BREECH PRESENTATION

Definition- occurs when baby’s buttocks or feet or both are in place to come out first during birth.
Causes- multiple pregnancy , uterine fibroids , placenta previa , preterm baby, prematurity , multiple
gestations , congenital and mullerian anomalies

Risk factors- prematurity , multiple gestation , multiparity , fetal hydrocephalus , oligohydramnios ,

placenta previa , gestational diabetes.

Types-
 complete breech (both legs are flexed)
 Frank breech (legs flexed at hips and extended at knee)
 Footing breech- (one or both legs extended at knee)

Symptoms- Subcoastal tenderness , soft irregular mass in pelvis , fetal heartbeat loudest at umbilicus.

Diagnostic test- abdominal exam using Leopold maneuvers , auscultation of fetal heartbeat. For
confirmation , transabdomibal ultrasound.

Management- External cephalic version , ceasearean section , vaginal breech birth.

Complication- Cord prolapsed , fetal head entrapment , prom, birth asphyxia , intracranial
hemorrhage.

FACE PRESENTATION
Definition- presentation of fetal face at the mouth of uterus during delivery.

Etiology- Multiple gestations , grand multiparity , fetal malformations , prematurity , cephalopelvic

disproportion.

Causes-hydrocephalus, neck masses, prematurity , low birth weight, macrosomia , cephalopelvic

disproportion , anencephaly.

Risk factors- small fetus , large fetus , high parity , previous c section, fetopelvis disproportion ,
hypertensive disorders ,polyhydramnios.
Types- mentum anterior (chin facing front of mother ), mentum posterior (chin facing mothers back) ,
mentum transverse.

Diagnostic test- usually diagnosed during first or second stage of labour through examination of
cervix.

Management-Careful monitoring of fetal heart rate , c section when indicated.

Complication- facial edema , breathing problems due to edema, prolonged labour , fetal distress ,
spinal cord injuries , brain damage, neonatal death.

BREAST DISORDERS
 GYNECOMASTIA
Definition- enlargement of breast in males.
Pathogenesis –imbalance of hormones estrogen and testosterone.
Causes – medications , hormonal imbalance , hypogonadism , hyperthyroidism,
Symptoms –swollen breast tissue , breast tenderness , nipple sensitivity
Diagnostic test – serum testosterone , estradiol , LH , hCG
Management – androgens , estrogen receptor modulators , arotamase inhibitors, surgery.

 BREAST CYST
Definition – fluid filled sac inside breast. Common in 35-50 years old ,premenopausal women
and postmenopausal women on hormone therapy.
Causes – unknown
Symptoms – smooth movable lump in breast, nipple discharge , breast pain or tenderness
Types – simple (fluid filled ) , complicated (solid fragments in fluid ) , complex (solid tissue)
Diagnosis – breast examination , ultrasound ,mammogram , fna , biopsy
Management – usually self limited . drainage in certain circumstances.

 FIBROADENOMA
Definition- common benign breast tumor . common between 15-35
Symptoms – firm , round , smooth , rubbery , painless
Cause – unknown
Diagnosis – mammogram , ultrasound , fna , biopsy
 Management – excisisonal biopsy , surgery

 BREAST CANCER
Causes – mutations in tumor suppressor genes (BRCA1 , BRCA2)
Risk factors – early menarche , late menopause, medications containing estrogen, ionizing
radiation ( CT , MRI), family history

Types –
 fibroadenoma of the breast (benign)
 ductal carcinoma (invasive )- most common type . it begins growing in the milk duct and
invades tissue outside the breast.
 Lobular carcinoma ( no invasion ). Starts in lobules which is collection of alveoli that secretes
milk.
o Paget disease. Rare. Starts at nipple and spreads to areola.
Complications – fibrosis , invasion of tissues , lymph buildup in interstitial space , spread of
tumour cells via blood and lymph.
Symptoms – hard , painless lump , swelling in breast , swelling under armpit ,immobile and fixed
breast , dimpling of skin , itching , redness, crusting , discharge from nipple, inverted nipple.
Diagnosis – breast examination , mammograpghy , ultrasound , MRI , biopsy ,FNA and cytology.
Treatment – based on type and stage. (TNM – tumour node metastasis staging ) surgery
( partial /total mastectomy ) radiation , chemo , hormonal therapy. Medications blocking effects of
estrogen.

OVARIAN TORSION
Causes – pcos , ovarian cyst/ mass , longer ovarian ligament , pregnancy , fertility treatment

Symptoms – adnexal / pelvic mass , nausea , severe pelvic pain , fever , vomiting , abdominal
bleeding , sudden onset , unilateral lower abdominal pain.

Diagnosis –ultrasound , Doppler sonography

Treatment – surgery , laproscopy

Complication- infection , peritonitis ,sepsis , chronic pain.

POLYHYDRAMNIOS
Definition- Increased volume of amniotic fluid (>2000cc) , above 95th centile, or deepest pool
greater than 8 cm.

Etiology- Idiopathic, fetal anomalies ,diabetes , multifetal gestation ,immune and nonimmune
hydrops ,fetal infection , placental hemangiomas, failure of fetal swallowing (neurological,
chromosomal anomalies), fetal GI tract abnormality (duodenal/oesophageal atresia), congenital
infections, fetal polyuria (diabetes, TTTS).

Causes – gestational diabetes , rh disease , intrauterine infection , multiple pregnancy ,

esophageal/dudodenal atresia , renal disorders , chromosomal abnormalities.

Epidiomology- Affects 1–4% of pregnancies.

Symptoms – dyspnea , venous stasis , heartburn , nausea , swelling in lower extremities and
abdominal wall, decreased perception of fetal movements

Examination- Abdomen: " fundal height> gestational age, impalpable fetal parts, tense uterine wall ,
ultrasound,

Pathogenesis - Raised amniotic fluid volume caused by increased fetal urine production or failure of
fetal swallowing/intestinal absorption.

Investigations – ultrasound (amniotic fluid index >24 , sdp>8). assessment of liquor volume, fetal
growth, umbilical artery Dopplers, exclude fetal anomalies. Other: Exclude maternal diabetes.

Management - Amnioreduction: Only if gross polyhydramnios is causing significant discomfort.

Cyclo-oxygenase inhibitors: Occasionally used to decrease fetal urine output. Diabetes: Optimise
diabetic control. Other: Paediatrician present at delivery.antacids for heartburn and nausea ,
indomethacin ,sugar control, hospitalization , bed rest.

Complications- preterm labour, malpresentation, placental abruption, cord prolapse, complications

of underlying pathology, postpartum hemorrhage, " risk Caesarean section.

Prognosis- Increased perinatal morbidity and mortality, related to preterm labour/congenital

anomalies.

OLIGOHYDRAMNIOS
Definition - Decreased volume of amniotic fluid, below fifth centile, or deepest pool less than 2 cm.

Etiology - Rupture of membranes, placental insufficiency, fetal urinary tract pathology/

malformations.
Causes – maternal:preeclampsia ,HTN , nephropathy , medications (ACE , NSAIDs) , maternal
dehydration , TORCH infections

Fetal: renal agenesis , rom , chromosomal abnormalities , IUGR , placental infarction.

Risk factors - Chromosomal abnormalities, post-term pregnancies, IUGR, pre-eclampsia, medication

(ACE inhibitors, indomethacin), multiple pregnancy (e.g. TTTS).

Symptoms – low maternal weight gain , prom, abdominal discomfort , sudden drop in fetal heart
rate.

Epidimology- Affects 4% of pregnancies.

History - History of fluid leak pre vaginal with rupture of membranes (note: commonly asymptomatic).

Examination - Abdomen: # fundal height< gestational age, fetal parts easily palpable. Speculum:
Assess for ruptured membranes if clinically appropriate.

Pathogenesis - Reduced amniotic fluid volume by loss of fluid or reduced fetal urine output (#
placental function or fetal urinary tract pathology).

Investigations – transabdominal ultrasound (amniotic fluid index <5 , SDP<2 ) Diagnosis þ

assessment of liquor volume, fetal growth, umbilical artery Dopplers, exclude fetal anomalies. CTG: Fetal
wellbeing.

Management- If PROM/PPROM: See relevant sections. Term: Delivery is appropriate (Induction of

labour if no contraindications). Pre-term: Monitor with serial USS for growth, liquor volume and
Dopplers, regular CTGs, deliver if further abnormalities arise (note: amnioinfusion has a very limited role
in modern obstetrics

Complications - Labour: " incidence CTG abnormalities, meconium liquor, emergency Caesarean
section. Neonate: pulmonary hypoplasia, limb deformities, miscarriage , preterm birth.

Prognosis - Dependent on gestation at time of presentation: increased perinatal mortality rates with
early-onset oligohydramnios.

PRENATAL CARE
History –
 Health history: last period started on

menstrual cycles are regular and how long they usually last;

details about any gynecological problems

details about any previous pregnancies.

medical history: including chronic conditions and medications used to treat them, drug
allergies, psychiatric problems, and any past surgeries or hospitalizations

ask about activities such as smoking, drinking, and drug use that could affect pregnancy.

Family history - ask if any of relatives or baby's father or his relatives have had any chronic or
serious diseases

Genetic history –chromosomal / genetic disorder , structural defect , exposure to toxins.

Physical assessment –
 Weight
 Urine for glucose & protein
 Vital signs
 Doppler of the fetal heart beat
 Leopold’s maneuvers to determine presentation of the fetus
 Assessment of fundal height

FIRST CONTACT WITH HEALTH PROFESSIONAL

Nutrient advice Ensure folic acid supplements (until 12/40), avoid vitamin A supplementation,
ensure adequate vitamin D intake.

Food/hygiene advice To reduce the risk of Listeria, Salmonella and toxoplasmosis, avoid
unpasteurised milk and cheese, raw/undercooked food (especially meat and eggs), pate, ripened soft
cheese, unwashed vegetables. Promote handwashing prior to food preparation and after handling soil.
Avoid cat litter.

Lifestyle advice Smoking cessation, moderate exercise safe (avoid scuba diving, activities with high
risk of joint stress or abdominal trauma), avoid alcohol in first trimester and recommend limit of 1–2
units per week afterwards, seatbelt advice (above and below the bump), travel advice (avoid longhaul
flights, wear compression stockings with air travel

AT BOOKING APPOINTMENT (BY 10 WEEKS)

General- Height, weight, BMI, BP, identify risk factors. Urine Urinalysis, MSU (screen for asymptomatic
bacteruria).

Booking -bloods FBC, group and screen (identify Rhesus-negative women/red cell alloantibodies), Hb
electrophoresis (haemoglobinopathies), rubella immunity, syphilis, hepatitis B, HIV.

Other -Give information regarding antenatal classes, organise dating USS at 10–14/40 weeks. Offer
screening for Down’s syndrome (associated with " nuchal translucency, "HCG, " inhibin A, #AFP, # PAPP-
A and #estriol)..

11–14 weeks: Combined test (NT þ hCG þ PAPP-A).

15–20 weeks: Double test (hCG, unconjugated estriol), triple test (hCG, unconjugated estriol, AFP) or
quadruple test (hCG, unconjugated estriol, AFP, inhibin A).

Both 11–14 and 15–20 weeks: Integrated test (combined test at 11–14 weeks, followed by AFP,
unconjugated estriol and inhibin A at 15–20 weeks) or serum integrated test (PAPP-A and hCG at 11–14
weeks, followed by AFP, unconjugated estriol and inhibin A at 15–20 weeks).

Concerns exist regarding the practicality of (3), so (1) and (2) are recommended depending on gestation
at booking.

SUBSEQUENT CHECKS
16 weeks: BP, urinalyis, review booking tests.

18–21 weeks: Fetal anomaly USS.

25 weeks: (Nulliparous) antenatal appointment including BP, urinalysis, fundal height.

28 weeks: BP, urinalysis, fundal height, anti-RhD for Rhesus-negative women, FBC (screen for anaemia
requiring iron supplementation), group and screen (red cell alloantibodies), GTT performed for women
at risk of GDM.

32 weeks: Further USS for women with low-lying placenta at anomaly scan. 31 weeks: (Nulliparous) BP,
urinalysis, fundal height.

34 weeks: BP, urinalysis, fundal height, second dose anti-RhD for Rhesus-negative women, discuss birth
plan.

36 weeks: BP, urinalysis, fundal height, fetal presentation/lie (offer ECV if breech), discuss breastfeeding
and neonatal vitamin K (to prevent haemorrhagic disease of the newborn). 38 weeks: BP, urinalysis,
fundal height, fetal presentation/lie.

40 weeks: (Nulliparous) BP, urinalysis, fundal height, fetal presentation/lie, can offer membrane sweep.
41 weeks: (If not delivered) BP, urinalysis, fudal height, fetal presentation/lie, offer membrane sweep,
organise induction of labour within the next week.
42 weeks: Offer twice-weekly CTG and USS (maximum amniotic pool depth) for women who decline
induction.

DELAYED PUBERTY
Definition –absence of sexual maturity and secondary characteristics (breast/testicle growth , pubic
hair development and voice changes) in girls by age 12 and in boys by age 14.

Causes – constitutional delay , genetic disorders ( turner syndrome , klienfelter sundrome) , mullerian
agenesis , PCOS , hypogonadotropic hypogonadism , hypothalamic/pituitary tumors , chronic disorders
(DM , CF, inflammatory bowel diseases, renal disorders), kallmann syndrome.

History –
 Present illness :symptoms regarding current illness , new symptoms . signs of puberty like breast
development , testicular enlargement , body odour , axillary/pubic hair, acne.
 Medical history:birth history , immunization status . asthma , CF?
 Medications
 Surgical history : any surgical correction of cryptoorchidism.
 Family history – any late bloomers in family.
 Social history
 Development – any developmental delay
 Physical examination-vital signs , height , weight, BMI

Clinical criteria
 Measurement of testosterone or estradiol, luteinizing hormone (LH), and follicle-
stimulating hormone (FSH)
 Imaging studies.
 Genetic testing

Treatment –hormone therapy ,

Boys: testosterone , monthly injection for 4-6 months

Girls : low dose estrogen for 4-6 months

CERVICAL CANCER
Definition – usually due to HPV 16 , 18
Types – squamous cell carcinoma , cervical adenocarcinoma

Causes – HPV infection

Risk factors – unprotected sex , multiple sex partners , sex at young age , weak immune system as in
HIV , smoking

Symptoms – abnormal vaginal bleeding especially after intercourse , dyspareunia , vaginal

discomfort , pelvic pain , discharge with odour , constipation , hematuria

Diagnosis –cervical screening followed by colposcopy and biopsy, abdominal/vaginal masses.imaging

(X ray ,CT,MRI ) for metastasis

Treatment –cryosurgery , conisation ,surgery (hysterectomy , lymphadnectomy ) radiation, chemo

with brachytherapy+cisplatin, combination of therapies.

Metastasis – extrapelvic lymph nodes , liver ,lungs , bone

Prevention -regular pap smear every 3 years from the start of sexual intercourse or age between 21-
65.

HPV vaccines , sexual intercourse with condoms.

Prognosis -5 year survival stage.

BARTHOLIN GLAND ABSCESS AND CYST

Definition - Cyst or abscess of the Bartholin’s gland.

Etiology -Obstruction of the Bartholin’s duct leads to accumulation of fluid and distension of the
gland.

Risk factors - Generally occur in women aged 20–30 years. Infection , surgery , injury , primigravida,
STD

Epidemiology - Affects 2% of women of reproductive age.

Symptoms -Unilateral vulval swelling. Cyst: often painless. Abscess: pain, difficulty walking/ sitting,
dyspareunia. Fever , chills , drainage from cyst

Examination - Unilateral swelling in region of Bartholin’s gland. Abscess will be tender, fluctuant,
warm, erythematous, surrounding cellulitis.
Pathogenesis- Superinfection now predominantly caused by Streptococcus, Staphylococcus and E.
coli (previously C. trachomatis and N. gonorrhoeae).

Investigations - Microbiology: Cyst fluid/cavity swab for MC&S.pelvic exam , sample of secretions
from vagina /cervix

Management - Small painless cysts: Conservative treatment. Small abscesses: May respond to
antibiotics. Large abscesses: Require marsupialisation (incision of the gland and formation of a tract
from the interior wall of the cyst to the exterior), surgical drainage .

Complications – Recurrence, bleeding ,cellulitis ,dyspareunia.

Prognosis - Recurrence rate of 20%

FIBROIDS
Definition - Benign tumours (leiomyomas) arising from myometrium.

Etiology - Hormone dependent: contain large numbers of oestrogen and progesterone receptors.
Enlarge in pregnancy (" oestrogen) and shrink in menopause (# oestrogen). Exact cause unknown.

Risk factors -Nulliparity,early menarche,late menopause , family history, obesity, Afro-Caribbean

race. Reduced risk: smoking, long-term hormonal contraceptive use , increased parity , late menarche

Epidemiology -Affect 30% of women of reproductive age.

Symptoms -Menorrhagia,intermenstrual bleeding , dysmenorrhoea, abdominal swelling, urinary

frequency ,bowel/bladder dysfunction, dyspareunia, miscarriage, infertility (note: often asymptomatic).
Signs of anemia.

Examination –Abdomen examination :palpation for masses.

Classification -
 Can be submucosal (protrude in endometrium and uterine cavity ),
 intramural (within myometrium )
 subserosal– (perimetrium )round whorls of smooth muscle and connective tissue.

May undergo secondary changes:

(i) hyaline degeneration (mucopolysaccharides deposits around muscle fibres), asymptomatic softening
and liquefaction of fibroid
(ii) calcification (often postmenopausal),

(iii) red degeneration (coagulative necrosis and hemorrhage within fibroid often in 2nd trimester of
pregnancy with acute pain),

(iv) cystic change (liquefaction). Asymptomatic central necrosis of fibroid leaving cystic spaces at center

Investigations -Bloods: FBC (anaemia). USS: TVS, . Other: Hysteroscopy (submucosal), saline infusion
, sonohysterography , MRI

Management -No treatment if asymptomatic. Medical: Tranexamic acid (menorrhagia), mefenamic

acid (dysmenorrhoea), COCP, IUS, GnRH analogues. Surgical: Endometrial ablation, transcervical
resection of fibroids (submucosal), uterine artery embolisation, myomectomy, hysterectomy.

Complications- Anaemia (menorrhagia), miscarriage, infertility, malignant change in 0.1%

(leiomyosarcoma). In pregnancy: red degeneration, miscarriage, malpresentation, PPH.

Prognosis - Ten-year recurrence rate after myomectomy 15–25% (note: fibroids regress and calcify
after the menopause).able pelvic mass. Vaginal: Uterine enlargement.

ADENOMYOSIS
Definition – endometrial tissue grows into muscular wall of the uterus.usually find between 35-50

Causes –unknown

Risk factors –prior uterine surgery , c section , fibroid removal , childbirth , middle age

Symptoms –menorrhagia , dysmenorrhea , prolonged menstrual bleeding ,chronic pelvic pain ,

irritation of urinary bladder , dyspareunia , infertility

Diagnosis –pelvic examination , transvaginal ultrasound , MRI

Treatment – NSAIDs (ibuprofen, naproxen ) , hormone modulators, hysterectomy, oral

contraceptives, (uterine artery embolization)

Complications – anemia

LABOR
The most common way of childbirth is a vaginal delivery.[6] It involves three stages of labor
STAGES OF LABOR
First stage -20 hours .begins with uterine contractions and ends with full cervix dilation at 10 cm.
There is rupture of membranes. Divided into

Latent phase Active phase

Irregular contractions Regular contractions Intense contractions

Every 5-30 min Every 3-5 min 60-90seconds

Last 30 seconds Last 1 + min Every 0.5-2 min

Cervix dilation 0-3 cm Dilation 3-6 cm Dilation 6-10 cm

Second stage – begins with cervical dilation and ends with delivery of the baby.involves 7 cardinal
movements of labour : engagement , descent , flexion ,internal rotation , extension , external rotation ,
expulsion

Factors:

Fetal size : fetal head

Fetal lie : longitudinal (ideal ) ,oblique and transverse

Fetal attitude :normally fully flexed. Chin on chest , rounded back , flexed arms and legs

Fetal presentation : cephalic . breech , shoulder

Third stage – expulsion of placenta.

Fourth stage – extending from birth of the baby to 6wks postpartum. includes postnatal care
The most prominent sign of labour is strong repetitive uterine contractions.

Onset of labour include: Regular uterine contractions at least every six minutes with evidence of change
in cervical dilation or cervical effacement between consecutive digital examinations.[36]

Induction of labor
Definition -Artificial initiation of labour.

Indications - Maternal: Diabetes (pre-existing or GDM), cardiac disease, pre-eclampsia, obstetric

cholestasis, poor obstetric history, fetal death.

Fetal: Post dates (most common indication), IUGR, fetal abnormality, antepartum
hemorrhage , prolonged rupture of membranes (>24 hours).

Contraindications - Previous Caesarean section, abnormal lie, placenta praevia, severe IUGR with
abnormal Doppler results.

Advantages - Expedition of delivery to treat clinical indication.

Diasadvantages - Requires continuous CTG monitoring. See complications below. Requires

continuous CTG monitoring.

Complication - Uterine hyperstimulation (and subsequent fetal compromise), failed induction (5%),
cord prolapse, uterine rupture, PPH. May be more painful than spontaneous labour (" epidural uptake).

METHOD
i. Assess favourability of cervix with Bishop score (see below).
ii. If BS<6, adminster prostaglandin (gel , tablet , pessary )
iii. Repeat 6 hourly
iv. when bishop score >6 perform amniotomy
v. After amniotomy, if poor progress/contractions commence intravenous oxytocin infusion

Augmentation of labor
Definition -Speeding labor up, or an augmentation of labor means that medical or natural techniques are used
to help labor back on its path. more common ways to try to speed up your labor:2

 Breaking your water

 Nipple stimulation
 Other natural techniques
 Pitocin
 Walking

Augmentation will be done when:

 Active labor has started, but your contractions are weak or irregular or have
stopped entirely.
 You have gone into active labor, but the amniotic sac has not ruptured on its
own. In this case, your doctor or nurse midwife may rupture the amniotic sac
(amniotomy) to augment labor. If labor still does not progress, oxytocin (Pitocin)
may be given to make the uterus contract.
  Active labor has started and the amniotic sac has ruptured on its own, but labor
still is not progressing. Oxytocin (Pitocin) may be given to make the uterus
contract.

If labor fails to progress in spite of membrane sweeping, an amniotomy, oxytocin, or

a combination of these measures, delivery by cesarean section may be considered.

Mechanism of labor
As the fetus descends through the birth canal, it undergoes changes in position and attitude, in order to
pass through the pelvis. In a typical (gynaecoid) pelvis, the transverse diameter (13 cm) is wider than the
anteroposterior diameter (11 cm) at the pelvic inlet. The mid-cavity is circular in cross-section (12 cm
diameter). At the pelvic outlet the AP diameter (13.5 cm) is wider than the transverse (11 cm).

Engagement : The fetal head enters the pelvis in the OT position. The head is engaged when the
widest part of the presenting part has passed through the inlet . This occurs prior to labor in nulliparous
women.

Descent : Occurs with uterine contractions.

Flexion : As the head enters the midcavity it flexes ( chin touching chest ), remaining in the OT
position

Internal rotation : As the head reaches the pelvic oultlet it encounters levator ani muscles of pelvic
floor and rotates to OA position

Extension : The head descends beyond ischial spines . Upward pressure from pelvic floor causes head
to expand.

Crowning : Occiput emerges from underneath the symphysis pubis and distends the vulva.

External rotation : Shoulder rotates into oblique or anterior/posterior plane.

Restitution : head aligns itself with shoulders and delivery occurs.

ANDROGEN INSENSITIVITY SYNDROME

Definition -Androgen insensitivity syndrome is a disorder of sex development due to androgen receptor dysfunction

46xy,person is genetically male but body is unable to respond to male sex hormone

So mostly female exterior with both male and female sexual development
External sex characteristic of female but no uterus and male internal sex organ(testes) but undescended

Cause —mutation in androgen receptor gene

Symptoms –little to no pubic /underarm hair ,short vagina , undermasculinized genitalia

Diagnosis—check for presence or absence breast ,uterus ,testis, pubic or axillary hair

ultrasound of the pelvis may be performed to look for internal testes., androgen receptor gene sequencing

TREATMENT- full disclosure and psychological support ,gonadectomy due to risk of testicular
malignancy , HRT

Vaginal dilation reconstruction for penetration

MYOMETRIAL HYPERPLASIA
Definition -Myometrial hyperplasia (MMH) is a structural variation with irregular zones of
hypercellularity and increased nucleus/cell ratio that appears in adolescence, can progress during the
childbearing years.

“myometrial hypertrophy” is symmetrically enlarged uteri weighing 120 grams or more in which no pathologic
changes other than increased size. Increase in weight of the uterus is due to hypertrophy of the smooth muscle
fibers of the myometrium.

Seen in multiparous women

Menorrhagia due to myometrial hypertrophy:

treatment with tamoxifen

FETAL THERAPY
Definition -interventions performed on a “sick” fetus with the aim of achieving fetal well being. These
interventions include medical (i.e. non-invasive) and surgical procedures. In general a medical
intervention is performed by administering medication to the mother. The drug crosses through the
placenta and reaches the blood circulation of the fetus. Surgical intervention on the fetus may involve
either a direct operation of the fetus or an intervention on the placenta

Fetal surgical therapy

 Fetal surgery is a procedure performed on an unborn baby (fetus) in the uterus (in
utero) to help improve the long-term outcome of children with specific birth
defects.
 Because these defects often worsen as a fetus develops, fetal surgery done by a
team of experts focuses on treating and improving the conditions before birth.

fetal surgery expertise and experience can treat many birth defects in utero,
including:

 Amniotic band syndrome

 Congenital high airway obstruction syndrome (CHAOS)

 Congenital diaphragmatic hernia

 Congenital heart disease

 Spina bifida

 Twin twin transfusion syndrome

Types –

 Open fetal surgery – opening the uterus and operating on the fetus.
 Minimally invasive fetoscopic surgery - with small incisions guided by
fetoscopy and sonography
 Percutaneous fetal therapy – placing catheter under continuous ultrasound
guidance

 Lower urinary tract obstruction (LUTO)

 Neck mass

 Spina bifida (myelomeningocele)

 Twin-twin transfusion syndrome (TTTS)

Types

Methods for treating these conditions at highly specialized health care centers with
fetal surgery expertise include:

 Fetoscopic endoluminal tracheal occlusion (FETO) for severe CDH

 In utero open or fetoscopic repair of myelomeningocele, the most severe form of

spina bifida

 Open fetal surgery f

 Shunt placements

 Fetal vesicoamniotic shunt (VAS) and fetal cystoscopy for bladder obstruction

 Fetoscopic laser ablation Bipolar cord coagulation for TRAP sequence

 Radiofrequency ablation for fetal tumors

 Intrauterine blood transfusion

Risks include rupture of the uterus after surgery (uterine rupture), fetal death,
operative complications, early labor and potential failure to treat the birth
defect.

CONGENITAL STRUCTURAL
ABNORMALITIES
Definition -can be defined as structural or functional anomalies that occur during the intrauterine
life

Structural Birth Defects

Structural birth defects are physical abnormalities that occur when a baby’s body doesn’t develop normally in the
womb. Most structural defects occur in the earliest weeks of pregnancy when the baby’s organs and skeleton are
forming.

Examples include:

 Heart defects,
 Cleft lip or cleft palate
 Missing or abnormal limbs,
  Neural tube defects (problems with the development of the brain and spinal cord), such as spina bifida
 Lower urinary tract obstructions that block fetal urination

Causes
 Genetic disorders
 Lack of folic acid
 Infections during pregnancy
 Smoking, drinking alcohol or using recreational drugs during pregnancy
 Uncontrolled diabetes
 Obesity
 Advanced age

Prenatal screening and diagnostic tests for structural birth defects include:

 Ultrasound scans
 Maternal serum screening
 Fetal echocardiographY
 Fetal MRI
 Amniocentesis

NEURAL TUBE DEFECT

Birth defects of brain , spine and spinal cord. Neural tube defect is the most common
congenital anomaly in the CNS

NTD is caused by defective closure of neuropore

Risk factors
 folic acid deficiency
 diabetes ,maternal obesity
 MTHFR gene mutation
 drugs and alcohol

TYPES OF DEFECTS
1) cranial ntd
 ancephaly (absence of brain and skull) ,enephalocele
 Iniencephaly = retroflexion of head , star gaze posture , occipital bone
defect
2) caudal ntd (mc)
 spina bifida oculta most common
 spina bifida cystica –
menegiocele : protrusion of meninges
meningomyelocele : protrusion of meneges + spinal nerve roots
 DAIGNOSIS
antenatal dx – 1)USG, 2)amniosinthesis
2)MARKERS – alpha fetoprotein , ACETYLCHOLINESTERASE (specific)

Prevention = folic acid preconceptional

TREATMENT
Surgical closure of defects 1-2 days after birth

Increased risk of LATEX allergy in NTD (use latex free gloves and catheters)

Ruptured meningocele or meningomyelocele – emergency closure of defect immediately after

birth

VASA PREVIA
Vc -splitting of cord,umbilical vessels exposed before entering. Fetal blood vesselspresent near the opening of the
uterus

Definition -Vasa praevia is a condition in which exposed fetal blood vessels run near the internal opening of
the uterus. These vessels are at risk of rupture when the supporting membranes rupture, as they are unsupported by
the umbilical cord or placental tissue

Risk factors – low lying placenta, previous c section or uterine delivery , in vitro fertilization , multiple
pregnancy

Symptoms - painless vaginal bleeding, rupture of membranes, and fetal bradycardia.

Diagnosis -Transvaginal ultrasonography

Treatment -Prenatal monitoring to detect cord compression, Cesarean delivery

INFERTILITY
Definition - Failure to conceive following at least one year of regular unprotected sexual
intercourse.

Primary infertility: No previous pregnancy.

Secondary infertility: Previous pregnancy.

Etiology - Idiopathic (15%)

 Female factor (50%): Tubal disease, anovulatory (PCOS, hypogonadotrophic hypogonadism,
premature ovarian failure), endometriosis, uterine factors (anomalies, fibroids, Asherman’s
syndrome).

Male factor (35%): Chromosomal abnormalities, endocrine causes, drugs, irradiation, infection
(STI, mumps), reproductive tract obstruction, trauma (including torsion), varicocele, ejaculatory
disorders, autoimmune causes (anti-sperm antibodies), previous maldescended testes.

Risk factors - See the aetiologies noted above. Also: smoking, alcohol, marijuana use, excess
exercise, extremes of bodyweight, female age >35years.

Epidemioliogy - Affects 10–15% of couples of reproductive age, incidence increases with

increasing age of female partner (>30% over 35 yrs).

History - Duration and type of infertility, coital frequency, menstrual history, PCOS symptoms,
contraceptive history, previous STIs, medical history, surgical history, medication history, social
history (alcohol, smoking).

Examination - General: BMI, signs of PCOS, signs of thyroid dysfunction, development of

secondary sexual characteristics. Speculum/vaginal: Uterine size and mobility, evidence of
infection.

Investigations - Couples proceeding to assisted reproduction techniques require screening for

HIV, hepatitis B and C.

Males Semen analysis (volume, pH, sperm concentration, motility, white blood cells). If
abnormal, consider FSH/LH levels, karyotype, USS testes.

Females Bloods: Day-21 progesterone (confirms ovulation), day-2 or day-3 LH/FSH (ovarian
reserve), serum TFTs, testosterone, androstenedione, SHBG, prolactin, rubella immunity.
Microbiology: Screen for Chlamydia. Imaging: USS pelvis (uterine anomalies, ovarian cysts,
polyps, fibroids), HSG (tubal patentcy).

Other: Laparoscopy and dye test (tubal patency), may require hysteropscopy

Management - Management of identified social/environmental factors. Unexplained:

ovulation induction with clomiphene citrate or gonadotrophins, IUI, IVF.

Male factor : May require specialist urological input. May need Intrauterine insemination ,
Intracytoplasmic sperm injection, IVF. If azoospermic and sperm not retrievable on testicular
biopsy, counsel regarding donor sperm
Female factor : Anovulatory: Correction of endocrinopathies, ovulation induction, IVF. With
PCOS, consider metformin, ovulation induction, laparoscopic ovarian drilling (if no reponse to
ovulation induction). Counsel women with high FSH regarding use of egg donation. Uterine
factors: May require hysteroscopic management. Tubal factors: Consider laparoscopic
prodedures, often requires IVF. Endometriosis: Should be offered surgical management of
endometriosis, may require IVF, psychological support.

Complications -Psychological distress, complications of fertility interventions (OHSS,

multiple pregnancy, ectopic pregnancy).

. Prognosis - Dependent on underlying aetiology

DOWN SYNDROME
Definition -genetic disorder caused when abnormal cell division results in an extra
full or partial copy of chromosome 21 . intellectual and structural problems may be
mild, moderate or severe

some of the more common features include:

 Flattened face

 Small head

 Short neck

 Protruding tongue

 Upward slanting eye lids (palpebral fissures)

 Unusually shaped or small ears

 Poor muscle tone

 Broad, short hands with a single crease in the palm

 Relatively short fingers and small hands and feet

 Excessive flexibility

 Tiny white spots on the colored part (iris) of the eye called Brushfield's
spots

 Short height
  Delayed physical growth

 Intellectual disability

 Hearing and vision disorders

 Congenital heart diseases

Life spans have increased dramatically for people with Down syndrome. live more
than 60 years, depending on the severity of health problems.

Screening tests include the first trimester combined test and the integrated
screening test.

The first trimester combined test, which is done in two steps, includes:

 Blood test. This blood test measures the levels of pregnancy-associated

plasma protein-A (PAPP-A) and the pregnancy hormone known as human
chorionic gonadotropin (HCG).

 Nuchal translucency test. During this test, an ultrasound is used to

measure a specific area on the back of your baby's neck. When
abnormalities are present, more fluid than usual tends to collect in this
neck tissue.

Second trimester. The quad screen measures your blood level of four
pregnancy-associated substances: alpha fetoprotein, estriol, HCG and inhibin A.

Diagnostic tests that can identify Down syndrome include:

 Chorionic villus sampling (CVS).

 Amniocentesis

Treatment – Early intervention for infants and children with Down syndrome can
make a major difference in improving their quality of life. Because each child with
Down syndrome is unique, treatment will depend on individual need. Speech ,
physical , occupational / educational therapy.

MENOPAUSAL TRANSITION
 Menopausal transition known as perimenopause begins four years before a woman’s final menstrual
cycle

 Perimenopause lasts up until menopause, the point when the ovaries stop releasing
eggs. In the last 1 to 2 years of perimenopause, this drop in estrogen speeds up. At
this stage, many women have menopause symptoms
 length of perimenopause is 4 years, but for some women this stage may last only a
few months or continue for 10 years. Perimenopause ends when women have gone
12 months without having their period.

80 percent of women experience symptoms such as hot flashes, sleep disturbances, mood changes
and vaginal dryness during perimenopause. Other symptoms include:

 Headache
 Vertigo (dizziness)
 Itchy skin
 Restless leg symptoms
 Heart palpitations
 Difficulty concentrating
 Breast tenderness
 Constipation
 Bloating
 Muscle and joint aches

How Is Perimenopause Diagnosed?

Often your doctor can make the diagnosis of perimenopause based on your symptoms.
A blood test to check hormone levels may also help, but your hormone levels are changing
during perimenopause

Can I Get Pregnant If I Am Perimenopausal?

Yes. Despite a decline in fertility during the perimenopause stage, you can still become
pregnant. If you do not want to become pregnant, you should use some form of birth control
until you reach menopause (you have gone 12 months without having your period).

Treatment

Medications are often used to treat perimenopausal symptoms.

 Hormone therapy. Systemic estrogen therapy — which comes in pill, skin patch,
spray, gel or cream form — remains the most effective treatment option for
relieving perimenopausal and menopausal hot flashes and night sweats

 Vaginal estrogen. Estrogen can be administered directly to the vagina using a

vaginal tablet, ring or cream. It can help relieve vaginal dryness, discomfort with
intercourse and some urinary symptoms.
  Antidepressants. Certain antidepressants related to the class of drugs called
selective serotonin reuptake inhibitors (SSRIs) may reduce menopausal hot
flashes.

 Gabapentin (Neurontin). Gabapentin is approved to treat seizures, but it has also

been shown to help reduce hot flashes. This drug is useful for women who can't
use estrogen therapy for health reasons and for those who also have migraines.

SCREENING OF 1ST AND 2ND

TRIMESTER
First trimester screening
First trimester screening may include combines fetal ultrasound and blood tests for the mother. It’s done during the
first trimester of pregnancy, during weeks 1 to 12 or 13. It can help find out the risk of the baby having certain birth
defects. This includes chromosome defects such as Down syndrome (trisomy 21), or trisomy 18 or 13.

:
 Ultrasound test for fetal nuchal translucency (NT). This test uses ultrasound to look at the back of the baby's
neck. It checks for increased fluid or skin thickening. These might mean a defect.
 Blood tests. The blood tests measure 2 substances found in the blood of all pregnant women:
o Pregnancy-associated plasma protein-A (PAPP-A). This protein is made by the placenta in early pregnancy.
Abnormal levels could mean an increased risk for a chromosome defect.
o Human chorionic gonadotropin (hCG). This hormone is made by the placenta in early pregnancy. Abnormal
levels could mean an increased risk for a chromosome defect.
 Cell-free fetal DNA screening. This tests the baby's DNA that is in your blood. It checks for certain abnormal
chromosomes. It can also check for defects in the fetal sex chromosomes (X or Y). Cell-free fetal DNA screening
does not find structural birth defects, such as spina bifida or defects in the abdominal wall.
If first trimester screening is abnormal, you may need more testing for diagnosis. This may include chorionic villus
sampling, amniocentesis, or another ultrasound.

Second Trimester Prenatal Screening Tests

Second trimester prenatal screening may include several blood tests, called multiple markers. These markers provide
information about a woman's risk of having a baby with certain genetic conditions or birth defects. Screening is
usually done by taking a sample of the mother's blood between the 15th and 20th weeks of pregnancy (16th to 18th
is ideal). The multiple markers include:
 Alpha-fetoprotein screening (AFP). This blood test measures the level of alpha-fetoprotein in the mothers' blood
during pregnancy. AFP is a protein normally produced by the fetal liver and is present in the fluid surrounding the
fetus (amniotic fluid), and crosses the placenta into the mother's blood. The AFP blood test is also called MSAFP
(maternal serum AFP).
Abnormal levels of AFP may signal:
o Open neural tube defects (ONTD), such as spina bifida
o Down syndrome
o Other chromosomal abnormalities
o Defects in the abdominal wall of the fetus
o Twins. More than one fetus is making the protein
o A miscalculated due date, as the levels vary throughout pregnancy
 hCG. Human chorionic gonadotropin hormone (a hormone made by the placenta).
 Estriol. A hormone made by the placenta.
 Inhibin. A hormone made by the placenta.
Abnormal test results of AFP and other markers may mean more testing is needed. Usually an ultrasound is done to
confirm the dates of the pregnancy and to look at the fetal spine and other body parts for defects. An amniocentesis
may be needed for accurate diagnosis.

MISCARRIAGE
Definition- Pregnancy loss under 24 weeks’ gestation.
Types –
 Threatened miscarriage: PV bleeding with fetal heart seen. Common , bleeding from
closed cervix.
 Inevitable miscarriage: PV bleeding with open cervical os. Abdominal cramping pain.
Uterine contents visible during pelvic exam.
 Incomplete miscarriage: Passage of products of conception through open cervix, uterus
not empty on USS.
 Complete miscarriage: Passage of products of conception, uterus empty on USS.
 Missed miscarriage: USS diagnosis of miscarriage in absence of symptoms. Fetus not
viable but cervix closed.
 Recurrent miscarriage (RMC): Three or more consecutive miscarriages.
Etiology - Ninety percent result from chromosomal abnormalities in the embryo (commonly
trisomy 16).
Causes –chromosomal abnormalities , failure of blastocyst to implant itself in endometrium
lining , lack of progesterone secreted by corpus luteum , lack of placental hormones , teratogens ,
alcohol , smoking , trauma , uterine abmormalities , infection , maternal disease .
risk factors –Increasing maternal age. More than 95% of miscarriages occur in the first
trimester. If RMC, consider structural abnormalities (fibroids, uterine septae), cervical
incompetence (late miscarriage), medical conditions (renal disease, diabetes, SLE), clotting
abnormalities (factor V Leiden, antithrombin III deficiency, primary antiphospholipid
syndrome).
Epidemiology -Affects 10–20% of recognised pregnancies.
Symptoms - PV bleeding (?tissue passed), cramping abdominal pain, ?fever (infection).
Examination –
 General: Assess for signs of shock, ?pyrexia (infection). Abdomen: May have mild lower
abdominal tenderness.
 Speculum: Assess quantity of bleeding, assess whether cervical os open (if products seen
in os, remove with spongeholding forceps).
 Vaginal: Uterine size, cervical dilatation, exclude ectopic (unilateral tenderness, cervical
excitation, adnexal mass).
Investigation – Urine: Pregnancy test. Bloods: FBC, G&S. USS: Pelvis (confirm
miscarriage/RPOC). RMC: Cytogenetic analysis of products of conception. Outpatient
investigation for RMC: Pelvic transvaginal USS (structural abnormalities), lupus anticoagulant,
antiphospholipid antibodies, anticardiolipin antibodies, consider screen for BV.
Management -Heavy bleeding: ABC, stabilise patient, requires surgical evacuation.
Administer anti-RhD if Rhesus-negative and >12/40 or surgical evacuation. Missed/incomplete
miscarriage: Management options are conservative, medical (mifepristone/prostaglandin),
surgical (ERPC). RMC: May require low-dose aspirin/LMWH if thrombophilia identified.
Closed monitoring , misoprostol , d&c uterine aspiration , social and mental support.
Complications - Haemorrhage, infection, complications of ERPC, psychological sequelae.
Prognosis - Most patients have subsequent successful pregnancies.

SPONTANEOUS MISCARRIAGE
Definition –spontaneous loss of pregnancy prior to viability.
Etiology –chromosomal abnormalities (trisomy , monosomy) , maternal disease

(antiphospholipid syndrome , diabetes , thyroid disease ), drugs ( methotrextae , antiepileptics )

Uterine abnormalities: the role of fibroids is uncertain but they may be implicated.Infection: varicella, rubella and

other viral illnesses.

 Cervix: cervical injury from surgery, cone biopsy and large loop excision of the transformation zone

• Infection: may occur with or without ruptured membranes. May be local to the genital tract or systemic .
• Thrombophilias.
• Uterine abnormalities: submucous fibroids and con- genital distortion of the cavity (uterine septae) may be

implicated

• Chromosomal abnormalities: these too may not become apparent until the second trimester.

Diagnosis -
 History-taking
 Examination /General examination
 Abdominal palpation
 Vaginal examination
 Differential diagnosis

Diagnostic tools :Ultrasound /Progesterone

 Ultrasound has a role to play, but caution must be excercised when diagnosing miscarriage on a single
scan
 Wide variation in normal levels of hCG at any gestation limits its use for assessment of viability.
  Progesterone levels do not correlate sufficiently well with viability to be a useful tool in diagnosing

Management
surgical management involves evacuation of the uterus by dilatation and suction curettage. Cervical dilatation can

be assisted by cervical priming with a prostaglandin (e.g. misoprostol) a minimum of 1 hour prior to the procedure
and is strongly recommended when the woman has not had a previous vaginal delivery
 Medical management of miscarriage involves using uterotonic therapy, alone or in conjunction with
antihormone therapy, to achieve evacuation of the uterine cavity.
 Available uterotonic agents include gemeprost and misoprostol, both of which are prostaglandin (PG)E1
ana- logues.
 Anti-D immunoglobulin should be given to all non- sensitized RhD-negative women who have a
spontaneous miscarriage after 12 weeks of pregnancy

MCROBERTS MANUERVER
employed in case of shoulder dystocia during childbirth and involves hyperflexing the mother's legs
tightly to her abdomen. It is effective due to the increased mobility at the sacroiliac joint during
pregnancy, allowing rotation of the pelvis and facilitating the release of the fetal shoulder.[2] If this
maneuver does not succeed, an assistant applies pressure on the lower abdomen (suprapubic
pressure). Current guidelines strongly recommend against pulling on the infants head, as this could
lead to brachial plexus injury. Instead, support while keeping the neck straight is indicated.

C SECTION
Definition- A surgical procedure by which the fetus is delivered through abdominal and
uterine incisions.

Indications - Whenever fetal/maternal risks from vaginal delivery exceed those of

Caesarean section. Indications include: Elective: Malpresentation, multiple pregnancy,
placenta praevia, severe IUGR, infections (e.g. HIV, active primary HSV), previous classical
Caesarean section (" scar rupture with vaginal delivery), previous anal sphincter injury,
previous Caesarean section, certain maternal medical conditions. Emergency: Fetal distress,
failure to progress, maternal conditions for which delay in delivery may compromise her
safety, malpresentation, placental abruption, cord prolapse, APH

Method
1. Preparation: The patient is anaesthetized (usually spinal/epidural, occasionally GA) and
placed on left tilt to prevent caval compression. An indwelling urinary catheter is inserted.
2. Abdominal entry: A transverse skin incision is made 2 finger-breadths above the pubic
symphysis. Occasionally, a midline vertical incision is used if difficulties are envisaged (e.g.
multiple fibroids). Subcutaneous tissues are divided followed by the rectus sheath. The
peritoneum is identified and entered high to avoid the bladder. The urinary bladder is reflected
from the lower uterine segment.
 3. Uterine entry: More than 95% of incisions to the uterus are transverse incisions to the lower
segment (# blood loss, # postnatal morbidity, # morbidity in future pregnancies). The classical
(vertical) incision is used in selected cases (e.g. lower uterine segment fibroids, placenta
praevia, prematurity).
4. Delivery: The presenting part is delivered through the incision with assistance of firm
fundal pressure. Wrigley’s forceps may be used. The placenta is delivered and the uterus
checked to ensure the cavity is empty.
5. Peritoneal closure: The uterus is closed in two layers. Peritoneal closure is not currently
recommended. The rectus sheath is closed. Camper’s fascia is approximated if >2 cm
subcutaneous fat. Skin is closed with either subcuticular sutures or staples.

Advantages -Important for avoiding maternal/neonatal morbidity and mortality when used
appropriately.

Complications - Bleeding (need for blood transfusion), infection, visceral damage (e.g.
bladder, ureter), VTE, fetal laceration, hysterectomy rare (" risk with multiple previous
uterine incisions, fibroids, placental site abnormalities).

Prognosis - Chance of future vaginal delivery with one uncomplicated previous Caesarean
section: 72–76% (risk of uterine scar rupture: 22–74 per 10 000). Increased risk of placental
site abnormalities in future pregnancies (0.4–0.8%). 0.4% risk of antenatal still-birth in future
pregnancies.

HYSTEROSCOPY
Hysteroscopy is inspection of the uterine cavity by endoscopy with access through cervix which is thin telescope
like device. It is inserted through vagina into the uterus. It is best carried out after menstruation when the
endometrium is thin. The patient is placed in lithotomy position.

can be used to diagnose and treat causes of abnormal bleeding

Indications
 Abnormal menstruation (age >40 years)

 Abnormal menstruation not responsive to medical treatment (age <40 years)

 Intermenstrual bleeding despite normal cervical smear Post-coital bleeding despite

normal cervical smear Postmenopausal bleeding (persistent or endometrial thickness
≥4mm)

 Abnormal pelvic ultrasound findings (e.g. endometrial polyps, submucous fibroids)

  Subfertility

 Recurrent miscarriage

 Asherman’s syndrome

 Mullerian anomalies

 Lost intrauterine contraceptive device

 Endometrial polyp

 adenomyosis

Contraindications
o Pelvic infection

o Pregnancy

o Cervical cancer(Heavy uterine bleeding)

Operative hysteroscopic procedures.

If abnormalities are found specialized instruments can be entered through hysteroscope to perform surgery.
Procedures include endometrial ablation , submucosal fibroid resection , endometrial polypectomy.

Advantages - Visualisation of endometrium and histological diagnosis

Complications - Infection, bleeding, uterine perforation (and subsequent damage to bowel or

bladder), failure to enter cavity.

Prognosis -Complications are rare (2 per 1000). Mortality is 3 per 100 000

HYSTERECTOMY
Definition - Surgical removal of the uterus, may be performed with removal of the ovaries
(bilateral salpingo-oophorectomy).

Types :

 Total: Uterus including the cervix.

  Subtotal: Uterus excluding the cervix.
 Radical: Uterus, cervix, fallopian tubes, ovaries, parametrium, upper third of vagina and
pelvic lymph nodes.

Indications
 Heavy menstrual bleeding
 Pelvic pain
 Uterine prolapse (vaginal hysterectomy)
 Gynaecological malignancy (usually ovarian, uterine or cervical)
 Adenomyosis, endometrial cancer
Contraindications
 Pelvic radiation.
 Large uterus
 Prior pelvic surgeries.
 Suspected severe pelvic adhesion and anatomical distortion from PID (pelvic inflammatory
disease) or endometriosis.
 obesity.
 Nulliparity.
 Lack of uterine descent,

Method –
 Abdominal hysterectomy: For malignancy, fibroids or immobile uterus (e.g. adhesions,
endometriosis).
 Vaginal hysterectomy:Preferred route for prolapse and heavy menstrual bleeding if
clinically and technically feasible. The uterus should be mobile and normally sized.
 Laparoscopically assisted vaginal hysterectomy : Ovarian and uterine pedicles are
secured under laparoscopic guidance. The remainder of the procedure is performed
vaginally. This enables removal of tubes and ovaries

Complications - Immediate: Damage to other organs (e.g. ureters, bladder, bowel),

haemorrhage. Early: Infection, VTE, pelvic haematoma, urinary retention.

Vaginal prolapsed , adhesion formation, bowel obstruction, wound infection

Late: Menopausal symptoms if ovaries removed; if ovaries conserved, 50% chance of entering
menopause within 5 years, psychosexual problems.

Prognosis -Depends on the indication. Overall risk of serious complications following TAH
for benign conditions is 4%

LAPROSCOPY
Laparoscopy is a type of diagnostic surgical procedure that doctor use to look inside your body at your abdominal
and reproductive organs. This procedure can also be used to collect samples of tissue (biopsies) for testing.

A laparoscope — a thin tube similar to a telescope — is passed through a small incision (cut) in your abdomen.
Using the laparoscope, your provider can look directly at the outside of your:Uterus. Ovaries. Fallopian tubes. Liver.
Pancreas. Gallbladder. Spleen. Stomach.

INDICATIONS Acute or chronic pelvic pain , Ectopic pregnancy , Pelvic inflammatory disease (including
TB) , Endometriosis , Adnexal torsion , Subfertility , Congenital pelvic abnormality , Abnormal pelvic scan , Unexplained pelvic
mass, Staging for ovarian malignancy

Contraindications Mechanical or paralytic bowel obstruction, Diaphragmatic hernia , ( shock), Severe

cardiorespiratory disease, Obesity, Inflammatory bowel disease, Large abdominal mass, Advanced pregnancy , Multiple
abdominal incisions

Advantages – reduced pain due to smaller incisions , reduced hemorrhage , shorter recovery time

Disadvantages limited range of motion at surgical site , poor depth perception ,

Complications – bleeding ,hematoma , infection , hernia , adverse reactions to anesthesia , abdominal

inflammation ,blood clots , injury to visceral organs , intraabdominal adhesion

LAPROTOMY
Definition -is a surgical procedure that involves a surgeon making one large incision in the abdomen.Doctors
use laparotomy to look inside the abdominal cavity to diagnose or treat abdominal health conditions.

Indications – signs of peritonitis , uncontrolled shock or hemorhhage , hemoperitoneum

Contraindications – unfitness for general anesthesia , peritonitis with severe sepsis , advanced
malignancy , comorbid conditions .

Complications – damage to internal organs , adhesions , bowel blockages , abdominal pain due to
adhesions,hemorrhage , infection.

UTERINE SARCOMA
Uterine sarcoma is when malignant cells forms in the muscles or tissues of the uterus.

Women who have had radiation therapy in the pelvis area, or who have been treated with the drug tamoxifen for
breast cancer, have a greater risk of developing uterine sarcoma.

The main signs and symptoms of uterine sarcoma are:

  Unusual bleeding from the vagina that is not related to menstrual periods, or that happens after
menopause
 A mass (lump or growth) in the vagina
 Pain in the abdomen
 Feeling full at all times
 Having to urinate often

uterine sarcoma diagnosis

Pap test

Transvaginal ultrasound

Endometerial biopsy

Dilation and curettage (D&C)

TREATMENT

 Hysterectomy: removal of the uterus and cervix.

 Total hysterectomy with salpingo-oophorectomy:
 Lymphadenectomy:
 Laparotomy

PLACENTAL TUMOURS
There are many tumours that can involve the placenta.

These can be of very different pathology and can include

PLACENTAL TUMOURS ARE BROADLY divided into trophoblastic and nontrophoblastic tumours.

 placental chorioangioma (considered the most common primary tumour of the placenta 1)

o placental chorioangiomatosis (multiple chorioangioma)

 placental teratoma

 placental metastases

 placental site trophoblastic tumour

What is chorioangioma?
Chorioangioma is a tumor of the placenta. The placenta is the organ that develops in the uterus
during pregnancy and attaches to the uterine wall, nourishing the growing fetus via the umbilical
cord.

 Chorioangiomas are vascular tumors, meaning they are made up of blood vessels. In the majority
of cases the tumor is benign (noncancerous).
  Small chorioangiomas typically cause no symptoms and complications. If the chorioangioma is
large, measuring more than 4 cm, in some cases it can pose serious risks to the pregnancy and
the fetus, including fetal heart failure.
 The cause of chorioangioma is unknown. The abnormal masses form in the chorionic tissue, the
tissue on the fetal side of the placenta

Risks to the fetus include:

 Anemia (lack of red blood cells)

 Thrombocytopenia (inability to clot due to lack of platelets)
 Non-immune hydrops (fluid buildup and swelling in multiple areas of the baby’s body)
 Enlargement of the heart (cardiomegaly)
 Fetal heart failure
 Intrauterine growth restriction, caused by a mass protruding into the amniotic cavity)
 Fetal stroke

Potential maternal complications include:

 Polyhydramnios, a build-up of amniotic fluid in the womb

 Premature delivery
 Preeclampsia (high-blood pressure with signs of organ damage)
 Placental abruption (placenta detaches from the uterus before delivery, causing bleeding)
 Malpresentation (baby abnormally positioned at delivery)
 Need for a cesarean delivery

Location
They tend to occur on the fetal side of the placenta (close to cord insertion).

Markers
 raised maternal alpha-fetoprotein (MSAFP)

Radiographic features
Ultrasound
Typically a chorioangioma is located near the insertion of the cord and protrudes into the amniotic cavity.

 often seen as a hypoechoic, rounded mass, located near the chorionic plate +/- umbilical cord insertion site

 Doppler: often demonstrates low resistance pulsatile flow within the anechoic 'cystic' areas, which represent enlarged
vascular channels

 MRI , fetal echocardiography

TREATMENT
  Small tumours are often monitored with ultrasound ~every 6-8 weeks, whereas large tumours require serial ultrasound
examinations more frequently ~every 1-2 weeks. Some tumours may even regress spontaneously during pregnancy

Mother and baby will be closely monitored throughout pregnancy with frequent ultrasounds and fetal
echocardiograms to assess the growth of the tumor, amniotic fluid level, fetal heart function, and fetal
growth, among other factors, for early detection of complications

In some cases, fetal intervention may be recommended. Treatment strategies during pregnancy may
include:

 Steroids to accelerate fetal lung maturity if early delivery becomes necessary

 Amnioreduction, a procedure used to reduce the amniotic fluid level, decreasing the risk of preterm labor
(similar to an amniocentesis)
 Fetal blood transfusions to treat anemia
 In fetuses at risk of heart failure, treatment to stop or reduce the blood supply to the tumor, such as
fetoscopic or interstitial laser ablation (using laser energy to seal blood vessels)

OVARIAN TUMOURS
Definition - Malignant neoplasm of the ovary

Etiology - Exact aetiology unknown: ?increased number ovulatory cycles (?abnormal repair of ovarian
surface), BRCA1 gene associated with breast–ovarian cancer syndrome.

Risk factors - Nulliparity, " older age, history of fertility treatment, family history, history of breast
cancer, obesity,postmenopausal HRT , endometriosis, early menarche , late menopause, HNPCC.
Protective factors: Parity, oral contraceptive use, breastfeeding, hysterectomy.

Epidemiology- Most common gynaecological malignancy in the UK (5% female cancers): 12.9–15.1
cases per 100 000 people, 1 in 70 lifetime risk.

Symptoms - Often late presentation. Vague early symptoms: abdominal/pelvic discomfort,

abdominal distension/mass, fatigue, weight loss, pressure symptoms (urinary frequency/dyspepsia).

Examination -General: Signs of malignancy (anaemia, cachexia etc.). Chest: Signs of metastasis,
pleural effusion. Abdomen: Abdominal/pelvic mass, ascites, hepatomegaly. Pelvis: Pelvic mass.

Pathogenesis - Multiple histological types including: Epithelial tumours (>90%): Include serous
cystadenocarcinoma (most common, fluid-filled cystic components), mucinous cystadenocarcinoma
(mucin-filled cysts), endometrioid carcinoma (resembles endometrial adenocarcinoma), clear cell
carcinoma (cells have clear cytoplasm). Germ cell tumours <5%: Dysgerminoma most common. Sex-cord
stromal tumours (rarely malignant): Most common granulosa cell tumour.
Investigation - Bloods: FBC (?anaemia), U&E (obstruction, renal failure), LFT (liver metastasis, #
albumin/ total protein), clotting (if LFTs abnormal), tumour markers (Ca 125, HCG, AFP, CEA, Ca 15-3, Ca
19-9). Imaging: TVS (" suspicion if solid areas, septae, thickened walls), MRI (for surgical planning).

management -Staging laparotomy: TAH/BSO, peritoneal washings, omentectomy, peritoneal

biopsies, assessment of pelvic/para-aortic lymph nodes. Advanced disease: Debulking procedure
(TAH/BSO, omentectomy, resection of metastases). Chemotherapy: Includes platinum compounds and
taxanes. Radiotherapy: Primarily for palliation.

Complications - Ovarian cyst accident, metastatic spread, surgical morbidity, complications of

chemotherapy (bone marrow suppression, infection, nephrotoxicity), ascites, pleural effusion.

Prognosis - Five-year survival: stage I 80–100%, stage III 15–20%, stage IV 5%. Overall survival low
owing to late-stage at presentation.

CERVICAL INTRAEPITHELIAL NEOPLASIA

Definition - Premalignant cells within the squamous epithelium of the cervix.

Etiology -HPV implicated in >95% cases, HPV 16 and 18 predominate.

Risk factors -Smoking, multiple sexual partners, # age at first intercourse, # socioeconomic status,
HIV.

Epidemiology - Peak incidence at 25–29 years, difficult to assess UK prevalence (only CIN3 recorded
in cancer registries).

Symptoms - Asymptomatic, detected on cervical screening.

Examination - Speculum: Cervix often unremarkable.

Pathogenesis -Histology: Dysplastic epithelial changes – "nuclear-to-cytoplasmic ratio, "nuclear size,

abnormal nuclear shape (poikilocytosis), "nuclear density (koilocytosis), # cytoplasm. CIN grades: CIN I –
mild dysplasia confined to lower third of the epithelium; CIN II – moderate dysplasia affecting two-thirds
of the epithelial thickness; CIN III – severe dysplasia extending to upper third of epithelium (carcinoma-
in-situ). CIN I is referred to as low-grade, CIN II and III as high-grade.

Investigations - Colposcopy biopsy.

Management - CIN I: Conservative (may resolve), but if persistent may require

excision/cryotherapy, conisation (differing opinions on timing of intervention).
OPERATIVE DELIVERY
Operative vaginal delivery involves application of forceps or a vacuum extractor to the fetal
head to assist during the 2nd stage of labor and facilitate delivery.

Indications for forceps delivery and vacuum extraction are essentially the same:
 Prolonged 2nd stage of labor (from full cervical dilation until delivery of the fetus)
 Suspicion of fetal compromise (eg, abnormal heart rate pattern)
 Need to shorten the 2nd stage for maternal benefit—eg, if maternal cardiac dysfunction (eg,
left-to-right shunting) or neurologic disorders (eg, spinal cord trauma) contraindicate
pushing or maternal exhaustion prevents effective pushing
A prolonged 2nd stage is defined as follows (1):
 In nulliparous women: Lack of continuing progress for 4 hours with a regional anesthetic or
3 hours without a regional anesthetic
 In multiparous women: Lack of continuing progress for 3 hours with a regional anesthetic or
2 hours without a regional anesthetic
.
Before starting an operative vaginal delivery, the clinician should do the following:
 Confirm complete cervical dilation
 Confirm an engaged fetal vertex at station +2 or lower
 Confirm rupture of membranes
 Confirm that fetal position is compatible with operative vaginal delivery
 Drain the maternal bladder
 Clinically assess pelvic dimensions (clinical pelvimetry) to determine whether the pelvis is
adequate
Also required are informed consent, adequate support and personnel, and adequate analgesia or
anesthesia. Neonatal care providers should be alerted to the mode of delivery so they can be
ready to treat any neonatal complications.

Contraindications include unengaged fetal head, unknown fetal position, and

certain fetal disorders such as hemophilia. Vacuum extraction is typically considered
contraindicated in preterm pregnancies of < 34 weeks because risk of intraventricular hemorrhage
is increased.
Major complications are maternal and fetal injuries and hemorrhage, Significant perineal
trauma and neonatal bruising are more common with forceps delivery; shoulder dystocia,
cephalohematoma, jaundice, and retinal bleeding are more common with vacuum-assisted delivery

FEMALE OVULATORY DYSFUNCTION

Ovulatory dysfunction is abnormal, irregular (with ≤ 9 menses/year), or absent ovulation.
Menses are often irregular or absent. Diagnosis is often possible by history or can be
confirmed by measurement of hormone levels or serial pelvic ultrasonography. Treatment is
usually induction of ovulation with clomiphene or other drugs.

Etiology of Ovulatory Dysfunction

Chronic ovulatory dysfunction in premenopausal women is most commonly
caused by
 Polycystic ovary syndrome (PCOS)
But it has many other causes, including
 Hyperprolactinemia
 Hypothalamic-pituitary dysfunction (most commonly, functional
hypothalamic amenorrhea)
 Other conditions that can cause anovulation (eg, diabetes, depression,
certain antidepressants, ex9ouiucessive exercise, use of drugs that
contain estrogens or progestins)
Symptoms and Signs of Ovulatory Dysfunction
In women with ovulatory dysfunction, menses may be absent, irregular, or not
preceded by symptoms, such as breast tenderness, lower abdominal bloating, or
moodiness (collectively termed molimina).
Diagnosis of Ovulatory Dysfunction
 Menstrual history
 Sometimes basal body temperature monitoring
 Measurement of urinary or serum hormones or ultrasonography
 Home testing kits, which detect an increase in urinary luteinizing hormone (LH) excretion
24 to 36 hours before ovulation (requiring daily testing for several days around midcycle,
usually beginning about or after cycle day 9)
 Pelvic ultrasonography, which is used to monitor increases in ovarian follicle diameter
and collapse of the follicle (monitoring should begin in the late follicular phase)
 Measurement of serum progesterone and urinary pregnanediol glucuronide (a
urinary metabolite of progesterone
Serum progesterone levels of ≥ 3 ng/mL (≥ 9.75 nmol/L) or elevated levels of pregnanediol
glucuronide in urine (measured, if possible, 1 week before onset of the next menstrual period)
indicate that ovulation has occurred.

Treatment of Ovulatory Dysfunction

 Clomiphene or letrozole
 Possibly metformin if body mass index is ≥ 35
 Gonadotropins if clomiphene is ineffective
Ovulation can usually be induced with drugs.
IUGR
Definition -when a baby in the womb (a fetus) does not grow as expected.
Etiology - Maternal: Hypertension, pre-eclampsia, diabetes, drug/alcohol abuse, smoking, renal
disease, thrombophilia, "maternal age. Fetal: Chromosomal abnormalities, infection (e.g. CMV,
rubella), multiple pregnancy. Other: Placental insufficiency.
Risk factors - As for aetiology; previous IUGR.
Epidemiology -Affects 3–5% of pregnancies.
History -History of any aetiological factors noted above; enquire about fetal movements.
Examination - Abdomen: #fundal height, USS, AFI, Abd circumference/ head circumference.
Pathogenesis –
SYMMETRICAL IUGR: effects begins early in gestation, uniform effect-Head and body are
proportionally small, seen in chromosomal abnormalities or infection.

ASYMETRICAL IUGR: affects fetus in late 2nd 3rd trimester

Low nutrition delivery to fetus
abdominal circumference disproportionately smaller than the head, seen with placental
insufficiency. Or HC normal, length normal, weight affected mostly low.
Investigations - USS: Anomaly scan, growth (abdominal and head circumference), liquor
volume (?oligohydramnios), umbilical artery Doppler (abnormal if end-diastolic flow absent or
reversed), middle cerebral artery Doppler (may show redistribution of blood to brain). CTG:
Fetal wellbeing.
Management - Normal Doppler results: Aim delivery >37/40 unless abnormalities arise, with
regular fetal monitoring. Abnormal Doppler results: Steroids if pre-term, consider delivery,
paediatrician at delivery, continuous CTG intrapartum. Tx- IV glucose
Complications - Stillbirth, PTL, preterm birth, intrapartum fetal distress, birth asphyxia,
meconium aspiration, postnatal hypoglycaemia, neurodevelopmental delay, " risk type 2 diabetes
and hypertension in adult life.
Prognosis - Increased perinatal morbidity and mortality, increased neurodevelopmental delay
if onset

TRISOMY 13
 Triosomy 13 also called as patau syndrome is a chromosomal condition associated with severe
intellectual disability and physical abnormalities like spinal cord abnormalities ,poorly developed
eyes, cleft lip, cleft palate,Small head (microcephaly),Extra fingers or toes

Trisomy 13 is a genetic disorder that your baby gets when they have an extra 13th chromosome

chances a woman will have a baby with any chromosome abnormality go up after age 35.

How Is It Diagnosed?
physical signs of trisomy 13 during your routine first-trimester fetal ultrasounds.
Or it could show up in tests such as cell-free DNA screening (NIPT) or the PAPP-A (pregnancy-associated plasma
protein A).

There is no cure for trisomy 13,

TRIOSOMY 18
Trisomy 18 is a chromosomal abnormality. It's also called Edwards syndrome, baby gets a extra 18th chromosome

Trisomy 18 is the second most common type of trisomy syndrome, after trisomy 21 (Down syndrome).

many babies with trisomy 18 don't survive past the second or third trimester of pregnancy.

PRESENTATION

 Cleft palate
 Clenched fists with overlapping fingers that are hard to straighten
 Defects of the lungs, kidneys, and stomach/intestines
 Deformed feet (called "rocker-bottom feet" because they're shaped like the bottom of a
rocking chair)
 Feeding problems
 Heart defects, including a hole between the heart's upper (atrial septal defect) or lower
(ventricular septal defect) chambers
 Low-set ears
 Severe developmental delays
 Chest deformity
 Slowed growth
 Small head (microcephaly)
 Small jaw (micrognathia)
 Weak cry

Diagnosis
a pregnancy ultrasound, although this isn't an accurate way to diagnose

precise methods take cells from the amniotic fluid (amniocentesis)

Karyotyping-A blood sample can be taken to look for the chromosome abnormality.

Chorionic villus sampling

Treatment
There is no cure for trisomy 18. Treatment for trisomy 18 consists of supportive medical care to provide the child

CHORIOAMNIOTIS
 Definition -is inflammation of the fetal membranes (amnion and chorion), usually due
to bacterial infection.
symptoms -
fever, leukocytosis (>15,000 cells/mm³), maternal (>100 bpm)[8] or fetal (>160
bpm) tachycardia, uterine tenderness and preterm rupture of membranes., Sore or painful uterus , A bad
smell from the amniotic fluid
Risk factors - Your bag of waters (amniotic sac) breaks long before you actually deliver
 You have a long labor
 You have frequent vaginal exams during labor
 This is your first pregnancy
 You have a sexually transmitted infection or other vaginal infection
 You use alcohol or tobacco
 You have internal fetal monitoring
 You get epidural anesthesia during labor
 You have group B strep

Diagnosis - Chorioamnionitis is diagnosed from a histologic (tissue) examination of the fetal

membranes
Diagnosis can be confirmed histologically or through amniotic fluid tests such as gram staining, glucose
levels, or other culture results consistent with infection.

Treatment - Standard
o Ampicillin + gentamicin
 Alternative
o Ampicillin/sulbactam
 Cesarean delivery
o Ampicillin and gentamicin plus either clindamycin or metronidazole
 Penicillin-allergy
o Vancomycin + gentamicin
o Gentamicin + clindamycin

PCOS
Definition - Ovarian dysfunction associated with hyperandrogenism and polycystic ovarian
morphology.

Etiology - Genetic basis widely implicated.

Risk factors - Family history, obesity, insulin resistance, hypertension, autoimmune thyroid disease.

Epidemiology -Most common endocrinopathy of women of reproductive age (5–10%).

Symptoms - Anovulatory symptoms (oligomenorrhoea, amenorrhoea, infertility), hyperandrogenic
symptoms (hirsuitism, acne, male-pattern baldness), weight gain.

Examination - General: BMI, BP, evidence of hyperadrogenism (hirsuitism, acne), rarely acanthosis
nigricans. Gynaecological: Often unremarkable.

Pathogenesis - LH and hyperinsulinaemia are thought to cause increased ovarian androgen

production.

Investigations - Bloods: LH, FSH ("LH:FSH ratio now not essential for diagnosis), oestradiol, prolactin,
testosterone, androstenedione, SHBG (#), TFT, GTT ("diabetes). Imaging: USS pelvis, polycystic ovarian
morphology defined as 12 or more follicles in an ovary or ovarian volume >10 mL.

Management - Diet, exercise (5% weight reduction can lead to resumption of ovulation), cosmetic
hair removal. Medical: Metformin, COCP including those with anti-androgenic effects (caution with
obesity) or intermittent progestogens (endometrial protection), ovulation induction (for infertility).
Surgical: Laparoscopic ovarian drilling.

Complications -Type 2 diabetes, complications in pregnancy (pre-eclampsia, gestational diabetes),

endometrial carcinoma, ovarian carcinoma, increased cardiovascular risk factors.

Prognosis - Weight management key to successful management and mitigating long-term risks

ENDOMETRIOSIS
Definition -Presence of endometrial tissue outside the uterus. Affects ovaries , fallopian tube ,
uterine ligaments , perimetrium , rectovaginal septum , recto uterine pouch , intestines .

Etiology - Suggested theories include: (i) retrograde menstruation (Sampson’s theory), the passage of
endometrial tissue through the fallopian tubes into the pelvis during menstruation; (ii) metaplasia of
coelomic epithelium into endometrial glands (Meyer’s theory); (iii) vascular and lymphatic
dissemination; (iv) immune; (v) genetic.

Risk factors - Nulliparity, family history, short menstrual cycle, long periods. EPIDEMIOLOGY Affects
10–15% of women of reproductive age.

Symptoms – bleeding , Cyclical dysmenorrhoea (starting premenstrually and reaching peak at onset
of menstruation), dyspareunia, chronic pelvic pain, infertility. Rarely symptoms of involvement of other
organs/distant sites: cyclical haematuria, PR bleed, epistaxis, haemoptysis, dyschaezia , urgent frequent
painful urination

Examination – Vaginal: (Often unremarkable) pelvic tenderness, immobile uterus, tender

uterosacral ligaments, palpable uterosacral nodules.
Pathogenesis -Ectopic endometrial tissue induces a chronic, inflammatory reaction. Can cause
fibrosis/adhesions. Classic ‘Powder-burn’ or ‘gun-shot’ lesions seen on pelvic surfaces. On the ovary, an
endometriotic cyst can form which enlarges with blood during each menstrual cycle
(endometrioma/chocolate cyst).

Investigations - USS: Endometrioma, differential diagnosis. Laparoscopy: Gold standard for

diagnosis.

Management -Medical: Analgesia (NSAIDs),combined estrogen progesterone oral contraceptive pills

, suppression of ovulation (COCP, progestogens analogues, Mirena IUS, GnRH analogues). Surgical:
Laparoscopic ablation/excision of lesions, adhesiolysis, ovarian cystectomy, rarely TAH/BSO (last resort).

Complications - Ovarian cyst accident (endometrioma), infertility, chronic pelvic pain, adhesions,
sexual dysfunction.

Prognosis -Medical management improves symptoms in 80–90%, but recurs if treatment stopped.
Symptoms subside in pregnancy and menopause

ENDOMETRITIS
Definition - Infection of the endometrium.

Etiology - Ascending infection from lower genital tract, may occur secondary to instrumentation of
the uterus.

Risk factors - Obstetric: Caesarean section, prolonged rupture of membranes, prolonged labour,
retained products of conception, manual removal of placenta. Gynaecological: PID/infection(Chlamydia,
bacterial vaginosis, tuberculosis), instrumentation of uterus (e.g. TOP).

Epidemiology - Incidence after vaginal delivery 1–3%, after Caesarean section 15–40%.

HISTORY Fever, abdominal pain, offensive discharge/lochia, dyspareunia.

Examination - General: Pyrexia, tachycardia. Abdomen: Lower abdominal tenderness. Vaginal:

Offensive discharge, uterine tenderness, adnexal tenderness.

Pathogenesis -Acute: Neutrophils present in endometrial glands.

Chronic: Plasma cells and lymphocytes in endometrial stroma.

Pathogens include: Gram-positive (Staphylococcus, Streptococcus), Gram-negative (E. coli, Klebsiella,

Proteus, Enterobacter, Gardnerella, Neisseria), and anaerobes (Bacteroides).
Investigations - Bloods: FBC, CRP (acute infection).

Microbiology: HVS, endocervical/Chlamydia swab, blood culture.

Management -Broad-spectrum antibiotics, surgery may be indicated if retained products of

conception (after 24-hour antibiotic cover).

COMPLICATIONS- PID, Asherman’s syndrome, pyometra, infertility.

Prognosis - Ninety percent resolve after 48–72 hours with antibiotic therapy

TURNER SYNDROME
Definition - genetic condition in which a female is partially or completely missing an X chromosome

Symptoms - short stature, heart defects, neck webbing, delayed or absent puberty, and infertility.
swollen hands and feet are seen at birth.[1] Typically, those affected do not develop menstrual
periods and breasts Heart defects, diabetes, and low thyroid hormone Vision and hearing problems

Diagnosis - amniocentesis or chorionic villus sampling during pregnancy

Treatment - there is no cure for Turner syndrome. Hormone replacement therapy such as Growth

hormone, either alone or with a low dose of androgen , Estrogen replacement therapy such as the birth
control pill,

HYPERPROLACTINEMIA
Prolactin is a hormone which is mostly produced in the pituitary gland

Causes – physiologic (pregnancy , lactation ) , prolactinoma , hypothyroidism , dopamine antagonist

, estrogen , trauma , surgery

Hyperprolactinemia is a condition of elevated serum prolactin.

Symptoms
 long or irregular cycles.
 anovulation
 amenorrhea (absence of periods)
 oligomenorrhea (irregular periods)
 infertility.
 galactorrhea
 sexual dysfunction
  hirsutism (abnormal hair growth)

CAUSES
a small tumor in their pituitary gland called a prolactinoma

Damage to other parts of the body can also affect prolactin production. damage to the kidneys, liver, and
thyroid can cause hyperprolactinemia

Medications can cause hyperprolactinemia.

A high level of prolactin in the body is normal during and after pregnancy, and while breastfeeding

Diagnosis – serum PRL , TSH , MRI

Treatment
For hyperprolactinemia caused by a benign tumor on the pituitary gland (prolactinoma), (dopamine
agonists - bromocriptine).

hormonal contraceptives or hormone replacement therapy (HRT)

surgery if medication not working

PROLACTINOMA
is a noncancerous tumor of the pituitary gland. (uncontrolled growth of lactotrophs) This tumor causes
the pituitary to make too much of a hormone called prolactin.

The major effect of prolactinoma is decreased levels of some sex hormones —

estrogen in women .

Symptoms

 amenorrhea

 galactorrhea

 dyspareunia

 hypogonadism

 Acne and hirsutism

 Bitemporal hemianopia, headache

 Visual changes
Diagnosis

BLOODTEST – increased Prolactin, TSH,

MRI OF HEAD

Treatment -dopamine agonist-bromocriptine,

Surgery ,

PELVIC ORGAN PROLAPSE

Definition – displacement of one or more organs from the anatomical position (uterus,
bladder, bowel or top of vagina)
Causes - gynecological cancer treatment, childbirth, heavy lifting, obesity, constipation, hysterectomy,
respiratory problems with chronic long-term cough.
Risk factors – pregnancy, vaginal childbirth, ageing, chronically increased intrabdominal pressure,
constipation, obesity, copd, multiple pregnancy, prior pelvic surgery, giving birth to large baby,
multigravida

Stages-
grade 0 – no prolapse,
grade 1–halfway to hymen,
grade 2 – to hymen,
grade 3 – halfway past hymen,
grade 4 –maximum descent (AKA procidentia)

Symptoms – pressure on lower abdomen and around genitals, discomfort in vagina , low back
pain , urinary problems , spotting or bleeding from vagina, sensation of vaginal or perineal bulge, seeing
or feeling bulge, heaviness in pelvis or vagina, urinary SX- urgency frequency incontinence, feeling of
incomplete voiding
Diagnosis – pelvic examination , bladder function test , imaging (X ray , CT , ultrasound )
Management – physical therapy for pelvic floor muscles, surgery, vaginal pessaries
Complications – permanent nerve damage , incontinence, constipation , sexual problems .

ANALGESIA
Definition - : Analgesia is used when only the pain relief is required, such as in post-surgical patients.
Types
 Inhaled analgesia – nitrous oxide. Short acting and mild relief .
Side effects : lightheadedness , nausea
Use : later stages of labor

 Systemic analgesia – narcotics are given IV . short acting and used for mild pain.

 Local analgesia – pudendal nerve block . used for operative vaginal delivery or repair of laceration . great
pain among nerve distribution.

 Regional analgesia –
Epidural anesthesia : catheter is placed in epidural space to inject medication. Used in 2 nd stage of labor.
Assist in vaginal delivery by relaxing women and allows head to descend and rotate .
Spinal anesthesia : more effective and faster onset . Spinal needle is passed through epidural space into
subarachnoid space and drug is injected.
Use – C section , manual removal of retained placenta , repair of perineal and vaginal tear

 General anesthesia – Used only in emergency C section

Side effects – vomiting which may cause pulmonary aspiration.

Indication – prolonged labor , maternal HTN , multiple pregnancy.

Contraindication – coagulation disorders , sepsis , hypovolaemia

CONTRACEPTION
Definition - a device or drug used to prevent pregnancy
NATURAL METHODS
1. Rhythm: avoidance of sexual intercourse during fertile period by monitoring body temperature
(0.2–0.4 degree celsius rise after ovulation) and cervical secretions (spinnbarkheit during
ovulation).
2. Withdrawal: removal of penis before ejaculation.
3. Lactation. Breastfeeding can be used as a method of birth control. This is called the lactational
amenorrhea method (LAM). a breastfeeding woman produces less oestrogen than normally,
she does not ovulate and cannot become pregnant.
4. Persona hormone monitoring kits: measure daily urinary concentrations of hormones to detect
the LH surge (precedes ovulation).

Barrier methods
 Sterilization

Most Effective: > 99%

1. Implant (progestin-only implant)------------Inhibits ovulation; ↑ cervical mucus

viscosity
2. Copper T IUD-----------Foreign body results in inflammation; copper has a spermicidal
effect
3. Intrauterine device (IUD) with progestin----Progesterone leads to cervical mucus
thickening and endometrial decidualization
4. Medroxyprogesterone------------IM injection (progestin) Suppresses ovulation and
decidualizes endometrium
5. Transdermal patch (“the patch”) --------Combined weekly estrogen and progestin
dermal patch
6. OCPs (combination estrogen and progestin) ------Inhibit FSH/LH, suppressing
ovulation; thicken cervical mucus; decidualize endometrium
7. Progestin-only “minipills” ---------Thicken cervical mucus
8. Male condoms--------A latex sheath covers the penis
9. Female condom-------A barrier sheath is inserted into the vagina
10. Fertility awareness methods (natural family planning)-----------Sexual intercourse is
avoided on days in the menstrual cycle on which conception is likely (near the time of
ovulation

Emergency Contraceptive Methods

1. Morning-after pill”a (progesterone agonist/ antagonist)
2. Copper T IUD (99% effective)

STERILIZATION
 Sterilization is a permanent method of birth control. Sterilization procedures for women are
called tubal occlusion. The procedure for men is called vasectomy.
 Tubal occlusion closes off the fallopian tubes. This prevents the egg from moving down the
fallopian tube to the uterus and keeps the sperm from reaching the egg.
 Sterilization is a highly effective way to prevent pregnancy
 A risk common to all female sterilization methods is ectopic pregnancy.

Sterilization methods
 There are three ways that sterilization for women can be performed:
 1) minilaparotomy,
 2) laparoscopy,
 3) hysteroscopy
  Minilaparotomy—A small incision is made in the abdomen. The fallopian tubes are brought up through
the incision. A small section of each tube is removed, or both tubes can be removed completely. Less
often, clips are used to close off the tubes. This approach frequently is used for postpartum sterilization
 Laparoscopy—In laparoscopy, an instrument called a laparoscope is inserted through a small incision
made in or near the navel. Another small incision may be made for an instrument to close off or remove
the fallopian tubes. The fallopian tubes can be closed off by bands or clips. They also can be cut and closed
with special thread or sealed with an electric current. The laparoscope then is withdrawn. The incisions are
closed with stitches or special tape.

 Hysteroscopy—Hysteroscopic sterilization does not require incisions in the skin. It can be done
with local anesthesiain a health care professional’s office. Small devices are placed into the openings of
the fallopian tubes. The devices cause scar tissue to form that blocks the fallopian tubes. After having the
procedure, it takes 3 months for the scar tissue to form. During this time, must use another form of birth
control to prevent pregnancy. A test called hysterosalpingography must be done to ensure that the
tubes are blocked before you can use it as your only method of birth control.

TUBAL LIGATION

UTERINE BLEEDING
Definition -. vaginal bleeding from the uterus that is abnormally frequent, lasts excessively long,
is heavier than normal, or is irregular.

Causes - ovulation problems, fibroids, the lining of the uterus growing into the uterine wall, uterine
polyps, underlying bleeding problems, side effects from birth control, or cancer.

Symptoms – menorrhagia, longer duration of menstruation, postcoital bleeding, intermenstrual

bleeding

Diagnosis – blood test , pelvic ultrasound , Laboratory assessment of thyroid stimulating

hormone (TSH), pregnancy, and chlamydia is also recommended.[6]

Treatment - hormonal birth control, gonadotropin-releasing hormone (GnRH) agonists, tranexamic

acid, NSAIDs, and surgery such as endometrial ablation or hysterectomy.

FETAL DISTRESS IN LABOR

Deifinition - Fetal distress refers to the compromise of the fetus due to inadequate oxygen or nutrient supply.
This can occur due to maternal, fetal or placental factors

Pathogenesis
 The main cause of antepartum fetal distress is uteroplacental insufficiency
 processes such as uteroplacental vascular disease, reduced uterine perfusion, intrauterine sepsis, reduced
fetal reserves and cord compression can be involved alone or in combination.

Risk factors Includes women with a history of:

Stillbirth.Intrauterine growth restriction (IUGR). Placental abruption

Oligohydramnios or polyhydramnios. Multiple pregnancy.

Rhesus sensitisation.Hypertension.

Obesity. Smoking.Diabetes and other chronic diseases.

Pre-eclampsia or pregnancy-induced hypertension. Decreased fetal movements.

Recurrent antepartum haemorrhage. Post-term pregnancy.

Maternal age over 35 years, and particularly over 40, is an independent risk factor for uteroplacental
insufficiency, fetal distress and stillbirth; the highest risk is in older women who are also nulliparous

Examinantion - General: Assess maternal pulse (maternal tachycardia can cause fetal
tachycardia), BP (maternal hypovolaemia), temperature (signs of infection/chorioamnionitis).
Abdomen: Check for hypertonic/irritable uterus (hyperstimulation,
abruption), clinical assessment of fetal growth/liquor (IUGR, oligohydramnios).
Vaginal: Assess cervical dilatation, colour of liquor, bleeding, check for cord
prolapse
Fetal distress presents in varied ways and to differing degrees. It may be suspected
by the following, which may also be used for further evaluation of suspected fetal
distress:
 Clinical suspicion when decreased fetal movements are felt by the mother or there is a
slowing or stopping of the growth of serial symphysis fundal height.
 Abnormal sonographic biometric parameters when IUGR or macrosomia is suspected.
 Doppler ultrasound is particularly valuable when performed up to 34 weeks of gestation:
o Umbilical artery Doppler may detect changes that reflect increasing placental
vascular resistance.

 Cardiotocography (CTG)
 Antenatal CTG
 Intrapartum CTG
 Biophysical profile (BPP)
Amniotic fluid volume,
Fetal scalp blood sampling

How is fetal distress managed?

 The first step is usually to give the mother oxygen and fluids. Sometimes, moving position, such
as turning onto one side, can reduce the baby’s distress.
 If you had drugs to speed up labour, these may be stopped if there are signs of fetal distress. If
it’s a natural labour, then you may be given medication to slow down the contractions.
 Sometimes a baby in fetal distress needs to be born quickly. This may be achieved by an assisted
(or instrumental) delivery which is when the doctor uses either forceps or ventouse (vacuum
extractor) to help you deliver the baby, or you might need to have an emergency caesarean.
 General: Left tilt, IV access, stop oxytocin infusion if in progress.
 Fetal bradycardia >6 minutes: Necessitates emergency delivery.
 Persistent CTG abnormalities: (See Cardiotocography appendix) may require FBS.
 Delivery: If fully dilated, <1/5 palpable abdominally and vertex at or below spines , consider
instrumental delivery otherwise deliver by c section.

Complications -Maternal: Complications of operative delivery.

Fetal: Hypoxic ischaemic encephalopathy, death.

PREECLAMPSIA
Definition- is a complication of pregnancy characterized by new onset hypertension along
with proteinuria after 20 weeks of gestation, last up to 6 wks after delivery..

Risk factors -Nulliparity, "maternal age>35, family history, previous history of pre-
eclampsia, pre-existing hypertension, multiparity, pre-existing renal disease, diabetes, PCOS,
multiple pregnancy, obesity.

Epidemiology - Affects 2–5% of pregnancies.

Symptoms - Headache, oedema, visual disturbance, right upper quadrant pain due to liver
capsule swelling (note: often asymptomatic). proteinuria , nausea ,vomiting ,new headache
that don’t go away after taking pain medication.

Examination - General: "BP,

Oedema proteinuria, (especially facial), hyperreflexia, clonus, ?papilloedema Abdomen: ?

RUQ tenderness, ?reduced fundal height.

Pathogenesis - Increased resistance due to fibrosis of spiral arteries in the uteroplacental

circulation leads to hypoperfusion/ ischaemia releasing inflammatory mediators which cause
widespread endothelial damage, end-organ dysfunction and oedema. Spiral arteries get
fibrous causing narrowing of vessels.

Investigations –BP – 140/90 (in severe cases 160/110)

Bloods: FBC (low platelets, haemoconcentration),

U&E and urate (renal impairment),

LFT (" transaminases), clotting.

Urine: Urinalysis (proteinuria),

MSU (exclude UTI), 24 h urine collection (significant proteinuria >0.3 g protein per 24 hours).
USS: Fetal growth, liquor volume and

umbilical artery Dopplers. CTG: Fetal wellbeing. Pulmonary edema.

Management - Depends on gestational age and severity of condition. The condition will
not resolve until after delivery.

Mild/moderate pre-eclampsia: Regular monitoring of BP with urinalysis, regular blood

testing, serial USS for fetal growth, regular CTGs, antihypertensives (e.g. methyldopa,
hydralazine , labetalol, nifedipine), aim for delivery after 37 weeks.

Severe pre-eclampsia/evidence of fetal compromise: (Note: requires delivery in severe)

antihypertensives (labetalol, nifedipine, hydralazine), seizure prophylaxis (IV magnesium
sulphate), fluid restriction and strict fluid balance (catheterise, consider CVP monitoring),
corticosteroids for lung maturity if preterm.

Complications -Maternal: Eclampsia, hemorhhagic shock , placental abruption, CVA,

pulmonary oedema, cerebral oedema, renal failure, liver failure, DIC, HELLP syndrome
(haemolysis, elevated liver enzymes, low platelets) Fetal: IUGR, death.

Prognosis - Severe pre-eclampsia has 10% recurrence in subsequent pregnancies.

ECLAMPSIA
Definition – new onset of seizures /coma in pregnant women with preeclampsia.

Etiology - Unclear: see pathology/pathogenesis.

Risk factors -Pre-existing pre-eclampsia.

Epidemiology - UK incidence is 4.9 per 10 000 maternities, 44% postpartum, 18%

intrapartum and 38% antenatal.

Symptoms - Symptoms of impending eclampsia: headache, epigastric tenderness, visual

disturbance, oedema, previous examination findings of hyperreflexia, clonus , seizures , loss
of consciousness , agitation

Examination -Grand mal seizure.

 Pathogenesis - Unclear. Mechanism related to cerebral vasospasm, hypertensive
encephalopathy, tissue oedema, ischaemia and haemorrhage have been proposed.

Investigations -Bloods: (As for pre-eclampsia) FBC, clotting, U&E, urate, LFT, G&S,
consider ABG. Urine: ? proteinuria. Imaging (post-seizure): CT head, CXR if chest signs.

Management - Airway and breathing: Apply oxygen, maintain patency, ventilation if

appropriate.

Circulation: Manage on left tilt, ensure large-bore IV access, evaluate pulse and blood
pressure.

Drugs: IV magnesium sulphate: 4 g loading dose followed by 1 g/h (monitor urine output,
respiratory rate, patellar reflexes).

Recurrent seizures: Consider – further bolus magnesium sulphate, thiopentone, diazepam,

IPPV and muscle relaxation.

Post-seizure: Assess chest, control blood pressure (consider IV labetalol/hydralazine), strict

fluid management, (85 mL/h input, urine output >25 mL/h), may require CVP monitoring,
deliver baby (only when mother stabilised), consider ITU.

Complications - Cardiac arrest, death, permanent CNS damage (e.g. cortical blindness),
CVA (1–2%), DIC, renal failure, ARDS.

Prognosis - Maternal mortality rate 1.8%; significant morbidity in 35%.

3 TRIMESTERAL ULTRASOUND
Ultrasound allows doctor to check your baby's health and development, monitor your pregnancy,
and look for any physical abnormalities.

First-trimester ultrasound:
If you have an ultrasound in the first trimester, it's usually too early to get a good look at your fetus's organs and limbs. But your
provider can:

 Confirm that your pregnancy is in your uterus (not an ectopic pregnancy)

 Confirm your dating. How far along are you? What's your due date?

 Confirm the number of babies you're carrying (one baby, twins, or multiples)

 Help screen for certain genetic disorders

 Identify any problems with your placenta, uterus, or ovaries

 Confirm viability by seeing the heartbeat. You're likely to see your baby's heart beating if you're at least 6 weeks pregnant.

Second-trimester ultrasound:
A second-trimester (mid-pregnancy) ultrasound allows your provider to:

 Tell you for certain whether you're carrying one baby or multiples

 Check your baby's heartbeat, position, and movement

 Measure your baby's size

 Check the location of your placenta

 Check your cervical length

 Assess the amount of amniotic fluid in your uterus

 Check your baby for physical abnormalities

 Try to determine your baby's sex

Third-trimester ultrasound:
A third-trimester ultrasound allows your provider to:

 Check on your baby's growth

 Check your amniotic fluid level

 Check on your baby's well-being

 Learn whether you may need a c-section, perhaps if your baby is especially large or in breech position

 Determine the cause of vaginal bleeding, if you're having any

CHLAMYDIA
Definition - A sexually transmitted infection caused by Chlamydia trachomatis.

Etiology - Transmission by sexual contact (30–40%) or vertical (50%).

Risk factors -Multiple sexual partners,unprotected sexual intercourse, age <25 years , history of
STIs , low socioeconomic status,

Epidemiology - Most common sexually transmitted disease, affecting 1% of sexually active women
aged 15–25 years.
Symptoms - PV discharge, dyspareunia, intermenstrual bleeding, post coital bleeding, abdominal
pain, dysuria (note: asymptomatic in 75%).

Examination –
 Abdomen: Lower abdominal tenderness.
 Speculum: Cervicitis, cervical/urethral discharge.
 Vaginal: May have tenderness/cervical excitation.

Pathogenesis - Gram-negative intracellular bacterium infects epithelial cells of the cervix and
urethra. Consists of an infectious elementary body and an intracellular reticular body. The elementary
body attaches to and is taken up by epithelial cells. The intracellular reticulate body replicates by binary
fission. The cell bursts releasing more infectious elementary bodies.

Investigations - There is a national Chlamydia screening programme for under-25s. Microbiology:

Endocervical swabs, HVS, first-void urine samples (NAAT). , cell culture

Management - Medical: Doxycycline 100 mg 2 daily for 1 week, or single dose of azithromycin 1 g.
In pregnancy: Erythromycin/amoxicillin (tetracyclines contraindicated). Other: Requires full STI screen
and contact tracing.

Complications -Pelvic inflammatory disease, chronic pelvic pain, infertility, ectopic pregnancy,
Reiter’s syndrome (arthritis, conjunctivitis, urethritis), Fitz–Hugh–Curtis syndrome (perihepatitis).
Pregnancy: PTL, PPROM, post-partum endometritis. Vertical transmission: Neonatal conjunctivitis (35–
50%), neonatal pneumonia (10–20%).

Prognosis - Good with prompt treatment, but many cases are asymptomatic. Longer term infection is
associated with higher morbidity, especially fertility problems.

GONORRHEA
Definition - Sexually transmitted infection caused by Neisseria gonorrhoeae

Etiology -Transmission by sexual contact (75%) or vertical (neonatal conjunctivitis).

Risk factors - Unprotected sexual intercourse, multiple partners, presence of other STIs, HIV, age <
25 year

Epidemiology - Second most common sexually transmitted bacterial infection in the UK, with
increasing prevalence: 22 000 cases in 2004.

Symptoms - PV discharge, IMB, PCB, dysuria, dyspareunia, ?lower abdominal pain (note: 50%
asymptomatic).
Examination - Abdomen: ?lower abdominal tenderness. Speculum: Mucopurulent endocervical
discharge, easily induced endocervical bleeding. Vaginal: ?pelvic tenderness, cervical excitation.

Pathogenesis -Highly infectious Gram-negative diplococcus affects mucous membranes (e.g.

urethra, endocervix, rectum, pharynx, conjunctiva), transmitted by inoculation of infected secretions
from one mucosal surface to another.

Investigations - Microbioogy: Endocervical swab/HVS, requires full STI screens

Management - Antibiotics: Cephalosporin, penicillin, tetracycline or quinolone (usually single dose).

Other: Contact tracing and treatment of partner.

Complications -PID, chronic pelvic pain, infertility, ectopic pregnancy, conjunctivitis, Fitz–Hugh–
Curtis syndrome (perihepatitis), " susceptibility to HIV, disseminated disease (1–2%, may lead to fever,
skin rash, arthralgia, septic arthritis, meningitis or endocarditis). Vertical transmission: ophthalmia
neonatorum (bilateral conjunctivitis).

Prognosis -Cure rate is 95% with treatment.

BACTERIAL VAGINOSIS
Definition -Overgrowth of predominantly anaerobic organisms in the vagina.

Etiology - Overgrowth by anaerobic organisms replacing lactobacilli and causing an increase in vaginal
pH (note: not sexually transmitted).

Risk factors - Smoking, IUS/IUCD, vaginal douching.

Epidemiology - Prevalence is 30%.

Symptoms - Typically an offensive ‘fishy’ PV discharge, not usually associated with pain , pruritus
(note: 50% asymptomatic). , dysuria

Examination - Thin white homogenous discharge adherent to vaginal wall, characteristic smell.

Pathogenesis - Organisms often implicated: Gardnerella vaginalis, Prevotella sp., Mycoplasma

hominis.

Investigations - Amsel’s criteria (3 out of 4 required): (i) thin white homogenous discharge; (ii) clue
cells (epithelial cells with attached bacteria) on microscopy; (iii) pH of vaginal fluid >4.5; (iv) ‘fishy’ odour
on alkalinisation with 10% KOH.

Management - Medical: PO metronidazole or topical clindamycin. Other: Avoid vaginal douching.

Complications - Associated with increased risk of endometritis following TOP and vaginal cuff
cellulitis after a vaginal hysterectomy. In pregnancy: associated with miscarriage, PTL, PPROM,
endometritis.

Prognosis -50% recurrence.

ANEMIA IN PREGNANCY
When you're pregnant, you may develop anemia. When you have anemia,
your blood doesn't have enough healthy red blood cells to carry oxygen to
your tissues and to your baby.

During pregnancy, your body produces more blood to support the growth of
your baby. If you're not getting enough iron or certain other nutrients, your
body might not be able to produce the amount of red blood cells it needs to
make this additional blood.

types

 Iron-deficiency anemia
 Folate-deficiency anemia
 Vitamin B12 deficiency

Symptoms

 Pale skin, lips, and nails

 Feeling tired or weak
 Dizziness
 Dyspnea
 Tachycardia
 Trouble concentrating

Untreated iron-deficiency anemia risk

 A preterm or low-birth-weight baby

 A blood transfusion (if you lose a significant amount of blood during
delivery)
 Postpartum depression
 A baby with anemia
 A child with developmental delays
Untreated folate deficiency can increase your risk of having a:

 Preterm or low-birth-weight baby

 Baby with a serious birth defect of the spine or brain (neural tube
defects)

Diagnosis

 Hemoglobin test. It measures the amount of hemoglobin -- an iron-rich

protein in red blood cells that carries oxygen from the lungs to tissues in
the body.
 Hematocrit test. It measures the percentage of red blood cells in a
sample of blood.

at the beginning of your pregnancy, your doctor will most likely recommend that
you get another blood test to check for anemia in your second or third trimester.

Treatment for Anemia

If you are anemic during your pregnancy, you may need to start taking an iron
supplement and/or folic acid supplement in addition to your prenatal
vitamins. Your doctor may also suggest that you add more foods that are
high in iron and folic acid to your diet. Green leafy vegetables , iron enriched
cereals and grains ,eggs ,meat , fish , citrus fruits

FETAL ANEMIA
Fetal anemia occurs when the amount of circulating red blood cells and hemoglobin in a fetus fall below normal levels

. fetal anemia can have several adverse effects, including cardiac complications. Fetal anemia is a relatively rare but
serious condition.

Causes – alloimmunization , maternal parvovirus b19 infection , fetal blood loss , structural
abnormalities , alpha thalasemmia , metabolic disorders , placental tumours .

An immune-related cause is most common,

 red-blood-cell (RBC) alloimmunization,/hemolytic disease of the fetus

 Rh(D)-negative women who deliver a D-positive baby she may sensitise do the RH antigen and develop
antibodies this antibodies cross the placenta and cause hemolysis of the fetal rbcs and this leads to
fetal anemia
 Alloimmunization does not usually cause problems during a first pregnancy because the baby often is
born before many of the antibodies develop. However, once the antibodies have formed, body does
 not get rid of them, so any subsequent babies are more likely to have problems if they have the same
blood type as the first baby
 All mothers are tested for the development of antibodies three times during pregnancy: at their first
prenatal visit, at 28 weeks’ gestation, and at delivery.
 If there is Alloimmunization during pregnancy, it is important that fetus be evaluated by a Maternal-Fetal
Medicine specialist for hemolytic disease of the fetus.
 If newborn has hemolytic disease he/she should be evaluated by a Neonatologist.

Symptoms of hemolytic disease in fetus or newborn may include:

 An abnormally large amount of amniotic fluid
 Jaundice (yellowing of the skin and eyes)
 Decreased muscle tone
 Lethargy
 Signs of red blood cell destruction in your baby’s blood

non-immune causes

 such as parvovirus B19 infection

it is also known as 5th disease parvovirus infection may cause fetal infection which may lead to
suppression of erythrocyte precursor of bone marrow and this leads to fetal anemia

complications can be fetal abortion, still birth

treatment will be self-care, fluids rest
hospitalization for blood transfusion, immunoglobulin injection for weak immune system

 Infection - Several maternal infections may cause fetal anemia.

 Blood loss - Loss of blood from the baby’s circulatory system can lead to anemia.
 Structural abnormalities - Defects in the structure of the baby’s heart or blood vessels
may contribute to anemia.

Diagnosing Fetal Anemia

Fetal anemia may be detected during pregnancy through prenatal testing. Some tests may be
routine, while others may be performed to check specifically for fetal anemia.

 A blood test to detect antibodies that are stuck to the surface of red blood cells (known as a direct Coombs
test)
 Testing of either or both the father of the baby or the fetus by amniocentesis to determine the fetus’ blood
type
 Ultrasound examination of the blood flow velocity in the fetal brain, Doppler
  Directly testing the fetal blood type and blood count by cordocentesis, amniocentesis , chorionic villus
sampling
 A blood test to look for higher-than-normal levels of bilirubin in baby’s umbilical cord blood

TO PREVENT ALLOIMMUNIZATION
Rh negative women are given injections of a medicine called Rh immune globulin (RhoGAM) to keep their
body from making Rh antibodies

How is Maternal Alloimmunization treated?

 If there is severe hemolytic disease of the fetus, then a Maternal-Fetal Medicine specialist can
give fetus in-utero transfusions. These can be lifesaving and prevent many of the complications
of hemolytic disease.
 After delivery, if baby has a mild case of hemolytic disease doctor may treat the condition with
phototherapy (light therapy). In some cases, baby may also need one or more blood
transfusions.
 An intrauterine transfusion provides blood to an Rh-positive fetus when fetal red blood cells are
being destroyed by Rh antibodies.

POSTPARTUM HEMORHHAGE
Definition - Blood loss of >500 mL at vaginal delivery or >1000 mL at Caesarean section.
Primary PPH: Within 24 hours. Secondary PPH: 24 hours to 6 weeks.

Etiology - Primary PPH: Uterine atony (80%), trauma to perineum/vagina/cervix, retained

placenta/ membranes, coagulopathy , eclampsia . Secondary PPH: Endometritis, retained
placenta/membranes.

Risk factors - Multiple pregnancy, polyhydramnios, APH, grand multiparity, fibroid uterus,
previous PPH, prolonged labour, augmented labour, instrumental delivery, high birthweight
infant, personal or family history of bleeding disorder, anticoagulant use, Caesarean section,
pyrexia in labour, episiotomy, placental site abnormalities.

Epidemiology - Affects 5% of deliveries.

History - Primary: Excessive PV bleed after delivery (note: verify whether placenta is
complete). , hypotension , tachycardia , decreased hematocrit , hematoma Secondary: PV bleed,
abdominal pain, PV discharge, fever.

Examination - Primary General: Shock (tachycardia, hypotension), signs of anaemia.

Abdomen: ?atonic uterus (above umbilicus)

Speculum: Exclude trauma (perineal/vaginal/cervical).

Vaginal: Evacuate clots from cervix (inhibits contraction).

 Secondary Abdomen: Tender uterus. Speculum: Assess bleeding, ?cervical os open.
Vaginal: ?uterine tenderness.

Pathogenesis - See the aetiologies noted above. Placental blood flow >500 mL /min at term.
With atony, poor uterine contraction (compresses spiral arteries) leads to heavy blood loss.

Investigations - Primary Bloods: FBC, U&E, clotting, X-match

Secondary Bloods: FBC, U&E, clotting, X-match, CRP. Microbiology: HVS. USS: ?retained
products.

Management – treatment of underlying cause , manual massage of uterus , medications for

stimulating contractions , removal of retained products . Primary Airway, breathing, circulation
(two large-bore IV cannulae), fluid resuscitation, blood transfusion if necessary. Atony:
Bimanual compression, uterotonics (oxytocin bolus þ infusion, IM ergometrine, IM carboprost,
PR misoprosol), transfer to theatre. Consider: Intra-uterine balloon insertion, uterine artery
embolisation, laparotomy and insertion of brace suture, hysterectomy. Trauma: Requires suturing
(consider transferring to theatre). Retained products: Manual evacuation in theatre.
Coagulopathy: Correct with FFP/cryoprecipitate/platelets.

Secondary Resuscitate as appropriate, IV antibiotics, ERPC only if unavoidable (increased risk

of uterine perforation).

Complications - Death, hysterectomy, "VTE, renal failure, DIC, Sheehan’s syndrome

(pituitary hypoperfusion following massive PPH causes pituitary necrosis and hypopituitarism).

Prognosis - Fourth most common cause of maternal death in the UK. Leading cause of
maternal mortality worldwide.

PRETERM LABOR
Definition -Onset of labour prior to 37 weeks’ gestation.

Etiology – May be idiopathic. Infection (often subclinical) contributes increasingly to aetiology

with decreasing gestation. See pathology/pathogenesis below.

Risk factors - Infection of genital tract, UTI, multiple pregnancy, polyhydramnios, cervical
incompetence/previous cervical surgery, systemic infective illness, previous PTL, uterine
abnormalities, APH , smoking , drug use , chronic conditions

Epidemiology -Affects 6% of deliveries in the UK.

Symptoms – regular frequent contractions , low back pain , abdominal cramps , preterm
rupture of membranes ,
 Examination -General: Signs of infection (tachycardia, fever). Abdomen: Contractions,
abdominal tenderness (may indicate abruption, chorioamnionitis). Speculum: ?liquor pooling.
Vaginal: Assess cervical dilatation.

Pathogenesis - Relationship with systemic infective illness may be due to direct spread of
infection or release of inflammatory mediators. Decidual haemorrhage is also associated with
release of inflammatory mediators. PTL in polyhydramnios/multiple pregnancy is related to
uterine over-distension.

Investigations - Bloods: FBC, CRP (evidence of infection). Microbiology: MSU, LVS/HVS.

CTG: Fetal wellbeing. USS: Confirm presentation, estimated fetal weight, cervical length. Fetal
fibronectin: (Sample taken at speculum examination) predictive of likelihood to labour (used for
high negative predictive value).

Management - Administer corticosteroids (fetal lung maturation), tocolysis used to allow

steroid cover e.g. oxytocin antagonists (atosiban), nifedipine or GTN (contraindicated if APH or
evidence of infection), antibiotics if SROM, fetal monitoring.

Complications -Respiratory distress syndrome, intracranial haemorrhage, sepsis, necrotising

enterocolitis, neurodevelopmental delay, cerebral palsy, neonatal death.

Prognosis - Dependent on gestation at delivery, accounts for over 20% of perinatal mortality.
There is 20% risk of PTL in subsequent pregnancies

CYSTITIS
Definition – inflammation of bladder

symptoms

 Urinary urgency

 dysuria

 oliguria

 (hematuria)

 Passing cloudy or strong-smelling urine

 Pelvic discomfort

 A feeling of pressure in the lower abdomen

 Low-grade fever

Causes - urinary tract infection (UTI)

  taking certain drugs
 exposure to radiation
 ongoing use of a catheter
 irritating hygiene products

types –
 bacterial ,
 drug induced – chemotherapy drugs , cyclophosphamide
 foreign body – long term use of catheter
 radiation
 chemicals – feminine hygiene sprays / spermicidal jellies
 associated with other conditions – diabetes , kidney stones , spinal cord injuries

risk factors – sexually active , using birth control , pregnancy , menopause , obstruction , prolonged
use of catheters , immunocompromised patients .

diagnosis – urinalysis , cytoscopy , ultrasound

treatment –
home care -applying heating pads to your abdomen or back

 over-the-counter pain relievers, such as ibuprofen and acetaminophen

 sitz baths to cleanse the pelvic area
 craneberry juice or tablets
 drinking lots of fluids
 wearing cotton underwear and loose fitting clothes
 avoiding any food or beverages that you suspect make your symptoms worse
 antibiotics

complications – chronic/recurrent UTI , hematuria , pyelonephritis , acute renal failure , sepsis ,

kidney stones

WELL WOMAN EXAM

What Is A Well Woman Exam?
A Well Woman Exam is a preventive annual gynaecological and breast exam. Well Women Exams are extremely
important in preventive care and early detection of diseases.

Physical Screening
Your height. weight. & blood pressure will be taken. You will be asked your age, your most recent menstrual period,
questions about any pregnancy experiences, any form of birth control and a review of your family history will be
asked for good measure.
ASK ABOUT VACCINATIONS

PRECONCEPTIONAL COUNCELLING

Clinical breast exam

The first of the two major specialized exams during your visit, this is to screen for lumps or other signs of
possible disease in the breast tissue.

Visual inspection, palpation

Pelvic exam
The pelvic exam is part of the physical examination of the internal pelvic organs (uterus, cervix, ovaries), vagina, and
external genitalia. This exam often includes three parts:

1. Inspection of the external genitalia

2. Bimanual examination
3. Inspection of the cervix and vagina using a speculum

Screening tests
Samples for screening tests may be collected during the pelvic exam. These screening tests include:

1. Cervical Cancer Screening - A Pap smear and/or HPV testing may be performed as a screening test for
cervical cancer.[18]
2. Sexually Transmitted Infection Screening - Depending on age and risk factors, clinicians may
recommend gonorrhea or chlamydia testing at the time of the well-woman exam. Additional screening tests
include blood tests for hepatitis C, HIV, and syphilis.[20]

Pap smears & annual pelvic exam

 USPSTF and ASCCP recommend cytology screening every 3 years from ages 21 to 29

 From ages 30 to 64, screening can be cytologic every 3 years or cytology with high-risk HPV testing every 5
years (co-testing)

Colorectal cancer screening

 ACS recommends screening average-risk patients at age 45

Breast cancer screening

 USPSTF recommends mammography every 2 years for women > 50

Hypertension, CVD, diabetes

 The AHA-approved cut-off for diagnosis of hypertension is now 130/80 mg/Hg

Osteoporosis screening

 BMD should be performed in women > 65 with no risk factors for osteoporosis

Well women care extras

1) Any examination should always be carried out with the patient’s consent and with
appropriate privacy and sensitivity.
2) Check and explain that the door is closed, check the patient’s comfort before
proceeding.
3) A female chaperone must be present throughout the examination.

4) HISTORY TAKING

1 General Name, age and occupation.

2 History of presenting complaint

3 Menstrual history

4 Cervical screening.

5 Sexual and contraceptive history

6 Other gynaecological conditions

7 Previous gynaecological history

8 Previous medical history

9 Medication and allergies.

10 Family history

11 Systems enquiry

Inspection- erythema, retraction, scaling, oedema, colour change.

Palpation- lymph node,

breast (supine position, hands above), check for breast pain, nipple discharge, nipple inversion,
dimpling, ulcer oedema. Breast lymph nodes,

Pelvic exam
Check in lithotomy position, inguinal lymph node and perineal inspection.

Speculum insertion-
Check ectocervix, vaginal wall and cervix for mass, ulceration, depigmentation and unusual discharge.

Bimanual exam-
With gloved fingers and lubricant.
 To check for cervix and uterus size, mobility, tenderness, position, shape, adnexal mass, consistency,
contour and os.

Rectovaginal exam-
Change gloves.

Physical exam-
Height, weight, BP, abdominal exam, rectal exam, bimanual, speculum, breast exam

Social history
woman’s social situation including details of her occupation, who she lives with, her housing and
whether or not she is in a stable relationship. A history regarding smoking and alcohol intake should also
be obtained

UTRINE ANATOMY
The uterus is a secondary sex organ

The uterus is a thick-walled muscular organ capable of expansion to accommodate a

growing fetus. It is connected distally to the vagina, and laterally to the uterine tubes.

The uterus has three parts;

 Fundus – top of the uterus, above the entry point of the uterine tubes.

 Body – usual site for implantation of the blastocyst.

 Cervix – lower part of uterus linking it with the vagina. This part is structurally and
functionally different to the rest of the uterus. See here for more information about the
cervix.

 the uterus normally lies immediately posterosuperior to the bladder, and anterior
to the rectum.
 The fundus and body of the uterus are composed of three tissue layers;

 Perimetrium– a double layered membrane, continuous with the abdominal peritoneum.

Also known as the perimetrium.

 Myometrium – thick smooth muscle layer. Cells of this layer undergo hypertrophy and
hyperplasia during pregnancy in preparation to expel the fetus at birth.

 Endometrium – inner mucous membrane lining the uterus. It can be further subdivided into
2 parts:
o Deep stratum basalis: Changes little throughout the menstrual cycle and is not shed at
menstruation.
o Superficial stratum functionalis: Proliferates in response to oestrogens, and becomes
secretory in response to progesterone. It is shed during menstruation and regenerates from
cells in the stratum basalis layer.

The tone of the pelvic floor provides the primary support for the uterus. Some ligaments
provide further support, securing the uterus in place.

 Broad Ligament: This is a double layer of peritoneum attaching the sides of the uterus to
the pelvis.
 Round Ligament: .
 Ovarian Ligament: Joins the ovaries to the uterus.
 Cardinal Ligament.
 Uterosacral Ligament

FEMALE ANATOMY
External :

Mons pubis
The mons pubis, or public mound, is the fleshy area on the pelvic bone where females typically grow
pubic hair.
Vulva - The vulva refers to the external parts of a female’s genitals. It consists of several parts, including
the labia majora, the labia minora, and the glans clitoris.
The list below provides more detail on these parts:

 Labia majora. These are the fleshy outer lips on either side of the vaginal opening. The word
“labia” is Latin for “lips.” These outer lips usually grow pubic hair.
 Labia minora. These are the inner lips. They sit inside the outer lips but can be varying sizes. In
some females, for example, the inner lips extend beyond the outer lips.
 Clitoris. The glans clitoris sits at the top of the vulva, located where the inner lips meet. It is
usually around the size of a pea, though size varies from person to person. Only the tip of the
clitoris is visible, but it has two shafts that extend into the body by as much as 5 inches. The
clitoris contains many nerve endings that are very sensitive, especially during sexual stimulation.
 Clitoral hood. The clitoral hood is the fold of skin that surrounds the head of the clitoris. It
protects the clitoris from friction.
  Urethral opening. The opening to the urethra sits above the vaginal opening. The urethra
connects to the bladder, and the opening is where urine exits the body.

Internal anatomy
The internal female anatomy begins at the vagina, which is the canal that leads from the vulva to the uterus.
The cervix separates the vagina from the uterus, and the fallopian tubes connect the ovaries with the uterus.
The following sections discuss these organs in more detail.

Vagina
As mentioned above, the vagina is the canal that connects the vulva with the uterus. The opening to the vagina is
part of the vulva.
The vagina can vary in size, but the average length is about 2.5 to 3 inches. That said, it expands in length during
arousal.
It also contains special structures called Bartholin’s glands. These are two “pea-sized Trusted Source” glands that sit
on either side of the vaginal opening. These glands are responsible for secreting lubrication to keep the vaginal
tissues from becoming too dry.

Cervix
The cervix is the lower portion of the uterus. It is a cylinder-shaped area of tissue that separates the vagina from the
rest of the uterus.
During birth, the cervix dilates to allow the baby to move through the vagina.

Uterus
The uterus is located in the middle of the pelvic cavity. This muscular sac will house the fetus during
pregnancy.
During a female’s monthly menstrual cycle, the lining of the uterus thickens with blood in preparation for
the release of an egg from one of the ovaries. This is to prepare a nourishing environment for a fetus if
pregnancy occurs.
If pregnancy does not occur, the uterine lining sheds. This is called the menstrual period. It occurs every
around 28 days, though cycle length varies between females.
The upper portion of the uterus is connected to the ovaries by the fallopian tubes.

Ovaries
The ovaries are egg-shaped organs attached to fallopian tubes on the left and right sides of the body.
Each ovary is roughly the size of an almond. Most females are born with two ovaries that produce eggs.
In addition to producing eggs, the ovaries also produce hormones. Namely, they
release estrogen and progesterone.

Fallopian tubes
The fallopian tubes connect the ovaries to the uterus. When the ovaries release an egg, the egg travels
down the fallopian tube toward the uterus for potential fertilization.
If a fertilized egg implants in the fallopian tube, doctors call this an ectopic pregnancy. An ectopic
pregnancy is a medical emergency because the fallopian tube can rupture.
Hymen
The hymen is a membrane of tissue that covers the external vaginal opening. Not all females have a
hymen, however.
The hymen can rupture as a result of pelvic injury, sports activity, pelvic examination, sexual intercourse,
or childbirth. The absence of a hymen does not mean that a female has been sexually active.
Types- imperforate, annular, septate, cribriform, parous introitus.

Breasts
Many people consider breasts “accessory organs” to the female reproductive system, as they are
responsible for supplying milk to an infant after childbirth.
The major external components of the breasts include the:

 Nipple. The nipple is the rounded area where milk drains to feed a baby. They have many nerve
endings that can make them an area of sexual stimulation. Nipples do not always protrude. Some
females have flat or inverted nipples Trusted Source.
 Areola. The areola is the pigmented area that surrounds the nipple. It is circular and varies in
size from person to person. It contains small glands, called Montgomery glands, that secrete
lubrication to keep the nipple from drying out, especially when nursing.
 Breast tissue. The breast is the area of skin on the chest that is composed of fat, muscle, and
ligament tissue, as well as an intricate network of blood vessels and glands. These areas are
specialized for breastfeeding. Breast tissue size varies greatly from person to person, often due
to a combination of individual genetics and body mass.
Internally, the breasts are primarily composed of fat. The amount of fat can determine breast size.
However, breast size has no bearing on the amount of milk someone is able to produce.
The internal anatomy of the breasts include the:

 Alveoli. These are milk secreting cells grouped into clusters inside the breasts.
 Lactiferous ducts. These are special channels that open on the nipple’s surface. Breast milk
exits through these ducts to nourish a baby.
 Lobules. These are collections of alveoli in the breast that secrete milk. The lobules drain into
lactiferous ducts, then into lactiferous sinuses that promote milk flow from the nipple.
 Mammary glands. These are responsible for producing breast milk.

Mullerian abnormalities
Definition - The anomaly is considered a 'congenital disorder', meaning it occurs during fetal
development and is present at birth.
Types
Agenesis & hypoplasia: all or part of the müllerian tract fails to form, or is extremely underdeveloped.

Unicornuate uterus (UU): When one müllerian duct is underdeveloped or fails to develop, a banana-
shaped half-uterus is formed. A missing kidney or other kidney problems accompany this asymmetric
anomaly. Treatment- laproscopic surgery
Uterus didelphys (UD): Commonly referred to as a 'double uterus'. There may be complete duplication of
the vagina, cervix and uterus, and the two halves may be divided by a ligament of connective tissue
Bicornuate uterus (BU): This is the most common form of müllerian anomaly. Described as a womb with
two horns. The womb is not pear-shaped, instead it is shaped like a heart, with a deep indentation at the
top. This means that the baby has less space to grow than in a normally shaped womb. Treatment-
Strassman metroplasty surgery
Septate uterus: Occurs when the inside of the uterus is divided by a wall or the septum. The septum may
extend only part way into the uterus or it may reach as far as the cervix.
DES-related uterus: A T-shaped uterine cavity, dilated horns and malformed cervix and upper vagina
may characterize this anomaly.

Arcuate uterus (AU): The fundus of the uterus may be indented slightly both inside and outside. The
shape is so slight that it is considered a variation of normal.

Cervical duplication ,cervical agenesis , cervical hypoplasia

Symptoms – miscarriage , infertility , amenorrhea , pelvic pain , preterm labor

Diagnosis - recognized at the onset of puberty — when an adolescent begins to menstruate or
when a young female fails to get her menstrual period. The condition may also be diagnosed when a
woman has trouble conceiving, or maintaining a pregnancy. pelvic ultrasound three dimensional
ultrasound magnetic resonance imaging (MRI) hysterosalpingogram (HSG) laparoscopy hysteroscopy

Treatment – surgery

PELVIC INFLAMMATORY DISEASE

Definition -This occurs when there is ascending infection from the endocervix to the higher
reproductive tract. It is a recognized complication of chlamydia and less frequently of gonorrhoea, but
they are often not isolated and other implicated organisms include Mycoplasma genitalium as well as
those in the vaginal microflora.

Etiology - Commonly caused by STIs (often Chlamydia and gonorrhoea).retrograde menstruation ,

sexual intercourse , surgery /abortion , childbirth . May occur following instrumentation of the uterus.
Other bacteria involved include anaerobes, coliforms and Mycoplasma genitalium.

Symptoms- lower bilateral abdominal pain, dyspareunia, altered vaginal discharge and IMB or PCB.
Systemic symptoms of infection may be present.

Characteristic clinical findings include lower abdominal and cervical motion tenderness and cervicitis.

Risk factors - Previous STI, IUCD/IUS (within 20 days of insertion), multiple sexual partners, age < 25
years , young age at first intercourse

Epidemiology - True incidence unknown, but accounts for 1 in 60 general practitioner consultations
in women < 45 years

History - May be asymptomatic, presenting with infertility, or presents as chronic pelvic pain. Acute
presentation: bilateral lower abdominal pain, discharge PV, fever, irregular PVB, dyspareunia, dysuria ,
intermenstrual bleeding
Examination - General: Signs of infection (tachycardia, fever). Abdomen: Lower abdominal
tenderness. Speculum: PV discharge. Vaginal: Cervical excitation, bilateral adnexal tenderness,?adnexal
mass (tubo-ovarian abscess).

Investigations –clinical findings ( pelvic pain , cervical motion tenderness , tenderness in RUQ ) ,
NAAT , ultrasound Bloods: FBC, CRP. Microbiology: MSU, HVS, endocervical/Chlamydia swabs. USS: ?
tubo-ovarian abscess Other: Exclude pregnancy.

Management – ceftriaxone IV followed by 14 days of doxycycline and metronidazole ,

acetaminophrn (pain ) , surgery for removal of adhesions or complications . Medical: Analgesia,
antibiotics based on current guidelines (may include cephalosporin, metronidazole, doxycycline). If IUCD
in situ and no recent unprotected sexual intercourse, consider removal. Surgical: If there is an abscess.
Other: Consider contact tracing.

Complications -Increased risk of future ectopic pregnancy, tubal infertility in up to 50%, chronic
pelvic pain. Right upper quadrant pain due to perihepatitis is an unusual complication called Fitz-Hugh–
Curtis syndrome.

Prognosis Depends on promptness of treatment. As it is often asymptomatic, there is high fertility-

related morbidity

ASHERMANS SYNDROME
Definition - Presence of intrauterine adhesions that may partially or completely occlude the uterine
cavity

Etiology - Damage to the endometrium involving the basal layer, owing to factors such as trauma
(from instrumentation) or infection. Leads to fibrosis and adhesion formation.

Risk factors - Endometrial resection, excessive curettage (e.g. following miscarriage, TOP), surgery
(myomectomy, Caesarean section), endometritis.

Epidemiology - Uncommon although incidence and prevalence vary widely.

Symptoms -Menstrual disturbance (often amenorrhoea), cyclical abdominal pain, subfertility.
Examination - No external physical signs.
Pathogenesis - Adhesions may be filmy consisting of basal endometrium, or fibromuscular covered by
endometrium, or entirely composed of connective tissue.

Investigations - Imaging: HSG (radiological filling defects), saline hysterosonography. Other:

Hysteroscopy.

Management -Surgical: Hysteroscopic adhesiolysis (myometrial scoring may increase cavity

dimensions in severely narrowed cavities). Post-procedure: Copper IUCD placed in cavity to prevent
adhesion formation, PO oestrogens (induce endometrial proliferation), reassess cavity 2–3 months after
treatment.

Complications -Infertility, miscarriage, menstrual disturbance, abnormal placentation in future

pregnancies, complications of operative treatment.

Prognosis - Menstrual disturbance often improves after treatment. Post-treatment pregnancy rates
of 50% are reported (although increased complication rates)

SHEEHAN SYNDROME
Definition -is postpartum hypopituitarism caused by necrosis of the pituitary gland. It is usually the result of
severe hypotension or shock caused by massive hemorrhage during or after delivery. Patients with SS have varying
degrees of anterior pituitary hormone deficiency.

Signs and symptoms of Sheehan's syndrome occur because of having too little of the
hormones the pituitary gland produces.

Causes – thrombosis , DIC , restriction of pituitary blood supply , vasospasm

Signs and symptoms include:

 agalctorrhea,

 amenorrhea , oligomenorrhea

 Inability to regrow shaved pubic hair

 hypothyridism

 Low blood pressure , hypoglycemia ,Fatigue , irregular heartbeat , Breast

shrinkage

Diagnosis

Diagnosing Sheehan's syndrome can be difficult. Many symptoms overlap with those
of other conditions.

 Collect a thorough medical history. It's important to mention any childbirth

complications you've had, no matter how long ago you gave birth. Also, be sure to
tell your doctor if you didn't produce breast milk or you failed to start
menstruating after delivery — two key signs of Sheehan's syndrome.
 Run blood tests.

 Request a pituitary hormone stimulation test.

 Request imaging tests , MRI

Treatment for Sheehan's syndrome is lifelong hormone replacement therapy for

the hormones you're missing.

Corticosteroids. Hydrocortisone (Cortef) or prednisone (Rayos), replace the adrenal

hormones that aren't being produced because of an adrenocorticotropic hormone
(ACTH) deficiency.

Levothyroxine ,estrogen ,growth hormone

ECTOPIC PREGNANCY
Definition -Pregnancy outside the uterus, usually in the fallopian tubes (98%) – mainly in ampulla
region. Can also occur in ovary, uterus (cornua, cervix), broad ligament, and abdomen.

Etiology - Damage to the fallopian tube e.g. infection, surgery, endometriosis.

Risk factors - STI/PID, previous tubal surgery, previous ectopic pregnancy, pregnancy with IUCD/IUS
in situ, assisted conception. , in vitro fertilization

Epidemiology -Affects 1% of pregnancies (increasing incidence related to higher rates of PID and
assisted conception).

Symptoms - Abdominal pain, pelvic pain, amenorrhoea (4–10 wks) PV bleeding (often scanty dark
blood), shoulder tip pain (referred), dizziness (note: ruptured ectopic may present with circulatory
collapse).

Examination - Abdomen: Tenderness rebound/guarding if rupture has occurred.

Vaginal: Cervical excitation, adnexal tenderness, adnexal mass.

Pathogenesis - Tubal damage interferes with tubal transport mechanisms, cilial dysfunction
increases the chance of the fertilised ovum implanting in the tube.

Investigations -Urine: bHCG. Bloods: FBC, clotting, X-match, serum bHCG. if diagnosis uncertain
repeat after 48 hours. Levels in intrauterine pregnancy will usually double, with a sub-optimal rise in
ectopic pregnancy. USS: TVS.

Management -All Rhesus-negative women should receive anti-RhD prophylaxis. Conservative: Only
permissible in a stable, asymptomatic patient with falling bHCG levels (tubal abortion). Medical:
Methotrexate injection – if patient clinically stable, asymptomatic, no blood in the pouch of douglas on
USS, normal renal and liver function, bHCG <3000iu/L , ectopic <4 cm in sizeand no FH detected.
Surgery: If patient is stable, laparoscopic salpingectomy is procedure of choice; if patient unstable or
laparoscopy not possible, laparatomy. Salpingotomy may be considered in the presence of contralateral
tubal disease, with increased risk of future ectopic pregnancy.

Complications -Rupture, haemorrhage, death, tubal infertility, psychological sequelae.

Prognosis -Reported 5 deaths per year from ectopic pregnancy in the UK, 15% risk of ectopic in
future pregnancies.

PRECONCEPTUAL COUNSELLING
 is a meeting with a health-care professional by a woman before attempting to become
pregnant.
 It allows planning or prevention of pregnancy, and access to the appropriate multidisciplinary
specialized services if necessary.

General pre-conception advice

 Diet, Supplements
 No Smoking, No Alcohol
 Body weight
 Advice regarding medications
 Advice related to maternal age
 Genetic counselling

 Women should modify their diet, stop or reduce smoking and alcohol intake, aim to enter
pregnancy with a normal BMI and take folic acid supplementation periconceptionally.
 Your provider may also discuss how to chart to your menstrual cycles and when you ovulate each
month. You may be given a prenatal vitamin with 400 to 800 micrograms of folic acid. You should start
taking this before you are pregnant. Your baby can benefit from a prenatal vitamin before you may even
know you are pregnant

Maternal risks of obesity

Subfertility Miscarriage

Hypertensive disease

Gestational diabetes

Thromboembolism Infection

Cardiac disease Instrumental deliveries Caesarean section

Postpartum haemorrhage Maternal death Neural tube defects

Large for dates, Preterm delivery, Shoulder dystocia

Increase in birth weight, neonatal hypoglycaemia

Drugs that are harmful in pregnancy

NSAIDs (except low-dose aspirin)

Warfarin Statins ,Retinoids

Tetracycline, doxycycline, ciprofloxacin Paroxetine

ACE inhibitors, angiotensin receptor blockers

 Most commonly used medications have good safety data and can continue to be taken in
pregnancy in the smallest effective dose. Inform women of any risks to pregnancy of
medications they are taking.
 Change teratogenic medications before pregnancy if possible (may not be appropriate with
some known teratogens (e.g. antiepileptic drugs).

ADVANCED MATERNAL AGE

 Delaying childbirth is associated with worsening reproductive outcomes, with more

infertility, miscarriage, chromosomal abnormalities and medical comorbidity and an
increase in maternal and fetal morbidity and mortality.

Vaccination: Your provider may need to update or give you additional vaccinations before you
become pregnant. Some of these vaccinations may require time between when they are given to you
and when you become pregnant. (MMR)

 Lab tests: These tests are used to check for various diseases and conditions. Lab tests may include:
o Testing for rubella.
o Testing for hepatitis.
o Complete blood count (CBC).
o A pap smear.
o Diabetes screening.
o Testing for thyroid issues.
o Testing for HIV.

GESTATIONAL DIABETES
Definition - Pre-existing or new-onset diabetes in pregnancy.

Etiology -Pre-existing: Type 1 – failure of pancreas to produce insulin; type 2 – relative insulin
deficiency associated with increased peripheral insulin resistance. Gestational diabetes (GDM): Altered
glucose tolerance in pregnancy.

Risk factors - GDM: " maternal age, ethnicity (South Asian, Middle Eastern, Afro-Caribbean), obesity,
smoking, PCOS, family history, previous macrosomic baby.
Epidemiology - Prevalence is 2–5% but estimates vary. GDM accounts for 90% of diabetes in
pregnancy.

History - Pre-existing: Usually known to mother. GDM: Usually asymptomatic, detected on screening.

Examination - Abdomen: Fundal height (macrosomia/polyhydramnios).

Pathogenesis -Type I: Autoimmune destruction of pancreatic islet cells. Type II: Genetic component
þ influence of age and obesity on peripheral insulin resistance. GDM: " insulin resistance in pregnancy ("
secretion of insulin antagonists, including HPL, glucagon and cortisol), altered carbohydrate metabolism,
failure of normal pregnancy increase in insulin production. Fetus: Hyperglycaemia in early pregnancy
may affect development (congenital abnormalities); hyperglycaemia causes fetal hyperinsulinaemia and
macrosomia. Neonatal: Hypoglycaemia can occur (withdrawal of maternal glucose while fetal insulin
levels remain high).

Investigation – screening at 24-28 wks of gestation . glucose challenge test , oral glucose tolerance
test ,urine glucose test. Sliding scale in labour. Pre-existing: Detailed anomaly scan, fetal cardiac scan,
ophthalmic examination. GDM: Screening (universal or selective) by GTT at 26–28/40.

Management - Pre-existing Preconceptual: Optimisation of glucose control.

Medical: Optimise diet, consider converting oral hypoglycaemics to insulin. Likely to require increasing
doses of insulin.

Pregnancy: Capillary blood glucose monitoring, monitor for pre-eclampsia, serial USS for fetal growth.
Delivery: Sliding scale in labour.

Postpartum: Return to pre-pregnancy doses of medications.

bGDM Medical: Diet control. Persistent hyperglycaemia may require insulin treatment.
Pregnancy/delivery: As for pre-existing. Postpartum: Stop insulin after delivery, fasting blood glucose
6/52 postpartum.

Complications - Maternal: Progression of pre-existing nephropathy/neuropathy/retinopathy,

miscarriage, pre-eclampsia, operative delivery

Fetal/neonatal: Congenital abnormalities (pre-existing only), fetal death, polyhydramnios,

polycythaemia, macrosomia ( þ traumatic delivery), respiratory distress syndrome, neonatal
hypoglycaemia, neonatal jaundice.

Prognosis - Dependent on adequacy of control. GDM: 70% recurrence in future pregnancies, " risk
(40–60%) for type 2 diabetes

Dysmenorrhea – painful menstrual periods

Types –

Primary – recurrent , aren’t due to other diseases. Pain last 12-72 hours along with other symptoms
such as nausea , vomiting , fatigue , diarrhea . cause - too much prostaglandin

Secondary – because of disorder or infection in reproductive organs. last longer than menstrual cramps
. cause – endometriosis , adenomyosis , pid , fibroids

Risk factors – smoking, alcohol, early menarche, obesity, nulliparity.

Symptoms – abdominal pain , pressure in abdomen , pain in hips , lower back and inner thighs ,
nausea , vomiting , fatigue , weakness , syncope

Diagnosis – careful history taking and complete physical exam . other test include – ultrasound ,
MRI , hysteroscopy

Management – NSAID s , prostaglandin inhibitors , oral contraceptives , regular exercise , abdominal

massage , heating pads , avoiding caffeine , alcohol , smoking, breathing exercises , acupuncture.

Dyspareunia –pain before, during or after sexual intercourse.

Causes – vaginal dryness , skin disorders such as ulcers , cracks , UTI , trauma , vaginitis ,
endometriosis , cystitis , pid , fibroids , irritable bowel syndrome , oral contraceptive pills

Risk factors – viral/ bacterial infection , postmenopausal women

Diagnosis –pelvis ultrasound , culture , urine test

Management – topical estrogen , antibiotics , antifungals , corticosteroids

Dysuria – pain , burning , discomfort while urinating

Causes – UTI ,STI , diabetes , advanced age , kidney stones , placement of urinary catheter

Diagnosis – urinalysis , urine dipstick ,cbc

Treatment – antibiotics , drinking more water

Klienfelter syndrome
 Definition -is a condition that occurs in males when they have an extra X chromosome
 Adults with Klinefelter syndrome may also have primary hypogonadism (decreased testosterone
production), undescendent testes (cryptorchidism), enlarged breast tissue (gynecomastia), tall stature
,infertility, as well as an abnormal opening of the penis (hypospadias), and an small penis
(micropenis) ,Social, psychologic and behavioral problems
KS is not inherited, but usually occurs as a random event during the formation of reproductive cells (eggs
and sperm) that results in the presence of one extra copy of the X chromosome in each cell (47,XXY)

DIAGNOSIS = A diagnosis of Klinefelter syndrome is often suspected based on the presence of

characteristic signs and symptoms. Additional testing can then be ordered to confirm the diagnosis. This
generally includes a chromosomal analysis (called a karyotype)

It is also possible to diagnosis Klinefelter syndrome before birth through chorionic villous
sampling or amniocentesis.

When a diagnosis is made, treatment is based on the signs and symptoms present in each person,
especially the problems related to hypogonadism, gynecomastia, and psychosocial problems. Treatment
may include

 Testosterone replacement:

 Breast removal or reduction surgery.

 Educational interventions:
 Several forms of therapy such as physical, speech, occupational, behavioral, mental health, and
family therapy can often help reduce or eliminate some of the symptoms

Premature ovarian failure

is the cessation of ovarian function before 40 years of age or before normal onset of menopause.

What causes primary ovarian insufficiency (POI)?

In about 90% of cases, the exact cause of POI is unknown. POI is related to problems with the follicles. Follicles are
small sacs in your ovaries. Your eggs grow and mature inside them. One type of follicle problem is that you run out of
working follicles earlier than normal. Another is that the follicles are not working properly. In most cases, the cause of
the follicle problem is unknown. But sometimes the cause may be

 Genetic disorders such as Fragile X syndrome and Turner syndrome

 A low number of follicles

 Autoimmune diseases, including thyroiditis and Addison disease

 Chemotherapy or radiation therapy

 Metabolic disorders
 Toxins, such as cigarette smoke, chemicals, and pesticides
 The first sign of POI is usually irregular or missed periods. Later symptoms may be similar to
those of natural menopause:

Hot flashes,Night sweats , Irritability , Poor concentration, Decreased sex drive,Pain during sex , Vaginal
dryness

 Anxiety and depression.

 Infertility.
 Low thyroid function. Osteoporosis.

How is primary ovarian insufficiency (POI) diagnosed?

To diagnose POI, your health care provider may do

 A medical history, including asking whether you have relatives with POI
 A pregnancy test, to make sure that you are not pregnant
 A physical exam, to look for signs of other disorders which could be causing your symptoms
 Blood tests, to check for certain hormone levels
 A pelvic ultrasound, to see whether or not the ovaries are enlarged or have multiple follicles
 Follicular monitoring

How is primary ovarian insufficiency (POI) treated?

 Hormone replacement therapy (HRT). HRT is the most common treatment. It gives your body the estrogen and other
hormones that your ovaries are not making. HRT improves sexual health and decreases the risks for heart disease and
osteoporosis.You usually take it until about age 50; that's about the age when menopause usually begins.
 Calcium and vitamin D supplements. Because women with POI are at higher risk for osteoporosis,
 In vitro fertilization (IVF). If you have POI and you wish to become pregnant, you may consider trying IVF.
 Regular physical activity and a healthy body weight
 Treatments for associated conditions. If you have a condition that is related to POI, it is important to treat that as well.
Treatments may involve medicines and hormones.

Precocious puberty
Onset of 2° sexual characteristics in a child < 8 years of age

TYPES
Central precocious puberty: Early activation of hypothalamic GnRH production.

 Central (GnRH Dependent)

 Constitutional (idiopathic) ,Hypothalamic lesions (hamartomas, tumors, congenital malformations)
 Dysgerminomas , Hydrocephalus , CNS infections CNS trauma/irradiation , Pineal tumors (rare) ,
Neurofibromatosis with CNS involvement Tuberous sclerosis
Peripheral precocious puberty: Results from GnRH-independent mechanisms

 Peripheral (GnRH Independent)

 Congenital adrenal hyperplasia ,Adrenal tumors , McCune-Albright syndrome (polyostotic fibrous
dysplasia)
 Gonadal tumors (especially granulosa cell tumor, which secretes estrogen)
 Exogenousestrogen, oral (OCPs) or topical Ovarian cysts (females)

History/PE/DX-
 Signs of estrogen excess (breast development and possibly vaginal bleeding) suggest ovarian cysts or
tumors.
 Signs of androgen excess (pubic and/or axillary hair, enlarged clitoris, and/ or acne) suggest adrenal
tumors or CAH.
 GnRH agonist (leuprolide) stimulation test
 Central precocious puberty = MRI
 Peripheral precocious puberty = Ultrasonography of ovaries, gonads, and/or adrenals

Treatment
Central precocious puberty: Leuprolide (suppresses gonadotropin secretion of luteinizing hormone and follicle-
stimulating hormone that subsequently suppresses gonadal sex steroid production) is first-line therapy; physical
changes regress or cease to progress.
Peripheral precocious puberty: Treat the cause.
Ovarian cysts: No intervention is necessary, as cysts will usually regress spontaneously.
CAH (congenital adrenal hyperplasia): Treat with glucocorticoids. Surgery is not required for the
treatment of ambiguous genitalia.
Adrenal or ovarian tumors: Require surgical resection.
McCune-Albright syndrome (disorder that affects the bones, skin, and several hormone-producing (endocrine)
tissues): Antiestrogens (tamoxifen) or estrogen synthesis blockers (ketoconazole or testolactone) may be
effective

Malpresentation
DEFINITION Any presentation where the presenting part is not the fetal vertex.
AETIOLOGY Associated with fetal/maternal factors that affect rotation.
ASSOCIATIONS/RISK FACTORS
Maternal: Placental site abnormalities, uterine abnormalities, obstructed lower segment
(fibroids, pelvic abnormalities) grand multiparity (uterine laxity).
Fetal: Multiple gestation, prematurity, fetal malformation, polyhydramnios, macrosomia.
EPIDEMIOLOGY Prevalence at term: breech 3–4%, transverse lie 0.3%, face 0.002%, brow
0.001%, compound 0.1%.
HISTORY Asymptomatic, detected on examination.
EXAMINATION
Breech Abdomen: Palpable head at fundus, soft breech in pelvis. Vaginal: Soft presenting part,
ischial tuberosities, anus or genitalia may be felt. Footling breech: Foot felt/seen through the
cervix.
Transverse lie Abdomen: No presenting part felt in pelvis, uterus appears wide, fundal height
may be low. Vaginal: No presenting part felt in pelvis.
Face Vaginal: Facial landmarks felt.
Brow Vaginal: Supraorbital ridges base of nose felt.
. INVESTIGATIONS- Breech or transverse: USS to confirm lie.
MANAGEMENT- Breech ECV (external cephalic version) may be attempted after 37 weeks.
Persistent breech: Recommend Caesarean section (" fetal/neonatal morbidity with vaginal
delivery).
Transverse lie Requires delivery by Caesarean section, ECV occasionally attempted.
Brow If persistent or second stage, deliver by Caesarean section.
Face Mentoposterior position: Deliver by Caesarean section. Mentoanterior: May attempt
vaginal delivery.
Compound Commonly this is fetal arm alongside fetal head – manage expectantly.
COMPLICATIONS-
Maternal: Morbidity resulting from operative delivery, prolonged/obstructed labour, uterine
rupture (especially transverse), PPH, " perineal injury (mentoanterior face presentation). 26
OBSTETRICS Fetal: " perinatal mortality/morbidity (difficult delivery, prematurity, congenital
abnormalities), cord prolapse (asphyxia).
PROGNOSIS Dependent on aetiology, presentation and timeliness of appropriate
management.

Shoulder dystocia
DEFINITION Difficulty with delivering the fetal shoulders following delivery of the head.
AETIOLOGY Bony impaction of the anterior fetal shoulder behind the maternal symphysis
pubis.
ASSOCIATIONS/RISK FACTORS High birthweight baby (although 50% occur with normal
birthweight babies), post-dates, previous shoulder dystocia, diabetes, obesity, instrumental
delivery, prolonged labour.
EPIDEMIOLOGY Affects 1% of deliveries.
HISTORY Delay in delivery of fetal shoulders, ‘turtle-necking’ of fetal head.
EXAMINATION Evidence of shoulder dystocia as above.
MANAGEMENT The mnemonic HELPERR below is often used. Each manoeuvre should be
attempted for up to 30 seconds. Meticulous documentation is mandatory.
H: Call for help.
E: Evaluate for episiotomy.
L: Legs – the McRoberts manoeuvre, hyperflexing the maternal thighs on to the abdomen.
P: Pressure suprapubically on to the posterior aspect of the fetal shoulder.
E: Enter manoeuvres – for internal rotation of the fetal shoulders into the oblique plane.
R: Remove the posterior arm.
R: Roll the patient on to all-fours. Manoeuvres of last resort include deliberate clavicular
fracture, symphysiotomy, general anaesthesia and the Zavanelli manoeuvre (replacement of
the fetal head followed by Caesarean section).

COMPLICATIONS Maternal: PPH, uterine rupture, extensive perineal tears (" third/fourth
degree tears), symphyseal separation.
Fetal: Death, hypoxic–ischaemic encephalopathy, fractured humerus/clavicle, brachial plexus
injury

Menopause
DEFINITION Permanent cessation of menstruation, defined as 12 months after the final period.
AETIOLOGY Physiological: Menopause occurs due to ovarian failure associated with a dramatic
decline in the quantity of oocytes and a reduction in ovarian sensitivity to gonadotrophins.
Iatrogenic: Bilateral oophorectomy, radiotherapy, chemotherapy.
ASSOCIATIONS/RISK FACTORS Increasing age, smoking, autoimmune disorders, living at high
altitude, chemotherapy, radiotherapy, ovarian surgery.
EPIDEMIOLOGY Average age of menopause is 51 years in UK.
HISTORY Persistent amenorrhoea (often initial oligomenorrhoea or irregular/shortened cycles),
vasomotor symptoms (hot flushes, night sweats, palpitations, headaches), urogenital
symptoms (vaginal dryness, dyspareunia, frequency, dysuria, recurrent UTIs), psychological
symptoms (poor concentration, lethargy, mood disturbance, reduced libido).
EXAMINATION General: Thin, dry skin, breast tissue atrophy. Vaginal: Atrophy, may have pelvic
organ prolapse.
PATHOLOGY/PATHOGENESIS Decreased follicular activity results in increased levels of FSH/
LH. Oestrogen and progesterone levels fall. Low/falling oestrogen levels are responsible for the
majority of symptoms in the menopausal and perimenopausal (climacteric) periods.
INVESTIGATIONS Bloods: " FSH (>30 IU/L).
MANAGEMENT Hormone replacement therapy Oestrogen replacement is indicated for the
relief of vasomotor symptoms. HRT should contain progesterone unless the woman has
undergone hysterectomy (prevents endometrial hyperplasia). Tibolone is a synthetic steroid
with weak oestrogenic, progestogenic and androgenic properties that has been used for
hormone replacement. Routes of administration: oral, transdermal (patches), vaginal (creams,
gels, pessaries), implants. Other SERMs, calcium supplementation and bisphosphonates are
occasionally used to maintain bone health. Natural supplements containing phytoestrogens are
frequently self-prescribed but do not currently carry an evidence base. Vaginal lubricants may
relieve symptoms of vaginal dryness.
COMPLICATIONS The incidence of osteoporosis and coronary heart disease increases after
menopause (note: HRT is not recommended for prevention of coronary heart disease).
Depression increases during the perimenopausal period. The contribution of menopause to
Alzheimer’s risk is currently under investigation

AMENORRHEA
Definition – absence of menses.
Types
 Primary – no menarche by 16 / no menarche by 13 and no signs of puberty. causes –
turner syndrome , mullerian agenesis ,androgen insensitivity syndrome, kallmann
syndrome, streaked gonads
 Secondary – no menstruation for at least 3 cycles who had regular cycles / 6 months
who had irregular cycles. causes – pregnancy, functional hypothalamic amenorrhea,
hyperprolactinemia prolactinoma, hypothyroidism, POF, asherman syndrome
History –LMP , menarche onset , menstrual history , medications , weight change , exercise ,
chronic illness , acne , endocrine disorders , galactorrhoea
Examination –
 Primary-assess stature . secondary sexual characteristics, anatomical abnormalities
 Secondary – weight, hirsutism, alopecia, acne, visual fields, vaginal atrophy
Diagnosis –
 rule out pregnancy
 Serum levels of FSH , LH, TSH , estrogen, testosterone , prolactin
 Karyotype for turner syndrome , androgen insensitivity syndrome
 Hysteroscopy for asherman syndrome
Treatment –
 Hormone replacement therapy ( turner , PCOS , POF )
 Dopamine agonist – prolactinoma, hyperprolactinemia
 Surgery – asherman, mullerian agenesis
 psychotherapy
complications – osteoporosis, endometrial hyperplasia, PCOS, infert ility

PLACENTA PREVIA
Definition – placenta implants itself lower in the uterus covering/ closing internal os which
leads to bleeding . this usually occurs after 20 wks of gestation .
Causes – unclear . upper endometrium not well vascularised. Damage from previous c section ,
abortion , uterine surgery , multiparity , low implantation of fertilised egg , uterine fibroids ,
scarring of endometrium.
Risk factors - having twins / triplets , maternal age >35 , smoking , intrauterine fibroids
Symptoms –bright red bleeding without pain from vagina during 2nd half of pregnancy ,
contractions along with bleeding
Classification – complete , partial , marginal
Association – placenta accrete
Diagnosis – prenatal ultrasound
Treatment – corticosteroids to enhance fetal lung maturity , bed rest (minor bleeding ), blood
products / IV fluids ( major bleeding ) , c section in severe cases
Complication – maternal blood loss , fetal hypoxia , preterm delivery

PLACENTAL ABRUPTION
Definition – premature separation of all or part of placenta . usually after 20 wks of gestation .
separation of uterine wall or deciduas basalis .
Cause – by degeneration of uterine arteries due to smoking , HTN,
Classification – partial , complete
Risk factors – blunt trauma like car accident, domestic violence , fall , drugs like cocaine and
methamphetamine , multiparity , maternal age >35 , previous abruption
Symptoms – vaginal bleeding , abdominal and back pain , uterine contractions , tenderness and
rigidity
Diagnosis – ultrasound, blood stained amniotic fluid from vagina
Treatment – IV fluids, blood products, c section in severe cases
Complications – maternal: hypovolemic shock, Sheehan syndrome, DIC, renal failure
Fetal : intrauterine hypoxia , asphyxia , premature birth

SURFACE EPITHELIAL STROMAL TUMOUR

Classification
Mucinous – from epithelial cells , large and multiloculated cyst
Benign – mucinous cystadenoma . develops on 1 ovary
Malignant – mucinous cystadenocarcinoma, inflamed and swollen lining ,postmenopausal
women .
Forms pseudomyxoma peritonei,mucinous material that collects in peritoneal cavity

Serous – from epithelial cells , serous filled , single cyst

Benign – serous cystadenoma . most common . on both ovaries . premenopausal women .
Malignant – serous cystadenocarcinoma ,inflamed and swollen lining , postmenopausal women
Forms psammoma body : plaques with ca and cellular debris .

Endometriod – endometriod like cells . ectopic and out of place .

Benign – cyst with dark blood , chocolate cyst
Malignant – can spread to fallopian tube and peritoneal cavity.

Transitional – Brenner tumours , from transitional cells – found normally in lining of bladder. Is
rare . usually solid

Decreased risk – pregnancy , oral contraceptives , breastfeeding

Increased risk – endometriosis PCOS , BRCA 1 and 2 mutations , hereditary nonpolyposis
colorectal cancer.

Symptoms – abdominal distension/ bloating , abdominal / pelvic pain ,ascites , abdominal

masses, bowel obstruction , dyspareunia
Diagnosis – tumour markers ,TVS ,biopsy , imaging ( CT , MRI )
Treatment –chemo ,surgery , radiotherapy.