Repro 5 Flashcards

1
Q

Molar pregnancy

A

Abnormal proliferation of trophoblastic tissue (1-2.5/1000). Also known as hydatidiform mole. Due to imbalance in number of chromosomes originating from the mother and father during conception. Parents tend to be <16 or >45

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2
Q

Types of molar pregnancy

A
  1. Complete hydatiform mole: no normal fetal tissue forms
  2. Partial hydatidiform mole: incomplete fetal tissue develops alongside molar tissue
  3. Invasive mole: contain many villi, but these may grow into or through the muscle layer of the uterus wall, persistently high HCG
  4. Choriocarcinoma: have cytotrophoblasts and syncytiotrophoblasrs but no villi form
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3
Q

Complete mole

A
  1. Most common type of hydatidiform mole. Diffuse thropoblastic hyperplasia, swelling of chorionic villi, no fetal tissue or membrane present
  2. Formed from a single sperm and an empty egg with no genetic material. Sperm replicates to provide a normal number of chromosomes
  3. Hydropic villi and focal trophoblastic hyperplasia are associated with 46XX or 46XY
  4. 10% INVADE AND 3% CHORIOCARCINOMA
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4
Q

Clinical features of a molar pregnancy

A
  1. Vaginal bleeding
  2. Uterine larger than date
  3. Hyperemesis gravidarum
  4. Thyrotoxicosis
  5. B-hcg > 100,000
  6. No fetal heart beat
  7. Presentation similar to threatened/ spontaneous/ missed miscarriage
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5
Q

Incomplete mole

A
  1. Often triploid (69(XXY,XYY,XXX) with chromosome complement from both parents 2 sperm fertilize 1 egg or 1 sperms with reduplication.
  2. Both paternal and maternal genetic material are present and there is variable evidence of foetal parts
  3. 1% RISK OF INVASION, does not become choriocarcinoma
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6
Q

Investigations for molar pregnancy

A
  1. UPT: B-hcg level
  2. U/S Complete – no fetus, classic snow storm
  3. U/S Incomplete – molar degeneration of placenta +/- fetal anomalies, multiple echogenic regions corresponding to hydropic villi and focal intrauterine haemorrhage
  4. CXR – may show metastatic lesions
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7
Q

Molar pregnancy: features of high risk neoplasm

A
  1. Local uterine invasion
  2. Beta hG >100,000
  3. Excessive uterine size
  4. Prominent theca- lutein cyst
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8
Q

Molar pregnancy- treatment

A
  1. Immediate referral to specialist centre
  2. Suction and curettage
  3. Anti-D in rhesus -ve
  4. If bleeding hysterectomy may be needed or if fertility preservation is not a concern
  5. Chemotherapy for chorio-carcinoma
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9
Q

Molar pregnancy- follow up

A
  1. If partial mole: repeat hCG is done 4 weeks later if normal discharged from surveilance
  2. Register with the national centres
  3. B-hcg 2/52 till normal
  4. Follow up monthly for 1 year
  5. Follow up 3 monthly in 2 year
  6. Occasionally the mole can metastasise and the patient may need systemic chemotherapy
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10
Q

Types of twins

A
  • Dizygotic twins: non-identical, develop from two separate ova that were fertilized at the same time
  • Dizygotic twins are all dichorionic and diamniotic (two separate outer and inner sacs) and have separate placentas
  • Monozygotic: identical, develop from a single ovum which has divided to form two embryos. Around 80% of twins are dizygotic
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11
Q

Types of monozygotic twins and USS findings

A
  • Depends on when the fertilised egg has split:
  • Dichorionic and diamniotic (two different sacs): lambda sign or twin peak sign which is a triangle sign
  • Monochorionic and diamniotic (same outer sac, two inner sacs): T sign
  • Monochorionic and monoamniotic (same sacs): no membrane
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12
Q

Monoamniotic monozygotic twins are associated with

A
  • increased spontaneous miscarriage, perinatal mortality rate
  • increased malformations, IUGR, prematurity
  • twin-to-twin transfusions: recipient is larger with polyhydramnios (Tx laser ablation of interconnecting vessels). When the fetus’s share a placenta, one twin (recipient) receives the majority of blood whilst the other (donor) is starved
  • Twin anaemia polycycthaemia sequence: one twin becomes anaemic the other develops polcythaemia
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13
Q

Predisposing factors for dizygotic twins include

A
  • previous twins
  • family history
  • increasing maternal age
  • multigravida
  • induced ovulation and in-vitro fertilisation
  • race e.g. Afro-Caribbean
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14
Q

Twins: antenatal complications

A
  • polyhydramnios
  • pregnancy induced hypertension
  • anaemia
  • antepartum haemorrhage
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15
Q

Twins; fetal complications

A
  • perinatal mortality (twins * 5, triplets * 10)
  • prematurity (mean twins = 37 weeks, triplets = 33)
  • light-for date babies, miscarriage, congenital abnormalities
  • malformation (*3, especially monozygotic)
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16
Q

Twins: labour complications

A
  • PPH increased, polyhydramnios
  • malpresentation
  • cord prolapse, entanglement
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17
Q

Twins management

A
  • rest
  • 2 weeks scans from 16 weeks for monochorionic twins
  • 4 weekly scans from 20 weeks for dichorionic twins
  • additional iron + folate: FBC check (for anaemia) at booking clinic, 20 weeks gestation and 28 weeks
  • more antenatal care (e.g. weekly > 30 weeks)
  • precautions at labour (e.g. 2 obstetricians present)
  • 75% of twins deliver by 38 weeks, if longer most twins are induced at 38-40 wks.
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18
Q

Multiple pregnancies; timing of births

A
  • 32 and 33 + 6 weeks for uncomplicated monochorionic monoamniotic twins (C-section)
  • 36 and 36 + 6 weeks for uncomplicated monochorionic diamniotic twins
  • 37 and 37 + 6 weeks for uncomplicated dichorionic diamniotic twins
  • If diamniotic can have vaginal if first baby is cephalic
  • Before 35 + 6 weeks for triplets
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19
Q

Risks of obesity in pregnancy

A

Risks pre-conception: Subfertility/ Miscarriage, VTE, GDM, Hypertensive disease: Double risk of pre-eclampsia with booking BMI >35

Risks intrapartum; Slow progress in labour, C-Section, Shoulder dystocia, Anaesthetic risk, Epidural/spinal failure, PPH, Aspiration, Difficult intubation, Post-op atelectasis, Stillbirth

Risks to baby: Neural tube defects, Macrosmia, prematurity, Admission NNU, Neonatal death

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20
Q

Management for BMI >30

A

Women with BMI >30 should be advised to take 5mg Folic acid daily, starting at least one month before conception and continuing during first trimester to reduce the risk of NTDs. Dont advise weight loss by dieting when pregnant

Obesity is defined as a BMI >30kg/m at the first antenatal visit

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21
Q

Antenatal care: BMI 30-35

A
  1. Discuss risks of obesity:
  2. Pre-eclampsia
  3. VTE - Consider antenatal LMWH (weight adjusted dose) if additional risk factors for VTE
  4. Gestational diabetes mellitus - screen with OGTT at 24-28 weeks
  5. High dose Vitamin D (10 micrograms daily) throughout pregnancy and breastfeeding, due to increased risk of Vitamin D deficiency in obesity
22
Q

Management if BMI >35

A
  1. Offer serial fetal growth USS as measurement of SFH can be unreliable
  2. Consider starting Aspirin 75-150mg if there are additional moderate risk factors for pre-eclampsia
23
Q

Management if BMI >40

A

If BMI >40 - will need antenatal anaesthetic review to identify potential problems with venous access and anaesthesia. Should have an antenatal consultation with an obstetric anaesthetist and a plan made

BMI should be re-measured at 28 weeks (for everyone)

24
Q

Labour and delivery

A
  1. If BMI >35, advise to give birth in a consultant-led obstetric unit
  2. Obesity alone is not an indication for induction of labour
  3. BMI >40: continuous midwifery care when in established labour & venous access in early labour
  4. Risk of difficult delivery if macrosomic baby eg. shoulder dystocia, maternal and fetal injuries
  5. Increased risk of emergency c-section, and operation may be more technically difficult
  6. Active management of third stage, to reduce the risk of PPH
  7. Postpartum: all women with a BMI >40 should have a LMWH
25
Q

Obstetric cholestasis

A
  • Multifactorial disease characterised by pruritus in the absence of a skin rash with abnormal liver function tests (LFTs), neither of which has an alternative cause and both of which resolve after birth.
  • Other causes of pruritus and abnormal LFTs must be ruled out (eg. Viral hepatitis, gall stones, autoimmune causes).
  • Typically manifests after the 24th week of pregnancy.
  • Impaired bile flow due to the accumulation of bile acids. Bile acids build up in the blood
26
Q

Obstetric cholestasis associated risks and risk factors

A
  • Maternal: pruritis, sleep deprivation, C-Section
  • Fetal: preterm labour, fetal death (physiology of stillbirth risk not well understood. Not associated with hypoxia, placental insufficiency or IUGR. Possibly related to bile acid toxicity to cardiomyocytes increasing risk of fetal arrhythmia)

Risk Factors: Previous OC, family history of OC, multiple pregnancy, gallstones, Hepatitis C

27
Q

Obstetric cholestasis clinical features

A
  1. Pruritus: particularly hands & feet, usually worse at night & starts in 3 trimester
  2. Other: mild jaundice, pale stools, dark urine, abdominal pain, anorexia, fatigue, malaise
  3. Increased risk of premature birth
28
Q

Obstetric cholestasis investigations- to rule out alternative Dx

A
  • Bedside: Blood Pressure, Urine dip for proteinuria
  • Bloods: LFTs, Bile Acids, Viral screen – Hepatitis, CMV, EBV; Liver autoimmune screen, HELLP screen
  • Imaging: Liver USS
29
Q

Obstetric cholestasis management

A
  • Emollients- reduce itch.
  • Chlorphenamine; Help sleeping
  • Ursodeoxycholic acid: off label
  • Weekly bloods and CTGs (though stillbirth not thought to be hypoxic)
  • Induction of labour – timing depends on level of bile acids but tends to be 37-38 weeks
  • If >100 consider from 35 weeks (as risk of stillbirth greater in this group), if <100 can wait until 39 weeks (unless symptoms debilitating, other indications etc).
  • Vitamin K if clotting is deranged
30
Q

Pelvic inflammatory disease definition and presentation

A

Definition: inflammation of the upper female reproductive tracts

Presentation
- Bilateral lower abdominal pain
- Deep dyspareunia, post coital bleeding
- Purulent discharge
- Abnormal uterine bleeding
- Nausea and Vomiting
- Urinary symptoms
- Fever > 38 C but can be afebrile
- Cervical excitation

31
Q

Management and investigations of placental abruption

A
  • US: can exclude placental praevi
  • Antenatal steroids given between 24 and 34+6 weeks
  • Rhesus D negative women require anti-D prophylaxis
32
Q

PID signs on examination

A
  • CERVICAL EXCITATION (MOTION TENDERNESS) – Key finding
  • Inflamed cervix (Cervicitis)
  • Adnexal tenderness
  • Mucopurulent cervicitis on speculum examination
33
Q

PID causes

A
  • Untreated chlamydial or gonorrhoeal infection can progress to PID
  • Neisseria Gonorrhoea or Chlamydia trachomatis. Or Mycoplasma genitalium
34
Q

PID risk factors

A
  • Increased risk in women with multiple sexual partners
  • <20s
  • Termination of pregnancy can introduce bacterial infection to the upper reproductive tract
  • Iatrogenic due to invasive gynaecological procedures
35
Q

Concealed abruption

A

where the cervical os remains closed and the bleeding occurs within the uterine cavity. The bleeding can be significantly underestimated

36
Q

PID management

A
  • If patient is severely unwell, consider admission for IV antibiotics
    • Fever >38 C
    • Severe nausea or vomiting
    • Ectopic pregnancy cannot be ruled out
    • Patient is haemodynamically unstable
  • Start empirical antibiotics as soon as diagnosis is confirmed
  • IM ceftriaxone + oral doxycycline + oral metronidazole
  • Or oral Ofloxacin + oral metronidazole
  • Avoid unprotected intercourse
  • Removal of IUD should be considered
36
Q

PID investigations

A
  • Bimanual
  • Endocervical Swabs for Chlamydia and Gonorrhoea with nucleic acid amplification tests
  • Urine dipstick and culture – Rule out UTI
  • Pregnancy Test- rule out ectopic which can also present with cervical excitation
  • Bloods: CRP, ESR
  • Pelvic USS – Rule out other pathology
  • Gold Standard: Laparoscopic visualisation
    • Invasive procedure only to be performed if clinical uncertainty
36
Q

Placenta praevia definition and risk factors

A

When the placenta lies wholly or partly in the lower uterine segment and may cover the cervical os. Suspect if vaginal bleeding after 24 weeks of pregnancy

Associated factors= Multiparity, multiple pregnancies, previous caesarean section

36
Q

PID complications

A
  • Subfertility caused by scarring and inflammation of the reproductive tract
  • Chronic Pelvic Pain
  • Reiter’s syndrome
  • Increased likelihood of future ectopic pregnancy
  • Increased risk of preterm delivery
  • Increased foetal and maternal morbidity in future pregnancies
  • Perihepatitis (Fitz-Hugh Curtis syndrome)- causes inflammation and infection of the liver capsule, RUQ pain
37
Q

Placenta praevia clinical features

A
  • Shock in proportion to visible loss
  • No pain
  • Uterus not tender
  • Lie and presentation may be abnormal
  • Fetal heart usually normal
  • Coagulation problems rare
  • Small bleeds before large (bright red)
  • Malpresentation of the foetus may be found on examination
37
Q

Placental praevia diagnosis

A
  • Digital vaginal examination should not be performed before an ultrasound as it may provoke a severe haemorrhage
  • Placenta praevia is often picked up on the routine 20 week abdominal ultrasound
  • Painless bleeding from 13 weeks: TV US
37
Q

Placental praevia classical grading

A
  • I - placenta reaches lower segment but not the internal os
  • II - placenta reaches internal os but doesn’t cover it
  • III - placenta covers the internal os before dilation but not when dilated
  • IV (‘major’) - placenta completely covers the internal os
38
Q

If low lying placenta at the 20 week scan

A
  • Rescan at 32 weeks
  • No need to limit activity or intercourse unless they bleed
  • If still present at 32 weeks and grade I/II then scan every 2 weeks
  • Final ultrasound at 36-37 weeks to determine the method of delivery: elective caesarean section for grades III/IV between 37-38 weeks. If grade I then a trial of vaginal delivery may be offered
  • If a woman with known placenta praevia goes into labour prior to the elective caesarean section an emergency caesarean section should be performed due to the risk of post-partum haemorrhage
39
Q

Placenta praevia with bleeding

A
  • admit
  • ABC approach to stabilise the woman
  • if not able to stabilise → emergency caesarean section
  • if in labour or term reached → emergency caesarean section
  • Corticosteroids if 24-34 weeks and risk of preterm labour
  • Placenta pravi with no bleeding and not in labour: monitor with US and pelvic rest, no penetrative sexual intercourse
40
Q

Placenta praevia prognosis

A
  • death is now extremely rare
  • major cause of death in women with placenta praevia is now PPH
41
Q

Placental abruption

A

Placental abruption describes separation of a normally sited placenta from the uterine wall, resulting in maternal haemorrhage into the intervening space

42
Q

Risks of PPH

A
  • Antepartum haemorrhage
  • Emergency caesarean section
  • Emergency hysterectomy
  • Maternal anaemia and transfusions
  • Preterm birth and low birth weight
  • Stillbirth
43
Q

Causes of placental abruption-

A
  • proteinuric hypertension
  • Pre-eclampsia or hypertension
  • Polyhydramnios
  • cocaine use, existing coagulation disorders
  • Trauma, smoking
  • multiparity
  • maternal trauma
  • increasing maternal age
44
Q

Placental abruption- clinical features

A
  • shock out of keeping with visible loss (hypotension and tacchycardia)
  • Reduced fetal movement and abnormal CTG
  • pain constant
  • tender, tense uterus
  • Woody hard uterus
  • Contractions
  • normal lie and presentation
  • fetal heart: absent/distressed
  • coagulation problems
  • beware pre-eclampsia, DIC, anuria
45
Q

Management of placental abruption; fetus alive and <36 weeks

A
  • fetal distress: immediate caesarean
  • no fetal distress: observe closely, steroids, no tocolysis, threshold to deliver depends on gestation
46
Q

Management of placental abruption: >36 weeks

A

Fetus alive and > 36 weeks
- fetal distress: immediate caesarean
- no fetal distress: deliver vaginally

Fetus dead= induce vaginal delivery

47
Q

Complications of placental abruption

A
  • Maternal= shock, DIC, renal failure, PPH
  • Fetal= IUGR, hypoxia, death
  • Prognosis= associated with high perinatal mortality rate, responsible for 15% of perinatal deaths