Week 4 Flashcards
Defining contraception
Aims to prevent pregnancy
Achieved by preventing:
-ovulation
-fertilisation
-implantation
Pregnancy occurs at implantation- contraception does not include abortifacients
Why is contraception important
30% pregnancies unplanned
Spacing pregnancy improves outcome
Prevent pregnancy related risk
Choice/empowerment/human rights
Lower teenage pregnancy
Background fertility
<35 years 80-90 pregnancies per 100 women per year
55 years natural conceptions are rare
Failure rates
No method is 100% effective
Effectiveness of some methods depends on correct and consistent use
Pearl index= failure rate per 100 women years of exposure
-if 100 women use the method for a year x will become pregnant
Typical use- failure rate when used as in real life -not always correct
-perfect use- failure rate when method used consistently and correctly at all times
Types of contraception
Methods with no user failure:
-copper coil (CuIUD)- copper
-hormonal coil (LNGIUD)- levonorgestrel
-implant
-sterilisation
Methods with user failure:
-barrier- external and internal condoms, diaphragm
-hormonal- combined pill/ patch/ ring, POP, injectables
-natural family planning and lactational amenorrhoea
Emergency contraception
For each contraceptive method the key things to know are
What it is/what it contains
How it’s used
How does it work- mode of action
How well does it work- failure rate
How long does it work for- duration
Advantages and disadvantages
Any major contraindications- refer to the UKMEC
UK medical eligibility criteria
Defines the safety of a contraceptive for individuals with certain characteristics, physical states or medical conditions
Does not advise on best methods nor effectiveness
1- condition for which theres no restriction for use
2-advantages of using methods generally outweigh theoretical or proven risks
3- condition where theoretical or proven risks usually outweigh advantages of using method
4- condition which represents an unacceptable health risk if method used
Long acting reversible contraception
Methods that require administration less than once per cycle or month
Effectiveness does not depend on memory/user
More effective
Longer lasting
Convenient
Cost effective
-hormonal coil LNGIUD
-copper coil CuIUD
-implant
-injectable
All are fully reversible with no long term impact on fertility
Implants
Nexplanon subdermal implant
Etonogestrel (progesterone)
Single rod
Duration- 3 years
Mode of action
-inhibition of ovulation
-thickened cervical mucus
Failure rate- typical and perfect use= 0.03%
Implants advs and disadvs
Advantages:
-highly effective and reversible
-reduce HMB and dysmenorrhea may cause amenorrhoea
-quick return of fertility when removed
Disadvantages/side effects:
-fitting and removal procedure required
-irregular menstrual bleeding
-hormonal side effects- headache, breast tenderness, changes to skin, mood changes
-affected by enzyme inducers
-no STI protection
Hormonal coils LNGIUD
Small plastic T shaped device- inserted into the uterus, short threads for removal
Gradual release of progesterone levonorgesterel (LNG)
Mirena/levosert/benilexa/kyleena/jaydess
Mode of action
-thin endometrium
-thickens cervical mucus
-inhibits ovulation in some people
Duration of use: between 3-8 years depending on type
Effectiveness >99%
Hormonal coils advs and disadvs
Non contraceptive benefits:
-reduces menstrual bleeding/may induce amenorrhoea
-reduced dysmenorrhea
-may reduce pain from endometriosis or adenomyosis
Disadvantages:
-requires pelvic examination and speculum to fit
-hormonal- headache, breast tenderness, acne
-irregular bleeding- can last up to 9 months
-benign ovarian cysts
-ectopic risk if pregnancy does occur
-expulsion -<1:20
-no STI protection
Copper coil CuIUD
Small plastic T shaped device inserted into uterus, short threads for removal
Has copper on stem +/- banded arms
Mode of action:
-foreign body reaction in uterus- prevents implantation
-copper is toxic to sperm and ova
Duration use 5 or 10 years depending on device
Effectiveness >99%
Intrauterine device IUD
Advantages:
-effective immediately
-can be used as emergency contraception
-non hormonal
Disadvantages:
-requires pelvic exam and speculum to fit
-may increase menstrual blood loss
-may worsen dysmenorrhoea
-expulsion -<1:20
-Ectopic risk if pregnancy does occur
-no STI protection
Contraindications IUD
Refer to UKMEC for full list of
->48hr or <4wk postpartum
-post partum sepsis
-PID
-unexplained vaginal bleeding
-gestational trophoblastic disease
-cervical cancer
-cardiac arrhythmias
Injectables
Depo-provera: 150mgs depo medroxyprogesterone acetate IM 12-14 weekly
Sayana press: 104mg S/C 12-14 weekly
Mode of action:
-inhibit ovulation
-thicken cervical mucus
-thin endometrium
Effectiveness:
-perfect use >99%, typical use 96% due to late injections
Injectables advs and disadvs
Advantages:
-highly effective, convenient, reversible
-not affected by other medications/enzyme inducers
-reduces bleeding and pain, improved PMS
-reduces severity of sickle cell crises
Disadvantages:
-once given cannot be removed
-menstrual irregularities
-weight gain
-no STI protection
-may delay return of fertility- up to 1 year
-hormonal side effects- same as implants/POP
-decrease bone mineral density- returns after stopping
Combined hormonal contraceptives
Contain oestrogen and progestogen
Pill
Patch
Vaginal ring
Mode of action:
-primary mode- prevent ovulation
-additional- thickens cervical mucus, endometrial thinning
Efficacy;
-perfect use- 0.3% failure
-typical use- 8% failure
Combined pills COC
Contains 2 hormones
-oestrogen: ethinyl-oestradiol
-progestogen: synthetic progestogens
One pill per day
Same time each day
Missed pill rules
Combined patch Evra
Ethinyl oestradiol and norelgestromin
Transdermal
5x5cm adhesive patch
Pale pink
1 patch for 1 week for 3 weeks
Perfect use 1% failure, typical use 9% failure
Efficacy may be reduced if >90kg
Not affected by GI upsets
Combined vaginal ring Nuvaring
Ethinyl oestradiol and etonogestrel
Flexible transparent ring 54mm wide
Mode of action- inhibition of ovulation
One ring per 21 days
Removed for 7 days- withdrawal bleed
Not a LARC
Perfect use 1% failure
Typical use 9% failure
Combined hormonal contraceptives
Benefits:
-regular, lighter, less painful periods
-reduced risk of ovarian/endometrial and colon cancer
-may reduce premenstrual symptoms
-may improve acne
Disadvantages/risks:
-venous or arterial thrombosis risk
-heart attack and stroke risk
-breast cancer- reduces with time after stopping the pill
-cervical cancer with longer use
Combined hormonal contraceptives side effects
Temporary: headaches, nausea, breast tenderness, mood changes
Breakthrough bleeding
Effectiveness affected by enzyme inducers
Pilll effectiveness affected by diarrhoea/vomiting
No STI protection
Combined hormonal contraceptives, oestrogen can increase risk of blood clots
Oestrogen containing contraceptives have more contraindications:
-high BMI
-migraines
-smoking
-age
-VTE <45 (patient or 1st degree relative)
-hypertension
-thrombophilias
How to take: standard- take for 21 days, 7 day break (hormone free interval)
Tailored regimens
Progestogen only pill
Synthetic progesterone
-desogestrel/levonorgestrel/norethisterone/drospirenone
Should be taken daily at the same time each day, every day
No pill free interval
Mode of action:
-prevent ovulation
-thicken cervical mucus
-thin endometrium
Failure rates:
-perfect use 1% failure
-typical use 9% failure
Be aware- traditional vs desogestrel POPs
Progestogen only pill advs and disadvs
Benefits:
-effective, reversible
-now available OTC
Disadvantages:
-menstrual irregularities
-same time each day- 12 hour window for desogestrel (3 hours traditional POPs)
-functional ovarian cysts
-hormonal (headaches, changes to mood, depression, bloating, breast tenderness)
Progestogen only methods
Much fewer contraindications than combined methods
No increased stroke risk
See UKMEC for full list
-current breast cancer
-severe liver disease/liver tumours
-stroke/IHD
Barrier methods condoms
External condom:
-latex/latex free, placed over an erect penis before any contact
-acts as barrier to stop sperm entering the vagina
-Perfect use 2% failure, typical 17%
-single use only, check date, kite mark, not damaged, avoid -oil based lubricants, STI and HIV protection
Internal condom:
-inserted before sex, loosely lines vagina/rectum, partially covers vulva, acts as barrier to sperm
-perfect use 5% fail, typical use 21%
-single use only, STI and HIV protected
Barrier methods diaphragm
Reusable flexible latex or silicone device
Put into vagina to cover cervix
Acts as barrier to sperm
Used with spermicide
Can be inserted up to 3 hours before sex
Needs to be left in for 6 hours after sex
Perfect use 4-8% failure
Typical use 12-29% failure
Do not offer STI or HIV protection
Natural family planning
2 categories:
-fertility awareness methods FAM
-lactational amenorrhoea
Fertility awareness methods
Identify a fertile window and avoid UPSI around this time
The main fertility indicators are which should be recorded daily:
-basal body temperature
-cervical secretions (cervical mucus)
-the length of your menstrual cycle
Failure rate between 1-25%
Apps available
Fertility awareness methods advs and disadvs
Advantages:
-can be used to avoid pregnancy or plan for one
-no physical side effects
-in couples control/may improve communication
-avoids hormones/devices
-acceptable to all faiths/cultures
Disadvantages:
-there are much more reliable methods
-need to have regular cycles
-takes 3-6 menstrual cycles to learn effectively
-traditionally time consuming, requires high motivation
-illness, lifetsyle, stress or travel may make fertility indicators harder to interpret
-need to avoid sex or use condoms during fertile time
-no STI protection
Lactational amenorrhoea
For post partum women
-baby <6m old
-woman must be amenorrhoeic
-exclusively breast feeding- 4hrly in day, 6hrly at night
If all 3 criteria are met:
-typical failure rate -2%
-perfect use failure rate -0.5%
Sterilisation male
Male- vasectomy -cutting /tying vas deferens
Failure rate 1 in 2000
Permanent and irreversible on NHS
Doesn’t affect sex drive or erections
Ejaculation occurs but no longer contains sperm
Use contraception for 8-12 weeks after until semen analysis
Female sterilisation
Works by tubal occlusion- preventing egg and sperm meeting
-filshie clips
-salpingectomy
Failure rate 1 in 200
Permanent and irreversible on NHS
Age/parity is not a restriction
Emergency contraception
To be given after sex
2 categories: copper IUD- gold standard, oral methods: ulipristal acetate (ellaOne), levonorgestrel (levonelle)
Copper IUD:
-can be inserted up to 120 hours after first UPSI
-or within 5 days of the earliest expected ovulation
-overall efficacy 99.9%, benefits and risks as for non emergency copper IUD
-can be used for ongoing contraception or removed once pregnancy excluded
Emergency contraception pill
Ulipristal acetate:
-current brand ellaOne single 30mg tablet, licensed for up to 120 hours after sex
-synthetic progesterone receptor modulator
-primary mode of action- delays ovulation
Prevents about 60-80% of expected pregnancies
Effectiveness decreased by progestogen contraception used 7 days before or 5 days after
Can be used multiple times per cycle
Levonorgestrel:
-single tablet- 1.5mg levonorgestrel (3mg if BMI>26)
-efficacy up to 96 hours
-high dose progesterone- delays ovulation
-use >72 hours outside the produce licence
-efficacy approx 60%
-can use multiple times per cycle
Menopause
Defined as the cessation of menses for:
-12 months >50 years
-24 months <50 years
Average age menopause in UK is 51
Early menopause <45
Premature ovarian insufficiency <40 years
Menopausal symptoms
Occur due to reduced oestrogens
Hot flushes and night sweats
Loss of libido
Vaginal dryness
Skin dryness/dry hair/thinner hair
Frequency of micturition, urgency, nocturia
Lethargy and fatigue
Low mood/anxiety
Arthralgia/myalgia
Poor sleep/insomnia
Palpitations
Long term effects of oestrogen deficiency
Increased cardiovascular risk:
-MI
-stroke
Reduction in bone mineral density
Increased total cholesterol and LDL cholesterol
Decreased glucose tolerance and insulin sensitivity
Hormone replacement therapy
Types HRT:
-with a uterus
—combined oestrogen and progestogen
—-cyclical (sequential)
—-continuous
Without a uterus
–oestrogen only
HRT routes
Transdermal: patch, gel, spray
Oral
LNGIUD- as progestogen component of HRT
Implants
Low dose vaginal oestrogen for vaginal symptoms (can be used with systemic HRT)
HRT risk and benefits
Benefits:
-eases symptoms
-reduces cardiovascular risk as long as started within 10 years menopause
-protects bone mineral density
Risks;
-transdermal HRT has a safer risk profile than oral
-oral preparations: DVT/PE risk, stroke and MI risk
-increased risk of breast cancer 1 per 1000 per year, needs to be considered in context
Risk of endometrial cancer is unopposed oestrogen is given to women with a uterus
HRT is not a contraceptive
Formation of placenta
1st trimester
Receptive endometrium
Mid-luteal phase:
-secretory activity peaks- endometrial cells rich in glycogen and lipids ~14mm thick
-glands increase in number and size
-maintained by high progesterone and oestrogen levels
-endometrial receptivity is marked by changes on surface epithelium
Implantation window
Pinopode formation day 16-20, reduce volume of uterus
Implantation
Embryo attached and penetration of the endometrium and maternal circulatory system to form the placenta
Embryo enters uterus bathed in the uterine secretions for 1-3 days prior to hatching from the zona pellucida
“Apposition”= blastocyst loosely associates with uterine wall
“Attachment”= firm adhesion
“Invasion”= blastocyst attachment to the uterine wall triggers enzyme production.
-degrades and invades the glycogen rich endometrial stroma
-provides further nutritional support
Decidualisation of the endometrium
Induced by progesterone
Oedema, changes in ECM, vascular remodelling/angiogenesis , leukocyte infiltration (uNK cells)
-uterine natural killer cells- set up environment to remodel endoemetrium, recognise embryo allowing tolerance to embryo
Endometrial stromal cells undergo morphological and biochemical changes
-fibroblast like-> polygonal (epithelial like)
Store glycogen and lipids support blastocyst
Secrete decidual proteins (characteristic markers): prolactin, IGFBP-1, tissue factor, VEGF, PIGF, LIF, IL-15
The decidua completely surrounds the implanted blastocyst by day ~10. Most is shed at parturition
Placenta
Plakous- flat cake
At term-discoid 15-25cm, 2.5-3cm thick, 500g
Structure of the placenta
Chorionic plate: you have layer of vascularised fetal tissue (the chorion) that goes across. From there the umbilical cord arises with vessels that go off to the fetus
From the maternal side: the endometrium comes around the placenta, you have lots of intervillous spaces, this is where maternal blood pools and circulates around chorionic villi
Functional units of placenta- cotyledon/lobe, placental septum’s
Some villi make contact with other side- anchoring villi
Maternal blood transferred through whole thing from spiral arteries from endometrium to allow for exchange nutrients and gases to fetus via villi then drain back via endometrial veins
Placental classification
3 main types based on structural organisation and separation of fetal and maternal blood supplies
Haemochorial- the chorion is in direct contact with the blood. Human placenta
Endotheliochorial- the maternal blood vessel endothelium comes in direct contact with chorion (dog and cat)
Epitheliochorial- the most primitive form- The maternal epithelium of the uterus comes into contact with the chorion (cows and pigs)
Trophoblast cells
Trophectoderm gives rise to 3 main types of trophoblast
-cytotrophoblasts (villous cytotrophoblast)
-fusion of these form syncytiotrophoblasts (multinucleate very invasive)
Extravillous trophoblasts EVT: interstitial, or endovascular
Implanting embryo at ~day 15
O2 and nutrients reach the developing embryo by diffusion from the surrounding decidua (histiotrophic nutrition)
The initial phases of development occur at low O2 tensions
Lacunae formation
Lacunae form in the syncytiotrophoblast
Syncytiotrophoblast invades and erodes maternal capillaries
These anastomose with trophoblast lacunae to form sinusoids
Intervillous space develops
Start of villous development
Primary villi
Day 11-13 cytotrophoblasts invade
Cytotrophoblast extend invade into syncytiotrophoblast layer form finger like projections in the decidua
Primary villi cover the entire surface of blastocyst
Secondary villi
Extra embryonic mesoderm (mesoblast) invades core of primary villous day 16
Mesoderm covers the entire surface of the chorionic sac
Villi continue to extend into the decidua between the blood filled lacunae/sinusoids
Tertiary villi
Mesodermal cells differentiate to form endothelial cells and other cell types
Blood vessels form an arteriocapillary network in the villi
These vessels fuse with developing vessels in the stalk- to link the foetal blood system via invading vessels from the umbilical cord
Structure of mature placental villi
Stem villi- basal part of villi- attached to chorionic plate
Branch/intermediate villi- project from sides of stem villi
Terminal villi- swellings at the tips of branch villi contain terminal vessels- form convoluted knots where the majority of exchange takes place- continue to be produced throughout gestation
The cytotrophoblast layer becomes very thin but remains mostly intact 80% coverage in full term placenta
Remodelling of the maternal blood vessels
Essential to establish a low resistance high flow blood supply to the intervillous space
Critical for normal pregnancy
Spiral arteries:
-resistance vessels supplying the endometrium/decidua
-coiled appearance in the inner myometrium and decidua
-100-150 arteries are transformed
-diameter is increased 10 fold
Extravillous trophoblast outgrowth
First trimester:
-cytotrophoblast columns form at tips of anchoring villi
-Extravillous trophoblasts EVT differentiate and form interstitial and endovascular EVT
EVT invade the decidua and occlude the spiral arteries
Replace the endothelium and smooth muscle cells forming the endovascular trophoblast layer
Establish normal utero placental dynamics
Anchoring villi- cross the intervillous space- migrate deeply and attach to maternal decidua
EVT plug spiral arteries- reduce blood flow to the developing placenta
Creates low oxygen environment- protects fetus from oxidative stress
EVT plugs breakdown initiating blood flow to intervillous space>14 weeks
UNK ~70% of inflammatory cells in decidua- produce many cytokines and initiate/promote remodelling
Vessels remodel outwards, lay down lots fibroid material, ECM, rigid structures. SMC undergo apoptosis or de differentiate migrate away
Phases of nutrition
Histiotrophic phase: week 8 [O2]=20mmHg
Placental perfusion- initiated week 12-14
Haemotrophic phases: week 14 [O2]=60mmHg
Maternal adaptations to meet the increasing oxygen/nutrient demand of the growing fetus
Increased maternal blood volume ~40% during first trimester
Uterine blood flow increases ~20 fold during pregnancy via uterine (and ovarian) arteries
Cardiac output increases by 30-40%
->25% cardiac output goes to placenta
Heart rate increases 10-15bpm
Increased ventilation rate
Fetal blood flow in placenta
Umbilical arteries (deoxygenated)
Fetal capillaries within villi: stem villi, intermediate, terminal
Umbilical vein (oxygenated)
Transport across the placenta
Parabiotic relationship between mother and fetus:
-fetus is dependent on maternal provision of nutrition, O2, salts, organic precursors etc and removal waste products CO2, urea etc across the placenta
Diffusion: O2, CO2, Na+, urea, fatty acids, sugars (facilitated), non conjugated steroids, thyroxine T4
Active transport: amino acids, iron, ca2+
Not transported: conjugated steroids most bacteria
Harmful: cocaine, alcohol, caffeine, tetracycline,
Placental barrier
Haemotrophic nutrition >wk 14- maternal blood delivers nutrients to fetal circulation across the placenta
~3-4cell layers separate the maternal and fetal circulations: syncytiotrophoblast, cytotrophoblasts, connective tissue, fetal capillary endothelium
The intervillous spaces of a mature placenta contains ~150ml of blood exchanged 3-4x every minute
Gas exchange across the placenta
O2 and CO2 by passive diffusion
~40% more haemoglobin in fetal blood vs adult
Fetal haemoglobin ~80% late gestation
Higher affinity for O2 achieves saturation at lower pO2
-pO2 40-50mmHg ~90% Fetal Hb staurated, ~60% adult
Simultaneous movement of CO2 on a concentration gradient back to the mother
Double Bohr effect results in increase of ph on fetal side- promotes uptake at lower PO2
Glucose carbohydrate metabolism
Uptake by insulin insensitive hexose transporters GLUT3 GLUT1
Maternal insulin regulates glucose- increases glycogen and adipose stores
Maternal tissues show insulin insensitivity/resistance (due to human placental lactogen) promoting transfer of blood glucose to placenta
Glucose is also metabolised to lactate which is used as an energy sourced by the fetus
Amino acids and urea
Fetus regulates maternal amino acids metabolism through progesterone
Mother retains extra amino acids and transports them to fetal circulation
Some are metabolised eg serine-> glycine
Fetal urea diffuses passively into the maternal blood
Water and electrolytes
Exchange in water occurs in placenta and non placental chorion at the amnion- amniotic fluid increases from 15ml at 8 wks to 450ml at wk 20, net production decreases to 0 by wk 34
Na+ and other electrolytes transfer readily across placenta
Iron: in fetal and maternal blood both free and bound to transferrin, enhanced absorption (10% 1st tri, to 30% 3rd) to cover loss to fetus, placenta, blood loss in labour
Calcium: demand for fetal ossification in 3rd trimester, Ca2+ absorption is enhanced and transferred to fetal circulation
Vitamins: folic acid and vit B12
The syncytiotrophoblast is the primary barrier
Lipids: extracellular lipases release fatty acids from maternal lipoproteins- intracellular binding proteins FABPs transport the fatty acids in the cytosol of the syncytiotrophoblast
Maternal antibodies
IgG transferred by pinocytosis
Provide passive post natal immunity:
-diphtheria
-small pox
-measles
-chicken pox
-whooping cough
Infectious agents that cross the placenta
Viruses:
-CMV
-rubella
-coxsackie- hand foot and mouth
-varicella
-polio
-HIV
Bacteria:
-spirochetes
-syphilis, listeria, lymes disease
Protozoa:
-toxoplasma
-toxoplasma gondii
Poor EVT invasions of the maternal spiral arteries
Migration of EVTs is under tight temporal-spatial control- disturbances in this process can result in significant loss of placental function
IUGR/early onset pre-eclampsia due to insufficient penetration by EVTs shallow invasions of decidua
Premature loss of EVT plugs in spiral arterioles- early initiation of blood flow to placenta may lead to miscarriage
Disturbed placental blood flow in placental insufficiency
Leads to high pressure flow
Vasoconstriction- pulsatile flow
Ischaemia reperfusion injury/oxidative stress
Damage to villi
Failure to fully remodel maternal spiral arterioles
-in PE reduced external myometrial spiral artery diameter
Pre eclampsia
Maternal systemic syndrome caused by abnormal placentation in the first trimester- clinical symptoms present from 20 weeks onwards
3-5% pregnancies in west
-severe early onset PE<32 weeks -0.5%
~30% PE cases associated with IUGR
Only cure delivery placenta
Maternal symptoms of pre eclampsia
Symptoms develop in 2nd-3rd trimester <20wks
Hypertension >140/90mmHg 2 readings >4hrs apart
Proteinuria >300mg/l 2+ dipstick
Headache
HELLP (haemolysis, elevated liver enzymes, low platelets syndrome 20% cases)
Disseminated intravascular coagulopathy DIC 20% HELLP cases
Seizures- eclampsia
Early onset <32wks tends to be more severe
Risk factors for PE
7-fold greater is previous PE pregnancy
Maternal or paternal history PE
Increased inter pregnancy interval
Multiple gestation
Maternal age>40
Insulin resistance, diabetes, obesity, metabolic syndrome, vascular inflammation, pre existing hypertension
Underlying pathology in pre eclampsia
Placenta:
-abnormal trophoblast invasion
-reduced differentiation and transport
-altered trophoblast secretions
-enhanced trophoblast apoptosis
-increased fibrin deposition
Maternal: systemic endothelial activation, systemic inflammatory response
Intra-uterine growth restriction IUGR
Occurs in 8-14% of normal pregnancies- associated with pregnancy induced hypertension particularly early onset PE
Blood flow to both sides placenta compromised
O2 passes across by simple diffusion- reduced flow leads to fetal hypoxia
Glucose transfer is generally not affected by
Reduced fatty acid transfer
Amino acid transport compromised
-lysine, taurine, leucine, phenylalanine reduced in fetal plasma
Reduced ion transport
Acidosis-increased fetal lactate levels
Reduced bone mineralisation in 3rd trimester
Placenta previa
3-6 per 1000
Blastocyst usually implants high on posterior wall of uterus
Increased risk of placental abruption/haemorrhage
Marginal type II/III, complete IV, low lying I
Classified as degree of coverage of cervix
Placenta accreta
Results from excessive trophoblast invasion
Placenta invades and is inseparable from uterine wall 3 in 1000
Identified before parturition on US
Can lead to vaginal bleeding in 3rd trimester
Associated cases of placenta previa
Associated with myometrial scarring from previous C sections
Risk of maternal haemorrhage
Pre term C section/hysterectomy
