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OBSTETRICS

Placenta- HCG (doubles every 48hrs


until 12 wks)

Antenatal care

+ve pregnancy test- Attend GP


Referred for booking at hospital
Booking USS scan to date pregnancy
Full Hx and booking bloods
Identify LOW risk (Community/Green)
or HIGH risk (Consultant/Red)

Booking Investigations

FBC (Rpt 28 wks)


Blood group and abs. (rpt 28wks)
Rubella status
HEP B/C, HIV, Syph. If no Hx chicken pox
do Varicella
Dip urine

OGTT, Haemoglobinopathy screen

Each visit

BP
Dip urine
Fundal height (1 cm/week)
Fetal heart with Doptone
Palpate abdomen for
presentation/station

Screening

CUBS -11-13 wks


Free fetal DNA
14-20 wks screening bloods
Gives risk for trisomy 21. Not
definitive. (DS , SB ) If > 1in 150,
referred for counselling
20 wks anomaly scan Structural
abnormalities/ Spina Bifida
CVS (9-11 wks)/ Amniocentesis (>15
wks). Karyotype. 1% risk of
miscarriage.

Labour
Primiparous- 12-24 hrs
Multiparous- 6-12 hrs
Usually defined as the onset of
painful, regular contractions, more
than one every ten minutes, with
progressive cervical effacement and
dilatation accompanied by descent of
the presenting part.

Initiation
Physiological factors largely
unknown.
Occurs when factors which inhibit
contractions and maintain a closed
cervix diminish and are succeeded
by the actions of factors which do the
opposite.
Increase in intracellular free calcium
brings about contraction.
Prostaglandins and oxytocin increase

Stages in Labour
Stage I- Onset of labour to full
dilatation. latent and active phase
(>3cm dilated.)
Stage II- Full dilatation to delivery of
baby (<4hrs in prim, <3hrs in Multi)
Passive and active.
Stage III- Birth of baby to delivery of
placenta. (<1hr) Can be active
(Syntocinon/Syntometrine) or
Physiological.

Progress
Confirm presentation
Monitor FH -Intermittent/ Continuous
Uterine muscle Contractions- 3-5
good contractions in 10 mins.
Examine for Cx dilatation/
effacement/ station and position
every 4hrs. Expect minimum
progress 0.5-1cm/hr.

Progress
Confirm presentation
Monitor FH -Intermittent/ Continuous
Uterine muscle Contractions- 3-5
good contractions in 10 mins.
Examine for Cx dilatation/
effacement/ station and position
every 4hrs. Expect minimum
progress 0.5-1cm/hr.

Partogram

Fetal Monitoring.

Presentation

Station

Position
Related to OCCIPUT (posterior
Symphysis Pubis

fontanelle)

Direct
L

R
Right

ANTERIOR

TRANSVERSE

TRANSVERSE
R

Left

POSTERIO
R
Direct
Sacrum

Position
Related to OCCIPUT (posterior
fontanelle)

Symphysis Pubis
Direct
L

R
Right

ANTERIOR

TRANSVERSE

TRANSVERSE
R

Left

POSTERIO
R
Direct
Sacrum

Analgesia in labour
Breathing/ TENS/ Bath/ Co-codamol
Entonox (Nitrous oxide/ oxygen)
Morphine- can cause CTG changes/
neonatal resp depression.
Remifentanyl PCA.
Epidural- L3/4 ( Needs IV fluids,
Catheter, Continuous CTG)
Can be topped up if needs LUSCS.

Problems.

Prolonged latent phase


Arrest of dilatation
Arrest of descent of presenting part.
Fetal compromise.

Types of delivery

SVD
Assisted delivery
Vaginal breech delivery.
LUSCS (lower uterine segment
caesarean section)

SVD

Engagement
Descent
Internal rotation
Crowning/Extension
Restitution
Delivery of ant then
post shoulder.

Third stage

Delivery of placenta.
Controlled cord traction.
Guard uters.
Syntocinon/ Syntometrine.
Risk of PPH

Emergencies
Malpresentation- Breech, face, Brow,
compound- LUSCS.
Cord prolapse- Cord comes out with
fluid. Elevate presenting part- Crash
LUSCS
Shoulder dystocia- Head delivered.
Shoulders stuck. Manoeuvres to try
disimpact.

The puerperium

6 wks post natal


Uterus shrinks- Lochia produced
PPH (secondary)
DVT/PE
Haemarrhoids/ Constipation
Postnatal depression

Breast feeding
Oestrogen and Progesterone

stimulate breast proliferation


Prolactin stimulates milk production
and descent into alveoli
Oxytocin stimulates milk ejection
First thick yellow fluid- Colostrum
Maintained by suckling

Breast feeding

Breast feeding
Skin to skin contact/ Bonding
Receives all required nutrients
Passive immunity of antibodies
Cant breast feed with certain
medications or if HIV +ve

Complications

Cracked nipples
Mastitis
Milk stasis
Poor supplyDomperidone

PRE TERM LABOUR

Definition
Onset of labour before 37 weeks
Presence of uterine contractions of

sufficient frequency and intensity to


cause dilation of the cervix prior to
term gestation

Cause largely unknown- no cause


found in 50% cases

Risk Factors
Social factors
-

low social class


young mother
low maternal weight
smoking

Over distension of uterus


- multiple pregnancy
- polyhydramnios

Fetal anomaly

Risk Factor
Uterine anomaly
- congenital
- cervical incompetence

Infection
-maternal pyrexial illness
-chorio-amnionitis (caused by premature rupture of
membranes)

Trauma
-injury
-surgery during pregnancy

Drug treatment -Tocolysis


Descision to treat depends on

gestation and steroids


Treatment does not have any benefit
on peri-natal mortality
Valuable for delaying delivery until
transfer to unit with suitable
neonatal care can be provided
Allows time for corticosteroids to be
given to accelerate fetal lung
maturity.

Drug treatment
DHP Calcium channel blockers
(nifedipine)
Inhibit uterine muscle contraction
No proven benefit over
betamimetics, other than fewer side
effects
Dose of 20mg given followed by 1020mg given 3-4times daily
depending on uterine activity

Tocolysis
Oxytocin receptor antagonist
(atosiban)
Blocks action of oxytocin on uterus
which stimulates contractions
Given IV, maximum duration 48hours
Licensed for inhibition of premature
labour between 24 and 33 weeks
gestation

POST PARTUM
HAEMORRHAGE

PPH
>500mls blood loss PV
Primary or secondary
Secondary- endometritis/RPOC

Primary PPH
Emergency
ABC
A- talk to pt
B- facial O2
C- IV Access (2 large venflons)
FBC, Coag, X-match
IV fluids

Causes

T- Tone
T- Tissue
T- Trauma
T- Thrombin

Tone

Atonic uterus 90%


Catheterise
Bimanual compression
IM syntocinon 10iu
IM ergometrine 500mcg
IV Syntocinon infusion 40iu
IM Haemabate (PGF2 ) 250mcg

Bimanual compression

Tissue
Check placenta
Manual removal

Trauma
Genital tract trauma
Repair

Thrombin

Chase Coag result


Contact haematology
Watch for signs of DIC

ANTE PARTUM
HAEMORRHAGE

APH
Bleeding from the genital tract after
24 wks gestation
2-5% of pregnancies
Important cause of maternal and
fetal morbidity and mortality

Dont forget Anti D in Rh-ve women

Causes

Placenta praevia
Placental abruption
Show
Local causes

Vasa praevia

Placenta praevia
Placenta develops in lower uterine
segment. 0.5% of all pregnancies
Risk factors- increased age
-multiparous
- prev LUSCS
- Smoking
- prev history
- multiple pregnancy

Classification

Presentation
20 wk USS (97% will migrate)
Painless vaginal bleedingunprovoked
Post coital bleeding
Malpresentation

Massive haemorrhage may follow


warning bleed

Diagnosis
VE/ Speculum should not be carried
out if PP suspected
USS (TV scan best)
MRI scanning can
help detect accreta

Management (Major)
If symptomatic- admit
Large cannula, G&S
Delivery at 37-38wks by LUSCS
(earlier if indicated)
Best to have blood, cell salvage and
interventional radiology ready

If haemorrhage- ABC, stabilise


mother then emergency LUSCS

Placental Abruption
Bleeding following separation of
normally sited placenta. 0.5-1.5% of
all pregnancies
Risk factors- Increased age
- Multiparous
- Smoking
- Recreational drug use
- Abdominal trauma

Classification
Revealed/
Concealed

Presentation
PV bleeding- Amount may not
correlate with significance of
haemorrhage
Abdominal pain/ tension
Shock/ collapse
Fetal distress

Diagnosis
Usually clinical
USS (only
if mother
and baby
stable)

Management

ABC
Resuscitation
Delivery if required
Increased risk of PPH
Watch for signs of DIC

MISCARRIAG
E

Miscarriage

15 % of all confirmed pregnancies


Threatened
Inevitable
Complete/Incomplete
Missed
Recurrent
Molar

Threatened miscarriage

PV bleeding +/- abdo pain


Mild
Os closed
USS confirms viable pregnancy
May lead on to miscarriage

Inevitable miscarriage
Heavy PV bleeding and pain
Open cervix
Products in canal

Complete/ Incomplete
Complete- products passed and
uterus empty

Incomplete- Not all products passed


but no FH on USS and PV bleeding

Missed miscarriage
Pregnancy Loss with no sx
Can be picked up at booking scan
Pregnancy sx usually gone away

Management
Expectant- Await body to pass
pregnancy
Surgical- Evac
MVA manual vacuum aspiration
Medical- Mifepristone and Misoprostol

Recurrent miscarriage

3 or more miscarriages
1% of all women
Chromosomal abnormality
Congenital uterine abnormalities
Cervical incompetence
Infection
PCOS
Thrombophillia

Molar pregnancy
High HCG, Large uterus
PV Bleeding
PARTIALMOLE

Where part of placenta overgrows


(proliferates) May be developing fetus
present, but is genetically abnormal and
cannot survive outside the womb. Two
sperm enter egg and instead of forming
twins forms an abnormal foetus. Triploid.

Molar pregnancy
COMPLETEMOLE
Whole placenta is abnormal and
grows rapidly. No developing fetus.
One sperm enters the egg but only
half of one set of chromosomes are
present. Aneuploid.

Diagnosed on USS
Snow storm
appearance

Management
Surgical evac
Products sent to lab for conformation
Register with Molar pregnancy unit
(Dundee)- They will follow up
Track HCG to 0
No new pregnancy for 1 yr but need
to avoid combined hormonal
contraception

Can progress to.....


PERSISTENT GESTATIONAL
TROPHOBLASTIC DISEASE
Part of the mole remains in any part of the
body despite initial treatment -can grow
quickly
CHORIOCARCINOMA
Rare but curable form of cancer- placenta
becomes malignant
Can spread throughout the body, usually
to lungs, liver and brain. Treatment is
chemotherapy

MULTIPLE
PREGNANCY

Multiple pregnancy
Incidence of twins ~1/100
Triplets ~1/4000
Predisposing factors Increased age
-Family/personal
Hx
- Fertility
treatment
-Race

Terms
Mono/Dizygotic- No. of embryos
Chorionicity- No. of placentas
Amnionicity- No. of amniotic sacs

Dizygotic twins
Non identical
2 embryos implant
Always 2 placentas and 2 sacs

Monozygotic twins
Identical
1 embryo splits
Split <3 days- DCDA
4-7 days- MCDA
8-12 days- MCMA- rare
13-15 days - conjoined twins

Diagnosis
Booking scan
Before if hyperemesis/ fertility Rx

Antenatal complications
FETAL
Increased pre-term delivery and
sequalae
Increased risk of anomalies
Increased risk IUGR/IUD

In MC twins- Twin to Twin Transfusion


syndrome (TTTTS)

Antenatal complications
MATERNAL
Severe hyperemesis
Increase risk miscarriage
Increase risk of anaemia, Preeclampsia, Pelvic pain, APH,
Placental praevia, Gestational
diabetes and PPH.
Cord accidents

Antenatal care
High Risk
More visits
Anomaly scan at 18-20 wks. (cant
really do CUBS/AFP)
Iron tablets
Serial Growth scans
Delivery ~38wks

Delivery
Vaginal vs LUSCS
If twin I is Breech or significantly

smaller- LUSCS
If twin I is cephalic- could try Vaginal
delivery
Continuous monitoring (FSE on twin
I)
IV access
Difficulty is with twin II- Should be 60
mins after I at most

Twin to Twin Transfusion


Monochorionic twins
Placental arteriovascular
anastamosis
Uneven distribution
Donor twin anaemic, IUGR,
oligohydramnios
Recipient twin- Polycythaemic,
Polyhydramnios, Ascites and pleural
effusions

TTTS

Treatment
Risky
Laser ablation of anastomosis
vessels
Early delivery

Small for dates


fetus

Small for Dates


Constitutionally small baby
Fetal growth restriction (FGR)
Usually picked up by measuring
fundal height
Confirmed on USS (Growth scan)

Fetal growth chart

Constitutionally small
Small mother
Symmetrically small.
Less that 10th centile but growing
appropriately
Normal liquor volume
Normal umbilical artery dopplers

IUGR
Asymmetrical growth
Low liquor volumes/ Abnormal
Dopplers
Not growing along centiles
Sometimes fetal distress

Causes

Placental insufficiency
Fetal anomalies
Drugs
Infection

Placental insufficiency
Most Common
Abnormalities in placental

development
Diabetes
Pre-eclampsia
Thrombophilia
Connective tissue diseases
Placental infarction/abruption

Drugs

Smoking (2-fold risk)


Alcohol
Recreational drugs
Beta-Blockers

Management
Increased monitoring
Growth scans, liquor volumes and
umbilical artery dopplers every 2
weeks
Early delivery

Pre- eclampsia
Increased BP and proteinuria +/- oedema
> 30 mmHg systolic or >15mmHg

diastolic above booking BP or


Systolic >150mmHg
Only 20% of patients with increased BP in
pregnancy have pre-eclampisa (80% are
PIH- pregnancy induced hypertension

Severe
Defined severe if:
3+ protein or more in urinalysis
BP >170/110
Visual disturbances/headache/ papilloedema
RUQ/Epigastric pain/tenderness
Clonus
Oliguria/ Renal failure
HELLP syndrome (Haemolysis, Elevated Liver
enzymes, Low Platelets)
All above suggest eclampsia could be imminent.

Aetiology
Largely unknown
Immunological disturbance decreased

invasion of maternal spiral arteries into


placenta decreased placental function
Endothelial cell damage Fibrin fragments
which break away and deposit inkidney Renal failure, proteinuria
CNS convulsions

Risk factors
Primigravida
<20yrs age and >35yrs age.
Family/ Personal history of Pre

eclamsia
Multiple pregnancy
Obesity
Non smokers
Pre-existing hypertension or renal
disease

Risks to mother

Renal/Hepatic failure
HELLP
Stroke
Disseminated intravascular
coagulopathy (DIC)
Pulmonary oedema
Convulsions
Death

Risks to baby

IUGR (growth restriction)


Placental abruption
Prematurity
Hypoxic damage
Death

Investigations
History
Exam (inc ando exam, reflexes,

fundoscopy)
Dip urine, regular BPs
Bloods (Large cannula, FBC, LFTs Urate,
U&Es, Coag and Grp and save)
If severe- Urinary catheter- monitor
output..
Invasive monitoring- central line,
ECG.

Treament
Treatment does not cure pre-eclampsia, its aim is

to prevent eclampsia
Only cure is to DELIVER BABY
Mild- Antihypertensives (Labetalol 200mg 3xday
or Methyldopa orally)
If <35wks gestation- steroids. 12mg
betamethasone IM.
Severe- IV Labetalol/hydralazine
- IV Magnesium sulphate 4g bolus and
1g/hr
Monitor BP, Urine output, Reflexes, Resp rate and
Mag levels if ? Toxicity

Cont..
CTG- for fetal wellbeing
Decide when safe to deliver baby. (can be

C-section or Induction of labour)


There is an increased risk of PPH. (Post
partum haemorrhage)
Continue management for 24hrs post
delivery
If has eclamptic seizure- treat with MgSO4

Future pregnancies.
Prophylaxis in future pregnancies
-Low dose aspirin (75mg)
Careful BP monitoring
Growth scans

Diabetes in
pregnancy

Diabetes
Pre existing Diabetes
Gestational Diabetes
Pregnancy is state of Insulin
resistance.
Placenta produces anti insulin
hormones (hPL, cortisol and
gulcagon)

Gestational Diabetes
Onset with pregnancy
Assess clinical risk and consider

HbA1c at booking and OGTT at 28


wks
Refer to Diabetic Obstetric clinic.
Milder risks than IDDM
Can progress to Type II DM
postnatally
Diet controlled vs Metformin/ Insulin

How pregnancy effects


Diabetes?
Insulin requirements rise
Decrease in Renal function
(proteinuria)
Increased episodes of hypoglycaemia
Worsening of Retinopathy
Hyperglycaemia in Steroid use!

How Diabetes effects


pregnancy?
Increased risk of congenital

abnormalities
Increases risk IUD/Neonatal death
Increased risk Pre-eclampsia
Polyhydramnios
Macrosomia/IUGR
Prematurity
Postnatal hypogycaemia and
Jaundice.

Antenatal care

Pre-conception counselling
Multi-disciplinary approach
Strict Diabetic control
Detailed Anomaly scan
ANC every 2 weeks at minimum with
growth scans
Induction at 38 wks

Labour
Continuous GTG
Sliding scale in certain cases- Half as
soon as placental delivered
6 wk follow up- GTT

BREAK

GYNAECOLOG
Y
Normal
Menstruation

Normal Menstruation

Cycle 22-35 days


Duration of bleeding <7 days
Blood loss <80mls
Menstrual Phase- endometrium shed
Discharged through Cx by uterine
contractions

Normal cycle

Proliferative (Follicular)
phase

Day 5-13
Ovarian follicular growth
Increasing oestrogen
Growth and vascularisation of
endometrium
Ovulation occurs day 14
Ovulation occurs 14 days prior to
next period in a cycle that is not 28
days

Secretory (luteal) phase


Day 15-28
Progesterone increases. Produced by
corpus luteum
Maintains endometrial thickness,
preparing for implantation
Ends with demise of corpus luteum

Menstrual phase
Day 1-5
Decline of oestrogen and
progesterone
Breakdown of endometrium- sheds

Heavy
Menstrual
Bleeding

Heavy Menstrual bleeding


Defined as > 80mls blood loss
/month
Heavy menstrual blood loss affecting
QOL or causing anaemia
10% of all women
Most common gynaecology referral

Causes
PALM COEIN
Polyp
Coagulopathy
Ademomyosis
Ovulatory
Dysfunction
Leiomyoma
Endometrial
Malignancy
Iatrogenic
Not yet classified

Assessment
History
Menstrual cycle length, duration
Heavy clots, flooding, tampons/pads
IMB, PCB
Associated pain
Examination
Abdominal
PV
Speculum- smear/swabs

Investigations
Pelvic USS
FBC, clotting, TFTs
In older women (>40yrs)
Pipelle biopsy
Hysteroscopy +/- biopsy

Causes

Dysfunctional Uterine bleeding


Fibroids
Polyps
Endometrial ca

Fibroids (leiomyoma)
Benign tumours of myometrium
20% incidence in women >40yrs old

Management
Medical
Non-hormonal
Hormonal
Surgical
Minor
Major

Medical
Non- hormonal
Mefenamic acid (NSAID)
Tranexamic acid (antifibrinolytic)
Both taken during period only

Medical
Hormonal
Progestogens- Norethisterone
- Provera
- POP (Cerazette)
Mirena coil
COC, Depoprovera, GnRH analogues
Esmya

Radiological
Fibroids
Uterine artery embolisation
Requires MRI

Surgical (Minor)
Endometrial ablation
75% satisfied
Must have biopsy prior
to carrying out
Family should be complete
LASH alternative
Myomectomy (fibroids)

Surgical (Major)
Hysterectomy +/- BSO
Should not be considered unless tried
alternative treatment or has very
large fibroids

Endometriosis
Ectopic endometrial tissue
Usual sites:
Pouch of Douglas
Uterosacral ligaments
Ovarian fossae
Bladder
Within uterine muscle (adenomyosis)
Very rare: lungs, brain, muscle
Usually present with pain/infertillity
Graded I-IV
Treatment COCP, progesterones, GnRH, surgical

Urinary
Incontinance and
prolapse

Prolapse
Downward displacement- weakening of
support (pelvic floor)

Definitions

Uterovaginal- uterus and cx


Cystocele- Bladder
Rectocele- Large bowel
Enterocele- small bowel

Uterovaginal
Grade I

Uterovaginal
Grade II

Uterovaginal
Grade III- complete eversion

Grade III

Procedentia
Ulceration

Rec

Sypmtoms

Something coming down


Discomfort
Urinary sx
Recurrent UTIs
Constipation/ Difficulty emptying bowel

Treatment
Mild- Oestrogen cream
- Pelvic floor exercises

Mod/Severe- Conservative (Pessary) vs


Surgical (pelvic floor repair/ Vaginal
hysterectomy/Mesh)

Pessaries

Urinary incontinence
Urge
Overactive bladder
Inability to delay following sensation to
void
e.g. Key in the door
Detrusor instability, neurogenic bladder,
infection
Stress
Loss of urine when intra-abdominal
pressure increased
Weak pelvic floor or sphincter

Treatments Urge

Lifestyle changes (weight, caffeine, fluid)


Frequency volume chart
Out patient continence programme
Anti-cholinergic medications
Botox (rare)

Treatments- Stress
Physio (PFE, Electrical stimulation of

muscles)
Urethral bulking
Sub-urethral sling (TVT-O)
Colposuspension

90% happy after surgery


Prolapse surgery can make urinary
symptoms worse and for urodynamics first

Gynaecological
cancers

Endometrial cancer

Most common gynae cancer


Adenocarcinoma most common 80-85%
Mean age 60yrs
Risks- Nulliparous
obesity
E2 only HRT
late menopause
(Oestrogen!)

Symptoms and Diagnosis


PMB
Heavy irregular bleeding
None
TV USS (Assess endometrial thickness)
12mm premenopause 4mm

postmenopause
Pipelle biopsy
Hysteroscopy, D&C

Staging
Stage I

Confined to uterus

Stage Ia

No myometrial invasion

Stage Ib

Myometrial invasion <50%

Stage Ic

Myometrial invasion >50%

Stage II

Involvement of cervix

Stage III

Pelvic spread

Stage IV

Bladder/rectum/distant (lung)

Treatment
Hysterectomy
Pelvic clearance

omentectomy/appendicectomy
Chemotherapy/ Hormone therapy
(advanced)
Stage I
75%
5 yr survival
Stage II

58%

Stage III

30%

Stage IV

10%

Ovarian cancer

Most deadly
Peak age 68-85yrs old
90% sporadic, 10% genetic
Epithelial tumours 85%
Increased risk: Nulliparous, higher social
class, ovulation induction
Decreased risk- COC use

Symptoms and Diagnosis


Abdo distension/mass
Abdo pain
Weight loss/loss of appetite

Ca125 >35 post menopausal


Ascitic tap
Imaging- TV USS, CT, MRI, CXR
Laparotomy

Ovarian tumour

Staging
Stage I -25%

Confined to ovaries

Stage Ia

One ovary

Stage Ib

Both ovaries

Stage Ic

+ve ascitic cytology

Stage II -10%

Confined to pelvis

Stage III -45%

Confined to peritoneal cavity

Stage IV -20%

Distant spread

Treatment
Pelvic clearance +

chemotherapy
Radiotherapy
5 yr survival

Stage I

67%

Stage II

51%

Stage III

20%

Stage IV

5%

Cervical cancer
Peak age 45-55 (can occur as young as 20)
Risks Defaulting smears
Multiple partners
HPV 16+18 (80-90%)
COC use
Smoking

Cervical screening

Cx smear- NICE guidelines


Every 3 yrs from age 20-65yrs
Liquid based cytology
Registered with SCCRS
Abnormal results referred to Colposcopy
for cold coagulopathy/LLETZ
Jade Goody effect Increase 21% uptake

Cervical smear

Pre-cancerous changes
Transformation

zone
Dyskaryosis
Cervical
intraepithelial
neoplasia (CIN)
May persist for
years
Can revert to
normal
30% CIN 3 will

CIN 1 Abnormal cells in


lower 1/3
epithelium only.
CIN 2 Abnormal cells in
lower only.
CIN 3 Carcinoma in-situ.
Full thickness of
epithelium

Cervical cancer

Symptoms and Diagnosis

Post coital bleeding


Abnormal discharge/ bleeding
Weight loss
Pain

EUA, cystoscopy, proctoscopy


Cone biopsy
LLETZ

Staging
Stage Ia

Micro <3mm in depth

Stage Ib

Confined to Cx

Stage II

Extends to upper vagina

Stage III

Extends to pelvic side wall or lower


vagina
Distant spread- bladder/rectum/beyond.

Stage IV

Treatment
Hysterectomy

Radical
Radiotherapy
Chemotherapy
5yr survival

Stage I

80%

Stage II

61%

Stage III

32%

Stage IV

15%

Vaccination

Gardasil
Protects against HPV 16 & 18, 6 & 11
99% effective
Girls age 12-13 yrs old
Will still need smears as rare Cx
cancers and current population not
protected.

Vulval cancer

Least common
Peak age 65-70 yrs old
Squamous carcinoma 92%
Risks- HSV
HPV (16/18)
Smoking
Immunosuppresion
VIN

Symptoms and Diagnosis


Pruitus vulva
Vulval pain/ discharge
Lump or ulcer
Diagnosed by vulval biopsy

Vulval cancer

Staging
Stage I

<2cm lesion confined to vulva

Stage II

>2cm lesion confined to vulva

Stage III

Local spread or node involvement

Stage IV

Advanced local spread or bilateral


node involement. (inguinal, femoral,
pelvic.)

Treatment
Stages I-III Radical

vulvectomy
Radiotherapy/
Chemotherapy
Stage IV- Palliative
only
5 yr survival

Stage I

97%

Stage II

85%

Stage III

74%

Strage IV

30%

Poly cystic ovarian


syndrome
PCOS

PCOS
Varying degrees
Unknown aetiology
Clinical signs- Oligomenorrhoea
- Obesity
- Hirsutism

Endocrine measurements
Increased LH/ Low FSH---> increased

LH:FSH ratio
Increased testosterone
Decreased SHBG
Insulin resistance and impaired glucose
tolerance. (11%)
Moderate hyperprolactinaemiaoccasionally

USS assessment
Increased ovarian volume
10-15 microcysts <10mm in diameter
String of pearls

PCOS

PCOS
Diagnosis can be made if has 2 of 3:
Clinical features
Endocrine findings
USS findings

Treatment

Weight loss
Metformin
Laser Rx for hirsuitism
COC, Mirena, Depo provera
Fertility Rx with clomid

Ectopic
pregnancy

Ectopic pregnancy
Implantation outside uterus
1.2% of pregnancies
Incidence rising
Tubal -97%
Cervix
Ovary
Peritoneum
Abdominal

Risk factors

STI/PID
IUD/Mirena
Previous Ectopic
Sterilisation/ Tubal Surgery
Assisted reproduction

Presentation

Amenorrhoea, +ve pregnancy test


Typically at 6-8 wks gestation
No symptoms
Pain (LIF/RIF/Shoulder tip) -90%
PV spotting- 70%
Faint, collapse, haemodynamic
compromise -15%

Diagnosis
Clinical (peritonism, adnexal mass,

unstable)
Serum HCG tracking
TV USS (no IU pregnancy, adnexal mass,
free fluid)
Laparoscopy

TV USS

Management

IV Access, FBC, G&S/ X-match


Resuscitation if required
Anti D if Rh-ve
Surgical vs Medical vs Conservative

Surgical
Laparoscopic

Salpingectomy
Any signs of
rupture
Laparotomy
Check other tube
is not damaged

Medical
Methotrexate- 50mg/m2
Must fit criteria and be

compliant to follow up
Check U&Es and LFTs
HCG tracking- may initially
rise
5-10% require surgery
No pregnancy for 3 months
Avoid alcohol/ sunlight

Conservative

Risky
Must be asymptomatic and stable
Falling HCG
Track to zero

Follow up/ Future


pregnancies
6 week follow up appt
De brief
Good contraception
Single ectopic- 60-70% will have IU

pregnancy
Subsequent pregnancies 10-15% will be
ectopic
Early Ultrasound