Obstetrics Flashcards
What is the normal foetal position of engagement
occiput anterior position
Classification of delay in failure to progress in labour
Primigravida: 1 hour suspect delay
2hours dx delay within active phase
Multiparous: 30 minutes suspect delay
1 hour dx delay
List the risk factors for a difficult labour
High BMI HTN Previous C section Multifoetal pregnancies Small women large babies Gestational DM Foetal position
Types of malpresentation
Abnormal lie
- longitudinal
- transverse
Occiputposterior/transverse
Breech
Brow
Face presentation
Discuss the potential causes of meconium stained liquor, the potential adverse effect associated with it and the management?
Indicator of foetal distress
Cx: placental insufficiency HTN Oligohydraminos Smoking Cocaine Increase in maternal age
Risks: Meconium aspiration syndrome
Rx: Continous foetal monitoring
Obstetrician led-care
Foetal blood sample pH > 7.2 emergency c-section
Progesterone challenge test
Give 5mg of methoxyprogesterone for five days if positive vaginal bleeding will follow
Negative result may indicate an absent womb
Gestational trophoblastic disease
Bleeding in early pregnancy Severe hyperemesis New onset HTN Uterus that is large than expected Extremely elevated HCG No foetal parts id on USS USS looks like a snow storm Strongly associated with thyroid dysfunction
Complications of polyhydraminos
Postpartum haemorrhage
Preterm labour
Role of progestins and oestrogens in the normal physiology of labour
Progestins
- Proliferation, vascularisation and differentiation of endometrial stroma
- Myometrium quiescence
- Represses contractile proteins
- Impairs Oxycontin and PGF2alpha synthesis
Oestrogens
- Foetal wellbeing
- Endometrial proliferation and differentiation
Discuss the physiology of pregnancy. Make reference to implantation, endovascular invasion, immunity and myometrial quiescence.
Hormones involved
- HCG
- Progestins
- Oestrogen
- Prolactin
- Oxytocin
Implantation Dedidual reaction Placenta develops floating and anchoring villi Differentiation of cells under hypoxic conditions Cells 1. CTB 2.ScTB (terminal differention) 3. Anchoring villi
Endovascular invasion by the spiral arteries
wide bore low resistance veins
Pre-eclampsia: poor endovascular remodelling
reduced foetal o2
Reduced immune response especially humeral related immunity
Myometrial quiescence based on cell signalling cascades and secondary messengers phosphorylation of intracellular proteins = inactivation of actin/myosin ATPase
Define screening and discuss the antenatal screening programmes carried out
Screening: a process of identifying apparently health individual who may be at increased risk of a disease or a condition
Detection rate: % of affected individuals identified by the test
Programmes
- Foetal anomaly screening
- Infectious diseases (Hep B, HIV and syphillis)
- Sickle cell and thalasaemia
Foetal anomaly screening programme
First semester
- crown-rump measurement
- blood sample (measure levels of PAPP-A, HCG-B)
- measure nuchal translucency
Second trimester
- Serum markers
- Nuchael translucency
+ve results
CVS (11-13)
Amniocentesis (post 15 weeks)
Apart from FA what other conditions are screened for in antenatal clinic
Infectious disease (Hep B, HIV, Syphillis, Rubella) Haemoglobinopathies (alpha and beta thalasaemias, sickle cell disease)
What conditions are tested for in the newborn screening programme
Sickle cell disease Cystic fibrosis Congenital hypothyroidism Phenylketonuria MCADD Maple syrup disease Isovaleric acidaemia Glutamic acidaemia Homocystinuria
Define gestational diabetes and the diagnostic criteria
Carbohydrate intolerance which is diagnosed during pregnancy. May or may not resolve post pregnancy.
Fasting glucose > 5.6mmol/L
2 hour glucose tolerance test >7.8mol/L
List the risk factors for GDM
BMI >30 Previous macrocosmic baby weighting >4.5kg Previous gestational diabetes Previous gestational diabetes 1st degree relative with diabetes Ethnicity - South Asian - Black Caribbean - Middle eastern
Foetal risks associated with having GDM
Congenital abnormalities Preterm labour Increased birthweight Increased likelihood of polyhydraminos Increase risk of birth trauma/ dsytocia Increased risk of later developing DMII Increased risk of jaundice
Maternal risks associated with GDM
Ketoacidosis Hypoglycaemia UTI Endometrial infection Increased likelihood of a C-section Increased likelihood of an instrumental delivery
Treatment and screening of GDM
Treatment
- Advise re diet and exercise
- Treat with metformin. If not well controlled on metforim treat with insulin
- Perform serial growth scans
- During delivery patient requires a sliding scale of insulin and dextrose
Screening
- 28 weeks GTT as part of routine antenatal screening
Preconceptual care for women with pre-existing DM
Optimising glycemic control Education of the patient Pre-conceptual folic acid (5mg) Screen for retinopathy/nephropathy HbA1c > 85mmol/mol DO NOT get pregnant Stop all hypoglycaemic except metformin
Epilepsy in pregnancy
Epilepsy drugs can be tetrogenic
Seizure free monotherapy should be a the lowest possible dose
Patients require detailed USS to observe
- cardiac function
- neural tubal defects
- skeletal condition
Risk factors for pre-term labour
Previous preterm labours Smoking Low socio-ecconomic group BMI <19 Lack social support Extremes of reproductive age Chronic medial conditions
List the potential causes of preterm labour
Infections Uterine overextension Ureoplacental ischaemia Cervical incompetence Foetal abnormality Iatrogenic
Name the pathogens which are involved in pre-term labour
STD; Chylamydia, Trichomonas,Syphilli
Enteric orgnaism: E.coli and strep faecsali
Bacterial vaginosa: Gardnerella, Mycoplasma
Grp B strep
Management of a potential pre term
1)Tocolysis: drugs to reduce uterine contractions. Depends on cervical dilation, administer steroids and need for inter transfer.
Drugs
Oxytocin antagonists -Atosiban
Calcium channel blockers - Nifedipin
B blockers- Ritodrine, acts on the beta receptors in the myometrium to relax
NSAID’s- act on cox enzyme that catalyses the production of prostaglandins
Nitric oxide acts on the myometrium in vitro to cause reaction
2)Abs therapy
Erythromin given prophylactically in PROM _ protect the foetus from an ascending infection
3) Cervical cleavage
Premature rupture of membranes
Main risk = SEPSIS
Dx: Confirmed by a pool of liquid in the poster fornix
Expectant management: Erythromycin and steroids
Outline the role corticosteoirds play in preterm labour
x2 IM injections 12-24hrs apart
reduce neonatal distress
Pree 24+0 weeks and post 34+6 weeks
Define APH
Any bleeding from the genital tract that occurs after 24 weeks of gestation till before the birth of the infant
List the causes of APH
Placenta previa Placenta abruption Uterine rupture Infection Post coital
Classify the types of APH
Minor < 50mL
Major < 50-100mL
Massive 1000mL
How does APH commonly present
Bleeding (painful/painless)
Uterine contractions
Foetal distress
Management of APH
ABC 15L O2 IV access wide bore cannula Group and save - order blood Cathertise (maintain urine output > 30mL) Perform a USS Do NOT perform a VE
Define placenta previa and classify the grades
Placenta previa is the placenta wholly or partially attached to the lower uterine segment
1: % of the placenta does not sit in the lower segment
2: Placenta reaches the internal os, on dilation =bleeding
3: Placenta is covering the os asymmetrically
4: All of the placenta is in the lower segement
Risk factor for APH
Previous c-section Advanced maternal age Multiparity Multiple pregnancy Smoking
Discuss the key presenting feature of placenta previa and discuss the management of these patients
PAINLESS BLEEDING occurs unprovoked. Degree of maternal shock will correlate with the degree of blood loss
Internal Os should be 3cm away from the leading placental edge
Grade 1: May be able to deliver vaginally
Grade 2-4: Delivery via c-section. Avoid penetrative intercourse.
May require inpatient care @ 34 weeks
Cross match 4 units of blood
Define placenta abruption
Placenta attachement to the uterus is disrupted by haemorrhage as the blood dissects under the placenta
Risk factors for placenta abruption
Previous abruption Increase maternal age Multiparity HTN Smoking Cocaine use ECV
Clinical presentation of placenta abruption
PAINFUL bleeding
Revealed haemorrhage vs concealed haemorrhage
Pain may be out of proportional with the perceived loss of blood
Hardy woody uterus and guarding of the abdomen
Management of placenta abruption
ABC Oxygen Wide bore cannula IV access If foetus remain alive Give steroids and emergency c-section
Explain the pathophysiology of vasa previa
Foetal blood
Umbilical cord = x2 arteries x1 veins
Arteries carry C02 from the baby to the placenta
Veins carry O2 and nutrients from the placenta to the baby
Umbilical cord inserts into the membranes
SROM or AROM can tear the vessels
BABY EXSANGUINATE = cold white baby
Must c-section immediately
Define PPH
Bleeding from the genital tract of more than 500mL after delivery of the infant
Primary PPH: bleeding of more than 500mL within 24hours after delivery
Secondary PPH: bleeding of more than 500mL that starts 24hours after delivery
> 2000mL = massive obstetric haemorrhage
Haematological changes in the mother during pregnancy and immediately afterwards
Pregnancy Increase in VWF Increase in Factor 8 Increase in Factor 9 Increase in in Factor 10 Increase in Protein resistance C Decrease in Protein resistance S Decrease in fibrinolytic activity
++ve coagulation state
@pregnancy: Increase RCV and plasma volume
@post partum: increase in RCV, plasma volume returns to normal = VTE is common
List the causes of PPH
TONE
- Atonic delivery
- Multiparous
- Gestational DM
- Increased foetal size
- Multifoetal birth
- Polyhydraminos
- Long labour
TISSUE
-Retained products of conception
commonest cause of 2nd PPH
TRAUMA
- Laceration the the uterus, cervix and vagina
1: injury to the perennial skin
2: injury to the perinial skin + muscles
3: Injury to the perineal skin + muscles+ anal sphincter
4: Injury to the perineal skin+ muscles+ anal sphincter + anal muscles
THROMBIN
Disseminated intravascular coagulation
Consumptive coagulopathy = all the clotting factors and the platelets are consumed
2 PPH: very commonly due to retained products of placenta.
Very common in molar pregnancies
Patient presents with fever, increased RR, increased HB, decreased BP
Discuss the management of PPH
ABC APPROACH ALWAYS
Atony:
- Bimanual compressions
- Syntometrin
- Misoprostolol
- Ballon compression
- Bilateral ligation of the arteries
- Hysterectomy
Retained Products of Placenta
- Controlled cord traction
- Placenta examined ( cotyledons + membranes intact)
Uterine Inversion (RARE) Uterine rupture (RARE)
List the physiological adaptions that occur during pregnancy
RESP
- CO2 levels decreased
- Tidal volume increases
- Compensated resp alkalois
CV
- Increased cardiac output
- Increase blood volume = physiological anaemia
- systolic ejection murmur
URINARY
- Kidneys increase in size
- Increase in eGFR
- Decrease in plasma urea and creatine
- Increased frequency of urination
ENDO
- All increase except
- Decrease in FSH/LH/GH/Oxytocin
List the causes of prolonged labour
3 P’s
Power
- Poor uterine activity
- Ruptured uterus
Passenger
- Malposition
- Malpresentation
- Size of infant
Passage
Cephalopelvic disproportion
Cervical dystocia
Dx criteria for polyhydraminos
Amniotic fluid index > 25cm
Deepest vertical pool > 8cm
Define early pregnancy
First trimester of pregnancy, up to and including the 12th week
List the complications of early pregnancy
Miscarriage: loss of pregnancy before 24 weeks of gestation
Ectopic pregnancy: pregnancy which is implanted outside of the uterus
Can occur in the ovary, cervix, corneal or most commonly in the fallopian tube.
Trophoblastic disease: partial or completel molar pregnancies. Can be followed by a choriocarcinoma
List the different types of miscarriage
Threatened: Bleeding, cervical os is closed
Inevitable: Heavy bleeding with clots and pain, cervical os is open
Missed/delayed/silent: Non viable foetus or empty intrauterine sac on scan. Cervical os is closed o/e
Complete: No products of conception in uterus on scan. Cervical os is closed
Incomplete: products of conception are only partially expelled. Cervical os is open
Causes of miscarriage
Foetal abnormality Infection (TORCH) Maternal age Abnormal uterine cavity Maternal illness Intervention
Management of miscarriage
Expectant management to expel the products of conception
Medical can give vaginal misoprostolol or oral misoprostolol
Evacuation of retained products of conception
Discuss endometritis: fever, feeling unwell, lower abdominal pain and change in vaginal bleeding
Rheusus negative: require anti-D is after
Define recurrent miscarriage
Three or more consecutive first trimester miscarriages
Possible causes of recurrent miscarriage
Abnormal uterine cavity Antiphospholipid antibodies Cervical weakness Foetal abnormalities (Karotype both partners and the products of conception if possible) Bacterial infection
Define ectopic pregnancy
Pregnancy implanted outside of the uterine cavity
Causes of ectopic pregnancy
Damage to the uterine tubes or the ciliary lining PID Tubal surgery Pelvic surgery IUCD IVF Endometriosis
Clinical features of an ectopic pregnancy
Abdominal pain Pelvic pain Shoulder tip pain Missed period Empty uterus on scaning
Ruptured
Shock
Intense pain
Bleeding
In a viable pregnancy B-HCG will double every 48hrs . In ectopic the level will either plateau or rise but not double
Treatment of an ectopic pregnancy
Medical
- Methotrexate
- not in significiant pain
- unruptured ectopic pregnancy adrenax mass <35cm and no visible heart beat
- Serum B-HCG <1500UI/L
- use contraception for 3-6 months as tetraogenic
Surgical
- Salpingectomy (complete or partial) tube fully or partially removed
- Salpingotomy ( incision made into the tube and tube allowed to heal by secondary intention)
Define gestational trophoblastic disease
Covers complete and partial molar pregnancies as well as the choriocarcinoma which can follow
Complete molar: Pregnancy consisting of a mass of trophoblastic tissue, no evidence of a foetus, all maternal genetic material has been deleted, all genes are paternal.
Partial molar: Pregnancy consisting of a mass of trophoblastic proliferation, foetus is visible (non-viable)
Chpriocarcinoma: trophoblastic cells which secrete hCG when molar pregnancies do not regress after surgical evacuation.
Clinical evaluation of a molar pregnancy
Bleeding early in the pregnancy Uss: bunch of grapes High levels of hCG Severe hyperemesis Vaginal bleeding Uterus is large for dates
Management of a molar pregnancy
Surgical evacuation
Fortnightly samples of hCG to confirm levels are falling and the tumour is regressing
Levels normal: monthly samples tested monthly for either 6 months (if normalised in 8 weeks or 2 years)
Avoid hormonal contraception or conceiving for a least 6 months post normal levels
Causes of polyhydraminos
Multiple pregnancy Infection (TORCH) Gestational diabetes Oesophageal atresia Neural tubal defect Foetal anomaly Genetic disorders Maternal substance abuse
Management of polyhydraminios
Treat the cause
Give steroid prenatally in case of preterm labour
Progesterone synthase inhibitors maybe given for up to max 48hrs
Induction of labour in case of foetal distress
Risk factors associated with polyhydraminos
Preterm delivery and labour Increased incidence of C-sections Low birth weight Low APAGAR Scores Malpresentation Cord prolapse PPH
Complications of GDM
Foetal
- Congenital abnormalties
- Preterm labour
- Increased risk of birth trauma (shoulder dystocia)
- Increase birth weight
Maternal
- Ketoacidosis (rare)
- Hypoglycaemia
- UTI
- Endometrial infection
- Increased likelihood of c-section
Signs of hypothyroidism in pregnancy
Lethargy Tiredness Weight gain Dry skin Hair loss
Note for the first 12 weeks foetus relies on maternal thyroid hormone. If absent = miscarriage, reduced intelligence, near-developmental delay and brain damage
Treatment of hypoparathyroidism in pregnancy
Thyroxine
Check TSH and T4 levels regularly
Treatment of hyperparathyroidism in pregnancy
Anti thyroid meds: Proplythioruracil or carbimazole
B-Blockers to improve symptoms
Monitor TFT’s throughout
Pathophysiology of VTE
Prothrombotic state
Increase in clotting factors
Increase in fibrionogen levels
Risk factors for VTE in pregnancy
Thrombophilia Age >35 BMI > 30 Parity > 3 Smoker Immobility Gross varicose veins Multiple pregnancy Medical comorbities Systemic infection
Management of high risk VTE patients
Antenatal risk assessment
General measures of mobilisation and maintenance or hydration
Compression stockings
LMW heparin
Postpartum prophylaxis ( high risk up to 6 weeks)
Treatment of VTE
Therapeutic dose of LMW heparin
Warfarin is tetraogenic
Anaemia in pregnancy
Common disorder
Physiological anaemia
<11g/dl at booking
<10.5g/dl at 28 weeks
Iron supplements to be given
Increase vitamin C consumption to aid with absorption
Will reduce the need for a transfusion following delivery
Define the Bishops score
Cervix scoring system to assist in predicting of induction of labour will be required
Based on
- Cervical dilation in centimeters
- Cervical effacement as a percentage
- Cervical consistency by provider assessment/judgement
- Cervical position
- Foetal station, the position of the fetal head in relation to the pelvic bones
Classify the types of HTN in pregnancy
- Pre-existing HTN: Bp >140 before pregnancy. Increased risk of pre-pre-eclampsia
- Pregnancy induced HTN : HTN presenting after 20 weeks of gestation. No proteinuria
- Pre-eclampsia: HTN presenting after 20 weeks of gestation
- HTN
- Proteinuria
- Oedema
Treatment of HTN in pregnancy
Pre-existing: Pregnancy appropriate medication. Low-dose aspirin (75mg) has been shown to be beneficial in reducing the risk of developing PET
Pregnancy induced: Start on laneetalol ( methlydopa/ nifedipine) regular urine dips to rule out proteinuria
Define pre-eclampsia
New onset HTN after 20 weeks with significant proteinuria. Multi system disorder
- HTN
- Proteinuria
- Oedema
Placental in origin
Risk factors for developing pre-eclampsia
Nulliparity Previous hx Family hx Increase age Chronic HTN Twin pregnancies Autoimmune disease Renal disease Obesity
Pathophysiology of pre-eclampsia
Stage one: DEVELOPMENT OF THE DISEASE
- incomplete trophoblastic invasion
- Spiral artery flow reduction
- Uteroplacental blood flow reduction
- Exaggerated inflammatory response
- Endothelial cell damage
Stage two: MANIFESTATION OF THE DISEASE
- Increased vascular permeability = Oedema, HTN and proteinuria
- Vasoconstriction = HTN, eclampsia, liver damage
Clinical features of pre-eclampsia
Asymptomatic (often) Headaches Drowsiness Visual disturbance Nausea/ Vomiting Epigastric pain
Treatment of pre-eclampsia
- Labetalol: alpha and beta blocker
- Nifedipine: Calcium channel blocker
- Methyldopa: alpha agonist. prevents vasoconstriction
- Hydralazine: IV causes vasodilation
Severe risk of eclampsia: give MgSO4 IV
Define eclampsia
Occurrences pf seizures in pregnancy following from pre-eclampsia
Management of eclampsia
Airway: protect
Breathing: give high flow O2
Circulation: Obtain IV access and take bloods
Give MgSO4 4 gram bolus over 20 mins
MgSO4 1g/hr over 24 hours following last seizure
Treat HTN
Consider delivery
Clinical features of sepsis
Pyrexia Tachycardia Hypotension Rigors Confusion Collapse
Cord prolapse
Cord is the presenting part
Often leads to foetal death
Exposure of the cord = vasospasm
Foetus is starved of oxygen
Risk factors for cord prolapse
PROM Polyhydraminos Long umbilical cord Low lying placenta Low birth weight Malpresentation
Define shoulder dystocia
Failure of the anterior shoulder to pass under the symphysis pubis after delivery of the foetal head that requires specific manoeuvres
Risk factors for shoulder dystocia
Macrosomia
Maternal DM
Distortion between the mother and the foetus
Maternal obesity
Discuss how a CTG should be interpreted
DR.C.Bravdo
Define risk: (PC, age, primi, multi,gravida, para, BMI )
Contractions: Number of contractions present in a 10 minute window
Baseline rate: Average foetal heart rate over a 10 minute window (110-160bpm)
Accelerations: abrupt increase in baseline heart rate. 2 acceleration every 15 minutes
Variability: variation of foetal HR from one beat to another
Overall impressions: reassuring, suspicious, pathological
List the potential causes of oligohydramnios
Ruptured membranes Foetal abnormality Aneuploidy IUGR Foetal infection Maternal drugs (atenolol)
Describe the stages of labour
1st stage
- Latent stage: cervix effaces and dilates <4cm
- Active stage: contractions, dilation >4cm
2nd stage
- Passive: complete dilation
- Active: pushing
3rd Stage
- Passage of the placenta
Define cervical ripening
Physical softening and distensibility of the cervix
Occurs prior to the onset of labour
Enzymatic dissolution of the collagen and increase in the water content
Outline the timeframes for delay in labour
1st stage
- Primi <1cm/ hour
- Multi <1cm/30 minutes
2nd stage
- Multi: delivery not imminent within 1hr of active pushing
- Primi: Delivery not imminent within 2hrs of active pushing
Explain the role of prostaglandins and oxytocin
PROSTAGLANDINS
- Local application of prostaglandin E2 can help with the ripening of the cervix
- Uterine contractions
- Expulsion of the placenta
- Feedback mechanism
OXYTOXIN
- Uterine contractions
- Syntocin
List the factors recorded on a partogram and the role of an alert and action line
Foetal HR: monitor wellbeing of the infant
Cervix dilation: progression of labour
Contractions per minute: speed of labour
Indicates slow progression and measures that should be taken
Maternal and foetal consequences of failure to progress
MATERNAL
- Long labour
- Increased risk of tears
- Increased risk of bleeding
FOETAL
- Foetal hypoxia
- Increase risk of mortality or morbidity
Outline the descent of the foetus in the birth canal
Descent Flex Internal rotation Crown Extention
Define small for gestational age
Weight of the foetus is less than the tenth centile for gestational age
Define large for gestational age
Weight of the foetus is greater than the 95th centile
Define intrauterine growth restriction
Foetus has failed to reach their growth potential, often due to placental dysfunction
List the cause of intrauterine growth restriction
FOETAL
- Chromosome abnormalities (trisomies)
- Infections (TORCH)
- Multiple pregnancy
PLACENTAL
- Abnormal trophoblastic infiltration ( pre-eclampsia/infraction/abruption)
MATERNAL
- Chronic disease
- Behavioural ( smoking/durgs/alcohol)
List the risk factors for small for gestational age
MAJOR
- Maternal age >40
- Smoker
- Cocaine use
- Previous SGA baby
- Previous stillbirth
- Chronic hypertension
- Diabetes
- Renal impairment
- Antiphospholipid
- Low PappA
MINOR
- Maternal age >35
- Nulliparity
- BMI >20
Management of an abnormally sized baby
SMALL
- Umbilical artery doppler ( if normal), serial growth scans every 2-3 weeks
- If abnormal consider delivery via CS
- Give glucocorticoids
- Feed within 2hrs of birth due to the likelihood of hypoglycaemia
LARGE
- Monitor with growth scans
- Rule out potential causes ( GDM)
- Consider CS
- Prone to hypoglycaemia and hypocalcaemia
Causes of breech
Idiopathic Uterine abnormalities Fibroids Prematurity Placenta previa Oligohydraminos Foetal abnormalities
Principle of ECV
Turn the baby through a forwards somersault
Contraindications
- Placenta previa
- Multiple pregnancy
- APH
- Ruptured membranes
- IUGR
Signs of uterine rupture
Pain ( variable, can just be tenderness over the uterus)
Variable vaginal bleeding
Continued bleeding with a well contracted uterus
Shock
Management of uterine rupture
ABCD
C- section
May require a hysterectomy
Define cord prolapse
Descent of the cord through the cervix below the presenting part after the rupture of the membranes
Cord compression and vasospasm results in foetal asphyxia
CF: Foetal braycardia (always do a VE)
Visible cord
Define shoulder dystocia
A delivery requiring obstetric manoeuvres to release the shoulder after gentle downward traction has failed.
Risk factors for shoulder dystocia
Large foetus Maternal BMI >30 Induced or augmented labours Prolonged labours Previous shoulder dystocia Diabetes mellitus
Management of shoulder dystocia
Legs in McRoberts position
Suprapubic pressure
Group B streptococcus infection in pregnancy
No screened for
Found on routine swabs
Can lead to neonatal infections Give all women IV antibiotics in labour - Previous GBS infected baby - Gestation <37wks - PROM
Components of the quadruple test
@ 16 weeks Dating scan + - AFP - Unconjugated oestriol - Free B-HCG - Inhibin A
Takes into account the women age in the 2nd trimester
Components of the combined test
Nuchael translucency ( <3.5cm)
hCG
PAPP-A
Womens age must also be taken into account
Role of PAPP-A
Large glycoprotein
1st trimester
- poor placentation
- trisomies
2nd trimester
- Pre-eclampsia
- Growth restriction
- Preterm delivery
- Foetal demise
Treatment of a UTI in pregnancy
Often asymptomatic
Cefalexin 500mg
Avoid trimethoprim in first semester antidotal action
Features of multiple pregnancy
Uterus large for dates
Hyperemesis
Plyhydraminos
Complications of multiple pregnancy
PREGNANCY
- Polyhydraminos
- Pre-eclampsia
- Anaemoa
- Increase risk of APH
- Gestational DM
FOETAL
- Prematurity
- IUGR
- Twin-twin transfusion
Management of a multiple pregnancy
Aspirin >12 wks to prevent pre-eclampsia
Consultant led care
Elective birth @ 37 weeks
Give steroids @ 36wks
What is the APGAR scoring system and what does it assess
APGAR is a method of assessing infants rapidly at 1 minute of age to see if they require assistance. It assesses - Pulse - Respirations - Muscle tone - Colour - On suction
A score above 7 is reassuring
Risk factors for maternal sepsis
Obesity Impaired glucose tolerance Immunosuppression Anaemia Vaginal discharge HX of Grp B streph
Causes of maternal sepsis
Grp A betahaemolytic strep
E.coli
Bacteroides
Treatment of maternal sepsis
IV broad spec: Tazocin (piperacillin-tazobactam) 4.5g/8hr
Crystalloid fluid bolus
Vasopressors to maintain the blood pressure
Puerperal period check wound sites and consider necrotising fasciitis
Define cervical show
Mucus plug and blood
Principle of chorionic villus sampling
Dx procedure for karyotyping during the first trimester
@ 11-13weeks
sample of chorionic villi from the foetal placenta
Potential sensitisation event give anti-D
Principle of amniocentesis
Sample of amniotic fluid
Karotype foetal cells within the fluid
@ 15 weeks and above
Potential sensitisation event
