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MD3 > Obstetrics > Flashcards

Obstetrics Flashcards

1
Q

Antenatal visit frequency

A

> 28/40: monthly
28-36: biweekly
36: weekly

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2
Q

Medications that cross the placenta so should be changed in pregnancy are

Medical conditions advised AGAINST getting pregnant

A

Anti-epileptic drugs
Warfarin (swap for LMW hep)

Pulm HTN
Renal failure (until on dialysis or receive a transplant)
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3
Q

SX of pregnancy

A

Nausea
Tender breasts
Missed period
Urinary frequency

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4
Q

Naegle’s rule

A

Date of conception is first day of last normal period + 9 months and 7 days

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5
Q
  1. When does the uterus first become palpable?

2. When do fetal movements first become noticeable?

A
  1. 12 weeks

2. ~20 weeks

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6
Q

What supplements should pregnant women be taking?

A

Folate
Vitamin D
Iron
Ca

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7
Q

Routine bloods at first antenatal visit (12 weeks)

A 
FBE
Blood group and antibody screen (ABO, Rh)
HIV, HBV, HCV, syphilis 
Rubella immunity 
MSU for MCS (?asymptomatic bacteriuria)

+/- VZV immunity
+/- Down syndrome serum screen (free betaHCG, PAPP-A)

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8
Q

Components of combined down syndrome serum screen

A

12 week ultrasound - gestational age and nuchal translucency
Serum free bHCG + PAPP-A

OR as an alternative, non-invasive pre-natal screen for cell-free DNA from 9 weeks. tests for aneuploidies. 99% NPV. If pos, refer for invasive testing. Takes 3 days but costs $450.

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9
Q

IF a women’s combined serum screen comes back as high risk, what is the next step in investigations for diagnosis?

A

Refer her for diagnostic invasive testing (chorionic villus sampling at 10-13 weeks or amniocentesis at 15-18 weeks) anti-D if mum is Rh neg

+ FISH and full karyotype

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10
Q

when do routine USS in low-risk pregnancies typically occur.

A

Ultrasound @ 12 weeks: gestational age and down syndrome screen

18-20weeks: morphology and wellbeing

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11
Q

What bloods get done in the second trimester and when?

A

28 week bloods:

  • FBE
  • Oral glucose challenge
  • AB screen in Rh neg women (will need anti-D injections if no Anti-D detected)
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12
Q

Who needs anti-D injections and when are these given?

A

Rh neg women who are negative for anti-D antibodies
Given at 28 and 36 weeks

To Rh(neg) women with M/C, invasive procedures, abruption, trauma etc

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13
Q

What 2 medical conditions do we screen for every visit and how do we do this?

A

Placental insufficiency - ask about fetal movements + SFH

Pre-Eclampsia - HTN (BP), proteinuria (urine dipstick) , oedema (exam/Hx)

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14
Q

When should women stop working?

A

34 weeks onwards

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15
Q

What routine Inx get done in the third trimester and when?

A

36 weeks:

  • FBE
  • AB screen in Rh neg women (will need anti-D injections if no Anti-D detected)
  • GBS swab! (lower vaginal)
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16
Q

Physiological changes in third trimester

A

Breast enlargement, colostrum production
Uterine contractions/tightenings, painless at first and becoming more painful closer to labour
Cervical ripening (effacement and dilation), evidenced by incr loss of D/C or mucus plug

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17
Q

Advise to women in third trimester as to when to come to hospital

A

Contractions are regular and painful, occurring ~1x5min (2:10) OR:

  • DFM
  • Bleeding
  • SROM
  • Psychological distress
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18
Q

When does the GBS swab get done?

A

36 weeks, lower vaginal and anal swab

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19
Q

When does the oral glucose challenge test get done?

A

28 weeks

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20
Q

How do you assess fetal wellbeing antenatally (5)

A
  1. fetal movements
  2. maternal SFH
  3. USS
  4. Infection screen +/- karyotype (aneuploidy screen)
  5. CTG
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21
Q

Assessing fetal wellbeing in labour

A
  1. CTG
  2. fetal movement
  3. Doppler
  4. Fetal scalp blood sampling
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22
Q

At what gestation does the uterus sit at the

  1. umbi
  2. xiphisternum
A
  1. 20 weeks

2. 38 weeks

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23
Q

Causes of:

  1. Oligohydramnios
  2. Polyhydramnios
A
  1. Decr fetal urine production (kidney or urinary tract problems) or ruptured/leaking membranes
    - Placental insufficiency
    - Post-date pregnancy
    - Maternal problems (HTN, PE, dehydration, GDM)
  2. Fetal inability to swallow or excess amniotic fluid production (polyuria in GDM)
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24
Q

What arteries does the doppler measure blood flow in and what is the clinical significance of each?

A

Umbilical arteries: fetal blood flow to placenta. Placental resistance to flow should be low and cardiac activity high so good flow in diastole.
Placental insufficiency or cardiac impairment can lead to absent or reversed diastole flow and high resistance to flow.

MCA: blood from circle of willis to brain. Resistance to flow should be HIGH. Fetal hypoxia -> MCA dilates -> reduces resistance to flow.

Uterine arteries: reflects maternal perfusion of uterus and normal placental implantation. Resistance should start high and reduce after 23 weeks.

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25
Q

what growth scan patterns do you see in IUGR babies?

GDM babies?

A

asymmetrically small: HC is relatively larger than AC

Asymmetrically large: AC to HC ratio high (due to glycogen deposits in liver)

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26
Q

What doppler USS features do you see in IUGR babies?

A

Umbilical arteries: increased resistance and reduced end diastolic flow (incr SDR, PI and RI). OR absent end diastolic slow (RI=1) OR reversal of end diastolic flow

MCA: decr resistance

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27
Q

Differentials for small fetus

A
  • Normal
  • Incorrectly diagnosed (earlier in gestation than thought)
  • Abnormally small (chromosomal/structural/genetic syndrome)
  • IUGR
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28
Q

Management of IUGR

A

Maternal CS administration if expected pre-term

NVD w continuous CTG monitoring if near term

If v small and v preterm, may need elective LUSCS

Maternal and fetal condition dictates need/timing of delivery

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29
Q

Differential causes of macrosomia

A

Normal
Incorrectly diagnosed
Maternal GDM
Beckwith-Wiedemman Syndrome

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30
Q

Indications for elective C/S delivery for large babies

A

If EFW >97th centile
GDM
High AC: HC ratio (risk of shoulder dystocia)

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31
Q

Risk factors for ovarian cancer

Protective factors

A
  • Age
  • Obesity
  • Incr # ovulations (nulliparity)
  • Family HX ovarian/breast/colorectal cancer:
    Lynch syndrome (HNPCC) - 10% risk
    BRCA1 (50% risk)
    BRCA2 (20% risk)
  • HRT/unopposed oestrogen

Protected: OCP, multiparty, breast feeding

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32
Q

Most common histo subtype of ovarian cancer

A

Serous adenocarcinoma

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33
Q

Clinical présentation of ovarian cancer

A 
Bloating, abdo swelling
Abdo pain
Dyspepsia 
Urinary freq
Weight change
Irreg bleeding
SX metastatic disease: ascites, pleural effusions, SBO/LBO
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34
Q

Inx for suspected ovarian cancer

A

TVUSS

Bloods: CA125 and CEA ; hcG, LDH, alpha fetoprotein

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35
Q

Management of ovarian cancer

A
  1. Pre-op CT or MRI
  2. Surgical staging and debunking (aim for <1cm residual) - laparotomy or hysterectomy + bilateral salpingo-oophrectomy
    OR Chemo if disease is widespread/metastatic at diagnosis
  3. Post-op: 6 cycles cytotoxic chemo
  4. Regular monitoring: imaging and CA125 levels
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36
Q

Stages of ovarian cancer

A
  1. limited to ovaries
  2. ovaries + pelvic spread (uterus, tubes, bowel, bladder etc)
    • disease outside pelvis +/- positive retroperitoneal or inguinal lymph nodes
    • distant mets /liver parenchymal disease
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37
Q

Risk factors uterine cancer

A
  • Age
  • Caucasian
  • nulliparity
  • early menarche, late menopause
  • Hx infertility
  • HRT/tamoxifen
  • Obesity
  • Diabetes
  • PCOS
  • Endometrial hyperplasia
  • HNPCC
  • Endometrial polyps
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38
Q

screening for ovarian cancer

A

NOT Recommended in asymptomatic women.

Only in women w Lynch syndrome - are high risk so annual endometrial sampling is recommended

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39
Q

Main histo subtypes for endometrial cancers

-prognosis

A

endometriod and mucinous adenocarcinoma

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40
Q

2 types of uterine cancers and he relative proportions of each

What are the prognoses of each?

A

95% Endometrial (good prognosis)

5% Sarcoma (myometrial cancer) - aggressive, younger onset and poor prognosis

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41
Q

How do you diagnose endometrial cancer?

A

Endometrial biopsy for histology, via D&C, O/P pipelle, or hysteroscopy

+ Evidence of spread via CT or MRI abdo, chest, pelvis

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42
Q

Management of uterine cancer

A

REFER TO GYNAE ONC

Pre-op CT/PET/MRI to assess for risk of lymph node mets - may need lymphadenectomy for high risk tumours (ex: Lynch)

Total hysterectomy + bilateral salpingooophrectomy +/- pelvic and para-aortic lymphadenectomy
NEED To assess involvement of ovaries via histopath- determines stage and prognosis

Younger women: want to conserve fertility so trial progesterone therapy (high dose oral or IUD)
If this fails, need hysterectomy + conservation of ovarian reserve

Long-term follow up evaluating for recurrence (13% risk overall, higher if metastatic spread at DX)

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43
Q

2 main Histological subtypes of cervical cancers

A

80% SCC

20% Adenocarcinoma

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44
Q

Presentation of cervical cancer

A

Early stage:
Asymptomatic
Post-coital bleeding, AUB, PMB, vaginal D/C

Late stage:

  • pelvic or back pain
  • Sciatica/neuropathy
  • enlarged groin nodes
  • bladder/bowel SX, lower limb oedema
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45
Q

How does cervical cancer spread?

What nodes does it spread to first?

A 
Local extension (perineum, vagina bladder, bowel, 
Lymphatics

Nodes: Pelvic -> common iliac -> Paraaortic nodes (rarely inguinal nodes involved)

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46
Q

How is staging of cervical cancer performed?

A

Clinically at first (spec, bimanual, cystoscopy, PR etc).

Further accuracy based on PET/MRI/CT +/- surgery.

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47
Q

FIGO Staging of cervical cancer

A

0 - carcinoma in situ (full thickness but no stromal invasion)
1 - confined to cervix
2 - spread beyond uterus but not to pelvic wall or lower 1/3 of vagina
3 - extends to pelvic wall and/or to lower 1/3 vagina
4 - involves mucosa of bladder/bowel OR mets in distant organs

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48
Q

Treatment of cervical cancer

A

MANAGED by gynae onc! REFER!

Stage 1-2a: surgery (cone biopsy or trachelectomy or hysterectomy +/- staging lymphadenectomy) or chemoradiation
Stage 2b-4A (bladder/bowel): chemoradiation
Stage 4b: systemic chemotherapy

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49
Q

What is a trachelectomy?

A

Remove cervix, parametric with cuff of vagina and suture uterus back to top of vagina

Fertility-sparing measure in treatment of cervical cancer for young patients with stage 1-2a disease

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50
Q

The different ‘layers’ of the cervix (endo/exo/trans zone etc)

A

Endocervix: columnar mucus -secreting epithelium

Transformation zone: squamo-columnar junction, area of active cellular change! cells constantly changing over from columnar to squamous when exposed to acidic pH of vagina (undergoing metaplasia), hence are prone to making mistakes and becoming dysplastic (esp w infected w HPV).

Ectocervix: non-keratinising squamous epithelium

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51
Q

Risk factors for cervical cancer

A 
SMOKING
Long term OCP use
HIV, immune suppression 
High parity
Chlamydia trachoma's, HSV infection
Uncircumcised male partner
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52
Q

What can HPV virus cause?

A 
Genital warts (warts elsewhere too, like plantar warts etc)
Cervical cancer 
Vulval/vaginal cancer
Anal cancer
Penile cancer
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53
Q

Natural history of HPV infection of cervix

A

Normal cervix HPV infected cervix with mild-cytological abnormalities. This can be cleared by the immune system so the cervix goes back to normal, or can progress to a precancerous lesion (CIN 1 and 2 which are LGSIL or CIN3 which is HGSIL). Most LGSIL regress without treatment.
Most HGSIL will progress over 7-10 years, if not treated, to invasive cancer (carcinoma in situ)

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54
Q

When is the guardasil vaccine given and what HPV strains does it protect against?

A

Given at 0, 2, 6 months of age

HPV 16,18,11

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55
Q

What is the screening process for cervical cancer?

A

Currently women aged 18-70 who have ever been sexually active need 2 yearly pap tests

Options:

  • Smear test
  • Liquid based cytology (thin prep or sure pap)
  • HPV test (detects HPV DNA presence, 99% NPV)
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56
Q

Management of LGSIL found on pap test

A

Mostly acute/transient HPV infection that the body clears within 12 months

NO TREATMENT. Repeat smear yearly until 2 consecutive neg results, then return to normal bi-yearly screening.

If a second LGSIL -> colposcopy and biopsy -> if confirmed normal or LGSIL, screen again in 12 months; if confirmed HGSIL, treat.

If any progression to HGSIL on repeat smears, straight to colposcopy and biopsy

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57
Q

Management of HGSIL found on pap

A 
Colposcopy and biopsy
Confirmation on biopsy needs tx:
Conservative 
- Diathermy
- Laser
- Cryotherapy
- LLETZ (most common tx mode) = large loop excision of transformation zone
- Cone biopsy (only used for adenocarcinoma in situ due to incr risk profile)

Definitive
- Hysterectomy (fertility not desired)

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58
Q

Follow up protocol post HGSIL dx and tx

A
  1. 4-6 monthly pap test and colposcopy
  2. 12 monthly pap test, HPV test (test of cure as 99% NPV). Repeat annually until woman has tested negative to both tests on 2 consecutive occasions, then return to normal 2 yearly screening.
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59
Q

Risks to pregnancy w LLETZ procedure

A

If > 2x LLETZ, incr risk of cervical incompetence -> preterm labour

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60
Q

Ovarian germ cell tumours
- which type are most common?

-when is their peak incidence?

A

most common - 95% benign, mature cystic teratomas (dermoid cysts)

Other types can be malignant

peak incidence in fertile years (young women and teens)

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61
Q

How might an ovarian germ cell tumour present?

A

Non specific abdo sx

  • abdo distension and pain (? ruptured cyst or torsion)
  • mass effects (bladder, bowel sx)
  • Menstrual irregularities
  • SX of pregnancy
  • SX of metastatic disease (ascites, lymphadenopathy)
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62
Q

Investigating suspected germ cell tumour

A 
Tumour markers (AFP, LDH, CA125, CA19.9, bHCG)
TV USS
CT abdo pelvis if malignancy suspected
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63
Q

MX of ovarian germ cell tumours

A

Surgery

  • cystectomy w ovarian preservation (dermoid cysts only)
  • Unilat salpingooophrectomy +/- …

Adjuvant chemotherapy

Follow up (Hx, exam, tumour markers) for 10 years after

Any recurrence gets chemo, not surgery!

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64
Q

What is GTD?

A

tumours arising from the fetal trophoblast -> abnormal proliferation of trophoblast, capable of invasion and metastatic spread

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65
Q

How does GTD present?

A

Usually presents as miscarriage <10weeks and is diagnosed on post-mortem histopath

Sx of pregnancy

Early pregnancy PV bleeding

irregular vaginal bleeding

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66
Q

What hormone does GTD produce and how is this helpful clinically?

A

produces hCG, used as a tumour marker for diagnosis (serial hCG) and follow-up/monitoring

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67
Q

Types of GTD

A

Benign (hydatidiform mole=molar pregnancy)
- partial or complete

Malignant or persistant = gestational trophoblastic neoplasm
- diagnosed after attempted evaluation of molar pregnancy, when it persists/hCG levels fail to decrease

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68
Q

Which type of benign molar pregnancy has a higher risk of progression to neoplasia?

A

Complete mole

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69
Q

How do complete vs partial moles originate/their genotypes?

A

Complete: sperm fertilises an empty egg and then duplicates it’s genetic material to form a full set -> 46XX or 46XY (YY not seen)

Partial: 2 sperm fertilise a normal egg -> 69XXY (triple karyotype)

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70
Q

Treatment benign moles

A

Suction curette with simultaneous US exam, oxytocic support and D&C
Anti-D to Rh neg women (risk of haemmhorage)

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71
Q

Spread of malignant GTD

A

Local spread

+ via blood to liver, lungs, brain

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72
Q

Treatment and prognosis of malignant GTD

A

Treatment: chemo +/- surgery (if no desire for future fertility or chemo-resistant mets)

Follow up via serial HCG and early surveillance in future pregnancies due to risk of recurrence

Prognosis - 100% cure rate if caught before metastatic stage

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73
Q

complications of genital prolapse

A

Hydronephrosis (obstruction of ureters in severe cases)

Urinary retention (outflow obstruction)

Faecal incontinence
Rectal prolapse
Haemmharoids

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74
Q

Risk factors for prolapse

A 
Age
Smoking
Obesity
Incr post-menopausal status (decr oestrogen)
Incr parity 
Incr birthweight

CLD

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75
Q

types of genital prolapse

A

cystocoele (anterior compartment collapse)
Rectocele (posterior compartment collapse)
Enterocoele (Small intestine)

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76
Q

SX of genital prolapse to ask about

A 
Dragging/heavy sensation in vagina
Lump/bulge in vagina 
Difficulty emptying bladder/bowels
Difficulty inserting tampons
Urinary/fecal incontinence
Haemmharoids 
lower back pain
DC/bleeding from ulceration
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77
Q

Management of genital prolapse

A

Reassurance
Reversible risk factor identification and lifestyle changes (weight loss, stop smoking, constipation)

Pelvic floor exercises - liase w physio and continence nurse

Vaginal oestrogen supplements (topical creams)

Vaginal pessaries!

Surgery last line

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78
Q

Side effects of pessaries

A 
Ulceration, bleeding
incr rates infection and D/C
Expulsion
Constipation
Pain
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79
Q

causes of urinary incontinence

A

Pregnancy

Injury/trauma (pregnancy/malignancy/direct trauma/pelvic radiotherapy, complications following surgery )

Medications

Medical conditions (DM, UTI, MS,

Excessive fluid intake

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80
Q

Causes of Fecal incontinence

A

Most common cause is childbirth!

  • traumatic delivery causing nerve damage or direct trauma to anal sphincter
  • fetal macrosomia
  • 3rd and 4th deg perineal tear/epis
  • instrumentation
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81
Q

types of incontinence

A
  1. Stress incontinence: loss of urine with IAP incr
  2. Urge incontinence: loss of urine assoc w uncontrollable desire to void
  3. Detrusor overactivity: urodynamic dx made when detrusor contraction is assoc w strong desire to void in a person trying NOT to
  4. Overactive bladder - urinary freq and urgency +/- urge incontinence
  5. Voiding dysfunction
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82
Q

How do you assess the progress of a woman in labour?

A
  1. Abdo palpation hourly
  2. Contractions - duration, freq, intensity
  3. VE - 4 hourly (as long as membranes are NOT ruptured)
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83
Q

Indications for giving Abx intrapartum (and what antibiotic?)

A

GBS positive mum or GBS status unknown (i.e. preterm)
Maternal fever
Prolonged ROM >18 hours
Previous baby with widespread GBS disease

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84
Q

Options for intrapartum pain relief

A

Support person

NO mask

PCA Narcotics (morphine has longer half life than fentanyl or pethidine)

Regional anaesthesia using lignocaine or bupivicaine (epidural for labour ward; spinal for theatre, faster onset action but shorter t1/2)

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85
Q

How do you assess the mother and baby during labour?

A

Mother:

  • Vitals (BP, temp, HR) hourly
  • contractions (should be ~4:10)
  • Urine 4 hourly
  • PV loss?

Baby:

  • Doppler USS if no risk factors
  • CTG if high risk
  • Amniotic fluid - colour and vol
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86
Q

Criteria for incr risk baby needing additional monitoring

A

DM, HTN/PE, IUGR, bleeding, mea stained liquor, abnormal FHR

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87
Q

SE of regional analgeisa

A

Hypotension
Pruritus, headache
URinary retention (req IDC)
Paralysis (rare)

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88
Q

Explain the mechanics of 2nd stage of labour

A
  1. maternal effort (urge to push)
  2. gravity
  3. uterine contractions

baby

  1. head moulding to change shape
  2. flexion of head onto chest (OE smallest diameter)
  3. rotation (baby undergoes internal rotation, head extension then external rotation of head)
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89
Q

active management of third stage

A
  1. oxytocin/syntocinon to stimulate uterine contraction to deliver placenta/prevent PPH
  2. controlled cord traction
  3. fundal pressure
  4. cord clamping within 5 min
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90
Q

Causes of PPH

A

Tone
Tissue
Trauma
Thrombin (rare)

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91
Q

when is the foetus most susceptible to teratogens?

A

first trimester, when organogenesis occurs

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92
Q

Effects of smoking on fetus

A 
Prematurity
IUGR/LBW
Miscarriage
Stillbirth
Placental abruption
SIDs
Premature rupture of membranes
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93
Q

What defines Hyperemesis gravidarum. What complications do you have to watch for?

A

Excessive pregnancy related vomiting and nausea that prevents adequate food and fluid intake and is assoc w >5% LOW, usually peaking mid-first trimester

Complications: dehydration, malnutrition, electrolyte imbalance, mallory-weiss tear with prolonged/severe vomiting, hyperthyroid (due to cross-reactivity between TSH and HCG)

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94
Q

RF for hyperemesis gravidarum

A 
Previous HG
Multi-pregnancy
Molar pregnancy
Female embryos
Increase free beta HCG (molar pregnancies)
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95
Q

Investigations for vomiting in pregnancy and why

A

UEC, LFTs, TFTs, FBE +/- CRP
urine MCS and dipstick

Exclude UTI, gastro/other infection, biliary disease, appendicitis, Addison’s disease, Thyroid disease, electrolyte disturbances from extreme dehydration

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96
Q

What is pre-eclampsia?

A

De novo HTN (>140/90, or >30/50 over baseline) arising after 20/40 and returning to normal within 3 months postpartum + evidence of dysfunction in at least one other organ (kidney, liver, neuro, haem, fetus)

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97
Q

Pathyphys of PE

A

Placental disorder! Placenta demands more O2 and nutrients that the mother can provide, so becomes hypoxic.
Hypoxic placenta releases toxic products which damage mum’s vasculature, causing vasospasm, and vasoconstriction -> HTN and ischaemia to other organs

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98
Q

RF for PE

A 
First pregnancy or new paternity 
Age extremes (teens and >40)
Obesity
Smoking 
Previous PE
Family HX
Assisted reproduction

Medical conditions: essential HTN, GDM, RA, SLE, renal disease etc

Large placenta - Multi pregnancies, GDM, GTD

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99
Q

Clinical features of PE

A

Stage 1: isolated HTN
Stage 2: + Proteinuria + Generalised swelling (facial and lower limb)

Stage 3 = Eclampsia
Signs of multi system dysfunction…
Neuro: SEIZURES!! Headaches +/- visual changes; hyper-reflexia and/or clonus
Renal: Oliguria, renal failure
Hepatic dysfunction: Epigastric/RUQ pain/lower abdo pain
CV: CCF, Pulm oedema (SOB)
Haem: thrombocytopenia, haemolysis, DIC
Uteroplacental: decr FM, IUGR, abruption, FDIU

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100
Q

Investigations for PE

A

FBE (plt, Hb)
UEC (renal function and uric acid)
LFTs (ALT deranged w liver dysfunction)
24 hour urine collection or spot Cr:urea ratio

CTG and USS (assess growth, AF, UA)

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101
Q

Definition of Eclampsia

A

Seizures assoc w PE due to hypo perfusion of brain

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102
Q

Prevention of PE.

Which women should get this?

A

Low-dose Aspirin and Ca supplements in high risk women
High dose folate
Diet (antioxidants, Mg, zinc, fish oil), exercise, bed rest
Salt restriction

+/- LMWH for women with genetic/acquired thrombophilias

High risk: HTN, renal disease, obesity, insulin resistance, GDM, assisted reproduction, and a history of preeclampsia in a previous pregnancy,

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103
Q

MX of (pre-)eclampsia

A

DELIVERY of placenta is curative (but not necessarily right away)
- timing and ode of delivery depends on stage
Stage 1: monitor, educate, antiHTN If >160/100, wait until >38 weeks

Stage 2: Close monitoring - bidaily CTG, 2 weekly USS; education; labetalol if >160/100; IOL or C/S past 34-36 weeks

Stage 3: immediate delivery once mum stable
Admit!
Monitor fluid balace/renal function (replace if necessary)
4 hourly bloods (FBE, UEC, LFTs)
Fetal surveillance (CTG)
Stabilise mother
- IV MgSO4 if they have had a convulsion (bolus + infusion) - will help to bring down BP (vasodilation)
- Epidural and anaesthetics R/V - will help to bring down BP
- Antihypertensives if SBP>=160 and DBP >=100 despite MgSo4 and epidural ( IV labetalol)
- Steroids if preterm

Surveillance postpartum (fluid-balance) and F/U post-delivery

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104
Q

When is the highest risk for VTE?

A

peri-puertum (6 weeks post delivery)

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105
Q

Inx for suspected VTE

A

Doppler for VTE

VQ scan or CTPA for PE

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106
Q

Treatment of PE

A

LMWH for 6 weeks post part and for remaining duration of pregnancy
Can change to warfarin postpartum
+ needs LMWH throughout next pregnancy up to 6 weeks postpartum for prevention

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107
Q

Consequences of GDM

A

Fetal

  • Macrosomia
  • Shoulder dystocia
  • Birth Trauma (fractures)
  • Birth asphyxia
  • Polyhydramnios (polyuria)
  • Congenital abnormalities
  • Stillbirth

Maternal

  • HTN disorders
  • Infection
  • Caesarian/instrumental delivery
  • ?PPH and Perineal trauma
  • 50% incr lifetime risk of developing T2DM

Neonatal:

  • hypoglycaemia
  • hypocalcaemia
  • RDS
  • jaundice
  • NICU/SCN admission
  • perinatal mortality and morbidity (incr risk obesity, DM)
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108
Q

Clinical presentation of GDM

A

Asymptomatic, picked up on routine 28 week GTT

SX of hyperglycaemia (polyuria, polydipsia)

Incr SFH

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109
Q

MX of GDM

A

Multidisciplinary care
1. Education. Diabetic education nurse, dietician, endocrinologist, obs/gynae input
2. Frequent self monitoring of capillary BSL (fasting <5mmol, 1hr post prandial <8mmol)
3. Diet and exercise daily
Add insulin and/or sulfonyelurea/metformin if targets not met
4. Antenatal Fetal monitoring
- Additional routine growth scans
- Regular clinical assessments of growth (SFH)
5. Consider IOL/electice LUSCUS after 38 weeks if poorly controlled /evidence of fetal involvement
6. Close fetal monitoring intrapartum
7. Postpartum neonatal follow-up monitoring for jaundice, RDS, hypoglycaemia, hypocalcaemia
8. Screening GCT early in future pregnancies

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110
Q

What is the definition of a miscarriage?

When is the risk of this highest?

A

Spontaneous loss of pregnancy <20weeks gestation

Highest risk <12/40

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111
Q

Definition of recurrent miscarriage.

What investigations would you perform?

A

> 3 consecutive miscarriages

Inx:
Cytogenic analysis on products of conception
Karyotypes of parents
Inx for thrombophilia, structural abnormalities, medical disorders etc

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112
Q

Aetiology for miscarriage

A

Advancing maternal age -> chromosomal (aneuploidy, 45XO etc)

Chronic disease (thrombophilia, APLS, SLE, Coeliac, GDM etc)

Structural abnormalities of uterus (bicornuate, subseptate)

Incompetent cervix

Toxins (smoking, cytotoxic drugs, high dose radiation)

TORCH infections

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113
Q

How does M/C present?

A

PV bleeding

Lower abdo pain

114
Q

What is a threatened MC?

MX

A

Ongiong/live pregnancy but PV bleed/spotting +/- lower abdo pain in 1st trimester

MX: reassurance and follow up

115
Q

What is an inevitable MC?

MX

A

A miscarriage that will definitely happen. PV bleed/lower abdo pain in presence of an open internal os in first trimester (means the body is already in process of expelling the embryo).

But POC still present, yet to be passed.

MX: Nothing can be done about it.
Psychol support, close follow up and expectant management

116
Q

What is an incomplete MC?

MX

A

PV bleeding and lower abdo pain have have passed some POC but some POC yet to be passed, and are visible on USS.
Cervix still open.

MX: expectant MX or can use Misoprostol (PGE analogue) or Mifepristone (anti-progesterone) to help expel products

117
Q

What is a complete MC?

MX

A

All POC have been passed; the cervix is now closed and the uterine cavity is empty on USS

MX: f/u with serum HCG measurements

118
Q

What is a missed MC?

MX

A

No SX of miscarriage - it is picked up on routine AN care due to lack of FHR, small for dates. May be complete or incomplete.

MX: expectant MX or can use Misoprostol (PGE analogue) or Mifepristone (anti-progesterone) to help expel products

119
Q

When would you do surgical D&C as treatment for miscarriage?

A

If the woman is haemodynamically unstable (heavy bleeding etc)

120
Q

Advice after a M/C

A

Pain and bleeding similar to a period is normal for ~2 weeks, treat w over the counter analgesia

Strong pain/heavy bleeding/abnormal DC/fever -> see doctor or ED

Avoid sex until bleeding stops, pain lessens

Use pads, NOT tampons until bleeding stops

Need anti-D injection if Rh(D)neg and Ab neg.

Wait until after next normal pregnant to try getting pregnant again (slightly incr risk of m/C again if you get pregnant within 4-6 weeks)

121
Q

What is the leading cause of maternal death in the first trimester?

A

Ectopic pregnancy

122
Q

Risk factors for ectopics

A 
STIs
Smoking
Prior ectopic
Incr age
Prior tubal surgery/ligation
IVF
Progestogens
Contraceptive failures (pregnant with IUD)
123
Q

Presentation of ectopic pregnancy

A

Pelvic pain (unilateral or generalised)
Delayed period
Abnormal bleeding
Pallor, hypotension, tachycardia, guarding/peritonism indicate ruptured ectopic -> shock

On exam: PV bleeding, closed cervix, adnexal mass, Localised tenderness

124
Q

Inx for suspected ectopic

A

TVUSS (free fluid, adnexal or fallopian tube mass, absence of IU gestational sac)

Serial betaHCG high (>1000) but rising less than 60% over 48 hours

FBE, blood group and cross match

125
Q

MX of ectopic

A

If in shock: emergency laparotomy

Not in shock:
- If HCG<1000: Admit for Observation, await natural resolution (betaHCG and USS monitoring)
- If HCG>1000 or keeps rising:
Medical (for small tubal ectopics and minimal bleeding): Methotrexate IM
Surgical (for large ectopics or IU bleeding): laparoscopy and salpingectomy/salpingostomy

Follow up: serum B-HCG on days 4 and 7, should decr to ensure complete removal

Psych support

126
Q

Impact of ectopic on future pregnancies

A

Incr risk of future ectopic so future pregnancies require early TVUSS at 5-6 weeks to ensure they are intra-uterine

Take folate when trying to get pregnant in future.
Wait 2 months post surgery and 4 months post medication to try for another baby

127
Q

CI to the COCP

A 
Women with IHD
Previous stroke, VTE
Breast cancer
Severe liver/biliary disease
Breast feeding with infants <6mo
Migraine with aura
128
Q

Mechanism of action of the COCP

A

Progesterone

  • prevents LH surge which prevents ovulation
  • thickens the cervical mucus impeding sperm passage
  • thins endometrium making it less favourable for implantation
  • decr motility within fallopian tubes

Oestrogen

  • stabilises endometrium to reduce irreg bleeding
  • prevents follicular maturation
129
Q

What happens if you miss one COCP pill?

What happens if you miss 2 or more?

A

1 missed pill: take it as soon as you remember

2+ missed pills: take the last missed pill as soon as you remember even if it means taking 2 on one day. Don’t worry about other missed pills. Then use condoms/abstinence in conjunction with active pills for another 7 days, even if this means skipping the placebo pills and running 2 packs together.

130
Q

Advice for starting the COCP

A

Start on days 1-5 of menstrual cycle (period) and you will be protected immediately, OR use back-up contraception until you have taken 7 active pills

You can start at any time if you are SURE you aren’t pregnant (abstinent etc)

131
Q

Risks vs benefits of the COCP

A

Benefits:

  • reversible contraception
  • decr PMS SX, can help w acne and PCOS
  • decr painful/heavy bleeding
  • predictable, regular bleeding
  • controls vasomotor SX around menopause

Risks:

  • hormonal SE
  • user dependent
  • incr risk VTE, stroke, breast cancer, cervical cancer
132
Q

Which women is the progesterone only mini pill good for?

A

Breast feeding women (COCP CI for babies <6mo)

Women in whom oestrogen is CI (breast cancer, risk of VTE etc)

133
Q

How does the mini pill work?

SE

A

Continuous release of low dose progesterone keeps the lining thin and thickens cervical mucus, can also prevent ovulation.

SE - unpredictable bleeding and spotting because there are no scheduled withdrawal bleeds.

134
Q

How does the nuva ring work?

A

Soft vinyl ring placed in vagina that releases constant dose of oestrogen and progesterone to vessels underlying vaginal skin

Stays in place 3 weeks then is removed for a week, in which a withdrawal bleed occurs. Put a new one in after that.

135
Q

Advantages and disadvantages of nuvaring

A

Adv: avoids first pass hepatic metabolism
- low dose local release of hormone means fewer side effects

Disadv: expensive!

136
Q

How does Depot Provera work?

Adv and disadv?

A

Injectable (IM) progesterone-only contraceptive lasting 3 months.

Adv: only need it 4x year; can lighten periods (not in everyone though)

Disadv: Irregular bleeding/spotting, irreversible, delay in return of ovulation after sensation by ~8mo, weight gain, not for long-term use due to risk of osteopenia/osteoporosis with lack of oestrogen

137
Q

What is implanon and it’s advantages and disadvantages

A

rod-implant that releases progesterone

adv: efficacy ~99.9%, no decr in bone density, is immediately reversible, not user dependent
disadv: intermittent bleeding and hormonal SEs

138
Q

How does the copper IUD work and what are side effects

A

Cu is toxic to sperm
Acts as a IU foreign body which interferes with implantation
Lasts 10 years or 5 years

SE: incr bleeding and pain with periods after insertion
Expulsion, perforation, infection, bleeding, pain on insertion

139
Q

How does the progesterone IUD work and what are advantages and disadvantages?

A

Delivers progesterone to uterus at constant rate, thickens cervical mucus and thins endometrium

Adv: minimal systemic SEs, 90% women report lighter or no periods after 6 months
lasts 5 years, cheap

Disadv: risk of perf, infection, pain, bleeding, expulsion, vasovagal on/soon after insertion
Incr relative risk of ectopic or miscarriage if you get pregnant with it in situ (but 99.7% protection)

140
Q

Advice on natural family planning

A

Most fertile from day 8-19 inclusive (5 days either side of day 14) so avoid unprotected sex on these days to avoid getting pregnant (only reliable in women w regular cycles)

  • Thin fertile mucus and 0.3C rise in temp during ovulation are other indicators
  • only 75% accurate
141
Q

How does a female diaphragm work?

A

Individually fitted silicone done-shaped cup attached to flexible circular springs. Sit in front of cervix and vaginal vault and held in place by pelvic muscles.
Insert anytime before sex but must remove within 6 hours after.

Note: only 94/84 perfect/typical use efficacy

142
Q

explain the pathophys behind GDM and fetal growth

A

GDM is a state of insulin resistance: blood glucose isn’t taken up into maternal tissues due to factors released by placenta (CRH, GH, placental lactogen).
Leads to maternal hyperglycaemia -> fetal hyperglycaemia -> fetal pancreas produces it’s own insulin -> incr fetal insulin -> incr glucose uptake into fetal tissues -> incr fetal grwoth

143
Q

Resp physiological changes

A

20% incr O2 consumption via incr tidal volume (not RR)

Diaphragmatic breathing (uterus pushes up on diaphragm and increases IAP)

Decr functional residual volume, exp and insp volume due to displacement of diaphragm. Mild decr in TLC.

Incr central resp drive -> relative hyperventilation (incr O2 and decr CO2) -> mild compensated resp alkalosis

144
Q

CV physiological changes

A

Increase CO by 40% (to supply placenta) from incr HR and SV

Decr systemic vasc resistance due to widespread vasodilation

Decr BP

Supine hypotension effect of position in late pregnancy

145
Q

Haem physiological changes

A

40% incr plasma volume -> periph oedema, pulm oedema
20% incr in RBC volume
Anaemia common (due to haemodilution)
Haemodiluition -> decr [albumin] -> oedema
Incr clotting factors -> Pro-thrombotic state

146
Q

MSK physiological changes

A 
Incr BMI by 10-14kg
lower back pain
Lordosis
Carpal tunnel due to oedema
Sciatica due to oedema
Calf cramp
147
Q

Derm physiological changes

A 
Incr skin pigmentation
Distension and proliferation of blood vessels
Spider nivae
Striae gravidarum 
Facial flushing
148
Q

Gynae physiological changes

A

Breast enlargement (oestrogen causes incr adipose tissue and in ductal system; progesterone causes enlargement of breast lobule)

Areola pigmentation
Cervical gland hypertrophy and formation of mucus plug
Vaginal lactobacilli proliferation
Uterine hypertrophy and hyperplasia

149
Q

Endocrine physiological changes

A

Anterior pituitary

  • incr prolactin
  • fish and lh suppressed
  • decr TSH in first trim due to HCG levels

Posterior pituitary: incr oxytocin

Pregnancy hormones

  • BetaHCG
  • Oestrogen and progesterone released by implanted embryo
  • Human placental lactogen (released by placenta, implicated in GDM)

Physiological insulin resistance and relative glucose intolerance
Incr maternal lipolysis (mother uses fats for fuel and preserves carbs for fetes)

150
Q

Renal physiological changes

A

Incr renal blood flow -> incr renal size; and incr GFR -> incr urinary frequency and incr clearance of creatinine, glucose and aa -> glycosuria and aminoaciduria

Ureteric dilation/enlargement (smooth muscle relaxation due to progesterone)

Uterine enlargement compresses bladder -> urinary frequency

Compression of ureter may lead to hydronephrosis - generally asymptomatic

151
Q

GI physiological changes

A

GORD due to relaxation of smooth muscle sphincter by progesterone, and incr IAP

Incr aspiration risk under anaesthesia

Haemmharoids due to incr IAP

Constipation due to smooth muscle relaxation by progesterone

Gallstones (decr gallbladder motility)

152
Q

Thyroid physiological changes

A

Incr levels T3 and T4
TSH levels decr in Trim1 due to thyrotrophic effects of beta HCG but incr again in Trim2 and 3

Incr HCG levels assoc w hyperthyroid

Pregnancy aggravates I deficiency (transported to fetes and lost in urine) -> goitre can result in I-deficient women

153
Q

What factors does O2 delivery to placenta and fetes depend on?

A 
Maternal O2 saturation
Hb concentration
Uterine blood flow (10% of CO)
LEFTWARD shift of Hb sat curve -> allowing higher Hb saturation at lower pO2 
O2 has higher affinity for HbF than HbA
154
Q

Breast milk production physiology

A

Anterior pituitary produces prolactin which stimulates milk production.

During pregnancy the embryo/placenta releases oestrogen and progesterone which inhibit the production of prolactin. Oestrogen and progesterone levels decrease after delivery, prolactin is no longer inhibited so milk production begins.

Sensory signals from baby suckling stimulate release of oxytocin from posterior pituitary which causes release of milk

155
Q

Role of umbilical artery and vein

A

Umbilical vein transports O2 and nutrients from placenta to fetal circulation (x1)

Umbilical arteries (x2) transport deoxy blood from fetus to placenta

Uterine artery is from mother to placenta

Uterine vein is from placenta to mother

156
Q

DDX genital itch (females)

A

Infection

  • candida albicans
  • Bacterial vaginosis
  • Trichomonas vaginosis
  • Genital warts
  • Pinworms (night time itch)
  • Pubic lice

Inflammation

  • irritant contact dermatitis
  • lichen sclerosis
  • psoriasis
  • allergic dermatitis
  • allergic urticaria

Neoplasm

  • VIN
  • vulval cancer (SCC)

Atrophic vaginitis in post-menopausal women

157
Q

What is bacterial vaginosis?

SX
Diagnosis
Tx

A

Disturbance of normal bacterial equilibrium in the vagina - overgrowth of anaerobic bacteria

SX: abnormal vaginal discharge (alkaline white-grey discharge with fishy odour) + EXTREME ITCH in women of reproductive age

DX: high vaginal swab -> microscopy and culture

Tx: oral metronidazole; topical in pregnant women to reduce systemic side effects.

158
Q

How does trichmononas vaginalis present?
What sort of bug is it?
How do you diagnose it?
How do you treat it?

A

Males - asymptomatic
Females - malodorous vaginal (frothy yellow-green fishy) discharge + ITCH

Protozoan parasite

Dx: high vaginal swab for microscopy and culture

Tx: oral metronidazole

159
Q

Chlamydia Trachomatis:

SX
What sort of bug is it?
How do you diagnose it?
How do you treat it?

A

SX: Males - urethritis
females - asymptomatic but may get vaginal d/c, dysuria, dyspareunia, post-coital bleed
Long-term can result in PID, ectopic, infertility, pain

Bacteria

DX: endocervical swab (women) or urine (males) for PCR

tx: single dose azithromycin OR doxycycline 7 days bd + test for cure 2-3 months post-treatment

160
Q

Gonorrhoea

SX
What sort of bug is it?
How do you diagnose it?
How do you treat it?

A

SX: males are 75% asymptomatic
females - dyspareunia, irregular bleeding, abnormal discharge, bartholin’s abscess, infertility/ectopic, chronic pelvic pain (but can be asymptomatic)

Bacteria

DX: endocervical swab for PCR and MCS

Tx: single dose IM ceftriaxone

161
Q

What are notifiable STIs?

A 
Chlamydia
Gonorrhoea 
HBV
HCV
HIV 
Syphilis
162
Q

What HPV strains cause genital warts?

A

6 and 11

163
Q

Candida albicans

SX
DX
TX

A

Cottage cheese DC + itchy, irritated vulva
RF: immunosuppression, diabetes, pregnancy, use of broad-spectrum abx or exogenous steroids

High vaginal swab for MCS

Tx - fluconazole for 1 week

164
Q

HSV

SX
How do you diagnose it?
How do you treat it?

A

type 1 causes oral lesions and type 2 causes genital ulcers
Tiny punched out extremely painful ulcers with discharge
Primary episode is severe +/- flu-like illness, with recurrent episodes more mild

Dx- swab lesions for viral PCR, and serology (IgM and IgG)

MX - acyclovir within 2-3 days of sx, especially in third trimester of pregnancy (+ LUSCS)
+/- topical lignocaine for pain

165
Q

When is the HIV virus first detectable in the blood?

what factors indicate progression of disease?

A

2-3 months post infection HIV Ab is detectable

Incr viral load and decr CD4 count indicates progression

166
Q

Management of pregnant patients w HIV

A

Antiretrovirals antenatally to suppress viral load

Antiretrovirals to mama and bub postpartum

Elective LUSCS

Avoid breast feeding

167
Q

What do the various HBV serum markers indicate:

  1. HBsAg
  2. ABsAb
  3. HBcAb
  4. HBeAg
A
  1. HBsAg - ACTIVE infection (Acute or chronic)
    -> persisting beyond 6 month indicates chronic HBV which is more common when infected in infancy -> likely to progress to chronic disease and incr risk of transmission
    If this is positive, no immunity has been developed yet. Should be NEGATIVE in vaccinated individuals
  2. ABsAb (immunity following vaccine or infected)
    - positive in vaccinated individuals or in individuals with resolved past infection.
  3. HBcAb (only follows natural infection-past or current)
  4. HBeAg (highly infectious carrier)
168
Q

What is the risk of syphilis in pregnancy?

Tx for syphilis

A

Spread transplacentally to fetes -> 40% risk of prematurity and perinatal death

tx: Penicillin

169
Q

What is the supine hypotensive effect of pregnancy?

How do you prevent/treat this?

A

Due to vena caval compression by gravid uterus, which can decr CO by ~30% and result in hypotension -> collapse

Position mother in left lateral tilt to reduce aortocaval compression

170
Q

Preterm birth risk factors

A 
Previous preterm birth
Polyhydramnios
Multi pregnancy 
Antepartum haemmhorage 
Low SES
Smoking, drugs
Young maternal age
2x previous LLETZ /cone biopsy resulting in cervical incompetence
Poor antenatal care
Chorioamnionitis
171
Q

Definition and Treatment of cervical incompetence

A

Cervical length of <1.5cm at <24 weeks gestation

Prostaglandins (pessary/local vaginal)
Cerclage suture

172
Q

how do you diagnose preterm birth?

A

Clinical (uterine activity + cervical effacement and dilatation)

+/- posterior vaginal swab for fetal fibronectin test (99% NPV but only 20% PPV)

173
Q

Management of preterm birth

A 
Admit 
Analgesia 
Tocolysis (nifedipine, other Ca channel blockers) to buy time for: 
- 2 doses steroids over 48 hours 
- Transfer to tertiary centre if <32/40

ABX (oral erythromycin) if PPROM or chorioamniotitis (maternal fever, pain/tender, looks septic, mec stained liquor)

Delivery immediately if chorioamnionitis suspected!

Otherwise try to buy time and D/C if contractions settle

174
Q

Prevention of preterm birth

A

Stop smoking
Vaginal progesterone or cerclage/cervical suture if cervical incompetence or previous preterm birth (Former only)
Treatment of asymptomatic bacteriuria

175
Q

Triggers for preterm birth

A

Infection (ascending, UTI, dental)
Ruptured membranes
Cervical insufficiency (note - painless and brief!)
Stretching of uterus - multi pregnancy, polyhydramnios
Antepartum haemmhorage

176
Q

Definition and Causes of antepartum haemmhorage

A

Defintion: Bleeding PV from 20 weeks gestation onwards

Causes:
placental abruption and placenta praaevia most common

Also Placenta accreta, vasa praevia, infection, malignancy

177
Q

How do you diagnose placental abruption?

A

Clinical diagnosis - USS is not sensitive for this.
Features: VAGINAL BLEEDING +/- ABDO PAIN in 2nd 1/2 of pregnancy +/- uterine tightenings
OE: Uterine tenderness on palpation, increase uterine tone (woody/hard)

178
Q

RF for abruption

A

PE/eclampsia, smoking/cocaine, PPROM, previous abruption, multi pregnancy, polyhydramnios, trauma to abdo/cervix, low lying placenta

179
Q

Management of suspected abruption

A

Aim to buy time if pre-term!

  • Admit for Steroid loading (2 doses over 48 hours)
  • AntiD if Rhneg and Abneg
  • MgSO4 if <30weeks (prevent CP)
  • FBE and iron-> IV infusion if significant/ongoing bleeding
  • D/C once not bleeding for 24 hours and mum and bub are stable
  • F/U: Monitor via freq growth scans, SFH for IUGR

If term and no fetal compromise -> Induce

If fetal or maternal compromise -> immediate delivery via emergency LUSCS

180
Q

Definition of placenta praevia

A

Implantation of placenta within 2cm of os (lower segment)

Dx - routine 20week morph USS with follow up scans to see if it has moved (90% move away on their own)

181
Q

RF for placenta praecia

A 
INCR number previous caesarians
incr age and multiparty
smoking
IVF
uterine surgery
182
Q

Mx of placenta praevia

A

DO NOT do VE
Expectant management if mum and bub are well -> ELECTIVE LUSCS ~37 weeks with regional anaesthesia (don’t want them going into labour - NVD Ci if <2cm from os). If recurrent bleeds, deliver at 34 weeks.

If presenting with bleed, follow routine antepartum haemmhorage care (admit, steroid load, +/- anti-D, +/- volume resus, deliver if mum or bub are unstable otherwise D/C once not bleeding and stable for 24 hours)

183
Q 
What is placenta accreta? 
RF
DX
Risk
Management
A

Placenta morbidly adherent to uterine wall
RF - incr # C/S (esp. classical), placenta praaevia, previous intrauterine procedures
Dx: USS +/- MRI
Risk: life-threatening PPH or APH
Mx: transfer to tertiary centre for elective caesarian hysterectomy (NVD CI!!)

184
Q 
What is vasapraevia?
RF
DX
Risk
Management
A

Fetal blood vessels run in amniotic membranes below presenting part of fetes in front of the cervix
RF - IVF, abnormal placenta, low-lying placenta, multi pregnancy
Dx- clinical palpation of fetal vessels on VE or visualisation with an amnioscope. TV colour Doppler USS can confirm if suspected.

Risk - fetal haemmhorage and death

MX - Immediate LUSCS if bleeding and maternal or fetal compromise.
If confirmed vasa praaevia but not bleeding, admit between 28-32 weeks for steroids, observation and elective LUSCS between ~37 weeks. If labour or ROM -> LUSCS.

185
Q

Inx and MX of antenatal haemmhorage

A 
CTG, USS
FBE
Anti-D and antibody status for Rhneg women
Group and hold 
Kleihauer test for Rhneg women

MX: Admit for anti-D and Steroids.
IV infusion (Hartmans if stable; RBC if deteriorating) if significant/ongoing bleed
if in labour -> continuous CTG monitoring
If maternal or fetal compromise -> emergency C/S
If at term or close to full dilation, can try for NVD (as long as placenta accreta, praaevia vasa praaevia are ruled out)

Home if just light spotting and USS has ruled out praevia and abruption
Home once bleeding has stopped and mum and bub are stable for 24 hours
F/U - monitor for IUGR

186
Q

What other compilations of labour are associated with placenta praaevia?

A

Placenta accreta, vasa praaevia, abruption

Malpresentation

187
Q

RF of cord prolapse

A 
breech and other malpresentation
disengaged fetal head and beginning of labour 
multi pregnancy
grand multi 
instrumentation
preterm
188
Q

Risk associated w cord prolapse

A

Perinatal mortality due to umbilical artery vasospasm or cord compression

189
Q

Management of cord prolapse

A

IMMEDIATE delivery

  • call for help
  • try to displace cord manually above presenting part, or dislodge the presenting part to relieve pressure on cord and re-place cord
  • emergency caesarian if NVD not possible
190
Q

How do you diagnose amniotic fluid embolism

A

Diagnosis of exclusion!

Diagnosed post-mortem - fetal Saumes found on biopsy

191
Q

RF for shoulder dystocia

A 
Maternal obesity 
Previous SD
GDM
Fetal macrosomia
Post-date pregnancy
Prolonged 1st and 2nd stages labour
IOL
192
Q

Risks associated w shoulder dystocia (5)

A

1 .Cord compression, perinatal death

  1. Fracture of humerus or clavicle
  2. Damage to brachial plexus
  3. Maternal soft tissue trauma/damage to bladder, rectum, urethra
  4. PPH
193
Q

MX of shoulder dystocia

A

Early identification!
Call for help

Discourage maternal pushing - may exacerbate impaction

McRobert’s position (extended lithotomy) is 1st line +/- Suprapubic pressure

Internal manoeuvres (may need episiotomy to gain access)

  • Delivery of posterior arm
  • rotational manœuvres

2nd line: reposition to all 4s (slim, mobile women without epidural)

POST DELIV: neonatal assessment of baby and pay attention to blood loss! (PPH)

194
Q

Definition of PPH

A

> 500ml blood loss during 3rd stage or within 24 hours of delivery (primary)

24hr-6 weeks is secondary PPH

195
Q

Prevention of PPH

A

Placenta out within 20 min!
Active management of 3rd stage
- syntometrin (syntocinon +ergometrine) as prophylactic uterotonic
- controlled cord traction
- fundal massage after placental delivery
2 large bore cannulas on admission for high-risk women

196
Q

Management of PPH

A

Early recognition - call for help!

Freq/ongoing vital monitoring - signs of shock?

RESUS- ABCs

  • O2 - high flow (10L/min)
  • IV fluid replacement via 2 large bore cannulas (crystalloids, or blood products if going to theatre, Hb<70 or unstable despite 2-3L crystalloids)

Bloods - FBE, UEC, coag screen, cross match
Check placenta for completeness
Check perineum for trauma, stitch any 3-4deg tears

Treat underlying cause

  • fundal massage
  • uterotonics (syntocinon IV, ergometrine IM, PR misoprostol)
  • IDC to empty bladder
  • Tranexamic acid (coag abnormalities)

May need surgical exploration for retained productions (PGF2alpha in theatre)

  • brace suture, IU balloon, embolisation or ligation
  • hysterectomy last-line
197
Q

Stage 1 of labour

A

regular painful uterine contractions with cervical effacement and dilation
stage 1 - passive (up to 3-4cm dilation); oxytocin and prostaglandins cause uterine contractions which help baby’s head to defend and stretch the cervix leading to its effacement and dilation

stage 2 -active (4cm-10cm); contractions continue under oxytocin and PGE2; also increase IAP which lead to rupture of amniotic sac (SROM)

198
Q

Complications of labour and their respective management

A

Failure of SROM
- amniotomy to artificially rupture membranes

Premature ROM

  • rupture before 37 weeks, will need antibiotics (erythromycin)
  • if term, admission for observation and IOL
  • if preterm, also give corticosteroids and deliver at 34 weeks

Failure to progress
- try amniotomy, oxytocin infusion +/- ECV if malpresentation

Fetal distress (CTG or doppler auscultation)
- do a fetal scalp lactate -> acidosis is indication for immediate delivery (C/S if in S1 or instrumental if fully dilated and head engaged)

Perineal trauma

  • incidental trauma or episiotomy
  • repair second-fourth degree tears with sutures, in layers.

Malpresentation

  • OP or OT usually spontaneously revert but may need instrumentation
  • Face and brow: emergency C/S may be necessary
  • Breech - supported NVD w manoeuvres or elective C/S
  • Transverse/oblique - stabilise lie w ECV and IOL, or C/S
199
Q

Complications of instrumentation

A

Perineal trauma
Subgaleal haemorrhage
Cephalohematoma

200
Q

Things done in third stage of labour

A
  1. syntometrine injection
  2. deliver placenta (prolonged >1hr)
  3. check placenta - membranes and cotyledons, insertion and vessels for completeness
  4. check uterine tone and fundal massage
  5. Umbilical cord bloods
  6. Check pack and pad need count
201
Q

Indications for C/S

A

Failure to progress
Fetal distress
Abnormal lie or malpresented at onset of labour
Elective if NVD poses significant risk to mother and/or fetes

202
Q

Complications of C/S

A

Surgical risks
prolonged recovery time
Risk of uterine dehiscence and rupture with future pregnancies
Incr risk of placenta accreta, vasa praaevia, placenta praaevia

203
Q

How do you induce labour?

A
  1. VE to assess fetal engagement and cervical ripeness (Bishop’s score)
  2. BS<6: Cervix is Unfavourable and needs to be primed:
    - PGE2 or mechanical balloon
    - takes 1-2 days
  3. BS>6: Cervix IS favourable -> amniotomy and oxytocin to stimulate uterus
    - takes <16hours
  4. Continuous fetal CTG monitoring
204
Q

Risks of IOL

A

fetal distress due to hyper stimulation of uterus -> may need to revert to C/S

205
Q

Initial investigations for infertility

A 
Hormones (FSH, Lh, oestrogen, androgens)
Genetic karyotype +/- CF screen (males)
Semen analysis (men)
Imaging - USS testes; ovaries, uterus
206
Q

Causes of female infertility

A

Egg factors - Advanced maternal age is #1!; aneuploidy

Anovulation

Endocrine - hypothyroid, hyperprolactinoma

Anatomy 
- Mullein abnormalities
- Endometriosis
- Chronic infection (PID), scarring
- Fibroids (distortion) 
Idiopathic
207
Q

Causes of male infertility

A 
Sperm - poor sperm count or abnormal sperm
Genetics - CF or Kleinfelter
Hypo-Monadism
Vasectomy/testicular removal previously
Varicocele, torsion, undescended testes
Anabolic steroids
208
Q

Causes of anovulation

and management of each

A

Normal FSH (MX: lifestyle - weight loss, diet +/- ovulation induction)

  • obesity
  • PCOS (+/- metformin)

Incr FSH (ovarian failure) - MX: IVF

  • Age >45
  • iatrogenic (radio/chemo)
  • autoimmune (SLE, RA)
  • Genetic (45XO, fragile X etc)

Decr FSH (HPO failure) - MX: lifestyle +/- ovulation induction

  • anorexia, stress, chronic illness, over-exercising
  • Pituitary tumour
  • infiltrative disease (sarcoid)

Idiopathic (Mx: IVF)

209
Q

management - male infertility

A

Lifestyle - stop smoking, drinking, increase exercise and dietary antioxidants

Intra-cytoplasmic sperm injections (donor sperm)

210
Q

Management of infertility

A
  1. Lifestyle - weight loss, exercise and diet (PCOS, obesity and incr sperm count)
  2. Ovulation induction (for PCOS, obesity, HPO failure)
    - Clonifine first line for PCOS; Letrozol; FSH; pulse dose LH/GnRH analogue/HCG triggers ovulation
  3. IVF (for ovarian failure)
    - Serum AMH predicts response to IVF
  4. Cryopreservation (if <35years old)
  5. Consider male-infertility and Tx for that
211
Q

What is HELLP syndrome?

A

A complication/variant of pre-eclampsia
Features: Haemolysis
Elevated liver enzymes
Low plt count

Sx - malaise, epigastric pain, ROQ tenderness (from liver dysfunction and capsular distention)
\+Ft of PE: 
N and V
Headache
Swelling, oedema
HTN, proteinuria
212
Q

RF for malpresentation

A

Pre-term
Placenta praaevia
Fetal anomaly
Polyhydramnios

213
Q

MX of malpresenation

A

CONFIRM presentation - abdo palpation + bedside USS

options:

  1. NVD
    - Admit and await labour if >=37 weeks
    - ok for breech, req CTG monitoring and senior obstetrician skilled in breech deliveries available
  2. ECV (with IOL and ROM if >=37 weeks)
  3. Emergency LUSCS if fetal distress or ECV unsuccessful

PLUS all need IV access, continuous C TG monitoring +/- epidural

214
Q

Risks and CI to ECV

A

Risks: fetal distress, placental abruption, cord prolapse, ROM, APH

CI: recent APH, abnormal CTG, Ruptured membranes, multi pregnancy, major uterine abnormalities

215
Q

Mx of breech via NVD

A

CTG monitoring and IV access
skilled senior obstetrician present
Position: dorsal lithotomy
+/- episiotomy
- Lovset monoeuvre to deliver arms + suprapubic pressure to assist head flexion
- Head delivery with forceps, Marceiu-Smellie-Velt or Burns-Marshall method

NOTE: if above fails, -> emergency c/s

216
Q

Causes of reduced variability on CTG

A 
4 Ss:
Sick
Sleeping
Sedated
Sub-mature
217
Q

What does absent variability indicate on CTG. what next?

A

hypoxia -> confirm w scalp pH - metabolic acidosis confirms

218
Q

cause of variable decels

Types of variable decelerations

A

Cord compression

Simple - rapid onset and recovery, occurring with contractions; shouldering present (reassuring)

Compound - increased baseline; slow to return to baseline; prolonged (>15s) = broad-based (bad!)

219
Q

MX of variable decels

A
  1. Conservative
    - fluid resus
    - change position
    - decr syntocinon IV rate

Fetal scalp electrode

Terbutaline (beta agonist)

  1. Do nothing
  2. Deliver!
    - lower threshold for intervention if known IUGR or thick mea-stained liquor
220
Q

Early vs late vs prolonged decels

A

Early and late are both repetitive and persistent with slow onset and recovery

Early: occur with contraction (due to head compression in labour)
Late: peak AFTER contraction (indicate fetal hypoxia and acidosis)

Prolonged: Last >2min duration = sustained bradycardia = sustained hypoxia

221
Q

RED FLAGS on fetal CTG monitoring

A

Lack of accelerations
Rising baseline
Persistent prolonged decels with prolonged recovery
REduced/absent variability -> fetal hypoxia
Contractions >5:10 despite decr synt infusion

222
Q

Criteria for diagnosis of PCOS

A

Rotterdam criteria: 2 of the following

  1. Oligomenorrhoea reflecting an ovulation
  2. Hyperandrogenism (clinical or biochemical with incr free testosterone and decr SHBG)
  3. Polycystic ovaries on USS
223
Q

SX of PCOS

A 
Obesity
Acne
Hirsutism
Sub fertility
Oligo or anovulation
224
Q

Risks assoc w PCOS

A 
Glucose intolerance and insulin sensitivity -> T2DM
Hyperlipidaemia
Obesity
OSA
Depression, anxiety
Endometrial hyperplasia -> endometrial cancer 
CVD
NAFLD
225
Q

Screening of women with PCOS

A

Lipid profile and OGTT every 2years
BP every year
Mental wellbeing and desire for pregnancy

226
Q

Management of PCOS

A

Diet and exercise firstling

Rest of MX depends on SX
- Oligomenorrhoea/anovulation (COCP to restore ovulation; cyclic progestins ex: IUD; metformin)

  • Hirsutism (Diane trial for 6 mo 1st line; Spironolactone 2nd line; laser therapy, creams, doxycycline)
  • Subfertility (diet and exercise, smoking cessation, folate supplement; ovulation induction ex: clomiphene +/- metformin)
  • Cardiometabolic risk (metformin)
227
Q

Which type of twin is more risky and what are some of the complications/associated risks?

A 
TTTS
Conjoined twins
Death of a co-twin
Discordant fetal anomalies
TOPS - Twin oligohydramnios polyhydramnios syndrome
Perinatal mortality
Preterm
LBW, IUGR
NICU admission, NEC etc
GDM
228
Q

What additional antenatal care considerations do women pregnant w twins need?

A

Education/counselling around additional risks (fetal + maternal GDM, PE, APH, PPH, depression, anaemia, marital problems) and support services

Nutritional advice - incr requirements of energy, protein, folate, Ca, iron,

Aspirin from 12-36 weeks as PE prevention
Early GTT at 12 weeks if other RFs for GDM

229
Q

When should twins be delivered?

A

DCDA: ~37 weeks

MCDA: no later than 37+6
MCMA: 32+0 to 33+6 with daily CTG monitoring after 26 weeks (MOST RISKS)

230
Q

MX of labour of twins

A

NVD fine as long as twin 1 is cephalic. if not -> LUSCS

Presence of skilled doctors (senior obstetrician, paeds, anaesthetics)
IV access
Epidural MANDATORY (for easy manipulation of twin 2 if necessary)
Deliver twin 1 then ensure long. lie of twin 2 (breech or vertex both ok)

Start syntocinon to restart contractions
ARM when twin 2 is in pelvis
Vaginal delivery of twin 2`

231
Q

What is TTTS

Consequences

A

Twin-twin transfusion syndrome
- net shunt of blood from donor to recipient in MC twins

Donor: anaemia, oliguria, hypovolaemia, oligohydramnios, IGUR, FDIU

Recipient: Polycythaemia, polyuria, hypervolaemia, polyhydramnios, cardiomyopathy

232
Q

Mx of TTTS

A
  1. amniodrainage - 70% survival but poor long term outcomes.

2. laser photocoagulation - creates functionally DC (only in severe cases)

233
Q

What features does USS look at?

A

Fetal biometry (AC, HC, FL, HC:AC)
Liquor volume
Fetal activity
Doppler USS -> umbilical artery waveform, uterine artery, MCA

234
Q

What umbilical artery waveforms are associated with placental gas exchange abnormalities

A

Raised Systolic diastolic ratio

Absent end-diastolic flow

235
Q

Management of pregnant women with influenza

A 
Empiric antiviral (tamiflu etc) therapy for pregnant women exposed to influenza virus or within 2 weeks either side of delivery (pre and postpartum)
Infection control measures
236
Q

Antibiotics for UTI in pregnancy

A

Empiric cephalexin or augmentin

237
Q

Risks of Rubella infection in pregnancy

SX

A

Highest risk with maternal viraemia in 1st trimester
Infx <16 wks -> congenital rubella syndrome (blind, deaf, CP, heart abnormalities)
Infx>16wks -> growth restriciotn

SX - asympt or may have mild febrile illness and fleeting rash

238
Q

MX of a women NOT immune to rubella antenatally

A

Paired IgM and IgG testing 14-21 days apart
Confirmed infection in first 12 weeks, offer termination
Confirmed infection > 16 weeks: fetal growth surveillance
Vaccine post-partum (live attenuated)

239
Q

CMV
SX
Risks associated with this?

A

SX - mum asymptatomic

Risks - congenital non-genetic deafness, blindness, intellectual disability/neurodegenerative problems

240
Q

Diagnosis and management of CMV

A

DX: no routine screening;
CMV IgG and avidity of IgG if high-risk or if USS or neonatal abnormalities have been detected.
Amniocentesis and serial USS if IvIg positive antenatally.

MX- insider termination if picked up early. no tx exists.

241
Q

SX of maternal and congenital VZV

A

maternal: vesicular rsh +/- varicella pneumonia several days after rash onset
congenital: cicatricial skin lesions, limb hypoplasia, microcephaly, eye lesions (evident on USS)

242
Q

Mx of a mother seronegative for VZV

A

If exposed:
VZVIg (ZIG) within 96 hours of exposure
Oral Acyclovir if you miss the 96hr window

IV Acyclovir if complications present (varicella pneumonia)

Babies born to infected mothers: ZIG +breastfeeding

If not exposed: postpartum vaccination

243
Q

Mx of syphilis in pregnancy. when is risk of transmission greatest?

A

Penicillin!

risk of perinatal transmission highest in primary, secondary syphillis, followed by early latent syphilis.

244
Q

What does listeria infection in pregnancy cause?

How do you prevent this infection?

A

Maternal sepsis and chorioamnionitis with intact membranes
Miscarriage

Transmitted by food so prevent via:
- safe food hygeine/handling; avoid high risk foods (unpasteurised diary, pre-prepared salads, uncooked seafood and chicken, processed meats)

245
Q

When does GBS sepsis present and what are risk factors for the congenital infection?

A

First 24 hours of life

RF: premature, PROM >18 hours, maternal fever, GBS positive mother (carries it in her GI/GU tract)

246
Q

MX of a GBS positive mother

A

IV intrapartum antibiotics: 2 doses 4 hours apart, starting at onset of labour (IV benpen or cephazolin if allergic)

Neonatal obs for 24 hours following delivery +/- neonatal abx if clinical suspicion of sepsis

247
Q

outcomes of maternal toxoplasmosis infection

How do you test for this?

A

10% of intrapartum infection -> miscarriage, still birth, congenital birth defects ( chorioretinitis, intracranial calcification and hydrocephaly )

Inx: not routine but can order serum IgM and IgG -> if positive, amniocentesis for confirmation

248
Q

What infection are child-care workers predisposed to in pregnancy?
SX

A

CMV infection (asymptomatic) and parvovirusB19 (slapped-cheek/lacy trunkal rash)

249
Q

Consequences of maternal parvovirus B19 infection in pregnancy

A

If primary infection in pregnancy, small risk (3-5% of maternal infections) of fetal hydrous and intrauterine death secondary to fetal anaemia

250
Q

Diagnosis and MX of parvovirus B19

A

DX: paired parvovirus B19 IgG and IgM serology in mum.
MX:
Close USS surveillance for development of fetal anaemia and hydrous in bub (polyhydramnios, ascites, incr SDR)

No tx for mum.
If fetal anaemia detected, refer to tertiary centre for care -> intrauterine infusion (O-neg blood) via umbilical cord

251
Q

Mx of intrapartum HSV

A

Highest risk of neonatal transmission with primary infection in 3rd trimester of pregnancy with viral shedding at time of vaginal delivery

Late primary infection: Antivirals (acyclovir) and C/S to reduce neonatal risk

Early primary infection: antivirals from 36 weeks, can try NVD unless there are active lesions at labour onset (in which case LUSCS is necessary)

252
Q

Risk factors for chorioamniotis

A

PROM
Prolonged labour
Multiple intrapartum VEs
Internal fetal HR monitoring (scalp electrode)
Genital tract infections (STIs, GBS positive)

253
Q

Clinical features of chorioamnionitis

A 
Maternal fever or fetal tachycardia
Uterine pain/tenderness
PV blood loss
Preterm labour
Malodorous or purulent amniotic fluid 
FBE: Incr WCC + incr CRP
254
Q

Management of chorioamnionitis

A

Erythromycin for 10 days + steroids

Immediate delivery if baby is unstable (even if preterm, if infected - i.e. baby tachycardia, offensive D/C, pain, bleeding)

255
Q

Management of pROM

A

If baby is stable, buy more time!
Antibiotics (10days erythromycin) and discharge with biweekly O/P appointments and at-home vital monitoring

IOL at 37 weeks
IOL pre-term if ?Chorio/unstable baby

256
Q

Pathophys of menopause

how do hormones change with this?

A

Physiological - loss of ovarian function from exhaustion of primordial follicles due to atresia/atrophy

Iatrogenic - gynae surgery (bilateral oophorectomy; chemo, radiation to pelvis)

Decr Estrogen and progesterone
Incr FSH

257
Q

Symptoms of menopause and what do they relate to?

A

SX Related to decr oestrogen
Vasomotor SX (hot flushes, night sweats, palpitations)
Sleep problems
Urogenital problems (dry vaginal, atrophic vaginitis, urinary frequency)
Locomotor sx (joint pain, backache, muscle aches)
Psychological SX (anxiety, depression, feeling unloved etc)
Loss of libido
Osteoporosis and incr fracture risk

258
Q

Common sites for osteoporotic fractures

A

Vertebral
Hip
Wrist

259
Q

Definition of osteoporosis

A

Bone density (DEXA scan) <2.5 SD below mean

Osteopenia is 1.5 - 2.5 SD below the mean

260
Q

Management of osteoporosis in menopause

A

All women with risk factors get 2 yearly DEXA scans

T-scores <2.5 get treatment:
Lifestyle/conservative: Ca, vit D supplements and daily exercise
<60: HRT
>60: Bisphosphonates (SE: GORD, osteonecrosis of the jaw)

261
Q

Risk factors for osteoporosis

A 
Low BMI
Smoking
Family Hx
excessive caffeine
steroids
IBD/malabsorption
Decr VitD
262
Q

Definition of menopause

normal age range

A

final menstrual period, determined after 12 months of amenorrhoea
normal age range: 45-57

263
Q

Non-hormonal management of menopause

A

Lifestyle:

  • stop smoking
  • weight mx (exercise and diet)
  • <2SD alcohol
  • Decr caffeine
SX-treatment
Vasomotor SX
- SNRI (Venlafaxine, fluoxetine, citalopram)
- GABApentin 
- Clonidine/nifedipine (Ca ch blocker)

Vaginal dryness

  • vaginal oestrogen pessary
  • lubricants and gels, moisturisers and oils

Locomotor SX: analgesia, NSAIDs, exercise
Psych SX: Antidepressants, anxiolytics, counselling

264
Q

Hormonal management of menopause

A
  1. HRT (only for women <60 to limit risks of CVD, VTE, stoke etc)
    Relieves menopausal SX and incr bone density
    With uterus: Oestrogen and progesterone (protects from incr risk of endometrial cancer)

Method: local cream/pessary/tablet if vaginal dryness (no need for prog)
- tablets, patches, subcut implant, skin gel (combined preparations)

Without uterus: oestrogen alone

  1. Tibolone: synthetic steroid with weak oestrogen, progesterone and anti androgen effects (helps w vasomotor SX, vaginal lubrication and libido; incr bone mass density and decr fracture risk; no incr risk endometrial cancer)
265
Q

SE of HRT and CI

A

SE:
incr risk stroke, VTE, CVD (oestrogen)
incr risk breast cancer (combined - prog)
incr risk endometrial, ovarian cancer and cholecystitis w unopposed estrogen

CI:
HX breast, ovarian, endometrial cancer
HX VTE or thrombophilia
HX stroke or heart disease
Uncontrolled HTN
Active liver or cholestatic disease 
Migraine w aura 
Abnormal vaginal bleeding
266
Q

Investigations for premature menopause (<45)

A

FSH (elected on 2 occasions is diagnostic)
Decr E2

Inx for other causes
prolactin, TFTs, betaHCG
Karyotype (turner’s) and fragile X screen
pelvic USS

267
Q

Differentials deep dyspaerunia

A 
Endometriosis
Adenomyosis
Adhesions
PID
Fibroid 
Neoplasia
268
Q

Differentials superficial dyspareunia

A

Vulvovaginitis (inflammation) - thrush, STIs, herpes, UTI
Dermatological - lichen sclerosis, eczema, psoriasis, contact dermatitis, atrophic vaginitis
Inadequate lubrication - menopause, oestrogen deficiency, radio/chemotherapy, drugs
Trauma
Vaginismus (spasm of vaginal muscles)
Vulvodynia
Rigid hymen
Neoplasia

269
Q

Aetiology post-menopausal bleeding

A

Anovulatory cycles (lack of ovulation leads to endometrial build up that outgrows blood supply)

Endometrial cancer until proven otherwise!
Cervical cancer (70% SCC due to HPV; 30% adenocarcinoma)

Benign causes :

  • Urogenital atrophy (due to lack of oestrogen, thinning of vaginal and cervical epithelium and endometrium)
  • Endometrial polyps
  • Fibroids
  • Endometrial hyperplasia (simple; atypical - 40% progress to carcinoma)
270
Q

Inx and Mx of post-menopausal bleeding

A

Inx: TVUSS and hysteroscopy D&C or O/P pipelle for endometrial sampling (colposcopy if pap spec and pap smear abnormal)

MX:
Medical
- vaginal oestrogen therapy for urogenital atrophy
- Progesterones (mirena, depot provera injections) for SIMPLE endometrial hyperplasia
- COCP if <60 and low risk for CVD, VTE

Surgical

  • Hysterectomy for atypical endometrial hyperplasia (+/- bilateral sapling-oophrectomy with lymph node sampling for endometrial cancer; +/- pelvic lymph node sampling for cervical cancer)
  • Endometrial ablation + contraception or tubal ligation
271
Q

Complications in the puerperium

A 
Secondary PPH (retained products or endometritis)
Infection 
- Sepsis (GAS)
- Endometritis 
- Wounds (C/S, Epis/perineal tears)
- epidural or IV site
- UTI
- Mastitis, other lactation problems

VTE risk
Urinary retention or incontinence (urethral damage etc)
Constipation or faecal incontinence
Mood disorders

272
Q

Time course of breastfeeding

A

Exclusive breastfeeding for up to 6 months post delivery with gradual introduction of solids and continued (non-exclusive) breastfeeding into 2nd year

273
Q

CI to breastfeeding

A

HIV

Methotrexate, cyclosporin

274
Q

Benefits of breast feeding

A

Infant - Decr risk of RTIs, gastro illness, DM, obesity, HTN, CV disease, NEC, SIDS; incr IQ

Mother - contraception, decr risk of ovarian cancer, breast cancer, osteoporosis, faster return to pre-pregnancy weight

275
Q

Complications of breast feeding

A

Mastitis (staph infection) +/- Breast abcess
Cracked/grazed/bleeding nipples - due to incorrect attachment
Engorgement
Low supply

276
Q

Presentation of mastitis

A

Red, hot, tender breast lump; Fever, pain, malaise +/- systemic SX
MX: encourage mum to keep feeding to drain the breast
AbX (fluxclox) only if SX unresolved for 12 hours -> if unstable, admit for IV antis + breast milk culture

277
Q

Risk factors for T21

A

age >= 37 is high risk
Prev chromosomal abnormalities (T21, T18, T13, 45XO)
2 or more minor or 1 major abnormality on USS
Chrom. abnormality in either partner

278
Q

MX of termination of pregnancy

A
  1. offer SW and psych referral
  2. Inx: blood group and Ab (if Rh neg give antiD); STI swabs

If 1st trim: Surgical D&C (day procedure but surgical risks)
Medical: Misoprostil/mifepristone (painful, takes 3 days; 15% fail and need D&C)

2nd trim: Surgical: D&C or hysterotomy
-Medical: IOL + KCL + Mifepristone + Misoprostil

279
Q

At what point does a terminal panel and 2 doctors need to agree on performing a termination?

A

24 weeks onwards

280
Q

Features of trisomy 21

A 
1/2 are FDIU
Low IQ
Congenital abnormalities
Dysmorphic features
Heart, hearing problems
Short stature

MD3 (7 decks)

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