Pregnancy Complications, Fetal Morbidity And Assisted Reproduction Flashcards
Hypertension during pregnancy
5-10% of pregnancies
BP > 140/90 on 2 occasions 6 hours apart
Hypertension needs to be controlled to prevent organ damage in long term
Hypertension present at booking is not pre eclampsia
What is chronic hypertension
Present at booking or before 20 weeks
No significant proteinuria
What is gestational hypertension
Presenting after 20 weeks with no significant proteinuria
What is pre eclampsia
Hypertension present at 20 weeks and significant proteinuria
Caused by pregnancy
Cured by delivery of placenta
Endothelial cell disorder
Excessive inflammatory response to pregnancy
Features of pre eclampsia
Hypertension Proteinuria Oedema Multi organ involvement Fetal compromise
Risk factors socio demographic for pre eclampsia
Extremes of reproductive age
Ethnic groups
Risk factors for pre eclampsia (pregnancy factors)
Multiple pregnancy
Primigravida
Assisted conception
Previous pre eclampsia
Abnormal placentation
Trophoblast cells fail to invade into maternal endometrium and myometrium
Maternal spinal arteries: persistent thick muscular walls
Reduced perfusion of placenta with maternal blood and possible vasospasm
Leads to increased apoptosis (cell death)
Release of circulating factors or placental syncytial fragments
Endothelial cell dysfunction
Increased capillary permeability - tissue oedema
Hypertension secondary to disturbed control of vascular tone by endothelial cells
Altered production of vasodilator substances
Clotting dysfunction secondary to abnormal production of procoagulants by endothelial cells, activation and clumping of platelets
Plasma volume loss and organ hypoperfusion
Symptoms of pre eclampsia
Headache: usually frontal but may be occipital due to cerebral oedema and hypertension
Visual disturbances: blurred, flashes of light or blindness
Epigastric or right upper quadrant pain due to enlargement of subcapsular haemorrhage of liver
Nausea and vomiting due to congestion of gastric mucosa and or cerebral oedema
Oliguria or anuria due to kidney pathology
Maternal complications of pre eclampsia
Neurological: seizures, retinal detachments, cortical blindness, intra cerebral or subarachnoid haemorrhage
Cardiovascular complications of pre eclampsia
LVF, pulmonary oedema, hypertension
Fetal complications of pre eclampsia
Asymmetrical FGR Intrauterine hypoxia Prematurity Abruption Still birth Hypertension / metabolic disease in later life
Maternal monitoring for pre eclampsia
BP 4-6 hourly Urinalysis Symptoms and signs Blood tests (FBC, U&E, LFT, fibrinogen) Fluid balance
Fetal monitoring for pre eclampsia
Movements U/S Size and growth Umbilical artery Doppler Liquor volumes Biophysical tests CTG >26 weeks monitoring of fetal heart beat
Drug targets for pre eclampsia
Aim to keep BP <150/100mmHG
Decreases the maternal cerebral and cardiovascular complications but not fetal outcomes
Consider MgSO4 to reduce risk of seizures and mortality
Death rate is now less than 1:1,000,000
How often should you test sugars in diabetes in pregnancy
Depends on severity but usually before and after a meal and before bedtime (7 times)
Changes in carbohydrate metabolism in normal pregnancy
Feto placental unit uses glucose therefore lower fasting blood glucose
Peripheral resistance to effects of insulin due to hormones eg HPL from the placenta, oestrogen, progesterone, cortisol
Insulin resistance increases with gestation
Mostly higher post prandial glucose
Diabetes occurs if B cells of pancreas are unable to produce sufficient insulin to prevent hyperglycaemia
Prevalence of diabetes in pregnancy
5-10% of all pregnancies in UK
Screening for gestational diabetes
Incidence increasing
Selective screening misses up to 30% of cases
Test: 2 hour 75g oral glucose tolerance test 24-28 weeks
Risk factors for GDM
BMI above 30
Previous macrosmic baby weighing mroe than 4.5kg
Previous gestational diabetes
First degree relative with diabetes
Family origin with high prevalence eg south Asian, black Caribbean or Middle Eastern
Effect of pregnancy on diabetes
Greater importance of tight glucose control (target HbA1c <6,5%)
Change in eating pattern
Hypoglycaemia more common
May lose warning signs for hypos (vomiting)
Increase in insulin dose requirements at 18-28 weeks
Increased risk of severe hypoglycaemia
Risk of deterioration in pre existing retinopathy
Risk of deterioration of established nephropathy
Lower renal threshold for glycosuria
How to achieve good glycaemic control
Regular meals and snacks including late night supper (high fibre improves maternal sensitivity to insulin)
Regular capillary blood glucose tests
Medication, often multiple injections of insulin
Effects of diabetes on pregnancy
Hypoglycaemia UTI Recurrent vulvovaginal candidiasis Pregnancy induced hypertension / pre eclampsia Pre term labour Obstructed labour Operative deliveries Increased retinopathy Increased nephropathy Cardiac disease
Fetal growth in diabetes disorders
Macrosomia is >90th centile birth of more than 4000g
What is asignificant proteinuria
> 300mg protein in a 24 hour urine collection or >30mg/ml in a spot urinary protein: creatinine sample
Personal medical history risk factors for pre eclampsia
Obesity Chronic renal disease Chronic hypertension DM and connective tissue diseases Certain thrombophilia
Respiratory maternal complications of pre eclampsia
Laryngeal oedema, respiratory distress syndrome (ARDS)
Hepatic maternal complications of pre eclampsia
Hepatocellular dysfunction, ischaemia pain, subcapsular haemorrhage and liver rupture
Renal maternal complications of pre eclampsia
Oliguria, renal failure (cortical or tubular necrosis)
Haematological maternal complications of pre eclampsia
Thrombocytopaenia, haemolytic, HELLP, DIC, thromboembolism
Drugs used fore emergency blood pressure control
Hydralazine, labetalol, nifedipine SR
Lifestyle changes as a first line Rx in GDM
Diet:
1 hour post prandial glucose strongly associated with birth weight: target level 7.8mmol/L
Inverse relationship between birth weight and proportion of dietary energy obtained from carbohydrate
Exercise: beneficial effects on glucose metabolism and reduces weight gain
Fetal growth in diabetes
High maternal blood glucose crosses placenta and stimulates fetal insulin production which acts as a growth promoter (bone, muscle, adipose tissue)
Excess glucose is laid down as glycogen in liver and adipose tissue
Different parts of the ovary
Outer covering of epithelium continuous with pelvic peritoneum
Stroma: support and hormones
Gamete producing structures
Different parts of the cervix
Endocervix: mucus secreting columnar epithelium
Ectocervix: stratified squamous epithelium
Different parts of uterus
1) endometrium - cuboidal epithelium overlying stroma
2) myometrium : smooth muscle
Most common type of tumour in the uterus
Affects the endometrium (glands) most often an adenocarcinoma
Normal cellular changes in the cervix
Occur at puberty, pregnancy and cyclical changes
Repositioning of the squamo-columnar junction exposes columnar cells to low pH environment of the vagina
Red appearance of exposed columnar cells - ectopy
Squamous metaplasia of cells in this transformation zone
These cells are vulnerable to dysplasia and neoplasia
Abnormal cellular changes in the cervix
Detected by Pap smear
‘Smear’ of desquamated cells on a slide from a spatula (being replaced by liquid cytology)
CN I - mild dysplasia (lower 1/3 epithelial thickness)
CIN II- moderate dysplasia (lower 2/3 epithelial thickness)
CIN III- severe dysplasia and carcinoma in situ (upper 1/3 and full thickness but intact BM)
Appearance of CIN cells
Increased nuclear to cytoplasmic ratio, clumped chromatin and a clear zone around the nucleus indicative of HPV infection
What does CIN stand for
Cervical intraepithelail neoplasia
Cervical cancer risk factors
Sexual intercourse (HPV infection) Age of first intercourse History of STD Socioecomic status Smoking
What are uterine neoplasms
Benign
- polyps (epithelial)
- fibroids (smooth muscle - leiomyoma)
Malignant - uterine carcinoma - risk factors: Obesity Diabetes Hypertension Infertility
What is endometriosis
Ectopic and endometrial material that is under the influence of cyclic hormones
Occurs anywhere but commonly in Fallopian tubes and Adnexa
Theories include retrograde menstruation / differentiation of stem cells
Up to 10% of women
Can be very disabling and painful even when just a few foci are present
Leads to chronic cyclical inflammation, scarring and adhesions
May impact fertility
Describe ovarian tumours
5th most common cancer in women
5th cause of cancer death in women
Complex pathology due to abundance of pluripotent and totipotent cell types
Risk factors:
Nuliparity
Family history BRAC1 and 2 gene mutations
Where are ovarian tumours derived from
Surface epithelium 70%
Stroma 10%
Follicles (germ cells) 20%
Metastases from elsewhere
Presenting symptoms: none until advanced
Staging, treatment and prognosis as we go along
Staging of ovarian cancer
Stage 1: limited to ovary
Stage 2: involvement of other pelvic structures
Stage 3: intra abdominal spread beyond pelvis
Stage 4: distant metastases
What are teratomas
Neoplasms of germ cell origin
90% are benign and occur in patients <20
Mixture of mature tissues mainly derived from ectoderm- hair, skin, skin appendages and teeth
Can occasionally have tissues derived from endoderm and mesoderm
Presence of immature (less differentiated) tissues indicates malignancy - rare
Functions of breast
Provision of food
Provision of nursing, extended period of parental care and proximity
Risk factors for breast cancer
Cyclical changes in oestrogen and progesterone
Ageing
Can be hereditary (mutation in BRCA1 and BRCA2 genes- more frequent screening - mammography and MRI)
Describe area of breast
Highly modified area of skin with specialised sweat glands which produce nutritious secretions under hormonal influences
Ductal system within a mammary lobule
Each ductal system in a lobule ends in a cluster of blind ending terminal ductules. These blind ends will transform to alveoli at pregnancy and produce milk at lactation
Nipple, lactiferous duct and extra lobular ductal system
Extra lobular ducts from mammary lobules drain into lactiferous ducts
Lactiferous sinus (dilated milk can gather here during lactation)
Lactiferous duct opening into nipple (arranged in a ring, normally plugged with keratin)
Nipple (pigmented, raised skin which darkens after pregnancy)
Areola (melanin pigmentation, sebaceous gland and pressure receptors)
Development of the breast
1) fetus / neonate, male / female before puberty. Minimal ductal system
2) puberty- branching of ductal system, blind ends of ducts form small solid spheroidal masses of cells. Increase in fibrocollagenous and adipose tissue with successive exposure to oestrogen
3) pregnancy - formation of alveoli in terminal ductules. Hypertrophy of ductal lobular alveolar system.
4) lactating breast: secretion of milk from alveoli. Pituitary prolactin and oxytocin
5) resting - regressing of alveoli and ductal system
Breast changes in pregnancy
Under the influence of the placental hormones: progesterone, oestrogen, prolactin
Increase in vascularity and melanin pigmentation in the nipple and areola
Hyperplastic proliferation of terminal ductile epithelium, vacuoles in luminal epithelial cells, formation of true alveoli
2nd and 3rd trimester of pregnancy: increasing lipid rich proteinaceous secretion into alveoli
Increase in support tissue
Lactating breast (after parturition)
After parturition, progesterone levels drop, prolactin receptors are now expressed on surface of breast alveolar cells
True milk production can begin
What is milk fat
Synthesised in the smooth ER of the alveolar epithelial cells
Membrane bound droplets traffic towards the lumen
Droplets pinched off and released
Milk protein passes through golgi system into vacuoles and is released by exocytosis to the lumen
Female breast in resting (non secreting state)
Alveoli can still be distinguished
Evidence of mechanical atrophy
Alveolar distension, capillary occlusion and alveolar hypoxia leads to gradual involution. The ductule system rather than alveolar system again predominates
Preparations for postnatal nutrition
1) inhibition of expression of prolactin receptors by pregnancy levels of oestrogen and progesterone. This makes placental prolactin ineffective as far as lactogenesis is concerned
2) the drop in levels of oestrogen and progesterone after expulsion of placenta allows dominance of mothers pituitary prolactin and this activates alveolar prolactin receptors
Suckling induced reflex
When baby suckles, sensory information causes release of the neuropeptide prolactin from anterior lobe of pituitary gland. This then causes more milk production
Nipple stimulation by sucking is essential for keeping prolactin levels high
Strength and duration of suckling influences amount of prolactin released
Cessation of breast feeding results in inhibition of lactation
Psychosocial advantages of breast milk
Breastfeeding enhances attachment; frequent direct skin, smell, visual contact between newborn and mother
Disadvantages of breast feeding
Most drugs and alcohol taken by mother are transmitted through breast milk
Mums poor nutritional, physical or mental health or personal aversion to breast feeding may be a contraindication to nursing
Transmission of HIV can be halved by bottle feeding
(WHO recommends breast feeding up to 12 months with anti viral treatment)
What is gestational preparatory behaviour
Nest building
What is post parturient behaviour
Providing warmth, comfort, food and protection
Baby: need for contact, clinging, olfactory and rooting response in babies, characteristic cry patterns
Retrieval from harm, carrying baby with you etc
What is weaning behaviour
Leads to gradual gain of independence
Mother / fathers proximity allows infants to resolve explore-retreat tendencies
Why are infections different in pregnancy
Physiological / immunological changes may increase susceptibility eg stasis in urinary tract and alter clinical manifestations
Many drugs are contraindicated in pregnancy
Consequences of infections in pregnancy
Infection of the fetus may have catastrophic consequences on fetal development
Neonatal immune systems not fully mature at birth, therefore infection may be devastating
Congenital infection may give rise to long term life threatening consequences eg blood borne viruses
UTI in pregnant women
May be asymptomatic
May lead to pyelonephritis
Women are screened during pregnancy so can be detected early
Varicella (chickenpox) in pregnant woman
More dangerous
Can cause varicella pneumonia ( more likely in pregnancy)
Antivirals are not licensed for use in pregnancy
Cytomegalovirus (CMV) in pregnancy
Common infection
Almost always asymptomatic but can be life threatening in pregnancy - can cross placenta and infect fetus
Baby born with rash and hepatomegaly and enlarged spleen
3-4 per 1000 live births
5-10% half evident at birth
5% minor eg unilateral deafness
Why is screening of CMV not advocated
1) there is no sensible advice to give to seronegative women
2) recurrent CMV infection may also cause symptomatic congenital infection
Maternal rash in pregnancy
Must exclude maternal rubella - risk of congenital rubella syndrome - cataracts, heart problems
First 12 weeks - baby severely affected
12-18 weeks - most likely deafness
After 18 weeks - no risk
Parvovirus B19
Most likely diagnosis with a maternal rash in pregnancy
- no congenital parvovirus syndrome
Increased risk of miscarriage (if not baby will be fine)
Can cause fetal hydrops ( affects cells that cause red blood cells - baby becomes anemic - heart failure - fluid retention)
Congenital toxoplasmosis
Transplacental transmission during maternal infection - risk increases with duration of pregnancy
Leads to brain damage, choroido-retinitis (may not present until later in life) carried in cat faeces, pregnant women advised not to change cat litter
Risk of fetal damage greatest in early pregnancy
Congenital syphilis
May be multi system
Range of clinical features which present at 5-15 years
Hence routine antenatal screening and treatment
Congenital varicella aka varicella embryopathy
Skin loss, scarring, usually unilateral, segmented
Impaired limb bud development
Many others, less specific features eg microcephaly, cataracts
Zika virus infection
Outbreak in Brazil with coincident rise in reports of microcephaly
Evidence linking zika to fetal damage is convincing
Magnitude of risk unknown likely to be in the order of 1-10% if maternal infection in first trimester- impairment of brain development
Blood borne virus infections
HIV
Hep B, C
Transmission may arise antenatally, perinatally (birth canal), postnatally
Mother to baby HIV
Overall risk around 20%
Almost entirely preventable by maternal antiretroviral therapy to reduce viral load
Elective c section
No breast feeding
Mother to baby hep B
Neonatal infection leads to very high carriage rates
Preventable by vaccine
Mother to baby hep C
Rates very low compared to hep B eg 3-5%
No intervention
Therefore no rationale for screening
Neonatal septicaemia / meningitis
Baby coming out of birth canal may be contaminated with organisms from maternal gut
Group B streptococcus, E. coli
Known carried of group B strep are given antibiotics during labour
Group B strep
Important cause of neonatal pneumonia septicaemia and meningitis
Commonly found as normal GI flora
Colonises perineum / vagina in around 1/4 pregnant women
If colonised risk of c. 1/200 of neonatal infection
IV antibiotics during delivery reduces risk to 1/4000
Management of maternal chickenpox in late pregnancy
Delivery > 7 days after onset maternal rash - nothing
VZIg to neonates born within 7 days of onset of maternal rash
Prophylactic acyclovir
Neonatal herpes
Most infections acquired from primary maternal genital herpes at term
50% cases have internally disseminated infection without external lesions
Transmitted by someone with a cold sore kissing a baby
Opthalmia neonatorum
Infection of conjunctivae with discharge
Caused by gonorrhoea or staphylococcus - acquired from mother
Can cause neonatal pneumonia
What does it mean if there is a break or a crack in Shentons line
A sign of a femoral neck fracture
Air in X-rays
Should only be seen in stomach, bowel and lung bases
Air outside of these regions is invariably pathological
Appearance of free air can differ according to the position of the patient
Why is good communication with children important
Makes treatment easier
Child more cooperative, less upset, mroe likely to follow instructions
Helps doctor reach a better understanding of child’s condition
Promotes health literacy - helps child to understand about illness and treatment therefore child will be less frightened, better able to make informed decisions
What is Piagets theory of childrens thinking stages
Young children
Age 18months - 6/7 years (pre operational)
Found confusion about causation of illness eg get a cold from trees so may view treatment or pain as a punishment
Usually define illness by its external signs eg heart attack is falling on your back
What is piagets theory of children thinking (age 7-11)
More sophisticated understanding of causation but may be preoccupied by contamination eg germs
Still tend not to think about under the skin
Still difficulties with abstract reasoning eg implications for future
Eg concepts of health promotion
What is piagets theory of childrens thinking age 11+
Formal operational thinking
Ability to reason about using abstract ideas
Useful for understanding the unobservable ie germs, DNA
Ability to start forming hypothesis (will be able to consider different treatment options)
What is the role of ‘able instruction’
Vygotsky accepted piagets stage theory but argued that children could be helped to understand new information
The teacher provides scaffolding to allow child to build an existing understanding
Examples of adverse pregnancy conditions or sub optimal intrauterine conditions
Poor maternal diet (low calorie/ low protein / high saturated fats)
Maternal stress (cortisol can cross placenta)
Hypoxia - smoking
Drugs / endocrine disrupting chemicals / alcohol abuse
Consequences to placenta of sub optimal intrauterine conditions
Placental insufficiency: poor placental growth, poor transport mechanisms, impaired barrier properties, vascular dysfunction, aberrant invasion, increased cortisol secretion, growth factor secretions
Consequences to offspring of sub optimal intrauterine conditions
Small baby and intra uterine growth restriction, metabolic changes, altered neurological development
Catch up growth in infants, obesity in children
Impaired glucose tolerance, insulin resistance, dyslipidemia, obesity, T2 diabetes, metbaolic syndrome when adult
What is catch up growth
Small baby will try to catch up with growth when born but can then lead to obesity in childhood
Reasons for low birth weight
Preterm pregnancy Multiple pregnancy Placental insuffiency (maternal height) Genetics Sub optimal maternal environment
What does IUGR stand for
Intrauterine growth restriction
What does small for date mean
2 standard deviations below the expected weight at a particular gestational age using population growth centile charts
Fetal physiology : oxygen and CO2
Fetus needs oxygen in relatively small continuous supply
Fetal stores of oxygen are very small
3kg fetus near term needs 18ml O2/min but stores 36ml, 2 mins worth of oxygen
Difference between adult haemoglobin and fetal haemoglobin
Adult has 2 a and 2 B globin chains
Fetal has 2 alpha, 2 gamma globin chains. At any given time HbF has a higher affinity to and will bind more O2 than maternal Hb leading to high oxygen saturation of fetal blood
When does the switch from HbF to HbA occur
Several months after birth
What factors mitigate the fact that a fetus can only store 2 minutes worth of oxygen
Oxygen tension: PO2 in umbilical vein is low relative to PO2 in maternal blood so oxygen readily diffuses across placenta from mother to fetus
CO2 tension: CO2 from fetal metabolism diffuses back across the placenta as PCO2 is always higher in umbilical artery and vein compared to maternal blood
O2 saturation is always higher in fetal blood - 70%. Different O2 trapping property
Describe the double Bohr effect as an oxygen trapping property of fetal blood
Uptake of fetal CO2 by maternal blood leads to a fall in the pH of maternal blood. This drives release of maternal O2
At the same time the rise in fetal pH due to removal of its CO2 facilitates uptake of O2
This facilitates transfer of extra 10% oxygen in the fetal direction
Fetal response to maternal nutrition stress
There is a survival value for selecting genes that reduce fetal growth in response to maternal nutritional stress as a way of preparing the offspring for optimised survival in a resource poor world
Role of placenta nutrient sensor
Can upregulate or downregulate transport of nutrients. Eg amino acid transport is down regulated prior to IUGR in rats fed a low protein diet
What is the barker hypothesis
Lower the weight of the baby at birth and during infancy the higher the risk for coronary heart disease in later life
Other studies have shown that low birth weight is associated with increased risk of hypertension, stroke and T2 diabetes
Define epigenetics
Mechanism of regulating gene expression, maintained across cell divisions without altering DNA sequence itself
Define epigenome
The machinery that regulates gene expression and thus may alter phenotype
Gene silencing due to DNA methylation or histone modification
How do epigenetic modifications to chromatin occur
1) DNA methylation
2) histone modification
3) chromatin remodelling through non coding RNAs
Describe DNA methylation
Addition of a methyl group to a cytosine residue on a cytosine-guanine dinucleotide. In mammals nearly all DNA coding for genes have methylated CpG dinucleotides
Describe histone modification
Binding of acetyl or methyl groups to histone tails altering wrapping of DNA
When can epigenetic modifications occur
1) epigenetic reprogramming during gametogenesis
Behind uniparental imprinting of alleles. Genes affected by epigenetic changes in the spermatogenic lineage differ from those imprinted in the oogenetic lineage
2) epigenetics in early development: important dpi-genetic processes can occur during development in the periconceptual period
3) epigenetics after fertilisation: upon fertilisation there is rapid demethylation of the entire parental genome in all genes. However some genes remain imprinted (1% of genes in the genome)
Epigenetic mechanisms can be modulated throughout life
Twin studies: monozygotic twins with different environmental exposures resulting in different phenotypes regardless of identical genomes
Roles of growth factors
Insulin like growth factors 1 and 2 are produced by fetal cells (inc placenta) synthesis of both rise with pregnancy (IGF2 is 2-3 fold higher)
IGF1- production is reposnsive to nutrient levels, declining when nutrients fall. It is sensitive to insulin, thyroxine, glucocorticoids (matching fetal growth to nutrient supply)
IGF2 stimulates placental growth and transport mechanisms - optimal transplacental transport of nutrients is essential for fetal growth
Why is IGF2 a paternally expressed gene
Argued to result from males dominating an evolutionary conflict controlling the extent of resources which are extracted from the mother
Expression of fathers allele in humans favours a bigger baby where’s expression of mothers allele favours a smaller child
Define altruism
A behaviour benefitting another individual which incurs a direct cost for the individual performing the altruistic action
Purpose of antenatal care
Used to detect early signs of complications, followed by a timely intervention if any found
Focuses on educating the pregnant woman on a range of topics including wellbeing, birth preparedness, complication readiness and breastfeeding
What is the neural tube
The embryonic precursor to the central nervous system
Closed by day 28 (4th week)
Folic acid supplements reduces the risk of neural tube defects
Vitamin D supplementation in pregnancy
10 mcg daily in high risk groups
Needed for our bowel to absorb sufficient quantities of phosphate and calcium
Essential for adequate bone mineralisation
Deficiency results in rickets in children and osteomalacia in adults, neonatal tetany
What are the different screening tests done before 10 weeks
Sickle cell anaemia and thalassaemia
What are the screening tests done at 8-10 weeks
HIV
Hep B
Syphilis
Blood group and rhesus status
What are the screening tests done at 11-14 weeks
Downs
Edwards
Patau’s
What happens if an Rh- mother is carrying a Rh + fetus
Father is Rh+
Rh antigens from developing fetus can enter the mothers blood during delivery
The mother will produce anti Rh antibodies
If the woman becomes pregnant with another Rh+ fetus her anti Rh antibodies will cross the placenta and damage fetal red blood cells
How is rhesus disease prevented
15% of population are rhesus negative
Prevent rhesus disease by giving the mother anti Rh immunoglobulin
Without this 16% of women become sensitised
Screening for trisomies (presence of an extra chromosome)
Combined test 10-14 weeks
Blood test and an ultrasound to measure nuchal translucency
Diagnostic test: amniocentesis (from 15 weeks)
Chorionic villus sampling (11-14 weeks)
How does non invasive prenatal testing (NIPT) for trisomies work
Works by analysing the DNA fragments in the maternal blood during pregnancy = cell free dna
Most comes from the mother but around 10-20% of it comes from the placenta which is representative of the unborn baby (cell free fetal DNA)
Screening for HIV
Universal HIV screening introduced in 1999- 97% uptake
1200 women per year in UK
Risk of mother to child transmission with undiagnosed = 25%
Risk with diagnosed HIV and appropriate management = 0.27%
1) viral suppression (combination anti retro viral therapy)
2) mode of delivery (C section)
3) not breastfeeding
4) ART for neonate
Screening for syphilis
Universal antenatal syphilis screening 97% uptake
Congenital syphilis almost entirely preventable
Single dose of IM penicillin
Risk of smoking during pregnancy
11% of pregnant women in UK smoke at the time of giving birth
Increases vascular resistance in the placenta and impairs oxygen exchange
Causes up to 2200 premature births, 5000 miscarriages and 300 perinatal deaths every year in UK
Fetus more likely to have low birth weight, ENT problems, respiratory conditions, obesity or diabetes
Complications of pre eclampsia
Maternal: fits, HELLP syndrome (rare liver and blood clotting disorder), stroke, liver failure, renal failure, pulmonary oedema
Fetal: fetal growth restriction, stillbirth, prematurity
High risk factors for pre eclampsia
Hypertensive disease in a previous pregnancy
Chronic kidney disease
Autoimmune disease such as systemic lupus erythematosus or antiphospholipid syndrome
T1 or T2 diabetes
Chronic hypertension
Moderate risk factors for pre eclampsia
First pregnancy
Age 40+
Pregnancy interval of more than 10 years
BMI of 35kg/m2 or more at first visit
Family history of pre eclampsia
Multiple pregnancy
Prevention of pre eclampsia
Low dose aspirin
75mg daily
What is gestational diabetes
Diabetes that occurs during pregnancy and disappears after giving birth
5% of all pregnant women
Screen high risk groups at 28 weeks with an oral glucose tolerance test
Majority of women treated with dietary changes
10% of women require metformin and / or insulin
Complications of gestational diabetes
Maternal: pre eclampsia; polyhydramnios; prolonged labour, obstructed labour; Caesarean section; uterine atony; postpartum haemorrhage
Fetal: congenital abnormalities; fetal macrosomia; stillbirth; birth injuries ; neonatal hypoglycaemia
What is fetal growth restriction
3% of all pregnancies
Condition in which fetus’ growth slows or stops during pregnancy
Majority of cases due to placental dysfunction
Benefit of folic acid supplementation
Reduces risk of neural tube defects
Benefit of vitamin D supplementation
Deficiency results in rickets (children) and osteomalacia (adults), neonatal tetany
Define intrauterine growth restriction (IUGR)
Birth weight <2.5kg
Define macrosomia
Birth weight > 4kg
Changes in carbohydrate metabolism in normal pregnancy
Foetus uses glucose, lower fasting maternal blood glucose
Insulin resistance increases with gestation, peripheral insulin resistance due to hormones
Diabetes occurs if B cells of pancreas are unable to produce sufficient insulin to prevent hyperglycaemia
List potential neonatal complications (diabetes)
Respiratory distress syndrome Polycythaemia Hyperbilirubinaemia and jaundice Hypoglycaemia Hypocalcaemia Hypomagnesaemia Hypothermia Cardiomegaly Birth trauma Delayed gastric emptying
Why is the risk of macrosomia higher due to diabetes mellitus
High maternal blood glucose crosses the placenta and stimulates foetal insulin production which acts as a growth promoter
Excess glucose laid down as glycogen in the liver and adipose tissue
Postnatal care for patients presenting with diabetes mellitus
Stop all hypoglycaemics, return to pre pregnnacy medication
Less tight glycaemic control
Encourage breastfeeding
Other maternal complications of diabetes
Hypoglycaemia
Retinopathy
Nephropathy
Cardiac disease
Define essential hypertension in pregnancy
Increase of 30/+ systolic mmHg or 15/+ diastolic mmHg
Indications for delivery in pre eclampsia
Hypertension remaining uncontrolled despite maximal anti-hypertensives
Eclampsia
Renal, hepatic or coagulation impairment
Pulmonary oedema
Foetal distress
Milder pre eclampsia at term
Maternal hepatic complications of pre eclampsia
Hepatocellular dysfunction
Ischaemic pain
Subcapsular haemorrhage
Liver rupture
Define severe hypertension
BP >160/110 mmHg on 2 occasions, 6 hours place
Define hypertension
BP >140/90 mmHG on 2 occasions, 6 hours place
Define significant proteinuria
> 300mg protein in a 24 hour urine collection or >30mg/mL in a spot urinary protein: creatinine sample
Different types of hypertension in pregnancy
Chronic: present at booking / before 20 weeks, no proteinuria
Gestational, present after 20 weeks, no proteinuria
Pre-eclampsia, present after 20 weeks, significant proteinuria
4 pathophysiological mechanisms in pre eclampsia
Abnormal placentation
Endothelial cell dysfunction
Organ hypoperfusion
Plasma volume loss
Which hormone is released after ovulation occurs and can be used as a marker of fertility
Progesterone as it is a sign that an egg is being released
What is haemodilution
Occurs in pregnancy because plasma volume increases by 50% and RBC increases by only 20% so even though maternal blood volume increases by 30% the ratio of plasma to RBC is unmatched
What are the key pointers of placental abruption
Age (increase in risk with age)
High parity (>5 pregnancies, >25 weeks gestation)
Onset of clincial shock
Tender, hard uterus on examination
Presenting symptoms of placental praevia
Painless vaginal bleeding
