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Obs & Gynae > antenatal care > Flashcards

antenatal care Flashcards

1
Q

what is the booking visit and what are the routine investigations offered to a mother during this appt?

A

Ideally by 10 weeks to discuss pregnancy and do health review of mum ID those higher risk, advice diet, pelvic floor exercises, how baby develops pregnancy, antenatal screening, pregnancy care pathway, place of birth, breastfeeding,
Bloods: FBC (anaemia), Rhesus, ABO, Haemoglobinopathies Electrophoresis (sickle cell + thalassemia), urine test- proteinuria + bacturia + G (DM) + culture, HIV, Hep B, Rubella immunity, Syphilis, offer chlamydia screen for <25.
Imm: Flu, Pertussis.

Obs/ Hx/ Exam: Height, weight, BMI, BP, screen for pre-eclampsia, gest diabetes, ask about mental health + current mood, occupation, FGM identify.

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2
Q

What screening is done for fetal anomalies?

A
  1. “combined” serum test for Trisomy 13 (Patau), 18 (Edwards), 21 (DS) BHcG and PAPP-A, Combo with maternal age + NT to assess risk [11-14 weeks].
  2. USS (increased nuchal translucency common to trisomy babies) for fetal abnormalities [18-20/52].
  3. Triple/ Quadruple test - 15-20 weeks HcG, Alpha feto- Protein, Inhibin A, uncongugated oestriol. (if USS not poss/ mum too big)
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3
Q

How is pregnancy dating + gest age carried out?

A
  • USScan: crown–rump measurement used to estimate gest age from weeks 11-13 +6.
  • Detection of multiple pregnancy.
  • Also allows Nuchal Translucency to be assessed.
    Head circumference (using biparietal diameter or occipital frontal diameter) / Femur length from 13-25 completed weeks.
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4
Q

what is gestational hypertension? How is it managed?

A

HT> or = to 140/90 that develops after 20 weeks of gestation and resolves within 12 weeks of delivery.
It can be mild, moderate or severe.
BP in pregnancy falls at the beginning of pregnancy to lowest point during the second trimester by approx 30/15 and then returns to pre-pregnancy levels by delivery. BP drops due to reduction in SVT.
Managed- oral labetalol is used first line. measure BP at least once/ week (mild), Biweekly (moderate), 4x daily (severe). Test for proteinuria, bloods at presentation for mod HT (U + E, FBC (platelets), LFTs, Bili) and weekly for severe HT. Severe HT req admission.
Fetal monitor: If before 34 weeks, do umbilical artery doppler, USS fetal growth + amniotic fluids volume check (mild- mod). If severe HT

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5
Q

what is pre-eclampsia? What are the signs and symptoms?

A

HT ie anything above 140/90 and proteinuria, defined as >30mg/ mmol Urinary protein: creatinine ratio or >300mg/ 24hours.
Early onset: causes complications before 34/52 ie growth restriction.
Late onset: causes complications after 34/52.
S &S: may be asymptomatic. Headaches, blurred vision, sudden oedema in face, hands, feet, vomiting, acute epigastric pain, drowsiness. Clonus.

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6
Q

what are the RF for pre-eclmapsia development? How are those at risk of pre-eclampsia managed?

A

HT during previous pregnancy, chronic HT, CKD, autoimmune SLE/ antiphospholipid syndrome, DM.
Moderate risk– nullip, >40yrs old, >10 years pregnancy interval, multiple pregnancies (twins etc), BMI >35, fhx pre-eclampsia.
Aspirin 75mg from 12/52 to birth if high risk and same if more than 1 from mod risk group

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7
Q

what are the classifications of HT/ pre-eclampsia?

A

Mild: BP >/= 140/ 90- 149/99
Mod: BP >/= 150/100 - 159/ 109
Severe: BP > 160/110

Severe pre-eclampsia= above definition OR HT + proteinuria + symptoms or biochemical/ haematological impairment.

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8
Q

what are the complications of pre-eclampsia?

A

HELLP: haemolysis (anaemia + dark urine), elevated liver enzymes (liver failure, epigastric pain, deranged clotting), low platelets
Kidney failure due to Acute Tubular Necrosis
Eclampsia: generalised tonic clonic seizures
Haemorrhagic stroke
Pulmonary oedema
Disemminated Intravascular Coagulation
IUGR, still birth, pre-term birth, oligohydramnios, placental abruption.

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9
Q

how is pre-eclampsia managed?

A
  1. regardless of severity, admit to hospital
  2. monitor BP at least QDS
  3. mod-severe HT : tx with labetalol
  4. at least biweekly U + E, FBC, LFTs, Bilirubin
  5. Offer birth between 34-37 weeks
    lots of monitoring of BP + symptoms of pre-eclampsia after birth.
  6. During labour monitor BP hourly or if severe continuous.
  7. at dx, CTG, umbilical artery doppler, fetal growth, amniotic volume fluid check and then every 2-4 weeks.
    Induction with PGs if required. If before 34weeks + IUGR/ CTG abnormal c-section usually req.
    Severe pre-eclampsia:
    IV MgSO4 (anticonvulsant)
    PO/ IV Labetalol; IV Hydralazine; PO Nifedipine
    Betamethasone IM for fetal lung maturation
    Limit maintenance fluids to prevent pulmonary oedema
    If severe HT persists, c-section req. .

After birth: lots of monitoring of BP + symptoms of pre-eclampsia after birth. Bloods still required U + E, LFTs, Platelets. fluid monitoring vital (remember maintenance is 80ml/hr).

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10
Q

what is the pathophysiology behind Gestational Diabetes?

A

During normal pregnancy, insulin resistance increases due to HPL (Human placental lactogen) prod by placenta. Gestational Diabetes dx requires a 2hour post-75g Glucose load of >7.8mmol (Glucose Tolerance Test done @ 28/52)

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11
Q

what are the fetal complications of (pre-existing) Diabetes in pregnancy?

A
  • macrosomia Birthweight is increased as fetal pancreatic islet cell hyperplasia leads to hyperinsulinaemia and fat deposition. This leads to increased urine output and polyhydramnios (increased liquor) is common. (increased risk of CS delivery)
  • increased risk of miscarriage
  • pre-eclampsia 2x risk (leading to IUGR)
  • congenital abnormalities: cardiac + neural tube defects
  • premature labour second to UTI
  • fetal lung development (Insulin reduces surfactant prod + CS rates higher in these babies + more likely prem)
  • shoulder dystocia + birth trauma more common due to baby’s size
  • massive increase (4-5x) stillborn risk
  • hypoglycaemia in neonatal period
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12
Q

what are the maternal complications of Diabetes in pregnancy?

A

diabetic retinopathy, nephropathy, diabetic ketoacidosis, pre-eclampsia + HT, UTI, wound infection, VTE risk

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13
Q

what is the inheritance of Rhesus blood group type? What is the pathophysiology of Rhesus isoimmunisation?

A

Rhesus positive Ag is autosomal dominant (therefore takes dd to be -ve)
A sensitisation event occurs where Rh-ve mum is exposed to Rhesus +ve RBC and mum therefore mounts an immune response to the Ag Rhesus and forms Ab against them. Sensitisation events may be during a previous pregnancy when fetal blood cells enter maternal circulation (e.g. at delivery), TOP/ removal of retained products following miscarriage, ectopic, external cephalic version, amniocentesis/ Chorionic villus sampling, Intrauterine Death, during the current pregnancy (e.g. vaginal bleed due to placental abruption), or a former blood transfusion. Following this event, if mum is re-exposed to this Ag, Ab cross the placenta and bind to fetal RBC resulting in haemolysis.

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14
Q

How is rhesus isoimmunisation prevented?

A

Mum’s Rh status checked at booking and then again at 28weeks.
Injection of Anti-D (500iu) at 28 weeks + 34 weeks provided mum has NOT been sensitised to Rhesus (ie has no Ab vs Rhesus +ve) or else this will be of no use to mum/ baby.
Also Injections of Anti-D provided within 72h of poss sensitisation events such as miscarriage or threatened miscarriage after 12 weeks, or before 12w if the uterus is instrumented (e.g. ERPC), termination of pregnancy and ectopic pregnancy.
Anti-D is also given after in utero
procedures such as amniocentesis and after external cephalic version, fetal death or antepartum haemorrhage.

If mum is 20+ weeks, must do Kleihauer testing to confirm if > 500 iu of Anti-D are required.

Also given within 72h of delivery if baby is proven to be Rh+.

All babies born to Rh- mums are checked following birth with FBC, Bilirubin, blood film.

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15
Q

What is the consequence of Rhesus disease of the newborn?

A

anaemia
Heart Failure
Hydrops (fluid in any compartment usually ascites + oedema) due to the heart failure
kernicterus haemolysis releases bilirubin. In utero this is cleared by the placenta and is not harmful. After birth the neonatal liver cannot cope with the excess production of bilirubin, and this leads to jaundice. if left untreated, high levels of bilirubin can result in damage to specific areas of the neonatal brain, causing permanent brain damage. This can lead to a range of neurodevelopmental problems, such as cerebral palsy, deafness, and motor and speech delay

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16
Q

If mum has been sensitised to Rh+ baby, how is fetus monitored + treated to prevent Rhesus disease?

A

MCA doppler recording peak velocity at systole has a high sensitivity for detecting fetal anaemia. It is used fortnightly for fetuses at risk.
Anaemia is detected as fetal hydrops. If suspected, fetal blood is sampled from the umbilical vein (preferred) or intrahepatic vein.
If anaemia detected, blood transfusion is performed into the u vein with Rh-ve, high haematocrit blood. This is done reg until 36 weeks when delivery is advised. When born they are given more blood transfusions + exchanges to treat hyperbilirubinaemia due to haemolysis + phototherapy.

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17
Q

what is antepartum haemorrhage? What are the complications for mum + fetus?

A

Bleeding after 24 weeks gestation from the vagina
common causes: placenta previa, placental abruption
Rarer: incidental genital tract pathology, uterine rupture, vasa previa, domestic violence.
Complications:
Fetal Hypoxia, Small for gest. age, IUGR, prematurity, fetal death
Mum- Anaemia, infection, shock, Acute Tubular Necrosis, PPH, consumptive coagulopathy, blood transfusion complication.

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18
Q

What is placenta previa? What are the RF for its development?

A

When placenta is located in the lower part of the uterus. Many are thought to be low lying prior to the third trimester but then subsequently “move” due to growth of the lower segment of the uterus during the final weeks.
It can be classified as minor or major (if covering os in any way) depending on the distance from the internal os of the cervix. If the placenta is located on the anterior wall of the uterus this increases the risk further of PPH due to the need to cut through the placenta to access the baby during c-section.
Uterine scarring e.g. due to previous c-section, Advanced maternal age, multiple pregnancies, and tobacco use, assisted conception, advanced maternal age, previous TOP.

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19
Q

what is vasa praevia? how does it present?

A

fetal vessels coursing through the membranes over the internal cervical os and below the fetal presenting part, unprotected by placental tissue or the umbilical cord. This is due to either the placenta being multi-lobed or the cord inserting into the fetal membranes and then running towards the placenta within the membranes rather than attaching straight into the placenta.
Fresh vaginal bleeding when waters break and Fetal compromise - CTG decelerations, bradycardia etc. Fetal death is quick and they require immediate delivery + resus. It requires c-section delivery imminently.

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20
Q

What are the complications of placenta previa?

A

usually necessitates c-section delivery because it obstructs the engagement of the foetus’s head. May also cause lie to be transverse.
Haemorrhage is the most serious complication either before, during or after delivery due to the lower segment of the uterus being unable to contract down to prevent blood loss.

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21
Q

How does placenta previa present?

A

Intermittent Painless antepartum bleeding (poss postcoital) which increase in freq + intensity over weeks. Not all women bleed, a third reach delivery with no bleeds. Often baby is transverse lie + breech presentation, high presenting part.
Vaginal Exam is CONTRAINDICATED IN P.PREVIA DUE TO BLEEDING RISK

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22
Q

How is placenta previa investigated and managed?

A

Investigation: USS for definitive diagnosis. For asymptomatic women with suspected minor pp, reimaging at 36 weeks is appro. If suspected major / placenta accreta but asymptomatic, reimage at 32 weeks for definitive diagnosis to allow planning.

Management: If present with bleeding, admit to hospital, do FBC, G + S, Clotting, CTG. Anti-D for Rh-ve mums. Steroids if mum <34 weeks. If asymptomatic wait until delivery to admit mum.
Delivery via c-section. Intrapartum + postpartum haemorrhage is common bc lower segment does not contract properly or there placenta accreta. Blood recycling + transfusion on hand in case. If haemorrhage too large, hysterectomy is a rare but possible outcome.

23
Q

what is placenta accreta? What are the RF?

A

when the placenta implants too deep into the uterine wall through decidua basalis into the myometrium and sometimes beyond this. (percreta into surrounding structures)
Previous c-section + pprevia / anterior placenta overlying old scar are at increased risk. MRI to help ID women at high risk.
Also different degrees- increta + percreta
Will cause massive haemorrhage if at all incised during c-section so incision must be made well away from it. Often involves resection of part of the uterus if not a total hysterectomy bc the placenta is too aherent to the uterus. Management of placenta include uterotonic agents to prevent blood loss.

24
Q

How would you differentiate between placenta previa + abruption clinically?

A
  • Abruption is painful often severely so + uterus is often hard “woody”, praaevia is not
  • Praaevia shock = amt of blood lost seen via naked eye, this is not the case in abruption
  • Bleeding is often red, and profuse in praveia but dark and may be none in abruption
  • Fétus engagement + lie usually normal in abruption, often high in abdomen + abnormal lie in previa
  • HR usually normal in previa, distressed/ dead fetus in abruption
  • US placenta often normal + not low in abruption but def low in previa.
25
Q

whjat is placental abruption? How does it present?

A

When part/ all of placenta Is separated from uterus before delivery of fetus. likely that many antepartum haemorrhages of undetermined origin are caused by small abruptions. When this happens, maternal bleeding occurs and can go in three directions, out into the vagina, into the liquor, or into the myometrium. May lead to further separation of placenta, and acute fetal distress, and sometimes fetal death. ALWAYS IMP TO CONSIDER CONCEALED BLEEDING.
vaginal bleeding + abdominal pain + contractions second half of pregnancy. Pain is constant during exacerbations.

26
Q

what are the trimesters of pregnancy? what is the age of viability?

A

Trimester 1: 0-12 weeks
Trimester 2: 13-27 weeks
Trimester 3: 28- 40 weeks
Age of viability: 24/52

27
Q

What are the RF for placental abruption? What are the s&s? What is the immediate management?

A

IUGR, maternal smoking, pre-eclampsia, pre-existing HT, previous abruption, autoimmune disease, cocaine use, high parity, polyhydramnios, advanced maternal age, low BMI.
Signs: Tachycardia poss if profound loss, uterus tender and often contracting (often go into labour), hypotension if MASSive bleed, woody uterus + fetus distressed, coagulopathy, poor urine output
Symptoms: abdo pain (constant with exacerbations), dark bleeding.
Immediate management:
- Admission for mum if more than spotting
- ABC: mum takes priority until stabilised
- monitoring BP, pulse, volume intake, and urine output. blood and fluid replacement Hb levels should be kept above 100 g/L (10 g/dL) and Hct above 30%. Urine output should be at least 30 mL/hour.
- Assess maternal wb, assess CV condition of mum, presence of pain. Fetal movements. Continuous pain = Abruption (intermittent- labour more likely ddx).
- Single course Steroids between 24-35 weeks if at risk of pre-term birth, significant reduction in rates of neonatal death, respiratory distress syndrome and intraventricular haemorrhage.
- Tocolytic therapy to delay delivery in Placental Abruption is CONTRAINDICATED!
- If prem, Consultant-led care + growth scans until later in pregnancy if mum + fetus well
- If term/prem + fetus + mum are compromised, c-section;
- if fetus + mum well vaginal.
- if fetus dead, vaginal delivery.
- Intrapartum CTG is required.
- Active management of Stage 3 labour to prevent PPH (ergometrine-oxytocin if not HT)

28
Q

What examinations should be performed on a woman presenting with APH?

A

ABC
Fetal HR
BP + Pulse
Abdo Palp (tense/ woody uterus), any tenderness.
Speculum
VE UNLESS SUSPECTING PP IN WHICH CASE CI
Kleihauer (if mum Rh-ve) to determine fetal maternal haemorrhage - guides amt AntiD given
USS for PP, does not help in determining abruption
U + E + LFT
FBC- platelets may be low if massive abruption, Hb if anaemia but not reliable in immediate bleed
Coag + Cross Match
CTG once mum stabilised, if cannot be detected USS to detect fetal HR

29
Q

what diagnostic tests are done for fetal anomalies?

A
  • Non-invasive prenatal diagnosis- samples free fetal DNA in mum’s blood but expensive and not 100% accurate
  • Anomaly scan (20/52) finds structural abnormalities
  • Invasive:
    CVS: Biopsy of trophoblast from 11/52 gest, needle into placenta, uses same as Amniocentesis but enables detection quicker and allows earlier TOP. Risk miscarriage higher bc spont miscarriage rate higher earlier in pregnancy.
    Amniocentesis: removal of Amniotic fluid US guided using fine needle. safest from 15/52 and allows chromosomal abnormalities dx, dx infection + inherited disorders eg CF/ Sickle Cell. 1% miscarry post-procedure.
30
Q

what are the blood test findings that might indicate the trisomies?

A 
DS: High HcG, low PAPP-A, low AFP, High Inhibin A, severe IUGR
Trisomy 18 (Edward's): low AFP
Trisomy 13 (Patau's): ADD TOO
31
Q

What are the outcome of Trisomy 18 + 13, and what are the genetics of Klinefelter’s and Turner’s?

A

13/18 die in utero or shortly after birth. 13: Patau, 18: Edward’s.
Klinefelter’s 47XXY
Turner’s 46 XO

32
Q

what is polyhydramnios? What are its causes? How is it managed? What are the complications?

A

Increased liquor volume. Severe in 1% pregnancy. Usually pool >10cm abnormal. Causes: idiopathic, maternal DM/ gest DM, Renal Failure, twins (partic twin-twin transfusion), fetal anomaly e.g. Upper GI obstruction.
Presents with: maternal discomfort, large for dates, diff to palpate
Complications; preterm labour, maternal discomfort, abnormal lie + malpresentation.
Management: Detailed USS (fetal anomaly), GTT, to reduce liquor if severe + < 34/52, use Amnioreduction (amniocentesis)/ NSAIDs to reduce urine output of fetus.
Vaginal delivery unless other indication

33
Q

What is important to gather as part of the Obs Hx?

A

Pregnancies include miscarriage, TOP, stillbirth
IVF/ Natural?
Problems during pregnancy(current or previous)? HT/ DM/ Bleeding/ Infections
Deliveries- gest age, type delivery + added forceps etc, Birth weight, issues post delivery: Shoulder Dystocia, Bleed, Tear (urinary/ faecal incontinence), Retained Products. If CS/ intervention: cause. Anaesthetic problems.

Gynae/ Abdo surgery

ADD TO

34
Q

Broadly explain twins. What are the risks of multiple pregnancy?

A
  • Usually dizygotic (ie two eggs fertilised by two sperm), diamnioitic, dichorionic, dizygotic (non-identical).
  • Monozygotic one egg + one sperm can result in multiple outcomes: diff sacs + diff placenta + monozygotic, or monochorionic + diamniotic (shared placenta but 2 amniotic sacs) - most common. or other rarer types.
  • RF: IVF, genetics, maternal age, parity
  • RISK: GDM, Pre-Eclampsia, Maternal Anaemia (more iron + folic acid req), APH/PPH (bigger placenta + larger uterus), Prolonged Labour, IUGR (more common Monochorionic same placenta- insufficient),
    Polyhydramnios, congenital abnormalities (in shared placenta), malpresentation, miscarriage (partic if TTTS) + preterm labour, stillbirth, Twin-twin transfusion syndrome (monochorionic- SAME PLACENTA), IUFD.
    Much higher rate of mortality + morbidity which increases with higher number of kids.
35
Q

How is multiple pregnancy managed antenatally?

A

High risk, CLC, MDT
Iron + Folic Acid
Low Dose Aspirin if risks of Pre-Eclampsia
Early USS indicates # placenta, Gest Age, screen DS (chorionicity - lambda sign indicates thicker membrane + two placentas) (λ) In monochroionic It is a thin T sign
Preterm birth CANNOT be prevented with P/ Cervical cerclage.
Serial growth scans to detect IUGR: at least 4wkly from 28/52 but more if monochorionic
Monochorionic: USS from 12/52, 2wkly and then 2-3wkly until delivery. Allows detection of TTTS.
IUGR- careful surveillance + induction preterm.
Deliver 37/52 for dichorionic; 36/52 for uncomplicated monochorionic

36
Q

What is twin-twin transfusion syndrome? How is it managed?

A

Common 16-24 weeks.
Only happens in monochorionicity ie where the placenta is shared. 15% time. Due to unequal blood distribution through vascular anastomoses of shared placenta. One twin is called the Donor and is volume depleted leading to suffering from anaemia, IUGR, Oligohydramnios. The Recipient twin however, becomes volume overloaded, polycythaemia (increased [Hb] ), HF, massive polyhydramnios which may enlarge uterus massively. Both twins at risk of IUFD/ severe preterm delivery.
Laser ablation of entire placental interface using US + fetoscope. Survival of both is 50%, one 80%, 10% neurodisability.

37
Q

How is multiple pregnancy managed Intrapartum?

A

Malpresentation of first twin 1/5 will require CS
Complications: Fetal Distress common particularly in second twin due to Cord Prolapse, Hypoxia, Tetanic uterine contraction, placental abruption, breech presentation, PPH.
Epidural
CTG monitoring due to risk of hypoxia/ distress particularly of second twin. Syntocin if contractions slow after first baby.
Ext Cephalic version of second twin if incorrect lie. Once Twin 2 enters pelvis, ARM
Syntocinon for active management of third stage to prevent PPH.

38
Q

What is the antepartum care for pre-existing DM?

A

CLC
MDT approach: Diabetic cons, specialist nurse, specialist MW, dietician, Obs cons. contact with joint diabetes and ANC every 1–2 weeks throughout pregnancy (NICE).
HbA1c at Booking
- Stop Statins / ACE-I
- Low dose Aspirin 75mg from 12/52 prevent PET
- Take Metformin (no chance of Hypo) + Insulin
- Admission for Hyperglycaemia/ unwell- Ketoacidosis
Counsel RE risk of Hypo partic impaired awareness Tri1
Growth Scans: Indicates IUGR/ Macrosomia + polyhydramnios which is an earlier sign of poor sugar control from 28/52 (at least 4 wkly)
7/day blood sugar testing: before + after every meal + before bed
Sugars should be kept below: 5.3mmol/L fasted
7.8mmol/L 1 hour after meals
Offer retinal + renal screening if not done within last 3/12 @ Booking + again at 28/52
Anaesthetics review during Tri3
IOL at 37+0 - 39/52 or CS if indicated. No later birth 40+ 6 due to risks of stillborn.

39
Q

What is important for Pre-conception counselling existing DM? What is important in Intrapartum care for women with pre-existing DM?

A
  • PREGNANCY NEEDS TO BE PLANNED! Contraception until HbA1c can be controlled to req tight range.
  • Support available but need freq contact with HC team.
  • 5mg Folic Acid until 12/52 pregnant
  • Offer monthly HbA1c
  • Advice for women to have waking (fasted) G of 5-7mmol/L
    Pre-meal G: 4-7mmol/L
    Normal range Hba1c: <10mmol/L at conception associated with congenital abnormality rate 5% which increases to 25% if >13 mmol/L, if cannot keep below 13 advise VS PREGNANCY.
    Intrapartum: IOL
    During labour v imp to maintain good glycaemic control to prevent Hypo in baby + jaundice in neonatal period. 1hrly Glucose measured, Sliding scale of insulin given.
40
Q

How are Blood Glucose levels managed in DM/ GDM during pregnancy?

A

Diet + Exercise (partic for GDM)
Metformin first line GDM
Insulin + Metformin as adjunct if bad GDM

41
Q

How should postpartum hypoglycaemia in neonates be managed? How should woman be managed postpartum?

A

Breastfeed asap within 30mins + every 2-3 hours to maintain pre-feed blood sugar levels of 2mmol/L minimum. IV Dextrose if not maintained.
Woman- reduce insulin immediately post-partum ( usually increased by 2-3x pre-pregnancy amts). Women at increased risk of Hypo postpartum esp if breastfeeding so snack during/ after feed. GDM Stop all Insulin/ Metformin immediately after delivery.

42
Q

What is involved in pre-conceptual care for normal pregnancy?

A

Folic Acid if normal risk of NTD: 400mcg/day until 12/52
Folic acid if higher risk ie Epileptic on meds, Obese, Malabsorption (coeliac), DM, Sickle Cell/ Thalassemia: 5mg/ day until 12/52. 10mcg Vitamin D (25 if BMI/ PET risk)

Healthy Diet: high in fibre, low in sugar + fat, base around starchy foods, 5 portions fruit + veg/ day. Avoid unpasteurised foods (Listeria risk)

Women > 30kg/m2 advise to lose weight, 5-10% pre-pregnancy have significant health benefits for them + baby + chance of becoming pregnant.

Stop smoking without nicotine replacement therapy if they can. Stop drinking, stop using drugs include illegal highs. Advise against exposure to radiation + hazard at work.

Cervical screening pre-pregnancy. Stop any unnecessary meds/ herbal remedies.

Immuniz: Rubella, Hep B, VZV

43
Q

What are the risks associated with obesity? Might be helpful to divide based on stage ie preconception, antenatal etc.

A

Preconception
Reduced Fertility

Antenatal
Increased risk miscarriage
GDM
GHT/ Pre-eclampsia
IUGR (pre-eclampsia)/ Macrosomia (GDM)
Congenital Abnormalities- might miss due to diff scanning

Intrapartum
Shoulder distocia (Macrosomia)
palpate + auscultate diff, CTG req + confined to bed but diff therefore do FSC of baby’s head.
Diff site epidural, aspiration risk in GA, intubation diff.
Preterm delivery (UTI)
Birth trauma
CS

Postpartum
VTE
Haemorrhage
Infection
Stillbirth
44
Q

What is involved in the Booking visit history?

A

History: Age (under 17 and over 35) increased chance of complications. Over 35- miscarriage, chr abnormalities, DM/HT/IHD pre-exist, DVT risk, stillbirth risk.
Under 17- pre-eclampsia, pre-term labour.
Prev Obs Hx: ever pre-term/ CS CLC; >4.5kg or <2.5kg CLC. Prev AN problems- HT, IP problems- Bleed, tear, shoulder, retained placenta. PN issues- depression, Birth wt, outcome.
Gynae hx- surgery, Smears, STIs, LETTS- preterm
Med Hx- HT, DM, CKD, VTE, CVD, autoimmune disorders, haemoglobinopathies, mental illness
Drugs- changed but ideally pre-conception done
Fhx- DM, Pre-eclampsia, HT, VTE, autoimmune, congenital
Social- Domestic violence, smoking, drink, drugs

45
Q

What is the inheritance pattern of CF and haemoglobinopathies?

A

CF: Autosomal Recessive (white Europeans)
Sickle Cell: Autosomal recessive (Carriers have sickle cell trait)
B Thalassemia: Autosomal recessive
A Thalassemia: Four genes encode. 4 copies= IUD, 3 copies= transfusion dependent, 1-2 copies= asymptomatic carrier.
Sickle Cell- Afrocarribean
Thalassemias: South East Asian, Mediterranean

46
Q

How is VTE risk managed in pregnancy?

A

Increased risk of VTE by 6x. Clotting factors are increased, fibrinolytic activity is reduced and blood flow is altered by mechanical obstruction and immobility.

If 4 or more RF for VTE, LMWH (Clexane) during AN period until 6/52 PP. [If Antithrombin deficiency/ Antiphospholipid syndrome + on longterm anticoagulant, give 50-75% full dose tx LMWH] – Ideally change from warfarin before w6.
If 3 RF for VTE, LMWH from week 28 and usually until 6/52 PP.
If 2 RF for VTE, LMWH for 10d PP.

47
Q

what are the risks of prolonged pregnancy?

A

increased risk of perinatal mortality (infant death/ stillbirth) increases between 41-42 weeks. Increased risk of neonatal illness, encephalopathy, meconium passage + fetal distress.
Aim to balance risk of induction of labour (failing and having CS) vs fetal distress due to prolonged pregnancy + CS. NNT= 500 to prevent 1 fetal death + IOL between 41-42 weeks reduces CS rate.
If woman refuses, perform cervical sweep + daily CTG.

48
Q

What is twin reversed arterial perfusion?

A

A rare complication in monochorionic twins
One twin is massively deformed often acardiac/ deformed heart therefore other twin (normal but small) acts as the “pump” and is at risk of cardiac failure. The deformed twin is incompatible with life but acts as a parasite receiving all deoxygenated blood from normal twin.

49
Q

what are the risks of substance misuse in pregnancy?

A

IUGR, preterm delivery, congenital abnormalities, infectious disease- HIV, Hep C.

Opiates- preterm delivery, IUGR, stillbirth, SIDS, Development Delay, Convulsions + withdrawal
Cocaine- IUGR, Abruption, Intel Impairment, Preterm, stillbirth, SIDS
Ecstasy- cardiac defects, gastroschisis
Benzos- facial cleft, neonatal hypotonia, withdrawal
Cannabis- IUGR, affect on development
Alcohol- early miscarriage, IUGR, FAS- face abnormalities + development delays, birth defects
Smoking- IUGR, stillbirth, preterm birth, abruption, SIDS

50
Q

How is Anaemia classified during pregnancy?

A

Tri1: <110 g/L
Tri2: <105g/L
Postpartum: <100 g/L

Increased blood volume of pregnancy is not matched by increase in RBC number therefore get net drop in Hb. Also increase in Iron + Folic Acid req.

51
Q

How is Anaemia diagnosed?

A

FBC at booking and again at 28w. (if multiple pregnancy, third FBC at 20-24w)
usually asymptomatic unless Hb <90.
Iron deficiency anaemia: MCV and Ferritin reduced
For Microcytic or Normocytic Anaemia, trial of Oral Iron to test whether iron deficiency anaemia. +ve if Hb rises in two weeks. (Oral iron commonly causes constipation)
Folic Acid/ Vitamin B12 deficiency: usually F.A., suspect if MCV is normal or increased.

52
Q

How is anaemia managed?

A

Oral Iron 100–200mg for Iron Deficiency +/- Folic Acid
Oral Iron for Haemoglobinopathy (sickle cell)
Advice on Dietary intake + how to ensure best absorption.
If late in pregnancy, gest >34 or Hb <70, IV Iron is required.

Intrapartum: IV Access, Group + Save, Active management of Stage 3 to minimise blood loss.
Once Hb is in the normal range supplementation should continue for 3months and at least until 6weeks postpartum
Consider blood transfusion in an emergency.

53
Q

What are the signs of VTE/ PE?

A

Chest pain, dyspnoea common but Tachycardia, tachypnoea, raised JVP and chest abnormalities are Imp signs

54
Q

What is the screening pathway for Gestational Diabetes? Who is screened for it? When is it performed?

A 
Urinanalysis at every visit.
If Glucose + or more, refer for random plasma G. If 6-11mmol/L refer for GTT at 28w. 
GTT is done at 28w. 
- Fhx (1 1st degree or 2 2nd degree). 
- previous macrosomia >4.25kg at term
- AC> 95% centile or growth acceleration of AC in present pregnancy
- Polyhydramnios dx
- Prev stillbirth
- Obesity > 30 BMI
- History of PCOS
- Previous gest DM

Obs & Gynae (11 decks)

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