Obstetrics and gynaecology Flashcards

(557 cards)

1
Q

How is gestation estimated? What is the most accurate method?

A

Ultrasonography within the first 13 6/7 weeks of gestation is most accurate method to establish/confirm gestational age

Using LMP:
Expected date of delivery = 280 days (40 weeks) from 1st day of last menstrual period

Naegele’s rule
EDD = LMP + 1 year and 7 days - 3 months

If IVF - days since oocyte retrieval or co-incubation + 14 days

Physical examination:
After 20 weeks - pubic symphysis to fundal height in cm should correlate with week of gestation

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2
Q

Describe the normal process of fertilisation and implantation in pregnancy

A

Fertilisation in fallopian tube
Transportation of embryo along tube
Implantation in endometrium occurs approximately 6 days post-fertilisation

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3
Q

Describe the hormonal changes which occur in normal early pregnancy

A

HCG rises exponentially from 4-12 weeks gestation, then falls and levels off at 24 weeks until birth

Progesterone and oestrogen rise from early gestation until birth, initially progesterone higher then oestrogen higher

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4
Q

Describe the normal physiological changes which occur in the respiratory system in pregnancy and the clinical consequences of these changes

A

Diaphragm pushed up so decreased expiratory reserve volume, giving the sensation of SOB (increased tidal volume balances out so sensation only)

Reduced CO2 (to draw CO2 out of baby’s blood) so reduced bicarb = compensated respiratory alkalosis

Increased respiratory rate

Increased laryngeal oedema - difficult intubation

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5
Q

Describe the normal physiological changes which occur in the cardiovascular system in pregnancy and the clinical consequences of these changes

A

Reduced systemic and pulmonary vascular resistance, BP can fall in 2nd trimester and rise slightly in late pregnancy

Cardiac output and stroke volume peak by week 16 - highest risk if pre-existing CVD

Drop in BP causes RAAS activation, leading to sodium and water retention - blood volume increased, physiological (dilutional) anaemia

Constriction of peripheral circulation - Raynaud’s

Can have ejection systolic murmur/third heart sound

ECG’s look different due to different position of heart

Increased risk varicose veins

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6
Q

Describe the normal haematological changes which occur during pregnancy

A

Increased plasma volume - dilutional anaemia

EPO release - increased RBC but haemoglobin still low

Modest leukocytosis

High demand for additional iron - serum iron falls, transferrin and total iron binding capacity rise

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7
Q

Describe the normal physiological changes which occur in the urinary tract during pregnancy and the clinical consequences they have.

A

Increased blood volume and cardiac output - increased renal blood flow - increased GFR - increased excretion (frequent urination), reduced levels of urea, creatinine, urate and bicarbonate

Mild glycosuria/proteinuria as increase in GFR can exceed ability for reabsorption

Increased water retention, reduction in plasma osmolality

Smooth muscle of renal pelvis and ureter relaxes and dilates, kidneys increase in length and ureters become longer, more curved (increased risk UTI) and increase in residual urine volume

Bladder smooth muscle relaxes, increased capacity, increased risk UTI

Mechanical pressure of uterus on bladder - increased urination

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8
Q

Describe the normal physiological changes in the GI tract during pregnancy and the clinical consequences these have

A

Relaxation of smooth muscle - decreased LOS pressure, decreased gastric peristalsis, delayed gastric emptying, increased small and large bowel transit times, reduced gallbladder contraction

= GORD, nausea and vomiting, constipation, gallstones

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9
Q

Describe the normal physiological changes which occur in the skin during pregnancy and the clinical consequences these can have

A

Hyperpigmentation of umbilicus, nipples, abdominal midline (linea nigra) and face
Hyperdynamic circulation and high levels oestrogen - spider naevi and palmar erythema
Striae gravidarum (stretch marks)

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10
Q

Describe the normal physiological changes in the musculoskeletal system which occur during pregnancy and the clinical consequences these can have

A

Increased ligament laxity due to relaxin contribute to back pain and pubic symphysis dysfunction
Shift in posture with exaggerated lumbar lordosis - typical gait of pregnancy

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11
Q

Define the terms:

Miscarriage
Stillbirth
Livebirth

A

Miscarriage - any pregnancy loss before 24 weeks
Stillbirth - any fetus born dead at or after 24 weeks gestation
Livebirth - a fetus which shows signs of life after delivery at any gestation

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12
Q

Define these types of miscarriage:

Threatened
Inevitable
Incomplete
Complete
Delayed/missed/early embryonic demise
Septic
Recurrent

A

Threatened - painless bleeding with continuing intrauterine pregnancy, before 24 weeks, cervix closed

Inevitable - bleeding with non-continuing intrauterine pregnancy, cervix may be open

Incomplete - retained products of conception remain in uterus

Complete - full miscarriage has occurred, no products of conception left in uterus

Delayed/missed/early embryonic - fetus died in-utero prior to 24 weeks gestation, no symptoms

Septic - miscarriage complicated by intrauterine infection

Recurrent - 3 or more consecutive miscarriages

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13
Q

Describe the methods for estimation of gestational age by US in each trimester

A

First trimester - crown-rump length
Second trimester - head circumference, femur length
Third trimester - head circumference, femur length

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14
Q

List causes and risk factors for miscarriages

A

Spontaneous usually due to embryonic abnormalities - chromosomal abnormalities, placental defects
No cause found in 50% of recurrent miscarriages

Causes of recurrent:
Thrombophilic abnormalities - factor V leiden mutation, prothrombin gene mutation
Immunological abnormalities - antiphospholipid syndrome
Anatomical/structural - uterine abnormalities (bicornuate or arcuate uterus), cervical abnormalities (cervical incompetence)
Genetic abnormalities
Endocrinological - PCOS, hyperprolactinaemia, thyroid disease, poorly controlled DM
Infective causes - bacterial vaginosis

Risk factors
Maternal age
Previous miscarriages
Occupational/environmental factors - pesticides, radiation
Advanced paternal age
Lifestyle - stress, obesity, smoking

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15
Q

Describe the clinical presentation of miscarriage

A

Pregnant - positive pregnancy test or symptoms of pregnancy (amenorrhoea, missed period, breast tenderness)

Vaginal bleeding (brown spotting to heavy +/- tissue), lower abdominal cramping or backache

Can be asymptomatic

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16
Q

What is the differential diagnosis for miscarriage?

A

Ectopic pregnancy
Molar pregnancy - heavy, prolonged bleeding, uterus large for dates

Pregnancy related:
Ruptured ovarian corpus luteal cyst
Adnexal torsion
Pregnancy-related degeneration of a fibroid

Non-pregnancy related:
Cervicitis, cervical ectropion, cervical polyps
Cancer of cervix, vagina, vulva
Haemorrhoids
Urethral bleeding, UTI
Vaginitis
MSK pain
Constipation
IBS
PID
Appendicitis
Renal colic
Bowel obstruction
Adhesions
Ovarian cyst - torsion, rupture, bleeding
Torsion of fibroid
Pelvic vein thrombosis

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17
Q

Describe assessment/investigations for suspected miscarriages

A

A-E - haemodynamically stable?
Removal of POC (speculum)

US - transabdominal, transvaginal (investigation of choice for diagnosis)

Examination of POC

Serum HCG tracking

Assess FBC, group and save/crossmatch

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18
Q

Describe the ultrasound findings used to diagnose miscarriages

A

No fetal heart activity with crown-rump length >7mm on transvaginal scan - repeat scan after 1 week to confirm non-viable pregnancy

Empty sac (no fetal pole) when gestational sac diameter >25mm on transvaginal scan - repeat scan after 1 week to confirm anembryonic pregnancy

Retained tissue seen in incomplete miscarriage

Empty uterus - complete passage of tissue (complete miscarriage), pregnancy too early to visualise or ectopic pregnancy

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19
Q

What are the options for management of miscarriages? When is each option appropriate?

A

Expectant management - give 1-2 weeks for miscarriage to occur spontaneously
Used if <6 or >6 weeks gestation if no pain and no other complications or risk factors

Medical/surgical - if increased risk of haemorrhage/infection, previous adverse experience of pregnancy (e.g. stillbirth, miscarriage)

Medical management - misoprostol (oral or vaginal)

Surgical - misoprostol to soften cervix then manual or electric vacuum aspiration

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20
Q

Describe the mechanism of action and side effects of misoprostol

A

Prostaglandin analogue - binds and activates prostaglandin receptors

Prostaglandins soften cervix and stimulate uterine contractions

Side effects:
Heavier bleeding
Pain
Vomiting
Diarrhoea

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21
Q

Describe the methods of surgical management of miscarriages and when they are appropriate

A

Manual vacuum aspiration - local anaesthetic applied to cervix, syringe through cervix into uterus and aspiration of contents of uterus

Electric vacuum aspiration - general anaesthetic, cervix dilated and products of conception removed through cervix using electric-powered vacuum

Manual - <10 weeks gestation, parous
If products of conception retained or ongoing symptoms after expectant/medical management
Definite indications - infection of retained tissue, haemodynamic instability, gestational trophoblastic disease

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22
Q

When is anti-rhesus prophylaxis required in miscarriages? When is it not required?

A

Rhesus negative women
Surgical management of miscarriage <12 weeks
Any potential sensitising event >12 weeks

Not required:
Threatened or complete miscarriage
Medical management of miscarriage

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23
Q

How is an incomplete miscarriage managed? Why?

A

Medical management - misoprostol
Surgical management - evacuation of retained products of conception (dilation of cervix and removal through vacuum aspiration and curettage)

Retained product are infection risk

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24
Q

What is a key complication of evacuation of retained products of conception?

A

Endometritis

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25
Describe the success rates of different management options for miscarriages
Expectant - 60% Medical - 80-90% Surgical - 97%
26
How should women be followed up after expectant management of miscarriage?
Return if bleeding continues or pain develops Repeat urine pregnancy test after 7-10 days, return if positive, if negative miscarriage confirmed
27
List risk factors for ectopic pregnancy
Previous ectopic pregnancy Damage to fallopian tube - PID, tube surgery History of infertility Assisted reproduction techniques - IVF Smoking Maternal age >35 Multiple sexual partners Contraception - if contraception failure higher risk of ectopic pregnancy with IUD, POP, sterilisation compared to other methods of contraception
28
Describe the clinical presentation of ectopic pregnancy
Positive pregnancy test or symptoms of pregnancy (missed period etc.) Usually presents 6-8 weeks gestation Can be asymptomatic Lower abdominal/pelvic pain Can have referred shoulder tip pain (peritonitis) Vaginal bleeding - brown spotting to heavy Pain with opening bowels/urination Cervical motion tenderness Collapse/hypovolaemic shock
29
How is a suspected ectopic pregnancy investigated?
Transvaginal US is investigation for diagnosis Serum hCG Assess FBC, group and save/crossmatch
30
Describe US findings in ectopic pregnancies
Gestational sac with fetal pole in fallopian tube May just be non-specific mass in tube - blob/bagel/tubal ring sign Empty uterus Fluid in uterus - pseudogestational sac
31
How are serial hCG measurements used to dictate management of pregnancy of unknown location?
Measure 48 hours apart Used if PUL on US and patient stable Increase >66% - likely intrauterine pregnancy, US to determine location 7-14 days later, if hCG >1,500 should be visible <66% increase or <50% decrease - ectopic, requires close monitoring/management >50% decrease - failing PUL, repeat pregnancy test in 2 weeks to confirm miscarriage
32
Describe emergency and non-emergency management of ectopic pregnancies
Emergency: A-E resuscitation Early involvement from gynaecology, anaesthetics, haematology (+ blood) Theatre to remove source of bleeding and stabilise Non-emergency: Conservative Medical - methotrexate Surgical
33
When is conservative management of ectopic pregnancy appropriate? What does this involve?
Size <35mm Unruptured Asymptomatic No fetal heartbeat hCG <1,000 Compatible if another intrauterine pregnancy Closely monitor patient over 48 hours, if hCG levels rise or symptoms manifest need to intervene
34
When is medical management of ectopic pregnancy appropriate? What does it involve?
Size <35mm Unruptured No significant pain No fetal heartbeat hCG <5000 Not suitable if intrauterine pregnancy Able to return for follow up No medical contraindications - anaemia, renal/hepatic impairment, UC, peptic ulcer Methotrexate
35
When can a patient become pregnant again after medical management of ectopic pregnancy? Why?
12 weeks after hCG <5 Need to replenish folic acid
36
What are the key risks and side effects of medical management of ectopic pregnancy?
7% risk fallopian tubal rupture Side effects Vaginal bleeding Nausea and vomiting Abdominal pain Stomatitis
37
When is surgical management of ectopic pregnancy appropriate?
Size >35mm Rupture Pain Visible fetal heartbeat HCG >5,000 Compatible with another intrauterine pregnancy
38
Describe the options for surgical management of ectopic pregnancy
Laparoscopy or laparotomy depending on clinical situation 1st line - salpingectomy (if no other risk factors for infertility) Salpingotomy if risk factors for infertility e.g. contralateral tube damage 1 in 5 need further treatment - methotrexate or salpingectomy
39
Which women need Anti-D in management of ectopic pregnancy? Which don't?
Rhesus negative, surgical management - need anti-D Conservative or medical management - don't need anti-D
40
Describe the risk of recurrence of ectopic pregnancies
18.5% risk recurrence after ectopic pregnancy
41
Define gestational trophoblastic disease
A group of conditions characterised by abnormal proliferation of trophoblastic tissue with production of HCG Includes: Pre-malignant conditions (more common) - partial molar pregnancy and complete molar pregnancy Malignant conditions (rarer) - invasive mole, choriocarcinoma, placental trophoblastic site tumour, epithelioid trophoblastic tumour
42
What is a hyatidaform mole?
Pre-malignant tumour within uterus arising from an abnormality in chromosomal number during fertilisation Partial molar pregnancy - one ovum with 23 chromosomes fertilised by two sperm, each with 23 chromosomes, resulting in cells with 69 chromosomes (triploidy), may exist with viable fetus (triploid placenta only) Complete molar pregnancy - one ovum without any chromosomes is fertilised by one sperm which duplicates or by two different sperm, leading to 46 chromosomes of paternal origin
43
Describe the malignant types of gestational trophoblastic disease - tissue of origin, common presentations
Choriocarcinoma - malignancy of trophoblastic cells of placenta, commonly co-exists with molar pregnancy, metastasises to lungs Placental site trophoblastic tumour - malignancy of intermediate trophoblasts, normally responsible for anchoring placenta to uterus, can occur after normal pregnancy (most commonly), molar pregnancy or miscarriage Epithelioid trophoblastic tumour - malignancy of trophoblastic placental cells, can be difficult to distinguish from choriocarcinoma, mimics cytological features of squamous cell carcinoma
44
List risk factors for gestational trophoblastic disease
Maternal age <20 or >35 Previous gestational trophoblastic disease Previous miscarriage OCP use Asian ethnicity
45
Describe the clinical features of gestational trophoblastic disease
Early pregnancy: Vaginal bleeding Abdominal pain Larger uterus than expected for gestation with a soft, boggy consistency Shedding of molar vesicles PV Later symptoms: Hyperemesis - increased bHCG Hyperthyroidism - bHCG stimulates thyroid Anaemia Large for date uterus
46
How should suspected gestational trophoblastic disease be investigated?
Urine bHCG - confirm pregnancy Blood bHCG - elevated at diagnosis, used to monitor US - complete mole has granular/snowstorm appearance with central heterogeneous mass and surrounding multiple cystic areas/vesicles Histological examination of POC If metastatic spread - staging investigations e.g. MRI, CT, US
47
How is gestational trophoblastic disease managed?
Register with GTD specialist centre for follow-up and monitoring in future pregnancies Molar pregnancy Suction curettage more effective for complete and non-viable partial moles Partial mole with fetal development - medial evacuation with urinary bHCG post-treatment Histological assessment of POC Malignant GTD - specialist centre treatment, chemotherapy +/- surgery
48
Why is medical management of molar pregnancies not recommended?
Theoretical risk of embolisation of trophoblastic tissue if managed with oxytocic agents
49
Is Anti-D required for gestational trophoblastic disease?
If mother Rh negative and surgical management
50
Define hyperemesis gravidarum. What causes it?
Persistent vomiting in pregnancy causing weight loss (more than 5% of body mass), dehydration and electrolyte imbalance High bHCG levels - stimulates chemoreceptor trigger zone in brainstem
51
List risk factors for hyperemesis gravidarum
First pregnancy Previous history hyperemesis gravidarum Raised BMI Multiple pregnancy Gestational trophoblastic disease
52
How is the severity of hyperemesis gravidarum measured?
Pregnancy-Unique Quantification of Emesis (PUQE) <7 - mild 7-12 - moderate >12 - severe
53
When does nausea and vomiting of pregnancy typically occur? When should another diagnosis be considered?
4-7 weeks Consider alternative if symptoms start after 10+6 weeks
54
How should hyperemesis gravidarum be investigated?
Weight Urine dipstick - ketonuria Mid-stream urine FBC U&Es - hypokalaemia, hyponatraemia, dehydration Blood glucose - exclude diabetic ketoacidosis if diabetic Exclude other causes e.g. LFTs, amylase, TFTs, ABG US - confirm gestation, exclude multiple pregnancy/trophoblastic disease
55
How is hyperemesis gravidarum managed?
Mild - in community with oral antiemetics, hydration, dietary advice, reassurance Moderate - ambulatory day care for IV fluids, parenteral antiemetics, thiamine, until ketonuria resolves Severe - inpatient management IV rehydration with electrolyte repletion as required (add potassium chloride) H2 receptor antagonists/PPI for reflux, oesophagitis, gastritis Thiamine - prevent Wernicke's Thromboprophylaxis
56
Which antiemetics are recommended for hyperemesis gravidarium?
First line - cyclizine, prochlorperazine, promethazine, chlorpromazine Second line - metoclopramide (max. 5 days due to risk of EPS), domperidone, ondansetron Third line - hydrocortisone IV (convert to prednisolone PO once symptoms resolve, reduce dose according to response)
57
Define infertility
Failure to achieve pregnancy after 12 months or more of regular unprotected sex between a man and a woman Primary - couple never able to conceive Secondary - couple cannot get pregnant again, despite previously having been able to without any difficulty
58
Describe the incidence of infertility in the UK
1 in 7 couples will struggle to conceive naturally
59
List causes of infertility in terms of basic reproductive physiology
FEMALE Disorders of ovulation - hypothalamic-pituitary failure, hypothalamic-pituitary-ovulation dysfunction, ovarian failure, hyperprolactinaemia, pituitary tumours Tubal causes - PID, sterilisation, endometriosis, pelvic surgery Uterine/peritoneal causes - endometriosis, pelvic/cervical surgery, fibroids, Asherman's syndrome MALE Oligospermia - <15 million sperm per ml Teratospermia - <4% normal morphology Asthenospermia - <32% sperm motility Azoospermia - no sperm in ejaculate Obstructive infertility - previous vasectomy, cystic fibrosis, ejaculatory duct obstruction, epididymal obstruction Non-obstructive infertility - hormonal (hypogonadotropic hypogonadism, hyperprolactinaemia), varicocele, genetic causes (Klinefelter's, androgen insensitivity syndrome, Kallmann syndrome), cryptorchidism, previous testicular trauma (e.g. torsion), malignancy Coital infertility - ED, premature ejaculation, anejaculation (primary or secondary), retrograde ejaculation, penile deformities (Peyronie's, hypospadies)
60
Who should be investigated for infertility?
Trying to conceive for 1 year after frequent (every 2-3 days) unprotected sexual intercourse OR Investigation after 6 months if: Woman >36 Known cause of infertility History of predisposing factors
61
What advice should be given to couples trying to conceive?
Regular (every 2-3 days) sexual intercourse throughout cycle Preparation for pregnancy e.g. folic acid daily Smoking cessation for men and women Avoid drinking alcohol excessively (women should avoid entirely) Women should aim for BM 19-25 Reduce stress No need to time intercourse
62
How should infertility be investigated?
BMI Chlamydia screening Semen analysis Female hormone testing - serum LH and FSH (day 2-5 of cycle), serum progesterone (day 21 or 7 days before end of cycle), anti-Mullerian hormone (ovarian reserve), TFTs, prolactin Rubella immunity in mother US pelvis - polycystic ovaries or structural abnormalities Hysterosalpingogram - patency of fallopian tubes Laparoscopy and dye test - patency of fallopian tubes, adhesions and endometriosis Male genetic testing Male US - structural abnormality Male hormone analysis - testosterone, FSH, LH, prolactin
63
Describe management of female factor infertility
Medical - stimulate ovulation Clomiphene - anti-oestrogen, increases GnRH, FSH and LH Letrozole - aromatase inhibitor with anti-oestrogen effects Gonadotrophins - if clomiphene resistant infertility Pulsatile GnRH Dopamine agonists - if secondary to hyperprolactinaemia Ovarian drilling for PCOS Surgery Tubal surgery if mild tubal disease - catheterisation or cannulation Uterine surgery for polyps, adhesions or structural abnormalities
64
How is male factor infertility managed?
Medical Gonadotrophins for hypogonadotropic hypogonadism Surgical Correction of blockage in genital tract
65
List options for assisted conception
Surgical sperm retrieval - if blockage in male genital tract, collect sperm directly from epididymis Intrauterine insemination - partner or donor sperm, injected into uterus during natural or stimulated cycles In vitro fertilisation - used for more severe tubal disease with unexplained fertility, or other treatments unaffective Intracytoplasmic sperm injection - low sperm count or sexual dysfunction Donor inseminsation - persistent azoospermia Oocyte donation - ovarian failure or absence of ovaries Embryo donation
66
Define ovarian hyperstimulation syndrome, describe the cause and features
Complication of some infertility treatments - gonadotropin or hCG treatment (e.g. in IVF) High levels of vasoactive substances (e.g. VEGF) with multiple luteinised cysts resulting in increased membrane permeability and loss of fluid from intravascular compartment Features: Mild: Abdominal pain Abdominal bloating Moderate: Nausea and vomiting Ascites Severe: Oliguria High haematocrit Hypoproteinaemia Critical: Thromboembolism Acute respiratory distress syndrome Anuria Tense ascites
67
Describe the process of egg retrieval for IVF. What are the potential side effects?
1. GnRH analogue - down-regulation of pituitary 2. FSH - stimulate ovulation 3. hCG - egg maturation 4. Egg retrieval - US guided needle through vagina Risks/side effects - ovarian hyperstimulation syndrome, vaginal bleeding, cramps, multiple births, ectopic pregnancy
68
An ectopic pregnancy in which area of the fallopian tube is highest risk for rupture?
Isthmus
69
List the types of cysts which affect the ovaries and describe their malignant potential
Non-neoplastic (no malignant potential) Functional: Follicular cysts - developing follicle in first half of menstrual cycle Corpus luteal cysts - luteal phase after corpus luteum is formed Pathological Endometrioma - chocolate cyst, in endometriosis Polycystic ovaries - US appearance of >12 antral follicles in ovary or volume >10ml Theca lutein cyst - due to raised hCG, resolves with normal hCG Mullerian inclusion cyst - implantation of tubal epithelium in ovary at ovulation, can develop into epithelial ovarian cancer
70
List the cancers which affect the ovaries, if they are benign or malignant and the cells they originate from
71
Describe the incidence of ovarian cancer
6th most common cancer in women in the UK, 2nd most common gynaecological cancer Highest incidence in 75-79 year olds Poor prognosis if advanced - 10% survival stage IV
72
List risk factors and protective factors for ovarian cancer
Risk factors - more ovulations Nulliparity Age - peak 75 Early menarche Late menopause Oestrogen only HRT Smoking Obesity Protective factors - less ovulations Multiparity Combined oestrogen and progesterone contraception Breastfeeding Genetic risk Family history BRCA1&2 Hereditary nonpolyposis colorectal cancer (Lynch II syndrome)
73
Describe the clinical presentation of ovarian cancer
Non-specific symptoms GI symptoms - abdominal bloating, early satiety, loss of appetite, constipation or diarrhoea (change in bowel habit) Pelvic pain - chronic or acute (ovarian torsion) Mass effect - urinary symptoms (frequency, urgency), constipation, bowel obstruction, abdominal/pelvic mass, compression of obturator nerve (hip/groin pain) Weight loss Ascites Rarely - paraneoplastic syndrome, pleural effusion (SOB) PV bleeding
74
Describe the referral criteria for suspected ovarian cancer
2-week wait referral if: Ascites Pelvic mass (unless clearly due to fibroids) Abdominal mass Further investigations (initially CA125) in >50 with: New symptoms of IBS/change in bowel habit Abdominal bloating Early satiety Pelvic pain Urinary frequency or urgency Weight loss
75
Which investigations should be used in suspected ovarian cancer?
Initial investigations: CA125 blood test (>35 significant) Pelvic ultrasound CT Histology - CT guided biopsy, laparoscopy or laparotomy Paracentesis (ascitic tap) - test ascitic fluid for cancer cells <40 years with complex ovarian mass - check tumour markers for possible germ cell tumour: Alpha-fetoprotein HCG Calculate risk of malignancy index (RMI)
76
What is the risk of malignancy index for ovarian cancer? How is it calculated?
Can be used as risk stratification tool in patients with suspected ovarian cancer RMI = U (ultrasound score) x M (menopausal status) x CA125 Ultrasound score - 1 point if one feature from list, 3 points if 2 or more features from list: Multilocular cyst Solid areas Metastases Ascites Bilateral lesions Menopausal status 1 point - premenopausal 3 points - postmenopausal RMI >200, refer for CT scan and MDT input
77
What causes raised CA125?
Glycoprotein antigen Elevated in: Malignancies - ovary, pancreas, breast, lung, colon Benign - menstruation, endometriosis, PID, pleural/pericardial effusions, recent laparotomy
78
How are ovarian cancers staged?
FIGO staging Stage IA - confined to one ovary, capsule intact, negative washings Stage IB - both ovaries involved Stage IC - 1 or both ovaries with surgical spill/capsule rupture/malignant cells in pleural fluid or washings Stage IIA - extension to tubes +/- uterus Stage IIB - extension to other pelvic tissues Stage IIIA - positive retroperitoneal LNs +/- microscopic mets beyond pelvis Stage IIIB - macroscopic, extra-pelvic, peritoneal mets <2cm Stage IIIC - macroscopic, extra-pelvic, peritoneal mets >2cm Stage IVA - pleural effusion with positive cytology Stage IVB - hepatic/splenic mesenchymal metastasis, metastasis to extra-abdominal organs including inguinal nodes Basically: Stage 1 - confined to ovary Stage 2 - spread past ovary but within pelvis Stage 3 - spread past pelvis but inside abdomen Stage 4 - spread outside abdomen (distant metastasis)
79
Describe the prognosis of ovarian cancer and the factors which affect prognosis
1 year survival - 70% 5 year survival - 46% 10 year survival - 35% Affected by factors including: Histological subtype Grade Stage Co-morbidities Residual disease at time of surgery
80
List the management options available for ovarian cancer
Surgery - staging laparotomy for those with high RMI and attempt to de-bulk tumour Adjuvant/neoadjuvant chemotherapy - recommended for all except those with early, low grade disease, uses platinum-based compounds Other options - biological therapy (anti-VEGF e.g. bevacizumab), hormonal therapy (tamoxifen/aromatase inhibitor, if platinum resistant)
81
What tests could be used for ovarian cancer screening? Why is this not done?
CA125 - false positive rate too high as raised in many other conditions and not sensitive enough Transvaginal US - difficult to determine from scan if benign or malignant disease, would need to obtain biopsy to determine which would result in many unnecessary surgeries
82
Which women are high risk for ovarian cancer? How can this risk be reduced?
BRCA1(higher risk) or BRCA2 (lower risk), Lynch syndrome, Peutz-Jegher syndrome, Cowden syndrome Recommended for age 35-40 for BRCA1 and 40-45 for BRCA2 Risk reducing surgery - prophylactic bilateral salpingo-oopherectomy, usually laparoscopic Reduces risk of ovarian cancer by 96%, breast cancer by 53%
83
What is the most common kind of endometrial cancer?
Adenocarcinoma
84
List the types of cancer which affect the endometrium and their tissues of origin
Adenocarcinoma - glandular epithelium Type 1 - oestrogen dependent, endometrioid most common (75%) Type 2 - not oestrogen dependent, papillary serous (5%), clear cell (1%) Sarcoma - muscular Leiomyosarcoma most common Uterine carcinosarcoma - rare, aggressive, mixed undifferentiated carcinoma and sarcoma
85
Describe the prevalence of endometrial cancer
Most common gynaecological cancer 13th most common cancer UK 65% increase since 1970s Peak incidence in 70-75
86
Describe the aetiology of and list risk factors for endometrial cancer
Endometrial hyperplasia - precancerous condition, <5% progress to endometrial cancer (same aetiology and risk factors as type 1) Type 1 adenocarcinoma - unopposed oestrogen (oestrogen without progesterone) Causes of unopposed oestrogen: Early menarche or late menopause Low parity PCOS Oestrogen only HRT Tamoxifen Other risk factors: Age Obesity Genetic factors - Lynch syndrome, family history Type 2 diabetes
87
List protective factors against endometrial cancer
Increased progesterone: Combined contraceptive pill Mirena coil Multiparity Cigarette smoking - anti-oestrogenic so protective in post-menopausal women
88
How can the risk of endometrial cancer be reduced in women with PCOS?
Endometrial protection with: Combined contraceptive pill Intrauterine pill e.g. Mirena coil Cyclical progestogens to induce withdrawal bleed Maintain healthy BMI Avoid diabetes
89
Describe the genetic pattern and clinical features of Lynch syndrome
Lynch I - site-specific colorectal cancer Lynch II - autosomal dominant Predisposition to colorectal, breast, ovarian, endometrial, gastric, hepatobiliary, brain, skin, upper urinary tract and small bowel cancers
90
How is Lynch syndrome diagnosed?
Amsterdam criteria: Colorectal cancer in 3 or more relatives Involves at least 2 generations One case before age 50 Familial polyposis excluded
91
Describe the similarities and differences between FAP and Lynch syndrome in terms of genetics, clinical consequences and management
Both autosomal dominant and cause predisposition to colorectal cancer FAP - mutation in APC gene HNPCC - genetic alterations in DNA mismatch repair genes FAP - colon, rectum, bones, eyes, duodenum affected HNPCC - colon, endometrium, ovaries, upper urinary tract, skin, brain, stomach, hepatobiliary system affected FAP - numerous (>100) benign polyps from young age, 100% cancerous transformation HNPCC - few polyps, 50-70% cancerous transformation Management: FAP - prophylactic colectomy for all patients, regular endoscopic check of upper GI tract HNPCC - no prophylactic surgery recommended, regular colonoscopic/gynaecologic examinations recommended
92
Describe the clinical presentation of endometrial cancer
Post-menopausal bleeding - >1 year after periods have stopped Pre-menopausal - irregular, heavy or inter-menstrual bleeding Post-coital bleeding Rarely - Clear/white vaginal discharge Haematuria Anaemia Raised platelet count Abdominal/pelvic mass
93
What is the differential diagnosis for post-menopausal bleeding?
Endometrial causes - endometrial cancer, endometrial hyperplasia without malignancy, benign endometrial polyps, endometrial atrophy Vulval causes - vulval atrophy, vulval pre-malignant or malignant conditions Cervical causes - cervical polyps, cervical cancer
94
What is post-menopausal bleeding?
Unexplained bleeding from the vagina >12 months after menstruation has stopped because of the menopause
95
How should a woman presenting with post-menopausal bleeding be assessed and investigated?
History: Age Timing of menopause Parity Risk factors for endometrial cancer - obesity, PCOS, tamoxifen use, T2DM, HRT, Lynch syndrome Examination - whole lower genital tract including vulva, vagina and cervix, abdominal examination (masses), bimanual examination (size and axis of uterus) Investigations Transvaginal US - endometrial thickness Thickness >3mm or >5mm in COCP/HRT users - endometrial biopsy If high risk or unable to biopsy in clinic - hysteroscopy with biopsy If malignancy confirmed - MRI/CT for staging
96
Describe the staging of endometrial cancer
FIGO staging: Stage I: confined to uterus A - <50% myometrial invasion B - >50% myometrial invasion Stage II: cervical stroma invasion but not beyond uterus Stage III: tumour outside uterus but within pelvis A - invades serosa or adnexa B - vaginal/parametrial involvement C1 - pelvic node involvement C2 - para-aortic node involvement Stage IV - A - invasion into bowel/bladder mucosa B - distant mets including abdominal mets or inguinal lymph nodes
97
Describe the prognosis and survival of endometrial cancer
1 year - 90% survival 5 year - 79% survival 10 year - 78% survival 25% present with stage 4 disease
98
Describe the referral criteria for suspected endometrial cancer
2-week wait for post-menopausal bleeding Referral for TV US in >65 with unexplained vaginal discharge or visible haematuria plus raised platelets, anaemia or elevated glucose levels
99
Describe management of endometrial cancer by stage
Stage 1/2 - usually total abdominal hysterectomy with bilateral salpingo-oophorectomy, take peritoneal washings Stage 2 - may have radical hysterectomy (vaginal tissue around uterus and supporting ligaments of uterus also removed, assessment and removal of pelvic LNs) +/- adjuvant radiotherapy Stage 3 - maximal de-bulking surgery, chemotherapy, radiotherapy Stage 4 - maximal de-bulking surgery although many have palliative approach with low-dose radiotherapy or high dose oral progestogens
100
List side effects of radiotherapy for endometrial cancer
Proctitis Cystitis Lethargy Skin changes
101
Define endometrial hyperplasia, describe the types of endometrial hyperplasia and their malignant potential
Precancerous condition involving thickening of the endometrium Types Hyperplasia without atypia - 1-4% malignant potential Atypical hyperplasia - 23% malignant potential
102
How is endometrial hyperplasia managed?
Progestogens: IUS e.g. Mirena coil Continuous oral progestogens e.g. levorgestrel, medroxyprogesterone
103
What is the most common type of cervical cancer? List other histological types of cervical cancer and their prevalence
70% squamous cell carcinoma 15% adenocarcinoma - mucinous or adenoma malignum 15% mixed type - adenosquamous carcinoma Rarer - endometrioid, clear cell, serous, neuroendocrine
104
Describe the normal histology of the cervix
Inner surface (canal) lined by columnar epithelium Outer surface lined by squamous epithelium Junction is at transformation zone
105
Describe the incidence of cervical cancer by age
50% diagnosed <47, peak in 25-29 and second peak in 80s
106
Describe the aetiology and risk factors for cervical cancer
Usually a progression from cervical intraepithelial neoplasia (CIN) Most caused by persistent HPV infection - risk factors for early HPV infection e.g. early sexual activity, increased numbers of sexual partners, sexual partners who have had more partners, not using condoms Other risk factors: Smoking Other STIs Long-term (>8 years) COCP use Immunodeficiency e.g. HIV Not engaging with cervical screening Increased number of full-term pregnancies Family history Exposure to diethylstilbestrol during fetal development (used to prevent miscarriages before 1971)
107
Describe how HPV causes cancer
Produces E6 protein which inhibits p53 and E7 protein which inhibits pRb (p53 and pRb are tumour suppressor genes)
108
Which strains of HPV are associated with cancer? Which cancers are associated with HPV?
Type 16 and 18 responsible for 70% of cervical cancers HPV also associated with anal, vulval, vaginal, penis and head and neck cancers
109
Describe the clinical presentation of cervical cancer
Often asymptomatic in early stages and detected through screening Abnormal vaginal bleeding - post-coital, intermenstrual or post-menopausal Vaginal discharge - blood-stained, foul smelling Dyspareunia Pelvic pain Weight loss Pelvic masses Abnormal appearance of cervix - ulceration, inflammation, bleeding, visible tumour Advanced disease Oedema Loin pain Rectal bleeding Radiculopathy Haematuria Obstructive renal failure, hydronephrosis
110
Describe the investigation of women presenting with suspected cervical cancer
Pre-menopausal Test for chlamydia - if positive treat, if symptoms persist refer for colposcopy and biopsy, if negative usually require colposcopy and biopsy Post-menopausal - urgent colposcopy and biopsy Colposcopy - colposcopy used to view cervix, acetic acid stain to show dysplastic areas, biopsy taken (punch biopsy or large loop excision of transformation zone) If diagnosis confirmed, further investigations: CT chest/abdomen/pelvis - metastases +/- examination under anaesthesia with further biopsies
111
How should a woman with suspected cervical cancer be assessed?
History Smear history Risk factors - smoking, family history, immunocompromised Previous colposcopy or cervical treatments Examination Abdominal examination including PR - masses, rectal bleeding, hydronephrosis Bimanual examination - pelvic masses Speculum examination - evidence of bleeding, discharge and ulceration (early cervical changes may not be visible)
112
How is dysplasia graded based on colposcopy appearance of the cervix? What is the prognosis of each grade?
Cervical intraepithelial neoplasia - grading system for level of dysplasia in cells of cervix (premalignant change) CIN I - mild dysplasia, affects 1/3 thickness of the epithelial layer, likely to return to normal without treatment CIN II - moderate dysplasia, affects 2/3 thickness of epithelial layer, likely to progress to cancer if untreated CIN III - severe dysplasia, very likely to progress to cancer if untreated (cervical carcinoma in situ)
113
Describe the process and side effects of large loop excision of the transformation zone
Performed with local anaesthetic usually during colposcopy procedure Uses loop of wire with diathermy to removal abnormal epithelial tissue on cervix Side effects: Bleeding Abnormal discharge Infection - avoid intercourse and tampon use to reduce risk Preterm labour risk depending on depth of tissue removed from cervix
114
How is cervical intraepithelial neoplasia managed? What are the main risks of this?
Cone biopsy - sent to histology for analysis Under GA Pain Bleeding Infection Scar formation - stenosis of cervix Increased risk miscarriage and premature labour
115
How is cervical cancer staged?
FIGO staging: Stage 0 - carcinoma in-situ Stage 1 - confined to cervix A - only identifiable under microscopy B - gross lesions, clinically identifiable Stage 2 - beyond cervix but not pelvic sidewall/involves upper 2/3 vagina A - no parametrial involvement B - obvious parametrial involvement Stage 3 - extends to pelvic sidewall/involves lower 1/3 vaginal/hydronephrosis not explained by other cause A - no extension to sidewall, lower 1/3 vagina only B - extension to sidewall and/or hydronephrosis Stage 4 - A - spread to adjacent pelvic organs (bladder, rectum) B - spread to distant organs
116
Describe the prognosis of cervical cancer
1 year 83% 5 years - Overall 70% Stage 1 - 95% Stage 2 - 55% Stage 3 - 38% Stage 4 - 5% 10 years 63%
117
List options for management of cervical cancer by stage
MDT input for all Options - surgery, radiotherapy, chemotherapy Depends if fertility preservation is desired Gold standard for stage 1b - 3 = chemoradiotherapy Surgery: Stage 1a - radical trachelectomy if fertility preservation is priority, laparoscopic hysterectomy with pelvic lymphadenectomy if not Stage 1b/2a - radical (Wertheim's) hysterectomy is curative Stage 4a or recurrent disease - anterior/posterior/total pelvic extenteration
118
Describe the surgical options for management of cervical cancer
Early stage: Trachelectomy - fertility preserving, removal or cervix and upper vagina Radical hysterectomy - removal of uterus, vagina and parametrial tissues up to pelvic sidewall + lymphadenectomy Late stage/recurrent disease: Anterior/posterior/total pelvic extenteration - removal of all pelvic adnexae plus bladder (anterior), rectum (posterior) or both (total)
119
Describe palliative options for management of cervical cancer
Chemotherapy - cisplatin-based Single dose radiotherapy for heavy bleeding Bevacizumab - targets VEGF-A, used in metastatic/recurrent disease May need nephrostomy/ureteric stents
120
Who receives the HPV vaccine? When? What strains does it protect against?
Offered to every 12-13 y/o (previously only girls) Also available for MSM <45 at sexual health clinics Now use 9-valent HPV vaccine - protects against: 6 and 11 - genital warts 16 and 18 - cervical cancer and 31, 33, 45, 52, 58
121
Describe the current cervical screening programme in Scotland
Offered to those between 25-64, every 5 years Cytological sample - tested for high risk HPV, if positive cells examined for dyskaryosis, if negative return to routine screening schedule Results: If high risk HPV but no dyskaryosis - repeat screening in 12 months to check HPV cleared If high risk HPV and dyskaryosis - refer for colposcopy Smear only done if normal cervical appearance - if not refer for colposcopy
122
List the possible results from cervical screening cytology
Inadequate Normal Borderline Low-grade dyskaryosis High-grade dyskaryosis - moderate High-grade dyskaryosis - severe Possible invasive squamous cell carcinoma Possible glandular neoplasia (adenocarcinoma) Can also identify infections e.g. BV, candidiasis, trichomoniasis Acetinomyces-like organisms - often with IUS, do not require treatment unless symptomatic, if symptomatic may need to remove IUS
123
Describe the incidence of vulval cancers
Rare compared with other gynae cancers Used to be only older women (80s - 90s), but HPV has increased prevalence in young women
124
What is the most common histological type of vulval cancer? List the other histological types of vulval cancer.
Most common is squamous cell carcinoma (90%) Other types: Malignant melanoma Adenocarcinoma BCC Sarcoma Metastatic
125
Describe the aetiology and risk factors associated with vulval cancers
HPV Inflammation due to chronic skin conditions - lichen sclerosus, lichen planus Advanced age (>75) Immunosuppression
126
Describe the precancerous condition associated with vulval cancer
Vulval intraepithelial neoplasia VIN 1 - not a precursor for 2/3, low grade squamous intraepithelial lesion, caused by low-risk HPV, usually resolve without treatment VIN 2/3 - high grade squamous intraepithelial lesion, caused by ongoing infection with high-risk HPV, usually requires treatment, usually in 35-49 year olds, smokers, immunocompromised Differentiated VIN - 50-60 years, not usually linked to HPV, found in lichen sclerosus, higher risk of malignant transformation, usually requires surgery
127
Describe the clinical presentation of VIN
Pruritus most common Pain Ulceration Leukoplakia - thickened, white areas Lump/wart 20% asymptomatic, often identified at cervical screening
128
Describe the malignant potential of VIN
9% malignant transformation if untreated Differentiated and symptomatic have higher malignant potential
129
What are the management options for VIN?
Observation - watch and wait with close follow-up Wide local excision Laser ablation Imiquimod cream
130
Describe the clinical features of vulval cancer
Lump Ulceration Bleeding Pain Itch Lymphadenopathy in groin Lower limb lymphoedema Mostly occurs on labia majora (can also be clitoris, perineum)
131
How is suspected vulval cancer investigated?
Biopsy: Incisional - preferred, original lesion used to plan treatment Excisional Under LA as outpatient Local regional LN assessment - US, MRI, CT
132
Describe the staging of vulval cancer
FIGO Stage I - confined to vulva A <2cm B >2cm Stage II - involvement of lower 1/3 of vagina, urethra or anus Stage III - extends to upper 2/3 of vagina or urethra or invasion to bladder or rectal mucosa or lymph nodes (non-ulcerated) Stage IV - ulcerated LNs, disease fixed to pelvic bone or distant mets
133
Describe the prognosis of vulval cancer
5 year - 64% 10 year - 53% Stage 1 - 80% Stage 2 - 60% Stage 3 - 40% Stage 4 - 15%
134
List options for management of vulval cancer
Surgery is gold standard Early stage Wide local excision and groin lymphadenectomy (node surgery important for decreasing mortality) Advanced stage Radical vulvectomy with resection of bilateral inguinofemoral LNs Post-op radiotherapy to pelvis and groin
135
List the types of surgeries used for vulval cancers
Wide local excision - small cancers Partial radical vulvectomy - if unilateral or anterior/posterior only Complete radical vulvectomy - if covering a large area Lymphadenectomy Often also require reconstructive surgery with flaps/grafts
136
List potential complications of groin lymphadenectomy
Wound dehiscence Infection Lymphocyst formation Lymphoedema Immobility Prolonged hospitalisation
137
Define gravidity
Sum of all pregnancies regardless of outcome - includes live birth, pregnancies terminated at <6 months and those which did not result in live birth
138
Define parity
Number of births (including live and stillbirths) where pregnancies reached viable gestational age (24 + 0 in the UK) Multiple pregnancy e.g. twins still counted as one
139
Calculate gravidity and parity for these scenarios: 1. Patient is currently pregnant; had two previous deliveries 2. Patient is not pregnant, had one previous delivery 3. Patient is currently pregnant, had one previous delivery and one previous miscarriage 4. Patient is not currently pregnant, had a live birth and a stillbirth 5. Patient is not pregnant, had a twin pregnancy resulting in two live births
1. G3 P2 2. G1 P1 3. G3 P1+1 (+1 refers to pregnancy not carried to 24+0) 4. G2 P2 5. G1 P1
140
List the main parts of a gynaecological history
Presenting complaint History of presenting complaint - SOCRATES Gynaecological symptoms - abdominal/pelvic pain, post-coital/inter-menstrual/post-menopausal bleeding, vaginal discharge, dyspareunia, vulval skin changes/itching, systemic symptoms (fatigue, fever, weight loss) Menstrual history - frequency, duration, volume, date of LMP, dysmenorrhoea, age at menarche, menopause Reproductive plans - are they considering having children in the future or currently trying to fall pregnant Past medical history Pregnancies - births/miscarriages/abortions/ectopics, means of delivery, age of child and birth weight, obstetric complications Cervical smear - date of last smear, result Surgical history Previous gynaecological problems Previous STIs Drug history Contraception HRT Other medications Allergies Family history Breast/ovarian/endometrial cancer Diabetes Bleeding disorders Social history Occupation Living situation Smoking and alcohol Systemic enquiry
141
Define LMP
Last menstrual period - date of first day of last menstrual period
142
Describe the main hormones of the hypothalamic-pituitary-ovarian axis involved in the menstrual cycle
Gonadotropin releasing hormone (GnRH) from the hypothalamus stimulates luteinising hormone (LH) and follicular stimulating hormone (FSH) release from the anterior pituitary FSH - binds to granulosa cells to stimulate follicule growth, convert androgens from theca cells to oestrogens and stimulate inhibin secretion LH - acts on theca cells to stimulate production and secretion of androgens Controlled by feedback loops: Moderate oestrogen levels exert negative feedback on HPG axis High oestrogen levels (without progesterone) positively feedback on HPG axis Oestrogen in the presence of progesterone exerts negative feedback on the HPG axis Inhibin selectively inhibits FSH secretion from anterior pituitary
143
List the phases of ovarian activity during the menstrual cycle
Follicular phase - days 1-14 Ovulation - day 14 Luteal phase - days 14-28
144
Describe the hormonal changes which occur during the menstrual cycle and the effects they have on the ovaries
Follicular phase: Follicles begin to mature independently of steroid or gonadotropin hormones Due to low steroid and inhibin levels there is little negative feedback on HPG axis so increased FSH and LH levels, which stimulate follicle growth and oestrogen production As oestrogen rises, negative feedback reduces FSH levels so all follicles except one regress Follicular oestrogen becomes high enough to cause positive feedback to HPG axis, increases levels of GnRH and LH (FSH inhibited by inhibin) Ovulation: LH surge causes follicle rupture, oocyte migrates to fallopian tube for 24 hours viable for fertilisation Follicle secretes oestrogen and progesterone, exerts negative feedback to HPG axis - pauses cycle for fertilisation Luteal phase: Corpus luteum formed, produces oestrogens, progesterone and inhibin to maintain conditions for fertilisation and implantation In absence of fertilisation corpus luteum spontaneously regresses after 14 days, fall in hormones, HPG axis resets ready to begin cycle If fertilisation occurs embryo produces HCG which maintains corpus luteum
145
Describe the hormonal changes which occur during the menstrual cycle and the effect they have on the endometrium
Proliferative phase (follicular phase): Oestrogen causes thickening of endometrium, production of thin alkaline cervical mucus Secretory phase (luteal phase): Progesterone causes thickening of endometrium into glandular secretory tissue, thick acidic cervical mucus production (prevent polyspermy) Menses: Occurs in absence of fertilisation once corpus luteum breaks down, internal lining of uterus is shed due to lack of progesterone
146
Define menarche. What is the average age of menarche in the UK?
First menstrual period Average age 12 Caucasian, 4-8 months later in Afro-Caribbean
147
Which placental abnormality is associated with IVF?
Placenta praevia
148
Define menopause. What is the average age of menopause in the UK? What is premature menopause?
Retrospective diagnosis - permanent end to menstruation, diagnosed after no periods for 12 months Average age UK = 51, usually between 45-55 Premature menopause - <40
149
Define climacteric
Stage in life starting from decline in ovarian activity to end of ovarian function, including peri-menopause, menopause and post-menopause Gradual loss of cyclical ovarian activity due to declining numbers of ovarian primordial follicles
150
What causes premature menopause?
Premature ovarian insufficiency - follicular dysfunction or early loss of eggs 90% idiopathic Can also be due to: Autoimmune disease e.g. T1DM, pernicious anaemia, Addison's, Hashimoto's Genetic disorders e.g. Turner's, Fragile X Chemo/radiotherapy Pelvic surgery - oophorectomy, hysterectomy without oophorectomy Smoking
151
List the criteria for diagnosis of premature ovarian insufficiency
Amenorrhoea Hypergonadotropism Hypoestrogenism
152
Describe the changes in the HPO axis which lead to menopause
Reduction in circulating oestrogen due to reduced sensitivity of ovary to circulating FSH and LH - less follicles so less binding sites Reduced oestrogen leads to more anovulatory cycles Levels of FSH and LH increase during menopause as less negative feedback from oestrogen and less inhibin from follicles In anovulatory cycles there is no corpus luteum to produce progesterone so endometrial lining not supported and frequently breaks down leading to breakthrough bleeding, as frequent as every two weeks
153
What risks are associated with early menopause?
Infertility Osteoporosis Ischaemic heart disease Pelvic organ prolapse Urinary incontinence Higher endometrial cancer risk
154
How is menopause/perimenopause diagnosed?
If >45 can diagnose perimenopause based on typical vasomotor symptoms and menstrual history (irregular periods), menopause if not had period for 12 months If <45 or >45 with atypical symptoms should measure FSH and consider genetic testing
155
What FSH level is diagnostic of menopause in <45s?
Consistently >30mIU/ML (not a one-off value) and no menstrual period for >12 months
156
List symptoms associated with the menopause
Irregular menstrual cycle Vasomotor symptoms - hot flushes, night sweats, can be associated with sweating, palpitations, anxiety Cognitive impairment and mood disorders - anxiety, mood swings, irritability, sleep disturbance, low mood, poor concentration and memory Urogenital symptoms - vulvovaginal irritation, discomfort, burning, itching, dryness, dyspareunia, reduced libido, dysuria, urinary frequency/urgency, recurrent UTIs, prolapse Joint and muscle pains Headaches Fatigue Loss of bone density - increased risk fragility fractures Ischaemic heart disease
157
Describe the hormonal changes which cause symptoms and clinical consequences of the menopause
Vasomotor changes - pulsatile LH influences central temperature control Urogenital changes - lower circulating oestrogen causes atrophy of vagina, thinning of vaginal walls and dryness, atrophy of bladder and urethra causes urinary symptoms Bone density - lower circulating oestrogen causes increased bone reabsorption by osteoclasts Ischaemic heart disease - oestrogen reduces levels of LDL cholesterol and raises HDL cholesterol, less oestrogen causes reversal of this process
158
What are the indications for HRT?
Premature menopause even without symptoms Reducing vasomotor symptoms Improving symptoms such as low mood, decreased libido, poor sleep and joint pain Reducing risk of osteoporosis in women under 60
159
Describe the different preparations of HRT available
Oestrogen: Oral Transdermal - patches or gels Progesterone: Cyclical or continuous Oral Transdermal - patches IUS - Mirena coil Combined - Cyclical, continuous oestrogen with progesterone added at specific periods during cycle: Oral Patches
160
What are the risks associated with HRT? How can these risks be minimised?
Generally in under 60s, the benefits outweigh the risks - more significant in older women Increased risk breast cancer, particularly with combined HRT (oestrogen-only has lower risk, risk increases with length of use and returns to normal once stopped for 5 years) Increased risk endometrial cancer (oestrogen-only higher risk) Increased risk VTE (2-3x background risk with oral HRT, no difference in risk with patches) Increased risk stroke and CAD with long term use in older women (no risk with oestrogen-only HRT, risk only if >10 years post-menopausal) Inconclusive evidence about risk of ovarian cancer, minimal increased risk if any
161
List side effects of HRT (not risks)
Oestrogenic: Bloating Breast tenderness Nausea Headaches Leg cramps Progestogenic: Mood swings Bloating Fluid retention Weight gain Acne, greasy skin
162
List resources for information about HRT risks
British Menopause Society Royal College of Obstetricians and Gynaecologists Menopause matters website
163
List contraindications for HRT
Undiagnosed abnormal bleeding Endometrial hyperplasia or cancer Breast cancer Uncontrolled hypertension Venous thromboembolism Liver disease Active angina or myocardial infarction Pregnancy
164
How should HRT formulation be chosen?
Step 1 - do they have local or systemic symptoms? Local - topical e.g. oestrogen cream, pessary Systemic - go to step 2 Step 2 - do they have a uterus? No uterus - continuous oestrogen-only HRT Uterus - add progesterone (combined HRT), go to step 3 Step 3 - have they had a period in the past 12 months? Perimenopausal - cyclical combined HRT Postmenopausal - continuous combined HRT
165
Why is it important to give combined HRT to women with a uterus?
Addition of progesterone greatly decreases the incidence of endometrial hyperplasia and endometrial cancer
166
Describe fertility and contraceptives in peri/postmenopausal women
HRT is not contraception Recommended to use effective contraception until: 12 months after the last period in women > 50 years 24 months after the last period in women < 50 years Examples of contraceptive options: Mirena Coil Progesterone only pill in addition to HRT Good contraceptive options: Barrier methods Mirena or copper coil Progesterone-only pill Progesterone implant Progesterone depot injection (<45) Sterilisation
167
List non-hormonal options for management of vasomotor symptoms in menopause and describe the evidence for their efficacy
Prescribed - good evidence for efficacy: Clonidine SSRI/SNRI - paroxetine, venlafaxine, fluoxetine Gabapentin Non-prescribed: Black cohosh - Small RCTs show reduction in mild-moderate hot flushes Vitamin E - no benefit Evening primrose oil - no benefit Phytoestrogens - may reduce severity CBT - improved vasomotor symptoms and mood Alternative: Acupuncture Lifestyle - avoid triggers, light clothing etc. Stellate ganglion blockade - potentially efficacious
168
Describe the mechanism of action of clonidine in reducing vasomotor symptoms of the menopause
Alpha-2 adrenergic receptor and imidazoline receptor agonist Lowers BP, reduces heart rate
169
List common side effects of clonidine
Dry mouth Headaches Dizziness Fatigue Sudden withdrawal - rapid increase in BP, agitation
170
List potential adverse effects of alternative remedies used to manage vasomotor symptoms of menopause
Black cohosh - liver damage Dong quai - bleeding disorders Red clover - oestrogenic effects, concerning in oestrogen sensitive cancers Evening primrose oil - significant drug interactions, linked with clotting disorders and seizures
171
List non-hormonal therapies used for urogenital symptoms of the menopause
Vaginal moisturisers/lubricants Urinary incontinence - weight reduction, supervised pelvic floor training, bladder training, antimuscarinics
172
List non-hormonal therapies used for management of osteoporosis of the menopause
Calculate FRAX to determine if high, medium or low-risk Lifestyle - smoking cessation, exercise Calcium and Vitamin D supplementation Bisphosphonates
173
Define heavy menstrual bleeding
Technically >80ml blood loss during menstruation - not measured in practice Self-reported excessive menstrual loss which interferes with quality of life Also defined as - need to change menstrual products every 1-2 hours, passage of clots greater than 2.54cm
174
List causes of heavy menstrual bleeding
PALM-COPEEIN PALM - structural causes Polyp Adenomyosis Leiomyoma (fibroid) Malignancy and hyperplasia COPEEIN - non-structural causes Coagulopathy - anticoagulants, Von Willebrand Ovulatory dysfunction Pelvic inflammatory disease Endometrial - endometriosis, endometrial cancer, endometrial hyperplasia Endocrine - PCOS, diabetes, hypothyroidism Iatrogenic - copper coil Not yet classified
175
Describe the clinical assessment of a patient with heavy menstrual bleeding
History: Nature of bleeding and impact on QOL Symptoms of anaemia Age at menarche Cycle length, days menstruating, variation Intermenstrual and post-coital bleeding Contraceptive history Sexual history Possibility of pregnancy Plans for future pregnancies Cervical screening history Migraines with or without aura PMH, DH, SH, FH Examination: Abdominal palpation - palpable uterus or pelvic mass Speculum - cervical excitation, inflamed cervix, cervical polyp/tumour, vaginal tumour Bimanual examination - smooth or irregular uterus (fibroids), bulky uterus (adenomyosis) Investigations: Bloods - FBC, TFTs, hormone testing if clinically suspicious (e.g. of PCOS) Coagulation screening, test for VWD if suspicious of clotting disorder Biopsy - endometrial cancer US - structural abnormalities Cervical smear - no need if up to date High vaginal and endocervical swabs - infection
176
What are the options for management of heavy menstrual bleeding?
If does not want contraception: Treatment during menstruation for symptomatic relief - tranexamic acid (no associated pain), mefenamic acid (associated pain) If contraception is wanted/acceptable: Levonorgestral-releasing IUS (Mirena coil) - first-line Combined oral contraceptive pill Cyclical oral progestogens e.g. norethisterone (does not work as contraceptive) Progesterone-only contraception - pill, depot, implant If medical management failed: Endometrial ablation Hysterectomy - partial or total
177
Describe the mechanism of action of non-hormonal pharmacological management options for heavy menstrual bleeding
Tranexamic acid - antifibrinolytic, inhibits plasminogen activator reducing fibrinolytic activity in endometrium Mefenamic acid - NSAID, prostaglandin synthase inhibitors, reduces pain, and bleeding
178
Describe the mechanism of action of hormonal management options for heavy menstrual bleeding
Pseudo-pregnancy - endometrial decidualization and necrosis: Mirena coil COCP Progestogens Pseudomenopause: GnRH analogues - suppress FSH and LH, can be used short-term, improve Hb, shrink fibroids Progesterone receptor modulators: Esmya - ullipristal acetate Act directly on endometrium, induce amenorrhoea, shrink fibroids
179
Describe the surgical options for management of heavy menstrual bleeding
Endometrial ablation: Local or general anaesthetic Ablation of endometrium to myometrium For those who do not wish to conceive - will need to continue using contraception after Hysterectomy: Only definitive treatment - guaranteed amenorrhoea Abdominal or laparoscopic Associated morbidity and mortality Partial - uterus removed only (not cervix) Total - cervix and uterus removed Total with bilateral salpingo-oophorectomy only if ovaries are abnormal
180
Define primary amenorrhoea
Failure to menstruate by 13 with no evidence of pubertal development Failure to menstruate by 15 with signs of puberty e.g. breast bud development
181
Define secondary amenorrhoea
Cessation of periods for >6 months after menarche (after excluding pregnancy) Or >12 months if previous oligomenorrhoea
182
Define oligomenorrhoea
Cycle persistently longer than 35 days, menses less frequently than every 35 days (less than 9 periods per year)
183
List the most common causes of primary amenorrhoea
Physiological delay Weight loss/dieting/heavy exercise PCOS Imperforate hymen
184
List causes of primary amenorrhoea
Normal secondary sexual characteristics: Physiological - constitutional delay, pregnancy Genito-urinary malformations - imperforate hymen, transverse septum, absent vagina or uterus Endocrine disorder - hypothyroidism, hyperthyroidism, hyperprolactinaemia, Cushing's syndrome, PCOS Androgen insensitivity syndrome No secondary sexual characteristics: Primary ovarian insufficiency - genetic (Turner's, gonadal agenesis), chemo/radiotherapy, autoimmune disease Hypothalamic dysfunction - excessive exercise/weight loss, chronic systemic illness, hypothalamic or pituitary tumours, cranial irradiation, infection or head injury, Kallman's syndrome, empty sella symdrome, Laurence-Moon-Biedl syndrome, Prader-Willi syndrome Causes of ambiguous genitalia - 5-alpha reductase deficiency, androgen-secreting tumour, congenital adrenal hyperplasia
185
Define hypogonadotropic hypogonadism and list examples
Deficiency of LH/FSH leading to deficiency of sex hormones (oestrogen) Hypopituitarism Radiation/surgical damage to hypothalamus or pituitary Chronic conditions Excessive exercise or dieting Kallman's syndrome - reduced/absent sense of smell
186
Define hypergonadotropic hypogonadism and list examples
Gonads fail to respond to stimulation from LH/FSH, so increased amounts of FSH/LH produced (lack of negative feedback) Damage to ovaries Congenital absence of ovaries Turner's syndrome
187
Describe causes of amenorrhoea in terms of the HPO axis
Hypothalamic causes: Functional disorders - exercise, eating disorders Severe chronic conditions Kallman syndrome - failure of migration of GnRH cells Pituitary causes: Prolactinomas or other pituitary tumours e.g. acromegaly, Cushing's syndrome Sheehan's syndrome Destruction of pituitary - radiation, surgery, autoimmune disease Post-contraception amenorrhoea - Depo-Provera highest risk Ovarian causes: PCOS Turner's Premature ovarian failure Adrenal causes: Congenital adrenal hyperplasia Genital tract abnormalities: Ashermann's syndrome - instrumentation of uterus damages basal layer of endometrium, causes intrauterine adhesions which fail to respond to oestrogen Imperforate hymen, transverse vaginal septum Mayer-Rokitansky-Kuster-Hauser syndrome - agenesis of Mullerian duct system, congenital absence of uterus and upper 2/3 of vagina
188
How are secondary sexual characteristics in females assessed?
Tanner staging
189
List causes of secondary amenorrhoea
Physiological: Pregnancy Lactation Menopause Premature ovarian insufficiency Chemotherapy Radiotherapy Autoimmune disease Hypothalamic causes: Hypothalamic dysfunction due to stress, excessive exercise, and/or weight loss Chronic systemic illness Cranial irradiation, infection or head injury Pituitary causes: Prolactinoma, other hormone-secreting tumours Head injury, cranial irradiation Hypopituitarism Sheehan's syndrome Sarcoidosis TB Uterine causes: Cervical stenosis Asherman's syndrome Thyroid disease Iatrogenic: Contraceptive Drugs e.g. antipsychotics (hyperprolactinaemia), illicit drug use Surgery - hysterectomy, endometrial ablation, ovarian surgery With androgen excess: PCOS Cushing's Late-onset congenital adrenal hyperplasia Androgen-secreting tumours of the ovary or adrenal gland
190
Describe the diagnostic criteria for PCOS
Rotterdam criteria - 2/3 of: Oligo- and/or anovulation Clinical and/or biochemical signs of hyperandrogenism Polycystic ovaries on imaging (>12 developing follicles in one ovary), or ovarian volume >10
191
List features of hyperandrogenism in PCOS
Clinical: Hirustism Acne Male pattern hair-loss Biochemical: Raised testosterone Low SHBG Raised LH Normal FSH Low progesterone May have mildly elevated prolactin
192
List the clinical features and complications of PCOS
Oligomenorrhoea or amenorrhoea Infertility Hirsutism Obesity Chronic pelvic pain Depression Acne Acanthosis nigricans - insulin resistance Male pattern hair-loss Obesity Hypertension Insulin resistance and diabetes Hypercholesterolaemia Endometrial hyperplasia and cancer Obstructive sleep apnoea Sexual problems
193
How is PCOS managed?
Reduce risk of cardiovascular disease and diabetes: lifestyle (weight loss, exercise, smoking cessation), antihypertensives and statins where indicated Reduce risk of endometrial cancer - Mirena coil (continuous protection), inducing withdrawal bleed at least 3-4 monthly with cyclical progestogens or COCP Manage infertility - weight loss, clomifene, metformin, letrozole, laparoscopic ovarian drilling, IVF Manage hirsutism - weight loss, COCP, topical eflornithine, other options e.g. electrolysis, laser hair removal, spironolactone, finasteride, flutamide, cyproterone acetate Manage acne - COCP, topical retinoid, topical antibiotics, topical azelaic acid, oral tetracycline antibiotics COCP used for hirsutism/acne = cyprindiol, anti-androgenic but increased risk VTE
194
Define primary and secondary dysmenorrhoea
Dysmenorrhoea = painful cramping, usually in the lower abdomen often radiating to legs and back, occurs shortly before and/or during menstruation Can be accompanied by GI symptoms and malaise Primary = idiopathic, no identifiable underlying pelvic pathology Secondary = caused by underlying pelvic pathology
195
Describe the features of primary vs secondary dysmenorrhoea
Primary: Usually young females, 6-12 months after menarche once cycles are regular Pain most severe on day of or prior to start of menstruation Secondary: Usually starts many years after menarche after long period of painless periods
196
List common causes of secondary dysmenorrhoea
Endometriosis/adenomyosis Fibroids PID Ovarian cancer Cervical cancer IUD insertion
197
How should a woman presenting with dysmenorrhoea be assessed?
Need to consider and rule out causes of secondary before diagnosing primary - diagnosis of exclusion Examination - Abdominal - masses Pelvic (not appropriate in adolescents who are not sexually active) - speculum, bimanual, swabs Investigations - may not be needed if no features of secondary US - fibroids, adnexal pathology, endometriosis, IUS High vaginal and endocervical swabs Pregnancy test
198
How is primary dysmenorrhoea managed?
Reassurance Smoking cessation Pharmacological: Analgesia (first-line) - NSAIDs (ibuprofen, naproxen, mefenamic acid), inhibit prostaglandins Paracetamol 3-6 month trial of hormonal contraception (second-line) - monophasic COCP, IUS (Mirena), depo-Provera Non-pharmacological: Local application of heat TENS
199
Define intermenstrual bleeding
Bleeding between periods
200
Define post-coital bleeding
Bleeding after intercourse
201
List causes of inter-menstrual bleeding, post-coital bleeding and post-menopausal bleeding in terms of anatomical site
Uterine: Polyp Cancer IUS Fibroids Infection Pregnancy Cervix: Cancer Ectropion Infection Cervical erosion Vagina: Atrophic vaginitis Cancer Trauma Vulval: Cancer
202
Describe the assessment of inter-menstrual bleeding and post-coital bleeding
Cervical smear history - do not take if not due Speculum and bimanual examination - urgent colposcopy referral if suspicious of cancer STI screen and treat +/- GUM referral if appropriate Urine pregnancy test
203
Which patients should be urgently/routinely referred for inter-menstrual/post-coital bleeding?
Urgent: >35 with persistent (>4 weeks) post-coital or inter-menstrual bleeding Routine: <35 with post-coital or inter-menstrual bleeding for >12 weeks Single heavy episode of post-coital or inter-menstrual bleeding at any age Reassurance: <35 with normal findings and results
204
Define chronic pelvic pain
Intermittent or chronic pain in the lower abdomen or pelvis for >6 months, not occurring exclusively with menstruation or intercourse and not associated with pregnancy
205
List causes of pelvic pain in terms of anatomical location
Vulva: Bartholin abscess Lichen sclerosus Herpes Cancer Vulvodynia Uterus: Fibroids - degeneration or torsion causes acute pain Endometriosis Adenomyosis Cancer Fallopian tubes: Pelvic inflammatory disease Hydrosalpinx Ovaries: Ovarian cysts - torsion, haemorrhage, rupture (acute) Cancer GI system: IBS Urinary system: Interstitial cystitis MSK pain General: Adhesions Pelvic organ prolapse Nerve entrapment e.g. post C-section Psychological and social issues Chronic pelvic pain syndrome
206
List ovarian cyst accidents and describe their presentation
Rupture - sudden onset pelvic pain, can have acute peritonism, shock or be asymptomatic Haemorrhage - sudden onset pelvic pain, pelvic mass, bloating, vaginal spotting/bleeding, may be asymptomatic Torsion - common gynaecological emergency, usually sudden onset severe unilateral pelvic pain which gets progressively worse, associated with nausea and vomiting, or can be mild or intermittent pain. Localised tenderness, may have palpable mass.
207
Describe the investigation of pelvic pain where an ovarian cyst event is suspected
Pregnancy test MSU - rule out UTI Vaginal/cervical swabs - ?PID FBC + CRP CA125 Transvaginal US - 'whirlpool sign', free fluid in pelvic and oedema of ovary seen in torsion Definitive diagnosis - laparoscopic surgery
208
How are ovarian cysts managed?
Depends on type of cyst If ovarian cancer suspected - two-week wait to gynaecological oncology specialist Dermoid cysts - ?surgery Simple ovarian cysts Pre-menopausal - <5cm will likely resolve on their own, do not need management or follow-up scan, 5cm-7cm require routine referral to gynaecology and yearly US monitoring, >7cm consider MRI or surgical evaluation Post-menopausal - measure CA125, if raised two-week wait referral, if normal and <5cm may be monitored with US 4-6 monthly Persistent/enlarging cysts - surgical intervention, usually laparoscopic, ovarian cystectomy +/- oophorectomy
209
Define pelvic inflammatory disease
Ascending infection of the upper genital tract, spreads from endocervix to cause one or more of: Endometritis - endometrium Salpingitis - fallopian tubes Parametritis - parametrium (connective tissue around uterus) Oophoritis - ovaries Tubo-ovarian abscess - adnexa Pelvic peritonitis - peritoneal membrane
210
What are the most common causes of pelvic inflammatory disease?
STIs: Chlamydia trachomatis Neisseria gonorrhoea Mycoplasma genitalium Other: Gardnerella vaginalis Haemophilus influenzae E. Coli Streptococcus agalactiae Can commonly be pathogen-negative
211
List complications of pelvic inflammatory disease
Ectopic pregnancy Infertility Tubo-ovarian abscess Chronic pelvic pain Fitz-Hugh-Curtis syndrome - RUQ pain, peri-hepatitis, especially associated with chlamydia
212
Describe the presentation of pelvic inflammatory disease
Can be asymptomatic Lower abdominal/pelvic pain Deep dyspareunia Menstrual abnormalities e.g. menorrhagia, dysmenorrhoea, intermenstrual bleeding Post-coital bleeding Dysuria Abnormal vaginal discharge - purulent, malodorous If advanced - severe lower abdominal pain, fever, nausea and vomiting On examination Tenderness of uterus/adnexae or cervical excitation Palpable mass in lower abdomen Abnormal vaginal discharge
213
How should suspected pelvic inflammatory disease be investigated?
NAAT swab for gonorrhoea, chlamydia, mycoplasma genitalium HIV test Syphilis test High vaginal swab for bacterial vaginosis, candidiasis and trichomoniasis Microscopy of vaginal/endocervical swabs - pus cells, absence is useful for excluding PID but presence is not specific for PID diagnosis Pregnancy test - exclude ectopic pregnancy ESR/CRP MSU - exclude UTI Transvaginal US if tubo-ovarian abscess is suspected Laparoscopy if diagnosis uncertain or no improvement after initial management
214
How is PID managed?
Antibiotics - 14-day course, broad spectrum with good anaerobic coverage Start immediately, before swab results are available Options for Abx: Doxycycline + ceftrixone + metronidazole Ofloxacin + metronidazole Analgesics e.g. paracetamol Avoid sexual intercourse until Abx course complete and partner(s) are treated Referral to GUM - contact tracing, test all sexual partners from previous 6 months More severe - admission for IV antibiotics Pregnant (including ectopic), signs of sepsis/pelvic peritonitis, unresponsive to oral Abx
215
Define endometriosis
Chronic condition with growth of ectopic endometrium-like tissue outside the uterus
216
Describe the aetiology of endometriosis
Several theories: Retrograde menstruation - endometrial cells flow from uterine cavity through fallopian tubes and out into pelvic cavity where they implant on tissues and seed and grow Lymphatic or circulatory dissemination - endometriotic tissue travels through lymphatic system or in bloodstream to ectopic sites Genetic predisposition - well documented, no specific genes identified Metaplasia - cells in pelvis and abdominal area change into endometrial-type cells of the germinal epithelium Embryonic cells - embryonic cells remain outside uterus during development and later develop into ectopic endometrial tissue Environmental factors Immune dysfunction - those with endometriosis seem to have reduced immunity to other conditions, unknown if this is a contributor or consequence
217
List sites for endometriosis to develop
Pelvic most common: Ovaries Pouch of Douglas Uterosacral ligaments Pelvic peritoneum Rectum Sigmoid colon Bladder Distal ureter Extra-pelvic sites rarer: Bowel Diaphragm Umbilicus Pleural cavity
218
Describe the clinical presentation of endometriosis
Can be asymptomatic Cyclical pelvic pain - occurs during menstruation May be constant pain if adhesions have formed Dysmenorrhoea Dyspareunia Dysuria Dyschezia (painful defecating) Subfertility Urinary symptoms Bowel symptoms Examination: Fixed, retroverted uterus Uterosacral ligament nodules Endometrial tissue visible in vagina General tenderness
219
Describe the assessment and investigations of women with suspected endometriosis
Examination - abdominal and pelvic examination (speculum and bimanual) Gold standard for diagnosis = laparoscopy Typical findings - chocolate cysts, adhesions, peritoneal deposits, powder burn lesions Biopsy of lesions Can also be used as treatment - remove endometriomas, divide adhesions Pelvic US should be done before surgery - determine severity of endometriosis
220
List potential complications of endometriosis
Endometriomas - rupture, torsion Fertility problems - mechanism not clear Adhesion formation - chronic pelvic pain Bowel obstruction Chronic pain without visible disease Reduced quality of life ?Link between endometriosis and ovarian cancer - evidence not clear
221
List management options for endometriosis
Initial management: Analgesia as required for pain - NSAIDs and paracetamol first line (follow analgesic ladder) Hormonal management: COCP Progesterone only pill Depo-provera Nexplanon implant Mirena coil GnRH agonists (induce menopause-like state) Surgical management: Laparoscopic surgery to excise or ablate endometrial tissue + adhesiolysis (relapses likely, may need repeated surgery) Hysterectomy + bilateral salpingo-oophorectomy
222
Define adenomyosis
Endometrial tissue inside the myometrium
223
Describe the micturition cycle
Storage/continence phase: Controlled by pons continence centre, which control sympathetic continence centres of spinal cord --> hypogastric nerve (T10-T12) Storage requires relaxation of the detrusor muscle (via B3-adrenoreceptors) and contraction of the internal urethral sphincters (via A1-adrenoreceptors) and external urethral sphincters (via pudendal nerve S2-4 --> cholinergic receptors) As bladder fills detrusor relaxes and volume of bladder expands - intra-vesical pressure remains constant and lower than the urethral pressure = receptive relaxation Micturition/voiding phase: Under parasympathetic control, afferent signals from bladder travel through spinal cord to pontine micturition centre to excite sacral preganglionic neurons Parasympathetic stimulation of pelvic nerve (S2-4), release of acetylcholine which acts on muscarinic Ach receptors on detrusor muscle, which causes it to contract, also inhibition of Onuf's nucleus with reduction in sympathetic stimulation to internal urethral sphincter, causing it to relax Conscious reduction in voluntary contraction of external urethral sphincter from cerebral cortex, distension of urethra, passing of urine
224
List the structures which help to maintain continence in women
Brain - pons continence centre Spinal cord - spinal continence centre, T10-L2 Nerves - pelvic nerve, pudendal nerve Bladder - detrusor muscle Urethral sphincters - internal (sympathetic control) and external (voluntary control) Pelvic floor - supports pelvic organs and tightens urethral opening
225
Define urinary incontinence
Involuntary loss of urine which can be objectively demonstrate and which is a social or hygienic problem
226
Define the types of urinary incontinence in women
Stress urinary incontinence - involuntary leakage of urine on effort or exertion, or on sneezing/coughing (increased intra-abdominal pressure) Urgency urinary incontinence involuntary leakage accompanied by or immediately preceded by a sudden compelling desire to pass urine which is difficult to defer (urgency), part of larger symptom complex of overactive bladder syndrome Overactive bladder syndrome - urinary urgency (with or without urgency incontinence) usually associated with increased frequency and nocturia Mixed urinary incontinence - both stress and urgency Overflow incontinence - detrusor under activity or bladder outlet obstruction results in urinary retention and leakage of urine, may have straining to urinate or feeling of bladder incompletely emptying
227
List the clinical types of overactive bladder syndrome
OAB wet - incontinence present OAB dry - incontinence absent
228
Define urodynamic stress incontinence
Urodynamic proven leakage of urine with increased intra-abdominal pressure (old term = genuine stress incontinence)
229
List risk/aetiological factors for overactive bladder
Mostly idiopathic Systemic neurological conditions - Parkinson's, MS, injury to pelvic/spinal nerves Obesity T2DM Chronic UTI Drugs which cause detrusor overactivity - parasympathomimetics (muscarinic receptor agonists, acetylcholinesterase inhibitors), antidepressants, hormone replacement Diuretics, caffeinated, acidic or alcoholic drinks - increase urinary frequency
230
List risk/aetiological factors for stress incontinence
Increasing age Pregnancy and vaginal delivery - weakens muscles and connective tissue, damage to pudendal and pelvic nerves Obesity - pressure on pelvic tissues, stretching and weakening of muscles and nerves Constipation - straining can weaken pelvic floor muscles Deficiency in supporting tissues - prolapse, hysterectomy, lack of oestrogen at menopause Family history Smoking Drugs - ACE inhibitors (cause cough)
231
List the complications of urinary incontinence
Impaired quality of life - employment and leisure activities Psychological problems - depression, anxiety, embarrassment/shame, low self esteem Social isolation, avoidance of leaving home Sexual problems Loss of sleep Falls and fractures
232
List the important points in a history of urinary incontinence
Does it occur when coughing, sneezing or on exertion (stress)? Is there sudden urgency, frequency and nocturia (urge)? Is there difficulty voiding (overflow)? Ask about fluid intake - amount and type of fluids Red flag symptoms - haematuria, bladder or urethral pain, recurrent UTI, constant leakage (fistula) How often? At what times? Use of pads, changing of clothing Drug history - alpha-1 adrenoreceptor antagonists (tamsulosin, doxazosin), antipsychotics, anticholinergics, anti-Parkinsonism drugs, antidepressants, benzodiazepines, diuretics, HRT PMHx - urinary tract disorders, spinal surgery, prolapse, hysterectomy, O+G history, neurological conditions (MS, Parkinson's), systemic disease (DM, heart failure) SH - impact on QOL, insomnia, sexual functioning
233
How should a woman with urinary incontinence be examined?
General - weight, gait, indicators of neurological disease Abdominal - palpable bladder or mass Pelvic examination - Cough with comfortably full bladder - observe for leakage Assess pelvic muscle tone and contraction during bimanual examination - squeeze finger (Oxford grading system) Evidence of prolapse, atrophic vaginitis, urethral diverticulum
234
How should a woman with urinary incontinence be investigated?
Urine dipstick - all women with urinary incontinence Bladder diary for minimum 3 days Post-void residual volume measurement with bladder scan (or catheterisation) - symptoms suggestive of voiding dysfunction or recurrent UTI Cystoscopy and renal tract imaging - if haematuria, recurrent UTIs Urodynamic testing - urge incontinence, voiding dysfunction, prolapse, failed conservative management
235
List management options for urinary incontinence associated with overactive bladder syndrome
Conservative: Exclude/manage treatable causes Advice on fluid intake and lifestyle measures - reduce caffeine, avoid drinking excessive amounts, weight loss, smoking cessation Bladder training Medical management: Antimuscarinic - oxybutynin, tolterodine, darifenacin (if symptoms persist with bladder training) Beta-3 agonist if antimuscarinic contraindicated (Mirabegron) Surgical management: Botulinum toxin injection Detrusor myomectomy and augmentation cystoplasty - only if debilitating symptoms resistant to other treatment
236
List management options for stress incontinence
Conservative: Lifestyle - weight loss, caffeine reduction, smoking cessation Treat risk factors e.g. chronic cough Supervised pelvic floor muscle training for at least 3 months Medical: Duloxetine - SNRI Surgical: Burch colposuspension Laparoscopic colposuspension Tension free vaginal tape
237
Define uterovaginal prolapse and list types of prolapse
Protrusion of the uterus and/or vagina beyond normal anatomical confines Uterine prolapse - uterus descends into vagina Vault prolapse - in women who have had hysterectomy, vault (top of vagina) descends into vagina Rectocele - rectum prolapses forwards into vagina (due to defect in posterior vaginal wall) Cystocele - bladder prolapses backwards into the vagina (due to defect in anterior vaginal wall), most common Urethrocele - descent of the anterior vaginal wall where the urethra sits, second most common Enterocele - upper vagina, descent of vagina and peritoneal sac (pouch of Douglas), usually contains loops of small bowel
238
Describe the structure of the pelvic floor
Funnel shaped Attaches to walls of lesser pelvis, separating pelvic cavity from perineum inferiorly Two significant holes in pelvic floor - urogenital hiatus (anterior), rectal hiatus (central) Main muscles of pelvic floor - levator ani (pubococcygeus, puborectalis, iliococcygeus) and coccygeus
239
Describe the support of the uterus and vagina
Primary support is via tone of pelvic floor Also ligaments: Broad - double layer of peritoneum attaches sides of uterus to pelvis Round - from uterine horns to labia majora via inguinal canal Ovarian - ovaries to uterus Cardinal ligament - cervix to lateral pelvic valls, contains uterine artery and vein Uterosacral ligament - cervix to sacrum
240
List the aetiological factors which contribute to uterovaginal prolapse
Increasing age/menopause - loss of oestrogen and connective tissue strength Vaginal deliveries - particularly multiple, instrumental, prolonged or traumatic delivery Raised intra-abdominal pressure - obesity, chronic cough, chronic constipation Abnormal collagen metabolism
241
Describe the clinical presentation of uterovaginal prolapse
Can be asymptomatic Sensation of pressure, fullness, heaviness Dragging sensation Sensation of bulge, 'something coming down' Worse on straining or bearing down Urinary symptoms - incontinence, urgency, frequency, weak stream, retention Bowel symptoms - constipation, incontinence, urgency Sexual dysfunction - pain, altered sensation, reduced enjoyment
242
Describe how to examine for a vaginal prolapse
Patient empty bowels and bladder before examination Can use dorsal and left lateral position Sim's speculum used to support vaginal wall on one side to examine other sides - anterior wall to check for rectocele, posterior wall for cystocele Cough or bear down to assess full descent of prolapse Abdominal/bimanual examination - pelvic masses
243
Describe the grading system for uterovaginal prolapse
Pelvic organ prolapse quantification (POP-Q) system Grade 0: Normal Grade 1: The lowest part is more than 1cm above the introitus Grade 2: The lowest part is within 1cm of the introitus (above or below) Grade 3: The lowest part is more than 1cm below the introitus, but not fully descended Grade 4: Full descent with eversion of the vagina Introitus = opening of vagina
244
List the management options for uterovaginal prolapse
Conservative: Physiotherapy - pelvic floor exercises Weight loss Lifestyle changes for associated stress incontinence - reduce caffeine intake, anticholinergic medications Vaginal oestrogen cream Vaginal pessaries Ring, shelf/Gelhorn, cube, donut, hodge Surgical: Colporrhaphy (anterior for cystocele/posterior for rectocele) Vaginal hysterectomy Manchester repair - cervical amputation, shortening of transcervical ligament Sacrohysteropexy - mesh to attach uterus to anterior longitudinal ligament Sacrospinous ligament fixation Sacrocolpopexy - vault attached to sacrum using mesh Colpocleisis - vaginal closure, if do not wish to have vaginal intercourse
245
How can uterovaginal prolapse be prevented?
Weight reduction Treatment of constipation Treatment of chronic cough & smoking cessation Avoidance of heavy lifting Encourage pelvic floor exercises Good Intrapartum care - avoid unnecessary instrumental trauma and prolonged labour
246
Describe the visit schedule for antenatal care
Healthy with no risk factors/obstetric problems - all care by midwives in the community With risk factors/health problems/obstetric problems - see other members of MDT including obstetricians First contact - pre-booking Booking appointment, arrange screening - by 10 weeks 16 week, 18-20 week (anomaly scan), 28, 34, 36, 38, 41, 42 weeks + 25, 31, 40 in prims
247
What antenatal care is given in the first trimester?
Identify risks, including domestic abuse Screen for abnormalities or illness Develop rapport, encourage future attendance Health promotion - smoking cessation, dietician, dental care, folic acid, alcohol, food hygiene Social work involvement if required Baseline observations - BMI, BP, HR, abdominal exam, urinalysis Determine likely gestation Screening - FBC, blood group, sickle cell and thalassaemia, hep B/syphilis/HIV
248
Which investigations are offered for fetal screening? When?
Combined test at 11-14 weeks - Down's (T21), Edward's (T18), Patau's (T13) NIPT - cell free fetal DNA, if high risk from combined test Chorionic villus sampling (11 weeks) or amniocentesis (15 weeks) to confirm diagnosis if NIPT positive Fetal anomaly scan (18-22 weeks)
249
What antenatal care is given in the second trimester?
Fetal anomaly scan (18-22 weeks) AN appointments - BP, urinalysis, auscultation of fetal heart from 18 weeks Ask about pain/vaginal loss Identify and manage common problems in pregnancy e.g. nausea and vomiting, heartburn, haemorrhoids
250
What antenatal care is given in the third trimester?
BP, urinalysis, auscultation of fetal heart Ask about pain/vaginal loss Ask about common problems in pregnancy Ask about fetal movement Abdominal examination Evaluation of fetal growth - 24 weeks+
251
List factors which can make a pregnancy high risk
Personal history/current health: Fertility treatment Medical conditions Surgical history Low/high BMI Mental health issues Social difficulties Family history: Congenital abnormalities Medical conditions Mental health Obstetric history: Miscarriages >14 weeks/stillbirth/neonatal death Recurrent miscarriages Premature birth Gestation diabetes, rhesus disease, antepartum haemorrhage, induction of labour, pre-eclampsia Operative birth Post-partum haemorrhage Current pregnancy: Hyperemesis Vaginal bleeding Abdo pain USS findings
252
List screening tests offered at the booking appointment and the implications of these
FBC - anaemia, thrombocytopaenia Blood group - ABO, rhesus (anti-D treatment) Sickle cell and thalassaemia HIV - anti-retrovirals during pregnancy, bottle feed if viral load detectable Hepatitis B/C - B vaccine given to baby after birth, no preventative measures for C (less likely to pass on) Syphilis - treat with penicillin Rubella immunity - don't give MMR if not immune (live vaccine) Blood glucose
253
Which screening test results indicate higher risk of Down's syndrome?
Higher nuchal translucency Higher B-HCG Lower pregnancy associated plasma protein A Lower serum oestriol Higher inhibin-A
254
Describe the incidence of multiple pregnancies
15 per 1000 UK
255
List risk factors for multiple pregnancies
Assisted conception - IVF, ovulation induction Maternal age Ethnic origin - West African Family history - maternal inheritance
256
Define: Zygosity Chorionicity Amniocity
Zygosity - number of fertilised eggs Chorionicity - number of placentas Amniocity - number of sacs
257
List the types of multiple pregnancies in terms zygosity, chorionicity, amniocity
Dizygotic - two eggs, two sperm, as genetically similar as siblings Monozyogtic - start as one fertilised egg then split: Before day 4 - dichorionic, diamniotic (1/3) Day 4-8 - monochorionic, diamniotic (2/3) From day 9 - monochorionic, monoamniotic (rare)
258
List the maternal risks of multiple pregnancies
All minor complications increased Hyperemesis gravidarum Pre-eclampsia (x 2-3) Gestational diabetes Placenta praevia Polyhydramnios Hypertension Malpresentation Instrumental delivery or caesarean Post-partum haemorrhage
259
List the fetal risks of multiple pregnancies
Miscarriage Congenital anomalies Fetal growth restriction Prematurity Twin-twin transfusion syndrome Twin anaemia polycythaemia sequence
260
Describe the pathophysiology and consequences of twin-twin transfusion syndrome
In monochorionic pregnancies Connection between blood supplies of fetuses, recipient receives majority of blood, donor is starved of blood Recipient gets fluid overloaded, heart failure and polyhydramnios Donor has growth restriction, anaemia, oligohydramnios
261
What is twin anaemia polycythaemia sequence?
Similar to twin-twin transfusion syndrome but less acute - one twin anaemic, other polycythaemic
262
How are multiple pregnancies managed antenatally?
Managed by specialist obstetric team Additional monitoring for anaemia - FBC at booking clinic, 20 weeks, 28 weeks Additional USS for fetal growth restriction, unequal growth, twin-twin transfusion - 2 weekly scans from 16 weeks for monochorionic, 4 weekly scans from 20 weeks for dichorionic
263
Describe the management of multiple pregnancies in delivery
Planned birth offered between: 32-33+6 for uncomplicated monochorionic monoamniotic twins 36-36+6 - for uncomplicated monochorionic diamniotic twins 37-37+6 - uncomplicated dichorionic diamniotic twins Before 35+6 for triplets Delivery: Monoamniotic - elective caesarean section Diamniotic - vaginal delivery for first baby with cephalic presentation, caesarean for second baby Elective caesarean if presenting twin not cephalic Analgesia for mum - often epidural Monitoring during labour - BP, IV access, fluids, continuous CTG, abdominal and fetal scalp electrode,
264
Describe postnatal management of multiple pregnancy
Increased risk postpartum haemorrhage Increased risk of postnatal depression, anxiety, relationship difficulties - counselling, emotional support, low threshold for suspecting perinatal psychological disturbance
265
List the specific complications which are associated with monochorionic twin pregnancies
Acute transfusion Twin-twin transfusion syndrome Twin reversed arterial perfusion sequence
266
Define acute transfusion in monochorionic twin pregnancies
Death of one twin in utero leads to increased risk of hypoxic-ischaemic injury in survivor due to acute transfusion from healthy to dying twin
267
Define twin reversed arterial perfusion syndrome
Two cords linked by a large arterio-arterial anastamosis, retrograde perfusion - ‘pump twin’ and ‘perfused twin’ Pump twin - normal, drives blood flow through both fetuses, can develop heart failure Perfused twin - acardiac, no chance of survival
268
Describe the three stages of labour
First stage - onset of labour until cervix fully dilated, further divided into two stages: 1. Latent - onset of contractions until cervix fully effaced and 3-4cm dilated 2. Active - until full cervical dilatation (10cm) Second stage - from full cervical dilatation (10cm) until baby is delivered, further divided into two stages: 1. Propulsive - full dilatation until head has descended onto pelvic floor 2. Expulsive - from time mother has an irresistible urge to bear down and push until baby is delivered Third stage - from delivery of baby until expulsion of placenta and membranes
269
Define effacement and dilatation of the cervix and describe how these processes occur
Effacement - thinning, begins with internal os and proceeds downwards to external os until cervical tissue becomes continuous with uterine walls Dilatation - opening up of external os Prim: effacement before dilatation Parous: effacement and dilatation can occur simultaneously
270
List the signs that labour is starting and the criteria for confirming labour
Signs of labour starting: Contractions 'Show' - mucus plug in cervix falls out Back pain Urge to move bowels - baby's head pressed on bowel Waters breaking (spontaneous rupture of membranes) Labour confirmed if: Regular contractions and fully effaced cervix Spontaneous rupture of membranes and regular uterine activity
271
List the factors which lead to the initiation of labour
Inhibition of pro-pregnancy factors: Progesterone - levels same but difference in receptors? Nitric oxide? Catecholamines? Activation of pro-labour factors: Oxytocin - increase in receptor levels, increased frequency and force of contractions Prostaglandins - increased levels, cervical ripening and uterine contractility Inflammatory cells and cytokines - cervical ripening, membrane rupture
272
How is cervical ripening assessed?
Bishop score - 0, 1, 2 for: Dilatation - <1, 1-2, 3-4 Length of cervix (effacement) - >2, 1-2, <1 Station of presenting part - spines-3, spines-2, spines-1 Consistency - firm, medium, soft Position - posterior, central anterior
273
Define engagement and station
Engagement of the presenting part - on abdominal examination how many fifths of the fetal head are palpable above the pelvic brim, refers to widest part of fetal head descending into maternal pelvis Fully engaged when fetal head is 3/5th palpable or less Station of the presenting part - position of widest part of fetal head in relation to ischial spines, spines is zero station, above spines -1, -2 etc., below spines +1, +2 etc.
274
How is the position of the fetal head determined in labour? What is the normal orientation of the head during labour?
Orientate using position of fontanelles - posterior fontanelle is triangle shaped, anterior is diamond shaped Begins in right or left occipitotransverse at pelvic brim When head reaches pelvic floor, rotates to occipitoanterior Shoulders deliver in AP diameter, head follows in external rotation (restitution)
275
Describe the passage of the baby through the pelvis and the normal delivery of a baby
Cardinal movements of labour: Engagement - engaged when fetal head is 3/5ths or less palpable above pelvic brim Descent - measured in relation to ischial spines (engagement) Flexion - head at pelvic brim in R/L occipitotransverse position, neck flexed so that presenting part is suboccipitobregmatic (smallest diameter) Internal Rotation - rotates to occipitoanterior Extension - head delivers by neck extension Restitution and external rotation - shoulders rotate to AP diameter, continued descent, head follows in external rotation (restitution) Expulsion - anterior shoulder delivers with lateral flexion, posterior shoulder delivers
276
How is a CTG recorded?
Two transducers on abdomen - one records fetal heart rate using US, other monitors contractions of uterus by measuring the tension of the abdominal wall
277
How is a CTG interpreted?
Mnemonic - DR C BraVADO DR - define risk Is pregnancy high or low risk? Based on maternal PMHx, obstetric complications, SHx e.g. smoking C - contractions Number present in 10 minutes - peaks in 10 big squares Duration and intensity (palpation) Bra - baseline rate of fetal heart Average HR in 10 minutes (ignore accelerations and decelerations) Tachycardia >160 Bradycardia <110, severe prolonged is <80 for more than 3 minutes V - variability Normal (reassuring) - 5-25bpm Non-reassuring - <5bpm for 30-50 minutes or >25 for 15-25 minutes Abnormal - <5 for >50 minutes or >25 for >25 minutes, sinusoidal A - accelerations Abrupt increase in baseline HR of >15bpm for >15 seconds - reassuring D - decelerations Abrupt decrease in baseline HR of >15bpm for >15 seconds Early decelerations - start wen uterine contractions begin, recover when uterine contractions stop, physiological Variable decelerations - rapid fall in baseline HR with variable recovery phase, usually caused by umbilical cord compression Accelerations before and after variable decelerations = shoulders of deceleration, means fetus is adapting to reduced blood flow, not yet hypoxic, if persistent need close monitoring Without shoulders - suggests they are becoming hypoxic Late deceleration - begin at peak. ofcontraction, recover when contraction ends, indicates fetal hypoxia Prolonged deceleration - >2 minutes, 2-3 is non-reassuring, >3 minutes is abnormal Sinusoidal - smooth, regular wave, no beat-to-beat variability, very worrying with high mortality O - overall impression Reassuring Suspicious Abnormal
278
Describe the use of a partogram and the observations recorded on them
Provides a graphic record of clinical findings and any relevant events during labour Records maternal observations (BP, HR, temp), fetal heart rate, progressive cervical dilatation, descent of the presenting part, strength and frequency of contractions, and colour of amniotic fluid. Uterine activity recorded over a 10 minute period Two lines which indicate is labour is not progressing adequately, labelled 'alert' and 'action' - crossing alert line is an indications for an amniotomy and repeat examination in 2 hours, crossing action means care should be escalated to obstetric-led care
279
Describe the anatomical changes which occur in the uterus during pregnancy
Uterus increases in size - expands outside of pelvic cavity into abdominal cavity, displaces abdominal organs 100mg --> 1.1kg Hypertrophy of myometrium and blood vessels in uterus Fundus moves down after week 38 to prepare for labour
280
Describe the changes which occur in the cervix during pregnancy
Increased oestrogen may cause cervical ectropion and increased cervical discharge
281
List the uterotonic hormones commonly used in practice and describe their uses
Oxytocin (syntocinon): First line for stimulation of contractions during labour (failure to progress), infusion started at low rate and titrated up at intervals of at least 30 minutes as required, aim for 4-5 contractions per 10 minutes Active management of third stage of labour - reduces risk of primary postpartum haemorrhage, 5-10 units IM for vaginal deliveries, 5 units IV for CS Management of post-partum haemorrhage (primary/secondary) Other uterotonics: Syntometrine (oxytocin + ergometrine) Carboprost (prostoglandin F2) Misoprostol (prostaglandin E1)
282
Describe the mechanism of action, side effects and contraindications of uterotonic drugs
283
Define tocolysis and give examples of tocolytic drugs
Using medications to suppress uterine contractions in premature labour - short term measure for <48 hours First-line - nifedipine (CCB) Second-line - atosiban (oxytocin receptor antagonist)
284
Define pre-term birth
Birth before 37 weeks gestation Under 28 weeks - extreme preterm 28-32 weeks - very preterm 32-37 - moderate to late preterm
285
List the risk factors for pre-term delivery
Aetiology largely unknown Association with infection/inflammation - intrauterine infection, urinary tract infection, bacterial vaginosis Previous pre-term birth - strongest predictive factor Multiple pregnancy 1st or 2nd trimester bleeding Antepartum haemorrhage Placenta praevia Pre-labour rupture of membranes Fetal growth restriction Congenital fetal anomaly Polyhydramnios Congenital uterine anomaly Pre-eclampsia Psychological stress, DV
286
Define pre-term labour and pre-term pre-labour rupture of the membranes
Pre-term labour: regular uterine contractions accompanied by effacement and dilatation of the cervix after 20 weeks and before 37 weeks Pre-term Pre-labour rupture of the membranes (PPROM): rupture of the fetal membranes before 37 completed weeks and before the onset of labour
287
List complications associated with pre-term delivery
Perinatal mortality - non-viable before 23 weeks, 10% chance of survival Neonatal problems: Respiratory distress syndrome Hypothermia Hypoglycaemia Poor feeding Apnoea and bradycardia Neonatal jaundice Intraventricular haemorrhage Retinopathy of prematurity Necrotising enterocolitis Immature immune system and infection Long term effects: Long term disability in 10% overall e.g. chronic lung disease of prematurity, cerebral palsy, blindness, deafness Lesser developmental/behavioural problems Susceptibility to infections, especially respiratory tract infections
288
How is pre-term labour managed?
Prophylaxis - high risk e.g. previous pre-term birth or loss, cervical length <25mm Vaginal progesterone, cervical cerclage (stitch in cervix) Pre-term pre-labour rupture of membranes - prophylactic antibiotics Dilated cervix and unruptured membranes (16-27 weeks) - emergency cervical cerclage Unruptured membranes in suspected/diagnosed pre-term labour (24-33+6 weeks) - tocolysis with nifedipine Maternal corticosteroids (IM betamethasone or dexamethasone) - for suspected, diagnosed, established, planned pre-term labour or P-PROM, up to 2 cources, for 24-35+6 weeks
289
Why are maternal steroids given in pre-term labour?
Cross the placenta and increase the amount of pulmonary surfactant produced by type II fetal pneumocytes - reduces the incidence of respiratory distress syndrome (hyaline membrane disease) Also reduce - intraventricular cerebral haemorrhage, neonatal death, necrotizing enterocolitis, neonatal intensive care admission No adverse neurological or cognitive effects No identifiable increase in the incidence of maternal or fetal infection, but contraindicated if there is active maternal sepsis
290
Define post-dates/term pregnancy
Prolonged/post-term - pregnancy which persists up to and beyond 42 weeks gestation Post-dates - pregnancy extended beyond the estimates delivery date
291
What are the clinical problems of post-term pregnancy for the mother?
Labour dystocia Severe perineal lacerations Operative vaginal delivery Caesarean section Post-partum haemorrhage Chorioamnionitis
292
What are the clinical problems of post-term pregnancy for the fetus?
Increased perinatal mortality rate - stillbirths and early neonatal deaths Causes - meconium aspiration syndrome, neonatal acidosis, neonatal encephalopathy Macrosomia - shoulder dystocia, fractured humerus/clavicle, brachial plexus injury, prolonged labour Dysmaturity syndrome - utero-placental insufficiency
293
List the methods used for induction of labour
Unfavourable cervix (Bishop <6) Vaginal prostaglandins - tablet, gel, pessary, one cycle per 24 hours Cervical ripening (Cook's) balloon - silicone balloon inserted into cervix and inflated to dilate cervix Favourable cervix (Bishop >6) Artificial rupture of membranes - amniotomy using amnihook, with oxytocin infusion Membrane sweep - not full method of induction, used to assist before full IOL, used from 40 weeks
294
List indications for induction of labour
Post-term pregnancy - 41-42 weeks Prelabour rupture of membranes Fetal growth restriction Pre-eclampsia Obstetric cholestasis Existing diabetes Intrauterine fetal death
295
What should be done if a post-term women declines induction of labour?
Twice weekly CTG monitoring and USS with amniotic fluid measurement to identify fetal distress - may need CS
296
What are the contraindications for induction of labour?
Absolute: Cephalopelvic disproportion Major placenta praevia Vasa praevia Cord prolapse Transverse lie Active primary genital herpes Previous classical Caesarean section Relative: Breech Triplet or higher order Two or more previous low transverse caesarean sections
297
How should women in whom labour has been induced be monitored?
Bishop score CTG
298
What are the complications of IOL?
Failure of induction Uterine hyperstimulation - causes fetal distress, can be managed with tocolytic agents Cord prolapse - especially if fetal head position is high Infection Pain - often need epidural Increased rate further intervention vs spontaneous e.g. emergency CS Uterine rupture - rare
299
List the criteria for diagnosis of failure to progress at each stage of labour
First stage - less than 2cm cervical dilatation in 4 hours, slow of progress in multiparous women Second stage - 2 hours in nulliparous, 1 hour in multiparous Third stage - >30 minutes active management, >60 minutes physiological
300
How is failure to progress managed?
Amniotomy if intact membranes Oxytocin infusion Instrumental delivery Caesarean section
301
List the options for pain management in labour
Non-pharmacological: Breathing and relaxation techinques Massage techniques Birthing pool Environment - music, mobilise, different positions Education Other - acupuncture, acupressure, hypnosis, TENS (limited evidence) Pharmacological: Non-regional Inhalational analgesia - Entonox (50:50 mixture of oxygen and nitrous oxide) IV and IM opioids - pethidine, diamorphine, PCA (remifentanil) General anaesthetic Regional Epidural Spinal Pudendal nerve block
302
Compare the options for regional anaesthesia in labour
Epidural: Generally used for labour, can be topped up for instrumental delivery Usually given on maternal request, indications e.g. twin delivery Extra-dural catheter placement May have patchy analgesic effect Spinal: Used for operative delivery/surgical management of post-partum complications Subarachnoid injection One-off, lasts 2-4 hours Dense, reliable anaesthetic blockade
303
List potential adverse effects of regional anaesthesia in labour
Dural puncture headache Hypotension - blockage of sympathetic tone to peripheral vessels Local anaesthetic toxicity - if injected into blood vessel, CV collapse and death Accidental total spinal block - injection of epidural doses into subarachnoid space, travels up spinal column leading to loss of consciousness, respiratory depression, hypotension Neurological damage - abscess, stretch injury, nerve ischaemia Longer second stage of labour Increased chance of vaginal instrumental birth Motor weakness of legs Bladder dysfunction - overdistension due to loss of sensation, catheterise if voiding difficulties
304
List side effects of non-regional analgesia used during labour
Entonox - lightheadedness, nausea, drowsiness Opioids - drowsiness, nausea in mother (give anti-emetic), respiratory depression in baby if given too close to birth, may interfere with breastfeeding
305
How many pregnancies are affected by diabetes in the UK
5% of pregnancies in the UK affected by diabetes: 87.5% GDM 7.5% T1DM 5% T2DM
306
Define type 1 diabetes, type 2 diabetes and gestational diabetes
Diabetes = metabolic disorder characterised by persistent hyperglycaemia (random BM >11) with disturbances of carbohydrate, protein and fat metabolism resulting from defects in insulin secretion (leading to insulin deficiency), insulin action (leading to insulin resistance) or both Type 1 - absolute insulin deficiency causes persistent hyperglycaemia Type 2 - insulin resistance and relative insulin deficiency result in persistent hyperglycaemia Gestational diabetes - hyperglycaemia develops during pregnancy and usually resolves after delivery, although woman is at increased risk of type 2 diabetes in the future
307
Describe normal glucose physiology in pregnancy
Increasing insulin resistance (or reduced insulin sensitivity) - gluconeogenesis and fatty acid levels increase to counter this Fasting glucose decreased (dilutional due to blood volume increase, increased glucose utilisation by fetus) and post prandial increased compared to non-pregnant Placenta produces human placental lactogen which increases insulin resistance and human chorionic somatotrophin which increases production of insulin Normal women double insulin production from 1st to 3rd trimester Glycosuria common (filtered Glucose > tubular resorption capacity) Ketosis also more common in pregnancy
308
Describe how maternal insulin requirements change with gestation
1st trimester - static or decrease 2nd trimester - increase 3rd trimester - increase, may reduce slightly towards term
309
Describe the maternal risks of pre-existing diabetes in pregnancy
Infections, particularly UTI DKA Pre-eclampsia Hypoglycaemia Macrosomia - birth trauma (e.g. tears), induction of labour, instrumental and caesarean section deliveries (50% operative deliveries) Retinopathy Nephropathy
310
Describe the fetal risks of pre-existing diabetes in pregnancy
Polyhydramnios (fetal polyuria) - unstable lie, malpresentation, pre-term labour Miscarriage Congenital malformations Stillbirth Neonatal death Fetal macrosomia - birth trauma (e.g. dystocia) Transient neonatal morbidity - hypoglycaemia, hypocalcaemia, hyperbilirubinaemia, polycythaemia, idiopathic respiratory distress syndrome, delayed lung maturity Obesity/diabetes in later life
311
How can the risks of pre-existing diabetes in pregnancy be reduced?
Pre-conception care Avoid unwanted/unplanned pregnancy - contraceptive Good glycaemic control prior to pregnancy ideally - aim for HbA1c 48 or less (avoid if >86) Folic acid 5mg/day from 3 months pre-conception until 12 weeks gestation Education about risks Aim for BMI <27 How to manage pregnancy-associated hypoglycaemia, reduced hypoglycaemic awareness, pregnancy-related nausea and vomiting Pre-pregnancy retinal and renal assessment Antenatal care Increased monitoring - obstetric review 4 weekly until 28 weeks, 2 weekly until 36 weeks, then weekly Offer serum screening and detailed anomaly and cardiac scan Retinal and renal screening at booking and 28 weeks Intrapartum Planned delivery 37 - 38+6 weeks Usually sliding scale for type 1, keep BM 4-7 Post-partum Encourage breastfeeding - early and regular Rapid reduction of insulin requirement, usually back to pre-pregnancy dose immediately
312
Describe target blood glucose and HbA1c levels prior to pregnancy
Fasting plasma glucose - 5-7 on waking 4-7 before meals or other times of day Keep HbA1c <48 Avoid pregnancy if HbA1c >86
313
Describe the use of antihyperglycaemic medications and medications used in complications of diabetes in pregnancy
Metformin can be used during pregnancy, all other oral blood glucose-lowering agents should be stopped before pregnancy, use insulin instead Stop ACEi and ARBs before conception or as soon as pregnancy confirmed - use alternative anti-hypertensive agents suitable for pregnant women Stop statins before pregnancy or as soon as pregnancy confirmed
314
Who should be offered screening for gestational diabetes? How is this done?
Any of these risk factors: BMI >30 Previous macrosomic baby weighing 4.5kg or more Previous gestational diabetes Family history of diabetes (first-degree relative) Ethnicity with high prevalence of diabetes Use 75g 2-hour oral glucose tolerance test (OGTT) to rest for gestational diabetes in women with any risk factors, at 24-28 weeks Normal results: Fasting <5.6 At 2 hours <7.8
315
Describe the short term implications of gestational diabetes for the mother and fetus
Maternal: Gestational hypertension Pre-eclampsia Birth trauma Induction of labour Operative delivery Fetal: Macrosomia - shoulder dystocia and other birth trauma Fetal hypoglycaemia, hypocalcaemia Hyperbilirubinaemia Polycythaemia Respiratory distress Perinatal death ?Congenital anomalies
316
Describe the long term implications of gestational diabetes for the mother and fetus
Maternal: Increased risk subsequent gestational diabetes Increased risk persistent T2DM Fetal: Increased risk of obesity and T2DM Increased risk of cardiovascular disease
317
Describe the antenatal care of women with gestational diabetes
Diet and exercise - low glycaemic index diet Education - importance of good glycaemic control, teach how to monitor It blood glucose targets not met with diet and exercise changes within 1-2 weeks - give metformin If blood glucose targets not met with metformin, offer insulin as well Advise delivery no later than 40+6 weeks Retinal and renal assessment US screening including cardiac abnormalities at 20 weeks Monitor fetal growth and amniotic fluid volume every 4 weeks from 28-36 weeks 1-2 weekly joint diabetes and antenatal clinics
318
Describe intrapartum care of women with gestational diabetes
Advise to give birth no later than 40+6 weeks - elective birth by induced labour or CS if haven't given birth by this time (earlier if complications) Keep blood glucose 4-7 - use IV dextrose and insulin infusion
319
Describe postpartum care of women with gestational diabetes
Babies BM 2-4 hourly after birth Feed as soon as possible after birth (within 30 minutes), continue at frequent intervals until pre-feed BM is a minimum of 2 Only use additional measures (e.g. tube feeding, IV dextrose) if BM <2, abnormal clinical signs, baby will not feed orally Immediately reduce insulin/oral antihyperglycaemics after birth Give lifestyle advice Fasting plasma blood glucose 6-13 weeks post-partum to exclude diabetes - >7 indicates T2DM
320
Describe the prevalence of thyroid disease in pregnancy
Affects 5-7% of pregnancies
321
Describe the changes in thyroid function related to pregnancy
Fetal thyroxine is wholly obtained from maternal sources in early pregnancy since the fetal thyroid gland only becomes functional at 12 weeks Thyroxine is essential for fetal neurodevelopment  In pregnancy, iodide losses through the urine and the feto-placental unit contribute to a state of relative iodine deficiency Pregnant women require additional iodine intake - recommended 250 µg per day Total thyroid hormone concentrations in blood are increased in pregnancy, partly due to the high levels of oestrogen and due to the weak thyroid stimulating effects of human chorionic gonadotropin (hCG) that acts like TSH. Thyroxine (T4) levels rise from about 6–12 weeks, and peak by mid-gestation; reverse changes are seen with TSH.
322
How should thyroid function tests be interpreted in pregnant women?
Use pregnancy specific ranges Variable at different gestations
323
Describe the development of thyroid function in the fetus
Fetal thyroid gland develops 7-9 weeks Placental transfer of T4 prior to 12 weeks From 12 weeks fetal thyroid function independent (in presence of adequate iodine)
324
List the potential complications associated with maternal hypothyroidism in pregnancy
Miscarriage/stillbirth Anaemia Small for gestational age Pre-eclampsia Abnormal neurophysiological development - loss of IQ points Placental abruption Prematurity
325
How should women with hypothyroidism be managed before and during pregnancy?
Check TFTs before conception - if euthyroid on levothyroxine safe to conceive, if not euthyroid advise delaying conception to stabilise on levothyroxine Monitor TFTs throughout pregnancy using adjusted reference ranges - adjust levothyroxine dose as required Contentious - changing dose in early pregnancy even if euthyroid?
326
What possible complications are associated with maternal hyperthyroidism in pregnancy?
If uncontrolled: Miscarriage Intrauterine growth restriction Preterm delivery Perinatal morbidity
327
Describe the clinical features of hyperthyroidism in pregnancy
Pregnancy symptoms can be similar to hyperthyroidism symptoms so can be difficult to tell - heat intolerance, palpitations, palmar erythema, emotional lability, tachycardia, increased T4/decreased TSH Distinguishing features: Weight loss Eye signs Pre-tibial myxoedema Tremor
328
Describe the effect of pregnancy on thyrotoxicosis
Often improves, especially in 2nd/3rd trimester State of relative immunosuppression, fall in TSH-stimulating antibody No effect on Grave's ophthalmology
329
How is hyperthyroidism managed in pregnancy?
Antithyroid drugs - carbimazole or propylthiouracil Block thyroid hormone synthesis and immunosuppressive Both can cross placenta - use lowest effective dose as can potentially cause fetal thyroid suppression (at high doses) Propranolol (monitor fetal growth) Serial TFT monitoring - at least monthly Rarely surgery indicated Radioactive iodine contraindicated Check neonatal TFTs at regular intervals if breast feeding mother on high doses PTU or carbimazole (less PTU secreted in breast milk so safer)
330
Describe the immunological basis of Grave's disease and the relevance of this in pregnancy
TSH receptor antibodies - mimic TSH and stimulate production of thyroid hormone Antibodies can in theory cross placenta and stimulate fetal TSH receptor
331
How are women with Grave's disease monitored in pregnancy?
If currently thyrotoxic or history of thyrotoxicosis treated with surgery/radioactive iodine: Monitor signs of fetal hyperthyroidism - IUGR, fetal goitre, heart rate Measure antibodies in last trimester - if high consider neonatal hyperthyroidism TFTs monitored Plan for postnatal medication and suitability for breastfeeding
332
Describe how maternal Grave's disease can affect the fetus
Miscarriage Stillbirth IUGR Fetal/neonatal thyrotoxicosis
333
Define post-partum thyroiditis
Changes in thyroid function within 12 months of delivery, affecting women with a history of thyroid disease Can involve thyrotoxicosis , hypothyroidism or both
334
Describe the typical pattern of postpartum thyroiditis
Thyrotoxicosis - usually in first three months Hypothyroid - 3-6 months Thyroid function gradually returns to normal (usually within a year)
335
How is postpartum thyroiditis managed?
Low threshold for testing thyroid function, especially in postnatal depression - test TFTs 6-8 weeks after delivery Thyrotoxicosis - symptomatic control e.g. propranolol Hypothyroidism - levothyroxine Annual monitoring of TFTs to identify those with long-term hypothyroidism
336
Describe the incidence of epilepsy in pregnancy
0.3-0.7% of obstetric population Most common neurological condition in pregnancy
337
What is the impact of epilepsy on fertility and contraceptives?
Fertility: Doesn't affect fertility itself but some anti-epileptic drugs (AEDs) do e.g. phenobarbitol Contraceptives: Enzyme-inducing AEDs (carbamazepine, phenytoin, phenobarbital, primidone, oxcarbazepine, topiramate and eslicarbazepine) can affect efficacy of some hormonal contraceptives - if on these AEDs should be offered IUD (copper or Mirena) or medroxyprogesterone acetate injection, copper coil for emergency contraception Non-enzyme-inducing AEDs (e.g. sodium valproate, levetiracetam, gabapentin, vigabatrin, tiagabine and pregabalin) can be offered all methods of contraception
338
Why is pre-pregnancy planning necessary for women with epilepsy?
Discuss risks to unborn child of AEDs - assess risks and benefits of individual treatment options (specifically risk of sodium valproate - contraindicated in pregnancy), review medication options, importance of adherence to medications, do not stop medication without supervision High dose folic acid 5mg daily - higher risk of neural tube defects, AEDs reduce availability of folate
339
Describe the teratogenicity of anti-epileptic drugs
Sodium valproate - avoid pregnancy, causes neural tube defects e.g. spina bifida, congenital heart defects, withdrawal, neurodevelopmental problems (ADHD, ASD), facial malformation e.g. cleft palate, hypospadias, polydactyly Phenytoin - congenital malformations, neurodevelopmental problems, cleft lip Safer anti-epileptics in pregnancy - levetiracetam, lamotrigine, carbamazepine Worse with polypharmacy and higher doses
340
Describe the effects of pregnancy on seizure control
First trimester - 64% no change, 16% better, 17% worse Reduced compliance with AEDs, reduced absorption (N+V), reduced sleep, reduced drug levels (increased volume of distribution, increased metabolism - lamotrigine) Seizures not harmful to pregnancy other than risk of physical injury
341
Describe antenatal management of epilepsy
Notify pregnancy - UK epilepsy and pregnancy register Therapeutic drug monitoring - individual 'therapeutic target level' set pre-pregnancy Screening for birth defects - 11-13 weeks for acrania, nuchal 20 weeks for neural tube defect, heart, face, limbs +/- serum screening Advice on bathing etc.
342
Describe the complications of pregnancy associated with maternal epilepsy
May have increased seizure activity Sudden unexplained death with epilepsy - more common in pregnancy Teratogenic effects of AEDs - neural tube defects, cardiac malformations, neurodevelopmental defects, cleft lip Haemorrhagic disease of the newborn - AEDs induce fetal hepatic enzyme activity, lower Vitamin K, neonatal bleeding
343
Describe the intrapartum management of epilepsy
IV access Continue AEDs at normal time - give parenterally if can't be tolerated orally Avoid maternal exhaustion Adequate analgesia Long-acting benzodiazepines considered if high risk of seizures Should terminate seizures in labour as soon as possible to avoid maternal and fetal hypoxia and fetal acidosis
344
Describe postnatal management of epilepsy
Continue AEDs Minimise triggers - sleep deprivation, stress, pain Plasma levels of AEDs fluctuate (up to 8 weeks) - monitor and adjust dose Mostly no increased risk to baby with breastfeeding Consider contraceptives
345
Describe the varicella zoster virus and its method of spread and infectivity
DNA virus which causes chickenpox (primary infection), shingles (viral reactivation) Highly contagious, spread through direct contact with lesions or infected droplets from cough or sneeze Become symptomatic 10 days to 3 weeks after exposure Stop being contagious after lesions have crusted over
346
Describe the incidence of varicella zoster virus infection in pregnancy
>90% seropositive for IgG antibody Primary infection 1 in 1000
347
Describe maternal complications of varicella zoster virus infection in pregnancy
Pneumonia Encephalitis - ataxia Conjunctival lesions Dehydration Bacterial superinfection Reactivation later in life as shingles or Ramsay-Hunt syndrome
348
Describe the fetal complications of maternal varicella zoster virus infection before 20 weeks
Intrauterine infection --> fetal varicella syndrome - Skin scarring in dermatomal distribution Eye defects - microphthalmia, chorioretinitis, cataracts, optic atrophy Hypoplasia of limbs Neurological abnormalities - microcephaly, cortical atrophy, learning difficulties, dysfunction of bowel and bladder sphincters, seizures, Horner's syndrome
349
Describe the neonatal consequences of maternal varicella zoster virus infection in late pregnancy
If in the last 4 weeks of pregnancy there is significant risk (50%) of varicella infection of the newborn Infection can be transplacental, vaginal or through direct contact after birth Can be asymptomatic If symptomatic often severe chickenpox infection - fever, rash, can develop disseminated or haemorrhagic varicella
350
Describe the risk assessment of women exposed to varicella zoster virus in pregnancy
Assess risk from history - if known to be immune (previous chickenpox) then no further action required If unknown or no previous infections used serum varicella zoster IgG to confirm immunity status IgM serum testing/PCR for varicella zoster DNA can be used to confirm acute infection
351
How is varicella zoster managed in pregnancy and in neonates?
If seronegative for varicella zoster IgG pre-pregnancy or post-partum can be vaccinated - not recommended during pregnancy as is a live virus Suspected varicella contact and non-immune - <20 weeks - give varicella zoster immunoglobulin (VZIG) within 10 days of contract and before onset of rash >20 weeks - VZIG or aciclovir from days 7-14 following exposure Potentially infectious from 8-28 days Maternal chickenpox Aciclovir (800mg PO 5 tds) if within 24 hours rash onset and >20 weeks gestation Serial US examinations to identify fetal abnormalities Varicella of the newborn - VZIG +/- aciclovir
352
Describe the inheritance of rhesus status
D antigen gene (positive) is dominant, d (lacking D antigen so negative) is recessive If mother is negative (homozygous) and father is positive (heterozgous) child has 50% chance of being positive, if father is positive (homozygous) child has 100% chance of being positive
353
Describe the immunological response which occurs when an Rh negative mother carries a Rh negative baby
Mother exposed to fetal rhesus-D antigens e.g. during delivery, produces anti-D antibodies against these antigens = sensitisation Usually doesn't cause problems during first pregnancy, during subsequent pregnancies the anti-rheusus D antibodies can cross the placenta into the fetus, if fetus is rhesus positive maternal antibodies attack fetal red blood cells
354
List potential rhesus sensitising events
Management of ectopic pregnancy Management of molar pregnancy Therapeutic termination of pregnancy <12 weeks vaginal bleed which is heavy, repeated or associated with severe pain <12 weeks medical or surgical management of miscarriage Potentially sensitising event >12 weeks Obstetric interventions - CVS, amniocentesis, external cephalic version in breech presentation Abdominal injury e.g. fall, blow to abdomen Pre-pregnancy sensitisation - ?blood transfusions Intrauterine death Delivery - normal, instrumental or caesarean
355
Describe haemolytic disease and its presentation and consequence in the antenatal period
Polyhydramnios Thickened placenta Hydrops fetalis - Sub-cut oedema Pleural/pericardial effusions Ascites Hepato-splenomegally In-utero demise Anaemia
356
Describe haemolytic disease and its presentation and consequences for the newborn
Jaundice Hepato-spenolmegaly Pallor Kernicterus - bilirubin-induced brain dysfunction, causes movement disorders, auditory dysfunction, visual impairment, dental problems Hypoglycaemia Anaemia - can cause high-output heart failure
357
Describe the monitoring of pregnancy antenatally for rhesus incompatibility and the consequences of this
Maternal blood group and antibody titres at booking visit and 28 weeks - determine ABO and RhD groups and detect any antibodies directed against RBC surface antigens (previous sensitisation), if rhesus-positive no further management required If rhesus-negative without previous sensitisation - after delivery, rhesus status of baby should be checked, if RhD+ a feto-maternal haemorrhage test should be performed (Kleihauer test) - tests how much fetal blood has entered maternal circulation to determine dose of anti-D If rhesus-negative with previous sensitisation - anti-D not effective, pregnancy monitored more closely (frequent USS), can do fetal blood group amniocentesis, free fetal DNA, paternal blood group to determine fetal Rh status
358
Describe methods of preventing Rh disease and the use of Anti-D
All women who are RhD- are offered routine antenatal anti-D prophylaxis at 28 and 34 weeks gestation (some centres give single larger dose at 34 weeks) Management of sensitising events: <12 weeks - ectopic pregnancy, molar pregnancy, termination or heavy uterine bleeding, give 250 IU anti-D within 72 hours of event 12-20 weeks - any potential sensitising event, 250 IU anti-D within 72 hours of event >20 weeks - any potential sensitising event, 500 IU within 72 hours of event, dose increased depending on size of feto-maternal haemorrhage
359
How is in-utero haemolytic disease managed?
Neonatal exchange transfusion Early delivery
360
List the common physiological changes to the skin in pregnancy
Increased skin pigmentation due to increased melanocyte stimulating hormone - linea nigra and melasma Striae gravidarum - stretch marks on expanding abdomen Pruritus - can be normal, can indicate obstetric cholestasis Spider naevi Palmar erythema Greasier skin Hair and nail changes - increased growth during pregnancy then post-partum hair loss
361
Describe the presentation of atopic eruption of pregnancy
Onset early in pregnancy - <3rd trimester Trunk and limbs involved 20% have previous history of eczema Eczematous type - rough, red patches Prurigo - bumps
362
How is atopic eruption of pregnancy managed?
Emollients Aqueous cream and menthol 1-2% Topical steroids Antihistamines Narrow band UVB 2nd line Oral steroids if severe (30mg pred)
363
Describe the presentation of polymorphic eruption of pregnancy
3rd trimester or post-partum 3/4 primigravid Pruritic eruption lower abdomen and striae with umbilical sparing and distant spread
364
How is polymorphic eruption of pregnancy managed?
Provide self-care advice to relieve itching Prescribe symptomatic treatment where necessary Emollients can be used liberally to soothe the skin Moderately-potent topical corticosteroids can be used to reduce inflammation Offer a sedating antihistamine (such as chlorphenamine or promethazine) if itch is causing sleeping difficulties (off-label indication)
365
Describe the presentation of pemphigoid gestationis, its pathophysiology and associated risks
Rare 2nd/3rd trimester Urticarial lesions, wheals and bullae, umbilical area Pathophysiology Autoimmune - binding of IgG to basement membrane Risks are rare and include Premature delivery Fetal growth restriction Transient blistering on the infant that resolves with clearance of maternal antibodies (about 3-4 months) – 10% Secondary infection, which may leave scarring
366
How is pemphigoid gestationis managed?
Refer to derm and obs Mild - topical steroids, antihistamines Moderate and severe - systemic steroids Additional monitoring due to risk of pre-term birth and reduced fetal growth
367
Which antihypertensives are contraindicated in pregnancy and which are safe to use?
Should be stopped: ACE inhibitors ARBs Thiazide and thiazide-like diuretics Not known to be harmful: Labetalol (beta-blocker) Calcium channel blockers e.g. nifedipine Alpha blockers e.g. doxazocin
368
Describe the risk of VTE in pregnancy
Pregnancy is a major risk factor for VTE - 4-5x increased risk Risk increases as pregnancy progresses - highest risk is post-partum
369
List risk factors for VTE in pregnancy
Pre-existing factors: Age >35 BMI >30 Parity >3 Smoking Varicose veins Thrombophilia Medical co-morbidities e.g. cancer Obstetric factors: Multiple pregnancy Pre-eclampsia Caesarean section Prolonged labour Stillbirth Pre-term birth PPH Transient factors: Surgical procedures Dehydration e.g. hyperemesis Ovarian hyperstimulation syndrome Admission or immobility Systemic infection Long distance travel
370
How is VTE in pregnancy managed?
LMWH immediately following diagnosis - titrated against booking weight Anticoagulation maintained throughout pregnancy if confirmed VTE until 6-12 weeks post-partum Omit dose 24 hours before any planned induction of labour or caesarean section, and should not take dose if they think they are going into labour Warfarin never used - teratogenic, can lead to foetal loss through haemorrhage
371
Describe prophylaxis of VTE in pregnancy
Assess risk in early pregnancy, intrapartum and postnatal periods Thromboprophylaxis (LMWH) given if - >4 risk factors in first 2 trimesters, >3 in 3rd and >2 in post-partum period Continue until 6 weeks post-partum
372
What are the effects of CKD on pregnancy?
Increased risk of adverse outcomes e.g. pre-eclampsia, fetal growth restriction, pre-term delivery, accelerated loss of maternal renal function Some medications contraindicated e.g. myophenolate mofetil (teratogenic), antihypertensives (ACEi, ARBs) Risk of inherited renal diseases - genetic counselling Optimisation of management pre-pregnancy recommended including blood pressure control, glycaemic control Assess renal function in pregnancy with serum creatinine (eGFR not reliable) Increased risk VTE (LMWH prophylaxis?), anaemia (iron, erythropoietin stimulating agents), vitamin D deficiency,
373
Describe the presentation of obstetric cholestasis
Typically in 3rd trimester Pruritis - palms or hands and soles of feet Fatigue Dark urine Pale, greasy stools Jaundice No rash Deranged LFTs - ALT, AST, GGT, bilirubin
374
Describe the normal change in ALP which occurs during pregnancy
Placental produces ALP - rises during pregnancy
375
How is obstetric cholestasis managed?
Ursodeoxycholic acid Symptomatic management of itch - emollients, antihistamines Water-soluble vitamin K if clotting (prothrombin time) deranged Monitor LFTs during pregnancy and after delivery to ensure condition resolves May need planned pregnancy after 37 weeks if LFTs severely deranged, risk of stillbirth
376
Describe the pathophysiology of acute fatty liver or pregnancy
Impaired processing of fatty acids in the placenta due to fetal condition which impaires fatty acid metabolism (most common is long-chain 3-hydroxyacyl-CoA dehydrogenase deficiency, autosomal recessive) Fatty acids enter maternal circulation, accumulate in liver --> acute hepatitis
377
Describe the presentation of acute fatty liver of pregnancy
Symptoms of hepatitis: General malaise and fatigue Nausea and vomiting Jaundice Abdominal pain Anorexia Ascites Raised ALT/AST, raised bilirubin, raised WBC, deranged clotting, low platelets
378
How is acute fatty liver of pregnancy managed?
Obstetric emergency - admission and delivery Treatment of acute liver failure, consideration of liver transplant
379
How are women monitored for anaemia during pregnancy?
Screened for anaemia at booking clinic and 28 weeks Hb >110 at booking, >105 at 28 weeks, >100 post-partum Offered haemoglobinopathy screening at booking clinic for thalassaemia and sickle cell disease (sickle cell only in those with higher risk) Additional investigations to determine cause of anaemia e.g. ferritin, B12, folate
380
How is anaemia in pregnancy managed?
Iron replacement B12 replacement Folic acid supplement
381
How is anti-phospholipid syndrome managed in pregnancy?
LMWH + aspirin to reduce risk of complications
382
How are maternal deaths reported in the UK?
Mothers and Babies: Reducing Risk through Adult and Confidential Enquires across the UK (M-BRRACE) Surveillance of all maternal deaths, confidential enquiries into maternal deaths up to a year after the end of pregnancy, enquiries into cases of serious maternal morbidity, surveillance of perinatal deaths
383
Define maternal death
Death of a pregnant mother due to complications related to pregnancy, underlying conditions worsened by the pregnancy or management of these conditions
384
Define direct, indirect, coincidental and late maternal death
Direct - as a consequence of a disorder specific to pregnancy Indirect - deaths resulting from previous existing disease, or disease that developed during pregnancy and which was not due to obstetric causes but aggravated by pregnancy Coincidental - incidental/accidental deaths not due to pregnancy or aggravated by pregnancy Late - occurring more than 42 days but less than a year after the end of pregnancy
385
What is the leading cause of indirect maternal death in the UK?
Cardiac disease
386
What is the leading cause of direct maternal death in the UK?
Thrombosis and thromboembolism
387
What is the leading cause of late maternal death in the UK?
Incidental malignancy (then suicide)
388
Define antepartum haemorrhage
Bleeding from or in to the genital tract, occurring from 24+0 weeks of pregnancy and prior to the birth of the baby
389
List causes of antepartum haemorrhage
Plactental abruption Placenta praevia Vasa praevia Uterine rupture Circumvallate placenta Placental sinuses Lower genital tract sources - cervical polyps, cervical erosions and carcinoma, cervicitis, vaginitis, vulval varicosities
390
Define placenta praevia
Placenta fully or partially attached to lower uterine segment Minor (grade 1/2) - placenta low in uterus but does not cover the internal cervical os Major (grade 3/4) - placenta lies over internal cervical os
391
List risk factors for placenta praevia
Previous caesarean section High parity Maternal age >40 Multiple pregnancy Previous placenta praevia History of uterine infection (endometritis) Curettage of endometrium after miscarriage or termination
392
Describe the presentation of placenta praevia
Antepartum haemorrhage - painless vaginal bleeding, can be from spotting to major haemorrhage Can be pain if in labour Typically non-tender uterus Lie and presentation may be abnormal Low lying placenta on 20-week scan
393
How should a woman with antepartum vaginal bleeding be assessed?
History: How much? When did it start? Was it fresh red or brown, mixed with mucus? Could the waters have broken? Was it provoked (post-coital)? Abdominal pain? Fetal movements? Risk factors for abruptions - smoking, drug-use, trauma - especially domestic violence Examination: A-E if potentially clinically unstable Abdominal tenderness? Uterus consistency - woody, tense = abruption Palpable contractions? Lie and presentation of fetus CTG if >26 weeks Assess bleeding Cusco speculum examination - only after placenta praevia excluded by USS Genital swabs to exclude infection if bleeding minimal Digital vaginal examination - only when placenta praevia excluded, can determine cervical dilation, avoid if membranes have ruptured
394
How is placenta praevia diagnosed?
Ultrasound - short distance between lower edge of placenta and internal os
395
How is placenta praevia managed?
A-E approach if significant bleeding Definitive control of bleeding - emergency CS, uterine artery ligation or embolisation, intrauterine balloon tamponade, emergency hysterectomy (Give anti-D within 72 hours of onset of bleeding if rhesus D negative) If identified in asymptomatic patient on 20-week US Minor - repeat scan at 36 weeks, likely to have moved superiorly Major - repeat scan at 32 weeks, plan for delivery Confirmed placenta praevia - caesarean section is safety mode of delivery, usually elective at 38 weeks
396
Define placenta abruption and describe the main patterns of disease
Complete or partial detachment of the placenta from the uterine wall before delivery Revealed - blood tracks down from site of placental separation between membranes and out of cervix causing vaginal bleeding Concealed - bleeding remains within the uterus, typically forming a clot retroplacentally, bleeding is not visible but can be severe
397
List risk factors for placental abruption
Previous placental abruption Pre-eclampsia and other hypertensive disorders Abnormal lie of baby e.g. transverse Polyhydramnios Abdominal trauma Smoking or drug use e.g. cocaine Bleeding in first trimester Underlying thrombophilias Multiple pregnancy Increased maternal age
398
Describe the clinical presentation of maternal abruption
Antepartum haemorrhage - painful vaginal bleeding (may be concealed) Pain between contractions if in labour Back pain if posterior abruption Symptoms of shock - loss of consciousness, dizziness Woody uterus (constantly tense), painful on palpation Absent/distressed fetal heart
399
How is placental abruption diagnosed?
Clinical diagnosis USS if patient stable - identify location of bleeding, poor negative predictive value so should not be used to exclude abruption
400
How is placental abruption managed?
A-E approach if significant bleeding Emergency delivery if maternal/fetal compromise - usually CS unless spontaneous delivery is imminent or operative vaginal birth is possible Induction of labour - haemorrhage at term without maternal or fetal compromise Conservative management - partial or marginal abruptions not associated with maternal or fetal compromise Give anti-D within 72 hours of onset of bleeding if woman is rhesus D negative
401
What are the potential complications of placental abruption for the mother and fetus?
Mother: Major haemorrhage Shock - Sheehan syndrome DIC - due to release of thromboplastin from placental haematoma Post-partum haemorrhage Fetus: Placental insufficiency - hypoxia and intrauterine growth restriction Premature birth Stillbirth
402
Define vasa praevia
Fetal blood vessels (the two umbilical arteries and single umbilical vein) are within the fetal membranes and run across the internal cervical os
403
Describe the clinical presentation of vasa praevia
Painless vaginal bleeding Rupture of membranes Fetal bradycardia Soft-non-tender uterus
404
How is vasa praevia managed?
If seen on US - elective CS at 34-36 weeks Steroids given from 32 weeks to promote fetal lung maturity If antepartum haemorrhage - emergency caesarean section
405
Define uterine rupture
Full-thickness disruption of the uterine muscle and overlying serosa Incomplete - peritoneum overlying uterus is intact, uterine contents remain in the peritoneal cavity Complete - peritoneum is torn, uterine contents escape into peritoneal cavity
406
List risk factors for uterine rupture
Previous caesarean section - vertical (classical) incisions are highest risk Previous uterine surgery Induction or augmentation of labour - particularly with prostaglandins Obstruction of labour Multiple pregnancy Multiparity
407
Describe the clinical presentation of uterine rupture
Sudden severe abdominal pain which persists between contractions Shoulder-tip pain Vaginal bleeding Regression of presenting part Scar tenderness Palpable fetal parts Signs of hypovolaemic shock Fetal distress or absent heart sounds
408
How is uterine ruptured managed?
A-E assessment Resuscitation - protect airway, oxygen, assess circulatory compromise and manage, monitor GCS Delivery by caesarean section, uterus repaired or removed (hysterectomy) Decision-incision interval should be less than 30 minutes
409
Define post-partum haemorrhage and list types of PPH
Any bleeding from or in to the genital tract following delivery of the infant Primary – occurring within 24 hours of delivery Secondary – occurring between 24 hours and 12 weeks postnatally Minor – loss of 500-1000ml Moderate - loss of 1000-2000ml Severe – loss of >2000ml Moderat/severe = major
410
List causes of primary post-partum haemorrhage
Tone - uterine atony: Maternal factors - age >40, BMI >35, Asian Uterine over-distension - multiple pregnancy, polyhydramnios, fetal macrosomia Labour - induction, prolonged (>12 hours) Placental problems - placenta praevia, placental abruption, previous PPH Tissue - retention of placental tissue Trauma - damage sustained to reproductive tract during delivery e.g. vaginal tears, cervical tears Instrumental vaginal deliveries - forceps or ventouse Episiotomy C-section Thrombin - coagulopathies and vascular abnormalities which increase the risk of PPH Vascular - placental abruption, hypertension, pre-eclampsia Coagulopathies - VWD, haemophilia A/B, ITP, DIC, HELLP
411
Describe the clinical presentation of primary PPH
Bleeding from the vagina Dizziness, palpitations, SOB Haemodynamic instability - tachypnoea, prolonged CRT, tachycardia, hypotension Missing cotyledon or ragged membranes of placenta - could have retained tissue
412
Describe the general principles of management of primary PPH
Simultaneous T - teamwork R - resusciation I - investigations and monitoring M - measures to arrest bleeding (definitive management) Resusciation - A-E Investigations: FBC Crossmatch 4-6 units of blood Coagulation profile U&Es LFTs Definitive management - dependent on cause: Uterine atony - bimanual compression, pharmacological measures (uterotonics), surgical measures (balloon tamponade, haemostatic suture around uterus, bilateral uterine or internal iliac artery ligation, hysterectomy) Trauma - primary repair of laceration, hysterectomy Tissue - IV oxytocin, manual removal or placental, prophylactic antibiotics Thrombin - correct coagulation abnormalities with blood products
413
Describe measures which are used to manage primary PPH caused by uterine atony
Bimanual compression - insert gloved hand into vagina, form a fist inside anterior fornix to compress anterior uterine wall and other hand applies pressure on abdomen at posterior aspect of uterus (empty bladder with catherisation) Uterotonic drugs: Syntocinon (injection & infusion) Ergometrine (injection) Carboprost (Haemabate) (IM injection) Misoprostol (suppository) Surgical measures: Intrauterine balloon tamponade B-lynch suture - haemostatic suture around uterus Bilateral uterine or internal iliac artery ligation Hysterectomy
414
Describe the ABC approach to management of PPH
A Protect airway - reducing consciousness B Oxygen mask 15L C Fluid resuscitation - IV Hartmann's or blood transfusion Keep patient warm Investigations/monitoring 14G cannulae x2 FBC, coagulation, U&Es, LFTs Crossmatch - 4 units RBC, FFP, PLT, cryoprecipitate ECG Oximeter Foley catheter Hb bedside Consider central/arterial lines Weigh all swabs to estimate blood loss
415
List causes of secondary PPH
Uterine infection - endometritis Risk factors - caesarean section, premature rupture of membranes, long labour Retained placental fragments or tissue Abdominal involution of placental site - inadequate closure and sloughing of spiral arteries at placental attachment site Trophoblastic disease - rare
416
Describe the clinical presentation of secondary PPH
Excessive vaginal bleeding - usually not as severe as primary, 10% prevent with massive haemorrhage Endometritis - fever/rigors, lower abdominal pain, foul smelling lochia, lower abdominal tenderness Retained placenta - uterus high
417
How is secondary PPH managed?
Antibiotics - ampicillin + metronidazole + gentamicin if endomyometritis or overt sepsis Uterotonics - syntocinon, syntometrine, carboprost, misoprostol Surgical measures if excessive or continued bleeding Intrauterine balloon catheter Removal or retained products of conception (risk of uterine perforation)
418
What are the two main causes of significant haemorrhage in early pregnancy?
Miscarriage - usually visualised vaginally, can cause cervical shock if POC or clots in os Ectopic pregnancy - often concealed bleeding, can become unstable quickly
419
Describe the changes in blood pressure which occur during pregnancy
BP decreases during 1st and 2nd trimesters Increases during third trimester, returning close to preconception levels post-partum
420
Define hypertension in pregnancy and describe classification of hypertension in pregnancy
Hypertension - DBP 90-109 and/or SBP 140-159 Severe hypertension - DBP >110 and/or SBO >160 Chronic hypertension - hypertension present at or prior to booking visit or before 20 weeks gestation Gestational hypertension - new hypertension after 20 weeks gestation without significant proteinuria
421
Define pre-eclampsia and severe pre-eclampsia
New onset hypertension (>140 SBP and/or >90 DBP) after 20 weeks of pregnancy and the co-existence or 1 or more of the following new-onset conditions (end-organ dysfunction): Proteinuria Renal insufficiency - creatinine >90 Liver involvement - elevated ALT/AST, RUQ/epigastric pain Neurological complications - eclampsia, altered mental status, blindness, stroke, clonus, severe headaches, persistent visual scotoma Haematological complications - thrombocytopaenia, DIC, haemolysis Uteroplacental dysfunction - fetal growth restriction, abnormal umbilical artery doppler, stillbirth Severe pre-eclampsia - SBP >160 and/or DBP >110 with worsening maternal organ dysfunction or worsening fetal growth restriction
422
Define eclampsia
Occurrence of one or more seizures in a woman with pre-eclampsia (in the absence of any other neurological or metabolic causes)
423
List risk factors for pre-eclampsia
Moderate risk factors: Nulliparity Maternal age >40 Maternal BMi >35 Family history Pregnancy interval >10 years Multiple pregnancy High risk factors: Chronic hypertension HTN, pre-eclampsia or eclampsia in previous pregnancy Pre-existing CKD Diabetes Autoimmune diseases e.g. SLE, antiphospholipid syndrome
424
Describe the clinical presentation of pre-eclampsia
Severe headaches - usually frontal, increasing frequency not relieved by regular analgesics Visual disturbance - blurred vision, flashing lights, double vision, floaters Persistent new epigastric pain or RUQ pain Vomiting Breathlessness Sudden swelling of face, hands, feet Hyperreflexia Reduced urine output
425
Describe the pathophysiology of pre-eclampsia
High vascular resistance in the spiral arteries and poor perfusion of the placenta, causes oxidative stress in the placenta, and release of inflammatory chemicals into the systemic circulation, leading to systemic inflammation and impaired endothelial function in the blood vessels
426
List the potential maternal complications of pre-eclampsia
Eclampsia - seizures Acute renal failure Liver dysfunction Coagulation abnormalties - DIC Intracranial haemorrhage Cerebral infarction Cerebral oedema Acute respiratory distress syndrome Pulmonary oedema Hepatic rupture HELLP syndrome - haemolysis, elevated liver enzymes, low platelets Death
427
List the potential fetal complications of pre-eclampsia
Prematurity Intrauterine growth restriction Placental abruption Intra-uterine fetal death Stillbirth Neonatal death
428
Describe interventions used to reduce the risk of developming pre-eclampsia
75mg aspirin per day for women with 1 high risk factor or 2 or more moderate risk factors - from 12 weeks gestation until birth Monitored at every antenatal appointment for evidence of pre-eclampsia: Blood pressure Symptoms Urine dipstick for proteinuria
429
Describe the management of chronic hypertension in pregnancy
Lifestyle advice - exercise, healthy diet, restrict dietary salt Make aware of risk of pre-eclampsia Stop ACEi, ARBs, thiazide/thiazide-like diuretics Use anti-hypertensives safe for pregnancy - labetalol, nifedipine, methyldopa
430
List pharmacological anti-hypertensive agents used in pregnancy, describe their mechanism of action and common side effects
431
List investigations used in pre-eclampsia
Blood pressure Urinalysis for proteinuria - abnormal if >30 Bloods - FBC, U&Es, LFTs, coagulation (end-organ dysfunction Placental growth factor testing - measure between 20-35 weeks to rule-out pre-eclampsia, low in pre-eclampsia
432
Describe the principles of management of pre-eclampsia
Usually require inpatient management - scoring systems e.g. fullPIERS or PREP-S VTE prevention - LMWH Manage fluid balance - risk of renal failure vs pulmonary oedema Antihypertensives - reduce risk of maternal complications, don't alter disease course Delivery - definitive treatment, planned early birth if BP can't be controlled or complications occur, steroids given to help mature fetal lungs
433
Describe pharmacological therapy in pre-eclampsia
Antihypertensives: 1st line - labetalol Nifedipine Methyldopa IV hydralazine - in ICU IV magnesium during labour and during 24 hours after - prevent seizures
434
How is pre-eclampsia monitored post-natally?
Monitor for seizures for at least 24 hours post-partum Switch to one or combination of - enalapril (1st line), nifedipine or amlodipine, labetolol or atenolol
435
How is eclampsia managed?
IV magnesium sulphate
436
Define HELLP syndrome
Complication of pre-eclampsia and eclampsia Haemolysis Elevated liver enzymes Low platelets
437
Describe the ABC management of eclampsia
Call for help Control seizures - IV magnesium sulphate Airway - left-lateral position, intubation? Breathing - high flow oxygen Circulation - IV access and bloods
438
Describe the clinical presentation and management of magnesium sulfate toxicity
Signs: Loss of deep tendon reflexes Respiratory depression Respiratory arrest Cardiac arrest Management: Stop magnesium sulfate Start BLS IV calcium gluconate Intubate early and ventilate until respiration resumes
439
Describe the long-term implications of pre-eclampsia and eclampsia
Increased risk of pre-eclampsia in future pregnancies - 1 in 6 If severe pre-eclampsia/HELLP/eclampsia - early planned delivery in subsequent pregnancies Increased risk hypertension and complications in later life (3-4x increased risk)
440
Define maternal collapse
An acute event involving the cardiorespiratory systems and/or brain, resulting in a reduced or absent conscious level (and potentially death), at any stage in pregnancy and up to six weeks after delivery
441
Describe the incidence of maternal collapse and the significant of this
Rare - healthcare workers not used to managing, need to give training for initial resuscitation, initial investigations and diagnosis, directed continuing management
442
Describe the ABC approach to maternal collapse
Call for help Check responsiveness - A-E approach, aim for SpO2 94-98%, normal PaCO2, 12-lead ECG, treat precipitating cause, targeted temperature management Open airway Check for breathing If unresponsive and not breathing normally - ALS algorithm
443
List consideration for resuscitation in a pregnant patient
Cardiovascular: Increased plasma volume - dilutional anaemia, reduced oxygen carrying capacity Increased heart rate, cardiac output, decreased venous return - increased CPR circulation demands Cardiac output reduced by pressure of uterus on IVC Uterine blood flow - potential for rapid massive haemorrhage Arterial blood pressure lower - decreased reserve Respiratory: Respiratory rate increased, residual capacity decreased, arterial PCO2 decreased - acidosis more likely Oxygen consumption increased by 20% - hypoxia develops more quickly Laryngeal oedema - difficult intubation Other: Decreased gastric motility, lower oesophageal sphincter tone - increased risk aspiration Uterus aortocaval compression causes supine hypertension, reduced venous return, reduces residual capacity Increased weight makes ventilation more difficulty
444
Describe the resuscitation council ALS algorithm
Patient unresponsive and not beathing normally Call resusciation team CPR 30:2 - attach defibrillator/monitor, minimise interruptions Assess rhythm - shockable, non-shockable, return of spontaneous circulation
445
Describe the additional steps required for resuscitation of a pregnant women
Displace uterus (left lateral) >20 weeks Call obstetric team, resuscitation team, neonatal team 100 O2, intubate early, 2x wide bore cannulae If no response to CPR after 4 minutes proceed to delivery/perimortem caesarean section - primarily to save mothers life (makes resuscitation easier)
446
List the broad causes of collapse in obstetrics and gynaecology
4 Hs Hypoxia Hypovolaemia Hypo/hyperkalaemia Hypothermia 4 Ts Thromboembolism Toxic Tamponade Tension pneumothorax In pregnancy Eclampsia, including magnesium toxicity Amniotic fluid embolism
447
Describe the categorisation of caesarean sections
1 - immediate threat to life of woman or fetus 2- maternal or fetal compromise that is not immediately life-threatening 3 - no maternal or fetal compromise but needs early delivery 4 - elective
448
List endications for an elective caesarean section
Breech at term Other malpresentations e.g. unstable lie, transverse lie, oblique lie Twin pregnancy - first twin not cephalic Maternal medical conditions where labour would be dangerous for mother Fetal compromise - early onset growth restriction, abnormal fetal doppler (labour dangerous for fetus) Transmissible disease - HIV with detectable viral load Primary genital herpes in third trimester Placenta praevia Maternal diabetes - fetal weight >4.5kg Previous major shoulder dystocia Previous 3rd/4th degree perineal tear Maternal request
449
Describe the pre-operative management of women undergoing a caesarean section
FBC and group and save H2-receptor antagonist - risk of aspiration and pneumonitis Risk of VTE assessed - anti-thromboembolic stockings +/- LMWH
450
List the layers which have to be dissected during a caesarean section
Skin - pfannenstiel or Joel-Cohen incision Scarpa's fascia Rectus sheath Rectus muscle Abdominal peritoneum - parietal Parietal peritoneum Uterus
451
List complications of caesarean section
Immediate: PPH Wound haematoma Intra-abdominal haemorrhage Bladder/bowel trauma Neonatal - transient tachypnoea of the newborn, fetal lacerations Intermediate: Infections - UTI, endometritis, respiratory VTE Late: Urinary tract trauma (fistula) Subfertility Rupture/dehiscence of scar at next labour Placenta praevia/accreta Caesarean scar ectopic pregnancy
452
What are the options for delivery in a patient who has previously had a caesarean section?
Vaginal birth after Caesarean section (VBAC) Planned elective repeat Caesarean
453
Describe the risks and benefits of VBAC
Risks - Uterine rupture - 0.5% Anal sphincter injury Maternal death Transient respiratory difficulties for neonate Hypoxic ischamic encephalopathy in neonate Stillbirth risk >39 weeks while waiting for spontaneous labour Benefits - Lower risk of maternal death than elective CS Shorter hospital stay and recovery if successful Good chance of future successful VBACs if successful Lower risk transient neonatal respiratory morbidity than elective CS Lower risk placental problems vs elective CS
454
What are the contraindications to VBAC?
Absolute - classical caesarean scar, previous uterine rupture, contraindications to vaginal birth e.g. placenta praevia Relative - complex uterine scares or >2 prior lower segment caesarean sections
455
Describe management of VBAC
Continuous CTG monitoring Monitor for signs of uterine rupture e.g. increased analgesic requirements Avoid induction and augmentation
456
Define lie, presentation and position. What is considered normal for each of these?
Lie - relationship between long axis of fetus and mother e.g. transverse, longitudinal, oblique Longitudinal normal at term Presentation - fetal part that first enters the maternal pelvis Cephalic vertex normal Position - position of fetal head as it exists the birth canal Occipito-anterior normal
457
How is abnormal fetal lie managed?
Attempt external cephalic version - between 36-38 weeks 50% success in primiparous, 60% in multiparous If unsuccessful - trial of vaginal birth or elective caesarean section
458
What are the risks and contraindications of external cephalic version?
Risks - fetal distress, premature rupture of membranes, antepartum haemorrhage, placental abruption, need for emergency caesarean Contraindications - recent antepartum haemorrhage, ruptured membranes, uterine abnormalities, previous C-section
459
How is malpresentation managed?
Dependent on presentation: Breech - attempt ECV before labour, vaginal breech deliver or C-section Brow - C-section Face Chin anterior - normal labour, may be prolonged and require C-section Chin posterior - C-section Shoulder - C-section
460
How is malposition managed?
90% spontaneously rotate to normal If doesn't rotate - rotation and operative vaginal delivery can be attempted, or C-section
461
List the types of breech presentation
Complete (flexed) breech – both legs are flexed at the hips and knees (fetus appears to be sitting ‘crossed-legged’) Frank (extended) breech – both legs are flexed at the hip and extended at the knee, most common Footling breech – one or both legs extended at the hip, so that the foot is the presenting part
462
List risk factors for breech presentation
Uterine: Multiparity Uterine malformations e.g. septate utrus Fibroids Placenta praevia Fetal: Prematurity Macrosomia Polyhydramnios Multiple pregnancy Abnormality e.g. anencephaly
463
How is breech presentation managed?
ECV If unsuccessful C-section recommended - increased perinatal morbidity and mortality in planned vaginal breech birth in term babies, no difference in maternal outcomes Vaginal brrech birth - if maternal choice or prsenting in advanced labour Contraindicated in footling delivery Don't put traction on baby - can cause head to extend and get caught Need to flex knees, use Lovsett's manoeuvre to rotate body and delivery shoulders and use the Mauriceau-Smellie-Viet manoeuvre to deliver the head by flexion (or forceps)
464
List complications of breech presentation
Cord prolapse Fetal head entrapment Premature rupture of membranes Birth asphyxia Intracranial haemorrhage
465
Define polyhydramnios
Polyhydramnios refers to an abnormally large level of amniotic fluid during pregnancy. It is defined by an amniotic fluid index that is above the 95th centile for gestational age.
466
Describe the aetiology of polyhydramnios
Idiopathic in 50-60% Anything which stops fetus from swallowing - oesophageal atresia, CNS abnormalities, muscular dystrophies, congenital diaphragmatic hernia Duodenal atresia - 'double bubble' sign on US Anaemia Fetal hydrops Twin-to-twin transfusion syndrome Increased lung secretions Genetic or chromosomal abnormalities Maternal diabetes Maternal ingestion of lithium - fetal diabetes insipidus Macrosomia
467
Describe diagnosis of oligohydramnios/polyhydramnios
Via USS Amniotic fluid index - maximum cord-free vertical pocket of fluid in four quadrants, add together OR Maximum pool depth - vertical measurement in any area
468
How is polyhydramnios managed?
Usually no intervention required Severe maternal symptoms e.g. breathlessness can consider amnioreduction but risk of infection and placental abruption Indomethacin - enhances water retention, associated with premature closure of ductus arteriosis, not used >32 weeks If idiopathic baby should be examined by paediatrician before feeding - NG tube passed to ensure there is no oesophageal abnormalities
469
Define oligohydramnios
Low level of amniotic fluid during pregnancy Amniotic fluid index below the 5th centile for gestational age
470
List causes of oligohydramnios
Preterm prelabour rupture of membranes Placental insufficiency Renal agenesis - Potter's syndrome Non-functioning fetal kidneys Obstructive uropathy Genetic/chromosomal anomalies Viral infections - may cause polyhydramnios
471
How is oligohydramnios managed?
Ruptured membranes - labour likely to commence within 24-48 hours, if doesn't start induction should be considered around 34-36 weeks (in the absence of infection) Course of steroids for fetal lung development, antibiotics to reduce risk of ascending infection
472
Define placenta accreta
Abnormal trophoblast invasion of part or all of the placenta into the myometrium of the uterine wall Range of pathologic adherence of the placenta, including placenta increta, placenta percreta, and placenta accreta Accreta - implants in surface of myometrium but not beyond Increta - attaches deeply to myometrium Percreta - invades past myometrium and perimetrium, potentially reaching other organs such as bladder
473
List risk factors for placenta accreta
Previous placenta accreta Previous endometrial curettage procedures (e.g. for miscarriage or abortion) Previous caesarean section Multigravida Increased maternal age Low-lying placenta or placenta praevia
474
Describe the presentation of placenta accreta
Asymptomatic typically Can cause antepartum haemorrhage in third trimester May be noticed on US May only present at birth when difficult to deliver placenta Post-partum haemorrhage
475
How is placenta accreta managed?
Blood transfusion Intensive care for mother and neonate Planned delivery 35 - 36+6 weeks Hysterectomy recommended Can also do uterus preserving surgery with resection of myometrium with placenta Expectant management - leave placenta to be reabsorbed over time, risks of bleeding and infection
476
List types of barrier contraception and benefits/drawbacks of each
Male condom: Protective against many STIs Incorrect use/failure common - 16% failure with typical use Female condom: Less likely to tear May protect against some STIs 21% failure with typical use Diaphragm: Require planning to insert Require measuring and fitting Higher risk UTIs Don't protect against UTIs Higher failure rates than long acting reversible options but protection against STIs from some
477
Describe the mechanism of action of combined hormonal contraceptives
Inhibit ovulation due to negative feedback effect of oestrogen and progesterone on HPO axis, prevents LH surge thus preventing ovulation Progesterone also inhibits proliferation of endometrium, increases thickness of cervical mucus
478
List the forms of combined hormonal contraception
COCP: Monophasic - same level of oestrogen and progesterone throughout Phasic - levels change throughout cycle Transdermal patch Vaginal ring
479
List advantages and disadvantages of combined hormonal contraceptives
Advantages: Non-invasive More effective than barrier if taken correctly Doesn't interrupt sex Menses lighter, less painful, more regular Reduced risk of ovarian, uterine and colon cancer Reduced risk functional ovarian cysts Normal fertility immediately after stopping Disadvantages: User dependent Adverse effects - headaches, breast tenderness, mood changes BP increase VTE risk MI/stroke risk Breast/cervical cancer risk
480
What are the contraindications to combined hormonal contraception use?
BMI >35 Breast feeding Smoking over the age of 35 Hypertension History of or family history VTE Prolonged immobility due to surgery or disability Diabetes mellitus with complications e.g. retinopathy History of migraines with aura Breast cancer or primary liver tumours
481
List options for emergency contraception
Morning after pill - emergency hormonal contraception Levonorgestrel Ulipristal acetate Intrauterine device - copper coil
482
Describe the use and contraindications of emergency contraceptive options
Levonorgestrel - delays ovulation, licensed for use within 72 hours of UPSI, contraindicated in malabsorption, high BMI, with enzyme inducing drugs, if refuses IUD then double dose Ulipristal acetate - delays ovulation, licensed for use within 120 hours of UPSI, contraindicated in malapsorption, severe hepatic dysfunction, enzyme inducing drugs, breast feeding, uncontrolled asthma, drugs which increase gastric pH (omeprazole, ranitidine) Copper IUD - used within 5 days of UPSI, prevents implantation, provides cover for 5-10 years, contraindicated in conditions which distort uterine cavity e.g. fibroids, PID, STI
483
How should women taking emergency contraception be followed-up? List the potential adverse effect they may experience
Hormonal: Seek help if vomiting with 2 hours of levonorgestrel or 3 hours ulipristal No protection for rest of cycle Pregnancy test after >3 weeks to exclude pregnancy Adverse effects - nausea, dizziness, menstrual disturbance, abdominal pain IUD: Increased relative risk of ectopic pregnancy following IUD insertion - be alert if period is >5 days late especially with reduced bleeding and severe lower abdominal pain Adverse effects - pelvic infections, expulsion, bleeding, pelvic pain
484
How should the COCP be started?
Start on first day of cycle - protected straight away If started >5 days through cycle - require extra contraception (e.g. condoms) for first 7 days of consistent pill use Ensure not already pregnant when starting
485
How should missed COCPs be managed?
Missed pill = pill >24 hours late Missing one pill (<72 hours since last pill): Take missed pill ASAP, no extra protection required as long as pill before and after taken correctly Missing more than one pill (>72 hours since last pill): Take most recent pill ASAP Additional contraception needed until they have taken the pill regularly for 7 days straight If day 1-7 of packet need emergency contraception if they have had sex Day 8-14 - no emergency contraceptive needed Day 15-21 - no emergency contraception needed, take next pack back-to-back
486
When should the COCP be stopped prior to surgery?
Stop COCP four weeks before a major operation (lasting more than 30 minutes) or any operation or procedure that requires the lower limb to be immobilised
487
List options for propgesterone only contraceptives
Progesterone only contraceptive pill - traditional or desogestrel Progesterone only implant - nexaplanon Progesterone only injectable contraception - depo-provera
488
Describe the mechanism of action of progesterone-only contraceptives
Progesterone thickens cervical mucus to prevent entry of pserm and fertilisation of the oocyte Suppresses ovulation to varying degrees Thins endometrium to inhibit implantation
489
List advantages and disadvantages of progesterone only contraceptives
Advantages: Can be used when combined contraindicated Very effective Reduce risk endometrial cancer? Disadvantages: Pill user dependent Adverse effects - headaches, breast tenderness, skin changes Weight gain Increased risk breast cancer Injection - loss of bone mineral density with long-term use Altered bleeding patterns including persistent bleeding
490
Describe use of the POP
Traditional - can't be delayed >3 hours Desogestrel - can be taken up to 12 hours late Starting on day 1-5 of cycle - immediate protection Started at any other time in cycle - additional contraception for 48 hours
491
How are missed POPs managed?
Take a pill as soon as possible, continue with next pill at usual time, use extra contraception for next 48 hours of regular use Emergency contraception required if had sex since missing pill or within 48 hours of restarting pills
492
List the types of intra-uterine devices and describe their mechanisms of action
Copper coil - toxic to ovum and sperm, alters endometrium to inhibit implantation Levonorgestrel intrauterine system - thickens cervical mucus, alters endometrium, inhibits ovulation in some
493
List advantages, disadvantages and contraindications to intrauterine devices
Advantages: Reliable, long-term, reversible Copper - no hormones so safe for those with risk of VTE, history of hormone-related cancers, can be used as emergency contraceptive Hormonal - lighter periods or no periods, improve dysmenorrhoea, no increased VTE risk Disadvantages: Requires procedure for insertion No STI protection Increased risk ectopic pregnancies Can fall out Can cause pelvic pain Copper - heavy or intermenstrual bleeding Hormonal - irregular bleeding, systemic side effects Contraindications - PID of infection Immunosuppression Unexplained bleeding Pelvic cancer Uterine cavity distortion e.g. fibroids Wilson's disease - copper
494
Define uterine inversion
Rare complication of birth, where the fundus of the uterus drops down through the uterine cavity and cervix Incomplete/partial - fundus descends inside uterus or vagina, not as far as introitus Complete - descends through vagina to introitus
495
How is uterine inversion managed?
Johnson manoeuvre - 1st line, push fundus into correct position, give uterotonic medications create tendion to hold in place Hydrostatic methods - fill vagina with fluid to inflate uterus back to normal position Surgery - if both methods fail + Treatment of PPH
496
Define umbilical cord prolapse and describe types
Umbilical cord descends through the cervix, with (or before) the presenting part of the fetus Occult (incomplete) - cord alongside but not beyond presenting part Overt (complete) - cord past the presenting part Cord presentation - umbilical cord between presenting part and cervix, can occur with or without intact membranes
497
What are the clinical consequences of umbilical cord prolapse?
Fetal hypoxia because of: Occlusion - presenting part of fetus presses on umbilical cord, occluding blood flow to fetus Aterial vasospasm - exposure of umbilical cord to cold atmosphere causes arterial vasospasm
498
List risk factors for umbilical cord prolapse
Breech presentation – especially footling breech Unstable lie - >37 weeks consider admission until delivery Artificial rupture of membranes – particularly when the presenting part is high Polyhydramnios Prematurity
499
How does umbilical cord prolapse present?
Non-reassuring fetal heart rate pattern - especially fetal bradycardia Absent membranes Digital vaginal examination - feel cord
500
How is umbilical cord prolapse managed?
Avoid handling cord to reduce vasospasm Manually elevate presenting part Left lateral position or knee-chest position - reduce pressure on cord from presenting part Consider tocolysis - delay delivery for transfer e.g. to theatre Delivery by emergency C-section usually
501
Describe the presentation of amniotic fluid embolism
Acute onset: Hypoxia Hypotension Fetal distress Seizures Shock Confusion Cardiac arrest DIC
502
How is amniotic fluid embolism managed?
Resuscitation - A-E approach Perimortem section if cardiac arrest or severe maternal compromise occur to facilitate CPR ECG - ischaemic damage CXR - pulmonary oedema ICU admission
503
List common causes of sepsis in pregnancy
Chorioamnionitis UTIs
504
Describe the aetiology and presentation of chorioamnionitis
Infection of the chorioamniotic membranes and amniotic fluid Caused by variety of bacteria - gram-positive, gram-negative and anaerobes Presentation: Fever Signs of sepsis - tachycardia, tachypnoea, hypotension, altered consciousness, reduced urine output, fetal compromise on CTG Abdominal pain Uterine tenderness Vaginal discharge
505
Describe the aetiology of shoulder dystocia
After delivery of the head, the anterior shoulder of the baby becomes stuck behind the pubic symphysis of the pelvis
506
List risk factors for shoulder dystocia
Pre-labour: Previous shoulder dystocia Macrosomia - >4.5kg Diabetes Maternal BMI >30 Induction of labour Intrapartum: Prolonged 1st stage of labour Secondary arrest Prolonged second stage of labour Augmentation of labour with oxytocin Assisted vaginal delivery - forceps or ventouse
507
Describe the clinical presentation of shoulder dystocia
Difficulty in delivery of fetal head or chin Failure of restitution Turtle neck sign - fetal head retracts into pelvic so that neck is no longer visible
508
How is shoulder dystocia managed?
Call for help Tell mother to stop pushing Avoid downwards traction on fetal head - increases risk of brachial plexus injury Do not apply fundal pressure - increases risk of uterine rupture Consider episiotomy - makes access for manoeuvres easier 1st line manoeuvres: McRoberts - hyperflex maternal hips, 90% success rate Suprapubic pressure - sustained or rocking, pressure behind anterior shoulder to disimpact it from under the maternal symphysis 2nd line (internal) manoeuvres: Posterior arm - insert hand into sacral hollow and grasp posterior arm to deliver Internal rotation (corkscrew manoeuvre) - pressure to front of one shoulder and behind over to move baby 180 degrees or into an oblique position If these fail roll onto all fours and repeat Further manoeuvres: Cleidotomy - fracture fetal clavicle Symphysiotomy - cut pubic symphysis Zavenelli - fetal head back into pelvis to deliver via C-section Active management 3rd stage - risk of PPH
509
List maternal and fetal complications of shoulder dystocia
Maternal – 3rd or 4th degree tears, post-partum haemorrhage Fetal – humerus or clavicle fracture, brachial plexus injury, hypoxic brain injury
510
Describe the legal status of female genital mutilation
Female genital mutilation is illegal as stated in the Female Genital Mutilation Act 2003, and there is a legal requirement for healthcare professionals to report cases of FGM to the police
511
Describe the epidemiology of FGM
Highest rates: Somalia Ethiopia Sudan Eritrea Yemen Kurdistan Indonesia
512
List the types of FGM
Type 1 (clitoridectomy) – removing part or all of the clitoris Type 2 (excision) – removing part or all of the clitoris and the inner labia , with or without removal of the labia majora Type 3 (infibulation) – narrowing the vaginal opening by creating a seal, formed by cutting and repositioning the labia Type 4 - other harmful procedures to the female genitals, including pricking, piercing, cutting, scraping or burning the area
513
List complications of FGM
Immediate - pain, bleeding, infection, swelling, urinary retention, urethral damage and incontinence Long-term - vaginal infections, pelvic infections, UTIs, dysmenorrhoea, sexual dysfunction and dyspareunia, infertility and pregnancy complications, significant psychological issues
514
How is asymptomatic bacteriuria managed during pregnancy? Why?
Give antibiotic prescription Risk of adverse outcomes associated with UTIs - preterm delivery, low birth weight, pre-eclampsia, pyelonephritis
515
How are UTIs managed during pregnancy?
7 day course of antibiotics - options: Nitrofurantoin - avoid in 3rd trimester, risk of neonatal haemolysis Amoxicillin - after sensitivities known Cefalezin Trimethoprim contraindicated in first trimester - folate anatagonist (can cause neural tube defects), generally also avoided later in pregnancy
516
Describe the cause and consequences of congenital rubella syndrome
Maternal rubella infection during first 20 weeks - risk highest before 10 weeks Features: Congenital deafness Congenital cataracts Congenital heart disease - PDA and pulmonary stenosis Learning disability
517
Describe use of the MMR vaccine to protect against congenital rubella syndrome
Planning to become pregnant - ensure they have recieved MMR vaccine If unsure, can be tested for rubella immunity, if don't have antibodies can be vaccinated with two MMR doses, three months apart Should not receive MMR if pregnant - live vaccine
518
How is listeria transmitted? What are the effects of listeria infection in pregnancy?
Unpasteurised dairy products, processed meats and contaminated foods - avoid high-risk foods and practice good food hygiene Listeriosis has high rate of miscarriage or fetal death, can cause severe neonatal infection
519
What causes congenital toxoplasmosis? What are the effects of toxoplasmosis infection during pregnancy?
Infection with the Toxoplasma gondii parasite, primarily spread by contamination with faeces from infected cat Triad of features: Intracranial calcification Hydrocephalus Chorioretinitis
520
List complications of parvovirus B19 infection during pregnancy
Miscarriage or fetal death Severe fetal anaemia Hydrops fetalis Maternal pre-eclampsia-like syndrome
521
List the features of congenital Zika syndrome
Microcephaly Fetal growth restriction Other intracranial abnormalities, such as ventriculomegaly and cerebellar atrophy
522
What causes bacterial vaginosis?
Disruption of normal vaginal flora - reduction in numbers of lactobacilli, usually maintina acidic pH Increased pH allows growth of other microorganisms - polymicrobial, garnerella, anaerobes, mycoplasmas
523
List risk factors for BV
Sexual activity - new partner or multiple partners IUD STI Vaginal douching Recent antibiotics Ethnicity - black women Smoking
524
Describe the clinical presentation of BV
50% asymptomatic Offensive smelling vaginal discharge Thin, white/grey, homogenous vaginal discharge
525
How is BV diagnosed?
Microscopy - high vaginal smear (HVS) is gram stained and evaluated for: The presence of ‘clue cells’ – vaginal epithelial cells studded with Gram variable coccobacilli Reduced numbers of lactobacilli Absence of pus cells
526
How is BV managed?
Metronidazole - oral (5-7 days or single dose) or topical gel
527
What causes vulvovaginal candidiasis? List risk factors.
90% candida albicans Risk factors: Pregnancy Diabetes Antibiotics Steroids Immunosuppression
528
Describe the clinical presentation of vulvovaginal candidiasis
Pruritus White, curd-like and non-offensive discharge Dysuria Erythema and swelling of vulva Satellite lesions - red, pustular lesions with superficial white/creamy pseudomembraneous plaques that can be scraped off
529
How is vulvovaginal candidiasis managed?
Intravaginal antifungal - clotrimazole or fenticonazole Oral antifungal as alternative - fluconazole, itraconazole
530
What causes chlamydia?
Chlamydia trachomatis - gram-negative bacteria, intracellular
531
How is chlamydia diagnosed?
NAAT swab
532
How does chlamydia present?
Majority asymptomatic Abnormal vaginal discharge Pelvic pain Abnormal vaginal bleeding Dyspareunia Dysuria Epidiymo-orchitis Reactive arthritis Lymphogranuloma venereum - painless ulcer, lymphadenitis, proctitis
533
How is chlamydia managed?
Doxycycline 100mg BD for 7 days
534
List potential complications of chlamydia
PID Infertility Ectopic pregnancy Epididymo-orchitis Conjunctivities Lymphogranuloma venereum Reactive arthritis Pregnancy-related complications - pre-term delivery, premature ROM, low birth weight, endometritis, neonatal infection
535
What causes gonorrhoea?
Neisseria gonorrhoeae - gram-negative diplococcus bacteria Infects mucous membranes with a columnar epithelium, such as the endocervix in women, urethra, rectum, conjunctiva and pharynx Spreads via contact with mucous secretions from infected areas
536
Describe the clinical presentation of gonorrhoea
Likely to be symptomatic Female - odourless purulent discharge, green/yellow, dysuria, pelvic pain Male - odourless purulent discharge, green/yellow, dysuria, epididymo-orchitis Rectal/pharyngeal - more likely to be asymptomatic
537
How is gonorrhoea diagnosed?
NAAT swab
538
How is gonorrhoea managed?
Single dose IM ceftriaxone Test of cure recommended - NAAT if asymptomatic, cultures if symptomatic
539
List potential complications of gonorrhoea
PID Chronic pelvic pain Infertility Epididymo-orchitis Prostatitis Conjunctivitis Disseminated gonococcal infection Fitz-Hugh-Curtis syndrome Septic arthritis Endocarditis Gonococcal conjunctivitis in neonate
540
Describe the presentation and complications of mycoplasma genitalium
Usually asymptomatic Urethritis Epidiymitis Cervicitis Can lead to PID, reactive arthritis, preterm delivery in pregnancy, tubal infertility
541
How is mycoplasma genitalium investigated/managed?
NAAT - first urine sample in morning in men, vaginal swabs in women Doxycyclin then azithromycin
542
What causes trichomoniasis?
Trichomonas vaginalis - protozoa
543
Describe the clinical presentation of trichomonas vaginalis
50% asymptomatic Vaginal discharge - frothy, yellow-green, fishy smell Itching Dysuria Dyspareunia Balanitis Strawberry cervix
544
How is trichomonas vaginalis diagnosed?
Posterior fornix vagina swab Urethral swab or first-catch urine Charcoal swab with microscopy
545
How is trichomonas vaginalis managed?
Metronidazole
546
What causes genital herpes?
Typically herpes simplex virus 2 (HSV-2), can be HSV-1
547
Describe the presentation of genital herpes
Asymptomatic Can be asymptomatic for long time then develop symptoms months-years after initial infection Initial episode most severe, recurrent episodes milder Ulcers or blistering lesions around genital area Neuropathic pain - tingling, burning, shooting Flu-like symptoms Dysuria Inguinal lymphadenopathy
548
How is genital herpes diagnosed?
Clinical diagnosis Viral PCR swab can confirm
549
How is genital herpes managed?
GUM referral Aciclovir Symptom management - analgesia, lidocaine gel, warm salt bath
550
How is genital herpes managed during pregnancy? What are the potential complications?
Primary genital herpes <28 weeks - aciclovir during initial infection, then regular prophylactic aciclovir starting from 36 weeks to reduce risk of genital lesions during labour and delivery If asymptomatic can have vaginal delivery if >6 weeks after initial infection, CS if symptoms present Primary genital herpes >28 weeks - aciclovir during initial infection then immediately prophylactic aciclovir, CS recommended Recurrent genital herpes, regular prophylactic aciclovir considered from 36 weeks to reduce risk of symptoms at time of delivery Risk of neonatal herpes simplex infection - can cause disseminated herpes, CNS herpes
551
What causes syphilis? How is it transmitted?
Treponema pallidum - spirochete bacteria Transmission: Oral, vaginal, anal sex Vertical transmission from mother to baby IV drug use Blood transfusion and other transplants
552
Describe the natural course of syphilis infection and the clihnical features at each stage
Primary syphilis - chancre (painless ulcer) at initial site of infection, local lymphadenopathy, lasts 3-8 weeks Secondary syphilis - systemic symptoms, maculopapular rash, condylomata lata, fever, lymphadenopathy, alopecia, oral lesions Latent syphilis - asymptomatic, early <2 years, late >2 years Tertiary syphilis - gummatous lesions, aortic aneurysm, neurosyphilis (dementia, paralysis, Argyll-Robertson pupil)
553
How is syphilis diagnosed?
Antibody testing can be used for screening Confirmed with PCR or dark field microscopy
554
How is syphilis managed?
Single dose IM benzylpenicillin
555
Describe the classification of perineal tears
First-degree – injury limited to the frenulum of the labia minora (where they meet posteriorly) and superficial skin Second-degree – including the perineal muscles, but not affecting the anal sphincter Third-degree – including the anal sphincter, but not affecting the rectal mucosa Fourth-degree – including the rectal mucosa
556
How are perineal tears managed?
First degree usually don't need stitches, larger do 3rd/4th degree - repair in theatre Broad-spectrum antibiotics Laxatives Physiotherapy If symptomatic after 3rd/4th degree tears offered elective CS in subsequent pregnancies
557
List potential complications of perineal tears
Short-term: Pain Infection Bleeding Wound dehiscence or wound breakdown Long-term: Urinary incontinence Anal incontinence Rectovaginal fistula Sexual dysfunction and dyspareunia Psychological consequences