O+G Flashcards
Common symptoms in pregnancy
Nausea Heartburn Constipation SOB Diizziness Swelling Backache Abdominal discomfort
NB: These are generally due to physiological adaptations but may be due to an underlying serious cause
Main risks of smoking during pregnancy
FGR
Preterm labour
Placental abruption
Intrauterine foetal death
When should the booking visit have taken place by?
10 weeks
Antenatal risks associated with increased BMI in pregnancy
Difficulty accurately assessing growth and anatomy of foetus
Increased risk of GDM
Hypertensive disorders of pregnancy; increased risk of chronic hypertension, gestational hypertesnion and pre-eclampsia
Increased risk of VTE
Intrapartum risks of increased BMI during pregnancy
Difficulty with analgesia (epidurals and spinal) and GA if needed
Diffuclty with monitoring in labour
Increased instrumental delivery rate
Increase C-section rate
Postnatal risks of increased BMI during pregnancy
VTE risk
Wound breakdown and infeciton
Postnatal depression
Risks to foetus of increased BMI during pregnancy
Increased congenital malformations: if BMI>40, risk of neural tube defects is three times that of a woman with BMI < 30
Macrosomia and associated complications (e.g. shoulder dystocia)
Foetal growth restriction and associated complications
Miscarriage: overall miscarriage risk is 20%, which increases to 25% if BMI>30
Stillbirth risk doubled
Increased risk of childhood obesity and diabetes later in life
RCOG dietary and exercise advide during pregnancy
Do NOT eat for two - maintain your normal portion size and try and avoid snacks
Eat fibre-rich foods such as oats, beans, lentils, grains, seeds, fruit and vegetables as well as whole grain bread, brown rice and pasta
Base your meals on starchy foods such as potatoes, bread, rice and pasta, choosing whole grain where possible
Restrict intake of fried food, drinks and confectionary high in added sugars, and other foods high in fat and sugar
Eat at least 5 portions of a variety of fruit and vegetables each day
Dieting in pregnancy is NOT recommended but controlling weight gain in pregnancy is advocated
Aerobic and strength conditioning exercises in pregnancy are considered beneficial and safe
May help recovery following delivery, reduce back and pelvic pain during pregnancy and contribute to overall wellbeing
Avoid contact sports
Pelvic floor exercises during pregnancy may reduce the risk of urinary and faecal incontinence in the future
It is safe to resume exercise after delivery once the woman feels comfortable
WHO recommendations for breastfeeding after pregnancy
Initiation of breastfeeding within an hour of birth
Exclusive breastfeeding for first 6 months of age
Continued breastfeeding beyond 6 months at least up to 2 years
Home Birth pros and cons
ADVANTAGES: familiar surroundings, no interruption of labour to go to hospital, no separation from family members, continuity of care
DISADVANTAGES: 45% of first-time mothers are transferred to hospital, poor perinatal outcome is twice as likely for home births, limited analgesic options
Midwifery units or birth centre pros and cons
ADVANTAGES: continuity of care, fewer interventions, convenient location
DISADVANTAGES: 40% of nulliparous women require transfer to a hospital birth centre, limited access to analgesic options
Hospital birth centre pros and cons
Midwives provide care during labour but doctors are available should the need arise
DISADVANTAGES: lack of continuity of care, greater likelihood of intervention
What are the risks of asymptomatic bacteriuria in pregnancy?
Increased risk of preterm prdelivery
Increased risk of pyelonpehritis during pregnancy
An MSU should be sent for culture and sensitivity at the booking visit as a screening test
What is urine screened for at every antenatal visit?
Protein- detect renal disease or pre-eclampsia
Persistent glycosuria- pre-existing diabetes or GDM
Nitrites- detect UTIs (If nitrites are detected, an MSU is sent for MC+S to detect asymptomatic bareiuria. Treatment will be initiated if a positive culture is found)
What happens to blood pressure during pregnancy?
BP falls a small amount in the first trimester, and will rise to pre-pregnancy levels by the end of the second trimester
Measurement of BP in first trimester also allows identification of previously undiagnosed chronic hypertension- this allow early initiation of treatment (antihypertensives and aspirin)
Booking tests in pregnancy
FBC MSU Blood group and anitbody screen Haemoglobinopathy screening Infection screen Dating scan and first trimester screening
FBC antenatal screening
Allows identification of anaemia
NOTE: anaemia in pregnancy is defined as:
FIRST trimester < 110 g/L
SECOND and THIRD trimesters < 105 g/L
POSTPARTUM < 100 g/L
If anaemia is detected, MCV should be examined to identify the likely cause
Additional investigations include B12, folate or iron studies
If iron deficiency anaemia, a trial of oral iron should be considered (an increase in Hb at 2 weeks suggests positive response)
Women with a known haemoglobinopathy should have serum ferritin checked and offered oral supplements if ferritin < 30 mcg/L
FBC may show low platelets (may be due to ITP)
Gestational thrombocytopaenia rarely present in the first trimester
NOTE: it’s more common > 28 weeks
So, a low platelet count in the first trimester warrants further investigation
A baseline platelet count is also useful later in pregnancy if the patient is suspected of having developed pre-eclampsia or HELLP syndrome
Blood group antenatal screening
Mainly to identify Rhesus D-negative women
These women should be informed about the risks of rhesus isoimmunisation and sensitisation from a RhD-positive baby
Anti-D immunoglobulin is administered (ideally < 72 hours) in cases of potential sensitising events (e.g. CVS, amniocentesis, trauma)
In pregnancies < 12 weeks, anti-D prophylaxis is only indicated if:
Ectopic pregnancy
Molar pregnancy
Therapeutic TOP
Uterine bleeding that is repeated, heavy or associated with abdominal pain
Minimum dose of anti-D = 250 IU Women who are RhD-negative are offered prophylactic anti-D at 28 weeks This can be done as a single large dose at 28 weeks Or two doses at 28 and 34 weeks RhD-negative mothers will receive anti-D postpartum once the baby has been confirmed as being RhD-positive on cord blood testing
Gestational diabetes antenatal screening
Women with previous GDM should be offered a glucose tolerance test or random blood glucose in the first trimester- this hopes to identify pre-existing diabetes that may have developed since the previous pregnancy
What is the mode of inheritance of thalassemia?
Autosomal recessive
What chromosome encodes alpha chains of haemoglobin?
Four genes, two on each chromosome 16
Severity if disease depends on the number of alpha globin genes that are mutated
Which chromosome encodes beta globin chains?
Beta chains are produced by 2 genes, one on each chromosome 11
Who is offered screening for thalassemia?
ALL pregnant women at the booking visit using the Family Origin Questionnaire and/or FBC results. Those deemed at high risk will be referred to a foetal medicine unit to discuss options for more invasive testing
Sickle cell antenatal screen
Carrier rate of sickle cell trait (HbAS) is 1 in 10 in Afro-Caribbean people
Carrier frequency of haemoglobin C trait is around 1 in 30
HbSS is the most serious form with patients suffering chronic haemolytic anaemia and acute sickle cell crises
People with HbSC have a milder features but are still at risk of sickle cell crises
Partners should also be tested if at high risk
Which diseases are screened for in the first trimester infection screen?
Rubella (screening programme has stopped due to MMR. If a woman is idenitifed as not being immune, they should be advised to avoid conact with individuals known to be currently infected. They should be offered the MMR vaccination following delivery)
Syphilis
Hepatitis B
Hepatitis C (not routinely screened- may be offered to women at high risk e.g. IVDU, HIV)
HIV
What are the risks of syphilis to the pregnancy?
Can cause miscarriage or stillbirth
Routinely screened for in pregnancy
What interventions are in place if a abby is born to a woman with active Hepatitis B?
Hepatitis B vaccine
One dose of hep B immunoglobulin within 12 hours
This confers 95% protection. Additional doses of Hepatitis B vaccine will be needed at 1 and 6 months.
What interventions are in place to minimise transmission of HIV to the foetus?
Initiation of ART by 24 weeks if naive
Planned C-section if viral load > 400 copies/ml at 36 weeks
Exclusive formula feeding from birth
Women who decline initial screening should be offered screening again at 28 weeks
Treatment for women at high-risk of developing pre-eclampsia
NICE recommends that women at high risk of pre-eclampsia should be given 75mg aspirin form early in pregnancy (12 weeks) to delivery
All women should be screened at every antenatal visit for pre-eclampsia by measurement of blood pressure and urinalysis for protein
Women at high risk of dveloping pre-eclampsia:
Hypertensive disease during previous pregnancy
Chronic kidney disease
Autoimmune diseases such as SLE and antiphospholipid syndrome
Diabetes mellitus
Chronic hypertension
Women at moderate risk of developing pre-eclampsia:
Primiparity Advanced maternal age (>40 years) Pregnancy interval of more than 10 years BMI>35 at booking visit Family history of pre-eclampsia Multifoetal pregnancy
Women with 2 or more moderate risk factors should start aspirin
Women at risk of preterm birth:
Previous preterm birth
Previous late miscarriage
Multifoetal pregnancies
Cervical surgery (e.g. cone biopsy)
These women may be offered serial cervical length screening (with or without monitoring foetal fibronectin)
Foetal growth measurements
NICE recommends that SFH measurements should be performed at every antenatal appointment form 24 weeks
If there are cocnerns of slow or arrested foetal growth, an ultrasound scan should be performed
Typically, a dating scan is offered at the end of the first trimester and an anomaly scan at 20-22 weeks, but no further growth assessment unless clinically indicated
Vitamin D screening in pregnancy
NOt routinely screened
Those at risk (e.g. skin colour, obesity) may be given vitamin D supplementation (oral cholecalciferol or ergocalciferol)
NICE recommends that ALL pregnant and breasfteeding women should be advised to take 10micrograms of vitamin D supplements daily
When is the anomaly scan carried out?
20-22 weeks
Which conditions can be identified in the anomaly scan?
Spina bifida
Major congenital abnormalities
Diaphragmatic hernia
Renal agenesis
Risk factors for gestational diabetes mellitus
Previous GDM Previous macrosomia Raised BMI First-degree relative with diabetes Asian, black Caribbean or Middle-Eastern origin
If risk factors are present, the woman should be offered a 2-hour 75g oral glucose tolerance test at 24-28 weeks
Women with previous history of GDM should have an OGTT at 16-18 weeks and then a repeat should be performed at 24-28 weeks
Triple test for Down syndrome
Nuchal translucency
PAPP-A
BetahcG
What are the risk factors for twin pregnancy?
Advanced maternal age
Antiretroviral therapy
IVF
Family history
Treatment for twin-twin transfusion syndrome
Foetoscopic laser ablation
How does the mirena coil work?
Hormone in mirena reduces heavy menstrual bleeding by controlling the monthly development of the womb, making the lining thinner
Thickens cervical mucus
In some cases, it stops ovulation
What is Barker hypothesis?
This showed that there is an association between reduced foetal growth and increased susceptibility to several adult diseases (e.g. coronary heart disease, stroke and diabetes)
Small for gestational age
Foetus <10th centile
Many SGA foetuses may be constitutionally small, but many have failed to reach their full growth potential (FGR): this is associated with increased risk of perinatal morbidity and mortality. Growth-restricted foetuses are at increased risk of intrauterine hypoxia/asphyxia, so they are more likely to be stillborn or have features of HIE (e.g. seizures, multi-organ failure). Other complications that they are at increased risk of in the neonatal period: Hypoglycaemia Hypothermia Infection Necrotising entercolitis
Complications of foetal hyperinsulinaemia
Results in foetal macrosomia and excessive fat deposition, which can lead to:
Shoulder dystocia
Stillbirth
Neonatal hypoglycaemia
Chromosomal disorders which cause FGR
Patau syndrome (trisomy 13) Edward's syndrome (trisomy 18)
Genes from which parent encourage growth?
Evidence suggests that geners that are paternally expressed promote growth, whereas maternally expressed genes suppress growth
Maternal influences on foetal growth
Maternal height
Pre-pregnancy weight
Age
Ethnicity
Increasing parity (associated with increased birthweight)
Teenage pregnancy (associated with FGR)
Smoking, alcohol and recreational drug use (LBW)
Cocaine (associated with spontaneous preterm birth, LBW and small head circumference (placental abruption is also associated with cigarette smoking and recreational drug use)
Chronic maternal disease (e.g. hypertension, CF, cyanotic heart disease, maternal thrombophilia)
Placental influences on foetal growth
Causes of placental insufficiency:
Poor maternal uterine artery blood flow
Thicker placental trophoblast barrier
Abnormal foetus villous development
Placental infarction
Acute premature separation (e.g. in placental abruption)
Antepartum haemorrhage
What are the four shunts that ensure that oxygenated blood from the placenta is delivered to the foetal brain?
Umbilical circulation
Ductus venosus
Foramen ovale
Ductus arteriosus
Umbilical circulation
Carries foetal blood to and from the placenta for gas and nutrient exchange
Umbilical arteries arise from the caudal end of the dorsal foetal aorta
They carry deoxygenated blood from the foetus to the placenta
The umbilical vein returns oxygenated blood from the placenta to the foetal liver
Usually there are:
2 x foetal arteries
1 x foetal vein
A small proportion of blood is used to oxygenate the liver, but most of it will bypass the liver via the ductus venosus and joins the IVC
The ductus venosus is a narrow vessel with high blood velocities within it
The streaming of the ductus venosus blood, along with a membranous valve in the right atrium (crista dividens), prevents mixing of the well-oxygenated blood in the ductus venosus with the desaturated blood of the IVC
The ductus venosus stream will pass through the foramen ovale into the left atrium
The blood then passes through the mitral valve into the left ventricle
It is them pumped into the aorta, from which 50% goes to the head and upper extremities
The remainder will pass down the aorta and mix with blood of reduced oxygen saturation from the right ventricle (via the ductus arteriosus)
Deoxygenated blood returning from the foetal head and lower body flows through the right side of the heart into the pulmonary artery
It will then bypass the lungs and enter directly into the descending aorta via the ductus arteriosus
This means that deoxygenated blood from the right ventricle will pass down the aorta and enter the umbilical arterial circulation to be returned to the placenta for oxygenation
Why is the ductus arteriosus patent before birth?
Production of prostaglandin E2 and prostacyclin
What can cause premature closure of the ductus arteriosus?
COX inhibitors
Cardiopulmonary changes at birth
Cessation of umbilical blood flow causes cessation of flow into the ductus venosus, leading to a fall in the pressure in the right atrium –> closure of the foramen ovale
Ventilation of the lungs opens the pulmonary circulation, causing a rapid fall in pulmonary vascular resistance –> increasing pulmonary circulation
Ductus arteriosus closes within a few days of birth
Persistent foetal circulation
Sometimes, the transition from foetal to adult circulation is delayed, usually because the pulmonary vascular resistance fails to fall despite adequate breathing = persistent foetal circulation, which results in left-to-right shunting of blood from the aorta through the ductus arteriosus into the lungs.
The baby will be cyanosed and can suffer from life-threatening hypoxia
This delay in closure of the ductus arteriosus is most commonly seen in preterm infants (<37 weeks) and results in congestion of pulmonary circulation and a reduction in blood flow to the Gi tract and brain (also implicated in the pathogenesis of necrotising enterocolitis and intraventricular haemorrhage)
Failure of closure of what results in neural tube defects?
The CNS begins as a simple neural plate that folds to form a groove then a tube (initially open at each end). Failure of closure of these open ends leads to neural tube defects.
Later development of the foetal brain involves elaborate folding of the neurocortex (mainly in the second half of pregnancy).
There is a rapid increase in grey matter in the last trimester.
Respiratory system in utero
The lungs first appear as an outgrowth from the primitive foregut at about 3-4 weeks post-conception
By 4-7 weeks, epithelial tube branches and vascular connections are forming
By 20 weeks, the conductive airway tree and parallel vascular tree is well developed
By 26 weeks, type I and type II epithelial cells are beginning to differentiate
By 30 weeks, surfactant production has started
Up to delivery, dilatation of the airspaces, alveolar formation and maturation of surfactant continues
In utero the foetal lungs are full of fluid
What changes happen to the lungs at birth?
Production of flung fluid ceases
Fluid is absorbed
Adrenaline appears to play a major role in this process
The clearance of fluid and onset of breathing leads to a fall in pulmonary pressure and a rise in pulmonary blood flow
A consequent increase in left atrial pressure causes closure of the foramen ovale
What is the main constituent element of surfactant?
Surfactant prevents the collapse of small alveoli during expiration by lowering surface tension
The main phsopholipid in surfactant is phosphatidylcholine (lecithin)
Production of lecithin is enhanced by cortisol, growth restriction, prolonged rupture of membranes
Surfactant production is delayed in maternal diabetes mellitus
Acute complications of RDS
Hypoxia/asphyxia
Intraventricular haemorrhage
Necrotising enterocolitis
How can the incidence and severity of RDS be minimised?
Administration of steroids antenatally to mothers at risk of preterm delivery: the steroids will cross the placenta and stimulate premature release of stored foetal pulmonary surfactant in the foetal alveoli
What is the purpose of foetal breathing movements (FBM)?
Several intermittent FBM occur in utero especially during REM sleep
These movements help maintain a high level of lung expansion that is essential for normal lung growth and maturation
During the apnoeic episodes in between FBM, active laryngeal constriction opposes lung recoil by preventing the escape of lung liquid via the trachea
Prolonged absence or impairment of FBM is likely to result in reduced mean lung expansion and can lead to hypoplasia of the lungs. What are some other causes of pulmonary hypoplasia?
Oligohydramnios
Decreased intrathoracic space (e.g. diaphragmatic hernia)
Chest wall deformities
What does the foregut endoderm later give rise to?
Oesophagus Stomach Proximal duodenum Liver Pancreas
What does the midgut endoderm give rise to?
Distal half of duodenum Jejunum Ileum Caecum Appendix Ascending colon Transverse colon
Between weeks 5-6, due to a rapidly enlarging liver and elongation of the intestines accompanied by a lack of space in the small abdomen, the midgut extrudes into the umbilical cord as a physiological hernia
Whilst herniated, the gut will undergo rotation and then re-enter the abdominal cavity by 12 weeks gestation
What does the hindgut endoderm give rise to?
Descending colon
Sigmoid colon
Rectum
What can failure of the midgut to re-enter the abdominal cavity result in?
Omphalocele (exomphalos)
Malrotation can result in what?
Volvulus
Bowel obstruction
Atresia
When a segment of bowel has a lumen that is not patent.
Usually occur in the upper GI tract
The foetus continuously swallows amniotic fluid, so an obstruction that prevents passage of the amniotic fluid through the GI tract will cause polydramnios
Meconium in the amniotic fluid is associated with:
Post-term pregnancies
Foetal hypoxia
Aspiration of the meconium-stained liquor by the foetus at birth can cause meconium aspiration syndrome or RDS
Why are preterm infants at increased risk of low weight?
In the last trimester, water content decreases and glycogen and fat stores increase about fivefold. Consequently, preterm infants have virtually no fat and have a reduced ability to withstand starvation
This can be compounded by poor sucking, uncoordinated swallowing mechanisms, delayed gastric emptying and poor absorption
Growth-restricted foetuses also have reduced glycogen stores–> more prone to hypoglycaemia (glycogen is stored in small quantities in the liver from the 1st trimester and peaks in 3rd trimester)
Indications for expectant management in ectopic pregnancy
Low bhCG
No symptoms
Tubal ectopic pregnancy measuring <35mm
No heartbeat
Indications for methotrexate in ectopic pregnancy
Small (<35mm) unruptured pregnancy No visible heartbeat Serum bhCG<1500 No intrauterine pregnancy No pain
Patient must be able to attend follow-up
Methotrexate is an anti metabolite chemotherapeutic drug. It interferes with DNA synthesis and disrupts cell multiplication, thus preventing the pregnancy from forming.
Indications for surgical management of ectopic pregnancy
Laparoscopic salpingectomy (or salpingotomy if there is a risk of infertility)
Larger than 35mm
Causing severe pain
BhCG>1500
Risk of infertility if remaining Fallopian tube is problematic in the future
In utero, what performs the normal functions of the liver? (metabolic)
Placenta (e.g. unconjugated bilirubin from haemolysis in the foetus is transferred to the mother rather than being conjugated in the foetus)
What may cause physiological jaundice?
The foetal liver is less able to conjugate bilirubin than the adult liver because of deficiencies of enzymes (e.g. UGT)
After birth, loss of placenta and this immature ability to conjugate bilirubin (especially in prematuer infants) may result in transient unconjugated hyperbilirubinaemia
What causes pelvic kidney?
Failure of normal migration (as the foetus develops, the torso elongates and the kidneys rotate and migrate upwards within the abdomen causing the length of the ureters to increase)
What causes duplex kidneys?
Abnormal development of the collecting duct system can result in duplications such as duplex kidneys
What is the danger with severe ureteric obstruction in utero?
Can lead to hydronephrosis and renal interstitial fibrosis
Why are preterm infants at increased risk of acid-base homeostasis issues, even though the structures of the urinary system are already in place at 32-36 weeks?
The excretory and concentrating ability of foetal kidneys develops gradually and continues after birth –> preterm infants may experience abnormal water, glucose, sodium and acid-base homeostasis
What is a posterior urethral valve?
An obstructing membrane in the posterior male urethra
Renal agenesis results in what?
Oligohydramnios (foetal urine forms much of the amniotic fluid)
Bilateral renal agenesis causes Potter’s syndrome, which is associated with:
Widely-s[aced eyes Small jaw Low set ears Secondary oligohydramnios Renal failure (and death) Pulmonary hypoplasia
Preterm babies have no vernix (which is what the periderm sloughs off as) and thin skin:
This leads to insensible fluid loss
They also have poor thermal control due to having a large surface area to body weight ratio and little insulation
They also have immature vascular tone meaning that they cant use peripheral vasoconstriction to limit heat loss
When is lanugo hair shed?
Usually shed before birth
Why are there more Treg cells in the second trimester than at any other point in life?
It is important in the induction of tolerance
IgM or IgA in the newborn without IgG: what is this suggestive of?
Foetal infection
(much of the IgG in the foetus will be from the mother.
The foetus produces small amounts of IgA and IgM)
