1. Inspecon of cervix & vagina (pap smear, discharge, swab)
2. High vaginal swab
3. Conrm PROM
4. IUD inseron
Used to visualize the cervix and vagina for
1. Inspect vaginal wall for lesions (fistula, prolapse, neoplasm)
2. D&C
3. Exploration in PPH
1)
Prepared by: Salman Jan
Indications:
1.Fetal: distress, cord prolapse
2.Maternal:
*shorten the 2nd stage (cardic disease, pul.edema, hypertension, neurological dysfuncons)
*Maternal exhaustion
*Poor maternal effort
3.Elecve:
*After coming head in breech.del.
*During caesrean section
Pre-requisites:
- Fetal:
1. Head engaged ( staon +2 or lower)
2. Vertex or face presentation
3. Position of the fetus precisely known
- Maternal:
1. Cervice fully dilated
2. Membrane must be ruptured
3. No cephalopelvic disproporon
4. Bladder empty
5. Adequate analgesia & anesthesia
6. Generous episitomy
7. Lithotomy posion
8. Empty rectum
Contraindications are the opposite to them!
Complications:
- Fetal:
1. Facial n.or brachial pluxes injury
2. Skull fractures
3. Heamatoma (caput saccundum)
4. Intracranial Hmg
- Maternal:
1. Tear and laceration of the cervix
2. Rupture of bladder
3. Extension of episitomy
4. Bleeding
5. Infections
Types:
- simpson
- piper
- Kielland
Indications: Same as forceps.. PLUS few more points !
Prerequities:
Full term baby
Full flexion of the head
Sucon pressure < 600 mmHg
Not more than 3 applicaon
Dont twist the cup !
Contraindications:
1. Face or other than vertex presentation
2. Premature baby
3. Fetal coagulopathies
4. Fallowing fetal scalp sampling!
Complication:
1. Vaginal laceration and fistula
2. Fetal scalp heamatoma, laceration
Uses:
Obtain cytology smear form the cervice and vagina ( screening purposes)
Copmnants
- Ayre spatula (2 ends)
- Endocervical swab
- Fixator
- Slide
Use:
1.Obtain swab form any uid or discharge
2.High vaginal swab
Looks like a swab but has a yellow head ..
Used to confrim rupture of membrane: Alkaline aminotic fluid: Yellow >>>>> Blue
(internal moniter)
Uses:
Record fetal ECG by applying small clip to fetal scalp.
Indications:
1. Chorioaminois
2. Meuconium stained liquor
3. Twins
4. Excessive fetal movment
5. Unsasfactory CTG
6. High risk pregnancy
Advantages:
More reliable tracing to fetal heart beat & variability..
Disadvantages:
1. Rupture of membrane is a must; spontaneous or artificial
2. Little chance of infection; mother & fetus
3. Scalp trauma
Contraindictions:
1. Maternal infection e.g HIV, herpes simplex
2. Sever fetal coagulopathy
(ovum forcepse)
Curved
Stright
Uses:
1. Remove conceptional product, intrautrine, cervical polyp
2. To hold tissue e.g cervix during D&C
Use: non pharmacological induction of labor (Rupture membrane)
Complication:
1. Fetal & maternal injuries
2. Cord prolapse
3. Repture of vasa previa
4. Chorioaminoitis