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Phase 3a > Womens Health PTS > Flashcards

Womens Health PTS Flashcards

1
Q

Which cell type produces oestrogen in the menstrual cycle?

A

Granulosa cells

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2
Q

Which hormone surge acts to cause ovulation?

A

LH

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3
Q

Which hormone drops to cause the bleeding in the menstrual cycle and where is it produced?

A

Drop in progesterone levels causes bleeding

Progesterone is produced by the corpus luteum – when the corpus luteum degenerates, it stops producing progesterone, which is when the lining of the womb is shed

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4
Q

Which medication can be used to postpone a period, i.e. when on holiday?

A

Noresthisterone – take 3 a day from 3 days before period is due and stop taking when bleeding is acceptable

Or take 2 packets of COCP back to back

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5
Q

What is the definition of primary amenorrhoea?

A

Failure to menstruate by the age of 16

Or failure to menstruate by the age of 14 in someone with no secondary sexual characteristics

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6
Q

What are some causes of primary amenorrhoea?

A

Tuner’s syndrome
GU malformations (i.e. an imperforate hymen – especially if they are having cyclical pain)
Hypothalamic failure (exercise, stress, anorexia) – switches off the drive from the hypothalamus
Constitutional delay
Kallmann’s syndrome (also has anosmia – can’t hear, can’t smell, can’t see, no periods)
Sarcoidosis
Hyperprolactinaemia/ prolactinoma
Gonadal dysgenesis (i.e. they did not form ovaries or a uterus)
Swyer syndrome – XY but look like a girl
Late onset CAH

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7
Q

What is the definition of secondary amenorrhoea?

A

Absence of periods for ≥ 6 months

In someone who is not pregnant

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8
Q

What are some causes of secondary amenorrhoea?

A

Marathon runners – excessive exercise can stop them from menstruating
PCOS
Premature ovarian failure – loss of function before age of 40, risk factors include previous chemo and radiotherapy – NOT the same as menopause
Iatrogenic (after pill)
Rule out pregnancy
Sheehan’s syndrome – pituitary necrosis following PPH
Asherman’s syndrome – endometrial adhesions post. Surgery
Hyperthyroidism – oligomenorrhoea (only 4-9 periods per year)

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9
Q

What biochemical findings would be present in someone with premature ovarian failure?

A

Hypergondatrophism – they will have high levels of GnRH

Hypooestrogenism – low levels of oestrogen

Raised FSH

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10
Q

How would you investigate primary amenorrhoea?

A

Karyotype

Ultrasound scan to look for structural causes i.e. gonadal dysgenesis, imperforate hymen

Full history – find out if they are exercising too much etc, family history to find out if constitutional delay

Bloods – oestrogen, progesterone, LH, FSH, free androgen (testosterone)

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11
Q

How would you investigate secondary amenorrhoea?

A

Full history – rule out physical causes such as over-exercising
Pregnancy test (urinary beta-HCG)
Thyroid function
FSH and LH 🡪 high in premature ovarian failure, low in hypothalamic causes (stress, excessive exercise)
Mid luteal progesterone – so day 21 in a 28 day cycle, check for ovulation
Prolactin levels
Free androgen (increased in PCOS)

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12
Q

How would you treat primary amenorrhoea?

A

History including family history – if mum, sister and aunty were all late then it could be a constitutional delay – REASSURE IF SUSPICIONS CONFIRMED ON FAMILY HISTORY

Examination – other signs of puberty, vaginal examinatoin, BMI, visual fields (if suspect pituitary tumour)

Treat underlying cause – surgery to repair genital tract abnormalities, oestrogen replacement therapy, if pituitary tumour – surgery, chemo, radio

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13
Q

How is secondary amenorrhoea treated?

A

Cyclic progesterone

Bromocriptine – to treat hyperprolactinaemia

GnRH replacement – if the cause is hypothalamic failure

Thyroid replacement

Treat any other underlying cause – i.e. reduce exercise level, treat PCOS

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14
Q

What is the triad of features in PCOS?

A

ROTTERDAM CRITERIA – 2 out of 3 must be present:

12 cysts on the ovary OR an ovary > 10ml

Signs of clinical (excess hair) or biochemical (on a blood test) raised testosterone/hyperandrogenism

Oligo or amenorrhoea

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15
Q

How does PCOS usually present?

A

Oligomenorrhoea - irregular, unpredictable periods

Hirsutism

Infertility

Associated with obesity, metabolic syndrome, T2DM, sleep apnoea

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16
Q

What investigations would you do for someone with suspected PCOS?

A

Serum testosterone/free androgen levels
Thyroid function
Prolactin
Sex hormone binding globulin
Test for diabetes – random plasma glucose, fasting, HBa1c
USS

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17
Q

What are some long-term complications of PCOS?

A

Gestational diabetes
T2DM
CVD
Endometrial cancer – try and have 3-4 monthly withdrawal bleeds to reduce risk
NO increased risk of ovarian or breast cancer

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18
Q

What are some differential diagnoses for PCOS?

A

Other causes of irregular menstrual bleeding:

Thyroid dysfunction
Hyperprolactinaemia
Congenital adrenal hyperplasia
Androgen secreting tumours
Cushing’s syndrome

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19
Q

How is PCOS treated?

A

Weight loss
Smoking cessation
Find and treat any diabetes, hypertension, dyslipidaemia, sleep apnoea

Clomifene – induces ovulation
Metformin
Ovarian drilling to help them get pregnant
If finished family/not wanting to get pregnant – COCP with regular withdrawal bleeds
Hair removal cream for hirsutism

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20
Q

Define menorrhagia

A

Heavy menstrual bleeding that occurs at expected intervals of the menstrual cycle and interferes with quality of life

No measurable quantity of bleeding – it’s judged on impact on QOL and function

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21
Q

What is the name for menorrhagia with no identifiable underlying cause?

A

Dysfunctional uterine bleeding

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22
Q

What are some causes of menorrhagia?

A

Most common cause seen in gynae – FIBROIDS
Bleeding disorder (tends to present at menarche)
Hypothyroidism
Unknown – dysfunctional uterine bleeding
Polyps
Adenomyosis
Endometriosis
Cancer

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23
Q

What sort of questions do you need to ask in a history for menorrhagia?

A

Flooding
Clots
Interfering with life/work
Pain
Symptoms of anaemia – tiredness etc.
If it’s always been this way or if it’s a new development

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24
Q

What investigations do you do for menorrhagia?

A

FBC - look for anaemia
Physical examination – if they have fibroids the uterus will be bulky and non-tender
TSH if clinically hypothyroid
Cervical smear if due
STI screen
TVUS – look for fibroids, polyps, endometrial thickness
Endometrial biopsy
Hysteroscopy

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25
Q

How do you medically treat menorrhagia?

A

Reassure
Mirena coil – first line treatment if doesn’t want to get pregnant
Anti-fibrinolytics – e.g. tranexamic acid taken during bleeding
NSAIDS – e.g. mefanamic acid taken during bleeding
COCP – triphasing (take back to back for 3 months, then break)
Progestogens
Norethisterone when they don’t want to bleed e.g. on holiday

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26
Q

What are some surgical options for treatments of menorrhagia?

A

Endometrial ablation – ONLY IF THEY HAVE COMPLETED THEIR FAMILY as it would lead to a very high risk pregnancy

Uterine artery embolisation

Hysterectomy – last resort

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27
Q

Define dysmenorrhoea

A

Painful periods

+/- nausea and vomiting

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28
Q

What are the causes of primary and secondary dysmenorrhoea?

A

Primary – unknown, no underlying physical cause

Secondary – due to underlying cause:
Endometriosis
Adenomyosis
Fibroids
PID
Cancer

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29
Q

How should dysmenorrhoea be investigated?

A

Clinical assessment of the problem – full history and examination

USS
Endometrial biopsy
Laparoscopy
STI screen

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30
Q

How is primary dysmenorrhoea treated?

A

NSAIDs – mefenamic acid given during menstruation

Paracetamol

COCP

Smooth muscle anti-spasmodics – e.g. hyoscine butylbromide

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31
Q

How is secondary dysmenorrhoea treated?

A

NSAIDs – mefenamic acid

Paracetamol

Treat underlying cause – i.e. fibroids

Mirena coil

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32
Q

What is the main diagnosis to rule out if someone presents with post-coital bleeding? What are some other causes?

A

Cervical cancer

Other causes – polyps, cervical trauma, cervicitis, vaginitis, chlamidya

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33
Q

What is the main diagnosis to rule out when someone presents with post-menopausal bleeding? What are some other causes?

A

Endometrial cancer until proven otherwise

Other causes – vaginitis, foreign bodies (e.g. pessaries), carcinoma of cervix or vulva, polyps, oestrogen withdrawal

Ensure she is not confusing with rectal bleeding

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34
Q

What is the average age of onset of the menopause?

A

51 years

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35
Q

How is menopause diagnosed?

A

Retrospective diagnosis

After 12 months of amenorrhoea

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36
Q

What are the symptoms of the peri-menopause?

A

Irregular periods
Vasomotor symptoms – hot flushes, night sweats, impact on sleep, mood and QoL
Mood swings
Decreased sexual desire
Joint aches and muscle pain
Vaginal dryness
Headache, dry skin
Loss of energy

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37
Q

Before what age is menopause deemed premature?

A

Before the age of 40

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38
Q

What are the long-term complications of the menopause?

A

Osteoporosis - oestrogen inhibits osteoclasts and therefore once oestrogen levels drop, osteoclasts can become hyperactive

Cardiovascular disease

Dementia

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39
Q

How is the menopause managed?

A

Lifestyle advice – reduction of modifiable risk factors (smoking, heart disease, alcohol, diabetes)

Hormonal treatments – HRT, vaginal oestrogen

Non-hormonal – clonidine, alpha receptor agonist

CBT

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40
Q

What are the benefits and risks of HRT?

A

Benefits – relief of menopausal symptoms, bone mineral density protection, possibly prevents long term morbidity

Risks – breast ca, VTE, CVD, stroke

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41
Q

How is the risk of endometrial cancer from HRT reduced?

A

Progesterone given alongside the oestrogen replacement

Stops the oestrogen causing excessive proliferation of the endometrium by allowing shedding

Not necessary if – they have had a hysterectomy, they have the Mirena coil

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42
Q

Which route of HRT gives the highest increased risk of DVT and how is this risk reduced?

A

Oral HRT poses the highest risk

Reduced by giving a transdermal patch instead

Transdermal should always be offered to people with BMI > 30

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43
Q

How is the risk of cardiovascular disease managed in someone on HRT?

A

Aim to manage and optimise RF before commencing on HRT – i.e. control hypertension, diabetes, cholesterol

If someone has PREVIOUSLY HAD AN MI OR STROKE – they SHOULD NOT have HRT at all

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44
Q

What are the different preparations of HRT available?

A

Pessary
Cream applied with applicator for local vaginal symptoms – bleeding, pain, UTI
Patch
Oral tablet

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45
Q

What are some indications for a transdermal HRT patch?

A

Patient choice
Gastirc upset – malabsorption such as Crohn’s
Increased risk of VTE

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46
Q

What is the most common side effect of a transdermal HRT patch?

A

Skin irritation

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47
Q

What is the difference between the hormone levels in HRT and OCP?

A

COCP gives a SUPRAPHYSIOLOGICAL dose of oestrogen

HRT only gives a physiological dose of oestrogen – what the body is used to

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48
Q

What is the definition of premature ovarian failure?

A

When periods stop < 40 years of age

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49
Q

What are the causes of premature ovarian failure?

A

Idiopathic

Iatrogenic – chemotherapy (i.e. effect of childhood cancer treatment), radiotherapy, surgery

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50
Q

How does premature ovarian failure present?

A

Infertility

Amenorrhoea

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51
Q

What are the diagnostic criteria for premature ovarian failure?

A

Age < 40 years

FSH > 25 in 2 samples > 4 weeks apart

Plus 4 months of amenorrhoea

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52
Q

How is premature ovarian failure treated?

A

Oestrogen replacement – HRT, COCP. HRT encourage until they are at least 50

Androgen replacement – testosterone gel

Fertility – donor egg

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53
Q

Define miscarriage

A

The loss of a pregnancy before 24 weeks’ gestation

(after 24 weeks’ it would be classed as a still birth)

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54
Q

What proportion of pregnancies miscarry?

A

15-20%

Usually in the first trimester

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55
Q

Which parental ages pose the highest risk for miscarriage?

A

Maternal age ≥ 35 years

Paternal age ≥ 40 years

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56
Q

What are some factors that increase risk of miscarriage?

A

Increased maternal age
Smoking in pregnancy
Alcohol
Drugs
High caffeine intake
Obesity
Infections and food poisoning
Medicines such as ibuprofen
Health conditions – thyroid, severe HTN
Cervical incomptency

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57
Q

Factors that are not associated with increased risk of miscarriage (but people may believe do)?

A

Heavy lifting
Bumping tummy
Having sex
Air travel
Being stressed

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58
Q

What are the most common causes for one-off miscarriages?

A

Unknown
Chromosomal abnormalities
Abnormal foetal development
Maternal illness
Infection
Trauma
Cervical weakness
Chronic maternal disease (SLE)

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59
Q

What is the definition of recurrent miscarriage?

A

The loss of ≥ 3 consecutive pregnancies before 24 weeks’ with the same biological father

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60
Q

What are some causes of recurrent miscarriage?

A

Antiphospholipid syndrome
Uterine abnormalities
Thrombophilia e.g. Factor V Leiden, protein C or protein S deficiencies
Parental chromosomal abnormality – unbalanced Robertsonian translocation
Infection – bacterial vaginosis associated with 2nd trimester loss

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61
Q

What are the signs and symptoms of a threatened miscarriage?

A

Mild symptoms - i.e. mild abdominal pain and mild vaginal bleeding

CERVICAL OS IS CLOSED

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62
Q

What are the signs and symptoms of an inevitable miscarriage?

A

Severe abdominal pain
Vaginal bleeding

The cervical os is open
If you can get a finger into the os = inevitable miscarriage

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63
Q

What are some other classifications of miscarriage?

A

Incomplete miscarriage – most of the products have already been passed but the process may still be happening
Missed miscarriage – foetus dies but remains in utero, os is closed, may be completely asymptomatic. Will be confirmed at USS
Pregnancy of uncertain viability – small sac with no visible heart beat. Rescan in 10-14 days
Complete – os closed, empty uterus

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64
Q

How is a miscarriage managed?

A

ABCDE approach to bleeding

Expectant management (conservative)

Inevitable and incomplete miscarriages – can be managed with misoprostol or surgical evacuation

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65
Q

What are the 3 main causes of PV bleeding in early pregnancy?

A

Ectopic pregnancy

Miscarriage

Molar pregnancy

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66
Q

What is the definition of an ectopic pregnancy?

A

Implantation of a fertilised ovum outside the uterine cavity

97% occur in the fallopian tubes

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67
Q

What are some RF for ectopic pregnancy?

A

Damage to tubes – PID, surgery
Previous ectopic
Endometriosis
Copper coil
IVF
Smoking
Past infection of the tubes or appendicitis

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68
Q

What are the features of ectopic pregnancy?

A

In exam Qs – LMP 8 weeks ago

Vaginal bleeding

Pain – generalised abdominal pain or confined to an iliac fossa

Shoulder tip pain from haemoperitoneum

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69
Q

How would you investigate someone with a suspected ectopic pregnancy?

A

USS – intrauterine pregnancy? Foetal heartbeat?

Serial HCG measurements

Pelvic examination – CERVICAL EXCITATION /motion tenderness on speculum examination

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70
Q

How should an ectopic pregnancy be managed?

A

ABCDE approach to bleeding

Surgical options – salpingectomy is the best treatment option (but only do this if the other fallopian tube is viable), salpingotomy to remove the pregnancy if other tube not viable

Medical management – methotrexate if BHCG is low

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71
Q

What are the clinical features of a molar pregnancy?

A

Vaginal bleeding
Pain
Uterus larger than it should be for the expected dates
Very very high levels of BHCG
Clinical hyperthyroidism
Severe morning sickness

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72
Q

How is a molar pregnancy managed?

A

Removal by suction

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73
Q

What is lichen sclerosus and how is it treated?

A

Not an STI
Creates patchy, white, thin skin around the vulval area
Thought to be autoimmune

Observe if doesn’t respond to treatment – can be pre-malignant

Topical steroid cream or topic tacrolimus
In children – 50% resolve by menarche

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74
Q

What is the pre-malignant stage of cervical cancer that can be picked up in screening?

A

Cervical intra-epithelial neoplasia (CIN)

Pre-invasive
60% regress to normal within 2 years
Many develop into squamous carcinoma of the cervix

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75
Q

What should be done in an abnormal smear?

A

Refer to colposcopy

If there is abnormal cytology or HPV +ve

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76
Q

hen are women offered cervical screening?

A

Sexually active women aged 25-64

Every 3 years from 25-50

Every 5 years from 50-64

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77
Q

What proportion of cervical abnormalities are picked up by the screening?

A

95%

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78
Q

What are some risk factors for CIN?

A

HPV infection
Multiple partners
Smoking
Immune compromisation

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79
Q

How is CIN managed?

A

HPV vaccination – offered to school girls at 12 years before they’re sexually active – no benefit if already exposed to HPV

Colposcopy – used for further assessment of normal smear

Large loop excision of the transformation zone

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80
Q

Which is the cell type usually seen in cervical cancer?

A

Squamous cell carcinoma

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81
Q

What staging tool is used to stage cervical cancer?

A

FIGO staging – 1/2/3/4

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82
Q

What is stage 1 cervical cancer?

A

Confined to the cervix

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83
Q

What is stage 2 cervical cancer?

A

Spread into the top part of the vagina

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84
Q

What is stage 3 cervical cancer?

A

Spread into other nearby organs such as the ureter

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85
Q

What is stage 4 cervical cancer?

A

Distant metastasis

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86
Q

What are some risk factors for cervical cancer?

A

HPV infection
Early age intercourse (< 16 years)
STIs
Cigarette smoking – encourages persistence of HPV
Previous CIN/abnormal smear
Multiparity
History of other genital tract neoplasia

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87
Q

Which are the harmful forms of HPV most associated with cervical cancer?

A

HPV 16 and 18

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88
Q

Which oncoproteins do these HPV subtypes contain and why does this cause cancer?

A

Contain E6 and E7 oncoproteins

E6 prevents p53 tumour suppressor gene working

E7 attacks retinoblastoma tumour suppressor gene

Leading to overstimulation of growth of the cells of the cervix

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89
Q

What are the symptoms of cervical cancer?

A

Often asymptomatic and picked up on smear
Post coital bleeding
Post-menopausal bleeding
Watery vaginal discharge

Features of advanced disease – heavy vaginal bleeding, ureteric obstruction, weight loss, bowel disturbance, vesico-vaginal fistula, pain

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90
Q

How do you investigate someone with suspected cervical cancer?

A

History – ask when their last cervical screening was and whether it was abnormal
Physical examination – bimanual, speculum
Punch biopsy for histology
CT abdomen and pelvis –staging
MRI pelvis – staging and identifying suspicious lymph nodes

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91
Q

How is cervical cancer treated?

A

Large loop excision of the transformation zone

Knife cone biopsy +/- pelvic lymph nodes

Simple hysterectomy
Cervicetomy/ trachelectomy
Radical hysterectomy (total abdominal hysterectomy) and pelvic lymph nodes
Chemo/radiotherapy – if too large for surgery (impacts fertility)

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92
Q

Which histological cell type is usually seen in endometrial cancer?

A

Adenocarcinoma

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93
Q

What are the different stages of endometrial cancer?

A

Again staged with FIGO

Stage 1 – confined to the endometrium and uterus
Stage 2 – grown into the cervix
Stage 3 – into the ovaries, vagina and surrounding lymph nodes
Stage 4 – distant spread

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94
Q

Who is more at risk of endometrial cancer?

A

Post-menopausal women

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95
Q

What causes endometrial cancer?

A

UNOPPOSED OESTROGEN - so anything that causes unopposed oestrogen

Obesity
Early menarche
Late menopause
Nulliparity
PCOS
Lynch syndrome
HRT

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96
Q

What are some risk factors for endometrial cancer?

A

OBESITY is the biggest risk - adipose tissue releases oestrogen – obesity is the reason for an increase in incidence of endometrial cancer

Post-menopause – loss of progesterone so you have unopposed oestrogen

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97
Q

What are some protective factors against endometrial cancer?

A

Parity (long time where there has been very high progesterone and low oestrogen during pregnancy)

Combined OCP

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98
Q

How does endometrial cancer present?

A

Post-menopausal bleeding - anyone with PMB should be referred on 2 week wait

In pre-menopausal women – heavy or irregular periods, PV discharge, pyrometra (infection of the uterus – 50% of ladies with pyrometra will have endometrial cancer)

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99
Q

What investigations should be done for someone presenting with suspected endometrial cancer?

A

Transvaginal USS

Endometrial biopsy

Hysteroscopy

MRI

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100
Q

How is endometrial cancer treated?

A

Surgery – total abdominal hysterectomy +/- lymph nodes

Radiotherapy – adjuvant (brachytherapy/external beam)

Progesterone therapy

Good prognosis – 5 year survival for stage 1 disease 80%

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101
Q

What histological cell type would be seen in vulval cancer and what causes it?

A

Squamous cell

In younger women – HPV
In older women – lichen sclerosis

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102
Q

How does vulval cancer present?

A

Vulval itching
Vulval soreness
Persistent ’lump’
Bleeding
Pain on passing urine
Past history of VIN (vulval intra-epithelial neoplasia) or lichen sclerosis

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103
Q

What cell type is seen mainly in ovarian cancer?

A

Epithelial cell tumours

Some can be granulosa, germ cell (teratomas) or secondary i.e. associated with presence of upper GI cancers

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104
Q

What are the causes of ovarian cancer?

A

Gene mutation – BCRA 1 and 2, HNPCC (Lynch syndrome)

Ovulation – the more you have ovulated the higher your risk (early menarche, late menopause, never been pregnant, never taken the pill)

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105
Q

What are the main risk factors for ovarian cancer?

A

Nulliparity
Early menarche and/or late menopause
Family history – gene mutations

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106
Q

What are some protective factors against ovarian cancer?

A

Pregnancy

Breastfeeding

COCP

Tubal ligation (prevents ovulation)

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107
Q

How does ovarian cancer present?

A

Bloating/IBS like symptoms (esp. in someone with no history of IBS)
Abdominal pain/discomfort
Change in bowel habit
Urinary frequency – due to pressure on bladder
Bowel obstruction (late presentation)
Asymptomatic until much later

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108
Q

How do you investigate ovarian cancer?

A

Ca125 levels
Transabdominal ultrasound scan
Whether they are pre- or post-menopausal

Combine the USS, menopausal status and Ca125 levels to determine the risk of malignancy index

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109
Q

What are the ultrasound findings suggestive of ovarian malignancy?

A

Bilateral
Multilocular
Ascites
Solid areas
Metastasis

One point scored for each of these findings

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110
Q

What score on the risk of malignancy index warrants a referral to gynae?

A

250 or above

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111
Q

How is ovarian cancer treated?

A

Surgery – sometimes will also need bowel resections
Chemo
Biologics

“holistic approach to management” – involved specialist cancer nurse, psychological therapy, social support etc.

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112
Q

Define endometriosis

A

Presence of endometrial tissue outside the uterus

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113
Q

What are some sites that endometriosis can occur and what symptoms can this cause?

A

Pouch of Douglas - rectal bleeding during period
Lungs or pharynx – coughing up blood during period
Nose – nosebleeds during period
Umbilicus
Points of previous scarring – e.g. at appendix scar – “lump near by scar that gets big and painful when I’m on my period”
Endometrioma – bleeding into the ovaries during period

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114
Q

What are the 3 theories of how endometriosis develops?

A

Sampson’s - Retrograde menstruation

Meyer’s - Metaplasia of mesothelial cells

Halban’s - Via the blood or lymphatic system

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115
Q

What are the symptoms of endometriosis?

A

2 most common – PAIN AND SUB-FERTILITY

Heavy bleeding
Bleeding from other places during period – nosebleeds, haemoptysis, rectal bleeding, umbilicus

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116
Q

What are the features of the pain in endometriosis?

A

Cyclical pain due to endometrial tissue responding to menstrual cycle
Worse 2-3 days before periods
Gets better after period
Deep dyspareunia
Dysuria
Pain on defecation (if there’s endometriosis in the pouch of douglas)

IMPROVES during pregnancy (low oestrogen)

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117
Q

Why does endometriosis cause sub-fertility?

A

Areas of endometriosis release cytokines and harmful chemicals which can cause damage to various areas of the reproductive tract

The damage can cause – reduced fallopian tube motility, scarring, bleeding, toxicity to the oocyte, adhesions and ovarian dysfunction

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118
Q

What is the main differential diagnosis for endometriosis?

A

Adenomyosis – when the areas of endometrial tissue are localised to the myometrium

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119
Q

What is the gold standard diagnosis for endometriosis?

A

Laparoscopy

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120
Q

What are the 2 generic approaches to treatment in endometriosis?

A

Abolish cyclicity

Invoke glandular atrophy

In addition to this – also provide pain relief (mefenamic acid, paracetemol)

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121
Q

What are some treatment options for endometriosis that work by abolishing cyclicity?

A

COCP – triphasing method. Works well in young women who do not want to get pregnant

GnRH agonists – “induces menopause” but reversible once the treatment is stopped. Works quicker than triphasing but they need HRT added

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122
Q

What are some treatment options for endometriosis which work by invoking glandular atrophy?

A

USE OF PROGESTERONE:
Oral progestogens (mini pill) – stops the bleeding, but can cause PMS symptoms
Depot Provera
Mirena coil

These all work well for ladies who do not want to get pregnant

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123
Q

How can endometriosis be treated in ladies who wish to get pregnant?

A

Ablation – burning away of the endometriotic tissue

Excision – cutting away of the endometriotic tissue

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124
Q

What are some surgical options for endometriosis treatment in a woman who has completed her family?

A

Oophorectomy – no ovaries = no oestrogen = no menstrual cycle = no endometriosis

Hysterectomy

The woman can also be given low dose HRT afterwards to improve menopausal symptoms

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125
Q

What is adenomyosis? Which type of lady is it more commonly seen in?

A

Excess endometrial tissue in the myometrium (muscle layer of the uterus)

Unlike endometriosis (which is seen more commonly in younger ladies who haven’t had children), adenomyosis tends to happen in older women who have had lots of children

So presents much later than endometriosis

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126
Q

What causes adenomyosis?

A

Unknown

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127
Q

How does adenomyosis present?

A

Cyclic pain – gets worse when period starts

Can last for 2 weeks after period stops (much longer than pain with endometriosis)

Dysmenorrhoea
Dyspareunia

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128
Q

What is the gold standard diagnosis for adenomyosis?

A

MRI scan

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129
Q

How is adenomyosis treated?

A

Often hysterectomy – usually occur in women who have already completed their family

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130
Q

What are fibroids?

A

Benign smooth muscle tumours of the uterus, otherwise known as uterine leiomyomas

Very common – 20% of women of reproductive age

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131
Q

What causes fibroids?

A

Unknown

But they are OESTROGEN DEPENDANT - so they shrink after the menopause

Associated with mutation in the gene for fumarate hydratase

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132
Q

What are the risk factors for fibroids?

A

Increasing age (until menopause is reached)

Afro-Caribbean women

Family history

Early puberty

Obesity

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133
Q

How do fibroids present?

A

Many asymptomatic and found incidentally
Menorrhagia
Dysmenorrhoea
Fertility problems – submucosal fibroids may interfere with implantation
Miscarriage – large or multiple tumours can compete for space
Pain
Mass
Pressure symptoms – bladder frequency, varicose veins
Bloating, constipation

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134
Q

How are fibroids investigated?

A

Abdominal examination
Bimanual pelvic examination
Transvaginal ultrasound
Transabdominal ultrasound
Hysteroscopy

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135
Q

What would be felt on a pelvic examination in someone with fibroids?

A

Bulky NON TENDER uterus

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136
Q

How are fibroids managed?

A

< 3 cm – IUS, tranexamic acid, NSAID (mefenamic acid) or COCP

> 3 cm – Trans-cervical resection of fibroids (TCRF), myomectomy, hysterectomy, uterine artery embolisation

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137
Q

What are endometrial polyps?

A

Benign growths of the endometrium

Some can be cancerous or precancerous

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138
Q

What are some risk factors for endometrial polyps?

A

Being peri- or post-menopausal

Hypertension

Obesity

Taxing tamoxifen (breast cancer therapy)

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139
Q

How do polyps present?

A

Irregular menstrual bleeding
Menorrhagia
Inter-menstrual bleeding
Post-menopausal bleeding

Infertility in younger ladies – competing with the foetus for space

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140
Q

What is the main differential diagnosis for polyps?

A

Fibroids

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141
Q

How are polyps investigated?

A

Ultrasound – transvaginal and transabdominal

Hysteroscopy

Endometrial biopsy

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142
Q

How are polyps treated?

A

Can be left alone – but monitor/biopsy if concered could be malignant or pre-malignant

GnRH analogues (oestrogen sensitive)

Polypectomy – can be done hysteroscopically
Hysterectomy if symptoms severe

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143
Q

What are the main types of benign ovarian tumours?

A

Functional cysts – enlarged persistent follicle or corpus luteum. Normal < 5cm, resolve after 2/3 cycles. Can cause pain and peritonitis if they bleed. COCP inhibits
Mucinous cystadenomas – massive, unilateral, appear solid. Common in 30-40 years olds, 15% malignant – cause mucus ascites (pseudomyoxma peritonei) if rupture
Serous cystadenomas – most common epithelial tumours, commonly bilateral, 30-50 year olds, 25% malignant
Dermoid cyst - ’mature cystic teratoma’ – contain skin/hair/teeth. Most common cyst in < 30s. Bilateral 20-30%. Torsion most likely in dermoid cyst

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144
Q

How do benign ovarian tumours present?

A

Asymptomatic – may be incidental finding
Chronic pain – dull ache, dyspareunia, cyclical pain, pressure effects
Acute pain – unilateral - if bleeding, torsion or rupture
Irregular vaginal bleeding
Hormonal effects – e.g. sudden development of androgenic features
Abdominal swelling or mass – ascites suggests malignancy or rupture mucinous cystademona

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145
Q

How should benign ovarian tumours be investigated?

A

FBC
Ca125 (if > 40 years)
If < 40 years – check other tumour markers (AFP, CEA, HCG)
Transvaginal USS
Transabdominal USS
Consider MRI for masses >7cm
MRI and CT for staging malignancy

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146
Q

How should benign ovarian tumours be treated?

A

ABCDE and hospital admission if acute presentation

Pre-menopausal women – preserve fertility and exclude malignancy. If no features of malignancy, leave alone. If cyst >5cm or symptomatic – laparoscopic ovarian cystectomy (avoid spilling cyst contents – can lead to chemical peritonitis if dermoid)

Post-menopausal women – calculate risk of malignancy index, leave alone if <5cm, watch and wait. Remove if >5cm or symptomatic. Bilateral oopherectomy can be performed if moderate/high risk

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147
Q

What are some risk factors for ovarian torsion?

A

Pregnancy
Malformations
Tumours
Previous surgery

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148
Q

How does ovarian torsion present?

A

Acute unilateral abdominal pain (often during exercise)

Radiates – back, thigh, pelvis

Nausea and vomiting

Fever – indicates necrotic ovary

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149
Q

How do you investigate ovarian torsion?

A

Rule out ectopic – pregnancy test

USS with colour Doppler = diagnostic gold standard

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150
Q

How is ovarian torsion managed?

A

Laparoscopy

Plus analgesia and fluid resuscitation

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151
Q

How does rupture of an ovarian cyst present?

A

Acute abdominal pain (often during exercise)

PV bleed

N&V

Circulatory collapse +/- weakness, syncope
Fever/sepsis

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152
Q

How should a ruptured ovarian cyst be investigated?

A

Rule out ectopic – urinary HCG

USS

Laparoscopy = diagnostic gold standard

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153
Q

How should someone with a rupture ovarian cyst be managed?

A

ABCDE assessment

If stable – analgesia and supportive (fluids, painkillers)
If unstable/bleeding – surgery – laparotomy may be necessary

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154
Q

What is pelvic inflammatory disease?

A

A chronic infection of the upper genital tract

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155
Q

What causes PID?

A

STI – 25% due to chlamydia and gonorrhoea

Uterine instrumentation – hysteroscopy, insertion of IUCD, TOP

Post-partum (retained tissue)

Descend from other organs – appendicitis

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156
Q

What are the risk factors for PID?

A

Age < 25

History of STI

New and multiple sexual partners

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157
Q

What are some protective factors against PID?

A

Barrier contraception

Mirena

COCP

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158
Q

What are the symptoms of PID?

A

Lower abdominal pain
May be unilateral or bilateral
May be constant or intermittent (but usually chronic in nature – i.e. lasting several months)
Deep dyspareunia
Vaginal discharge
IMB
PCB
Dysmenorrhoea
Fever

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159
Q

How would you investigate someone with suspected PID?

A

History
Examination – vaginal bimanual examination and speculum examination
Full STI screen – high and low vaginal swabs, endocervical swabs, urine sample
TVS if abscess suspected
FBC, CRP and blood cultures – if acutely unwell/septic

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160
Q

What are some signs you’d seen on examination in someone with PID?

A

Cervical excitation (motion tenderness) on vaginal examination – BIG ONE FOR THE EXAMS
Vaginal discharge
Adnexal tenderness

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161
Q

What are some complications of PID?

A

Tubo-ovarian abscess
Fitz-Hugh-Curtis syndrome – liver capsule inflammation
Recurrent PID
Ectopic pregnancy
Subfertility from tubal blockage

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162
Q

How is PID managed?

A

Contact tracing

Antibiotics – start before cultures come back (quicker treatment = reduced risk of complications) – ceftriaxone, doxycycline, metronidazole, azithromycin

If very severe/very unwell – admit for ABX

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163
Q

What asymptomatic screening is offered in GUM clinics?

A

Female – self-taken vulvo-vaginal swabs for gonorrhoea/chlamidya NAAT (nulceic acid amplification test), bloods for HIV and STIs

Heterosexual male – first void urine, bloods

MSM – first void urine (chlamidya and gonorrhoea), pharyngeal swab, rectal swab, bloods – STI, HIV, HEP B

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164
Q

What are some tests available at GUM for people with symptoms?

A

Vulvovaginal swabs – Gonorrhoea and Chlamydia
High vaginal swabs – BV, TV, candida
Urethral swabs for men
First void urine for men
Dipstick urinalysis (looks for pus cells)
Bloods
Rectal and pharyngeal swabs and cultures for MSM

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165
Q

What are some symptoms that females with STI problems will present with?

A

Vaginal discharge
Vulval discomfort/soreness, itching or pain
Superficial dysparuenia
Deep dyspareunia
Chronic pelvic pain
Vulval lumps and ulcers
Inter-menstrual bleeding
Post-coital bleeding

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166
Q

What are some symptoms of STIs that males may present with?

A

Pain/burning during micturition
Pain/discomfort in the urethra
Urethral discharge
Genital ulcers, sores or blisters
Syphillis – primary shankra (can occur on the penis/glans)
Genital lumps
Rash on penis/genital area
Testicular pain/swelling – e.g. orchiditis

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167
Q

What is the importance of contact tracing?

A

Prevent re-infection of index patient

Identify and treat asymptomatic infected individuals as a public health measure - i.e. preventing the disease from spreading further

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168
Q

What is the definition of incontinence?

A

Involuntary leakage of urine at a time which is not socially acceptable

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169
Q

What proportion of women experience urinary incontinence?

A

20% of adult women

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170
Q

What are the different subtypes of incontinence?

A

Overactive bladder (destrusor overactivity) – caused by involuntary bladder contractions
Stress incontinence - caused by sphincter weakness
Fistula – between urinary tract and vagina/bowel
Neurological – nerve damage/MS
Overflow incontinence – due to retention/prostate enlargement
Functional
Mixed incontinence

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171
Q

What are some risk factors for urinary incontinence?

A

Age
Increasing parity
Obesity
Smoking
Previous surgery

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172
Q

What are some causes of urinary incontinence?

A

Nerve damage from previous surgery

Childbirth

Diabetes – neuropathy may affect bladder control, polyuria and polydipsia as diabetes symptoms, renal impairment, nephropathy, reduced immunity and increased risk of infection

Recurrent UTI – causing frequency

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173
Q

What is the clinical presentation of an overactive bladder?

A

Urgency
Urge incontinence
Frequency
Nocturia
Noctural enuresis
‘Key in the door’ and ‘Hand wash’ can act as a trigger for bladder contractions in overactive bladder
Intercourse

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174
Q

How does stress incontinence present?

A

Involuntary leakage when:

Cough
Laugh
Lifting
Exercise
Movement

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175
Q

What is the first line investigation for incontinence?

A

HISTORY is the most important factor

Bladder diary (frequency volume chart) – need to record when, how much and fluid intake

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176
Q

What other investigations can you do for incontinence?

A

MSU – infections, nephritis, cancer, stones, diabetes, renal disease
Residual urine measurement - in and out catheter, USS to measure how much urine left
ePAQ questionnaire – asks about urinary, vaginal, bowel and sexul symptoms
Urodynamics – measures the pressures in the abdomen and the bladder to figure out the detrusor pressure
Cystogram – with contrast to view the bladder

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177
Q

What conservative/lifestyle measures can help someone with incontinence?

A

Weight loss

Smoking cessation

Reduced caffeine intake

Avoidance of straining and constipation

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178
Q

What is the first line treatment for overactive bladder?

A

Bladder retraining

Can also use pads to absorb any leaked urine – may be prefered to surgery

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179
Q

What is the first line treatment for stress incontinence?

A

Pelvic floor exercises

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180
Q

What medications can be used in overactive bladder?

A

ANTICHOLINERGICS:
Oxybutinin
Solifenacin
Parasympathetic - pissing – decreasing the need to urinate

MIRABEGRON:
Beta-3-adrenergic receptor agonist (sympathetic – storage)
Relaxes detrusor and increases bladder capacity

BOTOX INJECTION – paralyses detrusor to stop it from being overactive

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181
Q

What are the side effects of anti-cholinergics such as oxybutinin?

A

Dry mouth
Blurred vision
Drowsiness
Constipation
Tachycardia

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182
Q

What are some surgical options for managing overactive bladder?

A

Augmentation cystoplasty

Indwelling catheters

Bypass (urostomy)

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183
Q

What are the treatment options for stress incontinence?

A

60% is cured by physiotherapy and conservative measures - pelvic floor exercises, pads, pessaries, skin care, odor control

Surgery – sling, suspension – supports the urethra to increase the urethral resistance

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184
Q

What are the different types of prolapse that can occur?

A

Cystocele – anterior wall of vagina and bladder – causes frequency and dysuria

Rectocele – lower posterior wall or vagina and rectum – may beed to insert finger to vagina or press on perineum to aid defecation

Enterocele – upper posterior wall of vagina and intestine

Uterine prolapse – protrusion of the uterus fown the vagina

Vault prolapse – if the woman has had a total hysterectomy

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185
Q

What is the pathological reason behind prolapse and what are the risk factors?

A

Cause – weakness of the ligaments and pelvic floor

Risk factors - age, obesity, childbirth, previous surgery

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186
Q

What are the symptoms of prolapse?

A

”something coming down” – dragging sensation, feels as if something will fall out their vagina
Pain
Lump
Discomfort
Incontinence
Sexual dysfunction
Unable to go to the toilet – may complain of having to stick their fingers up to pass urine of faeces

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187
Q

How should a prolapse be investigated?

A

Speculum examination – can see easily whether there’s something there

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188
Q

How is prolapse managed?

A

Conservative – reassure, pelvic floor exercises

Pessary – ring, shelf, gelhorn

Surgery if all else fails

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189
Q

What is the definition of subfertility?

A

Failure to conceive after 1 year or regular unprotected sex (2-3 times per week)

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190
Q

What are the causes of infertility?

A

Unexplained – 25%
Male factors – 30%
Ovulatory disorders – 25%
Tubal damage – 20%
Uterine disorders – 10%

In 40% - factors are due to both partners

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191
Q

What are some risk factors for subfertility?

A

Increasing age

Extremes of weight

192
Q

What are some ovarian factors in females that cause sub-fertility?

A

PCOS
Pituitary tumours
Sheehan’s syndrome
Hyperprolactinaemia
Premature ovarian failure
Turner’s syndrome
Hypothyroidism
Previous chemo or radiotherapy

193
Q

What are some tubal/uterine causes of subfertility in women?

A

PID
Sterilisation
Asherman’s syndrome (adhesions)
Fibroids
Polyps
Endometriosis
Uterine malformation

194
Q

How should sub-fertility be investigated?

A

See both partners together and write down everything you explain to avoid confusion
Ovulatory tests – mid-luteal progesterone levels (day 21 in a 28 day cycle, day 28 in a 35 day cycle)
Ovarian reserve testing – FSH, antral follicle count, antimullerian hormone
Semen analysis – count, motility, morphology
Other tests for the woman – prolactin levels, thyroid levels, free androgen levels, USS of uterus and tubes, karyotype

195
Q

What are some causes of male infertility?

A

Use of anabolic steroids
High prolactin
Cystic fibrosis – even carriers can have absence of vas deferens
History of undescended testes
Childhood measles
Working with a lot of heat – i.e. chefs

196
Q

How should male infertilty be investigated?

A

Semen analysis – sperm count, motility, morphology

Imaging – vasogram, ultrasound, urology

CF screen

Karyotype

197
Q

How should sub-fertility be managed?

A

Recommend couples to keep trying for 1 year
Inform about effect of age
Preconception advice – intercourse 2-3x a week, folic acid, smear, rubella, stop smoking, BMI between 19-30, no alcohol or drugs, good control of existing medical conditions
Refer to specialist after 1 more year or other criteria (covered next)

198
Q

What are the criteria for an early referral to specialist sub-fertility centres?

A

FEMALE:
Age > 35
Menstrual disorder
Previous abdominal/pelvic surgery
PID

MALE:
Previous genital pathology or urogenital surgery
Previous STI
Systemic illness

199
Q

What are some lifestyle measures to optimise male fertility?

A

Avoidance of extreme heat near the genitals
Looser fitting underpants
Stop smoking – smoking reduces fertility
Moderate alcohol intake
Avoid harmful chemicals in occupation
Diet/supplements - folic acid
Weight optimisation

200
Q

What are some treatments for male infertility?

A

Mild – intrauterine insemination
Moderate – IVF
Severe – Intracytoplasmic Sperm Injection (ICSI)

If azoospermia – surgical sperm recovery or donor insemination

Hormonal – bromocriptine if hyper-prolacintaemia, gonadotrophin replacement
Ensure they are not taking anabolic steroids

201
Q

How can infertility be treated in women?

A

Induction of ovulation
Treat any tubal disease
IVF
If endometriosis – medical treatment doesn’t improve changes of pregnancy, they need surgical ablation or excision of the endometriotic areas

202
Q

What are some methods of assisted conception?

A

Ovulation induction
Stimulated intrauterine insemination
IVF
ICSI
Donor insemination
Donor egg
Donor embryo
Host surrogacy (i.e. if the problem is with their uterus)

203
Q

What are some risks/complications of IVF?

A

Multiple pregnancy
Miscarriage
Ectopic
Ovarian hyper stimulation syndrome
Bleeding and infection at egg collection

204
Q

What are some patient factors which affect the success of IVF?

A

Age
Cause of infertility
Previous pregnancies – increases likelihood
Duration of infertility
Number of previous atempts
Medical conditions
Environmental factors

205
Q

What is the definition of FGM?

A

All procedures involving partial or total removal of female external genitalia or injury to female organs for non-medical reasons

Involves damaging or removing normal, healthy female genital tissue and hence intereferes with function

206
Q

What are the 4 different types of FGM?

A

Clitoridectomy – partial or total removal of the clitoris

Excision – partial or total removal of the clitoris and labia minora +/- labia majora

Infibulation - narrowing of the vaginal orifice by stiching the labia together

All other harmful procedures to the female genitalia for non-medical purposes

207
Q

What are some “reasons” given for FGM in certain cultures?

A

Brings status and respect
Preserves a girl’s virginity
Part of being a woman
Rite of passage
Upholding family honor
Cleanses and purifies the girl
Fulfils a religious requirement
Makes the girl acceptable for marriage
Sense of belonging to the community

208
Q

What are some dangers of FGM?

A

Blood borne viruses (no use of sterile equipments)

Haemorrhage could occur

Infection and sepsis

209
Q

How many women in the UK (aged 15-49) have been subject to FGM?

A

103,000

210
Q

What are the legal standings on FGM in the UK?

A

Illegal to perform FGM in England, Wales and northern Ireland
Illegal to assist in the carrying out of FGM (including helping them book the flights, taking them to have it done or even knowing about it and not doing anything)

If you see a child with FGM you need to phone the police

211
Q

What are some gynae complications of FGM?

A

Sexual dysfunction with anorgasmia
Chronic pain
Keloid scar formation
Dysmenorrhoea
Haematocolpos - period blood backs up in the uterus as it cannot get released during the period
Urinary outflow obstruction
Recurrent UTI
Difficulty conceiving – sexual intercourse can be very difficult
PTSD

212
Q

What are some obstetric complications of FGM?

A

Fear of childbirth
Increased likelihood of C-section, PPH, episiotomy, severe vaginal lacerations and fistula formation
Extended hospital stay
Difficulty in – performing vaginal examinations in pregnancy, applying fetal scalp electrodes and FBS
Difficulty in catheterising the bladder

Best to try and reverse infibulation before the woman falls pregnant

213
Q

What are the responsibilities of doctors with regards to FGM?

A

Report all cases of FGM in the medical notes (if adult)

Call the police if child

Ensure that families know FGM is illegal so they don’t keep doing it to their children

214
Q

What is the role of the hormones in pregnancy?

A

Synchronisation between maternal and blastocyst tissue

Maternal adaptions to pregnnancy

215
Q

What are the main pregnancy hormones?

A

HCG
Progestins
Oestrogens
Human placental lactogen
Prolactin
Oxytocin

216
Q

What is the role of HCG and where is it produced?

A

Secreted by – trophoblastic cells of the blastocyst

Role – to signal the presence of the blastocyst to the mother
Prevents the corpus luteum generating so it can persist until the placenta is formed

217
Q

What is the role of progestins and where are they produced?

A

Initially come from the corpus luteum
Then come from the placenta

Prepares the endometrium and uterus for implanation by causing proliferation, vascularisation and differentiation of the endometrial stroma
Facilitates myometrial quiescence (stops myometrium contracting too early)

218
Q

What is the role of oestrogens and where are they produced?

A

Comes from the ovary initially (mother only)
Then comes from the foetus too, later in pregnancy

Role = promotes changes in CVS and alters carbohydrate metabolism
Indicates foetal wellbeing (E3 - declines with foetal distress)
E2 – facilitates progesterone by increasing endometrial progesterone receptors

219
Q

What is the role of human placental lactogen (HPL) ?

A

Mobilises glucose from fat reserves
Diabetogenic (raises blood glucose levels) – to help increase nutrient supply to the blastocyst
Converts mammary glands into milk secreting tissue

220
Q

What is the role of prolactin and where is it produced?

A

Increased levels of prolactin allows milk production

But ONLY when oestrogen and progesterone have declined post-partum

Produced in the anterior pituitary

221
Q

What is the role of oxytocin and where is it produced?

A

Facilitates uterine contractions during labour

Milk ejection reflex post-partum

PRODUCED in the hypothalamus, SECRETED by the posterior pituitary

222
Q

Between which days of the menstrual cycle is the window of implantation?

A

Between day 20—24

WILL NOT implant outside this time frame

223
Q

What are the layers of the interface between the placenta and the myometrium?

A

Placenta
Decidua
Myometrium
Abdomen

224
Q

What are the varying degrees of morbid adherence of the placenta?

A

Normal placenta – invades into decidua

Placenta accreta – placenta invades into the superficial myometrium

Placenta increta - invades into the deeper myometrium

Placenta percreta – invades through myometrium, into nearby organs of the abdomen (bladder, bowel)

225
Q

What risks are associated with morbid adherence of the placenta?

A

Poor placental separation (becomes difficult to deliver the placenta after the baby has been delivered. Retained products leads to increased risk of infection)

Significant post-partum haemorrhage

226
Q

Which type of immunity remains unchanged during pregnancy and which type is dampened?

A

HUMORAL – remains unchanged, plenty of circulating Th2 cells meaning mother can fight infections

CELL MEDIATED – reduced during pregnancy. Progesterone down regulates the production of Th1 cells

The dampening of Th1 production causes there to be a shift to increased Th2 production (Th2 bias)

227
Q

Which conditions in pregnancy do not have a Th2 (humoral immunity) bias?

A

Pre-eclampsia
IUGR
Miscarriage

228
Q

Which type of immunoglobulin is secreted in breast milk?

A

IgA

229
Q

Which is the only antibody to cross the placenta?

A

IgG

Role in rhesus disease/haemolytic disease of the newborn

The primary immune deficiency hypogammaglobulinaemia can occur in babies who’s mother’s didn’t have high enough levels of IgG during pregnancy

230
Q

Who is at risk of rhesus disease?

A

If the MOTHER IS RH-VE

AND THE FATHER IS RH+VE

This is because 50-100% of their offspring will be Rh+ve also
Not a problem if dad is also Rh-ve

231
Q

Why does Rh disease not occur in the first pregnancy?

A

During first pregnancy – sensitisation occurs
Maternal immune reaction to the Rh+ve antigen of foetal RBC
Produces IgM which doesn’t cross the placenta to affect this pregnancy
However DOES produce memory cells – which means IgG can be produced in a subsquent pregnancy = CAN cross the placenta and CAN affect the baby

232
Q

What does Rh disease do to the feotus?

A

Causes RBC haemolysis

Leading to severe foetal anaemia and possible death if no intervention

233
Q

How to avoid rhesus disease?

A

Anti-D prophylaxis

Anti-D destroys anti-Rh+ve antibodies

Given at 28 and 34 weeks and after birth
Also given earlier in pregnancy if any sensitisation events occur

234
Q

What is the pathology behind maternal insulin resistance?

A

Post-prandial glucose peak is higher for longer to spare glucose for the foetus

GLUCOSE IS THE MAIN SOURCE OF NUTRIENTS for the foetus

235
Q

What are the risks to the foetus of diabetes mellitus during pregnancy?

A

Macrosomic infant (>4kg birthweight)

Which increases the risk of traumatic delivery (too big for the hole) and shoulder dystocia

Still birth

Congenital malformations – cleft palate most common

At risk of neonatal hypoglycaemia (due to hyperinsulinaemia)

236
Q

What are the increased risks to the mother of DM during pregnancy ?

A

Ketoacidosis

Pre-eclampsia

Coronary heart disease

Nephropathy (and all the other normal complications of diabetes)

237
Q

What is the biggest threat to maternal health?

A

OBESTIY

Massively increases their risk of problems during pregnancy

238
Q

Which drugs are used to promote myometrial quiescence (i.e. stop uterine contractions)?

A

B2 agonists – salbutamol and ritodrine
CCB - nifedipine
These are known as TOCOLYTIC DRUGS (stop labor)

Used as a treatment for coming in in early labour – B2 agonists stop smooth muscle contraction (same way as they do in asthma)

Causes MYOCYTES TO BECOME HYPERPOLARISED = which means they cannot depolarise = they cannot contract

239
Q

What serum marker can be measured to predict early labour?

A

Fetal fibronectin (fFN)

High levels related to early labour

If high level comes back – give IM steroids and keep a closer eye on the lady

240
Q

How is labour induced?

A

Firstly – membrane sweep is done before medication to try and encourage labour to start on its own (promotes positive feedback of stretch 🡪 oxytocin release)

Prostaglandin PGE2 – pessary or vaginal gel
Oxytocin – the analogue given is syntocinon

241
Q

Which scoring system can be used to assess whether induction of labour may be needed?

A

Bishop score

A score < 5 generally means induction will be needed

A score > 9 indicates labour will likely be spontaneous

242
Q

Which drugs are given to prevent/stop post-partum bleeding?

A

Oxytocin

Ergometrine

Combined form – syntometrine

Helps the placenta be delivered after the baby comes out
Then makes the uterus contract to stop bleeding

243
Q

What are the 3 stages of labour?

A

Cervical dilatation (remodelling)

Myometrial contraction (pushing stage)

Placental delivery

244
Q

Which drug stops the effect of oxytocin by blocking its receptor?

A

ATOSIBAN

Was one of the first drugs used against premature labour

Can inhibit premature myometrial contractions by blocking oxytocin (and oxytocin is why labour happens)

245
Q

What is the WHO definition of normal labour?

A

Spontaneous onset

Low risk throughout

Infant born spontaneously in the vertex position between 37 and 42 weeks of pregnancy

At birth, mother and infant in good condition

246
Q

What is defined as adequate progress of labour?

A

2cm dilatation per 4 hours of active labour

However there is no absolute time limit for labour and progress is assessed dynamically throughout

247
Q

What are the stages of labour?

A

FIRST STAGE (preparation phase):
Latent phase - painful, irregular contractions, cervical effacement and dilation to 4cm
Active phase – >4cm, regular contractions, majority of dilatation happens in this phase

SECOND STAGE (pushing stage):
Passive stage – complete diltation but no pushing
Active stage – maternal pushing until delivery

THIRD STAGE – delivery of the placenta

248
Q

What are the 3 main causes of failure to progress in labour?

A

Power

Passenger

Passage

NB – can be a combination of all these factors. Maternal exhaustion also contributes in 2nd stage

249
Q

Name some problems with ‘power’ which affect failure to progress in labour?

A

MOST COMMON CAUSE of failure to progress

Poor uterine contractions

Common in primigravida ladies

250
Q

Name some problems with the ’passenger’ which can cause failure to progress in labour

A

Malpresentation

Malposition of a large baby

251
Q

Name some problems with the ’passage’ that can cause failure to progress in labour

A

Indadequate pelvis

Cephalopelvic disproportion – big baby, small pelvis

252
Q

What are some risk factors for failure to progress in labour?

A

Large baby
Breach baby
First time mother
Previous delayed labour
Premature rupture of membranes

253
Q

How to assess someone in failure to progress?

A

Palpate abdomen for lie, head and contractions
CTG
Colour of amniotic fluid
Vaginal examination

254
Q

How to manage a delay in the first stage of labour?

A

Offer amniotomy
If membranes ruptured already – oxytocin infusion
CTG
FBS if concerns on CTG
Consider LCSC if none of this helps

255
Q

How to manage a delay in the 2nd stage of labour?

A

Allow to push - 2 hours if primip, 1 hour if multip

If still no imminent delivery – obstetric review for instrumental delivery or LSCS

256
Q

What are some foetal consequences of failure to progress in labour?

A

Foetal distress

Foetal hypoxia 🡪 HIE

Increased foetal morbidity and mortality

257
Q

What are some maternal consequences of failure to progress in labour?

A

Bleeding

Tears

258
Q

What are the foetal and maternal parameters recorded on the partogram?

A

FHR – monitors the wellbeing of the feotus
Cervical dilatation
Contractions per 10 minutes
Drugs and IV fluids given
Pulse and BP of the mother – ensures she is stable
Urine

259
Q

What is “normal” for progression of labour?

A

Nulliparous – 0.5cm/hour (1cm every 2 hours)
Multiparous – 1cm/hour

260
Q

What is “abnormal” in progression of labour?

A

Slow from the beginning (dysfunctional labour)

Sudden slowing of labour (secondary arrest)

261
Q

What is the role of the “action line” on a partogram?

A

Action line indicates slow progression
At the action line – ACTION needs to be taken
Provides clear guidelines on when to intervene
The point at which progression stops is useful in seeing where the problem is

262
Q

What is malpresentation?

A

When the foetus is not presenting by the vertex

263
Q

What is a breech presentation?

A

When the presenting part of the foetus is not the head

The foetus is in longitudinal lie with the buttocks or feet closest to the cervix

264
Q

What is the most common type of breech presentation?

A

Extended breech

Presenting part is the bottom

265
Q

What are some causes of breech presentation?

A

Idiopathic
Uterine abnormalities – bicornate uterus, fibroids
Prematurity (the baby hasn’t turned itself round yet)
Placenta praevia
Oligohydramnios
Foetal abnormalities e.g. hydrocephalus

266
Q

How is breech presentation diagnosed?

A

Try to diagnose antenatally with USS

30% present undiagnosed in labour – palpation via abdominal examination or feeling the breech vaginally

Mother may complain of pain under the ribs

267
Q

How is breech presentation managed?

A

External cephalic version (ECV) – manoeuvring the baby to correct the breech
This can be done at 37 weeks

LCSC – if ECV is unsuccessful or contrainidcated

268
Q

What are some contraindications for ECV?

A

Placenta praevia
Multiple pregnancies (except delivery of 2nd twin)
APH in last 7 days
Rupture membranes
Growth restricted babies
Abnormal CTG
Mothers with uterine abnormalities or scars (e.g. previous LCSC)
Foetal abnormality
Pre-eclampsia or HTN (increased risk of abruption)

269
Q

What is the correct positioning of a baby’s head when presenting?

A

Occipito-anterior

270
Q

What is malposition?

A

The presenting part is in the right place but wrong position

i.e. presenting occipito-posteriorly or occipito-transverse

271
Q

How is malposition managed?

A

Most can have normal delivery

Some may need forceps

Some may need LSCS

272
Q

How to manage someone failing to progress in the first stage of labour?

A

Admit to labour ward
Artificial rupture of membranes
CTG monitoring

May need oxytocin drip to speed up the labour
If this fails – may need LSCS

273
Q

What factors will influence the mode of delivery in someone failing to progress?

A

Size of baby
Well-being of mother and baby
Presentation of the baby
How long labour has been going on for
Maternal exhaustion
Adequacy of pelvis

274
Q

How to review someone failing to progress in the second stage of labour?

A

Determine presentation of the foetus as this will determine actions – if breech then no point giving oxytocin as will likely need LSCS

CTG monitoring
USS of foetus if unsure of lie
If not breech – oxytocin and keep assessing
If breech – external cephalic version or LSCS

275
Q

What causes meconium stained liquor?

A

Foetal distress

Foetal maturity (i.e. late baby – ready to be born)

Beware – aspiration of fresh meconium can cause severe pneumonitis

276
Q

Name some non-pharmacological ways in which pain can be managed in labour?

A

Relaxation techniques
Massage
Water births
Getting in a comfortable position/posture
Being in a comfortable setting/environment for their birth

277
Q

What pain relief medications can be used during labour?

A

Paracetamol and codeine useful in early stages of labour

Entonox – gas and air

Opiates - pethidine, morphine, diamorphine - can be IV or single shot IM

Epidural

278
Q

Name some side effects of entonox

A

(gas and air – N2O and O2 mixed)

Can cause nausea and vomiting

279
Q

Name some side effects of using opiates in labour

A

Foetal side effects – respiratory depression, diminishes breast seeking and feeding behaviour

Materanl – euphoria, dysphoria (unease), nausea/vomiting, can prolong 1st and 2nd stage of labour, respiratory depression, pruritis

280
Q

Name some side effects of using epidural pain relief during labour

A

Maternal – increased length of 1st and 2nd stage of labour, need for more oxytocin, increased need for instrumental, loss of mobility, loss of bladder control, pyrexia

Foetal – tachycardia, diminishes breast-feeding behaviour

281
Q

What spinal level is an epidural performed?

A

L3 – L4

Can use USS to aid them and avoid damage of the spinal cord

282
Q

What medications can be given epidurally?

A

Local anaesthetics – bupivacaine

Opioids – fentanyl, diamorphine

283
Q

What are some complications of an epidural?

A

Potential for damage to the spinal cord
Hypotension and bradycardia
Haematoma/abscess at injection site
Anaphylaxis if allergic to the medicatoin
Post dural puncture headache

284
Q

What are some indications for an epidural?

A

Maternal request
HTN/pre-eclampsia
Cardiac disease
Induced labour
Multiple births
Instrumental/operative delivery likely

285
Q

What are some absolute contraindications for an epidural?

A

Maternal refusal
Local infection
Allergy to local anesthetics

286
Q

What are the 2 options of anaesthesia for a LSCS?

A

Regional block

General anaesthetic

287
Q

What is the definition of screening?

A

A process of identifying apparently individuals who may be at increased risk of a disease/condition

288
Q

What are the criteria for a screening programme?

A

Disease has an acceptable test
Disease is an “important” problem - i.e. affects large numbers of people
Disease has a known latent phase
Disease has a known progression/natural course
Disease has a known treatment
Agreed policy on who to treat

289
Q

What are the limitations of screening?

A

Does not guarantee protection against developing the condition (can only help reduce risk)

False positives and negatives

Not the same as a diagnosis – only looks for risk markers of the disease

290
Q

What pre-test information is important to give to mothers?

A

The condition(s) being screened for
When and how the test will be carried out
How reliable the test is
Different possible results and their meanings
Options of the test is positive
False positive and negative rates
Detection rates

291
Q

What conditions are screened for in the foetal anomaly screening programme?

A

Down’s syndrome – trisomy 21

Edward’s syndrome – trisomy 18

Patau’s syndrome – trisomy 13

292
Q

How are foetal anomalies screened for?

A

First trimester – combination of nuchal translucency + serum B HCG + Papp-A (combined test) – produces risk results for the trisomies
Needs to be done before 13+6 weeks

Second trimester – quadruple test give if late booker or nuchal translucency not obtained

293
Q

What hormones are tested for in the triple test?

A

Alpha fetoprotein

Oestriol

B-HCG

294
Q

What hormones are tested for in the quadruple test?

A

AFP
BHCG
Oestriol
Inhibin A

Done if after 15 weeks pregnancy

295
Q

When should the booking visit be?

A

8 – 12 weeks

296
Q

When is the nuchal translucency scan?

A

11 – 13+6 weeks

297
Q

When is the anomaly scan performed?

A

18 – 20+6 weeks

298
Q

What risk score is considered a screen positive result?

A

If the risk is 1 in 150 or worse

299
Q

What further tests can be given in these higher risk pregnancies?

A

Diagnostic testing – can be done on the same day

AMNIOCENTESIS OR CHORIONIC VILLUS SAMPLING

300
Q

What is the role of the early USS and late USS in pregnancy?

A

Early – assess gestational age

Mid pregnancy scan – identify major abnormalities and conditions that may benefit from treatment before birth

If any abnormalities detected - further scans may be offered

301
Q

What are the 3 infectious diseases should be screened for in pregnant women?

A

HIV

Hepatitis B

Syphillis

302
Q

What diseases as newborns screened for on the blood spot programme?

A

Sickle cell disease (and thallassamia)
Congenital hypothyroidism
Cystic fibrosis
And 6 inborn errors of metabolism:
Maple syrup urine disease
Phenylketonuria
Homocysteinuria
3 more that I will never remember

303
Q

When is the NIPE check done and what does it screen for?

A

First = within 72 hours of birth
Second = by GP at 6-8 weeks

Screens for problems with:
Hips – DDH
Reflexes
Eyes – absent red reflex, congenital cataracts
Heart
Mouth and palate
Undescended testes/checks of the genitals

304
Q

What are the advantages of CTG monitoring?

A

Can pick up foetal distress
Can be on constantly to see any slight changes that need to be looked at

305
Q

What are some disadvantages of CTG monitoring?

A

Does not improve still birth rates despite its use in high risk pregnancies
Many women find the device uncomfortable to wear
Ambulatory monitoring not possible
Doesn’t give true beat to beat FHR monitoring

306
Q

When are CTG monitors used?

A

During labour for every women

During high risk pregnancies

307
Q

What are the 4 baseline parameters on a CTG?

A

Baseline foetal heart rate (FHR) – resting HR

FHR variability – variation in HR

Number of accelerations – rise in baseline HR

Number of decelerations - fall in baseline HR

308
Q

What is the difference between early and late decelerations on a CTG?

A

Early – most likely due to uterine contractions

Late – whilst the uterus is relaxing, sign of distress of the baby

309
Q

What is the most common cause of early deceleration?

A

Head compression due to uterine contraction

310
Q

What is the most common cause of late deceleration?

A

Uterine placental insufficiency /foetal distress

311
Q

What causes variable deceleration? (When there is NO relationship to the uterine activity)

A

Cord compression

312
Q

What are normal features on a CTG?

A

Baseline HR - 110-160bpm

Variability - >5bpm

Accelerations present

No decelerations present

313
Q

How do you interpret a CTG?

A

Define each parameter and whether it’s reassuring, non-reassuring or abnormal

314
Q

What time frame is a reduced level of variability acceptable for any why?

A

40 mins

Because the baby may be sleeping – but they never normally sleep for more than 40 mins

315
Q

How is a direct foetal ECG obtained during labour?

A

Via the baby’s scalp
Gold standard of FHR monitoring – gives a true beat to beat FHR measurement

316
Q

What are the limitations of a direct foetal (scalp) ECG?

A

Invasive
Can only be used during labour
Can only be performed when membranes have ruptured and >2cm dilated
Associated with scalp injury and perinatal infection

317
Q

What is the only available ambulatory method of FHR monitoring?

A

Abdominal foetal ECG
True beat to beat recording
Can be used ambulatory and at home
Should only be used in HIGH RISK

318
Q

What are some relative contraindications for prescribing the COCP?

A

> 35 year and smoking < 15 cigarettes/day
BMI > 35 kg/m2
Family history of thromboembolic disease in first degree relatives
Controlled hypertension
Immobility (e.g. wheelchair use)
Known carrier of BRCA1/2

🡪 these are situations in which the risk outweigh the benefits of the pill, but are not absolutely contraindicated

319
Q

What are some absolute contraindications for the COCP?

A

> 35 and smoking >15 a day
Migraine with aura
History of thromboembolic disease of thrombogenic mutatoin
History of stroke of IHD
Breast feeding < 6 weeks post-partum
Uncontrolled HTN
Current breast cancer
Major surgery with prolonged immobilisation

320
Q

Which HPV viruses cause genital warts?

A

HPV 6 and 11

321
Q

Define antepartum haemorrhage

A

Genital tract bleeding from 24 weeks’ gestation

322
Q

What are some dangerous causes of antepartum haemorrhage?

A

Placental abruption

Placenta praevia

Vasa praevia (here the baby may bleed to death)

Morbidly adherent placenta

323
Q

Name some other causes of antepartum haemorrhage

A

Cervical polyps
Cervicitis
Carcinoma
Vaginitis
Vulval varicosities

324
Q

Define placental abruption

A

When part of the placenta becomes detached from the uterus

325
Q

Name some risk factors for placental abruption

A

Previous abruption
Hypertension
Multiple pregnancy
Trauma
Vascocontrictor drugs (cocaine and crack)
Infection
Thrombophilias
Uterine abnormality
Smoking
Pre-eclampsia
Increasing maternal age

326
Q

How does placental abruption present?

A

Classically PAINFUL

“Hidden bleeds” – bleeding may be localised to once placental area meaning that it can occur for a long time before presenting as vaginal bleeding - means that the mother may present in SHOCK with a relatively small amount of PV bleeding as the bleed is actually happening internally

Posterior abruptions – backache

327
Q

What would be felt on examination of a uterus experiencing abruption?

A

“Tender woody uterus”

There will also be foetal distress (which you will not necessarily see in someone with placenta praevia – so can be another way to distinguish them)

328
Q

What are some complications of placental abruption?

A

Foetal death or anoxia leading to brain damage
May prevent good contractions in labour
Post partum haemorrhage
Uterine hyper-contractility (>5 contractions/10 mins)
Disseminated intravascular coagulation (DIC)
Renal failure
Sheehan’s syndrome (pituitary necrosis following PPH)

329
Q

How to manage placental abruption?

A

Admit to hospital - ABC
IV fluids
Oxygen
ABO Rh compatible blood or O –ve blood
If safe and term – delivery
Mum comes first so if bleeding cannot be stopped, need to deliver the foetus even if it’s unlikely to survive

330
Q

Define placenta praevia

A

A low lying placenta – any part of the placenta has implanted into the lower segment of the uterus

Major – fully covering the cervical os

Minor – encroaching the lower segment but not fully covering the os

331
Q

What should be avoided in a lady with a low lying placenta?

A

Digital PV examinations

Penetrative intercourse

SPECULUM EXAMINATION IS SAFE

332
Q

How does a low lying placenta present?

A

Diagnosed antenatally on ultrasound scan - 20 week anomaly scan

Can be re-checked closer to the time of delivery as can appear low lying at first but may change over the course of the pregnancy

333
Q

What kind of bleed will be caused by a low lying placenta?

A

PAINLESS
Large amount of blood

Which is very different to placental abruption which is painful with a smaller amount of blood

334
Q

What are some risk factors for a low lying placenta?

A

Previous c-section
Previous termination of pregnancy – uterine evacuation
Multiparity
Multiple pregnancy
Mother >40 years
Assisted conception
Manual removal of previous placenta
Fibroids
Endometriosis

335
Q

How is a low lying placenta managed?

A

Advise for which symptoms to look out for

If minor - aim for normal delivery unless the placenta comes within 2cm of the os

Major – elective C-section at 38-39 weeks

336
Q

Define vasa praevia

A

The major foetal vessels are presenting before the foetus

These vessels are exposed meaning they are prone to rupture which can be potentially fatal for the foetus

337
Q

How to manage vasa praevia?

A

ABC management of bleeding

Delivery by caesarean (elective if detected antenatally, emergency if present with bleeding)

Mortality 60%

338
Q

How do you manage a morbidly adherent placenta?

A

MRI scan if degree of adherence uncertain

Elective LSCS at 36-37 weeks’

Discuss possible interventions - caesarean hysterectomy, leaving the placenta in place

339
Q

What are some risks that may occur at delivery in someone with a morbidly adherent placenta?

A

Haemorrhage
Transfusion
Caesarean hysterectomy
ITU admission

340
Q

What are some complications of antepartum haemorrhage?

A

Post-partum haemorrhage
Premature labour/delivery
DIC
ITU admission
ARDS
Acute tubular necrosis
Death (mother or foetus)
Sheehan’s syndrome

341
Q

Define PRIMARY post-partum haemorrhage (PPH)

A

The loss of >500ml in the first 24 hours after delivery

342
Q

What are the causes of primary PPH?

A

The 4 T’s:

Tone – uterine atony

Tissue – retained products (i.e. placenta)

Trauma – i.e. a big tear in the genital tract

Thrombin – clotting disorder

343
Q

Which is the most common cause out of the 4 for primary PPH?

A

Uterine atony

344
Q

How would you diagnose uterine atony on abdominal examination?

A

Un-palpable uterus

The uterus should normally be palpable in the period following giving birth but if it’s atonic it will not be palpable

345
Q

How do you approach the management of PPH caused by uterine atony?

A

Emptying bladder can help
Rub the abdomen to help the uterus contract
Bimanual compression of the uterine

IV Syntocinon(combination of ergometrine and oxycotin to help the uterus contract)
IM Carboprost
Surgical options also available (B-lynch sutures, internal iliac artery ligation)

346
Q

Define SECONDARY PPH

A

Excessive blood loss from the genital tract area after 24 hours – 12 weeks from delivery

347
Q

What’s the most common cause of secondary PPH?

A

Retained placental tissue

348
Q

What are some risk factors for PPH?

A

Antepartum haemorrhage (and any of the causes of)
Previous PPH
Previous retained placenta
Maternal anaemia at onset of labour
BMI > 35
Maternal age > 35
First baby
Large baby
Twins/triplets
Operative delivery
Fast labour and delivery

349
Q

How to manage a post-partum haemorrhage

A

Medications to stop the bleeding – ergometrine, oxytocin, syntometrine (combination of ergo and oxy) - these cause the uterus to contract which should stop the bleeding
IM Carboprost if this doesn’t work

If mild/moderate – IV fluids, oxygen, blood products, try and find and prevent the source of bleeding

If severe (>1500mls) – medical emergency – call 2222

350
Q

What are the surgical options for management of PPH?

A

Ligation of the internal iliac or uterine artery

Uterine artery embolization

Hysterectomy

351
Q

What are the most common causes for vaginal bleeding in the first trimester?

A

Miscarriage

Ectopic pregnancy

352
Q

What is the commonest cause of direct maternal death?

A

Pulmonary embolism

High risk during the post-partum period

353
Q

How can this be prevented?

A

Thromboprophylaxis in labour and chilbirth 🡪 LMWH injection (i.e. deltaparin) and TEDS stockings

354
Q

What are some risk factors for maternal VTE?

A

Previous VTE
Family history
Thrombophilia (acquired disorder) – beware antiphospholipid syndrome – recurrent miscarriages and tendency to clot
BMI > 30
Smoking
Age > 35
Pre-eclampsia
C-section
Immobility

355
Q

How may a VTE present?

A

Shortness of breath
Chest pain
Leg pain or swelling

356
Q

What is the gold standard diagnosis for VTE?

A

DVT – ultrasound doppler

PE – CTPA

If suspicious – Well’s score and D-Dimer

357
Q

How would you treat a VTE?

A

Most importantly = prophylactic dose of LMWH given according to maternal weight

Embolectomy

Anti-coagulate afterwards

358
Q

Another big cause of maternal death is sepsis. What are some common causes for maternal sepsis?

A

Flu – DO NOT UNDERESTIMATE FLU
Pyelonephritis
Chorioamnionitis
Wound infection – i.e. C-section, episiotomy
Pneumonia
Pancreatitis
Etc. – basically any infection
GBS (group B strep)

359
Q

What are some risk factors for maternal sepsis?

A

Immunosuppressed – HIV, medication
Obesity
Diabetes
Anaemia
History of pelvic infection
Amniocentesis and other invasive procedures
Cervical stitch
Prolonged ROM

360
Q

How does maternal sepsis present?

A

Pyrexia or hypothermia
Tachycardia
Hypotension
Oliguria
Hypoxia
Impaired consciousness

361
Q

How to investigate maternal sepsis?

A

SEPSIS SIX – in the first hour

Blood cultures
IV fluids
Monitor hourly urine output – catheterise
Broad spectrum IV antibiotics
ABG – lactate
High flow oxygen

362
Q

What are some precautionary measures that can be done to prevent maternal sepsis?

A

Give all pregnant ladies seasonal flu vaccine – flu must not be underestimated
Sepsis 6
Give broad spec IV Abx BEFORE cultures come back – then alter when sensitivities come back if necessary
Involve senior team and experts early

363
Q

What is cord prolapse?

A

When the umbilical cord prolapses through the cervix when the membranes rupture

364
Q

Why is cord prolapse dangerous?

A

Exposure of the cord leads to vasospasm

Can cause significant risk of foetal morbidity and mortality from hypoxia

365
Q

What are some risk factors for cord prolapse?

A

Premature rupture of membranes
Polyhydramnios
Long umbilical cord
Malpresentation
Multiparity
Mutliple pregnancy

366
Q

How to manage a cord prolapse?

A

Call 999 or emergency buzzer if in hospital
Alleviate pressure on cord – put their feet up in the air (Trendelenberg position)
Transfer to theatre to prepare for delivery

367
Q

What’s the definition of shoulder dystocia?

A

Failure for the anterior shoulder to pass under the symphysis pubis after delivery of the foetal head

Requires specific manoeuvers to facilitate delivery

368
Q

What are the risk factors for shoulder dystocia?

A

Macrosomia (baby >4kg)
Maternal diabetes - causes macrosomic babies
Known small maternal pelvis/disproportion btween mother pelvis size and foetus size
Post-maturity that required induction of labour
Prolonged labour
Instrumental delivery

369
Q

How to manage shoulder dystocia?

A

MEDICAL EMERGENCY – so call for help/press emergency buzzer

Either rotate the baby/use manouvers

Or replace the head and deliver by LSCS

370
Q

What are some complications of shoulder dystocia for the mother?

A

PPH
Extensive vaginal tear
Psychological impact to mother and partner

371
Q

What are some complications of shoulder dystocia to the baby?

A

Hypoxia
Fits
CP
Brachial plexus injury/Erb’s palsy
Fractured clavical or humerus

372
Q

How do you approach pregnancy in someone who has a chronic disease?

A

Ensure optimum disease control – defer pregnancy until the condition is stable
Effective contraception until ready to conceive
Avoid use or teratogenic drugs (warfarin, valproate)
Council mum on the risks of pregnancy with the condition
MDT approach and regular check ups
Agreed care plan with patient and other healthcare experts

373
Q

What is the most common cause of anaemia in pregnancy?

A

Relative physiological anaemia due to increased blood volume

Iron deficiency

Folate deficiency

374
Q

What risk does iron deficiency anaemia pose to the pregnancy?

A

Low birthweight

Preterm delivery

375
Q

How can anaemia be managed during pregnancy?

A

Iron and folate supplements

376
Q

Which asthma medications can be used during pregnancy?

A

ALL of the normal asthma medications can be used in pregnancy (steroids, salbutamol, theophyllines etc.)

As the baby grows it can press up on the lungs and make the asthma worse, but because all of these medications can be used during pregnancy it should be easy to optimise control (dose adjustment may be required)

In asthma attack – prioritise mum

377
Q

What is the leading cause of indirect maternal death?

A

Cardiovascular disease

In older women = ischaemic heart disease
In younger women = congenital heart disease which is exacerbated by pregnancy e.g. coarctation of the aorta

378
Q

What type of heart disease is risky during pregnancy?

A

FIXED OUTPUT HEART DISEASE:

Aortic stenosis
Coarctation
Prosthetic valves (added issue of anti-coagulation)
Cyanosed patients

379
Q

What are some lower risk cardiac conditions during pregnancy?

A

Mitral regurgitation
Aortic regurg
ASD
VSD

380
Q

If someone has had a valve replacement but is wanting to get pregnant, what are some important factors of their management plan you’d need to consider?

A

THEY CANNOT TAKE WARFARIN DURING PREGNANCY

So take them off warfarin and get them on daltaparin instead – this is the ONLY LISCENSED ANTICOAGULANT IN PREGNANCY

Also need to do a HASBLED score and predict their bleeding risk as they are at higher risk of antepartum and post-partum haemorrhage

381
Q

What is the mot common liver disease during pregnancy and how does it present?

A

Obstetric cholestasis (unique to pregnancy)

Presents with itchy skin (mainly on hands and feet)

382
Q

How is obstetric cholestasis treated?

A

Ursodeoxycholic acid

Piriton helps the itching

Goes away after delivery – but increased risk during another pregnancy

383
Q

Which is more common during pregnancy - hypo or hyperthyroidism?

A

HYPOthyroidism

384
Q

What is a common symptom of hyperthyroidism during pregnancy?

A

Excessive vomiting

So if someone presents with excessive vomiting check their thyroid levels

385
Q

What are the side effects of anti-thyroid drugs during pregnancy?

A

Propylthiourail – maternal liver failure (so more likely to use this one as treatment)

Carbimazole – foetal abnormalities

386
Q

What are the risks of hypothyroidism during pregnancy?

A

Early foetal loss

Congenital hypothyroidism – leading to neurodevelopmental delay

387
Q

Define gestational diabetes mellitus

A

Carbohydrate intolerance first recognised during pregnancy

388
Q

Which ladies are at high risk of gestational diabetes mellitus (GDM)?

A

History of previous GDM
FH of diabetes
High BMI
Persistent glycosuria on dipstick

389
Q

What pre-conceptual advice should you give to someone who has diabetes?

A

Aim for HBA1c < 48 mmol/l
Take 5mg folic acid
Stop ACEi and statins
Retinal screening
Renal fucntion screening
Establish GOOD diabetic control before pregnancy (and stay on contraception until good control is achieved)
Good glycaemic control from conception improves the outcome of the pregnancy

390
Q

What are some maternal risks of diabetes during pregnancy?

A

DKA
Hypoglycaemia (common)
Progression of retinopathy and other microvascular complications
Pre-eclampsia
The usual micro and macrovascular complications of diabetes

391
Q

What are some foetal/neonatal risks of diabetes during pregnancy?

A

Miscarriage
Stillbirth
Macrosomia
Shoulder dystocia
Foetal abnormality
Neonatal hyperinsulinaemia 🡪 neonatal HYOPglycaemia (which can be dangerous)
Respiratory distress
Hypocalcaemia
Polycythaemia

392
Q

Which medications should be given to T1 and T2 diabetics during pregnancy?

A

Type 1- insulin (dose adjustment as necessary for the normal changes to glucose metabolism during pregnancy)

Type 2 – start with metformin but may need upgrading to insulin

Gliclazide is contraindicated in pregnancy

393
Q

How should GDM be treated?

A

Attempt to manage with diet first

Start on medication if this is inadequate

394
Q

What are some maternal risks of having chronic renal disease during pregnancy?

A

Severe hypertension
Deterioration in renal function/renal failure
Pre-eclampsia
Caesearian section

395
Q

What are some risks to the foetus of renal disease during pregnancy?

A

Premature delivery
IUGR
Stillbirth
Foetal abnormalities due to maternal drug therapy

396
Q

How do you manage chronic renal disease during pregnancy?

A

Pre-pregnancy risk assessment
MDT care
Close monitoring of renal function during pregnancy
Regular BP and urine dip checks – if any proteinuria have a high index of suspicious for pre-eclampsia
Regular foetal growth scans

397
Q

What are the risks to the mother of epilespy during pregnancy?

A

Increase frequency of seizures
Seizure could lead to falls which could cause trauma to the baby
Sudden unexpected death in epilepsy – can happen in mothers who are breastfeeding and are therefore reluctant to take their anti-epileptic medications

398
Q

What are the risks to the foetus of epilepsy during pregnancy?

A

Anti epileptic drugs are teratogenic
VALPROATE – worst by far
Neural tube defects, spina bifida
Inheritence of epilepsy
Risk of feotal hypoxia with maternal seizures

399
Q

How should epilepsy be managed during pregnancy?

A

Preconception assessment – high dose folic acid
Once pregnant – screen for abnormalities
Control seizures
Plan for delivery – pain relief, avoid prolonged labour

400
Q

Define chronic hypertension in pregnancy

A

Hypertension diagnosed before pregnancy or 20th week of gestation

401
Q

Define gestational hypertension

A

NEW HTN AFTER 20 WEEKS’ GESTATION
Systolic BP >140
Diastolic BP >90

402
Q

Define pre-eclampsia

A

Hypertension and proteinuria during pregnancy

(when the hypertension developed >20 weeks gestation)

403
Q

Define eclampsia

A

Proteinuria, hypertension and generalised tonic-clonic seizures during pregnancy

404
Q

Define pre-eclampsia superimposed on chronic hypertension

A

Hypertension in pregnancy present before 20 weeks gestation

Proteinuria develops after 20 weeks gestation

405
Q

What causes pre-eclampsia?

A

Unknown

406
Q

Name some risk factors for pre-eclampsia?

A

Smoking
Young female
First pregnancy
Black people (2x increased risk)
Multiple pregnancy
Hypertension
Diabetes
Previous pre-eclamspia
Family history

407
Q

Describe the pathophysiology of how pre-eclampsia develops

A

Inadequate arterial invasion of the placenta
Meaning that less blood can get from mum to baby (the blood vessels are not as thick and dilated as they should be)
So the body increases its blood pressure to try and get more blood through to the baby
Which means that mother ends up with systemic HTN in order to get adequate nutrients to the baby

408
Q

What is the pathophysiology behind the seizures in eclampsia?

A

Proteinuria of pre-eclampsia leads to hypoalbuminaemia
Leads to oedema
Fluid loss into 3rd space = hypovolaemia
Hypovolaemia = lack of perfusion to the vital organs (starts at kidneys and eventually effects the brain)
Hypo-perfusion to the brain 🡪 seizures

409
Q

How does pre-eclampsia affect the coagulation system?

A

Placenta ischaemia occurs due to inadequate invasion of spiral arteries
Placenta then produces thromboplastins – which can lead to DIC
You also get low platelets in pre-eclampsia

410
Q

What is HELLP syndrome?

A

H – haemolysis
E L– elevated liver enzymes (ALT and AST)
L P – low platelets

411
Q

What are the symptoms of pre-eclampsia?

A

Oliguria
CNS – visual changes, headache, blind spots in vision, change in mental status
Oedema – rings hard to get off, marks left in ankles by socks
Epigastric or RUQ pain – hepatic swelling and inflammation, liver capsule stretches
Rapid weight gain

412
Q

What are the signs of pre-eclampsia?

A

Raised blood pressure ( >140/90)
Proteinuria (+++ on dipstick if severe)
Papilloedema
RUQ tenderness
Ankle clonus - NB brisk reflexes are normal during pregnancy but ankle clonus is not

413
Q

What investigations would you do if you suspect pre-eclampsia?

A

BP
Urine dip-stick
Haemoglobin
Platelets
LFTs
Protein:creatinine ratio
Date pregnancy and assess foetal growth

414
Q

What test result is diagnostic for pre-eclampsia?

A

Protein-creatinine ratio of OVER 30

415
Q

How do you treat pre-eclampsia?

A

Admit to hospital
Only cure is to deliver the baby
If not at term – give hydrazaline or labetelol to lower BP
Give magnesium sulphate to prevent seizures
Induction of labour if safe
If pre-eclampsia very early onset then may need to terminate the pregnancy to save mum

416
Q

What prophylactic treatment should you give in subsequent pregnancies for someone with a history of pre-eclampsia?

A

Aspirin 75mg

From 10 – 36 weeks’ gestation

(the spiral arteries form around 12 weeks so aspirin is thought to help them develop properly)

417
Q

Which other high risk ladies should be given aspirin during pregnancy?

A

High BMI
Renal disease
Known hypertension

418
Q

Define premature infant

A

An infant born before 37 weeks’ gestation

419
Q

Define small for dates

A

Below the 10th centile for their gestational age

(so do need to consider their gestational age and then plot on the growth charts)

Also known as small for gestational age (SGA)

420
Q

What are the risk factors for a SGA baby?

A

Placental problems – pre-eclampsia, abruption
Foetal factors – genetic abnormalities (trisomies, other syndromes such as Turner’s)
Multiple pregnancy
Maternal risk factors – smoking, age >40, cocaine use, BMI <20
Previous SGA baby
Antepartum bleeding
Low PAPP-A

421
Q

Define large for dates

A

Above the 90th centile for their gestational age

422
Q

Define low birth weight

A

A baby born with a weight < 2.5 kg

This measurement is regardless of their gestational age (although premature babies are more likely to have low birth weight)

423
Q

Define macrosomia

A

A baby born weighing > 4kg

Regardless of gestational age

424
Q

What are the causes for large babies?

A

Constitutionally large – familial (mum and dad would’ve been big babies too)

Maternal diabetes

Obesity

425
Q

Define intrauterine growth restriction

A

A baby which has not maintained its growth potential

i.e. it drops below the centile line it was following

Most common cause = placental issue (smoking, pre-eclampsia)

426
Q

What are the risk factors for pre-term delivery?

A

No apparent RF in 50%
Antepartum haemorrhage (placenta praevia, abruption, etc.)
Mulitple pregnancy – very unlikely to reach term with more than one baby in there
Race
Previous pre-term birth
Genital infection or systemic infection
Cervical weakness (can be treated with a cervical stitch)

427
Q

What are the major complications of premature delivery (to the baby)?

A

Developmental delay
Cerebral palsy
Chronic lung disease
Retinopathy of prematurity
Necrotising enterocolitis

428
Q

How have improvements in neonatal intensive care contributed to survival in premature babies?

A

Neonatal steroids – given to mums expected to go into pre-term labour
Artificial surfactant
Ventilation
Nutrition
Antibiotics

429
Q

What are the diagnostic criteria for preterm labour?

A

Persistent uterine activity

PLUS change in cervical dilatation and/or effacement

430
Q

Name some ways that preterm labour can be predicted

A

Measure cervical length with transvaginal USS

Foetal fibronectin levels

431
Q

How to reduce the risk of pre-term birth in those at increased risk?

A

Cervical stitch if length < 3cm

IM or pessary progesterone can help reduce risk

432
Q

How to treat someone who is already in pre-term labour?

A

Admit to hospital and contact consultant obstetrician and neonatologist

Tocolytic drugs – salbutamol (this will delay it slightly but nothing can reverse labour once it has started)

Corticosteroids – to protect the baby’s lungs

433
Q

Define puerperium

A

From delivery of the placenta to 6 weeks following birth

434
Q

Define postnatal period

A

The period under which the woman and baby are still under midwife care

For at least 10 days and for as long as the midwife feels necessary

435
Q

Define maternal death

A

The death of a women during or up to 6 weeks after her pregnancy

Due to causes related to or aggrevated by the pregnancy

436
Q

Define direct maternal death

A

Mother dying as a result of obstetric complication (haemorrhage, PE)

437
Q

Define indirect maternal death

A

Death resulting from pre-existing disease or disease that developed during the pregnancy, but not as a direct result from obstetric causes

i.e. heart disease

438
Q

What are the signs of SIRS?

A

3 T’s, white with sugar:

Temperature (>38 or <36 *C)
Tachycardia (>90bpm)
Tachypnoea (>20 breaths per minute)
White blood cell count (< 4 or >12)
Sugar – blood glucose (> 7.7mmol in the absence of DM)

439
Q

What is the leading cause of death in the post natal period?

A

Suicide

440
Q

What are the risk factors for post natal depression?

A

Any past medical history of a mental health problem
Poor social networks/relationships
Unemployed
Poor living conditions/social isolation
Family history of mental health problems
History of abuse
Carer for other adults or children

441
Q

What are the symptoms of post-natal depression?

A

Low mood
Loss of energy
Anhedonia (loss of interest)
Expressing feelings of guilt about not loving the baby
Not wanting to hold/touch/feed the baby
Loss of appetite
Change in sex drive
Social withdrawal

442
Q

How does the foetus adjust to reduced placental function and perfusion?

A

Polycythaemia – to try and compensate for the reduced oxygen supply from the mother, the baby develops more RBCs

Blood redistribution – “head sparing effect” – blood is directed to the brain, heart and kidneys which means that their head and abdominal circumference may be bigger than their arms and legs and overall length

443
Q

How does polycythaemia present?

A

Neonatal jaundice
Need to follow-up to prevent kernicterus

444
Q

Name some problems at birth associated with IUGR

A

Hypogylcaemia – blood directed away from liver to brain and kidneys = glycogen stores not developed adequately
Increased risk of NEC – blood supply to bowel reduced for head sparing
Neonatal jaundice due to polycythaemia
Hypothermia – no fat stores developed if growth restricted so cannot thermoregulate
HIE/CP – if brain isn’t spared
Respiratory problems - if kidneys don’t get enough perfusion, not enough urine is produced = less amniotic fluid = inadequate lung developement

445
Q

What are the main factors that affect foetal growth in utero?

A

Adequate blood flow from placenta
Adequate maternal nutrient intake
Foetal physiology – ability to metabolise and utilise nutrients from the mother – GLUCOSE is the most important
Genetic factors

446
Q

How should SGA babies be managed during the pregnancy?

A

Growth scans every 2-3 weeks

Umbilical artery doppler to see whether the baby is getting enough blood

Offer corticosteroids for foetal lung maturity up to 35+6 weeks

447
Q

How should macrosomic babies be managed during the pregnancy?

A

Regular growth scans to assess progress

Advise mother to have a low sugar diet

Consider need for caesarean section delivery if the baby looks extremely large

448
Q

How can a diagnosis of foetal growth restriction be made?

A

Baby measured on USS

Symphysial-fundal height measured

Plot on the personalised growth chart for this lady – the baby may have dropped below its growth potential on the centile lines which could indicate growth restriction (or just < 10th centile if small for dates)

449
Q

What are some important Qs to ask in the history if you think someone’s baby is growth restricted?

A

Is the baby moving? – lack of movements is very worrying
Smoking/using cocaine
Any previous SGA babies?
Screen for signs of pre-eclampsia – urine, BP, headaches, ankle swelling?
Has the lady had any infections during pregnancy?
Has the lady had Down’s syndrome screening?

450
Q

How would a diagnosis of large for dates be made?

A

Estimated foetal weight on USS

Symphysial fundal height measured

Both plotted on personalised growth chart for this pregnancy - if >90th centile then large for dates

451
Q

What investigations would you do for someone with a large for dates baby?

A

Blood glucose test for diabetes
USS
Ask about previous pregnancies – did this lady have a big baby before?
Repeat ultrasound
Vital signs
Look at the amniotic fluid index

452
Q

What is the definition of a miscarriage?

A

The loss of a pregnancy before 24 week’s gestation

After this = would be a still birth

453
Q

What % of pregnancies miscarry?

A

15-20%

454
Q

What are 2 parental risk factors associated with miscarriage?

A

Maternal age >35 years

Paternal age >40 years

455
Q

What are some causes of miscarriage?

A

Foetal chromosomal abnormalities that are incompatible with life

Maternal illness – infections, pyrexia

Trauma

456
Q

What is the definition of recurrent miscarriage?

A

The loss of ≥ 3 consecutive pregnancies

Before 24 weeks’ gestation

457
Q

What are some causes of recurrent miscarriage?

A

50% unknown
Chronic maternal disease – poorly controlled DM, SLE
Anti-phospholipid syndrome
Abnormality of the uterus making it unable to support foetal development
Infection
Parental chromosomal abnormality – balanced Robertsonian translocation
Thrombophilia – factor V leiden deficiency, protein S an C deficiency

458
Q

What serum markers would you look for if you suspected anti-phospholipid syndrome?

A

Lupus anticoagulant antibodies

Anti-cardiolipin antibodies

Phospholipid antibodies

459
Q

What is a threatened miscarriage?

A

Mild symptoms

Cervical os closed

75% will settle

460
Q

How would you classify an inevitable miscarriage?

A

Severe symptoms

Cervical os is open – if you can pass 1 finger through the cervical os then miscarriage is inevitable

461
Q

What is an incomplete miscarriage?

A

Most of the products have already been passed

But there are some retained products of conception

462
Q

What is a missed miscarriage?

A

The foetus dies in utero without any symptoms of a miscarriage

Picked up on USS – the foetus will appear on the scan to be dated before the actual date of the pregnancy

E.g. 12 week scan finds a 9 week foetus with no heartbeat – missed miscarriage at 9 weeks

463
Q

How does a miscarriage present?

A

PV bleeding

464
Q

How do you investigate a miscarriage?

A

SPECULUM EXAMINATION – most important examination as it allows you to see the cervical os

Digital vaginal examination

USS

465
Q

How is a miscarriage managed?

A

Expectant management – let nature take its course and clear the foetus naturally

Ergometrine – can help stop perfuse bleeding

Medical management – mifepristone followed by misoprostol (bleeding may continue for ~3 weeks after)

Surgical management – if there is unacceptable bleeding, pain or significant retained products seen on USS

466
Q

How should recurrent miscarriage be investigated?

A

Refer to specialist recurrent miscarriage clinic
Test for anti-phospholipid antibodies
Thrombophilia screening
Pelvic USS to look at the structure of the uterus
Karyotype foetal products after 3rd foetal loss – if chromosomal abnormality is found then karyotype the peripheral blood of the parents

467
Q

What is the main differential for bleeding in early pregnancy?

A

Miscarriage

Ectopic pregnancy

468
Q

Define ectopic pregnancy

A

When a fertilised ovum implants outside the uterine cavity

469
Q

What is the most common site for an ectopic pregnancy?

A

In the ampulla of the fallopian tube

470
Q

What are the risk factors for an ectopic pregnancy?

A

Previous ectopic pregnancy
Pelvic inflammatory disease
Damage to the tubes – i.e. from PID or surgery (adhesions etc.)
Endometriosis
Copper coil
Progesterone only pill
Smoking
Tubal ligation

471
Q

How does an ectopic pregnancy present?

A

NB – ALWAYS consider ectopic in a sexually active woman with
abdominal pain, bleeding, fainting, diarrhoea or vomiting

Uncertain LMP and 6-8 weeks amenorrhoea
Abdominal pain, classically unilateral
Vaginal bleeding
Diarrhoea and vomiting
Dizziness and fainting
Shoulder pain due to haemoperitoneum - irritates the diaphragm

472
Q

How should an ectopic pregnancy be investigated?

A

Pregnancy test – urinary B-HCG
Vaginal and speculum examination – cervical motion tenderness/cervical excitation
Ultrasound scan
FBC
Group and save

473
Q

How should an ectopic pregnancy be managed?

A

Expectant management if HCG is falling, mild symptoms, no foetal heart activity on USS, woman is haemodynamically stable

Medical management – methotrexate (teratogenic so ensure woman on effective contraception for 3 months afterwards)

Surgical management – laparoscopy. If contralateral tube is healthy, then remove the whole tube that had the ectopic (salpingectomy). If Other tube unhealthy - salpingotomy (removal of the ectopic but leave the tube in place)

474
Q

What are some side effects of methotrexate?

A

Conjunctivitis
Stomatitis
Diarrhoea
Abdominal pain

475
Q

What signs/symptoms do you get with a molar pregnancy?

A

Aka hydatidiform mole
Uterus bigger than expected for gestation
Hyperthyroidism
Painless vaginal bleeding
Excessive morning sickness
High serum HCG (which causes hyperemesis gravidum and thyrotoxicosis)

476
Q
A

Phase 3a (11 decks)

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