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Year 4 > O&G > Flashcards

O&G Flashcards

1
Q

Describe how to calculate estimated delivery date?

A

280 days (40 weeks) from the 1st day of the LMP

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2
Q 
Describe the hormone levels of
- oestrogen
- progesterone
- beta-hCG
in early pregnancy
A

After ovulation and fertilisation, oestrogen and progesterone continue to gradually rise, but bHCG peaks around week 12 of pregnancy and then plateaus

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3
Q

Define miscarriage (early and late)

A

Miscarriage = spontaneous termination of pregnancy <24 weeks gestation

  • early = <12 weeks
  • late = 12-24 weeks
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4
Q

Define stillbirth

A

Any foetus born dead >24 weeks gestation

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5
Q

Define livebirth

A

Any foetus born at any gestation showing any signs of life after delivery

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6
Q

Define the following types of miscarriage:

  1. Threatened
  2. Inevitable
  3. Incomplete miscarriage
  4. Complete miscarriage
  5. Missed (silent)
  6. Septic
  7. Recurrent
  8. Anembryonic
A
  1. Threatened = vaginal bleeding, closed cervix, alive foetus with continuing intrauterine pregnancy
  2. Inevitable = vaginal bleeding and open cervix, non-continuing intrauterine pregnancy
  3. Incomplete miscarriage = retained POC in the uterus after miscarriage
  4. Complete miscarriage = all pregnancy tissue expelled after miscarriage and uterus now empty
  5. Missed (silent) = foetus no longer alive but no symptoms have occurred
  6. Septic = miscarriage complicated by intrauterine infection
  7. Recurrent = 3 or more consecutive miscarriages (before 24 weeks) with the same biological father
  8. Anembryonic = Gestational sac is present, but contains no embryo
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7
Q

What is the rate of miscarriage?

A

1/5 pregnancies

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8
Q

Describe how a miscarriage may present

A
  • pelvic pain
  • vaginal bleeding (from brown spotting to heavy +/- tissue)
  • asymptomatic
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9
Q

Describe how to investigate a miscarriage

A

Hx - quantify pain, bleeding, LMP…
Ex - are they haemodynamically stable?, is the cervix open or closed?
USS TV - look for 3 things…

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10
Q

Describe how USS is used as the gold standard method of investigating miscarriages

A

Look for 3 things:

  • mean gestational sac diameter
  • fetal pole and crown-rump length
  • fetal heartbeat

Heartbeat should be expected when CRL is >7mm (-> if there is no heartbeat, check 1 week later on scan before confirming non-viable pregnancy)

Fetal pole is expected once mean gestational sac diameter is >25mm (-> if the sac diameter is >25mm with no fetal pole, repeat scan one week later before confirming an anembryonic pregnancy)

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11
Q

List differentials of a miscarriage

A

Ectopic pregnancy

Ruptured ectopic pregnancy

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12
Q

Describe the management flowchart of miscarriage

A

<6 weeks gestation = expectant management
>6 weeks gestation = refer to early pregnancy assessment service, USS to rule out ectopic, then one of three management options (expectant, medical, surgical)

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13
Q

Describe the 3 management options of miscarriage

A
  1. Expectant - spontaneous passage with follow up scans 7-10 days later. Further referral if continued pain or bleeding.
  2. Medical - Mifepristone (an anti-progesterone drug) to prime and then 24-48hrs later… Misoprostol (a prostaglandin analogue - binds to prostaglandin receptors and activates them) which softens the cervix and stimulates uterine contraction, given orally or as a vaginal suppository, dose depending on gestation) can then do at home
    - 70% success
    - S/Ex: GI upset and pain, heavy bleeding, diarrhoea and vomiting -> provide anti-emetics
  3. Surgical - for unacceptable pain/bleeding or retained POC on scan
    - Can be MVA (manual vacuum aspiration = LOCAL ANAES.) or EVA (electric vacuum aspiration = GENERAL ANAES.) -> both >98% success
    - Requires cervical priming (usually misoprostol is given to soften the cervix)
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14
Q

Define an ectopic pregnancy

A

When a pregnancy is implanted outside of the uterus (most commonly in fallopian tube but can occur at entrance to fallopian tube/ovary/cervix/abdomen)

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15
Q

List RFx for ectopic pregnancies

A

Previous ectopic
Endometriosis
Pelvic infection particularly chlamydia/PID (causes scarring)
Previous STI - causes scarring
Pelvic surgery – including C-sec, sterilisation, appendicectomy
Contraception – progesterone only pill, IUD (contains copper)/IUS (contains progesterone)
Assisted conception techniques
Cigarette smoking
Age 40+

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16
Q

What is the incidence of ectopic pregnancies?

A

1/200 women

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17
Q

Describe how an ectopic pregnancy may present

A

Should be a differential for any sexually active woman who presents with pain, irregular bleeding and/or amenorrhea!!!

  • Missed period
  • Constant lower abdominal pain in the right or left iliac fossa
  • Vaginal bleeding
  • Lower abdominal or pelvic tenderness
  • Cervical motion tenderness (pain when moving the cervix during a bimanual examination)
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18
Q

How are ectopic pregnancies investigated?

A

Are they haemodynamically stable? (if not this could be an emergency)

Hx - possibility of pregnancy, unprotected sex, missed periods

Examination (bimanual)

USS - Transvaginal
□ May see an empty uterus
□ May see a gestational sac containing a yolk sac or fetal pole may be seen in the fallopian tube (or may see an empty gestational sac)
□ A mass moving separately to the ovary represents a tubal ectopic pregnancy
□ A mass moving with the ovary represents the corpus luteum

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19
Q

Describe pregnancy of unknown location and how a blood marker can be tracked to help with diagnosis

A

PUL = when woman has +ve pregnancy test but there is no evidence of pregnancy on USS scan
An ectopic cannot be excluded in this case, so the hormone hCG is measured (two readings taken 48hrs apart)

Normally the developing syncytiotrophoblast will produce this hormone.
- In an intrauterine pregnancy, hCG will double every 48hrs

If >63% increase in hCG after 48hrs - intrauterine pregnancy (repeat USS 1-2 weeks later)
If <63% increase in hCG after 48hrs - ectopic
Fall of <50% = miscarriage (repeat urine pregnancy test 2 weeks later to confirm pregnancy has ended)

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20
Q

At what hCG hormone level should a pregnancy be visible on USS?

A

> 1500 IU/L

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21
Q

Describe the management of ectopic pregnancy

A

All ectopics need to be terminated as they are not viable pregnancies!
3 options depending on clinical situation and the location of the ectopic

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22
Q

Describe expectant management of ectopic pregnancies and the criteria

A

Criteria:

  • Follow up needs to be possible to ensure successful termination
  • The ectopic needs to be unruptured
  • Adnexal mass < 35mm
  • No visible heartbeat
  • No significant pain
  • HCG level < 1500 IU / l
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23
Q

Describe medical management of ectopic pregnancies and the criteria

A

Methotrexate, can only be used if the following criteria are met:

  • HCG level must be < 5000 IU / l
  • Confirmed absence of intrauterine pregnancy on ultrasound
  • Able to return for follow up
  • No medical contraindications (e.g. anaemia, renal, hepatic impairment, UC, peptic ulcer)
  • Pain free
  • Unruptured ectopic
  • <35mm
  • No fetal heartbeat visible

Method:

  • Antifolate medication (injection) -> stops DNA synthesis
  • No new pregnancy until 3 months after HCG<5 (time required to replenish folic acid) methotrexate is teratogenic
  • Must use a reliable form of contraception for 3 months after as any future pregnancy could be harmed by remaining folate antagonist in the system! (omen advised not to get pregnant in these 3 months)
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24
Q

Describe surgical management of ectopic pregnancies and the criteria

A

Criteria:

  • If ruptured
  • Pain
  • Adnexal mass > 35mm
  • Visible heartbeat
  • HCG levels > 5000 IU / l

Methods:

  • Laparoscopic salpingectomy - removal of tube (where contralateral tube looks healthy no need to remove)
  • Laparoscopic salpingotomy - opening of affected tube and removal of POC
  • Requires HCG follow up
  • 1 in 5 require further management as pregnancy may not be removed (may need methotrexate or salpingectomy)

Anti-rhesus D is given to women who are rhesus negative and requiring surgical management of their ectopic

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25
Q

What are the side effects of methotrexate

A

S/Ex of methotrexate:

  • Vaginal bleeding
  • Nausea and vomiting
  • Abdominal pain
  • Stomatitis (inflammation of the mouth)
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26
Q

Describe the need for rhesus immunisation

A

RH- mother and RH+ father
Mother carried first RH+ child
RH + antigens from developing fetus can enter mothers blood stream during delivery
Mother then makes anti-RH antibodies
If a second baby then grows in the mother who is RH+, her pre-made antibodies will cross the placenta and damage this second fetus’ RBC’s

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27
Q

List the criteria which may mean a mother needs to receive anti-Rhesus D immunisation

A
  • Anti-D is required if mother is Rh negative
  • After management of ectopic pregnancy
  • Therapeutic termination of pregnancy
  • <12w vaginal bleed which is heavy, repeated or associated with severe pain
  • <12w medical or surgical management of miscarriage
    Any potentially sensitising event >12w
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28
Q

Describe haemolytic disease of the newborn (HDN), and how it may present antenatally and postnatally

A

When maternal RH antibodies cross the placenta and attack the developing foetus who is RH+ve

As these antibodies destroy the fetus’ RBC’s, chemicals are released (particularly bilirubin)
This causes jaundice -> kernicterus, and a haemolytic anaemia

Jaundice + haemolytic anaemia = HDN

Antenatal signs -> polyhydramnios, thickened placenta
Post-natal signs -> jaundice, hepatosplenomegaly, kernicterus

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29
Q

Give a basic recap of fertilisation and embryo formation:

A
  • Fertilised egg = zygote
  • 16 cell divisions = morula
  • Morula is surrounded by glycoprotein coat called zona pellucida (prevents tubal implantation on way to uterus)
  • Morula becomes blastocyte
  • > Cells of the inner mass are now called the embryoblast -> gives rise to embryo and embryonic tissues
  • > Cells of the outer mass are collectively called the TROPHOBLAST -> gives rise to placenta
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30
Q

What is gestational trophoblastic disease?

A

A group of conditions characterised by abnormal proliferation of trophoblastic tissue with production of HCG

  • affects 1/700 livebirths in the UK
  • has premalignant and malignant forms
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31
Q

What are the risk factors for GTD?

A
  • Extremes of maternal age (<20 or >40)
  • Previous molar pregnancy
  • Ethnicity (higher incidence in Asia and USA)
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32
Q

Describe the two ‘premalignant’ forms of GTD

A
  1. Partial hydatidiform mole
    - triploid (2 sperms and 1 egg)
  2. Complete hydatidiform mole
    - diploid (46 chromosomes all from father e.g. 2 sperms, and empty ovum)
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33
Q

Describe the ‘malignant’ forms of GTD

A
  1. Invasive mole
  2. Choriocarcinoma
  3. PSTT - placental site trophoblastic tumour
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34
Q

What are the clinical features of GTD?

A
  • PV bleeding
  • Enlarged uterus
  • Hyperemesis gravidarium
  • Hyperthyroidism
  • Early onset pre-eclampsia
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35
Q

How is GTD diagnosed and treated?

A
  • US features ‘snowstorm appearance’
  • Histology – ideally following suction curettage
  • > BHG tracking and registration with specialist centres (Dundee) for follow up and co-ordination of care
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36
Q

Describe N&V in pregnancy

A

Most common in 1st trimester (affects >50% women in 1st trimester)
Very severe in some cases with high hCG
- Multiple pregnancy
- Molar pregnancy
90% settle by 16w
Cause is unknown but may be associated with serum hCG levels (similar subunit to TSH)

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37
Q

What is hyperemesis gravidarium?

A

Persisitent vomiting in pregnancy causing weight loss (more than 5% of body mass) and ketosis
Hyperemesis affects 1% of pregnancy women associated with increased bHCG (i.e. twins)

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38
Q

What are the effects of hyperemesis gravidarium on mum and baby?

A

Mum:

  • Wernices (thiamine deficiency)
  • Central pontine myelinolysis (rapid correction of hyponatraemia)
  • Maternal death (rare)

Baby:

  • Higher incidence of intrauterine growth restriction
  • Significantly smaller at birth
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39
Q

How is hyperemesis gravidarium investigated?

A

Investigate if unable to keep food or fluids down, so check weight, hydration, electrolytes, BP

  • Urine – ketones, other causes (e.g. UTI causing vomiting)
  • Serum – renal, liver and thyroid function, transaminases may be abnormal and albumin low
  • US scan – multiple pregnancy, molar pregnancy?
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40
Q

How is hyperemesis gravidarium managed?

A

Admit if unable to keep anything down despite oral antiemetics – rehydration and correction of metabolic disturbances

  • Oral intake advice/ dietician
  • IV fluids (avoid dextrose as glucose can exacerbate Wernickes) tailor to correct electrolyte imbalance
  • Regular antiemetics – cyclizine, ondansetron
  • Thromboprophylaxsis
  • Vitamin replacement e.g. K, thiamine, folic acid
  • Total parenteral nutrition (extreme)
  • Psychological support
  • Assessment of fetal growth
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41
Q

Define gravidy

A

Total no. pregnancies, including misscarriages or stillbirths, and the current pregnancy

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42
Q

Define parity

A

The number of potentially viable pregnancies beyond 24 weeks that have been delivered, NOT including the current pregnancy, AND including still and livebirths

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43
Q

What does para 3 mean?

A

Three term deliveries

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44
Q

What does para 2 + 1 mean?

A

Two term pregnancies, and a miscarriage at 20 weeks

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45
Q

What does multiparous mean?

A

Has delivered live/potentially viable babies >24 weeks gestation

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46
Q

What does nulliparous mean?

A

Never delivered a live or potentially viable baby >24 weeks gestation

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47
Q

Describe how to term a woman who is currently pregnant (16 weeks) and has had two miscarriages in the past

A

Gravidum 3, parity 0 + 2

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48
Q

Define infertility

A

Also called subfertility
= inability of a couple to achieve a clinical pregnancy after 12 months of regular sexual intercourse

Primary = no previous pregnancy
Secondary = at least 1 previous pregnancy
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49
Q

List some factors affecting fertility

A

Age
Timing of intercourse (sperm lives 72hrs inside female and needs to be there before ovulation)
Body weight

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50
Q

How is infertility investigated?

A 
History
- previous pregnancies
- ask about female cycles, previous STD's, smears
- sexual habits
Examination
- look at ovaries with USS
- sperm testing
Primary care
- BMI, STI screening, semen analysis, hormone testing
Secondary care
- Pelvic USS
- Hysterosalpingogram (check tubes using x-ray + dye)
- Laparoscopy + dye
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51
Q

What is the cut off parameters for suitable semen?

A
  • concentration > 15 million/ml
  • total motility >40%
  • normal forms >4%
  • volume >1.5mls
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52
Q

What are the management options for infertility?

A
  • ovulation induction
  • egg retrieval
  • intra-uterine insemination
  • IVF
  • ICSI (intracytoplasmic sperm infection)
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53
Q

What is ovarian hyperstimulation syndrome?

A
  • serious complication of fertility treatment (esp. IVF)
  • ovaries over-respond to gonadotrophin injections
  • vasoactive hormones and chemicals released systemically from the ovaries
  • fluid accumulates in 3rd spaces causing abdominal swelling, N&V, abdo pain, thirst, dehydration (intravascular depletion)
  • patient can become prothrombotic and develop a DVT/PE
  • affects 1/3rd of women having IVF
  • managed conservatively
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54
Q

What is the main differential for a 40yr old woman presenting with weight loss and bloating with no obvious cause?

A

Ovarian cancer? -> SEND FOR SCAN

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55
Q

What is the most common pathological type of ovarian cancer?

A

EPITHELIAL (90%)
‘Serous’ epithelial is the most common type

Serous tumours can be high or low grade

  • high grade, resemble fallopian tube mucosa, has P53 mutations, often need BSO (to remove both ovaries and tubes)
  • low grade arise from ovarian surface epithelium
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56
Q

List some germ cell ovarian tumours

A

Teratoma (dermoid) = contain hair/teeth/cartilage, common 20-30 years

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57
Q

How can ovarian cancer spread?

A
  • direct (transcoelemic)
  • exfoliation into peritoneal cavity
  • lymphatic
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58
Q

List RFx for ovarian cancer

A
  • smoking
  • low parity
  • old age
  • FHx
  • HRT
  • obesity
  • early menopause/late menarche
  • genetics (BRCA 1/2)
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59
Q

Describe how the BRCA genes increase your risk of ovarian cancer

A

They are TSG’s which normally hault the cell cycle if there are faults
- However when mutated, they allow abnormal cells to continue cycling, leading to cancer development

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60
Q

Other than BRCA, what other gene mutation can increase your risk of ovarian/colon/endometrial cancers?

A

Lynch (HNPCC) cancer

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61
Q

List protective factors against ovarian cancer

A

Not smoking
COCP
Multiparity
Breast feeding

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62
Q

How may an ovarian cancer present?

A 
B symptoms
Vague
Bloating
Loss of appetite
GI upset
Painful intercourse
Pleural effusion/ascites (Meig's syndrome)
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63
Q

What is Meig’s syndrome

A

Triad:
Ovarian fibroma (a type of benign ovarian tumour)
Pleural effusion
Ascites

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64
Q

How is ovarian cancer investigated?

A

Bloods (FBC, LFT, U&E, tumour markers)
- CA125 (non-specific), CEA, LDH, b-HCG, AFP
USS (TV)
CXR (look for pleural effusion or metastasis)
CT (to determine initial treatment)
Calculate RMI = USS findings x menopausal status x ca125 level
- RMI > 250 = high risk of cancer
- RMI < 250 = low risk of cancer

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65
Q

Describe the difference between staging and grading

A

Staging = the gross size of the tumour and how it has spread through the body

Grading = microscopically, how differentiated the cells are (higher grade = less differentiated)

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66
Q

Describe roughly the FIGO staging for ovarian cancer

A

Stage 1 = limited to ovaries (Tx = surg)
Stage 2 = peritoneal deposits in pelvis (Tx = surg them chemo)
Stage 3 = peritoneal deposits outside pelvic (Tx = surg them chemo)
Stage 4 = distant mets (Tx = palliative surg)

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67
Q

Describe the major treatment options for ovarian cancer

A
  1. Surgery
  2. Chemo/radio/hormonal (neoadjuvant or adjuvant)
  3. Palliative
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68
Q

What is the most common type of endometrial cancer

A

~80% = adenocarcinoma

There are 2 types of adenocarcinoma

  • type 1 = oestrogen dependent
  • type 2 = non-oestrogen dependent
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69
Q

What is endometrial hyperplasia?

A
  • Pre-cancerous thickening of the endometrium
  • diagnosed on USS as thickening <4mm
  • can be
  • > hyperplasia without atypia
  • > atypical hyperplasia
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70
Q

How is endometrial hyperplasia treated?

A

Progesterone encourages regression!

  • mirena coil
  • oral progesterones
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71
Q

List risk factors for endometrial cancer

A

(UNOPPOSED OESTROGEN)

  • obesity
  • early menarche/late menopause
  • PCOS
  • diabetes
  • tamoxifen
  • oestrogen only HRT
  • HNPCC (breast/colon cancer)
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72
Q

List protective factors for endometrial cancer

A
  • COCP
  • copper IUD
  • SMOKING! (smokers metabolise oestrogen differently)
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73
Q

How may endometrial cancer present?

A
  • any abnormal bleeding e.g. PMB, PCB, IMB
  • vaginal discharge
  • altered menstrual pattern
  • anaemia
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74
Q

List differentials of PMB based on anatomy

A
  • ovarian cancer
  • uterine fibroids
  • cervical changes
  • atrophic vaginal changes
  • haematuria
  • vulvitis, vulval malignancy
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75
Q

How is endometrial cancer investigated?

A
  • Bloods
    1 - TV USS (measure endometrial thickness)
    2 - Pipelle biopsy
    3 - Hysteroscopy and biopsy
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76
Q

Describe the FIGO staging of endometrial cancer

A
  • Stage 1 = tumour confined to uterus
  • Stage 2 = cervical stroma invasion (not beyond uterus)
  • Stage 3 = tumour outside uterus
  • Stage 4 = invasion of bladder/bowel mucosa
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77
Q

Describe how endometrial cancer is treated

A

Surgical
Adjuvant treatment (chemo/radio/hormonal)
Palliative

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78
Q

Define the following procedures:

  1. Hysterectomy
  2. Subtotal hysterectomy
  3. Radical hysterectomy
  4. BSO
A
  1. Hysterectomy = removing uterus and cervix
  2. Subtotal hysterectomy = removing uterus, leaves cervix
  3. Radical hysterectomy = uterus, cervix and vaginal cuff removed
  4. BSO = removing ovaries and tubes
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79
Q

Describe the lining of the cervix

A
  • > squamous epithelium of outer cervix (continuous with vagina)
  • > then transformation zone
  • > then inner surface of cervix is lined with columnar epithelium
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80
Q

What is the
1. ectovervix
2. endocervix
lined with?

A
  1. Ectocervix - outer surface, squamous lining

2. Endocervix = inner surface = columnar, glandular cells

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81
Q

What is a cervical ectropion?

A

Extension of the endocervical columnar epithelium downwards, which bleeds easily
Common in pregnancy due to increased oestrogen
Can be cauterised with silver nitrate sticks if necessary

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82
Q

Describe CIN

A

Cervical intraepithelial neoplasia

  • precancerous changes
  • CIN grading looks at the level of DYSPLASIA in the cervix cells
CIN1 = mild dysplasia, affects 1/3rd thickness of the epithelial layer (return to normal without treatment)
CIN2 = moderate dysplasia, affects 2/3rd thickness of the epithelial layer (likely to progress to cancer without treatment)
CIN3 = severe dysplasia (likely to progress to cancer if left untreated, sometimes called cervical carcinoma in situ)
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83
Q

Describe the most common type of endometrial cancer

A 
80% = squamous cell carcinoma
20% = adenocarcinoma
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84
Q

Describe the HPV vaccine

A
  • Ideally given to girls and boys before they become sexually active, with the intention of preventing them contracting and spreading HPV once they are sexually active
  • 80% of general population will be infected with the virus at some point in their life
  • Nearly 99.7% of cervical cancers are caused by HPV = HPV IS THE BIGGEST RFx
  • Vaccine - 2 injections (6-12 months apart)
  • Currently ‘GARDISAL’ vaccine – covers for HPV 6, 11, 16, 18
  • 6 and 11 = genital warts
  • 16 and 18 are the high risk strains associated with cervical cancer
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85
Q

List RFx for cervical cancer

A
  • HPV - think of factors which increase exposure!
  • smoking
  • early 1st sexual intercourse
  • COCP (because then not using condoms??)
  • FHx
  • multiple sexual partners
  • immunosuppression
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86
Q

Describe clinical features of cervical cancer

A 
Post-coital bleeding
Intermenstrual bleeding
Post-menopausal bleeding
vaginal discharge
asymptomatic (found on smear)
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87
Q

List some differentials of cervical cancer

A

E.g. causes of IMB and PCB

  • cervical ectropion
  • cervical polyp
  • fibroids
  • endometrial hyperplasia
  • endometrial malignancy
  • hormonal breakthrough bleeding
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88
Q

How is cervical cancer investigated?

A
  • Bloods
  • Speculum and smear (DO NOT SMEAR IF CERVIX APPEARS ABNORMAL as smears are for screening only!)
  • Colposcopy (carried out following an abnormal smear)
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89
Q

Describe the purpose of colposcopy

A

Can be used to diagnose CIN
(remember smear tests show cell dyskaryosis = abnornal nucleus)
Can use
- acetic acid (causes abnormal cells to appear white as they have a higher nuclear:cyto ratio e.g. cancerous/CIN cells)
- Iodine (stains healthy cells a brown colour and abnormal cells will not stain)
- a punch or loop biopsy can also be carried out
- a Cone biopsy can be carried out to treat CIN

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90
Q

Describe the FIGO staging of cervical cancer

A

Stage 1 = limited to the cervix
Stage 2 = involves upper 2/3rds vagina
Stage 3 = involves lower 1/3rd vagina
Stage 4 = tumour has spread to other organs

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91
Q

Describe cervical screening, and possible smear results

A
  • aims to detect and treat abnormal changes in a woman’s cervix that may develop into cervical cancer
  • 3yrly 25-49
  • 5yrly 50-64

Smear results:
- sample tested for HPV first (if HPV negative then not examined!)

Inadequate sample - repeat in 3/12
HPV -ve = return to normal screening programme
HPV +ve, normal cytology = repeat in 1 year
HPV +ve, abnormal cells -> colposcopy!

  • Cells are either normal or the cells can be:
  • cancerous, or precancerous (low or high grade), and also borderline smear (i.e. they are abnormal but not sure if associated with precancer or not), can also be glandular abnormality (meaning the abnormal cells are arising from the glandular epithelium – i.e. arising from the endocervix)
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92
Q

What is lichen sclerosis?

A
  • Most common of vulval dystrophies
  • Usually presents in postmenopausal women but can affect any age
  • Thought to be an immune reaction - an autoimmune condition
  • Affected skin usually can be a figure of 8 pattern around the vulva and perianal area.
  • Skin is thin, shiny and can be white (leukoplakia) or red (due to inflammation)
  • Uncontrollable scratching an pruritis (worse at night)
  • Anatomical changes include shrinkage or loss of labia minora, shrinkage of introitus (opening of vagina), labial fusion due to adhesions
  • Diagnosis histologically made from vulval biopsy but typical appearance can be treated.
  • Treatment goal is to treat the itch and soreness
  • Simple emollient Rx may relieve mild symptoms
  • If severe – may need course of potent topical steroid
  • Tapering regime of every day for one month, alternate days for one month, then 2x weekly for one month.

Complications:

  • Unusual but include permanent anatomical change (labial fusion may persist)
  • Can cause dyspareunia, and if fusion is in the midline then may cause issues with micturition requiring separation of the labia.
  • Risk of malignancy – these ladies need to remain under annual review by GP to rule out conversion to VIN/vulval cancer
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93
Q

What is VIN and how may it present

A

Vulval intraepithelial neoplasia (premalignant condition of the vulva)
VIN 1 = low grade disease
VIN 2/3 = high grade disease

  • Pruritis (2/3 of cases)
  • Pain
  • Ulceration
  • Leukoplakia or red
  • Lump/wart (popular, polypoid, verruciform)
  • 20% asymptomatic
94
Q

What is the most common type of cancer affecting the vulva?

A

90% are squamous cell carcinomas

95
Q

Describe the FIGO staging of vulval cancer

A

Stage 1 = confined to vulva
Stage 2 = involves lower vagina, urethra, anus
Stage 3 = spread to lymph nodes
Stage 4 = spread to upper vagina, upper urethra, bladder or anus

96
Q

What type of swab is used to test for chlamydia/gonorrhoea?

A

Endocervical (smear) swab

97
Q

What type of swab is used to test for bacteria vaginosis, candida, group B strep and trichomonas?

A

High vaginal swab (taken from the posterior fornix)

98
Q

What is the function of LH

A

Acts on and supports the theca cells, causing them to release androgens, oestrogen precursors and progesterone

99
Q

What is the function of FSH

A

Acts on the granulosa cells causing them to release oestrogen and progesterone

100
Q

What is the function of oestrogen in the proliferative phase?

A

Causes uterine lining to thicken

101
Q

Define menopause

A

Period where menstruation has finished, refers specifically to the LMP but can only be diagnosed retrospectively after 1 year of absent cycles in women >45yrs

NICE recommend using FSH level to diagnose menopause in women <40 with suspected premature menopause, or in women 40-45 with menopausal symptoms/change in their menstrual cycle

102
Q

Describe the hormonal changes in the menopause

A

Hypothalamic-pituitary hyperactivity: high FSH and LH
Low/absent progesterone
Initially unopposed oestrogen, then low oestrogen
Low inhibin

103
Q

List side effects of the menopause

A

Vasomotor symptoms
- hot flushes, night sweats

Urogenital tract atrophy
- atrophic vaginitis, recurrent UTI’s, weaker pelvic floor and uterovaginal prolapse

Psychological
- insomnia, depression, poor concentration, irritable, los of libido

Bones
- osteoporosis

Cardiovascular/stroke
- IHD & stroke incidence increases

104
Q

How is the menopause treated?

A

General measures

  • Good diet, exercise and weight control
  • Treat any medical condition e.g. Hypertension or diabetes
  • Psychological support if appropriate
  • HRT -> various preparations available
105
Q

Why must HRT contain oestrogen and progesterone if the patient has a uterus?

List the three adverse effects of HRT

A

As unopposed oestrogen therapy increases the risk of endometrial cancer

  1. Breast cancer risk (increased with o+p therapies, but risk removed when HRT stops, no increased risk with oestrogen only preparations)
  2. VTE clot risk: higher with oral preparations than transdermal
  3. Stroke risk: higher with oral options, not transdermal
106
Q

What preparations of HRT are available?

What are the benefits of HRT?

A

Preparations

  • oral
  • transdermal
  • implants
  • gels/creams

Benefits

  • lowers LDL (so improved LDL:HDL ratio)
  • reduced vasomotor symptoms
  • improves bone mineralisation and reduces # risk
107
Q

What is the perimenopause?

Define climacteric

Define POI (premature ovarian insufficiency)

A
  • May last for several years
  • Average age of menopause in UK = 51yrs
  • Variable estradiol production by granulosa cells
  • Peripheral androgen conversion to estrone in peripheral tissues becomes the main source of oestrogen
  • Rise in gonadotrophin production
  • If you are investigating a patient for irregular periods and you are trying to determine if it is perimenopausal or another pathology, low AMH (anti-müllerian hormone) is diagnostic for little/no follicles therefore suggests perimenopause

Climacteric = stage in life where woman gradually loses her cyclical ovarian activity as follicle numbers reduce

POI = where ovaries stop functioning normally <40yrs

108
Q

Define heavy menstrual bleeding (menorrhagia)

A

= menstrual bleeding that has an adverse impact on a woman’s QOL
(is the commonest cause of IDA in the affluent world)

109
Q

List causes of HBM

A
  1. Uterine pathology e.g. fibroids, polyps
  2. Absence of uterine pathology e.g. anovulatory, ovulatory
  3. Medical issue e.g. thyroid disorders, clotting disorders
110
Q

What is adenomyosis

A
  • Adenomyosis = a condition in which the inner lining of the uterus (the endometrium) breaks through the muscle wall of the uterus (into the myometrium - rather than out the way like endometriosus!)
  • Can cause menstrual cramps, pressure in the lower abdomen, and bloating before menstrual periods and can result in heavy periods
111
Q

Which ethnicity is a RFx for uterine fibroids?

A

Afro-carribean

112
Q

Describe the management of heavy menstrual bleeding

A
  1. Exclude any underlying pathology
  2. If patient needs contraception:
    - mirena coil
    - COCP
    - oral/depo progesterone
  3. If patient does not need contraception
    - tranexamic acid (lightens bleeding)
    - mefenamic acid (lightens bleeding and reduced pain)
  4. Surgical options (if medical treatment fails)
    - endometrial ablation
    - hysterectomy
113
Q

Define amenorrhoea

A

Absence of menstruation (one or more missed periods)

114
Q

Define primary and secondary amenorrhoea

A

Primary = failure to menstruate by 16yrs (+/- secondary sec characteristics)

Secondary = defined as established menses stop for >6m in the absence of pregnancy in a woman who has previously had normal menstruation

115
Q

Why can stress cause secondary amenorrhoea?

A

Stress (emotional, exams etc.) inhibits GnRH release and body goes into a pre-pubertal state

116
Q

List 4 causes of primary amenorrhoea

A
  • Physiological delay
  • Weight loss/anorexia/heavy exercise
  • PCOS (hormonal issues)
  • Imperforate hymen (structural issue)
117
Q

List 4 categories of causes of secondary amenorrhoea

A

1) HPO axis issue (e.g. less GnRH when stressed)
2) Pituitary causes e.g. pituitary adenoma, hypothyroidism
3) Ovarian causes e.g. PCOS, premature ovarian failure (menopause)
4) Uterine causes e.g. PREGNANCY, breastfeeding, asherman’s syndrome

118
Q

What is asherman’s syndrome

A
  • A uterine cause of amenorrhoea
  • An uncommon acquired gynaecological condition characterised by reduced menstrual flow, increased cramping and abdominal pain, eventual cessation of menstrual cycles (amenorrhea), and, in many instances, infertility
  • Can be caused by excessive curettage/scraping of endometrial cavity -> stricture and scar formation inside the uterus meaning the lining cannot be shed in the menstrual cycle
  • Management: hysteroscopy and breakdown adhesions
119
Q

Define oligomenorrhoea

A

(Bleeding too little)

Infrequent menstrual periods (periods at intervals of >35 days with only 4-9 periods in a year)

‘Definition of oligo- = cycles which are persistently >35days in length’

Common during extremes of reproductive life

120
Q

What are the Rotterdam criteria for PCOS?

A

Need 2/3 for diagnosis:

  1. Hyperandrogenism (e.g. hirsuitism, acne)
  2. Oligo/anovulation
  3. USS features of PCOS (large volume ovaries +/- 12 follicles) -> bead of pearls
121
Q

Describe the pathophysiology of PCOS

A

Complex metabolic HPO interactions

  1. Obesity + genetics leads to insulin resistance
  2. Insulin resistance leads to increased insulin production
  3. Increased insulin leads to:
    - > reduced SHBG produced by the liver (sex hormone binding globulin)
    - > increased androgen release from thecal cells in the ovarian follicles
  4. Less SHBG and more androgens means higher free circulating levels of testosterone and PCOS! (oligo-ovulation hirsuitism)
122
Q

List the complications of PCOS

A
  1. Reduced fertility
  2. Insulin resistance and diabetes
  3. HTN
  4. Endometrial cancer (due to unopposed oestrogen)
123
Q

Describe how PCOS is treated

A
  1. Weight loss
  2. COCP to control menstrual cycle (something with progesterone in for sure!)
  3. Antiandrogens/cosmetic therapies to treat hirsuitism
  4. GnRH treatment to overcome infertility
  5. Screen early for CV RFx
124
Q

Define dysmenorrhoea and list primary and secondary causes

A

Painful bleeding

Primary -> idiopathic, without any organ pathology

Secondary -> due to pelvic pathology e.g. endometriosis, adenomyosis, PID, fibroids

125
Q

List causes of IMB/PCB

A
  • Infection - STI (chlamydia and gonorrhoea)
  • Progesterone only contraceptives (mini-pill/implant)
  • Cervical causes: polyp, ectropion, cancer
  • Vaginal causes: atrophy, hymen tear, cancer
  • Uterine causes: cancer
  • Ovarian causes: peri-menopausal, PCOS, early miscarriage, cancer
  • Trauma
  • Pregnancy
  • Other causes: vaginitis, foreign bodies, polyps, oestrogen withdrawal
126
Q

Define PMB (post-menstrual bleeding)

A

bleeding occurring >12m after LMP = endometrial carcinoma until proven otherwise -> do TV-USS -> if endometrial thickness is over 4mm then must get a biopsy

127
Q

Define acute and chronic pelvic pain

A 
Acute = <6 months e.g. PID and cysts
Chronic = >6 months e.g. endometriosis
128
Q

List differentials of acute pelvic pain

A 
PID
Early pregnancy complications e.g. miscarriage, ectopic
Ovarian - cyst, rupture, torsion
Fibroids
Ovulation pain
Cervix - ectropion, polyps
Vulval/vaginal
UTI
Renal calculi
Appendicitis
129
Q

List differentials of chronic pelvic pain

A 
Adenomyosis
Endometriosis
Gynae malignancy
Diverticulitis
IBD
130
Q

Describe the pathologies covered under the umbrella term ‘PID’

A
  • endometritis (endometrium inflamed)
  • salpingitis (tubes inflamed)
  • pelvic peritonitis
131
Q

What is the aetiology of pelvic inflammatory disease?

A

PID occurs due to ascending infection from the vagina/cervix
Not always, but commonly associated with STI’s
- chlamydia
- gonorrhoea

(infective organisms are not always found!)

132
Q

What complications can arise from PID?

What is hydrosalpinx?

A

Complications

  • subfertility/tubal blockage
  • chronic pain
  • ectopic pregnancy

Hydrosalpinx

  • A fallopian tube that is blocked with watery fluid (differential for PID)
  • Typically caused by previous infection/STI/pelvic surgery or endometriosis
  • Increased risk of ectopic pregnancy
133
Q

How is PID investigated?

A
  • pregnancy test
  • bloods
  • exclude UTI
  • swabs
  • TV USS (rule out tube-ovarian abscess)
134
Q

How is PID managed?

A

Antibiotics (14 days)
Analgesia
Partner testing +/- contact tracing
(may need surgery and percutaneous drainage of abscesses)

135
Q

What is endometriosis and its causes?

A

Where endometrium has grown out-with the endometrial cavity
It is HORMONALLY (oestrogen) DRIVEN and related to period

Cause is unclear, but three components:

  • retrograde menstruation
  • metaplasia of cells
  • impaired immunity (woman who have bad endometriosis in their immune system cannot get rid of the tissue which is abnormally located)
136
Q

What are the S/Sx of endometriosis

A 
dysmenorrhoea
dyspareunia
dysuria
pelvic pain (relative to cycle, or constant if there is scarring)
subfertility
137
Q

How is endometriosis diagnosed?

A

LAPAROSCOPY and biopsy is the gold standard investigation

also:

  • bloods (Ca125)
  • examine with speculum + bimanual examination to check for visible patches/fixed uterus
  • TVUSS
138
Q

How is endometriosis treated?

A
  1. Conservative (if asymptomatic)
  2. Medical - non-hormonal: NSAIDs
  3. Medical - hormonal: COCP, mirena coil, depo injection (reduce oestrogen levels which stops ovulation and reduces endometrial thickening)
  4. Psychological - to deal with chronic pain
  5. Surgical - hysterectomy/oophorectomy of pain is unbearable (even though there may be ectopic tissue outwith the uterine cavity that is not removed, hysterectomy + BSO induces menopause, which should stop hormonal flare ups of any remaining tissue)
139
Q

Define

  1. Antepartum haemorrhage
  2. Intrapartum haemorrhage
  3. Postpartum haemorrhage
A
  1. Bleeding from/into the genital tract, occurring between 24 weeks of pregnancy and prior to birth
  2. bleeding from onset of labour until baby is born
  3. PPH = bleeding from when baby is born until 6 weeks post delivery
140
Q

What are the two most important causes of antepartum haemorrhage to rule out (but not the most common)?

A
  1. Placental abruption

2. Placental praevia

141
Q

Describe placenta praevia and how it is managed

A

Placenta is implanted in the lower segment of the uterus

  • presents with painless bleeding, non-engaged presenting part, soft uterus
  • seen on USS (at 18-22 weeks) as placenta encroaching within 5cm of the internal os
  • placenta may ascend as pregnancy continues after 24 weeks, so get another scan in 3rd trimester to check
  • classed as minor/major based on location of placenta in relation to os
  • risk of haemorrhage during natural birth (as baby squeezes past placenta and damages it) or at C-section as lower segment of uterus cannot contract

Mgx: CS at 37 weeks. If mother presents with bleeding then treat A-E and either vaginal delivery or CS based on grade of praevia

142
Q

Describe placental abruption and its treatment

A

Abruption -> presents with painful bleeding with a hard ‘woody’ uterus

  • retroplacental haemorrhage (between placenta and uterus)
  • involves some form of placental separation where there is then reduced gas exchange between fetal and maternal circulations, which predisposes to fetal hypoxia and acidosis
  • RFx = PIPES
  • > previous abruption
  • > intrauterine growth restriction
  • > pre-eclampsia
  • > essential HTN
  • > smoking

Mgx: Fetal distress = emergency CS. No fetal distress = <36 weeks (give steroids and observe), >36 weeks (vaginal delivery)

143
Q

Define primary and secondary PPH

A 
Primary = within 24hrs delivery
Secondary = blood loss between 24hrs and 12 weeks post-delivery
144
Q

Describe the 4 main categories which cause PPH

A

4T’s

  • thrombin (coagulation issue)
  • tone (uterine atony, lack of myometrial contraction to stop bleeding)
  • tissue (retained placental tissue)
  • trauma (vaginal/perineal tears)
145
Q

In terms of infertility, what can go wrong with the sperm?

A
  • azoospermia (obstructive e.g. in CF, or non-obstructive e.g. kleinfelter’s)
146
Q

In terms of infertility, what can go wrong with the egg?

A

1) HPO failure (e.g. athletes)
2) HPO dysfunction (e.g. PCOS, hypothyroid)
3) Ovarian failure (e.g. Turners, gonadal dysgenesis, radiotherapy)

147
Q

What three drugs are used for ovulation induction?

A

1) Letrozole (an aromatase inhibitor)
2) Clomiphene (anti-oestrogen)
3) GnRH downregulation (by giving FSH/LH)

148
Q

List risk factors for early menopause

A
  1. Surgical (BSO)
  2. Medical (chemo/radioTx)
  3. Genetics (Turner’s syndrome)
  4. Cigarette smoking
149
Q

Compare a pregnant vs non-pregnant uterus

A

Pregnant:

  • weight 1kg
  • cell hyperplasia
  • cellular hypertrophy
  • 4-5x enlarged
  • 5L

Non-pregnant:

  • weight 70kg
  • 8cm long, 5cm wide
  • walls 2cm thick
150
Q

What are the three stages of labour?

A

1st stage = from onset of labour (true contractions) to 10cm dilated

2nd stage = from 10cm dilated to baby delivered

3rd stage = from delivery of baby to delivery of placenta

151
Q

Describe the 1st stage of labour

A
  • LAT-
    1) Latent phase (0-3cm dilated cervix, dilates at rate of 0.5cm/hr, irregular contractions)

2) Active phase (3-7cm dilated, dilates at rate of 1cm/hr, regular contractions)
3) Transition phase (7-10cm dilated, rate 1cm/hr, STRONG regular contractions)

152
Q

Describe the bishop score

A

A pre-labour score used to assess cervical ripening and if induction of labour will be needed.
- score from 0-13
>/= to 8 means IOL would be successful
<8 means cervical ripening is required

153
Q

Describe the natural changes that occur to the cervix and the role of prostaglandins

A

Cervix dilates and ‘effaces’ (gets thinner).
The “show” occurs when the mucus plug (that has been preventing ascending infection during pregnancy) falls out.
Prostaglandins are released which stimulate uterine contraction and “ripen” the cervix pre-delivery.

154
Q

What are braxton hick contractions

A

IRREGULAR uterine contractions in 2/3rd trimesters. Do not become regular and do not indicate true onset of labour. Treatment -> hydration

155
Q

Describe the 2nd stage of labour

A

Depends on the three P’s:

1) Power (strength of uterine contractions)
2) Passenger (describe the foetus in 4 ways = SALP)
- Size
- Attitude (it’s posture)
- Lie (longitudinal/transverse/oblique)
- Presentation (cephalic/shoulder/breech)
3) Passage (i.e. size and shape of pelvis)

Involves the 7 cardinal movements of labour (Every Darn Fool In Egypt EatsRaw Eggs)

  • engagement
  • descent
  • flexion
  • internal rotation
  • extension
  • external rotation
  • expulsion
156
Q

Describe the 3rd stage of labour

A

Delivery of placenta
Can be managed physiologically or actively
- physiological = placenta delivered by maternal effort without medications of cord traction
- active = midwife/doctor assists -> give IM oxytocin to help uterus contract + traction on cord

157
Q

Why is active management of the 3rd stage of labour often needed?

A

To reduce PPH

158
Q

Name the two uterotonic hormones and describe their actions naturally and interventionally

A

1) Oxytocin
- naturally controls contractions (slow tonic and fast phasic contractions)
- interventionally, used to induce labour and stimulate contractions

2) Prostaglandin
- naturally, controls myometrium contraction and relaxation
- interventionally, given LOCALLY (not systemically, to reduce S/Ex) as vaginal tablet/gel to ripen cervix

159
Q

Name a tocolytic agent and its use

A

Nifedipine

  • used to REDUCE UTERINE ACTIVITY based on
  • > how dilated the cervix is
  • > if steroids need time to be administered before baby is born
  • > to allow patient transfer to hospital
160
Q

Define preterm birth and name some risk factors

A 
= baby born <37 weeks
RFx:
- multiple pregnancy
- previous preterm birth
- cervical surgery
- uterine abnormalities
- pre-eclampsia
- IUGR
161
Q

How is preterm birth managed?

A
  • look for precipitant e.g. infection, pre-eclampsia, polyhydramnios…
  • monitor the foetus and the contractions
  • give Abx if: sign of sepsis, ruptured membranes
  • consider tocolysis
  • give steroids for foetal lung development!
162
Q

Define a post-dates pregnancy and what problems it can pose for a) mother, b) baby

A

Baby born >42 weeks (after 42 weeks, 30% occur spontaneously, and 50% require IOL)

a) Problems for mother:
- intrumental delivery/CS may be needed
- increased PPH risk
- longer delivery with more analgesia and psychological stress
- more risk of uterine rupture and perineal trauma

b) Problems for baby:
- still-birth
- meconium aspiration -> death
- shoulder dystocia
- intrapartum CS may be needed

163
Q

When is induction of labour (IOL) offered and describe the methods that can be used

A

Offered 41-42 weeks, or in situations where it is beneficial to start labour early e.g. GestDiab where baby is big, pre-eclampsia…

  • use bishop score to assess

Options:

  1. Membrane sweep
  2. Vaginal prostaglandin E2
  3. Cervical ripening balloon
  4. Oxytocin infusion
  5. Oral mifepristone + misoprostol (if intra-uterine death has occured)
164
Q

What is uterine hyperstimulation and what can it lead to

A

A complication with the use of vaginal prostaglandins
- causes prolonged, frequent uterine contractions which causes foetal distress and compromise
Can lead to:
- foetal compromise (acidosis and hypoxia)
- emergency C-section
- uterine rupture

165
Q

How is uterine hyperstimulation managed?

A
  1. Remove vaginal prostaglandins / stop oxytocin infusion

2. Tocolysis with terbutaline

166
Q

Describe options for pain management in labour

A
  1. Non-pharmacological
    - maternal support, good environment, good education, birthing pool, ?massage/?TENS
  2. Pharmacological
    - entonox, IM diamorphine, epidural, spinal, general anaesthetic + CS
167
Q

What is the difference between an epidural and a spinal?

A 
Epidural = indwelling catheter in the epidural space, can be topped up with analgesia
Spinal = subarachnoid numbing injection which only lasts 2-4hrs
168
Q

What can dysfunctional activation of uterine contraction cause?

A

1) failure to progress in labour (cervical dilation <2cm in 4hrs)
- RFx: older maternal age, high maternal BMI, genetics
- Mgx with artificial rupture of membranes/oxytocin infusion
- may result in assisted delivery

2) Atonic post-partum haemorrhage
- failure of contraction mechanisms after delivery
- blood loss >500ml

169
Q

Classify APH as minor, major and massive

A 
Minor = <50ml
Major = 50-1000ml
Massive = >1000ml +/- shock
170
Q

Describe vasa praevia

A

Rare, where umbilical cord runs in fetal membranes and can cross the internal OS, can rupture during labour leading to fetal exanguination

171
Q

List risk factors for uterine rupture and state how it is managed

A

RFx:

  • uterine overdistention (twins, polyhydramnios…)
  • XS uterotonic use
  • dystocia unrecognised (prolonged contractions against obstruction)
  • previous CS and scar rupture

Management: Laparotomy and CS +/- hysterectomy

172
Q

Compare and contrast placenta praevia vs placental abruption based on the following factors:

1) Shock
2) Pain
3) Bleeding
4) Tenderness
5) Foetus
6) Ultrasound

A

1) SHOCK: PP = shock is consistent with the blood loss, abruption = inconsistent blood loss to match shock
2) PAIN: PP = painless, abruption = painful
3) BLEEDING: PP: red, profound. Abruption = dark, often absent bleeding
4) TENDERNESS: PP = soft, non-tender uterus. Abruption = hard woody tender uterus
5) FOETUS: PP = Abnormal lie, high head, normal HR. Abruption = normal lie, engaged, distressed/dead
6) USS: PP = placenta low, abruption = often normal USS and placenta not low

173
Q

List risk factors for PPH

A
  • increasing maternal age
  • previous PPH
  • prolonged labour
  • pre-eclampsia
  • macrosomia
  • polyhydramnios
  • tocolytic agent use
  • CS
174
Q

Quantify the blood loss in the following classifications of PPH:

1) Minor
2) Major
3) Moderate
4) Severe

A

1) Minor - <1000ml
2) Major - >1000ml
3) Moderate - 1000-2000ml
4) Severe - >2000ml

175
Q

List 4 things which can be done to prevent PPH

A

1) Empty bladder during delivery (reduce contraction strength)
2) Treat anaemia antenatally
3) Give active management in 3rd stage of labour (IM oxytocin) which reduces PPH risk
4) IV tranexamic acid during CS

176
Q

How is PPH managed

  • stabilising the pt
  • mechanical Mg
  • medical Mg
  • surgical Mg
A

Stabilising the pt
- A-E, keep flat and warm, IV access x 2, FBC/U&E/coag screen, fluids and blood, ?oxygen, ?FFP

Mechanical Mg

  • rub uterus through abdomen
  • catheterise

Medical Mg

  • oxytocin (syntocinon / ergometrine)
  • IM carboprost
  • sublingual misoprostol
  • tranexsamic acid

Surgical Mg

  • Intrauterine balloon tamponade
  • B-Lynch suture
  • Uterine artery ligation
  • Hysterectomy
177
Q

What are the 2 main causes of bleeding in early pregnancy?

A

Miscarriage

Ectopic pregnancy

178
Q

Describe the first few steps in the resus pathway for maternal collapse

A
  1. DRS-ABC
  2. If unresponsive, start CPR
    * Use L-lateral displacement of uterus technique*
  3. CPR 30:2 and attach debrillator
    * If no response after 4 minutes, carry out perimortem CS* (if baby is >20 weeks, aim to delivery within 5 mins, increases venous return and reduces O2 requirement to try and save mothers life)
  4. Assess rhythm and shock if necessary
179
Q

List 3 physiological changes of
a) CVS system
b) Respiratory system
that occur in pregnancy which affect CPR/resuscitation

A

CVS:

  • increased HR and CO (increases CPR demands)
  • reduced venous return (increases CPR demands)
  • increased plasma volume (dilutional anaemia)

RESP:

  • increased RR (acidosis more likely)
  • increased O2 consumption (hypoxia occurs faster)
  • increased laryngeal oedema (intubation tricky)
180
Q

List the reversible causes of cardiac arrest in maternal collapse

A

4H’s

  • hypoxia
  • hypovolaemia
  • hypo/per K (or other electrolytes)
  • hypothermia

4T’s

  • toxins (MgSO4 toxicity from treating pre-eclampsia)
  • thrombus (amniotic fluid embolism)
  • tension pneumothorax
  • cardiac tamponade
181
Q

Define mild, moderate and severe HTN in pregnancy

A

Any BP >140/90

Mild = 140/90 - 149-99
Moderate = 150/100 - 159-109
Severe = >/=160/110
182
Q

Define essential vs gestational HTN

A

Essential (= chronic) (= pre-existing)
- HTN diagnosed pre-pregnancy of <20 weeks

Gestational HTN
- HTN diagnosed >20 weeks

183
Q

What are the risk factors for gestational HTN in pregnancy?

A

Nulliparous
Multiple pregnancy
Maternal age <20 or >35

184
Q

Define pre-eclampsia

A

New onset HTN >20 weeks + HTN +/- organ dysfunction

  • Proteinuria (ACR > 8)
  • (Uteroplacental) Organ dysfunction e.g. IUGR, stillborn
  • (Maternal) Organ dysfunction e.g. HELLP syndrome (haemolysis, elevated liver enzymes, low platelets)
185
Q

Define eclampsia

A

Seizures which occur as a result of pre-eclampsia

186
Q

Describe the pathophysiology behind pre-eclampsia

A

Increased vascular resistance due to abnormal formation of the spiral arteries of the placenta -> poor placental perfusion -> oxidative stress and chemicals released from placenta -> causes systemic inflammation and impaired endothelial function of blood vessels

187
Q

What are the S/Sx of pre-eclampsia?

A 
Headache
N&V
Epigastric pain
Visual changes
Oedema
Reduced urine output
188
Q

What are the maternal and foetal complications of pre-eclampsia

A

Maternal

  • Intracranial haemorrhage
  • eclampsia
  • HELLP syndrome
  • pulmonary oedema
  • placental abruption
  • DIC

Foetal

  • IUGR
  • placental abruption -> hypoxia
  • oligohydramnios
  • premature delivery
189
Q

List the high and moderate risk factors for pre-eclampsia

A

High:

  • pre-existing HTN
  • diabetes
  • CKD
  • previous HTN in pregnancy

Moderate:

  • > 40yrs maternal age
  • BMI > 35
  • 1st pregnancy
  • multiple pregnancy
  • FHx of pre-eclampsia
190
Q

What interventions are taken to reduce the risk of pre-eclampsia developing?

A

If 1 high or 2 moderate RFx:
- daily aspirin

Routine antenatal monitoring (BP, urine protein, symptoms)

191
Q

What are the main pharmacological agents used to manage HTN in pregnancy?

A 
1st line = labetalol 
2nd line = nifedipine (or 1st line if asthmatic)
Methyldopa
IV hydralazine
IV MgSO4 (given during labour for HTN, and 24hrs after delivery to prevent seizures)

Only definitive management of pre-eclampsia = deliver baby!!!

After delivery use 1/combo of:

  • enalapril (1st line)
  • nifedipine/amlodipine
  • labetalol/atenolol
192
Q

Describe the ABC management of eclampsia

A
  • Call for help
  • Airway (left lateral manouevre), breathing (oxygen) and circulation (IV access and bloods)

Loading dose of MgSO4 = 4g IV over 5 mins
Maintenance dose of MgSO4 = 1g/hour for 24hrs after last seizure
Recurrent seizures = 2g over 5 mins

193
Q

List some causes why baby may be LARGER than expected for date when measuring fundal height:

A

Macrosomia, polyhydramnios, multiple pregnancy, wrong dates, fibroids

194
Q

List some causes why baby may be SMALLER than expected for date when measuring fundal height:

A

IUGR, oligohydramnios, small baby

195
Q

Define mono/di

  • amniotic
  • zygotic
  • chorionic twins
A 
Mono = 1
Di = 2
'Amniotic' = how many amniotic sacs
'Zygotic' = how many eggs fertilised
'Chorionic' = how many placentas
196
Q

What is special about dizygotic twins?

A

They are always DCDA (di-chorionic, di-amniotic)

197
Q

What is the incidence of multiple pregnancy in the UK, and describe risk factors for it

A

1/65

RFx:

  • assisted conception
  • older maternal age
  • ethnicity (increased incidence in West Africans)
  • Family history (maternal history of dizygotic twins)
  • Previous twins
198
Q

List the maternal antenatal complications of multiple pregnancy

A

All complications increased (as there are 2 babies!) but mainly

  • hyperemesis gravidarum
  • pre-eclampsia
  • gestational DM
  • anaemia
  • placenta praevia
199
Q

List the maternal intrapartum complications of multiple pregnancy

A
  • PPH (larger uterus with less tone)
  • malpresentation
  • cord entanglement
  • placental abruption
200
Q

List foetal complications of multiple pregnancies

A
  • increased miscarriage risk
  • congenital anomalies (NTD, cardiac defects)
  • growth restriction
  • pre-term delivery
201
Q

Describe the changes to antenatal monitoring in multiple pregnancy

A

Check for anaemia, with FBC at

  • booking clinic
  • 20 weeks
  • 28 weeks

Additional USS scans to check for foetal growth restriction, unequal growth, or twin-twin transfusion syndrome

  • monochorionic = 2 weekly scans from 16 weeks
  • dichorionic = monthly scans from 20 weeks
202
Q

Describe twin-twin transfusion syndrome

A

When monochorionic twins (sharing one placenta) have a blood supply connection between them. One twin (recipient) recieves majority of blood from the placenta, and the other twin (donor) is starved of blood
Recipient = fluid overloaded, HF, polyhydramnios
Donor = growth restriction, anaemia, oligohydramnios

203
Q

Describe the timings of planned birth for twins

A 
MCMA = 32-33 weeks
MCDA = 36 weeks
DCDA = 37 weeks
Triplets = <35 weeks

(waiting beyond these times increases the risk of fetal death)

204
Q

What are the delivery options for monoamniotic twins?

A

Elective CS at 32-33 weeks

205
Q

What are the delivery options for diamniotic twins?

A

SVD (if twin 1 has cephalic presentation)
-> CS may then be required for 2nd twin
Elective CS (advised when presenting twin is not cephalic)

206
Q

When does the booking scan occur and what is included?

A

<10 weeks, involves:
Bloods: FBC, blood group, Rh status, sickle cell screen and thalassaemia screen
Infectious diseases screen: HIV, HepB, Rubella, syphilis

207
Q

What two supplements should mothers take during pregnancy and how much?

A

Folic acid = 400mcg daily, pre-pregnancy until 12 weeks

Vitamin D = 10mcg daily

208
Q

When is the dating scan and what is carried out?

A

At 10 to 13+6 weeks

Calculate accurate gestational age from crown-rump length

209
Q

What is CUBSS

A

Combined USS and biochemical serum screening
At 11-14 weeks
to look for DS (trisomy 21)
Involves:
- maternal age + nuchal translucency + PAPP-A + bHCG

210
Q

When are chorionic villus sampling and amniocentesis carried out and describe each

A

Chorionic villus sampling = sample of placental cells examined, from 11 weeks onwards

Amniocentesis = amniotic fluid aspirated and fetal cells analysed, from 16 weeks onwards

211
Q

When is the anomaly scan carried out

A

20 weeks

To identify any congenital abnormalities, allows parents to have option of TOP or they can prepare for a disabled child

212
Q

List 5 routine checks that are carried out at all antenatal appointments:

A
  1. Maternal urine microscopy and culture for asymptomatic infection
  2. Maternal urine check for protein on dipstick
  3. BP
  4. Symphysis fundal height
  5. Examine fetal presentation
213
Q

What 2 vaccines are offered to all pregnant women

A
  1. Whooping cough (pertussis, from 16 weeks)

2. Influenza (flu)

214
Q

What renal physiological changes occur in pregnancy?

A

Reduced urea and creatinine (as renal blood flow increases, and GFR can increase by 150%!)
Increased micturation
Proteinuria
Glycosuria

215
Q

What cardiac physiological changes occur in pregnancy?

A 
Increased CO and HR
Reduced PVR
Increased circulating volume
Peripheral oedema
Low albumin, low platelets
High WCC
216
Q

What respiratory physiological changes occur in pregnancy?

A

Increased tidal volume
Increased oxygen demands
Reduced FRC (as abdomen squashed!)

217
Q

What dermatological physiological changes occur in pregnancy?

A 
Palmar erythema
Linea nigra
Striae gravidarum
Spider naevi
Cholasma
218
Q

What GI physiological changes occur in pregnancy?

A

Reduced motility and gastric emptying
GORD
Constipation
Hyperemesis and nausea

219
Q

What is naegele’s rule

A

Used to calculate EDD, assuming gestation is 280 days (or 40 weeks)

EDD = LMP + 1 year, - 3 months, + 7 days

220
Q

List the top 5 reasons for elective CS

A
  1. Previous LUSCS
  2. Breech presentation or abnormal lie
  3. Multiple pregnancy with non cephalic presentation of first twin
  4. Previous traumatic delivery and/or maternal request
  5. Placenta praevia
221
Q

List 5 maternal and 5 fetal indications for emergency CS

A 
FETAL:
1. Fetal distress in first stage of labour
2. Fetal distress in second stage of labour and any contra indication to instrumental
delivery
3. Malpresentation
a. Breech
b. Shoulder
c. Arm
d. Brow
e. Face
4. Cord prolapse
5. Prolonged second stage and any contra indication to instrumental delivery

Maternal:

  1. APH
  2. Maternal morbidity during labour e.g sepsis
  3. Maternal cardiac arrest
  4. Absolute/relative cephalopelvic disproportion
  5. Uterine rupture
222
Q

How is hyperemesis managed?

A
  1. Fluid replacement
  2. Anti emetics (prochlorperazine/cyclizine)
  3. Thromboprophylaxis
  4. Vitamin replacement
  5. Dietician review
223
Q

Describe the seroconversion rate of VZV in pregnancy

A

90% of mothers have IgG already (i.e. they are immune) -> if they are not, they can be given VZIG (needs to be given within 10 days of exposure)

224
Q

Describe fetal varicella syndrome

A 
When fetus is infected <20 weeks
Causes:
- growth restriction
- microcephaly/hydrocephalus
- limb hypoplasia
- cataracts and chorioretinitis
225
Q

How are chlamydia and gonorrhoea diagnosed?

A

Endocervical swab -> NAAT

226
Q

What is the treatment for chlamydia?

A

7 days oral doxycycline 100mg

227
Q

What is the treatment for gonorrhoea?

A

IM ceftriaxone 1g

228
Q

What is the treatment for syphilis?

A

IM penicillin

229
Q

What infective agent causes chlamydia?

A

Chlamydia trachomatis

230
Q

What infective agent causes gonorrhoea?

A

Neisseria gonorrhoea

231
Q

What infective agent causes syphilis?

A

Trepomena pallidum bacteria

232
Q

Contrast the S/Sx of bacterial vaginosis from trichomonias

A

BV = fishy odour and thin discharge, NO ITCH

Trichomoniasis = offensive odour, itch and pain, dyspareunia and red vulva/vagina/strawberry red cervix

Year 4 (28 decks)

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