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Contraception

IUD OCP Natural mmethods Barrier methods


1- Interfere with implanatation : local foreign body inflammatory response – increased local 1- Estrogen : inhibit ovulation via suppression of GNRH Natural methods does not need any facilities : Prevent sperm egg
Mode of action PGL production –Cu inhibit carbonic anhydrase & alkaline phosphatase – progesterone induce 2- Progesterone : Endometrial effect ( atrophic changes ) / Coitus interr: prevent semen deposition in vagina
atrophic endometrial changes cervical effect ( thick mucus ) / tubal ( altered tubal motility ) / Safe period : avoiding intercourse in days of
2- Interfere withsperms : inhibiting sperm migration – Cu produce toxic effect on on sperm - ovarian ( interfere with ovulation ) suspected ovulation
progertrone produce thick cervical mucus 3- Also : excellent cycle control / prevent endometrial Prolonged lactation : suppress GNRH by high
hyperplasia when combined level of prolactin
 Copper IUD : Cu T 380 the most commonly used used for 4-6 years 1- Combined : contain estrogen 30 ug and gestagen in one phase 1- coitus interruptus : 1- Male & female condom : prevent STDs
Types  Copper + silver ( Nova T ) silver is added to prevent cu degradation , two or three tsken for 21 day then 7 days pill free period then 2- The safe period 2- Female diaphragm |& cervical cap :
 Progesterone releasing IUD _ ( Mirena ) release levonorgesterol 35 ug/d started In day 3-4 of menses 3- Prolonged lactation inserted 6 hours before intercourse
2- Progestogen only : taken continuously irrespective of cycle 3- Spermicides ( nonoxynol 9 ) : appliaed 30
for women contraindicated to take COC min before & failure rate 30 HWY if alone
1- Single choice withlong term protection - Most effective , failure rate 0.1-1HMY - excellent cycle Simple – readily accessible for no cost - Easy to initiate & terminate / nosystemic side
Advantages 2- Doesnot affexct lactation or interfere with sexual intercourse control - no effect on fertility or sexual intercourse effects / no effect on future fertility or lactation
3- Very low failure rate < 0.5 HWY / some may prevent transmission of STDs
1- Vaginal bleeding : psot insertion bleeding ( mild spontaneously stop few days after – profuse 1- Spotting : due to inappropriate content of pills → shift for 1- Coitus : pre-ejaculatory fluid may Difficult to use consistently and correctly /
Disavantages indicate either pathology , perforation , or contractions of explusions ) – Menorrhagia ( due to higher dose in the next cycle contain sperms may interrupt sexual activity / some reauire
increase PGL _ increased fibrinoltyic activity / if mild treated by antifibrinolytics & NSAID / if 2- Breakthrough bleeding : intermenstrual 2- In safe period : suitable only for partener participation / less effective than
sever exclude any organic pathology then you canremove and use progeertrone release to induce 3- Hypomenorrhea & amenorrhea intellectual couples – need regular other methods
atrophy ) 4- Thromboembolic disorders cycles
2- Pelvic pain : during insertion ( from forcible cervical dilatation – perforation – abmormal 5- Hypertension & DM 3- In prlonged lactation : continuation of
position ) acute abdominal ( in situ → abortion – PID // missed →perforation ) 6- Impairment of liver functions ovulation is unpredictable may be
3- Infection : either chronic cervicitis or PID both increased with IUD in amy of them treat 7- Depress lactation resumed at any time
infection then remove IUD 8- Nausea & vomting ? weight gain
4- Vag discharge : watery from congestion/mucopurulent in chronic cervicitis 9- Irritability & depressive disorders
5- Expulsion : due to contractions during menses or misplacement at time of insertion / it can be 10- Migraine headache
complete or incomplete – both removed & reinserted 11- Acne worsen & chloasma resemble that of pregnancy
6- Perforation : mostly at time of insertion → sharp stabbing pain – persistent vaginal bleeding 12- Decreased libido & breast engorgement
7- Pregnancy on IUD : if threads visible removed / if not visisble left in situ with more risk for 13- Vaginal discharge
septic abortion 14- Increased risk of cervical & breast cancer
8- Missed IUD : either threads indrawn – completely expelled or missed in peritoneal cavity in
perforation
 Reliable with low failure rate of < 0.5 HWY/ require little motivation as it is single choice / no The most effective method but needs daily use it also : ttt DUB Failure rate is high & efficacy is low Fairly reliable with failure rate < 10 HWY
Evaluation need for educated user / good for national programs in developing countries / postpone next cycle / ↓ risk of ovarian & endometrial cancer
1- Pregnancy & undiagnosed vaginal bleeding Thrombophelibitis & DVT history / coronary heart & stroke / No contraindications No contraindications except spermicidals may
Contraindication 2- Uterine anomiles & uterine cavity pathology due to lack of proper insertion liver disease & liver malignancy / abnormal genital bleeding / cause allergic vaginitis in some women
s 3- History of PID ( may be aggravated ) / or ectopic pregnancy ( risk increased ) suspected carcinoma of breast

Premalignant lesions
Endometrial hyperplasia CIN VAIN VIN
Prolonged unopposed effect of estrogen as in : obesity –PCOS- HRT 1. Early 1st sexual intercourse Uncommon premalignant lesion in They are 2 types :
Risk factors –infertility – nulliparity – late menopause 2. Multiple parteners vagina may be associated with CIN - Squamous Vin
3. HPV – HSV infections VIN - Non Squamous ( paget disease and
4. Poor hygiene melanoma )
5. Smoking
6. immunosuppression
- Simple hyperplasia 1% - CIN I : basal 1/3 dysplastic ( LSILs) Squamous type has grsdes as CIN I & II &III
Histology & Types - Complex hyper plasiawithioutatspia 3% - CIN II : basal ½ ( HSILs)
- Simple atypical hyper plasia 8% - CIN III : full thickness without invasion of BM
- Complex atypical HP 25%
 Abnormal uterine bleeding especially perimenaupausal Nearly asymptomatic and discovered accidently during regular check up  1/3 asympromatic but most presents with
Clinical presentation  Normal uterus or enlarged – may be myomata – or ovarian pruritis vulvae
enlargement  Signs : multicentric multifocal lesion with
variable color white – black – red
1. TVS : abnormal endometrial thickening  Pap smear : annually for high risk / every 3 years for females > 30 Y with 3 –ve - Pap smear : abnormal vaginal Pain vulva with 5 % acetic acid and biopsy aceto-
Invetigations 2. endometrila biopsy is the gold standard either by pipelle or full samples / discontinued for > 70 epithelial cells white areas
D&C with anaesthia  Coloposcopy directed biopsy from acetowhite areas or schiller iodine –ve areas - Coloposcoy guided biopsy :
 Endocervical curettage when abnormal areas not visualized
1. cyclic oral progestin for 3-6 M : for patients without atypia 1- Low grade lesions CIN I : 1- Local destruction ablation  Spontaneous regression
Trreatmant 2. Hysterectomy for : failed hormonal therapy – complex atypical – a. treat infection and reapt smear after 12 weeks 2- Surgical excision  Topical steroids
postmenopausal patients b. if progress to high : destruction by ablation – cauterization or cryotherapy 3- Topical chemotherapy  Excisional biopsy if small lesion
2- High grade lesions II & III : Excision by  Skinning vulvectomy if wide lesion
a. Cold knife conization  Close observation aftr manage
b. Loop electrosurgical excision procedure ( LEEP )
c. TAH in older patients

‫بفضله بلغت من العلم منزل‬.... ‫ولكن اشكر االله الذي‬ ‫ مھما بلغت من العلم جاھل‬.....‫ال تغتر بعلمك فإنك‬

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Uterine carcinoma Choriocarcinoma Cervical cancer
Risk factors Prolonged unopposed effect of estrogen as in : obesity –PCOS- HRT –infertility – Molar pregnancies – abortion – multiple Early 1st sexual intercourse / Multiple parteners
nulliparity – late menopause -estrogen producigovaarian tumors –genetic pregnancies / HPV – HSV infections / Poor hygiene /
predisposition Smoking / immunosuppression
Incidence The most common gynecologic malignancy mainly in postmenopausal women from 60% follow vesicular mole – 25% abortion - Decline in the last 3 decades commonly between
55 – 70 years < 15% pregnancy – rarely nongestational 45-55 years
Patholo Gross 1-localized type : nodule or polyp infundus or cornu Friable hemorrhagic nodule arise from body invade Friable necrotic mass – deep ulcer – indurated
2-diffuse : diffuse endometrial thickening or multiple polyps endo and myometrium – ovaries shows multiple nodule if SCC // if adenocarcinoma can give cervix
Gy theca lutein cysts barrel shaped appearance
Microscopi Adenocarcinoma – adenoacanthoma –adenosquamous – 1ry SCC – papillary serous Anaplastic cyto and sycitiotrophoblast with He and 1-squamous cell carcinoma of ectocervix seen at
carcinoma necrosis chorionic villi are absent portiovaginalis 2- adenocarcinoma of endocervix
Grading - Grade 1 : <5% solid parts - grade II : 5-50 % solid parts -grade 1 : well differentiated cells - grade 2 :
- Grade III : > 50% solid parts with poor prognosis moderate differentiation - grade 3 : poor
Spread 1- Direct : to the rest of the endometrium / invasion to the myometrium It is famous for early and wide spread blood borne 1- Direct :to body of uterus – vagina –
2- Lymphatic : fundus to para-aortic LN / cornu to inguinal / isthmus to metastasis to lungs –vagina liver CNS parametium - bladder –rectum
paracervical / also direct spread to myometrium 2- Lymphatic : paracervical –obturatoexternal/
3- Vascular : late to intrapelvic organs or distant ones internal / common iliac – para-aortic LNs
Clinc Symptoms 1-podtmenopausal bleeding is the commonest 2- Metrorrhagia: profuse –persistent Persistent vaginal bleeding> 6 weeks after molar 1-contact bleeding is the commonest 2-
and recurrent even after TTT 3- offensive discharge and menstrual cramps – deep pregnancy or abortion or term pregnancy metrorrhagia and postmenopausal bleeding 3-
al pelvic pain vaginal discharge 4- deep pelvic pain or loin
presentat Signs  Bimanual examinaaiton : symmetrically enlarged uterus may be adenexal mass Bimanual : symmetrically enlarged uterus soft in 1-General : urinary manifestations in uretricobst
felt consistency / soft hemorrhagic nodule in vagina if 2- speculum : friavle mass or ulcer if late
ion  Speculum exam : toexclude cervical involvement or nodule or ulceration of metastasis to it occur obliterate vaginal fornices 3- P V : bleeds
cervix profusely on touch – later cervix become fixed and
tender
4-Bimanual : uterus normal except if pyometra
5-PR :parametrialextention&uterosacralinvovle
Investigations 1- TVS : show abnormal endometrial thickening especially memoupausal if > 5mm Elevated levels of B-HCG after evacuation 1-Knife biopsy : from suscpicious lesion if seen
for biopsy ofmolar 2-coloposcopy guided biopsy if no lesion seen
2- Outpatient endometrial biopsy : may miss the malignancy if localized TVS : mass extend to myometrium – bilateral 3-cone biopsy : if pap +ve for malignant cells and
3- FC : the gold standered dividing the sample into ( endocervical –isthmus –ant & theca lutein cysts / low pulsatilty index by Doppler extent of lesion ot seen by knife –laser –LEEP
post walls – fundus-cornu ) MRI for myometrial invasion / CT for metastasis 4-FC ": from endocervix and endometerium
/ D& C not essential
Staging  Stage I : in corpus : A ) in endometrium / B) <inner 1/2 of myometrium C) > 1- Non metastaticchorio Stage I : in cervix : A1)invasion depth
inner 1/2 of myometrium 2- Metastaticchorio <5mm & width <7 A2) >5&7 B) to body
 Stage II : to cervix but not outside uterus : A) in cervical glands B) in a. Low risk Stage II : A) t oupper 2/3 of vagin a B) to
cervical stroma parametrium
b. High risk
 Stage III : outside uterus but not the true pelvis : A ) serosa or ovaries or Stage III : A ) lower 1/3 of vagina B) to
peritoneum B ) upper vagina C) LNs lateral pelvic wall
 Stage IV : other organs : A) bladder or rectum B) distant metastasis Stage IV : a) bladder & rectum B) others
1- Stage I : a & b : TAH-BSO / c : TAH-BSO followed by vaginal cuff radiotherapy and if Chemotherapt is indicated in all cases either : 1- Stage I a1 : TAH-BSO alone or conization
Management grade 3 - Single agent : methotrexate is drg of choice for non 2- stage I a2& b : weithem's operation
2- Stage II : weritheum operation / Radio for unfit for surgery metastatic and metastic low risk 3- SatgeIIa : surgery is equal to radio
3- Stage III & IV : palliative radio and chemotherapy - Combination : MTX + EToposide + Actinomycin D for 4- Stage IIb : radio is the 1st line of TTT
4- Radiotherapy used are : intracavitry in uterus & vagina in III & IV and in II not fit for mwtastatic high risk and cases resistant to MTX alone 5- Stage III & IV : radio and chemo as palliative
surgery // Brachytherapy : cylinders in vagina in Ic and grsde 3 /// EBRT ; to ttt LN - Surgical ( TAH ) : elderly high risk Pts / resistant to 6- Weirthumsi ( TAH-BSO +pelvic adenectomy +
extention combination therapy / complicated by sever HGE or removal of parametrium and upper 3 cm of vagina )
5- Chemotherapy : either hormonal ( progestagen ) for well-differentiated tumors with estrogen perforation --- the surgery preceded and followed by 7- Radiotherapy : either primary iib by EBRT or
receptors or non hormonal ( cisplatin 0paclitexel ) for advanced EC chemotherapy intracavitary or brachy /// or adjuvant
prognosis Depends on : stage –type – grade – myometrila invasion – LN involvement IA ;cure rate 95 %
- Stage 1 ( G1-2 ) : 85% 5 year survival rate after surgery alone Ib :5 year survival rate 85 %
- Grade 3 has poorer prognosis
- More depth in endometrium the poorer the progniosis II : 5 year survival is 50%
- +ve peritoneal wash convert stage 1 to 3 Iii & IV : 25 % and % % respectively

ً‫كلما ادبنً الدھر ارانً نقص عقلً ***واذا ماازددت علما زادنً علما بجھل‬

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Non Neoplastic ovarian cysts
Follicullar cyst Corpus luteum cyst Theca lutein cyst Endometriotic cyst Inflammatory
Incidence The commonest of all functional cysts mainly 2nd common – childbearing and Incease lately due to increase in Not uncommon especially with  Tubo-ovarian cyst or tubo-
occurraing at childbearing period early pregnancy ) use of induction of oulation infertility & pelvic endometriosis ovarian abscess
&perimenopause  Infection reach ovary by
1- Cystic overdistention of an atretic follicle Excessive hemorrhage in corpus OVARIAN hyperstimulation by Hemorrhagic cysts of ovary lined lymphatics or near by infected
Aetiolgy organ
2- Dominant Graffian failed to rupture luteum in stage of vascularization 1- Natural HCG : vesicular mole by endometrial tissue ( glands
3- So it is commoanly encountered in – choriocarcinoma – &stroma ) blood accumulate  Bilateral
Metropathiahemorrhagica& PCOS& fibroids mulifetalpreg ) during menses and serous content  Pt come with history of :
– endometriosis 2- Iatrogenic : HMG – HCG absorbed leaving RBC’s give o Recent delivary or abortion
injections for induction chochalteappearance o Recent surgical pelvic surger y
Spontaneous regression and complete resolution The same Spontaneous regression and o IUD insertion
Fate  Treatment :parentral antibiotics
within few weeks unless complicated by rupture complete resolution when HCG
– hemorrhage – torsion falls regimen (ofloxacin 400mg Iv /
12 H + metronidazole 500 mg
IV / 12 H )
Pathology Unilateral – unilocular single ( 3-7 cm ) Unilateral – unilocular single ( - Multiple –bilateral –bluish – thin Thick wall – surrounded by dense Germinal inclusion
contain clear fluid 3-7 cm ) contain blood walled – contain clear fluid – adhesions ( from reapted leakage
Thin wall lined by granulose cells Thin wall lined by luteinized may reach > 20 cm of cyst ) so rarely undergo torsion  Microscopic cyst s from
Secrete estrogen causing menstrual granuloza cells - Linedc by luteinzed theca cells invagination of germinal
disturbances Secrete progesterone causing epithelium in the substance
menstrual disturbances of the ovary
 Considerd forerunners of
epithelial cancers
Symptoms Asymptomatic Asymptomatic in the majority  History of vesicular mole or History of infertility especially if
Menstrual disturbance ( delayed menses – Menstrual disturbance ( induction of ovulation pelvic endometriosis –
irregular bleeding ) delayed menses – irregular  Lower abdominal & pelvic Dysmenorhea& chronic pelvic
Pain if large –rapidly growing – complicated bleeding ) pain pain increase at time of menses
Acute lower abdominal pain if
complicated
Signs 1- Abdominal examination : tenderness at one Same signs  If large can be felt Bimamual Exam : adenexal
ovarian point suprapupically tenderness & fullness felt at
2- Bimanual : tenderness at one vaginal fornices  If small can be felt on PV at vaginal fornices
vaginal fornices with pain If lage can be felt abdominally
&tendernes on palpation
Investigations TVS-TAS : is the gold standard show the TVS : cyst is echolucent filled TVS : echolucent thin wall cyst - TAS-TVS
character s of the cyst with no septa or internal with blood that appear as fine filled clear fluid + high HCG - Laproscopyespecially If
echos particlesin clear fluid inferilte
- CBC – HCG for DD - Ca 125 level is elevated
DD 1- Simple serous cystadenoma ( lined by low 1- Abortion &metropathia same
columnar epithrlium ) in bleeding
2- Iliac fossa pain ( appendicitis – uretric stones 2- Follicular cyst& simple serous
) cyst
3- Pain in rt iliac fossa as ectopic –
appendicitis
Management  Conservative till resolution by follow up by  Conservative till resolution by  Expectant manage : removal  Very small : IM depot injections
reapted US follow up by reapted US of source of HCG of GnRH agonists
 Combined OCP accelerate resolution  Ovarian cystectomy ( if  Laparotomy is avoided except  Small endometrioma< 3 cm :
 Ovarian cystectomy ( if ruptured or ruptured or persistent – or If complicated aspirated ,irrigated and wall
persistent – or increase in size ( to exclude increase in size ( to exclude vaporized laproscopacally
malignancy ) conseve ovary malignancy ) conseve ovary  Large 3-5 cm wall removed
laparoscopcally&>5 cm by
laparotomy
‫ إن هللا ٌحب العبد المحترف‬: ‫قال رسول هلل صلى هلل علٌه وسلم‬
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Ovarian Neoplasms
Incidence Gross & cut section Microscopic Complications Hormonal activity
Serous cystadenoma Commonest benign ovarian Simple type : unilocular thin walled – thin clear Lined by cuboidal cells ciliated & Simple : lowest malignant No hormonal activity
neoplasm ( 10-15 % ovary T serous fluid /// the papillary type contain non ciliatd ( tubal epithelium ) potential but papillary
) papillary growths highest malignant ( 50% )
Mucinouscystadenoma 2nd common benign ovarian Unilateral – bluish colo r – multilocular – Lined by tall columnar Very low malignant No Known hormonal
neoplasm contain thick mucin material – reach huge sizes epithet;ium rich in golat cells potentiality ( < 5% ) activity
( may fill abdomen ) similar to endocervical epithelium Pseudomyxomaperitonii
Brenner tumor Rare ( 1-2 % ) of ovarian Solid – small to oderate – incidental discovery Epithelial cell nests with coffee May be brderlin or Occasionally secrete
neoplasm bean nucleus malignant estrogen causin vaginal
bleeding
Bening cystic teratoma The commonest germ cell Bilateral – moderate size – has long pedicle // Lined by stratified squamous Very low malignant
tumor (50% of ovary mostly unilocular containing a mamilla& epithelium with sebaceous glands potentiality < 1 % (
neoplasm in females < 20 ) variable contents (hair – skin- cartilage in squamous cell carcinoma )
sebeseous material )
Stumoovarii Rare Monodermalteratom a Hormonally active thyroid tissue 5-10 % develop into cancer 5% only capable of
producing thyroid causing
symptoms
Gonadoblastoma Rare Benign solid Germ cells mixed with 50 % predispose to
grnulosa&sertoli dysgerminoma
Fibroma Rare tumor Solid –unilateral – long pedicle – lobulated Cells of fibroblasts Meig’s syndrome
Thecoma Rare in postmenopausal Solid unilateral Cells resemble theca interna cells Endometrial hyperplasia Many produce estrogen
Serous Epithelial ovarian cancers Bilateral 50 % - has solid & cystic components Adenocarcinoma of serous type – Risk factors for epithelial
cystadenocarcinoma are the commonest with extensive hemorrhage & necrosis Psammoma bodies are common cancers :
malignant ovarian Bilateral in 20% - multilocular – contain Adenocarcinoma of mucinous Increasing age ( mean age
Mucinous
neoplasms ( 60-70 % mucinous fluid – huge size type well or moderate or poorly is 59 )
cystadenocarcinom ovarian cancers ) – older age Nulliparity& infertility
differentiated
> 50 – poor prognosis / has White race
Endometriod tumors In 30 % cases coexsistant 2nd 1ry in endometriu Adenocarainoma
tumor marker CA125 – Prior history of
Brder line epithelial chemosensitive Low malignat – could be serous or mucinous Cellular features of malignancy endometrial &
tumors but no invasion of stroma breastcancer or family
history
Dysgerminoma Commonest malignant germ Solid –small to moderate –bilateral in 10 % - Germ cells arranged in alveoli Features of malignant 5% o cases occur in
cell tumor 1-3 % – in young grayish with lobulated surface – characterized separated by fibrous septa- germ cell tumors : abnormal gonads / LDH
females 10-30 year by early lymphatic spread lymphocytic infiltration common Affect young females considerd tumor marker
Endodermal sinus T 2nd common germ cell only Small solid tumor unilateral Shiller –duval bodies ( cystic Has tumor markers Serum AFP used as tumor
1% of ovarian cancers – spaces inside which glomerulus Associated with abnormal marker / teratoma are
young women (19y) like structure gonads found in 20 %
Choriocarcinoma Very rare Unilateral solid tumor Malignant cyto&syncytio Radiosensitive and chemo Secrete HCG – cause
Conservative surgey can psudo puberty
Rare in children under 15 Y Unilateral solid tmor Immature neural , epithelial be done ( low malignant Secrete hcg – AFP
Malignant teratoma
&mesenchymal tissue tumors )

Granulose cell T 5% of ovarian malignancies Unilateral solid yellowish Call-exner bodies are pathognomenic 75% scrte estrogen others
with good prognosis in 50% cases ( spaces surrounded by secrete inhibin – 50 % are
granulose cells in rosette shape associated with EH – 5% with
endometrial carcinoma
Sertolileydg-ig cell T Rarest of all ovarian tumors Unilateral solid small or moderate in size Sertoli or leydigcels accompanied by Androgenic tumors in 75%
<0.2% / low grade malignancy – stroma derived fibroblasts will cause defeminization then
in young females ( 20-30 ) virilizing effect // rarely some
produce estrogen

‫فطعم الموت فً أمر حقٌر***كطعم الموت فً أمر عظٌم‬ ‫اذاغامرت فً شرف مروم***فال تقنع بما دون النجوم‬
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Ovarian Neoplasms 2
Benign ovarian Neoplasm Malignant ovarian Neoplasm
Symptoms 1- Aymptomatic : discovered only accidentally during US 1- Aymptomaticearly
2- Abdominal swelling felt by patient if large tumor 2- Abdominal swelling
3- Lower abdominal pain either acute if complicared or chronic dullaching pain in large sized tumors as 3- Dull aching pelvic pain&haeaviness
Mucinous cystadenoma 4- Pressure symptoms : dyspepsia –indigestion – frequency - constipation
4- Pressure symproms : if huge or incarcerated : either abdominal ( epigastric pain – dyspnea ) or pevic ( 5- DUB : if estrogen producing
frequency or retention )
5- Menstrual disorders : only if functional as theca cell tumor
Signs 1- Small tumor : only detected by bimanual examination as a mass rounded smooth cystic mobile separate from Feature suggesting malignancy :
uterus 1- History : extremes of age –rapid wt loss – rapid growth of tumor – family history –
2- Large tumor : by abdominal examination : feminizing &virilizing effects
a. Inspection : symmetrical abdominal enlargement 2- General examination : Malignant cachexia-pleural effussio n-associated breast mass
b. Palpation : abdominal mass smooth or lobulated tense and commonly mobile from above downwards –unilateral LL edema –palpable supraclavicular LNs
c. Percussion : central dullness –resonant flanks except if ascites associated ( shifting dullnesss 3- Abdominal ;skin show peaud’orange – tumor solid fixed bilateral –ascites
3- Ovarian cachexia could develop in rapidly growing tumors 4- Pelvic :nodules in oduguls pouch –bilater\l soildadenexal mass –frozen pelvis
5- At laparotomy : ascites – nodules on omentum – peritoneal nodules – bilaterality
fixation invasion of capsule –variable consistency – papillae & adhesions
Investigations 1- U/S : help in - US : TAS-TVS is the gold standard - chest xray : pleural effusion &secondaries
a. Diagnose ovarian origin – - X-ray abdomen calcification - TC-MRI : spread to liver + LNs
b. differeniate benign from malignant ( hetrogenous echogenicity – low resistance Doppler – ascites ) - Barium meal & enema : for 1ry cancer colon or stomach - GI endoscopy : same
c. Laterality of tmor and size consistency /uni or multilocular - IVP : course of ureter & backpressure on kidney
2- Tumor markers : Ca125 in epithelial cancer & CA19-19 with mucinous carcinoma - Paracentesis : for cytologic examination
3- Laproscopy : to differentiate ovarian cysts from tubo-ovarian cystic masses /// solid ovarian fibroma from - Endometrial curettage : in cases of DUB
pedunculated SSM - Tumor markers : CA125 in epithelial cancers – HCG in choriocarcinoma – LDH in
4- IVP : to delinate course of ureter dysgerminoma – alpha fetoprotein in EST
Complications / Torsion HGE Infection Rupture incarceration Malignant  Stage I : confined to ovary : (a) one ovary wit hintact capsule –no tumor deposits on
Predis- Moderate size + Torsion / Puerperium / Torsion or Large size Higher in external surface – no ascites ( b) two ovaries with same characters (c) Ia or Ib with
staging posing long pedicle / free trauma / infected Hge / trauma imapacted in solid than Ascites -+ve peritoneal wash – ruptured capsule – deposits on external surface
mobility / pregnant during organ / during labor douglas pouch cystic  Stage II : pelvic extention : ( a) to uterus & tube (B) other pelvic tissues (c) IIa or
&purepurium pregnancy or rough PV IIb + previous criteria in Ic
C/P Acute abdomen Acute General P of Acute Pressure  Stage III : with peritoneal implants – or +ve retroperitoneal or inguinal nodes : (a)
abdomen infection abdomen - symptoms grossly limited to pelvis with –ve nodes \9 microscopic implants ) - (b) implants <2
cm on abdominal peritoneal surface nodes –ve (c) implants >2 cm nodes +ve
TTT Ovriotomy in Shock Antibiotic s Sedatives – Ovariotomy or
 Stage IV : distant metastasis : liver lung etc …
absence of healthy manage + – oviotomy resuscitation cystectomy
 Staging here can only reached surgically by exploratory Laparotomy
tissue / or ovarian Ovriotom via – ovariotomy
cystectomy y laparotomy – peritoneal
lavage
1- Young female :  TAH-BSO and infracolicomentectomy : standard TTT for stages I-IIa completed by peritoneal
Mangemnet wash & LN sampling
a. Small cyst : ovarian cystectomy ( enculation with ovarian preservation ) laparoscopacally except
dermoid cyst removed by lapparotomy due to risk of dissemination of irritant contents  Unilateralsalpino-oophorectomy only in Ia + young patient + low malignant tumor (malignant
germ cells – malignant sex cord – border line epithelial )
b. Large cyst : Oophorectomy ( removal of cyst together with the ovary ) by laparotomy due to risk  Initialdebulking : ( TAH-BSO + omentectomy + excision of pelvic masses & peritoneal deposits
of dissemination – malignancy – absence of heaklthy ovarian tissue > 1-2 cm + bowel resection if needed for rest of stages from IIb
2- Older femalenon diserous for further fertility : TAH-BSO to prevent against develop of ovarian cancer  Interval Debulking : chemotherapy prior to debulking to reduce size of tumor
 2nd look surgery : to asses residual tumor in abdominal cavity after operation & chemo / done
only these days for patient with –ve imaging and rising tumor markers
- Chemotherapy : in stage I-IIa used only if +ve peritoneal or ruptured capsule – in stages II-IV
used either as adjuvant after surgery if resectable tumor – or palliative
- Radiotherapy : little place in epithelial – canbe used as adjuvant in germ cell tumors
 Factors affect prognosis : histopathologic type ( epithelial worest ) – histologic grading (well or
Prognosis poor differentiation ) – staging – response of tumor to adjuvant therapy
 5 year survival rate is : 90% in stage I - 80% in stage II – 15-20 % in stage III – 5% in stage IV

‫ وأساس‬، ً‫ الن أساس اإلٌمان القلب الذك‬. ‫ والعمل من خصائص الشباب‬، ‫ والحماسة‬، ‫ واإلخالص‬،‫ اإلٌمان‬: ‫ وتكاد تكون ھذه األركان األربعة‬. ‫ ووجد االستعداد الذي ٌحمل على التضحٌة والعمل لتحقٌقھا‬، ‫ وازدادت الحماسة لھا‬، ‫ وتوفر اإلخالص فً سبٌلھا‬، ‫إنما تنجح الفكرة إذا قوي اإلٌمان بھا‬
) ‫ ( اإلمام الشهيد حسن البنا‬.‫ وفً كل فكرة حامل راٌتھا‬، ‫ وفً كل نھضة سر قوتھا‬، ‫ ومن ھنا كان الشباب قدٌما و حدٌثا فً كل أمة عماد نھضتھا‬.‫ وھذه كلھا ال تكون إال للشباب‬، ً‫ وأساس العمل العزم الفت‬، ‫ وأساس الحماسة الشعور القوي‬، ً‫اإلخالص الفؤاد النق‬

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Vaginitis
Bacterial vaginosis Candida vaginitis Trichomonas vaginalis Childhood vaginitis Atrophic vaginitis
Incidence the commonest cause of bacterial 30% of cases with vulvovaginitis – 3rd most common cause of Rare but occur due ( weak Occur in postmenopausal
vaginal infection – 50% of considered STD vaginitis ( 25 % of cases ) – epithelium – low vaginal PH ) women – breast feeding women
women attendening for STDs multifocal infction (STD )
Risk factors 2nd trimester abortion – premature 1- changes in PH to more acidic 1- Poor hygiene - Loss thickness of vaginal
labour - PID – endometritis pregnancy – OCP- spermicidal 2- Foreign body insertion epithelium
– abuse of douching 3- Pinworms ( - Decreased estrogen levels so
2- ↓ host immunity ( Daibetes ) entrobiusvermicularis ) low glycogen content and
3- Long use of antibiotics alkaline PH
Causative organism Gardenerllavaginalis– Bacteroid - Candida albicans : normal Trichomomnasvaginalis : E-coli – streptococci –gonococci - Leucorrhea – pruritis –
species – mycoplasma hominis ( inhabitant of bowel – peri-anal flagellated protozoon larger – staph vaginal burning
unexplained increase in vaginal region – 30% of female vagina than leucocytes - By speculum : atrophic
anerobes due to decrease in - Non albicans : candida tropicalis vagina – inflamed walls –
vaginal PH ) – not sexually – torulopsisglabrata 20% cases discharge
transmitted resistant to usual TTT
Clinical picture 50% asymptomatic – the main - Intense pruritis – vaginal burning 1- 25-50 % are asypmtomatic - Vanial discharge : purulent
symptom : vaginal discharge ( ( dyspareunia ) 2- Vaginal discharge : copious foul smell
profuse – non irritant – - vaginal discharge ( cottage cheese – frothy offensive - Pruritisvulcae
malodorous – thin- yellowish dysuria 3- Pruritis – vulvitis - Dysuria
white or whitishadherent to - Vulva red swollen /vagina : 4- Strawberry spots : on
vaginal walls- fishy amine smell ) patches of adherent cheesy speculum examination
discharge ( punctate hemorrhage on
vagina – cervix )
Investigations 1-saline wet mount preparation : 1- Wet mount examination with  Saline wet mount preparation 1- Cuture& Infection not usually identified
clue cells ( epithetlial cells coated saline & 10% KOH : hyphae – : numerous leucocytes – sensitivityofdischarge by wet mount preparation
by bacteriaobscuring its borders ) pseudohyphae with budding flagellated trichomonads 2- US or X-ray t odetect Vaginal PH is low < 4.5
2-10% KOH : on fresh sample of yeasts  PH : weak acidic ( 5- 6) foreign body
vaginal secretions give fishy 2- PH : < 4.5  PAP smear : to exclude 3- Investigations for entrobius
odour 3- Swab& culture not necessary cervical neoplasia – oxyuris
3-PH : > 4.5  Culture rarely
Treatment Systemic : Metronidazole 500 mg 1-Intravaginal antifungal : - Metronidazole either 1g 1- Antiseptics - Intravaginal estrogen cream
oral twice for 7 days / clotrimazole 1% cream ( 5g - for single oral dose – or 500 mg 2- Systemic antibitics every night for 2 weeks then
clindamycin same dose 7 days ) – Nystatin 100,000 unit twice for 7 days 3- Treatment of worms once weekly
Local : Metronidazole gel 0.75% vaginal tab for 14 day - Intravaginal therapy isnot so 4- Removal of foreign body if - Systemic HRT : to treat other
or clindamycin cream 2% one full 2-oral : fluconazole single oral effective ( multifocal ) found symptoms of menopause
applicator intravaginally once for dose 150mg / ketoconazole 200 - During Pregnancy : metro-
5 days mg twice for 5 days for recurrent nidazole from 2nd trimester
During Pregnancy : clindamycin  During pregnancy : - Male patener should be
used but metronidazole only from intravaginaal TTT is safer treated
2nd trimester  Reecurrent cases : due to (non- - Recurrent : ssearch for other
albicans strains – DM – infected STDs
male partener )
. ‫ إنك بحاجة الن تتعلم الصفح وغض الطرف كً تواصل مشوار الحٌاة‬.ً‫إنك بحاجة الن تكف عن الحٌاة داخل ذكرٌات الماض‬
. ‫ أو أال تستطٌع التعرف على أخطائك وجوانب ضعفك‬، ‫ ولكن لٌس لدرجة أن تلزم نفسك أن تكون كامالً طوال الوقت‬، ‫ إنك بحاجة الن تأخذ نفسك على محمل الجد‬. ‫إنك بحاجة الن تكون مستمعا ً جٌداً حتى تستخلص أفضل ما لدى اآلخرٌن من خبرة‬
) ‫ديفيد فيسكوت ( خبير تنمية بشرية‬

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Female genital tract infections
PID Chronic salpingitis Acute endocervicitis Chronic cervicitis Cervical erosion
Aetiology Organisms : Neisseria gonorrhea is the most common cause / 1- Sequlae of acute PID Sexually transmitted Sequel of acute cervicitis Bright red area around
chlamydia trachomatis : in 20-40% / endogenous bacteria :E- 2- TB start as chronic infection pathogen ( neiseria gonorrhea  Symptoms external os due to
coli- strept –klebseilla – chlamydia- trichomaonas ) o Vaginal discharge replacement of stratified
Routes of infection : ascending from endocervicitis- direct - Staph or strpt o Dyspareunia sq epithelium of
from infected organ – lymohatic from purepural infection – o Backache ectocervix by columnar
rarely blood born o Dysmenorrhea epithelium of endocervix
1- Young sexually active female / Multiple sexual parteners IUD insertion - - post abortive o Contact bleeding -chronic cervicitis
Predisposing o Infertility
/ After menses due to retrograde menses /Sexual intercourse – D&C procedure –part of -congenital erosion
factors facilitate ascending infection/ Iatrogenic as : IUD – D& C purepural sepsis o Frequency of micturition -hormnal erosion (excess
operation – HSG  Signs : estrogen with OCP )
1 – Endosalpingitis: mucosal destruction & cilia – catarrheal 1- Hydrosalpinx: follows acute cattarrheal o Mucopurulent offensive IN chronic : infected
Pathology discharge
or suppurative 2- Pyosalpin x : acute suppurative discharge erode
3- Interstitial &perisalpingitis : in musculosa& serosa 3- Chronic interstitial salpingitis o Cervical erosion epithelium at external os
4- Oophorits : micro-abscesses on ovarian surface 4- Tubo-ovarian cyst o Chronic hypertrophc and columnar
5- Pelvic peritonitis from direct extention 5- Tubo-ovarian abscess cervicitis epitheliiumcover area then
6- Chronic PID o Mucous polyp ( hyper – stratified grow beneath
 Recent surgical intervention : D&C or IUD or delivery –  History of acute PID 1- Mucopurulent plasia of epithelium ) 1- Vaginal discharge :
Symptoms o Nabothian cyst ( obst-
abortion in young active female  Pain : lower abdominal / pelvic / lower vaginal discharge excessive mucoid
 Acute lower abdominal pain backache / pelvic congestive symptoms 2- Dyspareunia truction of glandular 2- Contact bleeding
 Increased vaginal discharge ( discharge / menorrhag ) / Dysmenorrhea / 3- Mid fever ducts 3- Symptoms of chronic
 Picture of infection : fever – headache – malaise = nausea dyspareunia 4- Backache cervicitis
– vomiting  Infertility : tubo-peritoneal factor
Signs  Abdominal Exam : lower abdominal tenderness Adenexal swelling bilateral – tense – cystic – - Cervix red swollen – with Vaginal exam : contact
 Bimanual Exam : aadenexal tenderness – cervical motion tender fixed with fixed RVF by adhesions – dischare bleeding
tenderness chronic cervicitis - Tenderness on moving it Speculum : flat ,papillary
or follicular erosion
Invetigations  Examination of discharge : by gram stain for gonorrhea –  Pelvic US : detect adnexal mass Cuture& sensitivity of 1- Culture & sensitivity of Vaginal and cervical
search for achlamydial& gonorrheal antibodies  Laproscope; especially with infertility – discharge discharge smears to exclude
 CBC & ESR : leukocytosis &icreased ESR differentiate it from endometriosis 2- Exclusion of malignancy malignancy
 US: mostly norml in acute except if tubo-ovarian abscess –  Investigations of TB by vag&cervical smears
also to exclude ectopic &myomata  CBC & ESR : leukocytosis &icreased ESR
 Laproscopy :gold standard ( tubal hyperemia – edema –  HSG : show dilated blocked tube – done
purulent exudate ) done to confirm or in poor respone to after subsidence of acute phase
TTT after 72 H  Immunoflurescent antibody for chlamydia
 Culdocentesis : aspiration of fluid from douguls pouch for  CT : in some cases
culture & sensitivity
 Tests for STDs
DD Ectopic pregnancy / ruptured ovarian cyst / degenerating Pelvic endometriosis – pelvic malignancy
myoma / Endometriosis / inflammatory bowel disease
Treatment 1- Rest &analgesics antipyritics 1- Conservative : Antibiotics for acute Broad spectrum antibiotics 1- Oral & vaginal 1- Hormonal erosion : no
2- Empiric therapy of antibiotics : exacerbations – glycerineecthyol for pelvic _ it canbe complicated by : antibiotics ttt except prolonged
a. Mild to moderate cases : Broad spectrum antibiotics congestion 1- Turning into chronic 2- Cervical 2- Antibiotics for chronic
orally ( ofloxacin 400mg once orally for 14 day + 2- Surgical : infection due to branching cauterizationincase of cervicitis
Metronidazole 500 mg twice orally for 14 day ) a. Salpingostomy : infertility due to of endocervical glands erosion 3- Cauterization
b. Sever cases : parentral antibiotics regimen (ofloxacin hydrosalpinx of small size – no 2- Spread of infection to be :electrocautery –
400mg Iv / 12 H + metronidazole 500 mg IV / 12 H ) recurrent acute exacerbations PID cryocaytery – laser
c. Tubo-ovarian abscess: same as sever or Ampicillin 2g iv b. Salpinogectomy:frequent acute Vaporization –
/4 H + gentamycin + metronidazole 500 IV / 8 axacerbtions – large swelling Endocoagulation
3- Surgical ttt : sever cases and abscess formation either c. Hysterectomy : if both tubes affected
drainage of abscess or unilateral salpingo-oophorectomy d. Aspiration & drainagefor cystic swellin
e. ICSI & IVF for ttt of infertility
Whatever doesn't kill you really does make you stronger. Time heals almost everything. Give time, time.
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TB Bilharziasis Syphilis Gonorrhea Chlamydia HSV HPV HIV
Organism Ttuberculosis bacilli Treponema palladium Neisseria gonorrhea Chlamydia Herpes simplex II DNA virus Retovirus I-II
trachomatis
Route of Blood – lymphatics – Vascular Sexually transmitted Sexual – infected Sexual transmission – Sexual – t onew born Sexual – neonatal Sexual - - blood
direct extension from communication towels or toilet – baby perinatal trans during vaginal infection products –
infection peritoneum - infected between vaginal during labour delivery contaminated syringes
semen &vasical venous – tattooing –perinatal
plexus
Pathology Tubes show : sausage Deposition of ova :
shaped – surrounding - Sandy patches
adhesion – tubercules - Polyp formation
on surface – fimbriae - Ulceration
not indrawn - Fibrosis
Clinical picture 1- Infertility : - Vulva : multiple 1- 1ry syphilis: 1- Urethra : frequency 1- Endocervicitis: - 1st attack : multiple 1- Condylomaaccu 1- Initial infection :
2- Menstrual sessile papliomata> chancre on vulva or & burning asymptomatic small painful monata: mononucleosis like
disturbances ulcers cervix raised papule 2- Endoccervix: 2- Salpingitis: ectopic vesicles rapidly cauliflower like symptoms
3- Discharge - Vagina : any of 4 soon ulcerate + backache & or infertility ulcerates leaving lesions on vulva 2- Incubation : long
4- Pain lesions found enlarged inguinal discharge 3- Urethritis : shallow painful 2- Dysplastic variable 5-10 years
Signs : - Cervix : LNs 3- Bartholin gland : frequency & dysuria ulcers changes of cervix 3- AIDS related
1- Tender fixed papillomata mor 2- 2ry syphilis : skin tender – red edma 4- Perinatal infection : - Recurrent attacks : especially complex : fever –
adnexal swelling common rash – mucous 4- Salpingo-oophoritis conjunctivitis – milder than 1st serotypes 16-18 diarrhea for > 1 m-
2- Nodules in - Tubes /ovaries : patches – 5- Transientendometrit pneumonia attack due to weight loss all not
douglous pouch fibrosis condylomatalata – is reactivation of virus explained –
3- TB peritonitis - Uterus : very rarely generalized LN 6- Systemic infection : generalized LN
4- TB cervical ulcers 3- 3ry :gumma – CVS arthritis –iridocyclitis 4- AIDs :
affection – 7- No vag infection immunosuppression
neurosyphilis ( Kapsi sarcoma –
opportunistic )
Investigations 1- PEB : saline Urine –stool analysis 1) Smear from lesion : 1-smear & culture of 1-tissuecutlture : Complications - PAP smear : 1- Detection of viral
preserved – Zeil- To prove bilharziasis dark ground discharge at thyar Mccoys cells 1- 1ry attack in koilcytes ( antibodies by
nelsen stained – + picture of lesions illumination martin medium 2-complment fixation pregnancy lead to exfoliated ELISA –western
Lovenstein Jensen 2) Biopsy : show 2-complement 3-pap smear of cervix abortion squamous cells blot technique
cultured syphilitic fixation test +ve after 2- ROM > 4 H cause wrinkled &pyknotic 2- CD4 /CD8 ratio
2- HSG : Dwarf granulation tissue 6 weeks infection of fetus ) depressed
uterus – beading of 3) Serological tests : lead to its death - Coloposcopy: flat 3- Viral culture
tubes +ve in 2ry stage : 3- It is linked to small lesions with
3- Laproscopy: a. Non specific : cervical neoplasia vascular punctations
4- CBC : wasserman and cancer
Lymphoctosis ↑ reaction & VDRL
ESR b. Specific : TPI /
5- Tuberculin test FTA-abs/ Microh-
6- Chest x-ray emaglutination
assay
Treatment 1- Medical : Antibilharzial: Procaine penicillin : Procaine penicillin Antibiotics - Analgesics - Condylomatalatale No effective ttt –
combination of 2 praziquentel 600,000 U IM daily single dose 4.8 million prophylaxis to new - Acyclovir orally asions : painting by Azidothymidineused
antituberculus for Antibiotics for 2ry for 2 W or units IM combined by born 200 mg 5 times for podphylin resin 25 to ptolong survival
at least 6 M INH – bacterial infection Benzathinepenicillin 1 gm of probencid Tetracycline 500 mg 10 days or locally % in paraffin oil –
rifampicin : 2.4 milliom unit . orally /6 H for 1-2 w - Local gential violet cryocautry –
2- Surgical : Erythromycin for 1% electro- laser – 5
apnhysterectomy in penicillin sensitive - CS for pregnant flourouracil
large cases with infection - Precancerous
preceded - Cervical smear to lasions : cryo- laser
&followed by ATB rule out dysplasia – or surgical
remova l
)‫(مصطفي السباعي‬ .‫ وانصح عممك بإدامة النظر في مصادره‬،‫ و انصح مالك بالحكمة في إنفاقو‬،‫بالشح في شهواتو‬
ّ ‫ وانصح جسمك‬،‫ وانصح عقمك بالحذر من خطراتو‬،‫انصح نفسك بالشك في رغباتها‬
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Incotinence & fistulae
Stress UI Urge UI Vesicovaginal fistula Ureterovaginal Urethral F Rectovaginal F
Definition Involuntary escape of urine through urethra during Leakage of urine from urethra Abnormal communications between Between ureter & Rare
increased IAP during cough – sneezing –straining before starting to void bladder & vagina vagina
Aetiology 1- Childbirth trauma :damage pelvic floor 1) Idiopathic 1- Obstetric trauma :either necrotic Injury of ureter Obstetric 1- Traumatic :
muscles & fascia 2) Local bladder irritation : stone VVF ( obstructed labor ) or traumatic ( during gynecological childbirth complete perineal
2- Postmenopausal weakness : atrophy of fascia infection, ulcer ,polyp instruments ) operation as trauma / tear / post colpoperi
3- Fibrosis of urethra & periurethral support from 3) Neuropathy: DM , spinal cord 2- Pelvic surgery hysterectomy hysterectomy – surgical trauma 2- Inflammatory :
bladder neck surgery lesions espciallty with adhesions – pelvic wertheim's – anterior as correction of perianal abscess
4- Congenital weakness in pelvic support malignancy surgey - CS colporrhaphy difficult SUI 3- Malignant : extensio
+ chronic increase in IAP ( obesity – 3- Pelvic malignancy : 2% direct delivery by CS 4- Irradiation :
constipation – chronic cough ) 4- Pelvic radiation : 6 % 5- Congenital : rare
Symptoms Involuntary leakage of urine during coughing – Urgency , frequency , nocturia - Complete incontinence ;is the main Incomplete incontine- Continent all - Large fistula :
may be associated prolapse presentation ( continous – no desire ) in ce ( bladder fill empties through but incontenece of feces
Signs 1- cough stress test :elicit urine escape to see Same test of SUI to exclude SUI low or large
- Partial : if high or small
normal
1- Inspection : small
complain of
voidi of double
& flatus + 2ry
vaginitis ( vag
2- Bonney's test : differniate between SUI due to
bladder neck descent or due to weakness in - Cystitis –vulvitis – pruritis highly situated fistu stream of urine discharge )
bladder neck - History after labor – radio 2- Methylene blue test during voiding / - Small: escape of
3- Examination for associated prolapse - Feal fistula if large or fibrosis around it if todifferentiate it fom post micturation flatus from vagina
4- Q-tip test : detect descent & mobility of small in palpation vesicovaginal fistula vaginal
urethrovesical junction - Inspection by sims' speculum dribbling
Investigations 1- Urodynamic studies : Cystometry : (leakage of 1- Cystometry : detrosur 1- Retrograde coloured dyeinjection – Cystoscopy show Urethral
urine during increase IAP in abscene of overactivity as detrusor pressure inspection & 3 gauze test normal bladder with catheter –
detrusor contractions ) – urethral pressure filling > 15 cm/H2O 2- IVP ; for course & uretric F uretric efflux on one urethroscopy
profile  increased intravesical P over 2- Urine culture & sensitivity may 3- Cystoscopy & IV injection of indigo side –failure of passage
intraurethral reveal cystitis as a cause – carmine dye / urethroscopy of ureteric catheter on
2- Midstream urine specimen for culuture 3- IVP – cystoscopy – affected side
3- Postvoiding residual urine PVR incre urethoscopy
4- IVP – cystoscopy – urethroscopy
management 1- Conservative : 1- Bladder training exercise : 1- Conservative : 1-Prevention : Surgical 1- Fistula in lower 1/ 3
a. Pelvic floor muscle exercise : kegel exercise increase interval between voids a. If discovered during difficult labor a. Preoperative IVP reconstruction of vagina : convert it
or passive electrical stimulation difficult need cooperative Pt → inser t rubber catheter and left for to delineate course of urethra & into complete peri-
b. Scheduled voiding & avoid complete filliing 2- Anticholinergic drugs : 3-6 weeks till fistula heal or ureteric catheter closure of neal tear and suture
c. Estrogen therapy : local vaginal cream in detrusitol 2 mg twice daily b. If discovered some time after no b. Proper surgical defect it in layers
menopausal operation done except after 3-6 technique 2- Fistula in middle
d. Alphasympathomimetics to decrease IVP months c. Immediate repair 1/3 : dedoublemet
e. Pessary ttt : temporary ttt for sui with 2- Surgical : in operation if operation
prolapse a. 1st repair carries the best prognosis / discovered 3- Fistula in upper 1/3
2- Surgical : multirepair must be tension free 2- Re-implantation of : abdominal reapir
a. Colposuspension operation : suscpension of upper b. Preoperative preparation :
i. Proper assessment
ureter in bladder or due to dense fibrosis
vagina & upper 1/3 of urethra to cooper's ligament end to end 4- Preoperative :
by abdominal approach (standard operation – ii. Ttt of vulvitis & cover it b y Vaseline
highest success rate ) iii. Renal function test anastomosis purge & daily enema
b. Sling operation : suscpension of vescicourethral iv. Culture of urine 3- Implantation into & vaginal douche /
junction to anterior abdominal wall by rectus sheath c. Operations : segment of ileum if non residue diet /
– sutures – tension free vainal tape ( mesh like tape ) i. Vaginal : deboublement / saucerisation reimplantation is not neomycin orally 3
c. Kelly's placation with anterior coloporraphy ii. Abdominal : for large –high – recurrent possible days before
placation of parauretheral fascia vaginally –then ant – near ureter
5- Post operative :
coloporaphy is done by success rate 60-70 % d. Post-operative : vaginal pack for 24 h
/catheter for 10-14 day / no sexual course
vulva regularly
d. Periurethral injection of collagen : short term ttt
success after 5 years < 30 % for 3 m & pregnancy for 1 Y / subsequent washed / low residue
labor by CS diet continue /
intestinal antiseptic /
antibiotics for
infection

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- Surgical :
 Definition :
Prolapse Leiomyoma  Indications for surgery in myoma :
Prolapse of one or more of pelvic organs downwards into vagina  In asymptomatic patients : multiple large myoma > 14 week / rapid growth or rapid recurrence after removal / certain
 Definition : types ( pedunclated SSM / cervical or broad ligamentry / SMF protrude from cervix )
 Types of prolapse:
o Anterior vaginal wall prolapse : urethrocele – cystocele –
Benign tumor of uterine smooth mudscles ( myometrium )
 Incidence : commonest benign tumor of FGT 20% in over 30 women
 Symptomatizing Pts : sever intractable bleeding – infertility & RPL if proved to be the cause
cystourethrocele  Risk factors :  Operations are :
o Posterior vaginal wall prolapse: rectocele – enterocele
o Apical vaginal wall : utero-vaginal ( uterine descent with inversion
- Nulliparous & low parity morethan multiparois  Myomectomy :
of vaginal apex ) – vault prolapse ( sfter hysterectomy
- Positive family history / Dark races more common / Obese o Indications : done in symptomatic fibroid in women desirous for fertility after failure of medical ttt / associated
 Aetiology : infertility or PRL due to myoma .
 Degrees : - Hyper-estrenism : evidenced by appear only in childbearing period – increase in
o 1st degree : descent within vagina - 2nd degree : descent to the o Contraindications: During pregnancy except if torsion occur / after menopause / suspension of sarcomatous change /
pregnancy – decrease in menopause – associated endometrial hyperplasia multiple large myomata
introitus - Growth factors ( increased EGF – decreased GIF )
o 3rd degree : descent outside introtus ( complete descent of uterus - Genetic factors : play a role o Types : abdominal is the commonest / vaginal in SMF polyp or cervical fro portio vaginalis / hysteroscopic in SMM
called procidentia <5cm dimeter protrude >50 % inuterine cavity / laproscopic mainly SSM <4 in number <6 in diameter
 Pathology :
 Aetiology : - Macro : variable size – rounded – multiple usually – firm – asymmetrical uterine o Complications : excessive blood loss / postoperative fever ileus / persistent of symptoms / recurrence / intestinal
o Childbirth trauma : multiparity ( risk ↑1.5 times with each vaginal enlargement adheesions / rupture of uterus later in labor
delivery ) increased duration of 2nd stageof labor with high fetal - Cut section : whorled appearance paler from uterus – psudocapsule in which lie blood  Hysterectomy :
birth Wt or forceps use – direct pelvic floor injury vessels o Indications : multiple or very large especially in perimenopausal or multiparous / post menopausal wit
o Ageing : every decade of life 30-60 incidence doubles from collagen - Micro: smooth muscle cells in bundles with fibrous CT hsymptomaizing fibroids
loss  Pathological changes : o Types : Aabdominal / vagina lin uterine enlargement < 12 W with some prolapse / laproscopic in slightly enlarged
o Congenital weakness : of pelvic support or spina bifida defective
innervation ( nulliparous prolapse)
- Atrophy after menopause - hyaline degeneration : commonest
- Cystic degeneration if absorbed - fatty degeneration
 Uterine aartery embolization : with 60% reducation of size
o Iatrogenic : inadequate support of vaginal vault in hysterectomy - Calcification - red degeneration : with thrombosis of BVs  Lparoscopic myolysis : by laser –coagulation or cryo
o Any of this + increased IAP
 Anatomical changes :
- Necrosis - Infection - torsion of pedunculated SSM
- Rupture of surface vei of SSM - incarceration during pregnancy
 MRI guided focused US produce protein denaturation
o Vagina : keritinization ( being everted exposed to air-trauma ) / - Malignant transformation : very rare 0.5 %
ulceration ( from congestion & circulatory changes )  Effect on pelvic organs : Endometriosis
o Cervix : ulceration in most dependant part / hypertrophy from - Uterus : increased in size – enlargement of cavity – endometrial hyperplasia - increased
congestion / supravaginal elongation from stretch on mackenrodt's vascularity – displacement or inversion in large fundal ones  Definition :
o Urinary : descent of base of bluffer / kinking of ureter (hydroureter - Tubes : chronic salpingitis with infected SMF polyp – obstruction in corneal ones – Presence of functioning endometrial glands and stroma outside endometrial cavity
 Symptoms : elongation & stretch in broad ligamentry  Aetiology :
o Sensation of pelvic heaviness :↑by end of day - ↓ by rest - Urinary : frequency if press on bladder – retention if pressing on urethra – hyroureter o Retrograde menstrual flow through tube to peritoneum implanting ccausing irritation and celomic metaplasia
&hydronephrosis if press on ureter
o Mass filling vagina : on strainig or squatting - ↓ by lying down & o Hematogenous or lymphatic spread : explain endometriosis indistant tissues
 Symptoms :
reduction o Gentic and immunological influence : 7% in siblings – altered immunological influene is involved
- Menstrual disorders : menorrhagia ( increased endometrial surface area –interfere with
o Low backache : from stretch on uterosacral ligaments & uterus ↑ by  Pathology :
heavy work –weight lifting ↓by rest – lying down uterine contractions - ↑ vascularity –endometrial hyperplasia ) – metrorrhagia ( tip of SMF o Pelvic endometriosis : burned match head spots ( multiple small dark red or brown cysts )
o Urinary symptoms : common ( frequency from trigone irritation or polyp – sarcomatous change ) o Ovarian Endo : either powder burn ( tiny superficial hemorrhagic implants ) or chocolate cyst ( ovarian
cystitis / SUI / inability to complete micturation unless mass is - PAIN : dull aching ( infection /hyaline degeneration ) – coliky( extrusion of polyp ) – endometrioma cyst filled with dark alterd blood )
reduced ) acute abdominal ( red degeneration – torsion of SSM – loin ( hydronephrosis ) –  Symptoms :
o Rectal symptoms : heaviness in rectum / difficult defecation dysmenorrhea SMF o Type of patient : midreproductive age – nulliparous – high socioeconomic
o Menstrual symptoms : dysmenorrhea / leucorrhea - Pressure symptoms :on bladder→frquency – urethra→retention - ll veins→ edema – o Dysmenorrhea : intramenstraul increscendo ( with onset on menses ) decrescendo fashion ( toward end of cycle)
nerves→referd back pain -
 Signs o Dyspareunia : due to omplamts on douglas pouch – uterosacral ligament- ovarian – fixed uterus
- Infertility in 5-10 % interfere with implantation (SMM ) or sperm ascent ( cervical ) –
o General for causes of increased IAP o Chronic pelvic pain : > 6 months strongly suggestive of endometriosis
tubal obstruction (corneal or multiple SMM) – associated condition
o Examination of type & degree of mass / ppresence of ulcers / if o Infertility : Moderate to sever endo ( from periovsasrian adhesions lead to impaired ovum pick up / anovulation
 Signs :
there is complete procidentia / dyspareunia ) in mild ( luteal phase defect – increased tubal macrophage activity )
- Abdominal examination : only large ones felt mobile –firm non tender dull on percussion
o Test levator ani function by palpation of post vaginal wall & o GIT symptoms : pain in defecation due to implant on recto-sigmoid
asymmetrical except single ISM or SMM
perineum during cough & strain o Urinary : dysuria & frequency
- Pelvic examination : confirm large by mobilitywith cwervical motion – detect small
o Daignosis Of : supravaginal elongation of cervix by uterine sound to o Distant : lung ( hemoptysis ) – brain ( seizures ) – umblicud ( monthly bleeding )
byasymmetrical uterine enlargement – fell SMF or cervical – uterus fixed in cervical &
measure cervical length t ointernal os inrelation to fornices depth /  Signs :
broad
associated stress incontinence / enterocele feeling gurgling o In minimal lesion normal examination – but extensive : fixed RVF from adhesions /if chocolate cyst: felt as
- Speculum : diagnose SMF polyp protrude from cervix
 Investigstions : tender tense cystic fixed adenaxal swelling – nodules on dougles pouch : tenderness on vaginal examination
 Investigations :
o Urine analysis for culture & sensitivity / IVP for ureter  Investigations :
- US : gold standard daiagnose site –size –number / relation to endometrial cavity / exclude
o Urodynamic studies for incontinence / pelvic & Abd US o CA-125 : elevated in endometriosis useful for follow up of response to treatment
any pelvic pathology / SSH for SMF
o Routine preoperastive / silver nitrate on ulcers o Pelvic imaging : US & MRI can not detect typical endometriotic lesions only large ones – and ovarian endometrios
 Maneegement :
- HSG : detect uterine cavity enlargement – SMM as filling defect – test for tubal patency o Laparoscopy : gold standard in diagnosis indicated in cases of infertility –chronic pelvic pain – unresolved
- MRI : differentiate between adenomyosis & leimyoma / between broad ligamentry – solid adnexal masses : you see characteristic brown pigmentations surrounded by adhesions
o Conservative : Pessary treatment ( temporary reducation ) till : ovarian tumor  Treatment :
healing of ulcers – ttt of anemia & correction of liver and kidney
- Laparoscopy : rare mainly for ttt of ssm o Medical : create a state of pseudo pregnancy or pseudomenopause by
function / during pregnancy / medically unfit either ring or shelf type - Hysteroscopy : confirm SMF – SMM  OCP : reapted courses continuously administerated 4-6 M each creating a pseudo-pregnancy state & atrophy
o Surgical : - Preoperative investigations including IVP – resorption of ectopic endometrium
 cystocele : anterior colporrhaphy – rectocele ( posterior  Treatment :  Progestogen : continuous therapy of synthetic progestin either tablets 5mg orally of MPA or depot MMPA
colpoperine-rrhaphy ) –cystorectocele ( classical repair both
- Conservative : for asymptomatic small fibroid to be examined periodically each 6-12 M injections / 3 months
previous operations )
- Medical : in cases of menorrhagia & uterine enlargement < 12 W  GNRH agonists : block Pituitary GNRH receptors → suppression of FSH & LH → suppression of ovarian
 uterovaginal ( with cysto-rectoocele : classical repair with
 NSAID : ↓ PGL → ↓Menstrual flow estrogen & transient 2ry amenorrhea ( pseudo-menopause ) taken IM injection monthly
shortening of mackenrodt's / same condition + supravaginal
elongation : machester operation ( same + amputation of vaginal  Progestin : atrophic endometrium → control bleeding – regular shedding & cycles  Danazol : testosterone derivative lead to suppression of FSH & LH as well as ovarian estrogen & progesterone
portion of cervix ) /perimenpausal + marked prolapse ( vaginal  GNRH : lead to 2ry amenorrhea & ↓size –vascularity of myoma taken either : → atrophic endometrial changes & 2ry amenorrhea finally suppression of endometric focus
o Surgical : Laparoscopic excision or laser ablation of all visible lesions & associated adhesions in infertile patients
hysterectomy and repair )
 Enterocele ( either vaginal repair the commonest or abdominal
 Short term : Preoperatively for 2-3 M to control bleeding so correcting anemia without
to restore normal anatomy + 3 month course of GNRH preoperatively improve prognosis / TAH-BSO for pariens
with sacroccolppexy ) blood transfusion & ↓size of myoma to facilitate procedure who don not desire for further fertility

 vaginal vault prolapse ( abdominal sacrocolpopexy – vaginal
mesh repair – Leforte's operations )
Long term : for perrimeunopausal women to induce medical menopause avoiding
surgery till natural menopause comes
Make peace with your past so it won't screw up the present.

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- Pelvic endmetriosis : causing peritoneal & peritubal adhadions
- Pelvic peritonitis : from appendicitis –ruptured gall bladder
Amenorrhea Anovulation - Congenital anomiles : tubal aplasia or hypoplasia
 Definition:  Etiology :  Uterine factor :
o Primary amenorrhea : menses has never occurred by age of 14 without 2ry sexual characters or 16 in 1. Hypothalamic causes : Emotional stress- excessive weight loss- sever exercise – sever - Uterine myomata large or multiple interstitial or SMM if bicorneal or endometrial polyps
presence of 2ry sexual characters psychological disturbance / Kallman syndrome / brain tumors / Drug induced - Intrauterine synechae : over curettage of basal layer – acute septic endometritis – chronic
o Secondary amenorrhea : cessation of menstruation more than 6 months in reproductive age not due 2. Pituitary causes : pituitary adenomas/ empty sella syndrome / pituitary insufficiency TB
pregnancy 3. Ovarian causes : PCOS / premature ovarian failure / iatrogenic causes - Congenital uterine anomalies : bicornuate or septate – uterine hypoplasia or aplasia
 Etiology : 4. Endocrinal causes : hypothyroidism & cushing  Cervical factor :
o Outflow tract disorders :  Clincal presentation : - Change in cervical mucus properties : scanty or visid
a.Imperforate hymen : congenital absence of orifices in hymen → hematocolpos at time of puberty 1. Amenorrhea or oligo-hyomenorrhea mostly 2ry / infertility 1ry or 2ry - Infection either acute or chronic cervicitis
& cryptomenorrhea / in 0.1 % of born females / present with : 1ry amenorrhea with intact 2ry 2. Dysfunctional uterine bleeding / hirsutism - Antisperm antibodies in cervical mucus
sexual characteristics & cyclic lower abdominal pain & urinary retention premenstrual / bulge at  Investigations for detection of ovulation : - Conization or excessive cauterization destroying cervical glands
hymenal ring / confirmed by pelvic US / TTT cruciate incision 1. Basal body temperature chart : daily record for oral temp in morning to detect - Cervical fibroid elongating cervical canal
b. Transverse vaginal septum : congenital septum between hymenal ring & cervix → hematocolp- thermogenic effect of progesterone in luteal phase so in ovulatory cycle show biphasic 3. Coital disorders :
BBT chart / in anovulaotry cycles monophasic chart  Dyspareunia : painful coitus
os & cryptomenorrhea ( as imperforate ) // TTT : surgical excision
2. Folliculometry : serial TVS infollicular phase to monitor dominant follicle till rupture  Vaginism : reflex spasm of levators & gluteus & thigh muscles on any intercourse attempt
c. Asherman’s Syndrome : acquired intrauterine adhesions either from vigorus endometrial
3. Midluteal serum progesterone : in day 21 of cycle ( >10 ng/ml →ovulation / <5  Effluvium seminis : excessive escape of semen from vagina after intercourse
curettage or IU infection // present : 2ry amenorrhea + history of endometrial damage // invest :
anovulatory cycle / 5-10 means luteal phase defect ) 4. Unexplained infertility :
US & HSG & hysteroscopy /// TTT : lysis of adhasions by hysteroscopy or D&C
4. Urinary LH kits : detect preovulatory LH surge in urine for best time of coitus  Diagnosed by exclusion in 15 % of infertile cases . possible causes are : psychological
d. Mullerian agenesis ( Rokitansky $ ) : genticic defect lead to failure in development of uterus &
5. Premenstrual endometrial biopsy : show secretory changes → ovulatory cycle / factors – defective sperm fertilization – dcerased ovarian reserve – occult cervical infection
cervix & vagina / 20 % of cases with 1ry amenorrhea / 2ry sexual characters are normal
 Investigations :
e. Testicular feminization $ : X-linked recessive disorder causing defect in peripheral androgen proliferative → non ovulatory / weak secretory → LPD
1. Investigations of male factor : semen analysis by masturbation 3-4days abstinence / hormonal
receptors so he fail to develop male sexual characters & develop as a female but gentcally 46XY  Treatment :
with gonads at labia and failure of mullerian development due to Y gene assay ( FAH&LH & PRL & testosterone ) – Doppler US on testicles –testicular biopsy - karyo
1. Clomiphene citrate :
o Ovarian disorders : 2. Assessment of ovarian factor :
 Compete with estrogen for hypothalamic receptors → artificial hypoestrogenic state  History : irregular cycles with periods of 2ry amenorrhea suggestive of anovulatory disorder
a.Turner $ : 45-XO – commonest cause of 1ry amenorrhea 30% of cases // picture : low hairv line – →↑ GNRH →↑ FSH → follicular growth →↑ E2 → +ve feedback on LH→surge  Symptoms : midcycle pain –spotting – leucorrhea suggestive of ovulation
short stature – webbed neck – increased carrying angle // pathology : absence of Y → normal  Dose :50mgoraltab twicw ddaily for 5days from 5th day of menses  Investigations : BBT charts – folliculometry – MLSP – PEB- urinary LH kits /// serum
development of mullerian duct & but absent X lead to development of streak gonads  Indications : 1st line for induction in nnormal FSH & intact axis FSH&LH – serum prolactin –serum androgen ( discussed in anovulation )
b. Premature ovarian failure : exhaustion of primordial follicles before 40 either idiopathic  Side effects : flushes & headache / multifetal preg / OHSS I-II / LPD& hostile mucus 3. Assesment of uterine factor :
(autoimmune ) –karyotype abnormalities – or induced ( radiation – chemo- mumps )  Tamoxifen : antiestrogenic has same action usedfor breast cancer after mastectomy  Pelvic US : detect uterine myoma –endometrial plovyp – adnexal masses
c. Resistant ovary $ : follicles fail to respond to gonadotropins temporarly → 2ry amenorrhea  Cyclofenil : related to CC with weak estrogenic effect  Saline infusion sonography : saline injectied under TVS detect endometrial abnormalities &
d. PCOS : chronic anovulation + hyperandrogenism + morphologic changes in ovary 2. Pituitary gondaotropins : tubal patenecy
e. Iatrogenic : bilateral surgical oophorectomy or bilateral ovarian destruction  Types : HMG ( 75IU FSh + 75 IU LH ) / purified urinary FSH ( 75 FSH + 1LH ) /  HSG : visualization of uterine cavity abnormalities ( congenital anomalies – filling defect )
o Pituitary disorders : synthetic FSH by recombinant DNA and internal lumen of fallopian tubes
a. Pituitary adenomas : prolactinoma is the commonest →suppression of GNRH by elevated  Mode : stimulation of growth og primordial follicle  Hysteroscpy : direct visualization of uterine cavity by an optic lens also do minor procedures
prolactin / microadenoma : <10 mm more common than macroadenoma > 10 mm  Indications : CC resistant / hypogonadotrophic anovulation / ICSI & IVF protocols  PEB : to exclude TB endometritis
b.Empty sella $ : defect in diaphragm sella allows CSF to enlarge the sella → elevated PRL  Dose : repeated IM injections from midfollicular phase till complete maturation 4. Assessment of tubal & peritoneal factors :
c. Pituitary insufficiency : Sheehan’s $ - radiation necrosis – pituitary infarctions – infiltrations  Side effects OHSS III—IV / multifetal pregnancy  HSG : detect patency of tube – pelvic adhesions – hydrosaplinx – tubal peritoneal spill can
o Hypothalamic disorders : 3. HCG : detect peritoneal adhesions if limited or localized in control film – TB endometritis &
a.Congenital GNRH deficiency : Kallman $ : congenital deficiency + anosmia  Action : Induce atrificail LH surge leading to ovulation salpingitis – improves pregnancy rate in 1 st 3-6 months
b. Emotional stress : can cause 2ry amenorrhea / pseudocyecsis ( prl levels are elevated )  Indications Used after course of CC or HMG to induce LH surge  Laproscopy : direct visualization of pelvic peritoneum – organs and external surface of tubes
c. Rapid weight loss below 20% of ideal body Wt as in anorexia nervosa or bulimia  Dose : 2 ampoules each 5000 m/IU IM after full follicular maturation by optic lens detecting ( adhesions – pelvic pathology as endometriosis – ovarian pathology
d.Exercise when sever stressful compitive →↑ androphins & 2ry amenorrhea as marathon runners 4. GNRH agonists : PCO ) – also you can inject dye and observe its spillage through tube to ensure patency
e. Drug induced : GNRH causing intial stimulation then prolonged suppression for FSH & LH //  Action : in small doses ↑FSH → follicular maturation / in larger dose →down 5. Assessment of cervical factor :
Progestine : prevent endometrial shedding & inhibit GNRH pulses // combined estrogen regulation or receptors → gonadotrophins  Physical properites of cervical mucus : by microscopic examination & doning fering test &
progestine therapy : in continuous therapy /// Androgenic drugs : atrophic endometrial changes  Indications : IVF/ICSI protocols to prevent premature ovulation by suppression of LH thread test detect if mucus is preovulatory (profuse –thin ) or post ovulatory (thick-viscid )
f. Hypothalamic tumors craniopharyngioma / lymphoma & histiocytosis & sarcodiosis 5. Combined therapy ; CC/HMG/hCG or GnRH /HMG/ hCG  Post coital test : examination of cervical mucus 6-10 h afte intercourse at time of ovulation t
o Endocrine disorders : hypothyroidism & cushing’s 6. Drugs to assist in iinduction : osee number of living and dead sperms & presence of leukocytes
 History :  Bromocriptine : to TTT hyperprolactinemia 0.2mg 1-2 tab daily  Management :
o 1ry amenorrhea : developmental history / cyclic symptoms / history of anosmia  Metformin for insulin resistance in PCOS / thyroid for hypo /corticosteroids for 1. Male factor :
o 2ry amenorrhes : mense ( onset – regularity – LMP ) – exercise – stressful events – Drugs – Addison  General measures: vitamins & antioxidants – TTT impotence – stop smoking –change drugs
virilizing signs or menopausal symptoms 7. Surgical ( laproscopic ovarian drilling ) multiple small punctures by diathermy to  Hormonal TTT : CC & HMG for defective spermatogenesis
 Examination : decrease ovarian androgens / for selected cases of POCS / can cause ovarian damage –  Surgical TTT : ligation of varicocele
o 1ry amenorrhea : examine for female sexual characters / BMI / stigmata of turner / genital Exam peritubal adhasions / time limited effect 3-6 M  ART : IUI ( in coital dysfuncton –erection disorders – mild oligospermia – female cervical –
o 2ry amenorrhea : exclude pregnancy & lactation / PCOS & hyperandrogenism unexplained ) – IVF ( mild male factor – unexplained sever tubal damage – failed tuboplasty )
 Investigations : – ICSI ( sever male factor – failed oocyte fertilization after IVF )
o Hormonal profile : B-hCG / prolactin / FSH&LH / serum E2 & P / testosterone / thyroid functions Infertility 2. Female factor :
o Pelvic US : can detect mullerian agenesis / streak gonads & agensis / Asherman’s$ / PCOS  Etiology :  Ovarian factor : same TTT or induction of ovulation as in anovulation
o Karyotype : for detection of turner $ & testicular femiization 1. Male factor :  Tubo-peritoneal factor :
o Autoimmune screen : in premature ovarian failure for antibodies  Abnormal spermatogenesis: increased scrotal temp / genetic causes / drug induced  Grade I-II tubal damage : operative laparoscopy(adhesiolysis of fine inflammatory
o CT&MRI : for suspected intracranial lesions  Failure of transport : bilateral epididymal obstruction ( gonorrhea – vas absence ) – adhesions – or cauterization of small endometriosis )- laparotomy ( fimbrioplasy –
 Management : bilateral surgical obstruction of vas (vasectomy – inguinal hernia) –immotile cilia $ salpingostomty )
o Hormonal :  Failure of semen deposition : ejaculatory dysfunction (impotence – retrograde ejacualtio  Grade III –IV : IVF or ICSI
a. Cyclic HRT : cyclic OCP for 21 days in premature ovarian failure –PCOS-hypoplastic uterus not 2. Female factor :  Uterine factor : hysteroscopic removal of polyps or synechiae – SMM – resction of a septum
complaining of infertility or cyclic progersterone 7 days every month  Ovarian factor :  Cervical factor : treatment of cause ( cervicitis – hostile mucus –polyp removal ) – estrogen
b.Drugs of induction : clomphine citrate in eugonadotrophic / IM gonadotropin in - Hypothalamic : sever exercise or emotional stress – excessive wt loss- sever depression & mucolytic drugs to improve mucus – IUI to ccervix to endometrial cavity
hypogonadotrophic desirous for fertility – drug induced –kallaman $-brai tumrs 3. Unexplained infertility : Revalaution of both parteners and doing further tests not done –
c. TTT of hyperprolactinemia : bromocriptine or cabergoline - Pituitary causes : prolactinomas – epty sella $ - pituitary insufficiency – adenomas superovulation induction protocols with HMG – repeated IUI for 3 cycles – IVF/ICSI at last
d.TTT thyroid disturbace : Eltroxin for hyothyrodism / thiouracil for hyperthyroidism - Ovarian ; PCOS – premature ovarian failure – resistant ovary $
e. TTT of pituitary disorders : cyclic combined HRT for regular cycles or IM gonadotropin for - Endocrinal : hypothyroidism & cushing
 Tuboperitoneal factor :
fertility / adenoma if not responsive to medical need trans-spenoidal surgery or gamma knife
- Chronic salingitis : from STDs – purepural or post abortive – non specific or specific - You don't have to win every argument. Agree
o Surgical : cruciate incision of hymen in imperforate hymen / excision of septum / reconstruction for
neovagina in testicular feminization with gonadectomy after puberty then long life HRT - Mechanical obstrucstion : to disagree
- Surgical trauma :

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 Management :
PCOS Menopause o Primary sutures can be done if discovered within 24 hours – if seen later left 3-6 M after all signs of
inflammation disappear
 Definition :  Definition : o Preoperative care : purge & daily cleansing enema to empty boel / vaginal douche / non residue diet
o Chronic anovulation ( 2ry amenorrhea ) – hyperandrogenism ( hirsutism –elevated serum LH ) Permenant cessation of menstruation due to intrinsic ovarian failure with mean age 51.5y free of milk / intestinal antiseptics orally for 3 days
– characteristic US morphology \( increased ovarian size & volume – peripherall yarranged  Endocrinal changes : o Operation :
follicles . necklace appearance ) o Decreased serum inhibin & E2 produced by ovary  Recent 1st or 2nd degree : sutured I layers ( 1st levator ani then superficial perineal muscles lastly
 Prevelance : o Increase serum FSH followed by LH vagina & skin are sutured all by interrupted sutures )
o 5-10 women in reproductive age – commonest ovarian cause of 2ry amrnorrhea o Increase free T & decrease in SHBG  Recent 3rd degree : rectal wall is sutured in 2 layers 1st continuous then interrupted without suturing
 Pathogensis : o These changes occur in climacteric period ( few years preceding menopause ) mucosa till apex – then anal spinchter is sutured
o High LH : from increased LH pulse & frequency → stimulate androgen secretion by theca cells  Pathological changes :  Old 3rd degree : deep horizontal incision to separate vagina & rectum then 2 verticla ones at site of
– inhibit aromatase enzyme so increasing ovarian androgen o Urogenital atrophy : 2 dimples of anal sphincter – then repair as recent 3rd degree – posterior colpo-perineorrhaphy is
o Hyperandrogenemia : from stimulation of theca cells by high LH & inhibition of aromatase so  Vagina : atrophic epithelium – loss of rugae – increased PH done . then vainal pack & urinary catheter is put
lead to → atresia of follicles – high serum androgen – hirsutism – conversion of androgen into  Pelvic ligaments : weaker pridspose to POP o Post operative care :
 Uterus : smaller with atrophic endometrium < 5mm / fibroid decrease in size  Vulva regularly washed by antiseptic 3 time sdaily
estrone in fat cells
 Cervix : become flushed – squamo-columnar junction migrates higher  Continue low residue diet & intestinal antiseptic
o Hyperinsulionemia : due to peripheral insulin resistance lead to → increased sensitivity of theca
 Urethra & bladder: loss of elasticity → UTI – SUI  Antiobiotics for infection – pack removed after 24 hours & catheter
cells to LH – decreased aromatase activity – decreased production og SHBG
o Breast changes : smaller –flabby – progressive fatty replacement  On 5th day given oral puratgative solution then daily oral laxative to prevent constipation
 Clinical presentation :
o 2ry amenorrhea & infertility from chronic anovulation o Skin & hair : loss of collagen so lost thickness & elasticity – more alopecia
o CNS : affect cognitive function & mood
o Hirsutism from hyperandrogenemia
o Obesity & glucose intolerance / DUB may occur from EH due to unopposed action of estrogen  Clinical features : Vaginal discharge
 Investigations : o Hot flushes : recurrent waves of heat over chest –neck- face followed by cold sweating
 Types & causes :
o Hormonal assa y : and last for 1-5 min start in perimanopause / it is due to inappropriate stimmulatio of
o Leuchorrhea : excessive white noninfected vaginal discharge either physiological ( in puberty –
 LH levels : elevated with normal FSH lead to abnormal LH/FSH ratio > 2:1 thermoregulatory centers at hypothalamus lead to VD of skin
preovulatory – during pregnancy ) or pathological ( pelvic congestion as fibroids – adnexal mass )
 Elevated levels of : estrone – androstendiaone – free testosterone o Nervous Symptoms : anxiety – irritability – mood changes – sleep disturbances
o Coloured offensive : bacterial vaginosis , trichomonas
 Hyperinsulinemia from insulin resistance o GIT symptoms : constipation – abdominal distention
o Mucopurulent : chronic cervicitis
o US ; increased ovarian size & volume – necklace appearance – no dominant or mature follicle o Genital symptoms : dyspareunia form senile vaginitis / POP from ligament weakness
o Purulent offensive : any infecytion ( septic abortion –purperal sepsis – pyometra ..etc )
o Laparoscopic picture : Oyster shell ovary ( enlarged ovary – thick capsule – absent gyrii ) o Urinary symptoms : frequency , dysuria , SUI
o Blood stained : atrophic vaginitis – ulcers – cervical erosion –fibriod polyp )
 Long term risks : o Andronergic manifestations : increased facial hair - baldness
o Watery : intermittent hydrosalpinx – urinary fistla
 Remote health hazards :
o DM & CVS disease & obesity  History :
o Endometrial hyperplasia → endometrial carcinoma o CVS changes : estrogen deficiency → hyperchlosterolemia – increased LDL – o Age of onset – if recurrent and previous antibiotics
 Management : atherrosclerosis – hypertension – myocardial infarction o Vaginal hygienic practice
o Osteoporosis : estrogen deficiency lead to imbalance between osteoclasts & osteoblasts o Menstrual history , sexual history , obstetric history , contraceptive history , medical condition
o Weight reduction : reduces insulin & androgen – improve response to therapy
causing fractures of vertebrae & increased curvature of spine // TTT by : bisphosphonate o Symptoms : character of discharge – burning sensation – itching or pruritis
o Hormone therapy : cyclic gestagen for 10 days every cycle to induce regular cycle / combined
– calcitonin- HRT – selective estrogen receptor modulators - phytoestrogens  Signs :
OCP for 21 day for regular cycle
 Management : o Vulva is inspected for vulvitis
o Induction of ovulation for fertility : CC / purified HMG / recombinant FSH / HCG injections
o Insulin sensitizing drugs : metformin to improve insulin sensitivity o Reassurance & tell patients natural changes o vagina & cervix : inspected for white plaques – strawberry spots – frothy discharge
o Corticosteroids : t osuppress ACTH in case of adrenal hyperandrogenemia o Regulation of diet & regular exercise o Milking of urethra through vagina to deteat gonorrhea
o Surgical TTT : LOD t odecrease ovarian androgen o Sedatives |& tranquilizers on indivudal basis o Bimanual examination for adnexal masses
o Hirsutiam TTT : cypertorone acetate – laser depilation o Periodic examination and investigations ( TVS – mammogram – pap smear )  Investigations :
o Hormone replacement therapy o Wet mount preparation & microscopic examination
 Benefits : reduce menopausal symptoms – reduce vaginal dryness – prevent osteoprosis o Addition of 10% KOH for fishy amine odour of BV
Hirsutism  Risks : increased CVS risk – venous thromboembolism – breast cancer – EH & cancer o Vaginal swab & culture
 Indications : sever menopausal symptoms – premature menopause – risk of osteoprosis o Pap smear – biopsy suscpicious lesions
 Definition :
 Contraindications : undiagnosed bleeding – brest cancer – DVT history – liver disease
Excessive growth of androgen dependant sexual hair on upper lip –chin –inner thigh – trunk o X-ray for forign body in young infants
 Types : estrogen only therapy ( with absent uterus ) – cyclic estrogen & progesterone  Treatment :
Classification :
(regular endometrial shedding ) – continuous combined for 1-2 years
1.Mild : fine pigmented hair over chest – abdomen –perineum –face o Treatment of cause – proper genital hygiene inculiding douching
 Routes : oral route – transdermal patch – IM injections monthly – local intravag cream
2.Moderate : cotse pigmented hair at same places o Proper treatment of 1st attack
 Follow up : periodic clinical examination – breast examionation – TVS – pap smear –
‫ ولوال نصرة اهلل لمحق لما انتصر‬،‫ والحق شاة وادعة‬،‫الباطل ثعمب ماكر‬
3.Sever : coarse pigmented hair at face –tip of nose - ear lobes
periodic Mamo – Bone densitometry
 Etiology :
1.Idiopathic : increased receptor sensitivity to androgen with normal female androgen
2.Adrenal gland causes : congenital adrenal hyperplasia – adrenal tumors
3.Ovaian causes : PCOS – androgenic ovarian tumors as sertoli lyedig cell tumor
Perineal lacerations ‫عمى الباطل أبدا‬
4.Mixed ovarian & adrenal  Causes :
5.Pituitary causes : cushing $ - acromegaly
6.Androgenic drugs : danazol inendometriosis
- Bad management of 2nd stage of labour : premature extension of head – lack of adequate
perineal support – instrumantel delivery
‫أٌنما وجد المسلم الصحٌح وجدت معه أسباب النجاح‬
 Investigations :
1.Hormonal assay : plasma testosterone level( 0.2-0.8 ng/ml) – free T level – DHAS 1500-2500
- Inadequately performed episiotomy in : delivery of malpositions - usage of forceps –
rigid perineum – narrow suprapubic angle
‫جمٌعا‬
2.Radiological investigations : CT &MRI in pituitary causes / & abdominal –pelvic US for tumor - Rapid delivery of head : as in precipitate labour
 Treatment : - Sever edema of vulva : asin pre-eclampsia
1.Elimination of specific causes : removal of tumor – stoppage of drug - ttt of cushing - Direct external trauma :
2.Hair removal techniques : shaving & tweezing / Bleaching for mild cases / electrolysis-laseer  Degress :
3.Suppression of androgen synthesis:
 OCP : decrease ovarian androgen production – increase SHBG so decreasing free T
- 1st degree : involve skin & superficial perineal muscles
- 2nd degree : levator ani is involved as well but anal sphincter in intact Other works for 5th year :
 Corticosteroids : suppression adrenal androgen production in CAH - 3rd degree : external sphincter is invoved –rectal mucosa may be involved also Lissauer ‘s extra topics
 Spironolactone : diuretic that inhibt 5 alpha reductase  Complications :
 Cypreterone acetate : potent progestin & antiandrogen that inhibit LH & decrease androgen - PPH from bleeding from lacerations - infection of laceration Clinical pediatrics
level for 10 days - Patuolous vaginal introtius - genital prolapse obstetric revision
4.Androgen receptor blocker : inhibit binding of DHT to receptors → direct inhibition of hair - Incontinence of stool & flatus in complete tears
growth - Residul rectovaginal fistula - Dyspareunia from tender scar M.Behairy
 Prevention :
- Proper management of 2nd stage preventing premature extension
- Adequate episitomy in instrumatal delivery & risk for lacerations

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