Obstetrics & Gynaecology Flashcards
Reason for folic acid supplementation in pregnancy
↓ risk of neural tube defects
Standard folic acid supplementation in pregnancy
400 micrograms/day for ~3 months before conception until 12th week of pregnancy
take 5mg/day if high risk group
Groups requiring 5mg folic acid supplementation
previous neural tube defects family history of NTDs Diabetes Coeliacs Thalassaemia Anti-epileptic medication obese women (>30kg/m^2)
recommendation for alcohol intake in pregnancy
recommended to not consume any alcohol
but if women choses to drink ≤1-2 units/week
Complications of smoking in pregnancy
IUGR low birth weight miscarriage still birth premature delivery placental issues
foods to avoid in pregnancy
uncooked meat/fish, raw egg, unpasteurised milk, soft cheese, raw shellfish
epilepsy medication considered safe in pregnancy
lamotrigine
dangerous anti epileptics in pregnancy
sodium valproate
phenytoin
Antidepressants safe in pregnancy
Fluoxetine
amitriptyline
Mood stabiliser to avoid in pregnancy
lithium
Diabetes drugs and pregnancy
discontinue all hypoglycaemic agents except metformin
supplement metformin with insulin if needed
anithypertenisve medication in pregnancy
Stop ACE-Is & ARBs
Stop Statins
Timing of booking appointment
8-12 weeks
ideally at <10weeks
Purpose of booking visit (8-12 weeks)
General info e.g. diet/folic acid/Vit D/alcohol/smoking
BP
Urine dipstick
BMI check
Booking bloods (FBC,HIV, Hep B, Syphilis, Rhesus status, red cell allo antibodies, haemoglobinopathies)
Urine culture (for asymptomatic bacteriuria)
GDM screen if risk factors
10-13+6 weeks check
early scan to confirm dates & exclude multiple pregnancy
11-13+6 weeks check
Down syndrome screening (nuchal translucency, beta-hCG, PAPPA)
18 - 20+6 week check
anomaly scan (USS)
Extra antenatal care dates for primips
25 weeks
31 weeks
40 weeks
all routine care (BP, urine dip, SFH)
28 week check
routine care (BP, urine dip, SFH) second anaemia screening Give first dose of anti-D prophylaxis if Rh -ve
34 week check
routine care (BP, urine dip, SFH) Birth planning/labour info Give second dose of anti-D prophylaxis if Rh -ve
36 week check
check presentation & offer external cephalic version if indicated routine care (BP, urine dip, SFH)
Conditions screened for in all pregnant women
anaemia bacteriuria blood group Rh status anti-red cell antibodies Down's syndrome fetal anomalies Hep B HIV NTDs syphilis
Down syndrome screening
11-13+6 weeks gestation
consisting of nuchal translucency, beta-hCG, PAPP-A)
Results suggesting Trisomy 21
↑nuchal translucency
↑beta-hCG
↓PAPP-A
NB trisomy 13/18 give similar results but lower PAPP-A values
Triple/Quadruple test for Down syndrome screening
used if booked late, so offered at 15-20 weeks
Triple test = AFP, uncojugated oeastriol (uE3), beta-hCG, Quadruple test =AFP, uncojugated oeastriol (uE3), beta-hCG, inhibit-A
results suggestive of Downs:
AFP ↓, uncojugated oeastriol (uE3) ↓, beta-hCG ↑, inhibit-A ↑
Positive Down syndrome prenatal diagnosis
offer diagnostic testing with chronic villous sampling (<13 weeks) or amniocentesis (<15 weeks)
if diagnosed offer TOP or continue pregnancy with appropriate support
chronic villous sampling (<13 weeks) or amniocentesis (<15 weeks) risk of miscarriage
~1% (1/100)
Antenatal rubella infection
suspected Rubella infection in pregnancy should be discussed with health protection unit
offer MMR vaccination in postnatal period
Antenatal Varicella Zoster infection
Risk of fatal varicella syndrome
Management:
check maternal blood for varicella immunity
if not immune:
<20 weeks: give varicella-zoster immunoglobulin (VZIG)
>20 weeks: give VZIG or aciclovir days 7-14 post exposure
antenatal CMV infection
no effective treatment
ensure good personal hygiene and avoid infected individuals
HIV infection in pregnancy
screened for in all pregnant women
- Maternal antiretroviral therapy (Zidovudine + 2 other antiretrovirals)
- Elective C-section at 38-39 weeks (consider delaying to >39 weeks if viral load >50copies/ml)
- neonatal antiretorviral therapy (Zidovudine)
- avoid breastfeeding (bottle feeing only)
if all prophylactic steps taken then mother to child transmission <1%
Hep B in pregnancy
screened for in all pregnant women
give full immunisation + Hep B immunoglobulin to baby of Hep B infected mother
define theses alloimmunisation
Rh -ve mothers may develop anti-D IgG antibodies if sensitised e.g. previous Rh +ve pregnancy, delivery, miscarriage, TOP, ectopic pregnancy, antepartum haemorrhage
preventing Rh alloimmunisation
test for anti-D antibodies for all Rh -ve mothers at booking
routine anti-D prophylaxis at 28&34 weeks if not sensitised
if sensitising event in 2nd/3rd trimester = large dose of anti-D & perform Keinhauer test
When to give anti-D immunoglobulin
Give within 72h of event
delivery of Rh +ve infant (stillbirth/live) TOP Miscarriage at >12 weeks gestation ectopic pregnancy ECV antepartum haemorrhage amniocentesis chorionic villous sampling fatal blood sampling abdominal trauma
Nausea & vomiting in pregnancy
affects ~75% of pregnancies
usually resolves by 16 weeks of gestation
symptoms beginning at >12 weeks usually have other causes
hyperemesis gravidarum
severe protracted nausea & vomiting associated with weight loss >5% of pre-pregnancy weight, fluid loss, dehydration, electrolyte imbalance
usually occurs between 8-12 weeks
Admission criteria for hyperemesis gravidarum
continued N&V + unable to keep down liquids/oral antiemetics
continued N&V + ketonuria and/or weight loss >5%
Obstetric cholestasis/intrahepatic cholestasis of pregnancy
pruritic condition of pregnancy due to impaired bile flow allowing bile salts to be deposited into the skin & placeenta
risk of recurrence of ectopic pregnancy
10-20%
Conditions associated with obstetric cholestasis/intrahepatic cholestasis of pregnancy
↑ risk of foetal distress
↑ risk of intrauterine death
↑ risk of premature birth
↑ maternal morbidity
Investigating obstetric cholestasis/intrahepatic cholestasis of pregnancy
Bile acid ↑
LFTs (AST ↑, ALT ↑, Gamma-GT ↑, ALP ↑)
Bilirubin↑
Management of obstetric cholestasis/intrahepatic cholestasis of pregnancy
weekly LFTs
Ursodeoxycholic acid
Vit K supplement
induction of labour at 37-38 weeks
Gestational diabetes mellitus (GDM)
a degree of glucose intolerance with its first onset during pregnancy & usually resolving shortly after delivery
Diagnostic criteria for gestational diabetes mellitus (GDM)
Fasting glucose ≥ 5.6mmol/L
2h postprandial glucose ≥7.8mmol/L
NB: the rule is 5678
Screening for gestational diabetes mellitus (GDM)
oral glucose tolerance test at booking & 24-28 weeks
Managing gestational diabetes mellitus (GDM)
1st line: blood glucose monitoring, diet & exercise, weight loss
2nd line: add metformin if not controlled by diet after 1-2 weeks
3rd line: insulin
NB if fasting glucose ≥7mmol/L start insulin
Complications of gestational diabetes mellitus (GDM)
macrosomia large for gestational age pre-eclampsia ↑ risk of shoulder dystocia ↑ risk of neonatal hypoglycaemia
Managing pre-existing diabetes in pregnancy
aim for BMI<27
stop all oral hypoglycaemics except metformin & commence insulin
folic acid 5mg pre-conception till 12 weeks gestation
Pre-existing hypertension in pregnancy
BP >140/90 either at booking or prior to 20 weeks gestation, no protein uria/oedema
Stop ACE-Is & ARBs and switch medication
aim for BP <150/100
Gestational hypertension
BP >140/90 after 20 weeks gestation without proteinuria / oedema
usually resolves spontaneously after birth
Termination of pregnancy (TOP)
also referred to as termination or abortion
medically directed miscarriage prior to independent viability using surgical/pharmacological means
complications of gestational hypertension & pre-existing hypertension in pregnancy
↑ risk of placental abruption ↑ risk of cerebrovascular event ↑ risk of DIC ↑ risk IUGR ↑ risk of prematurity ↑ risk of intrauterine death
Pre-eclampsia
condition seen at >20 weeks gestation characterised by new onset hypertension >140/90 associated with proteinuria & oedema
Eclampsia
pre-eclampsia with the development of seizures/convulsions
Risk factors for pre-eclampsia/eclampsia
Primiparity BMI >30 ↑ maternal age (>40 yrs) multiple pregnancy FHx of pre-eclampsia/eclampsia pre-existing diabetes/HTN/CKD/SLE/antiphospholipid syndrome
Preventing pre-eclampsia/eclampsia
75mg - 150mg of aspirin from week 12 till delivery
Presentation of pre-eclampsia/eclampsia
BP >140/90 + ≥1+ protein on urine dipstick headaches upper abdo pain oedema visual disturbances/blurry vision papilloedema
Seizures if eclampsia
Investigating pre-eclampsia/eclampsia
Urinalysis
FBC/LFTs/U&Es/renal function
USS to assess foetal growth/amniotic fluid levels
Severe pre-eclampsia
BP >170/110 + proteinuria
or
proteinuria 3+/4+
headache, visual disturbances, blurry vision, papilloedema, RUQ/epigastric pain, hyperrefelxia
platelets <100x10^9/L
abnormal LFTs
HELLP syndrome
Management of pre-eclampsia/eclampsia
4x daily BP monitoring, 2-3x weekly FBC/U&Es/LFTs/renal function
Antihypertensives:
1st line: labetalol
2nd line: nifedipine
Seizure control: Magnesium sulphate (4g loading dose over 5-10min then 1g/h for 24h)
Delivery = only curative treatment, generally try to deliver at >34 weeks
HELLP syndrome
complication of pregnancy presenting in women with pre-eclampsia/eclampsia characterised by: -Haemolysis (H) -Elevated liver enzymes (EL) -Low platelets (LP)
Presentation of HELLP syndrome
nausea&vomiting hypertension brisk tendon reflexes RUQ pain headache oedema
Investigating HELLP syndrome
FBC (↓ Hb, ↓platelets) Blood film (fragmented RBCs) LDH (↑ >600IU/L) LFTs (AST/ALT ↑ >70IU/L) platelets (<100x10^9/L) bilirubin (↑)
Managing HELLP syndrome
definite treatment = delivery of baby
Chorioamnionitis
medical emergency, due to ascending infection leading to inflammation of the foetal membranes
Chorioamnionitis risk factors
Preterm premature rupture of membranes (PPROM)
smoking
alcohol use
↑ number of vaginal examinations
Chorioamnionitis presentation
maternal fever uterine tenderness baseline fetal tachycardia (>160) maternal leucocytosis purulent cervical discharge
Chorioamnionitis management
IV Abx e.g. ampicillin
prompt delivery of fetus
Anaemia in pregnancy
normal physiological changes in pregnancy include the ↑plasma volume causing haemodilution so the Hb drops to ~115g/L
most frequently caused by iron deficiency (↓MCV)
often asymptomatic
screening for anaemia of pregnancy
at booking visit & 28 weeks
definition of anaemia in pregnancy
Hb <110g/L at booking, or Hb <105/L in 2nd/3rd trimester
Management of placenta accreta
C-section (open at site distant to placenta, have blood products ready)
if placenta acreata confirmed do not remove it (high risk of major obstetric haemorrhage), but perform hysterectomy
Polyhydramnios
abnormally large amount of amniotic fluid associated with adverse pregnancy outcomes
uterus presents large for date on examination
Polyhydramnios causes
most often idiopathic congenital abnormalities/genetic disorders Gestational diabetes multiple pregnancy congenital infections
Oligohydramnios
too little amniotic fluid (<500ml at 32-36 weeks) associated with IUGR & ↑perinatal mortality
Oligohydramnios causes
rupture of membranes congenital absence of functional renal tissue (renal agenesis) ↓ renal perfusion post-term gestation placental abruption drugs (ACE-Is, indomethacin) pre-eclampsia PROM
VTE in pregnancy
pregnancy is a physiological hypercoaguable state, leading to a 10x ↑ risk compared to non pregnant women
Risk factors for VTE in pregnancy
hereditary hypercoaguable states e.g. Factor V Leiden obesity (BMI>30) immobilisation previous thrombotic event cancer antiphospholipid syndrome ↑ maternal age pre-eclampsia
VTE management in pregnancy
LMWH (prophylaxis & treatment)
NB IV UFH treatment of choice in acute VTE management
continue treatment till at least 6-12 weeks postpartum
Ectopic pregnancy
fertilised ovum implanting & maturing outside the uterine endometrial cavity, 97% are tubal, most commonly in the ampulla
NB the most dangerous place is an ectopic in the isthmus
Risk factors for an ectopic pregnancy
previous ectopic damage to tubes (e.g. PID) endometriosis IVF IUD/IUS
Ectopic pregnancy presentation
6-8 weeks of amenorrhoea
lower abdo pain/pelvic pain
abdo tenderness on palpation
PV bleeding ± clots
If ruptured: dizziness, fatigue, syncope, haemodynamic instability
Investigating an ectopic pregnancy
beta-hCG
transvaginal USS
if pregnancy of unknown location = serious beta-hCGs
Expectant management for ectopic pregnancy
if size <35mm, unruptured, asymptomatic, no fetal heart beat, serum eta-hCG <1000IU/L
monitor over 48h, if symptoms develop/ ↑ beta-hCG = intervene
Medical management of ectopic pregnancy
if size <35mm, unruptured, no significant pain, no fetal heart beat, serum eta-hCG <1500IU/L
single dose methotrexate
3-6 months of contraception as methotrexate = teratogenic
Surgical management of ectopic pregnancy
if size >35mm, ruptured/unruptured, significant pain, visible fetal heart beat, serum eta-hCG >1500IU/L
usually laparoscopic salpingectomy
laparoscopic salpingotomy if other infertility risk factors
risk of recurrence of ectopic pregnancy
10-20%
Miscarriage
involuntary loss of pregnancy before 24 weeks gestation
Threatened miscarriage
painless PV bleeding at <24 weeks with a closed cervical OS
Inevitable miscarriage
heavy PV bleeding + clots, painful, open cervical OS
Incomplete miscarriage
incomplete expulsion of products of conception, may often be unrecognised missed miscarriage
complete miscarriage
products of contraception fully expelled i.e. no pregnancy tissue on USS
Missed miscarriage
gestational sac containing dead fetus without symptoms of expulsion, often presents with light bleeding + dark brown discharge
recurrent miscarriage
≥3 consecutive pregnancies lost spontaneously at <24 weeks
most common causes include antiphospholipid syndrome, endocrine disorders e.g. PCOS, parental chromosomal abnormalities, cervial incompetence
Investigating miscarriage
Transvaginal ultrasound (TVUS) serum beta-hCG (2 tests 48h apart)
Expectant management of miscarriage
waiting for a spontaneous miscarriage
wait 7-14 days then repeat pregnancy test
Medical management of miscarriage
vaginal misoprostol (stimulates contractions)
review if bleeding not started in 24h
perform pregnancy test 3 weeks later
Surgical management fo miscarriage
vacuum aspiration (suction curettage) or surgical removal (evacuation of retained products of contraception -ERPC)
The law around termination of pregnancy (TOP)
1967 abortion act (amended in 1990)
2 registered medical professionals must sign a legal document (HSA1 form)
TOP legal before 24 weeks gestation
- if it reduces the risk to a woman life
- if it reduces risk to her physical/mental health
- if it reduces the risk of physical/mental health of her existing children
- if baby has substantial risk of being seriously mentally/physically handicapped
No limit to gestational age if
- risk to mother’s life
- risk of grave/permanent injury to mothers physical/mental health
- substantial risk that child born would have such physical mental abnormalities as to be seriously handicapped
Medical termination of pregnancy (TOP)
mifepristone followed after 48h by misoprostol
surgical termination of pregnancy (TOP)
cervical dilation followed by suction of uterine contents
Complete hydatiform mole
benign tumour of trophoblastic material, empty egg fertilised by 1 sperm
features: bleeding in 1st/early 2nd trimester with exaggerated symptoms of pregnancy & a large for date uterus
very high beta-hCG levels
partial mole
normal haploid egg fertilised by 2 sperms/1 sperm with duplicated paternal chromosomes
fetal parts may be seen
Breech presentation
when the caudal end of the fetus occupies the lower segment instead of the cephalic presentation
associated with ↑ morbidity & mortality for mother and baby
Management of breech presentation
offer external cephalic version (ECV) at 36 weeks if nulliparous or 37 weeks if multiparous
if unsuccessful then the mode of delivery is C-section
contraindications for external cephalic version
antepartum ahemorrhage in last 7 days abnormal CTG major uterine abnormality ruptured membranes other indications for c-section
Monoamniotic monozygotic twins risks
↑ risk of spontaneous miscarriage
↑ perinatal mortality
↑ rate of malformation/IUGR/prematurity
↑ risk of twin to twin transfusion syndrome
Fetal movements
first movements usually around 18-20 weeks
Red flag if not established by 24 weeks
Fetal distress
presents as ↓ fetal movements
investigate with handheld doppler to confirm heartbeat
consider USS if no heartbeat
otherwise monitor with CTG
Placenta praevia
defined as placenta overlying the cervial OS i.e. low-lying placenta that is partially/fully inserted into the lower segment
commonest cause of antepartum haemorrhage (bleeding at >24 weeks)
Risk factors for placenta praevia
uterine scarring (e.g. pervious c-section)
multiparity
multiple pregancy
prior placenta praevia
Presentation of placenta praevia
often incidental finding on USS e.g. at 20 week scan
Painless PV bleeding (usually sudden & profuse)
abnormal lie/presentation
NO uterine tenderness
Investigations for placenta praevia
have a high clinical suspicion PV bleeding at >20weeks gestation
TVUS/Abdominal ultrasound
Management of placenta praevia
if major placenta praevia do C-section at 37-38 weeks
if pt has bleeding then encourage hospital admission from 34 weeks
NB do not attempt vaginal examination if pt is actively bleeding
Placenta accreta
describes the attachment of the placenta to the myometrium due to defective decidua basalis, meaning the placenta is unable to properly separate during labour =↑ risk of PPH
Types of placenta accreta
defined by depth of implantation
accreta = attach to myometrium
increta = attach in myometrium
percreta = penetrate into peritoneum
Conditions associated with placenta accreta
retained placental products
PPH
preterm delivery
Risk factors for placenta accreta
previous C-section
placenta praevia
↑ maternal age
Placental abruption
premature separation of a normally located placenta from the uterine wall occurring before delivery of the fetus
Types of placental abruption
concealed: ~20%, haemorrhage confided to uterine cavity, more severe form as blood loss often underestimated
revealed: ~80%, blood draws from cervix, usually less severe, often incomplete detachment of palcenta
Presentation of placental abruption
PV bleeding constant abdo pain uterine contraction level of shock not correlating to visible blood loss tense, tender, woody uterus on palpation
Risk factors of placental abruption
smoking cocaine use trauma multiple pregnancy pre-eclampsia uterine malformation previous abruption
Investigating placental abruption
USS CTG platelet count FBC cross match blood
Management of placental abruption
NB Mother takes priority
fetus alive >36 weeks = emergency c-section if fetal distress otherwise vaginal delviery
fetus alive <36weeks = emergency c-section if fetal distress, otherwise close monitoring + corticosteroids
dead fetus = induced vaginal delivery
Uterine rupture
usually occurs during labour however C-section scars from previous pregnancies may rupture during the 3rd trimester
Dehiscence
incomplete separation of a uterine scar with intact serosa and ↑ risk of uterine rupture
Presentation of uterine rupture
sudden tearing uterine pain vaginal haemorrhage cessation of uterine contractions regression of fetus CTG abnormalities Scar pain/tenderness fetal parts may be palpable per abdomen as they pass into abdominal cavity
Management of uterine rupture
urgent surgical delivery
uterine repair or hysterectomy
Cord prolapse
involved the umbilical cord descending ahead of the presenting part of the fetus, if untreated can lead to cord compression or cord spasm which may cause fatal hypoxia
Risk factors of cord prolapse
prematurity multiple pregnancy breech/transverese lie placenta praevia high fetal station cephalopelvic disproportion artificial rupture of membranes (ARM)*
Presentation of cord prolapse
may occur with no outward physical features/normal fetal heart trace
ill fitting/non presenting part on abdominal examiantion
cord prolapse felt PV
cord visible beyond introitus
abnormal CTG
Management of cord prolapse
pushing presenting part back into uterus to avoid cord compression
use of tocolytics e.g. indomethacin/nifedipine
place pt on all fours (pt in doggy position as she is grown a tail i.e. the cord)
usually need emergency C-section
Most important risk factor for cord prolapse
artificial rupture of membranes (ARM)
Post partum haemorrhage (PPH)
excessive bleeding post delivery, usually defined as >500ml
Types of post partum haemorrhage (PPH)
Primary: within 24h of delivery
Secondary: 24h - 12 weeks after delivery
Causes of primary post partum haemorrhage (PPH)
4T’s of PPH
Tone (uterine atony, ~90% of PPH)
Trauma (to uterus/cervix/vagina)
Tissue (e.g. retained placenta i.e. delayed 3rd stage)
Thrombin (pre-existing/acquired coagulopathies)
Risk factors for primary PPH
previous PPH prolonged labour pre-eclampsia ↑ maternal age emergency C-section placenta praevia/accreta BMI >35 assisted vaginal delivery
Presentation of primary PPH
bleeding which fails to stop after delivery of placenta
signs of shock e.g. hypotension (this is then defined as a major obstetric haemorrhage (MOH), usually >1500ml lost)
Management of primary PPH
ABCDE assessment
bilateral large bore cannulas
cross match blood & make units ready
Medication: syntocinon (5 unit bolus + 40 units IV) TXA (1g IV) Ergometrin (500 micrograms) Carboprost (250 micrograms every 15 min up to 5 doses) Misoprostol (800 micrograms)
Surgical/physical:
Bimanual uterine compression & stimulation
Balloon tamponade
B-lynch compression sutures
ligation of uterine/internal iliac arteries
hysterectomy
Active management of 3rd stage of labour
done to ↓ risk of PPH
5 units of syntocinon IM
consider following with 40 units IV if necessary
Secondary post partum haemorrhage (PPH) causes
infection especially endometritis
retained products of conception
Presentation of secondary PPH
prolonged/excessive bleeding fever abdo pain offensive smelling lochia dyspareunia
Managing secondary PPH
Oral/IV Abx for endometritis
elective curetage + Abx if retained products
NB 95% of endometritis treated with Abs improves within 48-72h, if this is not the case you must reassess
Lochia
vaginal discharge containing blood mucous and uterine tissue which may continue for 6 weeks after childbirth.
Sheehan’s syndrome
postpartum pituitary necrosis leading to hypopituitarism which is usually caused by massive PPH leading to hypotension & shock
Presents as failure to lactate, breast convolution, amenorrhoea
Shoulder dystocia
a complication of vaginal cephalic delivery, which entails the inability to delivery the body of the fetus using gentle traction after the head has been delivered as the anterior shoulder impacts on maternal pubic synthesis
Associated injuries to fetus in shoulder dystocia
brachial plexus injuries (Erb’s/Klumpke’s palsy)
Risk factors for shoulder dystocia
Gestational diabetes fetal macrosomia BMI >30 induced labour prolonged labour
Management of shoulder dystocia
call additional help ASAP
Stop mother from pushing & avoid downward traction on fetal head
McRobert’s manoeuvre: hyper flex & abduct mothers hips (i.e. knees to chest) to flatten lumbrosacral angle
episiotomy to facilitate secondary manoeuvres e.g. Rubin’s & woods’ screw
consider C-section
Amniotic fluid embolus
when fetal cells/amniotic fluid enters the maternal systemic circulation & stimulates a sudden cardiovascular collapse
presentation of amniotic fluid embolus
sudden cardiovascular collapse acute LV failure pulmonary oedema DIC bleeding diathesis respiratory distress (similar to PE) uterine atony shivers, seizures, LOC arrythmia
Diagnosing amniotic fluid embolus
diagnosis of exclusion
Classic presentation of amniotic fluid embolus
older multiparous women in advanced labour that suddenly collapses
Preterm premature rupture of membranes (PPROM)
PPROM = rupture of membranes prior to onset of labour in a pt <37 weeks gestation
PROM = rupture of membranes occurring prior to onset of labour in a pt ≥37 weeks gestation
Preterm premature rupture of membranes (PPROM) risk factors
smoking
previous preterm delivery
vaginal bleeding during pregnancy
Presentation of Preterm premature rupture of membranes (PPROM)
popping sensation/ gush of fluid PV
continuous watery liquid draining PV after initial gush
wet pad/underwear
pooling of amniotic fluid in posterior vaginal vault on sterile speculum examination
Examinations to avoid in Preterm premature rupture of membranes (PPROM)
DO NOT perform a vaginal examination as it ↑ risk of ascending infection
management of Preterm premature rupture of membranes (PPROM)
admission & CTG monitoring
oral erythromycin for 10 days
antenatal corticosteroids
monitor for infection
Perineal tear classifications
1st degree: superficial damage with no muscle involvement
2nd degree: injury to perineal muscle but on involvement of anal sphincter
3rd degree: injury to perineum involving anal sphincter complex
4th degree: injury to perineum involving anal sphincter complex & rectal mucos
Risk factors for perineal tears
primigravida
macrosomia
shoulder dystocia
forceps delivery
Episiotomy
controlled cutting of the perineum to prevent tearing which is performed during the 2nd stage of labour
Complications of perineal tears
urinary/faecal incontinence
pain
infection
Prolonged labour
inability of women to proceed with childbirth upon going into labour
Failure to progress
can occur in 2 phases of labour :
- latent phase
- active phase (this is where problems arise)
Causes of failure to progress/prolonged labour
fetal malpresentation
poor uterine contractions
cervical stenosis
dystocia
Presentation of failure to progress/prolonged labour
labour >18h
maternal exhaustion
pain
fetal distress
Management of failure to progress/prolonged labour
assisted vaginal delivery
C-section
Requirements for assisted vaginal delivery
fully dilated cervix occipital-anterioir posiiton ruptured membranes cephalic presentation engaged presenting part pain relief adequate sphincter (bladder) empty
Indications for assisted vaginal delivery
maternal/fetal distress in 2nd stage of labour
failure to progress/inadequate progress in 2nd stage of labour (>3h)
Symphysis pubis dysfunction
pregnancy associated pain, instability & dysfunction of the symphysis pubis joint and/or the sacroiliac joint. Due to ligament laxity in response to hormonal changes occurring during pregnancy
common, effecting ~20% of pregnancies
Presentation of symphysis pubis dysfunction
pain over pubic synthesis
difficulty walking/ waddling gait
trouble weight bearing
pain/discomfort lying in certain positions
Management of pubic symphysis dysfunction
exercise
physiotherapy
analgesia
NB pain generally resolved within 6 months of delivery
Induction of labour
the process of starting labour artificially
used in ~20% of pregnancies
Bishops score
to calculate the chance of successful induction of labour
made up of:
cervical position, cervical consistency, cervical effacement, cervical dilation, fetal station
Score <5 indicates natural labour unlikely to start without induction
score >9 indicates labour will likely commence spontaneously
Indications for induction of labour
prolonged pregnancy
PROM where labour doesn’t spontaneously start
diabetic mother >38weeks
Rh incompatibility
IUGR
HTN/pre-eclampsia
planned delivery is in best interest of baby
Method of inducing labour
membrane swee/artificial rupture of membranes (ARM)
prostaglandin gell/pessary
Oxytocin + ARM
Postnatal blues
seen in ~50% of women
usually 3-10 days post delivery mother is tearful, anxious, irritable
Key is reassurance
Postnatal depression
seen in ~10% of women
screened for using Edinburgh postnatal depression scale
usually starts within 1 month of birth, with peak at 3 months
features include anhedonia, loss of libido, low mood, low energy, low self-esteem, feelings of worthlessness
Managed with reassurance, CBT, Sertraline (1st line med) or paroxetine
Puerperal psychosis
~0.2% of women post delivery
onset within 2-3 weeks post birth
features: mood swings, disordered perception, schizophrenic symptoms, major depression, may have high suicidal drive
requires urgent admission to mother-baby unit
Postpartum contraception
should be discussed within 1 week postpartum, with earliest date fo ovulation being at 27 days post partum contraception is needed from 21 days post partum
From when is postpartum contraception needed
21 days post partum
Recommendations regarding inter pregnancy periods
avoid pregnancy for at least 1 year postpartum
Options for post partum contraception
POP:
can be used while breastfeeding
give any time postpartum
COCP
contraindicated while breastfeeding
IUD/IUS
can be inserted immediately post birth or at 4 weeks
Lactational amenorrhoea method (LAM)
in women who is fully breastfeeding & amenorrhoeic <6 months post partum
Polycystic ovarian syndrome (PCOS)
complex condition of ovarian dysfunction, common in women of reproductive age
aetiology not fully understood
NB the majority of women with polycystic ovaries do not have PCOS
Polycystic ovarian syndrome (PCOS) presentation
sub fertility/infertility
menstrual disturbance (oligomenorrhoea/amenorrhoea)
hirsutism, acne, acanthosis nigricans, alopecia
obesity/difficulty loosing weight
psychological symptoms
Rotterdam criteria
diagnostic criteria for PCOS
pt with 2/3 of the following
-polycystic ovaries (≥12 follicles / ↑ovarian volume ?10cm^3)
-oligo-ovulation/anovulation
-clinical/biochemical signs of hyperandrogegism
Investigating Polycystic ovarian syndrome (PCOS)
Pelvic USS (multi cystic ovaries)
FSH/LH/prolactin/TSH/Testosterone (all ↑)
OGTT (commonly shows impaired glucose tolerance)
Management of Polycystic ovarian syndrome (PCOS)
Weight control/↓ weight & exercise (improve fertility & metabolic features)
COCP (to regulate cycles + manage hirsutism/acne)
Topical eflornithine (if hirsutism/acne don’t respond to COCP)
metformin/clomifene
Management of Polycystic ovarian syndrome (PCOS) related infertility
Weight loss
Clomifene (1st line) or metformin or both
Complications of Polycystic ovarian syndrome (PCOS)
↑ risk of CVS diabetes OSA endometrial hyperplasia/cancer infertility
Endometriosis
Presence of endometrial tissue outside the uterine cavity most commonly in the peritoneal cavity
A chronic oestrogen dependent condition
Adenomyosis
invasion of the myometrium by endometrial tissue
Risk factors for endometriosis
positive family history nulliparity early menarche late menopause late first sexual encounters
Presentation of endometriosis
dysmenorrhoea chronic/cyclical pelvic pain dyspareunia (especially deep) subfertility bloating, lethargy, constipation, lower back pain, urinary symptoms posterior fornix/adnexal tenderness
Investigating endometriosis
laparoscopy (gold standard) Transvaginal USS (TVUS)
Management of endometriosis
NSAIDs + paracetamol for pain relief
1st line: COCP (suppress ovarian function) or progesterones (e.g. medroxyprogesterone)
2nd line: IUS
surgical (laparoscopic excision / laser ablation)
Uterine fibroids
also known as leiomyomata, are benign tumours of the uterus primarily compromised of smooth muscle & fibrous connective tissue
Epidemiology of uterine fibroids
very common
~20% of white women
~50% of black women (more common in afro carribbean population)
Presentation of uterine fibroids
1/2 will be asymptomatic
usually presents between 30-50 yrs of age
menorrhagia
lower abdo pain (cramping pain often during menstruation)
bloating
sub fertility
palpable mass
Investigating uterine fibroids
Transvaginal USS (TVUS) endometrial biopsy
Management of uterine fibroids
Mirena coil (IUS)/COCP
TXA
GnRH agonist (to ↓ size of fibroids)
surgical: myomectomy to retain fertility or hysterectomy
Complications of uterine fibroids
red degeneration: haemorrhage into fibroid often occurring during pregnancy
Pelvic inflammatory disease (PID)
a spectrum of inflammatory disorders of the upper female genital tract usually due to ascending infection from cervix
Causes of Pelvic inflammatory disease (PID)
Chlamydia trichromatis
Neisseria gonorrhoea
mycoplasma genitalium
mycoplasma hominis
NB in 50% of cases no organism is identified
Presentation of Pelvic inflammatory disease (PID)
often mild/absent/atypical symptoms lower abdo pain deep dyspareunia abnormal PV bleeding (post-coital, intermenstrual, menorrhagia) purulent vaginal/cervical discharge fever cervical motion tenderness
Investigating Pelvic inflammatory disease (PID)
pregnancy test (rule out ectopic)
cervical/high vaginal swabs
vaginal secretion sampling for gonorrhoea/chlamydia
laparoscopy (gold standard)
Management of Pelvic inflammatory disease (PID)
Abx (if clinically suspected) e.g. IM ceftriaxone (Gonorrhoea) + PO metronidazole + PO doxycycline (chlamydia)
consider IUD removal
management of sexual partners including STI screening
complications of Pelvic inflammatory disease (PID)
perihepatitis (Fitz-Hugh Curtis syndrome)
infertility/subfertility
↑ risk of ectopic pregnancy
Normal physiological discharge
white/clear, non offensive discharge that varies with menstrual cycle
thickness/stickiness varies with hormonal cycle
bacterial vaginosis
most common cause of abnormal vaginal discharge in women of reproductive age, caused by overgrowth of predominantly aerobic bacteria in the vagine e.g. gardenella vaginalis which replace lactobacilli =↓lactic acid production leading to ↑pH
Presentation of bacterial vaginosis
offensive fishy smelling vaginal discharge
generally thin, off white/greyish discharge
Amsel’s criteria for diagnosis of Bacterial vaginosis
3/4 of the following
- thin white homogenous discharge
- clue cells on microscopy (stippled vaginal epithelia cells)
- vaginal pH >4.5
- positive whiff test (add KOH = fishy odour)
Management of bacterial vaginosis
avoid vaginal douching, wash outside of vagina only with pH neutral soap PO metronidazole (5-7 days)
NB do not treat asymptomatic women unless pregnant (may cause preterm labour/chorioamnionitis in pregnancy)
Vaginal candidiasis
yeast infection of the lower female reproductive tract, 90% of which are caused by candida albicans
also known as thrush
peak incidence age 20-40 yrs
Risk factors for vaginal candidiasis
diabetes
Abx/steroid treatment
pregnancy
immunosuppression
Presentation of vaginal candidiasis
white, 'cottage cheese' on offensive thick discharge pruritus vulvae vulval soreness dyspareunia vulval erythema/vaginal mucosa erythema satellite lesions/excortications
Treatment of vaginal candidiasis
no internal cleaning & good personal hygiene
1st line: intravaginal clotrimazole/miconazole pessary
2nd line: oral anti fungal e.g. fluconazole (if severe/systemic symptoms)
Recurrent candidiasis
≥4 episodes in 1 year
confirm initial diagnosis via high vaginal swab
Trichomonas vaginalis
common STI caused by a protozoa
Presentation of trichomonas vaginalis
green-yellow, frothy, offensive discharge
vulvovaginitis (erythema of vulva&vaginal mucosa)
strawberry cervix
Investigating trichomonas vaginalis
high vaginal swab for NAAT
pH > 4.5
wet microscopy (at GUM clinic)
contact tracing
Management of trichomonas vaginalis
avoid intercourse for minimum 1 week post treatment
2g single dose PO metronidazole (treat both partners)
Other causes of vaginal discharge
Chlamydia trachomatis: purulent/mucopurulent discharge
Neisseria gonorrhoea: purulent discharge
Foreign object e.g. tampon: foul smelling, bloody purulent discharge
Erosive lichen plans: visible on examination
Indications for emergency contraception
no contraception used in a consensual sexual intercourse/rape/sexual assault
contraceptive failure e.g. barrier methods
incorrect use of contraception
unprotected sexual intercourse (UPSI)
Levornogestrel emergency contraception MOA
stops ovulation & prevents implantation
can be used more than once per menstrual cycle
Levornogestrel emergency contraception timing
must be taken within 72h of UPSI as single 1.5mg dose
generally well tolerated, but repeat dose if vomiting within 3h of administration
Ulipristal (ellaOne) emergency contraception MOA
inhibits ovulation
can be used more than once per menstrual cycle
Ulipristal (ellaOne) emergency contraception timing
can be taken up to 120h post UPSI as single 30mg dose
can be used more than once per menstrual cycle
Ulipristal (ellaOne) emergency contraception interaction with hormonal contraception
may reduce effectiveness, so restart hormonal contraception 5 days after taking ellaOne & use barrier methods in the mean time
Copper IUD as emergency contraception MOA
inhibits fertilisation & implantation
most effective form of emergency contraception
Copper IUD as emergency contraception timing
insert within 5 days of UPSI
if ≥5 days after UPSI then can be fitted within 5 days of the likely ovulation date (usually length of period in days -14 i.e.if 28day cycle then day 14)
Copper IUD as emergency contraception removal
can be kept in long term as ongoing contraception
if client wants IUD removed then must stay in till at least the next period after insertion
Important points for emergency contraception
return for pregnancy test if no normal period within 7 days of their normal expected period date or if regular bleeding
Combined oral contraceptive pill (COCP) MOA
works by inhibiting ovulation, thickens cervical mucus, inhibits implantation
Risks of taking Combined oral contraceptive pill (COCP)
↑ risk of breast cancer
↑ risk of cervical cancer
↑ risk fo VTE
↑ risk of MI/Stroke
Advantages of the Combined oral contraceptive pill (COCP)
↓risk of ovarian/endometrial/colorectal cancer
menses tends to be lighter
improves PMS
Contraindications for Combined oral contraceptive pill (COCP)
migraine + aura BMI >35 smoking >15 cigarettes at age >35 history of VTE breastfeeding <6 weeks postpartum uncontrolled HTN breast cancer history of stroke/IHD >20 yrs of diabetes
Drugs ↓ effectiveness of Combined oral contraceptive pill (COCP)
rifampicin
phenytoin
carbamazepine
Starting the Combined oral contraceptive pill (COCP)
start on first day of menstrual bleed/within 5 days of this day = no additional contraception required
if started on other days of cycle must use other form of contraception for first 7 days
How to take Combined oral contraceptive pill (COCP)
take pill at same time everyday
take 21 days then 7 day pill free window
may be able to tricycling (3x 21 day packets back to back)
1 missed Combined oral contraceptive pill (COCP)
1 pill missed anywhere in packet, i.e. >24h without pill
take last pill asap even if it means taking 2 pills in one day, then continue as normal & take 7 day break as normal
NB if they are in week 4 of their packet i.e. the sugar pills then no action required (day 22-28)
≥2 missed Combined oral contraceptive pill (COCP)
take last missed pill ASAP & omit any earlier pills + used additional contraception for next 7 days
If pills missed in week 1 (days 1-7): consider emergency contraception if unprotected intercourse in pill free interval/week 1
If pills missed in week 2 (days 8-14): no need for emergency contraception if pills taken correctly the last 7 days, finish packets as normal
if pills missed in week 3 (days 15-21): finish current packet as per usually and omit pill free break
Progesterone only pill (POP) MOA
inhibits ovulation & thickens cervical mucous
Progesterone only pill (POP) contraindications
past breast cancer
SLE
Progesterone only pill (POP) advantages
can be used while breastfeeding
can be used when oestrogen contra indicated e.g. VTE
can be used when having major surgery
Starting the Progesterone only pill (POP)
if commenced up to & including day 5 of the cycle it provides immediate protection
otherwise requires 2 days of additional contraception after commencing
How to take Progesterone only pill (POP)
must be taken at exactly same time everyday (within a 3h window of when pill was taken previous day)
> 3h late = missed pill
Missed pill for Progesterone only pill (POP)
if a pill is >3h late = missed
If missed pill, then take missed pill as soon as possible, use extra contraception until regular pill taking reestablished for 48h
Injectable contraceptive (Depo Porvera) MOA
inhibiting ovulation & thickening cervical mucous
Slowly releases progestogen
How Injectable contraceptive (Depo Porvera) is used
IM injection every 12 weeks
Disadvantages of Injectable contraceptive (Depo Porvera)
not quickly reversible
weight gain*
irregular bleeding
Injectable contraceptive (Depo Porvera) contraindications
current/past breast cancer
avoid in <18y/o due to ↓ bone mineral density
Contraceptive proven to cause weight agin
injectable contraceptive (Depo Provera)
Implantable contraceptive (Nexplanon) MOA
inhibits ovulation & thickens cervical mucous
Slowly releases progestogen
how the Implantable contraceptive (Nexplanon) works
lasts 3 years
inserted in the proximal non-dominant arm, just overlying the tricep
take additional contraception for 7 days if not inserted on day 1-5 of cycle
Intrauterine contraceptive device (IUD)
also known as the copper coil
inhibits fertilisation & is cytotoxic for sperm
lasts for 5-10years
effective immediately after insertion
Intrauterine contraceptive device (IUD) complications
heavy/prolonged periods
↑risk of ectopic pregnancy
Intrauterine system (IUS) (mirena coil)
levornogestrel releasing device
inhibits endometrial proliferation = prevents implantation and thickens cervical mucous
lasts for 5 years
Intrauterine system (IUS) (mirena coil) advantages
can be used to manage menorrhagia, as HRT, endometrial hyperplasia, endometriosis
often lighter menses/amenorrhoea
Contraceptive of choice in younger people
Implantable contraceptive (nexplanon) is the LARC of choice in young people
Age of consent for sexual encounters
Age < 13 means a pt is unable to consent, so if a child comes in this should trigger child protection meausres
generally age of consent = 16 but can be lower if fraser competent
The Fraser guidelines
Used in those <16 years old
The following points should be fulfilled:
- the young person understands the professional’s advice
- the young person cannot be persuaded to inform their parents or allow the professional to contact them on their behalf
- the young person is likely to begin, or continue having, sexual intercourse with or without contraceptive treatment
- unless the young person receives contraceptive treatment, their physical or mental health, or both, is likely to suffer
- the young person’s best interests require them to receive contraceptive advice or treatment with or without parental consent
Menopause
onset of menopause is defined as the cessation of menses for at least 12 consecutive months without other causes of amenorrhoea
as women move towards menopause their mensturation may become erratic but if there is still bleeding it is not menopause
average age = 51 yrs
Contraception and menopause
contraception is indicated until 12 months after last period if >50y/o
if <50y/o contraception is indicated till 24 months after last period
Presentation of menopause
menstrual irregularity hot flushes/sweats vaginal dryness & atrophy urinary frequency sleep disturbances mood changes (anxiety, depression, difficulty concentrating) ↓ libido
Management of menopausal symptoms (excluding HRT)
lifestyle modifications e..g weight loss, regular exercise etc
fluoxetine/citalopram/venlafaxine for hot flushes/vasomotor symptoms
lubricants & moisturisers for vaginal dryness
vaginal oestrogen’s for vaginal atrophy
HRT (hormone replacement therapy)
in women with uterus = oestrogen + progestogen
in women without uterus = only oestrogen
give continuous combined regime if amenorrhoea >12 months/sequential HRT received for >12 months
give sequential combined regimes if amenorrhoea <12 months
HRT (hormone replacement therapy) contraindications
current/past breast cancer
oestrogen-sensitive cancer
undiagnosed vaginal bleeding
untreated endometrial hyperplasia
Complications of HRT (hormone replacement therapy)
↑ risk of breast cancer
↑ risk of endometrial cancer
↑ VTE risk
Premature ovarian failure
onset of menopausal symptoms & ↑ gonadotrophin levels before the age of 40
Investigating premature ovarian failure
FSH ↑ LH ↑ estradiol ↓ TVUS TFTs prolactin
Management of premature ovarian failure
specialist referral
Sex steroid replacement till at least 51 yrs of age (e.g. via HRT or COCP)
egg donation if attempting conception
Female genital mutation (FGM)
also known as female circumcision is widely practiced throughout africa & the middle east
WHO definition: all procedures that involve the partial or total removal of the external female genitalia or other injuries to the female genital organs for non medical reasons
Type I Female genital mutation (FGM)
clitoridectomy: partial/complete removal of the clitoral glans and/or the prepuce/clitoral hood
Type II Female genital mutation (FGM)
excision: partial or total removal of the clitoris & labia minor with or without excision of the labia major
Type III Female genital mutation (FGM)
infibulation: narrowing of the vaginal orifice with the creation of a covering seal by cutting/repositioning the labia minor and/or labia major
Type IV Female genital mutation (FGM)
all other harmful procedures to the female genitalia for non medical purposes e.g. piercing, pricking, scraping, cauterising
Female genital mutation (FGM) and the law
all HCPs are required to report/record FGM if they see it in a patient or if there is a family history of FGM
It is an offence for UK nationals/permanent UK residents to carry out FGM in the UK or abroad as well as to aid/abet/counsel/procure the carrying out of FGM abroad even in countries where the practice is legal
Cervical cancer
a human papilloma virus (HPV) related malignancy of the uterine cervical mucosa, 80% are SCC
peak incidence in those aged 29-25 yrs
HPV subtypes implicated in cervical cancer
types 16 & 18
Risk factors for cervical cancer
HPV infection* smoking early first intercourse multiple sexual partners immunosuppression (invasive cervical cancer = AIDS defining illness) lower socioeconomic class
Presentation of cervical cancer
often detected at routine cervical screening
abnormal vaginal bleeding (post coital/intermenstrual/postmenopausal)
vaginal discomfort
vaginal discharge
urinary/bowel symptoms
abnormal appearance of cervix on examination
Investigating cervical cancer
vaginal/speculum examination colposcopy cervical biopsy HPV testing (usually +ve) CT
Staging cervical cancer
FIGO staging
Cervical intraepithelial neoplasia (CIN)
-CIN I confined to lower 1/3 of epithelium
-CIN II confined to lower 2/3 of epithelium
-CIN III full thickness of epithelium affected
Stage I - confined to cervix
Stage II - spread beyond cervix but not to pelvic wall/ lower 1/3 of vagina
Stage III - tumour extends to pelvic wall/ into lower 1/3 of vagina
Stage IV - tumour spreads beyond pelvis, or involves bladder/bowel
Managing cervical cancer
Early on: radical hysterectomy ± lymph node clearance (Gold standard)
NB cone biopsy/local excision to retain fertility
Later on: radical hysterectomy + chemo/radiotherpay
Complications of cone biopsy/local excision of cervical cancer
(LLETZ procedure = loop excision of transformation zone)
↑ risk of preterm labour due to shortened cervix (cervical incompetence) but can be treated with cervical cerclage
cervical stenosis
pyometra (A pyometra is a collection of pus distending the uterine cavity. It occurs principally when there is a stenosed cervical os)
Prevention of cervical cancer
HPV vaccination for all boys & girls aged 12-13
quadrivalent vaccine vs types 16,18 (cervical cancer) & 6,11 (genital warts)
Cervical cancer screening
smear test offered to all women aged 25-64
age 25-49 = 3 yearly
age 50-64 = 5 yearly
screens for high risk HPV, if +ve then cytology is performed
Cervical screening in pregnancy
usually delayed until 3 months post partum unless missed screening or previous abnormal smear
Inadequate sample protocol for cervical smear
repeat sample after 3 months
if inadequate again then perform colposcopy
If negative cervical smear
normal recall
i.e.
25-49 years: 3-yearly screening
50-64 years: 5-yearly screening
if positive cervical smear with abnormal cytology
colposcopy
if positive cervical smear with normal cytology
repeat in 12 months time
if positive smear with normal cytology at 12 months then repeat in 12 months
if positive smear with normal cytology at 24 months then colposcopy
if repeat test after 12/24 months is negative then return to normal recall
Endometrial cancer
an epithelial malignancy of the uterine corpus mucosa usually in the form of an adenocarcinoma, its an oestrogen dependent tumour
classically seen in postmenopausal women
hormone related to endometrial cancer
oestrogen
Risk factors for endometrial cancer
nulliparity obesity early menarche/late menopause PCOS endometrial hyperplasia unopposed oestrogen tamoxifen diabetes
Presentation of endometrial cancer
classically postmenopausal PV bleeding
abnormal/intermenstrual PV bleeding if premenopausal
investigating endometrial cancer
TVUS
endometrial biopsy ± hysteroscopy
Management of endometrial cancer
if localised = radical hysterectomy + bilateral sapling-oophrectomy ± radiotherapy
progestogen therapy in those not fit for surgery
Ovarian cancer
malignancy arising form the ovaries often epithelial (cystadenocarcinoma) (90%)
leading cause of death from gynaecological cancer in the UK
peak incidence ~60 y/o
Risk factors for ovarian cancer
BRCA 1/BRCA2 smoking obesity nulliparity early menarche/late menopause
Protective factors for ovarian cancer
COCP
Presentation of ovarian cancer
insidious onset & vague early symptoms abdominal distension/bloating abdo discomfort early satiety diarrhoea urinary symptoms pelvic/abdo mass ascites
Investigating ovarian cancer
CA125 (>35IU/ml)
pelvic USS/ TVUS
CT/MRI pelvis
Management of ovarian cancer
explorative laparotomy + histopathology/staging
total abdominal hysterectomy + bilateral sapling-oophrectomy + platinum based chemo
Prognosis of ovarian cancer
~80% present with advanced disease
~5% of all UK female cancer death are due to ovarian cancer
Endometrial hyperplasia
abnormal proliferation of the endometrium greater than the normal proliferation that occurs during the menstrual cycle
Risk factors for endometrial hyperplasia
obesity tamoxifen unopposed oestrogen PCOS diabetes
Presentation of endometrial hyperplasia
abnormal PV bleeding (intermenstrual/irregular bleeding/menorrhagia/post menopausal bleeding)
Investigating endometrial hyperplasia
endometrial biopsy via hysteroscopy (if atypical hyperplasia = premalignant)
TVUS (↑ endometrial thickness, >3-4mm if postmenopausal, >7mm if premenopausal)
Management of endometrial hyperplasia
progestogen therapy
1st line = IUS (levornogestrel)
2nd line = continues oral progestogen (e.g. POP)
if atypical hyperplasia then total hysterectomy is advised
Adenomyosis
characterised by the presence of endometrial tissue within the myometrium leading to thickened utuerus
presents with dysmenorrhoea, menorrhagia, enlarged globular uterus
investigate with TVUS
managed with simple analgesia, IUS/COCP or GnRH agonist (e.g. danazol)
Cervical ectropion
when columnar epithelium of the endocervix is displayed beyond the cervical OS, ie a change in the cervical transformation zone
usually due to ↑ oestrogen levels (e.g. COCP use or pregnancy)
Presentation of cervical ectropion
often asymptomatic
vaginal discharge
post coital PV bleeding
red ring around cervical OS on examination
Management of cervical ectropion
stop COCP & conservative management
Ovarian cysts
very common benign growth that generally occur in premenopausal women
Presentation of ovarian cysts
mostly asymptomatic dull ache/pain in lower abdomen lower back pain dyspareunia palpable mass on examination torsion/rupture = serve abdo pain often after exercise
Investigating ovarian cysts
TVUS (gold standard)
pregnancy test
CA125
CT/MRI
Management of ovarian cysts
small cysts (<50mm) = usually self resolve, no follow up neded
larger cysts (>50mm) or complex cysts need USS follow up and consider surgical treatment fi conservative approach fails
Types of ovarian cysts
Follicular = most common, due to non rupture of dominant follicle, often regress spontaneously
Corpus luteum cysts = failure of corpus lute to break down, often presents as intraperiotneal bleeding
Dermoid cysts = may contain hair/nails/skin, most common benign tumour in <30y/o
serous cyst adenoma = most common bening epithelial tumour, may resemble serous carcinoma
mucinous cyst adenoma = often large and may become massive, may rupture causing pseudomyxoma peritonea (mucin in peritoneal cavity)
genitourinary prolapse
descent of one or more of the pelvic organs including the uterus/blader/rectum/vaginal vault
Risk factors of genitourinary prolapse
↑ age ↑ parity/multiparity vaginal delivery obesity previous hysterectomy previous prolapse
Presentation of genitourinary prolapse
mild prolapse is often asymptomatic sensation of pressure/fullness/heaviness sensation of bulge/protrusion difficulty retaining tampons feeling of bearing down urinary symptoms (incontinence, frequency, urgency, incomplete emptying) dyspareunia constipation
Management of genitourinary prolapse
conservative : weight loss, pelvic floor exercises, ring pessary
Surgical management
Urinary incontinence
involuntary loss of urine
common problem especially in elderly female,
Types of urinary incontinence
stress incontinence: involuntary leak on effort/exertion/sneezing/coughing , usually small amounts
urge incontinence: involuntary leak immediately proceed by urgency of micturition
Mixed: mix of urgency & stress
overflow incontinence: usually due to chronic bladder outflow obstruction
Risk factors for urinary incontinence
↑ age previous pregnancy/childbirth vaginal delviery ↑ BMI FHx hysterectomy pelvic organ prolapse congiuntive impairment
Investigations for urinary incontinence
bladder diary
vaginal/speculum examination
urine dipstick & culture
urodynamic studies
Management of urge urinary incontinence
1st line bladder retraining
2nd line bladder stabilising drugs (antimuscarinics e.g. oxybutynin, tolterodine)
Management of stress urinary incontinence
pelvic floor exercises
duloxetine
surgical management
Management of mixed urinary incontinence
pelvic floor exercises + bladder retraining
Infertility/subfertility causes
male factors ~30% unexplained ~25% ovulation failure/ovulatory disorders ~25% tubal damage ~15% other causes ~10%
Investigating Infertility/subfertility
semen analysis (after min 3 days abstinence) serum progesterone (7 days prior to next expected period, so for 28 day cycle = day 21, <16nmol/L = abnormal, >30nmol/L indicated ovulation) FSH/LH
Ovarian hyperstimulation syndrome (OHSS)
complication of induced ovulation as part of assisted conception
presents as bloating, abdo pain, ascites, anuria, acute respiratory distress
Bartholin’s cysts/abscess
Bartholins glands are a pair of glands located next to the entrance fo the vagina, the ducts of these glands may occlude leading to cyst formation
generally unilateral
usually in women of childbearing age
Bartholin’s cysts/abscess presentation
small cysts often asymptmatic
vulval/perineal mass
vulval pressure/fullness
abscesses may be painful, labial oedema/erythema
on examination = unilateral labial mass
cysts = soft, fluctuant, non-tender
abscess = tesne, ahrd, painful with surrounding erythema
Management of Bartholin’s cysts/abscess
conservative therapy (if small) simple incision & drainage Marsupialisation (gold standard & definitive treatment)
Postmenopausal bleeding
vaginal bleeding occurring after >12 months of amenorrhoea in a women at the age where menopause cane expected
Causes of postmenopausal bleeding
vaginal atrophy (most common) HRT endometrial hyperplasia endometrial cancer trauma polyps
Investigating postmenopausal bleeding
TVUS
urine dipstick
CA-125
endometrial biopsy/hysteroscopy
Managing vaginal atrophy
topical/vaginal oestrogens + lubrication
Dysmenorrhoea
characterised by excessive pain during menstrual periods
Primary dysmenorrhoea
no underlying pathology, affects ~50% of menstruating women, often developing soon after menarche
pain usually starts just before/within a few hours of period starting
management: NSAIDs e.g. mefenamic acid
COCP (2nd line)
Secondary dysmenorrhoea
often due to underlying pathology, generally develops years after menarche
pain starts 3-4 days pre period
Causes: PID, endometriosis, adenomysosis, fibroids
refer to gynaecologist
Menorrhagia
menstrual blood loss which interferes with a women physical/emotional/social/maternal QoL
generally if quantity >80ml or bleeding >7days
peak age 30-49 yrs
Causes of menorrhagia
dysfunctional uterine bleeding (DUB) i.e. primary menorrhagia, ~50% of cases anovulatory cycles fibroids endometrial polyps endometriosis adenoymyosis PID copper coil
Investigating menorhagia
TVUS
FBC
TFTs
Management of menorhagia
mefenamic acid + TXA 1g
Mirena coil (1st line if contraception required)
Amenorrhoea
absence or cessation of menstruation, which may be physiological as before the menarche, due to pregnancy, or after menopause
Primary amenorrhoea
Menses has not occurred by the time of expected menarche i.e. age 14 if absence of secondary sexual characteristics or age 16 if secondary sexual characteristics present
Causes include constitutional delay, imperforate hymen, ovarian failure, hypothalamic failure
Secondary amenorrhoea
menstruation absent for ≥6months but having previously been established
causes: pregnancy, hypothalamic amenorrhoea, PCOS, hyperprolactinaemia, premature ovarian failure
Investigations for amenorrhoea
pregnancy test gonadotrophin levels i.e. FSH/LH (↑ if ovarian cause, ↓ of hypothalamic cause) prolactin androgen levels TFTs pelvic USS
Complications of forceps delivery
Maternal:
perineal tear, vaginal lacerations, sphincter injury, pelvic organ prolapse
Fetal:
facial lacerations, ocular trauma, skull fracture, subgaleal haematoma
Complications of ventouse delviery
maternal:
extension of vaginal laceration, perineal tears
fetal:
scalp laceration, cephalohaematoma, retinal haemorrhage
Use of GnRH agonist in fibroids
e.g. Triptorelin or Goserelin
used to ↓ size of fibroids, especially in the short term while awaiting surgery
Hypothalamic amenorrhoea
Due to ↓GnRH = ↓ LH & ↓ FSH
causes include excessive weight loss, eating disorders, obesity, stress
Causes of inadequate cervical smear
failure to sample full 360° of cervical circumference
blood on smear
cervical inflammation
age related atrophic changes
Imperforate hymen
cause of primary amenorrhoea
usually presents as lower abdominal pain, which gets worse from time to time (usually when periods would be)
in a girl with present secondary sexual characteristics
usually treated with incision of the hymen
